Issues in Interdisciplinarity 2019-20/Evidence in the Causes of Homosexuality

This article examines evidence within the disciplines of developmental psychology, epigenetics and endocrinology when studying the causes of homosexuality, providing a wider understanding of the topic, due to the issues presented by evidence in these disciplines.

Developmental PsychologyEdit

A theory in Developmental Psychology, labelled ‘Exotic becomes Erotic’[1] (EBE) states that a child’s nature affects their interest for gender-conforming activities and peers. Applied to both homosexual and heterosexual individuals, children who do not conform to gender norms supposedly feel unfamiliarity with same-sex peers, producing increased autonomic arousal (i.e. erotic or romantic attraction) for members of the same sex[1].

Data taken from a study in San Francisco[2] concludes conformity to gender norms in childhood as being the most significant childhood indicator of sexual orientation for adult men and women. The study supporting this theory uses an observational research methodology - commonly found within developmental psychology.

The data from the San Francisco study[2] presents evidence in the form of quantitative data, with no clarification on the classification of ‘gay’, ‘lesbian’ or ‘heterosexual’ individuals in the study. Individuals who were bisexual or did not fit into these categories may have been included in the table. Moreover, the study defines ‘sex-typical activities’ as ‘baseball and football’ for boys and ‘hopscotch, playing house or jacks’ for girls. With no proof supporting these assumptions, we see a common weakness in observational studies within developmental psychology - where evidence is susceptible to researcher bias, and accurate quantitative data cannot be produced.

The study in San Francisco[2] suggests a clear causal link between gender non-conformity in childhood and a homosexual orientation in adulthood, yet observational studies cannot permit cause and effect conclusions[3]. Developmental psychology often uses the case study research method[3] - which do not allow conclusions to be generalised to a larger population. Therefore, there are clear flaws existing in the evidence presented within this discipline.


According to epigenetics, sexual orientation is determined by the epigenome. The evidence that support this hypothesis lies in a series of empirical studies conducted on identical twins and the analysis of their DNA. Tung Ngun looked at the DNA of 47 set of twins, where 37 of them were discordant --meaning that one was gay and the other heterosexual-- and 10 where both twins identified as gay. By collecting and analyzing their DNA, he found that discordant twins had indeed the same code, but the way it functioned differed[4].

Epigenetic marks (epi-marks) settle themselves on top of the genome and produce a chemical reaction which activates or deactivates parts of the gene. This process is called DNA methylation and acts according to the needs of a situation, affecting the overall expression of the gene[5]. In this case, epi-marks are responsible for switching on and off sex-specific traits: whether they be sexual identity, sexual preference or the development of genitals [6]. Indeed, they are closely linked to the amount of testosterone one is exposed to. The more testosterone one is exposed to, the higher the likeliness to be sexually inclined towards women (and vice versa)[5].

Ngun and his team later looked at “at the associations between specific epi-marks and sexual orientation in one group, then tested how well those results could predict sexual orientation in the second group”[7]. They reached a 70% of accuracy, which compared to previous studies is a leap forward, but still demonstrates a gap in the evidence manipulated[7].

As epigenetics remains a relatively new discipline, the studies may lack core information about epigenomes, which might hinder the validity of results when studying external subjects such as the etiology of sexual orientation. Furthermore, the small sample size render the results inapplicable to wider populations. It has also not looked at other degrees of sexual orientation on the Kinsey scale, such as bisexuality. Finally, although empirical evidence employed in genetics is presumably objective, the experts manipulating it are inevitably biased, and might alter end results.


According to the field of endocrinology, and more specifically neuroendocrinology, sexual orientation is determined prenatally by the action of hormones in the human brain, precisely involving the sexually dimorphic nucleus (SDN) located in the hypothalamus. The evidence supporting this thought lies in various experiments conducted on ferrets, among other animals[8]. This SDN which is usually around 2.2 times larger in male than in female brains[9], according to neurobiology, defines sexual orientation: A larger SDN as seen in men will lead to an attraction to females and a smaller SDN as seen in women will lead to an attraction to males[10].

Endocrinological studies and experiments have shown that the size of the SDN is conditioned by natural testosterone levels during the prenatal and perinatal period of a human’s life, thus explaining the usual preference of men for women and vice versa[11][12]. However, it is important to note that the field of endocrinology considers not only testosterone important to the development of the SDN but also estrogens formed from testosterone by aromatase. These claims are demonstrated through the evidence provided by multiple studies on test subject animals: rats or rams which possess sexually specific average SDN size differences similar to humans[13].

Homosexuality, then, would be caused by abnormalities regarding hormonal development affecting in turn the growth of the SDN, once again supported by the use of experimental evidence conducted on test subject animals, more specifically lab rats treated perinatally with hormones such as testosterone and estrogen or ATD, an aromatase inhibitor, to reverse their sexual partner preference[14][15][16].

