Widespread Problems in Biology: Dr. Joomi Kim on DarkHorse
Bret speaks with Dr. Joomi Kim on the discovery that some of the processes biologists use are not what they believe they are and the implications this could potentially have on science. Dr. Joomi Kim is a molecular biologist and author of the Substack, Let’s Be Clear where she challenges the mainstream narratives about COVID-19. Please note, Dr. Kim offers the following correction: “While describing the steps of western blots it may have sounded like antibodies get added before the blott...
I have the delight of sitting in person with a good friend of mine, Jumi Kim.
Jumi Kim is a molecular biologist.
She did her PhD at Rutgers studying diatoms.
And as I understand it from you moments ago, the arrest of the cell cycle that would allow you to fatten them up before taking them to market, something like that.
Yes, they make oils and you can use the oils for all kinds of things like biodiesel.
All right.
Well, if I need to make any biodiesel, I will be sure to arrest the cell cycle of the diatoms in question for that purpose.
Jumi also has a wonderful substack called Let's Be Clear.
We have mentioned it on Dark Horse many times.
And what she does there is she does deep dives on topics of relevance to the public using her background in biology and elucidates things with wonderful clarity.
So anyway, I'm a big fan of the substack.
I hope people will check it out.
And you happen to be, happen to be somehow in the San Juan Islands, which affords us the ability to do this in person.
So Jumi, welcome to the San Juan Islands and to the Dark Horse Podcast.
Thank you, very happy to be here.
All right, so I don't know where we should start.
There's a lot going on.
Your most recent Substack article was of great interest to me.
It involves a discussion of the discovery that some of the Processes, techniques, models that we use in the study of biology are not what it says they are in the catalog.
They don't work the way they're supposed to and the implication for science is potentially profound.
So do you want to start by describing what all that means and how it plays out?
Yeah, so what prompted this article was that recently there was a news article in Nature magazine, the journal, and it was talking about broken plasmids.
So plasmids are circular pieces of DNA That is used in molecular biology constantly for cloning, for making genetic transformations.
Normally, these circular pieces of DNA, you have some gene of interest, you know, that you then stick into bacteria, the bacteria multiply, now you have a whole bunch of copies of the gene of interest, then you can use it to To stick the plasmids into some other cell, now that cell can express that gene.
So here, just for the interest of getting people up to speed, please feel free to correct anything I say that's incorrect.
I am not a molecular biologist.
I certainly studied a bit of microbiology, but anyway, it's not my home territory.
Circular plasmids are a regular feature of bacteria in nature.
So in nature, very often a bacterium, which has a circular chromosome, will have auxiliary chromosomes that contain information.
And a famous example of this that people may be familiar with is that bacteria, which are vulnerable to antibiotics, sometimes will have an antibiotic resistance gene on a plasmid, and those genes can actually be exported from one individual bacterium to other bacteria, conveying that resistance horizontally across the population.
And so in some sense, like most or all of our best biological techniques, The use of plasmids in molecular biology to transmit genes into a population or the growth of antibiotics or other products using plasmids is us borrowing a technology that we found in nature and repurposing it for our own ends.
Anyway, that's kind of a nifty thing.
It's not like we invented these things.
We just stole them and it turns out they're terrifically useful.
Yeah, exactly.
Yeah.
Great.
Okay, so you were talking about this nature Yeah, so the problem, though, is that so you can order plasmids that are just synthetically made in the lab.
The problem is that sometimes the sequence, the DNA sequence, is not what you ordered.
It's different from what was intended, you know.
And then if you're using this, you think it's a certain sequence.
you have certain results in the paper and then somebody else tries to replicate it, they might find totally different results.
So some independent researchers, they looked at some laboratory-made plasmids and saw that the sequences were not what they were supposed to be.
And like half of the, I think half of the ones that they studied, the plasmids from these labs were broken in some way where the sequence was not correct.
Okay.
So give me an example of a plasmid you could order from a catalog.
Maybe something that, a common one might be something that creates a protein that glows in the dark.
Fluorescence.
Yeah and then it usually has other things attached to it like antibiotic resistance because it's useful to have that as a way to select for um the cells that you've successfully transformed you know but it has other things on the plasmid.
Let's say you've got a Antibiotic resistance coupled with a fluorescence protein, then that allows you to actually physically see where the thing has successfully gotten and where it hasn't.
So you could select for the places where you've transmitted it as you intended, and you could do your experiment.
And you're saying the sequences are, you know, you're looking for a sequence and so you order it from a catalog assuming that what comes in the vials or whatever form it comes in is the sequence that you ordered.
But somebody has gone through the process of actually sequencing what they got and discovered that actually it's not a match.
That there's a large number of these things that you ordered one thing and you got something that was Either not what you ordered or what you ordered but spelled badly right fair.
