The Biology of Sexual Orientation
© Simon LeVay, 2003
This page is an overview of theories and research on the topic of sexual orientation, with emphasis on biological studies. I welcome corrections, comments, and suggestions for other studies that should be covered (email me) (return to home page).
Early in the 20th century, Sigmund Freud postulated that family dynamics influence a child’s ultimate sexual orientation. For example, a dominant, close-binding mother, or an absent or distant father, might steer a boy toward homosexuality by disrupting his exit from the postulated “Oedipal phase” of psychosexual development (Freud, 1957). Girls might become lesbian because of unconscious hatred of their mothers, envy of a brother’s penis, and the like (Freud, 1955). Retrospective studies confirm that gay men tend to describe their relationships with their mothers as unusually close and with their fathers as distant or hostile (Bell et al., 1981; Freund and Blanchard, 1983).
Comment: These retrospective findings don’t necessarily mean that parental attitudes influence the child’s sexual orientation in the way Freud envisaged, however. A contemporary American analyst has suggested that parental attitudes to pre-gay children, such as a father’s withdrawal or hostility, may actually be a response to gender-variant traits in the child rather than a cause of them (Isay, 1989, 1996).
Learning theorists have suggested that gendered traits, including sexual orientation, emerge from a conscious or unconscious “training regimen” imposed by parents, teachers, peers, and society in general (Money and Ehrhardt, 1971). Most feminist thinkers have also attributed the development of gendered traits to socialization.
Comment: The main difficulty with these ideas is that heterosexual parents don’t seem to inculcate homosexuality or gender-nonconformity, in fact they often attempt to prevent these traits in children who nevertheless become gay. Parents who happen to be gay themselves might tolerate or even foster gender variance and homosexuality in their children, but in fact the children of gay parents usually become heterosexual (Stacey and Biblarz, 2001). One much-publicized attempt to change a child’s gender and future sexual orientation by parental socialization (after his penis was accidentally destroyed during circumcision) ended in failure (Colapinto, 2000).
It has been proposed that early sexual experiences (pleasant or traumatic) influence sexual orientation—that a girl who is raped by a man at an early age may be “turned off” men and thus become lesbian, for example, while a boy who is seduced by a man (or molested by an older brother) and who derives sexual pleasure from the experience may become gay (Cameron and Cameron, 1995; Churchill, 1967).
Comment: Such ideas fail to explain how it is that many people whose initial sexual experiences are heterosexual and consensual nevertheless become gay, or how it is that children who attend single-sex boarding schools, where consensual homosexual encounters are common, are no more likely to become homosexual adults that are children who do not attend such schools (Wellings et al., 1994).
This school of thought proposes that a person’s identity as gay, straight, or bisexual is a label imposed by society and internalized by the individual, rather than arising from within (Foucault, 1978; Halperin, 1990).
Comment: Social constructionism has contributed valuable insights to our understanding of human sexuality in its cultural context, but it has had relatively little to say about the question that interests us here, which is why specific individuals become gay, straight, or bisexual.
A contrasting view is that sexual orientation is determined or influenced by biological factors such as genes and hormones. Of course, there doesn’t have to be a sharp distinction between biological and life-experience theories. It’s conceivable, for example, that a close-binding mother might induce hormonal changes in the young child that in turn lead to adult homosexuality. Conversely, a biological trait such as facial beauty might influence parents to treat a son in such a way as to steer him toward homosexuality. At the very least, though, testing biological and life-experience theories require the application of very different techniques and thus tend to engage researchers with different training and backgrounds.
Biological theories of sexual orientation have a long history. Magnus Hirschfeld, the German sexologist and gay-rights pioneer, promoted such theories early in the 20th century. Still, Freudian, behaviorist, and social-constructionist thinking dominated thinking on the topic for most of the century. Only in the 1980s and 1990s did biological ideas re-emerge in a significant way. This re-emergence paralleled a remarkable increase in tolerance and acceptance of gay people in many Western societies. It seems likely that these parallel trends reflected a two-way interaction: increasing acceptance of (and familiarity with) gays fostered a belief in biological theories, and vice versa.
