AWA: Academic Writing at Auckland

In order to meaningfully discuss the question “is being gay innate?” we must first define what is meant by the terms ‘gay’ and ‘innate’. It is difficult, and perhaps flawed, to place a definitive, categorical label on what is gay and what is not, considering the vast variety in human psychology and the proposed sliding scale of sexuality, where an individual is attracted to both males and females to varying degrees. However, in any scientific enquiry, concrete and measurable definitions are essential to solid conclusions. Thus, we must draw a somewhat arbitrary line. Obviously, being gay involves sexual attraction to members of one’s own sex. Since attraction to both sexes has its own label – bisexuality – and varying proportions of attraction are hard to quantify, the easiest definition to use is that of exclusive attraction to members of one’s own sex. This is also a logical choice because it has been used in studies in the past, and we know that approximately 1-5% of the population falls within this category (LeVay & Hamer, 1994).

It also proves problematic to define innateness, mainly because it is contentious whether such a thing exists (Mameli & Bateson, 2011). A simple Google definition reflects the popular understanding of ‘innate’: synonymous with inborn, natural, intrinsic, instinctive, intuitive, spontaneous, unlearned, and so on (‘innate definition - Google Search’). It seems to be a concept that people believe in and are comfortable with (Mameli & Bateson, 2011). However, from a biological point of view, innateness is hard to pin down. Different definitions of innateness focus on different aspects of it, and none of them are sufficient on their own, but some of them are necessary; especially lack of learning. According to Mameli, innateness might not even be a useful concept, because it refers to a group of biologically distinct properties of phenotypic traits, which occur independently. These properties include a trait having genetic roots, being highly heritable or developing inevitably regardless of environmental conditions (Mameli & Bateson, 2011). The cluster hypothesis argues that some other factor tends to cause these properties to occur together, and that innateness is the presence of that factor, measurable only by the presence of the properties. The clutter hypothesis disregards the cluster hypothesis for lack of evidence, and claims that these distinctive properties are unrelated (Mameli & Bateson, 2011). In order to usefully discuss whether a certain trait (being gay) is innate, we will assume innateness is a cohesive concept, characterised always by being not learnt, and using the presence of genetic influences, heritability and developmental inevitability (canalisation) as a measure of the strength of the innateness.

Firstly, I argue that since there is consensus that any definition of innateness rules out the role of learning – that is, if something is learnt, it cannot be innate (Mameli & Bateson, 2011) – surely the possibility of something innate being a choice is also eliminated. In other words, if it were possible for homosexuality to be imposed on an individual, then it would not be inevitable, it would be contingent on the will and could not be innate. I also argue that, amongst sane people, legal responsibility for their actions reflects the role of choice in their behaviour, whatever their desires and tendencies. Conscious sexual behaviour is voluntary. Whatever influences have predisposed an individual to certain sexual acts, it is still remains the individuals decision to engage in such acts. This is true regardless of orientation, and therefore I argue homosexual behaviour cannot itself be innate. Thus, for the purposes of this essay, let us disregard whether homosexual acts are innate. From now on in my discussion of innateness, when I refer to homosexuality or gayness, I refer to the urge or desire of sexual attraction to members of the same sex. However, I assume homosexual acts are usually still an indicator of homosexual tendencies.

One theory on the origin of homosexuality is levels of androgens a foetus experiences in utero. This would be a biological basis, but for the foetus, it would originate in the environment of the womb and not in themselves, thus it could contribute to the discussion of innateness in terms of being ‘present at birth’, but not in being heritable, genetic or canalised. Of course, some genetic difference in the way the foetus handles androgens is possible, but importantly, no molecular difference has been found between the androgen receptors of straight and gay people (Macke et al., 1993). In a study by Roger Gorski, new- born male and female rats were treated by castration and androgen injections respectively, to see what would happen to their ‘sexual orientations’. The rats showed behaviour typical of the other sex. The females became prone to mounting other rats, and the males tended to bend their backs in response (lordosis) (Barraclough & Gorski, 1962). Since human sexual development is also affected by prenatal hormones, this study has been used to claim a link to human orientation (Byne, 1994). However, this assumes that ‘male-typical’ and ‘female- typical’ sexual responses in rats are analogous to sexual attractions in humans. Human sexual behaviour and human desires are clearly vastly more complex, nuanced, and socially influenced than lordosis and mounting between rats. Gay behaviour in human males is not necessarily ‘feminised’, and lesbian behaviour is not always ‘masculinised’. There is also an assumption in Gorski’s study which cannot be extrapolated to humans, and that is that orientation does not depend on the sex of your sexual partner, but rather the role or position you assume in the relationship. In a male-female pair of rats, both are considered homosexual if the female mounts and the male arches his back (Byne, 1994). This is obviously not the case in humans.

