Balancing selection and homosexuality (revisited)

Genetic traits predisposing to homosexuality decrease their bearers' genetic fitness. Therefore, they should be weeded out of the gene pool. However, such traits could persist if their expression in homosexuals was balanced by a reproductive advantage when they are expressed in heterosexuals.

This paper looks at the heterosexual brothers of homosexuals (who share half their genes), to see if they have increased reproductive success -- and they don't.

This is consistent with my hypothesis that a factor contributing to homosexuality is an excess of feminine (or deficiency of masculine) traits expressed in the wrong (i.e. male) gender. According to this hypothesis, male homosexuality would be associated with greater reproductive success in female family members, who would possess an excess of feminine traits: what's bad for the males in the family would be good for the females. You can read more about this in Beautiful Wives and Gay Sons.

I think that an interesting aspect of the homosexual paradox stems from the common variant/common trait assumption, which states that a relatively common phenotype should be the result of a relatively common genotype. Thus the question: how is such a genotype maintained in the gene pool at a non-trivial frequency?

The idea of balancing selection is certainly a mechanism which may solve the paradox. But, on the other hand, it's also possible that the genetic basis of homosexuality is not a population-wide phenomenon, but rather multiple independent mutations arising all over the population in each generation, and quickly dying out after a few generations.

So, it is not a question of how the "gay gene" is maintained at a high-enough frequency in the gene pool despite its obvious reproductive shortcomings. Such common population-wide gene(s) probably do not exist.

In my opinion, homosexuality is maintained by several factors:

1. The expression of feminizing (or masculinizing) genes in men (or women).
2. Deleterious loss-of-function genes appearing de novo in each generation and quickly weeded out by selection
3. Social pressures to produce offspring which limit the effects of selection.

An interesting consequence of #3 is that as social tolerance for this behavior increases, its genetic basis will decrease, as men who would -in previous generations- be involved in sham marriages are now free to engage in their preferred behavior, removing their genetic contribution to the gene pool. Of course, factors 1-2 in addition to environmental influences will suffice to reproduce the phenomenon in society.

Here is a previous post on balancing selection and homosexuality.

Evolution and Human Behavior doi:10.1016/j.evolhumbehav.2008.08.004

Testing Miller's theory of alleles preventing androgenization as an evolutionary explanation for the genetic predisposition for male homosexuality

Pekka Santtila et al.

Abstract

The genetic background of male homosexuality presents an evolutionary paradox, since homosexuality could be considered a reproductive disadvantage. We tested E.M. Miller's (2000) balanced polymorphism explanation, which states that alleles partially preventing androgenization in male fetuses during pregnancy would be associated with a homosexual orientation. Having all the alleles produces homosexuality, while heterosexual carriers with only a few of these alleles instead have a reproductive advantage; that is, they have more traits, which, by controlling for excessive aggressiveness and psychopathy, make them more attractive mates. Pairs of brothers were used to test these assumptions. If homosexuality is due to having all the androgenization-preventing alleles, then heterosexual men with homosexual brothers are more likely to also have some of the these alleles compared to heterosexual men with heterosexual brothers. These two categories were compared on variables related both directly and indirectly to reproductive success, with heterosexual men with a homosexual brother hypothesized to have an advantage on the variables. However, no statistically significant findings in support of the theory were detected. The results were discussed together with alternative explanations.

Link