tag:blogger.com,1999:blog-10454451876200040072024-03-08T00:59:35.642-05:00Neuropsychopharmacology News Eutimiahttp://www.blogger.com/profile/07836706907685752267noreply@blogger.comBlogger56125tag:blogger.com,1999:blog-1045445187620004007.post-48187436285250907242020-01-09T14:17:00.002-05:002020-01-09T20:35:47.225-05:002020<div dir="ltr" style="text-align: left;" trbidi="on">
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Other online Journals</h3>
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<b style="font-size: 14.85px;"><a href="https://www.nature.com/npp/volumes/45/issues/2" style="color: #6699cc;" target="_blank">Neuropsychopharmacology </a></b></div>
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<b><a href="https://link.springer.com/journal/213/237/1" style="color: #6699cc;" target="_blank">Psychopharmacology </a></b></div>
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<b><a href="http://jop.sagepub.com/content/current" style="color: #6699cc;" target="_blank">Journal of Psychopharmacology</a></b><br />
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<a href="https://www.bap.org.uk/guidelines" style="color: #6699cc; font-size: 14.85px;" target="_blank"><b>BAP Consensus Guidelines</b></a></div>
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<b><a href="http://ajp.psychiatryonline.org/toc/ajp/current" style="color: #6699cc;" target="_blank">The American Journal of Psychiatry </a></b></div>
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<b><a href="https://www.nature.com/neuro/volumes/23/issues/1" style="color: #6699cc;" target="_blank">Nature Neuroscience </a></b></div>
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<b><a href="https://www.nature.com/mp/volumes/25/issues/1" style="color: #6699cc;" target="_blank">Molecular Psychiatry </a></b></div>
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Eutimiahttp://www.blogger.com/profile/07836706907685752267noreply@blogger.comtag:blogger.com,1999:blog-1045445187620004007.post-49472877688431615922019-09-05T12:08:00.002-04:002019-09-12T22:04:52.888-04:00September 2019<div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px; text-transform: uppercase;">Treatments for the Prevention and Management of Suicide: A Systematic Review</span></h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Abstract</b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><span style="font-size: 14.85px;"><br /><i>Background</i></span></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Suicide is a growing public health problem, with the national rate in the United States increasing by 30% from 2000 to 2016.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Purpose</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To assess the benefits and harms of nonpharmacologic and pharmacologic interventions to prevent suicide and reduce suicide behaviors in at-risk adults.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Data Sources</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">MEDLINE, EMBASE, PsycINFO, and other databases from November 2011 through May 2018.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Study Selection</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Systematic reviews (SRs) and randomized controlled trials (RCTs) that assessed nonpharmacologic or pharmacologic therapies for adults at risk for suicide.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Data Extraction</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">One investigator abstracted data and assessed study quality, and a second investigator checked abstractions and assessments for accuracy.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Data Synthesis</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Eight SRs and 15 RCTs were included. The evidence for psychological interventions suggests that cognitive behavioral therapy (CBT) reduces suicide attempts, suicidal ideation, and hopelessness compared with treatment as usual (TAU). Limited evidence suggests that dialectical behavior therapy (DBT) reduces suicidal ideation compared with wait-list control or crisis planning. The evidence for pharmacologic treatments suggests that ketamine reduces suicidal ideation with minimal adverse events compared with placebo or midazolam. Lithium reduces rates of suicide among patients with unipolar or bipolar mood disorders compared with placebo. However, no differences were observed between lithium and other medications in reducing suicide.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Limitation</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Qualitative synthesis of new evidence with existing meta-analyses, methodological shortcomings of studies, heterogeneity of nonpharmacologic interventions, and limited evidence for pharmacologic treatments and harms.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusion</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Both CBT and DBT showed modest benefit in reducing suicidal ideation compared with TAU or wait-list control, and CBT also reduced suicide attempts compared with TAU. Ketamine and lithium reduced the rate of suicide compared with placebo, but there was limited information on harms. Limited data are available to support the efficacy of other nonpharmacologic or pharmacologic interventions.</span></span><br />
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<b style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;">Source:</b><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"> </span><a href="https://annals.org/aim/fullarticle/2748923/treatments-prevention-management-suicide-systematic-review" style="color: #6699cc; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;" target="_blank">https://annals.org/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; text-transform: uppercase;">Benzodiazepine Use During Pregnancy Alone or in Combination With an Antidepressant and Congenital Malformations: Systematic Review and Meta-Analysis</span></span></h2>
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<span style="color: #333333;"><span style="line-height: 20.79px;"><i><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>The Journal of Clinical Psychiatry</b></span></span></i></span></span><br />
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><b><br />Summary</b></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"><i>Objective </i><br />To summarize the effects of antenatal benzodiazepine exposure as monotherapy and in combination with antidepressants on the risk of congenital malformations.</span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Data Sources </i><br />MEDLINE, PsycINFO, CINAHL, Embase, and the Cochrane Library were searched from inception to June 30, 2018, using controlled vocabulary and keywords (eg, prenatal, benzodiazepines, malformation).</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Study Selection</i><br />English-language cohort studies with prospectively collected data on the risk of malformations in benzodiazepine-exposed and -unexposed offspring were evaluated. 23,909 records were screened, 56 studies were assessed for eligibility, and 8 studies were included.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Data Extraction</i><br />Quality was assessed by 2 independent reviewers and data extracted. Random-effects models were used for outcomes (≥ 3 studies). Subanalyses examined effect of potential moderators including study quality and timing of exposure, among others.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i><br />Prenatal benzodiazepine use was not associated with an increased risk of congenital malformations (odds ratio [OR] = 1.13; 95% CI, 0.99 to 1.30, 8 studies, n = 222/5,195 exposed and 64,335/2,082,467 unexposed), including with first trimester exposure specifically (OR = 1.08; 95% CI, 0.93 to 1.25, P = .33; 5 studies, n = 181/4,331 exposed and 64,308/2,081,463 unexposed). There was no significant association with cardiac malformation following exposure (OR = 1.27; 95% CI, 0.98 to 1.65, P = .07; 4 studies, n = 61/4,414 exposed and 19,260/2,033,402 unexposed). However, concurrent use of benzodiazepine and antidepressants during pregnancy was associated with a significantly increased risk of congenital malformations (OR = 1.40; 95% CI, 1.09 to 1.80, P = .008; 3 studies).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i><br />Benzodiazepine exposure during pregnancy does not appear to be associated with congenital malformations or with cardiac malformations specifically. There may be an increased risk of congenital malformations when benzodiazepines are used in conjunction with antidepressants, suggesting that caution with this combination is warranted.</span><span style="font-size: 14.85px;">es.</span></span></div>
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<b><br /></b><b>Source:</b> <a href="https://www.psychiatrist.com/JCP/article/Pages/2019/v80/18r12412.aspx" style="color: #6699cc;" target="_blank">https://www.psychiatrist.com/</a></div>
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<b style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;">Abstract</b><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><span style="font-size: 14.85px;"><br /><i>Objective</i></span></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">This study aimed to compare weight loss (WL) outcomes for patients taking antidepressants and/or antipsychotics with those not taking psychiatric medication.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">A total of 17,519 adults enrolled in a lifestyle WL intervention at the Wharton Medical Clinics in Ontario, Canada, were analyzed. Sex‐stratified multivariable linear regression analysis was used to examine the association of taking antidepressants, antipsychotics, both, or neither with WL when adjusting for age, initial weight, and treatment time.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Twenty‐three percent of patients were taking at least one psychiatric medication. Patients lost a significant amount of weight (P < 0.0001) regardless of psychiatric medication use. Women taking psychiatric medications lost a similar amount of weight as women who were not (P > 0.05). Conversely, men taking antidepressants lost only slightly less weight than men taking both classes or neither class of psychiatric medication (3.2 ± 0.3 kg vs. 5.6 ± 0.9 kg and 4.3 ± 0.1 kg; P < 0.05). However, taking psychiatric medications that cause weight gain was associated with similar significant decreases in weight as taking medications that are weight neutral or associated with WL for both sexes (P > 0.05).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">Results of this study suggest that those who participate in a weight management program can lose significant amounts of weight regardless of psychiatric medication use.</span></div>
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<b>Source:</b> <a href="https://onlinelibrary.wiley.com/doi/10.1002/oby.22567" style="color: #6699cc;" target="_blank">https://onlinelibrary.wiley.com/</a></div>
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A Comparison of Long-Acting Injectable Antipsychotics With Oral Antipsychotics on Time to Rehospitalization Within 1 Year of Discharge in Elderly Patients With Schizophrenia</h2>
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<span style="font-size: 14.85px; line-height: 20.79px;"><b><i>The American Journal of Geriatric Psychiatry </i></b></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Abstract</b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i style="font-size: 14.85px;"><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"><i>Objective</i></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The effectiveness of long-acting injectable antipsychotics (LAIs) in elderly patients with schizophrenia remains unclear. This study aimed to compare the effect of LAIs with oral antipsychotics (OAPs) on time to rehospitalization within 1 year of discharge in this population. Other factors potentially associated with time to rehospitalization and trends in LAI prescription rates during the study period were also investigated.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Patients over 60 years of age with schizophrenia discharged between 2006 and 2017 were followed for 1 year under naturalistic conditions. Survival analysis was used in the comparison between LAIs and OAPs regarding time to rehospitalization. Covariates thought to affect time to rehospitalization were also analyzed. The Cochran-Armitage trend test was used to evaluate whether a time trend existed for LAI prescription rates.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The LAIs group had a significantly lower rehospitalization rate and a significantly longer time to rehospitalization within 1 year of discharge than the OAPs group. Other factors that were associated with a longer time to rehospitalization included a shorter index hospitalization during the time of the study and fewer previous hospitalizations. No significant time trend was found for LAI prescription rates during the study period. However, the prescription rate of second-generation LAIs grew significantly.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusion</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">LAIs were found superior to OAPs in preventing rehospitalization. A continuous increase in second-generation LAI prescription rate may be due to the better side-effect profile of second-generation LAIs compared to first-generation LAIs. More studies investigating the effectiveness of LAIs in elderly patients with schizophrenia are needed in the future.</span></span><br />
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Environmental pollution is associated with increased risk of psychiatric disorders</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Abstract</b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b><br /></b></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">The search for the genetic factors underlying complex neuropsychiatric disorders has proceeded apace in the past decade. Despite some advances in identifying genetic variants associated with psychiatric disorders, most variants have small individual contributions to risk. By contrast, disease risk increase appears to be less subtle for disease-predisposing environmental insults. In this study, we sought to identify associations between environmental pollution and risk of neuropsychiatric disorders. We present exploratory analyses of 2 independent, very large datasets: 151 million unique individuals, represented in a United States insurance claims dataset, and 1.4 million unique individuals documented in Danish national treatment registers. Environmental Protection Agency (EPA) county-level environmental quality indices (EQIs) in the US and individual-level exposure to air pollution in Denmark were used to assess the association between pollution exposure and the risk of neuropsychiatric disorders. These results show that air pollution is significantly associated with increased risk of psychiatric disorders. We hypothesize that pollutants affect the human brain via neuroinflammatory pathways that have also been shown to cause depression-like phenotypes in animal studies.</span><br />
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<b>Source:</b> <a href="https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.3000353" rel="" style="color: #6699cc;" target="_blank">https://journals.plos.org/</a></div>
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Association of Cesarean Delivery With Risk of Neurodevelopmental and Psychiatric Disorders in the Offspring</h2>
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<i><b>JAMA Network</b></i><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b><i>Abstract</i></b></span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Importance </i><br />Birth by cesarean delivery is increasing globally, particularly cesarean deliveries without medical indication. Children born via cesarean delivery may have an increased risk of negative health outcomes, but the evidence for psychiatric disorders is incomplete.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective </i><br />To evaluate the association between cesarean delivery and risk of neurodevelopmental and psychiatric disorders in the offspring.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Data Sources </i><br />Ovid MEDLINE, Embase, Web of Science, and PsycINFO were searched from inception to December 19, 2018. Search terms included all main mental disorders in the Diagnostic and Statistical Manual of Mental Disorders (Fifth Edition).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Study Selection </i><br />Two researchers independently selected observational studies that examined the association between cesarean delivery and neurodevelopmental and psychiatric disorders in the offspring.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Data Extraction and Synthesis </i><br />Two researchers independently extracted data according to Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) and Meta-analysis of Observational Studies in Epidemiology (MOOSE) reporting guidelines and assessed study quality using the Newcastle-Ottawa Scale. Random-effects meta-analyses were used to pool odds ratios (ORs) with 95% CIs for each outcome. Sensitivity and influence analyses tested the robustness of the results.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures </i><br />The ORs for the offspring with any neurodevelopmental or psychiatric disorder who were born via cesarean delivery compared with those were born via vaginal delivery.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results </i><br />A total of 6953 articles were identified, of which 61 studies comprising 67 independent samples were included, totaling 20 607 935 deliveries. Compared with offspring born by vaginal delivery, offspring born via cesarean delivery had increased odds of autism spectrum disorders (OR, 1.33; 95% CI, 1.25-1.41; I2 = 69.5%) and attention-deficit/hyperactivity disorder (OR, 1.17; 95% CI, 1.07-1.26; I2 = 79.2%). Estimates were less precise for intellectual disabilities (OR, 1.83; 95% CI, 0.90-3.70; I2 = 88.2%), obsessive-compulsive disorder (OR, 1.49; 95% CI, 0.87-2.56; I2 = 67.3%), tic disorders (OR, 1.31; 95% CI, 0.98-1.76; I2 = 75.6%), and eating disorders (OR, 1.18; 95% CI, 0.96-1.47; I2 = 92.7%). No significant associations were found with depression/affective psychoses or nonaffective psychoses. Estimates were comparable for emergency and elective cesarean delivery. Study quality was high for 82% of the cohort studies and 50% of the case-control studies.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance </i><br />The findings suggest that cesarean delivery births are associated with an increased risk of autism spectrum disorder and attention-deficit/hyperactivity disorder, irrespective of cesarean delivery modality, compared with vaginal delivery. Future studies on the mechanisms behind these associations appear to be warranted.</span><span style="font-size: 14.85px;"> </span></span><br />
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<b>Source:</b> <a href="https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2749054" rel="" style="color: #6699cc;" target="_blank">https://jamanetwork.com/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b><i>JAMA </i></b></span><b style="font-size: 14.85px;"><i>Psychiatry</i></b></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Importance </i><br />Children and youths who are prescribed antipsychotic medications have multiple, potentially fatal, dose-related cardiovascular, metabolic, and other adverse events, but whether or not these medications are associated with an increased risk of death is unknown.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective </i><br />To compare the risk of unexpected death among children and youths who are beginning treatment with antipsychotic or control medications.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants </i><br />This retrospective cohort study was conducted from 1999 through 2014 and included Medicaid enrollees aged 5 to 24 years in Tennessee who had no diagnosis of severe somatic illness, schizophrenia or related psychoses, or Tourette syndrome or chronic tic disorder. Data analysis was performed from January 1, 2017, to August 15, 2018.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Exposures </i><br />Current, new antipsychotic medication use at doses higher than 50 mg (higher-dose group) or 50 mg or lower chlorpromazine equivalents (lower-dose group) as well as control medications (ie, attention-deficit/hyperactivity disorder medications, antidepressants, or mood stabilizers) (control group).</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures </i><br />Deaths during study follow-up while out of hospital or within 7 days after hospital admission, classified as either deaths due to injury or suicide or unexpected deaths. Secondary outcomes were unexpected deaths not due to overdose and death due to cardiovascular or metabolic causes.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results </i><br />This study included 189 361 children and youths in the control group (mean [SD] age, 12.0 [5.1] years; 43.4% female), 28 377 in the lower-dose group (mean [SD] age, 11.7 [4.4] years; 32.3% female), and 30 120 in the higher-dose group (mean [SD] age, 14.5 [4.8] years; 39.2% female). The unadjusted incidence of death in the higher-dose group was 146.2 per 100 000 person-years (40 deaths per 27 354 person-years), which was significantly greater than that in the control group (54.5 per 100 000 population; 67 deaths per 123 005 person-years) (P < .001). The difference was primarily attributable to the increased incidence of unexpected deaths in the higher-dose group (21 deaths; 76.8 per 100 000 population) compared with the control group (22 deaths; 17.9 per 100 000 population). The propensity score–adjusted hazard ratios were as follows: all deaths (1.80; 95% CI, 1.06-3.07), deaths due to unintentional injury or suicide (1.03; 95% CI, 0.53-2.01), and unexpected deaths (3.51; 95% CI, 1.54-7.96). The hazard ratio was 3.50 (95% CI, 1.35-9.11) for unexpected deaths not due to overdose and 4.29 (95% CI, 1.33-13.89) for deaths due to cardiovascular or metabolic causes. Neither the unadjusted nor adjusted incidence of death in the lower-dose group differed significantly from that in the control group.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance </i><br />The findings suggest that antipsychotic use is associated with increased risk of unexpected death and appear to reinforce recommendations for careful prescribing and monitoring of antipsychotic treatment for children and youths and to underscore the need for larger antipsychotic treatment safety studies in this population.</span></span></div>
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<b>Source:</b> <a href="https://jamanetwork.com/journals/jamapsychiatry/article-abstract/2717966" style="color: #6699cc;" target="_blank">https://jamanetwork.com/journals/</a></div>
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MITIGATION OF OLANZAPINE-INDUCED WEIGHT GAIN WITH SAMIDORPHAN, AN OPIOID ANTAGONIST: A RANDOMIZED DOUBLE-BLIND PHASE 2 STUDY IN PATIENTS WITH SCHIZOPHRENIA</h2>
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<b><i>American Journal of Psychiatry</i></b></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Preclinical evidence and data from a proof-of-concept study in healthy volunteers suggest that samidorphan, an opioid antagonist, mitigates weight gain associated with olanzapine. This study prospectively compared combination therapy of olanzapine plus either samidorphan or placebo for the treatment of schizophrenia.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">This was an international, multicenter, randomized phase 2 study of olanzapine plus samidorphan in patients with schizophrenia. The study had a 1-week open-label olanzapine lead-in period followed by a 12-week double-blind treatment phase in which patients were randomly assigned in a 1:1:1:1 ratio to receive olanzapine plus placebo (N=75) or olanzapine plus 5 mg (N=80), 10 mg (N=86), or 20 mg (N=68) of samidorphan. The primary aims were to confirm that the antipsychotic efficacy of olanzapine plus samidorphan was comparable to olanzapine plus placebo, to assess the effect of combining olanzapine with samidorphan on olanzapine-induced weight gain, and to assess the overall safety and tolerability of olanzapine plus samidorphan.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Antipsychotic efficacy, as assessed by total score on the Positive and Negative Syndrome Scale (PANSS), was equivalent across all treatment groups. Treatment with olanzapine plus samidorphan resulted in a statistically significant lower weight gain (37% lower weight gain compared with olanzapine plus placebo). The least square mean percent change from baseline in body weight was 4.1% (2.9 kg) for the olanzapine plus placebo group and 2.6% (1.9 kg) for the olanzapine plus samidorphan group (2.8% [2.1 kg] for the 5 mg group, 2.1% [1.5 kg] for the 10 mg group, and 2.9% [2.2 kg] for the 20 mg group). Adverse events reported at a frequency ≥5% in any of the olanzapine plus samidorphan groups and occurring at a rate ≥2 times greater than in the olanzapine plus placebo group were somnolence, sedation, dizziness, and constipation. Other safety measures were comparable between the olanzapine plus samidorphan groups and the olanzapine plus placebo group.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The antipsychotic efficacy of olanzapine plus samidorphan was equivalent to that of olanzapine plus placebo, and olanzapine plus samidorphan was associated with clinically meaningful and statistically significant mitigation of weight gain compared with olanzapine plus placebo. Olanzapine plus samidorphan was generally well tolerated, with a safety profile similar to olanzapine plus placebo.</span></span><br />
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<b style="font-size: 14.85px; line-height: 20.79px;">Read More:</b><span style="font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://ajp.psychiatryonline.org/doi/10.1176/appi.ajp.2018.18030280" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://ajp.psychiatryonline.org/</a></div>
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<span style="color: #333333; font-family: "arial" , sans-serif;"><span style="font-size: 18px; line-height: 22px; text-transform: uppercase;">MOOD STABILISERS AND RISK OF STROKE IN BIPOLAR DISORDER</span></span></h2>
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<i><b><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Abstract</span></span></b></i><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Background</i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Research on the risk of stroke following the use of mood stabilisers specific to patients with bipolar disorder is limited.</span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Aims</i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">In this study, we investigated the risk of stroke following the exposure to mood stabilisers in patients with bipolar disorder.</span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Method</i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Data for this nationwide population-based study were derived from the Taiwan National Health Insurance Research Database. Among a retrospective cohort of patients with bipolar disorder (n = 19 433), 609 new-onset cases of stroke were identified from 1999 to 2012. A case–crossover study design utilising 14-day windows was applied to assess the acute exposure effect of individual mood stabilisers on the risk of ischaemic, haemorrhagic and other types of stroke in patients with bipolar disorder.</span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Mood stabilisers as a group were significantly associated with the increased risk of stroke in patients with bipolar disorder (adjusted risk ratio, 1.26; P = 0.041). Among individual mood stabilisers, acute exposure to carbamazepine had the highest risk of stroke (adjusted risk ratio, 1.68; P = 0.018), particularly the ischaemic type (adjusted risk ratio, 1.81; P = 0.037). In addition, acute exposure to valproic acid elevated the risk of haemorrhagic stroke (adjusted risk ratio, 1.76; P = 0.022). In contrast, acute exposure to lithium and lamotrigine did not significantly increase the risk of any type of stroke.</span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Use of carbamazepine and valproic acid, but not lithium and lamotrigine, is associated with increased risk of stroke in patients with bipolar disorder.</span></span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://www.cambridge.org/core/journals/the-british-journal-of-psychiatry/article/mood-stabilisers-and-risk-of-stroke-in-bipolar-disorder/3A251309D4B5BEDB9352BFCFA85DFE46" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://www.cambridge.org/core/journals/the-british-journal-of-psychiatry/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; text-transform: uppercase;">PSYCHOSIS WITH METHYLPHENIDATE OR AMPHETAMINE IN PATIENTS WITH ADHD</span></span></h2>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b><br /></b></span></i></span><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">BACKGROUND</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The prescription use of the stimulants methylphenidate and amphetamine for the treatment of attention deficit–hyperactivity disorder (ADHD) has been increasing. In 2007, the Food and Drug Administration mandated changes to drug labels for stimulants on the basis of findings of new-onset psychosis. Whether the risk of psychosis in adolescents and young adults with ADHD differs among various stimulants has not been extensively studied.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">METHODS</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We used data from two commercial insurance claims databases to assess patients 13 to 25 years of age who had received a diagnosis of ADHD and who started taking methylphenidate or amphetamine between January 1, 2004, and September 30, 2015. The outcome was a new diagnosis of psychosis for which an antipsychotic medication was prescribed during the first 60 days after the date of the onset of psychosis. To estimate hazard ratios for psychosis, we used propensity scores to match patients who received methylphenidate with patients who received amphetamine in each database, compared the incidence of psychosis between the two stimulant groups, and then pooled the results across the two databases.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">RESULTS</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We assessed 337,919 adolescents and young adults who received a prescription for a stimulant for ADHD. The study population consisted of 221,846 patients with 143,286 person-years of follow up; 110,923 patients taking methylphenidate were matched with 110,923 patients taking amphetamines. There were 343 episodes of psychosis (with an episode defined as a new diagnosis code for psychosis and a prescription for an antipsychotic medication) in the matched populations (2.4 per 1000 person-years): 106 episodes (0.10%) in the methylphenidate group and 237 episodes (0.21%) in the amphetamine group (hazard ratio with amphetamine use, 1.65; 95% confidence interval, 1.31 to 2.09).</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">CONCLUSIONS</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Among adolescents and young adults with ADHD who were receiving prescription stimulants, new-onset psychosis occurred in approximately 1 in 660 patients. Amphetamine use was associated with a greater risk of psychosis than methylphenidate. </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><b style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://www.nejm.org/doi/full/10.1056/NEJMoa1813751" style="color: #6699cc; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://www.nejm.org/</a></div>
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<b><a href="http://journals.lww.com/psychopharmacology/Pages/currenttoc.aspx" style="color: #6699cc;" target="_blank">Journal of Clinical Psychopharmacology - September 2019 - Volume 39, Issue 5</a></b></div>
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<b><a href="https://link.springer.com/journal/213/236/9" style="color: #6699cc;" target="_blank">Psychopharmacology - Volume 236, Issue 9, September 2019</a></b></div>
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<b><a href="http://jop.sagepub.com/content/current" style="color: #6699cc;" target="_blank">Journal of Psychopharmacology - September 2019; 33 (9)</a></b></div>
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<b><a href="http://ajp.psychiatryonline.org/toc/ajp/current" style="color: #6699cc;" target="_blank">The American Journal of Psychiatry - September 2019, Vol. 176, Issue 9</a></b></div>
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<b style="color: #6699cc;"><a href="http://archpsyc.jamanetwork.com/issue.aspx" style="color: #6699cc;" target="_blank">JAMA Psychiatry - September 2019, Vol. 76, No. 9</a></b></div>
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<b><a href="https://www.nature.com/neuro/volumes/22/issues/9" style="color: #6699cc;" target="_blank">Nature Neuroscience - September 2019, Vol 22, N° 9</a></b></div>
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<b><a href="https://www.nature.com/mp/volumes/24/issues/9" style="color: #6699cc;" target="_blank">Molecular Psychiatry - Volume 24, Issue 9, September 2019</a></b></div>
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<b style="background-color: white; color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"><a href="http://www.biologicalpsychiatryjournal.com/current" style="color: #6699cc;" target="_blank">Biological Psychiatry - Volume 86, Issue 6, September 2019</a></b><br />
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<b><a href="https://academic.oup.com/brain/issue/142/9" style="color: #6699cc;" target="_blank">Brain - Volume 142, Issue 9, September 2019</a></b></div>
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Eutimiahttp://www.blogger.com/profile/07836706907685752267noreply@blogger.comtag:blogger.com,1999:blog-1045445187620004007.post-30671381710300880002019-07-08T12:35:00.002-04:002019-08-01T13:30:30.555-04:00July 2019<div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Abstract</b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">More than half of new drugs entering the German healthcare system have not been shown to add benefit. Beate Wieseler and colleagues argue that international drug development processes and policies are responsible and must be reformed</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">Medicines regulators around the world are pursuing a strategy aimed at accelerating the development and approval of drugs.12 These approaches are based on the assumption that faster access to new drugs benefits patients. The rhetoric of novelty and innovation creates an assumption that new products are better than existing ones.</span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">But although gaps in the therapeutic armamentarium undoubtedly exist, research covering drug approvals since the 1970s suggests only a limited number of new drugs provide real advances over existing drugs.3456789 Most studies put the proportion of true innovation at under 15%, with no clear improvement over time.</span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">No evidence of added benefit for most new drugs</span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">.</span><br />
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<b>Source:</b> <a href="https://www.bmj.com/content/366/bmj.l4340.full" style="color: #6699cc;" target="_blank">https://www.bmj.com/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; text-transform: uppercase;">Comparative efficacy and tolerability of 32 oral antipsychotics for the acute treatment of adults with multi-episode schizophrenia: a systematic review and network meta-analysis</span></span></h2>
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<span style="color: #333333;"><span style="line-height: 20.79px;"><i><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>The Lancet</b></span></span></i></span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Background</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Schizophrenia is one of the most common, burdensome, and costly psychiatric disorders in adults worldwide. Antipsychotic drugs are its treatment of choice, but there is controversy about which agent should be used. We aimed to compare and rank antipsychotics by quantifying information from randomised controlled trials.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We did a network meta-analysis of placebo-controlled and head-to-head randomised controlled trials and compared 32 antipsychotics. We searched Embase, MEDLINE, PsycINFO, PubMed, BIOSIS, Cochrane Central Register of Controlled Trials (CENTRAL), WHO International Clinical Trials Registry Platform, and ClinicalTrials.gov from database inception to Jan 8, 2019. Two authors independently selected studies and extracted data. We included randomised controlled trials in adults with acute symptoms of schizophrenia or related disorders. We excluded studies in patients with treatment resistance, first episode, predominant negative or depressive symptoms, concomitant medical illnesses, and relapse-prevention studies. Our primary outcome was change in overall symptoms measured with standardised rating scales. We also extracted data for eight efficacy and eight safety outcomes. Differences in the findings of the studies were explored in metaregressions and sensitivity analyses. Effect size measures were standardised mean differences, mean differences, or risk ratios with 95% credible intervals (CrIs). Confidence in the evidence was assessed using CINeMA (Confidence in Network Meta-Analysis). The study protocol is registered with PROSPERO, number CRD42014014919.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Findings</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We identified 54 417 citations and included 402 studies with data for 53 463 participants. Effect size estimates suggested all antipsychotics reduced overall symptoms more than placebo (although not statistically significant for six drugs), with standardised mean differences ranging from −0·89 (95% CrI −1·08 to −0·71) for clozapine to −0·03 (−0·59 to 0·52) for levomepromazine (40 815 participants). Standardised mean differences compared with placebo for reduction of positive symptoms (31 179 participants) varied from −0·69 (95% CrI −0·86 to −0·52) for amisulpride to −0·17 (−0·31 to −0·04) for brexpiprazole, for negative symptoms (32 015 participants) from −0·62 (−0·84 to −0·39; clozapine) to −0·10 (−0·45 to 0·25; flupentixol), for depressive symptoms (19 683 participants) from −0·90 (−1·36 to −0·44; sulpiride) to 0·04 (−0·39 to 0·47; flupentixol). Risk ratios compared with placebo for all-cause discontinuation (42 672 participants) ranged from 0·52 (0·12 to 0·95; clopenthixol) to 1·15 (0·36 to 1·47; pimozide), for sedation (30 770 participants) from 0·92 (0·17 to 2·03; pimozide) to 10·20 (4·72 to 29·41; zuclopenthixol), for use of antiparkinson medication (24 911 participants) from 0·46 (0·19 to 0·88; clozapine) to 6·14 (4·81 to 6·55; pimozide). Mean differences compared to placebo for weight gain (28 317 participants) ranged from −0·16 kg (−0·73 to 0·40; ziprasidone) to 3·21 kg (2·10 to 4·31; zotepine), for prolactin elevation (21 569 participants) from −77·05 ng/mL (−120·23 to −33·54; clozapine) to 48·51 ng/mL (43·52 to 53·51; paliperidone) and for QTc prolongation (15 467 participants) from −2·21 ms (−4·54 to 0·15; lurasidone) to 23·90 ms (20·56 to 27·33; sertindole). Conclusions for the primary outcome did not substantially change after adjusting for possible effect moderators or in sensitivity analyses (eg, when excluding placebo-controlled studies). The confidence in evidence was often low or very low.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">There are some efficacy differences between antipsychotics, but most of them are gradual rather than discrete. Differences in side-effects are more marked. These findings will aid clinicians in balancing risks versus benefits of those drugs available in their countries. They should consider the importance of each outcome, the patients' medical problems, and preferences.</span></span></div>
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<b><br /></b><b>Read More:</b> <a href="https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(19)31135-3/fulltext" style="color: #6699cc;" target="_blank">https://www.thelancet.com/</a></div>
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; text-transform: uppercase;">novel bacterial virulence factor inhibitor for the </span></span><span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px; text-transform: uppercase;">treatment of Alzheimer’s Disease </span></h2>
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<i style="line-height: 20.79px;"><span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><b>Alzheimer’s Association International Conference</b></span></span><b style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;"> (AAIC) 2019</b></i><br />
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<b style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;">Poster</b><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">The gingipain hypothesis of Alzheimer’s disease, with P. gingivalis as an etiologic agent, is supported by </span></span><span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;">scientific literature from multiple disciplines and several independent labs. COR388 is a promising drug </span><span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;">for the treatment of AD with a novel mechanism of action. COR388 inhibits the Kgp gingipain protease </span><span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;">secreted by P. gingivalis, essential for pathogen survival and virulence. COR388 is readily bioavailable after </span><span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;">oral administration with a favorable PK profile and CNS penetration in humans, with target plasma </span><span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;">concentrations for efficacy reached. COR388 was well tolerated and AD patients treated with COR388 for </span><span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;">28 days demonstrated significant reduction in several pharmacodynamic biomarkers including plasma </span><span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;">RANTES and pathological ApoE fragments in CSF. There was also a trend of improvement in some </span><span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;">cognitive tests in AD patients treated with COR388, in contrast to subjects receiving placebo. Cortexyme is </span><span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;">currently enrolling a 570 patient Phase 2/3 study of COR388 assessing the efficacy, safety, and tolerability </span><span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;">of two dose levels of COR388 for a 48-week treatment period in subjects with mild to moderate </span><span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;">Alzheimer’s disease. This potentially pivotal study is now ongoing. </span></div>
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<b>Source:</b> <a href="https://www.cortexyme.com/wp-content/uploads/2019/07/Poster-AAIC-July2019-FINAL2-RS.pdf" style="color: #6699cc;" target="_blank">https://www.cortexyme.com/</a></div>
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EFFICACY OF ANTI‐INFLAMMATORY TREATMENT ON MAJOR DEPRESSIVE DISORDER OR DEPRESSIVE SYMPTOMS: META‐ANALYSIS OF CLINICAL TRIALS</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Abstract</b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i style="font-size: 14.85px;"><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Background</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">No study has gathered evidence from all randomized clinical trials (RCTs) with anti‐inflammatory drugs measuring antidepressant effects including a detailed assessment of side‐effects and bias.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We performed a systematic review identifying RCTs published prior to January 1, 2018, studying antidepressant treatment effects and side‐effects of pharmacological anti‐inflammatory intervention in adults with major depressive disorder (MDD) or depressive symptoms. Outcomes were depression scores after treatment, remission, response, and side‐effects. Pooled standard mean differences (SMD) and risk ratios (RR) including 95% confidence intervals (95%‐CI) were calculated.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We identified 36 RCTs, whereof 13 investigated NSAIDs (N = 4214), 9 cytokine inhibitors (N = 3345), seven statins (N = 1576), 3 minocycline (N = 151), 2 pioglitazone (N = 77), and 2 glucocorticoids (N = 59). Anti‐inflammatory agents improved depressive symptoms compared to placebo as add‐on in patients with MDD (SMD = −0.64; 95%‐CI = −0.88, −0.40; I2 = 51%; N = 597) and as monotherapy (SMD = −0.41; 95%‐CI = −0.60, −0.22; I2 = 93%, N = 8825). Anti‐inflammatory add‐on improved response (RR = 1.76; 95%‐CI = 1.44–2.16; I2 = 16%; N = 341) and remission (RR = 2.14; 95%‐CI = 1.03–4.48; I2 = 57%; N = 270). We found a trend toward an increased risk for infections, and all studies showed high risk of bias.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusion</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Anti‐inflammatory agents improved antidepressant treatment effects. Future RCTs need to include longer follow‐up, identify optimal doses and subgroups of patients that can benefit from anti‐inflammatory intervention.</span></span><br />
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GLOBAL ALCOHOL EXPOSURE BETWEEN 1990 AND 2017 AND FORECASTS UNTIL 2030: A MODELLING STUDY</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Summary</b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b><br /></b></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Background</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Alcohol use is a leading risk factor for global disease burden, and data on alcohol exposure are crucial to evaluate progress in achieving global non-communicable disease goals. We present estimates on the main indicators of alcohol exposure for 189 countries from 1990–2017, with forecasts up to 2030.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Adult alcohol per-capita consumption (the consumption in L of pure alcohol per adult [≥15 years]) in a given year was based on country-validated data up to 2016. Forecasts up to 2030 were obtained from multivariate log-normal mixture Poisson distribution models. Using survey data from 149 countries, prevalence of lifetime abstinence and current drinking was obtained from Dirichlet regressions. The prevalence of heavy episodic drinking (30-day prevalence of at least one occasion of 60 g of pure alcohol intake among current drinkers) was estimated with fractional response regressions using survey data from 118 countries.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Findings</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Between 1990 and 2017, global adult per-capita consumption increased from 5·9 L (95% CI 5·8–6·1) to 6·5 L (6·0–6·9), and is forecasted to reach 7·6 L (6·5–10·2) by 2030. Globally, the prevalence of lifetime abstinence decreased from 46% (42–49) in 1990 to 43% (40–46) in 2017, albeit this was not a significant reduction, while the prevalence of current drinking increased from 45% (41–48) in 1990 to 47% (44–50) in 2017. We forecast both trends to continue, with abstinence decreasing to 40% (37–44) by 2030 (annualised 0·2% decrease) and the proportion of current drinkers increasing to 50% (46–53) by 2030 (annualised 0·2% increase). In 2017, 20% (17–24) of adults were heavy episodic drinkers (compared with 1990 when it was estimated at 18·5% [15·3–21·6%], and this prevalence is expected to increase to 23% (19–27) in 2030.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">Based on these data, global goals for reducing the harmful use of alcohol are unlikely to be achieved, and known effective and cost-effective policy measures should be implemented to reduce alcohol exposure.</span><br />
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<b>Source:</b> <a href="https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(18)32744-2/fulltext?" rel="" style="color: #6699cc;" target="_blank">https://www.thelancet.com/</a></div>
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FDA APPROVES ESKETAMINE NASAL SPRAY MEDICATION FOR TREATMENT-RESISTANT DEPRESSION</h2>
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<i><b>US FDA</b></i></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The U.S. Food and Drug Administration approved Spravato (esketamine) nasal spray, in conjunction with an oral antidepressant, for the treatment of depression in adults who have tried other antidepressant medicines but have not benefited from them (treatment-resistant depression). Because of the risk of serious adverse outcomes resulting from sedation and dissociation caused by Spravato administration, and the potential for abuse and misuse of the drug, it is only available through a restricted distribution system, under a Risk Evaluation and Mitigation Strategy (REMS).</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">"There has been a long-standing need for additional effective treatments for treatment-resistant depression, a serious and life-threatening condition," said Tiffany Farchione, M.D., acting director of the Division of Psychiatry Products in the FDA's Center for Drug Evaluation and Research. "Controlled clinical trials that studied the safety and efficacy of this drug, along with careful review through the FDA’s drug approval process including a robust discussion with our external advisory committees, were important to our decision to approve this treatment. Because of safety concerns, the drug will only be available through a restricted distribution system and it must be administered in a certified medical office where the health care provider can monitor the patient."</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Patients with major depressive disorder who, despite trying at least two antidepressant treatments given at adequate doses for an adequate duration in the current episode, have not responded to treatment are considered to have treatment-resistant depression.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The Spravato labeling contains a Boxed Warning that cautions that patients are at risk for sedation and difficulty with attention, judgment and thinking (dissociation), abuse and misuse, and suicidal thoughts and behaviors after administration of the drug. Because of the risk of sedation and dissociation, patients must be monitored by a health care provider for at least two hours after receiving their Spravato dose. </span></span><br />
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<b>Read More:</b> <a href="https://www.fda.gov/news-events/press-announcements/fda-approves-new-nasal-spray-medication-treatment-resistant-depression-available-only-certified" rel="" style="color: #6699cc;" target="_blank">https://www.fda.gov/news-events/press-announcements/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b><i>JAMA </i></b></span><b style="font-size: 14.85px;"><i>Psychiatry</i></b></span></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span><span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Importance </i><br />Children and youths who are prescribed antipsychotic medications have multiple, potentially fatal, dose-related cardiovascular, metabolic, and other adverse events, but whether or not these medications are associated with an increased risk of death is unknown.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective </i><br />To compare the risk of unexpected death among children and youths who are beginning treatment with antipsychotic or control medications.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants </i><br />This retrospective cohort study was conducted from 1999 through 2014 and included Medicaid enrollees aged 5 to 24 years in Tennessee who had no diagnosis of severe somatic illness, schizophrenia or related psychoses, or Tourette syndrome or chronic tic disorder. Data analysis was performed from January 1, 2017, to August 15, 2018.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Exposures </i><br />Current, new antipsychotic medication use at doses higher than 50 mg (higher-dose group) or 50 mg or lower chlorpromazine equivalents (lower-dose group) as well as control medications (ie, attention-deficit/hyperactivity disorder medications, antidepressants, or mood stabilizers) (control group).</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures </i><br />Deaths during study follow-up while out of hospital or within 7 days after hospital admission, classified as either deaths due to injury or suicide or unexpected deaths. Secondary outcomes were unexpected deaths not due to overdose and death due to cardiovascular or metabolic causes.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results </i><br />This study included 189 361 children and youths in the control group (mean [SD] age, 12.0 [5.1] years; 43.4% female), 28 377 in the lower-dose group (mean [SD] age, 11.7 [4.4] years; 32.3% female), and 30 120 in the higher-dose group (mean [SD] age, 14.5 [4.8] years; 39.2% female). The unadjusted incidence of death in the higher-dose group was 146.2 per 100 000 person-years (40 deaths per 27 354 person-years), which was significantly greater than that in the control group (54.5 per 100 000 population; 67 deaths per 123 005 person-years) (P < .001). The difference was primarily attributable to the increased incidence of unexpected deaths in the higher-dose group (21 deaths; 76.8 per 100 000 population) compared with the control group (22 deaths; 17.9 per 100 000 population). The propensity score–adjusted hazard ratios were as follows: all deaths (1.80; 95% CI, 1.06-3.07), deaths due to unintentional injury or suicide (1.03; 95% CI, 0.53-2.01), and unexpected deaths (3.51; 95% CI, 1.54-7.96). The hazard ratio was 3.50 (95% CI, 1.35-9.11) for unexpected deaths not due to overdose and 4.29 (95% CI, 1.33-13.89) for deaths due to cardiovascular or metabolic causes. Neither the unadjusted nor adjusted incidence of death in the lower-dose group differed significantly from that in the control group.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance </i><br />The findings suggest that antipsychotic use is associated with increased risk of unexpected death and appear to reinforce recommendations for careful prescribing and monitoring of antipsychotic treatment for children and youths and to underscore the need for larger antipsychotic treatment safety studies in this population.</span></span></div>
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<b>Source:</b> <a href="https://jamanetwork.com/journals/jamapsychiatry/article-abstract/2717966" style="color: #6699cc;" target="_blank">https://jamanetwork.com/journals/</a></div>
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MITIGATION OF OLANZAPINE-INDUCED WEIGHT GAIN WITH SAMIDORPHAN, AN OPIOID ANTAGONIST: A RANDOMIZED DOUBLE-BLIND PHASE 2 STUDY IN PATIENTS WITH SCHIZOPHRENIA</h2>
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<b><i>American Journal of Psychiatry</i></b></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Preclinical evidence and data from a proof-of-concept study in healthy volunteers suggest that samidorphan, an opioid antagonist, mitigates weight gain associated with olanzapine. This study prospectively compared combination therapy of olanzapine plus either samidorphan or placebo for the treatment of schizophrenia.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">This was an international, multicenter, randomized phase 2 study of olanzapine plus samidorphan in patients with schizophrenia. The study had a 1-week open-label olanzapine lead-in period followed by a 12-week double-blind treatment phase in which patients were randomly assigned in a 1:1:1:1 ratio to receive olanzapine plus placebo (N=75) or olanzapine plus 5 mg (N=80), 10 mg (N=86), or 20 mg (N=68) of samidorphan. The primary aims were to confirm that the antipsychotic efficacy of olanzapine plus samidorphan was comparable to olanzapine plus placebo, to assess the effect of combining olanzapine with samidorphan on olanzapine-induced weight gain, and to assess the overall safety and tolerability of olanzapine plus samidorphan.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Antipsychotic efficacy, as assessed by total score on the Positive and Negative Syndrome Scale (PANSS), was equivalent across all treatment groups. Treatment with olanzapine plus samidorphan resulted in a statistically significant lower weight gain (37% lower weight gain compared with olanzapine plus placebo). The least square mean percent change from baseline in body weight was 4.1% (2.9 kg) for the olanzapine plus placebo group and 2.6% (1.9 kg) for the olanzapine plus samidorphan group (2.8% [2.1 kg] for the 5 mg group, 2.1% [1.5 kg] for the 10 mg group, and 2.9% [2.2 kg] for the 20 mg group). Adverse events reported at a frequency ≥5% in any of the olanzapine plus samidorphan groups and occurring at a rate ≥2 times greater than in the olanzapine plus placebo group were somnolence, sedation, dizziness, and constipation. Other safety measures were comparable between the olanzapine plus samidorphan groups and the olanzapine plus placebo group.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The antipsychotic efficacy of olanzapine plus samidorphan was equivalent to that of olanzapine plus placebo, and olanzapine plus samidorphan was associated with clinically meaningful and statistically significant mitigation of weight gain compared with olanzapine plus placebo. Olanzapine plus samidorphan was generally well tolerated, with a safety profile similar to olanzapine plus placebo.</span></span><br />
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<i><b><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Abstract</span></span></b></i><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Background</i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Research on the risk of stroke following the use of mood stabilisers specific to patients with bipolar disorder is limited.</span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Aims</i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">In this study, we investigated the risk of stroke following the exposure to mood stabilisers in patients with bipolar disorder.</span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Method</i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Data for this nationwide population-based study were derived from the Taiwan National Health Insurance Research Database. Among a retrospective cohort of patients with bipolar disorder (n = 19 433), 609 new-onset cases of stroke were identified from 1999 to 2012. A case–crossover study design utilising 14-day windows was applied to assess the acute exposure effect of individual mood stabilisers on the risk of ischaemic, haemorrhagic and other types of stroke in patients with bipolar disorder.</span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Mood stabilisers as a group were significantly associated with the increased risk of stroke in patients with bipolar disorder (adjusted risk ratio, 1.26; P = 0.041). Among individual mood stabilisers, acute exposure to carbamazepine had the highest risk of stroke (adjusted risk ratio, 1.68; P = 0.018), particularly the ischaemic type (adjusted risk ratio, 1.81; P = 0.037). In addition, acute exposure to valproic acid elevated the risk of haemorrhagic stroke (adjusted risk ratio, 1.76; P = 0.022). In contrast, acute exposure to lithium and lamotrigine did not significantly increase the risk of any type of stroke.</span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Use of carbamazepine and valproic acid, but not lithium and lamotrigine, is associated with increased risk of stroke in patients with bipolar disorder.</span></span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://www.cambridge.org/core/journals/the-british-journal-of-psychiatry/article/mood-stabilisers-and-risk-of-stroke-in-bipolar-disorder/3A251309D4B5BEDB9352BFCFA85DFE46" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://www.cambridge.org/core/journals/the-british-journal-of-psychiatry/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; text-transform: uppercase;">PSYCHOSIS WITH METHYLPHENIDATE OR AMPHETAMINE IN PATIENTS WITH ADHD</span></span></h2>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b><br /></b></span></i></span><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">BACKGROUND</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The prescription use of the stimulants methylphenidate and amphetamine for the treatment of attention deficit–hyperactivity disorder (ADHD) has been increasing. In 2007, the Food and Drug Administration mandated changes to drug labels for stimulants on the basis of findings of new-onset psychosis. Whether the risk of psychosis in adolescents and young adults with ADHD differs among various stimulants has not been extensively studied.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">METHODS</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We used data from two commercial insurance claims databases to assess patients 13 to 25 years of age who had received a diagnosis of ADHD and who started taking methylphenidate or amphetamine between January 1, 2004, and September 30, 2015. The outcome was a new diagnosis of psychosis for which an antipsychotic medication was prescribed during the first 60 days after the date of the onset of psychosis. To estimate hazard ratios for psychosis, we used propensity scores to match patients who received methylphenidate with patients who received amphetamine in each database, compared the incidence of psychosis between the two stimulant groups, and then pooled the results across the two databases.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">RESULTS</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We assessed 337,919 adolescents and young adults who received a prescription for a stimulant for ADHD. The study population consisted of 221,846 patients with 143,286 person-years of follow up; 110,923 patients taking methylphenidate were matched with 110,923 patients taking amphetamines. There were 343 episodes of psychosis (with an episode defined as a new diagnosis code for psychosis and a prescription for an antipsychotic medication) in the matched populations (2.4 per 1000 person-years): 106 episodes (0.10%) in the methylphenidate group and 237 episodes (0.21%) in the amphetamine group (hazard ratio with amphetamine use, 1.65; 95% confidence interval, 1.31 to 2.09).</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">CONCLUSIONS</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Among adolescents and young adults with ADHD who were receiving prescription stimulants, new-onset psychosis occurred in approximately 1 in 660 patients. Amphetamine use was associated with a greater risk of psychosis than methylphenidate. </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><b style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://www.nejm.org/doi/full/10.1056/NEJMoa1813751" style="color: #6699cc; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://www.nejm.org/</a></div>
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<b><a href="http://journals.lww.com/psychopharmacology/Pages/currenttoc.aspx" style="color: #6699cc;" target="_blank">Journal of Clinical Psychopharmacology - August 2019 - Volume 39, Issue 4</a></b></div>
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<b><a href="https://www.nature.com/npp/volumes/44/issues/8" style="color: #6699cc;" target="_blank">Neuropsychopharmacology - Volume 44, Issue 8 (July 2019)</a></b></div>
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<b><a href="https://link.springer.com/journal/213/236/7" style="color: #6699cc;" target="_blank">Psychopharmacology - Volume 236, Issue 7, July 2019</a></b></div>
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<b><a href="http://jop.sagepub.com/content/current" style="color: #6699cc;" target="_blank">Journal of Psychopharmacology - Augustay 2019; 33 (8)</a></b></div>
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<b><a href="http://ajp.psychiatryonline.org/toc/ajp/current" style="color: #6699cc;" target="_blank">The American Journal of Psychiatry - August 2019, Vol. 176, Issue 8</a></b></div>
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<b style="color: #6699cc;"><a href="http://archpsyc.jamanetwork.com/issue.aspx" style="color: #6699cc;" target="_blank">JAMA Psychiatry - July 2019, Vol. 76, No. 7</a></b></div>
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<b><a href="https://www.nature.com/neuro/volumes/22/issues/7" style="color: #6699cc;" target="_blank">Nature Neuroscience - July 2019, Vol 22, N° 7</a></b></div>
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<b><a href="https://www.nature.com/mp/volumes/24/issues/7" style="color: #6699cc;" target="_blank">Molecular Psychiatry - Volume 24, Issue 7, July 2019</a></b></div>
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<b style="background-color: white; color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"><a href="http://www.biologicalpsychiatryjournal.com/current" style="color: #6699cc;" target="_blank">Biological Psychiatry - Volume 86, Issue 3, August 2019</a></b><br />
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<b><a href="https://academic.oup.com/brain/issue/142/8" style="color: #6699cc;" target="_blank">Brain - Volume 142, Issue 8, August 2019</a></b></div>
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Eutimiahttp://www.blogger.com/profile/07836706907685752267noreply@blogger.comtag:blogger.com,1999:blog-1045445187620004007.post-77448822203558300922019-05-07T20:39:00.000-04:002019-05-20T14:56:01.669-04:00May 2019<div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px; text-transform: uppercase;">Limbic-predominant age-related TDP-43 encephalopathy (LATE): consensus working group report</span></span></h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Abstract</b></span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We describe a recently recognized disease entity, limbic-predominant age-related TDP-43 encephalopathy (LATE). LATE neuropathological change (LATE-NC) is defined by a stereotypical TDP-43 proteinopathy in older adults, with or without coexisting hippocampal sclerosis pathology. LATE-NC is a common TDP-43 proteinopathy, associated with an amnestic dementia syndrome that mimicked Alzheimer’s-type dementia in retrospective autopsy studies. LATE is distinguished from frontotemporal lobar degeneration with TDP-43 pathology based on its epidemiology (LATE generally affects older subjects), and relatively restricted neuroanatomical distribution of TDP-43 proteinopathy. In community-based autopsy cohorts, ∼25% of brains had sufficient burden of LATE-NC to be associated with discernible cognitive impairment. Many subjects with LATE-NC have comorbid brain pathologies, often including amyloid-β plaques and tauopathy. Given that the ‘oldest-old’ are at greatest risk for LATE-NC, and subjects of advanced age constitute a rapidly growing demographic group in many countries, LATE has an expanding but under-recognized impact on public health. For these reasons, a working group was convened to develop diagnostic criteria for LATE, aiming both to stimulate research and to promote awareness of this pathway to dementia. We report consensus-based recommendations including guidelines for diagnosis and staging of LATE-NC. For routine autopsy workup of LATE-NC, an anatomically-based preliminary staging scheme is proposed with TDP-43 immunohistochemistry on tissue from three brain areas, reflecting a hierarchical pattern of brain involvement: amygdala, hippocampus, and middle frontal gyrus. LATE-NC appears to affect the medial temporal lobe structures preferentially, but other areas also are impacted. Neuroimaging studies demonstrated that subjects with LATE-NC also had atrophy in the medial temporal lobes, frontal cortex, and other brain regions. Genetic studies have thus far indicated five genes with risk alleles for LATE-NC: GRN, TMEM106B, ABCC9, KCNMB2, and APOE. The discovery of these genetic risk variants indicate that LATE shares pathogenetic mechanisms with both frontotemporal lobar degeneration and Alzheimer’s disease, but also suggests disease-specific underlying mechanisms. Large gaps remain in our understanding of LATE. For advances in prevention, diagnosis, and treatment, there is an urgent need for research focused on LATE, including in vitro and animal models. An obstacle to clinical progress is lack of diagnostic tools, such as biofluid or neuroimaging biomarkers, for ante-mortem detection of LATE. Development of a disease biomarker would augment observational studies seeking to further define the risk factors, natural history, and clinical features of LATE, as well as eventual subject recruitment for targeted therapies in clinical trials.</span></span><br />
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<b>Source:</b> <a href="https://academic.oup.com/brain/advance-article/doi/10.1093/brain/awz099/5481202" style="color: #6699cc;" target="_blank">https://academic.oup.com/brain/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; text-transform: uppercase;">FDA adds Boxed Warning for risk of serious injuries caused by sleepwalking with certain prescription insomnia medicines</span></span></h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The Food and Drug Administration (FDA) is advising that rare but serious injuries have happened with certain common prescription insomnia medicines because of sleep behaviors, including sleepwalking, sleep driving, and engaging in other activities while not fully awake. These complex sleep behaviors have also resulted in deaths. These behaviors appear to be more common with eszopiclone (Lunesta), zaleplon (Sonata), and zolpidem (Ambien, Ambien CR, Edluar, Intermezzo, Zolpimist) than other prescription medicines used for sleep.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">As a result, we are requiring a Boxed Warning, our most prominent warning, to be added to the prescribing information and the patient Medication Guides for these medicines. We are also requiring a Contraindication, our strongest warning, to avoid use in patients who have previously experienced an episode of complex sleep behavior with eszopiclone, zaleplon, and zolpidem.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Serious injuries and death from complex sleep behaviors have occurred in patients with and without a history of such behaviors, even at the lowest recommended doses, and the behaviors can occur after just one dose. These behaviors can occur after taking these medicines with or without alcohol or other central nervous system depressants that may be sedating such as tranquilizers, opioids, and anti-anxiety medicines.</span></span></div>
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<b><br /></b><b>Read More:</b> <a href="https://www.fda.gov/drugs/drug-safety-and-availability/fda-adds-boxed-warning-risk-serious-injuries-caused-sleepwalking-certain-prescription-insomnia" style="color: #6699cc;" target="_blank">https://www.fda.gov/drugs/drug-safety-and-availability/</a></div>
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<i style="font-size: 14.85px; line-height: 20.79px;"><b>Nature Neuroscience</b></i><br />
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<b style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;">Abstract</b><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The transition from adolescence to adulthood is a period when ongoing brain development coincides with a substantially increased risk of psychiatric disorders. The developmental brain changes accounting for this emergent psychiatric symptomatology remain obscure. Capitalizing on a unique longitudinal dataset that includes in vivo myelin-sensitive magnetization transfer (MT) MRI scans, we show that this developmental period is characterized by brain-wide growth in MT trajectories within both gray matter and adjacent juxtacortical white matter. In this healthy population, the expression of common developmental traits, namely compulsivity and impulsivity, is tied to a reduced growth of these MT trajectories in frontostriatal regions. This reduction is most marked in dorsomedial and dorsolateral prefrontal regions for compulsivity and in lateral and medial prefrontal regions for impulsivity. These findings highlight that psychiatric traits of compulsivity and impulsivity are linked to regionally specific reductions in myelin-related growth in late adolescent brain development.</span></span></div>
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<b>Source:</b> <a href="https://www.nature.com/articles/s41593-019-0394-3" style="color: #6699cc;" target="_blank">https://www.nature.com/</a></div>
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Efficacy of anti‐inflammatory treatment on major depressive disorder or depressive symptoms: meta‐analysis of clinical trials</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Abstract</b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i style="font-size: 14.85px;"><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Background</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">No study has gathered evidence from all randomized clinical trials (RCTs) with anti‐inflammatory drugs measuring antidepressant effects including a detailed assessment of side‐effects and bias.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We performed a systematic review identifying RCTs published prior to January 1, 2018, studying antidepressant treatment effects and side‐effects of pharmacological anti‐inflammatory intervention in adults with major depressive disorder (MDD) or depressive symptoms. Outcomes were depression scores after treatment, remission, response, and side‐effects. Pooled standard mean differences (SMD) and risk ratios (RR) including 95% confidence intervals (95%‐CI) were calculated.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We identified 36 RCTs, whereof 13 investigated NSAIDs (N = 4214), 9 cytokine inhibitors (N = 3345), seven statins (N = 1576), 3 minocycline (N = 151), 2 pioglitazone (N = 77), and 2 glucocorticoids (N = 59). Anti‐inflammatory agents improved depressive symptoms compared to placebo as add‐on in patients with MDD (SMD = −0.64; 95%‐CI = −0.88, −0.40; I2 = 51%; N = 597) and as monotherapy (SMD = −0.41; 95%‐CI = −0.60, −0.22; I2 = 93%, N = 8825). Anti‐inflammatory add‐on improved response (RR = 1.76; 95%‐CI = 1.44–2.16; I2 = 16%; N = 341) and remission (RR = 2.14; 95%‐CI = 1.03–4.48; I2 = 57%; N = 270). We found a trend toward an increased risk for infections, and all studies showed high risk of bias.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusion</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Anti‐inflammatory agents improved antidepressant treatment effects. Future RCTs need to include longer follow‐up, identify optimal doses and subgroups of patients that can benefit from anti‐inflammatory intervention.</span></span><br />
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<b style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;">Source:</b><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"> </span><a href="https://onlinelibrary.wiley.com/doi/full/10.1111/acps.13016" style="color: #6699cc; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;" target="_blank">https://onlinelibrary.wiley.com/</a></div>
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Global alcohol exposure between 1990 and 2017 and forecasts until 2030: a modelling study</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b><i>The Lancet</i></b></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Summary</b></span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Background</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Alcohol use is a leading risk factor for global disease burden, and data on alcohol exposure are crucial to evaluate progress in achieving global non-communicable disease goals. We present estimates on the main indicators of alcohol exposure for 189 countries from 1990–2017, with forecasts up to 2030.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Adult alcohol per-capita consumption (the consumption in L of pure alcohol per adult [≥15 years]) in a given year was based on country-validated data up to 2016. Forecasts up to 2030 were obtained from multivariate log-normal mixture Poisson distribution models. Using survey data from 149 countries, prevalence of lifetime abstinence and current drinking was obtained from Dirichlet regressions. The prevalence of heavy episodic drinking (30-day prevalence of at least one occasion of 60 g of pure alcohol intake among current drinkers) was estimated with fractional response regressions using survey data from 118 countries.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Findings</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Between 1990 and 2017, global adult per-capita consumption increased from 5·9 L (95% CI 5·8–6·1) to 6·5 L (6·0–6·9), and is forecasted to reach 7·6 L (6·5–10·2) by 2030. Globally, the prevalence of lifetime abstinence decreased from 46% (42–49) in 1990 to 43% (40–46) in 2017, albeit this was not a significant reduction, while the prevalence of current drinking increased from 45% (41–48) in 1990 to 47% (44–50) in 2017. We forecast both trends to continue, with abstinence decreasing to 40% (37–44) by 2030 (annualised 0·2% decrease) and the proportion of current drinkers increasing to 50% (46–53) by 2030 (annualised 0·2% increase). In 2017, 20% (17–24) of adults were heavy episodic drinkers (compared with 1990 when it was estimated at 18·5% [15·3–21·6%], and this prevalence is expected to increase to 23% (19–27) in 2030.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Interpretation</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">Based on these data, global goals for reducing the harmful use of alcohol are unlikely to be achieved, and known effective and cost-effective policy measures should be implemented to reduce alcohol exposure.</span><br />
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<b>Source:</b> <a href="https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(18)32744-2/fulltext?" rel="" style="color: #6699cc;" target="_blank">https://www.thelancet.com/</a></div>
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FDA approves ESKETAMINE nasal spray medication for treatment-resistant depression</h2>
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<i><b>US FDA</b></i></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The U.S. Food and Drug Administration approved Spravato (esketamine) nasal spray, in conjunction with an oral antidepressant, for the treatment of depression in adults who have tried other antidepressant medicines but have not benefited from them (treatment-resistant depression). Because of the risk of serious adverse outcomes resulting from sedation and dissociation caused by Spravato administration, and the potential for abuse and misuse of the drug, it is only available through a restricted distribution system, under a Risk Evaluation and Mitigation Strategy (REMS).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">"There has been a long-standing need for additional effective treatments for treatment-resistant depression, a serious and life-threatening condition," said Tiffany Farchione, M.D., acting director of the Division of Psychiatry Products in the FDA's Center for Drug Evaluation and Research. "Controlled clinical trials that studied the safety and efficacy of this drug, along with careful review through the FDA’s drug approval process including a robust discussion with our external advisory committees, were important to our decision to approve this treatment. Because of safety concerns, the drug will only be available through a restricted distribution system and it must be administered in a certified medical office where the health care provider can monitor the patient."</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Patients with major depressive disorder who, despite trying at least two antidepressant treatments given at adequate doses for an adequate duration in the current episode, have not responded to treatment are considered to have treatment-resistant depression.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The Spravato labeling contains a Boxed Warning that cautions that patients are at risk for sedation and difficulty with attention, judgment and thinking (dissociation), abuse and misuse, and suicidal thoughts and behaviors after administration of the drug. Because of the risk of sedation and dissociation, patients must be monitored by a health care provider for at least two hours after receiving their Spravato dose. </span></span><br />
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<b>Read More:</b> <a href="https://www.fda.gov/news-events/press-announcements/fda-approves-new-nasal-spray-medication-treatment-resistant-depression-available-only-certified" rel="" style="color: #6699cc;" target="_blank">https://www.fda.gov/news-events/press-announcements/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b><i>JAMA </i></b></span><b style="font-size: 14.85px;"><i>Psychiatry</i></b></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Importance </i><br />Children and youths who are prescribed antipsychotic medications have multiple, potentially fatal, dose-related cardiovascular, metabolic, and other adverse events, but whether or not these medications are associated with an increased risk of death is unknown.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective </i><br />To compare the risk of unexpected death among children and youths who are beginning treatment with antipsychotic or control medications.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants </i><br />This retrospective cohort study was conducted from 1999 through 2014 and included Medicaid enrollees aged 5 to 24 years in Tennessee who had no diagnosis of severe somatic illness, schizophrenia or related psychoses, or Tourette syndrome or chronic tic disorder. Data analysis was performed from January 1, 2017, to August 15, 2018.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Exposures </i><br />Current, new antipsychotic medication use at doses higher than 50 mg (higher-dose group) or 50 mg or lower chlorpromazine equivalents (lower-dose group) as well as control medications (ie, attention-deficit/hyperactivity disorder medications, antidepressants, or mood stabilizers) (control group).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures </i><br />Deaths during study follow-up while out of hospital or within 7 days after hospital admission, classified as either deaths due to injury or suicide or unexpected deaths. Secondary outcomes were unexpected deaths not due to overdose and death due to cardiovascular or metabolic causes.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results </i><br />This study included 189 361 children and youths in the control group (mean [SD] age, 12.0 [5.1] years; 43.4% female), 28 377 in the lower-dose group (mean [SD] age, 11.7 [4.4] years; 32.3% female), and 30 120 in the higher-dose group (mean [SD] age, 14.5 [4.8] years; 39.2% female). The unadjusted incidence of death in the higher-dose group was 146.2 per 100 000 person-years (40 deaths per 27 354 person-years), which was significantly greater than that in the control group (54.5 per 100 000 population; 67 deaths per 123 005 person-years) (P < .001). The difference was primarily attributable to the increased incidence of unexpected deaths in the higher-dose group (21 deaths; 76.8 per 100 000 population) compared with the control group (22 deaths; 17.9 per 100 000 population). The propensity score–adjusted hazard ratios were as follows: all deaths (1.80; 95% CI, 1.06-3.07), deaths due to unintentional injury or suicide (1.03; 95% CI, 0.53-2.01), and unexpected deaths (3.51; 95% CI, 1.54-7.96). The hazard ratio was 3.50 (95% CI, 1.35-9.11) for unexpected deaths not due to overdose and 4.29 (95% CI, 1.33-13.89) for deaths due to cardiovascular or metabolic causes. Neither the unadjusted nor adjusted incidence of death in the lower-dose group differed significantly from that in the control group.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance </i><br />The findings suggest that antipsychotic use is associated with increased risk of unexpected death and appear to reinforce recommendations for careful prescribing and monitoring of antipsychotic treatment for children and youths and to underscore the need for larger antipsychotic treatment safety studies in this population.</span></span></div>
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<b>Source:</b> <a href="https://jamanetwork.com/journals/jamapsychiatry/article-abstract/2717966" style="color: #6699cc;" target="_blank">https://jamanetwork.com/journals/</a></div>
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Mitigation of Olanzapine-Induced Weight Gain With Samidorphan, an Opioid Antagonist: A Randomized Double-Blind Phase 2 Study in Patients With Schizophrenia</h2>
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<b><i>American Journal of Psychiatry</i></b></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Preclinical evidence and data from a proof-of-concept study in healthy volunteers suggest that samidorphan, an opioid antagonist, mitigates weight gain associated with olanzapine. This study prospectively compared combination therapy of olanzapine plus either samidorphan or placebo for the treatment of schizophrenia.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">This was an international, multicenter, randomized phase 2 study of olanzapine plus samidorphan in patients with schizophrenia. The study had a 1-week open-label olanzapine lead-in period followed by a 12-week double-blind treatment phase in which patients were randomly assigned in a 1:1:1:1 ratio to receive olanzapine plus placebo (N=75) or olanzapine plus 5 mg (N=80), 10 mg (N=86), or 20 mg (N=68) of samidorphan. The primary aims were to confirm that the antipsychotic efficacy of olanzapine plus samidorphan was comparable to olanzapine plus placebo, to assess the effect of combining olanzapine with samidorphan on olanzapine-induced weight gain, and to assess the overall safety and tolerability of olanzapine plus samidorphan.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Antipsychotic efficacy, as assessed by total score on the Positive and Negative Syndrome Scale (PANSS), was equivalent across all treatment groups. Treatment with olanzapine plus samidorphan resulted in a statistically significant lower weight gain (37% lower weight gain compared with olanzapine plus placebo). The least square mean percent change from baseline in body weight was 4.1% (2.9 kg) for the olanzapine plus placebo group and 2.6% (1.9 kg) for the olanzapine plus samidorphan group (2.8% [2.1 kg] for the 5 mg group, 2.1% [1.5 kg] for the 10 mg group, and 2.9% [2.2 kg] for the 20 mg group). Adverse events reported at a frequency ≥5% in any of the olanzapine plus samidorphan groups and occurring at a rate ≥2 times greater than in the olanzapine plus placebo group were somnolence, sedation, dizziness, and constipation. Other safety measures were comparable between the olanzapine plus samidorphan groups and the olanzapine plus placebo group.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The antipsychotic efficacy of olanzapine plus samidorphan was equivalent to that of olanzapine plus placebo, and olanzapine plus samidorphan was associated with clinically meaningful and statistically significant mitigation of weight gain compared with olanzapine plus placebo. Olanzapine plus samidorphan was generally well tolerated, with a safety profile similar to olanzapine plus placebo.</span></span><br />
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<b style="font-size: 14.85px; line-height: 20.79px;">Read More:</b><span style="font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://ajp.psychiatryonline.org/doi/10.1176/appi.ajp.2018.18030280" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://ajp.psychiatryonline.org/</a></div>
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<span style="color: #333333; font-family: "arial" , sans-serif;"><span style="font-size: 18px; line-height: 22px; text-transform: uppercase;">Mood stabilisers and risk of stroke in bipolar disorder</span></span></h2>
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<i><b><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Abstract</span></span></b></i><br />
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<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Background</i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Research on the risk of stroke following the use of mood stabilisers specific to patients with bipolar disorder is limited.</span></span><br />
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<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Aims</i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">In this study, we investigated the risk of stroke following the exposure to mood stabilisers in patients with bipolar disorder.</span></span><br />
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<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Method</i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Data for this nationwide population-based study were derived from the Taiwan National Health Insurance Research Database. Among a retrospective cohort of patients with bipolar disorder (n = 19 433), 609 new-onset cases of stroke were identified from 1999 to 2012. A case–crossover study design utilising 14-day windows was applied to assess the acute exposure effect of individual mood stabilisers on the risk of ischaemic, haemorrhagic and other types of stroke in patients with bipolar disorder.</span></span><br />
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<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Mood stabilisers as a group were significantly associated with the increased risk of stroke in patients with bipolar disorder (adjusted risk ratio, 1.26; P = 0.041). Among individual mood stabilisers, acute exposure to carbamazepine had the highest risk of stroke (adjusted risk ratio, 1.68; P = 0.018), particularly the ischaemic type (adjusted risk ratio, 1.81; P = 0.037). In addition, acute exposure to valproic acid elevated the risk of haemorrhagic stroke (adjusted risk ratio, 1.76; P = 0.022). In contrast, acute exposure to lithium and lamotrigine did not significantly increase the risk of any type of stroke.</span></span><br />
