The Journal of Physical Chemistry 最新文献

{"title":"Prenatal and Perinatal Risk Factors and the Promise of Birth Cohort Studies: Origins of Obsessive-Compulsive Disorder.","authors":"Thomas V Fernandez, James F Leckman","doi":"10.1001/jamapsychiatry.2016.2092","DOIUrl":"10.1001/jamapsychiatry.2016.2092","url":null,"abstract":"","PeriodicalId":58,"journal":{"name":"The Journal of Physical Chemistry ","volume":"67 12","pages":"1117-1118"},"PeriodicalIF":25.8,"publicationDate":"2016-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5180419/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50623988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Are There Still Too Few Suicides to Generate Public Outrage?","authors":"Megan C Lytle, Vincent M B Silenzio, Eric D Caine","doi":"10.1001/jamapsychiatry.2016.1736","DOIUrl":"10.1001/jamapsychiatry.2016.1736","url":null,"abstract":"","PeriodicalId":58,"journal":{"name":"The Journal of Physical Chemistry ","volume":"70 6","pages":"1003-1004"},"PeriodicalIF":25.8,"publicationDate":"2016-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5082695/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50623912","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evidence for Genetic Overlap Between Schizophrenia and Age at First Birth in Women.","authors":"Divya Mehta, Felix C Tropf, Jacob Gratten, Andrew Bakshi, Zhihong Zhu, Silviu-Alin Bacanu, Gibran Hemani, Patrik K E Magnusson, Nicola Barban, Tõnu Esko, Andres Metspalu, Harold Snieder, Bryan J Mowry, Kenneth S Kendler, Jian Yang, Peter M Visscher, John J McGrath, Melinda C Mills, Naomi R Wray, S Hong Lee, Ole A Andreassen, Elvira Bramon, Richard Bruggeman, Joseph D Buxbaum, Murray J Cairns, Rita M Cantor, C Robert Cloninger, David Cohen, Benedicto Crespo-Facorro, Ariel Darvasi, Lynn E DeLisi, Timothy Dinan, Srdjan Djurovic, Gary Donohoe, Elodie Drapeau, Valentina Escott-Price, Nelson B Freimer, Lyudmila Georgieva, Lieuwe de Haan, Frans A Henskens, Inge Joa, Antonio Julià, Andrey Khrunin, Bernard Lerer, Svetlana Limborska, Carmel M Loughland, Milan Macek, Patrik K E Magnusson, Sara Marsal, Robert W McCarley, Andrew M McIntosh, Andrew McQuillin, Bela Melegh, Patricia T Michie, Derek W Morris, Kieran C Murphy, Inez Myin-Germeys, Ann Olincy, Jim Van Os, Christos Pantelis, Danielle Posthuma, Digby Quested, Ulrich Schall, Rodney J Scott, Larry J Seidman, Draga Toncheva, Paul A Tooney, John Waddington, Daniel R Weinberger, Mark Weiser, Jing Qin Wu","doi":"10.1001/jamapsychiatry.2016.0129","DOIUrl":"10.1001/jamapsychiatry.2016.0129","url":null,"abstract":"<p><strong>Importance: </strong>A recently published study of national data by McGrath et al in 2014 showed increased risk of schizophrenia (SCZ) in offspring associated with both early and delayed parental age, consistent with a U-shaped relationship. However, it remains unclear if the risk to the child is due to psychosocial factors associated with parental age or if those at higher risk for SCZ tend to have children at an earlier or later age.</p><p><strong>Objective: </strong>To determine if there is a genetic association between SCZ and age at first birth (AFB) using genetically informative but independently ascertained data sets.</p><p><strong>Design, setting, and participants: </strong>This investigation used multiple independent genome-wide association study data sets. The SCZ sample comprised 18 957 SCZ cases and 22 673 controls in a genome-wide association study from the second phase of the Psychiatric Genomics Consortium, and the AFB sample comprised 12 247 genotyped women measured for AFB from the following 4 community cohorts: Estonia (Estonian Genome Center Biobank, University of Tartu), the Netherlands (LifeLines Cohort Study), Sweden (Swedish Twin Registry), and the United Kingdom (TwinsUK). Schizophrenia genetic risk for each woman in the AFB community sample was estimated using genetic effects inferred from the SCZ genome-wide association study.</p><p><strong>Main outcomes and measures: </strong>We tested if SCZ genetic risk was a significant predictor of response variables based on published polynomial functions that described the relationship between maternal age and SCZ risk in offspring in Denmark. We substituted AFB for maternal age in these functions, one of which was corrected for the age of the father, and found that the fit was superior for the model without adjustment for the father's age.</p><p><strong>Results: </strong>We observed a U-shaped relationship between SCZ risk and AFB in the community cohorts, consistent with the previously reported relationship between SCZ risk in offspring and maternal age when not adjusted for the age of the father. We confirmed that SCZ risk profile scores significantly predicted the response variables (coefficient of determination R2 = 1.1E-03, P = 4.1E-04), reflecting the published relationship between maternal age and SCZ risk in offspring by McGrath et al in 2014.