This paper reflects the research and thoughts of a student at the time the paper was written for a course at Bryn Mawr College. Like other materials on Serendip, it is not intended to be "authoritative" but rather to help others further develop their own explorations. Web links were active as of the time the paper was posted but are not updated.

Contribute Thoughts | Search Serendip for Other Papers | Serendip Home Page

Biology 202
2003 First Web Paper
On Serendip

Sexual Differentiation and its Effects on Sexual Orientation

Tiffany Litvine

What controls a human's sexual orientation? The long-standing debate of nature versus nurture can be extended to explaining human sexual orientation. Is it biological or environmental? The biological explanation has been gaining popularity amongst the scientific community although it is only based on speculations. It is argued that sexual orientation is linked to factors that occur during sexual differentiation. The prenatal exposure to androgens and their affect on the development of the human brain play a pivotal role in sexual orientation (2). Heredity is also part of the debate. Does biology merely provide the slate of neural circuitry upon which sexual orientation is inscribed? Do biological factors directly wire the brain so that it will support a particular orientation? Or do biological factors influence sexual orientation only indirectly?

Gender is determined by the sex chromosomes, XX produces a female, and XY produces a male. Males are produced by the action of the SRY gene on the Y chromosome, which contains the code necessary to cause the indifferent gonads to develop as testes (1). In turn the testes secrete two kinds of hormones, the anti-Mullerian hormone and testosterone, which instruct the body to develop in a masculine fashion (1). The presence of androgens during the development of the embryo results in a male while their absence results by default in a female. Hence the dictum "Nature's impulse is to create a female" (1). The genetic sex (whether the individual is XX or XY) determines the gonadal sex (whether there are ovaries or testis), which through hormonal secretions determines the phenotypic sex. Sexual differentiation is not driven by the sex chromosomes directly but by the hormones secreted by the gonads (3).

Hormones are responsible for sexual dimorphism in the structure of the body and its organs. They have organizational and activational effects on the internal sex organs, genitals, and secondary sex characteristics (1). Naturally these effects influence a person's behavior not only by producing masculine or feminine bodies, but also by causing subtle differences in brain structure. Evidence suggests that prenatal exposure to androgens can affect human social behavior, anatomy, and sexual orientation.

Androgens cause masculinization and defeminization of developing embryos. Masculinization is the organizational effect of androgens that enables animals and humans to engage in male sexual behavior in adulthood. This is accomplished by stimulating the development of neural circuits controlling male sexual behavior (1). Defeminization is the organizational effect of androgens that prevents animals and humans from displaying female sexual behavior in adulthood. This is accomplished by suppressing the development of neural circuits controlling female sexual behavior (1). For example if a female rodent is ovariectomized and given an injection of testosterone immediately after birth she will not respond to a male rat as an adult, when she is given estradiol and progesterone. This demonstrates that she has been defeminized. If the same female rodent is given testosterone in adulthood, rather than estradiol and progesterone, she will mount and attempt to copulate with receptive females (3). This on the other hand is an example of masculinization.

For example in the congenital adrenal hyperplasia (CAH) disorder, the adrenal glands secrete abnormal amounts of androgens. The secretion begins prenatally and causes prenatal masculinization and defeminization (1). Boys born with CAH develop normally. However girls with CAH are born with an enlarged clitoris and fused labia. Sometimes surgical intervention is needed and the person will be given a synthetic hormone that suppresses the abnormal secretion of androgens (1). Money and his colleagues performed a study on 30 women with a history of CAH. They were asked to give their sexual orientation and 48% described themselves as homosexual or bisexual. They also exhibited more masculinized behavior (4). These results suggest that an abnormally high exposure to prenatal androgens affects sexual orientation.

Androgen insensitivity syndrome affects people who are insensitive to androgens. These genetic males develop as females with female external genitalia, but also with testes and no uterus or Fallopian tubes (1). If they are raised as girls, they seem to do fine and function sexually as women in adulthood. Women with this problem lead normal sex lives. There is no indication of sexual orientation toward women. Thus, the lack of androgen receptors appears to prevent both the masculinizing and defeminizing effects of androgens on a person's sexual interest (1).

