Some of the most compelling research regarding biological bases for homosexuality involves prenatal hormonal mechanisms (Bogaert 2018).
It is well established that physical sexual development and cognitive sexual development occur by similar, but not identical, biological mechanisms (Daae et al 2020). For example, the embryonic processes that masculinize physical anatomy can occur at different times or in different locations than those that masculinize the brain, and it is hypothesized that the disruption of one of these processes may result in a neurobehavioral gender that is incongruent with the individual’s anatomical gender. Subsequently, if an -XY embryo proceeds through normal physical development, but undergoes an atypical feminine or non-masculine cognitive development, then the result may be a biological male with feminine neurobehavioral inclinations, which may include attraction towards other males.
The Fraternal Birth Order Effect
One often referenced finding in this area of developmental biology is the Fraternal Birth Order Effect which posits that males with two or more older brothers are more likely to be homosexual (Balthazart 2018). In response to this phenomenon, the website explains:
“Other studies have found that the more older brothers a male child has, the more likely he is to develop a homosexual orientation (McConaghy, et al. 2006). This study also found that homosexual men had a greater than expected proportion of brothers among their older siblings (229 brothers: 163 sisters) compared with the general population (106 males: 100 females). Subsequent, larger studies found that older brothers did not affect male sexual orientation (Zietsch, et al. 2012; Bogaert 2010).”
In a more recent 2020 systematic review, one author concludes, “Since its establishment, the FBOE has been replicated many times, including in national probability, cross-cultural, and in non-cisgender samples" (Balthazart 2018). Multiple metanalyses, some including over 7,000 homosexual participants, have conclusively proved the Fraternal Birth Order Effect, which blatantly contradicts the website’s claims (Blanchard 2020). In reality, the mentioned Zietsch et al. and Bogaert articles that found no evidence for this effect were two rare exceptions among dozens of other, more recent experiments that did find evidence for this effect (Zietsch et al. 2012)(Bogaert 2010).
Furthermore, the website incorrectly states that these studies were larger; while one involved close to 11,000 participants, only 207 of those were homosexual/bisexual, a dramatically smaller sample size than most other experiments (Zietsch et al 2012).
Other experiments have concluded that this extremely consistent birth-order effect suggests a prenatal, hormonal mechanism for homosexuality (Bogaert 2018).
It is hypothesized that, while in gestation with a male fetus, the mother develops an immune reaction to certain substances important for male fetal development. With every additional gestation of a male fetus, more of these antibodies accumulate and eventually alter these integral substances for male brain development.
One 2018 article found compelling evidence for this hypothesis; immunoassays of mothers of homosexual men and mothers of heterosexual men found that antibodies to NLGN4Y, a male-specific protein expressed in the fetal brain, were much more prevalent in mothers of homosexual men. The study explained:
“Thus, mothers of gay sons had an increased likelihood of an immune reaction against, and presumably altered the function of, this brain-related, male protein during their pregnancies with gay sons" (Balthazart 2018).
The implicated effect is that these sons subsequently developed with more feminine neurobehavioral characteristics, including sexual attraction towards men.
Congenital Adrenal Hyperplasia
Congenital Adrenal Hyperplasia is an autosomal, recessive disorder that causes a deficiency in the enzyme 21-hydroxylase, a limiting factor in cortisol synthesis. As a result, precursors for cortisol are instead synthesized into androgens, and affected individuals experience high levels of adrenal androgens during fetal development ( El-Maouche et al 2017). Because this disease involves altered prenatal hormone levels, it has been comprehensively studied in terms of outcomes on sexual orientation (Bogaert 2018). Despite providing some of the compelling evidence for a biological basis of sexual orientation, these experiments are mentioned by the website only briefly:
“A meta-analysis of 18 CAH studies shows that 91.5% of those women suffering from CAH end up with a heterosexual orientation (Meyer-Bahlburg, et al. 2008), despite having a severe imbalance of testosterone during fetal development. These studies show that hormonal influences in utero are not the major reason for female SSA.”
The article argues that since the majority of women participants (91.5%) were heterosexual, altered prenatal androgen levels must have no effect on sexual orientation. However, not only were several, unmentioned measured of homosexuality (such as history of same-sex partners) much higher than 8.5%, but even this statistic is 60% higher than the average 5.1% prevalence of homosexuality in women (Meyer-Bahlburg et al 2008).
The website incorrectly drew its own subjective conclusions from the paper, while ignoring the authors’ statement that “Our data clearly showed increased sexual orientation towards females (i.e., bisexuality and homosexuality) in women with classical CAH (SV and SW combined) compared to non-CAH controls . . . and [severity of disease] correlated with the degree of prenatal androgenization" (Meyer-Bahlburg et al. 2008)."
Furthermore, this study in particular demonstrated some of the lowest frequencies of homosexuality in the literature, and other publications have reported figures as high as 41%, 50%, and 55.6% among the most severe form of the disease (Meyer-Bahlburg et al. 2008). The vast majority of available literature similarly agree that high levels of androgens in the womb are conducive to male development which, in -XX fetuses, often leads to females with masculine neurobehavioral tendencies, such as attraction towards women.