</p><p><strong>Conclusions and relevance: </strong>This study provides evidence for a significant overlap between genetic factors associated with risk of SCZ and genetic factors associated with AFB. It has been reported that SCZ risk associated with increased maternal age is explained by the age of the father and that de novo mutations that occur more frequently in the germline of older men are the underlying causal mechanism. This explanation may need to be revised if, as suggested herein and if replicated in future studies, there is also increased genetic risk of SCZ in older mothers.</p>","PeriodicalId":58,"journal":{"name":"The Journal of Physical Chemistry ","volume":"76 21","pages":"497-505"},"PeriodicalIF":25.8,"publicationDate":"2016-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5785705/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50623443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Structural Brain Abnormalities in Youth With Psychosis Spectrum Symptoms.","authors":"Theodore D Satterthwaite, Daniel H Wolf, Monica E Calkins, Simon N Vandekar, Guray Erus, Kosha Ruparel, David R Roalf, Kristin A Linn, Mark A Elliott, Tyler M Moore, Hakon Hakonarson, Russell T Shinohara, Christos Davatzikos, Ruben C Gur, Raquel E Gur","doi":"10.1001/jamapsychiatry.2015.3463","DOIUrl":"10.1001/jamapsychiatry.2015.3463","url":null,"abstract":"<p><strong>Importance: </strong>Structural brain abnormalities are prominent in psychotic disorders, including schizophrenia. However, it is unclear when aberrations emerge in the disease process and if such deficits are present in association with less severe psychosis spectrum (PS) symptoms in youth.</p><p><strong>Objective: </strong>To investigate the presence of structural brain abnormalities in youth with PS symptoms.</p><p><strong>Design, setting, and participants: </strong>The Philadelphia Neurodevelopmental Cohort is a prospectively accrued, community-based sample of 9498 youth who received a structured psychiatric evaluation. A subsample of 1601 individuals underwent neuroimaging, including structural magnetic resonance imaging, at an academic and children's hospital health care network between November 1, 2009, and November 30, 2011.</p><p><strong>Main outcomes and measures: </strong>Measures of brain volume derived from T1-weighted structural neuroimaging at 3 T. Analyses were conducted at global, regional, and voxelwise levels. Regional volumes were estimated with an advanced multiatlas regional segmentation procedure, and voxelwise volumetric analyses were conducted as well. Nonlinear developmental patterns were examined using penalized splines within a general additive model. Psychosis spectrum (PS) symptom severity was summarized using factor analysis and evaluated dimensionally.</p><p><strong>Results: </strong>Following exclusions due to comorbidity and image quality assurance, the final sample included 791 participants aged youth 8 to 22 years. Fifty percent (n = 393) were female. After structured interviews, 391 participants were identified as having PS features (PS group) and 400 participants were identified as typically developing comparison individuals without significant psychopathology (TD group). Compared with the TD group, the PS group had diminished whole-brain gray matter volume (P = 1.8 × 10-10) and expanded white matter volume (P = 2.8 × 10-11). Voxelwise analyses revealed significantly lower gray matter volume in the medial temporal lobe (maximum z score = 5.2 and cluster size of 1225 for the right and maximum z score = 4.5 and cluster size of 310 for the left) as well as in frontal, temporal, and parietal cortex. Volumetric reduction in the medial temporal lobe was correlated with PS symptom severity.</p><p><strong>Conclusions and relevance: </strong>Structural brain abnormalities that have been commonly reported in adults with psychosis are present early in life in youth with PS symptoms and are not due to medication effects. Future longitudinal studies could use the presence of such abnormalities in conjunction with clinical presentation, cognitive profile, and genomics to predict risk and aid in stratification to guide early interventions.</p>","PeriodicalId":58,"journal":{"name":"The Journal of Physical Chemistry ","volume":"79 10","pages":"515-24"},"PeriodicalIF":22.5,"publicationDate":"2016-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5048443/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50623801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genome-wide Association Study of Cannabis Dependence Severity, Novel Risk Variants, and Shared Genetic Risks.","authors":"Richard Sherva, Qian Wang, Henry Kranzler, Hongyu Zhao, Ryan Koesterer, Aryeh Herman, Lindsay A Farrer, Joel Gelernter","doi":"10.1001/jamapsychiatry.2016.0036","DOIUrl":"10.1001/jamapsychiatry.2016.0036","url":null,"abstract":"<p><strong>Importance: </strong>Cannabis dependence (CAD) is a serious problem worldwide and is of growing importance in the United States because cannabis is increasingly available legally. Although genetic factors contribute substantially to CAD risk, at present no well-established specific genetic risk factors for CAD have been elucidated.