Your disappointingly vapid opinion piece is not going to encourage your book, Benjamin Oldroyd. There’s nothing there. I’m referring to an article titled Epigenetics and evolution: ‘the significant biological puzzle’ of sexual orientation. The author is plugging a new book, Beyond DNA, and is trying to persuade us that maybe he has an answer to why gay people exist by going through a couple of hypotheses.
The first hypothesis is that it is a product of kin selection.
Briefly, the kin selection idea is that a gene that promotes homosexual behaviour can spread in a population if homosexual people contribute significantly to the reproduction of close relatives. Although this idea is plausible, the lack of any genetic marker that is reliably associated with sexual orientation is a strong argument against it.
There is no such thing as a gay gene, though, so you can’t postulate the existence of one and build up an adaptive scenario around it. I agree with Oldroyd. It’s a useless hypothesis.
Another idea is that there are antagonistic alleles.
The “antagonistic alleles” idea is that there are certain genes that are selected in different directions, that is, positively selected in males, but negatively selected in females and vice versa. Hypothetically, because no such gene has been identified, a gene that promotes testosterone production could be at a selective advantage in males if it promoted traits such as muscle development, risk taking, opposite-sex sexual attraction and increased sexual attractiveness to females. But if the same gene were expressed in the same way in females it might be disadvantageous for reciprocal reasons. This means that selection could pull in different directions in males and females, maintaining different gene variants in a population. By that I mean, gene variants that have different selective advantages in males and females can potentially coexist in a population because neither is unambiguously better. If so, sexual orientation may be more fluid than one might expect based on biological sex alone. (Well, “der”, I suspect you are now thinking, but please don’t shoot your even-handed messenger.)
He explains it well, but…”might” and “could be” are not evidence. Again, this hypothesis falls apart because there is an absence of evidence for the existence of such alleles undergoing differential competition in males and females. It’s another adaptive just-so story. It’s a useless hypothesis.
Therefore, if you rule out two hypotheses, the third alternative must be the answer, right? Cue dramatic entrance of
Intelligent Design…no wait, not that. Oldroyd knows better than that. But it’s the same rationale: we think we have evidence against the conventional alternatives, therefore that counts as evidence for a different hypothesis.
No, it does not. Now the magical mcguffin we’re all looking for is epigenetics.
The epigenetic hypothesis for the widespread occurrence of human homosexuality is based on the possibility of epigenetic inheritance of adjustments to a foetus’s testosterone sensitivity. Like most other epigenetic marks, sex-specific epigenetic marks are established anew in the early embryo following fertilisation.
Substituting hypothetical “epigenetic marks” for a hypothetical “gay gene” gets us nowhere unless you’ve got something concrete and specific. If you do, that would be very interesting…but epigenetics, by it’s nature, is fuzzy and hard to pin down. That is not to say that epigenetics is non-existent — it’s very real and important — but that you can’t slap a simple causal explanation on many complex phenomena, whether it’s a gene or a epigenetic marker.
My preferred explanation is also a bit fuzzy. We have to get beyond the bogus genetic determinism that appeals so strongly to naive minds, and epigenetic determinism would be just as bad. I think we have to accept that human behavior is sloppy and variable as hell. We are built by a long chain of probabilistic interactions, from molecules bouncing around in a messy cell, to a tangle of cells communicating chaotically with one another, to incompletely specified individuals that are shaped by interactions with a variable, changing environment to end up as people with mostly unpredictable characteristics. Physics and chemistry are biased by biological constraints, but the end result is not rigidly locked in by your genes — there is a messy cascade of genetic, epigenetic, and environmental interactions that is skewed by evolution to produce a generally viable outcome, but is tolerant of variability.
We have to abandon these mechanistic notions of a clockwork biology that spits out adults who were specified at conception by the chemistry of nucleic acids. It just doesn’t work that way. We are all products of stochastic processes.
My personal belief is that evolution has worked to take a population of apes and favor a hierarchy of properties that are all weakly specified, and we’re lucky if the majority of individuals conform to that hierarchy. First in priority is cooperation, building a social environment that promotes mutual aid (we all know how poorly that often works out). The way I look at it is that biology is telling us to love one another…and then it is far less fussy about the details. We don’t need a deterministic explanation for why individuals vary, it’s the nature of how they are built.