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.

Emotion dysregulation is thought to be critical to the development of negative psychological outcomes. Gross (1998b) conceptualized the timing of regulation strategies as key to this relationship, with response-focused strategies, such as expressive suppression, as less effective and more detrimental compared to antecedent-focused ones, such as cognitive reappraisal. In the current study, we examined the relationship between reappraisal and expressive suppression and measures of psychopathology, particularly for stress-related reactions, in both undergraduate and trauma-exposed community samples of women. Generally, expressive suppression was associated with higher, and reappraisal with lower, self-reported stress-related symptoms. In particular, expressive suppression was associated with PTSD, anxiety, and depression symptoms in the trauma-exposed community sample, with rumination partially mediating this association. Finally, based on factor analysis, expressive suppression and cognitive reappraisal appear to be independent constructs. Overall, expressive suppression, much more so than cognitive reappraisal, may play an important role in the experience of stress-related symptoms. Further, given their independence, there are potentially relevant clinical implications, as interventions that shift one of these emotion regulation strategies may not lead to changes in the other.

Does trauma exposure impair retrieval of autobiographical memories? Many theorists have suggested that the reduced ability to access specific memories of life events, termed overgenerality, is a protective mechanism helping attenuate painful emotions associated with trauma. The authors addressed this question by reviewing 24 studies that assessed trauma exposure and overgenerality, examining samples with posttraumatic stress disorder, acute stress disorder, depression, traumatic event exposure, and other clinical disorders. Limitations are discussed, including variations in assessment of events, depression, and overgenerality and the need for additional comparison groups. Across studies, there was no consistent association between trauma exposure and overgenerality, suggesting that trauma exposure is unlikely to be the primary mechanism leading to overgenerality. Instead, psychopathology factors such as depression and posttraumatic stress appear to be more consistently associated with overgenerality. Alternative overgenerality theories may help identify key overgenerality mechanisms, improving current understanding of autobiographical memory processes underlying psychopathology.

Symptom exacerbation (i.e., treatment side effects) has often been neglected in the psychotherapy literature. Although prolonged exposure has gained empirical support for the treatment of chronic posttraumatic stress disorder (PTSD), some have expressed concem that imaginal exposure, a component of this therapy, may cause symptom exacerbation, leading to inferior outcome or dropout. In the present study, symptom exacerbation was examined in 76 women with chronic PTSD. To define a "reliable" exacerbation, we used a method incorporating the standard deviation and test-retest reliability of each outcome measure. Only a minority of participants exhibited reliable symptom exacerbation. Individuals who reported symptom exacerbation benefited comparably from treatment. Further, symptom exacerbation was unrelated to dropout. Thus, although a minority of individuals experienced a temporary symptom exacerbation, this exacerbation was unrelated to outcome.