There were two sets of analyses conducted on additional samples. For MDD replication, we used meta-analysis to combine the autosomal discovery results (554 SNPs with P< 0.001) with summary association results from independent samples42–48 (6783 MDD cases and 50 695 controls). The discovery SNP results were grouped into regions defined by linkage disequilibrium using an iterative process after ranking all SNPs by association P-value: for SNPs with r2 > 0.2 in a 1Mb window (based on HapMap3 CEU+TSI), the most strongly associated SNP was retained. In addition, given the close genetic and phenotypic relationships between MDD and BIP, we combined the MDD discovery sample and the PGC BIP mega-analysis36 to evaluate 819 autosomal SNPs with P < 0.0001 in either of the separate analyses. (See Sklar et al.36 for complete description). In effect, we tested for associations with a more broadly defined mood disorder phenotype. After resolving overlapping control samples, there were 32 050 independent subjects (9238 MDD cases/8039 controls and 6998 BIP cases/7775 controls).
