Homosexual Brains?

Much like the media hype surrounding the alleged “gay gene,” a great deal of attention and speculation still surrounds the published study (1) of the brains of 19 homosexual males. Simon LeVay studied a neuron group (known as INAH-3) in the anterior hypothalamus and noted a difference in size compared to that of a group comprised of 16 presumably heterosexual males and 6 females. The author, the editors of Science, and the media rashly related this size difference to “sexual orientation.” The New York Times headlined it “Zone of Brian Linked to Men’s Sexual Orientation,” the Washington Post ran “Node Seen as Key to Gay Orientation,” and Newsweek wrote “A Study Pinpoints a Difference in the Brain.”

Although LeVay’s report was first published five years ago, it is still frequently cited by gay activists, the media, and others as a basis for the supposedly biological cause of homosexuality. Simon LeVay himself has parlayed the attention given to that one article into two additional books on the research into biological explanations of homosexuality, including The Sexual Brain, published in 1993. Along with the “gay gene” study and research on the sexual orientation of identical versus fraternal twins, LeVay’s “homosexual brains” study has become one of the three “pillars” in the argument supporting the notion that homosexuals are “born that way.” As such it is well worth understanding and reviewing in detail.

While the technical aspects of LeVay’s small study approximate those of other researchers in the field, the interpretations of the findings are fanciful and unrelated to any evidence that this locus of neurons has any function whatsoever. It is highly speculative to suggest that this neuron group is associated in any way with human sexual function, let alone sexual behavior. To suggest that “sexual orientation” can be located in this group of nerve cells strains credulity and calls into question the scientific sensibilities of those claimsmakers.


In 1989, a group of investigators (2) seeking gender-related dimorphisms [sex differences in anatomic structure] in the preoptic-anterior hypothalamic area of the brain discovered that thionin (a histologic stain) “stained darkly” ” (4) relatively discrete cell groups” in 11 male and 11 female brains. These cell groups were named Interstitial Nuclei of the Anterior Hypothalamus (INAH). It must be noted that this was a hunt for microscopic structural differences – no attempt was made to tie any structural differences to any function, sexual or otherwise. These investigators noted that they “were unable to identify any cell group clearly homologous to a sexually dimorphic nucleus of another species,” but they decided to study these 4 nuclei anyway, of which INAH-2 and INAH-3 seemed to be dimorphic at least in their human subjects.

Further, they noted that “without knowledge of connectivity or neurochemical characteristics of these nuclei, it is difficult to assign any as a homolog to a sexually dimorphic nucleus of another mammalian species.” In other words, it is not known if animals have such a group of cells (so animal experiments could not help in deciding the function of the group) – a major drawback to future studies. Indeed, despite extensive “histological and histochemical characterization of sex differences in the [medial preoptic nucleus] of the rodent, little is known about its functions.” Scientists have dissected and studied the brains of countless rats in the pursuit of such knowledge, but for all of their efforts we still know “little.” Because “the human being cannot be manipulated experimentally as can laboratory animals, it is difficult to extrapolate from animals to humans regarding structural, behavioral, or physiological sex differences.”

In short, the findings of Allen et al relate to 4 areas of the hypothalamus that stain darkly to thionin, but: 1) these nuclei may merely have a common locus – it is possible that propinquity [i.e., physical closeness] is the only thing that these particular neurons have in common; 2) these nuclei have no known function and do not correspond to nuclei of animals whose function is known; thus, 3) there is no evidence that INAH-2 and INAH-3 are related to sexual function and certainly no evidence whatsoever that they are related to “sexual orientation,” if such a relationship could ever be established.

The first report of a difference between male and female brains came out of Swaab’s laboratory in the Netherlands (3). He reported on what Allen et al consider to be INAH-1. The typical course of “new” findings regarding the brain is illustrated by this study of INAH-1. In 1985, Swaab found that for his sample of males and females, INAH-1 was 2.5 times larger in his sample of males than it was in his females. In 1989 Allen et al found INAH-1 only 1.2 times larger in males (not a statistically significant difference) and in 1991 LeVay found INAH-1 slightly smaller in his sample of men than it was in his small sample of women. In other words, LeVay’s findings contradict previous studies. Such seems to be the fate of findings based upon small samples gathered hither and yon.

The first report of a difference between homosexual and heterosexual brains came out of Swaab’s laboratory in 19904. Swaab found that the suprachiasmatic nucleus (SCN) of the hypothalamus was 1.7 times larger in a sample of 10 homosexual men who died of AIDS than it was in 18 other men, and in 6 heterosexuals (including women) who died of AIDS. He construed this and his finding regarding another nucleus as evidence that does “not support the global hypothesis that homosexual men have a ‘female’ brain.” Of course, the hypothesis that male homosexuals are different from heterosexuals because they have brains structured like females is the basis for all recent research seeking a link between the brain and sexual orientation.