Yeah Okay, and so then that creates so you can't replicate some of the work where that where researchers have not checked, you know, so They're gonna get different results In that Should we keep talking about that or I can talk about some of the other examples of like problems not just with Cosmids?
Let me ask a question or two before we move on to the other examples.
I'm old enough that I remember when it was pretty hard to sequence stuff.
It was an arduous process, an expensive and arduous process.
It's gotten a lot easier.
How hard is it for somebody who has ordered plasmids to spot check them for sequence to see whether or not what they have is what they thought they had?
It's not that hard.
I mean, most people just get it sent off to be sequenced themselves.
They may not have the facilities to do it themselves, but they often just use a third party.
So it's just a matter of paying a bit of money, not exorbitantly expensive.
And just for my own interest, The process of sequencing a plasmid, can you just send it blind and say, tell me what's on this?
Do you have to send them a primer sequence?
What has to happen in order to be able to get back a report that tells you what's actually on the plasmid that you ordered?
I'm not an expert in sequencing, but there are ways to a sequence where you don't need to give hints or primers, you know, because people do it like where they just take environmental samples, they have no idea what's there, right?
So supposedly, there are ways to do it.
Now, I can't tell you how good those ways are.
But theoretically, there are ways to do that.
Okay.
So somebody checks A consumer good that ought to have high quality control and discovers the quality control isn't there, which raises not only problems for the reproducibility of results, but it raises questions about the results in the first place.
They're not reproducible, but even if they were, because you had the same badly spelled plasmid, A badly spelled plasmid may give you an experimental result that, you know, falsifies a hypothesis that's actually true, for example.
Yeah.
I mean, one way in which you might use the plasmid is that you use it to genetically transform some cells and say, okay, how different does this cell look when it's expressing this new gene that we've introduced, which is on the plasmid?
But if that gene that you introduced is actually not the gene you think, it's expressing some protein that isn't exactly what you thought it was.
So now all the behavior of the cell that you're measuring is not a result of the protein you think it made.
It's something else.
Right, so let me, this is a crude analogy, but I think it works.
Imagine that you were trying to test the effectiveness of a set of instructions for increasing the speed with which somebody could build an object, right?
Like let's say you were trying to, you were going to test instructions for assembling furniture.
And you ordered the instructions, but you didn't look at them.
Maybe they're in a language you don't speak, right?
And so you get a set of instructions and you assume that they are whatever you intended to encode, translated into a language you don't know.
But let's say that they were gibberish, and you discovered actually including instructions doesn't actually increase the chances of somebody assembling this object quickly, so instructions don't work.
The answer is no.
You don't know that instructions don't work.
You know that whatever you gave them didn't constitute effective instructions.
So if that happens in an experiment, you could easily conclude something scientifically on the basis of a hidden assumption, which is that, you know, that what you said in the methods section is actually what you introduced into your sample.
And if it isn't, you don't know what you know.
So that's a cryptic, very large obstacle to correct science.
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Once you've published your result, If it was predicated on a bad plasmid.
Then it will be taken as an assumption for the person who runs the next experiment.
They will say, well, this had no effect over here.
OK, but what had no effect?
Some badly spelled plasmid.
The correctly spelled plasmid might well have had the effect that they were looking for.
But then the next experiment is predicated on the idea, well, we know this has no impact.
So this compounds over time.
And it raises a question.
And I know you raise it in your Substack article.
But the replication crisis, in which we discovered that in sciences that require statistics, that there was a huge amount of gaming of the system by effectively
Creating the impression of statistical significance where if you understood the entire context there was no statistical significance which then resulted in us discovering that in social science most of the things that we had come to believe were true based on what seemed like scientific studies were not reproducible because they weren't true.
So this creates a whole new landscape of that where you're not even now talking about statistical techniques that are broken you're talking about A supply issue with the very materials used to run experiments that invalidate the experiments and the question is, well, okay, how much of what we think we know from molecular biology has been compromised in one way or another by this process?
Yeah.
Any guess at how much of it is broken?
I'm starting to think that, honestly, most papers probably have at least a problem in it, and it may not be a problem that nullifies the entire main story of the paper, but there's some problem, you know?
Could even be in papers that I've written, you know?
Because I've used these techniques, you know?
I talk later on about antibodies in that paper, used antibodies too.
When I read about the problem with antibodies, I was like, ooh, was my own work affected, you know?
Again, it doesn't necessarily nullify the whole story, you know, the hypothesis, but I'm starting to think, yeah, that most papers might have at least a problem like that.
Okay, so that sounds like incredibly widespread.
Yeah.
So let's talk about the antibody version of this.
That will begin to make the pattern more obvious.
Yeah, so antibodies are, well, people have heard of them because, you know, They think of immunity.
