Psychophysiological and Neural Mechanisms of Emotion Dysregulation in Alcohol Disorders Comorbid with PTSD

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 DESCRIPTION (provided by applicant): Many individuals with alcohol use disorders (AUD) also have posttraumatic stress disorder (PTSD) and these individuals have greater AUD severity than individuals with AUD-only. This study is based on the intersection of research conducted by Drs. Kevin Oschsner and Scott Coffey. Dr. Coffey identified an AUD/PTSD symptom cross-over effect where trauma-related cues elicit not only PTSD symptoms but also alcohol craving. Poor emotion regulation is theorized to underlie this link between AUD and PTSD via a pattern where emotion dysregulation makes individuals both more likely to develop PTSD and also reinforces alcohol use to regulate negative emotions. Dr. Ochsner, meanwhile, has studied emotion regulation extensively in his lab and developed a model of the cognitive control of emotion (MCCE). Within that model there are many different strategies that individuals employ to control emotion. One of these, "reinterpretation," has been the extensively studied and found to be more effective in reducing negative emotions than other strategies. Reinterpretation is based on the premise that emotional reactions to stimuli depend upon the nature of cognitive appraisals of (i.e., the meaning assigned to) stimuli, which is a central tenet of cognitive behavioral therapy. Research has identified aberrant neural processes in AUD and PTSD during stressors. Since these are brain regions and neural networks also associated with emotional control, researchers hypothesize that participants are attempting to regulate emotional responses to these stressful cues but failing. However, we do not know of alcohol comorbidity studies that specifically test the purposeful emotional regulation of stress using a known and well-tested strategy (reinterpretation), or where objective physiological measures of emotion regulation failure are collected, so that abnormal neural networks associated with failures can be objectively identified. In this study we will determine first the ability of particpants with AUD/PTSD, compared to participants with (1) AUD only, (2) PTSD only, and (3) no AUD or PTSD, to regulate emotional responses to personalized trauma cues (symptom provocation). We will also determine whether decreasing emotional responses reduces associated alcohol craving (behavior and subjective distress). Second, we will determine physiological indices (heart rate, skin conductance, heart rate variability) associated with poor emotion regulation (objective measure of distress). Finally, guided by those physiological indices and using fMRI, we will determine neural networks (stress circuit and AUD circuit interaction) associated with dysfunctional emotional regulation. This topic is a priority at NIAAA, who has stated that neurobiological mechanisms underlying AUD/PTSD must be found, and stress circuit and AUD circuit interaction must be clarified. Once these neurobiological mechanisms are identified and the relationship between stress circuits and AUD circuits is clear, we can apply this knowledge to improving treatment approaches, not only for AUD/PTSD patients, but also for those suffering from AUD comorbid with other disorders characterized by emotion regulation problems.