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Neurobiological Bases of Homosexuality? Some Evidence and Inquiries

Jen Benson's picture
Web Paper 1

Presented here is some evidence for biological factors involved in homosexual orientation and behavior, including microanatomy, psychoendocrinology, and genetics, though much of the research literature supports the view that it is due to an interaction of biological, psychological, and social or factors, as is the current understanding of much human behavior. I do not aim to fully endorse either a biological or environmental explanation for homosexuality, but merely to present some evidence for the influence of both on sexual orientation.
Until December 1973 the Diagnostic and Statistical Manual of Mental Disorders (DSM-1 and DSM-II) classified homosexuality as a mental disorder, before the American Psychological Association (APA) voted to replace such a description with “sexual orientation disturbance” (3). A 1992 documentary film “Changing Our Minds” presents some of the treatments that have been used on homosexuals, such as hysterectomies, estrogen injections, transorbital lobotomies, aversion therapy, and even castration, none of which were shown to effectively reverse homosexuality (2). One of the first people to research the issue was Alfred Kinsey, whose report Sexual Behavior from 1948 showed homosexuality to be rather common in males of different socioeconomic classes and educational and geographical backgrounds. He and his researchers could not find a single case in which sexual orientation had been successfully reversed (2). A study by Evelyn Hooker presented to the APA in 1956 showed an equal distribution of pathology and mental health across heterosexuals and homosexuals, as determined by use of the Rorschach test administered by researchers blind to the subjects’ orientations. Hers was followed by many studies showing that homosexuality is not a pathology (2). In the 1980’s “sexual orientation” replaced “sexual preference,” implying a biological root to homosexuality and reflecting growing cultural acceptance of the notion of homosexuality as something which is not chosen (9).
Sexual Dimorphism and Dimorphism by Sexual Orientation
Investigations into how homosexuals and heterosexuals differ biologically stemmed first from investigations into how females and males differ biologically. Charles Barraclough at the University of California in Los Angeles in 1959, found that injecting female rats with testosterone shortly before or after birth suppressed ovulation, while male rats could ovulate if castrated and given estrogen (2). Newborn males, however, would experience ovulation (characteristic of females), if deprived of testosterone, while newborn females would develop as females even in the absence of estrogen. Later studies at Oxford University in 1971 by Geoffrey Raisman and Pauline Field found a strong difference between the brains of male and female rats in that females had more synaptic connections between brain cells in the hypothalamus and where structurally shaped differently (2). Roger Gorski extended this research into sexual dimorphism (or differences in male and female brains) of rats and found that the male rat’s hypothalamus is five times larger than that of the female (2). Sexual dimorphism was then found in the brains of human beings, beginning in 1982 with the work of Christine de Lacoste-Utamsine and Ralph Holloway, who found that the splenium in the corpus callosum differs in size and shape between men and women (2). In 1985 Dick Swaab’s research at the Netherlands Institute for Brain Research in Amsterdam found other evidence for sexual dimorphism in human brains, the same difference that Gorski had found in rats. Five years later he discovered that the suprachiasmatic nucleus was dimorphic, though according to sexual orientation rather than sex; this cluster of cells was almost twice as large in homosexual men as it was in heterosexual men (2). Inspired by this finding, Simon LeVay, who was at the time conducting research at the Salk Institute in La Jolla, California, investigated dimorphism of the hypothalamus, a region thought to be more involved in sexual behavior than the suprachiasmatic nucleus. He dissected the brains of forty-one cadavers from hospitals in New York and California, nineteen of which were of homosexual men who had died of AIDS, and sixteen of which were presumed to be heterosexual men. He found that the cluster of neurons commonly known as INAH3, or the third interstitial hypothalamus, was more than twice as large in heterosexual men than in homosexual men (9). This study has been widely criticized for its small sample size, its lack of a control group, and the possible confound of all the gay men having died of AIDS, which certainly could affect their brains. Other researchers have cited dimorphism as evidence for the neurobiological bases of sexual orientation. For example, McCormick and Witelson (4) found that homosexual men and women showed no association between handedness and their magnitude of perceptual asymmetry, showing different patterns of functional cerebral asymmetry in homosexuals compared with heterosexuals. Since Le Vay’s study, however, the research on anatomical differences between heterosexuals and homosexuals has been conflicted and inconclusive and besides could not determine causality between biology and behavior (2).