Gorski found that in rats, the medial preoptic area of the hypothalamus is sexually dimorphic. This region is sensitive to androgens (only around the time of birth), and many cells die if there is no surge of testosterone at this time, leading to a female-differentiated brain region, as well as female-typical lordosis in mating (Barraclough & Gorski, 1962). Some have wondered if this is parallel to human females with congenital adrenal hyperplasia (who have been exposed to excess androgens prenatally). These women can have masculinised genitals, and there is some evidence that they are more likely to be homosexual (LeVay & Hamer, 1994). However, it is completely unknown whether any brain structures are affected by these unusual hormone levels, and if that is the cause of changed sexual tendencies.

There is statistical evidence that prenatal hormones are related somehow to orientation, but the mechanism is unknown.

Another line of enquiry in the question of innateness involves brain structure. Simon LeVay carried out an important study on size differences in the INAH3 region of the brain between straight and gay men, and found that it is larger in heterosexual men (LeVay, 1991). The reason LeVay decided to analyse the hypothalamic region in the medial preoptic area in humans was because of animal studies. Gorski found that the region was larger in male than in female rats, but did not specifically test its role in behaviour, so we do not know what physiology it is involved in (Barraclough & Gorski, 1962). He also found that the same area of the brain is involved in sexual behaviour in male monkeys, but he didn’t find the same structural dimorphism he found in rats. So in LeVay’s study of the different sizes of INAH3 in humans of different sexual orientations, he goes two steps beyond these animal studies; he draws a direct link between hypothalamus dimorphism and sexual activity (which has been suggested only in part by each of Gorski’s rat and monkey studies), and he raises the possibility that the dimorphism is based on sexual orientation rather than biological sex (LeVay, 1991). He then goes on to suggest that the difference in INAH3 sizes between gay and straight men is a causal determinant in their sexual orientations. LeVay admits that his study does not provide evidence for the causal relationship between orientation and brain structure. He believes that brain structure is a causal factor in determining gayness, and points out that both could be the result of a third developmental factor. He doubts the possibility of homosexual behaviour influencing brain structure, however, for a few reasons. For instance, rat brains show plasticity in response to androgens only around the time of birth, and not into adulthood (when human sexual behaviour would be able to exert influence) (LeVay & Hamer, 1994). However, hormones are not the only physiological result of certain behaviour patterns; there are a multitude of ways the architecture and connections of the brain can be influenced by behaviour in ways we don’t fully understand (Byne, 1994).

Studies on whether homosexuality is genetic are all important to the question of innateness. These follow a few lines of evidence. Firstly, some studies have looked at families with a gay son and measured how often the man’s brother is also gay. The baseline frequency of homosexuality in the population is 1-5%, but it was found that identical twins have a 52% chance of concordance, fraternal twins 22%, non-twin brothers 9% and adopted brothers 11% (LeVay & Hamer, 1994). Immediately, this suggests that homosexuality is in some way genetic, since the chance of both brothers being gay increased, mostly, with increasingly shared genes. What it also tells us is that there is, without a doubt, an environmental influence on homosexuality. If it were purely genetic, we would expect 100% concordance between identical twins, and we see only half. We would also expect that fraternal twins and non-twin brothers should show equal concordance, because they share the same amount of genes with the gay brother, and unrelated adopted brothers should not be significantly more concordant than the general population (1-5%). This raises the question, what role does environment play? An experiment like this cannot be disentangled from the social learning that takes place in a family, and although it is clear that homosexuality has some genetic basis, if it is as affected by learning as it appears, to what extent can we call it innate?

Another study has found that homosexuality seems to ‘run in families’ significantly more on the maternal than the paternal side. The most likely reason for this family clustering is that the responsible genetic locus is on the X chromosome (Hamer et al., 1993). One particular region, Xq28, large enough to contain several hundred genes, seems to have a link to homosexuality that no other region has shown. Females carry two copies of the X chromosome, and therefore Xq28, while males carry only one. There are several different versions of the Xq28 region in the population, and every male receives his Xq28 region randomly from his mother’s set of two. Thus, by chance, if mothers were never homozygous, you would expect 20 out of 40 pairs of brothers to have the same version of Xq28. However, in Hamer’s study, 33 out of 40 gay pairs of brothers had the same version of Xq28. These results have been popularly misinterpreted as the discovery of a ‘gay gene’, but in fact no one version of Xq28 is linked to homosexuality. The correlation is between homosexuality and brothers sharing the same version of Xq28, but no version in particular. This is rather confusing, for how can sharing a gene with a sibling increase your chances of homosexuality, if not through the action of the gene itself?

