Posttraumatic stress disorder (PTSD) and alcohol use disorder (AUD) commonly co-occur and are associated with many negative public health outcomes. There are several etiological models that explain the overlap between PTSD and AUD, including shared genetic risk and phenotypic causality, but the predominant model of etiologic association is the drinking-to-cope self-medication model. Although the self-medication model is conceptually appealing and has been widely accepted within the literature examining alcohol use and anxiety (e.g., PTSD) phenotypes, the findings are inconsistent and there is a lack of rigorous empirical evidence in support of this model. This review, which was, to our knowledge, the first systematic review of the self-medication model in relation to PTSD to date, aimed to synthesize the current literature on the association between PTSD and problematic alcohol use within the context of the self-medication model. In total, 24 studies met the inclusion criteria for the review and assessed the self-medication hypothesis using a variety of measurement instruments and data analytic approaches, such as mediation, moderation, and regression. Overall, the included studies provide evidence for the self-medication hypothesis but are limited in rigor due to methodological limitations. These limitations, which include issues with the operationalization (or lack thereof) of trauma-related drinking to cope, are discussed, and directions for future research are presented. Posttraumatic stress disorder (PTSD) and alcohol use disorder (AUD) are prevalent, with lifetime general population estimates of PTSD ranging from 0.5% to 14.5%, depending on trauma timing and type (Koenen, Ratanatharathorn, Bromet, Karam, & Stein, 2018) and AUD at around 29% (Grant et al., 2015). Further, PTSD and AUD frequently co-occur, with comorbidity estimates ranging from approximately 30% to 50%

Objective This study examined the prevalence and correlates of sexual assault (SA) pre-college, college onset, and repeat SA within a representative student sample. Participants A representative sample of 7,603 students. Methods Incoming first year students completed a survey about their exposure to broad SA prior to college, prior trauma, personality, relationships, and mental health. Broad SA was then re-assessed each spring semester while enrolled. Results Nearly 20% of the sample reported experiencing broad SA, with women endorsing significantly higher rates compared to males. Prior victimization before coming to college was related to a greater risk of victimization in college and there was no statistically significant difference between males and females who reported revictimization. Correlates of college onset broad SA were found and are discussed. Conclusions Given the need for SA intervention and prevention on college campuses, identification of factors potentially contributing to exposure within this population is essential.

Multiple etiological models have been proposed to explain posttraumatic stress disorder (PTSD) and alcohol use disorder (AUD) comorbidity, but the predominant model to date is the “drinking to cope” self-medication model. Despite its popularity, the self-medication model lacks rigorous empirical support related to inconsistencies and methodological limitations, particularly the failure to operationalize drinking to cope with trauma symptoms specifically. The present study sought to measure trauma-related drinking to cope (TRD) in order to provide a more specific test of the self-medication model among a representative sample of 1,896 undergraduates with a history of trauma exposure and alcohol use. Using a model-building approach in Mplus, a correlated multiple mediator model tested the association between PTSD symptoms and alcohol use problems (AUPs) through TRD and more generalized drinking to cope motives (as assessed by the coping subscale of the Drinking Motives Questionnaire; DMQ-Cope) as moderated by sex. Results indicated that, while accounting for the effects of generalized drinking to cope motives, TRD partially mediated the relation between PTSD symptoms and AUPs and that this relationship was stronger for males than for females. With the exception of moderation by sex, results were substantiated using longitudinal data. Findings were consistent with the self-medication model, suggesting that TRD motives may serve as a mechanism through which PTSD symptoms influence AUPs. TRD may serve as a more specific screening tool for AUP risk among individuals endorsing PTSD symptoms compared with the commonly used DMQ-Cope.

Military personnel returning from conflicts in Iraq and Afghanistan often endorse pain and posttraumatic stress disorder (PTSD) symptoms, either separately or concurrently. Associations between pain and PTSD may be further complicated by blast exposure from explosive munitions. Although many studies have reported on the prevalence and disability associated with polytraumatic injuries following combat, less is known about symptom maintenance over time. Accordingly, this study examined longitudinal interactive models of co-occurring pain and PTSD symptoms in a sample of 209 military personnel (Mage = 27.4 years, SD = 7.6) who experienced combat-related blast exposure. Autoregressive cross-lagged analysis examined longitudinal associations between self-reported pain and PTSD symptoms over a one-year period. The best-fitting model indicated that pain and PTSD were significantly associated with one another across all assessment periods, χ2(3) = 3.66, p = .30; TLI = .98; CFI = 1.00; RMSEA = .03, and PTSD had a particularly strong influence on subsequent pain symptoms. The relationship between pain and PTSD is related to older age, race, and traumatic brain injury characteristics. Results further the understanding of complex injuries among military personnel and highlight the need for comprehensive assessment and rehabilitation efforts addressing the interdependence of pain and co-occurring mental health conditions. Perspective This longitudinal study demonstrates that pain and posttraumatic stress disorder strongly influence one another and interact across time. These findings have the potential to inform the integrative assessment and treatment of military personnel with polytrauma injuries and who are at risk for persistent deployment-related disorders.

Background Insomnia is comorbid with internalizing and externalizing psychiatric disorders. However, the extent to which the etiologic influences on insomnia and common psychopathology overlap is unclear. There are limited genetically-informed studies of insomnia and internalizing disorders and few studies of overlap exist with externalizing disorders. Methods We utilized twin data from the Virginia Adult Twin Studies of Psychiatric and Substance Use Disorders (total n = 7500). Insomnia, internalizing disorders (major depressive disorder [MDD], generalized anxiety disorder [GAD]), and alcohol abuse and dependence (AAD) were assessed at two time points, while antisocial personality disorder (ASPD) was assessed once. Cholesky decompositions were performed in OpenMx and longitudinal measurement models were run on available phenotypes to reduce measurement error. Results The latent additive genetic influences on insomnia overlapped significantly (56% for females, 74% for males) with MDD and were shared completely (100%) with GAD. There was significant overlap of latent unique environmental influences, with overlap ranging from 38% to 100% across disorders. In contrast, there was less genetic overlap between insomnia and externalizing disorders, with 18% of insomnia’s heritability shared with AAD and 23% with ASPD. Latent unique environmental overlap between insomnia and both externalizing disorders was negligible. Conclusions The evidence for substantial genetic overlap between insomnia and stable aspects of both internalizing disorders suggests that there may be few insomnia-specific genes and investigation into unique environmental factors is important for understanding insomnia development. The modest overlap between insomnia and externalizing disorders indicates that these disorders are genetically related, but largely etiologically distinct.