In this 186th in a series of live discussions with Bret Weinstein and Heather Heying (both PhDs in Biology), we discuss the state of the world through an evolutionary lens. In this episode we discuss the mechanism of action by which the mRNA vaccines cause heart damage, following the publication of relevant research in Science Immunology. We discuss the nature of science, both empirical and theoretical, and why the eclipsing of theoretical science by the empiricists is dangerous. We disc...
Hey folks, welcome to the Dark Horse Podcast live stream 187.
Why are we so slow today?
What?
186.
186?
Yes.
Oh, okay.
186.
All right.
Yes, it is the 186th live stream.
I'm Dr. Brett Weinstein.
This is Dr. Heather.
We're on super speed.
Okay.
All right.
Apparently the dial which adjusts my speed has been set on the setting in which it makes large jumps rather than small jumps.
We're going to dial this in over the next few minutes.
There we go.
Don't worry too much about it.
All right.
But anyway.
It is 186.
I believe, unless I've got that wrong.
It's 186 in the shade.
Let's not linger on that question, right?
You are Dr. Bret Weinstein.
I'm Dr. Heather Hying.
Here we are with the livestream evolutionary lens of the Dark Horse Podcast.
We've been coming at you with this for a good A long time now.
Yes.
Over three years.
It has been over three years.
And we're just, we're just going to keep on going.
So you can join our watch party at Locals right now, or you can join in what would be a chat elsewhere.
But that is, that is the, the place, the only place that the chat is happening.
And we encourage you to join our Locals for both that reason, and because the private Q&A that we've been doing at my Patreon for almost three years, or actually over three years now, We're going to be moving to our locals as of this month, so that'll be on the last Sunday of the month, and we very much encourage you to go there, and you'll also be able to get to our Discord server there from our locals.
We're going to talk about all the other places that you can find us and such at the end, but for now, we'll also do a Q&A, live Q&A, after this episode.
The one remaining piece of business that we want to talk about before we launch into content is, of course, our sponsors, for whom we are very grateful, whom we take seriously and vet carefully.
And we have three, as always, at the top of the hour.
And who literally make this all possible.
They make this all possible, yes.
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To be fair, only Brett saw the puffins.
On the entire boat, I may be the only person who saw the puffins.
Yes, but you got a beautiful picture.
Oh, man.
Yeah.
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Yeah, well, sometimes that's me, but it wasn't this time.
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And I feel like my My tempo dial is now inching up.
Oh, we're going to bring it down a little bit, folks.
Yeah, I find myself thinking back to that cruise regularly.
I have been all summer, which is a very good sign about the quality of it.
It wasn't just great while we were there, but it gave us lots to think about.
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Oh.
Yeah, no, we're podcasting.
Oh, we're back.
Oh, sorry.
I was just reading my issue of County Highway that came this week.
County Highway, the first issue of County Highway, if I'm not mistaken.
Yeah, this is awesome.
This piece I was reading, Son of Joshua Tree.
I was actually just looking back at the lead because I finished this yesterday.
Son of Joshua Tree, Coachella babies overrun desert paradise, Airbnb schemers displace weirdos and freaks, mysterious energies remain.
It's like four different sets of headlines.
For those of you unaware, County Highway is a new publication, the brainchild of a number of people, including but not limited to David Samuels and Walter Kern.
They have at the top America's only newspaper, which is obviously a bit tongue-in-cheek, but they are responding to The need for good, honest, and enjoyable both journalism and just stuff that you would find in newspapers.
And so here it is.
This County Highway is not online.
I mean, they have a website and you can go and subscribe online and then you will get it to your mailbox.
And they've got in this issue a piece by R.F.K.
Jr.
on falcons.
And they've got stuff on logging camps and a number of things, including Call Him By Me.
But that is not the reason to subscribe.
You can also find it across the country in a number of bookstores, feed stores, record stores, lots of places that such publications, magazines and such might be sold, you will find this.
And once you pick up a copy, you'll probably want to subscribe.
Yeah, super cool.
And you know, America's only newspaper where you don't have to put news in scare quotes.
That's right.
That's right.
Actual news.
Yeah.
Wheat crop disaster.
Worst since 1917.
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It's just fabulous, fabulous stuff here.
So I recommend this as well.
Not a paid sponsor at all, but But friends of the show and we are enthusiastic about this amazing and very unique project.
Indeed.
All right.
Oh, actually, before we before we move on to the serious stuff of the episode about which you have many things, I want to consider your observation in that last ad that cinnamon is a bark.
Now, this reminds me of and I think we've mentioned this on the on the show before, that we were Gosh, 15 years ago, probably, in an Ikea in their, like, second's room, because Ikea wasn't cheap enough, we had to go to their second's room.
And there's actually some interesting stuff to be found in Ikea's second's room, as it turns out, including, as it turns out, a solid wood bench that we still have in our entry today.
It was, like, slightly marred, you know, just a tiny bit of marring, but it was 100% mango wood.
Because mango is not just a fruit, of course.
Mango is a species of plant that happens to have as its growth habit, it's a tree form.
And of course, therefore, you know, lots of trees wouldn't make good furniture, but it turns out that mango wood does.
And when we were interested in it, but in the second part of IKEA, it's not really clear.
It's not the same sort of thing that you do to go and check out.
We had to find someone who worked at IKEA to get him to, you know, Get it to us.
And he objected mightily to our characterization of a piece of furniture as being made of mango.
Mango, right.
Yeah, he said, we don't we don't do that here.
Mango is a fruit.
We don't make furniture out of fruit.
He claimed to have tasted the bench and it didn't taste remotely of mango.
No, he did not.
But the rest of the story is actually true, right?
And it was Both surprising and not surprising to hear from someone who had just never been in the place where mangoes are grown, that they have internalized what they occasionally find in their market as if delivered by gods.
This fruit just comes down from the sky and shows up in plastic clamshell cases.
That's all it is.
There's nothing else known as mango out there.
That story reminded me I was reminded of that when you said that cinnamon was a bark.
When I said it's not a fungus because that's sort of a list of mostly fungus and then you get to cinnamon.
The part of cinnamon that is used in mud water is the bark of the cinnamon tree.
But cinnamon isn't a bark.
Cinnamon the product is a bark.
Cinnamon itself is a bark.
I didn't see it until the very end.
You caught me.
You caught me.
I was speaking in shorthand, and I was doing that while we are recalibrating the speed at which I talk in regular hand.
Why I'm talking with my hands, I don't know.
But, you know, it's kind of an ethnic thing, I guess.
Yep.
Well, I'm glad we covered that topic-ish.
Yeah.
It's just one of the ways that biologists, at least organismal biologists such as ourselves, wander around the world seeing how people categorize things as the bit that humans use, right?
And I know you don't do that.
You said it that way in line in an ad read.
I'm following my interruption, so I was already throwing you, right?
But I'm reminded that, for the most part, we tend to see the whole organisms in things.
And it makes, for instance, shopping at a grocery store a rather longer process, because you're considering, you know, what is this?
What was the original plant?
Does it make sense, for instance, to be buying apples in August?
Mostly not.
Those are going to be pretty old apples.
Those are going to be old apples or apples from afar removed.
Whereas stone fruits and cherries and berries, yeah, this is the moment.
This is the moment.
So thinking about what the organism is and where it grows and when it grows and how it was grown is all part of the sort of organismal biology approach to the world.
And it results in lots of practical advice.
Like if you were to encounter a cinnamon tree and feel inclined to eat directly from it, stop when you get past the bark.
Yeah, actually, so where is cinnamon native?
I think it's going to be tropical Asia.
I don't actually know.
I don't know, and I feel confident that we've never seen it.
I've never seen it in the wild, whereas we have seen nutmeg trees in forests, and not just in human-produced farms for nutmeg.
You run into nutmeg and balsa and various other things that people will have heard of, but when you're wandering around neotropical rainforests, you see these trees if you know what you're looking for.
I don't think I've ever seen a cinnamon tree.
Therefore, I don't have any idea what the fruits look like.
Therefore, I don't know who tends to eat the fruits.
My guess is going to be birds, but I don't know.
And I don't know if it's bird distributed.
It's probably not very good for humans, but it's a possibility.
Yeah, if it's even a fruiting tree, which is very likely, but not certain.
Not dead certain.
I think it's a dicot, which is going to make it fruiting.
We're going to know soon enough.
Yeah.
Yeah.
Okay.
All right.
Anyway, you were hoping to talk about some things.
