Are there other theories on the origins of male homosexuality? Yes, quite a few. These theories generally fall into two categories: those that explain the relatively small variance due to genetic factors (30-45%) and those that explain the larger variance due to some environmental factor. Conceivably, we could be looking at an interaction between the two, i.e., an environmental factor (a pathogen, prenatal trauma, or perhaps environmental estrogens) interacting with a genetic predisposition (partly feminized male brains, as postulated by Ed Miller).
This week, we will look at another theory. Like Miller, Zietsch et al. (2008) postulate a genetic predisposition maintained by a balanced polymorphism. Unlike Miller, they believe this predisposition somehow increases mating success, rather than offspring survival.
Using twin data, they found that heterosexuals tend to have more sexual partners over a lifetime if they have a homosexual twin than if they have a heterosexual twin. This increased mating success, however, was significant only when the heterosexual was female. The authors attribute these findings to a genetically influenced behavioral trait.
Our hypothesis is that a number of pleiotropic (more than one effect) genes predispose to homosexuality but also contribute to reproductive fitness in heterosexuals. In the case of males, there are a number of alleles that promote femininity: if only a few of these alleles are inherited, reproductive success is enhanced via increased levels of attractive but typically feminine traits such as kindness, sensitivity, empathy, and tenderness. However, if a large number of alleles are inherited, even the feminine characteristic of attraction to males is produced. In females, the converse explanation could be used—a low dose could lead to advantageous typically masculine characteristics such as sexual assertiveness or competitiveness, and a large dose could further lead to attraction to females. (Zietsch et al., 2008)
The authors attribute this hypothesis to Ed Miller, although Miller’s theory has more to do with increased offspring survival (due to increased paternal investment) than to increased success on the mate market.
Does this hypothesis explain the authors’ findings? Does it predict that hetero women with gay or lesbian siblings have more lifetime sexual partners? No. First, it doesn’t explain why such an effect is confined to female heterosexuals. Nor is it clear why this hypothesis should account equally well for hetero women with gay brothers and for hetero women with lesbian sisters. The authors seem to be arguing that these women have more lifetime partners than do other women because they’re more feminine in some cases and more masculine in others.
Hmm … Could we be looking at a shared family environment effect? Parental attitudes toward homosexuality in offspring tend to correlate with parental attitudes toward promiscuity in offspring, especially in daughters. This correlation is especially high if we compare religious families with non-religious ones. If a mother and father accept expression of homosexuality in their children, they would probably also accept their daughters having more sexual partners. On these grounds alone, a gay or lesbian child is likelier to have a sister who has more sexual partners on average. But this correlation would not be a cause-and-effect one. It would flow from a common cause: parental permissiveness.
One could shoot back: “Homosexuals are not made by permissive parents. They’re born that way.” True, but the participants in this study were asked to self-identify as heterosexual or homosexual (on a scale of 1 to 6). Even if family environment doesn’t determine latent sexual orientation, this factor would probably influence one’s willingness to affirm it, both to oneself and to others.
Zietsch, B.P., Morley, K.I., Shekar, S.N., Verweij, J.H., Keller, M.C., Macgregor, S. Wright, M.J., Bailey, J.M., & Martin, N.G. (2008). Genetic factors predisposing to homosexuality may increase mating success in heterosexuals. Evolution & Human Behavior, 29, 424-433.