Sexual orientation is a gendered trait: most men are sexually attracted to women more than they are to men, and most women are sexually attracted to men more than they are to women. Homosexual people are sex-atypical, at least with respect to their sexual orientation. Biological theories of sexual orientation commonly, though not always, include the idea that sexual orientation is embedded within a larger constellation of gendered traits, and that biological factors influence multiple gendered traits simultaneously. Whatever ultimate biological factors influence a person to become homosexual, these factors may promote the development of other characteristics—anatomical, physiological, molecular-genetic, or psychological—that are sex-atypical. Given that the ultimate factors may not be directly detectable (if they operated during fetal life, for example), the presence of other sex-atypical traits in gay people may be taken as an indicator that those undetectable factors were in fact at work. Still, the presence of sex-atypical traits in gay people doesn’t always compel a biological interpretation—it might be that certain life experiences promote both homosexuality and other sex-atypical characteristics.
To give a concrete example: it’s been well documented that gay people, on average, display some sex-atypical psychological characteristics during childhood (Bailey and Zucker, 1995). Gay men, for example, tend to report that they had less interest in rough-and-tumble sports than other boys. A prospective study showed that boys who are very strongly gender-nonconformist have a high likelihood of developing into gay or bisexual adults (Green, 1987). But this connection between childhood gender-nonconformity and adult homosexuality could arise for genetic reasons (genes promoting a spectrum of gender-nonconformist traits including homosexuality) or for environmental reasons (e.g., parental encouragement these same traits). It’s also possible that genes cause childhood gender-nonconformity and that environmental factors (e.g. the hostile reactions of peers) cause gender-nonconformist children to become gay. Thus the fact that there is a correlation between homosexuality and some other trait doesn’t in itself distinguish between different possible causes.
Sibling studies. Most of the evidence for a genetic influence on sexual orientation comes from family and twin studies. Homosexuality clusters in particular families, especially among siblings. Thus, the brothers of gay men are reported to have about a 22 percent chance of themselves being gay, whereas the brothers of heterosexual men have only about a 4 percent chance of being gay (Pillard and Weinrich, 1986). Similarly, the sisters of lesbians have an increased chance of being lesbian (Bailey and Benishay, 1993). This clustering in largely sex-specific: the existence of a lesbian in a family has little effect on the chances that her brothers will be gay, or vice versa.
Comment: Family clustering is consistent with a genetic influence, but it does not by itself distinguish between genetic and environmental causes. For example, a mother who treats one son in such a way as to make him gay might well do the same with another son. To the extent that the clustering does have a genetic cause, the sex-specificity of the clustering would imply that different genes contribute to male and female homosexuality. This is hardly surprising since they are really different phenomena: male homosexuality is sexual attraction to males and female homosexuality is sexual attraction to females.
Twin studies. Most twin studies have focused on the concordance rate for homosexuality. This is the likelihood that, if one twin is gay, his or her co-twin will be gay too. If genes influence sexual orientation, the concordance rate should be higher for twin pairs who are monozygotic (“identical”) than for twin pairs who are dizygotic (“fraternal”). That’s because monozygotic twins share all the same genes, whereas dizygotic twins share only about half their genes. If genes absolutely determined sexual orientation the concordance rate for monozygotic twins should be 100%.
One early study did report a near-100% concordance rate for male monozygotic twins (Kallmann, 1952). More recent studies have come up with much lower figures, but have generally reported higher concordance rates for monozygotic than for dizygotic twins, consistent with a genetic influence on sexual orientation. In one study the concordance rate was 52% for male monozygotic twins compared with 22% for male dizygotic twins (Bailey and Pillard, 1995). A comparable study of female twins came up with concordances of 48% and 16% respectively (Bailey et al., 1993).
