Comparing our GWAS to recent GWAS of alcohol consumption measures suggests that the liability underlying normative patterns of alcohol intake and AD are only partially overlapping. Genome-wide, genetic correlations were significantly < 1 with log-scaled alcohol consumption by participants in AlcGen and CHARGE+ Consortia cohorts16 (rg = 0.695) and in the UK Biobank17 (rg = 0.371). We also observe only partial replication of the 8 loci significantly associated with consumption in the UK Biobank, with strongest results from SNPs in the ADH region, including a proxy for rs1229984. In addition there was no significant correlation with GWAS of log-scaled AUDIT scores in 23andMe participants18 (rg = 0.076). Subsequent analyses suggest these estimates are sensitive to sample characteristics, with somewhat higher genetic correlations reported in analysis of alcohol consumption in the full UK Biobank29 (rg = 0.75) and of AUDIT in combined data from 23andMe participants and UK Biobank30 (rg = 0.39). Importantly, initial UK Biobank data inclusion of a subset of participants recruited for a study of smoking and lung function in the first analysis17, which may have resulted in collider bias31 and contributed to the initial lower genetic correlation.