Yeah, I want to lead us through a series of connections that proceed from something that we talked about, in fact, last week.
It wasn't the first time we discussed this, but Last week we talked about a clip from an interview that Gadsad did with Paul Offit.
And in that clip...
Paul Offit suggested that the myocarditis and pericarditis that is observed after mRNA vaccinations for COVID might be the result of the fact that the spike protein mimics the chemical
...shape, effectively, of the actin protein in heart cells, and that therefore the unfortunate choice of the spike protein might result in the immune system attacking those proteins, doing damage to the heart, which would be truly unfortunate.
But what I said was that this looked like a limited hangout.
Because what it did by blaming the spike protein as the root cause was liberate us to start loading other proteins onto the mRNA platform for other diseases or potentially other proteins even for COVID.
So, my claim was that he was missing something that he should know, and in fact choosing to blame the spike protein because what it did is limit the bad press surrounding the destruction of hearts by these vaccines to the choice of antigen, which can easily be fixed the next time.
It effectively exonerates the mRNA platform.
If true.
Oh, yes.
Yeah.
Obviously.
So that's a hypothesis, and what I pointed out was a hypothesis that you and I have talked about quite a number of times here on Dark Horse.
I went back and, with the help of our Clips guy, David, found the original place where I had presented the hypothesis to begin with, and it was February of 22.
In February of 22, I laid out a hypothesis, an hypothesis, for the damage to hearts.
Remember, myocarditis means inflammation.
Inflammation is a symptom of heart damage.
And we have since seen quite a number of pieces of evidence about things related to this damage.
But anyway, it's become a central focus because it is the most obvious form of damage that results from these vaccines, and so there's been a lot of battling back and forth over what it does and doesn't mean, how it compares to COVID itself, etc.
But the hypothesis that I first deployed in February of 22 that we revisited in our last live stream and compares, it is a distinct mechanism from the one Paul Offit lays out, suggests that the vaccines by their very nature will result in the cells that translate the mRNAs into proteins.
Proteins?
I don't know why I Proteins?
No.
Proteins.
Any cell that translates these mRNA messages into proteins is going to be targeted by the immune system which will incorrectly regard them as virally infected because they are putting out the signature of a virally infected cell.
The signature of a virally infected cell being that it has molecules that look like your own molecules and it has molecules that look foreign.
Any cell that gives that signal, is suggesting to the immune system that it is virally infected, and destroying it is, while bad, the best thing to do, because that cell, if it is virally infected, is not going to become uninfected.
It's making the best of a bad situation so far as the immune system can see.
Right.
Now, a paper emerged this week, And I don't know whether this is just a simple coincidence or whether Offit was trying to seed the world with the idea that the problem was the spike protein molecular structure looking like heart muscle proteins or not.
It could be just a coincidence or it could be mere coincidence or it could be meaningful maintenance.
Maybe he was trying to get ahead of this paper that was going to emerge in Science Immunology, which is a high-profile, top-tier journal.
And so, Zach, do you want to show the paper?
I've got it on my screen, too, if you want to show that.
Okay, so here we have the paper.
The title is Cytokinopathy with Aberrant Cytotoxic Lymphocytes and Profibric Myeloid Response in SARS-CoV-2 mRNA Vaccine-Associated Myocarditis.
And what this paper does is it looks at the
pathology in people who are experiencing myocarditis following mRNA vaccination for COVID, and it analyzes at the level of the cellular and molecular environment in which the myocarditis is happening, it analyzes the various components in order to test competing hypotheses about what might be causing this pathology.
And so what I'm proposing to do is to go through, I think we should go, there's a little paragraph that has been inserted that describes the work, and then there is the abstract of the work, which summarizes the work.
The authors themselves summarize the work in the abstract as a standard scientific process.
Interesting.
I don't have, in the official PDF of the paper, I don't have the lay abstract.
The lay abstract.
But I think we should go through the real abstract, and I will say, I did take a course in immunobiology many years ago.
I speak immunobiology for this reason, but I'm not fluent in it, and I'm not current in it.
This is, you know, What I learned in immunobiology has stood the test of time.
It's high quality stuff, and among the best things I did as an undergraduate was taking this course.
It has paid back dividends each and every year since.
I learned a tremendous amount.
But anyway, I'm going to use what I understand to try to translate as much of this abstract as possible, and you will see the relevance to this question Raised by Offit and his proposal and my proposal from February of 22, which is now finally getting some traction.
Okay, the abstract says, And you will help me if I screw it up because there are a lot of complex technical terms here.
Rare immune-mediated cardiac tissue inflammation can occur after vaccination, including after SARS-CoV-2 mRNA vaccines.
Now they have to say rare because you have to kowtow to the appropriate gods on this.
You can't possibly be caught in a major journal like this admitting that the injuries from these vaccines are actually shockingly common.
Yeah, most of the abstracts we have seen that have in any way found damage associated with these vaccines have ended with a sentence that is something to the effect of, but despite all of this, it is still necessary that everyone go out and get vaccinated right away, right?
So this does not have that, but it begins with rare.
It has to say that, and then somewhere you hear an echo across the academy where everyone goes, Amen, right?
Okay.
However, the underlying immune, cellular, and molecular mechanisms driving this pathology remain poorly understood.
Here, we investigated a cohort of patients who developed myocarditis and or pericarditis.
And I should say, myocarditis is inflammation of the heart itself.
Pericarditis is inflammation of the pericardium, which is the sac in which the heart sits.
So these are both heart-associated inflammation but in a slightly different tissue.
Yeah.
With elevated troponin, you've heard us mention troponin recently in the study that we covered that John Campbell had covered, where instead of waiting for people to walk in with some sort of a pathology that caused them to seek medical help, they simply assessed troponin levels in people who had been vaccinated and found them in something like 1 in 35 people, indicating an awful lot of damage that's subclinical, that doesn't cause you to seek attention from a doctor, but is enough that it's measurable in your blood.
But I'm sure it'll be fine.
It'll be just fine, of course.
Amen.
B-type natriuretic peptide and C-reactive protein levels, as well as cardiac imaging abnormality shortly after SARS-CoV-2 mRNA vaccination.
So these are just markers that they're using.
Contrary to early hypotheses, patients did not demonstrate features of hypersensitivity myocarditis, nor did they have exaggerated SARS-CoV-2-specific neutralizing antibody responses consistent with hyperimmune humoral mechanisms.
Specific or neutralizing antibody responses.
So what this is going to take a little unpacking, but what they're saying is people have suggested that there might be some folks who I think this is what they're saying.
Some folks may have sensitivities which make them prone to myocarditis and they may be just simply triggered by this vaccine.
They don't see evidence of that.
They also say that there's no evidence with hyperimmune humoral mechanisms.
Now what they're talking about here, humoral mechanisms are not entirely limited to, but they are primarily talking about antibodies of the kind that you have heard overly focused upon with discussions of these COVID vaccines.
What they're saying is we do not see an overabundance of SARS-CoV-2 antibodies causing the heart To be inflamed.
Okay, so they are ruling out these proposals.
We additionally found no evidence of cardiac targeted antibodies.
Oops.
Autoantibodies.
Autoantibodies.
This is what Paul Offit was suggesting, right?
That autoimmune antibodies created because the spike protein mimicked what he said was the heavy chain of the actin molecule in the hearts would result in those antibodies being findable.
They didn't find them.
Instead, unbiased, systematic immune serum profiling revealed elevations in circulating interleukins of a number of different kinds, chemokines of a number of different kinds, and matrix metalloproteases.
Metalloproteases.
I don't know the significance of those second two classes of molecules.
These are enzymes.
I don't know.
I don't know much about it, so they're saying they didn't find it.
Subsequent deep immune profiling using single cell RNA repertoire sequencing of peripheral blood mononuclear cells during acute disease Revealed expansion of activated CXCR3 cytotoxic T cells and NK cells.
Now this is where the rubber meets the road, and I realize that was not a sentence to make you think anything important had happened, but what they're saying... Well, no.
I mean, many people would read that sentence and say, I have no idea what's going on here.
Maybe there's something important here, but I can't interpret it.
But NK.
So NK is natural killer.
Cytotoxic T-cells, these are T-cells that kill your own cells.
Also sort of colloquially called killer T-cells.
Yep.
Both phenotypically resembling cytokine-driven killer cells.
Now what they're saying is Inflammation, and actually people who listen to the Umberto Maduri Palmaric Podcast, which I highly recommend, we'll maybe come back to it later, will remember a discussion that we had in there about the fact that inflammation is part of the body's adaptive response to disease and that it gets away from us for various reasons.
