In defence of Semenya et al, many argue: 1. athletes with 5ARD are female; 2. features associated with 5ARD are normal female variation; 3. these athletes should be included in female sports.
The first claim is incoherent.
To understand 5ARD, let's look at healthy reproductive development.
Both male and female development are well-understood.
Male development 1. Y chromosome carrying functional SRY that directs testes development 2. testes produce hormones, notably testosterone (T) 3. T first drives male internal genitalia development 4. T>DHT conversion drives male external genital development
Female development 1. No Y chromosome and no SRY, so ovarian development is triggered 2. low/no testosterone production from ovaries 3. female internal genitalia can develop in low/no T environment 4. female external genitalia can develop in low DHT environment
I often describe reproductive development as:
Sequential | structures develop in a known chronological order
Coordinated | reproductive anatomy develops as a system, with each part linked mechanistically to others
The "cluster account" of sex attempts to classify individuals by the sum of their parts.
"These Male Bits plus Those Female Bits equals This Sex."
This completely ignores developmental biology, which describes the sequential, coordinated development of a functional system.
So given a functional account of sex that actually reflects biology, let's look at the disorder of sex development that is 5ARD.
The sequential development of 5ARD is mapped against healthy sex development here.
Keen eyes will spot that I omitted the word "coordinated" when describing 5ARD.
That's because it's not coordinated. There has been a break in the chain of development.
And that's because people with 5ARD are missing the enzyme needed in a healthy male to convert T>DHT to make a penis.
External genitalia differentiate from a bipotential tissue field.
A DHT signal (in healthy males) pushes the development of that field towards a penis and scrotum.
No DHT signal (in healthy females) pushes the development of that field towards a clitoris and labia.
People with 5ARD have mutations in a gene called SRD5A2 and this means the enzyme converting T>DHT doesn't work properly.
As a result, people with 5ARD have defects in external genital development. We say they are undervirilised (virile = manly 😉) compared to healthy males.
People with 5ARD might have some, low or no DHT.
This means that external genital field might develop as clearly male but with issue like a micropenis, but it might also develop to look like that of a female, or ambiguous between the two.
Consider a person with 5ARD and male external genitalia.
Now work backwards along their developmental pathway. Mostly typical, except for the mutation that has affected penis growth.
Of course, as a male, they have XY chromosomes and an SRY gene and testes and so on...
What about those argued to be female?
Well, they've got a ton of stuff wrong with them.
Their genetic information is all backwards. How odd.
And their hormones? OK, they are up in male range and that's unusual for a female.
And their anatomy? Apart from their external genitals, it's all atypical, unusual, aberrant.
None of the "female" schema makes any sense in terms of developmental biology.
Why would you anchor the endpoint metric as "sex" and therefore have to label everything else about the system "wrong", rather than acknowledge that the endpoint metric may be the issue here?
Especially when you know precisely why that endpoint metric has emerged.
But further, advocates of 5ARD as "female" must face up to the implications of their claims.
A male with 5ARD has a mutation in SRD5A2, and this gene is required for penis growth. This is simple, and maps perfectly onto well-established developmental processes.
"This is the chain, here is the break, this is the result."
A female with 5ARD however? The genetics world will be shook, I tell you.
Because she can't have a mutation in SRD5A2, can she? After all, the sequence she carries is perfectly concordant with being female.
Further, SRD5A2 must now be considered the master switch of sex determination in humans.
Not only that.
Possession of what was previously thought to be a perfectly healthy XY karyotype is now a chromosome defect, and possession of what was previously thought to be a perfectly healthy SRY sequence is now a mutation.
The special pleading is bonkers.
What they desperately try to argue is female with a ton of disparate features is actually, quite simply, male with a vulva.
Learn some dev bio, would be my suggestion.
Even further, according to their schema, Semenya doesn’t, in fact, have 5ARD.
😂
I’m reminded of this passage from Eve by Cat Bohannon.
Genetically male, but external appearance of girl. “They have two testes where their ovaries would normally be”.
Their ovaries wouldn’t normally be anywhere. Ovaries are not part of their developmental sequence.
The chain break is downstream of them being genetically male and having testes.