There are some criticisms about the methodology of Hamer’s study. Identical twins are more likely to be concordant in their sexuality than fraternal siblings – whether from genetics, environment or both is contentious. Either way, this may have contributed to selection bias, in which they recruited only families with two gay sons. Identical twins always share Xq28, and there was most likely a higher proportion of identical twins in the homosexual group than in the presumably heterosexual control group. That is one criticism of Hamer’s study, which so far has failed to be replicated (Rice, Anderson, Risch, & Ebers, 1999).

In conclusion, I argue that homosexual behaviour, as with all sexual behaviour, is a choice in adult humans, and is therefore not considered in my discussion except as an indication of underlying homosexual urges, which may or may not be ‘innate’. Referring to the minimal condition of innateness (if, indeed, innateness is not an illusory conflation of distinct properties), I also argue that ‘being gay’ – being exclusively sexually attracted to members of your own sex – is not in itself innate either. This is because environment, and most likely social learning, undeniably plays a significant role in the development of homosexuality (Byne, 1994). This violates the minimal condition that if a trait is innate it is not mediated by learning, and it also undermines the concept of canalisation; that an innate trait will inevitably and reliably develop, regardless of environmental influence. However, I do not come to the same conclusion regarding the biological basis of homosexuality. It seems clear to me that there is, without a doubt, a genetic or epigenetic reason that some individuals are much more likely than others to become gay, whatever the environment. In other words, it appears that the tendency or disposition to become gay is an innate trait. Some properties, such as canalisation or heritability, are very hard to measure for this trait, since the visible phenotype of individuals is also affected by learning and environment. But, until we come up with a better way of measuring traits, I feel the weight of evidence supports that gayness is the result of the interaction between an innate tendency and environment – both biological and social.

I believe what this debate really goes to show is that ‘innateness’ is not a useful concept. We should rather continue to focus on discovering the biological, social and psychological basis of homosexuality, and forget about arbitrary terms.

References

Barraclough, C. A., & Gorski, R. A. (1962). Studies on Mating Behaviour in the Androgen-Sterilized Female Rat in Relation to the Hypothalamic Regulation of Sexual Behaviour. Journal of Endocrinology, 25(2), 175–182. http://doi.org/10.1677/joe.0.0250175

Byne, W. (1994). The Biological Evidence Challenged. Scientific American. Retrieved from http://www.nature.com.ezproxy.auckland.ac.nz/scientificamerican/journal/v270/n5/pdf/scientificamerican0594-50.pdf

Hamer, D. H., Hu, S., Magnuson, V. L., Hu, N., & Pattatucci, A. M. (1993). A linkage between DNA markers on the X chromosome and male sexual orientation. Science, 261(5119), 321–327. http://doi.org/10.1126/science.8332896

innate definition - Google Search. (n.d.). Retrieved 24 April 2016, from https://www.google.co.nz/webhp?sourceid=chrome- instant&ion=1&espv=2&ie=UTF-8#q=innate%20definition

LeVay, S. (1991). A Difference in Hypothalamic Structure between Heterosexual and Homosexual Men. Science, 253, 1034–1037.

LeVay, S., & Hamer, D. H. (1994). Evidence for a Biological Influence in Male Homosexuality. Scientific American. Retrieved from http://www.nature.com.ezproxy.auckland.ac.nz/scientificamerican/journal/v270/n5/pdf/scientificamerican0594-44.pdf

Macke, J. P., Hu, N., Hu, S., Bailey, M., King, V. L., Brown, T., … Nathans, J. (1993). Sequence variation in the androgen receptor gene is not a common determinant of male sexual orientation. American Journal of Human Genetics, 53(4), 844–852.

Mameli, M., & Bateson, P. (2011). An evaluation of the concept of innateness. Philosophical Transactions of the Royal Society B: Biological Sciences, 366(1563), 436–443. http://doi.org/10.1098/rstb.2010.0174

Rice, G., Anderson, C., Risch, N., & Ebers, G. (1999). Male Homosexuality: Absence of Linkage to Microsatellite Markers at Xq28. Science, 284(5414), 665–667. http://doi.org/10.1126/science.284.5414.665