Biological Basis of Gender Identity

Below you'll find part of a research paper that I wrote for a graduate level psychology class that reviews some of the research literature on the biological factors that influence both gender identity and homosexuality. A large portion of the paper also covers why gender identity disorder should be removed from the DSM as a mental disorder. If you want to skip directly to the biological stuff click here: Biological Factors of Transgendered Behavior & Homosexuality

Trangenderism as a Physiological Variation of Prenatal Development

Gender assignment in our society is based on the appearance of the genitals. It is expected that the gender identity and gender role of the individual will be consistent with the appearance of their genitals (Seil, 2001). This means that if a person has male genitals that they should identify with a male gender identity, and if a person has female genitals that they should identify with a female gender identity. This also means that they are expected to conform to society's expected gender roles based on the appearance of the genitalia. As a result, the diagnosis of gender identity disorder is often given to children, adolescents, and adults who do not conform to society's expected gender roles based on the appearance of their genitals.

Gender identity disorder is currently listed as a mental disorder in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV). Gender identity disorder is characterized by wishing to be a sex, other than one's biological sex, wishing to live or be treated as the other sex, and a belief that the person's feelings and reactions are typical of the other sex.

There has been some controversy surrounding the inclusion and criteria of gender identity disorder in the DSM-IV (e.g., Bower, 2000; Cantor, 2002). A lot of the controversy seems to be based on those that are unhappy about the nature of the DSM-IV criteria or those that don't feel that having a gender identity inconsistent with the appearance of ones' genitals constitutes a mental disorder.

The inclusion of certain mental illnesses in the DSM are largely based on public opinion and the opinions of mental health professionals when deciding what to include as a mental disorder in the DSM. For example, the American Psychological Associated removed homosexuality from the third edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III) in 1973. Before homosexuality was taken out of the DSM, being homosexual was considered to be a mental illness that should be, and supposedly could be, treated by psychotherapy.

Before homosexuality was removed from the DSM it was thought that a person's sexual orientation was able to be changed by psychotherapy. After homosexuality was removed from the DSM, it was no longer considered an illness, and it was no longer considered to be a behavior that can or should be changed through psychotherapy.

It is interesting to note that after removing homosexuality as an illness in DSM-III, gender identity disorder in children was included as a mental illness in DSM-III and remains as a mental disorder in the DSM-IV. One reason this is particularly interesting is because long-term follow up data has shown that most, but not all, children diagnosed with gender identity disorder grow up to have homosexual behavior (Green, Roberts, Williams, & Goodman, 1987; Money & Russo, 1981; Zuger, 1984, 1988). If homosexuality in itself is not an illness then a condition that may eventually lead to homosexuality should not be considered an illness either.

Given this, it is also interesting that some forms of therapy for gender identity disorder in children and adolescents have as one of their goals, the prevention of homosexuality as an outcome for gender identity disorder (e.g., Rekers & Lovaas, 1974; Green, 1987). Based on this, it seems that some medical and mental health professionals may be using the diagnosis of gender identity disorder in the DSM-IV as a way of indirectly trying to "cure" individuals of their homosexuality.

Transgenderism is considered to be relatively rare, but it is possible that it is often under diagnosed. The prevalence of transgenderism is estimated to be approximately 1 in 10,000 males and 1 in 30,000 females (van Kesteran, Gooren, & Megens, 1996). These numbers are generally based on the number of individuals who actually seek sexual reassignment and may not reflect the number of persons that are actually transgendered, but instead may only tell us how many people seek sexual reassignment. Because not every transsexual is going to seek sexual reassignment surgery for a variety of reasons (e.g., cost associated with the surgery, not wanting to go through such drastic measures to change their sex), the number of transgendered individuals is most likely underrepresented.

This next is only speculation on my part, but it is also a possibility that a lot of people who are considered gay or lesbian are in fact gender disordered. This idea does not seem to have been examined by researchers yet, but this may be an area that should be researched in the future. The idea that many homosexuals may be gender disordered is based on the following: homosexual males often have many more feminine traits than heterosexual males, and lesbians often have more masculine traits than heterosexual women. It is also interesting to note that the most common outcome for childhood gender identity disorder is adult homosexuality (Green, Roberts, Williams, & Goodman, 1987; Money & Russo, 1981; Zuger, 1984, 1988). The possibility exists that transgendered persons may be reluctant to openly state that they are trans because it is more socially acceptable to be gay or lesbian than to be transgender, especially in light of the fact that homosexuality is not considered a mental illness, but being gender disordered is.

