The primary conclusion from these analyses is that, as for many other complex phenotypes (e.g. body-mass index: (39)), effect sizes for the contribution of individual genetic variants to differences in heaviness of alcohol consumption and alcoholism risk are small, perhaps accounting for as little as one-tenth of one percent of the variance. The approximately log-normal distribution of alcohol consumption in the general population is consistent with the hypothesis that this variation is being explained by small effects of many variants acting additively, rather than a few rare family-specific variants (40). For traits such as height (41) cumulative results do appear to support an important polygenic contribution to variation; and it seems plausible, given the many central and peripheral effects of alcohol, that this will also be true for variation in alcohol consumption and alcoholism.
