Biology and sexual orientation is the concept that there is, at least in part, a biological basis for sexual orientation. An increasing number of studies have investigated this link, but no scientific consensus exists as to the specific biological factors that may play a role, nor to the precise nature of their influence on sexual orientation. Causal areas these studies have examined include morphological brain structure, prenatal environment, chromosomes, and viral genetic influence. Methodologically, some studies have used twins as controls.
The main biological determinants of sexual orientation are generally thought to be genetic and hormonal, with some writers suggesting either one or the other are the key factor, and many suggesting that both play a role. Most scientists agree that it is unlikely that there is a single "gay gene" that determines something as complex as sexual orientation, and that it is more likely to be the result of a number of biological factors. Many also agree that social and environmental factors intersect with biology to produce sexual orientation, while many strongly believe that sexual orientation is purely biological and inborn. The view that post-natal environmental influence is the sole determinant of sexual orientation and gender was prominent in the 20th century, but is less widely held in the 21st century.Biological explanations of homosexuality have become more popular with the public over the past several years: In 1983, 16% of Americans believed that "homosexuality is something that people are born with"; by 1993, that figure had nearly doubled to 31% (Moore, D. W. (1993, April). Public polarized on gay issue. The Gallup Poll Monthly, 30-34).
Evidence is increasing that homosexuality is a result of a complex interaction of many genes which are spread throughout human populations Mustanski, B. S., Dupree, M. G., Nievergelt, C. M., Bocklandt, S., Schork, N. J., & Hamer, D. H. (2005). A genomewide scan of male sexual orientation. Human Genetics, 116, 272-278. It has been suggested that male homosexuality represents an excess of genes coding for female-like traits which tip gay males over a 'liability threshold' into homosexuality. Females selecting 'gay-enabled' men may have increased the viability of their offspring. Wilson, G. and Rahman, Q., (2005). Born Gay. London: Peter Owen Publishers. p64.
Some have suggested that homosexuality is adaptive in a non-obvious way. By way of analogy, the allele (a particular version of a gene) which causes sickle-cell anemia (when two copies are present) may also confer resistance to malaria with no anemia (when one copy is present).
The so-called "gay uncle" theory posits that people who do not themselves have children may nonetheless increase the prevalence of their genes in future generations by providing resources (food, supervision, defense, shelter, etc.) to the offspring of close relatives. The primary criticism of this theory has to do with the fact that children share on average 25% of their genes with their uncles and aunts, but on average 50% with their parents. This means that to be adaptive, a "gay uncle" would need to save from death (or other lineage-terminating events) on average two nieces or nephews for every one of their own offspring they give up. Critics of the theory find this trade-off to be unlikely to produce a net reproductive gain.
Another theory in support of positive adaptiveness of homosexuality and bisexuality is that these sexual orientations provide some benefit to the local community in general. Communities that are so supported would be stronger and more likely to survive in the future. The primary criticism of this theory is that genetic evolution works on the level of individuals, not communities. If heterosexuals have an individual reproductive advantage over homosexuals and bisexuals in a given community, after a very long period of time, the community should be composed solely of heterosexuals, regardless of how this affects the community as a whole.
Finally, some posit that homosexuality would indeed be purely anti-adaptive, but like poor eyesight, still exists in the population because it has not, in the past, greatly affected an individual's chances of reproducing. Homosexual individuals in societies with no understanding of homosexuality and without a stigma placed on homosexuality have been observed to marry someone of the opposite sex and have children just like heterosexuals. The phenotype of the alleged "homosexual" genes is different and may actually be adaptive in such an environment.
Many objections to the idea of an innate cause of homosexuality come from religious groups and conservatives who focus on a moral rather than medical interpretation of sexual orientation, and seeing an individual's sexuality as a matter of personal choice or upbringing. However, seeing homosexuality as a "medical" rather than a "moral" issue does not guarantee better treatment for homosexuals. Indeed, many medical explanations of the innateness of sexual orientation have pathologised homosexuality and bisexuality as a kind of disability, and if a "gay gene" was discovered, parents might choose to screen and terminate embryos that carry the gene.
A few such studies began to examine homosexuality in the early 20th century, using small, non-random samples. The first relatively large-scale twin study on sexual orientation was reported by Kallman in 1952. Examining only male twin pairs, he found a 100% concordance rate for homosexuality among 37 monozygotic (MZ) twin pairs, compared to a 12%-42% concordance rate among 26 dizygotic (DZ) twin pairs, depending on definition. In other words, every identical twin of a homosexual subject was also homosexual, while this was not the case for non-identical twins. This study was criticised for its vaguely-described method of recruiting twins and for a high rate of psychiatric disorders among its subjects.
