Integrated Treatment of PTSD and Substance Use Disorders: The Mediating Role of PTSD Improvement in the Reduction of Depression

Posttraumatic stress disorder (PTSD) represents one of the most common mental health disorders, particularly among veterans, and is associated with significant distress and impairment. This highly debilitating disorder is further complicated by common comorbid psychiatric disorders, such as substance use disorders (SUD). Individuals with PTSD and co-occurring SUD also commonly present with secondary symptoms, such as elevated depression. Little is known, however, about how these secondary symptoms are related to treatment outcome. The aim of the present study, therefore, was to examine (1) the effects of treatment of comorbid PTSD/SUD on depressive symptoms; and (2) whether this effect was mediated by changes in PTSD severity or changes in SUD severity. Participants were 81 U.S. military veterans (90.1% male) with PTSD and SUD enrolled in a randomized controlled trial examining the efficacy of an integrated, exposure-based treatment (Concurrent Treatment of PTSD and Substance Use Disorders Using Prolonged Exposure; n = 54) versus relapse prevention (n = 27). Results revealed significantly lower depressive symptoms at post-treatment in the COPE group, as compared to the relapse prevention group. Examination of the mechanisms associated with change in depression revealed that reduction in PTSD severity, but not substance use severity, mediated the association between the treatment group and post-treatment depression. The findings underscore the importance of treating PTSD symptoms in order to help reduce co-occurring symptoms of depression in individuals with PTSD/SUD. Clinical implications and avenues for future research are discussed

Effects of oxytocin on stress reactivity and craving in veterans with co-occurring PTSD and alcohol use disorder

© 2018 American Psychological Association. Posttraumatic stress disorder (PTSD) and alcohol use disorder (AUD) are highly prevalent and commonly co-occur. The dual diagnosis of PTSD/AUD is associated with serious negative sequalae, and there are currently no effective pharmacological treatments for this comorbidity. Both PTSD and AUD are characterized by dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, which helps modulate stress reactivity. Oxytocin, a neuropeptide that attenuates HPA axis dysregulation, may be beneficial for individuals with co-occurring PTSD/AUD. Thus, the current study examined the effects of intranasal oxytocin (40 IU) as compared with placebo on stress reactivity (e.g., cortisol) as well as subjective alcohol craving in response to a laboratory stress task (Trier Social Stress Task). Participants were 67 male U.S. military veterans with current PTSD and AUD (oxytocin n = 32, placebo n = 35; overall mean age = 49.06 years). Baseline cortisol levels were examined as a moderator of outcome. The findings revealed that oxytocin marginally attenuated cortisol reactivity in response to the stress task. Furthermore, oxytocin\u27s effect was moderated by baseline cortisol level, such that oxytocin mitigated cortisol reactivity to a greater extent among participants with higher, as compared with lower, baseline cortisol. Oxytocin did not reduce craving. Although preliminary, the findings are the first to examine oxytocin in co-occurring PTSD/AUD. The findings from this study contribute to the growing literature examining the potential utility of oxytocin among individuals with psychiatric disorders, such as PTSD and substance use disorders

Oxytocin moderates corticolimbic social stress reactivity in cocaine use disorder and healthy controls

Social stress can contribute to the development of substance use disorders (SUDs) and increase the likelihood of relapse. Oxytocin (OT) is a potential pharmacotherapy that may buffer the effects of social stress on arousal and reward neurocircuitry. However, more research is needed to understand how OT moderates the brain's response to social stress in SUDs. The present study examined the effect of intransasal OT (24 IU) versus placebo (PBO) on corticolimbic functional connectivity associated with acute social stress in individuals with cocaine use disorder (CUD; n = 67) and healthy controls (HC; n = 52). Psychophysiological interaction modeling used the left and right amygdala as seed regions with the left and right orbitofrontal and anterior cingulate cortex as a priori regions of interest. Moderators of the OT response included childhood trauma history and biological sex, which were examined in independent analyses. The main finding was that OT normalized corticolimbic connectivity (left amygdala-orbitofrontal and left amygdala-anterior cingulate) as a function of childhood trauma such that connectivity was different between trauma-present and trauma-absent groups on PBO, but not between trauma groups on OT. Effects of OT on corticolimbic connectivity were not different as a function of diagnosis (CUD vs HC) or sex. However, OT reduced subjective anxiety during social stress for CUD participants who reported childhood trauma compared to PBO and normalized craving response as a function of sex in CUD. The present findings add to some prior findings of normalizing effects of OT on corticolimbic circuitry in individuals with trauma histories and provide some initial support that OT can normalize subjective anxiety and craving in CUD