Extensive family, twin and adoption study literatures have documented the strong familial transmission of alcoholism, and its genetic underpinnings (1–4). Large-sample studies with widely varying operationalizations of alcoholism have been remarkably consistent in documenting moderately strong genetic contributions to variation in alcohol dependence (AD), typically accounting for 40–60% of variation in risk. This literature has generated gene-discovery efforts through genetic linkage methods (5–12), with successful follow-up of positive linkage regions (13–15), and through genomewide association studies of alcoholism (16,17). However, with the exception of genetic analyses of individual alcoholism symptoms (18,19), the specific aspects of AD symptomatology that best define its core heritable phenotype(s) has received inadequate attention. Alcohol abuse, for example, is commonly ignored as genetically uninformative, though the evidentiary basis for this assumption is weak (20). Despite widespread reliance on a binary dependence measure, evidence supporting a continuum of alcohol problems has been found repeatedly in both clinically ascertained (21) and general community (22–24) samples. From such analyses have come proposals for a quasi-continuous characterization of AD symptoms for DSM-V (25,26).