By Dr. Nadia El-Awady
IslamOnline’s Health & Science Editor

Homosexuality-Related Research

Much research has been done over the years to discover the scientific origins of homosexuality. Mostly it has been to disprove the fact that homosexuality is a matter of choice. None of the research done up to this date, however, is conclusive. Only varying theories exist according to the results of such research.

Research available on the topic of homosexuality can be divided into three categories:

  1. Anatomical differences
  2. Genetic investigations
  3. Biological causes
  4. Anatomical differences

Simon LeVay, a self-proclaimed homosexual, presented research in 1991 that was much publicized by the media. His report found neuroanatomic differences between homosexual and heterosexual men. Much of the field’s current visibility is due to the wide publicity surrounding this study of INAH3, the third interstitial nucleus of the anterior hypothalamus, which is normally three times larger in men than in women. LeVay examined hypothalamic tissue from 19 homosexual men, all of whom died of AIDS; 16 heterosexual men, six of whom had died of AIDS; and six women of unknown sexual orientation. He found that INAH3 was two to three times larger in heterosexual men than in homosexual men.

This study was the first ever to imply that there were neuroanatomic differences between homo and heterosexual men; thus, naturally, it was the subject of much controversy relating to both its scientific and its social implications. Many homosexual activists argued that the study bolstered their contentions that some people are born gay and that becoming gay was not a matter of choice. They thus arrived at the conclusion that homosexuals should be granted protection against discrimination. Many scientists, however, assailed LeVay’s methodology and the conclusions of his work. These counter-arguments did not receive the same amount of media attention.

Another neuroanatomical difference between homo and heterosexual men was reported in 1992 by University of California at Los Angelos investigators Laura S. Allen, a research scientist, and Roger Gorski, a professor of neurobiology (L.S. Allen, R. Gorski, Proceedings of the National Academy of Sciences, 89:7199-202).

The anterior commissure, a relatively small bundle of axons connecting the two brain hemispheres, which is larger in women than in men, was found to be also larger in gay men than it is in heterosexual men. In a related study, Dick F. Swaab and coworkers at the Netherlands Institute for Brain Research reported that a hypothalamic structure, known as the central subdivision of the bed nucleus of the stria terminalis, is larger in men than in women, and also larger in men than in male-to-female trans-sexuals. (J.N. Zhou et al., Nature, 378:68-70, 1995).

This anatomical work came under heavy criticism by William Byne, director of the Neuroanatomy Laboratory of Neuropsychiatric Disease at New York’s Mount Sinai Medical Center. “A general problem with this work is that there have been dozens and dozens of reports of sex differences in the human brain since the middle of the last century. But not a single one of these has been corroborated, except for the one that men tend to have slightly larger brains than women. The reason for that is that it’s tremendously difficult to do morphometric studies in the human brain. I would be surprised if there weren’t sex differences in the human brain, since there are sex differences in just about every organ system in humans. But to date, we can’t say with any confidence where the sex differences are.”

Byne also thinks that even if the sex differences are real, LeVay’s findings could have been confounded by the fact that all his original gay subjects died of AIDS. LeVay maintains that he controlled this by examining the brains of heterosexual men who died of AIDS, as well as one gay man who died of other causes. Dr. William Byne argued that, “[LeVay’s] inclusion of a few brains from heterosexual men with AIDS did not adequately address the fact that at the time of death virtually all men with AIDS have decreased testosterone levels as the result of the disease itself or the side effects of particular treatments. Thus it is possible that the effects on the size of the INAH3 (hypothalamus) that he attributed to sexual orientation were actually caused by the hormonal abnormalities associated with AIDS.” (E. Byne, “The Biological Evidence Challenged,” Scientific American (May 1994): 50-5)

Byne gives as an example the fact that many people with AIDS suffer testicular atrophy before death, and since gonadal hormones are known to regulate the size of several hypothalamic nuclei in animals, disease effects can not be excluded.