Hormones have also been studied as a contributing factor to homosexuality. Male rats injected with estrogen and female rats injected with testosterone have been found to show reproductive behaviors characteristic of the opposite sex (2). In 1984 Heino Meyer-Bahlburg from Columbia University could find no difference in testosterone or estrogen levels between homosexual and heterosexual men. Research into prenatal human exposure to hormones has, however, provided some insight into how it could contribute to sexual orientation. Congenital adrenal hyperplasia (CAH) is a condition caused by a defective enzyme that prevents the fetus’s adrenal gland from producing cortisol, resulting in an overproduction of masculinizing androgens by the adrenal gland; a female CAH baby will have genitalia that look more masculine than feminine. A 1984 study by John Money at the Johns Hopkins University found that 37 percent of CAH women claimed to be lesbian or bisexual, suggesting some influence of prenatal exposure on sexual orientation (2). Others have found similar trends, for example, a study by Meyer-Bahlburg and colleagues from 1995 (5) found that more women exposed prenatally to diethylstilbestrol (DES), a no steroidal synthetic estrogen, were rated as bisexual or homosexual than were controls, supporting the possibility that prenatal estrogen plays a role in sexual orientation, at least in females. Other research into the prenatal-hormone theory of sexual orientation, such as into the luteinizing-hormone (LH) feedback process, is as of yet largely inconclusive.
Inquiries into the possible genetic basis of homosexuality have examined identical and fraternal twins. A study by Michael Bailey and Richard Pillard at Boston Univeristy examined a sample of fifty-six monozygotic (identical) twins, fifty-four dizygotic (fraternal) twins, and fifty-seven unrelated adopted brothers (2). They found a gay-gay correspondence of 11% for the adopted brothers, 22% for the dizygotic twins, and 52 percent for the monozygotic twins, suggesting a considerable genetic factor in homosexuality. Thus they have determined up to 70% of the variance homosexuality to be attributable to heritability, other factors affecting variability potentially stemming from many sources, environmental or otherwise. Another study by Bailey, Dunne, and Martin (1) recruited twins from the Australian Twin Registry and assessed their sexual orientation as well as two related traits: childhood gender nonconformity and continuous gender identity. They found lower concordances for no heterosexual orientation than in prior studies, but that familial factors largely influenced sexual orientation, childhood gender nonconformity, and continuous gender identity. This study also found greater difficulty in separating genetic and shared environmental influences on variance in these factors, though childhood gender nonconformity was found to be significantly heritable in both males and females. A study by Richard Green of UCLA found that gender-atypical play in prepubescent boys (2) can indicate homosexual orientation 75 percent of the time, suggesting that sexual orientation may indeed be quite deeply rooted as some indicative behaviors may be observed so early.
Perhaps the most controversial study that sparked much of this recent debate was by Deam Hamer of the National Cancer Institute in 1993, who introduced the possibility of a “gay gene” (9). He examined 40 pairs of brothers who were homosexual, hypothesizing that some genetic marker on the X chromosome was partly responsible for their homosexual orientations. Because men inherit the X chromosome maternally, he theorized that sons may inherit homosexuality from their mothers. In his gene linkage studies, he found that families having more than one homosexual son showed greater incidence of homosexuality in relatives on the maternal side than on the paternal side. Among these twins he also found that 33 of the 40 sets of homosexual brothers had the same variants on the q28 marker of the X chromosone, leading him to conclude that homosexuality is influenced by gene Xq28. This study has been widely challenged, for example, by the Office of Research Integrity of the Department of Health and Human Services, and his results have yet to be replicated (9). A twin study of lesbian twins by Bailey and Pillard in 1991 found that about half of the lesbians in their sample of lesbian twins had a twin who was a lesbian, suggesting a possible genetic contribution (9) Yet another study by Martin and Bailey, that studied 1,912 women from ages 17 to 50 found no difference in the rate of lesbianism in identical or fraternal twins, suggesting that being raised in the same household by the same parents seems to influence sexual orientation much more than genetics, for lesbians (9). The suggestion that a gene itself could be directly responsible for psychological dispositions or behaviors is misleading. Genes merely direct a certain pattern of RNA synthesis, which may influence the development of psychological dispositions or behaviors, with many intervening factors between a gene and behavior (9).
Research into the biological bases of homosexuality has been both condoned and challenged by gay rights activists. Some believe such evidence may be grounds for discrimination and serve merely to showcase the behavior as something abnormal, while others believe that understanding homosexuality as something other than a choice might lead people to be less judgmental of it (8). My research into this topic has been largely disorienting in dealing with such a large mass of controversial and often conflicting information. One factor that sparked my interest in the topic is the fact that homosexuality has been documented in humans for centuries and yet appears to serve no reproductive or adaptive function. (The Alliance Theory of the evolution of male-male sexual behavior does posit, however, that such behavior reinforces alliances that contribute directly to male survival and thus indirectly to male survival (6). Homosexuality has been tied to fraternal birth order in males, childhood gender nonconformity, and certain gene loci on the X chromosone, as well as prenatal development (7). Until such studies can successfully establish lines of causality, however, consideration of other non-biological factors may not be dismissed.