While Kallman's was the largest relevant study until the 1990s, other studies did provide examples of MZ twin pairs of both sexes who were discordant for sexual orientation; that is, they found that both male and female homosexuals did sometimes have twins that were not homosexual themselves. The existence of such twins demonstrates that genes are not the only factor involved in determining sexual orientation, at least not for everybody. Environmental factors, in the womb or during life, must play a role.
However, studies such as Kallman's did suggest the existence of a significant genetic component to sexual orientation, and later researchers have attempted to use twin studies to quantify the size of such an effect. The most highly publicized was reported by J. Michael Bailey and Richard Pillard in "A Genetic Study of Male Sexual Orientation" in the Archives of General Psychiatry, December 1991. These researchers recruited gay male subjects through advertisements in the gay media and sent questionnaires, which included questions on sexual orientation, to their male siblings. They reported that:
were also gay themselves. The researchers estimated that the heritability of male homosexuality was between 31% and 74%. A similar study carried out by the same researchers on the siblings of lesbian women reported concordance rates of:
Heritability was estimated as between 27% and 76%.
Being based on samples of people who volunteered for studies specifically targeting gay men and lesbians, these results could only be suggestive. However, a number of more recent studies have examined sexual orientation in large "twin registries" recruited without reference to sexual orientation. Estimates of heritability for male and female homosexuality derived from these are shown below.
| Study | Male | Female |
|---|---|---|
| Hershberger, 1997 | 0% | 48% |
| Bailey et al., 2000 | 40% | 0% |
| Kendler et al., 2000 | 28–65% | |
| Kirk et al., 2000 | 30% | 50–60% |
One criticism often levelled at comparisons of MZ/DZ twins in general is that they depend upon an assumption that MZ and DZ twins share a similar amount of their environments with their twins. This assumption has been questioned.
To consider specifically the studies under discussion here, the results of the Bailey and Pillard volunteer studies pose some problems for interpretation. Consider the male study. The higher concordance rate among MZ twins compared to DZ twins is consistent with substantial heritability. However, the lower rate among non-twin brothers compared to DZ twins (both share on average 50% of genes), and the high rate of homosexuality among adoptive brothers of gay men compared to the general population (when adoptive brothers are no more genetically similar than men from different families) provide evidence for environmental factors. It is also worth stressing that the MZ concordance was well short of 100%, which also points to a role for environmental factors.
It is considered likely by some authors, including Bailey, that the heritability of homosexuality has been overstated by volunteer studies. For example, a gay man with a gay brother may be more likely to volunteer for a study of gay men and their brothers than will a gay man with a heterosexual brother, perhaps because he feels that his brother will be more willing to cooperate. The prevalence of stigmatization and discord within families occasioned by the "coming out" of a gay member might also reduce the likelihood of a heterosexual brother being willing to participate in the study. The lower heritability estimates from the more recent, probably more representative, studies seem to confirm this.
However, there is still considerable variation even between these studies. It is interesting to note that the Kirk et al. study (see table above) was a reanalysis of the same data used by Bailey et al. (same table), using different definitions of homosexuality. The striking difference in results, particularly for women, underlines the lack of definitive results at this point. One problem is that, for most definitions, the prevalence of homosexuality in the general population is low, which means that registries will contain relatively few twin pairs of which one is gay or lesbian. The lack of statistical power resulting from this may explain some of this lack of consistency. Meta-analysis might be of use in resolving this difficulty.
Overall, data appear to indicate that genetic factors play some role in the development of sexual orientation, but that they probably account for only a minority of variation and that further work will be needed to quantify their influence more precisely.
Any genetic component must be rooted in evolution by natural selection, and many non-scientists assume that a homosexual orientation would necessarily result in decreased reproduction. Gene prevalence and therefore selection, however, can be influenced by increasing the reproductive success of individuals with whom we share genes in common. While it may be unclear to some how homosexuality could offer a selective advantage to individuals, many hypotheses exist that explain why an inherited tendency toward this orientation might offer a selective advantage to the genes they carry. Most hypotheses speculate that the presence of homosexual members may also promote intragroup harmony. These are hypotheses: hard empirical data is lacking. Apparent homosexual behavior provides a stealth mechanism for slipping past alpha males in some species; like most putative explanations, that does not explain inheritance of female homosexuality. Some twin effects could be the result of their shared environment from conception to birth.
However, the best-known work of this type is that of Simon LeVay, reported in "A Difference in Hypothalamic Structure Between Hetero-sexual and Homosexual Men" in the journal Science, August 1991. LeVay studied four groups of neurons in the hypothalamus, called INAH1, INAH2, INAH3 and INAH4. This was a relevant area of the brain to study, because of evidence that this part of the brain played a role in the regulation of sexual behaviour in animals, and because INAH2 and INAH3 had previously been reported to differ in size between men and women.
