Posttraumatic stress disorder (PTSD) and alcohol/substance use disorder (A/SUD) are frequently comorbid. Comorbidity is associated with poorer psychological, functional, and treatment outcomes than either disorder alone. This review outlines biological mechanisms that are potentially involved in the development and maintenance of comorbid PTSD and A/SUD including neurotransmitter and hypothalamic-pituitary-adrenal dysregulation, structural differences in the brain, and shared genetic risk factors. The literature regarding pharmacological treatments that have been investigated for comorbid PTSD and A/SUD is also reviewed. Empirical data for each proposed mechanism and pharmacological approach is reviewed with the goal of making recommendations for future research.

Aims: Alcohol acutely reduces agitation and is widely used in social situations, but the neural substrates of emotion processing during its intoxication are not well understood. We examine whether alcohol's social stress dampening effect may be via reduced activity in the cortical systems that subserve awareness of bodily sensations, and are associated with affective distress. Methods: Blood oxygen level-dependent activation was measured through 24 functional magnetic resonance imaging sessions in 12 healthy volunteers during an emotional face-processing task following ingestion of a moderate dose of alcohol and a placebo beverage. Results: Results revealed that bilateral anterior insula response to emotional faces was significantly attenuated following consumption of alcohol, when compared with placebo (clusters >1472 μl; corrected P < 0.05). Conclusion: Attenuated response in the anterior insula after alcohol intake may explain some of the decreased interoceptive awareness described during intoxication.