And that's when it's pathological.
It's not that inflammation is inherently bad.
It's part of the immune response.
But then it can get away from you, which is where things become serious.
But what they say is that you've got cytokine... you've got these cytotoxic T cells, natural killer cells, both phenotypically resembling cytokine-driven killer cells.
So what they're describing is they're peering into the process of So-called vaccine-induced myocarditis, and they are finding the body reacting as if it is fending off an infection in the heart, exactly as I proposed.
In addition, patients displaying signatures of inflammatory and pro-fibric CCR2 and CD163 plus monocytes coupled with elevated serum soluble CD163 that may be linked to late Gatolinium enhancement on cardiac MRI.
So they're talking about something that they're seeing, you know, they're looking into these hearts with magnetic resonance imaging, and they're seeing pathologies that are grossly evidenced.
These are not molecular level pathologies, but they're seeing them.
There's a lot of specifics here that are going to be inside baseball, even for us, with regard to what are the indicators that are useful, since by and large you cannot detect damage directly.
So what we're seeing here is a lot of proxies for damage measured in a lot of different ways.
A lot of proxies.
A lot of different proxies, a lot of different measurements.
But they say, so that last sentence, we go back to the beginning of it.
In addition, patients displayed signatures of inflammatory and pro-fibrotic, which means this is basically scar tissue formation.
That's what that means.
And so what we're talking about is not, okay, this patient had a transient inflammation of the heart, which went away, and thank goodness they got away with it, and now they can go back to life.
The point is, they lost capacity in the heart.
This is not proven, but what they're saying is we see a pathology that is consistent with a heart damaged by natural killer cells and cytotoxic T cells in which scarring is the best repair that can be made, so that heart is now damaged for life, it now scars in the best case, and this person is now vulnerable to things like arrhythmias, they are less capable than they once were, and this is a potentially life-shortening pathology.
Right, and so let me, I know we're not done with the abstract yet, you're in the middle here still, but you mentioned, you know, this is therefore not transient.
How then have they been getting away with calling the myocarditis and the pericarditis transient in so many cases?
In part, and some of this will no doubt be intentional, but much of it will probably be utterly unintentional because doctors, like everyone in any field, will often conflate the underlying thing with the thing that they are measuring and imagine that they are the same.
If what you are measuring is inflammation in its acute phase, that acute inflammation will indeed be transient.
And so then you take that conclusion out into the world and say, ah, yes, damage, wow, or bad, but It's over and done with after a while, because we can't see it anymore, can we?
So the thing that is being measured is indeed transient, but there was never any reason to conclude, therefore, that the damage that that inflammation was indicating would be transient as well.
Right.
So it's a little bit like if you had a Building collapse, and you detected it by the dust that was kicked up.
The dust might clear, but it doesn't put the building back up, right?
So anyway, they're using proxies, which is frankly what you just simply have to do with all of this stuff, because we're dealing with mechanisms inside a living person, and it's difficult to assess.
Right, but I mean I think I also I just want to point to the media that grabbed onto this like it's transient, it's fine.
The it's fine thing was their conclusion based on a misunderstanding in part because of the misunderstanding of the people actually doing the research of what what transient is a reference to.
Transient is not a reference to the damage.
Transient is a reference to the particular thing that was measured as an indicator of the damage.
And so whenever you see any of these conclusions being trotted out in the media, you have to wonder what actually Are you talking about?
Right?
Like, transient in this case is true, and people will, you know, go to their graves saying, no, but it's transient!
It's like, yes, but the thing that's transient isn't anything worth talking about, actually.
The only reason we're talking about that is because that was what was measurable, and, you know, the map is not the territory at some level.
You remember the Spin Doctors?
The group?
The band?
The 1990s band?
Yeah.
Had a great album.
Yeah.
The Spin Doctors were named after a phenomenon that was very real called Spin Doctors.
Spin Doctors were people who went, I believe, to presidential debates and maybe other things, and they were there in the room, ready, they were listening to the debate, and if their candidate, the one they had been hired to protect, screwed up, they would immediately lodge in the room of people who were trying to figure out how they were going to report the story, they would lodge the interpretation that minimized the damage, or flipped it into a win, or whatever.
Now the idea is, okay, how are we going to take the dire fact of these radically novel transfection agents producing heart damage?
How are we going to get the blue team faithful to all, you know, look down their noses at people who are concerned and say, you're obviously a right-wing nutjob, everyone knows the myocarditis is You know, and then transient is going to be the way they're going to spin this very devastating indictment of that technology.
Alright, so let's just finish this out here.
Together, our results demonstrate upregulation of inflammatory cytokines and corresponding lymphocytes with tissue-damaging capabilities, suggesting a cytokine-dependent pathology, which may further be accompanied by myeloid cell-associated cardiac fibrosis.
What they're saying is, what we see is a reaction consistent with the body damaging its own heart.
Why would it do that?
Because it's programmed to fend off viruses if they get in there.
As bad as heart damage is, an infected heart is worse.
So that's what they see, is a pattern consistent with that, that results then in cell-associated cardiac fibrosis.
That is to say, scarring, which is the best case.
It's bad, but it's the best case.
These findings likely rule out some previously proposed mechanisms of mRNA vaccine-associated myopericarditis and point to new ones with relevance to vaccine development and clinical care.
So, what that means is the OFIT mechanism that he proposed last week, I don't know if he proposed it before that, is not consistent with the findings that they made.
And what is consistent, they say that this is a new proposal or a new set of observations but the point is you ought to notice that that new set of observations is consistent with a hypothesis that we put together on camera on Dark Horse.
I do want to say I say my hypothesis.
I do not mean this is my hypothesis alone and in fact I went back to the original This is important, where you're about to go, and this takes us far from this paper.
Can I just share a couple of excerpts from the end of the paper first?
Sure.
Because we're probably not going to come right back to this paper.
The very end of the discussion of the paper.
On the basis of our findings, longitudinal clinical monitoring of vaccine-associated myopericarditis patients may be warranted to assess potential persistence of cardiac abnormalities.
Yes.
Then in the same paragraph, future studies building on the translational relevance of our work will be important to further optimize the excellent safety profile of mRNA vaccines among specific demographic subgroups.
Amen.
Amen, right.
Now, they do have specific demographic subgroups, but you know, it is becoming acceptable, nay, it will be required soon to reflect back and say, yes, maybe we shouldn't have been vaccinating the young men after all, our bad.
Right?
That is becoming the thing that is now not only acceptable, but necessary.
And this specific demographic subgroups is the nod to that future orthodoxy.
But will we ever get to a legitimate orthodoxy in which there is widespread understanding that As you are saying, and this is where I'm going to just hand it right back to you, actually, these were not ready.
These were not ready.
They couldn't have possibly been ready.
This platform is not ready, and no one should have gotten it.
Yeah.
Nowhere near ready.
Right.
But, I mean, look, I don't want to say anything negative about these authors.
My guess is these authors faced a problem.
They did good work.
It successfully advances the ball in terms of how much we know.
This now goes out of the realm of hypothesis.
We now have a mechanism that appears is now the presumptive mechanism, right?
We know what it is, and we now know what it implies, and frankly that's hugely important.
But the fact that they have to riddle this piece of excellent work with, you know, various incantations designed to placate various powerful gods is absurd.
And that last one— Probably wouldn't have gotten published in Science Immunology, but for those nods to the orthodoxy.
Right, and the orthodoxy is—I don't like the term evil, but if you're going to take a radical, dangerous technology like this, and you're going to claim that it's only really bad for certain demographics.
Don't like the term evil.
But if you're going to take a radical, dangerous technology like this, and you're going to claim that it's only really bad for certain demographics, young, healthy men, like that's not a certain demographic.
Young, healthy men?
Like, that's not a certain demographic.
And what's more, the paper that we talked about either last week or the week before that found the one in 35 vaccinated people had elevated troponin levels.
It was actually women who were more commonly showing this sign.
So, hey, we don't know how extensive the damage is.
And these aren't limited subgroups.
Healthy young men, is that a demographic that half the population is supposed to pass through?
You can talk about demographic groups and know that there are some, you know, who they are intending to keep in the line of fire for these and future mRNA vaccines is older and immune compromised people and people who otherwise have comorbidities that put them at particular risk for whatever the pathogen is that we're talking about.
No, I'm sorry, I'm pushing back because the very sentence, I think it was the same sentence, they say optimize the excellent safety profile.