Another weakness of LeVay’s study is that even in his sample there were exceptions. In other words, there were some homosexuals who had larger hypothalamic structures than some of the heterosexuals examined. Even LeVay admits that these exceptions “hint at the possibility that sexual orientation, although an important variable, may not be the sole determinant of INAH3 (hypothalamus) size.”

Since the release of LeVay’s study, other researchers have found that brain structures can change as a result of life experiences. In 1997, University of California at Berkeley psychologist Marc Breedlove released a study that showed that sexual activities of rats actually structurally changed aspects of the brain at the base of the spinal chord. “These findings give us proof for what we theoretically know to be the case – that sexual experience can alter the structure of the brain, just as genes can alter it,” Breedlove commented. “You can’t assume that because you find a structural difference in the brain, that it was caused by genes. You don’t know how it got there.” He also states that, “It is possible that differences in sexual behavior cause (rather than are caused by) differences in the brain.” (Pat McBroom, “Sexual Experience May Affect Brain Structure,”Berkeleyancampus newspaper [University of California at Berkeley], 19 November 1997).

Indeed LeVay himself offered the following criticisms of his own research: “It’s important to stress what I didn’t find. I did not prove that homosexuality is genetic, or find a genetic cause for being gay. I didn’t show that gay men are born that way, the most common mistake people make in interpreting my work. Nor did I locate a gay center in the brain. INAH3 is less likely to be the sole gay nucleus of the brain than part of a chain of nuclei engaged in men and women’s sexual behavior…Since I looked at adult brains, we don’t know if the differences I found were there at birth, or if they appeared later.” LeVay also made an interesting observation about the emphasis on the biology of homosexuality. He noted, “…people who think that gays and lesbians are born that way are also more likely to support gay rights.” (The Innate-Immutable Argument Finds No Basis in Science.In Their Own Words:Gay Activists Speak About Science, Morality, Philosophy. A. Dean Byrd, Ph.D.; Shirley E. Cox, Ph.D.; Jeffrey W. Robinson, Ph.D., Salt Lake City Tribune: May 27th, 2001).

  1. Genetic Investigations

Twin Studies

In studies on male and female homosexuals who are twins, Northwestern University’s J.M. Bailey and his associates claimed that they found clear evidence for genetic transmission. In a study of gay men, 52% of their identical twins, 22% of their fraternal twins of the same sex, and only 11% of their adopted brothers were also gay (J.M. Bailey, R.C. Pillard, Archives of General Psychiatry, 48:1089-1096, 1991).

Among lesbian women, 48% of their identical twins, 16% of their fraternal twins of the same sex, and only 6% of their adopted sisters were also lesbian (J.M. Bailey et al., Archives of General Psychiatry, 50:217-223, 1993). Aside from these twin studies, there have been few, if any, firm results showing neuroanatomical or genetic correlates for female homosexuality.

The findings of the male twin study appear to support the argument for biology, since identical twins share the same genes. However, the rate of non-twin conformity should mirror that of fraternal twins. In the Bailey and Pillard study, the rate was only 9.2%. And the rate in adopted – which, if the biological hypothesis were true, should have been even lower than non-twin brothers – was actually higher (11%). (J.M. Bailey, R.C. Pillard, “A Genetic Study of Male Sexual Orientation,” Archives of General Psychiatry48 [1991]: 1089-96).

In his analysis of the medical evidence supporting a biological cause of homosexuality, Dr. William Byne noted other twin studies. He wrote, “Without knowing what developmental experiences contribute to sexual orientation, the effects of common genes and common environments are difficult to disentangle. Resolving this issue requires studies of twins raised apart.” Other physicians have also criticized the study for overvaluing the genetic influence.

Byne also criticizes Bailey’s study noting that subjects were recruited by ads placed in gay publications. “Some people have suggested that identical twins who are concordant on a variety of measures are more likely to respond to these ads than ones who are different, which would lead to an increased estimate of heritability.”

