My initial inspiration for starting this blog was a brief piece I had written about why Lady Gaga’s song, “Born This Way”, really got under my skin. The general premise of the song is, unless I’m badly mistaken, that homosexuality is genetic in nature, and, accordingly, should be socially accepted. The song is full of very selective logic and a poor grasp of the state of scientific knowledge, all of which is accepted in the service of furthering a political goal. For what it’s worth, I agree with that goal, but the means being used to achieve it in this case were misguided because:
“…I’m not so sure Lady Gaga – or any gay-rights supporter – wants to base their claims to equal rights on the supposition that homosexuality is a trait people are “born” with…If further research uncovers that people can come to develop a homosexual orientation for a number of reasons that have nothing to do with being “born like that”, I wouldn’t want to see the argument for equal rights slip away.”
Today, I’m going to be stepping back into that same political minefield that I did on the topic of race, and discuss a hypothesis regarding the cause of male homosexuality that some people may not like. People will not like this hypothesis for reasons extrinsic to the hypothesis itself, but do your best to contain any moral outrage you may be feeling. My first task in presenting this hypothesis will be to convince you that male homosexuality is not genetically determined – despite what an eccentric young pop-star might tell you – and is also not an adaptation.
Convincing critics is always such a pleasure.
For some, it might seem insulting that homosexuality requires an explanation, whereas heterosexuality does not. Aren’t both just different sides of a very bisexual coin? There’s a simple answer to that concern: heterosexual intercourse is the only means to achieve reproduction. An exclusive homosexual orientation is the evolutionary equivalent to sterility, and if three to five percent of the male population was consistently sterile – despite neither of anyone’s parents being sterile, by definition – that would raise some questions as to how sterility persists. There would be an intense selective pressure away from sterility, and any genes that actively promoted it would fail to reproduce themselves. That homosexuality seems to persist in the population, despite it being a reproductive dead-end, requires an explanation. Heterosexuality poses no such puzzle.
The first candidate explanation for the persistence of homosexuality is that it’s part on an adaptation for assisting the reproduction of one’s kin. While homosexuals themselves may suffer a dramatic reduction in their lifetime reproduction, they activity assist other genetic relatives, delivering enough benefits to offset their lack of personal reproduction, similar to how ants or bees would assist the queen, forgoing reproduction themselves. This suggestion is implausible on three levels: first, it would require that homosexuals deliver enormous benefits to their relatives. For each one child a gay man wouldn’t have, they would need to ensure a brother or sister would have an additional two that they wouldn’t otherwise have without those benefits. This would require an intense amount of investment. Second, there’s no theoretical reason that’s ever been provided as to why homosexuals would develop a homosexual orientation, as opposed to, say, an asexual orientation. Seeking out intercourse with same-sex individuals doesn’t seem to add anything to the whole investment thing. Finally, this explanation doesn’t work because, as it turns out, homosexuals don’t invest anymore in their relatives than heterosexuals do (Rahman & Hull, 2005). So much for kin selection.
A second potential explanation for homosexuality is that it’s the byproduct of sexually antagonist selection; a gene that damages the reproductive potential of males persists in the population because the same trait is beneficial when it’s expressed in female offspring (Ciani, Cermelli, & Zanzotto, 2008; Iemmola & Ciani, 2009). Another potential explanation is that a homosexual orientation is like sickle cell anemia: while it hurts the reproductive prospects of those who express it, it provides some unspecified benefit that outweighs that cost in some carriers, as sickle cell protects against malaria. Both explanations have a large issues to contend with but one of the most prominent shared issues is this: despite both hypotheses resting on rather strong genetic assumptions, half or more of the variance in male homosexual orientation can’t be attributed to genetic factors (Kirk et al., 2000; Kendler et al., 2000). Identical twins don’t seem to be concordant for their sexual orientation anymore than 30 to 50% of the time when one of the twins identifies as non-heterosexual. If homosexuality was determined solely by genes, there should be a near complete agreement.