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<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Use of carbamazepine and valproic acid, but not lithium and lamotrigine, is associated with increased risk of stroke in patients with bipolar disorder.</span></span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://www.cambridge.org/core/journals/the-british-journal-of-psychiatry/article/mood-stabilisers-and-risk-of-stroke-in-bipolar-disorder/3A251309D4B5BEDB9352BFCFA85DFE46" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://www.cambridge.org/core/journals/the-british-journal-of-psychiatry/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">BACKGROUND</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The prescription use of the stimulants methylphenidate and amphetamine for the treatment of attention deficit–hyperactivity disorder (ADHD) has been increasing. In 2007, the Food and Drug Administration mandated changes to drug labels for stimulants on the basis of findings of new-onset psychosis. Whether the risk of psychosis in adolescents and young adults with ADHD differs among various stimulants has not been extensively studied.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">METHODS</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We used data from two commercial insurance claims databases to assess patients 13 to 25 years of age who had received a diagnosis of ADHD and who started taking methylphenidate or amphetamine between January 1, 2004, and September 30, 2015. The outcome was a new diagnosis of psychosis for which an antipsychotic medication was prescribed during the first 60 days after the date of the onset of psychosis. To estimate hazard ratios for psychosis, we used propensity scores to match patients who received methylphenidate with patients who received amphetamine in each database, compared the incidence of psychosis between the two stimulant groups, and then pooled the results across the two databases.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">RESULTS</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We assessed 337,919 adolescents and young adults who received a prescription for a stimulant for ADHD. The study population consisted of 221,846 patients with 143,286 person-years of follow up; 110,923 patients taking methylphenidate were matched with 110,923 patients taking amphetamines. There were 343 episodes of psychosis (with an episode defined as a new diagnosis code for psychosis and a prescription for an antipsychotic medication) in the matched populations (2.4 per 1000 person-years): 106 episodes (0.10%) in the methylphenidate group and 237 episodes (0.21%) in the amphetamine group (hazard ratio with amphetamine use, 1.65; 95% confidence interval, 1.31 to 2.09).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">CONCLUSIONS</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Among adolescents and young adults with ADHD who were receiving prescription stimulants, new-onset psychosis occurred in approximately 1 in 660 patients. Amphetamine use was associated with a greater risk of psychosis than methylphenidate. </span></span><br />
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<b style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://www.nejm.org/doi/full/10.1056/NEJMoa1813751" style="color: #6699cc; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://www.nejm.org/</a></div>
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<b><a href="http://journals.lww.com/psychopharmacology/Pages/currenttoc.aspx" style="color: #6699cc;" target="_blank">Journal of Clinical Psychopharmacology - May 2019 - Volume 39, Issue 3</a></b></div>
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<b><a href="https://www.nature.com/npp/volumes/44/issues/7" style="color: #6699cc;" target="_blank">Neuropsychopharmacology - Volume 44, Issue 7 (June 2019)</a></b></div>
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<b><a href="https://link.springer.com/journal/213/236/2" style="color: #6699cc;" target="_blank">Psychopharmacology - Volume 236, Issue 2, February 2019</a></b></div>
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<b><a href="http://jop.sagepub.com/content/current" style="color: #6699cc;" target="_blank">Journal of Psychopharmacology - May 2019; 33 (5)</a></b></div>
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<b><a href="http://ajp.psychiatryonline.org/toc/ajp/current" style="color: #6699cc;" target="_blank">The American Journal of Psychiatry - May 2019, Vol. 176, Issue 5</a></b></div>
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<b style="color: #6699cc;"><a href="http://archpsyc.jamanetwork.com/issue.aspx" style="color: #6699cc;" target="_blank">JAMA Psychiatry - May 2019, Vol. 76, No. 5</a></b></div>
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<b><a href="https://www.nature.com/neuro/volumes/22/issues/5" style="color: #6699cc;" target="_blank">Nature Neuroscience - May 2019, Vol 22, N° 5</a></b></div>
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<b><a href="https://www.nature.com/mp/volumes/24/issues/5" style="color: #6699cc;" target="_blank">Molecular Psychiatry - Volume 24, Issue 5, May 2019</a></b></div>
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<b style="background-color: white; color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"><a href="http://www.biologicalpsychiatryjournal.com/current" style="color: #6699cc;" target="_blank">Biological Psychiatry - Volume 85, Issue 10, May 2019</a></b><br />
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<b><a href="https://academic.oup.com/brain/issue/142/5" style="color: #6699cc;" target="_blank">Brain - Volume 142, Issue 5, May 2019</a></b></div>
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<b><span style="font-size: large;">Follow us on <a href="https://www.facebook.com/neuropsychopharmacology/" target="_blank">Facebook</a> or <a href="https://twitter.com/luismariani" target="_blank">Twitter</a></span></b></h2>
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Eutimiahttp://www.blogger.com/profile/07836706907685752267noreply@blogger.comtag:blogger.com,1999:blog-1045445187620004007.post-27729104125083103342019-03-04T14:43:00.003-05:002019-03-04T17:54:04.906-05:00March 2019<div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px; text-transform: uppercase;">The neuroactive potential of the human gut microbiota in quality of life and depression</span></span></h2>
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<i style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"><br /></i><i style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;"><b>Nature Microbiology</b></i><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Abstract</b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The relationship between gut microbial metabolism and mental health is one of the most intriguing and controversial topics in microbiome research. Bidirectional microbiota–gut–brain communication has mostly been explored in animal models, with human research lagging behind. Large-scale metagenomics studies could facilitate the translational process, but their interpretation is hampered by a lack of dedicated reference databases and tools to study the microbial neuroactive potential. Surveying a large microbiome population cohort (Flemish Gut Flora Project, n = 1,054) with validation in independent data sets (ntotal = 1,070), we studied how microbiome features correlate with host quality of life and depression. Butyrate-producing Faecalibacterium and Coprococcus bacteria were consistently associated with higher quality of life indicators. Together with Dialister, Coprococcus spp. were also depleted in depression, even after correcting for the confounding effects of antidepressants. Using a module-based analytical framework, we assembled a catalogue of neuroactive potential of sequenced gut prokaryotes. Gut–brain module analysis of faecal metagenomes identified the microbial synthesis potential of the dopamine metabolite 3,4-dihydroxyphenylacetic acid as correlating positively with mental quality of life and indicated a potential role of microbial γ-aminobutyric acid production in depression. Our results provide population-scale evidence for microbiome links to mental health, while emphasizing confounder importance.</span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"> </span></div>
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<b>Source:</b> <a href="https://www.nature.com/articles/s41564-018-0337-x" style="color: #6699cc;" target="_blank">https://www.nature.com/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Background</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Tamoxifen is an oral medication that has been proposed as a potential treatment for bipolar disorder. Tamoxifen acts to inhibit the intracellular action of protein kinase C, which is also an action of well-established treatments such as lithium and valproate. Here we aimed to identify randomised controlled trials (RCTs) of tamoxifen in the treatment of bipolar disorder and synthesise their results using meta-analysis.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">RCTs were identified by searching of electronic databases and from discussion with experts in the field. Data were extracted, and meta-analyses performed in R.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Five placebo-controlled RCTs of tamoxifen in the treatment of acute mania were identified. There were no trials in the treatment of episodes of bipolar depression, or for relapse prevention. The studies of mania treatment were of between three and six weeks duration. Tamoxifen was studied either as monotherapy (two trials) or as augmentation of lithium or valproate (three trials). Change in mania scale scores favoured tamoxifen over placebo: SMD −2.14 (95% CI −3.39 to −0.89; 4 trials), as did endpoint mania scale scores SMD 1.23 (95% CI 0.60–1.87; 5 trials). Response rates were also higher: RR 4.35 (1.99–9.50; 4 trials). Acceptability was similar to placebo: RR 1.03 (0.94–1.13; 5 trials).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Tamoxifen appears to be a promising potential treatment for episodes of mania. Future studies could investigate its effects as an adjunct to dopamine antagonists for improved anti-manic efficacy, and establish its longer term effects on mood, particularly depression and relapse.</span></span></div>
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<b><br /></b><b>Source:</b> <a href="https://journals.sagepub.com/doi/full/10.1177/0269881118822167" style="color: #6699cc;" target="_blank">https://journals.sagepub.com/</a></div>
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<i style="font-size: 14.85px; line-height: 20.79px;"><b>JAMA Psychiatry</b></i><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Importance </i> <br />The effectiveness of antipsychotic polypharmacy in schizophrenia relapse prevention is controversial, and use of multiple agents is generally believed to impair physical well-being.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective </i> <br />To study the association of specific antipsychotic combinations with psychiatric rehospitalization.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants </i> <br />In this nationwide cohort study, the risk of psychiatric rehospitalization was used as a marker for relapse among 62 250 patients with schizophrenia during the use of 29 different antipsychotic monotherapy and polypharmacy types between January 1, 1996, and December 31, 2015, in a comprehensive, nationwide cohort in Finland. We conducted analysis of the data from April 24 to June 15, 2018. Rehospitalization risks were investigated by using within-individual analyses to minimize selection bias.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures</i> <br />Hazard ratio (HR) for psychiatric rehospitalization during use of polypharmacy vs during monotherapy within the same individual.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results </i> <br />In the total cohort, including 62 250 patients, 31 257 individuals (50.2%) were men, and the median age was 45.6 (interquartile range, 34.6-57.9) years. The clozapine plus aripiprazole combination was associated with the lowest risk of psychiatric rehospitalization in the total cohort, being superior to clozapine, the monotherapy associated with the best outcomes, with a difference of 14% (HR, 0.86; 95% CI, 0.79-0.94) in the analysis including all polypharmacy periods, and 18% in the conservatively defined polypharmacy analysis excluding periods shorter than 90 days (HR, 0.82; 95% CI, 0.75-0.89; P < .001). Among patients with their first episode of schizophrenia, these differences between clozapine plus aripiprazole vs clozapine monotherapy were greater (difference, 22%; HR, 0.78; 95% CI, 0.63-0.96 in the analysis including all polypharmacy periods, and difference, 23%; HR, 0.77; 95% CI, 0.63-0.95 in the conservatively defined polypharmacy analysis). At the aggregate level, any antipsychotic polypharmacy was associated with a 7% to 13% lower risk of psychiatric rehospitalization compared with any monotherapy (ranging from HR, 0.87; 95% CI, 0.85-0.88, to HR, 0.93; 95% CI, 0.91-0.95; P < .001). Clozapine was the only monotherapy among the 10 best treatments. Results on all-cause and somatic hospitalization, mortality, and other sensitivity analyses were in line with the primary outcomes.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance </i><br />Combining aripiprazole with clozapine was associated with the lowest risk of rehospitalization, indicating that certain types of polypharmacy may be feasible in the treatment of schizophrenia. Because add-on treatments are started when monotherapy is no longer sufficient to control for worsening of symptoms, it is likely that the effect sizes for polypharmacy are underestimates. Although the results do not indicate that all types of polypharmacy are beneficial, the current treatment guidelines should modify their categorical recommendations discouraging all antipsychotic polypharmacy in the maintenance treatment of schizophrenia.</span></span></div>
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<b>Source:</b> <a href="https://jamanetwork.com/journals/jamapsychiatry/fullarticle/2725088" style="color: #6699cc;" target="_blank">https://jamanetwork.com/</a></div>
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Severity and Variability of Depression Symptoms Predicting Suicide Attempt in High-Risk Individuals</h2>
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<span style="font-size: 14.85px; line-height: 20.79px;"><b><i>JAMA Psychiatry </i></b></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Abstract</b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i style="font-size: 14.85px;"><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"><i>Importance</i> </span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Predicting suicidal behavior continues to be among the most challenging tasks in psychiatry.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objectives </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To examine the trajectories of clinical predictors of suicide attempt (specifically, depression symptoms, hopelessness, impulsivity, aggression, impulsive aggression, and irritability) for their ability to predict suicide attempt and to compute a risk score for suicide attempts.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">This is a longitudinal study of the offspring of parents (or probands) with mood disorders who were recruited from inpatient units at Western Psychiatric Institute and Clinic (Pittsburgh) and New York State Psychiatric Institute. Participants were recruited from July 15, 1997, to September 6, 2005, and were followed up through January 21, 2014. Probands and offspring (n = 663) were interviewed at baseline and at yearly follow-ups for 12 years. Lifetime and current psychiatric disorders were assessed, and self-reported questionnaires were administered. Model evaluation used 10-fold cross-validation, which split the entire data set into 10 equal parts, fit the model to 90% of the data (training set), and assessed it on the remaining 10% (test set) and repeated that process 10 times. Preliminary analyses were performed from July 20, 2015, to October 5, 2016. Additional analyses were conducted from July 26, 2017, to July 24, 2018.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The broad definition of suicide attempt included actual, interrupted, and aborted attempts as well as suicidal ideation that prompted emergency referrals during the study. The narrow definition referred to actual attempt only.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The sample of offspring (n = 663) was almost equally distributed by sex (316 female [47.7%]) and had a mean (SD) age of 23.8 (8.5) years at the time of censored observations. Among the 663 offspring, 71 (10.7%) had suicide attempts over the course of the study. The trajectory of depression symptoms with the highest mean scores and variability over time was the only trajectory to predict suicide attempt (odds ratio [OR], 4.72; 95% CI, 1.47-15.21; P = .01). In addition, we identified the following predictors: younger age (OR, 0.82; 95% CI, 0.74-0.90; P < .001), lifetime history of unipolar disorder (OR, 4.71; 95% CI, 1.63-13.58; P = .004), lifetime history of bipolar disorder (OR, 3.4; 95% CI, 0.96-12.04; P = .06), history of childhood abuse (OR, 2.98; 95% CI, 1.40-6.38; P = .01), and proband actual attempt (OR, 2.24; 95% CI, 1.06-4.75; P = .04). Endorsing a score of 3 or higher on the risk score tool resulted in high sensitivity (87.3%) and moderate specificity (63%; area under the curve = 0.80).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The specific predictors of suicide attempt identified are those that clinicians already assess during routine psychiatric evaluations; monitoring and treating depression symptoms to reduce their severity and fluctuation may attenuate the risk for suicidal behavior.</span></span><br />
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<b style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;">Source:</b><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"> </span><a href="https://jamanetwork.com/journals/jamapsychiatry/article-abstract/2726611" style="color: #6699cc; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;" target="_blank">https://jamanetwork.com/</a></div>
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Association of Fetal Growth With General and Specific Mental Health Conditions</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b><i>JAMA Psychiatry</i></b></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Abstract</b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><span style="font-size: 14.85px;"><br /></span></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><span style="font-size: 14.85px;"><i>Importance </i></span></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">It is unclear if the associations between fetal growth and later mental health conditions remain after controlling for familial factors and psychiatric comorbidity.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To examine the associations between fetal growth and general and specific mental health conditions, controlling for familial factors.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">This register-based study conducted in Sweden analyzed 546 894 pairs of full siblings born between January 1, 1973, and December 31, 1998. Sibling pairs were followed up through December 31, 2013. First, population-based and within-sibling pair associations (which controlled for time-invariant familial confounders) between fetal growth and the outcomes were estimated. Second, exploratory factor analysis was applied to the outcomes to derive 1 general factor and 4 specific and independent factors. Third, the general and specific factors were regressed on fetal growth. Statistical analysis was performed from March 27, 2017, to October 27, 2018.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcome and Measures </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The outcomes were 11 psychiatric diagnoses (depression, anxiety, obsessive-compulsive disorder, posttraumatic stress disorder, bipolar disorder, alcohol abuse, drug use, attention-deficit/hyperactivity disorder, autism, schizophrenia, and schizoaffective disorder) and court convictions of violent crimes. Birth weight (in kilograms) statistically adjusted for gestational age was the exposure.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The mean (SD) age of the 1 093 788 participants was 27.2 (6.8) years (range, 15.1-40.9 years) and 51.5% were male. Nine outcomes were significantly associated with birth weight in the population at large: depression (odds ratio [OR], 0.96; 95% CI, 0.95-0.98), anxiety (OR, 0.94; 95% CI, 0.92-0.95), posttraumatic stress disorder (OR, 0.91; 95% CI, 0.89-0.93), bipolar disorder (OR, 0.94; 95% CI, 0.89-1.00), alcohol abuse (OR, 0.89; 95% CI, 0.87-0.91), drug use (OR, 0.83; 95% CI, 0.80-0.85), violent crimes (OR, 0.85; 95% CI, 0.83-0.86), attention-deficit/hyperactivity disorder (OR, 0.88; 95% CI, 0.86-0.90), and autism (OR, 0.95; 95% CI, 0.92-0.97). Only depression (OR, 0.95; 95% CI 0.92-0.98), obsessive-compulsive disorder (OR, 0.93; 95% CI, 0.87-0.99), attention-deficit/hyperactivity disorder (OR, 0.86; 95% CI, 0.82-0.89), and autism (OR, 0.72; 95% CI, 0.69-0.76) remained significantly associated within sibling pairs. An exploratory factor analysis indicated that 1 general and 4 specific factors (capturing anxiety, externalizing, neurodevelopmental, and psychotic conditions) fit the outcomes well. Across almost all sensitivity analyses, an increase in birth weight by 1 kg significantly reduced the general (β, −0.047; 95% CI, −0.071 to −0.023) and the specific neurodevelopmental factors (β, −0.159; 95% CI, −0.190 to −0.128) within sibling pairs.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Controlling for familial confounders, reduced fetal growth was associated with a small but significant increase in the general factor of psychopathology and a moderate increase in a specific neurodevelopmental factor.</span></span></div>
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<b>Source:</b> <a href="https://jamanetwork.com/journals/jamapsychiatry/fullarticle/2722846" rel="" style="color: #6699cc;" target="_blank">https://jamanetwork.com/</a></div>
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Association of Cannabis Use in Adolescence and Risk of Depression, Anxiety, and Suicidality in Young Adulthood</h2>
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<i><b>JAMA Psychiatry</b></i></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Abstract</b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Importance </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Cannabis is the most commonly used drug of abuse by adolescents in the world. While the impact of adolescent cannabis use on the development of psychosis has been investigated in depth, little is known about the impact of cannabis use on mood and suicidality in young adulthood.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To provide a summary estimate of the extent to which cannabis use during adolescence is associated with the risk of developing subsequent major depression, anxiety, and suicidal behavior.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Data Sources </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Medline, Embase, CINAHL, PsycInfo, and Proquest Dissertations and Theses were searched from inception to January 2017.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Study Selection </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Longitudinal and prospective studies, assessing cannabis use in adolescents younger than 18 years (at least 1 assessment point) and then ascertaining development of depression in young adulthood (age 18 to 32 years) were selected, and odds ratios (OR) adjusted for the presence of baseline depression and/or anxiety and/or suicidality were extracted.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Data Extraction and Synthesis </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Study quality was assessed using the Research Triangle Institute item bank on risk of bias and precision of observational studies. Two reviewers conducted all review stages independently. Selected data were pooled using random-effects meta-analysis.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The studies assessing cannabis use and depression at different points from adolescence to young adulthood and reporting the corresponding OR were included. In the studies selected, depression was diagnosed according to the third or fourth editions of Diagnostic and Statistical Manual of Mental Disorders or by using scales with predetermined cutoff points.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">After screening 3142 articles, 269 articles were selected for full-text review, 35 were selected for further review, and 11 studies comprising 23 317 individuals were included in the quantitative analysis. The OR of developing depression for cannabis users in young adulthood compared with nonusers was 1.37 (95% CI, 1.16-1.62; I2 = 0%). The pooled OR for anxiety was not statistically significant: 1.18 (95% CI, 0.84-1.67; I2 = 42%). The pooled OR for suicidal ideation was 1.50 (95% CI, 1.11-2.03; I2 = 0%), and for suicidal attempt was 3.46 (95% CI, 1.53-7.84, I2 = 61.3%).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Although individual-level risk remains moderate to low and results from this study should be confirmed in future adequately powered prospective studies, the high prevalence of adolescents consuming cannabis generates a large number of young people who could develop depression and suicidality attributable to cannabis. This is an important public health problem and concern, which should be properly addressed by health care policy.</span></span><br />
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<b>Source:</b> <a href="https://jamanetwork.com/journals/jamapsychiatry/article-abstract/2723657" rel="" style="color: #6699cc;" target="_blank">https://jamanetwork.com/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b><i>Child and Adolescent </i></b></span><b style="font-size: 14.85px;"><i>Psychiatry</i></b></span></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span><span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Parental age at birth has been shown to affect the rates of a range of neurodevelopmental disorders, but the understanding of the mechanisms through which it mediates different outcomes is still lacking. We used a population-based cohort to assess differential effects of parental age on estimates of risk across pediatric-onset neuropsychiatric disorders: autism spectrum disorder (ASD), attention-deficit hyperactivity disorder (ADHD), obsessive-compulsive disorder (OCD) and Tourette syndrome/chronic tic disorder (TS/CT).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Method</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Our study cohort included all singleton births in Denmark between 1980 and 2007 with full information on parental ages (N=1,490,745), followed through December 31, 2013. Cases of ASD, ADHD, OCD and TS/CT were identified in the Danish Psychiatric Central Register and the National Patient Register. Associations with parental age were modeled using a stratified Cox regression, allowing for changes in baseline diagnostic rates across time.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Younger parental age was significantly associated with increased estimates of risk for ADHD and TS/CT, while older parental age was associated with ASD and OCD. Except for OCD, we did not observe any evidence for differential effects of parental ages on male vs. female offspring.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusion</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We provide novel evidence for the association between age at parenthood and TS/CT and OCD, and show for the first time in a population-based sample that parental age confers differential risk rates for pediatric-onset psychiatric disorders. Our results are consistent with a model of both shared and unshared risk architecture for pediatric-onset neuropsychiatric conditions, highlighting unique contributions of maternal and paternal ages.</span></span></div>
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<b>Source:</b> <a href="https://www.jaacap.org/article/S0890-8567(19)30126-1/fulltext" style="color: #6699cc;" target="_blank">https://www.jaacap.org/</a></div>
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FDA APPROVES NEW DOSAGE STRENGTH OF BUPRENORPHINE AND NALOXONE SUBLINGUAL FILM AS MAINTENANCE TREATMENT FOR OPIOID DEPENDENCE</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The U.S. Food and Drug Administration today approved Cassipa (buprenorphine and naloxone) sublingual film (applied under the tongue) for the maintenance treatment of opioid dependence. This action provides a new dosage strength (16 milligrams/4 milligrams) of buprenorphine and naloxone sublingual film, which is also approved in both brand name and generic versions and in various strengths.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">“There’s an urgent need to ensure access to, and wider use and understanding of, medication-assisted treatment for opioid use disorder. The introduction of new treatment options has the potential to broaden access for patients. For example, the FDA recently described a streamlined approach to drug development for certain medication-assisted treatments that are based on buprenorphine. This streamlined approach can reduce drug development costs, so products may be offered at a lower price to patients and we can broaden access to treatment,” said FDA Commissioner Scott Gottlieb, M.D. “The FDA is committed to helping those with opioid use disorder transition to lives of sobriety. We’ve taken a number of steps to advance the development of new FDA-approved treatments for opioid dependence and encourage health care professionals to ensure patients are offered an adequate chance to benefit from these therapies. We’re also working to address the unfortunate stigma that’s sometimes associated with the use of opioid replacement therapy as one approach to the successful treatment of addiction. Despite what some may think, individuals who successfully transition onto medication-assisted treatment are not swapping one addiction for another. Opioid replacement therapy can be an important part of effective treatment. Opioid use disorder should be viewed similarly to any other chronic condition that is treated with medication.”</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Medication-assisted treatment (MAT) is a comprehensive approach that combines FDA-approved medications (currently methadone, buprenorphine, or naltrexone) with counseling and other behavioral therapies to treat patients with opioid use disorder (OUD). Regular adherence to MAT with buprenorphine reduces opioid withdrawal symptoms and the desire to use opioids, without causing the cycle of highs and lows associated with opioid misuse or abuse. At proper doses, buprenorphine also decreases the pleasurable effects of other opioids, making continued opioid abuse less attractive. According to the Substance Abuse and Mental Health Services Administration, patients receiving MAT for treatment of their OUD cut their risk of death from all causes in half.</span></span><br />
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<b style="font-size: 14.85px; line-height: 20.79px;">Read More:</b><span style="font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm619864.htm" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://www.fda.gov/</a></div>
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<span style="color: #333333; font-family: "arial" , sans-serif;"><span style="font-size: 18px; line-height: 22px; text-transform: uppercase;">ORGANOPHOSPHATE EXPOSURES DURING PREGNANCY AND CHILD NEURODEVELOPMENT: RECOMMENDATIONS FOR ESSENTIAL POLICY REFORM</span></span></h2>
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<i><b><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Abstract</span></span></b></i><br />
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<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">• Widespread use of organophosphate (OP) pesticides to control insects has resulted inubiquitous human exposures.</span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">• High exposures to OP pesticides are responsible for poisonings and deaths, particularly in developing countries.</span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">• Compelling evidence indicates that prenatal exposure at low levels is putting children atrisk for cognitive and behavioral deficits and for neurodevelopmental disorders.To protect children worldwide, we recommend the following:</span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">• Governments phase out chlorpyrifos and other OP pesticides, monitor watersheds andother sources of human exposures, promote use of integrated pest management (IPM)through incentives and training in agroecology, and implement mandatory surveillanceof pesticide-related illness.</span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">• Health professions implement curricula on the hazards from OP pesticides in nursingand medical schools and in continuing medical education courses and educate theirpatients and the public about these hazards.</span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">• Agricultural entities accelerate the development of nontoxic approaches to pest controlthrough IPM and ensure the safety of workers through training and provision of protec-tive equipment when toxic chemicals are to be used.</span></span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://www.scribd.com/document/391463803/OP-Pesticide-Paper-PLOS-Medicine" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://www.scribd.com/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; text-transform: uppercase;">CORROBORATION OF A MAJOR ROLE FOR HERPES SIMPLEX VIRUS TYPE 1 IN ALZHEIMER’S DISEASE</span></span></h2>
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<span style="color: #333333; line-height: 20.79px;"><i><span style="line-height: 20.79px;"><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Frontiers in Aging Neuroscience</b></span></span></span></i></span><br />
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b><br /></b></span></i></span><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Strong evidence has emerged recently for the concept that herpes simplex virus type 1 (HSV1) is a major risk for Alzheimer’s disease (AD). This concept proposes that latent HSV1 in brain of carriers of the type 4 allele of the apolipoprotein E gene (APOE-ε4) is reactivated intermittently by events such as immunosuppression, peripheral infection, and inflammation, the consequent damage accumulating, and culminating eventually in the development of AD. Population data to investigate this epidemiologically, e.g., to find if subjects treated with antivirals might be protected from developing dementia—are available in Taiwan, from the National Health Insurance Research Database, in which 99.9% of the population has been enrolled. This is being extensively mined for information on microbial infections and disease. Three publications have now appeared describing data on the development of senile dementia (SD), and the treatment of those with marked overt signs of disease caused by varicella zoster virus (VZV), or by HSV. The striking results show that the risk of SD is much greater in those who are HSV-seropositive than in seronegative subjects, and that antiviral treatment causes a dramatic decrease in number of subjects who later develop SD. It should be stressed that these results apply only to those with severe cases of HSV1 or VZV infection, but when considered with the over 150 publications that strongly support an HSV1 role in AD, they greatly justify usage of antiherpes antivirals to treat AD. Three other studies are described which directly relate to HSV1 and AD: they deal respectively with lysosomal changes in HSV1-infected cell cultures, with evidence for a role of human herpes virus type 6 and 7 (HHV6 and HHV7) in AD, and viral effects on host gene expression, and with the antiviral characteristics of beta amyloid (Aβ). Three indirectly relevant studies deal respectively with schizophrenia, relating to antiviral treatment to target HSV1, with the likelihood that HSV1 is a cause of fibromyalgia (FM), and with FM being associated with later development of SD. Studies on the link between epilepsy, AD and herpes simplex encephalitis (HSE) are described also, as are the possible roles of APOE-ε4, HHV6 and HSV1 in epilepsy. </span></span><br />
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<b style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://www.frontiersin.org/articles/10.3389/fnagi.2018.00324/full" style="color: #6699cc; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://www.frontiersin.org/</a></div>
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<b><a href="http://journals.lww.com/psychopharmacology/Pages/currenttoc.aspx" style="color: #6699cc;" target="_blank">Journal of Clinical Psychopharmacology - March 2019 - Volume 39, Issue 2</a></b></div>
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<b><a href="https://www.nature.com/npp/volumes/44/issues/4" style="color: #6699cc;" target="_blank">Neuropsychopharmacology - Volume 44, Issue 4 (March 2019)</a></b></div>
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<b><a href="https://link.springer.com/journal/213/236/1" style="color: #6699cc;" target="_blank">Psychopharmacology - Volume 236, Issue 1, January 2018</a></b></div>
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<b><a href="http://jop.sagepub.com/content/current" style="color: #6699cc;" target="_blank">Journal of Psychopharmacology - February 2019; 33 (2)</a></b></div>
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<b><a href="http://ajp.psychiatryonline.org/toc/ajp/current" style="color: #6699cc;" target="_blank">The American Journal of Psychiatry - March 2019, Vol. 176, Issue 3</a></b></div>
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<b style="color: #6699cc;"><a href="http://archpsyc.jamanetwork.com/issue.aspx" style="color: #6699cc;" target="_blank">JAMA Psychiatry - February 2019, Vol. 76, No. 2</a></b></div>
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<b><a href="https://www.nature.com/neuro/volumes/22/issues/2" style="color: #6699cc;" target="_blank">Nature Neuroscience - February 2019, Vol 22, N° 2</a></b></div>
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<b><a href="https://www.nature.com/mp/volumes/24/issues/3" style="color: #6699cc;" target="_blank">Molecular Psychiatry - Volume 24, Issue 3, March 2019</a></b></div>
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<b style="background-color: white; color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"><a href="http://www.biologicalpsychiatryjournal.com/current" style="color: #6699cc;" target="_blank">Biological Psychiatry - Volume 85, Issue 6, March 2019</a></b><br />
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<b><a href="https://academic.oup.com/brain/issue/142/3" style="color: #6699cc;" target="_blank">Brain - Volume 142, Issue 3, March 2019</a></b></div>
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Eutimiahttp://www.blogger.com/profile/07836706907685752267noreply@blogger.comtag:blogger.com,1999:blog-1045445187620004007.post-64117965659138559242019-01-09T12:19:00.002-05:002019-01-09T12:36:26.999-05:00January 2019<div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Abstract</b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Strong evidence has emerged recently for the concept that herpes simplex virus type 1 (HSV1) is a major risk for Alzheimer’s disease (AD). This concept proposes that latent HSV1 in brain of carriers of the type 4 allele of the apolipoprotein E gene (APOE-ε4) is reactivated intermittently by events such as immunosuppression, peripheral infection, and inflammation, the consequent damage accumulating, and culminating eventually in the development of AD. Population data to investigate this epidemiologically, e.g., to find if subjects treated with antivirals might be protected from developing dementia—are available in Taiwan, from the National Health Insurance Research Database, in which 99.9% of the population has been enrolled. This is being extensively mined for information on microbial infections and disease. Three publications have now appeared describing data on the development of senile dementia (SD), and the treatment of those with marked overt signs of disease caused by varicella zoster virus (VZV), or by HSV. The striking results show that the risk of SD is much greater in those who are HSV-seropositive than in seronegative subjects, and that antiviral treatment causes a dramatic decrease in number of subjects who later develop SD. It should be stressed that these results apply only to those with severe cases of HSV1 or VZV infection, but when considered with the over 150 publications that strongly support an HSV1 role in AD, they greatly justify usage of antiherpes antivirals to treat AD. Three other studies are described which directly relate to HSV1 and AD: they deal respectively with lysosomal changes in HSV1-infected cell cultures, with evidence for a role of human herpes virus type 6 and 7 (HHV6 and HHV7) in AD, and viral effects on host gene expression, and with the antiviral characteristics of beta amyloid (Aβ). Three indirectly relevant studies deal respectively with schizophrenia, relating to antiviral treatment to target HSV1, with the likelihood that HSV1 is a cause of fibromyalgia (FM), and with FM being associated with later development of SD. Studies on the link between epilepsy, AD and herpes simplex encephalitis (HSE) are described also, as are the possible roles of APOE-ε4, HHV6 and HSV1 in epilepsy.</span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"> </span></div>
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<b>Source:</b> <a href="https://www.frontiersin.org/articles/10.3389/fnagi.2018.00324/full" style="color: #6699cc;" target="_blank">https://www.frontiersin.org/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">• </span><span style="font-size: 14.85px;">Widespread use of organophosphate (OP) pesticides to control insects has resulted inubiquitous human exposures.<br />• High exposures to OP pesticides are responsible for poisonings and deaths, particularly in developing countries.<br />• Compelling evidence indicates that prenatal exposure at low levels is putting children atrisk for cognitive and behavioral deficits and for neurodevelopmental disorders.To protect children worldwide, we recommend the following:<br />• Governments phase out chlorpyrifos and other OP pesticides, monitor watersheds andother sources of human exposures, promote use of integrated pest management (IPM)through incentives and training in agroecology, and implement mandatory surveillanceof pesticide-related illness.<br />• Health professions implement curricula on the hazards from OP pesticides in nursingand medical schools and in continuing medical education courses and educate theirpatients and the public about these hazards.<br />• Agricultural entities accelerate the development of nontoxic approaches to pest controlthrough IPM and ensure the safety of workers through training and provision of protec-tive equipment when toxic chemicals are to be used.</span><span style="color: #444444;"><span style="font-size: 14.85px;"> </span></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"> </span></div>
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<b><br /></b><b>Source:</b> <a href="https://www.scribd.com/document/391463803/OP-Pesticide-Paper-PLOS-Medicine" style="color: #6699cc;" target="_blank">https://www.scribd.com/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The U.S. Food and Drug Administration today approved Cassipa (buprenorphine and naloxone) sublingual film (applied under the tongue) for the maintenance treatment of opioid dependence. This action provides a new dosage strength (16 milligrams/4 milligrams) of buprenorphine and naloxone sublingual film, which is also approved in both brand name and generic versions and in various strengths.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">“There’s an urgent need to ensure access to, and wider use and understanding of, medication-assisted treatment for opioid use disorder. The introduction of new treatment options has the potential to broaden access for patients. For example, the FDA recently described a streamlined approach to drug development for certain medication-assisted treatments that are based on buprenorphine. This streamlined approach can reduce drug development costs, so products may be offered at a lower price to patients and we can broaden access to treatment,” said FDA Commissioner Scott Gottlieb, M.D. “The FDA is committed to helping those with opioid use disorder transition to lives of sobriety. We’ve taken a number of steps to advance the development of new FDA-approved treatments for opioid dependence and encourage health care professionals to ensure patients are offered an adequate chance to benefit from these therapies. We’re also working to address the unfortunate stigma that’s sometimes associated with the use of opioid replacement therapy as one approach to the successful treatment of addiction. Despite what some may think, individuals who successfully transition onto medication-assisted treatment are not swapping one addiction for another. Opioid replacement therapy can be an important part of effective treatment. Opioid use disorder should be viewed similarly to any other chronic condition that is treated with medication.”</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Medication-assisted treatment (MAT) is a comprehensive approach that combines FDA-approved medications (currently methadone, buprenorphine, or naltrexone) with counseling and other behavioral therapies to treat patients with opioid use disorder (OUD). Regular adherence to MAT with buprenorphine reduces opioid withdrawal symptoms and the desire to use opioids, without causing the cycle of highs and lows associated with opioid misuse or abuse. At proper doses, buprenorphine also decreases the pleasurable effects of other opioids, making continued opioid abuse less attractive. According to the Substance Abuse and Mental Health Services Administration, patients receiving MAT for treatment of their OUD cut their risk of death from all causes in half.</span></span></div>
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<b>Read More:</b> <a href="https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm619864.htm" style="color: #6699cc;" target="_blank">https://www.fda.gov/</a></div>
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DETERMINANTS OF SUBOPTIMAL MEDICATION ADHERENCE IN PATIENTS WITH A MAJOR DEPRESSIVE EPISODE</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i style="font-size: 14.85px;"><br />Background</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Major Depression (MD) is often a chronic condition requiring a long‐term pharmacologic treatment. Despite the efficacy of antidepressants, the medication adherence in those affected is usually very poor. In this scenario, further research concerning drivers of suboptimal adherence is needed. We aimed to explore medication adherence in patients with a MD episode, and to identify sociodemographic, clinical (psychiatric antecedents, comorbidities, medication, pain, and medication side effects), and psychosocial factors (negative life events, childhood trauma, and attitudes to medication) related to adherence status.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Method</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The Medication Adherence Rating Scale (MARS) was completed by 370 patients at hospital admission. Participants were divided into groups of optimal and suboptimal adherence based on the medication adherence behavior score (MARS's factor 1), and were compared with respect to the study variables.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Twenty‐nine percent of participants (n = 107) were found to be optimally adherents to their medication (score = 4/4). Compared to optimally adherents, suboptimally adherents (71%) presented a significantly higher depression severity, more psychiatric hospitalizations, suicidal ideation, physical pain, negative medication side effects, and antecedents of emotional maltreatment. Suboptimally adherents also had less favorable attitudes toward medication and were less in a relationship than optimally adherents. Multivariate analyses showed that depression severity, suicidal ideation, and physical pain increase the probability of belonging to the suboptimal adherent group.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusion</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">These results suggest a vicious circle in which more vulnerable patients are less adherent to medication, which could worsen the clinical picture maintaining, in turn, low adherence. More efforts are needed to develop interventions aiming to improve medication adherence in MD patients.</span><br />
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ANXIETY AS A RISK FACTOR FOR COGNITIVE DECLINE: A 12-YEAR FOLLOW-UP COHORT STUDY</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Anxiety might be a risk factor for cognitive decline, but previous studies had short follow-up or small sample sizes or studied general or single cognitive domain functioning.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Anxiety symptoms were assessed with the Symptom Checklist-90 in 918 participants of the Maastricht Aging Study aged 50 years or older. Anxiety was analyzed both dichotomously (highest versus lower quartiles as a group) and continuously. Neuropsychological tests measured executive function, memory, speed of information processing, and verbal fluency. Linear mixed models were conducted with anxiety symptoms as predictor and change in cognitive scores as outcome. Differences of associations by age and gender were studied with three-way interactions.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Higher anxiety symptoms were significantly associated with more decline in verbal memory in those aged 65 years and older (delayed recall: χ2 = 9.30, df = 2, p = 0.01; immediate recall: χ2 = 11.81, df = 2, p = 0.003). There were sex differences in executive function (χ2 = 6.63, df = 2, p = 0.036), fluency (χ2 = 6.89, df = 2, p = 0.032), and processing speed (χ2 = 8.83, df = 2, p = 0.012), with lower performance in women over time.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusion</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">In participants without cognitive impairments at baseline, anxiety symptoms were associated with a decline in verbal memory in older adults and with poorer performance in nonamnestic domains in women. Adequate treatment of anxiety symptoms could have a beneficial influence on the risk of developing neurodegenerative diseases. Further research is needed to elucidate whether this association is causal.</span></span></div>
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<b>Source:</b> <a href="https://www.ajgponline.org/article/S1064-7481(18)30483-4/abstract" rel="" style="color: #6699cc;" target="_blank">https://www.ajgponline.org/</a></div>
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MAPPING THE HETEROGENEOUS PHENOTYPE OF SCHIZOPHRENIA AND BIPOLAR DISORDER USING NORMATIVE MODELS</h2>
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<i><b>JAMA Psychiatry</b></i></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Abstract</b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Importance </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Schizophrenia and bipolar disorder are severe and complex brain disorders characterized by substantial clinical and biological heterogeneity. However, case-control studies often ignore such heterogeneity through their focus on the average patient, which may be the core reason for a lack of robust biomarkers indicative of an individual’s treatment response and outcome.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objectives </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To investigate the degree to which case-control analyses disguise interindividual differences in brain structure among patients with schizophrenia and bipolar disorder and to map the brain alterations linked to these disorders at the level of individual patients.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">This study used cross-sectional, T1-weighted magnetic resonance imaging data from participants recruited for the Thematically Organized Psychosis study from October 27, 2004, to October 17, 2012. Data were reanalyzed in 2017 and 2018. Patients were recruited from inpatient and outpatient clinics in the Oslo area of Norway, and healthy individuals from the same catchment area were drawn from the national population registry.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Interindividual differences in brain structure among patients with schizophrenia and bipolar disorder. Voxel-based morphometry maps were computed, which were used for normative modeling to map the range of interindividual differences in brain structure.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">This study included 218 patients with schizophrenia spectrum disorders (mean [SD] age, 30 [9.3] years; 126 [57.8%] male), of whom 163 had schizophrenia (mean [SD] age, 31 [8.7] years; 105 [64.4%] male) and 190 had bipolar disorder (mean [SD] age, 34 [11.3] years; 79 [41.6%] male), and 256 healthy individuals (mean [SD] age, 34 [9.5] years; 140 [54.7%] male). At the level of the individual, deviations from the normative model were frequent in both disorders but highly heterogeneous. Overlap of more than 2% among patients was observed in only a few loci, primarily in frontal, temporal, and cerebellar regions. The proportion of alterations was associated with diagnosis and cognitive and clinical characteristics within clinical groups. Patients with schizophrenia, on average, had significantly reduced gray matter in frontal regions, cerebellum, and temporal cortex. In patients with bipolar disorder, mean deviations were primarily present in cerebellar regions.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">This study found that group-level differences disguised biological heterogeneity and interindividual differences among patients with the same diagnosis. This finding suggests that the idea of the average patient is a noninformative construct in psychiatry that falls apart when mapping abnormalities at the level of the individual patient. This study presents a workable route toward precision medicine in psychiatry.</span></span></div>
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<b>Source:</b> <a href="https://jamanetwork.com/journals/jamapsychiatry/article-abstract/2705762" rel="" style="color: #6699cc;" target="_blank">https://jamanetwork.com/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The menopause transition is a time when women experience an increased risk for new onset depression, as well as relapse of depression. While there are overlapping symptoms between major depression and depression during menopause, differences suggest ‘perimenopausal depression’ may be a unique subtype of depression associated with characteristic symptoms. There is currently no validated scale designed to measure perimenopausal depression. The aim of the current study was to develop and validate the ‘Meno-D’, a self-reporting or clinician rated questionnaire, designed to rate the severity of symptoms of perimenopausal depression. The development phase of the Meno-D involved literature review, clinical observation, and focus groups. A 12-item questionnaire was developed and clinically reviewed for face validity for content. The Meno-D was administered to women experiencing symptoms of perimenopausal depression as part of a larger baseline assessment battery. Validation involved confirmatory factor analysis (CFA). The development of the Meno-D resulted in 12 items. A total of 93 participants with perimenopausal depression were involved in the baseline assessments, 82 completed the Meno-D. Factor analysis identified five sub-scales of the Meno-D “somatic; cognitive; self; sleep; sexual” with high-internal consistency; discriminant validity and a good construct and convergent validity. The Meno-D provides a unique tool for clinicians and researchers to measure the presence of perimenopausal depression.</span></span></div>
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<b>Source:</b> <a href="https://www.nature.com/articles/s41398-018-0172-0#Abs1" style="color: #6699cc;" target="_blank">https://www.nature.com/</a></div>
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VITAMIN D SUPPLEMENTATION MAY HELP EASE DEPRESSION</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b><i>Medscape</i></b></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Vitamin D supplementation may help reduce depressive symptoms, new results of an updated meta-analysis show.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">"People who were vitamin D deficient and depressed seemed to respond best to supplementation, but there was some evidence that supplementation improved depressive symptoms in people who had a normal level of vitamin D," Marissa Flaherty, MD, of the Department of Psychiatry, University of Maryland School of Medicine in Baltimore, told Medscape Medical News.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Globally, more than 300 million people suffer from depression. It's the number one cause of years lost to disability worldwide. In the United States, the overall prevalence of vitamin D deficiency hovers around 42%, with the highest rate seen in blacks.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">"In my third year of residency, I noticed that a lot of my depressed patients had very low vitamin D levels, and when I supplemented their vitamin D, their depressive symptoms, particularly their fatigue and energy levels, would improve," Flaherty said.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To investigate further, Flaherty and her colleagues conducted a systematic review and meta-analysis of five randomized controlled trials published from 2011 to 2016 that examined the effect of vitamin D supplementation (vs no supplementation) on depressive symptoms, as measured by the Beck Depression Inventory and Hamilton Depression Rating Scale.</span></span><br />
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<b style="font-size: 14.85px; line-height: 20.79px;">Read More:</b><span style="font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://www.medscape.com/viewarticle/896449" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://www.medscape.com/</a></div>
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<span style="color: #333333; font-family: "arial" , sans-serif;"><span style="font-size: 18px; line-height: 22px; text-transform: uppercase;">PRENATAL EXPOSURE TO ACETAMINOPHEN AND RISK FOR ATTENTION DEFICIT HYPERACTIVITY DISORDER AND AUTISTIC SPECTRUM DISORDER: A SYSTEMATIC REVIEW, META-ANALYSIS, AND META-REGRESSION ANALYSIS OF COHORT STUDIES</span></span></h2>
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<i><b><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Abstract</span></span></b></i><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">Acetaminophen is the analgesic and antipyretic most commonly used during pregnancy. Evidence of neurodisruptive properties is accumulating. Therefore, we sought to evaluate the risk for attention deficit hyperactivity disorder (ADHD) and autistic spectrum disorder (ASD) in the offspring of women exposed to acetaminophen during pregnancy. We searched MEDLINE, Embase, and Cochrane databases for relevant studies up to January 2017. Data were independently extracted and assessed by 2 researchers. Seven eligible retrospective cohorts included 132,738 mother-child pairs, with follow-up periods ranging from 3 to 11 years. The pooled risk ratio for ADHD was 1.34 (95% confidence interval (CI): 1.21, 1.47; I2 = 72%); for ASD, the risk ratio was 1.19 (95% CI: 1.14, 1.25; I2 = 14%), and for hyperactivity symptoms, it was 1.24 (95% CI: 1.04, 1.43; I2 = 93%). In meta-regression analysis, the association between exposure and ADHD increased with the child’s age upon follow-up (β = 0.03, 95% CI: 0.00, 0.07) and with the mean duration of exposure (β = 0.00, 95% CI: 0.00, 0.01). The available data is of observational nature only. Studies differed widely in exposure and outcome assessment. Acetaminophen use during pregnancy is associated with an increased risk for ADHD, ASD, and hyperactivity symptoms. These findings are concerning; however, results should be interpreted with caution given that the available evidence consists of observational studies and is susceptible to several potential sources of bias.</span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; text-transform: uppercase;">ESTIMATION OF LIFETIME RISKS OF ALZHEIMER'S DISEASE DEMENTIA USING BIOMARKERS FOR PRECLINICAL DISEASE</span></span></h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"><i>Introduction</i></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Lifetime risks are the probabilities of progressing to Alzheimer's disease (AD) dementia during one's lifespan. Here, we report the first estimates of the lifetime and ten-year risks of AD dementia based on age, gender, and biomarker tests for preclinical disease.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We used a multistate model for the disease process together with US death rates.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Lifetime risks of AD dementia vary considerably by age, gender, and the preclinical or clinical disease state of the individual. For example, the lifetime risks for a female with only amyloidosis are 8.4% for a 90-year old and 29.3% for a 65-year old. Persons younger than 85 years with mild cognitive impairment, amyloidosis, and neurodegeneration have lifetime risks of AD dementia greater than 50%.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Discussion</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Most persons with preclinical AD will not develop AD dementia during their lifetimes. Lifetime risks help interpret the clinical significance of biomarker screening tests for AD</span></span><br />
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://www.alzheimersanddementia.com/article/S1552-5260(18)30098-0/fulltext" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://www.alzheimersanddementia.com/</a></div>
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<b><a href="http://journals.lww.com/psychopharmacology/Pages/currenttoc.aspx" style="color: #6699cc;" target="_blank">Journal of Clinical Psychopharmacology - January 2019 - Volume 39, Issue 1</a></b></div>
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<b style="color: #6699cc;"><a href="http://archpsyc.jamanetwork.com/issue.aspx" style="color: #6699cc;" target="_blank">JAMA Psychiatry - November 2018, Vol. 75, No. 11</a></b></div>
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<b><a href="https://www.nature.com/neuro/volumes/21/issues/11" style="color: #6699cc;" target="_blank">Nature Neuroscience - November 2018, Vol 21, N° 11</a></b></div>
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<b><a href="https://www.nature.com/mp/volumes/23/issues/8" style="color: #6699cc;" target="_blank">Molecular Psychiatry - Volume 23, Issue 8, August 2018</a></b></div>
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<b style="background-color: white; color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"><a href="http://www.biologicalpsychiatryjournal.com/current" style="color: #6699cc;" target="_blank">Biological Psychiatry - Volume 84, Issue 11, December 2018</a></b><br />
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<b><a href="https://academic.oup.com/brain/issue/141/11" style="color: #6699cc;" target="_blank">Brain - Volume 141, Issue 11, November 2018</a></b></div>
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Eutimiahttp://www.blogger.com/profile/07836706907685752267noreply@blogger.comtag:blogger.com,1999:blog-1045445187620004007.post-85350080420463833672018-11-01T15:15:00.003-04:002018-12-12T15:57:06.350-05:00November 2018<div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px; text-transform: uppercase;">Corroboration of a Major Role for Herpes Simplex Virus Type 1 in Alzheimer’s Disease</span></span></h2>
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<i style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"><br /></i><i style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;"><b>Frontiers in Aging Neuroscience</b></i><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Abstract</b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><span style="font-size: 14.85px;"><br /></span></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Strong evidence has emerged recently for the concept that herpes simplex virus type 1 (HSV1) is a major risk for Alzheimer’s disease (AD). This concept proposes that latent HSV1 in brain of carriers of the type 4 allele of the apolipoprotein E gene (APOE-ε4) is reactivated intermittently by events such as immunosuppression, peripheral infection, and inflammation, the consequent damage accumulating, and culminating eventually in the development of AD. Population data to investigate this epidemiologically, e.g., to find if subjects treated with antivirals might be protected from developing dementia—are available in Taiwan, from the National Health Insurance Research Database, in which 99.9% of the population has been enrolled. This is being extensively mined for information on microbial infections and disease. Three publications have now appeared describing data on the development of senile dementia (SD), and the treatment of those with marked overt signs of disease caused by varicella zoster virus (VZV), or by HSV. The striking results show that the risk of SD is much greater in those who are HSV-seropositive than in seronegative subjects, and that antiviral treatment causes a dramatic decrease in number of subjects who later develop SD. It should be stressed that these results apply only to those with severe cases of HSV1 or VZV infection, but when considered with the over 150 publications that strongly support an HSV1 role in AD, they greatly justify usage of antiherpes antivirals to treat AD. Three other studies are described which directly relate to HSV1 and AD: they deal respectively with lysosomal changes in HSV1-infected cell cultures, with evidence for a role of human herpes virus type 6 and 7 (HHV6 and HHV7) in AD, and viral effects on host gene expression, and with the antiviral characteristics of beta amyloid (Aβ). Three indirectly relevant studies deal respectively with schizophrenia, relating to antiviral treatment to target HSV1, with the likelihood that HSV1 is a cause of fibromyalgia (FM), and with FM being associated with later development of SD. Studies on the link between epilepsy, AD and herpes simplex encephalitis (HSE) are described also, as are the possible roles of APOE-ε4, HHV6 and HSV1 in epilepsy.</span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"> </span></div>
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<b>Source:</b> <a href="https://www.frontiersin.org/articles/10.3389/fnagi.2018.00324/full" style="color: #6699cc;" target="_blank">https://www.frontiersin.org/</a></div>
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<span style="color: #333333;"><span style="line-height: 20.79px;"><i><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>PLOS Medicine</b></span></span></i></span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">• </span><span style="font-size: 14.85px;">Widespread use of organophosphate (OP) pesticides to control insects has resulted inubiquitous human exposures.<br />• High exposures to OP pesticides are responsible for poisonings and deaths, particularly in developing countries.<br />• Compelling evidence indicates that prenatal exposure at low levels is putting children atrisk for cognitive and behavioral deficits and for neurodevelopmental disorders.To protect children worldwide, we recommend the following:<br />• Governments phase out chlorpyrifos and other OP pesticides, monitor watersheds andother sources of human exposures, promote use of integrated pest management (IPM)through incentives and training in agroecology, and implement mandatory surveillanceof pesticide-related illness.<br />• Health professions implement curricula on the hazards from OP pesticides in nursingand medical schools and in continuing medical education courses and educate theirpatients and the public about these hazards.<br />• Agricultural entities accelerate the development of nontoxic approaches to pest controlthrough IPM and ensure the safety of workers through training and provision of protec-tive equipment when toxic chemicals are to be used.</span><span style="color: #444444;"><span style="font-size: 14.85px;"> </span></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"> </span></div>
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<b><br /></b><b>Source:</b> <a href="https://www.scribd.com/document/391463803/OP-Pesticide-Paper-PLOS-Medicine" style="color: #6699cc;" target="_blank">https://www.scribd.com/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The U.S. Food and Drug Administration today approved Cassipa (buprenorphine and naloxone) sublingual film (applied under the tongue) for the maintenance treatment of opioid dependence. This action provides a new dosage strength (16 milligrams/4 milligrams) of buprenorphine and naloxone sublingual film, which is also approved in both brand name and generic versions and in various strengths.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">“There’s an urgent need to ensure access to, and wider use and understanding of, medication-assisted treatment for opioid use disorder. The introduction of new treatment options has the potential to broaden access for patients. For example, the FDA recently described a streamlined approach to drug development for certain medication-assisted treatments that are based on buprenorphine. This streamlined approach can reduce drug development costs, so products may be offered at a lower price to patients and we can broaden access to treatment,” said FDA Commissioner Scott Gottlieb, M.D. “The FDA is committed to helping those with opioid use disorder transition to lives of sobriety. We’ve taken a number of steps to advance the development of new FDA-approved treatments for opioid dependence and encourage health care professionals to ensure patients are offered an adequate chance to benefit from these therapies. We’re also working to address the unfortunate stigma that’s sometimes associated with the use of opioid replacement therapy as one approach to the successful treatment of addiction. Despite what some may think, individuals who successfully transition onto medication-assisted treatment are not swapping one addiction for another. Opioid replacement therapy can be an important part of effective treatment. Opioid use disorder should be viewed similarly to any other chronic condition that is treated with medication.”</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Medication-assisted treatment (MAT) is a comprehensive approach that combines FDA-approved medications (currently methadone, buprenorphine, or naltrexone) with counseling and other behavioral therapies to treat patients with opioid use disorder (OUD). Regular adherence to MAT with buprenorphine reduces opioid withdrawal symptoms and the desire to use opioids, without causing the cycle of highs and lows associated with opioid misuse or abuse. At proper doses, buprenorphine also decreases the pleasurable effects of other opioids, making continued opioid abuse less attractive. According to the Substance Abuse and Mental Health Services Administration, patients receiving MAT for treatment of their OUD cut their risk of death from all causes in half.</span></span></div>
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<b>Read More:</b> <a href="https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm619864.htm" style="color: #6699cc;" target="_blank">https://www.fda.gov/</a></div>
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Determinants of suboptimal medication adherence in patients with a major depressive episode</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b><i>Abstract</i></b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i style="font-size: 14.85px;"><br />Background</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Major Depression (MD) is often a chronic condition requiring a long‐term pharmacologic treatment. Despite the efficacy of antidepressants, the medication adherence in those affected is usually very poor. In this scenario, further research concerning drivers of suboptimal adherence is needed. We aimed to explore medication adherence in patients with a MD episode, and to identify sociodemographic, clinical (psychiatric antecedents, comorbidities, medication, pain, and medication side effects), and psychosocial factors (negative life events, childhood trauma, and attitudes to medication) related to adherence status.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Method</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The Medication Adherence Rating Scale (MARS) was completed by 370 patients at hospital admission. Participants were divided into groups of optimal and suboptimal adherence based on the medication adherence behavior score (MARS's factor 1), and were compared with respect to the study variables.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Twenty‐nine percent of participants (n = 107) were found to be optimally adherents to their medication (score = 4/4). Compared to optimally adherents, suboptimally adherents (71%) presented a significantly higher depression severity, more psychiatric hospitalizations, suicidal ideation, physical pain, negative medication side effects, and antecedents of emotional maltreatment. Suboptimally adherents also had less favorable attitudes toward medication and were less in a relationship than optimally adherents. Multivariate analyses showed that depression severity, suicidal ideation, and physical pain increase the probability of belonging to the suboptimal adherent group.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusion</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">These results suggest a vicious circle in which more vulnerable patients are less adherent to medication, which could worsen the clinical picture maintaining, in turn, low adherence. More efforts are needed to develop interventions aiming to improve medication adherence in MD patients.</span><br />
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<b style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;">Source:</b><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"> </span><a href="https://onlinelibrary.wiley.com/doi/10.1002/da.22852" style="color: #6699cc; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;" target="_blank">https://onlinelibrary.wiley.com/</a></div>
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Anxiety as a Risk Factor for Cognitive Decline: A 12-Year Follow-Up Cohort Study</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b><i>The American Journal of Geriatric Psychiatry</i></b></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Abstract</b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i></span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">Anxiety might be a risk factor for cognitive decline, but previous studies had short follow-up or small sample sizes or studied general or single cognitive domain functioning.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">Anxiety symptoms were assessed with the Symptom Checklist-90 in 918 participants of the Maastricht Aging Study aged 50 years or older. Anxiety was analyzed both dichotomously (highest versus lower quartiles as a group) and continuously. Neuropsychological tests measured executive function, memory, speed of information processing, and verbal fluency. Linear mixed models were conducted with anxiety symptoms as predictor and change in cognitive scores as outcome. Differences of associations by age and gender were studied with three-way interactions.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">Higher anxiety symptoms were significantly associated with more decline in verbal memory in those aged 65 years and older (delayed recall: χ2 = 9.30, df = 2, p = 0.01; immediate recall: χ2 = 11.81, df = 2, p = 0.003). There were sex differences in executive function (χ2 = 6.63, df = 2, p = 0.036), fluency (χ2 = 6.89, df = 2, p = 0.032), and processing speed (χ2 = 8.83, df = 2, p = 0.012), with lower performance in women over time.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Conclusion</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">In participants without cognitive impairments at baseline, anxiety symptoms were associated with a decline in verbal memory in older adults and with poorer performance in nonamnestic domains in women. Adequate treatment of anxiety symptoms could have a beneficial influence on the risk of developing neurodegenerative diseases. Further research is needed to elucidate whether this association is causal.</span></span></div>
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<b>Source:</b> <a href="https://www.ajgponline.org/article/S1064-7481(18)30483-4/abstract" rel="" style="color: #6699cc;" target="_blank">https://www.ajgponline.org/</a></div>
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Mapping the Heterogeneous Phenotype of Schizophrenia and Bipolar Disorder Using Normative Models</h2>
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<i><b>JAMA Psychiatry</b></i></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Abstract</b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><span style="font-size: 14.85px;"><br /></span></span></span><span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Importance </i></span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">Schizophrenia and bipolar disorder are severe and complex brain disorders characterized by substantial clinical and biological heterogeneity. However, case-control studies often ignore such heterogeneity through their focus on the average patient, which may be the core reason for a lack of robust biomarkers indicative of an individual’s treatment response and outcome.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Objectives </i></span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">To investigate the degree to which case-control analyses disguise interindividual differences in brain structure among patients with schizophrenia and bipolar disorder and to map the brain alterations linked to these disorders at the level of individual patients.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants </i> </span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">This study used cross-sectional, T1-weighted magnetic resonance imaging data from participants recruited for the Thematically Organized Psychosis study from October 27, 2004, to October 17, 2012. Data were reanalyzed in 2017 and 2018. Patients were recruited from inpatient and outpatient clinics in the Oslo area of Norway, and healthy individuals from the same catchment area were drawn from the national population registry.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures </i> </span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">Interindividual differences in brain structure among patients with schizophrenia and bipolar disorder. Voxel-based morphometry maps were computed, which were used for normative modeling to map the range of interindividual differences in brain structure.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Results </i></span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">This study included 218 patients with schizophrenia spectrum disorders (mean [SD] age, 30 [9.3] years; 126 [57.8%] male), of whom 163 had schizophrenia (mean [SD] age, 31 [8.7] years; 105 [64.4%] male) and 190 had bipolar disorder (mean [SD] age, 34 [11.3] years; 79 [41.6%] male), and 256 healthy individuals (mean [SD] age, 34 [9.5] years; 140 [54.7%] male). At the level of the individual, deviations from the normative model were frequent in both disorders but highly heterogeneous. Overlap of more than 2% among patients was observed in only a few loci, primarily in frontal, temporal, and cerebellar regions. The proportion of alterations was associated with diagnosis and cognitive and clinical characteristics within clinical groups. Patients with schizophrenia, on average, had significantly reduced gray matter in frontal regions, cerebellum, and temporal cortex. In patients with bipolar disorder, mean deviations were primarily present in cerebellar regions.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance </i></span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">This study found that group-level differences disguised biological heterogeneity and interindividual differences among patients with the same diagnosis. This finding suggests that the idea of the average patient is a noninformative construct in psychiatry that falls apart when mapping abnormalities at the level of the individual patient. This study presents a workable route toward precision medicine in psychiatry.</span></span></div>
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<b>Source:</b> <a href="https://jamanetwork.com/journals/jamapsychiatry/article-abstract/2705762" rel="" style="color: #6699cc;" target="_blank">https://jamanetwork.com/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px; text-transform: uppercase;">DEVELOPMENT AND VALIDATION OF A NEW RATING SCALE FOR PERIMENOPAUSAL DEPRESSION—THE MENO-D</span></span></h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b><i>Translational Psychiatry</i></b></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The menopause transition is a time when women experience an increased risk for new onset depression, as well as relapse of depression. While there are overlapping symptoms between major depression and depression during menopause, differences suggest ‘perimenopausal depression’ may be a unique subtype of depression associated with characteristic symptoms. There is currently no validated scale designed to measure perimenopausal depression. The aim of the current study was to develop and validate the ‘Meno-D’, a self-reporting or clinician rated questionnaire, designed to rate the severity of symptoms of perimenopausal depression. The development phase of the Meno-D involved literature review, clinical observation, and focus groups. A 12-item questionnaire was developed and clinically reviewed for face validity for content. The Meno-D was administered to women experiencing symptoms of perimenopausal depression as part of a larger baseline assessment battery. Validation involved confirmatory factor analysis (CFA). The development of the Meno-D resulted in 12 items. A total of 93 participants with perimenopausal depression were involved in the baseline assessments, 82 completed the Meno-D. Factor analysis identified five sub-scales of the Meno-D “somatic; cognitive; self; sleep; sexual” with high-internal consistency; discriminant validity and a good construct and convergent validity. The Meno-D provides a unique tool for clinicians and researchers to measure the presence of perimenopausal depression.</span></span></div>
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<b>Source:</b> <a href="https://www.nature.com/articles/s41398-018-0172-0#Abs1" style="color: #6699cc;" target="_blank">https://www.nature.com/</a></div>
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VITAMIN D SUPPLEMENTATION MAY HELP EASE DEPRESSION</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Vitamin D supplementation may help reduce depressive symptoms, new results of an updated meta-analysis show.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">"People who were vitamin D deficient and depressed seemed to respond best to supplementation, but there was some evidence that supplementation improved depressive symptoms in people who had a normal level of vitamin D," Marissa Flaherty, MD, of the Department of Psychiatry, University of Maryland School of Medicine in Baltimore, told Medscape Medical News.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Globally, more than 300 million people suffer from depression. It's the number one cause of years lost to disability worldwide. In the United States, the overall prevalence of vitamin D deficiency hovers around 42%, with the highest rate seen in blacks.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">"In my third year of residency, I noticed that a lot of my depressed patients had very low vitamin D levels, and when I supplemented their vitamin D, their depressive symptoms, particularly their fatigue and energy levels, would improve," Flaherty said.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To investigate further, Flaherty and her colleagues conducted a systematic review and meta-analysis of five randomized controlled trials published from 2011 to 2016 that examined the effect of vitamin D supplementation (vs no supplementation) on depressive symptoms, as measured by the Beck Depression Inventory and Hamilton Depression Rating Scale.</span></span><br />
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<b style="font-size: 14.85px; line-height: 20.79px;">Read More:</b><span style="font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://www.medscape.com/viewarticle/896449" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://www.medscape.com/</a></div>
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<span style="color: #333333; font-family: "arial" , sans-serif;"><span style="font-size: 18px; line-height: 22px; text-transform: uppercase;">PRENATAL EXPOSURE TO ACETAMINOPHEN AND RISK FOR ATTENTION DEFICIT HYPERACTIVITY DISORDER AND AUTISTIC SPECTRUM DISORDER: A SYSTEMATIC REVIEW, META-ANALYSIS, AND META-REGRESSION ANALYSIS OF COHORT STUDIES</span></span></h2>
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<i><b><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Abstract</span></span></b></i><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">Acetaminophen is the analgesic and antipyretic most commonly used during pregnancy. Evidence of neurodisruptive properties is accumulating. Therefore, we sought to evaluate the risk for attention deficit hyperactivity disorder (ADHD) and autistic spectrum disorder (ASD) in the offspring of women exposed to acetaminophen during pregnancy. We searched MEDLINE, Embase, and Cochrane databases for relevant studies up to January 2017. Data were independently extracted and assessed by 2 researchers. Seven eligible retrospective cohorts included 132,738 mother-child pairs, with follow-up periods ranging from 3 to 11 years. The pooled risk ratio for ADHD was 1.34 (95% confidence interval (CI): 1.21, 1.47; I2 = 72%); for ASD, the risk ratio was 1.19 (95% CI: 1.14, 1.25; I2 = 14%), and for hyperactivity symptoms, it was 1.24 (95% CI: 1.04, 1.43; I2 = 93%). In meta-regression analysis, the association between exposure and ADHD increased with the child’s age upon follow-up (β = 0.03, 95% CI: 0.00, 0.07) and with the mean duration of exposure (β = 0.00, 95% CI: 0.00, 0.01). The available data is of observational nature only. Studies differed widely in exposure and outcome assessment. Acetaminophen use during pregnancy is associated with an increased risk for ADHD, ASD, and hyperactivity symptoms. These findings are concerning; however, results should be interpreted with caution given that the available evidence consists of observational studies and is susceptible to several potential sources of bias.</span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://academic.oup.com/aje/advance-article-abstract/doi/10.1093/aje/kwy086/4980325" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://academic.oup.com/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; text-transform: uppercase;">ESTIMATION OF LIFETIME RISKS OF ALZHEIMER'S DISEASE DEMENTIA USING BIOMARKERS FOR PRECLINICAL DISEASE</span></span></h2>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b>The Journal of the Alzheimer's Association</b></span></i></span><br />
<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b><br /></b></span></i></span><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b><br /></b></span></i></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"><i>Introduction</i></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Lifetime risks are the probabilities of progressing to Alzheimer's disease (AD) dementia during one's lifespan. Here, we report the first estimates of the lifetime and ten-year risks of AD dementia based on age, gender, and biomarker tests for preclinical disease.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We used a multistate model for the disease process together with US death rates.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Lifetime risks of AD dementia vary considerably by age, gender, and the preclinical or clinical disease state of the individual. For example, the lifetime risks for a female with only amyloidosis are 8.4% for a 90-year old and 29.3% for a 65-year old. Persons younger than 85 years with mild cognitive impairment, amyloidosis, and neurodegeneration have lifetime risks of AD dementia greater than 50%.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Discussion</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Most persons with preclinical AD will not develop AD dementia during their lifetimes. Lifetime risks help interpret the clinical significance of biomarker screening tests for AD</span></span><br />
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://www.alzheimersanddementia.com/article/S1552-5260(18)30098-0/fulltext" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://www.alzheimersanddementia.com/</a></div>
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<b><a href="http://journals.lww.com/psychopharmacology/Pages/currenttoc.aspx" style="color: #6699cc;" target="_blank">Journal of Clinical Psychopharmacology - December 2018 - Volume 38, Issue 6</a></b></div>
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<b><a href="https://www.nature.com/npp/volumes/43/issues/13" style="color: #6699cc;" target="_blank">Neuropsychopharmacology - Volume 43, Issue 13 (December 2018)</a></b></div>
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<b><a href="https://link.springer.com/journal/213/235/11/page/1" style="color: #6699cc;" target="_blank">Psychopharmacology - Volume 235, Issue 11, November 2018</a></b></div>
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<b><a href="http://jop.sagepub.com/content/current" style="color: #6699cc;" target="_blank">Journal of Psychopharmacology - November 2018; 32 (11)</a></b></div>
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<b><a href="http://ajp.psychiatryonline.org/toc/ajp/current" style="color: #6699cc;" target="_blank">The American Journal of Psychiatry - November 2018, Vol. 175, Issue 11</a></b></div>
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<b style="color: #6699cc;"><a href="http://archpsyc.jamanetwork.com/issue.aspx" style="color: #6699cc;" target="_blank">JAMA Psychiatry - November 2018, Vol. 75, No. 11</a></b></div>
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<b><a href="https://www.nature.com/neuro/volumes/21/issues/11" style="color: #6699cc;" target="_blank">Nature Neuroscience - November 2018, Vol 21, N° 11</a></b></div>
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<b><a href="https://www.nature.com/mp/volumes/23/issues/8" style="color: #6699cc;" target="_blank">Molecular Psychiatry - Volume 23, Issue 8, August 2018</a></b></div>
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<b style="background-color: white; color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"><a href="http://www.biologicalpsychiatryjournal.com/current" style="color: #6699cc;" target="_blank">Biological Psychiatry - Volume 84, Issue 11, December 2018</a></b><br />
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<b><a href="https://academic.oup.com/brain/issue/141/11" style="color: #6699cc;" target="_blank">Brain - Volume 141, Issue 11, November 2018</a></b></div>
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Eutimiahttp://www.blogger.com/profile/07836706907685752267noreply@blogger.comtag:blogger.com,1999:blog-1045445187620004007.post-63489814585900350342018-09-05T12:28:00.000-04:002018-11-01T15:11:05.957-04:00September 2018<div dir="ltr" style="text-align: left;" trbidi="on">
