Fourth, we found little evidence for shared genetic overlap between weekly alcohol consumption and reduction/cessation of problematic drinking. Prior studies have identified candidate variants related to treatment-dependent remission (e.g., (Karpyak et al., 2014)) and emerging evidence suggests high sibling concordance for abstinent remission (McCutcheon et al., 2017), suggesting heritable influences on the transition from active AUD to low-risk drinking and abstinence. However, while PRS distinguished those without a lifetime history of DSM-5 AUD from those with an active diagnosis or high-risk drinking, they were unrelated to low risk drinking or abstinence in those with a lifetime history of DSM-5 AUD. This could be partially due to a lack of power: only 16% of the individuals were in the category of low-risk drinking and abstinence. This finding could also suggest that even though there is polygenic overlap between alcohol consumption and severity of AUD (e.g., DSM5AUDSX), and that individuals who successfully reduce their problem drinking might have a less severe form of the disorder, the genetic propensity that extends beyond severity and specifically predicts cessation is distinct. One might speculate that
