Previous research has demonstrated important phenotypic, neurobiological, and genetic overlap among sensation seeking, alcohol consumption, and AUD. This research has informed current addictions theory and suggests that sensation seeking, especially in adolescence and emerging adulthood, functions as a significant risk factor for heavy alcohol consumption, which may subsequently lead to AUD development. 2 , 3 The current study's extensive examination of these traits and their overlap resulted in five main findings: (1) replication of associated loci for alcohol consumption and AUD; (2) identification of novel GWS loci for sensation seeking; (3) stronger genetic overlap between sensation seeking and alcohol consumption than between sensation seeking and AUD with alcohol consumption mediating the genetic relation between sensation seeking and AUD; (4) genetic overlap between sensation seeking and alcohol consumption was related to neural regions/circuits central to neurobiological models of addiction (e.g., midbrain dopaminergic neurons and anterior caudate); and (5) genetic overlap between alcohol consumption and AUD was characterised by decreased frontocortical thickness and by genetic variation in a gene region (BANK1‐SLC39A8) previously implicated in striatal volume. 26 , 30 These are discussed in turn.
