I'll document this case of aggressive dishonesty from @AviBittMD as a reference for why I will no longer be engaging him in the future, as he's heavy on the insults and light on the substance.
So, he claims that my claim was false because remdesivir succeeded in a similar trial.
To disprove my claim, he brings up a study that had even later start of treatment, and indeed succeeded at its primary endpoint. But that endpoint was very different (time to recovery) so not really the same study design.
@Grinman helpfully noted this, and got abuse back.
In his abusive response, he notes another study he referenced. Patients with 5 days from symptom onset, and title mentions "progression to severe disease".
When we try to see what they mean by "progression to severe disease", we see their endpoint:
"The primary efficacy end point was a composite of Covid-19–related hospitalization or death from any cause by day 28"
The I-TECH study had a super-early endpoint, that in the ivm group triggered in 3.2. days after start of treatment. So, the average patient didn't even have time to complete the treatment.
In fact, the I-TECH definition of severe disease classifies only as "mild disease" by the standards of the WHO.
The 2nd remdesivir study used nonhospitalized patients, and the endpoint was, roughly "hospitalization or death"
The ivm study used mostly (I think) hospitalized patients, endpoint was "does a Dr think you need oxygen to not drop below 95%"
The definitions of "severe disease" are very very different in these two studies. Also, the nonhosp. patients in the remdesivir trial were obviously in better condition, as none of the control group died, whereas in the similar sized I-TECH study, 10 died in the control group.
My entire point is that patients that already have significant momentum, combined with an endpoint that is super close to their initial condition, will not give an antiviral enough time to act. Again, my figure:
His response, other than vile insults, is a study with patients that are clearly in better shape, and an endpoint that is harder to trigger (and indeed, only 15 triggered it, even in the control group, vs 43 control group pts that triggered the endpoint in the ivm trial)
Now, everyone makes mistakes. That's not a problem.
The problem is his disgusting attitude, dripping with condescension and ridicule. Victory lapping and insults without even a hint of doubt or self reflection.
Attempting to discuss with this person constantly puts me in situations where I have to deal with sophisticated sophistry, and the payoff for showing him to be in error is nothing of value to me.
I have tolerated him thus far as I do believe pushback is valuable.
This stuff isn't honest pushback though. It's grandstanding in the hopes I won't have time to dig in, or at best, without actually understanding my claim or the studies he cites.
This isn't useful, and I don't owe him my time.
Aaand responds with a classic goalpost shift.
I couldn't conclude our interaction with a better demonstration of this man's inability to admit an error.
A 🧵 of cases where data has been withheld or updates suspended, explicitly because the Authorities did not want the Commoners to "misunderstand" and "misinterpret" it.
As usual, I'll start with the ones I know, and please respond with more cases you are aware of.
Let's do this slowly for the people in the back: @BretWeinstein was commenting on a piece by Scott Alexander which picked through many ivm RCTs and did a meta-analysis to show there is a very weak signal. Then he threw the worms hypothesis on top to explain the signal.
This is a huge shift in epistemic standards. We're going from published, most peer reviewed, randomized controlled trials, many of which have been pored over by opposing groups, and trying to explain them away with a hypothesis that existed as a set of tweets. Epistemic whiplash.
As for my position on Ιvermectin, it's been consistent since the summer. We don't know if it works or not because *appropriately sized studies with correct dosing and timing* aren't being done. But it's safe enough that it's not worth not giving.
You can see a prior review of the evidence I did a couple of months back here, showing that there is a clear, if uncertain, signal of efficacy. doyourownresearch.substack.com/p/a-conflict-o…
The real scandal is that the proper authorities don't seem interested in drugs like this, or even fluvoxamine, which has even stronger data.
Run a trial with the same parameters as Paxlovid or Molnupiravir. It can't be impossible, it's been already done for those medicines.
Briefly, an antiviral started avg 5.1 days after symptom onset, with a primary endpoint that is triggered 3.1 days after start of treatment, when treatment is for 5 days, will be almost impossible to show benefit.
The avg patient didn't even have time to complete the treatment.
In the case of Paxlovid, the average patient in this trial would not even have been eligible to receive Paxlovid, since they would have been deemed "too late". fda.gov/media/155050/d…
True. It only prevented death (3 vs 10) and ICU admission (4 vs 10). But who cares about that if it doesn't prevent... (*checks notes*) drop in O2 levels below 95%?
Did anyone claim it did that?
Read the results of the study yourselves and then the conclusions... 🙄
Some required reading for all those playing with words like "statistically significant" without any understanding that those words have a specific technical meaning that is not the same thing as what we mean by "significant" in everyday life.
The trial had decent dosing and recommended taking the medicine with a meal, which is good practice. On the minus side, people were enrolled 5.1 days after symptoms. Which means the average patient would've been excluded from the Paxlovid & Molnupiravir trials for being too late.
How much spike protein is produced in the body as a result of mRNA vaccination and how does it differ from ancestral SARS-CoV-2 spike? This will be one of the most important questions to answer moving forward. It will tell us a lot about the side-effects, among other things. 1/