Bailey conducted another study, published in the March 2000 issue of the Journal of Personality and Social Psychology, that revealed that the genetic influence on homosexuality he supposedly found earlier may actually be less. He sent a questionnaire to the entire Australian Twin Registry. Only three pairs of identical male twins were both homosexuals out of a total of 27 male identical twin pairs in which at least one was homosexual. Of the 16 fraternal male twins, in none of the pairs were both homosexuals. Bailey found similar results for lesbians.

Bailey says that his data in men lead to an estimate that the overall heritability of sexual orientation ranges from 25-75%, depending on a number of assumptions.

Bailey’s team also asked non-concordant identical twins (one was homosexual, one not) about their early family environment, and found that the same family environment was experienced or perceived by the twins in quite different ways. These differences led later to homosexuality in one twin, but not in the other. (N. E. Whitehead, Ph.D;

N.E. Whitehead, Ph.D. of the National Association for Research and Therapy of Homosexuality(NARTH) ponders over the results of concordant identical twins, whether their genes could have “made them do it”. He contends that they didn’t. According to him:

Genes could be a strong influence for a few, but even for those few, it is never overwhelming. The record strengths for genetic influence on behaviors are 79% in a group of highly addicted women cocaine addicts and about the same or somewhat higher, for ADHD. Because those figures are not 100%, even among addicts or those strongly pushed towards some other behavior, there is room for outside intervention and change. Hence even if homosexuality is as addictive as cocaine for a few individuals, their genes didn’t ‘make them do it.’

For perspective, it is valuable to compare genetic contributions to homosexuality with the question – is a girl genetically compelled to become pregnant at 15? Her genes might give her physical characteristics that make her attractive to boys – but whether she gets pregnant will depend greatly on whether her community is Amish or urban, conservative or liberal, whether they use contraceptives, and whether the parents are away for the evening.

So the influence of the genes is very indirect. We can see this by thinking further – if she was in solitary confinement all her life, would her genes make her become pregnant? Of course not! Some influence from the environment (in this case a boy) is essential! The effects of genes on behaviors are very indirect because genes make proteins, not preferences.

So the results of identical-twin studies are critical in understanding the biological influences on homosexuality. Only for physical traits like skin color are identical twins 100% concordant; otherwise they don’t necessarily follow either their parents’ genes…or their parents’ admonitions! In this, homosexuality proves to be no different from such unrelated behaviors as violence, being extroverted, or getting divorced. All may be influenced by genes, but not overwhelmingly determined by them.

The scientific truth is – our genes don’t force us into anything. But we can support or suppress our genetic tendencies. We can foster them or foil them. If we reinforce our genetic tendencies thousands of times (even if only through homoerotic fantasy), is it surprising that it is hard to change? Similarly, we have a genetic tendency to eat, but it is possible to foster this tendency and overeat for the pleasure it brings. If we repeat that often enough, we will not only reinforce a genetic tendency to become overweight, but find that “starving” the habit takes a long time! (

Another, quite obvious, example of what Dr. Whitehead is saying is that of alcoholism. It has been demonstrated that there may be a genetic predisposition towards the condition. If a person does not drink alcohol, however, he will not possibly become an alcoholic.

Thus it is the behavior one assumes during one’s life that determines the acquisition of a certain genetic predisposition, not the gene itself.

The “gay” gene

Dean H. Hamer, chief of the Gene Structure and Regulation Section of the National Cancer Institute’s Laboratory of Biochemistry, and his coworkers, conducted a study of the pedigrees of gay men who also had gay brothers. Hamer found that such people had an excess of gay relatives on the mother’s, but not the father’s side of the family. Reasoning that this might indicate that sexual orientation might be linked to the X chromosome, Hamer conducted a linkage analysis to determine if any DNA markers on the X chromosome would be inherited along with the putative gene for sexual orientation. In 33 of 40 pairs of gay brothers, he found such a marker near the tip of the long arm of the X chromosome, in a location called Xq28, an area that contains several hundred genes (D.H. Hamer et al., Science,261:321-7, 1993). Hamer later replicated this finding in a new set of families (S. Hu et al., Nature genetics, 11:248, 1995).