</p><p><strong>Objective: </strong>To report findings for DSM-IV CAD criteria from association analyses performed in large cohorts of African American and European American participants from 3 studies of substance use disorder genetics.</p><p><strong>Design, setting, and participants: </strong>This genome-wide association study for DSM-IV CAD criterion count was performed in 3 independent substance dependence cohorts (the Yale-Penn Study, Study of Addiction: Genetics and Environment [SAGE], and International Consortium on the Genetics of Heroin Dependence [ICGHD]). A referral sample and volunteers recruited in the community and from substance abuse treatment centers included 6000 African American and 8754 European American participants, including some from small families. Participants from the Yale-Penn Study were recruited from 2000 to 2013. Data were collected for the SAGE trial from 1990 to 2007 and for the ICGHD from 2004 to 2009. Data were analyzed from January 2, 2013, to November 9, 2015.</p><p><strong>Main outcomes and measures: </strong>Criterion count for DSM-IV CAD.</p><p><strong>Results: </strong>Among the 14 754 participants, 7879 were male, 6875 were female, and the mean (SD) age was 39.2 (10.2) years. Three independent regions with genome-wide significant single-nucleotide polymorphism associations were identified, considering the largest possible sample. These included rs143244591 (β = 0.54, P = 4.32 × 10-10 for the meta-analysis) in novel antisense transcript RP11-206M11.7;rs146091982 (β = 0.54, P = 1.33 × 10-9 for the meta-analysis) in the solute carrier family 35 member G1 gene (SLC35G1); and rs77378271 (β = 0.29, P = 2.13 × 10-8 for the meta-analysis) in the CUB and Sushi multiple domains 1 gene (CSMD1). Also noted was evidence of genome-level pleiotropy between CAD and major depressive disorder and for an association with single-nucleotide polymorphisms in genes associated with schizophrenia risk. Several of the genes identified have functions related to neuronal calcium homeostasis or central nervous system development.</p><p><strong>Conclusions and relevance: </strong>These results are the first, to our knowledge, to identify specific CAD risk alleles and potential genetic factors contributing to the comorbidity of CAD with major depression and schizophrenia.</p>","PeriodicalId":58,"journal":{"name":"The Journal of Physical Chemistry ","volume":"78 18","pages":"472-80"},"PeriodicalIF":25.8,"publicationDate":"2016-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4974817/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50623834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Analyzing the Role of MicroRNAs in Schizophrenia in the Context of Common Genetic Risk Variants.","authors":"Mads Engel Hauberg, Panos Roussos, Jakob Grove, Anders Dupont Børglum, Manuel Mattheisen","doi":"10.1001/jamapsychiatry.2015.3018","DOIUrl":"10.1001/jamapsychiatry.2015.3018","url":null,"abstract":"<p><strong>Importance: </strong>The recent implication of 108 genomic loci in schizophrenia marked a great advancement in our understanding of the disease. Against the background of its polygenic nature there is a necessity to identify how schizophrenia risk genes interplay. As regulators of gene expression, microRNAs (miRNAs) have repeatedly been implicated in schizophrenia etiology. It is therefore of interest to establish their role in the regulation of schizophrenia risk genes in disease-relevant biological processes.</p><p><strong>Objective: </strong>To examine the role of miRNAs in schizophrenia in the context of disease-associated genetic variation.</p><p><strong>Design, setting, and participants: </strong>The basis of this study was summary statistics from the largest schizophrenia genome-wide association study meta-analysis to date (83 550 individuals in a meta-analysis of 52 genome-wide association studies) completed in 2014 along with publicly available data for predicted miRNA targets. We examined whether schizophrenia risk genes were more likely to be regulated by miRNA. Further, we used gene set analyses to identify miRNAs that are regulators of schizophrenia risk genes.</p><p><strong>Main outcomes and measures: </strong>Results from association tests for miRNA targetomes and related analyses.</p><p><strong>Results: </strong>In line with previous studies, we found that similar to other complex traits, schizophrenia risk genes were more likely to be regulated by miRNAs (P < 2 × 10-16). Further, the gene set analyses revealed several miRNAs regulating schizophrenia risk genes, with the strongest enrichment for targets of miR-9-5p (P = .0056 for enrichment among the top 1% most-associated single-nucleotide polymorphisms, corrected for multiple testing). It is further of note that MIR9-2 is located in a genomic region showing strong evidence for association with schizophrenia (P = 7.1 × 10-8). The second and third strongest gene set signals were seen for the targets of miR-485-5p and miR-137, respectively.