They're proteins that we make in our bodies, but they're also just something that gets used in molecular biology all the time for studying proteins.
People may have heard of Western blots.
Antibody is a key to that.
But basically, what they found was that there was batch variability with antibodies.
So you might order an antibody from the very same company, it's the same antibody from the same company, one time, then order a few months later, it's a different batch, and they're acting different.
So there's batch variability.
And actually, if you look into how antibodies are often made, maybe this isn't so surprising, because they often use like animals like rabbits and goats and stuff to make the antibodies for them.
And there's some, you know, biological variability in how they're making it, you know.
So, because there's this variability, I mean, some researchers were just testing this out between different batches, and they found that, wow, some of the findings for one batch don't replicate, you know, with another batch.
All right, so I'm going to again translate from technical English to simple English.
And again, it's not my field of specialty, so you just correct anything I get wrong.
Antibodies are something produced by white blood cells, B cells, that have a very unique electromagnetic property.
So people will be familiar, and maybe we'll even include a diagram in the podcast here, They have a characteristic Y shape so they've got the tail of the Y and then they've got the two ends of the Y and at the tips of the two ends of the Y are the variable regions and when I say variable what I'm getting at is Electromagnetically variable.
So if you imagine that atoms and molecules have charges on them that function like magnets, so you've got north and south, or positive and negative, and that the distribution of magnets, let's imagine that you had a pad that had room for, I don't know, 700 magnets on it, and that you could arrange those magnets.
They would be distributed in a particular way, but you could flip them so that in any given location, at any basically pixel on that pad, you could have the positive side facing up or the negative side facing up.
And then you imagine that you made an inverse pad that had all of the magnets flipped the opposite way.
Those two pads would stick together really, really well.
If you flipped them all the same way, they would repel each other.
They wouldn't stick at all.
And if you took a random pad with the one that you had carefully arranged, it would not stick very well because for every magnet that attracted, there'd be one that repelled, so it wouldn't get nothing.
So anyway, what we've got is a system in which if you have an electromagnetically variable object in the world, like a protein, You can detect it by coming up with something that has the inverse pattern of electromagnetic positives and negatives because it sticks.
So if you take the Y part of the antibody, I mean the stem part, and you put a fluorescent or a radioactive marker on it, you can dump the antibodies into the system and then you can wash it and you can say, well, where do I still see them?
Wherever I still see them, they're sticking because of that electromagnetic match and That way you can use this as a quick and dirty technique, again borrowing from something that nature created, which is the ability to make these electromagnetically distinct detectors.
You can use that to assay the presence or absence of something that you're interested in.
You could look at a cell and you could say, is this protein that I'm interested in a component of this tissue, right?
Wash it in the stuff and just see whether the antibodies with their radioactive tag sticks to that tissue.
If so, then I know that that receptor is there.
So anyway, again, same theme.
We're borrowing something from nature that we couldn't have made.
We're using animals to produce it because it's the animals and their B cells that are making these things.
And what you're telling me is that if you order them from a supplier, you think you know what you're getting.
You're getting something that's looking for a particular inverse sequence.
But even the same supplier, two different batches, they may not work the same, which means that you could get an experimental result.
You might have the identical protein sitting somewhere, and you might conclude that the protein was different because the affinity of the antibodies from this batch is higher than the affinity of the antibodies from that batch.
Right.
Exactly.
I mean, it's mind-blowing.
If there's one thing you would want to be able to just rely on, it's that at least the equipment you're using, in this case the antibodies, is consistent.
Yeah, yeah.
And I mean, people have always been aware that also, you know, antibodies, they're supposed to be specific for a protein, but in reality, they might bind to things that, you know, you don't want them to bind, right?
That's an issue.
That was also something that was discussed in the article.
But this is literally about something where there's batch variability, so it's a bit worse.
And the reason, you know, when you had asked, like, you know, what percentage of research papers have some problem in it.
The reason I said that was that I think most papers have at least one problem is because Western blots, which use antibodies, they're in almost every molecular biology paper.
They're just everywhere.
They use antibodies.
So do you want to explain what a Western blot is?
I guess very briefly.
Yeah.
So, you can use a Western blot to see if there's the presence of some protein of interest.
Let's just pick the spike protein, if a cell is making spike protein or not.
And you can even try to quantify it, like, you know, at different time points is the cell Making more or less spike protein.
And then you can have an antibody that is supposed to be specific to the spike protein.
And you take your samples of this cell, which contains all kinds of proteins from the cells, including supposedly the spike protein.
You extract the proteins from the cells, and then you add your antibody, right?
And then let it bind to spike protein.
And the antibody is supposed to have something, some kind of tag that, you know, like, let's say gives off some color so that you, if there's a lot of that color, you know, you had a lot of the spike protein.