Although these studies suggest that there is a substantial influence of genes on sexual orientation in both men and women, there are problems of interpretation. For one thing, it is difficult to get from the concordance rates to a measure of heritability (meaning, simply put, the fraction of the total causation of homosexuality that is genetic). If it is the case that monozygotic twins experience a more similar environment than do dizygotic twins (being treated more similarly by their parents, for example), and these environmental factors influence sexual orientation, then the concordance rate would be higher for monozygotic twins for that reason alone. There is in fact no reason to think that this scenario is the case, but it is a theoretical possibility.
Another problem has to do with ascertainment bias. Typically, researchers do these twin studies by advertising for individuals who are gay and have a twin, then they check on the other twin’s sexual orientation. But if the likelihood that a person responds to the ad is affected by whether his/her twin is also gay or not, this could throw off the statistics. To get away from this problem, Bailey and colleagues did one study using a pre-existing twin registry (Bailey et al., 2000). This study came up with lower concordance rates than previous studies, especially in women. Interestingly, the researchers found that childhood gender nonconformity—a common precursor of adult homosexuality—was significantly heritable in both sexes.
There is one small study of monozygotic twins reared apart (Eckert et al., 1986). Of four female pairs in which one twin was lesbian, none of the co-twins were lesbian. Of two male pairs in which one twin was gay, one of the co-twins was also gay, while the other was bisexual.
Comment: There remains considerable uncertainty about the heritability of homosexuality: it is probably significantly heritable in men but may be only slightly heritable or not heritable at all in women.
Candidate-gene study. One approach to the question of genes influencing sexual orientation is to pick a gene that might conceivably play a role and to compare its DNA sequence in gay and straight people. One group of researchers picked the androgen receptor gene, a gene that plays the key role in mediating testosterone’s influence on the body and brain (Macke et al., 1993). They could not find any differences between gay and straight men, however.
Linkage studies. A contrasting approach is to scan the entire genome, looking for sites where pairs of gay siblings inherit the same DNA more frequently than would be expected on a chance basis (“linkage analysis”). Dean Hamer’s group reported finding (in pairs of gay brothers) such a site on the X chromosome—in a region called Xq28 (Hamer et al., 1993). They concluded that a gene influencing male sexual orientation was probably located in this region. Hamer’s group has replicated the finding but there has not been an independent confirmation and in fact one group has reported failing to replicate the finding (Rice et al., 1999). Thus the claim of a “gay gene” on the X chromosome remains unverified.
Comment: The fact that 10 years have passed without further progress on this issue, in spite of the complete sequencing of the X chromosome that has been accomplished in the meantime, could lead one to suspect that the hypothesis of a “gay gene” at Xq28 has been allowed to die a quiet death. As is often true in behavioral genetics, however, this gene may exist but its effects may only be discernible in certain populations.
Genomic imprinting. This is the phenomenon whereby some genes acquire different molecular labels depending on whether they are inherited from the mother or the father; this labeling affects gene expression and development in the offspring. A recent article speculates that imprinting could play a role in the development of sexual orientation (Bocklandt and Hamer, 2003).
Gay genes and evolution. The existence of genes promoting homosexuality is counter-intuitive, since such genes should reduce their owner’s reproductive success and thus, over many generations, they should be eliminated from the gene pool. A number of people have considered the various ways in which gay genes might persist (Bailey, 2003; Hamer and Copeland, 1994; Ridley, 1994; Ruse, 1988; Weinrich, 1987; Wilson, 1978). Here are some of the ideas that have been put forward:
1. Gay genes might persist if gay people, though having few children themselves, promote the reproductive success of their siblings (“kin selection”).
2. A gene might cause homosexuality and thus reduce reproductive success when present on two homologous chromosomes (homozygous state) but have some other, positive effect when present on one chromosome (heterozygous state). The analogy is to the sickle-cell gene which causes anemia when homozygous but confers resistance to malaria when heterozygous. If the heterozygous advantage is sufficiently great the gene will persist in the population.
