by Catriona Nguyen-Robertson MRSV
Science Engagement Officer

This article follows our second joint presentation with Queers in Science on 30 January, 2020 by biological scientist Professor Andrew Barron from Macquarie University and medical scientist Dr Riki Lane from Monash University to the Royal Society of Victoria.

How did homosexuality evolve? Does it have a biological basis?

Professor Andrew Barron posed these questions to the audience at the Royal Society of Victoria. But he then iterated that these are not in fact the right questions to be asking. As a neuroethologist, studying the neural mechanisms of animal and insect behaviour, he has observed homosexual behaviour throughout the animal kingdom. ‘[Homosexuality] is not uniquely human.’

Animals, including humans, are born with innate behaviours to provide them with advantages for survival in response to different environmental stimuli. Genes are increasingly being considered as contributors to complex behavioural traits such as sexuality and gender differences in combination with environmental factors and influences. Previous family and genome-wide association studies have revealed that sexual orientation is between 30-40% hereditable (Sanders, Beecham et al. 2017), which is the same amount of heritability that contributes to birthweight, and more than what contributes to whether we are left- or right-handed.

Human sexuality is a continuum, much in the same way that height and weight are. Not everyone fits into the categories of strictly straight or strictly gay.  If the variation between individuals is collapsed to a binary then the focus becomes on asking why one end of the spectrum exists, when the better question would be to ask how variation in sexuality evolved and came about.

When thinking about evolution, we often think of Darwin’s “survival of the fittest” theory; that those with particular survival advantages pass their genes on to their offspring. Andrew introduced the homosexuality evolutionary paradox: homosexuals, on average, will pass on their genes at a lower rate – so any variation in genes contributing to homosexuality would be expected to be lost as they are not passed on to the next generation as frequently. But sex is about more than just reproduction. It plays a role in various social contexts and therefore has social benefits as well as reproductive ones that have to be considered.

Brian Hare, professor of evolutionary anthropology at Duke University, wrote about his idea of “survival of the friendliest”, in which recent human cognitive evolution has been selected for prosocial behaviour (Hare 2017). It is beneficial for a species like ours to be sociable, and sex can be a part of that. The idea that Andrew poses is that perhaps as humans and other animals increased their social cognition, there was an increase in diversity among sexual behaviour and rise in sociosexuality (uncommitted sexual relationships).

Dr Riki Lane, Research Fellow at Monash Health, asks if the “why” behind sexuality and gender even matters? There are two sides of the coin when we search for biological reasons to explain sexuality and gender: while people may find comfort in the “born this way” argument, looking for a “gay gene” can indicate a level of non-acceptance. They agree with Andrew in that dichotomising sexuality and gender ignores the continuum or clusters of individuals who don’t fall into one of two (and only two) categories and we can fall prey to thinking that one is “normal”.

Riki has explored the scientific evidence societal views on the psychosocial and biological factors used to explain gender and sexual diversity. Theories of gender have ‘waxed and waned’ over time: it was once a sin to be gender diverse, then a curable pathology, and now a healthy variant.

There is evidence to suggest that transsexuality is strongly associated with the neurodevelopment of the brain: that pre-natal hormones and genetics lead to differences in cognition, behaviour and identity between males and females. This evidence is based on hormonally atypical individuals, such as individuals with congenital adrenal hypoplasia (XX individuals who make testosterone in the adrenal glands and complex androgen insensitivity syndrome (XY individuals who do not respond to testosterone), among whom there are higher levels of gender change later in life.

A study in 1995 also suggested that brain anatomy also has a role to play (Zhou, Hofman et al. 1995). This research group found that the size of the brain area essential for sexual behaviour (BSTc) is larger in men that in women, and that male-to-female transsexuals often have the same size BSTc as females. Subsequent genetic studies also revealed weak links with a number of genes and transsexuality (Hare, Bernard et al. 2009, Foreman, Hare et al. 2019). Family and twin studies are also used to determine heritability estimates of transsexuality, ranging from between 17-45%. Riki is concerned that these arguments are often weak and often not reproduced.

As Joan Roughgarden writes in Evolution’s Rainbow, there are more colours of gender than colours that we have names for. Evidence points to genetic heritability behind gender and sexual preference, but in the end, does it even matter? Andrew and Riki think not. We don’t investigate the reasons as to why some people are short, some people are tall, and others are in between. We are different in many different ways. Together, we are more colourful than any rainbow.

A livestream video of Andrew and Riki’s presentations is available online from https://www.facebook.com/201662943328320/videos/771920039968056/ .

Further reading:

• Foreman, M., et al. (2019). “Genetic Link Between Gender Dysphoria and Sex Hormone Signaling.” J Clin Endocrinol Metab 104(2): 390-396.