There's a little bit of the color, you know, you have only a little bit of spike protein.
You run it on something called a gel.
A gel is something that can separate out proteins by molecular weight, and you're supposed to know the size of your protein of interest, in this case spike proteins, so you know when you run this gel where your protein should be, roughly.
So once you run it, you can see where the protein is, then you transfer all the proteins onto something, a blot.
Paper.
is just a special kind of paper.
You wash your-- there's secondary antibodies, which are supposed to bind to the first antibodies, I don't know if this is getting into too much detail, but this is what allows you to visualize how much of your protein of interest is actually there.
If the band is looking really nice and thick and dark, there's more of your protein.
If it's very, very light, then there's Less of it.
Right.
Okay, so I'm going to add one thing just because I think it's really cool.
I remember learning about it a million years ago.
The process of separating out these proteins based on their molecular weight is pretty interesting.
You've got a gel, which is like a, it's a matrix of stuff.
that has is porous enough it's it's literally a gel but it's porous enough that these proteins are small enough that they can move through the spaces so what they do is they electrically motivate them to move right so you put them all at one end and then you electrically motivate them to move in other words you put a repulsive electromagnetic force at one end and so the proteins start fleeing from it
But the rate at which they flee is inversely proportional to how big they are.
Right.
So the bigger ones move slower because they're cumbersome and they bump into more stuff along the way and the smaller ones don't.
So what they tend to do is spread out by size as they move through this gel which means that you can actually physically then go to this gel later and at a particular place you can find your protein isolated from the others because your protein has the same Size, right?
How do you know where to look for your protein?
So again, not my area of expertise, but you would use some sort of a known... Yeah, like a standard.
A standard.
Of known molecular weights.
Known molecular weight that would migrate along with your separating out proteins so that you could find the band you were looking for and then you could do this blot technique to test how much of that protein is actually present.
So if you were, for example, In your example of the spike protein, let's say you were looking for the spike protein on heart cells and you liquefied the heart cells.
Let's say that it didn't stick to heart cells or that it wasn't being produced by heart cells.
Doesn't mean that you're not going to have any because maybe there's spike proteins circulating in the blood that happened to be in the heart at the moment that you pureed it.
So you don't want to just simply know presence or absence because that would give you a false positive potentially.
In this case, you would find a lot of spike protein because it was actually being produced by heart cells in this animal, and you would know that because you would use the western blot to assess the basically the density of the mark that you found on the blot after you had separated out your protein.
Is that all right?
Yeah.
Cool.
All right, I feel like I'm passing molecular biology, which is great!
Okay, so Antibodies, which are unfortunate, I mean and you know this is the same thing for plasmids.
The plasmids, again you just be courageous and correct me any place I get something wrong, plasmids are being manufactured by the companies that make them using bacteria to copy them.
Is that true?
Okay, so Well, you can also just use it without, make them without that carrot.
You can make them cell free.
Yeah, yeah.
Okay, but you're using a biological process.
You're using enzymes to do the copying, the polymerizing.
Yeah, yeah.
Okay, so you're Unfortunately, dependent on a complex biological system, which wasn't built for quality control.
It was built for other purposes, right?
It was, you know, the goat has an immune system to fend off goat pathogens, and you're borrowing that system to make a consumer product, which is antibodies to assess whatever.
And you're stuck with the complexities of that biological system, which can do things you don't anticipate.
Which, in theory, the manufacturer should be aware of that.
The manufacturer should be trying to figure out what a quality control step would look like, so that nothing went out the door that wasn't what they said it was, but apparently that doesn't happen.
Apparently.
Okay, so we've got plasmids, we've got antibodies.
What else looks like this?
So, I'm not saying I've looked at every single technique, and there are some techniques I'm not that familiar with.
Like I said, if there are problems in sequencing, I wouldn't be able to tell you, you know, what they are.
But randomly, just through looking at other topics, I just found problems in Other places.
Another example, and this is not used as widely as antibodies, but another example is staining, you know, like when you're trying to look at the subcellular organization, you know, like, Where in the cell does something appear, right?
Turns out it's not super straightforward.
There's different ways to do it.
But and one of them is using standing technique where you first have to fix the cell that kills the cell.
And actually, you are using antibodies, you know, for some processes of these.
But then it during this process, there could be some artifacts, you know, where the very process where you're fixing can make the protein that you're looking at, like move into a different part of the cell, you know, so maybe in nature, it would never be there.
But the process that you're using is making it go into like some other organelle, like let's say into the nucleus.
So that was one example.
Another was that which I bring up in that Substack article is just contamination, which is really rampant.
So there was, there's actually a lot of work about cell lines and how sometimes they end up contaminated.
And there's a lot of work on them and they don't realize that it's contaminated.
