From a strictly Darwinian viewpoint, homosexuality shouldn’t still be around. It isn’t the best way to pass along one’s genes, and to complicate the picture further, no “gay genes” have even been identified. According to a newly released hypothesis, the explanation may not lie in DNA itself. Instead, as an embryo develops, sex-related genes are turned on and off in response to fluctuating levels of hormones in the womb, produced by both mother and child. This tug of war benefits the unborn child, keeping male or female development on a steady course even amid spikes in hormones. But if these so-called epigenetic changes persist once the child is born and has children of its own, some of those offspring may be homosexual, the study proposes.
Evolutionary geneticist William Rice of the University of California, Santa Barbara, felt there had to be a reason why homosexuality didn’t just fade away down the generations. Research estimates that about 8% of the population is gay, and homosexuality is known to run in families. If one of a set of identical twins is gay, there’s a 20% probability that the other will be, too.
Furthermore, Rice notes, “homosexuality isn’t just a human thing.” Among California gulls, which he watches from his office window, about 14% of pairs are female-female. In Australian black swans, some 6% of pairs are male-male, and 8% of male sheep are attracted exclusively to male partners.
But many genetic screens have failed to turn up genes that are responsible for sexual orientation. So to find out what makes homosexuality persist, Rice and colleagues began a comprehensive survey of the literature.
According to conventional wisdom, an embryo becomes a boy when a gene on the Y chromosome triggers the development of testes, which then begin to produce male sex hormones, including testosterone, at about the 8th week of gestation. With no Y chromosome and hence no testosterone, the embryo becomes a girl.
But testosterone doesn’t explain everything, the researchers found. For one thing, female fetuses are exposed to small amounts of the hormone from their adrenal glands, the placenta, and the mother’s endocrine system. At many key points of gestation, male and female fetuses are often exposed to similar amounts of testosterone. Levels of the hormone can even be higher than normal in females and lower than normal in males without any effect on genital or brain structure.
Rice and his co-workers were more intrigued by studies showing that male and female fetuses respond differently to the hormones that surround them, even when one hormone is temporarily higher. In their study, published online today in The Quarterly Review of Biology, the authors propose that differences in sensitivity to sex hormones result from “epigenetic” changes. These are changes that affect not the structure of a gene but when, if, and how much of it is activated—by chemically altering a gene’s promoter region or “on” switch, for example. Epigenetic changes at key points in the pathway through which testosterone exerts its effects on the fetus could blunt or enhance the hormone’s activity as needed, the authors suggest.
Although epigenetic changes are usually temporary, they involve alterations in the proteins that bind together the long strands of DNA. Thus, they can sometimes be handed down to offspring. According to the hypothesis, homosexuality may be a carry-over from one’s parents’ own prenatal resistance to the hormones of the opposite sex. The “epi-marks” that adjusted parental genes to resist excess testosterone, for example, may alter gene activation in areas of the child’s brain involved in sexual attraction and preference. “These epigenetic changes protect mom and dad during their own early development,” Rice says. The initial benefit to the parents may explain why the trait of homosexuality persists throughout evolution, he says.
“The authors have done a terrific job providing a mechanism for genetic variation, especially a variation that might not be expected to persist because it’s so tightly bound to reproduction,” says evolutionary biologist Marlene Zuk of the University of Minnesota, Twin Cities. But she adds that to go from changes in gene expression to why someone is attracted to a person of the same sex is a question for which science may never fill in all the blanks.