We identified 14, 23, and 1 genomic risk loci for the residual-PAU, PTU, and CUD phenotypes, respectively, whereas the residual-OUD GWAS did not identify any genome-wide significant hits (Supplementary Table 5). Many of these loci were mapped to genes involved in pharmacokinetic (e.g., metabolism) or pharmacodynamic (e.g., drug targets) processes for specific substances. For example, residual-PAU loci were mapped to genes in the alcohol dehydrogenase family (ADH1B, ADH4, ADH5, ADH6), which is involved in metabolism of alcohol, and loci for residual-PTU were mapped to genes in the nicotinic acetylcholine receptor family of proteins (CHRNA3, CHRNA5, CHRNA6, CHRNB3, CHRNB4).