They think they're working with cells that are, say, from the throat muscles or something, but it turns out it was contaminated by HeLa cells.
HeLa cells are this well-known cell that was originally from a woman who had cervical cancer.
It was from Henry- Henry de Lack?
That's why they're called HeLa.
And apparently they're quite aggressive, you know, they grow really well in culture, and then they may just out-compete other cells, you know, in like your petri dish.
So you think you're, you know, looking at one type of cell, you know, like heart cell or brain cell or something like that, but actually you're looking at HeLa cells, you know.
There's a lot of papers where, you know, this cell line turns out to be HeLa and they think it's something else, you know.
All right.
Is that the extent of the examples that you found in terms of potentially broken techniques and orderable goods?
At the moment that I can think of, yeah.
OK.
So I want to put a hypothesis on the table, an evolutionary hypothesis.
Now we're back in home territory.
I feel safe.
Here's the idea.
In science, No, in the academy you have niches and the creatures in the academy, the professors and researchers, they're creatures and they evolve to fit those niches and the niches are described just as they are in nature by the presence or absence of resources that the creatures can use.
So unfortunately we've set up a system in which The resources flow to those who write the papers and file the grants that get funded.
They no longer flow to... I'm not saying they never do, but there's no longer a strong reward for being right in the long term, right?
So what I'm getting at is this sounds to me an awful lot like You got the system you ordered.
I'm not talking to you, of course, but you got the system you ordered because what you rewarded people for was producing stuff that looked like work.
The fact it was not in their interest to figure out that they were running experiments that didn't make any sense, because whether a paper gets gets its author advanced in their career, You know, or a job, or whatever, is based on crude proxies of success.
It's not based on whether or not you were insightful.
So, you know, somebody who steals ideas may outcompete somebody who generates ideas, because generating ideas is harder than stealing.
Somebody who runs experiments at large, at a rapid rate, and publishes lots of papers will outcompete somebody who runs experiments that are high quality.
Right?
Somebody who gets cited a lot will outcompete somebody who gets cited less even if the person who gets cited a lot is being cited for being wrong.
So when you have all those broken incentives, it's not so surprising That nobody checked whether or not these things were what they pretended to be, because that's not what we asked them to do.
Yeah.
In fact, it would slow them down, right?
If you, in your career, decide that you're going to check every, you know, you're going to calibrate every apparatus and you're going to check your cell lines and your plasmids and your... You just wouldn't get rewarded for doing that.
Like, it would just be a lot of extra work, right?
And you'd have less time to just churn out many, many papers, which is what you should be doing if you want to, if you want tenure.
Right.
So, that's a horrifying thought.
I will say when I heard about the replication crisis in the social sciences, my thought was, that ain't the social sciences.
That's going to be the entire apparatus, right?
Certainly every place where statistics are used you're going to see this p-value hacking, but There are so many places where a person who is sloppy is going to get ahead in the system and a person who's careful is going to fall behind.
You know, certainly there's no role for theorists anymore.
We treat that as an unimportant skill and in fact it's a necessary skill.
One which would in fact force you to do some checking because suddenly you'd get results that weren't consistent and you'd have to figure out why.
I want to get back to that, but just going off of what you were just talking about, I mean, it's even worse.
So, for example, with the HeLa cell contamination, people have brought it up, you know, and they brought it up to journal editors, you know, like, hey, there's this problem.
There's papers that you've published in your journal where the cells were contaminated.
And often they didn't do anything, you know, because it would have been inconvenient for them.
Because they would have to retract a whole bunch of papers.
Sometimes it was their colleagues, you know, it wouldn't be good for their career.
And I saw some fraud even during my PhD.
There was a postdoc I knew who discovered an artifact.
I don't want to go into the details.
I don't necessarily want to be like ruining someone's career, but he discovered an artifact.
He brought it up.
Unfortunately, the artifact went against the previous work of his boss, so his advisor.
And it never got published to this day, even though this person is not even in academia, he could publish it if he wants.
He doesn't, it'll burn some bridges, so nobody knows about it.
This is an example of a negative result, right?
It's just something that finds problems with previous findings.
Those often don't get published.
Right, which raises terrible questions about the whole idea of, obviously, follow the science is a joke, right?
So, Science isn't something you follow.
But even if you want to follow the scientific method, You want to be able to assume that the facts, as you find them reported, are at least true.
Right?
Yes, you have to leave open the possibility that any given thing could be wrong, but in general you want to imagine, okay, what are the set of observations about the world that I need to reconcile?
Right?
Where do I need to build out what we already know into some place that we don't know?
But if the stuff that we ostensibly already know Isn't even true.
Then what is this?
This isn't science at all.
It just, I mean, and Richard Feynman did nail this to a fairly well in his speech, which then became a famous article on Cargo Cult Science.
Oh yeah, yeah.