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<i style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"><br /></i><i style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;"><b>The Oficial Journal of the </b></i><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b><i>College of Family Physicians of Canada</i></b></span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Abstract</b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To develop an evidence-based guideline to help clinicians make decisions about when and how to safely taper and stop benzodiazepine receptor agonists (BZRAs); to focus on the highest level of evidence available and seek input from primary care professionals in the guideline development, review, and endorsement processes.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The overall team comprised 8 clinicians (1 family physician, 2 psychiatrists, 1 clinical psychologist, 1 clinical pharmacologist, 2 clinical pharmacists, and 1 geriatrician) and a methodologist; members disclosed conflicts of interest. For guideline development, a systematic process was used, including the GRADE (Grading of Recommendations Assessment, Development and Evaluation) approach. Evidence was generated by conducting a systematic review of BZRA deprescribing trials for insomnia, as well as performing a review of reviews of the harms of continued BZRA use and narrative syntheses of patient preferences and resource implications. This evidence and GRADE quality of evidence ratings were used to generate recommendations. The team refined guideline content and recommendations through consensus and synthesized clinical considerations to address front-line clinician questions. The draft guideline was reviewed by clinicians and stakeholders.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Recommendations</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We recommend that deprescribing (tapering slowly) of BZRAs be offered to elderly adults (≥ 65 years) who take BZRAs, regardless of duration of use, and suggest that deprescribing (tapering slowly) be offered to adults aged 18 to 64 who have used BZRAs for more than 4 weeks. These recommendations apply to patients who use BZRAs to treat insomnia on its own (primary insomnia) or comorbid insomnia where potential underlying comorbidities are effectively managed. This guideline does not apply to those with other sleep disorders or untreated anxiety, depression, or other physical or mental health conditions that might be causing or aggravating insomnia.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusion</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Benzodiazepine receptor agonists are associated with harms, and therapeutic effects might be short term. Tapering BZRAs improves cessation rates compared with usual care without serious harms. Patients might be more amenable to deprescribing conversations if they understand the rationale (potential for harm), are involved in developing the tapering plan, and are offered behavioural advice. This guideline provides recommendations for making decisions about when and how to reduce and stop BZRAs. Recommendations are meant to assist with, not dictate, decision making in conjunction with patients.</span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"> </span></div>
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<b>Read More:</b> <a href="http://www.cfp.ca/content/64/5/339" style="color: #6699cc;" target="_blank">http://www.cfp.ca/</a></div>
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<span style="color: #333333;"><span style="line-height: 20.79px;"><i><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>US FDA</b></span></span></i></span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The U.S. Food and Drug Administration approved Lucemyra (lofexidine hydrochloride) for the mitigation of withdrawal symptoms to facilitate abrupt discontinuation of opioids in adults. While Lucemyra may lessen the severity of withdrawal symptoms, it may not completely prevent them and is only approved for treatment for up to 14 days. Lucemyra is not a treatment for opioid use disorder (OUD), but can be used as part of a broader, long-term treatment plan for managing OUD.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">“As part of our commitment to support patients struggling with addiction, we’re dedicated to encouraging innovative approaches to help mitigate the physiological challenges presented when patients discontinue opioids,” said FDA Commissioner Scott Gottlieb, M.D. “We’re developing new guidance to help accelerate the development of better treatments, including those that help manage opioid withdrawal symptoms. We know that the physical symptoms of opioid withdrawal can be one of the biggest barriers for patients seeking help and ultimately overcoming addiction. The fear of experiencing withdrawal symptoms often prevents those suffering from opioid addiction from seeking help. And those who seek assistance may relapse due to continued withdrawal symptoms. The FDA will continue to encourage the innovation and development of therapies to help those suffering from opioid addiction transition to lives of sobriety, as well as address the unfortunate stigma that’s sometimes associated with the use of medication-assisted treatments.”</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Opioid withdrawal includes symptoms — such as anxiety, agitation, sleep problems, muscle aches, runny nose, sweating, nausea, vomiting, diarrhea and drug craving — that occur after stopping or reducing the use of opioids in anyone with physical dependence on opioids. Physical dependence to opioids is an expected physiological response to opioid use. These symptoms of opioid withdrawal occur both in patients who have been using opioids appropriately as prescribed and in patients with OUD.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">In patients using opioid analgesics appropriately as prescribed, opioid withdrawal is typically managed by slow taper of the medication, which is intended to avoid or lessen the effects of withdrawal while allowing the body to adapt to not having the opioid. In patients with OUD, withdrawal is typically managed by substitution of another opioid medicine, followed by gradual reduction or transition to maintenance therapy with FDA-approved medication-assisted treatment drugs such as methadone, buprenorphine or naltrexone; or by various medications aimed at specific symptoms, such as over-the-counter remedies for upset stomach or aches and pains. Other treatments may also be prescribed by a patient’s health care provider.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">“Today’s approval represents the first FDA-approved non-opioid treatment for the management of opioid withdrawal symptoms and provides a new option that allows providers to work with patients to select the treatment best suited to an individual’s needs,” said Sharon Hertz, M.D., director of the Division of Anesthesia, Analgesia and Addiction Products in the FDA’s Center for Drug Evaluation and Research.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Lucemyra is an oral, selective alpha 2-adrenergic receptor agonist that reduces the release of norepinephrine. The actions of norepinephrine in the autonomic nervous system are believed to play a role in many of the symptoms of opioid withdrawal. The safety and efficacy of Lucemyra was supported by two randomized, double-blind, placebo-controlled clinical trials of 866 adults meeting Diagnostic and Statistical Manual-IV criteria for opioid dependence who were physically dependent on opioids and undergoing abrupt opioid discontinuation. The studies evaluated benefit using the Short Opiate Withdrawal Scale of Gossop (SOWS-Gossop), which is a patient-reported outcome instrument that assesses opioid withdrawal symptoms. These symptoms include feeling sick, stomach cramps, muscle spasms/twitching, feeling of coldness, heart pounding, muscular tension, aches and pains, yawning, runny eyes and insomnia/problems sleeping.</span><span style="color: #444444;"><span style="font-size: 14.85px;"> </span></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"> </span></div>
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<b><br /></b><b>Read More:</b> <a href="https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm607884.htm" style="color: #6699cc;" target="_blank">https://www.fda.gov/</a></div>
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<i style="font-size: 14.85px; line-height: 20.79px;"><b>JAMA Psychiatry</b></i><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Importance </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Antipsychotic medications are commonly used to treat nonpsychotic disruptive behavioral disorders in youths.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To characterize the metabolic effects of first exposure to antipsychotics in youths using criterion standard assessments of body composition and insulin sensitivity.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">This randomized clinical trial recruited antipsychotic-naive youths aged 6 to 18 years in the St Louis, Missouri, metropolitan area who were diagnosed with 1 or more psychiatric disorders and clinically significant aggression and in whom antipsychotic treatment was considered. Participants were enrolled from June 12, 2006, through November 10, 2010. Enrolled participants were randomized (1:1:1) to 1 of 3 antipsychotics commonly used in children with disruptive behavioral disorders and evaluated for 12 weeks. Data were analyzed from January 17, 2011, through August 9, 2017.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Interventions</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Twelve weeks of treatment with oral aripiprazole (n = 49), olanzapine (n = 46), or risperidone (n = 49).</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Primary outcomes included percentage total body fat measured by dual-energy x-ray absorptiometry (DXA) and insulin sensitivity in muscle measured via hyperinsulinemic clamps with stable isotopically labeled tracers. Secondary outcomes included abdominal adiposity measured by magnetic resonance imaging (MRI) and adipose and hepatic tissue insulin sensitivity measured via clamps with tracers.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The intention-to-treat sample included 144 participants (98 males [68.1%]; mean [SD] age, 11.3 [2.8] years); 74 (51.4%) were African American, and 43 (29.9%) were overweight or obese at baseline. For the primary outcomes, from baseline to week 12, DXA percentage total body fat increased by 1.18% for risperidone, 4.12% for olanzapine, and 1.66% for aripiprazole and was significantly greater for olanzapine than risperidone or aripiprazole (time by treatment interaction P < .001). From baseline to week 12, insulin-stimulated change in glucose rate of disappearance increased by 2.30% for risperidone and decreased by 29.34% for olanzapine and 30.26% for aripiprazole, with no significant difference across medications (time by treatment interaction, P < .07). This primary measure of insulin sensitivity decreased significantly during 12 weeks in the pooled study sample (effect of time, F = 17.38; P < .001). For the secondary outcomes from baseline to week 12, MRI measured abdominal fat increased, with subcutaneous fat increase significantly greater for olanzapine than risperdone or aripiprazole (time by treatment, P = .003). Behavioral improvements occurred with all treatments.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Adverse changes in adiposity and insulin sensitivity were observed during 12 weeks of antipsychotic treatment in youths, with the greatest fat increases on olanzapine. Such changes, likely attributable to treatment, may be associated with risk for premature cardiometabolic morbidity and mortality. The results inform risk-benefit considerations for antipsychotic use in youths.</span></span></div>
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<b>Source:</b> <a href="https://jamanetwork.com/journals/jamapsychiatry/article-abstract/2683878" style="color: #6699cc;" target="_blank">https://jamanetwork.com/</a></div>
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GREATER DEPRESSIVE SYMPTOMS, COGNITION, AND MARKERS OF BRAIN AGING</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b><i>Abstract</i></b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b><i><br /></i></b></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We examined whether greater depressive symptoms were associated with domain-specific cognitive performance, change in cognition, and MRI markers of brain atrophy and subclinical cerebrovascular disease in a diverse sample of older adults from the Northern Manhattan Study.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Data were analyzed from the Northern Manhattan Study, a prospective cohort study of mostly Caribbean Hispanic, stroke-free, older adults. A total of 1,111 participants had baseline measures of depressive symptoms, measured as the Center of Epidemiological Studies–Depression Scale, MRI markers, and cognitive function. A Center of Epidemiological Studies–Depression score ≥16 was considered indicative of greater depressive symptoms. Multivariable linear and logistic regression models were used to examine the associations of interest.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results At baseline </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">22% of participants had greater depressive symptoms. Greater depressive symptoms were significantly associated with worse baseline episodic memory in models adjusted for sociodemographic, vascular risk factor, behavioral, and antidepressive medication variables (β [95% confidence interval] = −0.21 [−0.33 to −0.10], p = 0.0003). Greater depressive symptoms were also associated with smaller cerebral parenchymal fraction (β [95% confidence interval] = −0.56 [−1.05 to −0.07], p = 0.02) and increased odds of subclinical brain infarcts (odds ratio [95% confidence interval] = 1.55 [1.00–2.42], p = 0.05), after adjustment for sociodemographic, behavioral, and vascular risk factor variables. Greater depressive symptoms were not significantly associated with white matter hyperintensity volume, hippocampal volume, or change in cognition over an average of 5 years. Results were unchanged when stabilized inverse probability weights were applied to address selective attrition during the study period.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"><i>Conclusions </i></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">In this sample of mostly Caribbean Hispanic, stroke-free, older adults, greater depressive symptoms were associated with worse episodic memory, smaller cerebral volume, and silent infarcts.</span><br />
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<b style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;">Source:</b><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"> </span><a href="http://n.neurology.org/content/early/2018/05/09/WNL.0000000000005639.long" style="color: #6699cc; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;" target="_blank">http://n.neurology.org/</a></div>
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MULTISCALE ANALYSIS OF INDEPENDENT ALZHEIMER’S COHORTS FINDS DISRUPTION OF MOLECULAR, GENETIC, AND CLINICAL NETWORKS BY HUMAN HERPESVIRUS</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Investigators have long suspected that pathogenic microbes might contribute to the onset and progression of Alzheimer’s disease (AD) although definitive evidence has not been presented. Whether such findings represent a causal contribution, or reflect opportunistic passengers of neurodegeneration, is also difficult to resolve. We constructed multiscale networks of the late-onset AD-associated virome, integrating genomic, transcriptomic, proteomic, and histopathological data across four brain regions from human post-mortem tissue. We observed increased human herpesvirus 6A (HHV-6A) and human herpesvirus 7 (HHV-7) from subjects with AD compared with controls. These results were replicated in two additional, independent and geographically dispersed cohorts. We observed regulatory relationships linking viral abundance and modulators of APP metabolism, including induction of APBB2, APPBP2, BIN1, BACE1, CLU, PICALM, and PSEN1 by HHV-6A. This study elucidates networks linking molecular, clinical, and neuropathological features with viral activity and is consistent with viral activity constituting a general feature of AD.</span></span></div>
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<b>Source:</b> <a href="https://www.cell.com/neuron/fulltext/S0896-6273(18)30421-5" rel="" style="color: #6699cc;" target="_blank">https://www.cell.com/</a></div>
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3,4-METHYLENEDIOXYMETHAMPHETAMINE (MDMA)-ASSISTED PSYCHOTHERAPY FOR POST-TRAUMATIC STRESS DISORDER IN MILITARY VETERANS, FIREFIGHTERS, AND POLICE OFFICERS: A RANDOMISED, DOUBLE-BLIND, DOSE-RESPONSE, PHASE 2 CLINICAL TRIAL</h2>
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<i><b>The Lancet Psychiatry</b></i></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Summary</b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Background</b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Post-traumatic stress disorder (PTSD) is prevalent in military personnel and first responders, many of whom do not respond to currently available treatments. This study aimed to assess the efficacy and safety of 3,4-methylenedioxymethamphetamine (MDMA)-assisted psychotherapy for treating chronic PTSD in this population.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Methods</b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We did a randomised, double-blind, dose-response, phase 2 trial at an outpatient psychiatric clinic in the USA. We included service personnel who were 18 years or older, with chronic PTSD duration of 6 months or more, and who had a Clinician-Administered PTSD Scale (CAPS-IV) total score of 50 or greater. Using a web-based randomisation system, we randomly assigned participants (1:1:2) to three different dose groups of MDMA plus psychotherapy: 30 mg (active control), 75 mg, or 125 mg. We masked investigators, independent outcome raters, and participants until after the primary endpoint. MDMA was administered orally in two 8-h sessions with concomitant manualised psychotherapy. The primary outcome was mean change in CAPS-IV total score from baseline to 1 month after the second experimental session. Participants in the 30 mg and 75 mg groups subsequently underwent three 100–125 mg MDMA-assisted psychotherapy sessions in an open-label crossover, and all participants were assessed 12 months after the last MDMA session. Safety was monitored through adverse events, spontaneously reported expected reactions, vital signs, and suicidal ideation and behaviour. This study is registered with ClinicalTrials.gov, number NCT01211405.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b><br /></b></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Findings</b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Between Nov 10, 2010, and Jan 29, 2015, 26 veterans and first responders met eligibility criteria and were randomly assigned to receive 30 mg (n=7), 75 mg (n=7), or 125 mg (n=12) of MDMA plus psychotherapy. At the primary endpoint, the 75 mg and 125 mg groups had significantly greater decreases in PTSD symptom severity (mean change CAPS-IV total scores of −58·3 [SD 9·8] and −44·3 [28·7]; p=0·001) than the 30 mg group (−11·4 [12·7]). Compared with the 30 mg group, Cohen's d effect sizes were large: 2·8 (95% CI 1·19–4·39) for the 75 mg group and 1·1 (0·04–2·08) for the 125 mg group. In the open-label crossover with full-dose MDMA (100–125 mg), PTSD symptom severity significantly decreased in the group that had previously received 30 mg (p=0·01), whereas no further significant decreases were observed in the group that previously achieved a large response after 75 mg doses in the blinded segment (p=0·81). PTSD symptoms were significantly reduced at the 12-month follow-up compared with baseline after all groups had full-dose MDMA (mean CAPS-IV total score of 38·8 [SD 28·1] vs 87·1 [16·1]; p<0·0001). 85 adverse events were reported by 20 participants. Of these adverse events, four (5%) were serious: three were deemed unrelated and one possibly related to study drug treatment.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Interpretation</b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Active doses (75 mg and 125 mg) of MDMA with adjunctive psychotherapy in a controlled setting were effective and well tolerated in reducing PTSD symptoms in veterans and first responders.</span></span></div>
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<b>Source:</b> <a href="https://www.thelancet.com/journals/lanpsy/article/PIIS2215-0366(18)30135-4/fulltext" rel="" style="color: #6699cc;" target="_blank">https://www.thelancet.com/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b><i>Translational Psychiatry</i></b></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The menopause transition is a time when women experience an increased risk for new onset depression, as well as relapse of depression. While there are overlapping symptoms between major depression and depression during menopause, differences suggest ‘perimenopausal depression’ may be a unique subtype of depression associated with characteristic symptoms. There is currently no validated scale designed to measure perimenopausal depression. The aim of the current study was to develop and validate the ‘Meno-D’, a self-reporting or clinician rated questionnaire, designed to rate the severity of symptoms of perimenopausal depression. The development phase of the Meno-D involved literature review, clinical observation, and focus groups. A 12-item questionnaire was developed and clinically reviewed for face validity for content. The Meno-D was administered to women experiencing symptoms of perimenopausal depression as part of a larger baseline assessment battery. Validation involved confirmatory factor analysis (CFA). The development of the Meno-D resulted in 12 items. A total of 93 participants with perimenopausal depression were involved in the baseline assessments, 82 completed the Meno-D. Factor analysis identified five sub-scales of the Meno-D “somatic; cognitive; self; sleep; sexual” with high-internal consistency; discriminant validity and a good construct and convergent validity. The Meno-D provides a unique tool for clinicians and researchers to measure the presence of perimenopausal depression.</span></span></div>
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<b>Source:</b> <a href="https://www.nature.com/articles/s41398-018-0172-0#Abs1" style="color: #6699cc;" target="_blank">https://www.nature.com/</a></div>
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VITAMIN D SUPPLEMENTATION MAY HELP EASE DEPRESSION</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Vitamin D supplementation may help reduce depressive symptoms, new results of an updated meta-analysis show.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">"People who were vitamin D deficient and depressed seemed to respond best to supplementation, but there was some evidence that supplementation improved depressive symptoms in people who had a normal level of vitamin D," Marissa Flaherty, MD, of the Department of Psychiatry, University of Maryland School of Medicine in Baltimore, told Medscape Medical News.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Globally, more than 300 million people suffer from depression. It's the number one cause of years lost to disability worldwide. In the United States, the overall prevalence of vitamin D deficiency hovers around 42%, with the highest rate seen in blacks.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">"In my third year of residency, I noticed that a lot of my depressed patients had very low vitamin D levels, and when I supplemented their vitamin D, their depressive symptoms, particularly their fatigue and energy levels, would improve," Flaherty said.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To investigate further, Flaherty and her colleagues conducted a systematic review and meta-analysis of five randomized controlled trials published from 2011 to 2016 that examined the effect of vitamin D supplementation (vs no supplementation) on depressive symptoms, as measured by the Beck Depression Inventory and Hamilton Depression Rating Scale.</span></span><br />
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<b style="font-size: 14.85px; line-height: 20.79px;">Read More:</b><span style="font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://www.medscape.com/viewarticle/896449" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://www.medscape.com/</a></div>
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<span style="color: #333333; font-family: "arial" , sans-serif;"><span style="font-size: 18px; line-height: 22px; text-transform: uppercase;">PRENATAL EXPOSURE TO ACETAMINOPHEN AND RISK FOR ATTENTION DEFICIT HYPERACTIVITY DISORDER AND AUTISTIC SPECTRUM DISORDER: A SYSTEMATIC REVIEW, META-ANALYSIS, AND META-REGRESSION ANALYSIS OF COHORT STUDIES</span></span></h2>
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<i><b><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Abstract</span></span></b></i><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">Acetaminophen is the analgesic and antipyretic most commonly used during pregnancy. Evidence of neurodisruptive properties is accumulating. Therefore, we sought to evaluate the risk for attention deficit hyperactivity disorder (ADHD) and autistic spectrum disorder (ASD) in the offspring of women exposed to acetaminophen during pregnancy. We searched MEDLINE, Embase, and Cochrane databases for relevant studies up to January 2017. Data were independently extracted and assessed by 2 researchers. Seven eligible retrospective cohorts included 132,738 mother-child pairs, with follow-up periods ranging from 3 to 11 years. The pooled risk ratio for ADHD was 1.34 (95% confidence interval (CI): 1.21, 1.47; I2 = 72%); for ASD, the risk ratio was 1.19 (95% CI: 1.14, 1.25; I2 = 14%), and for hyperactivity symptoms, it was 1.24 (95% CI: 1.04, 1.43; I2 = 93%). In meta-regression analysis, the association between exposure and ADHD increased with the child’s age upon follow-up (β = 0.03, 95% CI: 0.00, 0.07) and with the mean duration of exposure (β = 0.00, 95% CI: 0.00, 0.01). The available data is of observational nature only. Studies differed widely in exposure and outcome assessment. Acetaminophen use during pregnancy is associated with an increased risk for ADHD, ASD, and hyperactivity symptoms. These findings are concerning; however, results should be interpreted with caution given that the available evidence consists of observational studies and is susceptible to several potential sources of bias.</span></div>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b>The Journal of the Alzheimer's Association</b></span></i></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"><i>Introduction</i></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Lifetime risks are the probabilities of progressing to Alzheimer's disease (AD) dementia during one's lifespan. Here, we report the first estimates of the lifetime and ten-year risks of AD dementia based on age, gender, and biomarker tests for preclinical disease.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We used a multistate model for the disease process together with US death rates.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Lifetime risks of AD dementia vary considerably by age, gender, and the preclinical or clinical disease state of the individual. For example, the lifetime risks for a female with only amyloidosis are 8.4% for a 90-year old and 29.3% for a 65-year old. Persons younger than 85 years with mild cognitive impairment, amyloidosis, and neurodegeneration have lifetime risks of AD dementia greater than 50%.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Discussion</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Most persons with preclinical AD will not develop AD dementia during their lifetimes. Lifetime risks help interpret the clinical significance of biomarker screening tests for AD</span></span><br />
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://www.alzheimersanddementia.com/article/S1552-5260(18)30098-0/fulltext" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://www.alzheimersanddementia.com/</a></div>
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<b><a href="http://journals.lww.com/psychopharmacology/Pages/currenttoc.aspx" style="color: #6699cc;" target="_blank">Journal of Clinical Psychopharmacology - August 2018 - Volume 38, Issue 4</a></b></div>
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<b><a href="https://www.nature.com/npp/volumes/43/issues/8" style="color: #6699cc;" target="_blank">Neuropsychopharmacology - Volume 43, Issue 8 (July 2018)</a></b></div>
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<b><a href="https://link.springer.com/journal/213/235/7/page/1" style="color: #6699cc;" target="_blank">Psychopharmacology - Volume 235, Issue 7, July 2018</a></b></div>
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<b><a href="http://jop.sagepub.com/content/current" style="color: #6699cc;" target="_blank">Journal of Psychopharmacology - June 2018; 32 (6)</a></b></div>
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<b><a href="http://ajp.psychiatryonline.org/toc/ajp/current" style="color: #6699cc;" target="_blank">The American Journal of Psychiatry - July 2018, Vol. 175, Issue 7</a></b></div>
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<b style="color: #6699cc;"><a href="http://archpsyc.jamanetwork.com/issue.aspx" style="color: #6699cc;" target="_blank">JAMA Psychiatry - July 2018, Vol. 75, No. 7</a></b></div>
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<b><a href="https://www.nature.com/neuro/volumes/21/issues/6" style="color: #6699cc;" target="_blank">Nature Neuroscience - June 2018, Vol 21, N° 6</a></b></div>
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<b><a href="https://www.nature.com/mp/volumes/23/issues/6" style="color: #6699cc;" target="_blank">Molecular Psychiatry - Volume 23, Issue 6, June 2018</a></b></div>
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<b style="background-color: white; color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"><a href="http://www.biologicalpsychiatryjournal.com/current" style="color: #6699cc;" target="_blank">Biological Psychiatry - Volume 84, Issue 2, July 2018</a></b><br />
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<b><a href="https://academic.oup.com/brain/issue/141/7?browseBy=volume" style="color: #6699cc;" target="_blank">Brain - Volume 141, Issue 7, July 2018</a></b></div>
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Eutimiahttp://www.blogger.com/profile/07836706907685752267noreply@blogger.comtag:blogger.com,1999:blog-1045445187620004007.post-84267222716696980732018-07-03T13:55:00.002-04:002018-07-04T18:02:20.483-04:00July 2018<div dir="ltr" style="text-align: left;" trbidi="on">
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<i style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"><br /></i><i style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;"><b>The Oficial Journal of the </b></i><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b><i>College of Family Physicians of Canada</i></b></span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Abstract</b></span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To develop an evidence-based guideline to help clinicians make decisions about when and how to safely taper and stop benzodiazepine receptor agonists (BZRAs); to focus on the highest level of evidence available and seek input from primary care professionals in the guideline development, review, and endorsement processes.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The overall team comprised 8 clinicians (1 family physician, 2 psychiatrists, 1 clinical psychologist, 1 clinical pharmacologist, 2 clinical pharmacists, and 1 geriatrician) and a methodologist; members disclosed conflicts of interest. For guideline development, a systematic process was used, including the GRADE (Grading of Recommendations Assessment, Development and Evaluation) approach. Evidence was generated by conducting a systematic review of BZRA deprescribing trials for insomnia, as well as performing a review of reviews of the harms of continued BZRA use and narrative syntheses of patient preferences and resource implications. This evidence and GRADE quality of evidence ratings were used to generate recommendations. The team refined guideline content and recommendations through consensus and synthesized clinical considerations to address front-line clinician questions. The draft guideline was reviewed by clinicians and stakeholders.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Recommendations</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We recommend that deprescribing (tapering slowly) of BZRAs be offered to elderly adults (≥ 65 years) who take BZRAs, regardless of duration of use, and suggest that deprescribing (tapering slowly) be offered to adults aged 18 to 64 who have used BZRAs for more than 4 weeks. These recommendations apply to patients who use BZRAs to treat insomnia on its own (primary insomnia) or comorbid insomnia where potential underlying comorbidities are effectively managed. This guideline does not apply to those with other sleep disorders or untreated anxiety, depression, or other physical or mental health conditions that might be causing or aggravating insomnia.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusion</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Benzodiazepine receptor agonists are associated with harms, and therapeutic effects might be short term. Tapering BZRAs improves cessation rates compared with usual care without serious harms. Patients might be more amenable to deprescribing conversations if they understand the rationale (potential for harm), are involved in developing the tapering plan, and are offered behavioural advice. This guideline provides recommendations for making decisions about when and how to reduce and stop BZRAs. Recommendations are meant to assist with, not dictate, decision making in conjunction with patients.</span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"> </span></div>
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<b>Read More:</b> <a href="http://www.cfp.ca/content/64/5/339" style="color: #6699cc;" target="_blank">http://www.cfp.ca/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The U.S. Food and Drug Administration approved Lucemyra (lofexidine hydrochloride) for the mitigation of withdrawal symptoms to facilitate abrupt discontinuation of opioids in adults. While Lucemyra may lessen the severity of withdrawal symptoms, it may not completely prevent them and is only approved for treatment for up to 14 days. Lucemyra is not a treatment for opioid use disorder (OUD), but can be used as part of a broader, long-term treatment plan for managing OUD.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">“As part of our commitment to support patients struggling with addiction, we’re dedicated to encouraging innovative approaches to help mitigate the physiological challenges presented when patients discontinue opioids,” said FDA Commissioner Scott Gottlieb, M.D. “We’re developing new guidance to help accelerate the development of better treatments, including those that help manage opioid withdrawal symptoms. We know that the physical symptoms of opioid withdrawal can be one of the biggest barriers for patients seeking help and ultimately overcoming addiction. The fear of experiencing withdrawal symptoms often prevents those suffering from opioid addiction from seeking help. And those who seek assistance may relapse due to continued withdrawal symptoms. The FDA will continue to encourage the innovation and development of therapies to help those suffering from opioid addiction transition to lives of sobriety, as well as address the unfortunate stigma that’s sometimes associated with the use of medication-assisted treatments.”</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Opioid withdrawal includes symptoms — such as anxiety, agitation, sleep problems, muscle aches, runny nose, sweating, nausea, vomiting, diarrhea and drug craving — that occur after stopping or reducing the use of opioids in anyone with physical dependence on opioids. Physical dependence to opioids is an expected physiological response to opioid use. These symptoms of opioid withdrawal occur both in patients who have been using opioids appropriately as prescribed and in patients with OUD.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">In patients using opioid analgesics appropriately as prescribed, opioid withdrawal is typically managed by slow taper of the medication, which is intended to avoid or lessen the effects of withdrawal while allowing the body to adapt to not having the opioid. In patients with OUD, withdrawal is typically managed by substitution of another opioid medicine, followed by gradual reduction or transition to maintenance therapy with FDA-approved medication-assisted treatment drugs such as methadone, buprenorphine or naltrexone; or by various medications aimed at specific symptoms, such as over-the-counter remedies for upset stomach or aches and pains. Other treatments may also be prescribed by a patient’s health care provider.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">“Today’s approval represents the first FDA-approved non-opioid treatment for the management of opioid withdrawal symptoms and provides a new option that allows providers to work with patients to select the treatment best suited to an individual’s needs,” said Sharon Hertz, M.D., director of the Division of Anesthesia, Analgesia and Addiction Products in the FDA’s Center for Drug Evaluation and Research.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Lucemyra is an oral, selective alpha 2-adrenergic receptor agonist that reduces the release of norepinephrine. The actions of norepinephrine in the autonomic nervous system are believed to play a role in many of the symptoms of opioid withdrawal. The safety and efficacy of Lucemyra was supported by two randomized, double-blind, placebo-controlled clinical trials of 866 adults meeting Diagnostic and Statistical Manual-IV criteria for opioid dependence who were physically dependent on opioids and undergoing abrupt opioid discontinuation. The studies evaluated benefit using the Short Opiate Withdrawal Scale of Gossop (SOWS-Gossop), which is a patient-reported outcome instrument that assesses opioid withdrawal symptoms. These symptoms include feeling sick, stomach cramps, muscle spasms/twitching, feeling of coldness, heart pounding, muscular tension, aches and pains, yawning, runny eyes and insomnia/problems sleeping.</span><span style="color: #444444;"><span style="font-size: 14.85px;"> </span></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"> </span></div>
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<b><br /></b><b>Read More:</b> <a href="https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm607884.htm" style="color: #6699cc;" target="_blank">https://www.fda.gov/</a></div>
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<i style="font-size: 14.85px; line-height: 20.79px;"><b>JAMA Psychiatry</b></i><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Importance </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Antipsychotic medications are commonly used to treat nonpsychotic disruptive behavioral disorders in youths.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To characterize the metabolic effects of first exposure to antipsychotics in youths using criterion standard assessments of body composition and insulin sensitivity.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">This randomized clinical trial recruited antipsychotic-naive youths aged 6 to 18 years in the St Louis, Missouri, metropolitan area who were diagnosed with 1 or more psychiatric disorders and clinically significant aggression and in whom antipsychotic treatment was considered. Participants were enrolled from June 12, 2006, through November 10, 2010. Enrolled participants were randomized (1:1:1) to 1 of 3 antipsychotics commonly used in children with disruptive behavioral disorders and evaluated for 12 weeks. Data were analyzed from January 17, 2011, through August 9, 2017.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Interventions</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Twelve weeks of treatment with oral aripiprazole (n = 49), olanzapine (n = 46), or risperidone (n = 49).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Primary outcomes included percentage total body fat measured by dual-energy x-ray absorptiometry (DXA) and insulin sensitivity in muscle measured via hyperinsulinemic clamps with stable isotopically labeled tracers. Secondary outcomes included abdominal adiposity measured by magnetic resonance imaging (MRI) and adipose and hepatic tissue insulin sensitivity measured via clamps with tracers.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The intention-to-treat sample included 144 participants (98 males [68.1%]; mean [SD] age, 11.3 [2.8] years); 74 (51.4%) were African American, and 43 (29.9%) were overweight or obese at baseline. For the primary outcomes, from baseline to week 12, DXA percentage total body fat increased by 1.18% for risperidone, 4.12% for olanzapine, and 1.66% for aripiprazole and was significantly greater for olanzapine than risperidone or aripiprazole (time by treatment interaction P < .001). From baseline to week 12, insulin-stimulated change in glucose rate of disappearance increased by 2.30% for risperidone and decreased by 29.34% for olanzapine and 30.26% for aripiprazole, with no significant difference across medications (time by treatment interaction, P < .07). This primary measure of insulin sensitivity decreased significantly during 12 weeks in the pooled study sample (effect of time, F = 17.38; P < .001). For the secondary outcomes from baseline to week 12, MRI measured abdominal fat increased, with subcutaneous fat increase significantly greater for olanzapine than risperdone or aripiprazole (time by treatment, P = .003). Behavioral improvements occurred with all treatments.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Adverse changes in adiposity and insulin sensitivity were observed during 12 weeks of antipsychotic treatment in youths, with the greatest fat increases on olanzapine. Such changes, likely attributable to treatment, may be associated with risk for premature cardiometabolic morbidity and mortality. The results inform risk-benefit considerations for antipsychotic use in youths.</span></span></div>
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<b>Source:</b> <a href="https://jamanetwork.com/journals/jamapsychiatry/article-abstract/2683878" style="color: #6699cc;" target="_blank">https://jamanetwork.com/</a></div>
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Greater depressive symptoms, cognition, and markers of brain aging</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b><i>Abstract</i></b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b><i><br /></i></b></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We examined whether greater depressive symptoms were associated with domain-specific cognitive performance, change in cognition, and MRI markers of brain atrophy and subclinical cerebrovascular disease in a diverse sample of older adults from the Northern Manhattan Study.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Data were analyzed from the Northern Manhattan Study, a prospective cohort study of mostly Caribbean Hispanic, stroke-free, older adults. A total of 1,111 participants had baseline measures of depressive symptoms, measured as the Center of Epidemiological Studies–Depression Scale, MRI markers, and cognitive function. A Center of Epidemiological Studies–Depression score ≥16 was considered indicative of greater depressive symptoms. Multivariable linear and logistic regression models were used to examine the associations of interest.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results At baseline </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">22% of participants had greater depressive symptoms. Greater depressive symptoms were significantly associated with worse baseline episodic memory in models adjusted for sociodemographic, vascular risk factor, behavioral, and antidepressive medication variables (β [95% confidence interval] = −0.21 [−0.33 to −0.10], p = 0.0003). Greater depressive symptoms were also associated with smaller cerebral parenchymal fraction (β [95% confidence interval] = −0.56 [−1.05 to −0.07], p = 0.02) and increased odds of subclinical brain infarcts (odds ratio [95% confidence interval] = 1.55 [1.00–2.42], p = 0.05), after adjustment for sociodemographic, behavioral, and vascular risk factor variables. Greater depressive symptoms were not significantly associated with white matter hyperintensity volume, hippocampal volume, or change in cognition over an average of 5 years. Results were unchanged when stabilized inverse probability weights were applied to address selective attrition during the study period.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"><i>Conclusions </i></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">In this sample of mostly Caribbean Hispanic, stroke-free, older adults, greater depressive symptoms were associated with worse episodic memory, smaller cerebral volume, and silent infarcts.</span><br />
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<b style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;">Source:</b><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"> </span><a href="http://n.neurology.org/content/early/2018/05/09/WNL.0000000000005639.long" style="color: #6699cc; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;" target="_blank">http://n.neurology.org/</a></div>
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Multiscale Analysis of Independent Alzheimer’s Cohorts Finds Disruption of Molecular, Genetic, and Clinical Networks by Human Herpesvirus</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Summary</b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Investigators have long suspected that pathogenic microbes might contribute to the onset and progression of Alzheimer’s disease (AD) although definitive evidence has not been presented. Whether such findings represent a causal contribution, or reflect opportunistic passengers of neurodegeneration, is also difficult to resolve. We constructed multiscale networks of the late-onset AD-associated virome, integrating genomic, transcriptomic, proteomic, and histopathological data across four brain regions from human post-mortem tissue. We observed increased human herpesvirus 6A (HHV-6A) and human herpesvirus 7 (HHV-7) from subjects with AD compared with controls. These results were replicated in two additional, independent and geographically dispersed cohorts. We observed regulatory relationships linking viral abundance and modulators of APP metabolism, including induction of APBB2, APPBP2, BIN1, BACE1, CLU, PICALM, and PSEN1 by HHV-6A. This study elucidates networks linking molecular, clinical, and neuropathological features with viral activity and is consistent with viral activity constituting a general feature of AD.</span></span></div>
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<b>Source:</b> <a href="https://www.cell.com/neuron/fulltext/S0896-6273(18)30421-5" rel="" style="color: #6699cc;" target="_blank">https://www.cell.com/</a></div>
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3,4-methylenedioxymethamphetamine (MDMA)-assisted psychotherapy for post-traumatic stress disorder in military veterans, firefighters, and police officers: a randomised, double-blind, dose-response, phase 2 clinical trial</h2>
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<i><b>The Lancet Psychiatry</b></i></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Summary</b></span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Background</b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Post-traumatic stress disorder (PTSD) is prevalent in military personnel and first responders, many of whom do not respond to currently available treatments. This study aimed to assess the efficacy and safety of 3,4-methylenedioxymethamphetamine (MDMA)-assisted psychotherapy for treating chronic PTSD in this population.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Methods</b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We did a randomised, double-blind, dose-response, phase 2 trial at an outpatient psychiatric clinic in the USA. We included service personnel who were 18 years or older, with chronic PTSD duration of 6 months or more, and who had a Clinician-Administered PTSD Scale (CAPS-IV) total score of 50 or greater. Using a web-based randomisation system, we randomly assigned participants (1:1:2) to three different dose groups of MDMA plus psychotherapy: 30 mg (active control), 75 mg, or 125 mg. We masked investigators, independent outcome raters, and participants until after the primary endpoint. MDMA was administered orally in two 8-h sessions with concomitant manualised psychotherapy. The primary outcome was mean change in CAPS-IV total score from baseline to 1 month after the second experimental session. Participants in the 30 mg and 75 mg groups subsequently underwent three 100–125 mg MDMA-assisted psychotherapy sessions in an open-label crossover, and all participants were assessed 12 months after the last MDMA session. Safety was monitored through adverse events, spontaneously reported expected reactions, vital signs, and suicidal ideation and behaviour. This study is registered with ClinicalTrials.gov, number NCT01211405.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Findings</b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Between Nov 10, 2010, and Jan 29, 2015, 26 veterans and first responders met eligibility criteria and were randomly assigned to receive 30 mg (n=7), 75 mg (n=7), or 125 mg (n=12) of MDMA plus psychotherapy. At the primary endpoint, the 75 mg and 125 mg groups had significantly greater decreases in PTSD symptom severity (mean change CAPS-IV total scores of −58·3 [SD 9·8] and −44·3 [28·7]; p=0·001) than the 30 mg group (−11·4 [12·7]). Compared with the 30 mg group, Cohen's d effect sizes were large: 2·8 (95% CI 1·19–4·39) for the 75 mg group and 1·1 (0·04–2·08) for the 125 mg group. In the open-label crossover with full-dose MDMA (100–125 mg), PTSD symptom severity significantly decreased in the group that had previously received 30 mg (p=0·01), whereas no further significant decreases were observed in the group that previously achieved a large response after 75 mg doses in the blinded segment (p=0·81). PTSD symptoms were significantly reduced at the 12-month follow-up compared with baseline after all groups had full-dose MDMA (mean CAPS-IV total score of 38·8 [SD 28·1] vs 87·1 [16·1]; p<0·0001). 85 adverse events were reported by 20 participants. Of these adverse events, four (5%) were serious: three were deemed unrelated and one possibly related to study drug treatment.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>Interpretation</b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Active doses (75 mg and 125 mg) of MDMA with adjunctive psychotherapy in a controlled setting were effective and well tolerated in reducing PTSD symptoms in veterans and first responders.</span></span></div>
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<b>Source:</b> <a href="https://www.thelancet.com/journals/lanpsy/article/PIIS2215-0366(18)30135-4/fulltext" rel="" style="color: #6699cc;" target="_blank">https://www.thelancet.com/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b><i>Translational Psychiatry</i></b></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The menopause transition is a time when women experience an increased risk for new onset depression, as well as relapse of depression. While there are overlapping symptoms between major depression and depression during menopause, differences suggest ‘perimenopausal depression’ may be a unique subtype of depression associated with characteristic symptoms. There is currently no validated scale designed to measure perimenopausal depression. The aim of the current study was to develop and validate the ‘Meno-D’, a self-reporting or clinician rated questionnaire, designed to rate the severity of symptoms of perimenopausal depression. The development phase of the Meno-D involved literature review, clinical observation, and focus groups. A 12-item questionnaire was developed and clinically reviewed for face validity for content. The Meno-D was administered to women experiencing symptoms of perimenopausal depression as part of a larger baseline assessment battery. Validation involved confirmatory factor analysis (CFA). The development of the Meno-D resulted in 12 items. A total of 93 participants with perimenopausal depression were involved in the baseline assessments, 82 completed the Meno-D. Factor analysis identified five sub-scales of the Meno-D “somatic; cognitive; self; sleep; sexual” with high-internal consistency; discriminant validity and a good construct and convergent validity. The Meno-D provides a unique tool for clinicians and researchers to measure the presence of perimenopausal depression.</span></span></div>
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<b>Source:</b> <a href="https://www.nature.com/articles/s41398-018-0172-0#Abs1" style="color: #6699cc;" target="_blank">https://www.nature.com/</a></div>
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Vitamin D Supplementation May Help Ease Depression</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Vitamin D supplementation may help reduce depressive symptoms, new results of an updated meta-analysis show.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">"People who were vitamin D deficient and depressed seemed to respond best to supplementation, but there was some evidence that supplementation improved depressive symptoms in people who had a normal level of vitamin D," Marissa Flaherty, MD, of the Department of Psychiatry, University of Maryland School of Medicine in Baltimore, told Medscape Medical News.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Globally, more than 300 million people suffer from depression. It's the number one cause of years lost to disability worldwide. In the United States, the overall prevalence of vitamin D deficiency hovers around 42%, with the highest rate seen in blacks.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">"In my third year of residency, I noticed that a lot of my depressed patients had very low vitamin D levels, and when I supplemented their vitamin D, their depressive symptoms, particularly their fatigue and energy levels, would improve," Flaherty said.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To investigate further, Flaherty and her colleagues conducted a systematic review and meta-analysis of five randomized controlled trials published from 2011 to 2016 that examined the effect of vitamin D supplementation (vs no supplementation) on depressive symptoms, as measured by the Beck Depression Inventory and Hamilton Depression Rating Scale.</span></span><br />
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<b style="font-size: 14.85px; line-height: 20.79px;">Read More:</b><span style="font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://www.medscape.com/viewarticle/896449" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://www.medscape.com/</a></div>
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<span style="color: #333333; font-family: "arial" , sans-serif;"><span style="font-size: 18px; line-height: 22px; text-transform: uppercase;">Prenatal Exposure to Acetaminophen and Risk for Attention Deficit Hyperactivity Disorder and Autistic Spectrum Disorder: A Systematic Review, Meta-Analysis, and Meta-Regression Analysis of Cohort Studies</span></span></h2>
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<i><b><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Abstract</span></span></b></i><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">Acetaminophen is the analgesic and antipyretic most commonly used during pregnancy. Evidence of neurodisruptive properties is accumulating. Therefore, we sought to evaluate the risk for attention deficit hyperactivity disorder (ADHD) and autistic spectrum disorder (ASD) in the offspring of women exposed to acetaminophen during pregnancy. We searched MEDLINE, Embase, and Cochrane databases for relevant studies up to January 2017. Data were independently extracted and assessed by 2 researchers. Seven eligible retrospective cohorts included 132,738 mother-child pairs, with follow-up periods ranging from 3 to 11 years. The pooled risk ratio for ADHD was 1.34 (95% confidence interval (CI): 1.21, 1.47; I2 = 72%); for ASD, the risk ratio was 1.19 (95% CI: 1.14, 1.25; I2 = 14%), and for hyperactivity symptoms, it was 1.24 (95% CI: 1.04, 1.43; I2 = 93%). In meta-regression analysis, the association between exposure and ADHD increased with the child’s age upon follow-up (β = 0.03, 95% CI: 0.00, 0.07) and with the mean duration of exposure (β = 0.00, 95% CI: 0.00, 0.01). The available data is of observational nature only. Studies differed widely in exposure and outcome assessment. Acetaminophen use during pregnancy is associated with an increased risk for ADHD, ASD, and hyperactivity symptoms. These findings are concerning; however, results should be interpreted with caution given that the available evidence consists of observational studies and is susceptible to several potential sources of bias.</span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://academic.oup.com/aje/advance-article-abstract/doi/10.1093/aje/kwy086/4980325" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://academic.oup.com/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; text-transform: uppercase;">Estimation of lifetime risks of Alzheimer's disease dementia using biomarkers for preclinical disease</span></span></h2>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b>The Journal of the Alzheimer's Association</b></span></i></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;"><i>Introduction</i></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">Lifetime risks are the probabilities of progressing to Alzheimer's disease (AD) dementia during one's lifespan. Here, we report the first estimates of the lifetime and ten-year risks of AD dementia based on age, gender, and biomarker tests for preclinical disease.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">We used a multistate model for the disease process together with US death rates.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">Lifetime risks of AD dementia vary considerably by age, gender, and the preclinical or clinical disease state of the individual. For example, the lifetime risks for a female with only amyloidosis are 8.4% for a 90-year old and 29.3% for a 65-year old. Persons younger than 85 years with mild cognitive impairment, amyloidosis, and neurodegeneration have lifetime risks of AD dementia greater than 50%.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Discussion</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Most persons with preclinical AD will not develop AD dementia during their lifetimes. Lifetime risks help interpret the clinical significance of biomarker screening tests for AD</span></span><br />
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://www.alzheimersanddementia.com/article/S1552-5260(18)30098-0/fulltext" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://www.alzheimersanddementia.com/</a></div>
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<b><a href="http://journals.lww.com/psychopharmacology/Pages/currenttoc.aspx" style="color: #6699cc;" target="_blank">Journal of Clinical Psychopharmacology - August 2018 - Volume 38, Issue 4</a></b></div>
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<b><a href="https://link.springer.com/journal/213/235/7/page/1" style="color: #6699cc;" target="_blank">Psychopharmacology - Volume 235, Issue 7, July 2018</a></b></div>
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<b><a href="http://jop.sagepub.com/content/current" style="color: #6699cc;" target="_blank">Journal of Psychopharmacology - June 2018; 32 (6)</a></b></div>
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<b><a href="http://ajp.psychiatryonline.org/toc/ajp/current" style="color: #6699cc;" target="_blank">The American Journal of Psychiatry - July 2018, Vol. 175, Issue 7</a></b></div>
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<b style="color: #6699cc;"><a href="http://archpsyc.jamanetwork.com/issue.aspx" style="color: #6699cc;" target="_blank">JAMA Psychiatry - July 2018, Vol. 75, No. 7</a></b></div>
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<b><a href="https://www.nature.com/mp/volumes/23/issues/6" style="color: #6699cc;" target="_blank">Molecular Psychiatry - Volume 23, Issue 6, June 2018</a></b></div>
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<b style="background-color: white; color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"><a href="http://www.biologicalpsychiatryjournal.com/current" style="color: #6699cc;" target="_blank">Biological Psychiatry - Volume 84, Issue 2, July 2018</a></b><br />
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<b><a href="https://academic.oup.com/brain/issue/141/7?browseBy=volume" style="color: #6699cc;" target="_blank">Brain - Volume 141, Issue 7, July 2018</a></b></div>
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Eutimiahttp://www.blogger.com/profile/07836706907685752267noreply@blogger.comtag:blogger.com,1999:blog-1045445187620004007.post-18229947636026030512018-05-05T17:01:00.002-04:002018-05-07T16:37:12.259-04:00May 2018<div dir="ltr" style="text-align: left;" trbidi="on">
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<i style="font-size: 14.85px; line-height: 20.79px;"><br /></i><i><b>The American Journal of Psychiatry</b></i><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">People who eat vegetables, fruit and whole grains may have lower rates of depression over time, according to a preliminary study released today that will be presented at the American Academy of Neurology’s 70th Annual Meeting in Los Angeles, April 21 to 27, 2018.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The study found that people whose diets adhered more closely to the Dietary Approaches to Stop Hypertension (DASH) diet were less likely to develop depression than people who did not closely follow the diet. In addition to fruit and vegetables, the DASH diet recommends fat-free or low-fat dairy products and limits foods that are high in saturated fats and sugar. Studies have shown health benefits such as lowering high blood pressure and bad cholesterol (LDL), along with lowering body weight.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">“Depression is common in older adults and more frequent in people with memory problems, vascular risk factors such as high blood pressure or high cholesterol, or people who have had a stroke,” said study author Laurel Cherian, MD, of Rush University Medical Center in Chicago and a member of the American Academy of Neurology. “Making a lifestyle change such as changing your diet is often preferred over taking medications, so we wanted to see if diet could be an effective way to reduce the risk of depression.”</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">For the study, 964 participants with an average age of 81 were evaluated yearly for an average of six-and-a-half years. They were monitored for symptoms of depression such as being bothered by things that usually didn’t affect them and feeling hopeless about the future. They also filled out questionnaires about how often they ate various foods, and the researchers looked at how closely the participants’ diets followed diets such as the DASH diet, Mediterranean diet and the traditional Western diet.</span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"> </span></div>
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<b>Read more:</b> <a href="https://ajp.psychiatryonline.org/doi/abs/10.1176/appi.ajp.2018.17070836" style="color: #6699cc;" target="_blank">https://ajp.psychiatryonline.org/</a></div>
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<span style="color: #333333;"><span style="line-height: 20.79px;"><i><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b>European Journal of Clinical Pharmacology</b></span></span></i></span></span><br />
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b><br /></b></i></span></span><span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b>Abstract</b></i></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Purpose</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To investigate associations between antidepressant use patterns and risk of fatal and non-fatal suicidal behaviours in older adults who initiated antidepressant therapy.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Method</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">A national population-based cohort study conducted among Swedish residents aged ≥ 75 years who initiated antidepressant treatment. Patients who filled antidepressant prescriptions between January 1, 2007 and December 31, 2013 (N = 185,225) were followed until December 31, 2014. Sub-hazard ratios of suicides and suicide attempts associated with use patterns of antidepressants, adjusting for potential confounders such as serious depression were calculated using the Fine and Gray regression models.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">During follow-up, 295 suicides and 654 suicide attempts occurred. Adjusted sub-hazard ratios (aSHRs) were increased for both outcomes in those who switched to another antidepressant (aSHR for suicide 2.42, 95% confidence interval 1.65 to 3.55, and for attempt 1.76, 1.32 to 2.34). Elevated suicide risks were also observed in those who concomitantly filled anxiolytics (1.54, 1.20 to 1.96) and hypnotics (2.20, 1.69 to 2.85). Similar patterns were observed for the outcome suicide attempt. Decreased risk of attempt was observed among those with concomitant use of anti-dementia drugs (0.40, 0.27 to 0.59).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusion</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Switching antidepressants, as well as concomitant use of anxiolytics or hypnotics, may constitute markers of increased risk of suicidal behaviours in those who initiate antidepressant treatment in very late life. Future research should consider indication biases and the clinical characteristics of patients initiating antidepressant therapy.</span><span style="color: #444444;"><span style="font-size: 14.85px;"> </span></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"> </span></div>
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<b><br /></b><b>Source:</b> <a href="https://link.springer.com/article/10.1007/s00228-017-2360-x" style="color: #6699cc;" target="_blank">https://link.springer.com/</a></div>
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<i style="font-size: 14.85px; line-height: 20.79px;"><b>US FDA</b></i><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">ISSUE: The FDA is warning that the medicine Lamictal (lamotrigine) for seizures and bipolar disorder can cause a rare but very serious reaction that excessively activates the body’s infection-fighting immune system. This can cause severe inflammation throughout the body and lead to hospitalization and death, especially if the reaction is not diagnosed and treated quickly. As a result, we are requiring a new warning about this risk be added to the prescribing information in the lamotrigine drug labels.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">BACKGROUND: The immune system reaction, called hemophagocytic lymphohistiocytosis (HLH), causes an uncontrolled response by the immune system. HLH typically presents as a persistent fever, usually greater than 101°F, and it can lead to severe problems with blood cells and organs throughout the body such as the liver, kidneys, and lungs.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Lamotrigine is used alone or with other medicines to treat seizures in patients two years and older. It may also be used as maintenance treatment in patients with bipolar disorder to help delay the occurrence of mood episodes such as depression, mania, or hypomania. Stopping lamotrigine without first talking to a prescriber can lead to uncontrolled seizures, or new or worsening mental health problems. Lamotrigine has been approved and on the market for 24 years, and is available under the brand name Lamictal and as generics.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">RECOMMENDATION: Healthcare professionals should be aware that prompt recognition and early treatment is important for improving HLH outcomes and decreasing mortality. Diagnosis is often complicated because early signs and symptoms such as fever and rash are not specific. HLH may also be confused with other serious immune-related adverse reactions such as Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Evaluate patients who develop fever or rash promptly, and discontinue lamotrigine if HLH or another serious immune-related adverse reaction is suspected and an alternative etiology for the signs and symptoms cannot be established. Advise patients to seek immediate medical attention if they experience symptoms of HLH during lamotrigine treatment. A diagnosis of HLH can be established if a patient has at least five of the following eight signs or symptoms:</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">- fever and rash</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">- enlarged spleen</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">- cytopenias</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">- elevated levels of triglycerides or low blood levels of fibrinogen</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">- high levels of blood ferritin</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">- hemophagocytosis identified through bone marrow, spleen, or lymph node biopsy</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">- decreased or absent Natural Killer (NK) Cell activity</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">- elevated blood levels of CD25 showing prolonged immune cell activation</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Patients or their caregivers should contact their health care professionals right away if they experience any symptom of HLH while taking lamotrigine. HLH can occur within days to weeks after starting treatment. A physical examination and specific laboratory blood tests and other evaluations are used to diagnose HLH. Signs and symptoms of HLH include but are not limited to:</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">- fever</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">- enlarged liver; symptoms may include pain, tenderness, or unusual swelling over the liver area in the upper right belly</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">- swollen lymph nodes</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">- skin rashes</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">- yellow skin or eyes</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">- unusual bleeding</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">- nervous system problems, including seizures, trouble walking, difficulty seeing, or other visual disturbances</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Read the patient Medication Guide, which explains the benefits and risks of lamotrigine, every time you get a new prescription because the information may change. Do not stop taking lamotrigine without talking to your health care professional first as doing so can cause serious problems.</span></span></div>
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<b>Source:</b> <a href="https://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm605628.htm" style="color: #6699cc;" target="_blank">https://www.fda.gov/Safety/MedWatch/</a></div>
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Altered Brain Developmental Trajectories in Adolescents After Initiating Drinking</h2>
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<span style="font-size: 14.85px; line-height: 20.79px;"><b><i>The American Journal of Psychiatry </i></b></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b><i>Abstract</i></b></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b><i><br /></i></b></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The authors sought evidence for altered adolescent brain growth trajectory associated with moderate and heavy alcohol use in a large national, multisite, prospective study of adolescents before and after initiation of appreciable alcohol use.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Method</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">This study examined 483 adolescents (ages 12–21) before initiation of drinking and 1 and 2 years later. At the 2-year assessment, 356 participants continued to meet the study’s no/low alcohol consumption entry criteria, 65 had initiated moderate drinking, and 62 had initiated heavy drinking. MRI was used to quantify regional cortical and white matter volumes. Percent change per year (slopes) in adolescents who continued to meet no/low criteria served as developmental control trajectories against which to compare those who initiated moderate or heavy drinking.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">In no/low drinkers, gray matter volume declined throughout adolescence and slowed in many regions in later adolescence. Complementing gray matter declines, white matter regions grew at faster rates at younger ages and slowed toward young adulthood. Youths who initiated heavy drinking exhibited an accelerated frontal cortical gray matter trajectory, divergent from the norm. Although significant effects on trajectories were not observed in moderate drinkers, their intermediate position between no/low and heavy drinkers suggests a dose effect. Neither marijuana co-use nor baseline volumes contributed significantly to the alcohol effect.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">Initiation of drinking during adolescence, with or without marijuana co-use, disordered normal brain growth trajectories. Factors possibly contributing to abnormal cortical volume trajectories include peak consumption in the past year and family history of alcoholism.</span><br />
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Alzheimer’s Disease Can Be Spared by Nonsteroidal Anti-Inflammatory Drugs</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Alzheimer’s disease (AD) is characterized by deposits of amyloid- protein (A) in brain which become foci of </span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">inflammation. Neurons are destroyed by this inflammatory process, leading to the cognitive deficits which define AD clinical </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">onset. Epidemiological studies indicate that nonsteroidal anti-inflammatory drugs (NSAIDs) can ameliorate this destructive </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">process if they are started well before clinical signs develop. Biomarker studies indicate that the disease process starts at </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">least a decade before cognitive deficits appear. This pre-clinical onset explains the NSAID effect. It also opens a window </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">of opportunity for preventive treatment that can be met with a simple diagnostic test. Salivary levels of A42 may fulfill </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">that need. They can be measured by a simple ELISA test we have developed using commercially available reagents. By this </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">ELISA test, normal controls, who are not at risk for AD, have levels of A42 close to 20 pg/ml. AD cases, as well as high </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">level controls, secrete levels in the range of 40–85 pg/ml. Widespread application of this test to detect high level controls, </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">followed by NSAID consumption, could substantially reduce the prevalence of AD.</span></div>
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<b>Source:</b> <a href="https://content.iospress.com/download/journal-of-alzheimers-disease/jad170706?id=journal-of-alzheimers-disease%2Fjad170706" rel="" style="color: #6699cc;" target="_blank">https://content.iospress.com/</a></div>
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Neural Markers of Resilience in Adolescent Females at Familial Risk for Major Depressive Disorder</h2>
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<i><b>JAMA Psychiatry</b></i></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">Mental illness affects one in six U.S. adults, but scientists' sense of the underlying biology of most psychiatric disorders remains nebulous. That's frustrating for physicians treating the diseases, who must also make diagnoses based on symptoms that may only appear sporadically. No laboratory blood test or brain scan can yet distinguish whether someone has depression or bipolar disorder, for example.</span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Now, however, a large-scale analysis of postmortem brains is revealing distinctive molecular traces in people with mental illness. This week, an international team of researchers reports that five major psychiatric disorders have patterns of gene activity that often overlap but also vary in disease-specific—and sometimes counterintuitive—ways. The findings, they say, might someday lead to diagnostic tests and novel therapies, and one has already inspired a clinical trial of a new way to treat overactive brain cells in autism.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Outsiders say the data mark a milestone in psychiatry. "This [work] is changing fundamental views about the nature of psychiatric illness," says Kenneth Kendler, a psychiatric geneticist at Virginia Commonwealth University in Richmond.</span></span></div>
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<b>Read more:</b> <a href="https://jamanetwork.com/journals/jamapsychiatry/article-abstract/2675295" rel="" style="color: #6699cc;" target="_blank">https://jamanetwork.com/journals/jamapsychiatry/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Adult hippocampal neurogenesis declines in aging rodents and primates. Aging humans are thought to exhibit waning neurogenesis and exercise-induced angiogenesis, with a resulting volumetric decrease in the neurogenic hippocampal dentate gyrus (DG) region, although concurrent changes in these parameters are not well studied. Here we assessed whole autopsy hippocampi from healthy human individuals ranging from 14 to 79 years of age. We found similar numbers of intermediate neural progenitors and thousands of immature neurons in the DG, comparable numbers of glia and mature granule neurons, and equivalent DG volume across ages. Nevertheless, older individuals have less angiogenesis and neuroplasticity and a smaller quiescent progenitor pool in anterior-mid DG, with no changes in posterior DG. Thus, healthy older subjects without cognitive impairment, neuropsychiatric disease, or treatment display preserved neurogenesis. It is possible that ongoing hippocampal neurogenesis sustains human-specific cognitive function throughout life and that declines may be linked to compromised cognitive-emotional resilience.</span></span></div>
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<b>Source:</b> <a href="https://www.cell.com/cell-stem-cell/fulltext/S1934-5909(18)30121-8" style="color: #6699cc;" target="_blank">https://www.cell.com/cell-stem-cell/</a></div>
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The effect of curcumin (turmeric) on Alzheimer's disease: An overview</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b><i>Annals of Indian Academy of Neurology</i></b></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">This paper discusses the effects of curcumin on patients with Alzheimer's disease (AD). Curcumin (Turmeric), an ancient Indian herb used in curry powder, has been extensively studied in modern medicine and Indian systems of medicine for the treatment of various medical conditions, including cystic fibrosis, haemorrhoids, gastric ulcer, colon cancer, breast cancer, atherosclerosis, liver diseases and arthritis. It has been used in various types of treatments for dementia and traumatic brain injury. Curcumin also has a potential role in the prevention and treatment of AD. Curcumin as an antioxidant, anti-inflammatory and lipophilic action improves the cognitive functions in patients with AD. A growing body of evidence indicates that oxidative stress, free radicals, beta amyloid, cerebral deregulation caused by bio-metal toxicity and abnormal inflammatory reactions contribute to the key event in Alzheimer's disease pathology. Due to various effects of curcumin, such as decreased Beta-amyloid plaques, delayed degradation of neurons, metal-chelation, anti-inflammatory, antioxidant and decreased microglia formation, the overall memory in patients with AD has improved. This paper reviews the various mechanisms of actions of curcumin in AD and pathology.</span></span><br />
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<b style="font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2781139/" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/</a></div>
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<span style="color: #333333; font-family: "arial" , sans-serif;"><span style="font-size: 18px; line-height: 22px; text-transform: uppercase;">The Impact of Antidepressant Dose and Class on Treatment Response in Pediatric Anxiety Disorders: A Meta-Analysis</span></span></h2>
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<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><span style="font-size: 14.85px;"><br /></span></span></span>
<i><span style="color: #444444; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">Objective</span></span></i><br />
<span style="color: #444444; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">To determine the trajectory and magnitude of antidepressant response as well as the effect of antidepressant class and dose on symptomatic improvement in pediatric anxiety disorders.</span></span><br />
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<span style="color: #444444; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">Weekly symptom severity data were extracted from randomized, parallel group, placebo-controlled trials of selective serotonin reuptake inhibitors (SSRIs) and selective serotonin−norepinephrine reuptake inhibitors (SNRIs) in pediatric anxiety disorders. Treatment response was modeled for the standardized change in continuous measures of anxiety using Bayesian updating. Posterior distributions for each study served as informative conjugate prior to distributions update subsequent study posteriors. Change in symptom severity was evaluated as a function of time, class and, for SSRIs, standardized dose.</span></span><br />
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<span style="color: #444444; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #444444; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">Data from 9 trials (SSRIs: n = 5; SNRIs, n = 4) evaluating 7 medications in 1,673 youth were included. In the logarithmic model of treatment response, statistically, but not clinically, significant treatment effects emerged within 2 weeks of beginning treatment (standardized medication−placebo difference = −0.054, credible interval [CI] = −0.076 to −0.032, p = .005, approximate Cohen’s d ≤ 0.2) and by week 6, clinically significant differences emerged (standardized medication−placebo difference = −0.120, CI = −0.142 to −0.097, p = .001, approximate Cohen’s d = 0.44). Compared to SNRIs, SSRIs resulted in significantly greater improvement by the second week of treatment (p = .0268), and this advantage remained statistically significant through week 12 (all p values <.03). Improvement occurred earlier with high-dose SSRI treatment (week 2, p = .002) compared to low-dose treatment (week 10, p = .025), but SSRI dose did not have an impact on overall response trajectory (p > .18 for weeks 1−12).</span></span><br />
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<span style="color: #444444; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">In pediatric patients with generalized, separation, and/or social anxiety disorders, antidepressant-related improvement occurred early in the course of treatment, and SSRIs were associated with more rapid and greater improvement compared to SNRIs.</span></span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://www.jaacap.org/article/S0890-8567(18)30053-4/fulltext" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://www.jaacap.org/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; text-transform: uppercase;">Safety and efficacy of maintenance ketamine treatment in patients with treatment-refractory generalised anxiety and social anxiety disorders</span></span></h2>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b>Journal of Psychopharmacology</b></span></i></span><br />
<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b><br /></b></span></i></span><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b><br /></b></span></i></span></div>
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i></span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">In this maintenance treatment study, we sought to evaluate the effect on anxiety ratings, safety and tolerability of 3 months of weekly ketamine in 20 patients with treatment-refractory DSM IV generalised anxiety disorder (GAD) and/or social anxiety disorder (SAD), and subsequent assessment of remission post-treatment.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">This was an uncontrolled open-label study in 20 patients who had been responders in an ascending dose ketamine study. The study was undertaken in a university clinic. Patients received one or two weekly ketamine doses of 1 mg/kg injected subcutaneously for 3 months. Data were collected from December 2015–June 2017.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">There were 10 women (50%) and 10 men (50%); 15 patients (75%) met criteria for GAD and 18 (90%) for SAD. One hour after dosing, Fear Questionnaire ratings decreased by ~50%, as did Hamilton Anxiety ratings. Clinician Administered Dissociative States Scale mean scores declined over time, from 20 points at week 1 to 8.8 points at week 14. Compared with pre-dose values, mean systolic and diastolic blood pressure increased by ~10 mm Hg at 30 min. The most common adverse events were nausea, dizziness and blurred vision. Of the 20 patients, 18 reported improved social functioning and/or work functioning during maintenance treatment.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Weekly ketamine dosing was safe and well tolerated, and post-dose dissociative symptoms tended to reduce after repeated dosing. Patients reported marked improvements in functionality and in their personal lives. Maintenance ketamine may be a therapeutic alternative for patients with treatment refractory GAD/SAD.</span></span><br />
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://journals.sagepub.com/doi/full/10.1177/0269881118762073" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">http://journals.sagepub.com/</a></div>
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<b><a href="http://journals.lww.com/psychopharmacology/Pages/currenttoc.aspx" style="color: #6699cc;" target="_blank">Journal of Clinical Psychopharmacology - June 2018 - Volume 38, Issue 3</a></b></div>
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<b><a href="https://www.nature.com/npp/journal/v43/n6/index.html" style="color: #6699cc;" target="_blank">Neuropsychopharmacology - Volume 43, Issue 6 (May 2018)</a></b></div>
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<b><a href="https://link.springer.com/journal/213/235/5/page/1" style="color: #6699cc;" target="_blank">Psychopharmacology - Volume 235, Issue 5, May 2018</a></b></div>
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<b><a href="http://jop.sagepub.com/content/current" style="color: #6699cc;" target="_blank">Journal of Psychopharmacology - May 2018; 32 (5)</a></b></div>
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<b><a href="http://ajp.psychiatryonline.org/toc/ajp/current" style="color: #6699cc;" target="_blank">The American Journal of Psychiatry - May 2018, Vol. 175, Issue 5</a></b></div>
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<b style="color: #6699cc;"><a href="http://archpsyc.jamanetwork.com/issue.aspx" style="color: #6699cc;" target="_blank">JAMA Psychiatry - May 2018, Vol. 75, No. 5</a></b></div>
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<b><a href="https://www.nature.com/neuro/volumes/21/issues/5" style="color: #6699cc;" target="_blank">Nature Neuroscience - May 2018, Vol 21, N° 5</a></b></div>
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<b><a href="https://www.nature.com/mp/journal/v23/n4/index.html" style="color: #6699cc;" target="_blank">Molecular Psychiatry - Volume 23, Issue 4, April 2018</a></b></div>
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<b style="background-color: white; color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"><a href="http://www.biologicalpsychiatryjournal.com/current" style="color: #6699cc;" target="_blank">Biological Psychiatry - Volume 83, Issue 10, May 2018</a></b><br />
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<b><a href="https://academic.oup.com/brain/issue/141/3?browseBy=volume" style="color: #6699cc;" target="_blank">Brain - Volume 141, Issue 3, March 2018</a></b></div>
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Eutimiahttp://www.blogger.com/profile/07836706907685752267noreply@blogger.comtag:blogger.com,1999:blog-1045445187620004007.post-20159610602111299512018-03-03T13:25:00.000-05:002018-03-24T15:03:49.618-04:00March 2018<div dir="ltr" style="text-align: left;" trbidi="on">
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<i style="font-size: 14.85px; line-height: 20.79px;"><br /></i><i><b>American Academy of Neurology</b></i><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">People who eat vegetables, fruit and whole grains may have lower rates of depression over time, according to a preliminary study released today that will be presented at the American Academy of Neurology’s 70th Annual Meeting in Los Angeles, April 21 to 27, 2018.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The study found that people whose diets adhered more closely to the Dietary Approaches to Stop Hypertension (DASH) diet were less likely to develop depression than people who did not closely follow the diet. In addition to fruit and vegetables, the DASH diet recommends fat-free or low-fat dairy products and limits foods that are high in saturated fats and sugar. Studies have shown health benefits such as lowering high blood pressure and bad cholesterol (LDL), along with lowering body weight.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">“Depression is common in older adults and more frequent in people with memory problems, vascular risk factors such as high blood pressure or high cholesterol, or people who have had a stroke,” said study author Laurel Cherian, MD, of Rush University Medical Center in Chicago and a member of the American Academy of Neurology. “Making a lifestyle change such as changing your diet is often preferred over taking medications, so we wanted to see if diet could be an effective way to reduce the risk of depression.”</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">For the study, 964 participants with an average age of 81 were evaluated yearly for an average of six-and-a-half years. They were monitored for symptoms of depression such as being bothered by things that usually didn’t affect them and feeling hopeless about the future. They also filled out questionnaires about how often they ate various foods, and the researchers looked at how closely the participants’ diets followed diets such as the DASH diet, Mediterranean diet and the traditional Western diet.</span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"> </span></div>
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<b>Read more:</b> <a href="https://www.aan.com/PressRoom/Home/PressRelease/1624" style="color: #6699cc;" target="_blank">https://www.aan.com/</a></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b>JAMA Psychiatry</b></i></span></span><br />