What in God's name does that mean?
That's why I read it.
But I don't think, you know, specific demographic subgroups is a legitimate way to understand populations.
You know, we know, we were talking about, as were some other people, the need to risk stratify both our understanding of COVID and our understanding of the mRNA vaccines.
Um, as they were being trotted out and almost no one was doing it.
And that was part of why you got, you know, parents living, you know, scared parents living in scared fear until they could get their tiny children vaccinated, uh, with, uh, so-called vaccines that, uh, were at much more risk of doing damage to their children than the virus ever would.
Right?
Risk stratification is a massively important thing that we need to be talking about.
So risk stratification is great.
But when you have a novel technology that is a threat to a huge fraction of the population and then you minimize it by talking about demographic groups instead of saying, actually, we don't know how big a threat this is.
And we don't know if we're noticing it in young, healthy people because it gets obscured by the pathologies that older, unhealthy people tend to have anyway.
So the point is this.
They're just way ahead of what we understand.
And they're using language to minimize it.
And that's not cool.
That said, again, the authors did excellent work, and they got it into a high-profile, top-tier publication, and they may have—these are compromises they may have had to do, and I don't judge them for that.
Okay.
Back to the other point.
I keep saying my hypothesis.
I do not mean it is my hypothesis alone, and I went back to the initial presentation of it on Dark Horse from February of 22.
And in fact, in that initial presentation, what I say is that I was working this out, and I presented it to some people privately, and they told me that they had heard a related hypothesis, or maybe the same hypothesis, deployed by others.
And I went and looked, and I found Peter McCullough had alluded to such a thing.
I now know Mark Girardot has alluded to such a thing.
I mean, in fact, his whole bolus theory, with which I have one significant disagreement, but his bolus theory is predicated on the same idea.
I ran into a new one this week.
David Wakefield, of all people, had described a similar mechanism.
So, why am I focused on this being my hypothesis if it wasn't mine alone?
I want to make this clear to people.
The system requires us to track where ideas come from and how well they stand up to test.
Now, when I say it's mine, what I mean is I didn't get it from anybody else.
Okay?
I put this together based on what I understood.
That means, if it turns out to be borne out by empirical tests, as it now has, that that tells you something about how good my model is.
Not perfect.
Maybe I could have been more precise.
I certainly could have been earlier and I wish I had.
But, nonetheless, the point is, one, if the system is supposed to work, people who have predictive power have to have their credibility elevated.
Now, You and I, so if the system does this badly, if you elevate thieves, for example, then you get the inverse effect where people who aren't responsible for a particular thing get credit and they have their credibility elevated.
The system to evolve in the right direction, you have to be able to track who was capable of seeing something coming, making a valid prediction, and then having that prediction borne out.
But the other thing is you and I have endured Shocking indictments of our credibility and effectively attacks on whether or not we belonged in a conversation about COVID and its treatment and this has gone on for a very long time and it's been in some very close quarters.
We have been ruthlessly attacked by Sam Harris of course who has indicted our credibility and he said he's not the guy to do any of this analysis because he doesn't know what's going on but clearly we don't either.
Now my point would be This doesn't have to be my hypothesis alone, but if you can see that I'm capable of taking the facts of this and somehow being way ahead of the folks at Pfizer who apparently still can't explain why myocarditis has anything to do with their damn shot, right?
And ahead of Paul Offit who is blaming molecular mimicry of heart proteins and all of that.
If you can see that, then you know that somehow This is legitimate analysis that is leading you to see things well ahead.
Even the authors of this paper call their observations new.
They say this suggests a new pathology.
Well, it's not.
It was predicted by hypothesis outside of any laboratory setting, and that is an important consideration.
A model that is capable of predicting results in the lab is a powerful model.
And so all I'm saying is somewhere we have to have the tables turned on all of the attacks that were made on our credibility because the fact is we have been right.
We didn't guess where we were wrong.
We corrected it.
And that is what you want in people who are analyzing situations on which our health depends.
That's right.
We've dipped in and out of philosophy of science and epistemology, that is, how it is that we make claims of truth.
On what basis do we make claims of truth?
Many times, on Dark Horse and elsewhere.
But it warrants a revisit here.
It's part of what you're doing.
It's part of what is implied by what you're talking about here.
And part of one way, one of many ways, to categorize science, types of science, ways of doing science, you know, the kinds of things that scientists engage in, is empirical versus theoretical work.
And empirical work is that which takes a hypothesis, and usually, hopefully, it is the researcher who is doing the empirical work who has himself or herself generated the hypothesis or hypotheses that they are testing, and describes and executes an experimental test or an observational test.
of said hypothesis and generates data, actual numbers, actual measurements, and then does the analysis on those data, and depending on the type of work, a statistical analysis perhaps, or some other analysis, and generates a result.
That is empirical work in which there is something that has actually been measured.
The generation of hypothesis, including the generation of hypothesis, where you do not have any intention of, nor do you have the background to, because you do not have the familiarity with the equipment, with the various molecules you might be measuring in a field, where you can look at what is out there and say, I think it's this.
This is the prediction that I make given what we can see right now, and here's what would have to be true if so.
That is theoretical work, because it does not include any measurement.
You do not have to be out there measuring and analyzing data in order to be doing theoretical work.
Both are necessary.
Both theoretical work and empirical work are necessary to do science.
For a variety of reasons, from something like the mid-20th century on.
And, you know, maybe to some degree from time immemorial, but empirical work has been privileged in big science, in academic science.
This is in part because it leaves a clear trace, and in part because it is expensive to do.
And expensive is a good thing for the purposes of academic science, because expensive science means big grants, means lots of overhead to the universities.
It's a favored thing.
It is the thing that the administrations of universities who house scientists want.
They want scientists to do expensive science, not inexpensive science, because expensive science forces the scientists to spend more of their time being grants getters and grant administrators as opposed to actually doing science.
Whereas theory, and the term theoretician is confusing with regard to our contention that it's not a theory until it's passed many, many, many tests, right?
It's a hypothesis to start.
But we call these theoreticians versus empiricists.
Theoreticians largely don't need big grants to do their work.
And so this is one of several reasons that theoretical work has been pushed to the wayside in modern scientific circles.
And as a result, you have a number of people who have degrees in science, who have the accoutrements of science, who appear to be doing science, who are who the media go to when they need something sciency to be said to them, who might not recognize a hypothesis with a testable prediction if it hit them in the head.
And that means that what they're doing may be absolutely necessary.
But it's a piece of science, and it's not all of science.
And frankly, it's not the hard part of science.
It's not the rigorous part of science.
Using equipment that other people have generated with molecules that are signifiers, that are proxies for things that other people have generated, is not actually that hard.
It's a little bit like following a recipe.
And you have to be good at following a recipe, but you don't have to actually be able to see the big picture, whereas theoreticians generally do.
So, one, it's worse than that for theory.
And the reason that it's worse than that is that not only is theory cheap to do, but theory eliminates a large fraction of the experimental work that gets done by giving you a map of where to look.
Say that more so.
What you mean there is, if you don't have an idea about what you're doing, if you don't have a map, if you don't have a theoretical understanding of the situation, you could throw the dice and do any number of, almost infinite number of experiments, and most of them will be irrelevant because all it would have taken was Having a theoretical approach to begin with, to narrow the subset of experiments or tests of hypothesis that you might have done in the first place.
Yeah, that are worth doing.
And in fact, you can see that right here, because let's say we take Paul Offit's feeble understanding of the danger of these things.
Okay, it's based on the antigen that the mRNA transcript produces.
Well, let's suppose you wanted to make some other so-called vaccines on the same platform.
You've got to run a test for every single one of them in order to figure out whether they are good or bad antigens.
On the other hand, if the theoretical viewpoint says actually no, the platform is fundamentally flawed and it's not You know, spike protein is bad, but it's not just the spike protein.
The lipid nanoparticles are bad, but it's not just the lipid nanoparticles.
It's actually the most fundamental element here, the one you can't swap out.
Pseudouridine is bad.
Well, it's the mRNA transcripts that produce a foreign protein in your cells, which is going to get your cells targeted, and then the pseudouridine stabilization of the mRNAs that make this process a long-term process rather than a short-term process.
If your theoretical understanding leads you to that, the point is you don't need to go test every antigen.
That's right.
It's not going to be productive.
As soon as you've got a foreign antigen, you know that you're stepping into the same mechanism.
Now, you might want to run a few tests, because it would tell you something.
