What are we to make of this? (
Hannah Devlin,
The Times, Feb 14th 2014).
"Scientists have found the strongest evidence yet for the existence of genes that increase the chance of a man being gay. The study, which involved more than 400 gay brothers, identified two small areas on the male genome that appear to be linked to sexuality.
Michael Bailey, from the Northwestern University in Chicago, who carried out the research, said: “Sexual orientation has nothing to do with choice. Our findings suggest there may be genes at play and we found evidence for two sets that affect whether a man is gay or straight.”
In the study, presented yesterday at the American Association for the Advancement of Science annual conference in Chicago, scientists took blood from 409 gay brothers and heterosexual members of their family. On average, siblings share 50 per cent of their DNA, but ought to have a higher chance of sharing any genes involved in determining sexuality.
In the 1990s the American geneticist Dean Hamer identified an area that appeared to influence male sexuality on the X chromosome, which men inherit from their mothers. The results, however, have remained controversial.
The latest research confirmed that this region on the X chromosome, known as Xq28, is more likely to be shared by the gay pairs of brothers than by the brothers and their other siblings. The study also identified a second genetic region, on Chromosome 8, which also appeared to predict whether a man would be homosexual.
While the pairs of brothers shared gene variants in these regions, however, there were not individual genes that stood out across all the participants in the study.
The findings suggested that overall a man’s sexuality depends about 30 to 40 per cent on genetic factors, while the rest depends on environmental factors, such as the hormones a baby is exposed to in the womb."
Putting aside discredited "nurturist" theories of homosexuality, a leading non-genetic explanation is the pathogen theory advocated by Paul W. Ewald, a biology professor at Amherst College in Massachusetts, and Gregory Cochran, an independent physicist in Albuquerque, New Mexico (outlined in
this article by Caleb Crain). Their argument against "gay genes" is that these are so detrimental to reproductive fitness that they would have been removed from the population through natural selection. However, Hannah Devlin's
Times article has this to say:
"Previously, homosexuality has been viewed as a “Darwinian paradox” because if male homosexuality were genetic, and gay men reproduced less than heterosexuals, the trait should eventually disappear from the population over time. This has led some critics to dismiss the genetic argument.
"However, there is now some evidence that genes linked to male homosexuality could increase fertility in women. One study by Italian scientists found that female relatives of gay men tended to have more children than those of straight men."
Ewald and Cochran rejected this argument as explained at the end of
the Caleb Crain article:
" ... perhaps homosexuality is an unintended side effect of a gene for something else—a side effect more marked in one gender than the other. That might explain why more men than women are exclusively homosexual. Hamer, the discoverer of the Xq28 link, favors this explanation. “Suppose you had a gene that tended to make men gay, but the same gene in women made them more reproductive,” Hamer suggests. He proceeds to give examples. “If you had a gene that made people more attractive and intelligent, it might make men gay, but it might make women more likely to reproduce. Or suppose you had a gene that made people attracted to men. If you gave it to a guy, he would probably be gay, but if you gave it to a woman, she would simply be . . . well, let’s say, ‘exceptionally attracted to men.’ ”
"But Cochran and Ewald doubt this explanation, too. Evolution tends to balance out any gender inequity as severe as Hamer describes. After a while, some mutation would come along that jiggered our hormones to reduce the gene’s fitness cost to men, while retaining its benefit for women. “In the long run,” Cochran says, “sex-antagonistic genes are tamed.”
The argument for a sex ratio of 1:1 male-female (which means
reproductively-capable males and females) was one of the first great triumphs of quantitative population genetics,
going back to Ronald Fisher in 1930. Here's the
argument as presented by W. D. Hamilton.
- Suppose male births are less common than female.
- A newborn male then has better mating prospects than a newborn female, and therefore can expect to have more offspring.
- Therefore parents genetically disposed to produce males tend to have more than average numbers of grandchildren born to them.
- Therefore the genes for male-producing tendencies spread, and male births become more common.
- As the 1:1 sex ratio is approached, the advantage associated with producing males dies away.
- The same reasoning holds if females are substituted for males throughout. Therefore 1:1 is the equilibrium ratio.
In modern language, the 1:1 ratio is the evolutionarily stable strategy (ESS). In a population of individuals playing the ESS (i.e. producing equal numbers of sons and daughters), any other strategy (e.g. 51% sons and 49% daughters) would have lower fitness, and hence would be selected against.
What would resolve this debate would be to know more about the genes hanging around the Xq28 region and on chromosome 8 and what they do. Then some modelling of the evolutionary dynamics. Without a quantitative analysis this debate will run and run, even without all the social agendas swirling around.
