a change in aversive states and stress responses. Although our data do not provide support for this idea, it is possible this putative stage requires more than a decade to development or that it exists only in those prone to negative affect or extremely aversive withdrawal. Alternatively, while certain tenets of the allostasis theory may relate to animal models, they may not translate to manifestations of AUD as observed within the demographics of the current study sample. Indeed, cross-sectional neuroimaging studies suggest that individuals with more severe heavy drinking histories exhibit a reduced activation of the nucleus accumbens after a single dose of alcohol (52–54). In contrast, our within-subject findings demonstrated that the perceived pleasurable alcohol effects are not diminished as AUD severity progressed over a 10-year period. Although it is difficult to reconcile the contrasting findings, given the differences in samples and methodologies, we may speculate that other neurobiological substrates (i.e. basal ganglia) or circuits underlie the persistent positive subjective response to alcohol. Nevertheless, this possibility highlights the necessity for studies employing both neurobiological techniques and validated subjective measures.
