Biological Basis of Homosexuality

Published 23 Feb 2017

There is an ongoing debate on whether homosexuality has a biological basis or not. The search is on for the genetic, chemical, neuranatomical and functional evidence that the “third sex” is innate and not just a choice or entirely the product of psychosocial factors. There have been several studies supporting this theory. However, they are not without their flaws and even the interpretation of the results leave room for criticism and alternative explanations. This paper aims to examine the so-called proof of the biological basis of homosexuality.

The theory that homosexuality is partly genetic is based on several twin studies. It was found that there is higher concordance of sexual orientation in identical twins compared to fraternal twins (Bailey et al., 1993 as cited in Byne et al., 1994). Because identical twins have the exact DNA composition, it was hypothesized that the reason for the high concordance rates for sexual orientation is that it is directly affected by our genes.

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There are some loopholes in this theory, however, as cited in the book Biology and Human Sexual Orientation (Byne et al., 1994). One is that the twins used in the studies were not reared apart. Hence, they may have had very similar childhood experiences, possibly causing them to have the same sexual orientation. For studies that did deal with identical twins reared apart, the fact remains that they looked alike and as such people around them may have treated them the same way which again leads them to have the same childhood experiences. Concordance rates only tell us the degree to which homosexuality is associated with genetics and not how genetics actually affect homosexuality. Furthermore, it was found that half of the identical twin sets did not have the same sexual orientation, therefore, if genetic does play a role in homosexuality, it is through its interaction with the environment and not direct (Byne et al., 1994).

Researchers even went as far as identifying the chromosome responsible for homosexuality. In the controversial study of Hamer, et al. ( 1993, as cited in Rice, et al., 1999), it was claimed that the gene for male homosexuality is localized in the X chromosome, particularly in position Xq28. This is based on their analysis of chromosomes in families with more than one male homosexual sibling. Their study included an investigation on the sexual orientation of first-, second-, and third-degree relatives as well and found that there are more cases of homosexuality in the mother’s side as compared to the father’s side, leading them to think that male homosexuality could be an X-linked trait. Indeed, molecular analysis revealed that there is an excess of allele sharing in the region of Xq28. These results were replicated in the study of 33 additional homosexual brothers (Hu et al., 1995 as cited in Rice et al., 1999). However, in the larger-scale study by Rice, et al. (1999), they did not find the shared Xq28 marker. It is unclear why this is so since the sample size differ by only six people. Regardless of the reason, the disparity in findings warrants further investigations into the X-chromosome claim before making any conclusions.

Scientists are now also linking homosexuality to androgen exposure early in the fetal development. The Prenatal Hormone Hypothesis is based on the assumption that the brain of a fetus has a potential to develop into a male or female brain depending on the amount of androgens it is exposed to inside the womb (Byne et al., 1994). The theory is that male homosexuality and female heterosexuality are a result of exposure to low levels of androgen while consequently female homosexuality and male heterosexuality are a result of high levels of androgen. The theory was derived from the observation in that female mating behavior such as lordosis can be induced in certain male mammals such as rats, ferrets, pigs, and dogs by reducing the amount of androgen during a critical phase in the early brain development (Adkins-Regan, 1988; Baum et al., 1990 as cited in Pinel, 2003). Likewise, male mating behavior such as mounting can be induced in the female counterparts when androgen levels are elevated during this period (Adkins-Regan, 1988; Baum et al., 1990 as cited in Pinel, 2003).

The main criticism of this hypothesis is that it may not be appropriate to generalize mating behaviors of animals to sexual orientation of humans. For one thing, lordosis is merely a reflex (Byne et al., 1994). Human sexual orientation is extremely complex, involving erotic responses, emotions, and self-identification. It is not just defined by the sexual position one assumes. The stand of Byne et al. (1994) is that it is unlikely that prenatal hormones affect sexual orientation as directly as they do mating behaviors in animals. However, it is also wrong to completely disregard the relevance of these mammalian studies, especially since the pattern is so consistent.
Another chemical implicated in male homosexuality is the protein Alpha 1-Antitrypsin. In the experiment conducted by Deam et al. (1989 as cited in Wolfe, 1999) this compound was identified in the blood of 16.3% of the homosexual group and only 8.7% in the heterosexual group. Although there was a significant difference, the study did not explain how this protein affects one’s sexual orientation. In addition, there was no way of determining whether this protein was really innate or was acquired through a homosexual lifestyle.

In relation to the Prenatal Hormone Hypothesis, as previously mentioned, the theory is that exposure to androgens in the womb affects the subsequent development of the brain. Indeed, they found certain structural differences between the brain of homosexuals and heterosexuals.

The fist breakthrough study was by Swaab and Hoffman (1990 as cited in Alexander, 2000). They focused on the suprachiasmatic nucleus (SCN) of the hypothalamus. It was already established that this region is sexually dimorphic and significantly larger in men compared to women. They, however, found a clear difference between homosexuals and heterosexuals as well. The region enclosing vasopressin-containing neurons was double the size in homosexual males as compared to their heterosexual counterparts.