<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b><br /></b></i></span></span><span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b>Abstract</b></i></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Importance </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The menopause transition and early postmenopausal period are associated with a 2- to 4-fold increased risk for clinically significant depressive symptoms. Although a few studies suggest that hormone therapy can effectively manage existing depression during this time, to our knowledge, there have been no studies testing whether hormone therapy can prevent the onset of perimenopausal and early postmenopausal depressive symptoms.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i> <br />To examine the efficacy of transdermal estradiol plus intermittent micronized progesterone (TE+IMP) in preventing depressive symptom onset among initially euthymic perimenopausal and early postmenopausal women. A secondary aim was to identify baseline characteristics predicting TE+IMP’s beneficial mood effects.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants</i> <br />Double-blind, placebo-controlled randomized trial at the University of North Carolina at Chapel Hill from October 2010 to February 2016. Participants included euthymic perimenopausal and early postmenopausal women from the community, aged 45 to 60 years.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Interventions</i> <br />Transdermal estradiol (0.1 mg/d) or transdermal placebo for 12 months. Oral micronized progesterone (200 mg/d for 12 days) was also given every 3 months to women receiving active TE, and identical placebo pills were given to women receiving placebo.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcome Measures</i> <br />Scores on the Center for Epidemiological Studies–Depression Scale (CES-D), assessed at baseline and months 1, 2, 4, 6, 8, 10, and 12 after randomization, and the incidence of clinically significant depressive symptoms, defined as a CES-D score of at least 16.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i> <br />Of 172 participants, 130 were white (76%), and 70 were African American (19%), with a mean household income of $50 000 to $79 999. The mean age was 51 years, and 43 developed clinically significant depressive symptoms. Women assigned to placebo were more likely than those assigned to TE+IMP to score at least 16 on the CES-D at least once during the intervention phase (32.3% vs 17.3%; odds ratio [OR], 2.5; 95% CI, 1.1-5.7; P = .03) and had a higher mean CES-D score across the intervention period (P = .03). Baseline reproductive stage moderated the effect of treatment (β, −1.97; SEM, 0.80; P for the interaction = .03) such that mood benefits of TE+IMP vs placebo were evident among women in the early menopause transition (β, −4.2; SEM, 1.2; P < .001) but not the late menopause transition (β, −0.9; SEM, 0.3; P = .23) or among postmenopausal women (β, −0.3; SEM, 1.1; P = .92). Stressful life events in the 6 months preceding enrollment also moderated the effect of treatment on mean CES-D score such that the mood benefits of TE+IMP increased with a greater number of events (β, 1.22; SEM, 0.40; P = .003). Baseline estradiol levels, baseline vasomotor symptoms, history of depression, and history of abuse did not moderate treatment effects.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i> <br />Twelve months of TE+IMP were more effective than placebo in preventing the development of clinically significant depressive symptoms among initially euthymic perimenopausal and early postmenopausal women</span><span style="color: #444444;"><span style="font-size: 14.85px;"> </span></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"> </span></div>
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<b><br /></b><b>Source:</b> <a href="https://jamanetwork.com/journals/jamapsychiatry/article-abstract/2668205" style="color: #6699cc;" target="_blank">https://jamanetwork.com/journals/jamapsychiatry</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"><i>Importance </i> </span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Approximately one-third of patients with major depressive disorder (MDD) do not respond to available antidepressants.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective </i><br />To assess the efficacy, safety, and dose-response of intranasal esketamine hydrochloride in patients with treatment-resistant depression (TRD).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants </i><br />This phase 2, double-blind, doubly randomized, delayed-start, placebo-controlled study was conducted in multiple outpatient referral centers from January 28, 2014, to September 25, 2015. The study consisted of 4 phases: (1) screening, (2) double-blind treatment (days 1-15), composed of two 1-week periods, (3) optional open-label treatment (days 15-74), and (4) posttreatment follow-up (8 weeks). One hundred twenty-six adults with a DSM-IV-TR diagnosis of MDD and history of inadequate response to 2 or more antidepressants (ie, TRD) were screened, 67 were randomized, and 60 completed both double-blind periods. Intent-to-treat analysis was used in evaluation of the findings.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Interventions</i> <br />In period 1, participants were randomized (3:1:1:1) to placebo (n = 33), esketamine 28 mg (n = 11), 56 mg (n = 11), or 84 mg (n = 12) twice weekly. In period 2, 28 placebo-treated participants with moderate-to-severe symptoms were rerandomized (1:1:1:1) to 1 of the 4 treatment arms; those with mild symptoms continued receiving placebo. Participants continued their existing antidepressant treatment during the study. During the open-label phase, dosing frequency was reduced from twice weekly to weekly, and then to every 2 weeks.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures </i> <br />The primary efficacy end point was change from baseline to day 8 (each period) in the Montgomery-Åsberg Depression Rating Scale (MADRS) total score.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i> <br />Sixty-seven participants (38 women, mean [SD] age, 44.7 [10.0] years) were included in the efficacy and safety analyses. Change (least squares mean [SE] difference vs placebo) in MADRS total score (both periods combined) in all 3 esketamine groups was superior to placebo (esketamine 28 mg: −4.2 [2.09], P = .02; 56 mg: −6.3 [2.07], P = .001; 84 mg: −9.0 [2.13], P < .001), with a significant ascending dose-response relationship (P < .001). Improvement in depressive symptoms appeared to be sustained (−7.2 [1.84]) despite reduced dosing frequency in the open-label phase. Three of 56 (5%) esketamine-treated participants during the double-blind phase vs none receiving placebo and 1 of 57 participants (2%) during the open-label phase had adverse events that led to study discontinuation (1 event each of syncope, headache, dissociative syndrome, and ectopic pregnancy).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance</i> <br />In this first clinical study to date of intranasal esketamine for TRD, antidepressant effect was rapid in onset and dose related. Response appeared to persist for more than 2 months with a lower dosing frequency. Results support further investigation in larger trials.</span></span></div>
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<b>Source:</b> <a href="https://jamanetwork.com/journals/jamapsychiatry/fullarticle/2666767" style="color: #6699cc;" target="_blank">https://jamanetwork.com/journals/jamapsychiatry/</a></div>
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The American Psychiatric Association Practice Guideline for the Pharmacological Treatment of Patients With Alcohol Use Disorder</h2>
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Reduction of PTSD Symptoms With Pre-Reactivation Propranolol Therapy: A Randomized Controlled Trial</h2>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b>The American Journal of Psychiatry</b></span></i></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The authors assessed the efficacy of trauma memory reactivation performed under the influence of propranolol, a noradrenergic beta-receptor blocker, as a putative reconsolidation blocker, in reducing symptoms of posttraumatic stress disorder (PTSD).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Method</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">This was a 6-week, double-blind, placebo-controlled, randomized clinical trial in 60 adults diagnosed with long-standing PTSD. Propranolol or placebo was administered 90 minutes before a brief memory reactivation session, once a week for 6 consecutive weeks. The hypothesis predicted a significant treatment effect of trauma reactivation with propranolol compared with trauma reactivation with placebo in reducing PTSD symptoms on both the Clinician-Administered PTSD Scale (CAPS) and the patient-rated PTSD Checklist–Specific (PCL-S) in an intention-to-treat analysis.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The estimated group difference in posttreatment CAPS score, adjusted for pretreatment values (analysis of covariance), was a statistically significant 11.50. The within-group pre- to posttreatment effect sizes (Cohen’s d) were 1.76 for propranolol and 1.25 for placebo. For the PCL-S, the mixed linear model’s estimated time-by-group interaction yielded an average decrease of 2.43 points per week, for a total significant difference of 14.58 points above that of placebo. The pre- to posttreatment effect sizes were 2.74 for propranolol and 0.55 for placebo. Per protocol analyses for both outcomes yielded similar significant results.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Pre-reactivation propranolol, a treatment protocol suggested by reconsolidation theory, appears to be a novel and efficacious treatment for PTSD. Replication studies using a long-term follow-up in various trauma populations are required</span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">.</span></div>
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<b>Source:</b> <a href="https://ajp.psychiatryonline.org/doi/abs/10.1176/appi.ajp.2017.17050481" rel="" style="color: #6699cc;" target="_blank">https://ajp.psychiatryonline.org/</a></div>
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Major mental illnesses unexpectedly share brain gene activity, raising hope for better diagnostics and therapie</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">Mental illness affects one in six U.S. adults, but scientists' sense of the underlying biology of most psychiatric disorders remains nebulous. That's frustrating for physicians treating the diseases, who must also make diagnoses based on symptoms that may only appear sporadically. No laboratory blood test or brain scan can yet distinguish whether someone has depression or bipolar disorder, for example.</span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Now, however, a large-scale analysis of postmortem brains is revealing distinctive molecular traces in people with mental illness. This week, an international team of researchers reports that five major psychiatric disorders have patterns of gene activity that often overlap but also vary in disease-specific—and sometimes counterintuitive—ways. The findings, they say, might someday lead to diagnostic tests and novel therapies, and one has already inspired a clinical trial of a new way to treat overactive brain cells in autism.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Outsiders say the data mark a milestone in psychiatry. "This [work] is changing fundamental views about the nature of psychiatric illness," says Kenneth Kendler, a psychiatric geneticist at Virginia Commonwealth University in Richmond.</span></span></div>
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<b>Read more:</b> <a href="http://www.sciencemag.org/news/2018/02/major-mental-illnesses-unexpectedly-share-brain-gene-activity-raising-hope-better" rel="" style="color: #6699cc;" target="_blank">http://www.sciencemag.org/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b><i>American Academy of Child and Adolescent Psychiatry</i></b></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Schizophrenia (SZ) is a devastating mental disease caused by complex genetic and environmental factors. The pathological process and clinical manifestation of SZ are heterogeneous among patients, which hampers precise diagnosis and treatment of the disease. Since no objective marker for SZ has been established today, to identify a subgroup of the patients with homogeneous biochemical traits will provide a new angle for both researchers and clinicians to understand and manage the disease. In this study, we employed the niacin skin-flushing test in Chinese population and confirmed a niacin-blunted subgroup of SZ patients distinguishable from mood disorders (MD) and normal individuals. This subgroup accounted for 30.67% of the total SZ patients with a specificity of 88.37% in male subjects and 83.75% in female subjects. We support the notion that bluntness in niacin skin test might reflect abnormalities in membrane fatty acid composition, which could be induced by increased PLA2 enzyme activity, in vivo oxidative stress or lipid metabolism imbalance in SZ. Further studies are encouraged to clarify the molecular origins of niacin-bluntness in SZ, which would provide extra clues for etiological research in schizophrenia and for new targeted treatment.</span></span></div>
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<b>Source:</b> <a href="http://www.jaacap.com/article/S0890-8567(17)31934-2/fulltext" style="color: #6699cc;" target="_blank">http://www.jaacap.com/</a></div>
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Clinical Consensus Recommendations for Urine Testing of Adherence to Antipsychotics Among People With Serious Mental Illness</h2>
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<b><br /></b><b>Abstract</b></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">This study developed clinical recommendations for the use of proven urine testing technologies to assess antipsychotic medication adherence among people with serious mental illness.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Guided by the RAND/UCLA Appropriateness Method, researchers conducted a literature review and semistructured interviews and convened an expert panel to develop clinical consensus recommendations for the use of urine monitoring to assess antipsychotic medication adherence.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The expert panel identified six circumstances in which urine monitoring was recommended at initial evaluation and five scenarios in which monitoring was recommended after initial evaluation. Conducting monitoring at the site where psychiatric medication is prescribed and providing education prior to testing and feedback after testing were recommended.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">A consensus was reached on clinical recommendations for use of urine monitoring at intake and during ongoing treatment. There was strong agreement that monitoring can be used to improve assessment and thence clinical care and outcomes.</span></span><br />
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<b style="font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://ps.psychiatryonline.org/doi/10.1176/appi.ps.201700082" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://ps.psychiatryonline.org/</a></div>
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<span style="color: #333333; font-family: "arial" , sans-serif;"><span style="font-size: 18px; line-height: 22px; text-transform: uppercase;">IMPACT OF SSRI THERAPY ON RISK OF CONVERSION FROM MILD COGNITIVE IMPAIRMENT TO ALZHEIMER’S DEMENTIA IN INDIVIDUALS WITH PREVIOUS DEPRESSION</span></span></h2>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b><br /></b></i></span></span><span style="color: #333333; font-size: 14.85px; font-style: italic; font-weight: bold; line-height: 20.79px;">The American Journal of Psychiatry</span><br />
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<i><b><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Abstract</span></span></b></i><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Depression is associated with an increased risk of Alzheimer’s disease. Research has shown that the selective serotonin reuptake inhibitor (SSRI) citalopram decreases amyloid-β generation and plaque load. The authors evaluated the impact of SSRI treatment on CSF biomarkers and progression from mild cognitive impairment (MCI) to Alzheimer’s dementia.</span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Method</i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Data sets from 755 currently nondepressed participants from the longitudinal Alzheimer’s Disease Neuroimaging Initiative were evaluated by Kaplan-Meier analysis and analyses of variance and covariance with ApoE4 status and age as covariates.</span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">In MCI patients with a history of depression, long-term SSRI treatment (>4 years) was significantly associated with a delayed progression to Alzheimer’s dementia by approximately 3 years, compared with short-term SSRI treatment, treatment with other antidepressants, or no treatment and compared with MCI patients without a history of depression. No differences in CSF biomarker levels were observed between treatment groups.</span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Long-term SSRI treatment may delay progression from MCI to Alzheimer’s dementia.</span></span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://ajp.psychiatryonline.org/doi/abs/10.1176/appi.ajp.2017.17040404?journalCode=ajp" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://ajp.psychiatryonline.org/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; text-transform: uppercase;">CORTICAL AND SUBCORTICAL BRAIN MORPHOMETRY DIFFERENCES BETWEEN PATIENTS WITH AUTISM SPECTRUM DISORDER AND HEALTHY INDIVIDUALS ACROSS THE LIFESPAN: RESULTS FROM THE ENIGMA ASD WORKING GROUP</span></span></h2>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b>The American Journal of Psychiatry</b></span></i></span><br />
<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b><br /></b></span></i></span><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
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<i><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Objective</span></span></i><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Neuroimaging studies show structural differences in both cortical and subcortical brain regions in children and adults with autism spectrum disorder (ASD) compared with healthy subjects. Findings are inconsistent, however, and it is unclear how differences develop across the lifespan. The authors investigated brain morphometry differences between individuals with ASD and healthy subjects, cross-sectionally across the lifespan, in a large multinational sample from the Enhancing Neuroimaging Genetics Through Meta-Analysis (ENIGMA) ASD working group.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Method</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The sample comprised 1,571 patients with ASD and 1,651 healthy control subjects (age range, 2–64 years) from 49 participating sites. MRI scans were preprocessed at individual sites with a harmonized protocol based on a validated automated-segmentation software program. Mega-analyses were used to test for case-control differences in subcortical volumes, cortical thickness, and surface area. Development of brain morphometry over the lifespan was modeled using a fractional polynomial approach.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The case-control mega-analysis demonstrated that ASD was associated with smaller subcortical volumes of the pallidum, putamen, amygdala, and nucleus accumbens (effect sizes [Cohen’s d], 0.13 to –0.13), as well as increased cortical thickness in the frontal cortex and decreased thickness in the temporal cortex (effect sizes, −0.21 to 0.20). Analyses of age effects indicate that the development of cortical thickness is altered in ASD, with the largest differences occurring around adolescence. No age-by-ASD interactions were observed in the subcortical partitions.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The ENIGMA ASD working group provides the largest study of brain morphometry differences in ASD to date, using a well-established, validated, publicly available analysis pipeline. ASD patients showed altered morphometry in the cognitive and affective parts of the striatum, frontal cortex, and temporal cortex. Complex developmental trajectories were observed for the different regions, with a developmental peak around adolescence. These findings suggest an interplay in the abnormal development of the striatal, frontal, and temporal regions in ASD across the lifespan.</span></span><br />
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://ajp.psychiatryonline.org/doi/abs/10.1176/appi.ajp.2017.17010100?journalCode=ajp" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://ajp.psychiatryonline.org/</a></div>
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<b><a href="http://journals.lww.com/psychopharmacology/Pages/currenttoc.aspx" style="color: #6699cc;" target="_blank">Journal of Clinical Psychopharmacology - April 2018 - Volume 38, Issue 2</a></b></div>
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<b><a href="https://www.nature.com/npp/journal/v43/n5/index.html" style="color: #6699cc;" target="_blank">Neuropsychopharmacology - Volume 43, Issue 5 (April 2018)</a></b></div>
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<b><a href="https://link.springer.com/journal/213/235/3/page/1" style="color: #6699cc;" target="_blank">Psychopharmacology - Volume 235, Issue 3, March 2018</a></b></div>
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<b><a href="http://jop.sagepub.com/content/current" style="color: #6699cc;" target="_blank">Journal of Psychopharmacology - February 2018; 32 (2)</a></b></div>
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<b><a href="http://ajp.psychiatryonline.org/toc/ajp/current" style="color: #6699cc;" target="_blank">The American Journal of Psychiatry - March 2018, Vol. 175, Issue 3</a></b></div>
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<b style="color: #6699cc;"><a href="http://archpsyc.jamanetwork.com/issue.aspx" style="color: #6699cc;" target="_blank">JAMA Psychiatry - March 2018, Vol. 75, No. 3</a></b></div>
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<b><a href="https://www.nature.com/neuro/volumes/21/issues/3" style="color: #6699cc;" target="_blank">Nature Neuroscience - March 2018, Vol 21, N° 3</a></b></div>
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<b><a href="https://www.nature.com/mp/journal/v23/n3/index.html" style="color: #6699cc;" target="_blank">Molecular Psychiatry - Volume 23, Issue 3, March 2018</a></b></div>
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<b style="background-color: white; color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"><a href="http://www.biologicalpsychiatryjournal.com/current" style="color: #6699cc;" target="_blank">Biological Psychiatry - Volume 83, Issue 8, April 2018</a></b><br />
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<b><a href="https://academic.oup.com/brain/issue/141/3?browseBy=volume" style="color: #6699cc;" target="_blank">Brain - Volume 141, Issue 3, March 2018</a></b></div>
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Eutimiahttp://www.blogger.com/profile/07836706907685752267noreply@blogger.comtag:blogger.com,1999:blog-1045445187620004007.post-23987232641241035102018-01-01T16:47:00.000-05:002018-01-14T15:16:08.675-05:00January 2018<div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The U.S. Food and Drug Administration approved the first drug in the U.S. with a digital ingestion tracking system. Abilify MyCite (aripiprazole tablets with sensor) has an ingestible sensor embedded in the pill that records that the medication was taken. The product is approved for the treatment of schizophrenia, acute treatment of manic and mixed episodes associated with bipolar I disorder and for use as an add-on treatment for depression in adults.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The system works by sending a message from the pill’s sensor to a wearable patch. The patch transmits the information to a mobile application so that patients can track the ingestion of the medication on their smart phone. Patients can also permit their caregivers and physician to access the information through a web-based portal.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">“Being able to track ingestion of medications prescribed for mental illness may be useful for some patients,” said Mitchell Mathis, M.D., director of the Division of Psychiatry Products in the FDA’s Center for Drug Evaluation and Research. “The FDA supports the development and use of new technology in prescription drugs and is committed to working with companies to understand how technology might benefit patients and prescribers.”</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">It is important to note that Abilify MyCite’s prescribing information (labeling) notes that the ability of the product to improve patient compliance with their treatment regimen has not been shown. Abilify MyCite should not be used to track drug ingestion in “real-time” or during an emergency because detection may be delayed or may not occur. </span></div>
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<b>Read more:</b> <a href="https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm584933.htm" style="color: #6699cc;" target="_blank">https://www.fda.gov/NewsEvents/Newsroom/</a></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b>The American Journal of Psychiatry</b></i></span></span><br />
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<i><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Objective</span></span></i><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The purpose of this study was to assess the relative risk of suicide attempt and suicide in users of hormonal contraception.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Method</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The authors assessed associations between hormonal contraceptive use and suicide attempt and suicide in a nationwide prospective cohort study of all women in Denmark who had no psychiatric diagnoses, antidepressant use, or hormonal contraceptive use before age 15 and who turned 15 during the study period, which extended from 1996 through 2013. Nationwide registers provided individually updated information about use of hormonal contraception, suicide attempt, suicide, and potential confounding variables. Psychiatric diagnoses or antidepressant use during the study period were considered potential mediators between hormonal contraceptive use and risk of suicide attempt. Adjusted hazard ratios for suicide attempt and suicide were estimated for users of hormonal contraception as compared with those who never used hormonal contraception.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Among nearly half a million women followed on average for 8.3 years (3.9 million person-years) with a mean age of 21 years, 6,999 first suicide attempts and 71 suicides were identified. Compared with women who never used hormonal contraceptives, the relative risk among current and recent users was 1.97 (95% CI=1.85–2.10) for suicide attempt and 3.08 (95% CI=1.34–7.08) for suicide. Risk estimates for suicide attempt were 1.91 (95% CI=1.79–2.03) for oral combined products, 2.29 (95% CI=1.77–2.95) for oral progestin-only products, 2.58 (95% CI=2.06–3.22) for vaginal ring, and 3.28 (95% CI=2.08–5.16) for patch. The association between hormonal contraceptive use and a first suicide attempt peaked after 2 months of use.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Use of hormonal contraception was positively associated with subsequent suicide attempt and suicide. Adolescent women experienced the highest relative risk.</span><span style="color: #444444;"><span style="font-size: 14.85px;"> </span></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"> </span></div>
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<b><br /></b><b>Source:</b> <a href="https://ajp.psychiatryonline.org/doi/abs/10.1176/appi.ajp.2017.17060616" style="color: #6699cc;" target="_blank">https://ajp.psychiatryonline.org/</a></div>
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<i style="font-size: 14.85px; line-height: 20.79px;"><b>Journal of Affective Disorders</b></i><br />
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<i><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Background</span></span></i><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Vegetarian diets are associate with cardiovascular and other health benefits, but little is known about mental health benefits or risks.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Aims</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To determine whether self-identification of vegetarian dietary habits is associated with significant depressive symptoms in men.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Self-report data from 9668 adult male partners of pregnant women in the Avon Longitudinal Study of Parents and Children (ALSPAC) included identification as vegetarian or vegan, dietary frequency data and the Edinburgh Post Natal Depression Scale (EPDS). Continuous and binary outcomes were assessed using multiple linear and logistic regression taking account of potential confounding variables including: age, marital status, employment status, housing tenure, number of children in the household, religion, family history of depression previous childhood psychiatric contact, cigarette and alcohol consumption.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Vegetarians [n = 350 (3.6% of sample)], had higher depression scores on average than non-vegetarians (mean difference 0.96 points [95%CI + 0.53, + 1.40]) and a greater risk for EPDS scores above 10 (adjusted OR = 1.67 [95% CI: 1.14,2.44]) than non-vegetarians after adjustment for potential confounding factors.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Vegetarian men have more depressive symptoms after adjustment for socio-demographic factors. Nutritional deficiencies (e.g. in cobalamin or iron) are a possible explanation for these findings, however reverse causation cannot be ruled out.</span></span></div>
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<b>Source:</b> <a href="http://www.jad-journal.com/article/S0165-0327(16)32391-6/abstract" style="color: #6699cc;" target="_blank">http://www.jad-journal.com/</a></div>
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<span style="font-size: 14.85px; line-height: 20.79px;">Machine learning of neural representations of suicide and emotion concepts identifies suicidal youth</span></h2>
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<span style="font-size: 14.85px; line-height: 20.79px;"><b><i>Nature Human Behaviour </i></b></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The clinical assessment of suicidal risk would be substantially complemented by a biologically based measure that assesses alterations in the neural representations of concepts related to death and life in people who engage in suicidal ideation. This study used machine-learning algorithms (Gaussian Naive Bayes) to identify such individuals (17 suicidal ideators versus 17 controls) with high (91%) accuracy, based on their altered functional magnetic resonance imaging neural signatures of death-related and life-related concepts. The most discriminating concepts were ‘death’, ‘cruelty’, ‘trouble’, ‘carefree’, ‘good’ and ‘praise’. A similar classification accurately (94%) discriminated nine suicidal ideators who had made a suicide attempt from eight who had not. Moreover, a major facet of the concept alterations was the evoked emotion, whose neural signature served as an alternative basis for accurate (85%) group classification. This study establishes a biological, neurocognitive basis for altered concept representations in participants with suicidal ideation, which enables highly accurate group membership classification.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><b style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;">Source:</b><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"> </span><a href="https://www.nature.com/articles/s41562-017-0234-y" style="color: #6699cc; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;" target="_blank">https://www.nature.com/</a></div>
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Nutritional Deficiencies and Clinical Correlates in First-Episode Psychosis: A Systematic Review and Meta-analysis</h2>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b>Eschizophrenia Bulletin</b></span></i></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">S</span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Diet is increasingly recognized as a potentially modifiable factor influencing the onset and outcomes of psychiatric disorders. Whereas, previous research has shown long-term schizophrenia is associated with various nutritional deficiencies, this meta-analysis aimed to determine the prevalence and extent of nutritional deficits in first-episode psychosis (FEP).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Method</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">A search of electronic databases conducted in July 2017 identified 28 eligible studies, examining blood levels of 6 vitamins and 10 minerals across 2612 individuals: 1221 individuals with FEP and 1391 control subjects. Meta-analyses compared nutrient levels in FEP to nonpsychiatric controls. Clinical correlates of nutritional status in patient samples were systematically reviewed.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Significantly lower blood levels of folate (N = 6, n = 827, g = −0.624, 95% confidence interval [CI] = −1.176 to −0.072, P = .027) and vitamin D (N = 7, n = 906, g = −1.055, 95% CI = −1.99 to −0.119, P = .027) were found in FEP compared to healthy controls. Synthesis of clinical correlates found both folate and vitamin D held significant inverse relationships with psychiatric symptoms in FEP. There was also limited evidence for serum level reductions of vitamin C (N = 2, n = 96, g = −2.207, 95% CI = −3.71 to −0.71, P = .004). No differences were found for other vitamins or minerals.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Deficits in vitamin D and folate previously observed in long-term schizophrenia appear to exist from illness onset, and are associated with worse symptomology. Further research must examine the direction and nature of these relationships (ie, mediator, moderator, or marker) with clinical status in FEP. Future trials assessing efficacy of nutrient supplementation in FEP samples should consider targeting and stratifying for baseline deficiency.</span></span></div>
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<b>Source:</b> <a href="https://academic.oup.com/schizophreniabulletin/advance-article/doi/10.1093/schbul/sbx162/4675234" rel="" style="color: #6699cc;" target="_blank">https://academic.oup.com/schizophreniabulletin/</a></div>
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Rates and Predictors of Conversion to Schizophrenia or Bipolar Disorder Following Substance-Induced Psychosis</h2>
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<i><b>The American Journal of Psychiatry</b></i></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To evaluate the effect of prenatal exposure to selective serotonin reuptake inhibitors (SSRIs) on children’s behavioral, emotional, and social development by age 5 years, and over time since age 1.5.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Method</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The prospective Norwegian Mother and Child Cohort Study was linked to the Medical Birth Registry of Norway. We included women who reported depressive/anxiety disorders before and/or during pregnancy. Children born to women who used SSRIs in early (weeks 0-16), mid (weeks 17-28), or late (> week 29) pregnancy were compared to unexposed. Children’s internalizing and externalizing behaviors (Child Behavior Checklist) and temperament traits (Emotionality, Activity and Shyness Temperament Questionnaire) were measured at 1.5, 3, and 5 years. Mean scores were calculated and standardized. We fit general linear marginal structural models to account for time-varying exposure and confounders, and censoring; three-level growth-curve models.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We included 8,359 mother–child dyads, and 4,128 children had complete outcome data at age 5. Children exposed to SSRIs in late pregnancy had an increased risk for anxious/depressed behaviors by age 5 compared with unexposed (adjusted β: 0.50, 95% CI: 0.04, 0.96). Such risk was not evident for earlier timings of exposure. There was no evidence for a substantial prenatal SSRI effect on externalizing, social, and emotional problems.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusion</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">These findings suggest no substantial increased risk for externalizing, emotional, and social problems in preschool-age children following prenatal SSRI exposure. While the role of chance and potential unmeasured confounding cannot be ruled out, late-pregnancy SSRI exposure was associated with greater anxious/depressed behaviors in the offspring.</span></span></div>
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<b>Source:</b> <a href="https://ajp.psychiatryonline.org/doi/10.1176/appi.ajp.2017.17020223" rel="" style="color: #6699cc;" target="_blank">https://ajp.psychiatryonline.org/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Schizophrenia (SZ) is a devastating mental disease caused by complex genetic and environmental factors. The pathological process and clinical manifestation of SZ are heterogeneous among patients, which hampers precise diagnosis and treatment of the disease. Since no objective marker for SZ has been established today, to identify a subgroup of the patients with homogeneous biochemical traits will provide a new angle for both researchers and clinicians to understand and manage the disease. In this study, we employed the niacin skin-flushing test in Chinese population and confirmed a niacin-blunted subgroup of SZ patients distinguishable from mood disorders (MD) and normal individuals. This subgroup accounted for 30.67% of the total SZ patients with a specificity of 88.37% in male subjects and 83.75% in female subjects. We support the notion that bluntness in niacin skin test might reflect abnormalities in membrane fatty acid composition, which could be induced by increased PLA2 enzyme activity, in vivo oxidative stress or lipid metabolism imbalance in SZ. Further studies are encouraged to clarify the molecular origins of niacin-bluntness in SZ, which would provide extra clues for etiological research in schizophrenia and for new targeted treatment.</span></span></div>
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<b>Source:</b> <a href="http://www.jaacap.com/article/S0890-8567(17)31934-2/fulltext" style="color: #6699cc;" target="_blank">http://www.jaacap.com/</a></div>
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Periaqueductal Gray Glutamatergic Transmission Governs Chronic Stress-Induced Depression</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><b><i>Neuropsychopharmacology</i></b></span></span></div>
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<b><br /></b><b>Abstract</b></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The mechanisms underlying chronic stress-induced dysfunction of glutamatergic transmission that contribute to helplessness-associated depressive disorder are unknown. We investigated the relationship of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors and stress, and the neuroplastic changes of stress-induced depression-like behavior in the ventrolateral periaqueductal gray (vlPAG). We conducted whole-cell patch-clamp electrophysiological recordings in the vlPAG neurons. Depression-like behavior was assayed using tail suspension test and sucrose preference test. Surface and cytosolic glutamate receptor 1 (GluR1) AMPA receptor expression was analyzed using western blotting. Phosphorylated GluR1 expression was quantified using western blotting and immunohistochemical analysis. Unpredictable inescapable foot shock stress caused reduction in glutamatergic transmission originating from both presynaptic and postsynaptic loci in the vlPAG that was associated with behavioral despair and anhedonia in chronic stress-induced depression. Pharmacological inhibition of GluR1 function in the vlPAG caused depression-like behavior. Diminished glutamatergic transmission was due to reduced glutamate release presynaptically and enhanced GluR1-endocytosis from the cell surface postsynaptically. Chronic stress-induced neuroplastic changes and maladaptive behavior were reversed and mimicked by administration of glucocorticoid receptor (GR) antagonist and agonist, respectively. However, chronic stress did not affect γ-aminobutyric acid (GABA)-mediated inhibitory synaptic transmission in the vlPAG. These results demonstrate that depression-like behavior is associated with remarkable reduction in glutamatergic, but not GABAergic, transmission in the vlPAG. These neuroplastic changes and maladaptive behavior are attributed to GR-dependent mechanisms. As reduced GluR1-associated responses in the vlPAG contribute to chronic stress-induced neuroplastic changes, this cellular mechanism may be a critical component in the pathogenesis of stress-associated neuropsychiatric disorders.</span></span><br />
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<b style="font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://www.nature.com/articles/npp2017199" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://www.nature.com/</a></div>
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<span style="color: #333333; font-family: "arial" , sans-serif;"><span style="font-size: 18px; line-height: 22px; text-transform: uppercase;">Impact of SSRI Therapy on Risk of Conversion From Mild Cognitive Impairment to Alzheimer’s Dementia in Individuals With Previous Depression</span></span></h2>
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<i><b><span style="color: #444444; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">Abstract</span></span></b></i><br />
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<span style="color: #444444; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">Depression is associated with an increased risk of Alzheimer’s disease. Research has shown that the selective serotonin reuptake inhibitor (SSRI) citalopram decreases amyloid-β generation and plaque load. The authors evaluated the impact of SSRI treatment on CSF biomarkers and progression from mild cognitive impairment (MCI) to Alzheimer’s dementia.</span></span><br />
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<span style="color: #444444; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Method</i></span></span><br />
<span style="color: #444444; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">Data sets from 755 currently nondepressed participants from the longitudinal Alzheimer’s Disease Neuroimaging Initiative were evaluated by Kaplan-Meier analysis and analyses of variance and covariance with ApoE4 status and age as covariates.</span></span><br />
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<span style="color: #444444; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #444444; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">In MCI patients with a history of depression, long-term SSRI treatment (>4 years) was significantly associated with a delayed progression to Alzheimer’s dementia by approximately 3 years, compared with short-term SSRI treatment, treatment with other antidepressants, or no treatment and compared with MCI patients without a history of depression. No differences in CSF biomarker levels were observed between treatment groups.</span></span><br />
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<span style="color: #444444; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #444444; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">Long-term SSRI treatment may delay progression from MCI to Alzheimer’s dementia.</span></span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://ajp.psychiatryonline.org/doi/abs/10.1176/appi.ajp.2017.17040404?journalCode=ajp" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://ajp.psychiatryonline.org/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; text-transform: uppercase;">Cortical and Subcortical Brain Morphometry Differences Between Patients With Autism Spectrum Disorder and Healthy Individuals Across the Lifespan: Results From the ENIGMA ASD Working Group</span></span></h2>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b><br /></b></span></i></span><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
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<i><span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">Objective</span></span></i><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">Neuroimaging studies show structural differences in both cortical and subcortical brain regions in children and adults with autism spectrum disorder (ASD) compared with healthy subjects. Findings are inconsistent, however, and it is unclear how differences develop across the lifespan. The authors investigated brain morphometry differences between individuals with ASD and healthy subjects, cross-sectionally across the lifespan, in a large multinational sample from the Enhancing Neuroimaging Genetics Through Meta-Analysis (ENIGMA) ASD working group.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Method</i></span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">The sample comprised 1,571 patients with ASD and 1,651 healthy control subjects (age range, 2–64 years) from 49 participating sites. MRI scans were preprocessed at individual sites with a harmonized protocol based on a validated automated-segmentation software program. Mega-analyses were used to test for case-control differences in subcortical volumes, cortical thickness, and surface area. Development of brain morphometry over the lifespan was modeled using a fractional polynomial approach.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">The case-control mega-analysis demonstrated that ASD was associated with smaller subcortical volumes of the pallidum, putamen, amygdala, and nucleus accumbens (effect sizes [Cohen’s d], 0.13 to –0.13), as well as increased cortical thickness in the frontal cortex and decreased thickness in the temporal cortex (effect sizes, −0.21 to 0.20). Analyses of age effects indicate that the development of cortical thickness is altered in ASD, with the largest differences occurring around adolescence. No age-by-ASD interactions were observed in the subcortical partitions.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The ENIGMA ASD working group provides the largest study of brain morphometry differences in ASD to date, using a well-established, validated, publicly available analysis pipeline. ASD patients showed altered morphometry in the cognitive and affective parts of the striatum, frontal cortex, and temporal cortex. Complex developmental trajectories were observed for the different regions, with a developmental peak around adolescence. These findings suggest an interplay in the abnormal development of the striatal, frontal, and temporal regions in ASD across the lifespan.</span></span><br />
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://ajp.psychiatryonline.org/doi/abs/10.1176/appi.ajp.2017.17010100?journalCode=ajp" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://ajp.psychiatryonline.org/</a></div>
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<b style="color: blue; font-size: x-large;"><br /></b><b style="color: blue; font-size: x-large;">Online Journals:</b></div>
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<b><a href="http://journals.lww.com/psychopharmacology/Pages/currenttoc.aspx" style="color: #6699cc;" target="_blank">Journal of Clinical Psychopharmacology - February 2018 - Volume 38, Issue 1</a></b></div>
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<b><a href="http://www.nature.com/npp/journal/v43/n2/index.html" style="color: #6699cc;" target="_blank">Neuropsychopharmacology - Volume 43, Issue 2 (January 2018)</a></b></div>
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<b><a href="https://link.springer.com/journal/213/235/1/page/1" style="color: #6699cc;" target="_blank">Psychopharmacology - Volume 235, Issue 1, January 2018</a></b></div>
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<b><a href="http://jop.sagepub.com/content/current" style="color: #6699cc;" target="_blank">Journal of Psychopharmacology - December 2017; 31 (12)</a></b></div>
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<b><a href="http://ajp.psychiatryonline.org/toc/ajp/current" style="color: #6699cc;" target="_blank">The American Journal of Psychiatry - January 2018, Vol. 175, Issue 1</a></b></div>
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<b style="color: #6699cc;"><a href="http://archpsyc.jamanetwork.com/issue.aspx" style="color: #6699cc;" target="_blank">JAMA Psychiatry - January 2018, Vol. 75, No.1</a></b></div>
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<b><a href="https://www.nature.com/neuro/volumes/21/issues/1" style="color: #6699cc;" target="_blank">Nature Neuroscience - January 2018, Vol 21, N° 1</a></b></div>
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<b><a href="http://www.nature.com/mp/journal/v23/n1/index.html" style="color: #6699cc;" target="_blank">Molecular Psychiatry - Volume 23, Issue 1, January 2018</a></b></div>
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<b style="background-color: white; color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"><a href="http://www.biologicalpsychiatryjournal.com/current" style="color: #6699cc;" target="_blank">Biological Psychiatry - Volume 83, Issue 4, February 2018</a></b><br />
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<b><a href="https://academic.oup.com/brain/issue/140/12?browseBy=volume" style="color: #6699cc;" target="_blank">Brain - Volume 140, Issue 12, December 2017</a></b></div>
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<b><span style="font-size: small;">Join us on LinkedIn:</span> </b><b><a href="http://www.linkedin.com/groups/Neuropsychopharmacology-Neuroscience-5147601" style="color: #6699cc;">Neurosychopharmacology News Group</a></b></h3>
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Eutimiahttp://www.blogger.com/profile/07836706907685752267noreply@blogger.comtag:blogger.com,1999:blog-1045445187620004007.post-8776755229916339102017-11-04T10:37:00.000-04:002017-11-19T17:47:28.306-05:00November 2017<div dir="ltr" style="text-align: left;" trbidi="on">
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<i style="font-size: 14.85px; line-height: 20.79px;"><br /></i><i><b>Journal of Psychopharmacology</b></i><br />
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<i><b>Abstract</b></i></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Background</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Recent studies suggest that anti-inflammatory medication may play a role in the treatment of mood disorders.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Aims</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The purpose of this study was to determine the efficacy of anti-inflammatory drugs in patients with major depressive disorder and bipolar disorder.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Method</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The Cochrane Central Register of Controlled Trials, PubMed, EMBASE, PsychINFO and Clinicaltrials.gov were searched from inception until 15 April 2017 for completed and on-going randomized controlled trials of anti-inflammatory agents for major depressive disorder and bipolar disorder. Data from randomized controlled trials assessing the antidepressant and anti-manic effect of adjunctive mechanistically diverse anti-inflammatory agents were pooled to determine standard mean differences (SMDs) compared with placebo and/or treatment as usual.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Patients receiving anti-inflammatory agents showed lower post-treatment depressive symptom scores compared with those receiving placebo with a standard mean difference of −0.71 (six randomized controlled trials, n=214, 95% CI −1.24 to −0.17, p=0.009). Anti-inflammatory treatment was found to reduce post-treatment manic symptom scores with a standard mean difference of −0.72 (three randomized controlled trials, n=96, 95% CI −1.31 to −0.13, p=0.02). Anti-inflammatories did not show a statistically significant improvement in the secondary outcome measure (change in symptom scores from baseline to outcome).</span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"> </span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"><br /></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">Further high quality trials are needed before making recommendations for the routine clinical use of anti-inflammatories in the treatment of mood disorders.</span></div>
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<b>Source:</b> <a href="http://journals.sagepub.com/doi/abs/10.1177/0269881117725711" style="color: #6699cc;" target="_blank">http://journals.sagepub.com/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px; text-transform: uppercase;">Elevated Translocator Protein in Anterior Cingulate in Major Depression and a Role for Inflammation in Suicidal Thinking: A Positron Emission Tomography Study</span></span></h2>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b>Biological Psychiatry</b></i></span></span></div>
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<i><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Background</span></span></i><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Major depressive disorder is associated with raised peripheral inflammatory markers. Mounting evidence also suggests that inflammation is involved in suicidal behavior. However, the involvement of inflammation in the brains of individuals with depression, and its association with suicidal ideation, needs further clarification. Translocator protein (TSPO), which is upregulated in activated glia (predominantly microglia), can be measured as an indication of neuroinflammation in vivo using positron emission tomography and TSPO-specific radioligands.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We used [11C](R)-PK11195 positron emission tomography to compare TSPO availability in the anterior cingulate cortex (ACC), prefrontal cortex, and insula between 14 medication-free patients in a major depressive episode of at least moderate severity and 13 matched healthy control subjects. In a post hoc analysis, we also compared TSPO availability between patients with and without suicidal thoughts.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Multivariate analysis of variance indicated significantly higher TSPO in patients compared with control subjects (p = .005). The elevation was of large effect size and significant in the ACC (p = .022, Cohen’s d = 0.95), with smaller nonsignificant elevations in the prefrontal cortex (p = .342, Cohen’s d = 0.38) and insula (p = .466, Cohen’s d = 0.29). TSPO was not elevated in patients without suicidal thinking but was significantly increased in those with suicidal thoughts compared with those without, most robustly in the ACC (p = .008) and insula (p = .023).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We confirm evidence for increased TSPO availability, suggestive of predominantly microglial activation, in the ACC during a moderate to severe major depressive episode. Our findings provide further incentive for evaluating anti-inflammatory therapies in major depressive disorder.</span><span style="color: #444444;"><span style="font-size: 14.85px;"> </span></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"> </span></div>
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<b><br /></b><b>Source:</b> <a href="http://www.biologicalpsychiatryjournal.com/article/S0006-3223%2817%2931857-7/fulltext" style="color: #6699cc;" target="_blank">http://www.biologicalpsychiatryjournal.com/</a></div>
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<i style="font-size: 14.85px; line-height: 20.79px;"><b>Molecular Psychiatry</b></i><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The amyloid-β protein (Aβ) protein plays a pivotal role in the pathogenesis of Alzheimer’s disease (AD). It is believed that Aβ deposited in the brain originates from the brain tissue itself. However, Aβ is generated in both brain and peripheral tissues. Whether circulating Aβ contributes to brain AD-type pathologies remains largely unknown. In this study, using a model of parabiosis between APPswe/PS1dE9 transgenic AD mice and their wild-type littermates, we observed that the human Aβ originated from transgenic AD model mice entered the circulation and accumulated in the brains of wild-type mice, and formed cerebral amyloid angiopathy and Aβ plaques after a 12-month period of parabiosis. AD-type pathologies related to the Aβ accumulation including tau hyperphosphorylation, neurodegeneration, neuroinflammation and microhemorrhage were found in the brains of the parabiotic wild-type mice. More importantly, hippocampal CA1 long-term potentiation was markedly impaired in parabiotic wild-type mice. To the best of our knowledge, our study is the first to reveal that blood-derived Aβ can enter the brain, form the Aβ-related pathologies and induce functional deficits of neurons. Our study provides novel insight into AD pathogenesis and provides evidence that supports the development of therapies for AD by targeting Aβ metabolism in both the brain and the periphery.</span></span></div>
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<b>Source:</b> <a href="https://www.nature.com/articles/mp2017204" style="color: #6699cc;" target="_blank">https://www.nature.com/</a></div>
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<span style="font-size: 14.85px; line-height: 20.79px;">Psilocybin for treatment-resistant depression: fMRI-measured brain mechanisms</span></h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Psilocybin with psychological support is showing promise as a treatment model in psychiatry but its therapeutic mechanisms are poorly understood. Here, cerebral blood flow (CBF) and blood oxygen-level dependent (BOLD) resting-state functional connectivity (RSFC) were measured with functional magnetic resonance imaging (fMRI) before and after treatment with psilocybin (serotonin agonist) for treatment-resistant depression (TRD). Quality pre and post treatment fMRI data were collected from 16 of 19 patients. Decreased depressive symptoms were observed in all 19 patients at 1-week post-treatment and 47% met criteria for response at 5 weeks. Whole-brain analyses revealed post-treatment decreases in CBF in the temporal cortex, including the amygdala. Decreased amygdala CBF correlated with reduced depressive symptoms. Focusing on a priori selected circuitry for RSFC analyses, increased RSFC was observed within the default-mode network (DMN) post-treatment. Increased ventromedial prefrontal cortex-bilateral inferior lateral parietal cortex RSFC was predictive of treatment response at 5-weeks, as was decreased parahippocampal-prefrontal cortex RSFC. These data fill an important knowledge gap regarding the post-treatment brain effects of psilocybin, and are the first in depressed patients. The post-treatment brain changes are different to previously observed acute effects of psilocybin and other ‘psychedelics’ yet were related to clinical outcomes. A ‘reset’ therapeutic mechanism is proposed.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><b style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;">Source:</b><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"> </span><a href="https://www.nature.com/articles/s41598-017-13282-7" style="color: #6699cc; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;" target="_blank">https://www.nature.com/</a></div>
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The Effect of a Single Dose of Intravenous Ketamine on Suicidal Ideation: A Systematic Review and Individual Participant Data Meta-Analysis</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Suicide is a public health crisis with limited treatment options. The authors conducted a systematic review and individual participant data meta-analysis examining the effects of a single dose of ketamine on suicidal ideation.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Method</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Individual participant data were obtained from 10 of 11 identified comparison intervention studies that used either saline or midazolam as a control treatment. The analysis included only participants who had suicidal ideation at baseline (N=167). A one-stage, individual participant data, meta-analytic procedure was employed using a mixed-effects, multilevel, general linear model. The primary outcome measures were the suicide items from clinician-administered (the Montgomery-Åsberg Depression Rating Scale [MADRS] or the Hamilton Depression Rating Scale [HAM-D]) and self-report scales (the Quick Inventory of Depressive Symptomatology–Self Report [QIDS-SR] or the Beck Depression Inventory [BDI]), obtained for up to 1 week after ketamine administration.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Ketamine rapidly (within 1 day) reduced suicidal ideation significantly on both the clinician-administered and self-report outcome measures. Effect sizes were moderate to large (Cohen’s d=0.48–0.85) at all time points after dosing. A sensitivity analysis demonstrated that compared with control treatments, ketamine had significant benefits on the individual suicide items of the MADRS, the HAM-D, and the QIDS-SR but not the BDI. Ketamine’s effect on suicidal ideation remained significant after adjusting for concurrent changes in severity of depressive symptoms.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Ketamine rapidly reduced suicidal thoughts, within 1 day and for up to 1 week in depressed patients with suicidal ideation. Ketamine’s effects on suicidal ideation were partially independent of its effects on mood, although subsequent trials in transdiagnostic samples are required to confirm that ketamine exerts a specific effect on suicidal ideation. Additional research on ketamine’s long-term safety and its efficacy in reducing suicide risk is needed before clinical implementation.</span></span></div>
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<b>Source:</b> <a href="http://ajp.psychiatryonline.org/doi/abs/10.1176/appi.ajp.2017.17040472" rel="" style="color: #6699cc;" target="_blank">http://ajp.psychiatryonline.org/</a></div>
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Interpreting Biomarker Results in Individual Patients With Mild Cognitive Impairment in the Alzheimer’s Biomarkers in Daily Practice (ABIDE) Project</h2>
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<i><b>JAMA Neurology</b></i></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Importance </i><br />Biomarkers do not determine conversion to Alzheimer disease (AD) perfectly, and criteria do not specify how to take patient characteristics into account. Consequently, biomarker use may be challenging for clinicians, especially in patients with mild cognitive impairment (MCI).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective </i> <br />To construct biomarker-based prognostic models that enable determination of future AD dementia in patients with MCI.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants </i><br />This study is part of the Alzheimer’s Biomarkers in Daily Practice (ABIDE) project. A total of 525 patients with MCI from the Amsterdam Dementia Cohort (longitudinal cohort, tertiary referral center) were studied. All patients had their baseline visit to a memory clinic from September 1, 1997, through August 31, 2014. Prognostic models were constructed by Cox proportional hazards regression with patient characteristics (age, sex, and Mini-Mental State Examination [MMSE] score), magnetic resonance imaging (MRI) biomarkers (hippocampal volume, normalized whole-brain volume), cerebrospinal fluid (CSF) biomarkers (amyloid-β1-42, tau), and combined biomarkers. Data were analyzed from November 1, 2015, to October 1, 2016.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures </i><br />Clinical end points were AD dementia and any type of dementia after 1 and 3 years.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i> <br />Of the 525 patients, 210 (40.0%) were female, and the mean (SD) age was 67.3 (8.4) years. On the basis of age, sex, and MMSE score only, the 3-year progression risk to AD dementia ranged from 26% (95% CI, 19%-34%) in younger men with MMSE scores of 29 to 76% (95% CI, 65%-84%) in older women with MMSE scores of 24 (1-year risk: 6% [95% CI, 4%-9%] to 24% [95% CI, 18%-32%]). Three- and 1-year progression risks were 86% (95% CI, 71%-95%) and 27% (95% CI, 17%-41%) when MRI results were abnormal, 82% (95% CI, 73%-89%) and 26% (95% CI, 20%-33%) when CSF test results were abnormal, and 89% (95% CI, 79%-95%) and 26% (95% CI, 18%-36%) when the results of both tests were abnormal. Conversely, 3- and 1-year progression risks were 18% (95% CI, 13%-27%) and 3% (95% CI, 2%-5%) after normal MRI results, 6% (95% CI, 3%-9%) and 1% (95% CI, 0.5%-2%) after normal CSF test results, and 4% (95% CI, 2%-7%) and 0.5% (95% CI, 0.2%-1%) after combined normal MRI and CSF test results. The prognostic value of models determining any type of dementia were in the same order of magnitude although somewhat lower. External validation in Alzheimer’s Disease Neuroimaging Initiative 2 showed that our models were highly robust.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance </i><br />This study provides biomarker-based prognostic models that may help determine AD dementia and any type of dementia in patients with MCI at the individual level. This finding supports clinical decision making and application of biomarkers in daily practice.</span></span></div>
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<b>Source:</b> <a href="https://jamanetwork.com/journals/jamaneurology/article-abstract/2657326" rel="" style="color: #6699cc;" target="_blank">https://jamanetwork.com/journals/jamaneurology/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Schizophrenia (SZ) is a devastating mental disease caused by complex genetic and environmental factors. The pathological process and clinical manifestation of SZ are heterogeneous among patients, which hampers precise diagnosis and treatment of the disease. Since no objective marker for SZ has been established today, to identify a subgroup of the patients with homogeneous biochemical traits will provide a new angle for both researchers and clinicians to understand and manage the disease. In this study, we employed the niacin skin-flushing test in Chinese population and confirmed a niacin-blunted subgroup of SZ patients distinguishable from mood disorders (MD) and normal individuals. This subgroup accounted for 30.67% of the total SZ patients with a specificity of 88.37% in male subjects and 83.75% in female subjects. We support the notion that bluntness in niacin skin test might reflect abnormalities in membrane fatty acid composition, which could be induced by increased PLA2 enzyme activity, in vivo oxidative stress or lipid metabolism imbalance in SZ. Further studies are encouraged to clarify the molecular origins of niacin-bluntness in SZ, which would provide extra clues for etiological research in schizophrenia and for new targeted treatment.</span></span></div>
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<b>Source:</b> <a href="https://academic.oup.com/schizophreniabulletin/advance-article/doi/10.1093/schbul/sbx150/4564459#98764316" style="color: #6699cc;" target="_blank">https://academic.oup.com/schizophreniabulletin/</a></div>
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Machine learning of neural representations of suicide and emotion concepts identifies suicidal youth</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The clinical assessment of suicidal risk would be substantially complemented by a biologically based measure that assesses alterations in the neural representations of concepts related to death and life in people who engage in suicidal ideation. This study used machine-learning algorithms (Gaussian Naive Bayes) to identify such individuals (17 suicidal ideators versus 17 controls) with high (91%) accuracy, based on their altered functional magnetic resonance imaging neural signatures of death-related and life-related concepts. The most discriminating concepts were ‘death’, ‘cruelty’, ‘trouble’, ‘carefree’, ‘good’ and ‘praise’. A similar classification accurately (94%) discriminated nine suicidal ideators who had made a suicide attempt from eight who had not. Moreover, a major facet of the concept alterations was the evoked emotion, whose neural signature served as an alternative basis for accurate (85%) group classification. This study establishes a biological, neurocognitive basis for altered concept representations in participants with suicidal ideation, which enables highly accurate group membership classification.</span></span><br />
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<b style="font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://www.nature.com/articles/s41562-017-0234-y" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://www.nature.com/</a></div>
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<span style="color: #333333; font-family: "arial" , sans-serif;"><span style="font-size: 18px; line-height: 22px; text-transform: uppercase;">FDA permits marketing of mobile medical application for substance use disorder</span></span></h2>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b><br /></b></i></span></span><span style="color: #333333; font-size: 14.85px; font-style: italic; font-weight: bold; line-height: 20.79px;">FDA</span><br />
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<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The U.S. Food and Drug Administration permitted marketing of the first mobile medical application to help treat substance use disorders (SUD). The Reset application is intended to be used with outpatient therapy to treat alcohol, cocaine, marijuana and stimulant SUDs. The application is not intended to be used to treat opioid dependence.</span></span><br />
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<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">“This is an example of how innovative digital technologies can help provide patients access to additional tools during their treatment,” said Carlos Peña, Ph.D., M.S., director of the Division of Neurological and Physical Medicine Devices in FDA’s Center for Devices and Radiological Health. “More therapy tools means a greater potential to help improve outcomes, including abstinence, for patients with substance use disorder.”</span></span><br />
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<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">According to the Substance Abuse and Mental Health Services Administration, SUD occurs when an individual’s recurrent use of alcohol and/or drugs causes clinically and functionally significant impairment, such as health problems, disability, and failure to meet major responsibilities at work, school or home. According to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, a diagnosis of substance use disorder is based on evidence of impaired control, social impairment, risky use and pharmacological criteria.</span></span><br />
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<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The Reset device is a mobile medical application system containing a patient application and clinician dashboard. The device delivers cognitive behavioral therapy to patients to teach the user skills that aid in the treatment of SUD and are intended to increase abstinence from substance abuse and increase retention in outpatient therapy programs. The system is intended to be used in conjunction with outpatient therapy and in addition to a contingency management system, a widely-used program for treating SUD that uses a series of incentives to reward patients for adherence to their treatment program.</span></span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Read More:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm576087.htm" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://www.fda.gov/NewsEvents/Newsroom/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; text-transform: uppercase;">Potential Biomarkers Of Tardive Dyskinesia: A Multiplex Analysis Of Blood Serum</span></span></h2>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b>Neuroscience Applied</b></span></i></span><br />
<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b><br /></b></span></i></span><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Introduction</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Long-term antipsychotic treatment of schizophrenia is associated </span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">with the emergence of tardive dyskinesia (TD), a motor syndrome </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">consisting of involuntary and hyperkinetic movements [1].</span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Pathogenesis of this drug-induced movement disorder is not yet fully </span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">established, but may be connected to oxidative stress-related indirect </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">pathway neurotoxicity [2]. Dysregulations in immune, hormonal and </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">neurotrophic systems have been postulated to be one of the </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">mechanisms underlying this form of neurotoxicity [3, 4]. Principle </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">aims of translational psychiatric research are searching for biomarkers </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">which can be used to diagnose pathological biochemical processes </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">and to identify molecular targets for treatment as well as development </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">of pharmacogenetic approaches to personalize this therapy.</span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Aims</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The aim is to study potential endocrine, neurotrophic and </span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">immunological markers of tardive dyskinesia in the blood serum of </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">patients with schizophrenia with antipsychotic therapy.</span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">After obtaining approval of the study protocol by the local ethical </span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">committee, suitable participants were recruited from psychiatric </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">hospitals. All subjects gave informed consent after proper explanation </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">of the study. TD was assessed cross-sectionally by the use of the </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">Abnormal Involuntary Movement Scale (AIMS) [1, 5]. The </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">concentrations of cortisol, brain-derived neurotrophic factor (BDNF), </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">prolactin, cytokines (tumor necrosis factor (TNFa), interleukin 1 (IL-</span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">1β), interleukin 3 (IL-3), interleukin 6 (IL-6), interferon gamma (INF-</span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">γ) and S100β were measured in blood serum using the </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">MILLIPLEX® MAP panels (Merck, Darmstadt, Germany) by the </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">multiplex analyzer MAGPIX (Luminex, USA). Statistical analyses were </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">performed using SPSS software for Windows. Results were expressed </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">as median and quartile intervals (Me [Q1; Q3]) or mean and standard </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">deviation (M±SD). Differences were considered significant at p≤0.05.</span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">In total 180 patients with schizophrenia, 128 males and 52 females (age </span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">39.2±12.1 years), receiving long-term antipsychotic treatment were </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">included. These patients were divided into two groups: 71 patients </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">with tardive dyskinesia and 109 patients without this movement </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">disorder. A significant (p=0.04) decrease in BDNF concentration was </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">observed in patients with TD (1.9 [1.01; 2.99] ng/ml) in comparison to </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">patients without TD (2.66 [1.29; 3.89] ng/ml) (Fig.1). An increase</span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">(p=0.05) of the serum IL-6 level of patients with TD (5.69 [3.55; 7.4] </span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">pg/ml) was detected relative to patients without TD (4.69 [2.82; 6.13] </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">pg/ml) (Fig.2). In addition, a statistical trend (p=0.06) of increased </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">serum S100β concentration was found in TD patients (85.29±5.53 </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">ng/L) compared to patients without this side effect (75.14±2.81 ng/L) </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">(Fig.3). No other significant differences were established concerning </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">the other assayed biomarkers.</span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Discussion</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The biological processes that might play a role in the </span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">development of TD are not confined to the human brain per se. </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">Hormonal and immune systems are also involved, which may be</span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">related to these systems being closely interrelated. Furthermore, </span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">these parameters may provide information about risk factors of </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">the movement disorder. Identifying markers that can be used as</span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">diagnostics or predictors of treatment response in people with </span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">tardive dyskinesia will be an important step towards being able to </span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">provide personalized treatment.</span><br />
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://www.ecnp.eu/presentationpdfs/71/P.3.d.028.pdf" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">https://www.ecnp.eu/presentationpdfs/</a></div>
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<b><a href="http://journals.lww.com/psychopharmacology/Pages/currenttoc.aspx" style="color: #6699cc;" target="_blank">Journal of Clinical Psychopharmacology - December 2017 - Volume 37, Issue 6</a></b></div>
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<b><a href="http://www.nature.com/npp/journal/v42/n13/index.html" style="color: #6699cc;" target="_blank">Neuropsychopharmacology - Volume 42, Issue 13 (December 2017)</a></b></div>
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<b><a href="https://link.springer.com/journal/213/234/23/page/1" style="color: #6699cc;" target="_blank">Psychopharmacology - Volume 234, Issue 24, December 2017</a></b></div>
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<b><a href="http://jop.sagepub.com/content/current" style="color: #6699cc;" target="_blank">Journal of Psychopharmacology - October 2017; 31 (10)</a></b></div>
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<b><a href="http://ajp.psychiatryonline.org/toc/ajp/current" style="color: #6699cc;" target="_blank">The American Journal of Psychiatry - November 2017, Vol. 174, Issue 11</a></b></div>
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<b style="color: #6699cc;"><a href="http://archpsyc.jamanetwork.com/issue.aspx" style="color: #6699cc;" target="_blank">JAMA Psychiatry - November 2017, Vol. 74, No. 11</a></b></div>
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<b><a href="http://www.nature.com/neuro/journal/v20/n11/index.html" style="color: #6699cc;" target="_blank">Nature Neuroscience - November 2017, Vol 20, N° 11</a></b></div>
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<b><a href="http://www.nature.com/mp/journal/v22/n11/index.html" style="color: #6699cc;" target="_blank">Molecular Psychiatry - Volume 22, Issue 11, November 2017</a></b></div>
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<b style="background-color: white; color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"><a href="http://www.biologicalpsychiatryjournal.com/current" style="color: #6699cc;" target="_blank">Biological Psychiatry - Volume 82, Issue 12, December 2017</a></b><br />
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<b><a href="https://academic.oup.com/brain/issue/140/11?browseBy=volume" style="color: #6699cc;" target="_blank">Brain - Volume 140, Issue 11, November 2017</a></b></div>
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<b><span style="font-size: small;">Join us on LinkedIn:</span> </b><b><a href="http://www.linkedin.com/groups/Neuropsychopharmacology-Neuroscience-5147601" style="color: #6699cc;">Neurosychopharmacology News Group</a></b></h3>
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Eutimiahttp://www.blogger.com/profile/07836706907685752267noreply@blogger.comtag:blogger.com,1999:blog-1045445187620004007.post-55667562722006752432017-09-07T13:49:00.003-04:002017-09-08T17:45:16.706-04:00September 2017<div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Teva Pharmaceuticals Ltd. on Wednesday announced that the Food and Drug Administration has approved Austedo (deutetrabenazine) tablets for the treatment of adults with tardive dyskinesia (TD). Deutetrabenazine is a small molecule vesicular monoamine 2 transporter (VMAT2) inhibitor that has FDA approval for the treatment of chorea associated with Huntington’s disease.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The approval was based in part on the results of two 12-week, randomized, double-blind, placebo-controlled, multicenter trials, which compared changes in involuntary movements in 335 patients with TD who took deutetrabenazine or placebo. A total of 62% of the patients had concurrent diagnoses of schizophrenia/schizoaffective disorder, and 33% had a mood disorder; 86% were receiving concomitant antipsychotics. </span></span><br />
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<b>Read More:</b> <a href="http://alert.psychnews.org/2017/08/fda-approves-deutetrabenazine-for.html" style="color: #6699cc;" target="_blank">http://alert.psychnews.org/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">There has not been, until recently, a comprehensive classification of psychotropic agents (Nutt, 2009). Indeed, these medications are generally considered to belong to one of the five classes: antipsychotics, antidepressants, anxiolytics, hypnotics, and mood stabilizers. It is obvious that, even when considering the strict regulatory guidelines, there are numerous medications that cross such denominations (Stahl, 2013). For instance, the ‘atypical antipsychotic’ aripiprazole has official indications for the treatment of schizophrenia, bipolar mania, and unipolar major depressive disorder (MDD) with inadequate response to antidepressants. Furthermore, another drug of that same family, quetiapine, is often used at doses of 100 mg or less at bedtime as a sedative, at doses of 150–300 mg per day in the treatment of MDD (alone or in combination with an antidepressant), at 300–600 mg per day in bipolar disorder, and at regimens above 600 mg per day for schizophrenia. Using the existing classification, quetiapine could actually belong to all five of the above-mentioned categories. The current approach is thus outdated and untenable.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">A task force of members of five scientific organizations (the American, Asian, European, and International Colleges of Neuropsychopharmacology, as well as the International Union of Basic and Clinical Pharmacology) started developing in 2008 a neuroscience-based nomenclature (NbN) with primary focus on neuronal targets rather than on clinical indications. This approach was deemed feasible and radically new because the pre-existing categories could not be logically enriched. The task force recognized that the current knowledge base would not always be sufficient to define the primary target or the correct mechanism of action for certain drugs. Consequently, a cutting-edge scientific framework as developed. The task force realized that as knowledge increases regarding targets and mechanisms of action, and new medications are developed, the framework may need to be adjusted. As such, the committee will continue to meet twice a year to update classifications.</span><span style="color: #444444;"><span style="font-size: 14.85px;"> </span></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"> </span></div>
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<b><br /></b><b>Read More:</b> <a href="http://www.nature.com/npp/journal/v42/n10/full/npp201733a.html" style="color: #6699cc;" target="_blank">http://www.nature.com/npp/journal/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i><br />To determine the relationship between sleep quality and CSF markers of Alzheimer disease (AD) pathology in late midlife.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i><br />We investigated the relationship between sleep quality and CSF AD biomarkers in a cohort enriched for parental history of sporadic AD, the Wisconsin Registry for Alzheimer's Prevention. A total of 101 participants (mean age 62.9 ± 6.2 years, 65.3% female) completed sleep assessments and CSF collection and were cognitively normal. Sleep quality was measured with the Medical Outcomes Study Sleep Scale. CSF was assayed for biomarkers of amyloid metabolism and plaques (β-amyloid 42 [Aβ42]), tau pathology (phosphorylated tau [p-tau] 181), neuronal/axonal degeneration (total tau [t-tau], neurofilament light [NFL]), neuroinflammation/astroglial activation (monocyte chemoattractant protein–1 [MCP-1], chitinase-3-like protein 1 [YKL-40]), and synaptic dysfunction/degeneration (neurogranin). To adjust for individual differences in total amyloid production, Aβ42 was expressed relative to Aβ40. To assess cumulative pathology, CSF biomarkers were expressed in ratio to Aβ42. Relationships among sleep scores and CSF biomarkers were assessed with multiple regression, controlling for age, sex, time between sleep and CSF measurements, and CSF assay batch.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i><br />Worse subjective sleep quality, more sleep problems, and daytime somnolence were associated with greater AD pathology, indicated by lower CSF Aβ42/Aβ40 and higher t-tau/Aβ42, p-tau/Aβ42, MCP-1/Aβ42, and YKL-40/Aβ42. There were no significant associations between sleep and NFL or neurogranin.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i><br />Self-report of poor sleep was associated with greater AD-related pathology in cognitively healthy adults at risk for AD. Effective strategies exist for improving sleep; therefore sleep health may be a tractable target for early intervention to attenuate AD pathogenesis.</span></span></div>
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<b>Source:</b> <a href="http://www.neurology.org/content/early/2017/07/05/WNL.0000000000004171" style="color: #6699cc;" target="_blank">http://www.neurology.org/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Importance </i><br />Maternal antidepressant medication use during pregnancy has previously been associated with adverse outcomes in offspring, but to our knowledge, the association with intellectual disability (ID) has not been investigated.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objectives </i><br />To examine the association of maternal antidepressant medication use during pregnancy with ID in offspring and investigate the importance of parental mental illness for such an association.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants</i> <br />A population-based cohort study of 179 007 children born from January 1, 2006, through December 31, 2007, with complete parental information from national registers who were followed up from birth throughout 2014.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures</i> <br />We estimated relative risks (RRs) and 95% CIs of ID in children exposed during pregnancy to any antidepressant medication or specifically to selective serotonin reuptake inhibitor (SSRI) antidepressants, all other non-SSRI antidepressants, or other nonantidepressant psychotropic medications. Analyses were adjusted for potential confounders. In addition to full population analyses, we used a subsample to compare mothers who used antidepressants during pregnancy with mothers who had at least one diagnosis of depression or anxiety before childbirth but did not use antidepressants during pregnancy.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results </i><br />Of the 179 007 children included in the study (mean [SD] age at end of follow-up, 7.9 [0.6] years; 92 133 [51.5%] male and 86 874 [48.5%] female), ID was diagnosed in 37 children (0.9%) exposed to antidepressants and in 819 children (0.5%) unexposed to antidepressants. With adjustment for potential confounders, the RR of ID after antidepressant exposure was estimated at 1.33 (95% CI, 0.90-1.98) in the full population sample and 1.64 (95% CI, 0.95-2.83) in the subsample of women with depression. Results from analyses of SSRI antidepressants, non-SSRI antidepressants, and nonantidepressant psychotropic medications and analyses in the clinically relevant subsample did not deviate from the full-sample results.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance</i> <br />The unadjusted RR of ID was increased in offspring born to mothers treated with antidepressants during pregnancy. After adjustment for confounding factors, however, the current study did not find evidence of an association between ID and maternal antidepressant medication use during pregnancy. Instead, the association may be attributable to a mechanism integral to other factors, such as parental age and mother’s psychiatric disorder.</span></span><br />
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The VA augmentation and switching treatments for improving depression outcomes (VAST-D) study: Rationale and design considerations</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Because two-thirds of patients with Major Depressive Disorder do not achieve remission with their first antidepressant, we designed a trial of three “next-step” strategies: switching to another antidepressant (bupropion-SR) or augmenting the current antidepressant with either another antidepressant (bupropion-SR) or with an atypical antipsychotic (aripiprazole). The study will compare 12-week remission rates and, among those who have at least a partial response, relapse rates for up to 6 months of additional treatment. We review seven key efficacy/effectiveness design decisions in this mixed “efficacy-effectiveness” trial.</span></span></div>