Context: There is a likely genetic component to gender dysphoria, but association study data have been equivocal. Objective: We explored the specific hypothesis that gender dysphoria in transgender women is associated with variants in sex hormone-signaling genes responsible for undermasculinisation and/or feminization. Design: Subject-control analysis included 380 transgender women and 344 control male subjects. Associations and interactions were investigated between functional variants in 12 sex hormone-signaling genes and gender dysphoria in transgender women. Setting: Patients were recruited from the Monash Gender Clinic, Monash Health, Melbourne, Australia, and the University of California, Los Angeles. Patients: Caucasian (non-Latino) transgender women were recruited who received a diagnosis of transsexualism [Diagnostic and Statistical Manual of Mental Disorders (DSM)-IV) or gender dysphoria (DSM-V)] pre- or postoperatively. Most were receiving hormone treatment at the time of recruitment. Main Outcome Measured: Genomic DNA was genotyped for repeat length polymorphisms or single nucleotide polymorphisms. Results: A significant association was identified between gender dysphoria and ERalpha, SRD5A2, and STS alleles, as well as ERalpha and SULT2A1 genotypes. Several allele combinations were also overrepresented in transgender women, most involving AR (namely, AR-ERbeta, AR-PGR, AR-COMT, CYP17-SRD5A2). Overrepresented alleles and genotypes are proposed to undermasculinise/feminize on the basis of their reported effects in other disease contexts. Conclusion: Gender dysphoria may have an oligogenic component, with several genes involved in sex hormone-signaling contributing.

• Hare, B. (2017). “Survival of the Friendliest: Homo sapiens Evolved via Selection for Prosociality.” Annu Rev Psychol 68: 155-186.

The challenge of studying human cognitive evolution is identifying unique features of our intelligence while explaining the processes by which they arose. Comparisons with nonhuman apes point to our early-emerging cooperative-communicative abilities as crucial to the evolution of all forms of human cultural cognition, including language. The human self-domestication hypothesis proposes that these early-emerging social skills evolved when natural selection favored increased in-group prosociality over aggression in late human evolution. As a by-product of this selection, humans are predicted to show traits of the domestication syndrome observed in other domestic animals. In reviewing comparative, developmental, neurobiological, and paleoanthropological research, compelling evidence emerges for the predicted relationship between unique human mentalizing abilities, tolerance, and the domestication syndrome in humans. This synthesis includes a review of the first a priori test of the self-domestication hypothesis as well as predictions for future tests.

• Hare, L., et al. (2009). “Androgen receptor repeat length polymorphism associated with male-to-female transsexualism.” Biol Psychiatry 65(1): 93-96.

BACKGROUND: There is a likely genetic component to transsexualism, and genes involved in sex steroidogenesis are good candidates. We explored the specific hypothesis that male-to-female transsexualism is associated with gene variants responsible for undermasculinisation and/or feminization. Specifically, we assessed the role of disease-associated repeat length polymorphisms in the androgen receptor (AR), estrogen receptor beta (ERbeta), and aromatase (CYP19) genes. METHODS: Subject-control analysis included 112 male-to-female transsexuals and 258 non-transsexual males. Associations and interactions were investigated between CAG repeat length in the AR gene, CA repeat length in the ERbeta gene, and TTTA repeat length in the CYP19 gene and male-to-female transsexualism. RESULTS: A significant association was identified between transsexualism and the AR allele, with transsexuals having longer AR repeat lengths than non-transsexual male control subjects (p=.04). No associations for transsexualism were evident in repeat lengths for CYP19 or ERbeta genes. Individuals were then classified as short or long for each gene polymorphism on the basis of control median polymorphism lengths in order to further elucidate possible combined effects. No interaction associations between the three genes and transsexualism were identified. CONCLUSIONS: This study provides evidence that male gender identity might be partly mediated through the androgen receptor.

• Sanders, A. R., et al. (2017). “Genome-Wide Association Study of Male Sexual Orientation.” Sci Rep 7(1): 16950.

Family and twin studies suggest that genes play a role in male sexual orientation. We conducted a genome-wide association study (GWAS) of male sexual orientation on a primarily European ancestry sample of 1,077 homosexual men and 1,231 heterosexual men using Affymetrix single nucleotide polymorphism (SNP) arrays. We identified several SNPs with p < 10(-5), including regions of multiple supporting SNPs on chromosomes 13 (minimum p = 7.5 x 10(-7)) and 14 (p = 4.7 x 10(-7)). The genes nearest to these peaks have functions plausibly relevant to the development of sexual orientation. On chromosome 13, SLITRK6 is a neurodevelopmental gene mostly expressed in the diencephalon, which contains a region previously reported as differing in size in men by sexual orientation. On chromosome 14, TSHR genetic variants in intron 1 could conceivably help explain past findings relating familial atypical thyroid function and male homosexuality. Furthermore, skewed X chromosome inactivation has been found in the thyroid condition, Graves’ disease, as well as in mothers of homosexual men. On pericentromeric chromosome 8 within our previously reported linkage peak, we found support (p = 4.1 x 10(-3)) for a SNP association previously reported (rs77013977, p = 7.1 x 10(-8)), with the combined analysis yielding p = 6.7 x 10(-9), i.e., a genome-wide significant association.

• Zhou, J. N., et al. (1995). “A sex difference in the human brain and its relation to transsexuality.” Nature 378(6552): 68-70.

Transsexuals have the strong feeling, often from childhood onwards, of having been born the wrong sex. The possible psychogenic or biological aetiology of transsexuality has been the subject of debate for many years. Here we show that the volume of the central subdivision of the bed nucleus of the stria terminals (BSTc), a brain area that is essential for sexual behaviour, is larger in men than in women. A female-sized BSTc was found in male-to-female transsexuals. The size of the BSTc was not influenced by sex hormones in adulthood and was independent of sexual orientation. Our study is the first to show a female brain structure in genetically male transsexuals and supports the hypothesis that gender identity develops as a result of an interaction between the developing brain and sex hormones.