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.
The trigger for these balls of cells to turn into ovaries and not testes is genetic. This is what is meant by sex being “determined” by genetics.
Given those genes were inherited at fertilisation, it is reasonable to say sex is determined at fertilisation.
This means you can look at that genetic information in a fertilised egg and understand what will happen in six weeks to those balls of cells, despite the balls of cells not yet existing.
In an IVF clinic, for example, you can sort embryos by this genetic information.
The genetic switch that turns the balls of cells into ovaries and not testes is the absence of a Y chromosome gene called SRY.
The female switch is often conceptualised in the OFF position. That is, unless you have the genes required to flip the switch to ON, you will differentiate ovaries and not testes.
Plenty of developing systems use ON/OFF switches to drive different tissue fates. Sometimes the ON position makes something happen, sometimes it stops something different happening.
ON is not inherently more interesting or important than OFF.
The OFF position is often labelled a “default” pathway.
That is, we ask: what will happen to these precursor cells or this precursor tissue if it doesn’t get positively switched to do something else instead? What do they turn into “by default”?
Because differentiating as male - making testes and not ovaries - requires a positive switch (the SRY gene), female differentiation has been framed as the “default” pathway.
This leads to the claim that because the differentiation of female reproductive anatomy is “default”, the embryo before differentiation of any reproductive anatomy is phenotypically female.
This makes no sense to me; it’s really random.
And while many who anchor sex as a karyotype/genotype argue that embryos are, in fact, female (or male) from fertilisation before any sex differentiation, not even this framework can translate into the idea that all embryos are female at fertilisation.
It is a bonkers claim, leaning heavily into misogynistic ideas that the absence of a penis and the presence of a precursor embryonic outlet tube - the cloaca, in both sexes - means female.
Because females are no-penis cavities, amirite?
In fact, what we know is that female development is not the result of “do nothing”. You need plenty of female-specific, positive signalling to make ovaries. They don’t just drift into existence for lack of anything better to do; they are busy little balls of cells.
The embryonic gonads - the first point of sex differentiation - are bipotential. They are “competent” to differentiate as either ovaries or testes.
Before differentiation, they are no more female than they are male.
Internal genitalia develops from two sets of ducts, one pair that can be fashioned into female bits and one pair that can be fashioned into male bits. All embryos contain both sets of ducts.
This set up is no more female than it is male.
External genitalia develops from a tissue field that is, like the gonads, bipotential.
And again, before differentiation, this tissue field is no more female than it is male.
The wording in Trump’s executive order is fine (well, I dislike “conception” but that’s a minor quibble).
Sex is determined at fertilisation. We can predict the sex class of an embryo well before any sex phenotype develops, and with almost-perfect reliability.
Human embryos do not all start as female. This is a scientifically-illiterate claim.
@Kindun526 But regardless, are you suggesting that de novo mutation post-fertilisation can switch someone’s sex?
How interesting.
How do you assess that their sex has been switched?
@Shatterface I mean, I could make the argument they have converged to the baseline of only one active X chromosome, which is a mechanism to control gene dose in females.
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A cell layer that has developed to protect your body from the outside doesn’t work like a cell layer that has developed to protect your body from the inside.
The cells lining my vagina are not the same cells, and they don’t have the same function, as the ones wrapping your penis.
There’s a name for what happens when you subject dry-adapted “outside skin” to wet-adapted “inside conditions”.
My vagina - “inside skin” - hothouses a healthy microbiome that promotes health and healing, and imparts immune function onto small humans that happen to come out of it.
Yours? Less so.
My vagina is a muscular organ, adapted to my healthy female function of receipt of peen, expelling menstrual products and pushing out small humans.
Let’s move the discussion from available techniques for sex screening and to matters of process.
Ross @Scienceofsport has described the need for detailed technical documents that inform sports federations in robust implementation of a sex screening policy. I’ll link to his video next.
But here, I’m going to take a wander through running an assay, highlighting standards and procedures.
First, this is Ross’ video of the overall process, highlighting the need for coherent implementation practices. He - correctly - evokes the reams of technical documents used by WADA in their anti-doping programmes.
Even the simplest of lab assays can have pages of instructions associated with it.
So, the assay for sex screening will be detection of the SRY gene. This is the ‘make male’ gene that is the master switch for testes-not-ovaries.
The assays out there are very sensitive and specific. That means they can detect SRY when it’s present, and they don’t give a signal when it’s absent. They aren’t 100% on either metric, but near as dammit.
In 2025, Jon Pike and I argued that exclusion of athletes with androgenising XY DSDs from female athletics is justified, because these athletes are male, not female.
@runthinkwrite This followed a 2024 paper where we, along with Ross Tucker, Tommy Lundberg, Cathy Devine and many others, argued for a return to sex screening to secure eligibility for female sport.
@runthinkwrite @Scienceofsport @TLexercise @cathydevine56 This followed another 2024 paper where we critiqued the (now former) IOC policy on inclusion of trans-identifying males in female sports.
Alvares 2025, n=7, fat mass is higher in females as both absolute and relative values. This is logged as "favours cisgender", which is kinda odd because high fat mass isn't usually considered favourable for sports, but whatever.
TIMS: 16.2 kg (24%). F: 19.5 kg (26%).
But Ceolin 2024 is also logged as "favours cisgender" when their values are:
There are little-to-no controls for physical fitness in the individual studies.
Yet they conclude: “transgender women do not exhibit significant differences in upper-body strength, lower-body strength or maximal oxygen consumption relative to cisgender women after 1–3 years of GAHT.”
You haven’t controlled for fitness!!!
Their "performance" data. Can you see one study that really sticks out as an outlier?
The claim that won't die: trans-identifying males are "underpowered" and therefore "disadvantaged" in sport.
"One can imagine a large car with a small engine competing against a small car with a small engine, and that summarizes the playing field." Joanna Harper, Huff Post, 2016.
"You have a bigger body, and you have a smaller engine to move that vehicle around." Yannis Pitsiladis, BBC, 2019.
"giving trans women the disadvantage of having to power larger skeletal frames with reduced strength and aerobic capacity." Jamie Agapoff, 2025.
What happens when a trans-identifying male suppresses testosterone?
They lose a bit of muscle mass.
Their haemoglobin drops to female-typical levels.
The claim that won't die rests on the idea that trans-identifying males retain their skeletal frame and most of their muscle mass, but become unable to move it around a sports fields, rendering them "disadvantaged".
The words "underpowered" and therefore "disadvantaged" are carefully chosen, and typically leave the reader to infer that this means "underpowered" and therefore "disadvantaged" compared to females.