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L ast century, when things were a whole lot worse for gay people than they are today, there was a widely held notion that human homosexual behaviour was a choice, and that a homosexual person could change their ways and become heterosexual. The existence of such genes would show that homosexuality was not a choice but an inevitable consequence of development and genetics. Indeed, gay genes were perhaps the only example where many left-leaning people heartily embraced genetic determinism.

Moreover, since homosexuality would generally be reckoned to reduce reproductive output of an individual, an allele a gene variant that directly causes homosexuality is unlikely to spread in a population. Nonetheless, human homosexuality in both sexes is widespread, as it is across the animal kingdom.

One study estimated that 3. Despite the lack of genetic markers that are predictive of human homosexuality, the trait is highly heritable in the sense that siblings are more similar in their sexual orientation than expected by chance. However, the level of concordance between identical twins is surprisingly low. I once had a friend who was the of Gay Liberation in Victoria as a young man during the s.

The burghers of the town were waiting to pick him up at the station, with evil intent. So much for genetic determinism. If homosexuality was solely genetically determined, identical twins should have identical sexual orientation. The widespread occurrence of homosexuality in humans and other animals, together with its high heritability but unpredictable genetics and lack of genetic markers, is a significant biological puzzle.

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There are three leading hypotheses for the common existence of homosexuality in human populations, one based on kin selection, one on sexually antagonistic alleles, and one on epigenetic inheritance. 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. 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. Finally, we have an epigenetic hypothesis. Epigenetics is the transfer of genetic information between generations, which is not coded in DNA. In most mammals, male sexual development is determined by SrY, a gene on the Y chromosome. Thus, the short story of mammalian sexual development is that if a foetus is bathed in oestrogen produced by its default ovaries, it develops a female body.

But if it is bathed in testosterone from its newly converted testes, it develops as a male. I cheerfully taught it in my first-year biology classes for more than two decades, in full knowledge that the story is more complex. Indeed, such individuals may be hyper-female, since they do not produce or respond to testosterone, whereas genetic females do both. This enzyme converts testosterone to a more potent male-determining hormone.

These kids, who are chromosomally male, are born with female-like genitalia and are often raised as girls. They then change to the male phenotype at puberty with its associated release of testosterone. Not only do male foetuses produce more androgens than female foetuses, they respond to it more strongly due to sex-specific epigenetic marks in genes that code for androgen receptors.