He obtained brains from 41 deceased hospital patients. The subjects were classified as follows: 19 gay men who had died of AIDS, 16 presumed heterosexual men (6 of whom had died of AIDS), and 6 presumed heterosexual women (1 of whom had died of AIDS).
The AIDS patients in the heterosexual groups were all identified from medical records as intravenous drug abusers or recipients of blood transfusions, though only 2 of the men in this category had specifically denied homosexual activity. The records of the remaining heterosexual subjects contained no information about their sexual orientation; they were assumed to have been mostly or all heterosexual "on the basis of the numerical preponderance of heterosexual men in the population".
LeVay found no evidence for a difference between the groups in the size of INAH1, INAH2 or INAH4. However, the INAH3 group appeared to be twice as big in the heterosexual male group as in the gay male group; the difference was highly significant, and remained significant when only the 6 AIDS patients were included in the heterosexual group. The size of the INAH3 in the homosexual male brains was similar to that in the heterosexual female brains. However, he also found some contrary results:
William Byne and colleagues attempted to replicate the differences reported in INAH 1-4 size using a different sample of brains from 14 HIV-positive homosexual males, 34 presumed heterosexual males (10 HIV-positive), and 34 presumed heterosexual females (9 HIV-positive). They found a significant difference in INAH3 size between heterosexual men and women. The INAH3 size of the homosexual men was apparently smaller than that of the heterosexual men and larger than that of the heterosexual women, though neither difference quite reached statistical significance.
Byne and colleagues also weighed and counted numbers of neurons in INAH3, tests not carried out by LeVay. The results for INAH3 weight were similar to those for INAH3 size; that is, the INAH3 weight for the heterosexual male brains was significantly larger than for the heterosexual female brains, while the results for the gay male group were between those of the other two groups but not quite significantly different from either. The neuron count also found a male-female difference in INAH3, but found no trend related to sexual orientation.
It is not clear from the research how HIV/AIDS may affect brain structure, a possible confounding factor. So rather than showing that differences in the neuron indicate homosexuality, LeVay's study may be showing that HIV/AIDS causes differences in neurons. It should be noted, however, that neither LeVay nor Byne found an HIV-related difference in INAH3 size.
The man considered the "dean of American sexologists", Johns Hopkins University psychologist John Money, concerning LeVay's studies, says, "Of course it orientation is in the brain. The real question is, when did it get there? Was it prenatal, neonatal, during childhood, puberty? That we do not know."
Simon LeVay's finding points out a correlation between physiology and sexual orientation, but does not necessarily establish by itself a genetic basis for sexual orientation.
A recent study supports X-linkage from a different perspective. Women have two X chromosomes, one of which is "switched off". In some cases, it appears that this switching off can occur in a non-random fashion. Bocklandt et al (2006)Bocklandt, S.B., Horvath, S., Vilain, E., Hamer, D.H. (2006). Extreme skewing of X chromosome inactivation in mothers of homosexual men. Human Genetics, 118:691-694 reported that the number of women with extreme skewing of X chromosome inactivation is significantly higher in mothers of homosexual men than in age-matched controls without gay sons. 4% of controls showed extreme skewing compared to 13% of the mothers with gays sons and 23% of mothers with two or more gay sons.
Male homosexuality appears likely to be influenced by a complex genetic interaction which may be mediated by H-Y antigens in the mother’s immune system (see below). Whichever genes are implicated they almost certainly cause male brains to differentiate in a female typical direction. As for female homosexuality, there remains little evidence from replicated genetic linkage studies.
A chemical called the histocompatibility Y-antigen (the "HY antigen") is found on the surface of the cells of male mammals. It is hypothesized (Wachtel, 1983; Blanchard & Bogaert, 1996) that the "fraternal birth order effect" may be related to increasing levels of antibodies produced by the mother in response to the presence of this chemical during pregnancy with the oldest son. These antibodies could then somehow trigger different brain development patterns in later male children, either in the uterus or in early childhood through breast milk. Later sons would then more likely to have a homosexual orientation as adults. At least one genetic study attempting to verify this theory claimed to find a correlation with a certain area of the X chromosome (of which all women carry two copies, and all men carry one), but these findings could not be replicated by other researchers.
An alternate theory was proposed by Italian researchers in 2004 (Camperio-Ciani et al. 2004), supported by a study of about 4,600 people who were the relatives of 98 homosexual and 100 heterosexual men. Female relatives of the homosexual men tended to have more offspring than those of the heterosexual men. Female relatives of the homosexual men on their mother's side tended to have more offspring than those on the father's side. The researchers concluded that there was genetic material being passed down on the X chromosome which both promotes fertility in the mother and homosexuality in her male offspring. The connections discovered, however, would explain only 20% of the cases studied, indicating that this might not be the sole genetic factor determining sexual orientation.