</p><p><strong>Conclusions and relevance: </strong>This study provides evidence for a role of miR-9-5p in the etiology of schizophrenia. Its implication is of particular interest as the functions of this neurodevelopmental miRNA tie in with established disease biology: it has a regulatory loop with the fragile X mental retardation homologue FXR1 and regulates dopamine D2 receptor density.</p>","PeriodicalId":58,"journal":{"name":"The Journal of Physical Chemistry ","volume":"85 19","pages":"369-77"},"PeriodicalIF":25.8,"publicationDate":"2016-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1001/jamapsychiatry.2015.3018","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50623410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Cross-Disorder Method to Identify Novel Candidate Genes for Developmental Brain Disorders.","authors":"Andrea J Gonzalez-Mantilla, Andres Moreno-De-Luca, David H Ledbetter, Christa Lese Martin","doi":"10.1001/jamapsychiatry.2015.2692","DOIUrl":"10.1001/jamapsychiatry.2015.2692","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Importance: &lt;/strong&gt;Developmental brain disorders are a group of clinically and genetically heterogeneous disorders characterized by high heritability. Specific highly penetrant genetic causes can often be shared by a subset of individuals with different phenotypic features, and recent advances in genome sequencing have allowed the rapid and cost-effective identification of many of these pathogenic variants.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Objectives: &lt;/strong&gt;To identify novel candidate genes for developmental brain disorders and provide additional evidence of previously implicated genes.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Data sources: &lt;/strong&gt;The PubMed database was searched for studies published from March 28, 2003, through May 7, 2015, with large cohorts of individuals with developmental brain disorders.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Data extraction and synthesis: &lt;/strong&gt;A tiered, multilevel data-integration approach was used, which intersects (1) whole-genome data from structural and sequence pathogenic loss-of-function (pLOF) variants, (2) phenotype data from 6 apparently distinct disorders (intellectual disability, autism, attention-deficit/hyperactivity disorder, schizophrenia, bipolar disorder, and epilepsy), and (3) additional data from large-scale studies, smaller cohorts, and case reports focusing on specific candidate genes. All candidate genes were ranked into 4 tiers based on the strength of evidence as follows: tier 1, genes with 3 or more de novo pathogenic loss-of-function variants; tier 2, genes with 2 de novo pathogenic loss-of-function variants; tier 3, genes with 1 de novo pathogenic loss-of-function variant; and tier 4, genes with only inherited (or unknown inheritance) pathogenic loss-of-function variants.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Main outcomes and measures: &lt;/strong&gt;Development of a comprehensive knowledge base of candidate genes related to developmental brain disorders. Genes were prioritized based on the inheritance pattern and total number of pathogenic loss-of-function variants identified amongst unrelated individuals with any one of six developmental brain disorders.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Study selection: &lt;/strong&gt;A combination of phenotype-based and genotype-based literature review yielded 384 studies that used whole-genome or exome sequencing, chromosomal microarray analysis, and/or targeted sequencing to evaluate 1960 individuals with developmental brain disorders.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Our initial phenotype-based literature review yielded 1911 individuals with pLOF variants involving 1034 genes from 118 studies. Filtering our results to genes with 2 or more pLOF variants identified in at least 2 unrelated individuals resulted in 241 genes from 1110 individuals. Of the 241 genes involved in brain disorders, 7 were novel high-confidence genes and 10 were novel putative candidate genes. Fifty-nine genes were ranked in tier 1, 44 in tier 2, 68 in tier 3, and 70 in tier 4. By transcending clinical diagnostic boundaries, the evidence level for 18 additional genes th","PeriodicalId":58,"journal":{"name":"The Journal of Physical Chemistry ","volume":"92 7","pages":"275-83"},"PeriodicalIF":25.8,"publicationDate":"2016-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5333489/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50623541","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early