William E. Copeland

Bio: William E. Copeland is an academic researcher from University of Vermont. The author has contributed to research in topics: Population & Young adult. The author has an hindex of 48, co-authored 141 publications receiving 11251 citations. Previous affiliations of William E. Copeland include Durham University & University of Vermont Medical Center.

Traumatic events and posttraumatic stress in childhood

Abstract: Results: More than two thirds of children reported at least 1 traumatic event by 16 years of age, with 13.4% of thosechildrendevelopingsomePTSsymptoms.FewPTS symptoms or psychiatric disorders were observed for individuals experiencing their first event, and any effects were short-lived. Less than 0.5% of children met the criteria for full-blown DSM-IV PTSD. Violent or sexual trauma were associated with the highest rates of symptoms.ThePTSsymptomswerepredictedbypreviousexposure to multiple traumas, anxiety disorders, and familyadversity.Lifetimeco-occurrenceofotherpsychiatric disorders with traumatic events and PTS symptoms was high, with the highest rates for anxiety and depressive disorders. Conclusions:In the general population of children, potentially traumatic events are fairly common and do not oftenresultinPTSsymptoms,exceptaftermultipletraumas or a history of anxiety. The prognosis after the first lifetime trauma exposure was generally favorable. Apart from PTSD, traumatic events are related to many forms of psychopathology, with the strongest links being with anxiety and depressive disorders. Arch Gen Psychiatry. 2007;64:577-584

Adult psychiatric outcomes of bullying and being bullied by peers in childhood and adolescence.

Abstract: Importance Both bullies and victims of bullying are at risk for psychiatric problems in childhood, but it is unclear if this elevated risk extends into early adulthood. Objective To test whether bullying and/or being bullied in childhood predicts psychiatric problems and suicidality in young adulthood after accounting for childhood psychiatric problems and family hardships. Design Prospective, population-based study. Setting Community sample from 11 counties in Western North Carolina. Participants A total of 1420 participants who had being bullied and bullying assessed 4 to 6 times between the ages of 9 and 16 years. Participants were categorized as bullies only, victims only, bullies and victims (hereafter referred to as bullies/victims), or neither. Main Outcome Measure Psychiatric outcomes, which included depression, anxiety, antisocial personality disorder, substance use disorders, and suicidality (including recurrent thoughts of death, suicidal ideation, or a suicide attempt), were assessed in young adulthood (19, 21, and 24-26 years) by use of structured diagnostic interviews. Results Victims and bullies/victims had elevated rates of young adult psychiatric disorders, but also elevated rates of childhood psychiatric disorders and family hardships. After controlling for childhood psychiatric problems or family hardships, we found that victims continued to have a higher prevalence of agoraphobia (odds ratio [OR], 4.6 [95% CI, 1.7-12.5]; P Conclusions and Relevance The effects of being bullied are direct, pleiotropic, and long-lasting, with the worst effects for those who are both victims and bullies.

Childhood and adolescent psychiatric disorders as predictors of young adult disorders.

Abstract: Context Most adults with a psychiatric disorder first met diagnostic criteria during childhood and/or adolescence, yet specific homotypic and heterotypic patterns of prediction have not been firmly established. Objective To establish which childhood and adolescent psychiatric disorders predict particular young adult disorders when accounting for comorbidities, disaggregating similar disorders, and examining childhood and adolescent predictors separately. Design Eleven waves of data from the prospective population-based Great Smoky Mountains Study (N = 1420) were used. Setting The Great Smoky Mountains Study is a longitudinal study of the development of psychiatric disorder and need for mental health services in rural and urban youth. A representative sample of children was recruited from 11 counties in western North Carolina. Participants Children in the community aged 9 to 16, 19, and 21 years. Main Outcome Measures Common psychiatric disorders were assessed in childhood (ages 9-12 years) and adolescence (ages 13-16 years) with the Child and Adolescent Psychiatric Assessment and in young adulthood (ages 19 and 21 years) with the Young Adult Psychiatric Assessment. Results Adolescent depression significantly predicted young adult depression in the bivariate analysis, but this effect was entirely accounted for by comorbidity of adolescent depression with adolescent oppositional defiant disorder, anxiety, and substance disorders in adjusted analyses. Generalized anxiety and depression cross-predicted each other, and oppositional defiant disorder (but not conduct disorder) predicted later anxiety disorders and depression. Evidence of homotypic prediction was supported for substance use disorders, antisocial personality disorder (from conduct disorder), and anxiety disorders, although this effect was primarily accounted for by DSM-III-R overanxious disorder. Conclusions Stringent tests of homotypic and heterotypic prediction patterns suggest a more developmentally and diagnostically nuanced picture in comparison with the previous literature. The putative link between adolescent and young adult depression was not supported. Oppositional defiant disorder was singular in being part of the developmental history of a wide range of young adult disorders.

Trends in psychopathology across the adolescent years: What changes when children become adolescents, and when adolescents become adults?