If, hey, it doesn't matter what antigen we swap in, as long as it's foreign, we see the same thing.
That would tell you, oh yeah, this model was correct.
Test from widely disparate antigens.
Right.
So the point is, The part of the academic system that has gone full bore on the idea that the data is king, that science is data-driven, right?
This is a coup and it is staged against theory.
Now you can't... doing theory alone isn't any good.
You have to do the empirical tests, but... Someone does.
Someone, and that's the other thing... The empirical tests have to be done.
The empirical tests have to be done, and I was going to argue... But the empirical tests also can't exist absent the theoretical work in the first place, and those can be done by the same people.
They can be.
Now there's a risk when they are done by the same people, and the risk is that the perverse incentives cause us to see a false scientific picture, because people who have a dog in the fight may run a test that, they may throw away the tests that falsify, and they may publish the tests that validate, Yeah, well, but I mean, just from our particular experience, you didn't do that much empirical work.
I did, and it was not in this scope at all.
And both of us 100% generated our own hypotheses.
We were acting as both, you know, theoreticians and empiricists for the fieldwork that we did.
And what we haven't spelled out here explicitly is when it is you who are going to then be doing the empirical work, it is even more necessary than under other circumstances that you look in advance to try to find the complete solution set of possible hypotheses.
Will you still have one that you favor?
Perhaps.
Perhaps.
And that is what the scientific process is supposed to help eradicate.
The individuals who are doing the science will have bias, and you cannot get rid of human bias, but the scientific method is one road Uh, to minimizing it.
Um, you may still have favorite hypotheses, but if you have many, all of which might explain a pattern that you have observed, then you are less likely to say, ah, um, you know, as, as you falsify one after another of your, you know, treasured hypotheses, well, that's just the way it goes.
I'm out here to try to figure out what is true, as opposed to, uh, validate what I think is true, even as I continue to see evidence that I was wrong.
That's all well and good in places where you don't have huge financial incentives.
You know, if you're studying frogs or bats or whatever, you can teach people that they have to have scientific integrity and it might work.
It doesn't work when you come close to the money.
That is what I learned from the the telomere debacle, was the closer you get to the money, the more ruthless people become, the more eager they are to steal, the more Clever they are at lying to themselves.
Which brings me to the next point here.
What you have now is what you might call a paradox.
Let's take Sam Harris's confused view.
Because I think in some ways he speaks well for the blue team myopia.
What Sam Harris says is, I acknowledge that the institutions are compromised in an unacceptable way, but you're far better off with the institutions than out in the Wild West trying to do your own research or whatever he wants to demonize.
Now here's what you now know.
That's not true.
You watched, if you saw that clip, which you can check out, Jimmy Dore and I spoke about the clip of the Pfizer execs in Australia being questioned where they couldn't Give any explanation at all of how myocarditis might arise from their shots.
We can give a perfectly coherent one.
Turns out, laboratory work bears it out.
They can't give any answer.
They can't say it might be one of four things and lay them out even in, you know, who are these people?
So, what you now know It's the various people, right?
You have Peter McCullough, Mark Girardeau, you have us all spotted this issue.
David Wakefield, that ought to make you think.
You have all of these folks who spotted that the, the brochure, if you will, of these vaccines, what we were told about how they were supposed to work, predicts this pathology if you simply extrapolate from it properly.
Zach, do you want to put up that Pfizer diagram of how their, their so-called vaccine works?
All right.
Here's Pfizer's own cartoon of how the vaccine works.
And I borrowed this from a tweet of Mark Gerardo's.
And this is, how do we know, is there a date on this?
I don't know.
Where is this from?
I don't know and I don't think it matters.
Okay.
But as far as you know, they still vouch for this.
This is still...
Yeah, and I don't think there's anything wrong with their diagram.
But the point is, what it is, is a cell that has picked up lipid nanoparticle-coated mRNAs, transcribed a foreign protein, and exported it to its surface.
That's all you need to know if you understand how the immune system works in order to spot that it is at least a question whether or not this is going to trigger your own system to attack your cells, and then that will lead you to the obvious question of, well, which cells are going to do the transcribing?
Well, they told us the cells that were going to do the transcribing were going to be in your deltoid.
As soon as you know that that's not true, you have a four alarm fire.
So, this was all deducible.
Why is it that the Academy didn't deduce it?
Why is it that the obviously excellent scientists who were capable of sorting out this mechanism and finding the empirical evidence that it exists, why is it that they haven't been thinking this was a likely explanation all along?
Or if they were thinking it, why they didn't lay it out as a pre-existing hypothesis here?
Well, I mean, you know the answer.
You've already said why.
It's the money.
It's the money, but... In many different both money scales and temporal scales.
So now I want to flip this question on its head and I want to give you the scariest observation of all that comes out of everything we saw during COVID.
It was very easy to outthink the experts.
Doesn't mean it was easy to do.
Outthinking experts is tough, but they were thinking so feebly that it was very easy to outpace them.
It was very easy to get ahead, and get ahead doesn't mean be more compelling.
Get ahead means be more predictive.
See things coming ahead of time that the experts claim not to have known were coming.
Now we don't know if they were lying or they're too dumb to get it, but it doesn't matter.
The lesson here is one that actually you will have heard hinted at many times on Dark Horse.
You may remember a conversation that I had with Steve Patterson in which Steve Patterson and I had both come up with the idea that we were living in a dark age.
Steve Patterson puts the beginning of that dark age earlier than I do, but it doesn't much matter.
The idea that this vibrant technological sphere in which we live is actually a cryptic dark age in which our scientific tools are artificially feeble because our belief structure is interfering with their use.
That's where we are and the evidence that that's where we are is now in plain sight.
You have a novel technological mechanism being deployed massively across the globe that was foreseeably going to do damage to all your tissues, including your heart.
That was foreseeable based on what was understood and the people who were supposed to do the foreseeing couldn't see it.
What do you have?
You have dissidents on the outside saying, here's a problem.
It's evident that it will be real.
Why are we not looking at it?
And the answer is, oh, well, those are quacks.
Those are quacks.
You can just look at their Wikipedia pages.
They're quacks.
These aren't people you'd listen to.
You've got to listen to the institutions, because as frustratingly flawed as they may be, they are the gold standard.
No, they are not.
They're not quacks.
Well, they are and they're not.
They are the official quacks, and the actual quacks don't quack at all.
Some of them.
That got very confusing.
It did get confusing.
Well, that's the way with ducks.
They're a confusing clade.
They are a confusing clade.
But anyway, point being, what I learned in graduate school Is that a stuck field is easy to beat.
Doesn't mean it's easy to get credit, doesn't mean it's easy to get heard, but if you just simply want to understand the world better than people in a stuck field, all you've got to do is free yourself from obligations to their sacred principles.
Right?
That works.
You've now seen it happen with COVID, where people who just simply were not part of that system, either freed themselves from it or weren't part of it in the first place, were able to figure out what was coming ahead of everybody else.
That ought to terrify you, because what that says is that all of those fields in which the so-called experts were minted are broken.
They are incapable of protecting your health.
And that includes medicine, it includes includes virology, it includes vaccinology, it includes the entire regulatory apparatus.
These things are broken and I would claim beyond repair.
That's not a good thing, but nonetheless the evidence is right there.
So That's where we are.
And it does suggest that this dark age is having implications in ways that are not abstract and theoretical.
This isn't some, you know, discussion to have in your speakeasy.
This is actually a material emergency in which we have vaccinated a good fraction of the people on planet Earth with something that never should have been injected into them.
And we did so even though there were foreseeable harms that some of us tried to to raise the alarm about and instead of listening to those people and saying hey that's a good point maybe we ought to study that we were demonized and belittled and okay that didn't work but it could have it worked better than it should have um so that's a that's a pretty dire picture but It is now a picture supported by the evidence, right?
We don't have to wonder whether or not Peter McCullough is a quack who was once well-published in his field, but now he's become a compromised marginal thinker.
Nope, he was right.
His colleagues who didn't see this and injected who knows how many people, they were wrong.
That's where we are.
Yep, that is where we are.
And I don't know if it will be recognized.
Well it has to be and I do have the feeling in the last week that the again we've been we've been talking about this issue of your own cells producing foreign proteins and triggering an autoimmune response that damages your own heart we've been talking about that since February of 22.
The right now August of 23 That idea is finally lodging in enough minds, in enough public discussion.
