Dr. Serani was reporting on research that suggested possible genetic factors in human homosexual orientation. I questioned the genetic hypothesis on natural selection grounds--a gene that promoted homosexual behavior would tend to be eliminated from the population because such behavior doesn't favor reproductive success.
(An exception would be a case where the positive effect of a partial expression of a gene balanced the negative effect of the complete expression, a condition known as "adaptive polymorphism.")
It's much more plausible that a strong homosexual orientation is the result of some kind of infectious agent, such as a virus. The idea is not original with me, but was presented in a paper by Paul Ewald and Gregory Cochran, which Steve Sailer reproduced on his blog. Here's an excerpt:
Phenomena that strongly reduce the evolutionary fitness of their bearers cannot be maintained by strictly genetic causation at frequencies far above the rates at which they could be generated by mutation. The fitness costs of male homosexuality place it in this category. Perhaps more importantly, each of the hypotheses that have been put forward to explain male homosexuality have critical flaws that, if not sufficient to cause their outright rejection, are sufficient to severely weaken them. A full consideration of these issues is beyond the scope of this essay, but we briefly summarize the most salient points below.Although the Ewald/Cochran hypothesis remains unproven, it certainly seems plausible on the surface.
Human homosexuality can be traced back at least several thousand years. A substantially genetic cause could not be maintained over this time because of the great fitness costs that homosexuality imposes, unless there is some compensating benefit. But no evidence for a compensating benefit exists. Inclusive fitness benefits, for example, seem insufficient to overcome the reduction in reproduction, because male homosexuals do not channel their resources into the well-being of kin at an increased level. One could try to rescue the genetic causation hypothesis by arguing that reproductive effects of homosexuality have changed substantially in recent generations, with homosexual men having had just as many offspring as heterosexual men in previous centuries. This possibility seems unlikely from what is known about modern homosexual behavior, but it could be investigated empirically from historical records. A primarily genetic basis, however, is negated by the low monozygotic twin concordance, which is about 20 percent. Accordingly, the allele that purportedly conferred homosexual orientation has not stood up to independent testing .
Another hypothesis is that male homosexuality results from novel sociocultural influences, but the attraction to reproductive partners of a reproductively feasible sex seems so critical to evolutionary fitness that one would expect these attractions to be strongly buffered against social effects that could generate a preference for exclusive sexual relations with members of the same sex. The occurrence of exclusive male/male sexual preferences in sheep shows that cultural "powers of suggestion" are not necessary to generate the phenomenon. (Sheep do not watch television, read newspapers, or discuss alternatives lifestyles.) A brief consideration of ungulate and human infections should be sufficient to counter the natural inclination to dismiss the phenomena in sheep as irrelevant to humans; many important human infectious agents, such as HIV, herpes viruses, the measles virus, Mycobacterium tuberculosis, borna disease virus, and prions, have related pathogens in sheep or other ungulates that have similar effects.
In contrast with difficulties of noninfectious explanations of homosexuality, the hypothesis of infectious causation does not incorporate critical logical flaws or contradictions of fundamental biological principles. Indeed, anecdotal reports indicate that changes in human sexual orientation have occurred following changes in the limbic area due to trauma or infection One possible route would be sexual, whereby homosexual behavior could facilitate spread because of the larger numbers of
partners homosexual males may have on average, relative to heterosexual males. Alternatively, transmission could be partly or entirely by one or more nonsexual routes, and homosexual orientation be a side effect of the infection that is unrelated to transmission.
Although this hypothesis of infectious causation may generate a negative knee-jerk response, such responses are not reliable indicators of the validity of scientific hypotheses. The critical weaknesses of the alternative hypotheses draw attention to the need for rigorous testing of any hypothesis that has a sound theoretical basis, even if we find the hypothesis disturbing and disorienting. The presence of the phenomenon in sheep allows for experimental tests.
In making this point, I am neither adopting nor rejecting any moral or policy view of homosexual conduct or orientation. That's a different subject for a different day, although the issue of causation is not entirely irrelevant to debate on these questions. Many homosexual advocates emphasize what they claim is the fixed nature of the orientation, no doubt hoping that a genetic cause would make homosexuality more like race, an inherent characteristic for which people should not be penalized.
Nor am I trying to bring the negative connotations of "infection" to bear on the question.
Other commenters have tried to be clever by asking about the causes of heterosexuality. From the point of natural selection, of course, that's a non-question. Heterosexuals breed, homosexuals much less so.
Investigation will tend to confirm or negate this hypothesis, regardless of its policy consequences. Nor should such investigations be discouraged because some people might not like the results.