This is not to state that all gay and lesbian people are transgendered, but that a large portion of those considered to be gay or lesbian may may simply be transgendered.

One reason many transgendered persons might present themselves as gay or lesbian instead of transgendered is that it has almost become socially acceptable to be gay or lesbian, but not transgendered. Recently, gays and lesbians have made much progress in society regarding discrimination and acceptability. This is not yet true for transgendered individuals.

In addition, obtaining hormones and sex reassignment surgery may not be an option for everyone that would like it. Perhaps some individuals can't afford it, or are afraid of what others close to them might think. Additionally, it is a lot easier to hide homosexuality than it is to hide a sex transformation from other people.

Finally, it seems that there may be similar biological pathways for the development of both homosexuality and gender identity disorder, which suggests that homosexuals and gender disordered persons may not be as different as they are thought to be.

Biological Factors of Transgendered Behavior & Homosexuality

There is a lot of controversy surrounding the etiology of gender identity disorder, but there is some evidence that gender identity disorder may be due to physiological causes (e.g., Allen & Gorski, 1992; Bosinski, Peter, Bonatz, Arndt, Heidenreich, Sippell, & Wille, 1997; Blanchard, Zucker, Cavacas, Allin, Bradley, & Schacter, 2002; Breedlove, 1994; Collaer, & Hines, 1995; Hamer, Hu, Magnuson, Hu, & Pattatucci, 1993; Hines, Allen, & Gorski, 1992; Hofman & Swaab, 1989; LeVay, 1991; LeVay & Hamer, 1994; Sadeghi & Fakhrai, 2000; Singh, Vidaurri, Zambarano, & Dabbs, 1999; Swaab, & Fliers, 1985; Swaab & Hofman, 1990; Zhou, Hofman, Gooren, & Swaab, 1995).

If one looks at the biological literature that has demonstrated that there are sexually dimorphic areas of the brains between males and females and also on the effects of prenatal hormones on these brain structures it becomes feasible that gender identity is rooted in biological causes. As yet there is no conclusive evidence for specific brain structures that may cause one to feel in a way opposite their biological sex, but research strongly suggests a possible biological basis for the feelings of transgendered persons, most specifically through the role of prenatal hormones.

It can be argued that because there is evidence that there is a biological basis for transgenderism that it is not a mental disorder, but is instead just a natural variation on sexual identity expression.

Although no conclusive evidence for the role of prenatal development and specific brain structures have been found, the evidence is strong enough that psychologists and other mental health professionals should at least question whether being gender disordered warrants an Axis I diagnosis in the DSM-IV.

It seems that there is enough evidence for a biological basis for gender identity that gender identity disorder should be removed as an Axis I disorder from the next edition of the DSM. At most, gender identity disorder should be listed as an Axis III disorder in the next edition of the DSM (Seil, 1991). The reason it is necessary to continue to list gender identity disorder as a disorder is so that transgendered individuals will be able to receive hormones to treat their condition as well as receive psychotherapy for psychological problems that may arise due to their condition. For example, it has been shown that individuals who cross gender boundaries are often ostracized by their peers (Zucker, 2004) and psychotherapy may assist in helping these individuals to cope with their rejection by their peers. Moving gender identity disorder from an Axis I disorder to an Axis III disorder in the DSM will serve two purposes: One will be to stop treating these people as if their feelings are not valid and that they are mentally ill. The other will be to change treatment methods for people who come to therapy with this disorder.

The reason that the axis placement of gender identity disorder in the DSM is so important is that axis placement will most likely dictate the type of treatment transgendered individuals receive. For example, although there is a lot of evidence for a physiological cause for gender identity disorder, many psychologists and medical professionals attempt to treat gender identity disorder through psychotherapy or medication. Through these methods they attempt to change the feelings and or behavior of transgendered individuals to behavior that is more consistent with what society generally expects based on one's genitalia (e.g., Bradley & Zucker, 1997; Meyer-Bahlburg, 2002, Loeb, 1999; Rekers, 1974).