Interestingly, LeVay, although aware of Swaab’s finding, chose to dismiss it [he said, because there “is little evidence, however, to suggest that SCN is involved in the regulation of sexual behavior”] in favor of looking at differences in INAH-2 and INAH-3. Note that the Swaab finding of a larger SCN in homosexuals, if it were to hold up to further testing, would make the homosexual male brain “super-male” rather than “female-like” as LeVay’s finding of smaller nuclei in homosexual males would imply.


Framing his research as a quest for the “biological substrate for sexual orientation,” Dr. LeVay explored the relative sizes of INAH-2 and INAH-3 in 19 homosexual males who had died of AIDS, 16 presumed heterosexuals (6 of whom died of AIDS) and 6 women (1 of whom died of AIDS). INAH-3 “was more than twice as large in the heterosexual men 1 as in the homosexual men 2” and “the women 3.” Countless explanations might account for the apparently smaller size of homosexual male INAH-3 nuclei, but to interpret the size differential as bearing upon a “biological substrate for sexual orientation” is reminiscent of how graduate students find “the solution” in almost every one of their projects.

Since there is no homolog to a nucleus governing sexual orientation (or even a sexual function) in animals [as the commentator in Science noted “there is no animal model for studying homosexuality (5)“], future studies using animals would not be helpful. Even if further work on many more human brains replicated the finding of generally larger INAH-3 among those not known to be homosexual, the emphasis would have to be placed on “generally.” The size differentials reported by LeVay denote the average or mean size of the INAH-3 nucleus. That is, the average size of the INAH-3 nucleus in the set of homosexuals was smaller than the average size of the INAH-3 in heterosexual males.

Despite some media misinterpretations that LeVay had shown all the homosexual brains to be smaller than all the heterosexual brains, there was actually a fair amount of variability in INAH-3 size from individual to individual and definite overlap in the size distributions among the three sets of brains. For instance, 3 out of the 19 homosexuals had a larger INAH-3 than the average size for LeVay’s group of ‘heterosexual’ males. In addition, 3 of the 16 ‘heterosexual’ male brains had a smaller INAH-3 than the average homosexual in LeVay’s study. If heterosexuals and homosexuals could truly be classified by size of the INAH-3 nucleus, why didn’t all the homosexuals have smaller INAH-3 nuclei and all the heterosexual males have larger INAH-3 nuclei?

Even the supposed sexual dimorphism [i.e., size difference between male and female] exhibited in INAH-3, as first reported by Allen et al, was less than clearcut in LeVay’s study. In one of LeVay’s females, INAH-3 was larger than the “heterosexual” male mean, while in 3 of the “heterosexual” males, INAH-3 was smaller than the female mean size. Of course, the small samples of individuals used in LeVay’s study make it difficult to determine what if anything these results really mean. In fact, it is not certain that LeVay’s ‘heterosexual’ males were all necessarily even heterosexual. LeVay did not verify the sexual orientation of his dead subjects before examining their brains. It appears suspicious that 6 of his 16 ‘heterosexual’ males had died of AIDS. But LeVay classified them as heterosexual anyway. If some of these individuals were really homosexual, the average INAH-3 sizes for the two groups of males would almost certainly change, increasing the degree of overlap between the heterosexual and homosexual brains and muddling the results even further.

Dr. William Byne (6) has also noted that “The reliance on the brains of AIDS victims poses a serious interpretive difficulty because decreased testosterone levels are common in their cases…. In some mammalian species the size of sexually dimorphic hypothalamic nuclei varies with the amount of testosterone circulating in the blood stream…. Furthermore, some of the drugs used to treat opportunistic infections associated with AIDS are also known to lower testosterone levels…. it is conceivable that the size of the INAH3 in the men in LeVay’s study reflected endocrine status at the time of death or some other aspect of AIDS or its treatment rather than sexual orientation. Unfortunately, the medical histories published in the LeVay study are inadequate to test this hypothesis.”


The key issue in the LeVay study is not whether INAH-3 is, in fact, smaller in homosexual men than in heterosexual men, but whether INAH-3 has anything at all to do with sexual function, let alone sexual orientation. Until and unless this is “nailed down,” talk about cause/effect [e.g., does INAH-3 affect sexual orientation or does sexual orientation cause changes in INAH-3?] is just so much groundless speculation. LeVay’s data is consistent with the hypothesis that sexually intimate contact with females causes growth in INAH-3 – after all, the bisexual in LeVay’s sample had an INAH-3 size in line with the “heterosexual” male mean. But his limited data is consistent with any number of alternative hypotheses. For instance, that promiscuity or exposure to bodily waste bears a relationship to the size of INAH-3; or that participation in competitive sports [which is reported infrequently by homosexuals] causes its growth, or that nonparticipation causes shrinkage; or even that a bigger INAH-3 enables one to better control his emotions. It could also be that exposure to the AIDS virus itself has an impact on the INAH-3 nucleus, at least in some cases, since so many of the individuals in LeVay’s study had died of the disease.

