By Caleb Crain. Originally published in Out magazine, August 1999, pp. 46–49.
Heart disease. Cervical cancer. Peptic ulcers. Homosexuality. What do these four things have in common? According to two scientists who are reshaping the way we think about disease and evolution, all are more likely to be caused by a germ than a gene.
Paul W. Ewald, a biology professor at Amherst College in Massachusetts, and Gregory Cochran, an independent physicist in Albuquerque, New Mexico, have a new theory about homosexuality: You catch it. Right now their theory is just that—a theory. They do not claim to have proof, and they have not named a particular virus or bacterium as the culprit. Homosexuality is not even the focus of their work, which takes on everything from kidney stones to Kaposi’s sarcoma. In an article in the February  issue of The Atlantic Monthly, writer Judith Hooper describes their ambitious, wide-ranging ideas as nothing less than “A New Germ Theory.” With diplomatic wariness, Cochran emphasizes that homosexuality “is just one aspect of [our work], not the biggest.” He’d rather talk about heart disease. In a carefully worded e-mail, Ewald, for his part, asserts only that “the argument about infectious causation of homosexuality is a feasible hypothesis and should be treated as such—no more and no less.”
But despite Ewald and Cochran’s caution, their idea could prove to be highly controversial. Few gay men and lesbians are likely to welcome with Vulcan impartiality the idea that their love lives got their distinctive twist from a germ. Asked about the risk of angering the gay community, Cochran responds by e-mail, “Should we drop a theory that has a chance of being correct on the grounds that it might upset people?” It’s a good question. But a few other good questions come to mind. For starters, are these guys crackpots? What led them to suggest that microbes cause gayness? Whatever happened to the much-hyped gay gene? And last but far from least: Are they right?
SEVERAL YEARS AGO, Cochran, who has worked as a consultant to a number of aerospace companies, had an unorthodox idea: What if homosexuality were caused by a germ that manipulated its human host’s behavior, perhaps to the germ’s advantage? Cochran wrote an article about his brainstorm and sent it off to a prestigious journal. It was rejected, but one of the journal’s anonymous reviewers—Ewald—contacted Cochran because he thought he saw the seed of something greater in the idea.
That something greater was a radical new view about the causes of disease. What Cochran suspected about homosexuality, he and his colleague now believe to be true for a large number of conditions—namely, that microbes, not genes, are responsible for them. Ewald and Cochran’s innovation is to consider disease from the perspective of human evolution. If your mother is obsessed with knowing when you are going to give her some grandchildren, then you are more or less familiar with the traditional perspective of human evolution: You were put on this earth to reproduce. Anything that gets in the way of reproduction is a problem that you better be prepared to explain. To judge the size of such a problem, evolutionary biologists assess its “fitness cost”—that is, the damage it does to your chances of procreating.
Genes with a substantial fitness cost do appear from time to time. Every so often a cell makes a mistake while copying its DNA—a mistake known as a random mutation—and this mutation may give rise to a gene harmful to the person carrying it. But in such a case, according to evolutionary theory, the new disease-causing gene would vanish after a hundred generations or so, gradually but inexorably, because damaged organisms reproduce less often and less prolifically than healthy ones. (There is an exception: Some disease-causing genes simultaneously provide a protective benefit—such as the gene for sickle-cell anemia, which also happens to ward off malaria.) The higher its fitness cost, the faster a gene disappears. Like the basis of most scientific paradigm shifts, Cochran and Ewald’s idea sounds obvious once they’ve pointed it out: It is almost never in our evolutionary interest to develop genes for diseases.
But what does this have to do with homosexuality? Remember your mother’s idée fixe. She doesn’t care about your hobbies; she wants to see infants. Unhappily for her, modern homosexuals have only one fifth as many children as heterosexuals do, according to a San Francisco study published in 1981. That puts the fitness cost of homosexuality at 80 percent—staggeringly high from the perspective of human evolution. If there is a gene for homosexuality, nobody has figured out why it survives.