A more effective treatment would be to allow transgendered people easier access to hormones so that they could change their bodies to be more in line with their internal image of themselves.

If the cause of gender identity disorder is due to brain structures that developed along a different sexual pathway than the reproductive system, then it is unlikely that trying to talk someone out of behaving in ways that are inconsistent with one's sex is going to be productive as far as changing the gender identity of these individuals.

Because there is strong evidence that gender identity is determined by prenatal hormones the remainder of this paper will give an overview of sexual differentiation during gestation and will review some of the studies that have found a biological basis for gender identity.

Hopefully, if enough biological evidence is presented then the diagnosis of gender identity disorder can be moved to Axis III in the next addition of the DSM and then the appropriate treatments for transgenderism will follow.

Organizational Hypothesis

The most popular and also the most viable explanation for the cause of gender identity disorder is based on the organizational hypothesis (Breedlove, 1994). The organizational hypothesis demonstrates how one could end up with brain structures that are opposite the sex of the genitalia. To explain more clearly how this can account for transgendered behavior and feelings, it is necessary to provide a brief overview of prenatal differentiation of the reproductive system.

Prenatal Development Overview

During the first two months of prenatal development, both male and female humans develop identically—everyone starts out with a female phenotype (Wilson, George, & Griffin, 1981). After two months have passed, a series of hormonal and chemical events occur that eventually determine whether the fetus develops a male or female phenotype. The development of the ovaries or testes are directed by the chromosomes. If the individual has a Y chromosome with a properly functioning SRY gene, then testes will develop.

If testes are present, they will secrete androgens that will in turn direct the future differentiation of the fetus into a male phenotype. The testes will also secrete müllerian inhibiting substance, which causes the rudimentary female internal reproductive organs that are present in everyone at this point to disintegrate.

If testes are not present then the fetus will develop a female phenotype. In the absence of androgens and müllerian inhibiting substance, the fetus will develop a female phenotype. Of course it isn't always quite this simple, and sometimes there are problems that occur during development. For example, there are cases in which individuals are exposed to unusual levels of prenatal hormones (Breedlove, 1994). This can occur for a variety of reasons, including stress experienced by the pregnant mother (Breedlove, 1992).

So how can abnormal levels of androgens lead to transgenderism? According to Breedlove (1994), androgen receptors are present in the brains of both developing male and female fetuses. This means that a fetus with a female genotype (XX) can undergo masculinization of the brain if exposed to high enough levels of androgens. Conversely, if a genetically male fetus (XY) is exposed to too little levels of androgen, then its brain may develop more similarly to the typical female brain. If this occurs then the individual can end up with a brain/genitals mismatch.

Known Sexual Differentiation Disorders

Androgen Sensitivity Disorder

Sexual differentiation is not a flawless process and errors sometimes occur. One of these is known as androgen insensitivity syndrome, in which genetically male (XY) individuals will develop a female exterior (Olsen, 1992). They will develop testes around gestational age of two months and the testes will secrete testosterone, but the non-gonadal tissues have a defective gene for the androgen receptor, which leads to the female exterior. This disorder is caused by a mutation of the AR gene, for the human androgen receptor, which is located on the Xq11-12 area of the X chromosome (Sinnecker, Hiort, Nitsche, Holterhus, & Kruse, 1997).

The SRY Gene

Another genetic disorder that may affect the sexual differentiation of XY individuals involves the SRY gene on the Y chromosome. The SRY gene must be present on the Y chromosome for an XY fetus to develop a male phenotype (Ravel, Chantot-Bastaraud, & Siffroi 2004). If the SRY gene is missing or defective then the person will develop a completely female exterior and the internal reproductive organs will be female, even though they are genetically male.

Congenital Adrenal Hyperplasia

A sexual developmental disorder that affects XX individuals is congenital adrenal hyperplasia. Congenital adrenal hyperplasia (CAH) is an autosomal recessive condition characterized by an insufficient production of cortisol and hypersecretion of adrenal androgens, which causes masculinization of the external genitalia of the female fetus.

