At least, that’s what you might have read on the internet. Unfortunately, it appears to be another case of science journalism telephone with bloggers misreading press releases misreading studies, ultimately leading to a sensationalist but erroneous conclusions. The phenomenon is sadly not a new one. Indeed, just last month, an over-excited NASA scientist gushing about Mars dust got the science press in a tizzy over potential aliens.
Regardless, even though the paper (accessible through jstor) does not “prove” anything about anything, it does set out an interesting hypothesis. They first argue, using evidence from previous research, that sex hormones alone cannot explain sexual determination in humans, as fetus hormone levels are too variable and inconsistent to reliably ensure sexual differentiation. Therefore, the body must have some trait that canalizes the process, making it less perturbable to flucuations in hormone levels. The authors suppose that sex-specific epi-markers (things like DNA methylation that change the physical structure of genetic material but do not alter the base-pair sequence) are precisely that canalizing agent and build a model to demonstrate how this could work (I should note for clarity that everything beyond this point is hypothetical and explicitly a hypothesis to be tested):
Now this hypothesis would be interesting on its own (and definitely worth further investigation), but the authors went a step further and proposed that, if true, their theory of epi-markers assisting in sexual determination would also help explain the evolutionary puzzle of homosexuality. They argue that, generally, the newly-formed embryo would create its own sex-specific genetic markers, based on the presence or absence of a Y chromosome (or even the SRY-gene itself). However, residual markers on the genetic material inherited by the embryo from its parents may remain, and, if from the opposite sex parent, could muck with the sensitivity of the embryo to testosterone levels during development, leading to partially masculinized/feminized fetuses, especially after the gonads are formed and fetus testosterone levels begin to approach one another. Using a mathematical fitness model, the researchers demonstrate that the canalizing sex-specific epi-markers would be evolutionarily advantageous and be expected to reach fixation in the gene pool, even if some cross-generational leakage led to homosexual offspring (which the researchers posit not unreasonably to be damaging to fitness in a vacuum).
In all honesty, it is a really interesting hypothesis, as it avoids the specious logic usually involved in arguing that homosexuality in and of itself is an evolutionary advantage while providing the details that proponents of pleiotropic explanations usually cannot (and is certainly superior to the germ of the gaps and other fringier explanations). I am really interested to see what the researchers and others do with the model and am curious if the gayness-as-parental-vestige hypothesis will ultimately pan out. I just wish the science press had not assumed it already had.