We performed a secondary GWAS focusing on three clinically recognized subtypes of bipolar disorder: BD1 (n=14,879 cases), BD2 (n=3,421 cases), and SAB (n=977 cases) (Supplementary Note, Supplementary Tables 1A & 11, Supplementary Figure 6). We observed variants in 14 loci with genome-wide significance for BD1, 10 of which were in genome-wide significant loci in the combined BD GWAS analysis. Not surprisingly given the sample overlap, 3 of the 4 remaining loci genome-wide significant for BD1 have P < 10−6 in either our discovery GWAS or combined analysis. The remaining locus (MAD1L1, chr7:1.9Mb, discovery GWAS p = 2.4×10−6) was recently published in two BD GWAS that included Asian samples 44,45. We did not observe genome-wide significant results for the smaller BD2 and SAB analyses. BD1, BD2 and SAB all have significant common variant heritabilities (BD1 h2snp = 0.25, se = 0.014, p = 3.2×10−77; BD2 h2snp = 0.11, se = 0.028, p = 5.8×10−5; SAB h2snp = 0.25, se = 0.10, p = 0.0071). Genetic correlations among BD subtypes show that these represent closely related, yet partially distinct, phenotypes (Supplementary Table 12).
