Objectives. We estimated prevalence and assessed correlates of emotional, physical, sexual, and financial mistreatment and potential neglect (defined as an identified need for assistance that no one was actively addressing) of adults aged 60 years or older in a randomly selected national sample. Methods. We compiled a representative sample by random digit dialing across geographic strata. We used computer-assisted telephone interviewing to standardize collection of demographic, risk factor, and mistreatment data. We subjected prevalence estimates and mistreatment correlates to logistic regression. Results. We analyzed data from 5777 respondents. One-year prevalence was 4.6% for emotional abuse, 1.6% for physical abuse, 0.6% for sexual abuse, 5.1% for potential neglect, and 5.2% for current financial abuse by a family member. One in 10 respondents reported emotional, physical, or sexual mistreatment or potential neglect in the past year. The most consistent correlates of mistreatment across abuse types were low social support and previous traumatic event exposure. Conclusions. Our data showed that abuse of the elderly is prevalent. Addressing low social support with preventive interventions could have significant public health implications.

The risk of posttraumatic stress disorder (PTSD) following trauma is heritable, but robust common variants have yet to be identified. In a multi-ethnic cohort including over 30,000 PTSD cases and 170,000 controls we conduct a genome-wide association study of PTSD. We demonstrate SNP-based heritability estimates of 5–20%, varying by sex. Three genome-wide significant loci are identified, 2 in European and 1 in African-ancestry analyses. Analyses stratified by sex implicate 3 additional loci in men. Along with other novel genes and non-coding RNAs, a Parkinson’s disease gene involved in dopamine regulation, PARK2, is associated with PTSD. Finally, we demonstrate that polygenic risk for PTSD is significantly predictive of re-experiencing symptoms in the Million Veteran Program dataset, although specific loci did not replicate. These results demonstrate the role of genetic variation in the biology of risk for PTSD and highlight the necessity of conducting sex-stratified analyses and expanding GWAS beyond European ancestry populations.

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.

Recent attention has been given to the role of emotion regulation in the development and maintenance of psychopathology. Gross (1998) provided a framework from which to understand emotion regulation processes, and it is within this framework that the literature on emotion regulation/ dysregulation in the anxiety disorder population is reviewed, with a focus on possible deficiencies that lead to or maintain the disorders. The present paper aims to (1) briefly introduce emotion regulation strategies of suppression and reappraisal; (2) summarize the empirical studies of emotion regulation within anxiety disorders; (3) discuss the neurobiological markers of emotion regulation within these disorders; (4) provide future directions for research; and (5) summarize possible treatment implications resulting from this important area of research.

Rape affects one in seven women nationwide. Historically, most rape victims do not report rape to law enforcement. Research is needed to identify barriers to reporting and correlates of reporting to guide policy recommendations that address such barriers. We investigated the prevalence of reporting rape among a national sample of women (N = 3,001) interviewed in 2006. The study also examined predictors of reporting as well as barriers to reporting, concerns about reporting, and women's experiences with the reporting process. Results demonstrated that the overall prevalence of reporting (15.8%) has not significantly increased since the 1990s. Differences were found between rape types, with rapes involving drug or alcohol incapacitation or facilitation being less likely to be reported than forcible rapes. Several predictors of reporting emerged in multivariable analyses. Implications for public health and public policy are discussed.

Post-traumatic stress disorder (PTSD) is a prevalent, disabling anxiety disorder that constitutes a major health care burden. Despite evidence supporting a genetic predisposition to PTSD, the precise genetic loci remain unclear. Herein we review the current state and limitations of genetic research on PTSD. Although recent years have seen an exponential increase in the number of studies examining the influence of candidate genes on PTSD diagnosis and symptomatology, most studies have been characterized by relatively low rates of PTSD, with apparent inconsistencies in gene associations linked to marked differences in methodology. We further discuss how current advances in the genetics field can be applied to studies of PTSD, emphasizing the need to adapt a genome-wide approach that facilitates discovery rather than hypothesis testing. Genome-wide association studies offer the best opportunity to identify novel “true” risk variants for the disorder that in turn has the potential to inform our understanding of PTSD etiology.

Objective There is great variability in response to stressful life events (SLEs), with some individuals demonstrating substantial psychiatric symptoms while others remain largely asymptomatic. The source of this variability is poorly understood. The present study aimed to examine the genetic and environmental underpinning of resilience, defined as the difference between the twins’ total score on a broad measure of internalizing symptoms and their predicted score based on their cumulative exposure to SLEs. Method SLE exposure and internalizing symptoms were assessed at two time points in 7,500 adult twins. Using the residual between actual and predicted internalizing symptom total score, twin modeling was conducted for each wave separately, as well as longitudinally. Quantitative and qualitative sex effects were also tested. Results Resilience was found to have a mild to moderate genetic heritability at each individual wave (~31%). Additionally, qualitative sex effects were found. Incorporating error of measurement into the model increased the estimated heritability for the latent construct of resilience (~50%). Unconfounded by measurement error and occasion specific effects, environmental influences contributed roughly equally to determining the individual level of resilience. Conclusions Genetic factors influence the level of psychiatric resilience, and are largely stable over time. The genes that impact on resilience are not entirely the same in males and females, although the degree of heritability is equal across the sexes. Environmental influences can also have an enduring effect on resilience. The present findings of the genetic and environmental influences on adaptation to SLEs clarify the sources of individual variation to environmental stressors.

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