Affected infants can have ambiguous genitalia or even erroneous gender assignment. Because testicles are not present to produce müllerian inhibiting factor, the internal female organs are intact (Cutler, 1990; New, 1992). CAH is caused by mutations in the CYP21 gene located on the short arm of chromosome 6. The prevalence of CAH in the USA and Europe is approximately 1:15 000-16 000 (Spandri, Coglardi, Maggi, De Giorgi, Masperi, & Beccaria, 2004). What is particularly interesting about this disorder in the context of gender identity is that these females were exposed to abnormal levels of prenatal androgens.

Research has shown that CAH females show higher rates of gender atypical play in childhood (Hines & Kaufman, 1994) and have more lesbian or bisexual experiences as adults (Dittman, Kappes, & Kappes, 1992; Money & Lewis, 1987; Money, Schwartz, & Lewis, 1984).

In addition, Meyer-Bahlburg (1993;1995) found that the prevalence of transgender behavior and feelings are higher in CAH females than in non-CAH control subjects.

Findings from Animal Studies

Additional findings from animal studies have also suggested that prenatal hormones play a role in shaping later sexual behavior. For example, exposure of a female animal that is adjacent in the uterus to male animals results in adult females that exhibit more masculine copulatory behaviors and more aggressive behavior (Meisel & Ward, 1981; vom Saal, 1989). It is thought that this occurs due to the influence of prenatal hormones because elevated levels of androgens have been found in the amniotic fluid and plasma of these females (vom Saal, 1989).

Given what we know about the role of prenatal hormones in the organizational development of the fetus, it comes as no surprise that some brain structures have been found to differ in males and females. Also, because we know that sometimes there are flaws in the developmental process and that at times there are higher or lower than normal levels of sex hormones present during prenatal development, it certainly seems plausible that there could be brain structures that are affected by hormones or other factors that may determine one's gender identity and behavior.

The lack of understanding and tolerance for transgendered individuals stems from the problem that these brain structures are not visible to others and people often have a difficult time believing in what they cannot see. The genitals are visible so people usually expect gender identity to be consistent with the biological sex of the persons genitals, despite that it is only the brain that determines whether a person feels like a male or a female.

Brain Structures Influenced by Prenatal Hormones

Research has shown that prenatal hormones do influence some brain structures. One brain area shown to differ in males and females is the anterior commissure (Allen & Gorski, 1991;1992). This structure is a fiber tract that is larger in its midsagittal area in women than in men (Allen & Gorski, 1991).

The anterior commissure is not thought to be related to reproductive or sexual behavior, but is thought to play a role in cerebral lateralization. Allen and Gorski (1992) examined the anterior commissure in ninety brains from heterosexual men and women, and homosexual men. They reported that the midsagittal area of the anterior commissure in homosexual men was 18% larger than in heterosexual women and 34% larger than in heterosexual men.

The significance of this finding is not only that the anterior commissure of the homosexual men was more similar in size to the heterosexual women than to the homosexual men, but also that this suggests that prenatal hormones don't just target areas of the brain responsible for sexual behavior, but that they affect the brain more globally (Allen & Gorski, 1992).

Another brain area found to differ in heterosexual and homosexual men is the suprachiasmatic nucleus (Swaab & Hofman, 1990). This area is involved in the regulation of circadian rhythms. More importantly, the suprachiasmatic nucleus was found to be 1.7 times larger in homosexual men than heterosexual men, which provides further evidence that brain structures develop differently during development for heterosexual and homosexual men.

Additionally, two nuclei in the hypothalamus, an area known to be involved with sexual behavior and reproduction, were found to be larger in men than in women (Allen, Hines, Shryne, & Gorski, 1989). These two nuclei were the second and third interstitial nucleus of the anterior hypothalamus (INAH2 and INAH3). This finding led to a famous study by Simon LeVay that is often cited as evidence for a biological etiology for homosexuality. In his study, LeVay (1991) hypothesized that the INAH2 and INAH3 would be larger in individuals sexually oriented towards women (e.g., heterosexual men and homosexual women) and smaller in individuals sexually oriented towards men (e.g., heterosexual women and homosexual men). LeVay found that the INAH3 of the homosexual men was more similar in size to the heterosexual women than to that of the heterosexual men, indicating that the INAH3 may play a role in attraction toward men. There were no significant size differences found in the INAH2 between the two groups.

