Consistent with models suggesting that alcohol consumption and AUD are driven, in part, by separable biological underpinnings, molecular genetics research has revealed separable genetic influences contributing to each phenotype despite substantial overlap between them, suggesting that alcohol consumption has limitations as a direct genetic proxy for AUD. 19 , 20 Thus, investigations examining differences in genetic associations among sensation seeking, alcohol consumption, and AUD are warranted. Prior evidence suggests that sensation seeking may be more strongly genetically correlated with alcohol consumption than AUD, 19 , 21 but direct comparisons of these relative associations have not been investigated. Further, investigations attempting to further elucidate the nature of the neurogenetic (i.e., genetic influences on individual differences in brain function) pathways linking sensation seeking, alcohol consumption, and AUD using large‐scale genomic data and advanced post‐multivariate genome‐wide association study (GWAS) approaches have not yet been performed.