And the chain break has resulted in them having a vulva where their penis would normally be.
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In our recent paper (cited by World Athletics @sebcoe) calling for the reintroduction of sex screening in the female category, we make it very clear that this type of screening must be:
1. Cohort-wide | performed in all athletes wishing to enter the female category, regardless of skin colour, religion, nationality etc.
2. Early | to protect privacy and dignity, and avoid athletes being front-page news.
With these parameters in mind, the sex screen itself cannot be considered “racist”.
Citing historic ethical issues won’t wash. We all acknowledge these. Early, cohort-wide screening will avoid the failures of the past.
So the cry of “racism” must be aimed elsewhere, presumably anchored on the premise that previous targeted screening (which is precisely what I and others advocate against) brought multiple black athletes and very few white athletes to our front pages.
Now, let’s grant that and think about what that means.
The charge against me and others is that we are “policing sex” in a way that excludes black women (when measured against “white femininity”).
My friends, I am here to tell you that I - an adult human female with white skin - am precisely the same quality and amount of female as any adult human female with black skin.
Black women aren’t female by some weird voodoo. They are women in precisely the same way as white women are women.
In fact, it starts to look a bit racist on your part to suggest that black women aren’t women in the same way as white women are women.
In sport, we are interested in the effects of male or female development on the body, not the booty.
The category boundary between males and females is male-pattern androgenisation - having testes that make testosterone (T) and a functional T response.
Disorders of sex development (DSDs) affect reproductive development, and sometimes challenge legal and social sex classification.
5ARD, for example, means a male baby doesn't make the hormone required for penis development. The baby may be misclassified as female at birth.
But there is no evidence that having 5ARD means you don't go through normal male "rest-of-body" development, and this gives performance advantages in sport.
At the level of anatomy, “female” describes a particular reproductive system - eggs in ovaries, oviducts, uterus, cervix, vagina and vulva.
This reproductive system begins to differentiate at around six weeks post-fertilisation, when the embryonic gonads - two balls of cells clumped in your pelvic area - turn into ovaries and not testes.
The ongoing development of internal and external genitalia follows this gonadal differentiation into ovaries.
This is what is meant by “organisation” - the coordinated, sequential development of multiple tissues that have evolved around a given reproductive function.
I ran a fairly straightforward analysis of track and field performances across junior ages in different track and field competitions.
The raw analysis looks like this for international records. Above the line is male advantage, below the line is female advantage.
This pattern its repeated across national and state-level competitions. You can see that for almost all events at all ages, boys hold advantage over girls.
Where female advantage is detected, this is easily explained.
At 10 years old, girls grow ahead of boys, and catch up/overtake them briefly in running.
The female advantage in discus at 15-16 years old is because girls throw lighter implements.
The distance drop off as boys move to the 2 kg discus is obvious.
But actually, while these data are good for getting a handle on the magnitude of advantage, I came up with a slightly different question to ask of them.
With help from @johnarmstrong5, I came up with a null hypothesis: if there is no difference between boys and girls pre-puberty, the frequency of boys and girls "winning" should be around 50/50.
So I collapsed the performances as wins or losses. See below for international records, scored as wins for the boys above the line and wins for the girls below the line.
Let’s have a think what hormone categories looks like. And let’s assume that @neiltyson is considering a high/low T category. This has also been proposed by @AliceDreger
The proposal only works if you don’t deny evolution and sexual selection. Remarkably, there are academics who argue there is no biological basis for why males run faster than females. While it is plausible ongoing underinvestment in female sport means female athletes have not yet reached their full potential, it is frankly ridiculous to think this can explain the entirety of the performance gap.
See Sheree Bekker et al for more details on why, because one time, this one female figure skater won a medal, Usain Bolt should be allowed to race against females.
The proposal only makes sense if we recognise that the action of T on a body gives advantage in sport. This is by no means universally-accepted. Many humanities types argue T is not a key part of sports performance, citing males with low T and people registered as female with high T. Even though both phenomena are explicable by factors like illness, doping and male DSDs, still this argument persists.
See Veronica Ivy, Katrina Karkazis et al for why we should pretend that the stupidly high prevalence of weightlifting males with low T is not because they have just finished an off-period jacking up.