The Pearson's correlation between the two PGRS for alcohol dependence derived from the SAGE and Yale‐Penn GWAS was 0.61. Polygenic risk for alcohol dependence in GS:SFHS was positively associated with alcohol consumption (SAGE: β = 0.045, P = 0.00003; Yale‐Penn: β = 0.042, P = 0.00009) (Table 1). The proportion of variance in alcohol consumption explained by risk scores was low: less than 0.2 percent (Fig. 1). Using the PGRS derived from the meta‐analysis of the SAGE and Yale‐Penn GWAS, the effect size and variance explained increased modestly (β = 0.049, P = 2.8 × 10−6, r 2 = 0.0022) (Table 1). The SAGE and Yale‐Penn alcohol scores remained significantly associated with alcohol consumption when chromosome 4 SNPs were removed (Yale‐Penn: β = 0.034, P = 0.001, r 2 = 0.00102 and SAGE: β = 0.036, P = 0.0006, r 2 = 0.0012) (Supporting Information Table S1). The effect size (β) was reduced by 14–24 percent (Yale‐Penn and SAGE scores, respectively). Although chromosome 4 SNPs explain some of the variance in alcohol consumption, a significant polygenic risk signal is present on the remaining chromosomes.
