examined two genes in relation to six related alcohol outcomes in an effort to systematically assess the association. Prior evidence for genetic association, along with the high degree of correlation between the alcohol phenotypes (r2 range from 0.35-0.96) and SNPs (r2 from 0.01-0.75), mitigates the concern that results are merely a consequence of multiple testing. Nevertheless, when we applied the Benjamini-Hochberg procedure to control the false discovery rate at 0.05 (Benjamini & Hochberg, 1995), all results remained significant except that ADH1B-rs1229982 was not associated with AUD severity. Last, in Israel, consuming several drinks on one occasion is common in religious practice (e.g., Purim and the Passover Seder), and might occur for cultural/environmental reasons even among individuals who would otherwise drink much less. As a sensitivity analysis, we conducted post-hoc analyses of another measure, “usual drinks,” which indicates how many drinks a respondent usually had in a single day. Association results were similar in that ADH1B was significantly related to usual drinks, and ADH1C, when analyzed jointly with ADH1B, was not related to usual drinks.