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<b>Source:</b> <a href="http://www.psy-journal.com/article/S0165-1781(15)00556-9/abstract" rel="" style="color: #6699cc;" target="_blank">http://www.psy-journal.com/</a></div>
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FDA Approves Long-acting Injectable ARIPIPRAZOLE for Bipolar I Disorder IN ADULTS</h2>
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<i><b>Medscape</b></i></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The extended-release formulation of aripiprazole (Abilify Maintena, Otsuka Pharmaceutical Co, Ltd, and H. Lundbeck A/S) has been approved by the US Food and Drug Administration (FDA) for use as an injectable suspension for maintenance monotherapy of bipolar I disorder (BP-I) in adults, the companies have announced.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Abilify Maintena, an atypical antipsychotic, is a sterile lyophilized powder that, when reconstituted with sterile water, forms a suspension that can be administered by injection. It was created by Otsuka in Japan and has been jointly developed and commercialized by Otsuka and Lundbeck.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">"Abilify Maintena provides healthcare professionals a new treatment option for their patients who have established tolerability with oral aripiprazole," Joseph Calabrese, MD, director, Mood Disorders Program, University Hospitals Cleveland Medical Center, and professor of psychiatry, Case Western Reserve University School of Medicine, Cleveland, Ohio, said in a press release.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">"Receiving Abilify Maintena each month as prescribed and administered by a healthcare professional provides patients an opportunity to be free from taking their daily antipsychotic for bipolar I disorder."</span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">He stressed that concomitant oral antipsychotic medication must be administered for 14 days after the first injection.</span></span></div>
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<b>Read More:</b> <a href="http://www.medscape.com/viewarticle/883591" rel="" style="color: #6699cc;" target="_blank">http://www.medscape.com/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Importance </i><br />Results from animal and human studies suggest that lithium in therapeutic doses may improve learning and memory and modify the risk of developing dementia. Additional preliminary studies suggest that subtherapeutic levels, including microlevels of lithium, may influence human cognition.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective </i><br />To investigate whether the incidence of dementia in the general population covaries with long-term exposure to microlevels of lithium in drinking water.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants </i><br />This Danish nationwide, population-based, nested case-control study examined longitudinal, individual geographic data on municipality of residence and data from drinking water measurements combined with time-specific data from all patients aged 50 to 90 years with a hospital contact with a diagnosis of dementia from January 1, 1970, through December 31, 2013, and 10 age- and sex-matched control individuals from the Danish population. The mean lithium exposure in drinking water since 1986 was estimated for all study individuals. Data analysis was performed from January 1, 1995, through December 31, 2013.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures </i><br />A diagnosis of dementia in a hospital inpatient or outpatient contact. Diagnoses of Alzheimer disease and vascular dementia were secondary outcome measures. In primary analyses, distribution of lithium exposure was compared between patients with dementia and controls.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results </i><br />A total of 73 731 patients with dementia and 733 653 controls (median age, 80.3 years; interquartile range, 74.9-84.6 years; 44 760 female [60.7%] and 28 971 male [39.3%]) were included in the study. Lithium exposure was statistically significantly different between patients with a diagnosis of dementia (median, 11.5 µg/L; interquartile range, 6.5-14.9 µg/L) and controls (median, 12.2 µg/L; interquartile range, 7.3-16.0 µg/L; P < .001). A nonlinear association was observed. Compared with individuals exposed to 2.0 to 5.0 µg/L, the incidence rate ratio (IRR) of dementia was decreased in those exposed to more than 15.0 µg/L (IRR, 0.83; 95% CI, 0.81-0.85; P < .001) and 10.1 to 15.0 µg/L (IRR, 0.98; 95% CI, 0.96-1.01; P = .17) and increased with 5.1 to 10.0 µg/L (IRR, 1.22; 95% CI, 1.19-1.25; P < .001). Similar patterns were found with Alzheimer disease and vascular dementia as outcomes.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance </i><br />Long-term increased lithium exposure in drinking water may be associated with a lower incidence of dementia in a nonlinear way; however, confounding from other factors associated with municipality of residence cannot be excluded.</span></span></div>
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<b>Source:</b> <a href="http://jamanetwork.com/journals/jamapsychiatry/article-abstract/2649277" style="color: #6699cc;" target="_blank">http://jamanetwork.com/journals/jamapsychiatry/</a></div>
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Retinal amyloid pathology and proof-of-concept imaging trial in Alzheimer’s disease</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Background</i>Noninvasive detection of Alzheimer’s disease (AD) with high specificity and sensitivity can greatly facilitate identification of at-risk populations for earlier, more effective intervention. AD patients exhibit a myriad of retinal pathologies, including hallmark amyloid β-protein (Aβ) deposits.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i><br />Burden, distribution, cellular layer, and structure of retinal Aβ plaques were analyzed in flat mounts and cross sections of definite AD patients and controls (n = 37). In a proof-of-concept retinal imaging trial (n = 16), amyloid probe curcumin formulation was determined and protocol was established for retinal amyloid imaging in live patients.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Histological examination uncovered classical and neuritic-like Aβ deposits with increased retinal Aβ42 plaques (4.7-fold; P = 0.0063) and neuronal loss (P = 0.0023) in AD patients versus matched controls. Retinal Aβ plaque mirrored brain pathology, especially in the primary visual cortex (P = 0.0097 to P = 0.0018; Pearson’s r = 0.84–0.91). Retinal deposits often associated with blood vessels and occurred in hot spot peripheral regions of the superior quadrant and innermost retinal layers. Transmission electron microscopy revealed retinal Aβ assembled into protofibrils and fibrils. Moreover, the ability to image retinal amyloid deposits with solid-lipid curcumin and a modified scanning laser ophthalmoscope was demonstrated in live patients. A fully automated calculation of the retinal amyloid index (RAI), a quantitative measure of increased curcumin fluorescence, was constructed. Analysis of RAI scores showed a 2.1-fold increase in AD patients versus controls (P = 0.0031).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusion</i><br />The geometric distribution and increased burden of retinal amyloid pathology in AD, together with the feasibility to noninvasively detect discrete retinal amyloid deposits in living patients, may lead to a practical approach for large-scale AD diagnosis and monitoring.</span></span><br />
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b><br /></b></i></span></span><span style="color: #333333; font-size: 14.85px; font-style: italic; font-weight: bold; line-height: 20.79px;">Brain</span><br />
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<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Individuals with schizophrenia typically suffer a range of cognitive deficits, including prominent deficits in working memory and executive function. These difficulties are strongly predictive of functional outcomes, but there is a paucity of effective therapeutic interventions targeting these deficits. Transcranial direct current stimulation is a novel neuromodulatory technique with emerging evidence of potential pro-cognitive effects; however, there is limited understanding of its mechanism. This was a double-blind randomized sham controlled pilot study of transcranial direct current stimulation on a working memory (n-back) and executive function (Stroop) task in 28 individuals with schizophrenia using functional magnetic resonance imaging. Study participants received 30 min of real or sham transcranial direct current stimulation applied to the left frontal cortex. The ‘real’ and ‘sham’ groups did not differ in online working memory task performance, but the transcranial direct current stimulation group demonstrated significant improvement in performance at 24 h post-transcranial direct current stimulation. Transcranial direct current stimulation was associated with increased activation in the medial frontal cortex beneath the anode; showing a positive correlation with consolidated working memory performance 24 h post-stimulation. There was reduced activation in the left cerebellum in the transcranial direct current stimulation group, with no change in the middle frontal gyrus or parietal cortices. Improved performance on the executive function task was associated with reduced activity in the anterior cingulate cortex. Transcranial direct current stimulation modulated functional activation in local task-related regions, and in more distal nodes in the network. Transcranial direct current stimulation offers a potential novel approach to altering frontal cortical activity and exerting pro-cognitive effects in schizophrenia.</span></span></div>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b>The American Journal of Psychiatry</b></span></i></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">This study evaluated rates of all-cause mortality and self-harm in association with clozapine treatment in individuals with treatment-resistant schizophrenia.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Method</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">A population-based cohort of 2,370 individuals with treatment-resistant schizophrenia after Jan. 1, 1996, was followed until death, first episode of self-harm, emigration, or June 1, 2013. Time to all-cause death and time to first episode of self-harm were analyzed in Cox regression models with time-varying treatment, adjusted for clinical and sociodemographic covariates.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The rate of all-cause mortality was higher for patients not receiving clozapine than for those given clozapine (hazard ratio: 1.88, 95% confidence interval [CI]: 1.16–3.05). This was driven mainly by periods of no antipsychotic treatment (hazard ratio: 2.50, 95% CI: 1.50–4.17), with nonsignificantly higher mortality during treatment with other antipsychotics (hazard ratio: 1.45, 95% CI: 0.86–2.45). Excess mortality was observed in the year after clozapine discontinuation (hazard ratio: 2.65, 95% CI: 1.47–4.78). The rate of self-harm was higher for nonclozapine antipsychotics than for clozapine (hazard ratio: 1.36, 95% CI: 1.04–1.78).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">The results demonstrate a nearly twofold higher mortality rate among individuals with treatment-resistant schizophrenia not treated with clozapine compared with clozapine-treated individuals. Furthermore, the results suggest a harmful effect of other antipsychotics regarding self-harm compared with clozapine. It remains to be investigated to what extent the observed excess mortality after clozapine discontinuation is confounded by nonadherence and other unobserved factors and to what extent it is mediated by adverse effects from recent clozapine exposure or deterioration in physical or mental health precipitated by clozapine discontinuation.</span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://ajp.psychiatryonline.org/doi/abs/10.1176/appi.ajp.2017.16091097" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">http://ajp.psychiatryonline.org/</a></div>
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<b><a href="http://journals.lww.com/psychopharmacology/Pages/currenttoc.aspx" style="color: #6699cc;" target="_blank">Journal of Clinical Psychopharmacology - October 2017 - Volume 37, Issue 5</a></b></div>
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<b><a href="http://www.nature.com/npp/journal/v42/n10/index.html" style="color: #6699cc;" target="_blank">Neuropsychopharmacology - Volume 42, Issue 10 (September 2017)</a></b></div>
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<b><a href="https://link.springer.com/journal/213/234/18/page/1" style="color: #6699cc;" target="_blank">Psychopharmacology - Volume 234, Issue 18, September 2017</a></b></div>
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<b><a href="http://jop.sagepub.com/content/current" style="color: #6699cc;" target="_blank">Journal of Psychopharmacology - August 2017; 31 (8)</a></b></div>
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<b><a href="http://ajp.psychiatryonline.org/toc/ajp/current" style="color: #6699cc;" target="_blank">The American Journal of Psychiatry - September 2017, Vol. 174, Issue 9</a></b></div>
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<b style="color: #6699cc;"><a href="http://archpsyc.jamanetwork.com/issue.aspx" style="color: #6699cc;" target="_blank">JAMA Psychiatry - September 2017, Vol. 74, No. 9</a></b></div>
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<b><a href="http://www.nature.com/neuro/journal/v20/n9/index.html" style="color: #6699cc;" target="_blank">Nature Neuroscience - September 2017, Vol 20, N° 9</a></b></div>
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<b><a href="http://www.nature.com/mp/journal/v22/n9/index.html" style="color: #6699cc;" target="_blank">Molecular Psychiatry - Volume 22, Issue 9, September 2017</a></b></div>
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<b style="background-color: white; color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"><a href="http://www.biologicalpsychiatryjournal.com/current" style="color: #6699cc;" target="_blank">Biological Psychiatry - Volume 82, Issue 7, October 2017</a></b><br />
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<b><a href="https://academic.oup.com/brain/issue/140/9?browseBy=volume" style="color: #6699cc;" target="_blank">Brain - Volume 140, Issue 9, September 2017</a></b></div>
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<b><span style="font-size: small;">Join us on LinkedIn:</span> </b><b><a href="http://www.linkedin.com/groups/Neuropsychopharmacology-Neuroscience-5147601" style="color: #6699cc;">Neurosychopharmacology News Group</a></b></h3>
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Eutimiahttp://www.blogger.com/profile/07836706907685752267noreply@blogger.comtag:blogger.com,1999:blog-1045445187620004007.post-71419240973079529502017-07-03T13:55:00.000-04:002017-07-30T13:58:17.714-04:00July 2017<div dir="ltr" style="text-align: left;" trbidi="on">
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<i style="font-size: 14.85px; line-height: 20.79px;"><br /></i><i><b>The Lancet</b></i></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Background</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Post-partum depression is a serious mood disorder in women that might be triggered by peripartum fluctuations in reproductive hormones. This phase 2 study investigated brexanolone (USAN; formerly SAGE-547 injection), an intravenous formulation of allopregnanolone, a positive allosteric modulator of γ-aminobutyric acid (GABAA) receptors, for the treatment of post-partum depression.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">For this double-blind, randomised, placebo-controlled trial, we enrolled self-referred or physician-referred female inpatients (≤6 months post partum) with severe post-partum depression (Hamilton Rating Scale for Depression [HAM-D] total score ≥26) in four hospitals in the USA. Eligible women were randomly assigned (1:1), via a computer-generated randomisation program, to receive either a single, continuous intravenous dose of brexanolone or placebo for 60 h. Patients and investigators were masked to treatment assignments. The primary efficacy endpoint was the change from baseline in the 17-item HAM-D total score at 60 h, assessed in all randomised patients who started infusion of study drug or placebo and who had a completed baseline HAM-D assessment and at least one post-baseline HAM-D assessment. Patients were followed up until day 30. This trial is registered with ClinicalTrials.gov, number NCT02614547.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Findings</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">This trial was done between Dec 15, 2015 (first enrolment), and May 19, 2016 (final visit of the last enrolled patient). 21 women were randomly assigned to the brexanolone (n=10) and placebo (n=11) groups. At 60 h, mean reduction in HAM-D total score from baseline was 21·0 points (SE 2·9) in the brexanolone group compared with 8·8 points (SE 2·8) in the placebo group (difference −12·2, 95% CI −20·77 to −3·67; p=0·0075; effect size 1·2). No deaths, serious adverse events, or discontinuations because of adverse events were reported in either group. Four of ten patients in the brexanolone group had adverse events compared with eight of 11 in the placebo group. The most frequently reported adverse events in the brexanolone group were dizziness (two patients in the brexanolone group vs three patients in the placebo group) and somnolence (two vs none). Moderate treatment-emergent adverse events were reported in two patients in the brexanolone group (sinus tachycardia, n=1; somnolence, n=1) and in two patients in the placebo group (infusion site pain, n=1; tension headache, n=1); one patient in the placebo group had a severe treatment-emergent adverse event (insomnia).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Interpretation</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">In women with severe post-partum depression, infusion of brexanolone resulted in a significant and clinically meaningful reduction in HAM-D total score, compared with placebo. Our results support the rationale for targeting synaptic and extrasynaptic GABAA receptors in the development of therapies for patients with post-partum depression. A pivotal clinical programme for the investigation of brexanolone in patients with post-partum depression is in progress.</span><br />
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<b>Source:</b> <a href="http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(17)31264-3/abstract" style="color: #6699cc;" target="_blank">http://www.thelancet.com/journals/lancet/</a></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b>JAMA Psychiatry</b></i></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Importance </i><br />For a small percentage of obsessive-compulsive disorder (OCD) cases exhibiting additional neuropsychiatric symptoms, it was proposed that neuroinflammation occurs in the basal ganglia as an autoimmune response to infections. However, it is possible that elevated neuroinflammation, inducible by a diverse range of mechanisms, is important throughout the cortico-striato-thalamo-cortical circuit of OCD. Identifying brain inflammation is possible with the recent advance in positron emission tomography (PET) radioligands that bind to the translocator protein (TSPO). Translocator protein density increases when microglia are activated during neuroinflammation and the TSPO distribution volume (VT) is an index of TSPO density.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective </i><br />To determine whether TSPO VT is elevated in the dorsal caudate, orbitofrontal cortex, thalamus, ventral striatum, dorsal putamen, and anterior cingulate cortex in OCD.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants</i> <br />This case-control study was conducted at a tertiary care psychiatric hospital from May 1, 2010, to November 30, 2016. Participants with OCD (n = 20) and age-matched healthy control individuals (n = 20) underwent a fluorine F 18–labeled N-(2-(2-fluoroethoxy)benzyl)-N-(4-phenoxypyridin-3-yl)acetamide PET scan. It is a high-quality second-generation TSPO-binding PET radiotracer. All participants were drug and medication free, nonsmoking, and otherwise healthy.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures</i> <br />The TSPO VT was measured in the dorsal caudate, orbitofrontal cortex, thalamus, ventral striatum, dorsal putamen, and anterior cingulate cortex. Compulsions were assessed with the Yale-Brown Obsessive Compulsive Scale.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i> <br />In the OCD and healthy groups, the mean (SD) ages were 27.4 (7.1) years and 27.6 (6.6) years, respectively, and 11 (55%) and 8 (40%) were women, respectively. In OCD, TSPO VT was significantly elevated in these brain regions (mean, 32%; range, 31%-36% except anterior cingulate cortex, 24%; analysis of variance, effect of diagnosis: P < .001 to P = .004). Slightly lower elevations in TSPO VT (22%-29%) were present in other gray matter regions. The Yale-Brown Obsessive Compulsive Scale measure of distress associated with preventing compulsive behaviors significantly correlated with TSPO VT in the orbitofrontal cortex (uncorrected Pearson correlation r = 0.62; P = .005).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance</i> <br />To our knowledge, this is the first study demonstrating inflammation within the neurocircuitry of OCD. The regional distribution of elevated TSPO VT argues that the autoimmune/neuroinflammatory theories of OCD should extend beyond the basal ganglia to include the cortico-striato-thalamo-cortical circuit. Immunomodulatory therapies should be investigated in adult OCD, rather than solely childhood OCD, particularly in cases with prominent distress when preventing compulsions.</span><span style="color: #444444;"><span style="font-size: 14.85px;"> </span></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"> </span></div>
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<b><br /></b><b>Source:</b> <a href="http://jamanetwork.com/journals/jamapsychiatry/article-abstract/2631893" style="color: #6699cc;" target="_blank">http://jamanetwork.com/journals/jamapsychiatry/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;">Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by social deficits and repetitive behaviors that typically emerge by 24 months of age. To develop effective early interventions that can potentially ameliorate the defining deficits of ASD and improve long-term outcomes, early detection is essential. Using prospective neuroimaging of 59 6-month-old infants with a high familial risk for ASD, we show that functional connectivity magnetic resonance imaging correctly identified which individual children would receive a research clinical best-estimate diagnosis of ASD at 24 months of age. Functional brain connections were defined in 6-month-old infants that correlated with 24-month scores on measures of social behavior, language, motor development, and repetitive behavior, which are all features common to the diagnosis of ASD. A fully cross-validated machine learning algorithm applied at age 6 months had a positive predictive value of 100% [95% confidence interval (CI), 62.9 to 100], correctly predicting 9 of 11 infants who received a diagnosis of ASD at 24 months (sensitivity, 81.8%; 95% CI, 47.8 to 96.8). All 48 6-month-old infants who were not diagnosed with ASD were correctly classified [specificity, 100% (95% CI, 90.8 to 100); negative predictive value, 96.0% (95% CI, 85.1 to 99.3)]. These findings have clinical implications for early risk assessment and the feasibility of developing early preventative interventions for ASD.</span></div>
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<b>Source:</b> <a href="http://stm.sciencemag.org/content/9/393/eaag2882" style="color: #6699cc;" target="_blank">http://stm.sciencemag.org/</a></div>
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<span style="font-size: 14.85px; line-height: 20.79px;">Association of Microvascular Dysfunction With Late-Life Depression</span></h2>
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<span style="font-size: 14.85px; line-height: 20.79px;"><b><i>JAMA Psychiatry </i></b></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Importance </i><br />The etiologic factors of late-life depression are still poorly understood. Recent evidence suggests that microvascular dysfunction is associated with depression, which may have implications for prevention and treatment. However, this association has not been systematically reviewed.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective </i><br />To examine the associations of peripheral and cerebral microvascular dysfunction with late-life depression.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Data Sources</i> <br />A systematic literature search was conducted in MEDLINE and EMBASE for and longitudinal studies published since inception to October 16, 2016, that assessed the associations between microvascular dysfunction and depression.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Study Selection</i> <br />Three independent researchers performed the study selection based on consensus. Inclusion criteria were a study population 40 years of age or older, a validated method of detecting depression, and validated measures of microvascular function.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Data Extraction and Synthesis </i><br />This systematic review and meta-analysis has been registered at PROSPERO (CRD42016049158) and is reported in accordance with the PRISMA and MOOSE guidelines. Data extraction was performed by an independent researcher.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures</i> <br />The following 5 estimates of microvascular dysfunction were considered in participants with or without depression: plasma markers of endothelial function, albuminuria, measurements of skin and muscle microcirculation, retinal arteriolar and venular diameter, and markers for cerebral small vessel disease. Data are reported as pooled odds ratios (ORs) by use of the generic inverse variance method with the use of random-effects models.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results </i><br />A total of 712 studies were identified; 48 were included in the meta-analysis, of which 8 described longitudinal data. Data from 43 600 participants, 9203 individuals with depression, and 72 441 person-years (mean follow-up, 3.7 years) were available. Higher levels of plasma endothelial biomarkers (soluble intercellular adhesion molecule–1: OR, 1.58; 95% CI, 1.28-1.96), white matter hyperintensities (OR, 1.29; 95% CI, 1.19-1.39), cerebral microbleeds (OR, 1.18; 95% CI, 1.03-1.34), and cerebral (micro)infarctions (OR, 1.30; 95% CI, 1.21-1.39) were associated with depression. Among the studies available, no significant associations of albuminuria and retinal vessel diameters with depression were reported. Longitudinal data showed a significant association of white matter hyperintensities with incident depression (OR, 1.19; 95% CI, 1.09-1.30).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance</i> <br />This meta-analysis shows that both the peripheral and cerebral forms of microvascular dysfunction are associated with higher odds of (incident) late-life depression. This finding may have clinical implications because microvascular dysfunction might provide a potential target for the prevention and treatment of depression.</span></span><br />
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Effect of Liraglutide Treatment on Prediabetes and Overweight or Obesity in Clozapine- or Olanzapine-Treated Patients With Schizophrenia Spectrum Disorder</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Importance</i> <br />Compared with the general population, patients with schizophrenia have a 2- to 3-fold higher mortality rate primarily caused by cardiovascular disease. Previous interventions designed to counteract antipsychotic-induced weight gain and cardiometabolic disturbances reported limited effects.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objectives </i><br />To determine the effects of the glucagon-like peptide-1 receptor agonist liraglutide added to clozapine or olanzapine treatment of schizophrenia spectrum disorders.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants</i> <br />This randomized clinical double-blind trial enrolled participants at 2 clinical sites in Denmark. Of 214 eligible participants with a schizophrenia spectrum disorder, 103 were randomized to liraglutide or placebo. Participants received stable treatment with clozapine or olanzapine, were overweight or obese, and had prediabetes. Data were collected from May 1, 2013, through February 25, 2016.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Interventions</i> <br />Treatment for 16 weeks with once-daily subcutaneous injection of liraglutide or placebo. Trial drug therapy was titrated during the first 2 weeks of the study.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures</i> <br />The primary end point was change in glucose tolerance estimated by a 75-g oral glucose tolerance test result. Secondary end points included change in body weight and cardiometabolic parameters.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i> <br />Of the 103 patients undergoing randomization (60 men [58.3%] and 43 women [41.7%]), 97 were included in the efficacy analysis, with a mean (SD) age of 42.5 (10.5) years and mean (SD) body mass index (calculated as weight in kilograms divided by height in meters squared) of 33.8 (5.9). The liraglutide and placebo groups had comparable characteristics (mean [SD] age, 42.1 [10.7] vs 43.0 [10.5] years; 30 men in each group; mean [SD] body mass index, 33.7 [5.1] vs 33.9 [6.6]). A total of 96 randomized participants (93.2%) completed the trial. Glucose tolerance improved in the liraglutide group compared with the placebo group (P < .001). Altogether, 30 liraglutide-treated participants (63.8%) developed normal glucose tolerance compared with 8 placebo-treated participants (16.0%) (P < .001; number needed to treat, 2). Body weight decreased with liraglutide compared with placebo (−5.3 kg; 95% CI, −7.0 to −3.7 kg). Reductions in waist circumference (−4.1 cm; 95% CI, −6.0 to −2.3 cm), systolic blood pressure (−4.9 mm Hg; 95% CI, −9.5 to −0.3 mm Hg), visceral fat (−250.19 g; 95% CI, −459.9 to −40.5 g), and low-density lipoprotein levels (−15.4 mg/dL; 95% CI, −23.2 to −7.7 mg/dL) occurred with liraglutide compared with placebo. Adverse events with liraglutide affected mainly the gastrointestinal tract.</span></span><br />
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<b>Source:</b> <a href="http://jamanetwork.com/journals/jamapsychiatry/article-abstract/2629288" rel="" style="color: #6699cc;" target="_blank">http://jamanetwork.com/journals/jamapsychiatry</a></div>
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Vitamin D Deficiency Associated With Cognitive Functioning in Psychotic Disorders</h2>
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<i><b>The Journal of Clinical Psychiatry</b></i><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Background </i><br />Cognitive dysfunctions are core features of psychotic disorders with substantial impact on daily functioning. Vitamin D deficiency has been found to be related to cognitive dysfunctions, but the associations between vitamin D deficiency and cognition in persons with a psychotic disorder are largely unknown.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br />Methods</i><br />This cross-sectional study included 225 patients with a DSM-IV psychotic disorder consecutively recruited from 2003 to 2014 and 159 randomly selected healthy controls, assessed by a cognitive test battery, a clinical protocol (including Structured Clinical Interview for DSM-IV Axis I Disorders and Positive and Negative Syndrome Scale), and a physical examination including vitamin D measurements. Multiple regression models were performed to evaluate the effect of vitamin D deficiency (defined serum 25-hydroxyvitamin D [25(OH)D] < 25 nmol/L) on key cognitive domains: processing speed, verbal learning, verbal memory, and executive functioning.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br />Results</i><br />Vitamin D deficiency was significantly associated with decreased processing speed (ie, Digit Symbol Coding) (t = −2.6, P = .01; total model: adjusted R2 = 0.40, F6, 374 = 43.8, P < .001) and decreased fluency (ie, verbal fluency) (t = −2.1, P = .04; total model: adjusted R2 = 0.35, F6, 373 = 34.2, P < .001) when the results were controlled for age, ethnicity, IQ, patient versus control status, and substance or alcohol abuse. Additional analyses indicated that negative symptoms diluted the association between vitamin D deficiency and processing speed (t = −1.72, P = .09) and verbal fluency (t = −1.35, P = .18) in patients.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /><i>Conclusion</i> <br />The associations between vitamin D deficiency and processing speed and verbal fluency are good arguments for planning large-scale randomized controlled studies in target populations so conclusions can be made about the potential beneficial effect of vitamin D on cognition in psychotic disorders.</span></span></div>
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<b>Source:</b> <a href="http://www.psychiatrist.com/JCP/article/Pages/2017/aheadofprint/16m10880.aspx" rel="" style="color: #6699cc;" target="_blank">http://www.psychiatrist.com/JCP/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The authors conducted a genome-wide association study of anorexia nervosa and calculated genetic correlations with a series of psychiatric, educational, and metabolic phenotypes.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Method</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Following uniform quality control and imputation procedures using the 1000 Genomes Project (phase 3) in 12 case-control cohorts comprising 3,495 anorexia nervosa cases and 10,982 controls, the authors performed standard association analysis followed by a meta-analysis across cohorts. Linkage disequilibrium score regression was used to calculate genome-wide common variant heritability (single-nucleotide polymorphism [SNP]-based heritability [h2SNP]), partitioned heritability, and genetic correlations (rg) between anorexia nervosa and 159 other phenotypes.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Results were obtained for 10,641,224 SNPs and insertion-deletion variants with minor allele frequencies >1% and imputation quality scores >0.6. The h2SNP of anorexia nervosa was 0.20 (SE=0.02), suggesting that a substantial fraction of the twin-based heritability arises from common genetic variation. The authors identified one genome-wide significant locus on chromosome 12 (rs4622308) in a region harboring a previously reported type 1 diabetes and autoimmune disorder locus. Significant positive genetic correlations were observed between anorexia nervosa and schizophrenia, neuroticism, educational attainment, and high-density lipoprotein cholesterol, and significant negative genetic correlations were observed between anorexia nervosa and body mass index, insulin, glucose, and lipid phenotypes.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Anorexia nervosa is a complex heritable phenotype for which this study has uncovered the first genome-wide significant locus. Anorexia nervosa also has large and significant genetic correlations with both psychiatric phenotypes and metabolic traits. The study results encourage a reconceptualization of this frequently lethal disorder as one with both psychiatric and metabolic etiology.</span></span></div>
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<b>Source:</b> <a href="http://ajp.psychiatryonline.org/doi/abs/10.1176/appi.ajp.2017.16121402" style="color: #6699cc;" target="_blank">http://ajp.psychiatryonline.org/</a></div>
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Suicidal Behavior During Lithium and Valproate Treatment: A Within-Individual 8-Year Prospective Study of 50,000 Patients With Bipolar Disorder</h2>
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<i><b>The American Journal of Psychiatry</b></i></div>
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<b><br /></b><b>Abstract</b></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Conclusions regarding lithium’s antisuicidal effect for bipolar disorder have been limited due to nonrepresentative subjects and potential confounding factors, including varying severity of illness. Findings regarding the effect of valproate, the most common alternative to lithium, are inconsistent for suicidal behavior. This study investigated the associations of these two drugs with the risk of suicide-related events, and possible differences between drugs, by using within-individual designs in a register-based longitudinal cohort.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Method</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Through linkage of multiple Swedish national registers, 51,535 individuals with bipolar disorder were followed from 2005 to 2013 for treatment with lithium and valproate. Stratified Cox regression was used to estimate the hazard ratios of suicide-related events during treated periods compared with untreated periods. For significant associations between medication and suicide-related events, the population attributable fraction was estimated to assess the public health impact for patients with bipolar disorder.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">During follow-up, 10,648 suicide-related events occurred. The incidence rate was significantly decreased by 14% during lithium treatment (hazard ratio 0.86, 95% confidence interval [CI] 0.78–0.95) but not during valproate treatment (hazard ratio 1.02, 95% CI 0.89–1.15). The difference in hazard ratios of suicide-related events between lithium and valproate was statistically significant. Estimates of the population attributable fraction suggested that 12% (95% CI 4%−20%) of suicide-related events could have been avoided if patients had taken lithium during the entire follow-up.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The results suggest that lithium should be considered for patients with bipolar disorder with suspected suicidal intentions, although risk for suicide is only one of the considerations when providing clinical care.</span></span></div>
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<b style="font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://ajp.psychiatryonline.org/doi/abs/10.1176/appi.ajp.2017.16050542" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">http://ajp.psychiatryonline.org/</a></div>
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<span style="color: #333333; font-family: "arial" , sans-serif;"><span style="font-size: 18px; line-height: 22px; text-transform: uppercase;">A 6-Year Posttreatment Follow-up of Panic Disorder Patients: Treatment With Clonazepam Predicts Lower Recurrence Than Treatment With Paroxetine</span></span></h2>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b><br /></b></i></span></span><span style="color: #333333; font-size: 14.85px; font-style: italic; font-weight: bold; line-height: 20.79px;">Journal of Clinical Psychiatry</span><br />
<span style="color: #333333; font-size: 14.85px; font-style: italic; font-weight: bold; line-height: 20.79px;"><br /></span><span style="color: #333333; font-size: 14.85px; font-weight: bold; line-height: 20.79px;">Abstract</span></div>
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<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Background </i><br />The aim of this study was to identify factors associated with relapse in panic disorder (PD).</span></span><br />
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<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i><br />This was an observational study conducted in the outpatient clinic of a psychiatric hospital in Rio de Janeiro, Brazil. In a previous study, 120 patients diagnosed as having PD according to Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria were randomized to receive clonazepam or paroxetine. After 3 years, treatment was discontinued in patients who had achieved remission. These subjects were included in the current study and were followed up for 6 years. The follow-up assessments were made at 1, 2, 3, 5, and 6 years after treatment discontinuation. Assessment included the number of panic attacks per month, Clinical Global Impression–Severity, and other measures. Patients who had initiated psychotherapy or pharmacological treatment because of PD symptoms or who had Clinical Global Impression–Severity scores greater than 1 or panic attacks in the month preceding the assessment were considered relapse cases. Data were collected from January 2003 to August 2012.</span></span><br />
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<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i><br />Eighty-five patients completed the follow-up. Cumulative relapse rates were 50% (n = 33) at 1 year and 89.4% (n = 76) at 6 years. One-year relapse rates were lower in patients previously treated with clonazepam (P = 0.001) compared with those treated with paroxetine. Low 6-year relapse rates were associated with high Hamilton Anxiety Rating Scale scores before treatment (P = 0.016) and previous treatment with clonazepam.</span></span><br />
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<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions </i><br />Relapse is a frequent problem in PD, and long-term treatment does not protect these patients in the long run. Treatment with clonazepam predicts lower relapse when compared with paroxetine.</span></span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://journals.lww.com/psychopharmacology/Citation/2017/08000/A_6_Year_Posttreatment_Follow_up_of_Panic_Disorder.8.aspx" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">http://journals.lww.com/psychopharmacology/</a></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px; text-transform: uppercase;">Brain Structural Signatures of Adolescent Depressive Symptom Trajectories: A Longitudinal Magnetic Resonance Imaging Study</span></span></h2>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b>Child and Adolescent Psychiatry</b></span></i></span><br />
<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b><br /></b></span></i></span><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Most evidence for structural brain abnormalities associated with adolescent depression is based on cross-sectional study designs that do not take into account the dynamic course of depressive symptoms and brain maturation across adolescence. In this study, a longitudinal design was used to investigate the association between different trajectories of depressive symptoms and longitudinal changes in brain structure throughout adolescence.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Method</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">One hundred forty-nine adolescents were assessed on depressive symptoms and underwent structural magnetic resonance imaging at 12 years of age and were followed up multiple times until 19 years. Three depressive symptom trajectories (low-stable [n = 97], early-decreasing [n = 33], late-increasing [n = 19]) were identified, and effects of group and group by time on hippocampus and amygdala volume and prefrontal cortical thickness and surface area were evaluated.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The early-decreasing symptoms group exhibited differences in cortical surface area compared to the low-stable and late-increasing symptoms groups, moderated by sex. Specifically, females in the early-decreasing symptoms group showed lower anterior cingulate and orbitofrontal cortex surface areas across adolescence compared to females in the other groups. Males in the early-decreasing symptoms group showed lower right orbitofrontal cortex surface area expansion over time compared to males in the low-stable and late-increasing symptoms groups. No effects were found for cortical thickness or for hippocampus and amygdala volume.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusion</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">Alterations in cortical surface area were specifically observed in young people experiencing depressive symptoms in early adolescence. These findings suggest that early adolescence is a particularly sensitive period for cortical surface area abnormalities associated with depressive symptoms and could provide a critical window for treatment of (subthreshold) depressive symptoms.</span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://www.jaacap.com/article/S0890-8567(17)30210-1/abstract" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px;" target="_blank">http://www.jaacap.com/article/</a></div>
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<b><a href="http://journals.lww.com/psychopharmacology/Pages/currenttoc.aspx" style="color: #6699cc;" target="_blank">Journal of Clinical Psychopharmacology - August 2017 - Volume 37, Issue 4</a></b></div>
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<b><a href="http://www.nature.com/npp/journal/v42/n9/index.html" style="color: #6699cc;" target="_blank">Neuropsychopharmacology - Volume 42, Issue 9 (Augst 2017)</a></b></div>
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<b><a href="https://link.springer.com/journal/213/234/15/page/1" style="color: #6699cc;" target="_blank">Psychopharmacology - Volume 234, Issue 15, August 2017</a></b></div>
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<b><a href="http://jop.sagepub.com/content/current" style="color: #6699cc;" target="_blank">Journal of Psychopharmacology - July 2017; 31 (7)</a></b></div>
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<b><a href="http://ajp.psychiatryonline.org/toc/ajp/current" style="color: #6699cc;" target="_blank">The American Journal of Psychiatry - July 2017, Vol. 174, Issue 7</a></b></div>
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<b><a href="http://www.nature.com/neuro/journal/v20/n8/index.html" style="color: #6699cc;" target="_blank">Nature Neuroscience - August 2017, Vol 20, N° 8</a></b></div>
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<b><a href="http://www.nature.com/mp/journal/v22/n8/index.html" style="color: #6699cc;" target="_blank">Molecular Psychiatry - Volume 22, Issue 8, August 2017</a></b></div>
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<b style="background-color: white; color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"><a href="http://www.biologicalpsychiatryjournal.com/current" style="color: #6699cc;" target="_blank">Biological Psychiatry - Volume 82, Issue 4, August 2017</a></b><br />
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<b><a href="https://academic.oup.com/brain/issue/140/8?browseBy=volume" style="color: #6699cc;" target="_blank">Brain - Volume 140, Issue 8, August 2017</a></b></div>
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<b><span style="font-size: small;">Join us on LinkedIn:</span> </b><b><a href="http://www.linkedin.com/groups/Neuropsychopharmacology-Neuroscience-5147601" style="color: #6699cc;">Neurosychopharmacology News Group</a></b></h3>
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Eutimiahttp://www.blogger.com/profile/07836706907685752267noreply@blogger.comtag:blogger.com,1999:blog-1045445187620004007.post-29566019996806005162017-05-07T16:07:00.002-04:002017-05-10T16:50:58.301-04:00May 2017<div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"><i>Importance </i><br />Osteoporotic fractures are a leading cause of disability, costs, and mortality. FRAX is a tool used to assess fracture risk in the general population. Mental disorders and medications to treat them have been reported to adversely affect bone health, but, to date, they have not been systematically studied in relation to osteoporotic fractures.</span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective </i><br />To examine the association of mental disorders and psychotropic medication use with osteoporotic fracture risk in routine clinical practice.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants</i> <br />In this population-based cohort study, bone mineral density and risk factors were used to calculate FRAX scores using data from the Manitoba Bone Density Program database of all women and men 40 years of age or older in Manitoba, Canada, referred for a baseline dual-energy x-ray absorptiometry scan from January 1, 1996, to March 28, 2013. Population-based health services data were used to identify primary mental disorders during the 3 prior years, psychotropic medication use during the prior year, and incident fractures. Cox proportional hazards regression models estimated the risk for incident fractures based on mental disorders and use of psychotropic medications. Data analysis was conducted from November 25, 2013, to October 15, 2016.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures </i><br />Incident nontraumatic major osteoporotic fractures (MOFs) and hip fractures.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results </i><br />Of the 68 730 individuals (62 275 women and 6455 men; mean age, 64.2 [11.2] years) in the study, during 485 322 person-years (median, 6.7 years) of observation, 5750 (8.4%) sustained an incident MOF, 1579 (2.3%) sustained an incident hip fracture, and 8998 (13.1%) died. In analyses adjusted for FRAX score, depression was associated with MOF (adjusted hazard ratio [aHR], 1.39; 95% CI, 1.27-1.51; P < .05) and hip fracture (aHR, 1.43; 95% CI, 1.22-1.69; P < .05) before adjustment for medication use, but these associations were not significant after adjustment for medication use. In contrast, the use of selective serotonin reuptake inhibitors (aHR for MOF, 1.43; 95% CI, 1.27-1.60; P < .05; aHR for hip fracture, 1.48; 95% CI, 1.18-1.85; P < .05), antipsychotics (aHR for MOF, 1.43; 95% CI, 1.15-1.77; P < .05; aHR for hip fracture, 2.14; 95% CI, 1.52-3.02; P < .05), and benzodiazepines (aHR for MOF, 1.15; 95% CI, 1.04-1.26; P < .05; aHR for hip fracture, 1.24; 95% CI, 1.05-1.47; P < .05) were each independently associated with significantly increased risk for both MOF and hip fracture. FRAX significantly underestimated the 10-year risk of MOF by 29% and of hip fracture by 51% for those with depression. It also underestimated the 10-year risk of MOF by 36% for use of selective serotonin reuptake inhibitors, by 63% for use of mood stabilizers, by 60% for use of antipsychotics, and by 13% for use of benzodiazepines. FRAX underestimated the 10-year risk of hip fracture by 57% for use of selective serotonin reuptake inhibitors, by 98% for use of mood stabilizers, by 171% for use of antipsychotics, and by 31% for use of benzodiazepines. FRAX correctly estimated fracture risk in people without mental disorders and those not taking psychotropic medications.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance</i> <br />Mental disorders and medication use were associated with an increased risk for fracture, but in simultaneous analyses, only medication use was independently associated with fracture. Depression and psychotropic medication use are potential risk indicators that are independent of FRAX estimates.</span></span><br />
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<b>Source:</b> <a href="http://jamanetwork.com/journals/jamapsychiatry/article-abstract/2618262" style="color: #6699cc; text-decoration-line: none;" target="_blank">http://jamanetwork.com/journals/jamapsychiatry/</a></div>
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<span style="color: #333333; font-size: 14.85px;">The U.S. Food and Drug Administration approved Ingrezza (valbenazine) capsules to treat adults with tardive dyskinesia. This is the first drug approved by the FDA for this condition. </span></div>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Tardive dyskinesia is a neurological disorder characterized by repetitive involuntary movements, usually of the jaw, lips and tongue, such as grimacing, sticking out the tongue and smacking the lips. Some affected people also experience involuntary movement of the extremities or difficulty breathing.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">"Tardive dyskinesia can be disabling and can further stigmatize patients with mental illness," said Mitchell Mathis, M.D., director of the Division of Psychiatry Products in the FDA’s Center for Drug Evaluation and Research. "Approving the first drug for the treatment of tardive dyskinesia is an important advance for patients suffering with this condition."</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Tardive dyskinesia is a serious side effect sometimes seen in patients who have been treated with antipsychotic medications, especially the older medications, for long periods to treat chronic conditions, such as schizophrenia and bipolar disorder. Tardive dyskinesia can also occur in patients taking antipsychotic medications for depression and certain medications for gastrointestinal disorders and other conditions. It is unclear why some people who take these medications develop tardive dyskinesia yet others do not.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The efficacy of Ingrezza was shown in a clinical trial of 234 participants that compared Ingrezza to placebo. After six weeks, participants who received Ingrezza had improvement in the severity of abnormal involuntary movements compared to those who received placebo.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 13px;"><span style="line-height: 20.79px;"><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Ingrezza may cause serious side effects including sleepiness and heart rhythm problems (QT prolongation). Its use should be avoided in patients with congenital long QT syndrome or with abnormal heartbeats associated with a prolonged QT interval. Those taking Ingrezza should not drive or operate heavy machinery or do other dangerous activities until it is known how the drug affects them. </span></span><span style="font-size: 14.85px;"> </span></span></span></div>
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<b><br /></b><b>Source:</b> <a href="https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm552418.htm" style="color: #6699cc; text-decoration-line: none;" target="_blank">https://www.fda.gov/NewsEvents/Newsroom/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Importance </i><br />There have been concerns raised by patients and regulatory agencies regarding serious psychiatric adverse effects associated with 5α-reductase inhibitors.</span></span><br />
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</i><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective </i><br />To determine if there is an increased risk of suicide, self-harm, or depression among older men starting a 5α-reductase inhibitor for prostatic enlargement.</span></span><br />
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</i><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants </i><br />A population-based, retrospective, matched cohort study using linked administrative data for 93 197 men ages 66 years or older (median [IQR] age, 75 [70-80] years) in Ontario, Canada, who initiated a new prescription for a 5α-reductase inhibitor during the study period (2003 through 2013). Participants were matched (using a propensity score that included 44 of our 96 covariates that included medical comorbidities, medication usage, and health care system utilization) to an equal number of men not prescribed a 5α-reductase inhibitor.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Exposures </i><br />Duration of finasteride or dutasteride usage.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures </i><br />Suicide. Secondary outcomes were self-harm and depression.</span></span><br />
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</i><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results </i><br />Men who used 5α-reductase inhibitors were not at a significantly increased risk of suicide (HR, 0.88; 95% CI, 0.53-1.45). Risk of self-harm was significantly increased during the initial 18 months after 5α-reductase inhibitor initiation (HR, 1.88; 95% CI, 1.34-2.64), but not thereafter. Incident depression risk was elevated during the initial 18 months after 5α-reductase inhibitor initiation (HR, 1.94; 95% CI, 1.73-2.16), and continued to be elevated, but to a lesser degree, for the remainder of the follow-up period (HR, 1.22; 95% CI, 1.08-1.37). The absolute increases in the event rates for these 2 outcomes were 17 per 100 000 patient-years and 237 per 100 000 patient-years, respectively. The type of 5α-reductase inhibitor (finasteride or dutasteride) did not significantly modify the observed associations with suicide, self-harm, and depression.</span></span><br />
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<span style="font-size: 14.85px;"><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance </i><br />In a large cohort of men ages 66 years or older, we did not demonstrate an increased risk of suicide associated with 5α-reductase inhibitor use. However, the risk of self-harm and depression were increased compared with unexposed men. This is in keeping with postmarketing experience and patient concerns, and discontinuation of the medication in these circumstances may be appropriate.</span></span></span></div>
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<b>Source:</b> <a href="http://jamanetwork.com/journals/jamainternalmedicine/article-abstract/2610105" style="color: #6699cc; text-decoration-line: none;" target="_blank">http://jamanetwork.com/journals/jamainternalmedicine/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Context</i><br />Preterm birth increases the risk for mental disorders in adulthood, yet findings on self-reported or subclinical mental health problems are mixed.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To study self-reported mental health problems among adults born preterm at very low birth weight (VLBW; ≤1500 g) compared with term controls in an individual participant data meta-analysis.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Data Sources</i><br />Adults Born Preterm International Collaboration.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Study Selection</i><br />Studies that compared self-reported mental health problems using the Achenbach Young Adult Self Report or Adult Self Report between adults born preterm at VLBW (n = 747) and at term (n = 1512).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Data Extraction</i><br />We obtained individual participant data from 6 study cohorts and compared preterm and control groups by mixed random coefficient linear and Tobit regression.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i><br />Adults born preterm reported more internalizing (pooled β = .06; 95% confidence interval .01 to .11) and avoidant personality problems (.11; .05 to .17), and less externalizing (–.10; –.15 to –.06), rule breaking (–.10; –.15 to –.05), intrusive behavior (–.14; –.19 to –.09), and antisocial personality problems (–.09; –.14 to –.04) than controls. Group differences did not systematically vary by sex, intrauterine growth pattern, neurosensory impairments, or study cohort.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Limitations</i><br />Exclusively self-reported data are not confirmed by alternative data sources.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i><br />Self-reports of adults born preterm at VLBW reveal a heightened risk for internalizing problems and socially avoidant personality traits together with a lowered risk for externalizing problem types. Our findings support the view that preterm birth constitutes an early vulnerability factor with long-term consequences on the individual into adulthood.</span></span><br />
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A translational approach for NMDA receptor profiling as a vulnerability biomarker for depression and schizophrenia</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">Altered NMDA receptor activity and glutamate signalling might underlie the pathogenesis of both schizophrenia and depression in subgroups of patients. In schizophrenia, pharmacological modelling, post-mortem and imaging data suggest reduced NMDA signalling. In contrast, recent clinical trials demonstrating the efficacy of the NMDA antagonist ketamine in severely depressed patients suggest increased NMDA receptor signalling. We conducted a proof-of-concept study to assess whether there is any in vivo evidence for an inverse association in depression and schizophrenia with respect to the NMDA receptor function. For this purpose, we used a translational approach, based on findings from animal studies that NMDA receptor is a key mediator of arginine vasopressin (AVP) release into the bloodstream. Using hypertonic saline to increase plasma osmolality (POsm) and thereby induce AVP release, as done in animal studies, we found that in depressed patients the NMDA receptor-mediated AVP release induced by hypertonic saline infusion was significantly increased [0.24 (0.15) pg ml−1 mosmol−1, P < 0.05] compared with schizophrenia patients [0.07 (0.07) pg ml−1 mosmol−1]. Slopes for healthy control subjects were 0.11 (0.09) pg ml−1 mosmol−1 which was less than the depressed group. These findings are consistent with implicated NMDA receptor-related abnormalities in depression and schizophrenia in subgroups of patients and provide the first in vivo evidence of this dichotomy.</span></div>
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<b>Source:</b> <a href="http://onlinelibrary.wiley.com/doi/10.1113/EP086212/full" rel="" style="color: #6699cc; text-decoration-line: none;" target="_blank">http://onlinelibrary.wiley.com/</a></div>
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Sugar- and Artificially Sweetened Beverages and the Risks of Incident Stroke and Dementia</h2>
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<i><b>Stroke</b></i><br />
<i><b><br /></b></i><b>Abstract</b></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Background and Purpose</i><br />Sugar and artificially-sweetened beverage intake have been linked to cardiometabolic risk factors, which increase the risk of cerebrovascular disease and dementia. We examined whether sugar- or artificially sweetened beverage consumption was associated with the prospective risks of incident stroke or dementia in the community-based Framingham Heart Study Offspring cohort.</span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i><br />We studied 2888 participants aged >45 years for incident stroke (mean age 62 [SD, 9] years; 45% men) and 1484 participants aged >60 years for incident dementia (mean age 69 [SD, 6] years; 46% men). Beverage intake was quantified using a food-frequency questionnaire at cohort examinations 5 (1991–1995), 6 (1995–1998), and 7 (1998–2001). We quantified recent consumption at examination 7 and cumulative consumption by averaging across examinations. Surveillance for incident events commenced at examination 7 and continued for 10 years. We observed 97 cases of incident stroke (82 ischemic) and 81 cases of incident dementia (63 consistent with Alzheimer’s disease).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i><br />After adjustments for age, sex, education (for analysis of dementia), caloric intake, diet quality, physical activity, and smoking, higher recent and higher cumulative intake of artificially sweetened soft drinks were associated with an increased risk of ischemic stroke, all-cause dementia, and Alzheimer’s disease dementia. When comparing daily cumulative intake to 0 per week (reference), the hazard ratios were 2.96 (95% confidence interval, 1.26–6.97) for ischemic stroke and 2.89 (95% confidence interval, 1.18–7.07) for Alzheimer’s disease. Sugar-sweetened beverages were not associated with stroke or dementia.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i><br />Artificially sweetened soft drink consumption was associated with a higher risk of stroke and dementia.</span></span></div>
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<b>Source:</b> <a href="http://stroke.ahajournals.org/content/early/2017/04/20/STROKEAHA.116.016027" rel="" style="color: #6699cc; text-decoration-line: none;" target="_blank">http://stroke.ahajournals.org/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Importance </i><br />Midlife vascular risk factors have been associated with late-life dementia. Whether these risk factors directly contribute to brain amyloid deposition is less well understood.</span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective </i><br />To determine if midlife vascular risk factors are associated with late-life brain amyloid deposition, measured using florbetapir positron emission tomography (PET).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants</i> <br />The Atherosclerosis Risk in Communities (ARIC)–PET Amyloid Imaging Study, a prospective cohort study among 346 participants without dementia in 3 US communities (Washington County, Maryland; Forsyth County, North Carolina; and Jackson, Mississippi) who have been evaluated for vascular risk factors and markers since 1987-1989 with florbetapir PET scans in 2011-2013. Positron emission tomography image analysis was completed in 2015.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Exposures</i> <br />Vascular risk factors at ARIC baseline (age 45-64 years; risk factors included body mass index ≥30, current smoking, hypertension, diabetes, and total cholesterol ≥200 mg/dL) were evaluated in multivariable models including age, sex, race, APOE genotype, and educational level.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures</i> <br />Standardized uptake value ratios (SUVRs) were calculated from PET scans and a mean global cortical SUVR was calculated. Elevated florbetapir (defined as a SUVR >1.2) was the dependent variable.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i> <br />Among 322 participants without dementia and with nonmissing midlife vascular risk factors at baseline (mean age, 52 years; 58% female; 43% black), the SUVR (elevated in 164 [50.9%] participants) was measured more than 20 years later (median follow-up, 23.5 years; interquartile range, 23.0-24.3 years) when participants were between 67 and 88 (mean, 76) years old. Elevated body mass index in midlife was associated with elevated SUVR (odds ratio [OR], 2.06; 95% CI, 1.16-3.65). At baseline, 65 participants had no vascular risk factors, 123 had 1, and 134 had 2 or more; a higher number of midlife risk factors was associated with elevated amyloid SUVR at follow-up (30.8% [n = 20], 50.4% [n = 62], and 61.2% [n = 82], respectively). In adjusted models, compared with 0 midlife vascular risk factors, the OR for elevated SUVR associated with 1 vascular risk factor was 1.88 (95% CI, 0.95-3.72) and for 2 or more vascular risk factors was 2.88 (95% CI, 1.46-5.69). No significant race × risk factor interactions were found. Late-life vascular risk factors were not associated with late-life brain amyloid deposition (for ≥2 late-life vascular risk factors vs 0: OR, 1.66; 95% CI, 0.75-3.69).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance</i> <br />An increasing number of midlife vascular risk factors was significantly associated with elevated amyloid SUVR; this association was not significant for late-life risk factors. These findings are consistent with a role of vascular disease in the development of Alzheimer disease.</span></span></div>
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<b>Source:</b> <a href="http://jamanetwork.com/journals/jama/article-abstract/2616396" style="color: #6699cc; text-decoration-line: none;" target="_blank">http://jamanetwork.com/journals/jama/</a></div>
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Functional Connectivity of the Subcallosal Cingulate Cortex And Differential Outcomes to Treatment With Cognitive-Behavioral Therapy or Antidepressant Medication for Major Depressive Disorder</h2>
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<i><b>The American Journal of Psychiatry</b></i></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The purpose of this article was to inform the first-line treatment choice between cognitive-behavioral therapy (CBT) or an antidepressant medication for treatment-naive adults with major depressive disorder by defining a neuroimaging biomarker that differentially identifies the outcomes of remission and treatment failure to these interventions.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Method</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Functional MRI resting-state functional connectivity analyses using a bilateral subcallosal cingulate cortex (SCC) seed was applied to 122 patients from the Prediction of Remission to Individual and Combined Treatments (PReDICT) study who completed 12 weeks of randomized treatment with CBT or antidepressant medication. Of the 122 participants, 58 achieved remission (Hamilton Depression Rating Scale [HAM-D] score ≤7 at weeks 10 and 12), and 24 had treatment failure (<30% decrease from baseline in HAM-D score). A 2×2 analysis of variance using voxel-wise subsampling permutation tests compared the interaction of treatment and outcome. Receiver operating characteristic curves constructed using brain connectivity measures were used to determine possible classification rates for differential treatment outcomes.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The resting-state functional connectivity of the following three regions with the SCC was differentially associated with outcomes of remission and treatment failure to CBT and antidepressant medication and survived application of the subsample permutation tests: the left anterior ventrolateral prefrontal cortex/insula, the dorsal midbrain, and the left ventromedial prefrontal cortex. Using the summed SCC functional connectivity scores for these three regions, overall classification rates of 72%−78% for remission and 75%−89% for treatment failure was demonstrated. Positive summed functional connectivity was associated with remission with CBT and treatment failure with medication, whereas negative summed functional connectivity scores were associated with remission to medication and treatment failure with CBT.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Imaging-based depression subtypes defined using resting-state functional connectivity differentially identified an individual’s probability of remission or treatment failure with first-line treatment options for major depression. This biomarker should be explored in future research through prospective testing and as a component of multivariate treatment prediction models.</span></span></div>
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<b style="font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://ajp.psychiatryonline.org/doi/abs/10.1176/appi.ajp.2016.16050518" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration-line: none;" target="_blank">http://ajp.psychiatryonline.org/</a></div>
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<span style="color: #333333; font-family: "arial" , sans-serif;"><span style="font-size: 18px; line-height: 22px; text-transform: uppercase;">Altered Thalamo-Cortical White Matter Connectivity: Probabilistic Tractography Study in Clinical-High Risk for Psychosis and First-Episode Psychosis</span></span></h2>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b><br /></b></i></span></span><span style="color: #333333; font-size: 14.85px; font-style: italic; font-weight: bold; line-height: 20.79px;">Schizophrenia Bulletin</span><br />
<span style="color: #333333; font-size: 14.85px; font-style: italic; font-weight: bold; line-height: 20.79px;"><br /></span><span style="color: #333333; font-size: 14.85px; font-weight: bold; line-height: 20.79px;">Abstract</span></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span></div>
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<span style="font-size: 14.85px;">Disrupted thalamo-cortical connectivity is regarded as a core psychopathology in patients diagnosed with schizophrenia. However, whether the thalamo-cortical white matter connectivity is disrupted before the onset of psychosis is still unknown. To determine this gap in knowledge, the strength of thalamo-cortical white matter anatomical connectivity in subjects at clinical-high risk for psychosis (CHR) was compared to that of first-episode psychosis (FEP) and healthy controls. A total of 37 CHR, 21 FEP, and 37 matched healthy controls underwent diffusion-weighted magnetic resonance imaging to examine the number of probabilistic tractography “counts” representing thalamo-cortical white matter connectivity. We also investigated the relationship with psychopathology. For FEP, the connectivity between the thalamus and parietal cortex was significantly increased ( F = 5.65, P < .05) compared to that of healthy controls. However, the connectivity between thalamus and orbitofrontal cortex was significantly reduced compared to both healthy controls ( F = 11.86, P < .005) and CHR ( F = 6.63, P < .05). Interestingly, CHR exhibited a similar pattern as FEP, albeit with slightly reduced magnitude. Compared to healthy controls, there was a significant decrease ( F = 4.16, P < .05) in CHR thalamo-orbitofrontal connectivity. Also, the strength of the thalamo-orbitofrontal connectivity was correlated with the Global Assessment of Functioning score in CHR ( r = .35, P < .05). This observed pattern of white matter connectivity disruptions in FEP and in CHR suggests that this pattern of disconnectivity not only highlights the involvement of thalamus but also might be useful as an early biomarker for psychosis.</span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://academic.oup.com/schizophreniabulletin/article-lookup/doi/10.1093/schbul/sbv169" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration-line: none;" target="_blank">https://academic.oup.com/schizophreniabulletin/</a></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px; text-transform: uppercase;">Largest GWAS of PTSD (N=20 070) yields genetic overlap with schizophrenia and sex differences in heritability</span></span></h2>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b>Molecular Psychiatry</b></span></i></span><br />
<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b><br /></b></span></i></span><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b><br /></b></span></i></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">The Psychiatric Genomics Consortium-Posttraumatic Stress Disorder group (PGC-PTSD) combined genome-wide case–control molecular genetic data across 11 multiethnic studies to quantify PTSD heritability, to examine potential shared genetic risk with schizophrenia, bipolar disorder, and major depressive disorder and to identify risk loci for PTSD. Examining 20 730 individuals, we report a molecular genetics-based heritability estimate (h2SNP) for European-American females of 29% that is similar to h2SNP for schizophrenia and is substantially higher than h2SNP in European-American males (estimate not distinguishable from zero). We found strong evidence of overlapping genetic risk between PTSD and schizophrenia along with more modest evidence of overlap with bipolar and major depressive disorder. No single-nucleotide polymorphisms (SNPs) exceeded genome-wide significance in the transethnic (overall) meta-analysis and we do not replicate previously reported associations. Still, SNP-level summary statistics made available here afford the best-available molecular genetic index of PTSD—for both European- and African-American individuals—and can be used in polygenic risk prediction and genetic correlation studies of diverse phenotypes. Publication of summary statistics for ~10 000 African Americans contributes to the broader goal of increased ancestral diversity in genomic data resources. In sum, the results demonstrate genetic influences on the development of PTSD, identify shared genetic risk between PTSD and other psychiatric disorders and highlight the importance of multiethnic/racial samples. As has been the case with schizophrenia and other complex genetic disorders, larger sample sizes are needed to identify specific risk loci.</span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://www.nature.com/mp/journal/vaop/ncurrent/full/mp201777a.html" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration-line: none;" target="_blank">http://www.nature.com/mp/journal/</a></div>
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<b style="color: blue; font-size: x-large;"><br /></b><b style="color: blue; font-size: x-large;">Online Journals:</b></div>
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<b><a href="http://journals.lww.com/psychopharmacology/Pages/currenttoc.aspx" style="color: #6699cc; text-decoration-line: none;" target="_blank">Journal of Clinical Psychopharmacology - June 2017 - Volume 37, Issue 3</a></b></div>
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<b><a href="http://www.nature.com/npp/journal/v42/n6/index.html" style="color: #6699cc; text-decoration-line: none;" target="_blank">Neuropsychopharmacology - Volume 42, Issue 6 (May 2017)</a></b></div>
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<b><a href="https://link.springer.com/journal/213/234/9/page/1" style="color: #6699cc; text-decoration-line: none;" target="_blank">Psychopharmacology - Volume 234, Issue 9, May 2017</a></b></div>
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<b><a href="http://jop.sagepub.com/content/current" style="color: #6699cc; text-decoration-line: none;" target="_blank">Journal of Psychopharmacology - May 2017; 31 (5)</a></b></div>
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<b><a href="http://ajp.psychiatryonline.org/toc/ajp/current" style="color: #6699cc; text-decoration-line: none;" target="_blank">The American Journal of Psychiatry - May 2017, Vol. 174, Issue 5</a></b></div>
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<b style="color: #6699cc;"><a href="http://archpsyc.jamanetwork.com/issue.aspx" style="color: #6699cc; text-decoration-line: none;" target="_blank">JAMA Psychiatry - March 2017, Vol. 74, No. 5</a>3</b></div>
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<b><a href="http://www.nature.com/neuro/journal/v20/n5/index.html" style="color: #6699cc; text-decoration-line: none;" target="_blank">Nature Neuroscience - May 2017, Vol 20, N° 5</a></b></div>
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<b><a href="http://www.nature.com/mp/journal/v22/n5/index.html" style="color: #6699cc; text-decoration-line: none;" target="_blank">Molecular Psychiatry - Volume 22, Issue 5, May 2017</a></b></div>
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<b style="background-color: white; color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"><a href="http://www.biologicalpsychiatryjournal.com/current" style="color: #6699cc; text-decoration-line: none;" target="_blank">Biological Psychiatry - Volume 81, Issue 10, May 2017</a></b><br />
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<b><a href="https://academic.oup.com/brain/issue/140/5?browseBy=volume" style="color: #6699cc; text-decoration-line: none;" target="_blank">Brain - Volume 140, Issue 5, May 2017</a></b></div>
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<b><span style="font-size: small;">Join us on LinkedIn:</span> </b><b><a href="http://www.linkedin.com/groups/Neuropsychopharmacology-Neuroscience-5147601" style="color: #6699cc; text-decoration-line: none;">Neurosychopharmacology News Group</a></b></h3>
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Eutimiahttp://www.blogger.com/profile/07836706907685752267noreply@blogger.comtag:blogger.com,1999:blog-1045445187620004007.post-46193008687861601182017-03-04T13:18:00.002-05:002017-03-11T14:56:12.662-05:00March 2017<div dir="ltr" style="text-align: left;" trbidi="on">
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<i style="font-size: 14.85px; line-height: 20.79px;"><br /></i><i><b>Depression and Anxiety</b></i></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"><i>Background</i></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">Due to its potent effects on social behavior, including maternal behavior, oxytocin has been identified as a potential mediator of postpartum depression and anxiety. The objective of this study was to examine the relationship between peripartum synthetic oxytocin administration and the development of depressive and anxiety disorders within the first year postpartum. We hypothesized that women exposed to peripartum synthetic oxytocin would have a reduced risk of postpartum depressive and anxiety disorders compared with those without any exposure.</span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">Population-based data available through the Massachusetts Integrated Clinical Academic Research Database (MiCARD) were used to retrospectively (2005–2014) examine this relationship and calculate the relative risk of peripartum synthetic oxytocin for the development of postpartum depressive and anxiety disorders in exposed (n = 9,684) compared to unexposed (n = 37,048) deliveries.</span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">Among deliveries to women with a history of prepregnancy depressive or anxiety disorder, exposure to peripartum oxytocin increased the risk of postpartum depressive or anxiety disorder by 36% (relative risk (RR): 1.36; 95% confidence interval (95% CI): 1.20–1.55). In deliveries to women with no history of prepregnancy depressive or anxiety disorder, exposure to peripartum oxytocin increased the risk of postpartum depressive or anxiety disorder by 32% compared to those not exposed (RR: 1.32; 95% CI: 1.23-1.42).</span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">Contrary to our hypothesis, results indicate that women with peripartum exposure to synthetic oxytocin had a higher relative risk of receiving a documented depressive or anxiety disorder diagnosis or antidepressant/anxiolytic prescription within the first year postpartum than women without synthetic oxytocin exposure.</span><br />
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<b>Source:</b> <a href="http://onlinelibrary.wiley.com/doi/10.1002/da.22599/full" style="color: #6699cc; text-decoration: none;" target="_blank">http://onlinelibrary.wiley.com/</a></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b>Schizophrenia Bulletin</b></i></span></span></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 13px;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br />Substance use is common in first-episode psychosis (FEP) and has been linked to poorer outcomes with more severe psychopathology and higher relapse rates. Early substance discontinuation appears to improve symptoms and function. However, studies vary widely in their methodology, and few have examined patients longitudinally, making it difficult to draw conclusions for practice and treatment. We aimed to investigate the relationship between substance use and early abstinence and the long-term course of illness in a representative sample of FEP patients. Out of 301 included patients, 266 could be divided into 4 groups based on substance use patterns during the first 2 years of treatment: persistent users, episodic users, stop-users and nonusers. Differences in clinical and functional measures during the follow-up period were assessed using linear mixed effects models for the analysis of repeated measures data. Patients who stopped using substances within the first 2 years after diagnosis had outcomes similar to those who had never used with fewer symptoms than episodic or persistent users. Both episodic and persistent users had lower rates of symptom remission than nonusers, and persistent users also had more negative symptoms than those who stopped using. Our findings emerge from one of very few long-term longitudinal studies examining substance use cessation in FEP with 10-year follow-up. The results convey hope that the detrimental effects of substance abuse on mental health may be significantly reversed if one stops the abuse in time. This can help patients who struggle with addiction with their motivation to embrace abstinence.</span></span> </span></span></div>
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<b><br /></b><b>Source:</b> <a href="https://academic.oup.com/schizophreniabulletin/article-abstract/doi/10.1093/schbul/sbw179/2987461/The-Effect-of-Substance-Use-on-10-Year-Outcome-in" style="color: #6699cc; text-decoration: none;" target="_blank">https://academic.oup.com/schizophreniabulletin/</a></div>
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<i style="font-size: 14.85px; line-height: 20.79px;"><b>The Journal of Neuropsychiatry</b></i><br />
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<span style="font-size: 14.85px;">Although major depressive disorder (MDD) and posttraumatic stress disorder (PTSD) are prevalent after traumatic brain injury (TBI), little is known about which patients are at risk for developing them. The authors systematically reviewed the literature on predictors and multivariable models for MDD and PTSD after TBI. The authors included 26 observational studies. MDD was associated with female gender, preinjury depression, postinjury unemployment, and lower brain volume, whereas PTSD was related to shorter posttraumatic amnesia, memory of the traumatic event, and early posttraumatic symptoms. Risk of bias ratings for most studies were acceptable, although studies that developed a multivariable model suffered from methodological shortcomings.</span></div>
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<b>Source:</b> <a href="http://neuro.psychiatryonline.org/doi/full/10.1176/appi.neuropsych.16090165" style="color: #6699cc; text-decoration: none;" target="_blank">http://neuro.psychiatryonline.org/</a></div>
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<span style="font-size: 14.85px; line-height: 20.79px;">Modafinil Improves Episodic Memory and Working Memory Cognition in Patients With Remitted Depression: A Double-Blind, Randomized, Placebo-Controlled Study</span></h2>
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<span style="font-size: 14.85px; line-height: 20.79px;"><b><i>Biological Psychiatry </i></b></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Background</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Cognitive dysfunction is a core feature of depression and tends to persist even after mood symptoms recover, leading to detrimental effects on clinical and functional outcomes. However, most currently available treatments have not typically addressed cognition. Modafinil has been shown to have beneficial effects on cognitive function and therefore has the potential to improve cognition in depression. The objective of this double-blind, placebo-controlled study was to investigate the effects of modafinil on cognitive functions in patients with remitted depression.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">In total, 60 patients with remitted depression participated in the study. Cognitive functions were evaluated with tests of working memory, planning, attention, and episodic memory from the Cambridge Neuropsychological Test Automated Battery at the baseline session and after treatment. A double-blind, randomized, placebo-controlled, parallel groups design was used to assess the effects of single-dose (200 mg) modafinil (n = 30) or placebo (n = 30) on cognition and fatigue. The main outcome measures were neurocognitive test scores from the Cambridge Neuropsychological Test Automated Battery. Visual analogue scales for subjective feelings and fatigue were used as secondary measures.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The modafinil group had significantly better performance on tests of episodic memory (p = .01, ηp2 = .10) and working memory (p = .04, ηp2 = .06). Modafinil did not improve planning or sustained attention.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">This study suggested that modafinil (200 mg) could improve episodic memory and working memory performance in patients with remitted depression. Modafinil may have potential as a therapeutic agent to help remitted depressed patients with persistent cognitive difficulties.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span><b style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;">Source:</b><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"> </span><a href="http://www.biologicalpsychiatrycnni.org/article/S2451-9022(16)30181-1/fulltext" style="color: #6699cc; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; text-decoration: none;" target="_blank">http://www.biologicalpsychiatrycnni.org/</a></div>
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Association of Serum Docosahexaenoic Acid With Cerebral Amyloidosis</h2>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b>JAMA Neurology</b></span></i></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Importance </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Higher dietary intake of the essential fatty acid docosahexaenoic (DHA) has been associated with better cognitive performance in several epidemiological studies. Animal and in vitro studies also indicate that DHA prevents amyloid deposition in the brain.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To determine the association between serum DHA levels, cerebral amyloidosis, and the volumes of brain areas affected by Alzheimer disease.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Design, Settings, and Participants </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Cross-sectional analysis of serum DHA levels together with measures of amyloid deposition (Pittsburgh Compound B index), brain volumes, and neuropsychological testing scores from 61 participants in the Aging Brain Study. The study was conducted between June 2008 and May 2013, and the data were analyzed between October 2015 and April 2016. Linear models were adjusted for age, sex, years of education, and apolipoprotein E status.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Serum DHA levels with cerebral amyloidosis measured using PIB PET.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Samples were available from 61 Aging Brain Study participants (41 women and 20 men) who underwent amyloid PET imaging. The mean (SD) age of the participants was 77 (6) years and ranged from 67 to 88 years. Serum DHA levels (percentage of total fatty acids) were 23% lower in participants with cerebral amyloidosis than those without (0.97 vs 1.25, P = .007) and were inversely correlated with brain amyloid load (r = −0.32, P = .01) independent of age, sex, apolipoprotein E genotype, and years of education. Moreover, greater serum DHA levels were positively associated with brain volume in several subregions affected by AD, in particular the left subiculum (r = 0.38, P = .005) and the left entorhinal volumes (r = 0.51, P = .001). Serum DHA levels were also associated with nonverbal memory scores (r = 0.28, P = .03).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">In this study, serum DHA levels were associated with pathogenesis of cerebral amyloidosis and with preservation of entorhinal and hippocampal volumes. These findings suggest an important role for DHA metabolism in brain amyloid deposition during the preclinical or early symptomatic stages of Alzheimer disease.</span></span></div>
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<b>Source:</b> <a href="http://jamanetwork.com/journals/jamaneurology/article-abstract/2538230" rel="" style="color: #6699cc; text-decoration: none;" target="_blank">http://jamanetwork.com/journals/jamaneurology/</a></div>
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Efficacy and Safety of Aripiprazole Once-Monthly in the Maintenance Treatment of Bipolar I Disorder</h2>
