The impact of substance use on posttraumatic stress disorder symptoms and treatment discontinuation.

This study examined the impact of ongoing substance use during posttraumatic stress disorder (PTSD) and substance use disorder (SUD) treatment on PTSD symptoms and treatment discontinuation. The study represents a secondary analysis of U.S. military veterans (N = 183) who participated in a randomized clinical trial for the treatment of both PTSD and SUD. Veterans mostly identified as Black (53.8%) or White (41.9%) and male (92.4%). Substance use, PTSD symptoms, and treatment discontinuation were measured at 4-week intervals throughout treatment. Predictors were the percentage of days with alcohol, cannabis, and other substance use (primarily cocaine and opioids) and the average number of alcoholic drinks per drinking day. Outcomes were PTSD symptoms and treatment discontinuation at concurrent and prospective assessments. Multilevel models accounted for the nested structure of the longitudinal data. Alcohol, cannabis, and other substance use did not predict PTSD symptoms or treatment discontinuation prospectively. Concurrently, we observed that as a participant's percentage of drinking days increased by 34.7% (i.e., 1 standard deviation), PTSD symptoms during the same period were 0.07 standard deviations higher (i.e., 1 point on the PCL), B = 0.03, p = .033. No other substances were related to PTSD symptoms concurrently. The findings demonstrate that PTSD symptoms improved regardless of substance use during exposure-based PTSD and SUD treatment, and treatment discontinuation was not associated with substance use. This study suggests that substance use during treatment cannot directly explain the poorer treatment outcomes observed in the literature on comorbid PTSD/SUD compared to PTSD-only populations.

Potentially Traumatic Events and the Association Between Gender Minority Stress and Suicide Risk in a Gender-Diverse Sample.

Transgender and gender diverse (TGD) individuals are at an elevated risk of trauma exposure and other negative mental and physical health outcomes. The present study examined the interaction between minority stressors, reported potentially traumatic events (PTEs), and suicide risk (i.e., ideation and behavior) in a TGD sample. A convenience sample of 155 self-identified TGD individuals completed questionnaires assessing distal (e.g., gender-related discrimination) and proximal (e.g., internalized transphobia) gender identity-related stressors, lifetime PTE history, and suicide risk. The results of a mediation analysis demonstrated that proximal stressors partially mediated the association between distal stressors and suicide risk, B = 1.12, t(152) = 3.72, p < .01, 95% CI [0.53, 1.72], and the results of a moderated mediation analysis showed that the interaction term was not significant, and that the number of PTEs did not moderate the mediation model that examined proximal stressors as a mediator of the association between distal stressors and suicide risk, F(3, 151) = 18.74, MSE = 0.75, R2 = 0.27, B = 0.07, t(151) = 0.89, p = .371, 95% CI [-0.08, 0.21]. These findings suggest that minority stressors may contribute to suicide risk in a TGD population above and beyond the impact of trauma exposure. Risk reduction efforts for suicide risk may be enhanced by attending to minority stressors in addition to PTEs.

Intimate Partner Violence and Psychological Maladjustment: Examining the Role of Institutional Betrayal Among Survivors.

Research has found that a majority of individuals, irrespective of gender, experienced their first intimate partner violence (IPV) victimization between the ages of 18 and 24 years. Indeed, researchers have found that college students' experiences of IPV are comparable if not higher than that of the general population. IPV victimization also places individuals at a higher risk for developing psychological conditions. In addition, when IPV experiences occur on college campuses, there are a variety of institutional factors that may impact the outcome of the traumatic event for the survivor. The present study seeks to examine whether institutional betrayal moderates the relationship between IPV and different psychological outcomes (i.e., depression, posttraumatic stress, anxiety). The study analyzed survey responses from a sample of 316 undergraduate students attending a Midwestern University. Three separate hierarchical regression analyses were conducted for each of the maladaptive psychological outcomes. Results showed that institutional betrayal was positively correlated with depressive symptoms, posttraumatic stress symptoms, and anxiety symptoms. Interestingly, institutional betrayal was a significant predictor of depressive symptoms, posttraumatic stress symptoms, and anxiety symptoms when controlling for the effects of physical violence, sexual violence, and psychological aggression. The present study highlights the significance of the impact of institutional betrayal, independent of interpersonal betrayal, on mental health.

Differentiating the symptoms of posttraumatic stress disorder and bipolar disorders in adults: Utilizing a trauma-informed assessment approach.

In adult populations, bipolar disorders (BDs) and posttraumatic stress disorder (PTSD) have overlapping symptoms, potentially leading to misdiagnosis. This misdiagnosis or failure to diagnose both co-occurring disorders can result in individuals not receiving the proper treatment to address their symptoms. This article highlights how trauma-informed psychological assessment can assist in differential diagnosis and improve the timely delivery of appropriate treatments. The overlapping symptoms of PTSD and BD are discussed to assist in differential diagnosis, and we suggest guidelines for conducting trauma-informed, evidence-based assessments to help clarify these diagnoses.

The impact of exposure, relaxation, and rescripting therapy for post-trauma nightmares on suicidal ideation.

OBJECTIVE: This study investigated whether a brief psychotherapy for post-trauma nightmares (exposure, relaxation, and rescripting therapy [ERRT]), reduced suicidal ideation (SI). We hypothesized that: (a) nightmare frequency and severity, post-traumatic stress disorder (PTSD), depression, and sleep quality would be related to SI at pretreatment; (b) SI would decrease from pre- to post-treatment; and (c) the decrease in SI would remain after controlling for change in PTSD and depression. METHOD: Seventy-five individuals exposed to a traumatic event and who experienced frequent nightmares (minimum one per week) participated in ERRT. Participants were not required to have a psychological diagnosis. Thirty percent endorsed SI at pretreatment. RESULTS: Depression and PTSD were related to SI at pretreatment. SI decreased following treatment; however, the third hypothesis was not supported. CONCLUSION: Results suggest brief psychotherapy targeting post-trauma nightmares may decrease SI. More research is necessary to determine what factors contribute to decreases in SI.

Isoprenoid-mediated control of SMAD3 expression in a cultured model of cystic fibrosis epithelial cells.

Several cellular signaling alterations have been identified in cystic fibrosis (CF) epithelium. One of these alterations is reduced SMAD3 protein expression and a corresponding reduction in SMAD3-mediated transforming growth factor-beta1 (TGF-beta1) signaling in CF epithelial cells compared with wild-type (wt) controls. The goal of this study was to identify a mechanism leading to reduced SMAD3 protein expression in CF epithelium. Based on previous work demonstrating isoprenoid-mediated regulation of CF-related alterations in signal transducer and activator of transcription-1 (Stat1) and inducible nitric oxide synthase (NOS2) expression, the hypothesis of this study is that inhibition of isoprenoid-dependent signaling will restore SMAD3 expression and signaling in a model of CF epithelium. Presented data will demonstrate that inhibition of both farnesyl and geranylgeranyl transferase activities partially restores SMAD3-mediated TGF-beta1 signaling and normalizes SMAD3 protein expression in one cultured model of CF cells. Analysis of the human SMAD3 promoter demonstrates that isoprenoid regulation of SMAD3 expression is dependent on Sp1/Sp3 activity, although farnesyl-mediated pathways may be acting through a secondary mechanism as well. Isoprenoid-mediated regulation of SMAD3 expression, coupled with previous data demonstrating isoprenoid control of Stat1 and NOS2 expression, suggest that the isoprenoid/cholesterol synthesis pathway is a critical intermediate in influencing CF-related cell signaling changes.