Where he describes exactly this process and basically his point about Cargo cult science.
He analogizes what goes on in science to these things, cargo cults, where people who, I believe these are Bornean natives, who watched during the war, they watched an amazing transformation of their island where
The military built airports and vast cargo planes landed and huge amounts of wealth were unloaded from these cargo planes and so there were actually people who attempted To make that happen by imitating the behaviors of the people that they saw involved with all this fantastic wealth.
So they, you know, carved headphones that looked like the control tower and they built phony control towers and cleared areas and they, you know, went around behaving like this, hoping that it would make the planes land.
And guess what?
It didn't.
Right?
So anyway, I think outsiders Do not know that the fact that what people are doing looks scientific means nothing.
Right?
It's really just like theater at that level.
Yeah, yeah.
No, and on top of that, add that there there is a lot of propaganda as well, you know, especially when you start to go into, you know, areas like medicine and there's a lot of money on the line, pharmaceutical products.
And I mean, if you can imagine, it gets even worse in those situations.
Yeah, the closer you get to the money, the worse this gets.
Yeah, yeah, yeah.
And then this is something, I mean, there's so many things you could talk about with this too.
I mean, problems with peer review as well.
Yeah.
Reciprocity networks.
Because the people who review your paper are in your immediate field.
So the point is, if you start slamming them for bad work, guess what's going to happen to you?
You're all going to fail.
And you've been citing each other.
Yeah, so there's this incentive to actually pretend other people's work is better than it is, so they'll pretend your work is better than it is, so you all advance faster than you should.
Yeah, yeah.
I mean, it could go the other way as well.
You know, you try to sabotage someone who's your competitor, too.
I mean, that's... it could go the other way, you know.
Peer preview.
That's the joke.
Yeah.
All right, so this all paints a rather dire picture.
And I must say, I'm reminded hearing you describe these failings of another topic on which you and I have talked frequently with a small group of COVID dissidents, which has to do with the dangers that arise when the manufacturer of something like a vaccine is immune from liability.
The feedback really requires that the manufacturer be afraid of what happens if they distribute a product that is not what they thought it was, or a product that's more dangerous than is warranted given the benefit that it provides.
And we see, you know, apocalyptic levels of malfeasance where manufacturers of medicines have immunity from liability.
But isn't this the same thing?
If nobody's checking whether the stuff that they send out in a particularly scientific-looking vial is what they say it is, why would you expect it to be consistent?
Yeah.
Well, I mean, in this case, some people have checked, right?
But and then they found some things that were really not good.
But luckily for the pharmaceutical companies, they have so much money that like they can, you know, they have ways that they can try to make those people look crazy, you know, or they're just conspiracy theorists or things like that.
You're talking about Kevin McKernan.
I am talking about Kevin McKernan.
So, for those who don't know, Kevin McKernan is a stalwart in the COVID dissident community who somebody gave him or he solicited vials from which the COVID vaccines, the mRNA vaccines, had been delivered.
So these were vials that had a little remainder in them because, of course, when they suck it into the syringe They don't suck it all the way to the bottom and, you know, get a bubbly mess.
There's more in there.
So anyway, they tested what was actually in these vaccines based on the residual and what they found, what Kevin found, was Plasmids, for one thing.
Yeah, DNA contamination.
Yeah, DNA contamination, where there's not supposed to be any DNA in these things in the first place, right?
We were told they were RNA short-lived, that didn't turn out to be true, but the process, the mechanism they used to make them involved bacteria and plasmids were left over, and the plasmids contained some Frightening stuff, like the SV40 promoter, right?
I mean, it's in fact the exact same thing.
So the SV40 promoter is a simian virus 40, I think, and it is a potential carcinogen.
Am I right about that?
That's what I hear.
I haven't looked too deeply in it, but yeah, possibly, yeah.
Yeah, so it really shouldn't be in there because for one thing, you know, the library of Biological, library is the wrong thing, the workshop of biological tools that exist in a living human being is immense.
You start dumping DNA messages in there and those things, you know, DNA can be edited in, you know, it can have all kinds of effects.
It can trigger... Yeah, at a small, at a very small rate, but it happens occasionally where it'll integrate into your genome.
Right, and integrated into your genome, you know, if you're talking about something like the SV40 promoter, which has a carcinogenic potential, then, you know, it only has to mess up one cell to kill you, right?
That's not saying that's very likely, but it means You should be very careful not to be introducing DNA messages that are coherent.
And I think, you know, I'm sure you know more about this than I do.
But Kevin then went on, in addition to just simply finding that there was DNA contamination in the form of plasmids that it contained SV40 promoter, there was also his discovery of
the range of RNA templates in there you know we were told at the beginning oh you're going to get an injection it's going to be a lipid nanoparticle covering an mRNA template and that template is going to encode this particular protein the spike protein But that's not what it was, right?