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<i><b>The Journal of Clinical Psychiatry</b></i><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To evaluate efficacy, safety, and tolerability of long-acting injectable antipsychotic aripiprazole once-monthly 400 mg (AOM 400) as maintenance treatment for bipolar I disorder (BP-I).</span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">In a double-blind, placebo-controlled, 52-week randomized withdrawal study conducted from August 2012 to April 2016, patients with a DSM-IV-TR diagnosis of BP-I currently experiencing a manic episode were stabilized sequentially on oral aripiprazole and AOM 400 and then randomized to AOM 400 or placebo. The primary end point was time from randomization to recurrence of any mood episode. Other end points included proportion of patients with recurrence of any mood episode and recurrence by mood episode type.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Of 266 randomized patients, 64 (48.1%) of 133 in the AOM 400 group and 38 (28.6%) of 133 in the placebo group completed the study. AOM 400 significantly delayed the time to recurrence of any mood episode compared with placebo (hazard ratio: 0.45; 95% CI, 0.30 to 0.68; P < .0001). Significantly fewer patients (P < .0001) experienced recurrence of any mood episode with AOM 400 (35/132; 26.5%) compared with placebo (68/133; 51.1%), with the effects observed predominantly on manic episodes (P < .0001). Patients were not depressed at study entry, and between-group differences in depressive episodes were not significant (P < .864). The treatment-emergent adverse events (incidence > 5%) that were reported at higher rates with AOM 400 than placebo were weight increase, akathisia, insomnia, and anxiety.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">AOM 400 delayed the time to and reduced the rate of recurrence of mood episodes and was generally safe and well tolerated. These findings support the use of AOM 400 for maintenance treatment of BP-I.</span></span><br />
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<b>Source:</b> <a href="https://www.ncbi.nlm.nih.gov/pubmed/28146613" rel="nofollow" style="color: #6699cc; text-decoration: none;" target="_blank">http://www.psychiatrist.com/JCP/</a></div>
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<i style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Geriatric Psychiatry</b></span></i></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span><span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i></span></span></div>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">To study whether antidepressant use is associated with an increased risk of hip fracture among community-dwelling persons with and without Alzheimer's disease (AD), and to compare the risk according to duration of use and between antidepressant groups.</span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">Retrospective cohort study, including 50,491 persons with AD (mean age 80) and 100,982 comparison persons without AD from Finnish register-based MEDALZ cohort. Antidepressant use was compared with nonuse with Cox proportional hazard models. Incident users were identified with a one year washout period from Prescription register data. Main outcome was hospitalization due to hip fracture.</span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">During antidepressant use, the age-adjusted rate of hip fractures per 100 person-years was 3.01 (95% CI 2.75–3.34) among persons with and 2.28 (1.94–2.61) among persons without AD. Antidepressant use was associated with an increased risk of hip fracture among persons with and without AD (adjusted HR 1.61, 95% CI 1.45–1.80 and 2.71, 2.35–3.14, respectively) compared with nonuse. The risk was most prominent in the beginning of use and was elevated even up to 4 years. The risk was increased with all of the most frequently used antidepressants.</span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusion</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">Antidepressant use is associated with an increased risk of hip fracture among older persons. </span></div>
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<b>Source:</b> <a href="http://onlinelibrary.wiley.com/doi/10.1002/gps.4667/full" style="color: #6699cc; text-decoration: none;" target="_blank">http://onlinelibrary.wiley.com/</a></div>
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Relation between resting amygdalar activity and cardiovascular events: a longitudinal and cohort study</h2>
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<i><b>The Lancet</b></i></div>
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<b><br /></b><b>Abstract</b></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Background</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Emotional stress is associated with increased risk of cardiovascular disease. We imaged the amygdala, a brain region involved in stress, to determine whether its resting metabolic activity predicts risk of subsequent cardiovascular events.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Individuals aged 30 years or older without known cardiovascular disease or active cancer disorders, who underwent 18F-fluorodexoyglucose PET/CT at Massachusetts General Hospital (Boston, MA, USA) between Jan 1, 2005, and Dec 31, 2008, were studied longitudinally. Amygdalar activity, bone-marrow activity, and arterial inflammation were assessed with validated methods. In a separate cross-sectional study we analysed the relation between perceived stress, amygdalar activity, arterial inflammation, and C-reactive protein. Image analyses and cardiovascular disease event adjudication were done by mutually blinded researchers. Relations between amygdalar activity and cardiovascular disease events were assessed with Cox models, log-rank tests, and mediation (path) analyses.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Findings</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">293 patients (median age 55 years [IQR 45·0–65·5]) were included in the longitudinal study, 22 of whom had a cardiovascular disease event during median follow-up of 3·7 years (IQR 2·7–4·8). Amygdalar activity was associated with increased bone-marrow activity (r=0·47; p<0·0001), arterial inflammation (r=0·49; p<0·0001), and risk of cardiovascular disease events (standardised hazard ratio 1·59, 95% CI 1·27–1·98; p<0·0001), a finding that remained significant after multivariate adjustments. The association between amygdalar activity and cardiovascular disease events seemed to be mediated by increased bone-marrow activity and arterial inflammation in series. In the separate cross-sectional study of patients who underwent psychometric analysis (n=13), amygdalar activity was significantly associated with arterial inflammation (r=0·70; p=0·0083). Perceived stress was associated with amygdalar activity (r=0·56; p=0·0485), arterial inflammation (r=0·59; p=0·0345), and C-reactive protein (r=0·83; p=0·0210).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Interpretation</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">In this first study to link regional brain activity to subsequent cardiovascular disease, amygdalar activity independently and robustly predicted cardiovascular disease events. Amygdalar activity is involved partly via a path that includes increased bone-marrow activity and arterial inflammation. These findings provide novel insights into the mechanism through which emotional stressors can lead to cardiovascular disease in human beings.</span></span></div>
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<b style="font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(16)31714-7/abstract" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration: none;" target="_blank">http://www.thelancet.com/journals/lancet/</a></div>
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<span style="color: #333333; font-family: "arial" , sans-serif;"><span style="font-size: 18px; line-height: 22px; text-transform: uppercase;">An epigenetic mechanism links socioeconomic status to changes in depression-related brain function in high-risk adolescents</span></span></h2>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b><br /></b></i></span></span><span style="color: #333333; font-size: 14.85px; font-style: italic; font-weight: bold; line-height: 20.79px;">Molecular Psychiatry</span><br />
<span style="color: #333333; font-size: 14.85px; font-style: italic; font-weight: bold; line-height: 20.79px;"><br /></span><span style="color: #333333; font-size: 14.85px; font-weight: bold; line-height: 20.79px;">Abstract</span></div>
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<span style="font-size: 14.85px;">Identifying biological mechanisms through which the experience of adversity emerges as individual risk for mental illness is an important step toward developing strategies for personalized treatment and, ultimately, prevention. Preclinical studies have identified epigenetic modification of gene expression as one such mechanism. Recent clinical studies have suggested that epigenetic modification, particularly methylation of gene regulatory regions, also acts to shape human brain function associated with risk for mental illness. However, it is not yet clear whether differential gene methylation as a function of adversity contributes to the emergence of individual risk for mental illness. Using prospective longitudinal epigenetic, neuroimaging and behavioral data from 132 adolescents, we demonstrate that changes in gene methylation associated with lower socioeconomic status (SES) predict changes in risk-related brain function. Specifically, we find that lower SES during adolescence is associated with an increase in methylation of the proximal promoter of the serotonin transporter gene, which predicts greater increases in threat-related amygdala reactivity. We subsequently demonstrate that greater increases in amygdala reactivity moderate the association between a positive family history for depression and the later manifestation of depressive symptoms. These initial results suggest a specific biological mechanism through which adversity contributes to altered brain function, which in turn moderates the emergence of general liability as individual risk for mental illness. If replicated, this prospective pathway may represent a novel target biomarker for intervention and prevention among high-risk individuals.</span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://www.nature.com/mp/journal/v22/n2/abs/mp201682a.html" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration: none;" target="_blank">http://www.nature.com/mp/journal/</a></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px; text-transform: uppercase;">Side Effects to Antidepressant Treatment in Patients With Depression and Comorbid Panic Disorder</span></span></h2>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b>The Journal of Clinical Psychiatry</b></span></i></span><br />
<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b><br /></b></span></i></span><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b><br /></b></span></i></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"><i>Objective</i></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">Side effects to antidepressant medication can affect the efficacy of treatment, but few predictors foretell who experiences side effects and which side effects they experience. This secondary data analysis examined whether depressed patients with comorbid panic disorder were more likely to experience side effects than those without panic disorder. The study also examined whether greater burden of side effects predicted a poorer treatment course for patients with panic disorder than those without panic disorder. To examine the specificity of these effects, analyses also examined 2 other anxiety disorders—social phobia and generalized anxiety disorder (GAD).</span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Between 2002 and 2006, a large sample (N = 808) of chronically depressed individuals (assessed using the Structured Clinical Interview for DSM-IV-TR Axis I Disorders [SCID-IV]) received antidepressants according to a predetermined algorithm for 12 weeks. Every 2 weeks, depressive symptoms (per the Hamilton Depression Rating Scale) and side effects (specific side effects as well as several indicators of side effect burden) were assessed.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Lifetime diagnosis of panic disorder (assessed using the SCID-IV) at baseline was associated with higher likelihood of gastrointestinal (OR = 1.6 [95% CI, 1.0–2.6]), cardiac (OR = 1.8 [95% CI, 1.1–3.1]), neurologic (OR = 2.6 [95% CI, 1.6–4.2]), and genitourinary side effects (OR = 3.0 [95% CI, 1.7–5.3]) during treatment. Increases in side effect frequency, intensity, and impairment over time were more strongly associated with increases in depressive symptoms for patients with panic disorder compared to those without panic disorder. Neither social phobia nor GAD was associated with these effects.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Potentially due to heightened interoceptive awareness of changes in their body, chronically depressed individuals with panic disorder may be at greater risk than those without panic disorder for antidepressant side effects and to experience a worsening of depressive symptoms as a result of these side effects over time.</span></span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://www.ncbi.nlm.nih.gov/labs/articles/28068460/" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration: none;" target="_blank">http://www.psychiatrist.com/JCP/</a></div>
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<b><a href="http://journals.lww.com/psychopharmacology/pages/currenttoc.aspx" style="color: #6699cc; text-decoration: none;" target="_blank">Journal of Clinical Psychopharmacology - April 2017 - Volume 37, Issue 2</a></b></div>
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<b><a href="http://www.nature.com/npp/journal/v42/n4/index.html" style="color: #6699cc; text-decoration: none;" target="_blank">Neuropsychopharmacology - Volume 42, Issue 4 (March 2017)</a></b></div>
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<b><a href="https://link.springer.com/journal/213/234/6/page/1" style="color: #6699cc; text-decoration: none;" target="_blank">Psychopharmacology - Volume 234, Issue 6, March 2017</a></b></div>
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<b><a href="http://jop.sagepub.com/content/current" style="color: #6699cc; text-decoration: none;" target="_blank">Journal of Psychopharmacology - March 2017; 31 (3)</a></b></div>
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<b><a href="http://ajp.psychiatryonline.org/toc/ajp/current" style="color: #6699cc; text-decoration: none;" target="_blank">The American Journal of Psychiatry - March 2017, Vol. 174, Issue 3</a></b></div>
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<b style="color: #6699cc; text-decoration: none;"><a href="http://archpsyc.jamanetwork.com/issue.aspx" style="color: #6699cc; text-decoration: none;" target="_blank">JAMA Psychiatry - March 2017, Vol. 74, No. </a>3</b></div>
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<b><a href="http://www.nature.com/neuro/journal/v20/n3/index.html" style="color: #6699cc; text-decoration: none;" target="_blank">Nature Neuroscience - March 2017, Vol 20, N° 3</a></b></div>
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<b><a href="http://www.nature.com/mp/journal/v22/n3/index.html" style="color: #6699cc; text-decoration: none;" target="_blank">Molecular Psychiatry - Volume 22, Issue 3, March 2017</a></b></div>
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<b><span style="font-size: small;">Join us on LinkedIn:</span> </b><b><a href="http://www.linkedin.com/groups/Neuropsychopharmacology-Neuroscience-5147601" style="color: #6699cc; text-decoration: none;">Neurosychopharmacology News Group</a></b></h3>
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Eutimiahttp://www.blogger.com/profile/07836706907685752267noreply@blogger.comtag:blogger.com,1999:blog-1045445187620004007.post-35804043867801958422017-01-05T12:11:00.001-05:002017-01-05T15:02:59.823-05:00January 2017<div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px; text-transform: uppercase;">Treatment-Resistant Schizophrenia: Treatment Response and Resistance in Psychosis (TRRIP) Working Group Consensus Guidelines on Diagnosis and Terminology</span></span></h2>
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<i style="font-size: 14.85px; line-height: 20.79px;"><br /></i><i><b>The American Journal of Psychiatry</b></i></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Research and clinical translation in schizophrenia is limited by inconsistent definitions of treatment resistance and response. To address this issue, the authors evaluated current approaches and then developed consensus criteria and guidelines.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Method</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">A systematic review of randomized antipsychotic clinical trials in treatment-resistant schizophrenia was performed, and definitions of treatment resistance were extracted. Subsequently, consensus operationalized criteria were developed through 1) a multiphase, mixed methods approach, 2) identification of key criteria via an online survey, and 3) meetings to achieve consensus.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Of 2,808 studies identified, 42 met inclusion criteria. Of these, 21 studies (50%) did not provide operationalized criteria. In the remaining studies, criteria varied considerably, particularly regarding symptom severity, prior treatment duration, and antipsychotic dosage thresholds; only two studies (5%) utilized the same criteria. The consensus group identified minimum and optimal criteria, employing the following principles: 1) current symptoms of a minimum duration and severity determined by a standardized rating scale; 2) moderate or worse functional impairment; 3) prior treatment consisting of at least two different antipsychotic trials, each for a minimum duration and dosage; 4) systematic monitoring of adherence and meeting of minimum adherence criteria; 5) ideally at least one prospective treatment trial; and 6) criteria that clearly separate responsive from treatment-resistant patients.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">There is considerable variation in current approaches to defining treatment resistance in schizophrenia. The authors present consensus guidelines that operationalize criteria for determining and reporting treatment resistance, adequate treatment, and treatment response, providing a benchmark for research and clinical translation.</span></span><br />
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<b>Source:</b> <a href="http://ajp.psychiatryonline.org/doi/full/10.1176/appi.ajp.2016.16050503" style="color: #6699cc; text-decoration: none;" target="_blank">http://ajp.psychiatryonline.org/</a></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b>Biological Psychiatry</b></i></span></span></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b><br /></b></i></span></span></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 13px;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Background</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Attention-deficit/hyperactivity disorder (ADHD) is associated with high rates of psychiatric comorbidity, including depression. However, it is unclear whether ADHD medication increases or decreases the risk for depression.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We studied all individuals with a diagnosis of ADHD born between 1960 and 1998 in Sweden (N = 38,752). We obtained data for prescription of ADHD medication, diagnosis of depression and other psychiatric disorders, and sociodemographic factors from population-based registers. The association between ADHD medication and depression was estimated with Cox proportional hazards regression.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">After adjustment for sociodemographic and clinical confounders, ADHD medication was associated with a reduced long-term risk (i.e., 3 years later) for depression (hazard ratio = 0.58; 95% confidence interval, 0.51–0.67). The risk was lower for longer duration of ADHD medication. Also, ADHD medication was associated with reduced rates of concurrent depression; within-individual analysis suggested that occurrence of depression was 20% less common during periods when patients received ADHD medication compared with periods when they did not (hazard ratio = 0.80; 95% confidence interval, 0.70–0.92).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333;"><span style="line-height: 20.79px;"><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Our study suggests that ADHD medication does not increase the risk of later depression; rather, medication was associated with a reduced risk for subsequent and concurrent depression.</span></span></span></span> <span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 13px;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b><br /></b></i></span></span></div>
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<b><br /></b><b>Read more:</b> <a href="http://www.biologicalpsychiatryjournal.com/article/S0006-3223(16)00130-X/abstract" style="color: #6699cc; text-decoration: none;" target="_blank">http://www.biologicalpsychiatryjournal.com/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px; text-transform: uppercase;">Characterization of Admission Types in Medically Hospitalized Patients Prescribed Clozapine</span></span></h2>
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<i style="font-size: 14.85px; line-height: 20.79px;"><b>Psychosomatics</b></i><br />
<span style="font-size: 14.85px; line-height: 20.79px;"><b><br /></b></span><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></div>
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<i style="font-size: 14.85px; line-height: 20.79px;"><b><br /></b></i></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Background</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Clozapine is the antipsychotic of choice for treatment-resistant schizophrenia; however, rigorous monitoring is required to prevent or detect adverse drug events that contribute to morbidity and mortality. In addition to the FDA boxed safety warnings specific to clozapine (agranulocytosis, hypotension, seizures, and cardiomyopathy/myocarditis), other adverse events such as pneumonia and gastrointestinal hypomotility have been reported in the literature to result in hospitalization.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To explore the reasons for medical hospitalization in patients prescribed clozapine, a retrospective chart review was completed.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Adults with schizophrenia or schizoaffective disorder prescribed clozapine were identified if they had a non-psychiatric medical admission between 1/1/2003 and 8/1/2015. Demographics, admitting diagnosis, admitting service type, psychiatric consult information, clozapine dosing, and drug-interactions were collected.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">104 patients, representing 248 hospitalizations, were admitted to a medical unit during the study period. The predominant admission types were for the management of either pulmonary (32.2%) or gastrointestinal (19.8%) illnesses. The most common pulmonary diagnosis was pneumonia, accounting for 58% of pulmonary admissions. 61.2% of the gastrointestinal admissions were related to hypomotility, ranging from constipation to death. Clozapine was discontinued due to neutropenia in 2 patients; in both cases concomitant chemotherapy had been given.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusion</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">In patients prescribed clozapine admitted to non-psychiatric medical settings, gastrointestinal and pulmonary illnesses were common but not illnesses related to boxed warnings. Additional research is needed to better assess the causality and true incidence of gastrointestinal or pulmonary events associated with clozapine. Furthermore, clinicians must be prepared to prevent, detect, and manage potentially life-threatening events associated with clozapine.</span></span></div>
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<b>Source:</b> <a href="http://www.psychosomaticsjournal.com/article/S0033-3182(16)30147-5/abstract?cc=y=" style="color: #6699cc; text-decoration: none;" target="_blank">http://www.psychosomaticsjournal.com/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The purpose of this multicenter, prospective, randomized, placebo-controlled study was to evaluate and compare the efficacy of two cognitive rehabilitation interventions (Memory and Attention Adaptation Training (MAAT) and Attention Builders Training (ABT)), with and without pharmacologic enhancement (ie, with methylphenidate (MPH) or placebo), for treating persistent cognitive problems after traumatic brain injury (TBI). Adults with a history of TBI at least four months prior to study enrollment with either objective cognitive deficits or subjective cognitive complaints were randomized to receive MPH or placebo and MAAT or ABT, yielding four treatment combinations: MAAT/MPH (N=17), ABT/MPH (N=19), MAAT/placebo (N=17), and ABT/placebo (N=18). Assessments were conducted pre-treatment (baseline) and after six weeks of treatment (post-treatment). Outcome measures included scores on neuropsychological measures and subjective rating scales. Statistical analyses used linear regression models to predict post-treatment scores for each outcome variable by treatment type, adjusting for relevant covariates. Statistically significant (p<0.05) treatment-related improvements in cognitive functioning were found for word list learning (MAAT/placebo>ABT/placebo), nonverbal learning (MAAT/MPH>MAAT/placebo and MAAT/MPH>ABT/MPH), and auditory working memory and divided attention (MAAT/MPH>ABT/MPH). These results suggest that combined treatment with metacognitive rehabilitation (MAAT) and pharmacotherapy (MPH) can improve aspects of attention, episodic and working memory, and executive functioning after TBI.</span></span><br />
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FDA Drug Safety Communication: FDA revises description of mental health side effects of the stop-smoking medicines Chantix (varenicline) and Zyban (bupropion) to reflect clinical trial findings</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Based on a U.S. Food and Drug Administration (FDA) review of a large clinical trial that we required the drug companies to conduct,1 we have determined the risk of serious side effects on mood, behavior, or thinking with the stop-smoking medicines Chantix (varenicline) and Zyban (bupropion)* is lower than previously suspected. The risk of these mental health side effects is still present, especially in those currently being treated for mental illnesses such as depression, anxiety disorders, or schizophrenia, or who have been treated for mental illnesses in the past. However, most people who had these side effects did not have serious consequences such as hospitalization. The results of the trial confirm that the benefits of stopping smoking outweigh the risks of these medicines.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">As a result of our review of the large clinical trial, we are removing the Boxed Warning, FDA’s most prominent warning, for serious mental health side effects from the Chantix drug label. The language describing the serious mental health side effects seen in patients quitting smoking will also be removed from the Boxed Warning in the Zyban label.† We are also updating the existing warning section in both labels that describes the side effects on mood, behavior, or thinking to include the results from the clinical trial. This decision is consistent with the recommendations of external experts at a September 2016 FDA Advisory Committee meeting. The patient Medication Guide that explains the risks associated with the use of the medicines will continue to be provided with every patient prescription; however, the risk evaluation and mitigation strategy (REMS) that formally required the Medication Guide will be removed.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Our review of the clinical trial results also confirmed that Chantix, Zyban, and nicotine replacement patches were all more effective for helping people quit smoking than was an inactive treatment called a placebo. These medicines were found to better help people quit smoking regardless of whether or not they had a history of mental illness.</span></span></div>
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<b>Read More:</b> <a href="http://www.fda.gov/Drugs/DrugSafety/ucm532221.htm" rel="" style="color: #6699cc; text-decoration: none;" target="_blank">http://www.fda.gov/Drugs/</a></div>
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Sex and Race Differences in the Association Between Statin Use and the Incidence of Alzheimer Disease</h2>
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<i><b>JAMA Neurology</b></i><br />
<i><b><br /></b></i><b>Abstract</b></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Importance </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To our knowledge, no effective treatments exist for Alzheimer disease, and new molecules are years away. However, several drugs prescribed for other conditions have been associated with reducing its risk.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To analyze the association between statin exposure and Alzheimer disease incidence among Medicare beneficiaries.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We examined the medical and pharmacy claims of a 20% sample of Medicare beneficiaries from 2006 to 2013 and compared rates of Alzheimer disease diagnosis for 399 979 statin users 65 years of age or older with high or low exposure to statins and with drug molecules for black, Hispanic, and non-Hispanic white people, and men and women of Asian, Native American, or unkown race/ethnicity who are referred to as “other.”</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The main outcome was incident diagnosis of Alzheimer disease based on the International Classification of Diseases, Ninth Revision, Clinical Modification. We used Cox proportional hazard models to analyze the association between statin exposure and Alzheimer disease diagnosis for different sexes, races and ethnicities, and statin molecules.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The 399 979 study participants included 7794 (1.95%) black men, 24 484 (6.12%) black women, 11 200 (2.80%) Hispanic men, 21 458 (5.36%) Hispanic women, 115 059 (28.77%) white men, and 195 181 (48.80%) white women. High exposure to statins was associated with a lower risk of Alzheimer disease diagnosis for women (hazard ratio [HR], 0.85; 95% CI, 0.82-0.89; P<.001) and men (HR, 0.88; 95% CI, 0.83-0.93; P<.001). Simvastatin was associated with lower Alzheimer disease risk for white women (HR, 0.86; 95% CI, 0.81-0.92; P<.001), white men (HR, 0.90; 95% CI, 0.82-0.99; P=.02), Hispanic women (HR, 0.82; 95% CI, 0.68-0.99; P=.04), Hispanic men (HR, 0.67; 95% CI, 0.50-0.91; P=.01), and black women (HR, 0.78; 95% CI, 0.66-0.93; P=.005). Atorvastatin was associated with a reduced risk of incident Alzheimer disease diagnosis for white women(HR, 0.84, 95% CI, 0.78-0.89), black women (HR, .081, 95% CI, 0.67-0.98), and Hispanic men (HR, 0.61, 95% CI, 0.42-0.89) and women (HR, 0.76, 95% CI, 0.60-0.97). Pravastatin and rosuvastatin were associated with reduced Alzheimer disease risk for white women only (HR, 0.82, 95% CI, 0.70-0.95 and HR, 0.81, 95% CI, 0.67-0.98, respectively). High statin exposure was not associated with a statistically significant lower Alzheimer disease risk among black men.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The reduction in Alzheimer disease risk varied across statin molecules, sex, and race/ethnicity. Clinical trials that include racial and ethnic groups need to confirm these findings. Because statins may affect Alzheimer disease risk, physicians should consider which statin is prescribed to each patient.</span></span><br />
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<b>Source:</b> <a href="http://jamanetwork.com/journals/jamaneurology/article-abstract/2591317" style="color: #6699cc; text-decoration: none;" target="_blank">http://jamanetwork.com/journals/jamaneurology/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Renal dysfunction has been linked with increased risk for cognitive impairment and dementia, but studies are conflicting. For that reason, the aim of the present systematic review and meta-analysis is to summarize the best available evidence on the prospective association between potential markers of renal dysfunction and development of cognitive impairment or dementia.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Medline, Embase, and Cochrane Database of Systematic Reviews were searched for potential publications until August 1, 2016. Studies were eligible if they fulfilled the following criteria: population-based study, prospective design, ≥100 participants, aged ≥45 years, ≥1 year follow-up, and cognition/dementia outcomes. Where appropriate, random effects meta-analyses were conducted yielding pooled odds ratios (OR) and 95% confidence intervals (CI).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Twenty-two out of 8,494 abstracts fulfilled the eligibility criteria. Sufficient evidence was found for albuminuria, mixed results for estimated glomerular filtration rate (eGFR), insufficient support for cystatin C, and tentative evidence for serum creatinine and creatinine clearance. Meta-analyses of 5 studies representing 27,805 persons showed a 35% increased risk of cognitive impairment or dementia in those with albuminuria (OR 1.35, 95% CI 1.06–1.73, p = 0.015), whereas eGFR <60 mL/min/1.73 m2 showed no significant association (OR 1.28, 95% CI 0.99–1.65, p = 0.063). No meta-analyses could be done for serum creatinine, creatinine clearance, or cystatin C.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The overall evidence for an association between renal dysfunction and cognitive impairment or dementia is modest. Evidence suggests that albuminuria is associated with higher odds of developing cognitive impairment or dementia</span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;">.</span></div>
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<b>Source:</b> <a href="http://www.neurology.org/content/early/2016/12/14/WNL.0000000000003482.abstract" style="color: #6699cc; text-decoration: none;" target="_blank">http://www.neurology.org/</a></div>
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Assessment of the Incremental Diagnostic Value of Amyloid PET With Florbetapir F 18 Imaging in Patients With Cognitive Impairment</h2>
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<i><b>JAMA Neurology</b></i></div>
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<b><br /></b><b>Abstract</b></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>I</i></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>mportance </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Cerebral amyloidosis is a key abnormality in Alzheimer disease (AD) and can be detected in vivo with positron emission tomography (PET) ligands. Although amyloid PET has clearly demonstrated analytical validity, its clinical utility is debated.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To evaluate the incremental diagnostic value of amyloid PET with florbetapir F 18 in addition to the routine clinical diagnostic assessment of patients evaluated for cognitive impairment.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The Incremental Diagnostic Value of Amyloid PET With [18F]-Florbetapir (INDIA-FBP) Study is a multicenter study involving 18 AD evaluation units from eastern Lombardy, Northern Italy, 228 consecutive adults with cognitive impairment were evaluated for AD and other causes of cognitive decline, with a prescan diagnostic confidence of AD between 15% and 85%. Participants underwent routine clinical and instrumental diagnostic assessment. A prescan diagnosis was made, diagnostic confidence was estimated, and drug treatment was provided. At the time of this workup, an amyloid PET/computed tomographic scan was performed, and the result was communicated to physicians after workup completion. Physicians were asked to review the diagnosis, diagnostic confidence, and treatment after the scan. </span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Primary outcomes were prescan to postscan changes of diagnosis, diagnostic confidence, and treatment.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Of the 228 participants, 107 (46%) were male; mean (SD) age was 70.5 (7) years. Diagnostic change occurred in 46 patients (79%) having both a previous diagnosis of AD and an amyloid-negative scan (P < .001) and in 16 (53%) of those with non-AD diagnoses and an amyloid-positive scan (P < .001). Diagnostic confidence in AD diagnosis increased by 15.2% in amyloid-positive (P < .001; effect size Cohen d = 1.04) and decreased by 29.9% in amyloid-negative (P < .001; d = −1.19) scans. Acetylcholinesterase inhibitors and memantine hydrochloride were introduced in 61 (65.6%) patients with positive scan results who had not previously received those drugs, and the use of the drugs was discontinued in 6 (33.3%) patients with negative scan results who were receiving those drugs (P < .001).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Amyloid PET in addition to routine assessment in patients with cognitive impairment has a significant effect on diagnosis, diagnostic confidence, and drug treatment. The effect on health outcomes, such as morbidity and mortality, remains to be assessed.</span></span></div>
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<b style="font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://jamanetwork.com/journals/jamaneurology/article-abstract/2578330" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration: none;" target="_blank">http://jamanetwork.com/journals/jamaneurology/</a></div>
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<span style="color: #333333; font-family: "arial" , sans-serif;"><span style="font-size: 18px; line-height: 22px; text-transform: uppercase;">Ziprasidone Augmentation of Escitalopram for Major Depressive Disorder: Cardiac, Endocrine, Metabolic, and Motoric Effects in a Randomized, Double-Blind, Placebo-Controlled Study</span></span></h2>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b><br /></b></i></span></span><span style="color: #333333; font-size: 14.85px; font-style: italic; font-weight: bold; line-height: 20.79px;">Journal of Clinical Psychiatry</span><br />
<span style="color: #333333; font-size: 14.85px; font-style: italic; font-weight: bold; line-height: 20.79px;"><br /></span><span style="color: #333333; font-size: 14.85px; font-weight: bold; line-height: 20.79px;">Abstract</span></div>
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<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective </i> </span></span></div>
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 13px;"><span style="font-size: 14.85px;">I</span></span><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To examine motoric, cardiovascular, endocrine, and metabolic effects of adjunctive ziprasidone in adults with major depressive disorder (MDD) and prior nonresponse to 8 weeks of open-label escitalopram.</span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span>
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Methods</i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">A multicenter, parallel, randomized, double-blind, placebo-controlled trial was conducted at 3 US academic medical centers from July 2008 to October 2013. Recruited were 139 outpatients with persistent DSM-IV MDD following an 8-week open-label trial of escitalopram. Subjects were then randomized to adjunctive ziprasidone (escitalopram + ziprasidone, n = 71) or placebo (escitalopram + placebo, n = 68) for 8 additional weeks. Cardiac and metabolic measures were obtained at each treatment visit. Barnes Akathisia Scale and Abnormal Involuntary Movement Scale (AIMS) scores were also obtained. Changes in outcome measures for each treatment group were compared by independent-samples t test.</span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span>
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">A trend toward significance (P = .06) in corrected QT interval (QTc) increase was observed for ziprasidone (mean [SD] = 8.8 [20.2] milliseconds) versus placebo (–0.02 [25.5] milliseconds). Ziprasidone-treated patients had a significantly greater increase in global akathisia scores (P = .01) and significant weight increase (mean [SD] = 3.5 [11.8] kg, or 7.7 [26.1] lb) compared to placebo (1.0 [6.4] kg, or 2.2 [14.1] lb) (P = .03). No significant changes in AIMS scores were observed for either treatment group.</span></span><br />
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<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Adjunctive ziprasidone, added to escitalopram, led to a greater weight gain and greater but modest akathisia compared to placebo. The effect of ziprasidone on QTc showed a trend toward significance, and therefore caution should be used in the administration of ziprasidone. While ziprasidone augmentation in patients with MDD appears safe, precautions should be taken in practice, specifically regular monitoring of electrocardiogram, weight, extrapyramidal symptoms, and involuntary movements.</span></span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://www.psychiatrist.com/JCP/article/Pages/2016/aheadofprint/15m10426.aspx" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration: none;" target="_blank">http://www.psychiatrist.com/JCP/</a></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px; text-transform: uppercase;">Association of Neurocognition With Transition to Psychosis</span></span></h2>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b>JAMA Psychiatry</b></span></i></span><br />
<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b><br /></b></span></i></span><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b><br /></b></span></i></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Importance </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Neurocognition is a central characteristic of schizophrenia and other psychotic disorders. Identifying the pattern and severity of neurocognitive functioning during the “near-psychotic,” clinical high-risk (CHR) state of psychosis is necessary to develop accurate risk factors for psychosis and more effective and potentially preventive treatments.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objectives </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To identify core neurocognitive dysfunctions associated with the CHR phase, measure the ability of neurocognitive tests to predict transition to psychosis, and determine if neurocognitive deficits are robust or explained by potential confounders.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">In this case-control study across 8 sites, baseline neurocognitive data were collected from January 2009 to April 2013 in the second phase of the North American Prodrome Longitudinal Study (NAPLS 2). The dates of analysis were August 2015 to August 2016. The setting was a consortium of 8 university-based, outpatient programs studying the psychosis prodrome in North America. Participants were 264 healthy controls (HCs) and 689 CHR individuals, aged 12 to 35 years.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Neurocognitive associations with transition to psychosis and effects of medication on neurocognition. Nineteen neuropsychological tests and 4 factors derived from factor analysis were used: executive and visuospatial abilities, verbal abilities, attention and working memory abilities, and declarative memory abilities.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">This study included 264 HCs (137 male and 127 female) and 689 CHR participants (398 male and 291 female). In the HCs, 145 (54.9%) were white and 119 (45.1%) were not, whereas 397 CHR participants (57.6%) were white and 291 (42.3%) were not. In the HCs, 45 (17%) were of Hispanic origin, whereas 127 CHR participants (18.4%) were of Hispanic origin. The CHR individuals were significantly impaired compared with HCs on attention and working memory abilities and declarative memory abilities. The CHR converters had large deficits in attention and working memory abilities and declarative memory abilities (Cohen d, approximately 0.80) compared with controls and performed significantly worse on these dimensions than nonconverters (Cohen d, 0.28 and 0.48, respectively). These results were not accounted for by general cognitive ability or medications. In Cox proportional hazards regression, time to conversion in those who transitioned to psychosis was significantly predicted by high verbal (premorbid) abilities (β = 0.40; hazard ratio [HR], 1.48; 95% CI, 1.08-2.04; P = .02), impaired declarative memory abilities (β = −0.87; HR, 0.42; 95% CI, 0.31-0.56; P < .001), age (β = −0.10; HR, 0.90; 95% CI, 0.84-0.97; P = .003), site, and a combined score of unusual thought content or delusional ideas and suspiciousness or persecutory ideas items (β = 0.44; HR, 1.56; 95% CI, 1.36-1.78; P < .001).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Neurocognitive impairment, especially in attention and working memory abilities and declarative memory abilities, is a robust characteristic of CHR participants, especially those who later develop psychosis. Interventions targeting the enhancement of neurocognitive functioning are warranted in this population.</span></span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://jamanetwork.com/journals/jamapsychiatry/article-abstract/2575728" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration: none;" target="_blank">http://jamanetwork.com/journals/jamapsychiatry/</a></div>
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<b style="color: blue; font-size: x-large;"><br /></b><b style="color: blue; font-size: x-large;">Online Journals:</b></div>
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<b><a href="http://journals.lww.com/psychopharmacology/pages/currenttoc.aspx" style="color: #6699cc; text-decoration: none;" target="_blank">Journal of Clinical Psychopharmacology - February 2017 - Volume 37, Issue 1</a></b></div>
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<b><a href="http://www.nature.com/npp/journal/v42/n2/index.html" style="color: #6699cc; text-decoration: none;" target="_blank">Neuropsychopharmacology - Volume 42, Issue 2 (January 2017)</a></b></div>
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<b><a href="http://link.springer.com/journal/213/234/2/page/1" style="color: #6699cc; text-decoration: none;" target="_blank">Psychopharmacology - Volume 234, Issue 2, January 2017</a></b></div>
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<b><a href="http://jop.sagepub.com/content/current" style="color: #6699cc; text-decoration: none;" target="_blank">Journal of Psychopharmacology - December 2016; 30 (12)</a></b></div>
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<b><a href="http://ajp.psychiatryonline.org/toc/ajp/current" style="color: #6699cc; text-decoration: none;" target="_blank">The American Journal of Psychiatry - January 2017, Vol. 174, Issue 1</a></b></div>
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<a href="http://archpsyc.jamanetwork.com/issue.aspx" style="color: #6699cc; text-decoration: none;" target="_blank"><b>JAMA Psychiatry - January 2017, Vol. 74, No. 1</b></a></div>
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<b><a href="http://www.nature.com/neuro/journal/v20/n1/index.html" style="color: #6699cc; text-decoration: none;" target="_blank">Nature Neuroscience - January 2017, Vol 20, N° 1</a></b></div>
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<b><a href="http://www.nature.com/mp/journal/v22/n1/index.html" style="color: #6699cc; text-decoration: none;" target="_blank">Molecular Psychiatry - Volume 22, Issue 1, January 2017</a></b></div>
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<b style="background-color: white; color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"><a href="http://www.biologicalpsychiatryjournal.com/current" style="color: #6699cc; text-decoration: none;" target="_blank">Biological Psychiatry - Volume 81, Issue 3, February 2017</a></b><br />
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<b><a href="http://brain.oxfordjournals.org/content/140/1" style="color: #6699cc; text-decoration: none;" target="_blank">Brain - Volume 140, Issue 1, January 2017</a></b></div>
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<b><span style="font-size: small;">Join us on LinkedIn:</span> </b><b><a href="http://www.linkedin.com/groups/Neuropsychopharmacology-Neuroscience-5147601" style="color: #6699cc; text-decoration: none;">Neurosychopharmacology News Group</a></b></h3>
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Eutimiahttp://www.blogger.com/profile/07836706907685752267noreply@blogger.comtag:blogger.com,1999:blog-1045445187620004007.post-40193350062830890832016-11-06T07:42:00.002-05:002016-11-12T11:17:14.450-05:00November 2016<div dir="ltr" style="text-align: left;" trbidi="on">
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<i style="font-size: 14.85px; line-height: 20.79px;"><br /></i><i><b>JAMA Psychiatry</b></i></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Importance</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Speech/language, scholastic, and motor disorders are common in children. It is unknown whether exposure to selective serotonin reuptake inhibitors (SSRIs) during pregnancy influences susceptibility to these disorders.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To examine whether SSRI exposure during pregnancy is associated with speech/language, scholastic, and motor disorders in offspring up to early adolescence.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">This prospective birth cohort study examined national population-based register data in Finland from 1996 to 2010. The sampling frame includes 845 345 pregnant women and their singleton offspring with data on maternal use of antidepressants and depression-related psychiatric disorders during pregnancy.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Exposures</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">There were 3 groups of offspring: 15 596 were in the SSRI-exposed group, ie, had mothers diagnosed as having depression-related psychiatric disorders with a history of purchasing SSRIs during pregnancy; 9537 were in the unmedicated group, ie, had mothers diagnosed as having depression-related psychiatric disorders without a history of purchasing SSRIs during pregnancy; and 31 207 were in the unexposed group, ie, had mothers without a psychiatric diagnosis or a history of purchasing SSRIs.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Cumulative incidence of speech/language, scholastic, or motor disorders (829, 187, and 285 instances, respectively) from birth to 14 years. All hypotheses tested were formulated before data collection.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Of the 56 340 infants included in the final cohort, 28 684 (50.9%) were male and 48 782 (86.6%) were 9 years or younger. The mean (SD) ages of children at diagnosis were 4.43 (1.67), 3.55 (2.67), and 7.73 (2.38) for speech/language, scholastic, and motor disorders, respectively. Offspring of mothers who purchased SSRIs at least twice during pregnancy had a significant 37% increased risk of speech/language disorders compared with offspring in the unmedicated group. The cumulative hazard of speech/language disorders was 0.0087 in the SSRI-exposed group vs 0.0061 in the unmedicated group (hazard ratio, 1.37; 95% CI, 1.11-1.70; P = .004). There was a significantly increased risk of these disorders in offspring in the SSRI-exposed and unmedicated groups compared with offspring in the unexposed group. For scholastic and motor disorders, there were no differences between offspring in the SSRI-exposed group and in the unmedicated group.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px; line-height: 20.79px;"><i>Conclusions and Relevance </i> </span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px; line-height: 20.79px;">Exposure to SSRIs during pregnancy was associated with an increased risk of speech/language disorders. This finding may have implications for understanding associations between SSRIs and child development.</span><br />
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<b>Source:</b> <a href="http://jamanetwork.com/journals/jamapsychiatry/article-abstract/2566206" style="color: #6699cc; text-decoration: none;" target="_blank">http://jamanetwork.com/journals/</a></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b>Molecular Psychiatry</b></i></span></span></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 13px;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333;"><span style="line-height: 20.79px;"><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We sought to determine whether high-dose folinic acid improves verbal communication in children with non-syndromic autism spectrum disorder (ASD) and language impairment in a double-blind placebo control setting. Forty-eight children (mean age 7 years 4 months; 82% male) with ASD and language impairment were randomized to receive 12 weeks of high-dose folinic acid (2 mg kg−1 per day, maximum 50 mg per day; n=23) or placebo (n=25). Children were subtyped by glutathione and folate receptor-α autoantibody (FRAA) status. Improvement in verbal communication, as measured by a ability-appropriate standardized instrument, was significantly greater in participants receiving folinic acid as compared with those receiving placebo, resulting in an effect of 5.7 (1.0,10.4) standardized points with a medium-to-large effect size (Cohen’s d=0.70). FRAA status was predictive of response to treatment. For FRAA-positive participants, improvement in verbal communication was significantly greater in those receiving folinic acid as compared with those receiving placebo, resulting in an effect of 7.3 (1.4,13.2) standardized points with a large effect size (Cohen’s d=0.91), indicating that folinic acid treatment may be more efficacious in children with ASD who are FRAA positive. Improvements in subscales of the Vineland Adaptive Behavior Scale, the Aberrant Behavior Checklist, the Autism Symptom Questionnaire and the Behavioral Assessment System for Children were significantly greater in the folinic acid group as compared with the placebo group. There was no significant difference in adverse effects between treatment groups. Thus, in this small trial of children with non-syndromic ASD and language impairment, treatment with high-dose folinic acid for 12 weeks resulted in improvement in verbal communication as compared with placebo, particularly in those participants who were positive for FRAAs.</span></span></span></span>
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<b>Read more:</b> <a href="http://www.nature.com/mp/journal/vaop/ncurrent/full/mp2016168a.html" style="color: #6699cc; text-decoration: none;" target="_blank">http://www.nature.com/mp/journal/</a></div>
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<i style="font-size: 14.85px; line-height: 20.79px;"><b>Proceedings of the National Academy of Sciences</b></i><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Amygdala circuitry and early life stress (ELS) are both strongly and independently implicated in the neurobiology of depression. Importantly, animal models have revealed that the contribution of ELS to the development and maintenance of depression is likely a consequence of structural and physiological changes in amygdala circuitry in response to stress hormones. Despite these mechanistic foundations, amygdala engagement and ELS have not been investigated as biobehavioral targets for predicting functional remission in translational human studies of depression. Addressing this question, we integrated human neuroimaging and measurement of ELS within a controlled trial of antidepressant outcomes. Here we demonstrate that the interaction between amygdala activation engaged by emotional stimuli and ELS predicts functional remission on antidepressants with a greater than 80% cross-validated accuracy. Our model suggests that in depressed people with high ELS, the likelihood of remission is highest with greater amygdala reactivity to socially rewarding stimuli, whereas for those with low-ELS exposure, remission is associated with lower amygdala reactivity to both rewarding and threat-related stimuli. This full model predicted functional remission over and above the contribution of demographics, symptom severity, ELS, and amygdala reactivity alone. These findings identify a human target for elucidating the mechanisms of antidepressant functional remission and offer a target for developing novel therapeutics. The results also offer a proof-of-concept for using neuroimaging as a target for guiding neuroscience-informed intervention decisions at the level of the individual person.</span></span></div>
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<b>Source:</b> <a href="http://www.pnas.org/content/113/42/11955.abstract" style="color: #6699cc; text-decoration: none;" target="_blank">http://www.pnas.org/</a></div>
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<span style="font-size: 14.85px; line-height: 20.79px;">Pharmacotherapy for Adults With Alcohol Use Disorders in Outpatient Settings</span></h2>
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<span style="font-size: 14.85px; line-height: 20.79px;"><b><i>JAMA </i></b></span><br />
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<span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Importance </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Alcohol use disorders cause substantial morbidity and early mortality yet remain greatly undertreated. Medications are considerably underused.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To conduct a systematic review and meta-analysis of the benefits and harms of medications (US FDA-approved and others) for adults with alcohol use disorders.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Data Sources </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">PubMed, Cochrane Library, PsycINFO, CINAHL, EMBASE, FDA website, and clinical trials registries (January 1, 1970, to March 1, 2014).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Study Selection </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Two reviewers selected randomized clinical trials (RCTs) with at least 12 weeks’ duration that reported eligible outcomes and head-to-head prospective cohort studies reporting health outcomes or harms.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Data Extraction and Synthesis </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We conducted meta-analyses using random-effects models and calculated numbers needed to treat for benefit (NNTs) or harm (NNHs).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Alcohol consumption, motor vehicle crashes, injuries, quality of life, function, mortality, and harms.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We included 122 RCTs and 1 cohort study (total 22 803 participants). Most assessed acamprosate (27 studies, n = 7519), naltrexone (53 studies, n = 9140), or both. The NNT to prevent return to any drinking for acamprosate was 12 (95% CI, 8 to 26; risk difference [RD], −0.09; 95% CI, −0.14 to −0.04) and was 20 (95% CI, 11 to 500; RD, −0.05; 95% CI, −0.10 to −0.002) for oral naltrexone (50 mg/d). The NNT to prevent return to heavy drinking was 12 (95% CI, 8 to 26; RD −0.09; 95% CI, −0.13 to −0.04) for oral naltrexone (50 mg/d). Meta-analyses of trials comparing acamprosate to naltrexone found no statistically significant difference between them for return to any drinking (RD, 0.02; 95% CI, −0.03 to 0.08) or heavy drinking (RD, 0.01; 95% CI, −0.05 to 0.06). For injectable naltrexone, meta-analyses found no association with return to any drinking (RD, −0.04; 95% CI, −0.10 to 0.03) or heavy drinking (RD, −0.01; 95% CI, −0.14 to 0.13) but found an association with reduction in heavy drinking days (weighted mean difference [WMD], −4.6%; 95% CI, −8.5% to −0.56%). Among medications used off-label, moderate evidence supports an association with improvement in some consumption outcomes for nalmefene (heavy drinking days per month: WMD, −2.0; 95% CI, −3.0 to −1.0; drinks per drinking day: WMD, −1.02; 95% CI, −1.77 to −0.28) and topiramate (% heavy drinking days: WMD, −9.0%; 95% CI, −15.3% to −2.7%; drinks per drinking day: WMD, −1.0; 95% CI, −1.6 to −0.48). For naltrexone and nalmefene, NNHs for withdrawal from trials due to adverse events were 48 (95% CI, 30 to 112) and 12 (95% CI, 7 to 50), respectively; risk was not significantly increased for acamprosate or topiramate.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Both acamprosate and oral naltrexone were associated with reduction in return to drinking. When directly compared with one another, no significant differences were found between acamprosate and naltrexone for controlling alcohol consumption. Factors such as dosing frequency, potential adverse events, and availability of treatments may guide medication choice.</span></span><br />
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<b style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;">Source:</b><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px;"> </span><a href="http://jamanetwork.com/journals/jama/fullarticle/1869208?resultClick=1" style="color: #6699cc; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; text-decoration: none;" target="_blank">http://jamanetwork.com/journals/jama/</a></div>
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Effect of High-Frequency Transcranial Magnetic Stimulation on Craving in Substance Use Disorder: A Meta-Analysis</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Repetitive transcranial magnetic stimulation (rTMS), a noninvasive, neuromodulatory tool, has been used to reduce craving in different substance use disorders. There are some studies that have reported conflicting and inconclusive results; therefore, this meta-analysis was conducted to evaluate the effect of high-frequency rTMS on craving in substance use disorder and to investigate the reasons behind the inconsistency across the studies. The authors searched clinical trials from MEDLINE, Cochrane databases, and International Clinical Trials Registry Platform. The PRISMA guidelines, as well as recommended meta-analysis practices, were followed in the selection process, analysis, and reporting of the findings. The effect estimate used was the standardized mean difference (Hedge's g), and heterogeneity across the considered studies was explored using subgroup analyses. The quality assessment was done using the Cochrane risk of bias tool, and sensitivity analysis was performed to check the influences on effect size by statistical models. After screening and assessment of eligibility, finally 10 studies were included for meta-analysis, which includes six studies on alcohol and four studies on nicotine use disorder. The random-model analysis revealed a pooled effect size of 0.75 (95% CI=0.29 to 1.21, p=0.001), whereas the fixed-model analysis showed a large effect size of 0.87 (95% CI=0.63 to 1.12, p<0.00001). Subgroup analysis for alcohol use disorder showed an effect size of –0.06 (95% CI=–0.89 to 0.77, p=0.88). In the case of nicotine use disorder, random-model analysis revealed an effect size of 1.00 (95% CI=0.48 to 1.55, p=0.0001), whereas fixed-model analysis also showed a large effect size of 0.96 (95% CI=0.71 to 1.22). The present meta-analysis identified a beneficial effect of high-frequency rTMS on craving associated with nicotine use disorder but not alcohol use disorder.</span></span></div>
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<b>Source:</b> <a href="http://neuro.psychiatryonline.org/doi/full/10.1176/appi.neuropsych.16040065" rel="" style="color: #6699cc; text-decoration: none;" target="_blank">http://neuro.psychiatryonline.org/</a></div>
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FMRP regulates an ethanol-dependent shift in GABABR function and expression with rapid antidepressant properties</h2>
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<i><b>Nature Communications</b></i><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Alcohol promotes lasting neuroadaptive changes that may provide relief from depressive symptoms, often referred to as the self-medication hypothesis. However, the molecular/synaptic pathways that are shared by alcohol and antidepressants are unknown. In the current study, acute exposure to ethanol produced lasting antidepressant and anxiolytic behaviours. To understand the functional basis of these behaviours, we examined a molecular pathway that is activated by rapid antidepressants. Ethanol, like rapid antidepressants, alters γ-aminobutyric acid type B receptor (GABABR) expression and signalling, to increase dendritic calcium. Furthermore, new GABABRs are synthesized in response to ethanol treatment, requiring fragile-X mental retardation protein (FMRP). Ethanol-dependent changes in GABABR expression, dendritic signalling, and antidepressant efficacy are absent in Fmr1-knockout (KO) mice. These findings indicate that FMRP is an important regulator of protein synthesis following alcohol exposure, providing a molecular basis for the antidepressant efficacy of acute ethanol exposure.</span></span></div>
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<b>Source:</b> <a href="http://www.nature.com/articles/ncomms12867" style="color: #6699cc; text-decoration: none;" target="_blank">http://www.nature.com/</a></div>
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<i style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>The American Journal of Psychiatry</b></span></i></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span><span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The authors sought to determine the risk of treatment-emergent mania associated with methylphenidate, used in monotherapy or with a concomitant mood-stabilizing medication, in patients with bipolar disorder.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Method</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Using linked Swedish national registries, the authors identified 2,307 adults with bipolar disorder who initiated therapy with methylphenidate between 2006 and 2014. The cohort was divided into two groups: those with and those without concomitant mood-stabilizing treatment. To adjust for individual-specific confounders, including disorder severity, genetic makeup, and early environmental factors, Cox regression analyses were used, conditioning on individual to compare the rate of mania (defined as hospitalization for mania or a new dispensation of stabilizing medication) 0–3 months and 3–6 months after medication start following nontreated periods.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Patients on methylphenidate monotherapy displayed an increased rate of manic episodes within 3 months of medication initiation (hazard ratio=6.7, 95% CI=2.0–22.4), with similar results for the subsequent 3 months. By contrast, for patients taking mood stabilizers, the risk of mania was lower after starting methylphenidate (hazard ratio=0.6, 95% CI=0.4–0.9). Comparable results were observed when only hospitalizations for mania were counted.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">No evidence was found for a positive association between methylphenidate and treatment-emergent mania among patients with bipolar disorder who were concomitantly receiving a mood-stabilizing medication. This is clinically important given that up to 20% of people with bipolar disorder suffer from comorbid ADHD. Given the markedly increased hazard ratio of mania following methylphenidate initiation in bipolar patients not taking mood stabilizers, careful assessment to rule out bipolar disorder is indicated before initiating monotherapy with psychostimulants.</span></span></div>
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<b>Source:</b> <a href="http://ajp.psychiatryonline.org/doi/full/10.1176/appi.ajp.2016.16040467" style="color: #6699cc; text-decoration: none;" target="_blank">http://ajp.psychiatryonline.org/</a></div>
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Association Between Androgen Deprivation Therapy and Risk of Dementia</h2>
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<i><b>JAMA</b></i></div>
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<b><br /></b><b>Abstract</b></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Importance </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">A growing body of evidence supports a link between androgen deprivation therapy (ADT) and cognitive dysfunction, including Alzheimer disease. However, it is currently unknown whether ADT may contribute to the risk of dementia more broadly.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To use an informatics approach to examine the association of ADT as a treatment for prostate cancer with the subsequent development of dementia (eg, senile dementia, vascular dementia, frontotemporal dementia, and Alzheimer dementia).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">In this cohort study, a text-processing method was used to analyze electronic medical record data from an academic medical center from 1994 to 2013, with a median follow-up of 3.4 years (interquartile range, 1.0-7.2 years). We identified 9455 individuals with prostate cancer who were 18 years or older at diagnosis with data recorded in the electronic health record and follow-up after diagnosis. We excluded 183 patients with a previous diagnosis of dementia. Our final cohort comprised 9272 individuals with prostate cancer, including 1826 men (19.7%) who received ADT.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We tested the effect of ADT on the risk of dementia using propensity score–matched Cox proportional hazards regression models and Kaplan-Meier survival analysis.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Among 9272 men with prostate cancer (mean [SD] age, 66.9 [10.9] years; 5450 [58.8%] white), there was a statistically significant association between use of ADT and risk of dementia (hazard ratio, 2.17; 95% CI, 1.58-2.99; P < .001). In sensitivity analyses, results were similar when excluding patients with Alzheimer disease (hazard ratio, 2.32; 95% CI, 1.73-3.12; P < .001). The absolute increased risk of developing dementia among those who received ADT was 4.4% at 5 years (7.9% among those who received ADT vs 3.5% in those who did not receive ADT). Analyses stratified by duration of ADT found that individuals with at least 12 months of ADT use had the greatest absolute increased risk of dementia (hazard ratio, 2.36; 95% CI, 1.64-3.38; P < .001). Kaplan-Meier analysis demonstrated that ADT users 70 years or older had the lowest cumulative probability of remaining dementia free (log-rank P < .001).</span></span><br />
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<span style="color: #333333; font-size: 14.85px;"><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance </i></span></span></span><br />
<span style="color: #333333; font-size: 14.85px;"><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Androgen deprivation therapy in the treatment of prostate cancer may be associated with an increased risk of dementia. This finding should be further evaluated in prospective studies.</span></span></span></div>
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<b style="font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://jamanetwork.com/journals/jamaoncology/article-abstract/2569059" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration: none;" target="_blank">http://jamanetwork.com/journals/jamaoncology</a></div>
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<span style="color: #333333; font-family: "arial" , sans-serif;"><span style="font-size: 18px; line-height: 22px; text-transform: uppercase;">Association Between Prescription of Major Psychotropic Medications and Violent Reoffending After Prison Release</span></span></h2>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b><br /></b></i></span></span><span style="color: #333333; font-size: 14.85px; font-style: italic; font-weight: bold; line-height: 20.79px;">JAMA Network</span><br />
<span style="color: #333333; font-size: 14.85px; font-style: italic; font-weight: bold; line-height: 20.79px;"><br /></span><span style="color: #333333; font-size: 14.85px; font-weight: bold; line-height: 20.79px;">Abstract</span></div>
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<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Importance </i> </span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Individuals released from prison have high rates of violent reoffending, and there is uncertainty about whether pharmacological treatments reduce reoffending risk.</span></span><br />
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<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i> </span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To investigate the associations between major classes of psychotropic medications and violent reoffending.</span></span><br />
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<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants </i> </span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">This cohort study included all released prisoners in Sweden from July 1, 2005, to December 31, 2010, through linkage of population-based registers. Rates of violent reoffending during medicated periods were compared with rates during nonmedicated periods using within-individual analyses. Follow-up ended December 31, 2013.</span></span><br />
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<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Exposures </i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Periods with or without dispensed prescription of psychotropic medications (antipsychotics, antidepressants, psychostimulants, drugs used in addictive disorders, and antiepileptic drugs) after prison release. Prison-based psychological treatments were investigated as a secondary exposure.</span></span><br />
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<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures </i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Violent crime after release from prison.</span></span><br />
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<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results </i> </span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The cohort included 22 275 released prisoners (mean [SD] age, 38 [13] years; 91.9% male). During follow-up (median, 4.6 years; interquartile range, 3.0-6.4 years), 4031 individuals (18.1%) had 5653 violent reoffenses. The within-individual hazard ratio (HR) associated with dispensed antipsychotics was 0.58 (95% CI, 0.39-0.88), based on 100 events in 1596 person-years during medicated periods and 1044 events in 11 026 person-years during nonmedicated periods, equating to a risk difference of 39.7 (95% CI, 11.3-57.7) fewer violent reoffenses per 1000 person-years. The within-individual HR associated with dispensed psychostimulants was 0.62 (95% CI, 0.40-0.98), based on 94 events in 1648 person-years during medicated periods and 513 events in 4553 person-years during nonmedicated periods, equating to a risk difference of 42.8 (95% CI, 2.2-67.6) fewer violent reoffenses per 1000 person-years. The within-individual HR associated with dispensed drugs for addictive disorders was 0.48 (95% CI, 0.23-0.97), based on 46 events in 1168 person-years during medicated periods and 1103 events in 15 725 person-years during nonmedicated periods, equating to a risk difference of 36.4 (95% CI, 2.1-54.0) fewer violent reoffenses per 1000 person-years. In contrast, antidepressants and antiepileptics were not significantly associated with violent reoffending rates (HR = 1.09 [95% CI, 0.83-1.43] and 1.14 [95% CI, 0.79-1.65], respectively). The most common prison-based program was psychological treatments for substance abuse, associated with an HR of 0.75 (95% CI, 0.63-0.89), which equated to a risk difference of 23.2 (95% CI, 10.3-34.1) fewer violent reoffenses per 1000 person-years.</span></span><br />
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<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance </i></span></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><span style="font-size: 14.85px;">Among released prisoners in Sweden, rates of violent reoffending were lower during periods when individiduals were dispensed antipsychotics, psychostimulants, and drugs for addictive disorders, compared with periods in which they were not dispensed these medications. Further research is needed to understand the causal nature of this association.</span></span></span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://jamanetwork.com/journals/jama/article-abstract/2576607" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration: none;" target="_blank">http://jamanetwork.com/journals/jama/</a></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px; text-transform: uppercase;">Association of Resting Heart Rate and Blood Pressure in Late Adolescence With Subsequent Mental Disorders</span></span></h2>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b>JAMA Psychiatry</b></span></i></span><br />
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Importance </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Differences in cardiovascular autonomic activity between individuals with psychiatric disorders and healthy controls have been observed, but whether cardiovascular autonomic abnormalities are associated with subsequent psychiatric disorders is unknown.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">To investigate whether differences in cardiac autonomic function as indexed by resting heart rate and blood pressure are associated with psychiatric disorders during the lifetime of men in Sweden.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">We conducted a longitudinal register-based study of Swedish men whose resting heart rate (n = 1 039 443) and blood pressure (n = 1 555 979) were measured at military conscription at a mean (SD) age of 18.3 (0.6) years during the period from 1969 to 2010, with register-based follow-up data available until the end of 2013. Analyses were performed from November 18, 2015, to June 9, 2016.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Dates of inpatient/outpatient diagnoses of anxiety disorders, obsessive-compulsive disorder, posttraumatic stress disorder, depressive disorders, bipolar disorder, schizophrenia, and substance use disorders and convictions for violent crimes, between 1973 and 2013, were obtained from nationwide registers. Adjustments were made for height, weight, body mass index, cardiorespiratory fitness, cognitive ability, and socioeconomic covariates.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Results </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">After adjustment for covariates, Cox regression models with up to 45 years of follow-up data showed that men (mean [SD] age of 18.3 [0.6] years at conscription) with resting heart rates above 82 beats per minute had a 69% (95% CI, 46%-94%) increased risk for obsessive-compulsive disorder, a 21% (95% CI, 11%-33%) increased risk for schizophrenia, and an 18% (95% CI, 13%-22%) increased risk for anxiety disorders compared with men with resting heart rates below 62 beats per minute. Similar associations were observed with systolic/diastolic blood pressure. In contrast, lower resting heart rate and lower systolic blood pressure were associated with substance use disorders and violent criminality.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">Our results suggest that for men, differences in heart rate and blood pressure in late adolescence are associated with lifetime major psychiatric disorders, with higher levels associated with obsessive-compulsive disorder, schizophrenia, and anxiety disorders and lower levels associated with substance use disorders and violent behavior. Differences in autonomic nervous system functioning may predate or represent an early marker of psychiatric disorders.</span></span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://jamanetwork.com/journals/jamapsychiatry/fullarticle/2569454" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration: none;" target="_blank">http://jamanetwork.com/journals/jamapsychiatry/</a></div>
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<b><a href="http://journals.lww.com/psychopharmacology/pages/currenttoc.aspx" style="color: #6699cc; text-decoration: none;" target="_blank">Journal of Clinical Psychopharmacology - December 2016 - Volume 36, Issue 6</a></b></div>
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<b><a href="http://www.nature.com/npp/journal/v41/n13/index.html" style="color: #6699cc; text-decoration: none;" target="_blank">Neuropsychopharmacology - Volume 41, Issue 13 (December 2016)</a></b></div>
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<b><a href="http://link.springer.com/journal/213/233/23/page/1" style="color: #6699cc; text-decoration: none;" target="_blank">Psychopharmacology - Volume 233, Issue 23, December 2016</a></b></div>
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<b><a href="http://jop.sagepub.com/content/current" style="color: #6699cc; text-decoration: none;" target="_blank">Journal of Psychopharmacology - November 2016; 30 (11)</a></b></div>
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<b><a href="http://ajp.psychiatryonline.org/toc/ajp/current" style="color: #6699cc; text-decoration: none;" target="_blank">The American Journal of Psychiatry - November 2016, Vol. 173, Issue 11</a></b></div>
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<a href="http://archpsyc.jamanetwork.com/issue.aspx" style="color: #6699cc; text-decoration: none;" target="_blank"><b>JAMA Psychiatry - November 2016, Vol. 73, No. 11</b></a></div>
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<b><a href="http://www.nature.com/neuro/journal/v19/n11/index.html" style="color: #6699cc; text-decoration: none;" target="_blank">Nature Neuroscience - November 2016, Vol 19, N° 11</a></b></div>
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<b><a href="http://www.nature.com/mp/journal/v21/n11/index.html" style="color: #6699cc; text-decoration: none;" target="_blank">Molecular Psychiatry - Volume 21, Issue 11, November 2016</a></b></div>
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<b style="background-color: white; color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"><a href="http://www.biologicalpsychiatryjournal.com/current" style="color: #6699cc; text-decoration: none;" target="_blank">Biological Psychiatry - Volume 80, Issue 12, December 2016</a></b><br />
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<b><a href="http://brain.oxfordjournals.org/content/139/11" style="color: #6699cc; text-decoration: none;" target="_blank">Brain - Volume 139, Issue 11, November 2016</a></b></div>
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<b><span style="font-size: small;">Join us on LinkedIn:</span> </b><b><a href="http://www.linkedin.com/groups/Neuropsychopharmacology-Neuroscience-5147601" style="color: #6699cc; text-decoration: none;">Neurosychopharmacology News Group</a></b></h3>
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Eutimiahttp://www.blogger.com/profile/07836706907685752267noreply@blogger.comtag:blogger.com,1999:blog-1045445187620004007.post-62201052609914127342016-10-02T18:46:00.003-04:002016-10-06T17:18:34.563-04:00October 2016<div dir="ltr" style="text-align: left;" trbidi="on">
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<i style="font-size: 14.85px; line-height: 20.79px;"><br /></i><i><b>Nature</b></i></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px; line-height: 20.79px;">Serotonin (also known as 5-hydroxytryptamine (5-HT)) is a neurotransmitter that has an essential role in the regulation of emotion. However, the precise circuits have not yet been defined through which aversive states are orchestrated by 5-HT. Here we show that 5-HT from the dorsal raphe nucleus (5-HTDRN) enhances fear and anxiety and activates a subpopulation of corticotropin-releasing factor (CRF) neurons in the bed nucleus of the stria terminalis (CRFBNST) in mice. Specifically, 5-HTDRN projections to the BNST, via actions at 5-HT2C receptors (5-HT2CRs), engage a CRFBNST inhibitory microcircuit that silences anxiolytic BNST outputs to the ventral tegmental area and lateral hypothalamus. Furthermore, we demonstrate that this CRFBNST inhibitory circuit underlies aversive behaviour following acute exposure to selective serotonin reuptake inhibitors (SSRIs). This early aversive effect is mediated via the corticotrophin-releasing factor type 1 receptor (CRF1R, also known as CRHR1), given that CRF1R antagonism is sufficient to prevent acute SSRI-induced enhancements in aversive learning. These results reveal an essential 5-HTDRN→CRFBNST circuit governing fear and anxiety, and provide a potential mechanistic explanation for the clinical observation of early adverse events to SSRI treatment in some patients with anxiety disorders.</span><br />
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<b>Source:</b> <a href="http://www.nature.com/nature/journal/v537/n7618/full/nature19318.html" style="color: #6699cc; text-decoration: none;" target="_blank">http://www.nature.com/nature/journal/</a></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b>Johnson & Johnson</b></i></span></span></div>
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">FDA action marks second Breakthrough Therapy Designation for intranasal esketamine, highlighting its potential as treatment for patients with major depressive disorder who are at imminent risk for suicide and for those with treatment-resistant depression</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px;">Janssen Research & Development, LLC, one of the Janssen Pharmaceutical Companies of Johnson & Johnson, announced that the U.S. Food and Drug Administration (FDA) has granted a Breakthrough Therapy Designation for esketamine, an investigational antidepressant medication, for the indication of major depressive disorder with imminent risk for suicide. If approved by the FDA, esketamine would be one of the first new approaches to treat major depressive disorder available to patients in the last 50 years.</span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">This also marks the second time esketamine has received a Breakthrough Therapy Designation from the U.S. regulatory authority. Esketamine was first granted this designation for treatment-resistant depression in November 2013. Breakthrough Therapy Designation is intended to expedite development and review timelines when preliminary clinical evidence indicates the drug may demonstrate substantial improvement on one or more clinically significant endpoints over available therapies for serious or life-threatening conditions.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">The esketamine Phase 2 clinical trial data presented by Janssen in May 2016 at the Society of Biological Psychiatry 71st Annual Scientific Meeting in Atlanta, Georgia, provided preliminary clinical evidence to support the Breakthrough Therapy Designation for major depressive disorder with imminent risk for suicide.</span></span><b style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"></b></div>
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<b>Read more:</b> <a href="http://www.jnj.com/news/all/Esketamine-Receives-Breakthrough-Therapy-Designation-from-US-Food-and-Drug-Administration-for-Major-Depressive-Disorder-with-Imminent-Risk-for-Suicide" style="color: #6699cc; text-decoration: none;" target="_blank">http://www.jnj.com/news/</a></div>
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<span style="font-size: 14.85px; line-height: 20.79px;"><b><br /></b></span><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Objective</i></span></span></div>
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">Insomnia is associated with increased risk for suicide. The Food and Drug Administration (FDA) has mandated that warnings regarding suicide be included in the prescribing information for hypnotic medications. The authors conducted a review of the evidence for and against the claim that hypnotics increase the risk of suicide.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Method</i></span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">This review focused on modern, FDA-approved hypnotics, beginning with the introduction of benzodiazepines, limiting its findings to adults. PubMed and Web of Science were searched, crossing the terms “suicide” and “suicidal” with each of the modern FDA-approved hypnotics. The FDA web site was searched for postmarketing safety reviews, and the FDA was contacted with requests to provide detailed case reports for hypnotic-related suicide deaths reported through its Adverse Event Reporting System.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">Epidemiological studies show that hypnotics are associated with an increased risk for suicide. However, none of these studies adequately controlled for depression or other psychiatric disorders that may be linked with insomnia. Suicide deaths have been reported from single-agent hypnotic overdoses. A separate concern is that benzodiazepine receptor agonist hypnotics can cause parasomnias, which in rare cases may lead to suicidal ideation or suicidal behavior in persons who were not known to be suicidal. On the other hand, ongoing research is testing whether treatment of insomnia may reduce suicidality in adults with depression.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px;">The review findings indicate that hypnotic medications are associated with suicidal ideation. Future studies should be designed to assess whether increases in suicidality result from CNS impairments from a given hypnotic medication or whether such medication decreases suicidality because of improvements in insomnia.</span></span></div>
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<b>Source:</b> <a href="http://ajp.psychiatryonline.org/doi/full/10.1176/appi.ajp.2016.16030336" style="color: #6699cc; text-decoration: none;" target="_blank">http://ajp.psychiatryonline.org/</a></div>
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<span style="font-size: 14.85px; line-height: 20.79px;"><b><i>JAMA Psychiatry</i></b></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Importance </i> </span></span></div>
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">Millions of women worldwide use hormonal contraception. Despite the clinical evidence of an influence of hormonal contraception on some women’s mood, associations between the use of hormonal contraception and mood disturbances remain inadequately addressed.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Objective </i><br />To investigate whether the use of hormonal contraception is positively associated with subsequent use of antidepressants and a diagnosis of depression at a psychiatric hospital.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants </i><br />This nationwide prospective cohort study combined data from the National Prescription Register and the Psychiatric Central Research Register in Denmark. All women and adolescents aged 15 to 34 years who were living in Denmark were followed up from January 1, 2000, to December 2013, if they had no prior depression diagnosis, redeemed prescription for antidepressants, other major psychiatric diagnosis, cancer, venous thrombosis, or infertility treatment. Data were collected from January 1, 1995, to December 31, 2013, and analyzed from January 1, 2015, through April 1, 2016.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Exposures </i><br />Use of different types of hormonal contraception.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Results </i><br />A total of 1 061 997 women (mean [SD] age, 24.4 [0.001] years; mean [SD] follow-up, 6.4 [0.004] years) were included in the analysis. Compared with nonusers, users of combined oral contraceptives had an RR of first use of an antidepressant of 1.23 (95% CI, 1.22-1.25). Users of progestogen-only pills had an RR for first use of an antidepressant of 1.34 (95% CI, 1.27-1.40); users of a patch (norgestrolmin), 2.0 (95% CI, 1.76-2.18); users of a vaginal ring (etonogestrel), 1.6 (95% CI, 1.55-1.69); and users of a levonorgestrel intrauterine system, 1.4 (95% CI, 1.31-1.42). For depression diagnoses, similar or slightly lower estimates were found. The relative risks generally decreased with increasing age. Adolescents (age range, 15-19 years) using combined oral contraceptives had an RR of a first use of an antidepressant of 1.8 (95% CI, 1.75-1.84) and those using progestin-only pills, 2.2 (95% CI, 1.99-2.52). Six months after starting use of hormonal contraceptives, the RR of antidepressant use peaked at 1.4 (95% CI, 1.34-1.46). When the reference group was changed to those who never used hormonal contraception, the RR estimates for users of combined oral contraceptives increased to 1.7 (95% CI, 1.66-1.71).</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance </i><br />Use of hormonal contraception, especially among adolescents, was associated with subsequent use of antidepressants and a first diagnosis of depression, suggesting depression as a potential adverse effect of hormonal contraceptive use.</span></span></div>
