🧵 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:

2⃣ *Bret still claims Covid vaccines are dangerous*

"Vaccines don't stay at the injection site"
"Spike protein is toxic"

Oh well, at least no more exploding rat ovaries, phew.

Here the clip with my comments:

3⃣ *Ivermectin is "natural" because it comes from soil bacteria*

Oh boy, that was quite a WTF moment:

"the fact ivermectin comes from soil bacteria, it's not a
completely synthetic molecule, means that it is likely to be similar to things that one's ancestors...
...have encountered before and there's therefore a good chance that the body has a reasonably elegant way of dealing with it rather than using some mechanism that's not so great"

I just have one comment to that: 🤦‍♂️
4⃣ *Heather has reading comprehension issues and claims we can't tell apart prophylaxis from treatment*

For some reason Heather thinks that the first paragraph in the screenshot of our article is all about prophylaxis.
No, Heather, see the italicized *any* word in the "any significant benefit" phrase? "Any" stands for either prophylactic or treatment benefit, and the reference to the JAMA study is meant to highlight that even as treatment (i.e. not as crazy...
...a suggestion as your proposal of using IVM as alternative to vaccines), IVM has no proven benefit when the clinical trial is done properly.

With that out of the way, the next paragraph then dives into the prophylactic comparison of IVM to vaccines, and it's not even close.
5⃣ *B&H still tout the Carvallo IVM prophylaxis study*

Yeah, the SARS2 origin skeptics suddenly seem to trust even the most unbelievable of studies when it comes to IVM.

Here is the clip and a detailed thread:

6⃣ *Heather claims that correlation between declines in cases and IVM use is "really good evidence" for IVM efficacy*

Yeah, this is just a clear example of mistaking correlation for causation with cherrypicking on top.

You know that cases rise and drop all the time, right?
There were plenty of other places which didn't use IVM and cases still fell. Like in Russia, or Sweden after the second wave. These countries didn't use IVM, didn't have lockdowns, Russia's vaccination rate was (and still is) dismal but numbers still fell.

So, no, not evidence.
7⃣ *Heather doesn’t understand IVM's teratogenicity, or drug development*

Here's a clip and a detailed thread:

8⃣ *Heather didn’t read or understand the papers on IVM’s testicular toxicity*

Yeah, another double standard: rat ovaries are important but rat testicles... not so much.

Clip/thread:

9⃣ *The Deigin Threshold or how IVM can do its magic without being present in the body*

Is IVM secretly a vaccine pretending to be a small molecule? Bret hints it might be.

🔟 *Heather reads a chapter from their book which further reveals their anti-scientific beliefs*

1⃣1⃣ *IVM could somehow interfere with vaccine effectiveness*

Yeah, B&H were far off into conjecture land by then.

1⃣2⃣ *Large-scale randomized controlled trials are very very expensive*

A good trial does not need to be "large scale". And randomization and double blinding don't add any significant overheard to a trial.
1⃣3⃣ That's all, folks!

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More from @ydeigin

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
13 Jul
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.
Read 10 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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