More than an XY tale: Sexual and Gender diversity and brain development.
Human sexuality and gender identity are increasingly accepted as more fluid and more diverse than in the past. The rigid binary of masculinity and femininity prescribed to a heterosexual and heteronormative framework is becoming increasingly challenged. Instead, a range of sexualities and gender identities, in a gradient from heterosexual to homosexual and masculine to feminine with everything in between, is giving new generations more freedom in their human experience. The complete failure of behavioral treatments aimed to “cure” homosexual or transgender individuals favors the role of nature in people’s sexuality and gender identity, instead of traits that can be changed.
The biological basis of sexual and gender diversity is not very clear. However, human and animal studies indicate that early brain development and in particular the influence of hormones during pregnancy can help us understand our own nature and diversity in this regard.
In broad terms, males and females are differentiated genetically by one chromosome pair; two X chromosomes determine biological female and an XY combination is present in males. A gene in particular in the Y chromosome, called SRY gene, leads to the formation of testicles, which in turn produce male hormones and secondary masculine features. In contrast, a different gene in the X chromosome, called DAXI, promotes formation of the ovaries and later on female hormonal production and secondary sexual differentiation. Damage in the SRY gene or absence of male hormones in XY individuals results in development of female genitalia and female characteristics. Therefore, even at the chromosome level, XY does not always mean masculine characteristics.
While the genitals differentiate during the first trimester of pregnancy, the brain develops at a later stage, around the second trimester. Hormones have a crucial role in the development of the brain, including formation of neuronal connections and neuronal differentiation. Male hormones result in “masculinization” of the brain, while its absence in brain “feminization”. In particular, testosterone peaks between the second and sixth month of pregnancy and 1–3 months postnatally. The conjunction of hormonal peaks and brain development, make these early developmental stages crucial for the maturation of the brain. As genital and brain development occur at different stages, both under hormonal influence, it is possible that these processes are disconnected and therefore individuals with either male of female genitalia do not identify with their biological sex as their brain may have developed under a different hormonal environment.
Indeed, structural and functional brain studies show that brain characteristics are more alike between transgender and cisgender people sharing the same gender identity (e.g. trans females and biological females), versus cis and trans individuals sharing the same biological sex (e.g. trans females and biological males). Further, sexual orientation is also influenced by embryonic hormonal exposure. Seminal studies in Rams found a brain region, called the sexually dimorphic preoptic nuclei, bigger in heterosexual males in comparison to heterosexual females and homosexual males, which correspond to 6–8% of male rams displaying court and mounting behaviors toward other males. This brain structure develops upon early testosterone exposure, but not hormonal exposure in adulthood. Similar patters have been found in humans, with findings of females exposed to abnormally high testosterone before birth displaying masculinized genitals and behavior.
All these studies are far from conclusive, but point out at the complexity of sexuality and gender identity, which are not reducible to a single genetic or environmental factor. A better understanding of our own biology will help us appreciate human complexity and diversity, hopefully with more acceptance for our differences.
References
Roselli CE. Neurobiology of gender identity and sexual orientation. J Neuroendocrinol. 2018 Jul;30(7):e12562. doi: 10.1111/jne.12562. PMID: 29211317; PMCID: PMC6677266.
