Clumping the ADH locus for linkage disequilibrium (LD; r2 < 0.1 within 500 kb) suggested multiple independent signals in both populations, with the differing leading alleles reflecting different LD structures and allele frequencies in each population (Table 2, Supplementary Figure S2). Conditional analyses controlling for rs1229984 and rs2066702 had limited power, but results showed limited attenuation of effect sizes between marginal and conditional analyses, consistent with the existence of additional independent effects in the region (Supplementary Table S3; Supplementary Figure S3). Suggestive independent signals in the genotyped cohorts included trialleleic variant rs894368 (marginal z = −4.57, p = 4.9E-6; conditional z = −4.53, p = 5.8E-6) and insertion rs112346244 (marginal odds ratio = 0.912, SE = .024, z = −3.81, p = 1.4E-4; conditional odds ratio = 0.883, SE = .025, z = −5.05, p = 4.5E-7; Supplementary Table S3). Several additional variants that were prioritized in the conditional analysis, while not significant, were in moderate to strong LD with rs698 (marginal odds ratio = 1.115, SE = .021, z = 5.19, p = 2.1E-7; conditional odds ratio = 1.084, SE = .021, z = 3.78, p = 1.6E-4), a functional ADH1C variant with a role in AD8,11.