Another brain area found to differ in males and females is the bed nucleus of the stria terminalis (Hines et al. 1992; Zhou et al. 1995). This brain structure is much larger in men than in women and has been shown to be important for sexual behavior. For example, the bed nucleus of the stria terminalis has been shown to be involved in aggression (Shaikh, Brutus, Siegel, & Siegel, 1986), rough and tumble play behavior of juvenile rats (Meany, Dodge, & Beatty, 1981), and male copulatory behavior (Shaikh et al. 1986).

This is particulary interesting because Zhou et al. (1995) found that the bed nucleus of the stria terminalis in male-to-female transsexuals was similar in size to that of hetersexual females. Most importantly they reported that the size of the bed nucleus of the stria terminalis is not influenced by sex hormones in adulthood. This finding further supports the hypothesis that gender identity develops as a result of an interaction between the developing brain and prenatal hormones.

Research has found that there are some biological markers outside the central nervous system that are found in gender atypical persons. For example, Singh, Vidaurri, Zambarano, and Dabbs (1999), conducted a study comparing masculine and feminine lesbians on a variety of physiological measures. They found that the more masculine lesbians had higher waist to hip ratios and higher saliva testosterone levels than the more feminine lesbians. Higher waist to hip ratios are an important marker in determining whether one has been previously exposed to high levels of prenatal androgens because research has shown that the level of sex hormones regulates fat distribution (Rebuffe-Scrive, 1988; Singh, 1993). The more masculine lesbians also recalled more childhood gender atypical behavior, and had less desire to give birth. What is important here is that those women that remembered more gender atypical behavior also had the highest waist to hip ratios, which suggests that there may be something physiologically different about women who are more masculine.

According to Collaer and Hines (1995) gender atypical behavior in childhood is "one of the most reliable correlates of prenatal exposure to androgens (testosterone) in genetic females." Interestingly, the more feminine lesbians did not differ significantly from heterosexual women on any of these measures.

Other indirect biological markers have also been reported. One of these is hand use preference which may reflect prenatally organized cerebral lateralization (Zucker et al. 2001). Zucker reported that both male and female transsexuals are left handed more often than control subjects. Additionally, transsexuals have been found to differ on fingerprint asymmetry patterns that develop prenatally and may be sex hormonally influenced (Green & Young, 2000). Fingerprint asymmetry refers to whether one has more ridges on their right versus their left hand.

Although most people have more ridges on their right than left hands, those who do have more ridges on the left tend to be women (Green & Young, 2000). Green and Young found that male-to-female transgendered individuals who were also attracted to men, had more ridges on their left hand than the heterosexual male controls did - a pattern more similar to heterosexual woman. This is an important finding because dermal ridges are formed prenatally, between gestational weeks 13-19 (Babler, 1987).

Conclusion

The above studies provide evidence that the determination of gender identity may be biological and not psychological. However, none of the studies discussed are considered conclusive evidence for a biological origin for gender identity. Unfortunately, the burden of proof seems to rest on finding unquestionable evidence for a biological basis for trangendered individuals.

It seems too that this burden of proof is asymmetrical—meaning that those that feel the disorder is purely psychological do not seem to need to prove transgenderism is purely psychological. For them, examining the genitals, and then determining if the gender role of the individual is consistent with the appearance of the genitals is considered conclusive evidence that the disorder is psychological, which seems analogous to examining one's arm or leg to determine if the person likes to read or not.

However, there are some problems in concluding that prenatal hormones are soley responsible for the occurrence of transgendered behavior and feelings. One of the problems with interpreting the data from biological studies of transgender and gay and lesbian individuals is that if they are based only on genetics and/or prenatal environment, then one would expect a 100% concordance rate in twin studies. Results from twin studies have been equivocal: some studies find that twins are concordant for transgenderism (e.g., Garden & Rothery, 1992; Coolidge, Thede, & Young, 2002) and others find that the twins are discordant for transgender behavior (Green & Stoller, 1971).

Because transgenderism occurs in only a small percentage of the population, it is difficult to get a large sample of twins to conduct research on, and often the results come from studies that consist of only one set of twins. This makes it hard to generalize the findings on transgenderism and homosexuality from twin studies.

Although there is a lot of evidence that suggests that one's gender identity is based on biological factors that occur before one is even born, the burden of proof seems to be placed on those that don't fit the developmental pathway of the majority in providing proof that there is a valid reason for the feelings of transgendered people.

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