As a response to the apparent fluctuation in human sexuality that is observable in our societies, endocrinologists affirm that sexual orientation and sexual behavior are separate: the prior being a definite set in stone biological preference determined by endocrinology which cannot be changed after development, and the latter being a non-reflective behavior adopted by humans in specific contexts[17]. Thus, they deny the possible use of sexual behavior as evidence on the cause and nature of homosexuality and choose to rely solely on empirical endocrinological experimentation.

Finally, Endocrinology falls short of fully explaining animal sexual orientation; humans have defined not only heterosexuality and homosexuality, but attraction to both sexes: bisexuality. Endocrinology cannot in the present day provide an explanation of bisexuality, as it lacks the required evidence to emit or test any hypotheses. This situation begs that question of whether it is therefore wise to make use of only empirical and endocrinological evidence to explore the causes of homosexuality, and if the attachment to this form of evidence only does not hold research back.

Evaluating evidenceEdit

Evidence can be presented in different manners through a range of disciplines, with there being no absolute method to collect data. Positivistic ideologies produce representative results which generalise and summarise in certain disciplines, whilst those with interpretivistic viewpoints produce results giving meaning and experience. Through all disciplines however, evidence can be manipulated to verify the truth or falsity of one's claim or the ideologies of their own discipline. The evidence disciplines choose to use differs from one another, creating differences in their views on the roots of homosexuality. By gathering the evidence of the studies made by developmental psychology, epigenetics and endocrinology, and looking at them together, one can achieve a more holistic vision of the issue.


  1. a b 1. Bem D. Exotic becomes Erotic: A Development Theory of Sexual Orientation. Psychological Review [Internet]. 1996 [cited 8 December 2019];103(2):320-335. Available from:
  2. a b c Bell, Alan P; Weinberg, Martin S; Hammersmith, Sue Kiefer; Alfred C. Kinsey Institute for Sex Research (1981), Sexual preference : its development in men and women, Indiana University Press, ISBN 978-0-253-16672-2 
  3. a b 2. Methods of Collecting Data | Boundless Psychology [Internet]. 2019 [cited 8 December 2019]. Available from:
  4. Healy M. Scientists find DNA differences between gay men and their straight twin brothers [Internet]. Los Angeles Times. 2015 [cited 9 December 2019]. Available from:
  5. a b National Geographic Explains the Biology of Homosexuality [Internet]. 2013 [cited 9 December 2019]. Available from:
  6. William R. Rice, Friberg, Urban and Sergey Gavrilets. "Homosexuality as a Consequence of Epigenetically Canalized Sexual Development." The Quarterly Review of Biology 87.4 (2012): n. pag. Print. PMID 23397798 doi:10.1086/668167
  7. a b Balter M. Homosexuality may be caused by chemical modifications to DNA [Internet]. Science. 2015 [cited 9 December 2019]. Available from:
  8. Paredes, R.G. & Baum, M.J. (1995) Altered sexual partner preference in male ferrets given excitotoxic lesions of the preoptic area anterior hypothalamus. J. Neurosci., 15, 6619–6630.
  9. Hofman, M A; D F Swaab (1989). "The sexually dimorphic nucleus of the preoptic area in the human brain: a comparative morphometric study". Journal of Anatomy. 164: 55–72. PMC 1256598. PMID 2606795.
  10. Swaab DF (2008). "Sexual orientation and its basis in brain structure and function". PNAS. 105 (30): 10273–10274. doi:10.1073/pnas.0805542105. PMC 2492513. PMID 18653758.
  11. Jacobson, C.D., Csernus, V.J., Shryne, J.E. & Gorski, R.A. (1981) The influence of gonadectomy, androgen exposure, or a gonadal graft in the neonatal rat on the volume of the sexually dimorphic nucleus of the preoptic area. J. Neurosci., 1, 1142–1147.
  12. Roselli C, Stadelman H, Reeve R, Bishop C, Stormshak F (2007). "The ovine sexually dimorphic nucleus of the medial preoptic area is organized prenatally by testosterone". Endocrinology. 148 (9): 4450–4457. doi:10.1210/en.2007-0454. PMID 17540718.
  13. Roselli, C.E., Larkin, K., Schrunk, J.M. & Stormshak, F. (2004) Sexual partner preference, hypothalamic morphology and aromatase in rams. Physiol. Behav., 83, 233–245.
  14. Houtsmuller, E.J., Brand, T., de Jonge, F.H., Joosten, R.N., van de Poll, N.E. & Slob, A.K. (1994) SDN-POA volume, sexual behavior, and partner preference of male rats affected by perinatal treatment with ATD. Physiol. Behav., 56, 535–541
  15. Jacobson, C.D., Csernus, V.J., Shryne, J.E. & Gorski, R.A. (1981) The influence of gonadectomy, androgen exposure, or a gonadal graft in the neonatal rat on the volume of the sexually dimorphic nucleus of the preoptic area. J. Neurosci., 1, 1142–1147.
  16. Henley, C.L., Nunez, A.A. & Clemens, L.G. (2009) Estrogen treatment during development alters adult partner preference and reproductive behavior in female laboratory rats. Horm. Behav., 55, 68–75.
  17. Jacques Balthazart (2011) The Biology of Homosexuality, Oxford