As lesbians and gay men have won liberation and come out of the closet, they have probably become less likely to marry and produce children; some researchers have suggested, therefore, that in the past, when homosexuals lived more closeted lives, they reproduced at a rate closer to that of heterosexuals. But even under a regime of compulsory heterosexuality, disinterest in the opposite sex would still have lowered the rate of reproduction. Nor will the current “gayby boom” turn the tide. Gay parents are still very far from matching the fertility rate of straight parents.
The math is unforgiving. If a genetic trait has a fitness cost of just 1 percent, it will sink to the very low rate of a random mutation after only 100 generations. Over the course of human evolution—roughly 800,000 generations so far—a trait would vanish even if its fitness cost were as low as 0.001 percent. According to the best available estimates, however, 3 to 4 percent of men and 1 to 2 percent of women in the United States are exclusively homosexual. That’s a lot of homosexuals. Too many, Cochran and Ewald believe, for the condition to be genetic.*
No one has found a virus or a bacterium for homosexuality. (So far no one seems to have looked.) But recently, a slew of ailments that were long thought to be caused by stress, high living, or genetic bad luck have instead been pinned on microbes. In an article published in Natural History in February , Ewald and Cochran list a few. Peptic ulcers, for instance, used to be attributed to stress, but it is now known that they are caused by a bacterium, Helicobacter pylori. And although long evenings of sitting on the sofa and eating ice cream have not been fully exonerated, new studies suggest that the trigger for atherosclerosis (clogged arteries) may be the Chlamydia pneumoniae bacterium. Scientists have linked viruses to cervical and liver cancers. And researchers now associate some kidney stones with the bacterium Nanobacter.
Ewald and Cochran boldly predict that we will eventually find germs for every condition that carries a high fitness cost, strikes more often than a random mutation (that is, more than one person in 50,000), and cannot be explained by a new environmental hazard such as pesticides or cigarettes. The only common diseases attributed to genes, they predict, will be those like sickle-cell anemia that are better understood as self-destructive defenses. If Ewald and Cochran are right, we’ll soon be hearing that scientists have found germs behind obsessive-compulsive disorder, polycystic-ovary syndrome, schizophrenia, breast cancer, Alzheimer’s disease, multiple sclerosis, cerebral palsy—and homosexuality.
DOES HOMOSEXUALITY BELONG on a list of diseases? On the one hand, William Byne, a brain researcher at the Mount Sinai School of Medicine in New York, suspects that Cochran and Ewald are guilty of pathologizing homosexuality. “It’s hard for most people to entertain the idea that homosexuality might be a natural variant of human sexual behavior,” says Byne. On the other hand, Michael Bailey, a professor of psychology at Northwestern University, gives Cochran and Ewald the benefit of the doubt. Bailey does worry that homophobes could use the germ theory as political ammunition—as “proof” that homosexuality is a disease. But that would be “a totally illegitimate conclusion,” in Bailey’s opinion. Not everything caused by a germ is a disease, he insists. “Suppose we found that a form of genius was also caused by a virus. Would that mean that genius is a disease?”
Some germs do help their hosts. The amicable bacteria you consume in yogurt, for example, continue to live in your gut and help break down food. The word disease is not a scientific term; it reflects how we feel about an infection. Science, by contrast, doesn’t care how we feel. As Ewald explains, “Scientific inquiry doesn’t make judgments about whether new understandings of nature are good or bad, pleasant or unpleasant.” But it is one thing for a germ to improve your digestion and another altogether for it to determine whether you like boys or girls. Science may not distinguish between the two cases, but society probably will. Furthermore, you can tell yourself that it might be nice to be infected by a virus, but you probably can’t get yourself to believe it.
AS COCHRAN AND EWALD venture into the minefield of public opinion, they will find the ground already occupied by another cadre of scientists—those who announced several years ago that homosexuality is inheritable. The gay-gene researchers are battle-hardened and hunkered down. They won’t be easy to rout.