There are two additional cases which show quite a strong correlation between sexual orientation and sexual differentiation. The first example is a genetically transmitted condition which is fairly common in one area of the Dominican Republic. It causes abnormal sexual differentiation in XY fetuses that produce an inadequate enzyme required to convert testosterone to DHT in the external genitalia (3). The child is born with ambiguous genitalia, labia (with testes inside) and an enlarged clitoris, causing partial masculinization. These individuals are usually raised as females, but at puberty the rise in testicular androgen secretion causes the phallus and the scrotum to grow and the body to develop in a male fashion. At this age the individuals start assuming male tasks and having girlfriends (3). These individuals prove that early testosterone masculinizes the human brain and influences sexual orientation and gender identity. The following example is with a set of identical twin boys. They were raised normally until seven months of age when the penis of one of the boys was accidentally burnt off during circumcision. The parents decided to perform a sex change on the child to remove the testes and raise it as a girl. It turned out that when the child reached adolescence she was unhappy and felt like she was really a boy. The family admitted to her what had happened and she got at sex change to become a boy again (1). This is another case that suggests that people's sexual identity and orientation is under the control of biological factors rather than environmental.

The brain is a sexually dimorphic organ. Neurologists discovered that the two hemispheres if a women's brain appear to share functions more than those of a man's brain. Men's brains are also larger on average than a woman's (1). Most researchers believe that the differences in the brain arise from different levels of exposure to prenatal androgens. Several studies have examined the brains of deceased heterosexual and homosexual men and heterosexual women. The studies have found differences in the size of three different subregions of the brain: the suprachiasmatic nucleus, the sexually dimorphic nucleus of the preoptic area (SDN-POA), and the anterior commissure (2). The suprachiasmatic nucleus was found to larger in homosexual mean and smaller in heterosexual men and women. The SDN-POA was found to be larger in heterosexual men and smaller in homosexual men and heterosexual women. The anterior commissure was found to be larger in homosexual men and heterosexual women and smaller in heterosexual men (2). It cannot be concluded that any of these brain regions are directly involved in people's sexual orientation. The results do suggest that the brains of heterosexual women, heterosexual men, and homosexual men may have been exposed to different patterns of hormones prenatally and that differences do exist.

If sexual orientation is affected by differences in exposure of the developing brain to androgens, there must be factors that cause exposure to vary. A study performed on rats showed that maternal stress decreased the secretion of androgens, causing an increased incidence of homosexual behavior and female-like play behavior in male rats (1). Prenatal stress has also been shown to reduce the size of the SDN-POA, which is normally larger in males (1).

The last biological factor that may play a role in sexual orientation is heredity. A study performed using identical and fraternal twins was performed. When both twins were homosexual, they were said to be concordant for that trait. If only one was homosexual, they were said to be discordant (1). There was 52% concordance of homosexuality in identical male twins and 22% in fraternal twins and a 48% concordance of homosexuality in identical female twins and 16% in fraternal twins (1). This study suggests that two biological factors may affect a person's sexual orientation, prenatal hormonal exposure and heredity.

Sexual orientation may be influenced by prenatal exposure to androgens as the studies strongly imply. So far, researchers have obtained evidence that suggests that the sizes of three brain regions are related to a man's sexual orientation. The case in the Dominican Republic and the twin whose penis was accidentally damaged shows that the effects or early androgenization are not easily reversed by the way a child is reared. The twins' studies suggest that heredity may play a role in sexual orientation. Despite all this evidence scientists are still unable to fully assert that biologically factors are responsible for sexual orientation. There are so many variations within society that could affect at person's sexuality, that it is impossible to make any assertions at this point. Therefore the nature and nurture debate is still open.


1) Carlson, Niel R. Physiology of Behavior. 7Th ed. Massachusetts: Allyn and Bacon,

2) Swaab, D.F., and Hofman, M. Sexual Differentiation of the Human Hypothalamus in
Relation to Gender and Sexual Orientation. Trends in Neuroscience. 18, 264-270.

3) Breedlove, M.S. Sexual Differnetiation of the Brain and Behavior. In Becker, J.B,
Breedlove, S.M, and Crews, D. (EDS). Behavioral Endocrinology. Pp 39-70.

4) Money, J. , Schwartz, M. and Lewis, V.G. Adult Erotusexual status and Fetal Hormonal Masculinization and Demasculinization:46, XX. Psychoneuroendocrinology, 1984, 9, 903-908.

Course Home Page | Course Forum | Brain and Behavior | Serendip Home |

Send us your comments at Serendip

© by Serendip 1994- - Last Modified: Wednesday, 02-May-2018 10:53:04 CDT