First and most important point: there is no way we’re going to cover in 750 words the whole of this field. Much will be left out. This small article is not going to be all things; it will discuss only one important point. Experience suggests I should warn certain readers of the danger of hyperventilating and apoplexy.
If same-sex attraction is heritable, which is to say genetic, how is it that this trait has been passed along? Men who are SSA and act on these proclivities are far less likely to pass on their genes. Yet we have been assured that SSA has always been with us as a race; that is, for thousands of years over many, many generations. But not everywhere. Certain areas of Africa report no SSA men. Of course, some men with SSA mate with women, but not nearly at the same rate men not so afflicted. Thus whatever genetic components to SSA exist should gradually disappear. Or already be gone.
The new peer-reviewed study “Genome-wide scan demonstrates significant linkage for male sexual orientation” by A. R. Sanders and a slew of others in journal Psychological Medicine suggests an answer to this puzzler. “Our findings may also begin to provide a genetic basis for the considerable evolutionary paradox that homosexual men are less motivated than heterosexual men to have procreative sex and yet exist as a stable non-trivial minority of the population,” they say.
The word “considerable” is apt, and an understatement; but you have to admire the euphemism “less motivated.” Anyway, they correctly note the observed population stability of men with SSA. This is important, this observation, because it highlights that we should be finding a theory which fits these facts and not finding facts which fit a theory. Now one particular gene that these authors noted is shared by some (not all) SSA brothers (and some half brothers) is called “Xq28”. Never mind why.
The authors state, “Linkage to Xq28 is especially relevant to the X-linked sexually antagonistic selection hypothesis that women with genetic variant/s predisposing to homosexuality in men have a reproductive advantage compared with other women, i.e. that fertility costs of variants that increase the likelihood of a man’s homosexuality are balanced by increased fecundity when expressed in a woman”.
In other words, this appears to be a theory in search of facts; that is, some folks start with the theory that SSA is genetic and work backwards. Women who mate with SSA men, it is suggested, are more fecund: they pump out more babies. What we have is a balancing act. Is it because the women who “go for” SSA men are more fertile, or is it the male gametes from SSA men are causing greater fecundity? And how much more fertile must these women be (by whatever cause) to match the rate of baby making seen in women who mate with non-SSA men?
That would seem to be (to reuse the apt word) considerable, especially these days when SSA behavior is seen as socially acceptable. SSA men aren’t making many babies. True, many SSA men in the past days were encouraged to take a wife and reproduce. Not so now. Yet SSA is on the rise. Another paradox—but only if you insist the heritability theory is (somehow) correct. There is no paradox if the diseugenic SSA trait is caused by environmental stressors. I have some colleagues who suspect SSA is caused by a yet-to-be-discovered virus. I doubt this strongly, because it seems that genetic non-immunity to this virus would also die out of the population (the virus could mutate, of course).
The environmental hypothesis, incidentally, also has going for it that in LGBT we have all kinds of other behaviors besides strict SSA. There are far more “B”S than “G”s, for instance. And nobody knows much about the genetic facets of “L”s. “T”s are surely just plain mentally ill.
What impressed me about this study was its coverage. Kelly Servick at Science Mag said of the methods used by Sander “the genetic linkage technique has largely been replaced with genome-wide association (GWA) studies.” She reported that the editor of the journal was surprised to see the study because it used such a blunt instrument, and she said, “Sanders admits that although the strongest linkage he identified on chromosome 8, using an isolated genetic marker, clears the threshold for significance, the Xq28 linkage does not.”
Also consider we do not know how pairs of non-SSA men would look on these same techniques. If these siblings also show similar patterns on chromosome 8, then we’re looking at something similar to brothers, not just to SSA status.
Lastly, Samantha Allen at The Daily Beast note (correctly) that SSA can be a choice.
Update I stupidly forgot to point to Robert Reilly’s and to Stephen Goldberg’s books which correctly point to the evidence that the rate of SSA in identical twins is far from 100%, thus proving the genetic component, if any, cannot be all important.