The Inter-relatedness of Gender Identity and Sexual Differentiation

Gender identity and sexual differentiation form a complex, interrelated paradigm involving genetic inheritance, internal and external physiology, endocrinology, neurological structure, sexual orientation, and socio-environmental factors. Before the 1950’s gender assignment at birth was a matter of ‘predominant sex’; in other words, dependent on the external genitalia, structure of gonads, and sex chromosomes (Cohen-Kettenis, 2005). In the wake of the behavioral-cognitive movement that sprang up shortly thereafter, the ‘psychosexual neutrality’ theory was embraced, built upon the supposed, all-encompassing mechanism of experiential learning. More recently a policy of ‘optimal gender’ has been adopted, in which gender assignment is based on reproductive abilities, overall psychological functionality, and psychosexual efficacy. Regardless of which policy is used for gender assignment, an understanding of the underlying genetic, hormonal, and environmental factors involved in sexual differentiation is the key to elucidating the more complicated subjects of gender identity and sexual orientation.

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When the 23 single chromosomes of the male sperm and female ovum combine to create a genetically unique human zygote, complete with 23 pairs of chromosomes, it is the 23rd chromosome that determines genetic sex (Wickens, 2005). If the alleles of the 23rd chromosome are both an X, then the zygote is genetically female; if one X and one Y, then the zygote is genetically male. Deviations from the standard XX/XY dichotomy include Turner’s syndrome (only one X allele), Klinefelter’s syndrome (one extra X or Y allele), and extra X chromosomes (triple, tetra, and penta). To varying degrees these syndromes can cause psychological, physiological, and sexual abnormalities; ranging from menstrual irregularities and premature menopause to mental retardation and violent tendencies. However, until the sixth week of normal gestation, the fetus has the potential to become both male and female, containing the precursors for both the male reproductive system (Wolffian duct) and the female reproductive system (Mullerian duct). However, if the fetus contains a Y allele on the 23rd chromosome, then in the sixth week of gestation the sex chromosome produces the chemical testis-determining factor. This chemical causes the maturation of the Wolffian duct and the degeneration of the Mullerian duct; conversely, if this chemical is not released, then the Mullerian duct develops and the Wolffian duct deteriorates. 

At this point, hormones take over sexual development—with the release of testosterone and Mullerian duct-inhibiting substance causing the development of the testes and the degeneration of the Mullerian duct in men—and the lack of testosterone causing the degeneration of the Wolffian duct and the development of ovaries at 12 weeks. Furthermore, androgens, such as testosterone and estrogen, have a twofold organizational/activational effect on the neurological structure and later behavioral stimulation, respectively. The neural circuitry of individuals seems to be organized during prenatal development by androgens, which subsequently affects sexual behavior in adulthood. 

In a discussion of the biological foundations of gender identity, it is important not to emphasize physical sexual differentiation to the exclusion of socio-environmental factors. Even in cases of congenital adrenal hyperplasia (CAH), androgen insensitivity, and enzyme defects (5a-RD-2 and 17b-HSD-3) sex assignment at birth is still the best indicator of gender identity later in life (Cohen-Kettenis, 2005). One study of 250 patients affected by CAH, raised as females, showed that only 32 individuals chose sex re-assignment after infancy, and 5.2% showed gender identity-related issues later in life, of which only 1.6% chose a gender change. Likewise, in a study of 99 individuals with partial androgen insensitivity (PAIS) and 156 with complete androgen insensitivity (CAIS), 9 of those with PAIS chose sex reassignment and none of those with CAIS chose reassignment. Lastly, in the case of enzyme defects, 56% of those affected by the 5a-RD-2 enzyme defect chose sex reassignment and 39% of those affected by the 17b-HSD-3 chose reassignment. Even though these numbers substantiate a large presentation of gender confusion in those affected by various intersex conditions, sex assignment at birth is still the best indicator of long-term gender identity efficacy.            

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Bi-sexual and homosexual orientations have been correlated with microsatellite markers on the Xq28 part of the X chromosome for gay men, but not lesbian females; elevated levels of in utero androgens, as evidenced by lower second to fourth finger ratios; prenatal exposure to nicotine; and structural differentiation of the suprachiasmatic nucleus, third interstitial nucleus of the anterior hypothalamus, and the commisura anterior (Swaab, 2004). Furthermore, Swaab (2004) has postulated that in women that have had many male children a biological mechanism might be in play that partially explains sexual orientation. Additionally, in several studies of a group of congenital adrenal hyperplasia (CAH) clients Bohlin et. al. (2003) observed a dose-response relationship with boy-like behaviors and prenatal androgen exposure. Their conclusion was that: 

“…socialization acts on a biological predisposition that is different than that of girls without CAH, and depending on the prevailing values and attitudes in the society, the CAH girls’ behavioral dispositions are more or less easily accepted within the female gender role” (Bohlin et. al., 2003, p. 448)      

Collectively, this evidence paints a complex picture of interrelated genetic, androgenic, and environmental predilections acting in relation to social factors to bring about gender identity and sexual orientation. 

In conclusion, genetic inheritance acting in conjunction with prenatal androgenic factors work together to influence the development of neurological and reproductive structures, which in turn affect later sexual behavior. The mediating effects of social factors can be seen in the predominant, life-long efficacy of sex assignment at birth. Furthermore, even though sex assignment at birth seems to be the best indication of gender identity, even in cases of intersex/transsexuals, the causal factors behind gender identity and sexual orientation cannot be explained through simple mechanisms of social determinism or social rebellion. Nor, is a purely physical explanation, dependent on sexual differentiation or androgenic action, adequate to explain gender identity or sexual orientation. The understanding of gender identity and sexual orientation is largely predicated on a complex interplay of genetic, hormonal, and neurological factors acting in conjunction with socio-environmental mediation, to bring about sexual and gender-related behavior.        

References

Bohlin, G., Larsson, A., Nordenström, A., & Servin, A. (2003). Prenatal androgens and gender-typed behavior: A study of girls with mild and severe forms of congenital adrenal hyperplasia. Developmental Psychology, 39(3), 440-450. Retrieved April 19, 2009, fromEBSCOHost Database. 

Cohen-Kettenis, P. (2005). Psychological long-term outcome in intersex conditions. Hormone Research, 64, 27-30. Retrieved April 19, 2009, from EBSCOHost Database. 

Swaab, D. F. (2004). Sexual differentiation of the human brain: Relevance for gender identity, transsexualism and sexual orientation. Gynecological Endocrinology, 19(6), 301-312. Retrieved April 19, 2009, from EBSCOHost Database. 

Wickens, A. (2005). Foundations of biopsychology, 2e. Upper Saddle River, N.J.: Pearson Hall. 

Paper Topic

  1. Prepare a 700 to 1,050-word paper in which you explain the interaction between hormones and behavior and how this interaction affects the determination of gender identity. In your paper be sure to also evaluate biological psychology and environmental influences on sexual differentiation and gender identity. Based on your evaluation, determine which has the greater influence.

Be sure to include at least three references in your paper from scholarly (peer-reviewed) sources.

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