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?
Alvares 2025, a study of 7 self-selected, trans-identifying males, who were 5cm shorter than the female comparators. Which is weird. The authors note this.
Also, they played lower level volleyball for about 30% of the hours put in by the female cohort. The authors consider that training volume and competitive level is, indeed, a confounder.
It's interesting when assessing lower body strength, this recent paper uses only jump heights and seems to ignore explosive power measurements.
That is, while acknowledging low-to-no control for fitness, they use a "fitness"" output instead of raw data like muscular power.
Why might unfit people not jump very well? Hmmm.
A spectacular pair of sentences.
Manipulating stats by adjusting for a sex difference is dishonest.
The bit about "not accompanied by increased functionality" is just riffing. They haven't provided evidence that functionality is impaired because they haven't compared like-for-like in terms of fitness.
I dispute "absence". Especially when you've ignored metrics like power (peak and relative).
They apparently ignore the second paper (Chiccarelli 2023) on an expanded USAF cohort, that showed advantages in push ups and sit-ups remain after two years.
Perhaps this tells us something about the cohort/type of data? Hmmm.
My friends, there is power data out there. Including in some of the papers you use.
He was the first author on a paper led by Peter Goodfellow, and they published side-by-side with a paper led by Robin Lovell-Badge.
This pair of papers showed that the “mysterious make male mammals molecule” was the product of the SRY gene.
Unequivocally.
Their joint discovery was hailed, including by Sinclair himself, as the answer to one of the most fundamental questions about human life: what makes us male or female?
This is, IMO, an entirely reasonable lauding of the impact.
Persistent Müllerian Duct Syndrome is a DSD that occurs in 46,XY males with normal testes and normal virilisation, who also retain Müllerian structures (uterus, cervix, fallopian tubes, upper vagina) that should have degenerated in utero.
How does it happen?
Early in development, every fetus has two duct systems: the paramesonephric/Müllerian (female) and mesonephric/Wolffian (male).
(The formal names will become relevant later).
In XY babies, carrying the “make male” SRY gene, testes are made on schedule.
These testes make testosterone that promotes development of the Wolffian ducts, because testes will need an epididymis, vas deferens and seminal glands to do their fathering job.
I think the Andes hantavirus data is being misread right now.
Claims are circulating that the evidence doesn’t seem to support.
I want to walk through them carefully.
The 40% fatality figure: an artefact of who gets counted.
The 40% case fatality rate (CFR) figure comes specifically from hantavirus pulmonary syndrome (HPS), an outcome in a subset of hanta infections.
This is the severe cardiopulmonary presentation. It excludes subclinical infections that resolved without anyone noticing more than “a touch of flu”.
In Jujuy Province, Argentina, the seroprevalence (rate at which people have antibodies due to hanta infection) is 6.5%. Hospitalised HPS cases had a CFR of 13.3%, but most patients were described as having a mild clinical course.
Disclaimer: although an Argentine outbreak, this has not been confirmed as ANDV.
The 40% is the fatality rate among people sick enough to be diagnosed and hospitalised.
It is not the infection fatality rate.
These are not the same thing, and conflating them is causing significant confusion.
The true attack rate: barely any data.
The Boat had approximately 180 exposed individuals, and around ten cases have been detected. Three - soon to be four, I predict - have died.
Without antibody analysis of the full cohort, we don’t know how many mild or subclinical infections were missed entirely.
Disclaimer: I am a biology PhD, but not virology/epidemiology. Husbandman is a virology PhD. But I’m told I’m good at communicating science, so here’s my take.
#Hantavirus
Humans get hantavirus from rodents who carry it.
Some people went to Argentina birdwatching in a landfill, and were exposed to hantavirus because rodents like landfills.
Looks like one - if not two - people brought the virus onto their cruise boat.
So now we have an isolated boat with an index case: someone who is infected.
That’s not good for the index case. Hantavirus has a high fatality rate, and that’s scary.