In fact, most of the variance appears to be due to our decadent Western lifestyle. Who knew, right?
Accordingly, any satisfying explanation for homosexuality needs to reference environmental factors, as all traits do; the picture is far from as crude as there being some genes “for” homosexuality. While there clearly are some genetically inherited components in the ontogeny of a homosexual orientation, it’s entirely unclear what those genetic factors are. It’s also far from clear how those genetic factors interact with their environment – or when, for that matter. They would seem to act sometime before puberty, but beyond that the door is open. What seems to have been established so far is that an exclusive homosexual orientation is detrimental to reproduction in a big way, and these costs are not known to be reliably offset.
There is one last hypothesis that may hold some potential, though, as I mentioned, I suspect many people won’t like it: the “gay germ” theory. The general idea is that some outside pathogen – be it a bacteria or a virus – manipulates development in some way, the end result being a homosexual orientation. This hypothesis seems to have potential for a number of reasons: first, it neatly deals with why homosexuality persists in the population, despite the massive reproductive costs. It could also account for why monozyogtic twins are often discordant for homosexual orientation, despite sharing genes and a prenatal environment. As of now, it remains an untested theory, but other lines of research suggest some preliminary success using the same basic idea to understand the persistence of disorders like schizophrenia and obsessive compulsive disorder, among many others. Of course, such a theory does come with some political baggage and questions.
Like: will two gay men ever be able to hold hands, post love-making, on top of an American flag, just like straight couples do?
The first set of questions concern the data speaking to the hypothesis: what pathogen(s) are responsible? When do they act in development? How do they alter development? Are those alterations an adaptation on the part of the pathogen or merely a byproduct? These are no simple questions to answer, especially because it won’t be clear which children will end up gay until they have matured. This makes narrowing the developmental window in which to be looking something of task. If concordance rates for monozyogtic twins are similar between adopted and reared together twins, that might point to something prenatal, depending on the age at which the twins were separated, but would not definitively rule out other possibilities. Further, this pathogen need not be specific to gay men; it could be a pathogen that much of the population carries, but, for whatever reason, only affects a sub-group of males in such a way that they end up developing a homosexual orientation.
The second set of questions concern potential implications of this theory, were it to be confirmed. I’ll start by noting these concerns have zero, absolutely nothing, to do with whether or not the gay germ theory is true. That said, these concerns are probably where most of the resistance to the hypothesis would come from, as concerns for data (or lack thereof) are often secondary to debates. Yes, the hypothesis cries out for supporting data so it shouldn’t be accepted just yet, but I’m talking to those people who would reject it as a possibility out of hand because it sounds icky. In terms of gay rights and social acceptance, it shouldn’t matter whether homosexuality is 100% genetically determined, caused by a pathogen, or just a choice someone makes one day because they’re bored with all that vanilla heterosexual sex they’ve been having. That something may be, or is, caused by a pathogen should really have no bearing on it’s moral status. If we discovered tomorrow that it was a virus that caused men to have larger-than-average penises, I doubt many people would cheer for the potential to cure the “disease” of large-penis.
References: Ciani, A.C., Cermilli, P., & Zanzotto, G. (2008). Sexually antagonistic selection in human male homosexuality. PLosone.org, 3, e,2282.
Iemmola, F. & Ciani, A.C. (2009). New evidence of genetic factors influencing sexual orientation in men: Female fecundity increase in the maternal line. Archives of Sexual Behavior, 38, 393-399
Kendler, K.S., Thornton, L.M., Gilman, S.E., & Kessler, R.C. (2000). Sexual orientation in a U.S. national sample of twins and nontwin sibling pairs. American Journal of Psychiatry, 157, 1843-1846
Kirk, K.M., Bailey, J.M., Dunne, M.P., & Martin, N.G. (2000). Measurement models for sexual orientation in a community twin sample. Behavior Genetics, 30, 345-356
Rahman, Q. & Hull, M.S. (2005). An empirical test of the kin selection hypothesis for male homosexuality. Archives of Sexual Behavior, 234, 461-467