Still, accumulating such data on one hundred thousand or more individuals (necessary to detect effect sizes of the order of 0.001% [one tenth of one percent] of the variance with reasonable power) would be feasible. The immediate clinical value of identifying a number of very weakly but significantly associated variants by such an approach may be low, but identification of genes and pathways involved in individual variation in liability to alcohol use disorders could be great. Perhaps more narrowly defined consequences of alcohol effects (alcoholic liver disease; severe alcohol withdrawal) will give more hopeful outcomes. It is also possible however that work on genomic profiling, using random effects modeling of genomewide SNP data (48) will point to new directions in biological psychiatry, yielding greater understanding of the genetic contributions to individual phenotypes and enabling better quantification of genetic risk, thereby overcoming one of the primary challenges in prospective research on high-risk groups, and in resilience research, namely the inability to achieve sharp differentiation of genetic risk between groups.
