So the Weinstein household is “a lot skeptical of pills”. Why? Based on Bret’s grad school “discovery” that lab mice have longer telomeres than wild type mice and so he made the leap that this somehow translates into a greatly improved capacity of tolerating toxic insults.
The next giant leap for Weinsteinkind is that this greatly improved capacity of tolerating toxic insults translates into toxicity being somehow underestimated for approved pharmaceuticals. Bret, even if lab mice *were* more tolerant of toxicity, have you heard of Phase I studies?
Phase I studies are clinical trials in healthy human volunteers designed to assess the drug safety in — wait for it — humans, precisely because animal testing does cannot guarantee human safety.
Moreover, for a drug to be allowed for Phase I studies, it must be proven safe in MULTIPLE animal species. Anyone with even a hint of drug dev experience knows this. That you didn’t bother to look into it but decided to fear approved meds based on your conjecture speaks volumes.
Now, concerning your conjecture that longer telomeres somehow better protect from drug toxicity. This is just ridiculous. Toxic substances kill not because of short telomeres. Telomere length also does not determine reparative capacity.
I won’t even get into the fact that fast-dividing tissues, progenitor cell populations, and stem cells all have active telomerase expression, which can elongate telomeres on demand.
Finally, even your “discovery” that lab mice somehow have critically longer telomeres than wild type mice is wrong and irrelevant. Tlmr len is highly variable even bw individuals, and it doesn’t affect much. Moreover, bw species, those with SHORTER telomeres actually live longer.
Many animal species have much longer telomeres than humans, and both mice and rats have very long telomeres, but squirrels have even longer ones. Have they been lab bred too?
In conclusion, it is very telling to see how you’ve been clinging to one erroneous conclusion for many years, and have built a whole narrative of lack of drug safety based on it. This explains well your fear of GMOs and “non-natural” chemicals. But this is not science.
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More from @ydeigin

13 Jul
🧵 RESPONSE THREAD TO @BretWeinstein and @HeatherEHeying Podcast #87

In this thread I will collect all of my responses to B&H's key counterarguments as I heard them on their podcast #87 today:

1⃣ *Bret thinks drugs are dangerous because telomeres*

This part set the stage very well for the festival of incompetence that the podcast turned out to be. Incompetence in drug development, pharmacology, data analysis, statistics, reading comprehension and even basic biology.
Here is the relevant clip and my analysis of Bret's telomere hypothesis:

Read 19 tweets
13 Jul
That’s why I do this.
Read 5 tweets
13 Jul
And here is the ultimate embarrassment — drawing parallels between how ivermectin might work and how vaccines “don’t depend on their concentration in the body”. Seriously??
To hypothesize even for a microsecond a parallel between the mechanism of action of a small molecule and a vaccine betrays a glaring misunderstanding of biology.
Also, just because *you* don’t know the pharmacokinetics of ivermectin doesn’t mean I didn’t bother to read the papers on it.

It’s quite clear the drug is eliminated from the body in exponentially decaying fashion with the half life being approximately 18 hours.
Read 9 tweets
13 Jul
Ah, the Carvallo Argentinian study that Bret and Heather still seem to trust.

Not sure where they see cowardice or unclear messaging. I have said many times that I don’t trust that study for a second.
And no, I don’t mistrust it because it was “too good to be true”, I don’t trust it because

(1) there’s a huge disparity between the control and treatment group infection rates (0% vs 92% for one hospital), while the background infection rate was 20% in hospital personnel.
(2) their findings are a huge outlier among the dozens of other studies assessing prophylactic efficacy of ivermectin.

Only a naïve person would think that this study must be true while all others must have had some methodological shortcomings.
Read 9 tweets
7 Jul
1/5

@BretWeinstein claims we know how IVM works because it binds the SARS2 spike protein. Is he correct? No.

The only evidence we have for IVM binding the spike comes from a computer modeling:
2/5

The computer model predicts that IVM binds to L91 of the 1300 aa spike AND that it binds to the ACE2 receptor.

ncbi.nlm.nih.gov/pmc/articles/P…
3/5

Where is L91 located in the spike? In NTD (blue), which it pretty far from the RBD (green) that interacts with the ACE2 receptor.

But it is also predicted to bind to the receptor itself! Isn’t that why people think the spike is toxic, as it interferes with ACE2 signaling?
Read 5 tweets
17 Jun
😱 Whoa. Could SARS2 have been an early ANIMAL vaccine candidate? A self-transmitting one.

And FCS was inserted to expand species tropism and thus enable its transmission between species?

nature.com/articles/s4155…
@SharriMarkson have you heard about Australian self-disseminating vaccine efforts mentioned in the above paper?

Also, doesn’t WIV long-time collaborator Linfa Wang work in Australia? Maybe you could talk to him. Image
I mean SARS2 already exhibits signs of cold adaptation which is a hallmark of vaccine attenuation (to make it prefer the upper respiratory tract, infection in which is less likely to be severe of fatal):
Read 4 tweets

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