Something about that Offit piece caused this now to be a question, because maybe presenting that hypothesis in isolation doesn't work, but presenting it as a competing, everybody's heard of spike protein, everybody knows that they're supposed to fear it, and then when Paul Offit overplayed his hand and tried to blame the spike protein for everything, it made it possible to say, here's why, as good as that sounds, as much as that sounds like an admission,
I don't know that the genie goes back in the bottle on this one.
I think they may have screwed this up now in the same way that they screwed up LabLeak, and I think we may finally be able to have this discussion in a sober way.
I hope you're right.
I think genies are going back in bottles all the time, not by actually stuffing genies back in bottles, but it's like the genie metaphor equivalent of dilution being the solution to pollution.
Like, there's so many genies out there, and there's so many misdirections.
There are so many things that you can draw people's attention to over there.
You know, will it be another new virus?
Will it be another new war?
Will it be another visit from aliens?
Like, there's a lot of places to distract people, and then coming back to this, like, oh god, COVID again?
Must we?
Well, I'll tell you how we're gonna know.
Oh, I think we'll know.
I just have little faith that it will actually happen, because I think we are up against something that is not willing to lose.
Well, I don't care.
I mean, it lost LabLeak.
It lost LabLeak, and it is now losing control of this one.
It is going to have to face up to this because if it tries to load other things into that mRNA platform and it has a repeat on myocarditis and pericarditis, which is effectively inevitable, then people are going to know what they're looking for.
So here's how I think we will know whether or not this one has finally crossed a threshold where they can't re-obscure it.
There are many people who have played A net positive role on COVID, some of whom I like very much personally and in terms of their professional contribution, but who have had what I would call a misplaced caution over what to do about COVID.
Their caution has caused them to stop short of saying things like what Peter McCullough has said, which is there needs to be an immediate halt to this vaccination campaign.
It should stop completely, right?
Others have said, well, maybe we should Limit it and stop injecting it into people who are comparatively unthreatened by COVID because they're young and healthy, etc.
Maybe we just limit it to people who are old or enfeebled or both.
And that has never been right.
It never made any sense because these inoculations are, just for starters, Not only are they structured in a way that should be presumed to cause this pathology, as soon as you know they don't stay in the deltoid.
Is there a way to keep them out of your heart?
Nope, it's not there.
Therefore, that's a risk.
But they are also a double violation of Nuremberg.
Nuremberg The way that they were deployed.
Yes.
It's not the technology itself, but the fact that it was injected into people who were led to believe that these things were safe and effective means that those people were not informed.
So they couldn't engage in informed consent because they were not informed.
And in fact, there was a systematic campaign designed to prevent them from becoming informed.
And then they were coerced.
And the fact is, both of these things are forbidden.
Informed consent has to not be coerced, and it has to be correctly informed, not misinformed.
So you have a double violation of Nuremberg, and my point would be there's no There's no principle by which Nuremberg should ever be violated.
The fact that we did violate it and now we have a huge population of people that can tell us something new about the pathologies and who they afflict most is irrelevant.
You don't get to inject some huge fraction of the population and then figure out what the dangers are and then, you know, back off your vaccination campaign and exclude some people from it.
These things were not properly tested.
They sped them right past all of the things that would have told us that this was true either in animals or told us this was true in a small number of unfortunate people who were part of a clinical trial.
And so...
What I want to know is when those folks are going to recognize that what's on the table, what we now know about the pathologies emerging from this, are serious, they are well supported by evidence, they are not rare, And that that means that nobody should be injected with these things, not another one.
And that was true from the beginning, now it's very, very clear it's true.
So I'm waiting to see all of those folks who have been advocating for a voluntary process of getting vaccinated with this stuff, or a limited process where we vaccinate the vulnerable, or whatever it is.
None of those things make any sense in light of what we now know, and I am expecting That those people in that group with integrity, which is a great many, are going to have to reconcile themselves to the idea that caution about backing off the vaccine program is not where it should be.
The caution should have been in deploying it, and halting it should be something we do instantaneously now, now that we know what we know, and we should have done it all along.
I agree, obviously, that we should have done it all along.
I do wonder to what extent Politics affects even the good people in a non-egregious way, such that some people who have been advocating for, you know, not giving these products to the young and healthy, and paying specifically attention to the risk stratification of both the disease and the vaccine,
um can't could begin to be heard just as we could begin to be heard uh more effectively by coming at it in stages and uh that that truth is not inherently nefarious i agree all i'm saying is i don't think that that was ever what was unknown about these inoculations
was substantial enough that objection to the entire process was correct from the beginning.
I do understand that people, you know, as the authors of this paper are caught in a bind, that many of the high integrity folks have been caught in a bind.
There's lots of stuff that you and I know, excuse me, that you and I know that we don't say.
Sure.
Right?
And that should be true for all intelligent people who are speaking publicly about things for which the majority of people have been sold a bunch of lies.
Right, but that's my point.
Whatever process led people to say less than they knew, or to understand less than they should have, That's gone.
At this point, any reasonable person looking at the evidence who has integrity should be on the side of, wait a minute, what did we do?
This should never have happened, and if it should never have happened, no part of it should be continuing, period, the end.
So that is what I am hoping for, and that is what I am expecting if those folks are up to the challenge.
And it's not going to be easy because, of course, as we started this discussion, Within the Academy, there is a religion that requires you to mumble the right kinds of words in order not to be viewed as a heretic.
So, okay, the question is, can you now join the heretics long enough for what should have happened long ago to happen now?
And I really hope that it does.
Indeed.
Did you want to talk about the paper in the strangely named journal Vaccine X?
Yes.
I thought you wanted to talk about that as part of this.
I'll set it up slightly, although I don't know much.
You can show my screen if you want.
You mentioned this paper existed.
Its title is Relapsing Myocarditis Following Initial Recovery of Post-COVID-19 Vaccination in Two Adolescent Males Case Reports.
So the paper is, as that title suggests, two case reports of relapsing, recurring myocarditis in a 15 and a 16 year old male after mRNA vaccination, but just a word first about the journal.
What a strange name for a journal.
It turns out that it's Elsevier, which is the most major of the academic publishing outfits.
The most predatory, I think, as well.
Maybe that just goes along with being major.
It likes to claim that it was Galileo's publisher.
That claim does not stand up to scrutiny.
They've used the name of Galileo's publisher.
But anyway, they like to claim that it's that old and important.
Yeah.
They publish a huge number of the influential scientific journals.
Also, I believe – correct me if I'm wrong, maybe you won't know – a number of textbooks.
I believe they're also textbook publishers as well, which of course is a totally separate – well, not totally separate – is a different way of getting money out of people who shouldn't have money extracted from them at that rate, which is to say undergraduates mostly and medical students.
Anyway, Vaccine X is basically the pay-for-play, the pay-to-play version of the journal Vaccine.
Vaccine is Elsevier's premium peer-reviewed journal, and Vaccine X is a pay-to-play journal where for $2,000 you can get your paper in Vaccine X. So I don't think there's anything wrong with it, but I think we should separate the term Pay-to-play, which I think is a good term for corruption, for pay-to-publish, in which you have a journal in which… There are editors, presumably.
Yeah.
Yes, and the fact is, this is not a peer-reviewed journal.
It looks like one, but it is not.
And that scheme is not uncommon.
And there's nothing inherently wrong with something in such a thing, and I would also point out...
Peer review is, of course, completely broken.
The idea that you need resources in order to publish on top of a system in which you basically need resources in order to do any research that is going to be recommended or recognized by an academic institution just further makes science an elite process that is not open to people who only know how to think, but don't also already have resources with which to publicize what they want to
Yeah, I did imply, but I did not mean to imply there's nothing wrong with the idea of a pay-to-publish journal.
There is nothing inherently wrong with the work in a pay-to-publish journal.
I think pay-to-publish journals are a despicable and predatory outgrowth of a very broken and corrupt system.
But the fact that something shows up and one doesn't count for it or against it, it's effectively like a different version of the archive where you have unpublished, unreviewed work that is available.
It just gives the veneer of legitimacy that comes from a journal that looks You can't tell just by looking at that page that this is pay to publish rather than peer review.
And I believe there are hybrids.
But nonetheless, never mind any of that.
What you have here is a paper And you know you could say well it's a very small study because it only involves two people but what it really is is two case reports it says so of adolescent males who got myocarditis following a administration of these COVID so-called vaccines and what it reports is something you want to read or should I just summarize it?
Yeah you can What they report is that even though these cases had appeared to clear up, that effectively they've got relapses, and those relapses appear to be about, I believe it says that they show new lesions upon investigating the hearts of these young people.