That was in there, but there were every... The quality control is so bad that there's mRNA encoding for who knows what else, and actually Western blots confirm this.
Like if you look at the products of the mRNA vaccines, you'll see that the The molecular weights of the proteins that you get as a result, they're not just what you'd expect from spike protein, but there's like other weights there.
What are those?
They're just these... Fragments.
Fragments, yeah.
Fragments of biologically active stuff, like of an actual information molecule that contains information which your system processes and reacts to.
So, you know, it's like if...
If Airbus ordered rivets from some supplier, right, and it ordered, you know, Inch and a half long rivets.
And it then loaded them into a robot that installed those rivets to keep their planes together.
But instead of getting inch and a half rivets, it got a mixture of, you know, rivets from, you know, a quarter of an inch to three inches.
And so, you know, the planes would all end up loosey-goosey because, you know, the rivets weren't consistent.
It's like that.
It's just inconceivable that you would Sell stuff.
You'd have to be indifferent to the harm to people to do so.
But anyway, the larger point was the parallel between the pharmaceutical manufacturer and the immunity from liability that caused really crappy quality control, right?
In addition to all of the other problems with the vaccines.
Terrible quality control for the vaccines seems to be mirrored It's not an immunity from liability, presumably, with these suppliers of experimental materials.
But, A, there isn't that much immunity there because, you know, a pharmaceutical company, if they kill your relative, you know, if they were liable, that would be expensive for them.
Yeah.
In the case of ruining your experiment, right, it's a lot lower risk.
But if nobody's checking, in general, Then the risk is very low.
Yeah.
And if everybody's happy because, look, I don't really care what, you know, I just got in that UPS package.
I'm just glad it's here so I can run this experiment so I can publish the paper and move on to the next one.
It's crazy.
Yeah.
Do you think the system could be rescued?
The scientific system?
Possibly.
I think the incentives would have to be set up, right?
I think that's the only way.
And I'm not sure how you would set that up.
I mean, that would be really hard.
You know, you have to incentivize truth-seeking and who's going to be the one to check whether, you know, you've arrived at the truth.
I think it would help though if you had More people looking at these kinds of things, you know, because right now we have a system where biology, it's not just in biology, scientists will produce papers.
And you don't really have a field where people are just looking and checking.
And then and then if they find a problem, like, okay, somebody comes in, like tries to redo the experiment the right way or something, you know, actually, you know, we can bring up this, you brought up like,
Theory, you know and you've brought up in the past that in physics They have theoretical physicists, you know people who whose job isn't really mainly to do experiments but You know, they're thinking about things they're looking at papers or reading the research and you don't really have this in biology where your main job is to just look at a lot of research and I mean, it's always good to have experimental experience, you know, when you're doing that.
But actually, like, I feel like I've learned more doing research for my sub stack, just looking at a whole bunch of papers than I did during my PhD, which is crazy.
Like, of course I learned more experimental stuff during my PhD, but I've looked at all these papers and, you know, sometimes things going back in the 60s, I'm like, wow, this is crazy.
How come no one's talking about this?
And I'm like, I'm just this random person.
How am I finding this?
And this is not on the front page of the New York Times or something that, you know, you can make all these connections.
All this information needs to be synthesized, too.
You can make all kinds of connections.
Sometimes something from one field will give you ideas about another field.
A random example turns out that in plant tissues you'll find bacteria or viruses, they're contaminated with these bacteria and viruses, but they seem harmless.
And now some people are thinking, maybe that happens in animals too.
So if you look at brain tissue and you're finding SARS-CoV-2 there, in the media, we'll fearmonger and say, "Oh my God, the SARS-CoV-2 infect neurons." But maybe it's just contamination, like if there's absolutely no symptoms, you know?
Yeah.
It's a possibility.
But this is something that they've known about in plant biology for a while.
Just a random example there, you know?
Yep.
But yeah, theory, theoretical biologists.
I mean, I think that could help.
Well, I mean, I will tell my piece of my story from my own graduate work because it tells this tale.
I found something very much in keeping with what you've been reporting on by accident.
And the way I found it was that I was looking at a wide Swath of literature and there was one thing that just didn't add up and I knew it couldn't possibly be true and yet it clearly was and when that happens The question is well, what's going on?
Why why is this thing that I know shouldn't be true apparently true, right?
Either there's something to discover or there's a problem with what I think is true so anyway, the story as you as you know is that I was working for my own Uh, my own reasons really was not part of my dissertation.
It ended up being part of my dissertation, but it was not what I was supposed to be working on.
I was supposed to be working on bats and tent making behavior, but I became interested in cancer and senescence because there was this very important field by George C. Williams, which Brilliantly explained why evolutionarily you would expect creatures like us to grow feeble and inefficient as we get old.
