Symptoms of posttraumatic stress (PTS) show significant comorbidity with alcohol use, but little is known about the mechanisms that might account for this comorbidity. Deficits in reward functioning have long been implicated in alcohol misuse and more recently in PTS reactions, but no study has examined whether reward deprivation may serve as a transdiagnostic risk factor for comorbid PTS-alcohol misuse. The current cross-sectional study sought to test the behavioral economic hypothesis that reward deprivation would be related to both PTS symptoms and alcohol problems, and would mediate the relation between PTS symptoms and alcohol problems in college students. We recruited a diverse sample of urban college students (N = 203, Mage = 21.5 years, SD = 5.5; 79.5% female; 56.8% White, 28.1% Black, .9% Asian, 9.8% Multiracial) who endorsed both alcohol use and PTS symptoms. Reward deprivation (lack of access to, and ability to, experience reward) was related to alcohol problems, and a lack of access to reward was related to PTS symptoms. Furthermore, reward access mediated the relation between PTS symptoms and alcohol problems and craving, after controlling for alcohol use, age, gender, and race. These data provide preliminary support for behavioral economic models of alcohol comorbidity and suggest that treatments for combined PTS and alcohol misuse should attempt to reduce barriers to accessing natural rewards. (PsycINFO Database Record

Trauma-informed beliefs often decrease during posttraumatic stress disorder (PTSD) treatment. This may also extend to anxiety sensitivity (AS), defined as a fear of anxiety-related sensations and beliefs that anxiety is dangerous and/or intolerable. However, little is known about how AS changes during exposure-based and psychopharmacological PTSD treatments. Further, high AS may be a risk factor for diminished PTSD symptom improvement and increased treatment dropout. To better understand how AS impacts and is impacted by PTSD treatment, we conducted a secondary analysis of a randomized clinical trial with a sample of 223 veterans (87.0% male, 57.5% White) with PTSD from four U.S. sites. Veterans were randomized to receive prolonged exposure (PE) plus placebo (n = 74), sertraline plus enhanced medication management (n = 74), or PE plus sertraline (n = 75). Veterans answered questions about PTSD symptoms and AS at baseline and 6-, 12-, 24-, 36-, and 52-week follow-ups. High baseline AS was related to high levels of PTSD severity at 24 weeks across all conditions, β = .244, p = .013, but did not predict dropout from exposure-based, β = .077, p = .374, or psychopharmacological therapy, β = .009, p = .893. AS also significantly decreased across all three treatment arms, with no between-group differences; these reductions were maintained at the 52-week follow-up. These findings suggest that high AS is a risk factor for attenuated PTSD treatment response but also provide evidence that AS can be improved by both PE and an enhanced psychopharmacological intervention for PTSD.