Large-scale GWAS reveals insights into the genetic architecture of same-sex sexual behavior

Abstract

Twin and family studies have shown that same-sex sexual behavior is partly genetically influenced, but previous searches for specific genes involved have been underpowered. We performed a genome-wide association study (GWAS) on 477,522 individuals, revealing five loci significantly associated with same-sex sexual behavior. In aggregate, all tested genetic variants accounted for 8 to 25% of variation in same-sex sexual behavior, only partially overlapped between males and females, and do not allow meaningful prediction of an individual’s sexual behavior. Comparing these GWAS results with those for the proportion of same-sex to total number of sexual partners among nonheterosexuals suggests that there is no single continuum from opposite-sex to same-sex sexual behavior. Overall, our findings provide insights into the genetics underlying same-sex sexual behavior and underscore the complexity of sexuality.

Mental Health Disparities Mediating Increased Risky Sexual Behavior in Sexual Minorities: A Twin Approach

“…In the first section of the indirect pathway, minority sexual orientation was significantly and comparably associated with increased mental health problems in men and women, and this has been linked to minority stress (Hatzenbuehler, 2009). Similar to prior findings (Frisell et al, 2010;Ganna et al, 2019;Zietsch et al, 2012), this relationship was further influenced by genetic and unique environmental factors. However, the influences of these factors were transmitted through phenotypic causal paths rather than as effects of common genetic and environmental factors.…”

“…This finding raises the possibility that common genetic and environmental factors may additionally influence the relationship between sexual orientation, and disparities in mental health and risky sexual behavior. This is further supported by evidence of genetic correlations between sexual orientation and depression (Ganna et al, 2019, Zietsch et al, 2012 and multiple sexual partners (Burri, Spector, & Rahman, 2015) with genetic factors explaining 60% and 78% of the phenotypic correlation of sexual orientation with depressive symptoms (r = .26;Zietsch et al, 2012) and with number of sexual partners (r = .13; Burri et al, 2015), respectively. Other support involves the genetic overlap between neuroticism, which is highly correlated with depression, and risky sexual behavior (r = .09, genetic correlation = .21; Zietsch, Verweij, Bailey, Wright, & Martin, 2010).…”

Prosociality and a Sociosexual Hypothesis for the Evolution of Same-Sex Attraction in Humans

“…SSSA persists both within and across cultures (Witham and Mathy, 1985;Crompton, 2006) and within families, since sexual orientation has high heritability (Pillard and Bailey, 1998;Mustanski et al, 2005;Santtila et al, 2008;Bailey et al, 2016). Evidence from human twin studies and genome-wide genetic association studies suggest that about one third of the variation in sexual orientation can be attributed to additive genetic factors (Santtila et al, 2008;Bailey et al, 2016;Ganna et al, 2019). For evolutionary biologists the puzzle is typically posed like this: how can a heritable SSSA persist in a population when homosexual sex of itself is non-reproductive and homosexual people have fewer offspring on average than heterosexual people (Bell et al, 1981;King et al, 2005;Wrangham, 2019).…”

“…Genetic changes underlying the evolution of such traits are likely to be complex and highly polygenic. Presently not much is known about the genetic basis of human SSSA, but as we learn more about it, it is clear human SSSA is also highly polygenic and a complex multicomponent trait (Mustanski et al, 2005;Prum, 2017;Sanders et al, 2017;Ganna et al, 2019;Swift-Gallant et al, 2019). The high heritability of human SSSA is caused by a large number of genes each with individually small effect.…”

It is time to get real when trying to predict educational performance

“…For example, researchers are exploring the use of these scores to predict the onset of complex diseases, such as cardiovascular disease, diabetes and cancer. It has also been proposed that polygenic scores could be used to predict educational attainment (Lee et al, 2018), and social behaviors such as loneliness (Abdellaoui et al, 2018) and same-sex sexual behavior (Ganna et al, 2019). However, even when the association between a polygenic score and a certain phenotype is statistically significant, this does not always guarantee the polygenic score will have a strong predictive power.…”