3. A gene for sexual attraction to men would cause homosexuality in men but might cause a “hyper-heterosexuality” in women, thus increasing their reproductive success—and vice versa. The positive effect on the reproductive success of one sex might balance the negative effect in the other sex.
4. It’s possible that, through much of human evolution, people have been socially compelled to marry and have children regardless of their sexual orientation. In this case, the negative effect of a gay gene on reproductive success might be small, and might be outweighed by some other, unknown benefit conferred by the gene.
5. The elimination of gay genes from the population (by non-reproduction of gay people) might be balanced by the occurrence of new mutations. For this to be the case, the mutation rate for gay genes would have to be exceptionally high.
Comment: None of these theories are particularly persuasive. The evolutionary value of gay genes may become clearer if and when such genes are identified and their mechanism of action determined.
Adult hormone levels. Most studies have failed to find significant differences in the levels of circulating sex hormones between homosexual and heterosexual adults of the same sex (Meyer-Bahlburg, 1984).
Prenatal hormones: background. In experimental animals it’s been well established that the sexual differentiation of the body and brain results primarily from the influence of sex hormones secreted by the testes or ovaries (Arnold, 2002). Males have high levels of testosterone in fetal life (after functional development of the testes) and around the time of birth, as well as at and after puberty. Females have low levels of all sex hormones in fetal life, and high levels of estrogens and progestagens starting at puberty. High prenatal testosterone levels organize the brain in a male-specific fashion; low levels testosterone permits it to organize in a female-specific fashion. Hormones at puberty activate the circuits laid down in prenatal life but do not fundamentally change them. Thus, the range of sexual behaviors that adult animals can show is determined in large part by their prenatal/perinatal hormone exposure—manipulating these hormone levels can lead to atypical sex behavior or preference for same-sex sex partners as well as a range of other gender-atypical characteristics.
Nevertheless, prenatal/perinatal hormones may not be the entire story. Changes in adult hormone levels can change brain anatomy in some cases (Cooke et al., 1999). Furthermore, some aspects of the prenatal sexual differentiation of the brain seem to be independent of sex hormones and probably reflect the direct effects of the brain’s chromosomal sex on its own development (Arnold, 2003). Whether these direct effects are significant for the development of any gendered traits in humans is unknown.
Based on this animal research a number of scientists, especially the German neuroendocrinologist Günter Dörner, have promoted a prenatal hormonal theory of homosexuality (Dörner, 1969). This theory postulated that in human fetuses destined to become homosexual adults, the sexual differentiation of the brain proceeds in a sex-atypical direction. The cause could be atypical levels of sex hormones (e.g., unusually low levels of testosterone in the case of a male fetus, or unusually high levels in a female fetus) or some difference in the way the brain responds to hormones, such as a genetic peculiarity of the androgen receptor (see above).
Dörner initially presented his theory as part of a pathological conception of homosexuality and even as a tool for preventing it through medical means. This did not endear him to the gay community. There is no intrinsic reason why his theory should be seen as less gay-friendly than other theories, however (LeVay, 1996). Although the prenatal hormonal theory has not been proved or disproved in the decades since Dörner proposed it, a body of supportive evidence has accumulated, and it is probably the dominant idea among those who think about sexual orientation from a biological perspective.
Attributing sexual orientation to prenatal hormone levels is not an ultimate explanation, because the question remains as to how those levels (or the brain’s response to them) come to be different in pre-gay and pre-straight fetuses. At one extreme, the reason for these differences might be genetic, as with the androgen receptor hypothesis mentioned above or the case of congenital adrenal hyperplasia, discussed below. At the other extreme the reason might be environmental, as with Dörner’s maternal stress theory, discussed below. It’s also possible that essentially random developmental processes could be responsible. In species such as rats where the mother carries multiple fetuses simultaneously, a female fetus that happens to be located next to a male fetus can absorb testosterone from its neighbor, resulting in some masculinization of her sexual behavior in adulthood (Clemens et al., 1978; Meisel and Ward, 1981). Since the sex of a fetus’s neighbor is random, the ultimate cause of the masculinized behavior is also random. There are probably countless such random processes occurring prenatally, even in fetuses who are singletons. (Human females who had a male twin are not thought to be especially likely to be lesbian. Some studies have reported other gender-atypical traits in these women (McFadden, 1993), but negative findings have also been reported (Henderson and Berenbaum, 1997)).
