Prenatal Hormones

The hormonal theory of sexuality holds that, just as exposure to certain hormones plays a role in fetal sex differentiation, such exposure also influences the sexual orientation that emerges later in the adult. Prenatal hormones may be seen as the primary determinant of adult sexual orientation, or a co-factor with genes, biological factors and/or environmental and social conditions. Differences in brain structure that come about from hormones and genes interacting on developing brain cells are believed to be the basis of sex differences in countless behaviors, including sexual orientation.

Prenatal factors that affect or interfere with the interaction of these hormones on the developing brain can influence later sex-typed behavior in children. This hypothesis is originated from countless experimental studies in non-human mammals, yet the argument that similar effects can be seen in human neurobehavioral development is a much debated topic among scholars. Recent studies, however, have provided evidence in support of prenatal androgen exposure influencing childhood sex-typed behavior.

Fetal hormones may be seen as either the primary influence upon adult sexual orientation or as a co-factor interacting with genes and/or environmental and social conditions. However, Garcia-Falgueras and Swaab (2010) disagree that social conditions influence sexual orientation to a large degree. As seen in young children as well as in vervet and rhesus monkeys, sexually differentiated behavior in toy preference is differing in males versus females, where females prefer dolls and males prefer toy balls and cars; these preferences can be seen as early as 3–8 months in humans. Further, differences in viewing preference can be seen as early as the first day of life, where females prefer human faces and males prefer mechanical mobiles. Despite this, is it impossible to completely rule out the social environment or the child’s cognitive understanding of gender when discussing sex typed play in androgen-exposed girls.

Conversely, environmental/social conditions may affect the presentation of sexually differentiated behavior in males more than females, as male-typical play behavior is much more encouraged and female behavior discouraged among male children. Children also tend towards objects which have been labelled for their own sex, or toys that they have seen members of their sex playing with previously. An endocrinology study by Garcia-Falgueras and Swabb postulated that ‘In humans, the main mechanism responsible [for] sexual identity and orientation involves a direct effect of testosterone on the developing brain.’

Their study puts forward the notion that intrauterine exposure to hormones is largely determinative. Sketching the argument briefly here, the authors say that sexual organs are differentiated first, and then the brain is sexually differentiated ‘under the influence, mainly, of sex hormones such as testosterone, estrogen, and progesterone on the developing brain cells and under the presence of different genes as well . . . . The changes brought about in this stage are permanent. . . . [S]exual differentiation of the brain is not caused by hormones alone, even though they are very important for gender identity and sexual orientation.’

Fetal gonads develop primarily based on the presence or absence of androgens; production of testosterone and conversion into dihydrotestosterone during weeks 6 to 12 of pregnancy are key factors in the production of a male fetus’ penis, scrotum and prostate. In a female, however, absence of these levels of androgens results in the continued development of typically female genitals. Following this, sexual differentiation of the brain occurs; sex hormones exert organizational effects on the brain that will be activated in puberty. As a result of these two processes occurring separately, the degree of genital masculinization does not necessarily relate to the masculinization of the brain. Sex differences in the brain have been found in many structures, most notably the hypothalamus and the amygdala (responsible for the ‘fight or flight’ response.

Hamman et al. (2003) conducted a study to investigate the role of the amygdala in human sexual behavior. Participants were shown a combination of sexual photos (a heterosexual couple engaging in sexual activity and opposite-sex nudes) and non-sexual photos (a man and woman engaging in non-sexual activity and a fixation cross). Hamman et al. found that males showed an increased level of amygdala activity in response to visually sexual stimuli while females reported a greater level of sexual arousal. Findings suggest that the amygdala may play an important role in mediating sex differences, especially in males, through the neural pathways responsible for emotionally-positive, desirable stimuli.

The study of the organizational theory of prenatal hormones can be difficult, as ethically researchers cannot alter hormones in a developing fetus; instead, scholars must rely on naturally occurring abnormalities of development to provide answers. Most extensively studied in organizational effects of hormones is the condition Congenital adrenal hyperplasia (CAH, deficient production of sex steroids). The theory being that, if human psychological sex differences are exerted on the fetus by androgens, then females with CAH should be more male-typed and less female-typed than comparison groups of females without CAH.

Another condition being examined by researchers is Androgen Insensitivity Syndrome (AIS, partial or complete inability of cells to respond to androgens). If androgen does affect behavior, partial AIS individuals should be less male-typed than typical boys, and more male-typed than typical girls. While effects of androgens have been implicated in sex-typed play behaviors, there seems to be no evidence of a large effect of androgens on gender identity; moderate levels during prenatal development have been shown to increase the probability of a male gender identity, but this is in no way a guarantee.  Since research suggests that hormones alone do not act on sexual orientation and differentiation of the brain, the search for other factors that act upon sexual orientation have led to the discovery of genes such as the SRY and ZRY.

