Genome-wide association studies (GWASs) of AUD and DPW have identified multiple risk loci. The largest GWAS of problematic alcohol use (PAU; N = 435,563) which meta-analyzed AUD with a GWAS of the problem-subscale of the Alcohol Use Disorders Identification Test (AUDIT-P) reported genome-wide associations at 29 loci encompassing 66 genes, the largest tranche of signals for any addictive disorder to date10. In comparison to Zhou and colleagues PAU GWAS, other comparatively large GWAS of alcoholism concentrated on the consumption aspect of addictive disorders. For example, the largest GWAS of typical alcohol intake (N = 941,280) identified more than 200 independent genome-wide significant variants within or near more than 150 genes at 81 independent loci11. Despite a genetic correlation (SNP-rg) of 0.77 between PAU and DPW (less so for AUD and DPW, SNP-rg=0.67), genetic correlations between these aspects of alcohol involvement and other anthropometric, cardio-metabolic, and psychiatric disorders revealed marked distinctions10–14. For instance, while AUD and PAU appear to be consistently associated with increased genetic liability for other psychiatric disorders and positively with liability to educational achievement, DPW is genetically uncorrelated
