Emma Hilton Profile picture
Aug 12, 2020 6 tweets 1 min read Read on X
Unpopular opinion incoming.

A matter of months ago, the NHS were advising that puberty blockers were reversible.

It is not unreasonable for the average person to take this on authority and to share this as an authority view.
It is not unreasonable for medics, scientists and other relevant experts to question the NHS advice on puberty blockers, and to draw attention to inaccuracies or misrepresentations.
It is not unreasonable for the NHS to alter or update their advice on puberty blockers after a fuller assessment of the evidence laid before them.
It is not unreasonable for those people who rely on the NHS as an authority opinion to remove/alter what they may now consider outdated, inaccurate and/or potentially harmful shared information to reflect more recent medical advice.
I am not blind to the politics and motivations here. And I think it's reasonable to question why people we might expect to "know better" (i.e. to have conducted their own research into puberty blockers) maintained a "party line".
I am simply pointing out that there are many more who simply quoted the NHS medical advice. And that is a perfectly reasonable thing to do.

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More from @FondOfBeetles

Jul 22
On Sinclair, SRY and the destruction of a legacy.

In 1990, Andrew Sinclair was the first author on a paper that reported the discovery of SRY as the gene that drives male development in mammals.
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.
Read 21 tweets
Jul 21
I recently spoke at the 2026 International Working Group (IWG) on Women and Sport.

Here are my slides. Image
Sport seeks to identify and reward talent.

We want to find the best swimmers and the best boxers. Athletes with the physicality, skill and mental strength to win.

And we identify and reward talent by measuring performance.

But performance is an output, and not just of talent. Image
Nurturing matters. Environment matters. Having an athletic parent matters.

Nurture can obscure talent.

But differential nurture is, at least in principle, fixable. Image
Read 22 tweets
Jul 20
A thread on PMDS 👀

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.

The Selfish Testes. 🤣
Read 15 tweets
Jul 13
We wrote to Amnesty @amnesty @AmnestyUK about their reports containing defamatory slurs against Sex Matters and others.
So did For Women Scotland. @ForWomenScot
@ForWomenScot So did LGB Alliance @AllianceLGB
Read 21 tweets
May 13
On hantavirus #ANDV #hantavirus

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.
Read 21 tweets
May 7
On Hantavirus: a (non-technical) thread.

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.
Read 20 tweets

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