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To test whether these aggregate estimates of genetic effects correlate with sexuality in other samples, we constructed polygenic scores for same-sex sexual behavior (14, 24). These polygenic scores were significantly associated with sexual identity in MGSOSO (Wald test, P = 0.001) and same-sex attraction in the Add Health (P = 0.017) and CATSS (P = 3.5 × 10?6) studies (tables S12, S13, and S14). In CATSS, polygenic scores were also significantly associated with sexual attraction in participants at age 15 years (P = 6.4 × 10?5), suggesting that at least some of the genetic influences on same-sex sexual behavior manifest early in sexual development. The purpose of these analyses is to further characterize the genetic influences on same-sex sexual behavior and not to predict same-sex sexual behavior on the individual level. In all cases, the variance explained by the polygenic scores was extremely low (<1%); these scores could not be used to accurately predict sexual behavior in an individual.
Overall, these findings suggest that genetic influences on same-sex sexual behavior are highly polygenic and are not specific to the discovery samples or measures. All the SNPs measured, when combined, do not capture the entirety of family-based heritability (8 to 25% from GWAS versus 32% from family-based methods). In this, same-sex sexual behavior is similar to many other complex traits; the ratio between family-based heritability and SNP-heritability estimated in the same sample is consistent with empirical findings for the other 16 traits we tested (family heritability approximately three times larger than SNP-heritability) (Fig. 3) (14). There are many possible reasons for this discrepancy, including, but not limited to, variants not captured by genotyping arrays, nonadditive genetic effects, and phenotypic heterogeneity.