Yeah, the CMR, which I can't remember what that stands for, showed new focal areas of edema in the first case report and stable lesions in the second one.
They reached full recovery with normalization of cardiac enzymes after a few days.
So full recovery being the measure of the cardiac enzymes.
Yep.
Only.
Okay, so anyway, the reason that we raised this is because, again, it puts the lie, and yes, it's two cases, but it suggests... Sorry, CMR, that's Cardiac Mechanic Resonance Scanning.
So these are... It's MRIs.
It's MRIs of the heart, yep.
The problem here is that we have been told again and again that we are terrible people for casting doubt on these marvelous inoculants, which they call vaccines, and that the fact that myocarditis, well of course, sure it may happen, but it's extremely rare and it clears up and so it's not a big deal and so who are we to worry?
And the answer is You don't know anything.
I'm not sure I would have predicted that it would clear up and recur, but the idea that people who've gotten a clean bill of health after having myocarditis, which no cardiologist would tell you is a minor condition, or no good cardiologist anyway, The fact that these relapses occur is extremely concerning.
Why are they occurring?
Is it an ongoing pathology even though the heart has cleared these mRNAs?
Are the mRNAs that have been hyperstabilized with these pseudouridines migrating around?
That is not obvious.
And in any case, the idea that people who had effectively no risk from COVID in the first place were inoculated with something that had this potential And then the concerns of other people who might think, well, maybe I shouldn't get one because myocarditis doesn't sound like something I want, we're told, well, if you do get it, and that's going to be very unlikely, which it isn't.
But if you do get it, it's likely to be transient and you'll go on your way.
No big deal.
And the answer is no.
How many times do we have to say it?
We're talking about hearts, and we're talking about heart damage, and the fact is, heart damage doesn't repair.
You get a scar, and a scar means you have a lesser heart.
That's a heart that can do less, it's less efficient, it's less capable of enduring insult in the future.
This is not a minor issue at all.
And the fact that these maniacs decided to inject people who stood to gain effectively nothing from it, in spite of the fact that the inoculations didn't prevent transmission, which still wouldn't have justified giving them to people who stood to gain no benefit personally.
But they don't block transmission.
It didn't control the disease.
So we harmed these people for no reason whatsoever.
And the harm is one that is going to adjust how long many of these people live and what they can do during that lifetime.
Is there anything more precious that you could rob someone of?
This is robbing them of their own physiologically generated freedom, the capacity to live a life that you don't have to worry that your heart was damaged by some stupid experiment that somebody ran on you in 20, Yeah.
No, we're just going to take your youthful vigor away from you.
That's all.
And, you know, make you potentially a lifelong...
consumer for pharmaceuticals to deal with the heart problems that they've caused and you know mind you also it's been weeks maybe months since we talked about it but the fact that these things were seem to have been driven to be injected into young people and put on the childhood schedule for cynical reasons of creating legal immunity for the shots that were injected into adults this is just this is disgusting
And I don't know how many different lines of evidence you need, but it seems really unambiguous that, as I've said many times, something has become Completely indifferent to the suffering and death of other people's children.
And anytime you're dealing with something that's that cold, you really have to wonder about anything connected to it.
And it is obviously riddled through our governmental regulatory structure, our universities, our journals.
It's censoring people on social media.
It is disparaging them on Wikipedia.
I mean, It's a dire emergency of criminality that has become so normal that we barely notice it.
That's right.
There are a number of other things we wanted to talk about today, but I'm wondering if we should just skip ahead and talk about bumblebees.
About bumblebees.
All right.
And save the rest for next week?
Fair enough.
All right.
There's some new, cool research, other than what you have just revealed to us this week, that has no political ramifications at all, I think.
We'll find something.
I don't think we need to.
It's about social learning and bumblebees.
Hymenopterans, which are the ants, bees, and wasps, as you know, are often highly social.
There are some solitary species of Hymenopterans, and that sociality is driven in large part by the eusociality that is downstream of their unusual genetics.
They're haplodiploid, which means that all of the females are diploid just like we are.
We have two copies of all of our chromosomes, but the males are haploid.
They only have one copy, and that has all sorts of fascinating effects, including that, for instance, full sisters are three-quarters related to one another, and they're only half related to their mothers, and so kin selection theory suggests they are more likely to be interested in the production of more sisters than they are in reproducing on their own.
Which, I'll just add, is why the stinging bees, the Stinging apparatus is actually the ovipositor.
It's the egg layer that has been modified into a weapon because they don't need it as an egg layer because they're better off facilitating the reproduction of their mother with full siblings than they are of retaining the capacity to reproduce themselves.
Right.
Now that logic only holds for full siblings.
For half-siblings, they're a little bit less related to their half-siblings than they would be three-eighths related to their half-siblings than they would be related to their own children.
And that three-eighths is a probability, whereas they'd be exactly half related to their own kids.
I'd be happy to go on endlessly about the genetics of haplodiploidy another time as I used to with my students, but this is not the place.
Although, one of the other interesting effects of the haplodiploid system in hymenopterans—again, ants, bees, and wasps—is that males don't have sons.
Males only have daughters.
And sons, therefore, males also don't have fathers.
They only have mothers.
So all of that is interesting.
Which makes for kind of a fraught relationship.
Yeah.
With whom?
between these fatherless sons and their mothers who are wrongly described as queens but are really slaves of the colony.
Anyway.
It's not fraud at all.
They're 100% related to their moms.
Right.
Which Could be rough.
I don't know.
No.
No.
Not helpful.
So it's been long assumed that the behaviors of the social insects were innate, genetic, right?
Not socially learned.
But new research suggests slightly otherwise.
So not yet.
Take my screen off while I scroll to the top.
Okay, now you can put my screen back on.
This published, I believe this week or at least very recently, in PLOS Biology.
So this is an open access journal, high quality journal.
Bumblebees acquire alternative puzzle box solutions via social learning.
Published by a number of people out of Queen Mary University of London.
And I will just read first the introduction and then the abstract and then we'll talk about it a little bit.
Or the first paragraph or so of the introduction.
The diversity of behaviors observed in some insect societies is on par with or exceeds that of some mammals and includes the construction of architecturally complex climate-controlled nests and the division of labor between foraging, brood care, and nest defense.
Indeed, outside the human realm, their nesting structures are unparalleled in terms of their regularity, sophistication, and their scale and proportion to body size.
There is profound variation in foraging specializations, architectures, and social organizations not just between related species of social insects, but more intriguingly, even within species.
While these specializations have historically been viewed as a limited set of pre-programmed responses to external stimuli resulting from evolutionary trial-and-error processes, this innate repertoire is supplemented by a remarkable capacity for learning that has been recognized for decades.
The acquisition of the honeybee dance language is perhaps the best characterized example of social learning described thus far in an invertebrate, and as early as 1884, Darwin suggested that nectar-robbing of flowers by bumblebees could spread socially.
I did not remember that, that Darwin had suggested this.
Then they've got, um, what they actually did here is, uh, to investigate social learning, a two-action control experimental design is helpful, as this can help exclude alternative explanations.
Such designs have been used to great effect to investigate social learning in chimpanzees, with demonstrators trained to obtain food from a pan pipes apparatus in one of two different ways, and observers acquiring their demonstrator's technique.
Meanwhile, without a demonstrator, no chimpanzees acquired either technique.
So you seed the culture of chimpanzees with a way to solve a problem, and the chimps pick up that way to solve the problem, but they don't solve the problem at all when you don't seed it, at least in the experiment here cited.
Meanwhile, without a demonstrator, more recently in Great Tits, demonstrators were trained to open a puzzle box in one of two possible ways before seeding them back into wild populations.
That's birds, by the way.
Great tits.
You knew that.
I did.
Yeah.
The demonstrators' preferences spread throughout these groups and were maintained long term, even when the alternative behavior was discovered, and even though the two variants were entirely arbitrary.
So interesting, right?
Two arbitrary, apparently equally good ways to solve a problem.
When one or the other is seeded into a population, that's the one that spreads when a demonstrator is fed into a population.
And it remains the consistently preferred one even when some other non-demonstrator birds stumble across, invent, whatever, learn the other way of doing things.
Their way, which is supposedly neither better nor worse, although that's going to be really hard to actually obtain in a real world situation, the newly discovered way does not end up winning the day.
For the present study- As you would expect, in my opinion.
Yeah.
With the big caveat that the two ways of doing things have to really be equivalently good, And that's, for me, that's a- All else being equal, you would expect that conservatism.
