Another observed source of overlap between alcohol consumption and AUD was in shared genetic correlations with decreased cortical thickness that was particularly pronounced in frontal regions. To date, research examining genetic correlations between alcohol use traits and neuroimaging phenotypes using large‐scale GWAS data is relatively limited. 58 , 67 Given that reduced frontocortical thickness has previously been associated with impulsive choice in adolescence, 72 alcohol consumption in young adults, 73 and AUD in middle‐aged adults, 74 the present results highlight a possible genetic pathway consistent with addiction theory whereby genetic liability for reduced cortical thickness leads to disinhibited behaviour, which may confer greater risk for transitions from heavy consumption to AUD. Future studies using longitudinal data to test this pathway more directly are needed to fully elucidate the neurogenetic features influencing progression to AUD.
