more biological and genetically relevant domains that one day could be incorporated into a diagnostic framework (Kwako et al., 2016). In particular, a more biologically-based diagnostic framework for AUD will undoubtedly aid discovery of more effective pharmacotherapies by reducing patient heterogeneity, for example. To this end, one of the most useful paradigms for conceptualizing AUD and drug addiction is taken from advances in the understanding of the neurocircuitry of addiction and the impact on the brain reward, stress, and executive function systems. (Koob and Volkow, 2016). As such, addiction has been defined as a three stage cycle containing: (1): binge/intoxication, (2): withdrawal/negative affect and (3): preoccupation/anticipation stages that represent distinct neurocircuitry and functional domains. Initial use of alcohol is driven by positive reinforcement mechanisms that involves patterns of binge-and-intoxication. Alcohol or stimuli associated with alcohol act as a positive reinforcer, to strengthen behavior, which engages the mesolimbic dopamine and opioid reward systems in the central nervous system. In addition, engagement of the dorsal striatum during alcohol addiction is thought to help to solidify habitual behaviors associated with drug seeking and taking. Namely, neuroadaptations in the dorsal striatum involve changes in glutamate, GABA and the endocannabinoid system (Koob and Volkow, 2010).
