Re: Evolution and homosexuality

Whenever biologists find a gene that seems likely to decrease its organism's reproductive success, the student of evolution wonders how this gene survived the process of natural selection. Discussion of such questions tends to resemble unconstrained speculation, since proposed explanations are often not testable by experiment; so don't be disappointed by the lack of rigor in this short note.

Some preliminaries:

A trivial explanation for a seemingly deleterious gene's existence is that the gene is the result of a recent mutation, and the selective process has not yet had time to eliminate it. For example, some claim that the haemophilia gene in the Russian royal family appeared by mutation at a specific point in the family tree, though I think it would be hard to prove this proposition. In any event, this sort of explanation is not applicable to a phenomenon as widespread as homosexuality.

Secondly, it is imporant to note that a gene is not always as damaging to reproductive success as it may seem on the surface. A gene that has devastating effects after its organism has passed reproductive age is somewhat sheltered from selection. Perhaps more pertinent to homosexuality, a successful gene may reduce its own organism's reproduction while aiding the reproduction of siblings. Finally, note that traditional social suppression of homosexual behavior would have the effect of reducing the selective pressure against a gene for such behavior. Recent trends toward public acceptance of blatantly nonreproductive behavior have presumably increased the selective pressure against such genes.

Now for more specific suggestions:

A gene that is deleterious (in the sense of reducing reproductive success) in large doses may be beneficial in small doses. A classic example is the gene for sickle cell anemia, which in large doses (i.e., in a person with two copies of the gene) produces a debilitating disease, but in small doses (i.e., in a person with a single copy of the gene) produces a heightened resistance to malaria. For any numerical values you care to pick for (a) the benefit of a little extra malaria resistance, and (b) the penalty for having the debilitating disease, you can compute an equilibrium frequency for the sickle-cell gene, below which the gene will, on the average, benefit the organisms bearing it more than it hinders them.

Similarly, there is evidence that a single dose of the cystic fibrosis gene, which produces disease in a double dose, may increase resistance to cholera. (more on this) The relevance to the homosexual-gene hypothesis is, of course, that such a gene might, in heterozygotes (people with a single copy), produce behavior that promotes reproductive success.

A slightly different observation is that practically all of our genes find themselves, during the evolutionary process, half the time in female bodies and half the time in male bodies. A gene that is somewhat detrimental to male owners can survive if it is sufficiently beneficial to female owners. Selective pressure, in this case, will not be to eliminate the gene, but to build for it a regulatory mechanism that will express it more in females than in males. The appearance of inherited behavior that is reproductively deleterious in one sex but beneficial in the other might merely reflect evolution's failure to surround some such gene with well functioning regulatory machinery.

- Peter Pearson