Intervention for Psychotic Disorders: Building Population Health Systems.","authors":"Vinod H Srihari, Anant Jani, Muir Gray","doi":"10.1001/jamapsychiatry.2015.2821","DOIUrl":"10.1001/jamapsychiatry.2015.2821","url":null,"abstract":"","PeriodicalId":58,"journal":{"name":"The Journal of Physical Chemistry ","volume":"89 23","pages":"101-2"},"PeriodicalIF":25.8,"publicationDate":"2016-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50623717","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Importance of Assessing Neural Trajectories in Pediatric Depression.","authors":"Ian H Gotlib, Sarah J Ordaz","doi":"10.1001/jamapsychiatry.2015.2453","DOIUrl":"10.1001/jamapsychiatry.2015.2453","url":null,"abstract":"","PeriodicalId":58,"journal":{"name":"The Journal of Physical Chemistry ","volume":"95 15","pages":"9-10"},"PeriodicalIF":25.8,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5522740/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50623208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epidemiology of DSM-5 Drug Use Disorder: Results From the National Epidemiologic Survey on Alcohol and Related Conditions-III.","authors":"Bridget F Grant, Tulshi D Saha, W June Ruan, Risë B Goldstein, S Patricia Chou, Jeesun Jung, Haitao Zhang, Sharon M Smith, Roger P Pickering, Boji Huang, Deborah S Hasin","doi":"10.1001/jamapsychiatry.2015.2132","DOIUrl":"10.1001/jamapsychiatry.2015.2132","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Importance: &lt;/strong&gt;Current information on the prevalence and sociodemographic and clinical profiles of individuals in the general population with DSM-5 drug use disorder (DUD) is limited. Given the present societal and economic context in the United States and the new diagnostic system, up-to-date national information is needed from a single uniform data source.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Objective: &lt;/strong&gt;To present nationally representative findings on the prevalence, correlates, psychiatric comorbidity, disability, and treatment of DSM-5 DUD diagnoses overall and by severity level.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Design, setting, and participants: &lt;/strong&gt;In-person interviews were conducted with 36,309 adults in the 2012-2013 National Epidemiologic Survey on Alcohol and Related Conditions-III, a cross-sectional representative survey of the United States. The household response rate was 72%; person-level response rate, 84%; and overall response rate, 60.1%. Data were collected April 2012 through June 2013 and analyzed from February through March 2015.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Main outcomes and measures: &lt;/strong&gt;Twelve-month and lifetime DUD, based on amphetamine, cannabis, club drug, cocaine, hallucinogen, heroin, nonheroin opioid, sedative/tranquilizer, and/or solvent/inhalant use disorders.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Prevalences of 12-month and lifetime DUD were 3.9% and 9.9%, respectively. Drug use disorder was generally greater among men, white and Native American individuals, younger and previously or never married adults, those with lower education and income, and those residing in the West. Significant associations were found between 12-month and lifetime DUD and other substance use disorders. Significant associations were also found between any 12-month DUD and major depressive disorder (odds ratio [OR], 1.3; 95% CI, 1.09-1.64), dysthymia (OR, 1.5; 95% CI, 1.09-2.02), bipolar I (OR, 1.5; 95% CI, 1.06-2.05), posttraumatic stress disorder (OR, 1.6; 95% CI, 1.27-2.10), and antisocial (OR, 1.4; 95% CI, 1.11-1.75), borderline (OR, 1.8; 95% CI, 1.41-2.24), and schizotypal (OR, 1.5; 95% CI, 1.18-1.87) personality disorders. Similar associations were found for any lifetime DUD with the exception that lifetime DUD was also associated with generalized anxiety disorder (OR, 1.3; 95% CI, 1.06-1.49), panic disorder (OR, 1.3; 95% CI, 1.06-1.59), and social phobia (OR, 1.3; 95% CI, 1.09-1.64). Twelve-month DUD was associated with significant disability, increasing with DUD severity. Among respondents with 12-month and lifetime DUD, only 13.5% and 24.6% received treatment, respectively.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions and relevance: &lt;/strong&gt;DSM-5 DUD is a common, highly comorbid, and disabling disorder that largely goes untreated in the United States. These findings indicate the need for additional studies to understand the broad relationships in more detail; estimate present-day economic costs of DUDs; investigate hypotheses regarding etiology, chronicity, and treatment use; ","PeriodicalId":58,"journal":{"name":"The Journal of Physical Chemistry ","volume":"98 24","pages":"39-47"},"PeriodicalIF":25.8,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5062605/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50622920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}