You have this backwards. They are saying to stay away from ibuprofen, not aspirin.

Which of course is a theory that is being walked back.

https://science.sciencemag.org/content/367/6485/1434.1

See also Wired: https://www.wired.com/story/the-ibuprofen-debate-reveals-the...

My mistake. Why would I have thought that a cyclooxygenase-inhibiting NSAID would have anything to do with a cyclooxygenase-inhibiting nsaid. These are entirely different kettle of fish, and I am a fool for thinking adverse effects of one would be at all related to the adverse effects of the other.

I was mistaken, and got snarky about it to boot. I was in a shit mood. Sorry.

This study was done in vitro. If I recall the counterindication of aspirin in C19 patients was accelerating pneumonia or something. So it's possible aspirin does both.

Look with suspicion on any in vitro data. There are so many differences between in vitro and a living organism. Nevermind the fact that in vitro tests usually use concentrations that would never be achieved in the body, a fact usually lost on the public. I’d definitely lean towards the “aspirin is bad with Coronavirus” camp on this one.

Source: Myself, a former tester of in vitro effects.

> Nevermind the fact that in vitro tests usually use concentrations that would never be achieved in the body, a fact usually lost on the public.

But the reason large doses are used in vitro is because it's easier to show that a chemical actually inhibits viral replication if you can slow down replication by 99.9%. But in real life, you might only need to slow down replication by 10% or whatever to meaningfully improve clinical outcomes.

That's true in theory and we should see aspirin doing something in vivo for coronavirus if it did, but we don't. Something else more important seems to be affecting it the other way.

In skimming the article it seems they used 20 mM doses and ranges which is an absolutely enormous amount of anything. We normally considered low uM the range where something is even beginning to be interesting.

Yeah about the in vitro thing.. I'm sure gasoline also kills the corona virus. Unfortunately the patient also goes.

Aspirin is a blood thinner it might cause your lungs to bleed once they sustain enough damage to their epithelial layer which might make your pneumonia worse.

>This study was done in vitro. If I recall the counterindication of aspirin in C19 patients was accelerating pneumonia or something. So it's possible aspirin does both.

Relavent: https://xkcd.com/1217/

Is there actual good data on aspirin/NSAIDs? Because what I've read was a theory communicated in a letter to the Lancet, and the actual data might suggest the opposite.

One of the first victim in Turkey wrote her twitter she was using vinegar and aspirin solution before she passed away. But she had also some permanent sickness which i can not recall. I also wonder how ahcc plays well with it because i have been using since a month and had asymp symtomps since 10 day so far i can say i recovered and my gf shows no symptoms at all (she is also using) atm asked my gp and waiting response him.

According to the Medcram youtube series, NSAIDs in general are known to impair virus replication, but also impair immune function. What is the net result? That is less clear. Many believe that aspirin had a negative effect during the 1918 flu epidemic though.

Video link here: https://www.youtube.com/watch?v=dT6mHi_8V5E

Apparently aspirin contributed to fatalities via aspirin poisoning, so it did not necessarily have a direct impact on the virus.

Reference: https://en.wikipedia.org/wiki/Spanish_flu#Aspirin_poisoning

According to https://academic.oup.com/cid/article/49/9/1405/301441, the aspirin doses that were used in 1918 (8.0 - 31.2 g/day) were much higher than what people normally take today (usually a max of 3.6g or so).

In this study the aspirin used is actually a salt of aspirin, tradename is Aspirin I.V.