Hamer’s results are often misunderstood. Many believe that the study found an identical sequence (Xq28) on the X chromosome of all homosexual brothers. In reality, what it found was matching sequences in each set of brothers who were both homosexuals. Dr. William Byne argues that in order to prove anything by this study, Hamer would have had to examine the Xq28 sequence of gay men’s heterosexual brothers. Hamer insisted that such an inclusion would have confounded his study. Byne responded, “In other words, inclusion of heterosexual brothers might have revealed that something other than genes is responsible for sexual orientation.”

In 1999, on the other hand, Drs. George Rice, Neil Risch and George Ebers published their findings in Science after attempting to replicate Hamer’s Xq28 study. Their conclusion: “We were not able to confirm evidence for an Xq28-linked locus underlying male homosexuality.” Moreover, they added that when another group of researchers (Sanders, et al.) tried to replicate Hamer’s study, they, too, failed to find the genetic connection to homosexuality.

Ebers explains:

We’ve been collecting families that have more than one gay person for five years, and we’ve gone through something like 400 pedigrees. In those [families] there is really no support for the idea that male homosexuality is X-linked. The DNA tests that were done didn’t even support Dean’s idea a bit. There wasn’t even a trend toward increased sharing of haplotypes down there at Xq28.

Ebers speculates that there may be a simple explanation for Hamer’s finding of maternal transmission:

There may be an excess of all kinds of things on the maternal side because mothers know more about their family history than fathers. Something of a personal nature like this is perhaps even more likely to be something that you would [learn] from the maternal side.


Rice concluded in the Rice et al study:

It is unclear why our results are so discrepant from Hamer’s original study. Because our study was larger than that of Hamer’s et al, we certainly had adequate power to detect a genetic effect as large as reported in that study. Nonetheless, our data do not support the presence of a gene of large effect influencing sexual orientation at position Xq28. (

Byne offers another possible confounding factor in Hamer’s work:

The hallmark of X-linked transmission is the absence of father-to-son transmission…It’s possible that just the relative absence of father-to-son transmission – because gay men tend not to have children – could have given Dean the impression of X-linked transmission in his first pedigree study. (

Hamer himself offered some conclusions regarding genetics and homosexuality:

We knew that genes were only part of the answer. We assumed the environment also played a role in sexual orientation, as it does in most, if not all behaviors…. Homosexuality is not purely genetic…environmental factors play a role. There is not a single master gene that makes people gay…I don’t think we will ever be able to predict who will be gay. (

Citing the failure of his research, Hamer further writes:

The pedigree failed to produce what we originally hoped to find: simple Mendelian inheritance. In fact, we never found a single family in which homosexuality was distributed in the obvious pattern that Mendel observed in his pea plants. (

Hamer’s research has been cast into doubt not only by arguments over his interpretation of the data, but also by allegations of scientific misconduct. According to a front-page article by John Crewdson in the Chicago Tribune (June 25, 1995), an anonymous former member of Hamer’s lab had alleged that Hamer engaged in selective presentation of data in his 1993 Science paper. Crewdson reported that an investigation had been launched by the Office of Research Integrity (ORI) of the United States Department of Health and Human Services.