Evidence exists in rats that the stress levels of the mother can also have an effect on fetal development. As Ellis & Cole-Harding (2001) outline, the chain of events in prenatal stress affecting brain sex differentiation appears to be that stress causes the mother’s adrenal glands to release high levels of stress hormones into the blood system, substantial proportions of which cross the placental barrier and interfere with the fetus’ production of sex hormones temporarily, most notably testosterone. These results have been applied to human sexual orientation, although studies of maternal stress often lack generalizability due to small sample sizes and the inherent difficulty of accurately measuring stress levels in pregnancy. Criticisms of this study outline that subprimate mammals are invalid measures of human sexual differentiation, as sex hormones follow a more ‘on-off’ role in sex-typed behavior than is found in primates.

Some studies do suggest that prenatal stress significantly increases the likelihood of homosexuality or bisexuality, although varying evidence exists for which trimester is most important. Evidence does not suggest that nicotine or alcohol consumption during pregnancy has any effect on male sexual orientation. In females, no significant relationship between prenatal stress or sexual orientation has been found. However, evidence has been found that prenatal stress alongside smoking increases the probability of homosexuality in females more than just smoking alone, which is in contrast to animal models of nicotine on gendered behavior. Studies of endocrinology have found implications for amphetamines and thyroid-gland hormones to increase homosexuality in female offspring as well, although it has not been examined in conjunction with prenatal stress levels.

Some have postulated that postnatal (e.g., social and environmental factors) development can play a role in the sexual orientation of an individual, yet solid evidence of this has yet to be discovered.Children born through artificial insemination with donor sperm and consequently raised by lesbian couples have typically been heterosexually oriented. Summed up by Bao and Swaab, ‘The apparent impossibility of getting someone to change their sexual orientation . . . is a major argument against the importance of the social environment in the emergence of homosexuality, as well as against the idea that homosexuality is a lifestyle choice.’

There is evidence of a correlation between sexual orientation and traits that are determined in utero. Williams et al. (2000) found that finger length ratio, a characteristic controlled by prenatal hormones, is different in lesbians than in straight women. However, they found no difference between gay and straight men. Another study by McFadden in 1998 found that auditory systems in the brain, another physical trait influenced by prenatal hormones is different in those of differing orientations; likewise the suprachiasmatic nucleus (SCN) in the brain (responsible for controlling circadian rhythms) was found by Swaab and Hofman to be larger in homosexual men than in heterosexual men. The SCN is also known to be larger in men than in women.

An analysis of the hypothalamus by Swaab and Hofmann found that the volume of the SCN in homosexual men was 1.7 times larger than a reference group of male subjects, and contained 2.1 times as many cells. During development, the volume of the SCN and the cell counts reach peak value at approximately 13 to 16 months after birth; at this age, the SCN contains the same number of cells as was found in adult male homosexuals, yet in a reference group of heterosexual males the cell numbers begin to decline to the adult value of 35% of the peak value. Gay men have also been shown to have higher levels of circulating androgens and larger penises, on average, than hetero men.

Gay men have more older brothers on average, a phenomenon known as the fraternal birth order effect (FBO). It has been suggested that the greater the number of older male siblings the higher the level of androgen fetuses are exposed to. No evidence of birth order effects have been observed in women. The theory holds that FBO is a result of a maternal immune response that is produced towards a factor of male development over several male pregnancies. Bogaert’s hypothesis argues that ‘the target of the immune response may be malespecific molecules on the surface of male fetal brain cells (e.g.,including those in the anterior hypothalamus). Antimale antibodies might bind to these molecules and thus interfere with their role in normal sexual differentiation, leading some later born males to being attracted to men as opposed to women.’ Garcia-Falgueras and Swaab state that ‘The . . . . fraternal birth order effect . . . is putatively explained by an immunological response by the mother to a product of the Y chromosome of her sons. The chance of such an immune response to male factors would increase with every pregnancy resulting in the birth of a son.’

In conjunction with fraternal birth order, handedness provides further evidence of prenatal effects on sexual orientation, because handedness is regarded by many as a marker of early neurodevelopment. Other correlates to handedness (e.g., cerebral laterality, prenatal hormonal profiles, spatial ability) have been linked to sexual orientation, either empirically and/or theoretically. In right-handed individuals, the number of older brothers increased the odds of homosexual orientation, but this effect was not seen in left-handed individuals.

