Evidence for important genetic contributions to the intergenerational transmission of alcohol use disorder has accumulated over many years. This began with the observation of pedigrees with multiple alcoholic family members (1), continuing with adoption study data suggesting that adopted-away offspring risk correlates with biological parent alcoholism (2,3) and twin studies suggesting that, across a range of phenotype definitions ranging from severe to broad, genetic factors may explain as much as 60% of the variance in risk of alcoholism (4,5). Genetic linkage studies (6,7,8) and, most recently, the first generation of GWAS studies of alcoholic case-control series(9,10,11), have sought to identify genes contributing to risk of alcohol use disorder. In parallel, a second literature has developed, mostly based on twin studies, showing comparably high genetic variance in alcohol consumption patterns (12) and noting genetic overlap between alcohol dependence and heaviness of consumption (13). This overlap persists even when consumption data from alcohol dependent individuals are omitted from the analysis, to avoid an artefactual correlation due to escalating consumption secondary to the onset of alcoholism (14). Studies of alcohol metabolism genes (ALDH2,
