But however much some of the researchers may have desired a particular outcome, the studies are objective and sound. There is no room for doubt that homosexuality is highly heritable. In one study, for example, among fifty-four gay men who were fraternal twins, there were twelve whose twin was also gay; and among fifty-six gay men who were identical twins, there were twenty-nine whose twin was also gay. Since twins share the same environment, whether they are fraternal or identical, such a result implies that a gene or genes accounts for about half of the tendency for a man to be gay. A dozen other studies came to a similar conclusion.12

Intrigued, Dean Hamer decided to seek the genes that were involved. He and his colleagues interviewed no families with gay male members and noticed something unusual. Homosexuality seemed to run in the female line. If a man was gay, the most likely other member of the previous generation to be gay was not his father but his mother’s brother.

That immediately suggested to Hamer that the gene might be on the X chromosome, the only set of nuclear genes a man inherits exclusively from his mother. By comparing a set of genetic markers between gay men and straight men in the families in his sample, he quickly found a candidate region in Xq28, the tip of the long arm of the chromosome. Gay men shared the same version of this marker seventy-five per cent of the time; straight men shared a different version of the marker seventy-five per cent of the time. Statistically, that ruled out coincidence with ninety-nine per cent confidence. Subsequent results reinforced the effect, and ruled out any connection between the same region and lesbian orientation.

To canny evolutionary biologists, such as Robert Trivers, the suggestion that such a gene might lie on the X chromosome immedi ately rang a bell. The problem with a gene for sexual orientation is that the version that causes homosexuality would quite quickly become extinct. Yet it is plainly present in the modern population at a significant level. Perhaps four per cent of men are definitively gay (and a smaller percentage bisexual). Since gay men, are, on average, less likely to have children than straight men, the gene would be doomed to have long since dwindled in frequency to vanishing point unless it carried some compensating advantage.
Trivers argued that, because an X chromosome spends twice as much time in women as it does in men, a sexually antagonistic gene that benefited female fertility could survive even if it had twice as large a deleterious effect on male fertility. Suppose, for example, that the gene Hamer had found determined age of puberty in women, or even something like breast size (remember, this is just a thought experiment). Each of those characteristics might affect female fertil ity. Back in the Middle Ages, large breasts might mean more milk, or might attract a richer husband whose children were less likely to die in infancy. Even if the same version of the same gene reduced male fertility by making sons attracted to other men, such a gene could survive because of the advantage it gave daughters.

Until Hamer’s gene itself is found and decoded, the link between homosexuality and sexual antagonism is no more than a wild guess. Indeed, it remains a possibility that the connection between Xq28 and sexuality is misleading. Michael Bailey’s recent research on homosexual pedigrees has failed to find a maternal bias to be a general feature. Other scientists, too, have failed to find Hamer’s link with Xq28. At present it looks as if it may have been confined to those families Hamer studied. Hamer himself cautions that until the gene is in the bag, it is a mistake to assume otherwise.14

Besides, there is now a complicating factor: a completely different explanation of homosexuality. It is becoming increasingly clear that sexual orientation correlates with birth order. A man with one or more elder brothers is more likely to be gay than a man with no siblings, only younger siblings, or with one or more elder sisters. The birth order effect is so strong that each additional elder brother increases the probability of homosexuality by roughly one-third (this can still mean a low probability: an increase from three to four per cent is an increase of thirty-three per cent). The effect has now been reported in Britain, the Netherlands, Canada and the United States, and in many different samples of people.15

For most people, the first thought would be a quasi-Freudian one: that something in the dynamics of growing up in a family with elder brothers might predispose you towards homosexuality. But, as so often, the Freudian reaction is almost certainly the wrong one. (The old Freudian idea that homosexuality was caused by a pro tective mother and a distant father almost certainly confused cause and effect: the boy’s developing effeminate interests repel the father and the mother becomes overprotective in compensation.) The answer probably lies, once more, in the realm of sexual antagonism.

An important clue lies in the fact that there is no such birth-order effect for lesbians, who are randomly distributed within their families. In addition, the number of elder sisters is also irrelevant in predicting male homosexuality. There is something specific to occupying a womb that has already held other males which increases the probability of homosexuality. The best explanation concerns a set of three active genes on the Y chromosome called the H-Y minor histocompatibility antigens. A similar gene encodes a protein called anti-Mullerian hormone, a substance vital to the masculinis ation of the body: it causes the regression of the Mullerian ducts in the male embryo — these being the precursors of the womb and Fallopian tubes. What the three H-Y genes do is not certain. They are not essential for the masculinisation of the genitals, which is achieved by testosterone and anti-Mullerian hormone alone. The significance of this is now beginning to emerge.

The reason these gene products are called antigens is because they are known to provoke a reaction from the immune system of the mother. As a result, the immune reaction is likely to be stronger in successive male pregnancies (female babies do not produce H-Y antigens, so do not raise the immune reaction). Ray Blanchard, one of those who studies the birth-order effect, argues that the H-Y antigens’ job is to switch on other genes in certain tissues, in particu lar in the brain – and indeed there is good evidence that this is true in mice. If so, the effect of a strong immune reaction against these proteins from the mother would be partly to prevent the masculini sation of the brain, but not that of the genitals. That in turn might cause them to be attracted to other males, or at least not attracted to females. In an experiment in which baby mice were immunised against H-Y antigens, they grew up to be largely incapable of success ful mating, compared with controls, though frustratingly the experimenter did not report the reasons why. Likewise, male fruit flies can be irreversibly induced to show only female sexual behaviour by the switching on at a crucial point in development of a gene called ‘transformer’.16

People are not mice or flies, and there is plenty of evidence that the sexual differentiation of the human brain continues after birth. Homosexual men are clearly not, except in very rare cases, ‘mental’ women trapped inside ‘physical’ men. Their brains must have been at least partly masculinised by hormones. It remains possible, how ever, that they missed some hormone during some early and crucial sensitive period and that this permanently affects some functions, including sexual orientation.

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