A gene of the Rh system has been discussed as a possible candidate for affecting fraternal birth order, as it has been linked to both handedness and immune system functioning. Gene variants in the Rh system are implicated in a maternal response to what is known as Hemolytic disease of the newborn. Rh is a factor in blood, and in cases where the mother is absent of this (Rh-) while carrying an Rh+ fetus, an immune response may develop with deleterious effects. The Rh gene hypothesis is a strong candidate because not only does it involve the maternal immune response, but it has been implicated in handedness as well. Variants of the androgen receptor (AR) gene have also been discussed, in that non-right-handedness in men has been linked with fewer repeats of the AR gene, which in turn is associated with lower testosterone. A theory that high prenatal testosterone leads to neuronal and axonal loss in the corpus callosum (connects the right and left hemispheres) is supported by this hypothesis.

In a 1991 study, Simon LeVay demonstrated that a tiny clump of neurons of the anterior hypothalamus—which is believed to control sexual behavior and linked to prenatal hormones— known as the interstitial nuclei of the anterior was, on average, more than twice the size in heterosexual men when contrasted to homosexual men. Due to this area also being nearly twice the size in heterosexual men than in heterosexual women, the implication is that the sexual differentiation of the hypothalamus in homosexuals is in a female direction. In 2003 scientists at Oregon State University announced that they had replicated his findings in sheep. Later studies in humans, however, have yet to confirm this finding.

Most empirical or theoretical research into women’s sexual orientation has, historically, been guided by the idea of lesbians as essentially masculine and heterosexual women as essentially feminine. Typically, this belief is traced to the early ‘inversion theory’ of sex researchers who state that homosexuality is a result of biological abnormalities that ‘invert’ sexual attraction and personality. Handedness research has provided implications; because more men than women present a preference for their left hand, the higher proportion of non-right handedness that has been discovered among lesbians when compared to heterosexual women demonstrates a possible link of prenatal masculinization and sexual orientation. Backing this up are reports that lesbians display more masculinized 2D:4D (index to ring finger) digit ratios than heterosexual women, based on data gathered from at least six different laboratories. This effect has not yet been observed between homosexual and heterosexual males. However, the validity of this measure of digit ratios remains controversial as a predictor of prenatal androgen, as many other prenatal factors may play roles in bone growth in prenatal stages of development. While many studies have found results confirming this hypothesis, others have failed to replicate these findings, leaving the validity of this measure unconfirmed.

Diethylstilbestrol (DES), a drug that has been in the past prescribed to prevent miscarriages, has also been studied in relation to women’s sexual orientation. It has been observed to exert a masculinizing/defeminizing effect on the developing brain of the fetus. When compared to controls, higher percentages of DES-exposed women (17% vs 0%) reported that they had engaged in same-sex relations; however, the great majority of DES women stated an exclusively heterosexual orientation. Girls with congenital adrenal hyperplasia (an autosomal recessive condition which results in high androgen levels during fetal development) have more masculinized sex role identities and are more likely to have a homosexual sexual orientation as adults than controls. An alternative explanation for this effect is the fact that girls with this condition are born with masculinized external genitalia, which leads their parents to raise them in a more masculine manner, thus influencing their sexual orientation as adults. However, the degree to which the girls’ genitals are masculinized does not correlate with their sexual orientation, suggesting that prenatal hormones are a stronger causal factor, not parental influence.

Prenatal androgen exposure has been associated with an increased chance of patient-initiated gender reassignment to male after being initially raised as female in early childhood or infancy. Gooren found that organizational effects of prenatal androgens are more prevalent in gender role behavior than in gender identity, and that there are preliminary findings that suggest evidence of a male gender identity being more frequent in patients with fully male-typical prenatal androgenization. Individuals with complete Androgen Insensitivity Syndrome are almost always brought up as females, and the differentiation of gender identity/role is feminine. This example is important in demonstrating that chromosomes and gonads alone do not dictate gender identity and role.

Because organ differentiation and brain differentiation occur at different times, in rare cases transsexualism can result. Drawing on some transsexualism cases, Garcia-Falgueras and Swaab state that ‘[f]rom these examples it appears that the direct action of testosterone on the developing brain in boys and the lack of such action on the developing brain in girls are crucial factors in the development of male and female gender identity and sexual orientation . . . .’ Countless studies have been run on peripheral levels of sex steroids in male and female homosexuals, a considerable number of which claimed to find ‘less ‘male hormone’ and/or more ‘female hormone’ in male homosexuals and vice versa in female homosexuals.’ However, these findings have been reviewed and have subsequently been dismissed by scholars as suffering from faulty design and interpretation.

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