An article on genes and behavior in Science magazine said:

The interaction of genes and environment is much more complicated than the simple “violence genes” and intelligence genes” touted in the popular press. Indeed, renewed appreciation of environmental factors is one of the chief effects of the increased belief in genetics’ effects on behavior. The same data that show the effects of genes also point to the enormous influence of non-genetic factors. (C. Mann, “Genes and behavior,” Science 264; 1687 (1994), pp. 1686-1689)

Among Jeffrey Satinover’s conclusions on the “gay gene” are:

  • There is a genetic component to homosexuality, but “component” is just a loose way of indicating genetic associations and linkages. “Linkage” and “association” do not mean “causation.”
  • There is no evidence that shows that homosexuality is genetic-and none of the research itself claims there is. Only the press and certain researchers do, when speaking in sound bites to the public.
  1. Biological Causes

In addition to the neuroanatomical and genetic work, several other studies argue for a biological basis for sexual orientation. In one, Lee Ellis indicated that “if the mother experiences a lot of stress – and it’s got to be severe – during the second trimester [of pregnancy], there will be a significantly higher chance that her male offspring would be homosexual when they became sexually mature” (L. Ellis et al., Journal of Sex Research, 25[1]: 152-7, 1988). Another study published in Behavioral Neuroscience suggests that, compared with heterosexual men, gay men show a leftward asymmetry in the number of fingerprint ridges on their thumbs and little fingers (J.A.Y. Hall, D. Kimura, Behavioral Neuroscience, 108[6]: 1203-6, 1994).

Bailey reports that a common behavioral finding about male homosexuals provides additional support for a biological hypothesis. “The most consistent finding about male homosexuality is that as children, gay men were feminine boys,” as judged by such factors as lack of interest in sports or rough play, reputation as a “sissy,” or a desire to be a girl.

Perhaps 75% of feminine boys grow up to be gay men, which is a huge increase over expected rates. That’s generally consistent with a biological hypothesis because you have these boys playing atypically at a very early age – three to five – in a way they haven’t been socialized to behave. In fact, they’re often punished for behaving that way (J.M. Bailey, K.J. Zucker, Developmental Psychology, 31[1]: 43-55, 1995).

In 1998, researchers Dennis McFadden and Edward G. Pasanen published a study that evaluated the auditory systems of heterosexuals and homosexuals. Specifically, the study considered differences in echo-like waveforms emitted from an inner ear structure of people with normal hearing. These waves are higher in women than in men, often attributed to the person’s exposure to androgen in his or her early development as a fetus.

The McFadden study found the level of these waveforms in the ears of self-acknowledged lesbian women ranged between those of men and those of heterosexual women. The researchers concluded that this evidence suggests that female homosexuality could be a result of increased exposure to the male hormone androgen in the womb (homosexual men did not show the same variation).

The researchers themselves, however, are not too quick to draw definitive conclusions. They caution that the results are only tentative. In the published study, they point out that exposure to “intense sounds, certain drugs, and other manipulations” can lower the level of these auditory waveforms. “Thus, it may be that something in the lifestyles of homosexual and bisexual females leads them to be exposed to one or more agents that have reduced the (waveforms), either temporarily or permanently.” Moreover, even if the hearing differences were caused by an increased exposure to androgen in the womb, scientists would still be a far cry away from proving that this exposure is a cause of homosexuality -especially since the difference was not apparent in the male homosexual sample.

In March 2000, yet another study on a biological link to homosexuality surfaced. Scientists reported that finger length indicated how much exposure a person had had to androgen while in the womb (Williams, T.J., Pepitone, M.E., Christensen, S.E., Cooke, B.M., Huberman, A.D., Breedlove, N.J., Breedlove, T. J., Jordan, C.L. & Breedlove, S.M. (2000): Nature 404, 455-456).

Typically, people’s index finger is slightly shorter than the ring finger – a difference that is seen more clearly on the right hand due to exposure to higher levels of androgen while the human is developing in the womb. In females, the ring finger and index finger are almost the same size, but in men the ring finger is generally shorter.

Niel Whitehead, Ph.D. of NARTH comments on this study by saying:

Williams et al. reported that the mean finger-length ratio for lesbians was significantly less than that for heterosexual women, and did this by comparing the two ratios by a statistical test. They used a large number of interviewees. In such circumstances, although the mean finger lengths may be statistically different, they are often so close that it is not practically useful to say they are different. That is what has happened in the present case.