Levay’s (1991 as cited in ) controversial study followed soon after. His area of focus was the interstitial nucleus of the anterior hypothalamus or INAH; INAH 3 to be exact. INAH 1 was found to vary with sex but not with sexual orientation but INAH 3 varies with both. It was found that INAH 3 is more than twice as large in heterosexual men as they are in women and homosexual men. This region is said to be responsible for the generation of male typical mating behavior (Alexander, 2000). There are, however, several faults in Levay’s methodology and furthermore, it does not automatically mean that the INAH 3 is in anyway the cause of homosexuality. The sample size used in Levay’s study was small and because they were conducted on dead bodies, it was impossible to get the accurate sexual history of the subjects. In addition, most of the subjects died of AIDS, this fact in itself a major confounding variable. Testosterone is said to alter the size of INAH 3 (Alexander, 2000). AIDS may cause testicular failure, which in turn decreases the levels of testosterone in the body, thereby possibly reducing the size of INAH 3. In addition, the effects of AIDS treatments on INAH 3 were not examined. The difference in size may be a result of either the treatment or the disease itself. Also, a difference in size does not necessarily mean a difference in function or capacity. Brains of males are generally larger than females’ but they are not more intelligent because female brains are denser. Alexander (2000) argued that the number of cells in INAH 3 should be compared and not the size.

Another area of interest is the anterior commissure. This is sexually dimorphic like the suprachiasmatic nucleus and INAH3. It was found to be larger in females and smaller in males (Pinel, 2003). The interesting thing is that the anterior commissure in homosexual males is not similar in size to that of the female nor was it intermediate between the two sexes. It is actually larger compared to both heterosexual female and heterosexual male (Allen & Gorsky 1992 as cited in Alexander, 2000) supporting the idea that they are indeed a separate third sex. However, despite the existence of group differences, as with all studies comparing brain structures of heterosexuals and homosexuals, the individual differences between individual brains actually exceed the differences found between groups (Byne et al., 1994). Therefore, one cannot tell a person’s orientation by looking at any brain structure.
As there are gender dimorphic structures in the brain, they too have found functional differences. Alexander and Sufka (1993 as cited in Alexander, 2000) compared patterns in brain activity among homosexual males, heterosexual males and females as they performed verbal, cognitive, and spatial tasks and also while making affective judgements.

Activity was measured via EEG in four locations in the left and right hemispheres. They found that the homosexual males displayed greater asymmetry compared to both heterosexual sexes during the verbal, cognitive, and spatial tasks. More precisely, homosexual subjects had greater inhibition in the right hemisphere compared to the heterosexual subjects during the verbal task, and greater inhibition in the left during spatial tasks. In heterosexuals, inhibition was not as pronounced and it was in the same hemisphere for both tasks. The same asymmetry was found in homosexual males when making affective judgments, and again these were not observed in heterosexual males and females. One limitation of this study, as with most studies on the biology of homosexuality, is that they did not use lesbian subjects. In addition, activity was only measured in eight locations.

If Alexander and Sufka found asymmetry in homosexual males and not in heterosexuals, the opposite is true in Reite and his colleagues’ (1995 as cited in Alexander, 2000) study of the M100. This auditory evoked response has also been established as a sexually dimorphic (Reite et al. 1991 as cited in Alexander, 2000). They recorded MEG M100 source location in the left and right hemispheres of nine heterosexual and nine homosexual males. In the heterosexual group, they found an auditory asymmetry in which the response was found substantially anterior on the right hemisphere. In the homosexual group, they did not find this asymmetry. Their findings suggest that there is a difference in either the structure, function, or both, of the superior temporal gyrus between homosexual and heterosexual males. The sample size, however, is too small to make such generalizations.

This is the main problem with all studies investigating the biological basis of homosexuality and perhaps the greatest criticism. The evidence cannot hold up due to methodological flaws such as a small sample size or confounding variables. The view that homosexuality is partly biological is not widely accepted because the evidence is not concrete enough to support it. In terms of genetic evidence, there is no way of telling whether specific chromosomes do influence homosexuality or the concordance is a result of a common environment twins and siblings grow up in. For neuranatomic and neurendocrine differences, they have not yet determined if these are innate or acquired through a homosexual lifestyle. Furthermore, individual differences exceed the differences found between homosexual and heterosexual groups.

A second criticism to the view that homosexuality has a biological basis is that sexual orientation is far too complex to be determined or directly influenced by just a few brain structures, chromosomes or hormones. This is not to say that it should be concluded that there is no biological basis for homosexuality or that the results of previous studies should be disregarded. However, researchers must always consider that psychosocial factors also play a key role in one’s sexual orientation and that it is a product of the interaction between biology and the environment. This may be another nature-nurture or choice debate that has no answer.


  • Alexander, J. E. (2000). Biological influences on homosexuality. Psychology, Evolution & Gender, 2, 241-252.
  • Byne, W. and Parson, B.(1994). Biology and human sexual orientation. Harvard Mental Health Letter, 10, 5.
  • Pinel, J.P. (2003). Biopsychology (5th ed.). Boston, MA: Allyn & Bacon.
  • Rice, G., C., Anderson,C., Risch, N., and Ebers, G. (1999). Male homosexuality: absence of linkage to microsatellite markers at Xq28. Science, 284, 665-667.
  • Wolfe, C. (1999). Homosexuality and American Public Life. Dallas, TX: Spence Publishing Company.
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