would be more readily available in other data-sets. We looked for consistency of evidence of genetic effects across phenotypes – between HOD and AUD-FS; for each with dependence diagnosis, and with other consumption measures. Finally, we used case-population control comparisons as a further check for consistency of evidence. To provide context for our findings, and guidelines for replication, we conducted power calculations for power to detect genetic association, under an additive genetic model, at alpha=5E-8, for a SNP in complete linkage disequilibrium, or with specified D′, with a variant, for a range of assumed effect sizes, using the Genetic Power Calculator (38).
