22 July 2011

Genetics, evolution, and sexual orientation: the gay extinction hypothesis

Three weeks ago, I went to the Cornerstone Music Festival with my two oldest kids. For the second year, I was an invited speaker in the festival's excellent seminar program. This year, my two series were entitled "Alien Worlds" and "Zombies on Jeopardy" – exploring extreme biology and human nature, respectively. It was fun, if a little too hot for a day or so.

At one point, I was discussing human intelligence and its genetic underpinnings. And I got a loaded question, paraphrased thus: "What happens when you substitute 'sexual orientation' for intelligence? Is homosexuality 'genetic' and if so, what does that mean for Christian views of sexuality?" (The Cornerstone Festival is a Christian music festival, known for embracing music at the 'fringes' while remaining consistent with most mainstream evangelical sensibilities, including a typically evangelical view of homosexuality.) I answered that sexual orientation also has a fairly significant heritable component, meaning that some of the variation in sexual orientation is accounted for by genetics. Then I got a followup question/comment, delivered with intriguing smugness, and paraphrased as follows: "Homosexuality can't be genetic, because homosexuals don't have kids and so the trait will be eliminated from the population." Without going into the complexity of sexual orientation as a biological phenomenon, I will critique this person's claim, since I hear it from Christians with disheartening frequency.

Let's call this claim the gay extinction hypothesis. It can be broken down into two basic assertions:
1. The trait reduces fitness (to near zero) by inhibiting (almost completely) reproduction.
2. Because the trait reduces fitness to near zero, the gene that causes it should have been eliminated from the human population.

Both assertions, when applied to sexual orientation, are incorrect.

Homosexuality does reduce reproduction, at least in men, but not to zero. According to a widely-known study from the 1990's, gay men have about 1/10 the number of children as straight men. That's surely an approximation, and it's a dramatic effect. But it's clearly not the case that homosexuals can't or don't reproduce, and we haven't even explored all the other ways (e.g., reproductive technologies) in which the assertion doesn't work.

Still, let's grant the reproductive disadvantage for the sake of argument and move to the second assertion. Shouldn't we expect any gene that reduces reproduction by 90% to be extremely rare in a population? No, not necessarily. This is the bigger error in the gay extinction hypothesis.

The main error, in my view, is the assumption that the gene that causes the trait is always expressed. (I'm simplifying things to a large extent by referring to one "gene" and one "trait." Correcting these simplifications makes the gay extinction hypothesis even more problematic.) And this would imply that the trait is dominant. (A dominant trait is one in which the individual will express the trait if he or she possesses just one copy of the dominant form of the gene.) But we have no reason to suppose that sexual orientation is a dominant trait. On the contrary, sexual orientation is the kind of complex trait that is expected to be influenced by multiple genes interacting with other factors. While we might postulate that certain gene forms can influence the trait to a much bigger extent than others, we would also expect that gene forms associated with homosexuality can be carried by heterosexual individuals. In other words, it is not the case that a "gay gene" (or genes) is expected to lead to homosexuality whenever it is present in an individual.

To see what I mean by all this, consider the example of cystic fibrosis (CF). This awful disease is as purely genetic as any human disease we know. It shortens life expectancy and, more to the point for our gay extinction hypothesis, leads to significant infertility. (At least 98% of males with CF  have no vas deferens and are therefore infertile; the disease also devastates female fertility.) Homosexuality looks tame by comparison. And yet, the gene form that causes CF is distressingly common in certain human populations (namely in those people of European descent). How can this be? How can such a gene form be present in the population at all? Note that this is exactly the challenge posed by the gay extinction hypothesis.

The basic answer is this: a person with just one of those lethal gene forms is unaffected. We call the person a "carrier." Before having an affected child (or a genetic test), such a person would never know that he or she is a carrier. One copy of that wrecked gene form would have no influence on that person's reproductive ability, a.k.a. the person's fitness.* My basic point is one that should be taught in any introductory biology course: there is nothing surprising about the presence of gene forms that lower fitness, and that should be clear with a single visit to the OMIM database. To be sure, we might wonder how they got into our genomes in the first place, and how they are maintained at particular frequencies in our population. We really needn't wonder at their existence, or even their ubiquity.

There is much, much more that could be said about sexual orientation, its genetic components, and evolutionary influences thereupon. But there should be no place for simplistic and bogus claims about the evolutionary impossibility of homosexuality. The extent to which sexual orientation is a "choice" is, I think, an open question. The validity of the gay extinction hypothesis is not.

* Interestingly, one model suggests that possession of one of the wrecked CF gene forms provides a small fitness advantage in the form of protection against tuberculosis. A conceptually identical model has been proposed to explain relatively high rates of human homosexuality.

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