Homosexuality has also been correlated with elevated testosterone levels in adult males, which may indicate an indirect genetic influence.
Studies involving mice have shown differences in female sexual behaviour depending on distance from testosterone sources in the womb (Ryan & Vandenbergh, 2002). Female mice flooded with higher levels of testosterone in the womb are prone to more masculine sexual behaviour, such as mounting other females, whereas their sisters exposed to lower levels of foetal testosterone act in more traditionally feminine ways, and are typically courted more by male mice (vom Saal, 1989; vom Saal & Bronson, 1980; Rines & vom Saal, 1984). This suggests a pivotal role of hormones, and specifically testosterone, in the development of sexual orientation.
Some have theorized that events in the womb may contribute to some subset of homosexual behavior (though certain individuals may be genetically predisposed to be vulnerable to such events, and the conditions inside the mother's reproductive system are of course influenced by her genetics).
Supporting evidence for this hypothesis includes:
It is unclear whether the observed anatomical and cognitive differences are signs of a (possibly genetic) mechanism that determines sexual orientation, or symptoms of the formation of an atypical sexual orientation during childhood.
One possible mechanism is differential fetal hormone exposure, especially to testosterone (and a compound it is transformed into, estradiol) and luteinizing hormone (LH) is proposed as the mechanism. The concentrations of these chemicals is thought to be influenced by fetal and maternal immune systems, maternal consumption of certain drugs, maternal stress, and direct injection.
Hormone levels may of course vary over time. Given the semi-sequential nature of fetal development, and because multiple hormones are involved, it is possible for the hypothesized "masculinization" or "feminization" process to affect only some body or brain systems. (This is necessary to explain why someone might be say, born with a male body but with a "feminized" sexual attraction.)
Prenatal hormones have been indicated both in Simon LeVay's study of the anterior hypothalamus in cadavers with homosexual contraction of AIDS as cause of death and Marc Breedlove's study of birth order and finger length ratios in living individuals. LeVay's study suggests that homosexual men are "feminized", Breedlove's study suggests that both heterosexual men and homosexual women are "masculinized".
Researchers at the University of Texas at Austin, lead by Dennis McFadden, found the response of the inner ear to soft sounds tended to be weaker in homosexual woman than in heterosexual women. The response among men tended to be weaker than either female group. Fetal exposure to androgens is hypothesized to affect this attribute, suggesting that fetal exposure to the same chemicals may also predispose a daughter to a lesbian orientation. However, lifestyle differences between the two female groups may lead to different sound exposures, and this could also explain the correlation.
Researchers in the Breedlove study found evidence correlating prenatal hormones to male homosexuality. Males exposed to high levels of androgens (sexual hormones) as fetuses are predominantly homosexual.
Based on the relatively high frequency of homosexuality in the population, and the assumption that it is evolutionarily very disadvantageous, some have proposed that the cause may be a bacterium or virus.
A sort of reverse sexual imprinting has been observed in heterosexual humans; see the section on the "Westermarck effect" in Behavioral imprinting.
Several different triggers for imprinting upon a particular sexual orientation have been proposed.
A common hypothesis, especially among non-scientists, is that something about what young children see in the gender-roles behavior of adults, or some differences (possibly unconscious) in the way adults treat young children, somehow influence or determine a child's eventual sexual orientation.
This hypothesis, however, has not been supported by research findings that children of homosexuals are just as likely to be heterosexual as the general population and in reverse for children of heterosexuals in prevalence of homosexuality.
The theory is based in part on the frequent finding that a majority of gay men and lesbians report being gender-nonconforming during their childhood years. A meta-analysis of 48 studies showed childhood gender nonconformity to be the strongest predictor of a homosexual orientation for both men and women (Bailey and Zucker, 1995, Developmental Psychology). For example, in a study by the Kinsey Institute of approximately 1000 gay men and lesbians (and a control group of 500 heterosexual men and women), 63% of both gay men and lesbians reported that they were gender nonconforming in childhood (i.e., did not like activities typical of their sex), compared with only 10-15% of heterosexual men and women. There are also six "prospective" studies--that is longitudinal studies that begin with gender-nonconforming boys at about age 7 and follow them up into adolescence and adulthood. These also show that a majority (63%) of the gender nonconforming boys become gay or bisexual as adults (reported by Zucker, 1990). There are no prospective studies of gender nonconforming girls.
This article is licensed under the GNU Free Documentation License.
It uses material from the
"Biology and sexual orientation".
Home Page • arts • business • computers • games • health • hospitals • home • kids & teens • news • physicians • recreation• reference • regional • science • shopping • society • sports • world