Other studies in endocrinology have found that the administration of DES, a synthetic estrogen, during pregnancy resulted in a homosexuality/bisexuality frequency of 24% in female offspring (Neibergall et al. 2019). In addition, progesterone therapy during pregnancy has consistently been found to increase frequency of homosexuality in both male and female offspring (Reinisch et al. 2017). Between these experiments, studies conducted on FBO and CAH, and numerous other endocrinological phenomena not mentioned for brevity, it is blatantly inaccurate to conclude, as the given article does, that
“All of the studies reporting possible hormonal influence on SSA suffer from the lack of any concrete evidence that hormones actually play any role in sexual orientation.”
While the website claims that “androgen gene variants do not play a role in male sexual orientation (Macke, et al. 1993),” the androgen receptor gene is only one of dozens of endocrinological mechanisms that influence fetal development, and furthermore, is not mentioned in any of the previous literature discussed (Bogaert 2018). Lastly, many of the website’s claims are either overgeneralizations that actually misconstrue experimental results or complete misunderstandings of the methodology:
“The fact that contradictory studies report increased vs. decreased androgens as a basis for SSA does not provoke confidence that the proxies are legitimate.”
In this example, the article is referring to an older study on the FBO effect which posits that third-born sons are exposed prenatally to more androgens (Williams et al. 2000). As stated before, the FBO effect was found to operate via antibody reactivity to male specific proteins in the brain, not over-general “high androgen exposure" (Balthazart 2018). According to the website, however, this study supposedly contradicted another idiosyncratic, outdated article claiming that differential bone length among different male sexualities is generally attributed to “less steroid exposure” during development (Martin et al. 2004). The website assumed that “less steroid exposure” in this experiment logically contradicts the “high androgen exposure” in the previous experiment. However, not only were dramatic overgeneralizations made, but the second experiment actually referred to androgen exposure in childhood development, not prenatal development.
Overall, this website’s attempts at disproving an endocrinological basis for homosexuality lacked critical understanding of the literature as well as general scientific integrity. The studies that this website promoted were largely hand-picked, outdated publications that were rare exceptions to the robust collection of research that all similarly attest to an endocrinological basis for homosexuality.
1. Bogaert, Anthony F., and Malvina N. Skorska. "A short review of biological research on the development of sexual orientation." Hormones and Behavior 119 (2020): 104659.
2. Daae, Elisabeth, et al. "Sexual Orientation in Individuals With Congenital Adrenal Hyperplasia: A Systematic Review." Frontiers in Behavioral Neuroscience 14 (2020): 38.
3. Balthazart, Jacques. "Fraternal birth order effect on sexual orientation explained." Proceedings of the National Academy of Sciences 115.2 (2018): 234-236.
4. Deem, Richard. “Genetics and Homosexuality: Are People Born Gay? The Biological Basis for Sexual Orientation by Richard Deem, MSc.” Are People Born Gay? The Biological and Genetic Basis for Homosexuality, Godandscience.org, 2017, www.godandscience.org/evolution/homosexuals_born_gay.html#frisch.
5. Bogaert, Anthony F., and Malvina N. Skorska. "A short review of biological research on the development of sexual orientation." Hormones and Behavior 119 (2020): 104659.
6. Blanchard, Ray. "Fraternal birth order, family size, and male homosexuality: Meta-analysis of studies spanning 25 years." Archives of Sexual Behavior 47.1 (2018): 1-15.
7. Zietsch, B. P., et al. 2012. "Do Shared Etiological Factors Contribute to the Relationship between Sexual Orientation and Depression?" Psychol Med 42, no. 3 (Mar): 521-32. http://dx.doi.org/10.1017/s0033291711001577.
8. Bogaert, A. F. 2010. "Physical Development and Sexual Orientation in Men and Women: An Analysis of Natsal-2000." Arch Sex Behav 39, no. 1 (Feb): 110-6. http://dx.doi.org/10.1007/s10508-008-9398-x.
9. Balthazart, Jacques. "Fraternal birth order effect on sexual orientation explained." Proceedings of the National Academy of Sciences 115.2 (2018): 234-236.
1. El-Maouche, Diala, Wiebke Arlt, and Deborah P. Merke. "Congenital adrenal hyperplasia." The Lancet 390.10108 (2017): 2194-2210.
2. Meyer-Bahlburg, Heino F. L., et al. 2008. "Sexual Orientation in Women with Classical or Non-Classical Congenital Adrenal Hyperplasia as a Function of Degree of Prenatal Androgen Excess." Archives of Sexual Behavior 37, no. 1: 85-99. http://dx.doi.org/10.1007/s10508-007-9265-1.
3. Neibergall, Nicholas C., Alex J. Swanson, and Francisco J. Sánchez. "Hormones, Sexual Orientation, and Gender Identity." The Oxford Handbook of Evolutionary Psychology and Behavioral Endocrinology (2019): 201.
4. Reinisch, June M., Erik Lykke Mortensen, and Stephanie A. Sanders. "Prenatal exposure to progesterone affects sexual orientation in humans." Archives of sexual behavior 46.5 (2017): 1239-1249.
5. Williams, T. J., et al. 2000. "Finger-Length Ratios and Sexual Orientation." Nature 404, no. 6777 (Mar 30): 455-6. http://dx.doi.org/10.1038/35006555.
6. Martin, J. T., and D. H. Nguyen. 2004. "Anthropometric Analysis of Homosexuals and Heterosexuals: Implications for Early Hormone Exposure." Horm Behav 45, no. 1 (Jan): 31-9. https://www.ncbi.nlm.nih.gov/pubmed/14733889.