Hacker News Reader

Comment by Infinitesimus | Hacker News Reader

Attempt at a simple summary:

From what I see, low testosterone is a risk because there is a strong link between lower respiratory muscle activity and lower testosterone levels and high testosterone is a risk because high test -> more androgen receptor expressions -> more binding opportunities for TMPRSS2 and that gene seems to be an active factor in transcription of covid-19.

Its not a magic bullet but the TMPRSS2 angle is quite interesting since we could target drugs that temporarily minimize androgen receptor affectiveness to control the spread ( which might complicate other things in the meantime..)

Tangent, what's the state of drug discovery when it comes to simulating interactions of hormonal treatments with cells?

View on HN

>> we could target drugs that temporarily minimize androgen receptor affectiveness to control the spread

Modifying key hormone functionality across the population, what could possibly go wrong? The impact on other diseases, not to mention behavior, is huge open question.

Presumably this would only be done for those found to be at risk based on tested testosterone levels.

Fortunately the linked paper doesn't recommend it, only notes the stats and details and concludes that "The elucidation of the role of testosterone in the battle towards COVID-19 infection turns out to be an urgent need."

Seems pretty even-handed to me.

That's the difference between treating patients and reducing spread. Appling a preventative to a small population of at-risk individuals will help them individually but won't decrease spread with the population, won't decrease their exposure. That requires preventing the infection from spreading amongst all people, including those who are at no real risk.

This is one of those special situations where one contemplates a applying treatment to patients A B and C not to protect them from harm but to protect them from spreading something to patients D and E. The ethical difficulty is how one balances the potential increased in risks to ABC against the benifits to DE. What if hormone therapy to ABC reduces their lifespan? What it if causes long term behavioral or repoductive changes? How should that be balanced against D and E's chances of infection/death?

Remember that any widespread COVID therapy will likely be with us as long as the disease. Altering hormone levels across a population, potentially for many years or even decades, is a radical approach. And to think of altering testosterone amongst the reproductive-aged population, potentially modifying sexual development of exposed children too, to safeguard those beyond reproductive age from COVID? That's a very dangrous area.

I mean the effects of spironolactone and cyproterone on people who are AMAB are well understood and any doctor in the country can titrate your dosage to get you at specific levels. It's not without effect, obviously, which is why trans women take it, but it's not unsafe or dangerous.

The distribution of testosterone in AMAB people ranges ranges from about 200 to 1000 ng/dl so there's a massive range for "normal" levels and trans women are proof that you can go much much lower for an indefinite period of time.

None of this is to say that this course of action is a good idea or would meaningfully help the spread of the rona but it's not as much an open question as you're making it seem.

The article doesn't say that low testosterone is a risk, it says that low testosterone might be a risk.

You also ignored the entire half of the article which says that high testosterone also might be a risk.

Looking forward to the cyproterone shortages after people start trying to suppress testosterone to avoid catching covid.

Reply on news.ycombinator.com