Yep.
For the present study, we designed two option puzzle box feeders formed by previous work in Bumblebee problem solving, which replicated those used to investigate the spread of arbitrary behavioral differences in great tit populations.
We then developed an open diffusion protocol that allowed the spread of box opening through the group to be recorded, and seeded colonies of bumblebees with demonstrators trained to perform one of the two possible behavioral variants.
These novel foraging techniques were successfully acquired by untrained bees via social learning.
And there's a lot more to say here, but as they allude to there in the introduction, which is odd, but they allude to the results of the discussion there, this box-opening behavior spread through colonies seated with a demonstrator trained to perform one of the two possible behavioral variants, and the observers acquired the demonstrated variant.
This preference persisted among observers even when the alternative technique was discovered, and in controlled diffusion experiments that lacked a demonstrator, some bees spontaneously opened the puzzle boxes but were significantly less proficient than those that learned in the presence of a demonstrator.
So, much as what has previously been described, discovered and described in both chimps and great tits, which are in turns mammal and bird, which are known to be, you know, have complex brains, highly social, highly capable of learning with cultural transmission of information, Here we have a very similar result in bumblebees.
Now these authors are not going so far as to call this evidence of culture because bumblebees die out.
Bumblebees are effectively annuals with only the queen surviving overwintering and so you don't have the acquisition of this learning taking place multi-generationally, but you do have it within the season that it is happening.
And thus, as the authors say, this is likely to be a necessary precursor to, if not sufficient to describe an organism as having culture.
Yeah.
Frankly, I find that distinction a little arbitrary.
I get why it is.
They're using a definition of culture that requires cross-generational transmission.
Yeah, and that is a real distinction.
On the other hand, all of the capabilities here transmitting a behavioral phenomenon like that across a population, I would say, A, it raises questions because not all hymenopterans are annuals.
And therefore, if the same capacity existed in something like, let's say, thatch ants, then you would expect it to transmit.
You would expect a colony to have this capacity and to transmit it through generations.
Generations being a little bit of a weird term because you've got presumably a single queen, although there are things that happen when a queen dies.
But anyway, all that aside, the reason that you would expect a group of bees who had learned a technique from a demonstrator to be resistant to the acquisition of a new technique, though equally good, is that it wouldn't be equally good because they would though equally good, is that it wouldn't be equally good because they would be less proficient at the one Precisely.
And so you expect this resistance to doing it the new way.
And the real question is, how much better does the new way have to be than the old way in order to overcome that conservatism, which then becomes a model for exactly what we have in civilization, where there's a tendency to want to do things the way we've done them, which is the right tendency.
And then there is sometimes a benefit that is worth engaging in the changeover cost.
Well, and I think here is one of the places where bumblebees being annuals, and humans decidedly not, will make the answer to that question potentially very different, right?
Like if you've got a colony that has a lifespan measured in months rather than a societal lifespan that could possibly be measured in millennia or at least centuries, It's a very different analysis to say, okay, like, I don't care how many times you manage to do the thing, you're going to be dead next month.
And it probably doesn't make sense for you to learn a totally new technique when what you're doing is equally good or even just slightly less good.
And I will say, actually, that with regard to the bee work, it was like they had like a turn a red thing counterclockwise or turn a blue thing counterclockwise.
I don't remember the specifics, but there was a red and a blue tag.
And red is right near the edge of what bumblebees can see very well.
And so when there is no demonstrator, blue tends to be the thing that is discovered.
They both work equally well, and the bees can see the red, but they don't find it first.
That said, when the demonstrator is trained on red, and blue is discovered in that colony, red still persists.
So that suggests that sensory exploitation is not going on here, right?
Like that, oh, well, we can see this thing, but actually, Georgina over here has discovered the thing that we can all see better, so let's go there.
It's like, you know what?
We're all going to be dead soon.
Let's just stick with what we know.
Well, again, this is
There's going to be a threshold of superiority, and in fact, I didn't read the paper so I'm just learning about the technique, but it does seem to me that you can actually, you've got a continuum of difficulty that you could deploy that would cause you to find the threshold at which the changeover was worth paying, and it would be interesting whether that changeover, that threshold was at a different place at a different point in the season.
Yes.
Right?
Precisely.
But anyway, that is really interesting, and that does sound like such a fun experiment.
Doesn't it?
There are a lot of boring things you can do in biology graduate school, but that sounds like fun.
Yeah, no, it does.
And yeah, social learning in bees and just reminding us again that we imagine ourselves the only ones who are capable of the things that we do on this planet at our peril.
It's silly, right?
There are a lot of other ways to be and many other organisms do things better than we do.
And many do things worse, but also there are a lot of other ways to arrive at similar kinds of skills.
And here we have an example of bumblebees.
Ways to be a bee.
Ways to be a bee, indeed. - Yeah.
All right, I think that's gotten us to the end of our first hour or two here.
We're going to take a break and come back with a Q&A that will only be on Rumble and later on Spotify as well, I think.
Are we putting these on Spotify?
Yeah.
The Q&As.
Okay, so you can ask questions in the live Q&A at darkhorsesubmissions.com.
That's where that happens.
We've got a lot of good guest episodes coming out right now.
You mentioned earlier the one that just came out on Saturday with... Berto Baduri and Paul Merrick.
And it's a conversation which Many people who have watched it have had a rather profound experience from it because it talks about a story, an unknown story.
In fact, we broke it on Dark Horse.
An unknown story where pharmaceutical skullduggery upended a safe therapy in favor of a new and highly profitable and not safe
therapy and this it ultimately ended up having something to do with COVID but this started 20 years before so anyway it's a very interesting story very well worth engaging and I would encourage you strongly to to go check it out.
Excellent.
Also, please check out Natural Selections, my sub stack.
This week I posted a piece I wrote a few years ago called In the Footsteps of Those Who Came Before, about walking the Yumbo Trails in the Andes, in the Ecuadorian Andes.
which in the in the mountains of South America the soils are such that when you walk a path a lot over time it wears it wears in and the trails some of the trails that you can now walk in the Andes specifically in the Makapakuna Reserve where we spent time with students The walls, they're very narrow.
It's basically single track.
You wouldn't want to bike there, but it's basically single track.
You can't go to a breast.
And the walls are sometimes over the height of a human head.
Often these are three, four foot high walls.
And that's not made mostly by moderns.
These were made by Yumbo people who coexisted with and were actually in some collaboration with the Inca and existed before the Inca came to Ecuador.
So, it is truly remarkable to know that you were literally walking in the footsteps of people from a thousand, two thousand years ago, and try to imagine what their lives were, and not make simplistic generalizations about what they must have been because they were agents.
So that's at Substack, that's at Natural Selections this week.
We, I would encourage you again to join our Locals.
The Discord is going to be on there soon.
We have the Watch Party right now for this and for our Q&A, for our live streams, and we're going to start doing our private Q&A only on Locals starting this month on the last Sunday of the month.
We have DarkHorseStore.org where you can get some stuff.
PsyOp until proven otherwise.
Dark Horse stuff.
EpicTabby.
Our EpicTabby has been absent lately, but he'll show up again soon, I would hope.
He's been on vacation.
No, it's August, I guess.
He's an extended walkabout.
No, he's fine.
He's good.
He's just been camera shy of late, as has Tesla, our panther cat.
You can get copies of Hunter Gatherer's Guide to the 21st Century everywhere books are sold, including at Darville's here in the San Juan Islands, where it's signed.
And we forgot to mention last week that you are continuing to have excellent conversations at your Patreon.
You had those this last weekend and you will continue to have those even as we try to encourage most people to move over into locals.
But your higher level patrons are still going to be having conversations with you on the first Saturday and first Sunday of every month.
Yep, Coalition of the Reasonable if you want to talk about current events, and Evolutionary Biology is the other discussion in which we talk about... sometimes it involves current events, but it often is focused around evolutionary principles and questions.
Anyway, they're both great.
Excellent.
And both at your Patreon, on my Patreon, and our locals, soon you're going to get access to our Discord server, which is just a wonderful, wonderful group of people engaging in difficult and not-so-difficult topics, having book clubs, karaoke, happy hour, Lots of great stuff, and every week that we do a Q&A, we start out with a question from them, so that's another way to interact with us.
Once again, we encourage you to check out our wonderful sponsors this week, which were Un-Cruise and American Hartford Gold and Mudwater.
And we will have links to those sponsors in the show notes as well as to the papers that we talked about this week.
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