Unlike heavy drinking or psychiatric comorbidity, which may arise as a consequence of problematic drinking patterns, PGS and EEG measures provide a glimpse into potential and preexisting neurobiological vulnerabilities. EEG and AUD PGS results generally echoed other findings. Specifically, theta EROs distinguished between individuals with low-risk and high-risk mild-to-moderate AUD and demonstrated similarly blunted neurophysiological responses in both high-risk mild-to-moderate and severe AUD groups in the cross-sectional cohort. AUD PGS primarily exhibited associations with criterion count and overall diagnostic status (AUD vs no AUD) across both ancestry subsamples. As these PGS are calculated using genome-wide association studies of broadly conceptualized AUD status often obtained from electronic health record–derived diagnostic codes,25,26,27,28 findings here highlight the need for criterion-focused genome-wide association studies to resolve key genetic mechanisms that might underlie specific clinical presentations.38,39,42,43,44