The original normal distributions can be reconstructed from the researchers’ data, and the results are shown in the figure below. (With its two large overlapping curves, this figure assumes that we are comparing an equal number of heterosexual women and lesbians).

There is obviously a very large overlap in the two populations (heterosexual women and lesbians), and although the two means may be statistically different, the difference is only 1% – which is a small effect, and not diagnostically useful in any sense.

Within the figure is also given the expected distribution of finger lengths for lesbians, assuming a United States nation-wide prevalence of 1.7% (which includes bisexual lesbians). For any finger-length ratio chosen, the lesbians in the population at large are outnumbered by their heterosexual counterparts by approximately 60:1.

The figure shows that there are large numbers of heterosexual women who have much more “masculine” finger-length ratios than most lesbians, but this is not considered by the researchers to be related to their sexual orientation.

Williams et al. invoke the idea of very high prenatal androgen levels (for which there is very scant evidence) to explain the difference in mean finger lengths which they find. But if this is indeed an explanation, it must rarely affect sexual orientation. An explanation which involved considerably less biological extrapolation would be preferable. For example, does a slightly more masculine pattern for a hand influence the self-image of a developing girl?

This study is rather similar to many other reported links between homosexuality and some biologically based phenomena. Although statistical connections may be shown, only a small percentage of subjects with that biological feature actually end up homosexual. (

Prominent research teams Byne and Parsons, and also Friedman and Downey, each concluded that there was no evidence to support a biologic theory, but rather that homosexuality could be best explained by an alternative model where “temperamental and personality traits interact with the familial and social milieu as the individual’s sexuality emerges.” (W. Byne and B. Parsons, “Human Sexual Orientation: The Biologic Theories Reappraised.” Archives of General Psychiatry 50, no. 3.)

Are homosexual attractions innate? There is no support in the scientific research for the conclusion that homosexuality is biologically determined (A. Dean Byrd, Ph.D.

Sociologist Steven Goldberg, Ph.D. states:

Virtually all of the evidence argues against there being a determinative physiological causal factor and I know of no researcher who believes that such a determinative factor exists…such factors play a predisposing, not a determinative role…I know of no one in the field who argues that homosexuality can be explained without reference to environmental factors.

He further says, “Gay criticism has not addressed the classic family configuration.” It has merely “asserted away the considerable evidence” for the existence of family factors. Studies which attempt to disprove the existence of the classic family pattern in homosexuality are “convincing only to those with a need to believe.” (S. Goldberg, When Wish Replaces Thought; Why So Much of What You Believe is False. Buffalo, New York: Prometheus Books, 1994)

Simon LeVay writes:

At this point, the most widely held opinion [on causation of homosexuality] is that multiple factors play a role. In 1988, PFLAG (Parents and Friends of Lesbians and Gays) member Tinkle Hake surveyed a number of well-known figures in the field about their views on homosexuality. She asked: “Many observers believe that a person’s sexual orientation is determined by one of more of the following factors: genetic, hormonal, psychological, or social. Based on today’s state-of-the-art-science, what is your opinion?” The answers included the following: “all of the above in concert” (Alan Bell), “all of these variables” (Richard Green), “multiple factors” (Gilbert Herdt), “a combination of all the factors named” (Evelyn Hooker), “all of these factors” (Judd Marmor), “a combination of causes” (Richard Pillard), “possibly genetic and hormonal, but juvenile sexual rehearsal play is particularly important” (John Money), and “genetic and hormonal factors, and perhaps also some early childhood experiences” (James Weinrich). (Simon LeVay, Queer Science, MIT Press, p. 273).

The role of the media in making information available on such research as mentioned above is of major importance. The media have been noted to put the spotlight on “pro-homosexual” research without even mentioning the fact that there are any arguments related to that research. It has become taboo in the West to be labeled a homophobe. Does Western media go to great lengths to prove themselves worthy of the very active and quite strong gay and lesbian movements? Do they selectively choose what reaches the reader and what does not, to that end?