In the early 1990s, two studies strongly suggested that genes could affect sexual orientation. First, in 1991, Michael Bailey and Richard C. Pillard, a professor of psychiatry at Boston University, showed that male identical twins were roughly twice as likely as male fraternal twins to share a homosexual orientation. A follow-up study found a similar ratio among female twins. Then in 1993, a team led by geneticist Dean H. Hamer at the National Cancer Institute found that in families where homosexuality ran on the mother’s side, homosexual brothers often shared genetic material at a spot on their X chromosomes known as Xq28.
Both the twin studies and the link to Xq28 have been challenged of late. In a new, still unpublished study of men and women listed in the Australian Twin Registry, researchers found that twins appeared to share a homosexual orientation much less frequently than earlier studies indicated. However, according to Bailey (who coauthored both the Australian study and the original twin studies it is said to refute), the Australian data, once they are analyzed, will reveal a similar estimate of the role that heredity plays in homosexuality—50 percent. (No serious researcher believes that homosexuality is 100 percent genetic. The “gay gene” is journalistic shorthand for the hypothesis that some genes make you susceptible to homosexuality.)
More controversy has dogged Hamer. In April, researchers at the University of Western Ontario reported in Science magazine that they found no evidence linking sexual orientation to Xq28—a flat refutation of Hamer’s results. But Alan Sanders, a professor of psychiatry at the University of Chicago, recently found that gay brothers tended to share genetic material at the exact spot on the X chromosome that Hamer had identified. In Sanders’ study, this sharing happened often enough to be significant but not often enough to fully vindicate Hamer’s results. “We’re probably in Hamer’s ballpark,” he says.
Under fire, the evidence for a gay gene seems to be holding its ground. Like all evidence, it is open to conflicting interpretations. It is worth repeating that there is no evidence for a gay germ yet.
COCHRAN AND EWALD presented their germ theory to the world in an unorthodox way. It debuted in the popular press; only now is an overview being prepared for a scientific journal to review. In other words, the hardest-hitting criticism—from fellow scientists—has yet to come. When I ask researchers for their advance opinions, reactions range from the curious to the dismissive.
Perhaps because his own work has undergone such scrutiny, Hamer wants to see hard facts. “I think it’s a very interesting idea,” he says. “The idea that homosexuality resulted from overprotective mothers was also an interesting idea. But when it was tested, it turned out to be completely untrue. Whether [Ewald and Cochran's theory is] true or false is an experimental question and needs to be answered by observation and by experimentation, not by chitchat.” Hamer is skeptical that Ewald and Cochran will find much supporting evidence. Infectious diseases, he notes, tend to appear in clusters, but the rate of homosexuality doesn’t seem to vary significantly from country to country or across historical time. Like Hamer, Bailey wonders about the evidence. “What would an empirical research program for this [theory] look like?” Bailey asks. One answer might come from studies of another complex psychological trait for which the cause is in dispute: schizophrenia.
Elaine Walker of Emory University investigates the relation between schizophrenia and prenatal complications, including infection. To show a link between schizophrenia and germs, she relies on two kinds of data: medical records and faces. Medical records tell her whether schizophrenia correlates with difficult births or prenatal complications. But she can get nearly the same information from a subject’s face. An infection in the womb is such a traumatic event that it leaves signs on the body that are still legible in adulthood. It turns out that schizophrenics are more likely to have “minor physical anomalies”—irregularities in the shape and position of eyes, ears, and other features—than healthy adults, probably because they more often suffered from infections in the womb. “Homosexuals do not show these kinds of irregularities,” Walker says. “At least, I am not aware of any data indicating that they do.” (In one study of gender-atypical boys, in fact, judges consistently rated them “cuter” and “prettier” than gender-typical boys.) Nor do homosexuals show the neuro-motor defects that are also associated with prenatal infection. In Walker’s best guess, Cochran and Ewald’s proposal “doesn’t seem very likely for homosexuality. Schizophrenia is highly debilitating, and sexual orientation is not.”
