Effectiveness of exposure therapy for posttraumatic stress disorder (PTSD) may be adversely influenced by comorbid disorders. The present study investigated behavioral activation and therapeutic exposure (BA-TE), a new integrated treatment designed specifically for comorbid symptoms of PTSD and depression. Combat veterans with PTSD (N = 117) completed eight sessions of BA-TE that included two phases of treatment: (a) behavioral activation (BA) in which some activities involved situational exposures and (b) BA and situational exposures with imaginal exposures. Findings supported improvements in symptoms of PTSD, and overlapping symptoms of PTSD and depression, but not in nonoverlapping symptoms of depression. The findings also demonstrated a relatively consistent rate of change in PTSD and depression symptoms during BA-TE, despite the addition of imaginal exposures midway through the treatment. Together, these findings provide preliminary support for BA-TE as a treatment for PTSD and depression, and highlight the utility of transdiagnostic treatments in addressing comorbidity and symptom overlap.

Negative mood increases smoking reinforcement and risk of relapse. We explored associations of gene variants in the dopamine, opioid, and serotonin pathways with smoking reward (“liking”) and reinforcement (latency to first puff, total puffs) as a function of negative mood and expected vs. actual nicotine content of the cigarette. Smokers of European ancestry (n=72) were randomized to one of four groups in a 2 × 2 balanced-placebo design, corresponding to manipulation of actual (0.6 mg vs. 0.05 mg) and expected (told nicotine, told denicotinized) nicotine “dose” in cigarettes during each of two sessions (negative vs. positive mood induction). Following mood induction and expectancy instructions, they sampled and rated the assigned cigarette, and then smoked additional cigarettes ad lib during continued mood induction. The increase in smoking amount due to negative mood was associated with: DRD2 C957T (CC>TT or CT), SLC6A3 (presence of 9 repeat > absence of 9), and among those given a nicotine cigarette, DRD4 (presence of 7 repeat > absence of 7) and DRD2/ANKK1 TaqIA (TT or CT > CC). SLC6A3 and DRD2/ANKK1 TaqIA were also associated with smoking reward and smoking latency. OPRM1 (AA > AG or GG) was associated with smoking reward, but SLC6A4 VNTR was unrelated to any of these measures. These results warrant replication but provide the first evidence for genetic associations with the acute increase in smoking reward and reinforcement due to negative mood.