Other neuroimaging work demonstrated that alterations in ventral striatal and amygdala activity in response to stress in problem drinkers was mediated by anxious/depressive symptomatology (Nikolova et al., 2016). Since AUD is also highly comorbid with mood and anxiety disorders, it remains especially important to consider clinical diagnoses in neuroimaging studies of AUD as these comorbidities are often not accounted for in study design or analysis. Overall, neuroimaging work should control for smoking status and other psychiatric comorbidities in studies of AUD, as this may improve our understanding of the differential effects of alcohol vs. tobacco smoking [or depression/anxiety, etc.] on the brain, and parse out whether these differences are SG-dependent. Importantly, future work, including the Adolescent Brain Cognitive Development (ABCD) and National Comorbidity Survey – Adolescent Supplement studies, will also be able to address SG differences in variability of brain development during adolescence as it relates to substance use (e.g., marijuana, e-cigarettes) and beyond (e.g., traumatic brain injury, sleep, psychopathology, psychosocial factors [parental income, family structure]) and how that may be associated with the development and maintenance of AUD in adulthood (Conway, Swendsen, Husky, He, & Merikangas, 2016; Volkow et al., 2018).