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<b>Source:</b> <a href="http://archpsyc.jamanetwork.com/article.aspx?articleid=2552796" style="color: #6699cc; text-decoration: none;" target="_blank">http://archpsyc.jamanetwork.com/</a></div>
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IDENTIFICATION OF 15 GENETIC LOCI ASSOCIATED WITH RISK OF MAJOR DEPRESSION IN INDIVIDUALS OF EUROPEAN DESCENT</h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Despite strong evidence supporting the heritability of major depressive disorder (MDD), previous genome-wide studies were unable to identify risk loci among individuals of European descent. We used self-report data from 75,607 individuals reporting clinical diagnosis of depression and 231,747 individuals reporting no history of depression through 23andMe and carried out meta-analysis of these results with published MDD genome-wide association study results. We identified five independent variants from four regions associated with self-report of clinical diagnosis or treatment for depression. Loci with a P value <1.0 × 10−5 in the meta-analysis were further analyzed in a replication data set (45,773 cases and 106,354 controls) from 23andMe. A total of 17 independent SNPs from 15 regions reached genome-wide significance after joint analysis over all three data sets. Some of these loci were also implicated in genome-wide association studies of related psychiatric traits. These studies provide evidence for large-scale consumer genomic data as a powerful and efficient complement to data collected from traditional means of ascertainment for neuropsychiatric disease genomics.</span></span></div>
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<b>Source:</b> <a href="http://www.nature.com/ng/journal/v48/n9/full/ng.3623.html" rel="" style="color: #6699cc; text-decoration: none;" target="_blank">http://www.nature.com/ng/journal/</a></div>
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Neurometabolic Disorders: Potentially Treatable Abnormalities in Patients With Treatment-Refractory Depression and Suicidal Behavior</h2>
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<i><b>The American Journal of Psychiatry</b></i></div>
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">Treatment-refractory depression is a devastating condition with significant morbidity, mortality, and societal cost. At least 15% of cases of major depressive disorder remain refractory to treatment. The authors previously identified a young adult with treatment-refractory depression and multiple suicide attempts with an associated severe deficiency of CSF tetrahydrobiopterin, a critical cofactor for monoamine neurotransmitter synthesis. Treatment with sapropterin, a tetrahydrobiopterin analogue, led to dramatic and long-lasting remission of depression. This sentinel case led the authors to hypothesize that the incidence of metabolic abnormalities contributing to treatment-refractory depression is underrecognized.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">The authors conducted a case-control, targeted, metabolomic evaluation of 33 adolescent and young adult patients with well-characterized histories of treatment-refractory depression (at least three maximum-dose, adequate-duration medication treatments), and 16 healthy comparison subjects. Plasma, urine, and CSF metabolic profiling were performed by coupled gas chromatography/mass spectrometry and high-performance liquid chromatography electrospray ionization tandem mass spectrometry.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">CSF metabolite abnormalities were identified in 21 of the 33 participants with treatment-refractory depression. Cerebral folate deficiency (N=12) was most common, with normal serum folate levels and low CSF 5-methyltetrahydrofolate (5-MTHF) levels. All patients with cerebral folate deficiency, including one with low CSF levels of 5-MTHF and tetrahydrobiopterin intermediates, showed improvement in depression symptom inventories after treatment with folinic acid; the patient with low tetrahydrobiopterin also received sapropterin. None of the healthy comparison subjects had a metabolite abnormality.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions</i></span></span><br />
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<b>Source:</b> <a href="http://ajp.psychiatryonline.org/doi/full/10.1176/appi.ajp.2016.15111500" style="color: #6699cc; text-decoration: none;" target="_blank">http://ajp.psychiatryonline.org/</a></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span><span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">Identification of moderators of the response to naltrexone hydrochloride treatment for alcohol dependence could improve clinical care for patients with alcohol use disorders.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Objective</i> <br />To investigate the preliminary finding that the sweet-liking (SL) phenotype interacts with a high level of craving for alcohol and is associated with an improved response to naltrexone in alcohol dependence.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants </i><br />This 12-week double-blind, randomized, placebo-controlled clinical trial was conducted from February 1, 2010, to April 30, 2012, in an academic outpatient medical center. Eighty actively drinking patients were randomized by the SL (n = 22) or the sweet-disliking (SDL) (n = 58) phenotype and by pretreatment high (n = 40) or low (n = 40) craving for alcohol, with high craving defined as greater than the median. Patients and staff were blinded to categorization. Patients were excluded for unstable medical or psychiatric illness, including dependence on drugs other than nicotine. Four patients (2 in the placebo arm and 2 in the naltrexone arm) stopped medication therapy because of adverse effects. Data were analyzed from January 15, 2013, to May 15, 2016, based on intention to treat.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Interventions </i><br />Oral naltrexone hydrochloride, 50 mg/d, or daily placebo with weekly to biweekly brief counseling.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures </i><br />The a priori hypothesis tested SL/SDL phenotype, pretreatment craving, and their interaction as moderators of frequency of abstinent and heavy drinking days during treatment, assessed with the timeline follow-back method.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Results </i><br />Eighty patients were randomized (57 men [71%]; 23 women [29%]; mean [SD] age, 47.0 [8.6] years). A nonsignificant effect of naltrexone on heavy drinking was noted (4.8 fewer heavy drinking days; Cohen d = 0.45; 95% CI, −0.01 to 0.90; F1,67 = 3.52; P = .07). The SL phenotype moderated the effect of naltrexone on heavy drinking (6.1 fewer heavy drinking days; Cohen d = 0.58; 95% CI, 0.12-1.03; F1,67 = 5.65; P = .02) and abstinence (10.0 more abstinent days; Cohen d = 0.57; 95% CI, 0.11-1.02; F1,67 = 5.36; P = .02), and high craving moderated heavy drinking (7.1 fewer heavy drinking days; Cohen d = 0.66; 95% CI, 0.20-1.11; F1,67 = 7.37; P = .008). The combination of the SL phenotype and high craving was associated with a strong response to naltrexone, with 17.1 fewer heavy drinking days (Cohen d = 1.07; 95% CI, 0.58-1.54; F1,67 = 19.33; P < .001) and 28.8 more abstinent days (Cohen d = 0.72; 95% CI, 0.25-1.17; F1,67 = 8.73; P = .004) compared with placebo.</span></span><br />
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<span style="color: #333333; line-height: 20.79px;"><span style="font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance </i><br />The SL phenotype and a high craving for alcohol independently and particularly in combination are associated with a positive response to naltrexone. The SL/SDL phenotype and a high craving for alcohol merit further investigation as factors to identify patients with alcohol dependence who are responsive to naltrexone.</span></span></span></div>
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<b>Source:</b> <a href="http://jamanetwork.com/journals/jamapsychiatry/article-abstract/2548275" style="color: #6699cc; text-decoration: none;" target="_blank">http://jamanetwork.com/journals/jamapsychiatry/</a></div>
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Meditation and vacation effects have an impact on disease-associated molecular phenotypes</h2>
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<i><b>Translational Psychiatry</b></i></div>
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<span style="color: #333333; font-size: 14.85px;">Meditation is becoming increasingly practiced, especially for stress-related medical conditions. Meditation may improve cellular health; however, studies have not separated out effects of meditation from vacation-like effects in a residential randomized controlled trial. We recruited healthy women non-meditators to live at a resort for 6 days and randomized to either meditation retreat or relaxing on-site, with both groups compared with ‘regular meditators’ already enrolled in the retreat. Blood drawn at baseline and post intervention was assessed for transcriptome-wide expression patterns and aging-related biomarkers. Highly significant gene expression changes were detected across all groups (the ‘vacation effect’) that could accurately predict (96% accuracy) between baseline and post-intervention states and were characterized by improved regulation of stress response, immune function and amyloid beta (Aβ) metabolism. Although a smaller set of genes was affected, regular meditators showed post-intervention differences in a gene network characterized by lower regulation of protein synthesis and viral genome activity. Changes in well-being were assessed post intervention relative to baseline, as well as 1 and 10 months later. All groups showed equivalently large immediate post-intervention improvements in well-being, but novice meditators showed greater maintenance of lower distress over time compared with those in the vacation arm. Regular meditators showed a trend toward increased telomerase activity compared with randomized women, who showed increased plasma Aβ42/Aβ40 ratios and tumor necrosis factor alpha (TNF-α) levels. This highly controlled residential study showed large salutary changes in gene expression networks due to the vacation effect, common to all groups. For those already trained in the practice of meditation, a retreat appears to provide additional benefits to cellular health beyond the vacation effect.</span></div>
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<b style="font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://www.nature.com/tp/journal/v6/n8/full/tp2016164a.html" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration: none;" target="_blank">http://www.nature.com/tp/</a></div>
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<span style="color: #333333; font-family: "arial" , sans-serif;"><span style="font-size: 18px; line-height: 22px; text-transform: uppercase;">Prediction of transition from ultra-high risk to first-episode psychosis using a probabilistic model combining history, clinical assessment and fatty-acid biomarkers</span></span></h2>
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<span style="color: #444444; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">Current criteria identifying patients with ultra-high risk of psychosis (UHR) have low specificity, and less than one-third of UHR cases experience transition to psychosis within 3 years of initial assessment. We explored whether a Bayesian probabilistic multimodal model, combining baseline historical and clinical risk factors with biomarkers (oxidative stress, cell membrane fatty acids, resting quantitative electroencephalography (qEEG)), could improve this specificity. We analyzed data of a UHR cohort (n=40) with a 1-year transition rate of 28%. Positive and negative likelihood ratios were calculated for predictor variables with statistically significant receiver operating characteristic curves (ROCs), which excluded oxidative stress markers and qEEG parameters as significant predictors of transition. We clustered significant variables into historical (history of drug use), clinical (Positive and Negative Symptoms Scale positive, negative and general scores and Global Assessment of Function) and biomarker (total omega-3, nervonic acid) groups, and calculated the post-test probability of transition for each group and for group combinations using the odds ratio form of Bayes’ rule. Combination of the three variable groups vastly improved the specificity of prediction (area under ROC=0.919, sensitivity=72.73%, specificity=96.43%). In this sample, our model identified over 70% of UHR patients who transitioned within 1 year, compared with 28% identified by standard UHR criteria. The model classified 77% of cases as very high or low risk (P>0.9, <0.1) based on history and clinical assessment, suggesting that a staged approach could be most efficient, reserving fatty-acid markers for 23% of cases remaining at intermediate probability following bedside interview.</span></span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://www.nature.com/tp/journal/v6/n9/full/tp2016170a.html" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration: none;" target="_blank">http://www.nature.com/tp/journal/</a></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px; text-transform: uppercase;">Incidence of Depression After Stroke, and Associated Risk Factors and Mortality Outcomes, in a Large Cohort of Danish Patients</span></span></h2>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b>JAMA Psychiatry</b></span></i></span></div>
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Importance </i> </span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">More than 30 million people live with a stroke diagnosis worldwide. Depression after stroke is frequent, and greater knowledge of associated risk factors and outcomes is needed to understand the etiology and implications of this disabling complication.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Objectives </i><br />To examine whether the incidence of and risk factors for depression differ between patients with stroke and a reference population without stroke and to assess how depression influences mortality.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Design, Setting, and Participants</i> <br />Register-based cohort study in Denmark. Participants were all individuals 15 years or older with a first-time hospitalization for stroke between January 1, 2001, and December 31, 2011 (n = 157 243), and a reference population (n = 160 236) matched on age, sex, and municipality. The data were analyzed between January and March 2016.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Main Outcomes and Measures </i><br />The incidence of depression and mortality outcomes of depression (defined by hospital discharge diagnoses or antidepressant medication use) were examined using Cox proportional hazards regression analyses.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i>Results</i> </span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;">In total, 34 346 patients (25.4%) with stroke and 11 330 (7.8%) in the reference population experienced depression within 2 years after study entry. Compared with the reference population, patients with stroke had a higher incidence of depression during the first 3 months after hospitalization (hazard ratio for stroke vs the reference population, 8.99; 95% CI, 8.61-9.39), which declined during the second year of follow-up (hazard ratio for stroke vs the reference population, 1.93; 95% CI, 1.85-2.08). Significant risk factors for depression for patients with stroke and the reference population included older age, female sex, single cohabitation status, basic educational attainment, diabetes, high level of somatic comorbidity, history of depression, and stroke severity (in patients with stroke). The associations were strongest for the reference population. In both populations, depressed individuals, especially those with new onset, had increased all-cause mortality (hazard ratio for new-onset depression, 1.89 [95% CI, 1.83-1.95] for patients with stroke and 3.75 [95% CI, 3.51-4.00] for the reference population) after adjustment for confounders. Similar patterns were found for natural and unnatural causes of death. In most models, the depression-related relative mortality was approximately twice as high in the reference population vs the stroke population.</span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px;"><i><br /></i></span></span></div>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="line-height: 20.79px;"><span style="font-size: 14.85px;"><i>Conclusions and Relevance</i> <br />Depression is common in patients with stroke during the first year after diagnosis, and those with prior depression or severe stroke are especially at risk. Because a large number of deaths can be attributable to depression after stroke, clinicians should be aware of this risk.</span></span></span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://jamanetwork.com/journals/jamapsychiatry/article-abstract/2547209" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration: none;" target="_blank">http://jamanetwork.com/journals/jamapsychiatry/</a></div>
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<b><a href="http://journals.lww.com/psychopharmacology/pages/currenttoc.aspx" style="color: #6699cc; text-decoration: none;" target="_blank">Journal of Clinical Psychopharmacology - October 2016 - Volume 36, Issue 5</a></b></div>
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<b><a href="http://www.nature.com/npp/journal/v41/n11/index.html" style="color: #6699cc; text-decoration: none;" target="_blank">Neuropsychopharmacology - Volume 41, Issue 11 (October 2016)</a></b></div>
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<b><a href="http://link.springer.com/journal/213/233/19/page/1" style="color: #6699cc; text-decoration: none;" target="_blank">Psychopharmacology - Volume 233, Issue 19, October 2016</a></b></div>
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<b><a href="http://jop.sagepub.com/content/current" style="color: #6699cc; text-decoration: none;" target="_blank">Journal of Psychopharmacology - October 2016; 30 (10)</a></b></div>
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<b><a href="http://ajp.psychiatryonline.org/toc/ajp/current" style="color: #6699cc; text-decoration: none;" target="_blank">The American Journal of Psychiatry - October 2016, Vol. 173, Issue 10</a></b></div>
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<a href="http://archpsyc.jamanetwork.com/issue.aspx" style="color: #6699cc; text-decoration: none;" target="_blank"><b>JAMA Psychiatry - October 2016, Vol. 73, No. 10</b></a></div>
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<b><a href="http://www.nature.com/neuro/journal/v19/n10/index.html" style="color: #6699cc; text-decoration: none;" target="_blank">Nature Neuroscience - October 2016, Vol 19, N° 10</a></b></div>
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<b><a href="http://www.nature.com/mp/journal/v21/n10/index.html" style="color: #6699cc; text-decoration: none;" target="_blank">Molecular Psychiatry - Volume 21, Issue 10, October 2016</a></b></div>
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<b style="background-color: white; color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"><a href="http://www.biologicalpsychiatryjournal.com/current" style="color: #6699cc; text-decoration: none;" target="_blank">Biological Psychiatry - Volume 80, Issue 7, October 2016</a></b><br />
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<b><a href="http://brain.oxfordjournals.org/content/139/10" style="color: #6699cc; text-decoration: none;" target="_blank">Brain - Volume 139, Issue 10, October 2016</a></b></div>
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<b><span style="font-size: small;">Join us on LinkedIn:</span> </b><b><a href="http://www.linkedin.com/groups/Neuropsychopharmacology-Neuroscience-5147601" style="color: #6699cc; text-decoration: none;">Neurosychopharmacology News Group</a></b></h3>
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Eutimiahttp://www.blogger.com/profile/07836706907685752267noreply@blogger.comtag:blogger.com,1999:blog-1045445187620004007.post-8959482427155294132016-09-04T18:44:00.002-04:002016-09-13T16:41:56.034-04:00September 2016<div dir="ltr" style="text-align: left;" trbidi="on">
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<i style="font-size: 14.85px; line-height: 20.79px;"><br /></i><i><b>Translational Psychiatry</b></i></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px; line-height: 20.79px;">Recent research efforts have progressively shifted towards preventative psychiatry and prognostic identification of individuals before disease onset. We describe the development of a serum biomarker test for the identification of individuals at risk of developing schizophrenia based on multiplex immunoassay profiling analysis of 957 serum samples. First, we conducted a meta-analysis of five independent cohorts of 127 first-onset drug-naive schizophrenia patients and 204 controls. Using least absolute shrinkage and selection operator regression, we identified an optimal panel of 26 biomarkers that best discriminated patients and controls. Next, we successfully validated this biomarker panel using two independent validation cohorts of 93 patients and 88 controls, which yielded an area under the curve (AUC) of 0.97 (0.95–1.00) for schizophrenia detection. Finally, we tested its predictive performance for identifying patients before onset of psychosis using two cohorts of 445 pre-onset or at-risk individuals. The predictive performance achieved by the panel was excellent for identifying USA military personnel (AUC: 0.90 (0.86–0.95)) and help-seeking prodromal individuals (AUC: 0.82 (0.71–0.93)) who developed schizophrenia up to 2 years after baseline sampling. The performance increased further using the latter cohort following the incorporation of CAARMS (Comprehensive Assessment of At-Risk Mental State) positive subscale symptom scores into the model (AUC: 0.90 (0.82–0.98)). The current findings may represent the first successful step towards a test that could address the clinical need for early intervention in psychiatry. Further developments of a combined molecular/symptom-based test will aid clinicians in the identification of vulnerable patients early in the disease process, allowing more effective therapeutic intervention before overt disease onset.</span><br />
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<b>Source:</b> <a href="http://www.nature.com/tp/journal/v5/n7/full/tp201591a.html" style="color: #6699cc; text-decoration: none;" target="_blank">http://www.nature.com/tp/journal/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">A U.S. Food and Drug Administration (FDA) review has found that the growing combined use of opioid medicines with benzodiazepines or other drugs that depress the central nervous system (CNS) has resulted in serious side effects, including slowed or difficult breathing and deaths. Opioids are used to treat pain and cough; benzodiazepines are used to treat anxiety, insomnia, and seizures. In an effort to decrease the use of opioids and benzodiazepines, or opioids and other CNS depressants, together, we are adding Boxed Warnings, our strongest warnings, to the drug labeling of prescription opioid pain and prescription opioid cough medicines, and benzodiazepines.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Health care professionals should limit prescribing opioid pain medicines with benzodiazepines or other CNS depressants only to patients for whom alternative treatment options are inadequate. If these medicines are prescribed together, limit the dosages and duration of each drug to the minimum possible while achieving the desired clinical effect. Warn patients and caregivers about the risks of slowed or difficult breathing and/or sedation, and the associated signs and symptoms. Avoid prescribing prescription opioid cough medicines for patients taking benzodiazepines or other CNS depressants, including alcohol.</span></span><b style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"></b></div>
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<b>Read more:</b> <a href="http://www.fda.gov/Drugs/DrugSafety/ucm518473.htm" style="color: #6699cc; text-decoration: none;" target="_blank">http://www.fda.gov/Drugs/DrugSafety/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px; text-transform: uppercase;">The Effect of Concomitant Treatment With SSRIs and Statins: A Population-Based Study</span></span></h2>
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<i style="font-size: 14.85px; line-height: 20.79px;"><b>The American Journal of Psychiatry</b></i><br />
<span style="font-size: 14.85px; line-height: 20.79px;"><b><br /></b></span><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Objective</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Both preclinical studies and clinical trials have indicated that the combination of a selective serotonin reuptake inhibitor (SSRI) and a statin may have superior antidepressant effects compared with SSRI treatment alone. The authors sought to assess whether this beneficial effect can be generalized to a more heterogeneous population of SSRI users.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Method</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">In a nationwide cohort study that included all incident SSRI users in Denmark between 1997 and 2012, the authors compared people who had periods of concomitant use of SSRIs and statins with people who had periods of SSRI treatment alone. Outcomes included the rates of psychiatric hospital contacts (any cause), psychiatric hospital contacts due to depression, suicidal behavior, and all-cause mortality. Using Cox regression and competing risk analysis, the authors calculated crude and adjusted hazard ratios for these outcomes.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">The authors identified 872,216 incident SSRI users, of whom 113,108 (13.0%) used a statin concomitantly. Compared with SSRI treatment alone, the combined use of an SSRI and a statin was associated with a significantly lower risk for both psychiatric hospital contacts (adjusted hazard ratio=0.75 (95% CI=0.69, 0.82) and psychiatric hospital contacts due to depression (adjusted hazard ratio=0.64, 95% CI=0.55, 0.75). Compared with SSRI treatment alone, the concomitant use of SSRIs and statins was not associated with significant increases in all-cause mortality (adjusted hazard ratio=1.04, 95% CI=0.96, 1.12) or suicidal behavior (adjusted hazard ratio=0.85, 95% CI=0.61, 1.18).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">In a large naturalistic cohort, concomitant treatment with SSRIs and statins resulted in robust advantages compared with SSRIs alone.</span></span></div>
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<b>Source:</b> <a href="http://ajp.psychiatryonline.org/doi/abs/10.1176/appi.ajp.2016.15040463" style="color: #6699cc; text-decoration: none;" target="_blank">http://ajp.psychiatryonline.org/doi/abs/10.1176/appi.ajp.2016.15040463</a></div>
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<span style="font-size: 14.85px; line-height: 20.79px;">Association of Acetaminophen Use During Pregnancy With Behavioral Problems in Childhood</span></h2>
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<span style="font-size: 14.85px; line-height: 20.79px;"><b><i>JAMA Pediatrics</i></b></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Importance </i> </span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Acetaminophen (paracetamol) is used by a large proportion of pregnant women. Research suggests that acetaminophen use in pregnancy is associated with abnormal fetal neurodevelopment. However, it is possible that this association might be confounded by unmeasured behavioral factors linked to acetaminophen use.</span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Objective </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">To examine associations between offspring behavioral problems and (1) maternal prenatal acetaminophen use, (2) maternal postnatal acetaminophen use, and (3) partner’s acetaminophen use.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Design, Setting, and Participants </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">From February 2015 to March 2016, we collected and analyzed data from the Avon Longitudinal Study of Parents and Children (ALSPAC), a prospective birth cohort. We studied 7796 mothers enrolled in ALSPAC between 1991 and 1992 along with their children and partners.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Exposures</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Acetaminophen use was assessed by questionnaire completion at 18 and 32 weeks of pregnancy and when the child was 61 months old.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Main Outcomes and Measures </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Maternal reports of behavioral problems using the Strengths and Difficulties Questionnaire (SDQ) when the children were 7 years old. We estimated risk ratios for behavioral problems in children after prenatal, postnatal, and partner’s exposure to acetaminophen and mutually adjusted each association.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Results</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Maternal prenatal acetaminophen use at 18 (n = 4415; 53%) and 32 weeks of pregnancy (n = 3381; 42%) was associated with higher odds of having conduct problems (risk ratio [RR], 1.42; 95% CI, 1.25-1.62) and hyperactivity symptoms (RR, 1.31; 95% CI, 1.16-1.49), while maternal acetaminophen use at 32 weeks was also associated with higher odds of having emotional symptoms (RR, 1.29; 95% CI, 1.09-1.53) and total difficulties (RR, 1.46; 95% CI, 1.21-1.77). This was not the case for maternal postnatal (n = 6916; 89%) or partner’s (n = 3454; 84%) acetaminophen use. We found the associations between maternal prenatal acetaminophen use and all the SDQ domains unchanged even after adjusting for maternal postnatal or partner’s acetaminophen use.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Conclusions and Relevance</i> </span></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;">Children exposed to acetaminophen prenatally are at increased risk of multiple behavioral difficulties, and the associations do not appear to be explained by unmeasured behavioral or social factors linked to acetaminophen use insofar as they are not observed for postnatal or partner’s acetaminophen use. Although these results could have implications for public health advice, further studies are required to replicate the findings and to understand mechanisms.</span></span></span></div>
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<b>Source:</b> <a href="http://archpedi.jamanetwork.com/article.aspx?articleid=2543281" style="color: #6699cc; text-decoration: none;" target="_blank">http://archpedi.jamanetwork.com/</a></div>
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Identification of 15 genetic loci associated with risk of major depression in individuals of European descent</h2>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b>Nature Genetics</b></span></i></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Despite strong evidence supporting the heritability of major depressive disorder (MDD), previous genome-wide studies were unable to identify risk loci among individuals of European descent. We used self-report data from 75,607 individuals reporting clinical diagnosis of depression and 231,747 individuals reporting no history of depression through 23andMe and carried out meta-analysis of these results with published MDD genome-wide association study results. We identified five independent variants from four regions associated with self-report of clinical diagnosis or treatment for depression. Loci with a P value <1.0 × 10−5 in the meta-analysis were further analyzed in a replication data set (45,773 cases and 106,354 controls) from 23andMe. A total of 17 independent SNPs from 15 regions reached genome-wide significance after joint analysis over all three data sets. Some of these loci were also implicated in genome-wide association studies of related psychiatric traits. These studies provide evidence for large-scale consumer genomic data as a powerful and efficient complement to data collected from traditional means of ascertainment for neuropsychiatric disease genomics.</span></span></div>
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<b>Source:</b> <a href="http://www.nature.com/ng/journal/v48/n9/full/ng.3623.html" rel="" style="color: #6699cc; text-decoration: none;" target="_blank">http://www.nature.com/ng/journal/</a></div>
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Suicide Attempt as a Risk Factor for Completed Suicide: Even More Lethal Than We Knew</h2>
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<i><b>The American Journal of Psychiatry</b></i></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Objective</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">While suicide attempt history is considered to robustly predict completed suicide, previous studies have limited generalizability because of using convenience samples of specific methods/treatment settings, disregarding previous attempts, or overlooking first-attempt deaths. Eliminating these biases should more accurately estimate suicide prevalence in attempters.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Method</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">This observational retrospective-prospective cohort study using the Rochester Epidemiology Project identified 1,490 (males, N=555; females, N=935) Olmsted County residents making index suicide attempts (first lifetime attempts reaching medical attention) between January 1, 1986, and December 31, 2007. The National Death Index identified suicides between enrollment and December 31, 2010 (follow-up 3–25 years). Medical records were queried for sex, age, method, and follow-up care for index attempt survivors. Coroner records yielded data on index attempt deaths.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">During the study period, 81/1,490 enrollees (5.4%) died by suicide. Of the 81, 48 (59.3%) perished on index attempt; 27 of the surviving 33 index attempt survivors (81.8%) killed themselves within a year. Males were disproportionately represented: 62/81 (11.2% of men, 76.5% of suicides) compared with 19/81 (2.0% of women, 23.5% of suicides). Of dead index attempters, 72.9% used guns, yielding an odds ratio for gunshot death, compared with all other methods, of 140 (95% CI=60–325). When adjusted for covariates, survivors given follow-up psychiatric appointments had significantly lower likelihood of subsequent suicide (odds ratio=0.212, 95% CI=0.089–0.507).</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;">At 5.4%, completed suicide prevalence in this community cohort of suicide attempters was almost 59% higher than previously reported. An innovative aspect of this study explains the discrepancy: by including index attempt deaths—approximately 60% of total suicides—suicide prevalence more than doubled. We contend that counting both index and subsequent attempt deaths more accurately reflects prevalence. Our findings support suicide attempt as an even more lethal risk factor for completed suicide than previously thought. Research should focus on identifying risk factors for populations vulnerable to making first attempts and target risk reduction in those groups.</span></span></span><br />
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<b>Source:</b> <a href="http://ajp.psychiatryonline.org/doi/10.1176/appi.ajp.2016.15070854" style="color: #6699cc; text-decoration: none;" target="_blank">http://ajp.psychiatryonline.org/</a></div>
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<i style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>The Journal of Clinical Psychiatry</b></span></i></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span><span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 13px; line-height: 18.2px;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Objective</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Studies of aging usually focus on trajectories of physical and cognitive function, with far less emphasis on overall mental health, despite its impact on general health and mortality. This study examined linear and nonlinear trends of physical, cognitive, and mental health over the entire adult lifespan.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Methods</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Cross-sectional data were obtained from 1,546 individuals aged 21–100 years, selected using random digit dialing for the Successful AGing Evaluation (SAGE) study, a structured multicohort investigation that included telephone interviews and in-home surveys of community-based adults without dementia. Data were collected from 1/26/2010 to 10/07/2011 targeting participants aged 50–100 years and from 6/25/2012 to 7/15/2013 targeting participants aged 21–100 years with an emphasis on adding younger individuals. Data included self-report measures of physical health, measures of both positive and negative attributes of mental health, and a phone interview–based measure of cognition.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Results</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Comparison of age cohorts using polynomial regression suggested a possible accelerated deterioration in physical and cognitive functioning, averaging 1.5 to 2 standard deviations over the adult lifespan. In contrast, there appeared to be a linear improvement of about 1 standard deviation in various attributes of mental health over the same life period.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Conclusions </i></span></span></span><br />
<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">These cross-sectional findings suggest the possibility of a linear improvement in mental health beginning in young adulthood rather than a U-shaped curve reported in some prior studies. Lifespan research combining psychosocial and biological markers may improve our understanding of resilience to mental disability in older age and lead to broad-based interventions promoting mental health in all age groups.</span></span></span></div>
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<b>Source:</b> <a href="http://www.psychiatrist.com/JCP/article/Pages/2016/v77n08/v77n0813.aspx" style="color: #6699cc; text-decoration: none;" target="_blank">http://www.psychiatrist.com/JCP/</a></div>
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Early Improvement in Work Productivity Predicts Future Clinical Course in Depressed Outpatients</h2>
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<i><b>The American Journal of Psychiatry</b></i></div>
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<b><br /></b><b>Abstract</b></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Objective</i></span></span></div>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Depression symptom severity, the most commonly studied outcome in antidepressant treatment trials, accounts for only a small portion of burden related to major depression. While lost work productivity is the biggest contributor to depression’s economic burden, few studies have systematically evaluated the independent effect of treatment on work productivity and the relationship between changes in work productivity and longer-term clinical course.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Method</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Work productivity was measured repeatedly by the Work Productivity and Activity Impairment self-report questionnaire in 331 employed participants with major depression enrolled in the Combining Medications to Enhance Depression Outcomes trial. Trajectories of change in work productivity during the first 6 weeks of treatment were identified and used to predict remission at 3 and 7 months.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Participants reported reduced absence from work and increased work productivity with antidepressant treatment even after controlling for changes in depression severity. Three distinct trajectories of changes in work productivity were identified: 1) robust early improvement (24%), 2) minimal change (49%), and 3) high-impairment slight reduction (27%). Compared with other participants, those with robust improvement had 3–5 times higher remission rates at 3 months and 2–5 times higher remission rates at 7 months, even after controlling for select baseline variables and remission status at week 6.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">In this secondary analysis, self-reported work productivity improved in depressed patients with antidepressant treatment even after accounting for depressive symptom reduction. Early improvement in work productivity is associated with much higher remission rates after 3 and 7 months of treatment.</span></span></div>
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<b style="font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://ajp.psychiatryonline.org/doi/abs/10.1176/appi.ajp.2016.16020176" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration: none;" target="_blank">http://ajp.psychiatryonline.org/</a></div>
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<span style="color: #333333; font-family: "arial" , sans-serif;"><span style="font-size: 18px; line-height: 22px; text-transform: uppercase;">Antipsychotic Use in Pregnancy and the Risk for Congenital Malformations</span></span></h2>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b><br /></b></i></span></span><span style="color: #333333; font-size: 14.85px; font-style: italic; font-weight: bold; line-height: 20.79px;">JAMA Psychiatry</span><br />
<span style="color: #333333; font-size: 14.85px; font-style: italic; font-weight: bold; line-height: 20.79px;"><br /></span><span style="color: #333333; font-size: 14.85px; font-weight: bold; line-height: 20.79px;">Abstract</span></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span></div>
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<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Importance </i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">The frequency of antipsychotic (AP) use during pregnancy has approximately doubled during the last decade. However, little is known about their safety for the developing fetus, and concerns have been raised about a potential association with congenital malformations.</span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Objective</i> </span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">To examine the risk for congenital malformations overall and cardiac malformations associated with first-trimester exposure to APs.</span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Design, Setting, and Participants </i> </span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">This nationwide sample of 1 360 101 pregnant women enrolled in Medicaid with a live-born infant constituted the pregnancy cohort nested in the Medicaid Analytic Extract database, which included data from January 1, 2000, to December 31, 2010. Participants were enrolled in Medicaid from 3 months before their last menstrual period through at least 1 month after delivery. Relative risks (RRs) were estimated using generalized linear models with fine stratification on the propensity score to control for the underlying psychiatric disorders and other potential confounders. Data were analyzed during 2015.</span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Exposures</i> </span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Use of APs during the first trimester, the etiologically relevant period for organogenesis.</span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Main Outcomes and Measures </i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Major congenital malformations overall and cardiac malformations identified during the first 90 days after delivery.</span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Results </i> </span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Of the 1 341 715 pregnancies that met inclusion criteria (mean [SD] age of women, 24.02 [5.77] years), 9258 (0.69%) filled at least 1 prescription for an atypical AP and 733 (0.05%) filled at least 1 prescription for a typical AP during the first trimester. Overall, 32.7 (95% CI, 32.4-33.0) per 1000 births not exposed to APs were diagnosed with congenital malformations compared with 44.5 (95% CI, 40.5-48.9) per 1000 births exposed to atypical and 38.2 (95% CI, 26.6-54.7) per 1000 births exposed to typical APs. Unadjusted analyses suggested an increased risk for malformations overall for atypical APs (RR, 1.36; 95% CI, 1.24-1.50) but not for typical APs (RR, 1.17; 95% CI, 0.81-1.68). After confounding adjustment, the RR was reduced to 1.05 (95% CI, 0.96-1.16) for atypical APs and 0.90 (95% CI, 0.62-1.31) for typical APs. The findings for cardiac malformations were similar. For the individual agents examined, a small increased risk in overall malformations (RR, 1.26; 95% CI, 1.02-1.56) and cardiac malformations (RR, 1.26; 95% CI, 0.88-1.81) was found for risperidone that was independent of measured confounders.</span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Conclusions and Relevance</i> </span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Evidence from this large study suggests that use of APs early in pregnancy generally does not meaningfully increase the risk for congenital malformations overall or cardiac malformations in particular. The small increase in the risk for malformations observed with risperidone requires additional study.</span></span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://archpsyc.jamanetwork.com/article.aspx?articleid=2545072" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration: none;" target="_blank">http://archpsyc.jamanetwork.com/</a></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px; text-transform: uppercase;">FDA allows marketing of first-of-kind computerized cognitive tests to help assess cognitive skills after a head injury</span></span></h2>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b>US FDA</b></span></i></span></div>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;">The U.S. Food and Drug Administration today permitted marketing of two new devices to assess a patient’s cognitive function immediately after a suspected brain injury or concussion. The Immediate Post-Concussion Assessment and Cognitive Testing (ImPACT) and ImPACT Pediatric are the first medical devices permitted for marketing that are intended to assess cognitive function following a possible concussion. They are intended as part of the medical evaluation that doctors perform to assess signs and symptoms of a head injury.</span></div>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">ImPACT and ImPACT Pediatric are not intended to diagnose concussions or determine appropriate treatments. Instead the devices are meant to test cognitive skills such as word memory, reaction time and word recognition, all of which could be affected by a head injury. The results are compared to an age-matched control database or to a patient’s pre-injury baseline scores, if available.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">“These devices provide a useful new tool to aid in the evaluation of patients experiencing possible signs of a concussion, but clinicians should not rely on these tests alone to rule out a concussion or determine whether an injured player should return to a game,” said Carlos Peña, Ph.D., M.S., director of the division of neurological and physical medicine devices at the FDA’s Center for Devices and Radiological Health.</span></span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Read more:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm517526.htm" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration: none;" target="_blank">http://www.fda.gov/NewsEvents/</a></div>
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<b style="color: blue; font-size: x-large;"><br /></b><b style="color: blue; font-size: x-large;">Online Journals:</b></div>
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<b><a href="http://journals.lww.com/psychopharmacology/pages/currenttoc.aspx" style="color: #6699cc; text-decoration: none;" target="_blank">Journal of Clinical Psychopharmacology - October 2016 - Volume 36, Issue 5</a></b></div>
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<b><a href="http://www.nature.com/npp/journal/v41/n11/index.html" style="color: #6699cc; text-decoration: none;" target="_blank">Neuropsychopharmacology - Volume 41, Issue 11 (October 2016)</a></b></div>
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<b><a href="http://link.springer.com/journal/213/233/19/page/1" style="color: #6699cc; text-decoration: none;" target="_blank">Psychopharmacology - Volume 233, Issue 19, October 2016</a></b></div>
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<b><a href="http://jop.sagepub.com/content/current" style="color: #6699cc; text-decoration: none;" target="_blank">Journal of Psychopharmacology - September 2016; 30 (9)</a></b></div>
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<b><a href="http://ajp.psychiatryonline.org/toc/ajp/current" style="color: #6699cc; text-decoration: none;" target="_blank">The American Journal of Psychiatry - September 2016, Vol. 173, Issue 9</a></b></div>
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<a href="http://archpsyc.jamanetwork.com/issue.aspx" style="color: #6699cc; text-decoration: none;" target="_blank"><b>JAMA Psychiatry - September 2016, Vol. 73, No. 9</b></a></div>
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<b><a href="http://www.nature.com/neuro/journal/v19/n8/index.html" style="color: #6699cc; text-decoration: none;" target="_blank">Nature Neuroscience - September 2016, Vol 19, N° 9</a></b></div>
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<b><a href="http://www.nature.com/mp/journal/v21/n9/index.html" style="color: #6699cc; text-decoration: none;" target="_blank">Molecular Psychiatry - Volume 21, Issue 9, September 2016</a></b></div>
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<b style="background-color: white; color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"><a href="http://www.biologicalpsychiatryjournal.com/current" style="color: #6699cc; text-decoration: none;" target="_blank">Biological Psychiatry - Volume 80, Issue 7, October 2016</a></b><br />
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<b><a href="http://brain.oxfordjournals.org/content/139/9" style="color: #6699cc; text-decoration: none;" target="_blank">Brain - Volume 139, Issue 9, September 2016</a></b></div>
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<b><span style="font-size: small;">Join us on LinkedIn:</span> </b><b><a href="http://www.linkedin.com/groups/Neuropsychopharmacology-Neuroscience-5147601" style="color: #6699cc; text-decoration: none;">Neurosychopharmacology News Group</a></b></h3>
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Eutimiahttp://www.blogger.com/profile/07836706907685752267noreply@blogger.comtag:blogger.com,1999:blog-1045445187620004007.post-45327958749889424752016-08-06T16:05:00.002-04:002016-08-13T16:57:52.552-04:00August 2016<div dir="ltr" style="text-align: left;" trbidi="on">
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<i style="font-size: 14.85px; line-height: 20.79px;"><br /></i><i><b>Bipolar Disorders</b></i></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Objectives</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px; line-height: 20.79px;">We have preciously documented that many individuals with acute mania have immune activation. However, the sources of immune activation have not been identified. We investigated whether individuals hospitalized with acute mania have evidence of bacterial infections as determined by the prescription of systemic antimicrobial agents.</span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px; line-height: 20.79px;">We assessed the recent prescription of systemic antimicrobial medications and the site of presumed bacterial infection in 234 individuals hospitalized for acute mania in either an inpatient unit or a day hospital. We also assessed individuals hospitalized for other psychiatric disorders (n=368) and controls (n=555). We employed logistic regression models to compare the rates of antibiotic prescription in individuals with the different diagnoses, employing demographic variables as covariates.</span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px; line-height: 20.79px;">We found that individuals hospitalized with acute mania had a substantially increased rate of recent antimicrobial prescription, defined as exposure within three days of ascertainment (adjusted odds ratio=5.5, 95% confidence interval: 2.2–14.1, P<.0002). Overall, a total of 18 of the 234 (7.7%) individuals hospitalized for acute mania were prescribed antibiotics as opposed to seven of 555 (1.3%) controls. The prescription of antibiotics was associated with being on an inpatient unit as opposed to being in the day hospital, and having increased mania symptom severity but not with other clinical ratings, demographic variables, or psychiatric medications. Hospitalization for other psychiatric disorders was not associated with the recent prescription of antimicrobial medications. The urinary tract was the most common site of infection in women, while the respiratory tract and mucosal surfaces were the most common sites in men.</span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px; line-height: 20.79px;">Individuals hospitalized with acute mania have a markedly increased rate of bacterial infections, as evidenced by the recent prescription of antimicrobial agents. The prevention and effective treatment of bacterial infections may be important interventions for the management of individuals with mania.</span><br />
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<b>Source:</b> <a href="http://onlinelibrary.wiley.com/doi/10.1111/bdi.12416/abstract" style="color: #6699cc; text-decoration: none;" target="_blank">http://onlinelibrary.wiley.com/</a></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b>Psychiatry Research</b></i></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">This study sought to explore the impact of smoking reduction on suicidality (suicide ideation and behaviour) among people with a psychotic disorder (n=235) who participated in a randomized trial of a healthy lifestyle intervention trial. Suicidality, measured by item −4 of the Brief Psychiatric Rating Scale (BPRS) was the main variable of interest. Measures were collected by research assistants blind to treatment allocation at baseline, at 15 weeks (mid-intervention) and 12 months after baseline. Mediation analysis, adjusted for confounders, was used to determine the relationship between smoking reduction and suicidality and to explore whether this was mediated through depression. At 12 months, smoking reduction was found to be significantly associated with suicidality change; an association was also seen between smoking reduction and depression and depression and suicidality. After adjusting for depression, the association between smoking reduction and suicidality was attenuated but remained statistically significant; the proportion of the total effect that was mediated through depression was 30%. There was no significant association between suicidality and treatment group (vs. controls) over time. Our study suggests that smoking interventions may have benefits over and above those for improved physical health, by reducing suicidal ideation in people with psychosis.</span></span><b style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"></b></div>
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<b>Source:</b> <a href="http://www.psy-journal.com/article/S0165-1781(15)30893-3/abstract" style="color: #6699cc; text-decoration: none;" target="_blank">http://www.psy-journal.com/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px; text-transform: uppercase;">White Matter Integrity Reductions in Intermittent Explosive Disorder</span></span></h2>
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<i style="font-size: 14.85px; line-height: 20.79px;"><b>Neuropsychopharmacology</b></i><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Intermittent explosive disorder (IED), as described in DSM-5, is the categorical expression of pathological impulsive aggression. Previous work has identified neurobiological correlates of the disorder in patterns of frontal-limbic brain activity and dysregulation of serotonergic neurotransmission. Given the importance of short- and-long range white matter connections of the brain in social and emotional behavior, studies of white matter connectivity in impulsive aggression are warranted. Diffusion tensor imaging (DTI) studies in the related conditions of antisocial and borderline personality disorder have produced preliminary evidence of disturbed white matter connectivity in these disorders, but to date there have been no DTI studies in IED. A total of 132 male and female adults between the ages of 18 and 55 years underwent Turboprop-DTI on a 3-Tesla MRI scanner. Of these, 42 subjects had IED, 40 were normal controls, and 50 were clinical psychiatric controls with psychiatric disorders without IED. All subjects were free of alcohol, psychotropic medications, or drugs of abuse. The diffusion tensor was calculated in each voxel and maps of fractional anisotropy (FA) were generated. Tract-based spatial statistics (TBSS) were used to compare FA along the white matter skeleton among the three subject groups. IED was associated with lower FA in two clusters located in the superior longitudinal fasciculus (SLF) when compared with the psychiatric and healthy controls. Impulsive aggression and borderline personality disorder, but not psychopathy or antisocial personality disorder, was associated with lower FA in the two clusters within the SLF. In conclusion, IED was associated with lower white matter integrity in long-range connections between the frontal and temporoparietal regions.</span></span></div>
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<b>Source:</b> <a href="http://www.nature.com/npp/journal/vaop/ncurrent/abs/npp201674a.html" style="color: #6699cc; text-decoration: none;" target="_blank">http://www.nature.com/npp/journal/</a></div>
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<span style="font-size: 14.85px; line-height: 20.79px;">An Individualized Risk Calculator for Research in Prodromal Psychosis</span></h2>
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<span style="font-size: 14.85px; line-height: 20.79px;"><b><i>The American Journal of Psychiatry</i></b></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Objective</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Approximately 20%–35% of individuals 12–35 years old who meet criteria for a prodromal risk syndrome convert to psychosis within 2 years. However, this estimate ignores the fact that clinical high-risk cases vary considerably in risk. The authors sought to create a risk calculator, based on profiles of risk indicators, that can ascertain the probability of conversion to psychosis in individual patients.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Method</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">The study subjects were 596 clinical high-risk participants from the second phase of the North American Prodrome Longitudinal Study who were followed up to the time of conversion to psychosis or last contact (up to 2 years). The predictors examined were limited to those that are supported by previous studies and are readily obtainable in general clinical settings. Time-to-event regression was used to build a multivariate model predicting conversion, with internal validation using 1,000 bootstrap resamples.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">The 2-year probability of conversion to psychosis was 16%. Higher levels of unusual thought content and suspiciousness, greater decline in social functioning, lower verbal learning and memory performance, slower speed of processing, and younger age at baseline each contributed to individual risk for psychosis. Stressful life events, trauma, and family history of schizophrenia were not significant predictors. The multivariate model achieved a concordance index of 0.71 and, as reported in an article by Carrión et al., published concurrently with this one, was validated in an independent external data set. The results are instantiated in a web-based risk prediction tool envisioned to be most useful in research protocols involving the psychosis prodrome.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;">A risk calculator comparable in accuracy to those for cardiovascular disease and cancer is available to predict individualized conversion risks in newly ascertained clinical high-risk cases. Given that the risk calculator can be validly applied only for patients who screen positive on the Structured Clinical Interview for Psychosis Risk Syndromes, which requires training to administer, its most immediate uses will be in research on psychosis risk factors and in research-driven clinical (prevention) trials.</span></span></span></div>
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<b>Source:</b> <a href="http://ajp.psychiatryonline.org/doi/abs/10.1176/appi.ajp.2016.15070890" style="color: #6699cc; text-decoration: none;" target="_blank">http://ajp.psychiatryonline.org/</a></div>
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A multi-modal parcellation of human cerebral cortex</h2>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b>Nature</b></span></i></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Understanding the amazingly complex human cerebral cortex requires a map (or parcellation) of its major subdivisions, known as cortical areas. Making an accurate areal map has been a century-old objective in neuroscience. Using multi-modal magnetic resonance images from the Human Connectome Project (HCP) and an objective semi-automated neuroanatomical approach, we delineated 180 areas per hemisphere bounded by sharp changes in cortical architecture, function, connectivity, and/or topography in a precisely aligned group average of 210 healthy young adults. We characterized 97 new areas and 83 areas previously reported using post-mortem microscopy or other specialized study-specific approaches. To enable automated delineation and identification of these areas in new HCP subjects and in future studies, we trained a machine-learning classifier to recognize the multi-modal ‘fingerprint’ of each cortical area. This classifier detected the presence of 96.6% of the cortical areas in new subjects, replicated the group parcellation, and could correctly locate areas in individuals with atypical parcellations. The freely available parcellation and classifier will enable substantially improved neuroanatomical precision for studies of the structural and functional organization of human cerebral cortex and its variation across individuals and in development, aging, and disease.</span></span></div>
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<b>Source:</b> <a href="http://www.nature.com/nature/journal/v536/n7615/full/nature18933.html" rel="" style="color: #6699cc; text-decoration: none;" target="_blank">http://www.nature.com/nature/</a></div>
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Amyloid proteotoxicity initiates an inflammatory response blocked by cannabinoids</h2>
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<i><b>Aging</b></i></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">The beta amyloid (Aβ) and other aggregating proteins in the brain increase with age and are frequently found within neurons. The mechanistic relationship between intracellular amyloid, aging and neurodegeneration is not, however, well understood. We use a proteotoxicity model based upon the inducible expression of Aβ in a human central nervous system nerve cell line to characterize a distinct form of nerve cell death caused by intracellular Aβ. It is shown that intracellular Aβ initiates a toxic inflammatory response leading to the cell's demise. Aβ induces the expression of multiple proinflammatory genes and an increase in both arachidonic acid and eicosanoids, including prostaglandins that are neuroprotective and leukotrienes that potentiate death. Cannabinoids such as tetrahydrocannabinol stimulate the removal of intraneuronal Aβ, block the inflammatory response, and are protective. Altogether these data show that there is a complex and likely autocatalytic inflammatory response within nerve cells caused by the accumulation of intracellular Aβ, and that this early form of proteotoxicity can be blocked by the activation of cannabinoid receptors.</span></span><br />
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<b>Source:</b> <a href="http://www.nature.com/articles/npjamd201612" style="color: #6699cc; text-decoration: none;" target="_blank">http://www.nature.com/</a></div>
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<i style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Psychiatric Service</b></span></i></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span><span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 13px; line-height: 18.2px;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Objective:</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">This study analyzed hospital readmission rates of patients with schizophrenia who were treated with long-acting injectable antipsychotics (LAIs) or with oral antipsychotics after being discharged from a hospitalization.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Medical claims of patients with schizophrenia who were ages 18–64 and had a first hospitalization for a serious mental illness (index hospitalization, October 2007 through September 2012) and at least one prescription for a first- or second-generation antipsychotic were analyzed from the Truven Health MarketScan Multi-State Medicaid Database. Analyses were conducted for patients with a sole diagnosis of schizophrenia (N=1,450) and for all patients with schizophrenia (N=15,556), which added patients with a codiagnosis of bipolar disorder or major depressive disorder. Probability of rehospitalization for any cause at 30 and 60 days after the initial hospitalization was assessed with multivariate logistic regression and propensity score matching (PSM) methods. The PSM model matched age, preindex use of LAIs or short-acting injectables, and select comorbidities between the LAI and the oral antipsychotics groups.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">LAIs were associated with significantly lower probability of rehospitalization compared with oral antipsychotics at 60 days for schizophrenia-only patients (adjusted odds ratio [AOR]=.60, 95% confidence interval [CI]=.41–.90) and for all patients (AOR=.70, CI=.52–.95). The absolute difference in probability of rehospitalization for all patients was significantly lower by 5.0% at 60 days in the LAI group compared with the oral antipsychotics group.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Compared with use of oral antipsychotics, use of LAIs was associated with fewer readmissions of Medicaid patients with schizophrenia within 60 days after an index hospitalization.</span></span></span></span></div>
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<b>Source:</b> <a href="http://ps.psychiatryonline.org/doi/abs/10.1176/appi.ps.201500455" style="color: #6699cc; text-decoration: none;" target="_blank">http://ps.psychiatryonline.org/</a></div>
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Gray matter maturation and cognition in children with different APOE ε genotypes</h2>
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<i><b>Neurology</b></i></div>
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<b><br /></b><b>Abstract</b></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Objective</i></span></span></div>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">The aims of the current study were to determine whether children with the 6 different APOE ε genotypes show differences in gray matter maturation, particularly for those with ε4 and ε2 alleles, which are associated with poorer outcomes in many neurologic disorders.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">A total of 1,187 healthy children (aged 3–20 years, 52.1% boys, 47.9% girls) with acceptable data from the cross-sectional Pediatric Imaging Neurocognition and Genetics Study were evaluated for the effects of 6 APOE ε genotypes on macroscopic and microscopic cortical and subcortical gray matter structures (measured with 3-tesla MRI and FreeSurfer for automated morphometry) and on cognition (NIH Toolbox).</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Among APOE ε4 carriers, age-related changes in brain structures and cognition varied depending on genotype, with the smallest hippocampi in ε2ε4 children, the lowest hippocampal fractional anisotropy in younger ε4ε4 children, the largest medial orbitofrontal cortical areas in ε3ε4 children, and age-dependent thinning of the entorhinal cortex in ε4ε4 children. Younger ε4ε4 children had the lowest scores on executive function and working memory, while younger ε2ε4 children performed worse on attention tasks. Larger parietal gyri in the younger ε2ε4 children, and thinner temporal and cingulate isthmus cortices or smaller hippocampi in the younger ε4ε4 children, predicted poorer performance on attention or working memory.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Conclusions</i></span></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;">Our findings validated and extended prior smaller studies that showed altered brain development in APOE ε4–carrier children. The ε4ε4 and ε2ε4 genotypes may negatively influence brain development and brain aging at the extremes of age. Studying APOE ε polymorphisms in young children may provide the earliest indicators for individuals who might benefit from early interventions or preventive measures for future brain injuries and dementia.</span></span></span></div>
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<b style="font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://www.neurology.org/content/early/2016/07/13/WNL.0000000000002939" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration: none;" target="_blank">http://www.neurology.org/</a></div>
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<span style="color: #333333; font-family: "arial" , sans-serif;"><span style="font-size: 18px; line-height: 22px; text-transform: uppercase;">Relative hypocortisolism is associated with obesity and the metabolic syndrome in recurrent affective disorders</span></span></h2>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b><br /></b></i></span></span><span style="color: #333333; font-size: 14.85px; font-style: italic; font-weight: bold; line-height: 20.79px;">Journal of Affective Disorders</span><br />
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<span style="color: #333333; font-size: 14.85px; font-weight: bold; line-height: 20.79px;">Abstract</span></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span></div>
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<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Background</i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Cardiovascular disease (CVD) is one of the main causes of excess deaths in affective disorders. Affective disorders are associated with increased frequencies of CVD risk-factors such as obesity, dyslipidemia, and metabolic syndrome. Stress-induced chronic cortisol excess has been suggested to promote obesity and metabolic syndrome. Chronic stress with frequent or persisting hypothalamic-pituitary-adrenal-axis (HPA-axis) hyperactivity may, over time, lead to a state of low HPA-axis activity, also denoted hypocortisolism. A low-dose weight-adjusted dexamethasone-suppression-test (DST) is considered to be a sensitive measure of hypocortisolism.</span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Methods</i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">245 patients with recurrent depression or bipolar disorder and 258 controls participated in a low-dose DST and were also examined with regard to metabolic status.</span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Results</i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Patients with hypocortisolism (low post-DST cortisol) compared with patients without hypocortisolism (normal or high post-DST cortisol) exhibited increased odds ratios (OR) for obesity (OR=4.0), overweight (OR=4.0), large waist (OR=2.7), high LDL (OR=4.2), low HDL (OR=2.4), high LDL/HDL ratio (OR=3.3), high TC/HDL ratio (OR=3.4) and metabolic syndrome (OR=2.0). A similar pattern but less pronounced was also found in the control sample.</span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Limitations</i></span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">The cross sectional study design and absence of analyses addressing lifestyle factors.</span></span><br />
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span>
<span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Conclusions</i></span></span><br />
<span style="font-size: 14.85px; line-height: 20.79px;"><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Our findings suggest that a substantial portion of the metabolic disorders and cardiovascular risk factors seen in recurrent affective disorders are found among individuals exhibiting hypocortisolism. This might indicate that long-term stress is a central contributor to metabolic abnormalities and CVD mortality in recurrent affective disorders.</span></span></span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://www.jad-journal.com/article/S0165-0327(16)30648-6/abstract" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration: none;" target="_blank">http://www.jad-journal.com/</a></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px; text-transform: uppercase;">Association Between Diabetes-Related Eye Complications and Symptoms of Anxiety and Depression</span></span></h2>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b>JAMA Ophthalmology</b></span></i></span></div>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b><br /></b></span></i></span><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span><br />
<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b><br /></b></span></i></span></div>
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Importance </i> </span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">This study is needed to clarify inconsistent findings regarding the association between diabetes-related eye complications and psychological well-being.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Objective </i></span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">To examine the association between severity of diabetic retinopathy (DR) and diabetic macular edema (DME) with symptoms of depression and anxiety in adults with diabetes.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Design, Setting, and Participants</i> </span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">A cross-sectional study was conducted in a tertiary eye hospital in Melbourne, Australia. The study comprised 519 participants with diabetes. The median duration of diabetes was 13.0 (interquartile range, 14.0) years. The study was conducted from March 1, 2009, to December 24, 2010.</span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Exposures </i> </span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Patients underwent a comprehensive eye examination in which dilated fundus photographs (disc and macula centered) were obtained and graded for the presence and severity of DR and DME. Presenting distance uniocular and binocular visual acuity were assessed using a 3-m logMAR chart.</span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span>
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Main Outcomes and Measures </i> </span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Symptoms of depression and anxiety were measured using the Hospital Anxiety and Depression Scale (HADS), which comprises 7 questions specific to anxiety and 7 specific to depression with scores ranging from 0 to 21; scores higher than 8 signify possible anxiety or depression. The ordinal raw scores of the HADS questionnaire were transformed to estimates of interval measure using Rasch analysis and evaluated as continuous variables. Participants also completed standardized interview-administered questionnaires. Blood samples were assessed for hemoglobin A1c, fasting blood glucose, and serum lipids. Multiple linear regression models were used to determine the associations between the severity of DR and DME with symptoms of anxiety and depression and commonality analysis was used to quantify the unique variance explained.</span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span>
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Results </i> </span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Of the 519 participants in the study, 170 individuals (32.8%) were female; mean (SD) age was 64.9 (11.6) years. Raw scores indicated that 80 individuals (15.4%) screened positive for depressive symptoms and 118 persons (22.7%) screened positive for symptoms of anxiety. In multivariate analysis using Rasch scores, severe nonproliferative DR (NPDR)/PDR was independently associated with greater depressive symptoms (regression coefficient [β] = 0.69; 95% CI, 0.03-1.34) after controlling for sociodemographic factors and clinical characteristics, including visual acuity. A history of depression or anxiety accounted for 60.6% (95% CI, 23.9%-83.2%) of the unique variance in depressive symptoms, and severe NPDR or PDR contributed to 19.1% (95% CI, 1.7%-44.4%) of the total explained variance of depressive symptoms. Diabetic macular edema was not associated with depressive symptoms. No association between DR and symptoms of anxiety was identified.</span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Conclusions and Relevance </i> </span></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;">Severe NPDR or PDR, but not DME, was independently associated with depressive symptoms. The severity of DR could be an indicator to prompt monitoring of depression in at-risk individuals with diabetes. Further work is required to replicate these findings and determine the clinical significance of the association.</span></span></span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://archopht.jamanetwork.com/article.aspx?articleid=2531482" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration: none;" target="_blank">http://archopht.jamanetwork.com/</a></div>
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<b style="color: blue; font-size: x-large;"><br /></b><b style="color: blue; font-size: x-large;">Online Journals:</b></div>
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<b><a href="http://journals.lww.com/psychopharmacology/pages/currenttoc.aspx" style="color: #6699cc; text-decoration: none;" target="_blank">Journal of Clinical Psychopharmacology - August 2016 - Volume 36, Issue 4</a></b></div>
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<b><a href="http://www.nature.com/npp/journal/v41/n9/index.html" style="color: #6699cc; text-decoration: none;" target="_blank">Neuropsychopharmacology - Volume 41, Issue 9 (August 2016)</a></b></div>
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<b><a href="http://link.springer.com/journal/213/233/15/page/1" style="color: #6699cc; text-decoration: none;" target="_blank">Psychopharmacology - Volume 233, Issue 15, August 2016</a></b></div>
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<b><a href="http://jop.sagepub.com/content/current" style="color: #6699cc; text-decoration: none;" target="_blank">Journal of Psychopharmacology - August 2016; 30 (8)</a></b></div>
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<b><a href="http://ajp.psychiatryonline.org/toc/ajp/current" style="color: #6699cc; text-decoration: none;" target="_blank">The American Journal of Psychiatry - August 2016, Vol. 173, Issue 8</a></b></div>
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<a href="http://archpsyc.jamanetwork.com/issue.aspx" style="color: #6699cc; text-decoration: none;" target="_blank"><b>JAMA Psychiatry - August 2016, Vol. 73, No. 8</b></a></div>
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<b><a href="http://www.nature.com/neuro/journal/v19/n8/index.html" style="color: #6699cc; text-decoration: none;" target="_blank">Nature Neuroscience - August 2016, Vol 19, N° 8</a></b></div>
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<b><a href="http://www.nature.com/mp/journal/v21/n8/index.html" style="color: #6699cc; text-decoration: none;" target="_blank">Molecular Psychiatry - Volume 21, Issue 8, August 2016</a></b></div>
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<b style="background-color: white; color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"><a href="http://www.biologicalpsychiatryjournal.com/current" style="color: #6699cc; text-decoration: none;" target="_blank">Biological Psychiatry - Volume 80, Issue 5, September 2016</a></b><br />
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<b><a href="http://brain.oxfordjournals.org/content/139/8" style="color: #6699cc; text-decoration: none;" target="_blank">Brain - Volume 139, Issue 8, August 2016</a></b></div>
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<b><span style="font-size: small;">Join us on LinkedIn:</span> </b><b><a href="http://www.linkedin.com/groups/Neuropsychopharmacology-Neuroscience-5147601" style="color: #6699cc; text-decoration: none;">Neurosychopharmacology News Group</a></b></h3>
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Eutimiahttp://www.blogger.com/profile/07836706907685752267noreply@blogger.comtag:blogger.com,1999:blog-1045445187620004007.post-44122290204737150692016-07-03T23:41:00.000-04:002016-07-10T14:42:03.401-04:00July 2016<div dir="ltr" style="text-align: left;" trbidi="on">
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<i style="font-size: 14.85px; line-height: 20.79px;"><br /></i><i><b>Mayo Clinic Proceedings</b></i></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px; line-height: 20.79px;"><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;">Antidepressants are commonly prescribed medications in the United States, and there is increasing interest in individualizing treatment selection for more than 20 US Food and Drug Administration–approved treatments for major depressive disorder. Providing greater precision to pharmacotherapeutic recommendations for individual patients beyond the large-scale clinical trials evidence base can potentially reduce adverse effect toxicity profiles and increase response rates and overall effectiveness. It is increasingly recognized that genetic variation may contribute to this differential risk to benefit ratio and thus provides a unique opportunity to develop pharmacogenetic guidelines for psychiatry. Key studies and concepts that review the rationale for cytochrome P450 2D6 (CYP2D6) and cytochrome P450 2C19 (CYP2C19) genetic testing can be delineated by serum levels, adverse events, and clinical outcome measures (eg, antidepressant response). In this article, we report the evidence that contributed to the implementation of pharmacokinetic pharmacogenetic guidelines for antidepressants primarily metabolized by CYP2D6 and CYP2C19.</span></span><b style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"></b></div>
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<b>Source:</b> <a href="http://www.mayoclinicproceedings.org/article/S0025-6196%2816%2930002-7/abstract" style="color: #6699cc; text-decoration: none;" target="_blank">http://www.mayoclinicproceedings.org/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Alzheimer's disease is one of the most significant healthcare problems nationally and globally. Recently, the first description of the reversal of cognitive decline in patients with early Alzheimer's disease or its precursors, MCI (mild cognitive impairment) and SCI (subjective cognitive impairment), was published. The therapeutic approach used was programmatic and personalized rather than monotherapeutic and invariant, and was dubbed metabolic enhancement for neurodegeneration (MEND). Patients who had had to discontinue work were able to return to work, and those struggling at work were able to improve their performance. The patients, their spouses, and their co-workers all reported clear improvements. Here we report the results from quantitative MRI and neuropsychological testing in ten patients with cognitive decline, nine ApoE4+ (five homozygous and four heterozygous) and one ApoE4-, who were treated with the MEND protocol for 5-24 months. The magnitude of the improvement is unprecedented, providing additional objective evidence that this programmatic approach to cognitive decline is highly effective. These results have far-reaching implications for the treatment of Alzheimer's disease, MCI, and SCI; for personalized programs that may enhance pharmaceutical efficacy; and for personal identification of ApoE genotype.</span></span><b style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"></b></div>
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<b>Source:</b> <a href="http://www.aging-us.com/article/9R5JsRe8k4Jq7uTXj" style="color: #6699cc; text-decoration: none;" target="_blank">http://www.aging-us.com/</a></div>
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<span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><i>Obje<span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;">c</span>tive</i><br />To determine whether treatment with methylphenidate in children and young people with attention-deficit/hyperactivity disorder (ADHD) was associated with cardiovascular events.</span></span><br />
<span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><br /><i>Design</i><br />Self controlled case series analysis.</span></span><br />
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<span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><i>Setting</i><br />Nationwide health insurance database, 1 January 2008 to 31 December 2011, in South Korea.<br /> </span></span><br />
<span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><i>Parti<span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;">c</span>ipants</i><br />1224 patients aged ≤ 17 who had experienced an incident cardiovascular event and had had at least one incident prescription for methylphenidate.<br /> </span></span><br />
<span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><i>Main Out<span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;">com</span>e Measures</i><br />A recorded diagnosis (either a primary or secondary cause) of any of the following cardiovascular adverse events: arrhythmias (ICD-10 (international classification of diseases, 10th revision) codes I44, I45, I47, I48, I49), hypertension (codes I10-I15), myocardial infarction (code I21), ischemic stroke (code I63), or heart failure (code I50). Incidence rate ratios were calculated with conditional Poisson regression and adjusted for time varying comorbidity and comedication.<br /><i> </i></span></span><br />
<span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><i><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;">R</span>esults</i><br />Increased risk of arrhythmia was observed in all exposed time periods—that is, periods of treatment<span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"> </span>with methylphenidate—(incidence rate ratio 1.61, 95% confidence interval 1.48 to 1.74), and the risk was highest in the children who had congenital heart disease. No significant risk of myocardial infarction was observed for all exposed time periods (1.33, 0.90 to 1.98), though risk was higher in the early risk periods between eight and 56 days after the start of treatment with methylphenidate. No significant increased risk was observed for hypertension, ischemic stroke, or heart failure.<br /> </span></span><br />
<span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><i>Conclusion</i><br />The relative risk of myocardial infarction and arrhythmias is increased in the early period after the<span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"> </span>start of methylphenidate treatment for ADHD in children and young people. Though the absolute risk is likely to be low, the risk-benefit balance of methylphenidate should be carefully considered, particularly in children with mild ADHD.</span></span></div>
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<b>Source:</b> <a href="http://www.bmj.com/content/bmj/353/bmj.i2550.full.pdf" style="color: #6699cc; text-decoration: none;" target="_blank">http://www.bmj.com/</a></div>
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<span style="font-size: 14.85px; line-height: 20.79px;">Cortisol awakening response in patients with psychosis: Systematic review and meta-analysis</span></h2>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">The cortisol awakening response (CAR), defined as the increase in cortisol release in response to waking up, shows associations with social and environmental risk factors of schizophrenia and has been studied as a potential biomarker in schizophrenia. We report a systematic review and meta-analysis of 11 studies and 879 participants focusing on the CAR of patients with schizophrenia, first-episode psychosis, and at-risk mental states. Random-effects meta-analysis showed that CAR is attenuated in patients with psychosis compared to healthy controls (g = −0.426, 95% CI −0.585 to −0.267, p < 0.001, 11 between-group comparisons, n = 879). Subgroup analysis showed flattened CAR in patients with schizophrenia (g = −0.556, 95% CI −1.069 to −0.044, p < 0.05, 2 between-group comparisons, n = 114) and first-episode psychosis (g = −0.544, 95% CI −0.731 to −0.358, p < 0.001, 6 between-group comparisons, n = 505), but not in individuals with at-risk mental states. These distinctive alterations of hypothalamic-pituitary-adrenal axis function may have important implications for CAR as a marker for transition risk. However, the lack of objective verification of sampling adherence in these studies may limit the interpretation of the results.</span></span><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"></span></div>
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<b>Source:</b> <a href="http://www.sciencedirect.com/science/article/pii/S0149763416300549" style="color: #6699cc; text-decoration: none;" target="_blank">http://www.sciencedirect.com/</a></div>
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7T Proton Magnetic Resonance Spectroscopy of Gamma-Aminobutyric Acid, Glutamate, and Glutamine Reveals Altered Concentrations in Patients With Schizophrenia and Healthy Siblings </h2>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i>Background</i><br />The N-methyl-D-aspartate receptor hypofunction model of schizophrenia predicts dysfunction in both glutamatergic and gamma-aminobutyric acidergic (GABAergic) transmission. We addressed this hypothesis by measuring GABA, glutamate, glutamine, and the sum of glutamine plus glutamate concentrations in vivo in patients with schizophrenia using proton magnetic resonance spectroscopy at 7T, which allows separation of metabolites that would otherwise overlap at lower field strengths. In addition, we investigated whether altered levels of GABA, glutamate, glutamine, and the sum of glutamine plus glutamate reflect genetic vulnerability to schizophrenia by including healthy first-degree relatives.<br /> </span><br />