Congenital adrenal hyperplasia (CAH). This condition is caused by a genetic defect in one of the enzymes that are involved in the synthesis of corticosteroid hormones. It is marked by excessive levels of androgens (testosterone-like hormones) that are secreted by the adrenal glands during fetal life. (The condition is generally recognized and successfully treated after birth.) Affected girls are often born with some degree of masculinization of the external genitalia, in which case the condition is considered a form of intersexuality. Numerous studies have reported that CAH-affected girls tend to display a variety of gender-atypical traits (Berenbaum et al., 2000), though the effects may be small (Henderson and Berenbaum, 1997). When adult they are much more likely to have experienced or to wish for homosexual relationships that comparison groups of women such as their unaffected sisters (Dittmann et al., 1992).
Comment: Although it’s been suggested that the tendency toward gender-atypicality and homosexuality in CAH-affected females is an indirect effect caused by their (or their family’s) reaction to the partially masculinized genitalia, it seems more likely to be a direct effect of the prenatal androgens on brain development. Supporting this conclusion is the observation that there seems to be no relationship between the degree of genital masculinization and the degree of psychological gender-atypicality (Berenbaum and Bailey, 2003). Of course, CAH is a rare condition and plays no role in the psychosexual development of most lesbian or bisexual women, but it supports the hypothesis that atypical prenatal hormone levels can influence adult sexual orientation.
Diethylstilbestrol (DES) exposure. DES is a synthetic, non-steroidal drug that activates estrogen receptors. It was widely prescribed to pregnant women before 1971. Women who were exposed to the drug during fetal life are significantly more likely to experience same-sex attraction than comparison groups such as their unexposed sisters, according to one small study (Meyer-Bahlburg et al., 1995), but a recent larger study found that exposed women were actually slightly less likely to have experienced a same-sex relationship (Titus-Ernstoff et al., 2003).
Comment: The equivocal or possibly non-existent effect of prenatal DES on female sexual orientation, which contrasts with the strong effects seen in CAH, may reflect the fact that DES does not activate androgen receptors. Although androgens are normally converted to estrogens in the brain and thus activate estrogen receptors as well as androgen receptors, the direct activation of androgen receptors may be more important for this particular gendered trait, and perhaps for others too.
Prenatal stress theory of male homosexuality. Stressing pregnant rats (for example, by close confinement and exposure to bright lights) causes the male offspring of those pregnancies to display atypical sex behavior in adulthood: they are relatively unwilling to mount females and they may show a female-type response (“lordosis”) to being mounted by males (Ward, 1972; Ward et al., 1994). The reason is that the stress activates the fetuses’ stress hormones which in turn lead to a diminution in the levels of testosterone during a critical period of brain development.
On the basis of Ward’s findings and his own animal studies, Dörner proposed that the mothers of homosexual men were exposed to severe stress during pregnancy, and he carried out retrospective studies that seemed to offer strong support for the hypothesis (Dörner et al., 1980; Dörner et al., 1983). But more recent studies have either completely failed to confirm Dörner’s hypothesis (Bailey et al., 1991; Schmidt and Clement, 1990) or have provided very equivocal support for it (Ellis et al., 1988). Prenatal stress also has no effect on the development of gender role behavior in boys (Hines et al., 2002).
Comment: The prenatal stress theory of male homosexuality seems to be incorrect, in spite of the animal results. Rats and humans probably differ in their stress-response mechanisms.
