Anyone wishing to spot changes from our pre-print:
1. We included a section on pre-pubertal differences (that is, even young boys outperform young girls, thus the performance gap is not solely down to pubertal T).
2. We extended our analysis of CV capacity changes and potential impact on endurance performance (although we had acknowledged a likely effect, we have drilled deeper into mechanism).
3. We have *significantly* extended our discussion of impact on athlete transwomen and the mitigating effects of exercise (that is, moderate training can mitigate or even reverse muscle/strength loss during T suppression).
The remaining differences are minor, and represent no significant change from the pre-print.
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.
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.