<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i>Methods</i><br />Proton magnetic resonance spectroscopy at 7T was performed in 21 patients with chronic schizophrenia who were taking medication, 23 healthy first-degree relatives of patients with schizophrenia, and 24 healthy nonrelatives. Glutamate, glutamine, and GABA were measured cortically and subcortically in bilateral basal ganglia and occipital cortex.<br /> </span><br />
<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i>Results</i><br />Patients with schizophrenia had reduced cortical GABA compared with healthy relatives and the combined sample of healthy relatives and healthy nonrelatives, suggesting that altered GABAergic systems in schizophrenia are associated with either disease state or medication effects. Reduced cortical glutamine relative to healthy control subjects was observed in patients with schizophrenia and the combined sample of healthy relatives and patients with schizophrenia, suggesting that altered glutamatergic metabolite levels are associated with illness liability. No group differences were found in the basal ganglia.<br /> </span><br />
<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i>Conclusions</i><br />Taken together, these findings are consistent with alterations in GABAergic and glutamatergic systems in patients with schizophrenia and provide novel insights into these systems in healthy relatives.</span></div>
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<b>Source:</b> <a href="http://www.sciencedirect.com/science/article/pii/S0006322316322831" rel="" style="color: #6699cc; text-decoration: none;" target="_blank">http://www.sciencedirect.com/</a></div>
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Association Between Religious Service Attendance and Lower Suicide Rates Among US Women</h2>
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<i><b>JAMA Psychiatry</b></i></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Importance </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Previous studies have linked suicide risk with religious participation, but the majority have used ecologic, cross-sectional, or case-control data.<br /><br /><i>Objective </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">To examine the longitudinal association between religious service attendance and suicide and the joint associations of suicide with service attendance and religious affiliation.<br /><br /><i>Design, Setting, and Participants </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">We evaluated associations between religious service attendance and suicide from 1996 through June 2010 in a large, long-term prospective cohort, the Nurses’ Health Study, in an analysis that included 89 708 women. Religious service attendance was self-reported in 1992 and 1996. Data analysis was conducted from 1996 through 2010.<br /><br /><i>Main Outcomes and Measures </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Cox proportional hazards regression models were used to examine the association between religious service attendance and suicide, adjusting for demographic covariates, lifestyle factors, medical history, depressive symptoms, and social integration measures. We performed sensitivity analyses to examine the influence of unmeasured confounding.<br /><i><br />Results </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Among 89 708 women aged 30 to 55 years who participated in the Nurses’ Health Study, attendance at religious services once per week or more was associated with an approximately 5-fold lower rate of suicide compared with never attending religious services (hazard ratio, 0.16; 95% CI, 0.06-0.46). Service attendance once or more per week vs less frequent attendance was associated with a hazard ratio of 0.05 (95% CI, 0.006-0.48) for Catholics but only 0.34 (95% CI, 0.10-1.10) for Protestants (P = .05 for heterogeneity). Results were robust in sensitivity analysis and to exclusions of persons who were previously depressed or had a history of cancer or cardiovascular disease. There was evidence that social integration, depressive symptoms, and alcohol consumption partially mediated the association among those occasionally attending services, but not for those attending frequently.<br /><br /><i>Conclusions and Relevance</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">In this cohort of US women, frequent religious service attendance was associated with a significantly lower rate of suicide.</span></span><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"></span></div>
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<b>Source:</b> <a href="http://archpsyc.jamanetwork.com/article.aspx?articleid=2529152" style="color: #6699cc; text-decoration: none;" target="_blank">http://archpsyc.jamanetwork.com/</a></div>
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<i style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Journal of Psychiatric Research</b></span></i></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span><span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span><span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Background</i> </span></span></span></span><br />
<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Transcutaneous electrical acupoint stimulation (TEAS) is thought to have potential to treat obsessive-compulsive disorder (OCD).<i><br /> </i></span></span></span></span><br />
<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Objective</i></span></span></span></span><br />
<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">The purpose of this study was to determine whether adding TEAS to cognitive behavioral therapy (CBT) and clomipramine would improve the efficacy of these conventional treatments in OCD.<i><br /> </i></span></span></span></span><br />
<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Methods</i></span></span></span></span><br />
<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">In this randomized controlled trial, 360 OCD patients were assigned to receive TEAS combined with CBT plus clomipramine (Group A, n = 120), TEAS combined with CBT plus placebo (Group B, n = 120), and simulated (placebo) TEAS combined with CBT plus clomipramine (Group C, n = 120) for 12 weeks. The primary outcome was measured using the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS).<i><br /> </i></span></span></span></span><br />
<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Results</i></span></span></span></span><br />
<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">OCD symptoms in all patients reduced over time, however Groups A and B had a significantly greater reduction in Y-BOCS total score and the subscale for obsession and compulsion between week 2 and week 12 compared to Group C. Groups A and B had similar scores on these measures. Both groups had significantly higher rates of clinical response than Group C (88.3% and 81.7% vs. 67.5%, respectively, p < 0.001); and higher rates of remission (30.0% and 22.5% vs. 9.2%, respectively, p < 0.001). Group B experienced fewer adverse events than the other two groups.<i><br /> </i></span></span></span></span><br />
<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;">C</span>onclusions</i> </span></span></span></span><br />
<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">TEAS enhances the efficacy of conventional OCD interventions and avoids the adverse effects associated with conventional pharmacological treatment. It can be considered as an effective adjunct intervention for OCD.</span></span></span></span></div>
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<b>Source:</b> <a href="http://www.journalofpsychiatricresearch.com/article/S0022-3956%2816%2930106-6/abstract" style="color: #6699cc; text-decoration: none;" target="_blank">http://www.journalofpsychiatricresearch.com/</a></div>
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Association of Cerebral Microbleeds With Cognitive Decline and Dementia</h2>
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<i><b>JAMA Neurology</b></i></div>
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<i><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Importance </span></span></i><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Cerebral microbleeds are hypothesized downstream markers of brain damage caused by vascular and amyloid pathologic mechanisms. To date, whether their presence is associated with cognitive deterioration in the general population remains unclear.<br /><br /><i>Objective </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">To determine whether microbleeds, and more specifically microbleed count and location, are associated with an increased risk for cognitive impairment and dementia in the general population.<br /><br /><i>Design, Setting, and Participants </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">The Rotterdam Study, a prospective population-based study set in the general community, assessed the presence, number, and location of microbleeds at baseline (August 2005 to December 2011) on magnetic resonance imaging studies of the brain in 4841 participants 45 years or older. Participants underwent neuropsychological testing at 2 points a mean (SD) of 5.9 (0.6) years apart and were followed up for incident dementia throughout the study period until January 1, 2013. The association of microbleeds with cognitive decline and dementia was studied using multiple linear regression, linear mixed-effects modeling, and Cox proportional hazards.<br /><br /><i>Exposures</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Cerebral microbleed presence, location, and number.<br /><br /><i>Main Outcomes and Measures</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Cognitive decline measured by a decrease in neuropsychological test battery scores (Mini-Mental State Examination, Letter Digit Substitution Task, Word Fluency Test, Stroop test, 15-word Verbal Learning Test, and Purdue Pegboard Test) and compound scores (eg, G factor, executive function, information processing speed, memory, motor speed) and dementia.<br /><br /><i>Results</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">In total, 3257 participants (1758 women [54.7%]; mean [SD] age, 59.6 [7.8] years) underwent baseline and follow-up cognitive testing. Microbleed prevalence was 15.3% (median [interquartile range] count, 1 [1-88]). The presence of more than 4 microbleeds was associated with cognitive decline. Lobar (with or without cerebellar) microbleeds were associated with a decline in executive functions (mean difference in z score, −0.31; 95% CI, −0.51 to −0.11; P = .003), information processing (mean difference in z score, −0.44; 95% CI, −0.65 to −0.22; P < .001), and memory function (mean difference in z score, −0.34; 95% CI, −0.64 to −0.03; P = .03), whereas microbleeds in other brain regions were associated with a decline in information processing and motor speed (mean difference in z score, −0.61; 95% CI, −1.05 to −0.17; P = .007). After a mean (SD) follow-up of 4.8 (1.4) years, 72 participants developed dementia, of whom 53 had Alzheimer dementia. The presence of microbleeds was associated with an increased risk for dementia after adjustment for age, sex, and educational level (hazard ratio, 2.02; 95% CI, 1.25-3.24), including Alzheimer dementia (hazard ratio, 2.10; 95% CI, 1.21-3.64).<br /><br /><i>Conclusions and Relevance </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">In the general population, a high microbleed count was associated with an increased risk for cognitive deterioration and dementia. Microbleeds thus mark the presence of diffuse vascular and neurodegenerative brain damage.</span></span><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"></span></div>
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<b style="font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="font-size: 14.85px; line-height: 20.79px;"> </span><a href="https://archneur.jamanetwork.com/article.aspx?articleid=2526492" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration: none;" target="_blank">https://archneur.jamanetwork.com/</a></div>
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<span style="color: #333333; font-family: "arial" , sans-serif;"><span style="font-size: 18px; line-height: 22px; text-transform: uppercase;">Pediatricians Urged to Routinely Screen Adolescents for Risk Factors for Suicide </span></span></h2>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b><br /></b></i></span></span><span style="color: #333333; font-size: 14.85px; font-style: italic; font-weight: bold; line-height: 20.79px;">Psychiatric News</span></div>
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<span style="font-size: 14.85px; line-height: 20.79px;">The American Academy of Pediatrics (AAP) published updated guidelines to assist pediatricians and other child and adolescent health care professionals in identifying and helping adolescents at risk of suicide. The report, which replaces recommendations made in 2007, acknowledges the role bullying and the internet may play in teen suicide risk and highlights the value of antidepressant medications to treat those at risk.<br /><br />According to most recent data, suicide is the second leading cause of death for adolescents aged 15 to 19. The guidelines recommend pediatricians routinely ask adolescent patients if they have thoughts of harming themselves, and screen for bullying, pathological internet use, and other risk factors including a family history of suicide, a history of physical or sexual abuse, and mood disorders.<br /><br />If an adolescent is considered to be at moderate or high risk of suicide, the guidelines recommend that arrangements for immediate mental health professional evaluation should be made during the office visit. For teens considered to be at low risk of suicide, the guidelines recommend close follow-up and/or a referral for a timely mental health evaluation.</span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Read More:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://alert.psychnews.org/2016/06/pediatricians-urged-to-routinely-screen.html" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration: none;" target="_blank">http://alert.psychnews.org/</a></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px; text-transform: uppercase;">Screening for Cognitive Impairments After Traumatic Brain Injury: A Comparison of a Brief Computerized Battery With the Montreal Cognitive Assessment </span></span></h2>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b>The Journal of Neuropsychiatry</b></span></i></span></div>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b><br /></b></span></i></span><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span><br />
<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b><br /></b></span></i></span></div>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Detecting cognitive dysfunction in a busy traumatic brain injury (TBI)
clinic is challenging given the length of conventional assessments and
the need for psychometric expertise. The authors report the utility of a
10-minute, easily administered computerized battery that is more
sensitive than the Montreal Cognitive Assessment in detecting cognitive
impairments in people with a TBI.</span></span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://neuro.psychiatryonline.org/doi/abs/10.1176/appi.neuropsych.16010005" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration: none;" target="_blank">http://neuro.psychiatryonline.org/</a></div>
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<b><a href="http://journals.lww.com/psychopharmacology/pages/currenttoc.aspx" style="color: #6699cc; text-decoration: none;" target="_blank">Journal of Clinical Psychopharmacology - August 2016 - Volume 36, Issue 4</a></b></div>
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<b><a href="http://www.nature.com/npp/journal/v41/n8/index.html" style="color: #6699cc; text-decoration: none;" target="_blank">Neuropsychopharmacology - Volume 41, Issue 8 (July 2016)</a></b></div>
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<b><a href="http://link.springer.com/journal/213/233/15/page/1" style="color: #6699cc; text-decoration: none;" target="_blank">Psychopharmacology - Volume 233, Issue 15, August 2016</a></b></div>
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<b><a href="http://jop.sagepub.com/content/current" style="color: #6699cc; text-decoration: none;" target="_blank">Journal of Psychopharmacology - July 2016; 30 (7)</a></b></div>
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<b><a href="http://ajp.psychiatryonline.org/toc/ajp/current" style="color: #6699cc; text-decoration: none;" target="_blank">The American Journal of Psychiatry - July 2016, Vol. 173, Issue 7</a></b></div>
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<a href="http://archpsyc.jamanetwork.com/issue.aspx" style="color: #6699cc; text-decoration: none;" target="_blank"><b>JAMA Psychiatry - July 2016, Vol. 73, No. 7</b></a></div>
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<b><a href="http://www.nature.com/neuro/journal/v19/n7/index.html" style="color: #6699cc; text-decoration: none;" target="_blank">Nature Neuroscience - July 2016, Vol 19, N° 7</a></b></div>
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<b><a href="http://www.nature.com/mp/journal/v21/n7/index.html" style="color: #6699cc; text-decoration: none;" target="_blank">Molecular Psychiatry - Volume 21, Issue 7, July 2016</a></b></div>
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<b style="background-color: white; color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"><a href="http://www.biologicalpsychiatryjournal.com/current" style="color: #6699cc; text-decoration: none;" target="_blank">Biological Psychiatry - Volume 80, Issue 2, July 2016</a></b><br />
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<b><a href="http://brain.oxfordjournals.org/content/139/7" style="color: #6699cc; text-decoration: none;" target="_blank">Brain - Volume 139, Issue 7, July 2016</a></b></div>
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<b><span style="font-size: small;">Join us on LinkedIn:</span> </b><b><a href="http://www.linkedin.com/groups/Neuropsychopharmacology-Neuroscience-5147601" style="color: #6699cc; text-decoration: none;">Neurosychopharmacology News Group</a></b></h3>
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Eutimiahttp://www.blogger.com/profile/07836706907685752267noreply@blogger.comtag:blogger.com,1999:blog-1045445187620004007.post-37999632451598061022016-06-03T12:20:00.002-04:002016-06-12T12:42:30.416-04:00June 2016<div dir="ltr" style="text-align: left;" trbidi="on">
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<i style="font-size: 14.85px; line-height: 20.79px;"><br /></i><i><b>The American Journal of Psychiatry</b></i></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Objective:</i></span></span></div>
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;">Cigarette smoking during pregnancy is a major public health problem leading to adverse health outcomes and neurodevelopmental abnormalities among offspring. Its prevalence in the United States and Europe is 12%–25%. This study examined the relationship between prenatal nicotine exposure (cotinine level) in archived maternal sera and schizophrenia in offspring from a national birth cohort.</span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Method:</i></span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">The authors conducted a population-based nested case-control study of all live births in Finland from 1983 to 1998. Cases of schizophrenia in offspring (N=977) were identified from a national registry and matched 1:1 to controls on date of birth, sex, and residence. Maternal serum cotinine levels were prospectively measured, using quantitative immunoassay, from early- to mid-gestation serum specimens archived in a national biobank.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Results:</i></span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">A higher maternal cotinine level, measured as a continuous variable, was associated with an increased odds of schizophrenia (odds ratio=3.41, 95% confidence interval, 1.86–6.24). Categorically defined heavy maternal nicotine exposure was related to a 38% increased odds of schizophrenia. These findings were not accounted for by maternal age, maternal or parental psychiatric disorders, socioeconomic status, and other covariates. There was no clear evidence that weight for gestational age mediated the associations.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Conclusions:</i></span></span></div>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>To the authors’ knowledge, this is the first study of the relationship between a maternal smoking biomarker and schizophrenia. It provides the most definitive evidence to date that smoking during pregnancy is associated with schizophrenia. If replicated, these findings suggest that preventing smoking during pregnancy may decrease the incidence of schizophrenia.</b></span></span></span></span></div>
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<b>Source:</b> <a href="http://ajp.psychiatryonline.org/doi/abs/10.1176/appi.ajp.2016.15060800" style="color: #6699cc; text-decoration: none;" target="_blank">http://ajp.psychiatryonline.org/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px; text-transform: uppercase;">Self-harm, Unintentional Injury, and Suicide in Bipolar Disorder During Maintenance Mood Stabilizer Treatment</span></span></h2>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b>JAMA Psychiatry</b></i></span></span></div>
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<b style="font-size: 14.85px; line-height: 20.79px;"><br /></b><b style="font-size: 14.85px; line-height: 20.79px;">Abstract</b></div>
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Importance </i></span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Self-harm is a prominent cause of morbidity in patients with bipolar disorder and is strongly associated with suicide. There is evolving evidence that lithium use may reduce suicidal behavior, in addition to concerns that the use of anticonvulsants may increase self-harm. Information is limited about the effects of antipsychotics when used as mood stabilizer treatment. Rates of unintentional injury are poorly defined in bipolar disorder, and understanding drug associations with this outcome may shed light on mechanisms for lithium’s potential antisuicidal properties through reduction in impulsive aggression.</span></span></div>
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span>
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Objective </i> </span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">To compare rates of self-harm, unintentional injury, and suicide in patients with bipolar disorder who were prescribed lithium, valproate sodium, olanzapine, or quetiapine fumarate.</span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span>
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Design, Setting, and Participants</i> </span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">This investigation was a propensity score (PS)–adjusted and PS-matched longitudinal cohort study in a nationally representative UK sample using electronic health records data collected between January 1, 1995, and December 31, 2013. Participants included all patients diagnosed as having bipolar disorder who were prescribed lithium, valproate, olanzapine, or quetiapine as maintenance mood stabilizer treatment.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Main Outcomes and Measures</i> </span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">The primary outcome was any form of self-harm. Secondary outcomes were unintentional injury and suicide.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Results</i> </span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Of the 14 396 individuals with a diagnosis of BPD, 6671 were included in the cohort, with 2148 prescribed lithium, 1670 prescribed valproate, 1477 prescribed olanzapine, and 1376 prescribed quetiapine as maintenance mood stabilizer treatment. Self-harm rates were lower in patients prescribed lithium (205; 95% CI, 175-241 per 10 000 person-years at risk [PYAR]) compared with those prescribed valproate (392; 95% CI, 334-460 per 10 000 PYAR), olanzapine (409; 95% CI, 345-483 per 10 000 PYAR), or quetiapine (582; 95% CI, 489-692 per 10 000 PYAR). This association was maintained after PS adjustment (hazard ratio [HR], 1.40; 95% CI, 1.12-1.74 for valproate, olanzapine, or quetiapine vs lithium) and PS matching (HR, 1.51; 95% CI, 1.21-1.88). After PS adjustment, unintentional injury rates were lower for lithium compared with valproate (HR, 1.32; 95% CI, 1.10-1.58) and quetiapine (HR, 1.34; 95% CI, 1.07-1.69) but not olanzapine. The suicide rate in the cohort was 14 (95% CI, 9-21) per 10 000 PYAR. Although this rate was lower in the lithium group than for other treatments, there were too few events to allow accurate estimates.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Conclusions and Relevance</i> </span></span></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Patients taking lithium had reduced self-harm and unintentional injury rates. This finding augments limited trial and smaller observational study results. It supports the hypothesis that lithium use reduces impulsive aggression in addition to stabilizing mood.</b></span></span></span></span><br />
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<b>Source:</b> <a href="http://archpsyc.jamanetwork.com/article.aspx?articleid=2521461" style="color: #6699cc; text-decoration: none;" target="_blank">http://archpsyc.jamanetwork.com/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px; text-transform: uppercase;">Whole-Body Hyperthermia for the Treatment of Major Depressive Disorder</span></span></h2>
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<i style="font-size: 14.85px; line-height: 20.79px;"><b>JAMA Psychiatry </b></i><br />
<span style="font-size: 14.85px; line-height: 20.79px;"><b><br /></b></span><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></div>
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Importance </i> </span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Limitations of current antidepressants highlight the need to identify novel treatments for major depressive disorder. A prior open trial found that a single session of whole-body hyperthermia (WBH) reduced depressive symptoms; however, the lack of a placebo control raises the possibility that the observed antidepressant effects resulted not from hyperthermia per se, but from nonspecific aspects of the intervention.</span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Objective</i> </span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">To test whether WBH has specific antidepressant effects when compared with a sham condition and to evaluate the persistence of the antidepressant effects of a single treatment.</span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Design, Setting, and Participants</i> </span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">A 6-week, randomized, double-blind study conducted between February 2013 and May 2015 at a university-based medical center comparing WBH with a sham condition. All research staff conducting screening and outcome procedures were blinded to randomization status. Of 338 individuals screened, 34 were randomized, 30 received a study intervention, and 29 provided at least 1 postintervention assessment and were included in a modified intent-to-treat efficacy analysis. Participants were medically healthy, aged 18 to 65 years, met criteria for major depressive disorder, were free of psychotropic medication use, and had a baseline 17-item Hamilton Depression Rating Scale score of 16 or greater.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Interventions</i> </span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">A single session of active WBH vs a sham condition matched for length of WBH that mimicked all aspects of WBH except intense heat.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Main Outcomes and Measures </i> </span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Between-group differences in postintervention Hamilton Depression Rating Scale scores.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Results </i></span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">The mean (SD) age was 36.7 (15.2) years in the WBH group and 41.47 (12.54) years in the sham group. Immediately following the intervention, 10 participants (71.4%) randomized to sham treatment believed they had received WBH compared with 15 (93.8%) randomized to WBH. When compared with the sham group, the active WBH group showed significantly reduced Hamilton Depression Rating Scale scores across the 6-week postintervention study period (WBH vs sham; week 1: −6.53, 95% CI, −9.90 to −3.16, P < .001; week 2: −6.35, 95% CI, −9.95 to −2.74, P = .001; week 4: −4.50, 95% CI, −8.17 to −0.84, P = .02; and week 6: −4.27, 95% CI, −7.94 to −0.61, P = .02). These outcomes remained significant after evaluating potential moderating effects of between-group differences in baseline expectancy scores. Adverse events in both groups were generally mild.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Whole-body hyperthermia holds promise as a safe, rapid-acting, antidepressant modality with a prolonged therapeutic benefit.</b></span></span></span></div>
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<b>Source:</b> <a href="http://archpsyc.jamanetwork.com/article.aspx?articleid=2521478" style="color: #6699cc; text-decoration: none;" target="_blank">http://archpsyc.jamanetwork.com/</a></div>
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<span style="font-size: 14.85px; line-height: 20.79px;">FDA warns about rare but serious skin reactions with mental health drug olanzapine (Zyprexa, Zyprexa Zydis, Zyprexa Relprevv, and Symbyax)</span></h2>
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">The U.S. Food and Drug Administration (FDA) is warning that the antipsychotic medicine olanzapine can cause a rare but serious skin reaction that can progress to affect other parts of the body. We are adding a new warning to the drug labels for all olanzapine-containing products that describes this severe condition known as Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS).</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Health care professionals should immediately stop treatment with olanzapine if DRESS is suspected. When prescribing the medicine, explain the signs and symptoms of severe skin reactions to your patients and tell them when to seek immediate medical care.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Olanzapine is an antipsychotic medicine used to treat mental health disorders schizophrenia and bipolar disorder. It can decrease hallucinations, in which people hear or see things that do not exist, and other psychotic symptoms such as disorganized thinking. Olanzapine is available under the brand names Zyprexa, Zyprexa Zydis, Zyprexa Relprevv, and Symbyax, and also as generics.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">DRESS may start as a rash that can spread to all parts of the body. It can include fever and swollen lymph nodes and a swollen face. It causes a higher-than-normal number of infection-fighting white blood cells called eosinophils that can cause inflammation, or swelling. DRESS can result in injury to organs including the liver, kidneys, lungs, heart, or pancreas, and can lead to death.</span></span><br />
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;">A search of the FDA Adverse Event Reporting System (FAERS) database identified 23 cases of DRESS reported with olanzapine worldwide since 1996, when the first olanzapine-containing product was approved. FAERS includes only reports submitted to FDA, so there are likely to be additional cases about which we are unaware. One patient taking olanzapine experienced DRESS and died; however, this patient was taking multiple medicines that could also have contributed to death (see Data Summary).</span></span></span></span></div>
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<b>Read More:</b> <a href="http://www.fda.gov/Drugs/DrugSafety/ucm499441.htm" style="color: #6699cc; text-decoration: none;" target="_blank">http://www.fda.gov/</a></div>
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FDA approves first drug to treat hallucinations and delusions associated with Parkinson’s disease </h2>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b>US FDA</b></span></i></span></span></div>
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">The U.S. Food and Drug Administration today approved Nuplazid (pimavanserin) tablets, the first drug approved to treat hallucinations and delusions associated with psychosis experienced by some people with Parkinson’s disease.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Hallucinations or delusions can occur in as many as 50 percent of patients with Parkinson’s disease at some time during the course of their illness. People who experience them see or hear things that are not there (hallucinations) and/or have false beliefs (delusions). The hallucinations and delusions experienced with Parkinson’s disease are serious symptoms, and can lead to thinking and emotions that are so impaired that the people experiencing them may not relate to loved ones well or take appropriate care of themselves. </span></span><br />
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">“Hallucinations and delusions can be profoundly disturbing and disabling,” said Mitchell Mathis, M.D., director of the Division of Psychiatry Products in the FDA’s Center for Drug Evaluation and Research. “Nuplazid represents an important treatment for people with Parkinson’s disease who experience these symptoms.”</span></span></span></span></div>
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<b>Read More:</b> <a href="http://www.fda.gov/newsevents/newsroom/pressannouncements/ucm498442.htm" rel="nofollow" style="color: #6699cc; text-decoration: none;" target="_blank">http://www.fda.gov/</a></div>
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FDA warns about new impulse-control problems associated with mental health drug aripiprazole (Abilify, Abilify Maintena, Aristada)</h2>
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<i><b>US FDA</b></i></div>
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">The U.S. Food and Drug Administration (FDA) is warning that compulsive or uncontrollable urges to gamble, binge eat, shop, and have sex have been reported with the use of the antipsychotic drug aripiprazole (Abilify, Abilify Maintena, Aristada, and generics). These uncontrollable urges were reported to have stopped when the medicine was discontinued or the dose was reduced. These impulse-control problems are rare, but they may result in harm to the patient and others if not recognized.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Although pathological gambling is listed as a reported side effect in the current aripiprazole drug labels, this description does not entirely reflect the nature of the impulse-control risk that we identified. In addition, we have become aware of other compulsive behaviors associated with aripiprazole, such as compulsive eating, shopping, and sexual actions. These compulsive behaviors can affect anyone who is taking the medicine. As a result, we are adding new warnings about all of these compulsive behaviors to the drug labels and the patient Medication Guides for all aripiprazole products.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;">Health care professionals should make patients and caregivers aware of the risk of these uncontrollable urges when prescribing aripiprazole, and specifically ask patients about any new or increasing urges while they are being treated with aripiprazole. Closely monitor for new or worsening uncontrollable urges in patients at higher risk for impulse-control problems. These include those with a personal or family history of obsessive-compulsive disorder, impulse-control disorder, bipolar disorder, impulsive personality, alcoholism, drug abuse, or other addictive behaviors. Consider reducing the dose or stopping the medicine if such urges develop.</span></div>
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<b>Read More:</b> <a href="http://www.fda.gov/Drugs/DrugSafety/ucm498662.htm" style="color: #6699cc; text-decoration: none;" target="_blank">http://www.fda.gov/</a></div>
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<i style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Journal of Clinical Medicine</b></span></i></div>
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">To examine the relationship between the choice of second-generation antidepressant drug treatment and long-term weight change.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">We conducted a retrospective cohort study to investigate the relationship between choice of antidepressant medication and weight change at two years among adult patients with a new antidepressant treatment episode between January, 2006 and October, 2009 in a large health system in Washington State. Medication use, encounters, diagnoses, height, and weight were collected from electronic databases. We modeled change in weight and BMI at two years after initiation of treatment using inverse probability weighted linear regression models that adjusted for potential confounders. Fluoxetine was the reference treatment.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">In intent-to-treat analyses, non-smokers who initiated bupropion treatment on average lost 7.1 lbs compared to fluoxetine users who were non-smokers (95% CI: −11.3, −2.8; p-value < 0.01); smokers who initiated bupropion treatment gained on average 2.2 lbs compared to fluoxetine users who were smokers (95% CI: −2.3, 6.8; p-value = 0.33). Changes in weight associated with all other antidepressant medications were not significantly different than fluoxetine, except for sertraline users, who gained an average of 5.9 lbs compared to fluoxetine users (95% CI: 0.8, 10.9; p-value = 0.02). </span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Conclusion</i></span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Antidepressant drug therapy is significantly associated with long-term weight change at two years. Bupropion may be considered as the first-line drug of choice for overweight and obese patients unless there are other existing contraindications.</span></span><br />
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<b>Source:</b> <a href="http://www.mdpi.com/2077-0383/5/4/48" style="color: #6699cc; text-decoration: none;" target="_blank">http://www.mdpi.com/</a></div>
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Evidence-based guideline: Treatment of tardive syndromes</h2>
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<i><b>Neurology</b></i></div>
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<b><br /></b><b>Abstract</b></div>
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Objective </i><br />To make evidence-based recommendations regarding management of tardive syndromes (TDS), including tardive dyskinesias (TDD), by addressing 5 questions: 1) Is withdrawal of dopamine receptor blocking agents (DRBAs) an effective TDS treatment? 2) Does switching from typical to atypical DRBAs reduce TDS symptoms? 3) What is the efficacy of pharmacologic agents in treating TDS? 4) Do patients with TDS benefit from chemodenervation with botulinum toxin? 5) Do patients with TDS benefit from surgical therapy?</span></span></div>
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">PsycINFO, Ovid MEDLINE, EMBASE, Web of Science, and Cochrane were searched (1966–2011). Articles were classified according to a 4-tiered evidence-rating scheme; recommendations were tied to the evidence.</span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Results and recommendations</i></span></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Clonazepam probably improves TDD and ginkgo biloba probably improves TDS (both Level B); both should be considered as treatment. </b>Risperidone may improve TDS but cannot be recommended as treatment because neuroleptics may cause TDS despite masking symptoms. Amantadine and tetrabenazine might be considered as TDS treatment (Level C). Diltiazem should not be considered as TDD treatment (Level B); galantamine and eicosapentaenoic acid may not be considered as treatment (Level C). Data are insufficient to support or refute use of acetazolamide, bromocriptine, thiamine, baclofen, vitamin E, vitamin B6, selegiline, clozapine, olanzapine, melatonin, nifedipine, fluperlapine, sulpiride, flupenthixol, thiopropazate, haloperidol, levetiracetam, quetiapine, ziprasidone, sertindole, aripiprazole, buspirone, yi-gan san, biperiden discontinuation, botulinum toxin type A, electroconvulsive therapy, α-methyldopa, reserpine, and pallidal deep brain stimulation as TDS treatments (Level U). Data are insufficient to support or refute TDS treatment by withdrawing causative agents or switching from typical to atypical DRBA (Level U).</span></span></span><br />
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<b style="font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://www.neurology.org/content/81/5/463.full" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration: none;" target="_blank">http://www.neurology.org/</a></div>
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<span style="color: #333333; font-family: "arial" , sans-serif;"><span style="font-size: 18px; line-height: 22px; text-transform: uppercase;">Association Between Genetic Traits for Immune-Mediated Diseases and Alzheimer Disease</span></span></h2>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b><br /></b></i></span></span><span style="color: #333333; font-size: 14.85px; font-style: italic; font-weight: bold; line-height: 20.79px;">JAMA Neurology</span><br />
<span style="color: #333333; font-size: 14.85px; font-style: italic; font-weight: bold; line-height: 20.79px;"><br /></span><span style="color: #333333; font-size: 14.85px; font-weight: bold; line-height: 20.79px;">Abstract</span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Importance </i></span></span></div>
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Late-onset Alzheimer disease (AD), the most common form of dementia, places a large burden on families and society. Although epidemiological and clinical evidence suggests a relationship between inflammation and AD, their relationship is not well understood and could have implications for treatment and prevention strategies.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Objective </i> </span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">To determine whether a subset of genes involved with increased risk of inflammation are also associated with increased risk for AD.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Design, Setting, and Participants</i> </span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">In a genetic epidemiology study conducted in July 2015, we systematically investigated genetic overlap between AD (International Genomics of Alzheimer’s Project stage 1) and Crohn disease, ulcerative colitis, rheumatoid arthritis, type 1 diabetes, celiac disease, and psoriasis using summary data from genome-wide association studies at multiple academic clinical research centers. P values and odds ratios from genome-wide association studies of more than 100 000 individuals were from previous comparisons of patients vs respective control cohorts. Diagnosis for each disorder was previously established for the parent study using consensus criteria.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Main Outcomes and Measures </i></span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">The primary outcome was the pleiotropic (conjunction) false discovery rate P value. Follow-up for candidate variants included neuritic plaque and neurofibrillary tangle pathology; longitudinal Alzheimer’s Disease Assessment Scale cognitive subscale scores as a measure of cognitive dysfunction (Alzheimer’s Disease Neuroimaging Initiative); and gene expression in AD vs control brains (Gene Expression Omnibus data).</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Results </i></span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Eight single-nucleotide polymorphisms (false discovery rate P < .05) were associated with both AD and immune-mediated diseases. Of these, rs2516049 (closest gene HLA-DRB5; conjunction false discovery rate P = .04 for AD and psoriasis, 5.37 × 10−5 for AD, and 6.03 × 10−15 for psoriasis) and rs12570088 (closest gene IPMK; conjunction false discovery rate P = .009 for AD and Crohn disease, P = 5.73 × 10−6 for AD, and 6.57 × 10−5 for Crohn disease) demonstrated the same direction of allelic effect between AD and the immune-mediated diseases. Both rs2516049 and rs12570088 were significantly associated with neurofibrillary tangle pathology (P = .01352 and .03151, respectively); rs2516049 additionally correlated with longitudinal decline on Alzheimer’s Disease Assessment Scale cognitive subscale scores (β [SE], 0.405 [0.190]; P = .03). Regarding gene expression, HLA-DRA and IPMK transcript expression was significantly altered in AD brains compared with control brains (HLA-DRA: β [SE], 0.155 [0.024]; P = 1.97 × 10−10; IPMK: β [SE], −0.096 [0.013]; P = 7.57 × 10−13).</span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span>
<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="color: #444444;"><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Conclusions and Relevance </i> </span></span></span></span></span></span></span><br />
<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="color: #444444;"><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Our findings demonstrate genetic overlap between AD and immune-mediated diseases and suggest that immune system processes influence AD pathogenesis and progression.</b></span></span></span></span></span></span></span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://archneur.jamanetwork.com/article.aspx?articleid=2514054" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration: none;" target="_blank">http://archneur.jamanetwork.com/</a></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px; text-transform: uppercase;">Effect of prenatal selective serotonin reuptake inhibitor (SSRI) exposure on birthweight and gestational age: a sibling-controlled cohort study</span></span></h2>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b>International Journal of Epidemiology</b></span></i></span></div>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b><br /></b></span></i></span><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span><br />
<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b><br /></b></span></i></span></div>
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Background</i></span></span></div>
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Up to 10% of women are exposed to selective serotonin reuptake inhibitors (SSRIs) during pregnancy. Information on their effect on birthweight and gestational age remains conflicting. The aim of this sibling-controlled prospective cohort study is to address shared geneticand family-level confounding to investigate the effects of prenatal SSRI exposure and maternal depression on birthweight and gestational age.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Methods</i></span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">We used the Norwegian Mother and Child Cohort Study (MoBa) and the Medical Birth Registry of Norway (MBRN). Our study population consisted of 27 756 siblings; 194 were prenatally exposed to SSRIs and 27 500 were unexposed to any antidepressant medication. Random and fixed effects analysis with propensity score adjustment was used to evaluate the effectson birthweight and gestational age.</span></span><br />
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<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">SSRI exposure during two or more trimesters was associated with a decrease in birthweight of 205 g [95% confidence interval (CI) −372 to − 38] and a decrease in gestational length of 4.9 days (95% CI − 9.1 to − 1.4). Neither maternal SSRI use in one trimester, lifetime history of major depression nor depressive symptoms during pregnancy were associated with these pregnancy outcomes (for non-pharmacologically treated depression in two periods in pregnancy, +5 g (95% CI − 56 to + 67) and +4.9 days (95% CI − 4.7 to + 14.7), respectively).</span></span><br />
<span style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="color: #444444;"><span style="font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Conclusions</i></span></span></span></span></span><br />
<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="color: #444444;"><span style="font-family: arial, tahoma, helvetica, freesans, sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Prenatal exposure to SSRIs during two or more trimesters may decrease birthweight and gestational length. Our results indicate that neither maternal depression nor shared genetics and family environment fully explain this association.</b></span></span></span></span></span><br />
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://ije.oxfordjournals.org/content/early/2016/05/16/ije.dyw049.short?rss=1" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration: none;" target="_blank">http://ije.oxfordjournals.org/</a></div>
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<b><a href="http://journals.lww.com/psychopharmacology/pages/currenttoc.aspx" style="color: #6699cc; text-decoration: none;" target="_blank">Journal of Clinical Psychopharmacology - June 2016 - Volume 36, Issue 3</a></b></div>
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<b><a href="http://www.nature.com/npp/journal/v41/n7/index.html" style="color: #6699cc; text-decoration: none;" target="_blank">Neuropsychopharmacology - Volume 41, Issue 7 (June 2016)</a></b></div>
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<b><a href="http://link.springer.com/journal/213/233/12/page/1" style="color: #6699cc; text-decoration: none;" target="_blank">Psychopharmacology - Volume 233, Issue 12, June 2016</a></b></div>
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<b><a href="http://jop.sagepub.com/content/current" style="color: #6699cc; text-decoration: none;" target="_blank">Journal of Psychopharmacology - June 2016; 30 (6)</a></b></div>
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<b><a href="http://ajp.psychiatryonline.org/toc/ajp/current" style="color: #6699cc; text-decoration: none;" target="_blank">The American Journal of Psychiatry - June 2016, Vol. 173, Issue 6</a></b></div>
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<a href="http://archpsyc.jamanetwork.com/issue.aspx" style="color: #6699cc; text-decoration: none;" target="_blank"><b>JAMA Psychiatry - June 2016, Vol. 73, No. 6</b></a></div>
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<b><a href="http://www.nature.com/neuro/journal/v19/n6/index.html" style="color: #6699cc; text-decoration: none;" target="_blank">Nature Neuroscience - June 2016, Vol 19, N° 6</a></b></div>
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<b><a href="http://www.nature.com/mp/journal/v21/n6/index.html" style="color: #6699cc; text-decoration: none;" target="_blank">Molecular Psychiatry - Volume 21, Issue 6, June 2016</a></b></div>
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<b style="background-color: white; color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"><a href="http://www.biologicalpsychiatryjournal.com/current" style="color: #6699cc; text-decoration: none;" target="_blank">Biological Psychiatry - Volume 79, Issue 12, June 2016</a></b><br />
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<b><a href="http://brain.oxfordjournals.org/content/139/6" style="color: #6699cc; text-decoration: none;" target="_blank">Brain - Volume 139, Issue 6, June 2016</a></b></div>
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<b><span style="font-size: small;">Join us on LinkedIn:</span> </b><b><a href="http://www.linkedin.com/groups/Neuropsychopharmacology-Neuroscience-5147601" style="color: #6699cc; text-decoration: none;">Neurosychopharmacology News Group</a></b></h3>
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Eutimiahttp://www.blogger.com/profile/07836706907685752267noreply@blogger.comtag:blogger.com,1999:blog-1045445187620004007.post-90804752337524913762016-05-01T13:51:00.003-04:002016-05-01T14:02:12.977-04:00May 2016<div dir="ltr" style="text-align: left;" trbidi="on">
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<i style="font-size: 14.85px; line-height: 20.79px;"><br /></i><i><b>The American Journal of Psychiatry</b></i></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Objective:</i></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Citalopram has been shown to improve agitation in patients with Alzheimer’s disease. The authors evaluated whether other neuropsychiatric symptoms improve with citalopram treatment compared with placebo.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Method:</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">In this planned secondary analysis of the Citalopram for Agitation in Alzheimer’s Disease study, the authors evaluated the effect of citalopram on the 12 neuropsychiatric symptom domains assessed by the Neuropsychiatric Inventory (NPI). They compared caregiver-reported NPI scores at week 9 in patients receiving citalopram (30 mg/day) or placebo with regard to both the presence or absence of individual neuropsychiatric symptoms and individual domain scores (reflecting severity) in participants who had symptoms at week 9.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Results:</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">At week 9, participants treated with citalopram were significantly less likely to be reported as showing delusions (odds ratio=0.40), anxiety (odds ratio=0.43), and irritability/lability (odds ratio=0.38). A comparison of median scores of participants with symptoms present at week 9 showed significant differences favoring citalopram for hallucinations and favoring placebo for sleep/nighttime behavior disorders.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Conclusions:</i></span></span></div>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>While dosage constraints must be considered because of citalopram’s adverse effect profile,</b> <b>this agent’s overall therapeutic effects in patients with Alzheimer’s disease and agitation, in addition to efficacy for agitation/aggression, included reductions in the frequency of irritability, anxiety, and delusions; among patients who had these symptoms at week 9, they included a reduction in the severity of hallucinations but an increase in the severity of sleep/nighttime behavior disorders.</b></span></span></span></div>
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<b>Source:</b> <a href="http://ajp.psychiatryonline.org/doi/abs/10.1176/appi.ajp.2016.15020248?journalCode=ajp" style="color: #6699cc; text-decoration: none;" target="_blank">http://ajp.psychiatryonline.org/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px; text-transform: uppercase;">A Double-Blind, Randomized, Placebo-Controlled, Dose-Frequency Study of Intravenous Ketamine in Patients With Treatment-Resistant Depression</span></span></h2>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b>The American Journal of Psychiatry</b></i></span></span></div>
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<b style="font-size: 14.85px; line-height: 20.79px;"><br /></b><b style="font-size: 14.85px; line-height: 20.79px;">Abstract</b></div>
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<i style="color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;">Objective:</i></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Ketamine, an N-methyl-d-aspartate glutamate receptor antagonist, has demonstrated a rapid-onset antidepressant effect in patients with treatment-resistant depression. This study evaluated the efficacy of twice- and thrice-weekly intravenous administration of ketamine in sustaining initial antidepressant effects in patients with treatment-resistant depression.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Method:</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">In a multicenter, double-blind study, adults (ages 18–64 years) with treatment-resistant depression were randomized to receive either intravenous ketamine (0.5 mg/kg of body weight) or intravenous placebo, administered over 40 minutes, either two or three times weekly, for up to 4 weeks. Patients who discontinued double-blind treatment after at least 2 weeks for lack of efficacy could enter an optional 2-week open-label phase to receive ketamine with the same frequency as in the double-blind phase. The primary outcome measure was change from baseline to day 15 in total score on the Montgomery-Åsberg Depression Rating Scale (MADRS).</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Results:</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">In total, 67 (45 women) of 68 randomized patients received treatment. In the twice-weekly dosing groups, the mean change in MADRS score at day 15 was −18.4 (SD=12.0) for ketamine and −5.7 (SD=10.2) for placebo; in the thrice-weekly groups, it was −17.7 (SD=7.3) for ketamine and −3.1 (SD=5.7) for placebo. Similar observations were noted for ketamine during the open-label phase (twice-weekly, −12.2 [SD=12.8] on day 4; thrice-weekly, −14.0 [SD=12.5] on day 5). Both regimens were generally well tolerated. Headache, anxiety, dissociation, nausea, and dizziness were the most common (≥20%) treatment-emergent adverse events. Dissociative symptoms occurred transiently and attenuated with repeated dosing.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Conclusions:</i></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Twice-weekly and thrice-weekly administration of ketamine at 0.5 mg/kg similarly maintained antidepressant efficacy over 15 days.</b></span></span></span><br />
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<b>Source:</b> <a href="http://ajp.psychiatryonline.org/doi/abs/10.1176/appi.ajp.2016.16010037" style="color: #6699cc; text-decoration: none;" target="_blank">http://ajp.psychiatryonline.org/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px; text-transform: uppercase;">Reduced Integrity of Right Lateralized White Matter in Patients with Primary Insomnia: A Diffusion-Tensor Imaging Study</span></span></h2>
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<i style="font-size: 14.85px; line-height: 20.79px;"><b>Radiology </b></i><br />
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<span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Purpose</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">To analyze the integrity of white matter (WM) tracts in primary insomnia patients and provide better characterization of abnormal WM integrity and its relationship with disease duration and clinical features of primary insomnia.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Materials and Methods</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">This prospective study was approved by the ethics committee of the Guangdong No. 2 Provincial People’s Hospital. Tract-based spatial statistics were used to compare changes in diffusion parameters of WM tracts from 23 primary insomnia patients and 30 healthy control (HC) participants, and the accuracy of these changes in distinguishing insomnia patients from HC participants was evaluated. Voxel-wise statistics across subjects was performed by using a 5000-permutation set with family-wise error correction (family-wise error, P < .05). Multiple regressions were used to analyze the associations between the abnormal fractional anisotropy (FA) in WM with disease duration, Pittsburgh Sleep Quality Index, insomnia severity index, self-rating anxiety scale, and the self-rating depression scale in primary insomnia. Characteristics for abnormal WM were also investigated in tract-level analyses.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Primary insomnia patients had lower FA values mainly in the right anterior limb of the internal capsule, right posterior limb of the internal capsule, right anterior corona radiata, right superior corona radiata, right superior longitudinal fasciculus, body of the corpus callosum, and right thalamus (P < .05, family-wise error correction). The receiver operating characteristic areas for the seven regions were acceptable (range, 0.60–0.74; 60%–74%). Multiple regression models showed abnormal FA values in the thalamus and body corpus callosum were associated with the disease duration, self-rating depression scale, and Pittsburgh Sleep Quality Index scores. Tract-level analysis suggested that the reduced FA values might be related to greater radial diffusivity.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Conclusion</i></span></span></div>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>This study showed that WM tracts related to regulation of sleep and wakefulness, and limbic cognitive and sensorimotor regions, are disrupted in the right brain in patients with primary insomnia. The reduced integrity of these WM tracts may be because of loss of myelination.</b></span></span></div>
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<b>Read more:</b> <a href="http://pubs.rsna.org/doi/abs/10.1148/radiol.2016152038" style="color: #6699cc; text-decoration: none;" target="_blank">http://pubs.rsna.org/</a></div>
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<span style="font-size: 14.85px; line-height: 20.79px;">Pharmacotherapy Relapse Prevention in Body Dysmorphic Disorder: A Double-Blind, Placebo-Controlled Trial</span></h2>
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<span style="font-size: 14.85px; line-height: 20.79px;"><b><i>The American Journal of Psychiatry</i></b></span></div>
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<i style="font-size: 14.85px; line-height: 20.79px;"> </i></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Objective</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Body dysmorphic disorder is common, distressing, and often severely impairing. Serotonin reuptake inhibitors appear efficacious, but the few existing pharmacotherapy studies were short term (≤4 months), and no relapse prevention studies or continuation phase studies have been conducted to the authors’ knowledge. The authors report results from the first relapse prevention study in body dysmorphic disorder.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Method</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Adults (N=100) with DSM-IV body dysmorphic disorder received open-label escitalopram for 14 weeks (phase 1); 58 responders were then randomized to double-blind continuation treatment with escitalopram versus switch to placebo for 6 months (phase 2). Reliable and valid outcome measures were utilized.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">In phase 1, 67.0% of treated subjects and 81.1% of subjects who completed phase 1 responded to escitalopram. Body dysmorphic disorder severity (in both the intent-to-treat and the completer groups) and insight, depressive symptoms, psychosocial functioning, and quality of life significantly improved from baseline to end of phase 1. In phase 2, time to relapse was significantly longer with escitalopram than with placebo treatment (hazard ratio=2.72, 95% CI=1.01–8.57). Phase 2 relapse proportions were 18% for escitalopram and 40% for placebo. Among escitalopram-treated subjects, body dysmorphic disorder severity significantly decreased over time during the continuation phase, with 35.7% of subjects showing further improvement. There were no significant group differences in body dysmorphic disorder severity or insight, depressive symptoms, psychosocial functioning, or quality of life.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Continuation-phase escitalopram delayed time to relapse, and fewer escitalopram-treated subjects relapsed than did placebo-treated subjects. Body dysmorphic disorder severity significantly improved during 6 additional months of escitalopram treatment following acute response; more than one-third of escitalopram-treated subjects experienced further improvement.</b></span></span></span></div>
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<b>Source:</b> <a href="http://ajp.psychiatryonline.org/doi/abs/10.1176/appi.ajp.2016.15091243?journalCode=ajp" style="color: #6699cc; text-decoration: none;" target="_blank">http://ajp.psychiatryonline.org/</a></div>
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Association of Androgen Deprivation Therapy With Depression in Localized Prostate Cancer </h2>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b>Journal of Clinical Oncology</b></span></i></span></span></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span><span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
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<i style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Purpose </i></div>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Androgen deprivation therapy (ADT) may contribute to depression, yet several studies have not demonstrated a link. We aimed to determine whether receipt of any ADT or longer duration of ADT for prostate cancer (PCa) is associated with an increased risk of depression.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Methods </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">We identified 78,552 men older than age 65 years with stage I to III PCa using the SEER-Medicare–linked database from 1992 to 2006, excluding patients with psychiatric diagnoses within the prior year. Our primary analysis was the association between pharmacologic ADT and the diagnosis of depression or receipt of inpatient or outpatient psychiatric treatment using Cox proportional hazards regression. Drug data for treatment of depression were not available. Our secondary analysis investigated the association between duration of ADT and each end point.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Results </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Overall, 43% of patients (n = 33,882) who received ADT, compared with patients who did not receive ADT, had higher 3-year cumulative incidences of depression (7.1% v 5.2%, respectively), inpatient psychiatric treatment (2.8% v 1.9%, respectively), and outpatient psychiatric treatment (3.4% v 2.5%, respectively; all P < .001). Adjusted Cox analyses demonstrated that patients with ADT had a 23% increased risk of depression (adjusted hazard ratio [AHR], 1.23; 95% CI, 1.15 to 1.31), 29% increased risk of inpatient psychiatric treatment (AHR, 1.29; 95% CI, 1.17 to 1.41), and a nonsignificant 7% increased risk of outpatient psychiatric treatment (AHR, 1.07; 95% CI, 0.97 to 1.17) compared with patients without ADT. The risk of depression increased with duration of ADT, from 12% with ≤ 6 months of treatment, 26% with 7 to 11 months of treatment, to 37% with ≥ 12 months of treatment (P trend < .001). A similar duration effect was seen for inpatient (P trend < .001) and outpatient psychiatric treatment (P trend < .001).</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span>
<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Conclusion </i></span></span></span></span></span><br />
<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Pharmacologic ADT increased the risk of depression and inpatient psychiatric treatment in this large study of elderly men with localized PCa. This risk increased with longer duration of ADT.</b> The possible psychiatric effects of ADT should be recognized by physicians and discussed with patients before initiating treatment.</span></span></span></span></span></div>
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<b>Source:</b> <a href="http://jco.ascopubs.org/content/early/2016/04/07/JCO.2015.64.1969.abstract" rel="nofollow" style="color: #6699cc; text-decoration: none;" target="_blank">http://jco.ascopubs.org/</a></div>
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Deep Brain Stimulation of the Ventral Anterior Limb of the Internal Capsule for Treatment-Resistant Depression</h2>
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<i><b>JAMA Psychiatry</b></i></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="color: #444444; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 13px; line-height: 18.2px;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Importance </i></span></span></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Patients with treatment-resistant depression (TRD) do not respond sufficiently to several consecutive treatments for major depressive disorder. Deep brain stimulation (DBS) is a promising treatment for these patients, but presently placebo effects cannot be ruled out.</span></span></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Objective </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">To assess the efficacy of DBS of the ventral anterior limb of the internal capsule (vALIC), controlling for placebo effects with active and sham stimulation phases.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Design, Setting, and Participants </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Twenty-five patients with TRD from 2 hospitals in the Netherlands were enrolled between March 22, 2010, and May 8, 2014. Patients first entered a 52-week open-label trial during which they received bilateral implants of 4 contact electrodes followed by optimization of DBS until a stable response was achieved. A randomized, double-blind, 12-week crossover phase was then conducted with patients receiving active treatment followed by sham or vice versa. Response and nonresponse to treatment were determined using intention-to-treat analyses.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Interventions </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Deep brain stimulation targeted to the vALIC.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Main Outcomes and Measures </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">The change in the investigator-rated score of the 17-item Hamilton Depression Rating Scale (HAM-D-17) was the main outcome used in analysis of the optimization phase. The primary outcome of the crossover phase was the difference in the HAM-D-17 scores between active and sham DBS. The score range of this tool is 0 to 52, with higher scores representing more severe symptoms. Patients were classified as responders to treatment (≥50% decrease of the HAM-D-17 score compared with baseline) and partial responders (≥25 but <50% decrease of the HAM-D-17 score).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Results </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Of 25 patients included in the study, 8 (32%) were men; the mean (SD) age at inclusion was 53.2 (8.4) years. Mean HAM-D-17 scores decreased from 22.2 (95% CI, 20.3-24.1) at baseline to 15.9 (95% CI, 12.3-19.5) (P = .001), Montgomery-Åsberg Depression Rating Scale scores from 34.0 (95% CI, 31.8-36.3) to 23.8 (95% CI, 18.4-29.1) (P < .001), and Inventory of Depressive Symptomatology–Self-report scores from from 49.3 (95% CI, 45.4-53.2) to 38.8 (95% CI, 31.6-46.0) (P = .005) in the optimization phase. Following the optimization phase, which lasted 51.6 (22.0) weeks, 10 patients (40%) were classified as responders and 15 individuals (60%) as nonresponders. Sixteen patients entered the randomized crossover phase (9 responders [56%], 7 nonresponders [44%]). During active DBS, patients scored significantly lower on the HAM-D-17 scale (13.6 [95% CI, 9.8-17.4]) than during sham DBS (23.1 [95% CI, 20.6-25.6]) (P < .001). Serious adverse events included severe nausea during surgery (1 patient), suicide attempt (4 patients), and suicidal ideation (2 patients).</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Conclusions and Relevance </i></span></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Deep brain stimulation of the vALIC resulted in a significant decrease of depressive symptoms in 10 of 25 patients and was tolerated well.</b> The randomized crossover design corroborates that vALIC DBS causes symptom reduction rather than sham.</span></span></span><br />
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<b>Source:</b> <a href="http://archpsyc.jamanetwork.com/article.aspx?articleid=2512238" style="color: #6699cc; text-decoration: none;" target="_blank">http://archpsyc.jamanetwork.com/</a></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px; text-transform: uppercase;">Mixed Depression in Bipolar Disorder: Prevalence Rate and Clinical Correlates During Naturalistic Follow-Up in the Stanley Bipolar Network</span></span></h2>
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<i style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>The American Journal of Psychiatry</b></span></i></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span><span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span><span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Objective</i></span></span></span></span></div>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">DSM-5 introduced the “with mixed features” specifier for major depressive episodes. The authors assessed the prevalence and phenomenology of mixed depression among bipolar disorder patients and qualitatively compared a range of diagnostic thresholds for mixed depression.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Method</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">In a naturalistic study, 907 adult outpatients with bipolar disorder participating in the Stanley Foundation Bipolar Network were followed longitudinally across 14,310 visits from 1995 to 2002. The Inventory of Depressive Symptomatology–Clinician-Rated Version (IDS-C) and the Young Mania Rating Scale (YMRS) were administered at each visit.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Mixed depression, defined as an IDS-C score ≥15 and a YMRS score >2 and <12 at the same visit, was observed in 2,139 visits (14.9% of total visits, and 43.5% of visits with depression) by 584 patients (64.4% of all patients). Women were significantly more likely than men to experience subthreshold hypomania during visits with depression (40.7% compared with 34.4%). Patients with one or more mixed depression visits had more symptomatic visits and fewer euthymic visits compared with those with no mixed depression visits. DSM-5-based definitions of mixed depression (ranging from narrower definitions requiring ≥3 nonoverlapping YMRS items concurrent with an IDS-C score ≥15, to broader definitions requiring ≥2 nonoverlapping YMRS items) yielded lower mixed depression prevalence rates (6.3% and 10.8% of visits, respectively) but were found to have similar relationships to gender and longitudinal symptom severity.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Conclusions</i></span></span></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Among outpatients with bipolar disorder, concurrent hypomanic symptoms observed during visits with depression were common, particularly in women. The DSM-5 diagnostic criteria for depression with mixed features may yield inadequate sensitivity to detect patients with mixed depression.</b></span></span></span></span></span></div>
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<b>Source:</b> <a href="http://ajp.psychiatryonline.org/doi/abs/10.1176/appi.ajp.2016.15091119" style="color: #6699cc; text-decoration: none;" target="_blank">http://ajp.psychiatryonline.org/</a></div>
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Association Between Anticholinergic Medication Use and Cognition, Brain Metabolism, and Brain Atrophy in Cognitively Normal Older Adults</h2>
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<i><b>JAMA Neurology</b></i></div>
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<b><br /></b><b>Abstract</b></div>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i>Importance </i> </span></div>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">The use of anticholinergic (AC) medication is linked to cognitive impairment and an increased risk of dementia. To our knowledge, this is the first study to investigate the association between AC medication use and neuroimaging biomarkers of brain metabolism and atrophy as a proxy for understanding the underlying biology of the clinical effects of AC medications.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Objective </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">To assess the association between AC medication use and cognition, glucose metabolism, and brain atrophy in cognitively normal older adults from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) and the Indiana Memory and Aging Study (IMAS).</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Design, Setting, and Participants</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">The ADNI and IMAS are longitudinal studies with cognitive, neuroimaging, and other data collected at regular intervals in clinical and academic research settings. For the participants in the ADNI, visits are repeated 3, 6, and 12 months after the baseline visit and then annually. For the participants in the IMAS, visits are repeated every 18 months after the baseline visit (402 cognitively normal older adults in the ADNI and 49 cognitively normal older adults in the IMAS were included in the present analysis). Participants were either taking (hereafter referred to as the AC+ participants [52 from the ADNI and 8 from the IMAS]) or not taking (hereafter referred to as the AC− participants [350 from the ADNI and 41 from the IMAS]) at least 1 medication with medium or high AC activity. Data analysis for this study was performed in November 2015.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Main Outcomes and Measures </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Cognitive scores, mean fludeoxyglucose F 18 standardized uptake value ratio (participants from the ADNI only), and brain atrophy measures from structural magnetic resonance imaging were compared between AC+ participants and AC− participants after adjusting for potential confounders. The total AC burden score was calculated and was related to target measures. The association of AC use and longitudinal clinical decline (mean [SD] follow-up period, 32.1 [24.7] months [range, 6-108 months]) was examined using Cox regression.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Results</i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">The 52 AC+ participants (mean [SD] age, 73.3 [6.6] years) from the ADNI showed lower mean scores on Weschler Memory Scale–Revised Logical Memory Immediate Recall (raw mean scores: 13.27 for AC+ participants and 14.16 for AC− participants; P = .04) and the Trail Making Test Part B (raw mean scores: 97.85 seconds for AC+ participants and 82.61 seconds for AC− participants; P = .04) and a lower executive function composite score (raw mean scores: 0.58 for AC+ participants and 0.78 for AC− participants; P = .04) than the 350 AC− participants (mean [SD] age, 73.3 [5.8] years) from the ADNI. Reduced total cortical volume and temporal lobe cortical thickness and greater lateral ventricle and inferior lateral ventricle volumes were seen in the AC+ participants relative to the AC− participants.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Conclusions and Relevance</i> </span></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;">The use of AC medication was associated with increased brain atrophy and dysfunction and clinical decline. Thus, use of AC medication among older adults should likely be discouraged if alternative therapies are available.</span></span></span><br />
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<b style="font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://archneur.jamanetwork.com/article.aspx?articleid=2514553" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration: none;" target="_blank">http://archneur.jamanetwork.com/</a></div>
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<span style="color: #333333; font-family: "arial" , sans-serif;"><span style="font-size: 18px; line-height: 22px; text-transform: uppercase;">Diagnostic and Prognostic Utility of the Synaptic Marker Neurogranin in Alzheimer Disease</span></span></h2>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><b><br /></b></i></span></span><span style="color: #333333; font-size: 14.85px; font-style: italic; font-weight: bold; line-height: 20.79px;">JAMA Neurology</span><br />
<span style="color: #333333; font-size: 14.85px; font-style: italic; font-weight: bold; line-height: 20.79px;"><br /></span><span style="color: #333333; font-size: 14.85px; font-weight: bold; line-height: 20.79px;">Abstract</span></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span></div>
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Importance </i></span></span></div>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Synaptic loss is an early pathologic substrate of Alzheimer disease (AD). Neurogranin is a postsynaptic neuronal protein that has demonstrated utility as a cerebrospinal fluid (CSF) marker of synaptic loss in AD.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Objective </i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">To investigate the diagnostic and prognostic utility of CSF neurogranin levels in a large, well-characterized cohort of individuals with symptomatic AD and cognitively normal controls.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Design, Setting, and Participants </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">A cross-sectional and longitudinal observational study of cognitive decline in patients with symptomatic AD and cognitively normal controls was performed. Participants were individuals with a clinical diagnosis of early symptomatic AD and cognitively normal controls who were enrolled in longitudinal studies of aging and dementia at the Charles F. and Joanne Knight Alzheimer Disease Research Center, Washington University School of Medicine, from January 21, 2000, through March 21, 2011. Data analysis was performed from November 1, 2013, to March 31, 2015.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Main Outcomes and Measures </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Correlations between baseline CSF biomarker levels and future cognitive decline in patients with symptomatic AD and cognitively normal controls over time.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><br /></span></span>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Results </i> </span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">A total of 302 individuals (mean [SE] age, 73.1 [0.4] years) were included in this study (95 patients [52 women and 43 men] with AD and 207 controls [125 women and 82 men]). The CSF neurogranin levels differentiated patients with early symptomatic AD from controls with comparable diagnostic utility (mean [SE] area under the receiver operating characteristic curve, 0.71 [0.03]; 95% CI, 0.64-0.77) to the other CSF biomarkers. The CSF neurogranin levels correlated with brain atrophy (normalized whole-brain volumes: adjusted r = −0.38, P = .02; hippocampal volumes: adjusted r = −0.36, P = .03; entorhinal volumes: adjusted r = −0.46, P = .006; and parahippocampal volumes: adjusted r = −0.47, P = .005, n = 38) in AD and with amyloid load (r = 0.39, P = .02, n = 36) in preclinical AD. The CSF neurogranin levels predicted future cognitive impairment (adjusted hazard ratio, 1.89; 95% CI, 1.29-2.78; P = .001 as a continuous measure, and adjusted hazard ratio, 2.78; 95% CI, 1.13-5.99; P = .02 as a categorical measure using the 85th percentile cutoff value) in controls and rates of cognitive decline (Clinical Dementia Rating sum of boxes score: β estimate, 0.29; P = .001; global composite scores: β estimate, −0.11; P = .001; episodic memory scores: β estimate, −0.18; P < .001; and semantic memory scores: β estimate, −0.06; P = .04, n = 57) in patients with symptomatic AD over time, similarly to the CSF proteins VILIP-1, tau, and p-tau181.</span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i><br /></i></span></span>
<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="color: #444444;"><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Conclusions and Relevance </i> </span></span></span></span></span></span><br />
<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="color: #444444;"><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>The CSF levels of the synaptic marker neurogranin offer diagnostic and prognostic utility for early symptomatic AD that is comparable to other CSF markers of AD. Importantly, CSF neurogranin complements the collective ability of these markers to predict future cognitive decline in cognitively normal individuals and, therefore, will be a useful addition to the current panel of AD biomarkers.</b></span></span></span></span></span></span></div>
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://archneur.jamanetwork.com/article.aspx?articleid=2506518" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration: none;" target="_blank">http://archneur.jamanetwork.com/</a></div>
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<span style="color: #333333;"><span style="font-size: 14.85px; line-height: 20.79px; text-transform: uppercase;">Adjunctive Nutraceuticals for Depression: A Systematic Review and Meta-Analyses</span></span></h2>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b>The American Journal of Psychiatry</b></span></i></span></div>
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<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><i><span style="font-size: 14.85px; line-height: 20.79px;"><b><br /></b></span></i></span><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><b>Abstract</b></span></span><br />
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<i><span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Objective</span></span></i></div>
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">There is burgeoning interest in augmentation strategies for improving inadequate response to antidepressants. The adjunctive use of standardized pharmaceutical-grade nutrients, known as nutraceuticals, has the potential to modulate several neurochemical pathways implicated in depression. While many studies have been conducted in this area, to date no specialized systematic review (or meta-analysis) has been conducted.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Method</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">A systematic search of PubMed, CINAHL, Cochrane Library, and Web of Science was conducted up to December 2015 for clinical trials using adjunctive nutrients for depression. Where sufficient data were available, a random-effects model analyzed the standard mean difference between treatment and placebo in the change from baseline to endpoint, combining the effect size data. Funnel plot and heterogeneity analyses were also performed.</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Results</i></span></span><br />
<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;">Primarily positive results were found for replicated studies testing S-adenosylmethionine (SAMe), methylfolate, omega-3 (primarily EPA or ethyl-EPA), and vitamin D, with positive isolated studies for creatine, folinic acid, and an amino acid combination. Mixed results were found for zinc, folic acid, vitamin C, and tryptophan, with nonsignificant results for inositol. No major adverse effects were noted in the studies (aside from minor digestive disturbance). A meta-analysis of adjunctive omega-3 versus placebo revealed a significant and moderate to strong effect in favor of omega-3. Conversely, a meta-analysis of folic acid revealed a nonsignificant difference from placebo. Marked study heterogeneity was found in a Higgins test for both omega-3 and folic acid studies; funnel plots also revealed asymmetry (reflecting potential study bias).</span></span><br />
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<span style="color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><i>Conclusions</i></span></span><br />
<span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="color: #444444;"><span style="font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif;"><span style="font-size: 14.85px; line-height: 20.79px;"><span style="font-size: 14.85px; line-height: 20.79px;">Current evidence supports adjunctive use of SAMe, methylfolate, omega-3, and vitamin D with antidepressants to reduce depressive symptoms.</span></span></span></span></span></span><br />
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<b style="color: #333333; font-size: 14.85px; line-height: 20.79px;">Source:</b><span style="color: #333333; font-size: 14.85px; line-height: 20.79px;"> </span><a href="http://ajp.psychiatryonline.org/doi/abs/10.1176/appi.ajp.2016.15091228?journalCode=ajp" style="color: #6699cc; font-size: 14.85px; line-height: 20.79px; text-decoration: none;" target="_blank">http://ajp.psychiatryonline.org/</a></div>
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<b style="color: blue; font-size: x-large;"><br /></b><b style="color: blue; font-size: x-large;">Online Journals:</b></div>
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<b><a href="http://journals.lww.com/psychopharmacology/pages/currenttoc.aspx" style="color: #6699cc; text-decoration: none;" target="_blank">Journal of Clinical Psychopharmacology - June 2016 - Volume 36, Issue 3</a></b></div>
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<b><a href="http://www.nature.com/npp/journal/v41/n6/index.html" style="color: #6699cc; text-decoration: none;" target="_blank">Neuropsychopharmacology - Volume 41, Issue 6 (May 2016)</a></b></div>
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<b><a href="http://link.springer.com/journal/213/233/10/page/1" style="color: #6699cc; text-decoration: none;" target="_blank">Psychopharmacology - Volume 233, Issue 10, May 2016</a></b></div>
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<b><a href="http://jop.sagepub.com/content/current" style="color: #6699cc; text-decoration: none;" target="_blank">Journal of Psychopharmacology - May 2016; 30 (5)</a></b></div>
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<b><a href="http://ajp.psychiatryonline.org/toc/ajp/current" style="color: #6699cc; text-decoration: none;" target="_blank">The American Journal of Psychiatry - April 2016, Vol. 173, Issue 4</a></b></div>
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<a href="http://archpsyc.jamanetwork.com/issue.aspx" style="color: #6699cc; text-decoration: none;" target="_blank"><b>JAMA Psychiatry - March 2016, Vol. 73, No. 4</b></a></div>
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<b><a href="http://www.nature.com/neuro/journal/v19/n5/index.html" style="color: #6699cc; text-decoration: none;" target="_blank">Nature Neuroscience - May 2016, Vol 19, N° 5</a></b></div>
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<b><a href="http://www.nature.com/mp/journal/v21/n5/index.html" style="color: #6699cc; text-decoration: none;" target="_blank">Molecular Psychiatry - Volume 21, Issue 5, May 2016</a></b></div>
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<b style="background-color: white; color: #333333; font-family: arial, tahoma, helvetica, freesans, sans-serif; font-size: 14.85px; line-height: 20.79px;"><a href="http://www.biologicalpsychiatryjournal.com/current" style="color: #6699cc; text-decoration: none;" target="_blank">Biological Psychiatry - Volume 79, Issue 10, May 2016</a></b><br />
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<b><a href="http://brain.oxfordjournals.org/content/139/5" style="color: #6699cc; text-decoration: none;" target="_blank">Brain - Volume 139, Issue 5, May 2016</a></b></div>
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Eutimiahttp://www.blogger.com/profile/07836706907685752267noreply@blogger.com