Abstract: Background: Little is known about changes in the prevalence of psychiatric disorders between childhood and adolescence, and adolescence and adulthood. Methods: We reviewed papers reporting prevalence rates of psychiatric disorders separately for childhood, adolescence, and early adulthood. Both longitudinal and cross‐sectional papers published in the past 15 years were included. Results: About one adolescent in five has a psychiatric disorder. From childhood to adolescence there is an increase in rates of depression, panic disorder, agoraphobia, and substance use disorders (SUD), and a decrease in separation anxiety disorder (SAD) and attention‐deficit hyperactivity disorder (ADHD). From adolescence to early adulthood there is a further increase in panic disorder, agoraphobia, and SUD, and a further decrease in SAD and ADHD. Other phobias and disruptive behavior disorders also fall. Conclusions: Further study of changes in rates of disorder across developmental stages could inform etiological research and guide interventions.

Impact of Bullying in Childhood on Adult Health, Wealth, Crime, and Social Outcomes

Abstract: Bullying is a serious problem for schools, parents, and public-policymakers alike. Bullying creates risks of health and social problems in childhood, but it is unclear if such risks extend into adulthood. A large cohort of children was assessed for bullying involvement in childhood and then followed up in young adulthood in an assessment of health, risky or illegal behavior, wealth, and social relationships. Victims of childhood bullying, including those that bullied others (bully-victims), were at increased risk of poor health, wealth, and social-relationship outcomes in adulthood even after we controlled for family hardship and childhood psychiatric disorders. In contrast, pure bullies were not at increased risk of poor outcomes in adulthood once other family and childhood risk factors were taken into account. Being bullied is not a harmless rite of passage but throws a long shadow over affected people's lives. Interventions in childhood are likely to reduce long-term health and social costs.

Human biochemical genetics

Abstract: So far in this course we have dealt entirely with the evolution of characters that are controlled by simple Mendelian inheritance at a single locus. There are notes on the course website about gametic disequilibrium and how allele frequencies change at two loci simultaneously, but we didn’t discuss them. In every example we’ve considered we’ve imagined that we could understand something about evolution by examining the evolution of a single gene. That’s the domain of classical population genetics. For the next few weeks we’re going to be exploring a field that’s actually older than classical population genetics, although the approach we’ll be taking to it involves the use of population genetic machinery. If you know a little about the history of evolutionary biology, you may know that after the rediscovery of Mendel’s work in 1900 there was a heated debate between the “biometricians” (e.g., Galton and Pearson) and the “Mendelians” (e.g., de Vries, Correns, Bateson, and Morgan). Biometricians asserted that the really important variation in evolution didn’t follow Mendelian rules. Height, weight, skin color, and similar traits seemed to

Integrative analysis of 111 reference human epigenomes

Abstract: The reference human genome sequence set the stage for studies of genetic variation and its association with human disease, but epigenomic studies lack a similar reference. To address this need, the NIH Roadmap Epigenomics Consortium generated the largest collection so far of human epigenomes for primary cells and tissues. Here we describe the integrative analysis of 111 reference human epigenomes generated as part of the programme, profiled for histone modification patterns, DNA accessibility, DNA methylation and RNA expression. We establish global maps of regulatory elements, define regulatory modules of coordinated activity, and their likely activators and repressors. We show that disease- and trait-associated genetic variants are enriched in tissue-specific epigenomic marks, revealing biologically relevant cell types for diverse human traits, and providing a resource for interpreting the molecular basis of human disease. Our results demonstrate the central role of epigenomic information for understanding gene regulation, cellular differentiation and human disease.

Lifetime Prevalence of Mental Disorders in U.S. Adolescents: Results from the National Comorbidity Survey Replication-Adolescent Supplement (NCS-A)

Abstract: Objective To present estimates of the lifetime prevalence of DSM-IV mental disorders with and without severe impairment, their comorbidity across broad classes of disorder, and their sociodemographic correlates. Method The National Comorbidity Survey–Adolescent Supplement NCS-A is a nationally representative face-to-face survey of 10,123 adolescents aged 13 to 18 years in the continental United States. DSM-IV mental disorders were assessed using a modified version of the fully structured World Health Organization Composite International Diagnostic Interview. Results Anxiety disorders were the most common condition (31.9%), followed by behavior disorders (19.1%), mood disorders (14.3%), and substance use disorders (11.4%), with approximately 40% of participants with one class of disorder also meeting criteria for another class of lifetime disorder. The overall prevalence of disorders with severe impairment and/or distress was 22.2% (11.2% with mood disorders, 8.3% with anxiety disorders, and 9.6% behavior disorders). The median age of onset for disorder classes was earliest for anxiety (6 years), followed by 11 years for behavior, 13 years for mood, and 15 years for substance use disorders. Conclusions These findings provide the first prevalence data on a broad range of mental disorders in a nationally representative sample of U.S. adolescents. Approximately one in every four to five youth in the U.S. meets criteria for a mental disorder with severe impairment across their lifetime. The likelihood that common mental disorders in adults first emerge in childhood and adolescence highlights the need for a transition from the common focus on treatment of U.S. youth to that of prevention and early intervention.

Multiple Imputation for Nonresponse in Surveys

Abstract: 25. Multiple Imputation for Nonresponse in Surveys. By D. B. Rubin. ISBN 0 471 08705 X. Wiley, Chichester, 1987. 258 pp. £30.25.