We identified 124 approximately independent SNPs (pairwise r2 < 0.1) that attained genome-wide significance (P < 5×10–8). These 124 “lead SNPs” are listed in Supplementary Table 3 and shown in Fig. 1a. All have coefficients of determination (R2’s) below 0.02%, and the SNP with the largest per-allele effect is estimated to increase general risk tolerance by ~0.026 standard deviations in our discovery sample (Supplementary Fig. 2). To test if the lead SNPs’ effect sizes are heterogeneous across the 23andMe and UKB cohorts, we generated an omnibus test statistic by summing Cochran’s Q statistics across all lead SNPs; consistent with our genetic correlation estimate of less than unity between the two cohorts, we rejected the null hypothesis of homogeneity (P = 4.32×10–5; Supplementary Note). To define genomic loci around the lead SNPs, we took the physical regions containing all SNPs in LD (pairwise r2 > 0.6) with the lead SNPs and merged loci within 250 kb of each other; the 124 lead SNPs are located in 99 such loci (Supplementary Table 3). We supplemented those analyses with a conditional and joint multiple-SNP (COJO) analysis13, which identified 91 genome-wide significant “conditional associations” (Supplementary Table 3).
