No statistically significant heterogeneity was observed across individual cohorts for the 30 genome-wide significant loci, as assessed with Cochran’s Q-test (Supplementary Fig. 32), the I2 statistic and the genomic structural equation modeling (GenomicSEM) \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$${Q}_{{\rm{SNP}}}$$\end{document}QSNP statistic16 (Supplementary Table 2). Genome-wide analyses of samples grouped by clinical, comorbid, biobank and 23andMe information (Supplementary Table 3 and Supplementary Figs. 33–37) showed evidence that sample ascertainment impacted results at a genome-wide scale, although not beyond what is observed with closely related psychiatric disorders17,18. We observed moderate to high genetic correlations across the subgroups (between 0.63, s.e. = 0.11 for biobanks and comorbid information and 0.92, s.e. = 0.07 for 23andMe and comorbid information; Supplementary Table 7) and a satisfactory fit for a one-factor GenomicSEM model (Supplementary Table 8 and Supplementary Fig. 39). A common factor GWAS based on the one-factor GenomicSEM model resulted in 20 significant loci, all of which were also significant in the primary GWAS (Supplementary Table 8 and Supplementary Fig. 40; analysis details in Supplementary Note 5). SNP heritability (assuming a 1%