Effects on anatomy, brain structure and function, and cognition. Prenatal sex hormones have numerous effects on the developing body and brain. Thus, if there are differences in the levels of these hormones between pre-gay and pre-straight fetuses, one might expect to see other differences between gay and straight adults than simply their sexual orientation. Presumably, this would particularly likely for traits that differ between the sexes. Numerous studies have compared body anatomy, brain anatomy, brain function, and cognitive and personality traits between gay and straight men and between lesbian and heterosexual women. The results of some of these studies are reviewed in the following sections.
Penis size. According to a re-analysis of old Kinsey Institute data derived from about 5,000 men, the penises of gay men are slightly but significantly longer (6.46 vs. 6.14 inches measured along the top surface) and fatter than those of straight men (Bogaert and Hershberger, 1999).
Comment: These findings are open to criticism because the measurements were made by the subjects themselves at home and not by an independent observer. (Gay men might be more tempted to exaggerate than straight men, or they might be more aroused by the sight of their erect penises, thus causing stronger erections.) If correct, the result is inconsistent with the simplest form of the prenatal hormone hypothesis, which would predict gay men’s penises to be smaller. There are various ways one could make the findings fit the hypothesis, but it may not be worth dwelling on this until a replication study has been done—which could be a while.
Finger length ratios. In men the index finger (D2) is usually significantly shorter than the ring finger (D4), whereas in women D2 is nearly as long as D4. In other words, the D2:D4 ratio is usually lower in men than in women. Presumably this results from hormonal differences between males and females during development of the fingers. This idea is supported by the observation that CAH-affected individuals, who were exposed to high prenatal androgen levels, have low D2:D4 ratios (Brown et al., 2002b).
Several groups have reported that the D2:D4 ratio is lower in lesbians than in heterosexual women (McFadden and Shubel, 2002; Rahman and Wilson, 2003b; Williams et al., 2000), consistent with the prenatal hormone theory. It’s also been reported that only one subgroup of lesbians, namely those who self-identify as “butch” (masculine), has low D2:D4 ratios (Brown et al., 2002a). This is one of the very few biological studies that look at the important differences that exist within the categories of “gay” and “lesbian.”
One study failed to confirm the relationship between D2:D4 ratios and sexual orientation in women, citing ethnicity as a confounding variable (Lippa, 2003a). The finding was confirmed, however, in another recent study that focused on female monozygotic twins who were discordant for sexual orientation: the lesbians twins had a lower 2D:4D ratio than their heterosexual co-twins (Hall and Love, 2003). This suggests that the 2D:4D effect is independent of genes.
Data for men have been inconsistent: gay men have been reported to have a D2:D4 ratio that is lower (McFadden and Shubel, 2002; Rahman and Wilson, 2003b), higher (Lippa, 2003a) or the same (Williams et al., 2000) as in straight men.
Fingerprints. A 1994 study reported a difference in the fingerprint patterns of gay and straight men: more specifically, the ratio of the numbers of ridges on the fingers of the left and right hands, which usually favors the right hand, was reported to be left-shifted in gay men (Hall and Kimura, 1994). Two subsequent studies have failed to replicate this finding, however (Forastieri et al., 2002; Mustanski et al., 2002).
Comment: None of these anatomical studies inspire tremendous confidence, though the D2:D4 findings in women seem the best documented, and are consistent with the prenatal hormone theory.
Suprachiasmatic nucleus (SCN). This is a small group of cells in the hypothalamus that plays a key role in the generation of circadian rhythms. A Dutch group has reported that the SCN is larger in gay men than in straight men (Swaab and Hofman, 1990).
Comment: This finding hasn’t been replicated (or refuted) by other labs. If it is correct, its significance is unclear since the SCN is not known to play a role in the generation of sexual feelings or behaviors.
