Extensive theory and empirical testing point to models of shared neurobiology underlying relations among sensation seeking, alcohol consumption, and AUD. For example, the ‘addiction cycle’ model argues that the initial binge/intoxication stage of the cycle is primarily driven by bottom‐up incentive‐reward systems localised to the basal ganglia and midbrain and impaired top‐down control of these approach systems by the prefrontal cortex linked via mesocorticolimbic pathways. 11 AUD progression follows from continuation of the cycle with withdrawal/negative affect (extended amygdala) and preoccupation/anticipation stages (i.e., craving; prefrontal cortex, insula) signalling a shift in the relative influence of the neurobiological circuits contributing to continued drinking behaviours. Neuroimaging studies provide corroborating evidence of some of these hypothesised addiction pathways 12 and demonstrate overlap between alcohol consumption and sensation seeking with respect to regional brain morphology and functional connectivity. For example, studies have demonstrated associations between sensation seeking and neuroanatomical differences in frontocingulate thickness and surface area, volume of basal ganglia structures (e.g., nucleus accumbens and globus pallidus), 13 , 14 and reward‐cued connectivity of frontostriatal pathways, 15 , 16 highlighting many of the same