Works Cited

1) Bailey, J. M., Dunne, M. P., and Martin, N. G. (2000). Genetic and Environmental Influences on Sexual Orientation and Its Correlates in an Australian Twin Sample. Journal of Personality and Social Psychology, 78(3), 524-536.

2) Burr, C. Homosexuality and Biology. Online. June 1997. <>

3) Homosexuality and DSM-IV. Online. May 2001. <>

4) McCormick, C. M., and Witelson, S. F. (1994). Functional Cerebral Asymmetry and Sexual Orientation in Men and Women. Behavioral Neuroscience, 3, 525-531.

5) Meyer-Bahlburg, H. F. L., Ehrhardt, A. A., Rosen, L. R., Gruen, R. S., Veridiano, N. P., Vann, F. H., and Neuwalder, H. F. (1995). Prenatal Estrogens and the Development of Homosexual Orientation. Developmental Psychology, 31(1), 12-21.

6) Muscarella, F. (2007). The Evolution of Male-Male Sexual Behavior in Humans: The Alliance Theory. Journal of Psychology and Human Sexuality, 18(4), 275-311.

7) Rahman, Q., and Wilson, G. D. (2003). Born Gay? The Psychobiology of Human Sexual Orientation. Personality and Individual Differences, 34, 1337-1382.

8) Sartelle, J. Rejectiong the Gay Brain (and Choosing Homosexuality). Online. May 1994. <>

9) Schneider, Y. C. The Gay Gene: Going, Going…Gone. Online. 24 April 2006. <>


Putt Williams's picture

Biology Yes! Environment, not so.

I cannot accept that environmental factors play a role in homosexuality. It may play a role in some same-sex activity. But such activity is mostly confined to sex. But when it comes to one's personality, creativity and finding oneself attracted to the same gender, that in my opinion is pure biological. If environmental factors were also a key factor, then what would be the cause of homosexuality in the most homophobic societies? Whether it is Uganda or Jamaica, you will find feminine men and masculine women. You will find that neither of these groups are entirely gay or straight. So surely what we see on the outside is a reflection of what is on the inside.

Paul Grobstein's picture

Sexual orientation and the brain

A nice bringing together of lots of material. Does one need to "endorse either a biological or an environmental explanation"? If brain = behavior, then what is the distinction? Maybe the issue is "genetic" and "environmental"? And the answer is ... both play a role? Where does "choice" fit into this framework?  For more along these lines, see Does Biology Have Anything to Contribute to Thinking About Sex and Gender?