Third interstitial nucleus of the anterior hypothalamus (INAH1). This small group of cells lies in a region of the hypothalamus known from animal studies to be involved in the generation of male-typical sex behavior. It is generally larger in men than women (Allen et al., 1989; Byne et al., 2001; LeVay, 1991). In a 1991 autopsy study, I reported that INAH3 was smaller in gay men than in straight men (LeVay, 1991). A more recent study replicated this finding, although the magnitude of the difference was less (Byne et al., 2001). This latter study also reported that there was a difference in cell density—a higher density (more cells per cubic millimeter) in the gay men. The researchers commented that the total number of cells in INAH3 may be the same in gay and straight men, but are packed more closely in the gay men, perhaps because they did not form so many synapses during development.
Comment: There has been concern that the small size of INAH3 in the gay men might be a consequence of the disease (AIDS) from which most of them died, rather than their sexual orientation. However, neither I nor Byne’s group found any evidence that AIDS by itself has any effect on the size of INAH3. The findings on INAH3 support the prenatal hormone theory, because it’s known that manipulating testosterone levels in rats, if performed during a critical prenatal/perinatal period of development, affects the ultimate size of the analogous cell group in the rat’s hypothalamus, (Rhees et al., 1990), as well as causing atypical sex behavior in adulthood (Grady et al., 1965). Still, the findings don’t absolutely compel us to accept that prenatal events influence sexual orientation, since (as mentioned above) there is evidence that some sexually dimorphic brain structures can be modified by hormonal or other changes in adulthood.
A group at
Comment: Of course I like this study because it offers such a close parallel to my own human study. Why some rams are homosexual is not known—exclusive homosexuality seems to be rare in the animal kingdom—but there are other studies suggestive of a neuroendocrinological mechanism (Pinckard et al., 2000).
There is a report that the anterior commissure, a fiber bundle connecting the left and right sides of the cerebral cortex, is larger in women than men, and larger in gay men than in straight men (Allen and Gorski, 1992).
Comment: This report has not been replicated or refuted. The significance of the finding, if correct, is unclear, though it might be related to the cognitive differences that have been reported between gay and straight men (see below).
Auditory system. There are differences between men and women in the functional properties of the inner ear and the central auditory system, as assessed by measurement of otoacoustic emissions (sounds produced by the inner ear) and auditory evoked potentials (recordings of brain activity following a brief sound). Dennis McFadden and his colleagues (McFadden, 2002) have reported that lesbian and bisexual women have partially masculinized otoacoustic emissions and auditory evoked potentials. They also report that women who had male twins (and who may therefore have been exposed to testosterone from their twin during prenatal life) are likewise masculinized in otoacoustic emissions, as mentioned above. They therefore interpret their findings as consistent with the prenatal hormonal theory of sexual orientation, i.e., that pre-lesbian or pre-bisexual fetuses are exposed to atypically high levels of androgens. Interestingly, the researchers found no difference in the otoacoustic emissions of gay and straight men, but they observed that some aspects of the evoked potentials of gay men were shifted in a “hypermasculine” direction—which if true is the opposite of what would be expected on the basis of the prenatal hormone theory, at least in its simplest form.
A British group (Rahman et al., 2003b) recently reported differences in the startle response (eyeblink following a loud sound) of lesbians compared with heterosexual women. It was previously known that men and women differ in the extent to which the startle response is inhibited when the loud sound is preceded by a weaker sound: this “prepulse inhibition” (PPI) is typically less evident in women than men. The researchers reported that the PPI was greater (i.e., masculinized) in the lesbian subjects, a finding that they interpreted in terms of the prenatal hormone theory. They did not find any difference between the startle responses of gay and straight men.
Comment: These specific findings await independent replication, but the Rahman and McFadden studies are consistent with each other.
Sexual arousal. A recent brief report from Bailey and Mesulam’s groups described the patterns of brain activity in gay and straight men while they were viewing sexually arousing and non-arousing images (Barch et al., 2003). The regions selectively active during arousing stimuli were generally the same ones in the two groups, but three regions (medial prefrontal cortex, left hippocampus, and right amygdala) were more selectively active in the gay men.
Comment: Probably the main message of this study is the similarity of activity patterns in the gay and straight men during sexual arousal, in spite of the differences in the kind of images they find arousing.
