Biological sex in humans has often been simplified to whether or not someone has XX chromosomes, for females, or XY chromosomes, for males. We create this binary in attempt to classify, and better understand ourselves and our identities – however this can often lead to hostile language and the “othering” of the many people who don’t fit this binary. But just like gender identity, biological sex isn’t all that simple.
For decades now, international sports organisations and the public alike have been outraged of the possibility that so called male athletes could be competing as unfair competitors in women’s sports. In the Olympic Games of 1960 we started to establish rules of eligibility for female athletes, which required physical examination. It was met with wide criticism, so in the 1968 Olympics, we started testing their genome.
After the first few methods being unsuccessful, they landed on testing for the SRY gene. This gene is generally located on the Y chromosome and is responsible for triggering the formation of testes. At first glance that seems fine – but in reality, it’s not a fair dividing line on what what a female is. SRY testing was banned, but that only lead to different methods of testing for an athletes sex.
Controversy around this issue has never died, it was only in 2009 that Caster Semenya, 18 at the time, was forced to undergo tests to “prove” her sex after an 800m World Champion win. It showed that she had hyperandrogenism, which meant she had three times as much testosterone as the “average” woman. She was subject to humiliating and misogynistic abuse purely because she couldn’t fit into the restrictive box we consider as female. A similar and more recent case is Dutee Chand, banned to compete in 2014, which she challenged, because of her hyperandrogenism.
Almost 60 years later, sports organisations have still been unsuccessful in finding a way to clearly classify between the sexes. So why is that the case?
Biological sex is classified in many different ways, Kieth Moore in 1968 described nine components of sexual phenotype: external genital appearance, internal reproductive organs, structure of the gonads (ovaries or testes or anything in between), endocrinologic sex, genetic sex, nuclear sex, chromosomal sex, psychological sex and social sex. The sex binary states that there are only two different routes of sexual differentiation – and all these nine components will line up. But when considering this complexity, a binary has never existed. In fact, some statistics indicate as many as 1 in 100 people have a form of DSD, a difference in sex development.
A DSD is not to be mistaken for true intersex variations. Intersex variations are more rare: about 1 in 4,500 having some sort of intersex condition. For more information on the social issues surrounding intersex people, written by intersex people, see here. The only component of Moore’s sexual phenotype theory I’ll be discussing is the genetic sex.
Sex can be determined by your chromosomes. The 23rd pair of chromosomes in your cells are vital in sex development; they have often been simplified to the “sex chromosomes” but this does not mean all the genes on the X or Y chromosome are responsible for sex development, and it also doesn’t mean genes on other chromosomes don’t have a role. Nevertheless, genes make up your primary sex determination: whether or not your gonads develop into testes or ovaries. So what are these genes that aid sexual differentiation?
The SRY gene
As mentioned previously, it’s the gene that triggers the formation of the testes. Generally located on the Y chromosome, most XY carrying individuals will have this gene. As complicated as genetics is, it’s not surprising that this gene can jump onto an X chromosome in the formation of a sperm cell. If this sperm cell with the SRY-having-X goes onto fertilise an egg, it results in individuals with XX chromosomes, but otherwise male sex characteristics. Few of these people will however have ambiguous genitalia, that may become more apparent during puberty. Sometimes individuals with XY chromosome formation can develop female sex characteristics because of mutations on the SRY gene that resulted in its silencing. This was one of the issues which arose in the SRY-testing for female athletes.
For a long time it was thought that developing ovaries and Fallopian tubes was the “default”, that if you didn’t have this SRY gene that you were destined to develop the typical female anatomy – until further discoveries were made of other genes that aid the development of the ovaries and silences further male development. This shows that there are genes on both sides of the spectrum that assist sexual differentiation.
There are other genes that have a role in sex differentiation (DAX1, Sox9, Fgf9 to name a few) and it has become increasingly evident that sex determination (in terms of genes) is all about balance. These genes interact with each other, controlling how often each one is expressed. Another layer of complexity is added when you consider epigenetics – the way in which environmental conditions can affect the expression of these genes. Epigenetics alone is a very new and accelerating area of science research, and the epigenetics of sex determination itself is still rather obscure. It’s the complexity of the wide array of genes and how these genes are expressed that opens the door to variation, and disproves the binary.
- Check out the Howard Hughes Medical Institute biointeractive test to see just how complicated sex verification of female athletes is.