Prenatal hormones and sexual orientation

Sexual orientation
Orientations
Asexual Bisexual Heterosexual Homosexual
Gender-based alternative concepts
Androphilia and gynephilia Human female sexuality Human male sexuality Intersexuality Third gender Two-Spirit
Research
Biology Demographics Environment Kinsey scale Klein Grid Neuroscience Non-heterosexual Psychology Queer studies Sexology Timeline of sexual orientation and medicine Non-human animals Homosexual behavior in animals (List)
Category

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. Fetal hormones may be seen as the primary determiner of adult sexual orientation, or a co-factor with genes and/or environmental and social conditions.

Prenatal hormones and sexuality-linked characteristics

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.

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.

A 2010 endocrinology study by Garcia-Falgueras and Swaab says that intrauterine exposure to hormones is largely determinative. Sketching the argument briefly here, it says that sexual organs are differentiated 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 [p. 24:] 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." ". . . . These fetal and neonatal peaks of testosterone, together with the functional steroid receptor activity, are thought to fix the development of structures and circuits in the brain for the rest of a boy's life (producing 'programming' or 'organizing' effects). Later, the rising hormonal levels that occur during puberty 'activate' circuits and behavioral patterns that were built during development, in a masculinized and de-feminized direction for male brains or in a feminized and de-masculinized direction for female brains." Because organ differentiation and brain differentiation occur at different times, in "rare" cases transsexualism can result (transsexualism resulting from having organs of one gender and feelings of the other). "The brain structure differences that result from the interaction between hormones, genes and developing brain cells are thought to be the basis of sex differences in a wide spectrum of behaviors, such as . . . sexual orientation (heterosexuality, homosexuality, or bisexuality) . . . . Factors that interfere with the interactions between hormones and the developing brain systems during development in the womb may permanently influence later behavior." "In humans, the main mechanism responsible of [sic] sexual identity and orientation involves a direct effect of testosterone on the developing brain." Drawing on some transsexualism cases, the authors say, "[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 . . . ." "There are no indications that postnatal social factors could be responsible for the occurrence of transsexuality." "With regard to sexual orientation, the most likely outcome of childhood gender identity disorder is homosexuality or bisexuality." "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." "The presence of a genetic component of over 50% in the development of sexual orientation is apparent from family and twin studies." "Women with gay sons appeared to have an extreme skewing of X-inactivation [referring to the "X-chromosome"] . . . ." "[S]ome two million pregnant women . . . were prescribed diethylstilbestrol (DES)[,] . . . . an estrogen-like substance[,] . . . [and] it [was] . . . found . . . to increase the chance of bisexuality or homosexuality in girls." "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." "Prenatal exposure to nicotine, amphetamine, or thyroid-gland hormones increases the chances of giving birth to lesbian daughters." Stress in pregnancy makes birth of a gay son likelier. "Although it has often been postulated that postnatal development is also important for the direction of sexual orientation, there is no solid proof for this."

Male homosexuality as hypermasculine

Main article: Hypermasculinity

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. [1] 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 was found by Swaab and Hopffman to be larger in homosexual men than in heterosexual men, [2], the suprachiasmatic nucleus is also known to be larger in men than in women. Gay men have also been shown to have higher levels of circulating androgens and larger penises, on average, than straight men.

Gay men have more older brothers on average, a phenomenon known as the fraternal birth order effect. It has been suggested that the greater the number of older male siblings the higher the level of androgen fetuses are exposed to.

Male homosexuality as hypomasculine

Main article: Hypomasculinity

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—was on average more than twice the size in heterosexual men when contrasted to homosexual men. In 2003 scientists at Oregon State University announced that they had replicated his findings in sheep.

Female homosexuality

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, which then influences 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 the causal factor, not parental influence.

See also

• Biology and sexual orientation
• Environment and sexual orientation
• Handedness and sexual orientation
• Genetics of gender
• Pathogenic hypothesis of homosexuality
• David Reimer
• Mental roots of sexual orientation

References

• Green, R. (1987). The "sissy boy syndrome" and the development of homosexuality. New Haven, CT: Yale University Press.
• Dailey, T. and Sprigg , P. (2001). Getting It Straight — What the Research Shows about Homosexuality, Family Research Council, Washington D.C.
• Dittmann RW, Kappes MH, Kappes ME, et al. (1990). "Congenital adrenal hyperplasia. I: Gender-related behavior and attitudes in female patients and sisters". Psychoneuroendocrinology 15 (5–6): 401–20. doi:10.1016/0306-4530(90)90065-H. PMID 2101963. 
• Dittmann RW, Kappes MH, Kappes ME, et al. (1990). "Congenital adrenal hyperplasia. II: Gender-related behavior and attitudes in female salt-wasting and simple-virilizing patients". Psychoneuroendocrinology 15 (5–6): 421–34. doi:10.1016/0306-4530(90)90066-I. PMID 2101964. 
• Dittmann RW, Kappes ME, Kappes MH (1992). "Sexual behavior in adolescent and adult females with congenital adrenal hyperplasia". Psychoneuroendocrinology 17 (2–3): 153–70. doi:10.1016/0306-4530(92)90054-B. PMID 1438641. http://linkinghub.elsevier.com/retrieve/pii/0306-4530(92)90054-B. 
• Rahman Q (2005). "The neurodevelopment of human sexual orientation". Neurosci Biobehav Rev 29 (7): 1057–66. doi:10.1016/j.neubiorev.2005.03.002. PMID 16143171. http://linkinghub.elsevier.com/retrieve/pii/S0149-7634(05)00032-1. 
• Williams TJ, Pepitone ME, Christensen SE, et al. (March 2000). "Finger-length ratios and sexual orientation". Nature 404 (6777): 455–6. doi:10.1038/35006555. PMID 10761903. http://msu.edu/~breedsm/pdf/breedlove2000.pdf. 
• Zucker KJ, Bradley SJ, Oliver G, Blake J, Fleming S, Hood J (December 1996). "Psychosexual development of women with congenital adrenal hyperplasia". Horm Behav 30 (4): 300–18. doi:10.1006/hbeh.1996.0038. PMID 9047259. http://linkinghub.elsevier.com/retrieve/pii/S0018-506X(96)90038-0. 

External links

• WEBMD: Pointing the Finger at Androgen as a Cause of Homosexuality
• Boston Globe: "What makes people gay?"