To have a “hunch” about something, then to argue that one’s hunch is proven by evidence that could just as plausibly be used by someone with a totally different “hunch” [e.g., a classical music instructor who “just knew” that smaller INAH-3 caused an appreciation of fine music], is much more like “wishful fishing” than serious scientific hypothesis testing. Since Science noted that there are no animal models for homosexuality, LeVay’s hunch could not have come from studies of any similar animal nuclei. It is certainly not “obvious” that women are more like homosexual men than they are like heterosexual men – there are numerous ways that heterosexual men are more like females than homosexual males are.

As an openly gay researcher, LeVay’s credibility must also be questioned on other grounds. LeVay promised publicly, both in debates with Dr. Paul Cameron of FRI shortly after publication of his article in Science and to various media reporters that he was going to replicate his findings on live subjects in the near future (presumably through MRI techniques). However, LeVay left the Salk Institute, the only plausible place he could have tried to carry out such experiments, in favor of starting his own Institute of Gay and Lesbian Education in West Hollywood, CA in 1992. In his 1993 book (7), LeVay claimed that MRI techniques were currently impractical for measuring such a small nucleus as INAH-3. It is now 1996 – five years later – and LeVay has not entered the refereed scientific literature again.

Perhaps this is because, as noted by Byne (6), “LeVay’s study was initially rejected by the in-house reviewers at Science…. the paper did not meet the minimal standards to which even animal research in this area is held. This paper had a single author who did all of the tissue processing as well as all of the anatomical measurements and statistical tests. Even in animal work, the standard has been that all measurements are made not only blindly but also by more than one investigator. Certainly, the editors at Science should have been more cautious and required that a co-investigator repeat and verify LeVay’s measurements prior to publication of a study that was sure to be of great interest to the general public as well as to the scientific community.”

Furthermore, with respect to another brain structure, Dr. Byne has noted that “Despite the lack of evidence for a sex difference in the corpus callosum, LeVay (New York Times, letter, October 7, 1991) suggests that male homosexuals may be found to have female-typical callosa. He erroneously asserts that the 1982 study of de Lecoste-Utamsing and Holloway has been replicated in its entirety and that the sex difference they reported is like that reported in laboratory animals. As shown above, however, the 1982 study (de Lecoste-Utamsing & Holloway) stands alone in finding women to have a larger splenium and is contradicted by nearly two dozen studies. Furthermore, when a sex difference in the corpus callosum has been reported in laboratory animals, it has been larger in males….”

LeVay’s explanation may be satisfying to some segments of society, but it remains nothing more than a wishful explanation – a hunch. LeVay’s hunch not only ignores some of Swaab’s earlier finding, but also fails to take into consideration the many other “hunches” that might explain the phenomena he was examining. To summarize, LeVay ignores previous studies, incongruities in his own data, and numerous alternative explanations for the “differences” he cites. Yet the media was quick to hail this study as the final proof. In Vancouver, Washington, The Columbian editorialized that INAH-3 “is always smaller in the brains of homosexual males than it is in other brains…. Now [gays] have evidence to back [their] faith [that they didn’t choose to be gay]. Anti-gay zealots won’t surrender their positions in the face of one scientific report; zeal may be defined as the refusal to see reason no matter what the evidence says. Anyone else should be able to see more clearly that hating a sexual preference is no more valid than hating eye color, skin tone, hair twist or any other characteristic based on biology.”

A similar media circus was generated in 1984, when Science published an analogous study (8) on physiological differences between 17 heterosexual and 14 homosexual males. In spite of all the excitement, it led nowhere – again, a study using an extremely small sample. The chances are good that LeVay’s study will meet the same fate.


1. LeVay, S. A difference in hypothalamic structure between heterosexual and homosexual men. Science 253 (1991): 1034—1037.

2. Allen, L.S., Hines, M. Shryne, J.E., and Gorski, R.A. Two sexually dimorphic cell groups in the human brain. J of Neuroscience 9 (1989): 497—506.

3. Swaab, D.F. and Fliers, E. A sexually dimorphic nucleus in the human brain. Science 228 (1985): 1112—1115.

4. Swaab, D.F. and Hofman, M.A. An enlarged suprachiasmatic nucleus in homosexual men. Brain Research 537 (1990): 141—148.

5. Barinaga, M. Is homosexuality biological? Science 253 (1991): 956—957.

6. Byne, W. Science and belief: psychobiological research on sexual orientation. J of Homosexuality 28 (1995): 303—344.

7. LeVay, S. The Sexual Brain. Cambridge, MA: MIT Press, 1993.

8. Gladue, B.A., Green, R. and Hellman, R.E. Neuroendocrine response to estrogen and sexual orientation. Science 225 (1984): 1496—1499.

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