Origins of male homosexuality - Conclusion

What causes exclusive male homosexuality? This is the question I’ve addressed in the last few posts. The answer is still elusive although there seems to be consensus on some points.

One such point is the relative importance of inborn causation versus environmental causation. In men, an exclusively homosexual orientation has a heritability of 30-45%. A genetic cause must therefore be interacting with an unknown but more important environmental cause (Bailey et al., 2000). The genes in question are likewise unknown but may be located near the ones for RH factor (Ellis et al., 2008).

This raises another question. Why would natural selection create a genetic predisposition, however minor, to become exclusively gay? The answer is probably the one put forward by Ed Miller (2000). Human evolution has seen a relatively recent increase in provisioning by men of their mates and offspring, together with a corresponding decrease in polygyny. Even among present-day humans, this evolutionary trend has gone further in some populations than in others. How, then, did natural selection change male behavior over so little time? Miller’s answer: by partially feminizing the male mind (i.e., by impeding cerebral masculinization during prenatal and neonatal development). This is the fastest way with the least genetic change, the only downside being an increased risk that some boys will grow up with the wrong sexual orientation.

For several reasons, I disagree with Miller on one point: I believe that the downside of this rapid natural selection has not been a certain proportion of exclusively homosexual men but rather a larger proportion of weakly heterosexual men. First, as noted earlier, the genetic predisposition is not acting alone. It seems to be interacting with a more important cause of environmental origin. Second, I have trouble believing that a balanced polymorphism could maintain 3-5% of all men in a state of sexual indifference to women. (I incidentally feel the same way about the ‘gay uncle’ theory, where the reproductive cost of indifference to women is balanced by care given to related children—the cost seems too high to offset the presumed benefit). Third, I have trouble believing that 3-5% of all men were sexually indifferent to women before the late 19th century. Male homosexuality is attested in earlier time periods but usually in a facultative form, i.e., older heterosexual men having sex with boys or with males of servile status.

In my opinion, the likeliest scenario is one where a genetic predisposition weakens male heterosexuality but is not enough, in itself, to cause exclusive male homosexuality. Something in the environment has to push some of these heteros over the borderline. If so, there must be a large population of weakly heterosexual men, certainly much larger than the 3-5% who end up being exclusively homosexual.

Alongside this scenario would be a residual of various other causes—random genetic mutations, psychological or environmental stresses during pregnancy, chimerism, etc.—that each occur at such a low rate that natural selection cannot effectively counter any one of them. These residual causes might account for a baseline of exclusive male homosexuality that has always been with us, perhaps less than 1% of all men.

The current level of 3-5%, however, is much harder to ascribe to longstanding causes. I suspect it’s recent, essentially since the late 19th century, and due either to a pathogen that is co-evolving with its host population or to a recent environmental factor that humans have not yet overcome through natural selection.

If a pathogen is responsible, it may have become more prevalent because of the great increase in urbanization at that time or perhaps because some other factor had increased transmissibility. The main problem so far with the ‘gay germ’ theory is simply lack of evidence. Where is the smoking gun?

If a new environmental factor is responsible, it may be some kind of estrogen or estrogen-like compound in the neonatal environment. The late 19th century, however, is too early for most candidates. In fact, there seem to be only two credible ones. One is borax, which was used as a food preservative until the 1950s. The other is estrogen-rich drinking and bathing water from sources contaminated by untreated wastewater. Such effluent greatly increased in volume with the introduction of modern sewer systems in the late 19th century and decreased only with conversion to secondary and tertiary wastewater treatment during the 1970s.

How should we test these different theories? First, we should do what researchers normally do: conduct controlled studies and debate the findings in academic journals. Unfortunately, very little of either is going on. J. Michael Bailey, Lee Ellis, and the people around them, seem to account for much of the current research (and even Bailey runs into a great deal of flak). Most real debate actually seems to be happening in the blogosphere. This may or not be a bad thing, but it does say a lot about the climate surrounding this subject.


References

Bailey, J.M., M.P. Dunne, & N.G. Martin. (2000). Genetic and environmental influences on sexual orientation and its correlates in an Australian twin sample. Journal of Personality and Social Psychology, 78, 524-536.

Ellis, L, Ficek, C, Burke, D, & Das, S. (2008). Eye color, hair color, blood type, and the rhesus factor: exploring possible genetic links to sexual orientation. Archives of Sexual Behavior, 37(1), 145-9.

Miller, E.M. (2000). Homosexuality, birth order and evolution: Toward an equilibrium reproductive economics of homosexuality. Archives of Sexual Behavior, 29, 1-34.