Some researchers object that homosexuality may not even be an evolutionary puzzle that needs solving. It is only recently and only in the West, Byne complains, that homosexuals have become a “pariah species” who do not reproduce. Rather than a problem, homosexuality might be an “eroticized form of affiliative behavior that’s crucial for survival of the species,” he suggests. According to Bruce Bagemihl, author of Biological Exuberance: Animal Homosexuality and Natural Diversity, homosexual animals find a great variety of ways to reproduce in the wild. Pairs of male black swans, for example, will mate with a female, allow her to lay eggs that they’ve fertilized, and then chase her off so that they can raise the young cygnets themselves. Bagemihl estimates that zoologists have documented homosexual behavior in 15 to 30 percent of the animal species that have been studied in depth.
At this point, there is only speculation pitted against speculation. Many gay men and women will hope Cochran and Ewald are wrong. But, as Cochran writes, “The facts of the natural world don’t seem to care what we feel, and our feelings don’t always help in figuring out how things really work.”
“WE ARE ALL housing countless cohabiting microbes,” Ewald reminds me when I ask about the reactions that his idea may provoke. It is strange to imagine that these microscopic hitchhikers may be responsible for the most intimate part of oneself. It makes one feel a bit like the Sigourney Weaver character who comes back as a cloned chimera in the fourth Alien movie—most of her the same good old Ripley who slew the alien in earlier installments but part of her now the alien itself.
In the middle of writing this article, I took a break and went to a birthday party for a childhood friend’s three-year-old son. The party’s theme was “Thomas the Tank Engine,” an earnest-looking choo-choo train that, like the Teletubbies, is part of the current British tot-culture invasion. The three-year-old’s grandfather is a research biologist, so he and I batted around the gay germ idea as a matter of recreational speculation. Any germ that changed sexual orientation, he suggested, would have to have an appetite for nerve tissue. Herpesviruses are neurotropic, which would make them eligible candidates. My biologist friend considered Hamer’s objection that infectious diseases ought to appear unevenly—sweeping through one culture, skipping certain islands altogether—but then speculated that perhaps the germ infected nearly everyone on the planet but caused homosexuality in only a small percentage. We wondered at what age the infection might take place. Certainly before puberty, the point at which most males become aware of their orientation. Maybe parents give the child the germ at the moment of conception. Would infection have to occur in the womb? Could it happen later?
At this point the three-year-old climbed onto the chair next to me to show me his battery-operated galloping horse. I froze. Suddenly all I could think was, What if you catch it when you’re three? I was afraid to touch or even breathe on him. My intellectual defenses had imploded; I had become a plague-carrying monster. But the boy’s grandfather kept talking, unperturbed, and a moment later, I returned to normal.
If Cochran and Ewald succeed in refashioning the study of disease, their speculations about homosexuality will take on new weight. The gay germ is a line of research that lesbians and gay men will want to watch closely. It may be hard to watch calmly, however, because even if we don’t yet know if the theory is true, we already know that it hurts.
* [An outtake. To streamline the argument, the following passage was cut from an early draft. It originally appeared in the spot marked by an asterisk above. The objections discussed in it have come up in subsequent debates.]
To reconcile the gay gene to the evolutionary requirement to reproduce, researchers have proposed genetic models that are more complex. One by one, Ewald and Cochran shoot these proposals down.
Perhaps homosexuality is like sickle-cell anemia, and it provides a great (though as yet unidentified) benefit to heterosexuals who carry the gene without expressing it fully. “Very unlikely,” writes Ewald. “These defenses tend to involve grossly defective proteins that inhibit pathogens more than they negatively affect the person carrying the trait. No one has yet identified any such defective proteins in gay men.” Strike one.
Perhaps homosexuals are exceptionally helpful to their nephews and nieces, so that families with homosexual aunts and uncles tend to be more successful than those without. This explanation “simply does not work,” says Cochran. A childless gay uncle “would have to cause, on average, four more nephews or nieces to survive than otherwise would have,” since a nephew and his uncle share only a quarter of their genetic material. (A child and his parent share half their genetic material.) That fourfold extra investment is “unfeasible,” Cochran thinks. Strike two.
Or 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.” Strike three.