The power of our study, because of its family-structured sampling, approximates that of a study using a random sample of 7600 individuals (a conservative figure, since it ignores the oversampling of individuals from the upper tail of the distribution of alcohol consumption). The range of effect sizes that we actually observed, of the order of 0.15–0.25% of the variance, implies that at least several hundred genetic variants are contributing to variation; but in a discovery sample, selecting top hits will overestimate true effect sizes. Thus in hindsight the achieved power of our study to detect the effect of a specific variant will be low (Table S11 in the Supplement). Given a median effect size of 0.0017 for SNPs associated with AUD-FS at p<.0001, replication of a true association with 90% probability at alpha=5E-8, in the ideal case of complete linkage disequilibrium between marker and trait variant, would require approximately 27000 unrelated individuals, with more realistic effect sizes of 0.001 or 0.00075 requiring samples of 45,000 or 61,000. Imperfect linkage disequilibrium (D’=.9) with a modest mismatch between genetic marker allele frequency