General. Men and women differ in a number of cognitive traits. Men tend to outperform women in certain kinds of visuospatial tasks, such as mental rotation, navigation, and targeting, as well as in mathematical reasoning, whereas women tend to outperform men in tests of verbal fluency (speed at coming up with words that correspond to some category), speed of calculation, recognition of facial expressions, and memory of object location (Kimura, 1999). Men are also typically more competitive and aggressive than women. There is evidence that these sex differences result at least in part from differences in prenatal sex hormone levels (Collaer and Hines, 1995). Thus, in terms of the prenatal hormone hypothesis it makes sense to ask whether gay people differ from straight people of the same sex in any of these traits.
Visuospatial tasks. A number of studies have reported that gay men perform worse than straight men on a variety of visuospatial tasks, such as mental rotation, judgment of line orientation, and targeting (Gladue et al., 1990; Hall and Kimura, 1995; McCormick and Witelson, 1991; Neave et al., 1999; Rahman and Wilson, 2003a; Wegesin, 1998). In these studies the gay men performed at the female-typical level or at an intermediate level. Two studies failed to find differences between gay and straight men (Gladue et al., 1990; Tuttle and Pillard, 1991). Findings for women have been mixed: one recent large study found that lesbians are moderately better than heterosexual women at mental rotation, but the difference was only in speed of response, not accuracy (Rahman and Wilson, 2003a).
Object location memory. One recent large study of object location memory found that gay men do better than straight men, and about at the level of heterosexual women. No difference between the performance of lesbian and heterosexual women was found (Rahman et al., 2003c).
Verbal fluency. A 1991 study reported that gay men outperform heterosexual men in this trait (McCormick and Witelson, 1991). Two subsequent studies came up with negative results (Gladue et al., 1990; Neave et al., 1999), but a recent large study reported that both gay men and lesbians have sex-atypical scores in verbal fluency tests (Rahman et al., 2003a).
Aggressiveness. Gay men are reported to be less physically aggressive than straight men (Ellis et al., 1990; Gladue and Bailey, 1995). No difference was found between lesbians and straight women (Gladue and Bailey, 1995).
Handedness. There seems to be little or no difference in the handedness of heterosexual men and women (Lippa, 2003b), but most studies have found that gay men and/or lesbians are significantly more likely to be non-righthanded (i.e. left-handed or mixed-handed) than straight people of the same sex (Lalumiere et al., 2000; Lippa, 2003b; Mustanski et al., 2002).
Comment: Hand preference is observable before birth (Hepper et al., 1991), though it can change as a result of birth trauma and the like. The observation of increased non-righthandness in gay people is therefore consistent with the idea that sexual orientation is influenced by prenatal processes.
A considerable number of studies, mostly by a Canadian group of researchers, have reported that gay men tend to be have more older brothers than do straight men (Blanchard and Bogaert, 1996; Bogaert, 2003b). By way of explanation, the researchers hypothesize that some women develop antibodies to male-specific antibodies during early pregnancies with male fetuses, and that these antibodies affect the development of subsequent male fetuses in such a way as to increase the likelihood of homosexuality. This might happen through a general retardation of fetal growth with resulting small statute in postnatal life (Bogaert, 2003a).
Comment: The birth-order effect seems to be robust across numerous samples. It is not a particularly large effect, however: it would take an improbable number of older brothers (I think about 10) to give one even a 50:50 chance of being gay by the birth-order effect alone. In general, birth-order effects on psychological traits are explained by family dynamics (e.g., in this case, by parents “permitting” younger sons to be gay). However, the researchers have offered some good arguments why family dynamics are not likely to be the main explanation in the case of sexual orientation. A more direct test of their hypothesis, such as the detection of anti-male antibodies in the mothers of gay men, remains to be done.
Although quite a few of the findings reported here are inconsistent between studies or await independent replication, my general conclusion is that biological processes, especially the prenatal, hormonally-controlled sexual differentiation of the brain, are likely to influence a person’s ultimate sexual orientation.
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