Caster Semenya: The three aspects to consider on testosterone rules that do not justify discriminating against her
I served on Semenya’s legal team as an expert witness in her Court of Arbitration for Sport appeal that ruled against naturally occurring genetic variation despite not assessing how this affects testosterone levels
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I was asked by Caster Semenya’s legal team to serve as an expert witness at the Court of Arbitration for Sport in Lausanne. She had challenged the new regulations of the International Association of Athletics Federation (IAAF) on the eligibility of athletes with certain ‘Differences in Sexual Development’ (DSDs) and naturally high levels of testosterone to compete in the female category.
The regulations mean that most women with DSDs cannot compete in certain running events, or must have medical treatment to lower their naturally occurring high levels of testosterone for at least six months before competing.
The case was about DSD athletes and not about transgender athletes, although there are clear links between the two categories of athlete.
I saw three aspects to the case:
- Are the kinds of genetic mutations found in DSD women comparable to or clearly different from other genetic mutations not affected by the regulations?
There is a range of DSD categories, each with their own causal genetic mutations. But a multitude of other genetic differences exist between people within a population and between populations. Everyone (except identical siblings) has unique DNA that interacts with our environment to affect our physical appearance, behaviours and physical capabilities.
The genetic mutations found in DSD women are entirely comparable to those we all possess – it’s just that the majority of our mutations don’t affect our sexual development, so sport doesn’t have regulations about them. In terms of sport performance, some of the genetic mutations found in DSD women are likely to give them advantages over most of their competitors. But other athletes also possess genetic differences that give them equivalent advantages over competitors – for example, increasing the ability of muscle to produce force quickly that is essential in sprinting, increasing muscle size or increasing the blood’s ability to transport oxygen to muscles.
So the genetic mutations found in DSD women are not exceptional and are comparable to other genetic differences not affected by any regulations.
- Do any performance advantages DSD women gain from increased testosterone make them equivalent to men?
Elite men outperform elite women by approximately 10 per cent in sports that have a major reliance on physical strength or endurance. One key biological difference between most men and most women is certainly testosterone level - in women it is usually less than 2nmol/L compared to 8-30nmol/L in most men. Higher testosterone levels usually do improve most aspects of physical performance, especially when comparing typical male levels to typical female levels. Smaller differences in testosterone within the normal male or female ranges don’t seem to have much effect on performance.
However, the degree of performance advantage provided by higher testosterone in DSD women is not always the same. For example, some categories of DSD women have only partially elevated testosterone so even on that simple basis they are not equivalent to men in terms of their potential for sport performance.
Other DSD women have testosterone levels in the typical male range but do not process testosterone in the same way as men. For example, one category of DSD is 5-alpha‐reductase type 2 deficiency, caused by a genetic mutation on chromosome 2. Due to that mutation, those individuals produce little or none of the enzyme that converts testosterone to dihydrotestosterone (DHT). DHT has direct effects on muscle structure and function as well as oxygen-carrying capacity of the blood and has been on the list of prohibited substances of the World Anti-Doping Agency (Wada) for many years. Ben Johnson, the Canadian sprinter, was stripped of the 100m gold medal at the 1988 Olympics because he used Stanozolol, a drug derived from DHT.
So DSD women with 5-alpha‐reductase type 2 deficiency can have testosterone levels of a typical man but don’t benefit from all of its performance-enhancing effects because of limited/no ability to convert it to DHT. They are not equivalent to men in terms of potential for sport performance.
- If testosterone levels alone are not a valid way of separating male and female categories in sport, what is?
The World Health Organisation (WHO) clearly states that no single biological factor determines sex. Sex is determined by a combination of genetic and other factors, including hormone levels and anatomy. WHO clearly states that while males usually have XY sex chromosomes and females usually have XX, there are also XY females and XX males.
In fact, there’s a range of DSDs that can involve either rare combinations of sex chromosomes (e.g. XXY or XYY) or genetic mutations on other chromosomes that affect sexual development. Thus, no single factor, genetic or otherwise, neatly determines whether an individual is male or female. Furthermore, no formula exists that uses genetic and other data to produce an answer of whether someone is male or female. The IAAF regulation disregards this reality and was surprisingly unenlightened considering the chequered history of genetic sex testing in sport.
It seems clear to me that if someone was assigned female sex at birth, has been reared and socialised as a woman, wishes to remain a woman, has always been legally recognised as a woman and has always competed in sport as a woman, they should be permitted to continue to compete in the female category without discrimination. I do not believe that a naturally occurring genetic variation in such a woman, regardless of whether it affects testosterone level or physical performance, justifies discrimination.
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