Beautiful paper that proposed that within our genomes we ought to have a lot of genes that do two things or more and one of those things should be a benefit to us early in our lives and the others should be harms late in life.
But we'd never found one and so I was curious why why haven't we found one and I thought I had a candidate and that candidate involved These repetitive genetic sequences at the ends of chromosomes called telomeres.
And what had become apparent in the years prior to my happening onto this topic was that when cells divide, these repetitive sequences at the ends of the chromosomes, which are not genes because they don't contain any information, but these sequences shrink every time a cell divides.
It loses some of this like it's like a leader on cassette tape which is a useless analogy for young people but um but if you have a cassette tape the tape doesn't go to the end of the spool there's a little bit of plastic at the end so the telomeres like that it shortens with every time the cell divides and in any case what i discovered what i happened on to was that there were two groups of people who were focused on telomeres you had people studying cancer
What they found was that in all of the cell lines in which they saw cancer, there was an enzyme called telomerase that was active, that was adding more telomere, right?
So they thought, hey, if we can turn off that process, maybe we can cure cancer.
And there was another group of people studying aging who found that cell lines were getting exhausted, and when their telomeres got short, they stopped dividing.
And so those people were thinking, hey, if we can turn on telomerase, we can live forever.
And my thought was, well, evolutionarily, I know what I'm looking for.
I'm looking for a gene that has an early life benefit and a late life cost.
And although the telomere isn't a gene, it does exactly this because What it would do is as a cell line got damaged and it started reproducing too much and would become a cancer, the fact that the telomere shrinks with every cell division would cause it to stop dividing so that it wouldn't kill you, right?
That would be an early life benefit.
You get no cancer for decade after decade of youth.
But what would the cost be?
Well, the cost would be you can't repair your tissues forever.
All right?
Isn't that a beautiful story?
Here's the problem.
Couldn't possibly be true, because mice were known to have ultra-long telomeres, and yet they live short lives.
So, something had to be off.
People argued, well, mice or rodents, they work differently.
I knew that wasn't going to be true.
They're mammals, they should work similarly.
In any case, I couldn't find a reason.
I thought at first, I thought, well, maybe this is one of those cases where one lab tested mouse telomeres and they mismeasured them and mouse telomeres aren't really long.
Oh, did I say that part?
I think I forgot to say that part.
Oh, I said it.
Mice have very long telomeres, or that's what people said.
So I thought maybe they don't have really long telomeres, and everybody's reporting one result that was erroneous because the experiment was done badly.
That would explain it, right?
Everybody's parroting one result.
No?
A bunch of different labs have measured telomeres.
They all found that mice had long telomeres.
Some papers said rodents have long telomeres, which was even more shocking because, you know, there are thousands of species of rodents, right?
We're extrapolating from mice.
But anyway, What I ultimately realized after a couple weeks of banging my head on the table over this was that there was something funny about the conclusion that mice have long telomeres and it was not that they had been mismeasured.
So I started looking into this question and what I found, much to my surprise, was that all the mice were coming from the same place.
There was a supplier called the Jax Lab which supplied all the mice in North America for science experiments and also, you know, the pet store mice.
And in any case, so they were all coming from one place and the deeper I dug, The more I realized that there was something fishy, that the colonies that they were raising these things in had their own evolutionary dynamics, and that nobody was paying attention to what was going on with the evolution of mice in these colonies.
And it didn't really seem like it could be that, because they hadn't been in captivity long enough.
It was like a hundred years.
And yet, something was off.
So anyway, I made a phone call to Carol Greider, and she didn't know me.
She was a famous person who later went on to get a Nobel Prize.
I called her.
I said, you don't know me, Carol.
I'm an evolutionary biology graduate student.
I respect what you're doing.
I got a question for you.
This conclusion that mice have long telomeres.
Is it possible that that's just wrong and that only laboratory mice have long telomeres?
And she said, I don't think so.
I think all mice have long telomeres, but it's kind of funny.
If you order Musbridis rather than Musmusculus, and you get them from Europe, how long their telomeres are varies a lot.
She said, maybe there's something to this.
So then she put her graduate student, Mike Heeman, on the case.
He measured a number of different strains of mice.
He measured their telomeres.
None of them were wild.
What I would have liked to have seen was wild mice.
None of them were wild.
But in any case, they were all in captivity for a much shorter period of time.
And actually, one of the species that they used wasn't even musk.
It was peromyscus, a deer mouse.
That had been kept in effectively natural conditions in this one colony.
But Mike Heman did this experiment.
He discovered that mouse telomeres are in fact short.
He sent me a very excited email.
The hypothesis is true.
Mice have short telomeres.
It's only laboratory mice that have long telomeres.
Yada yada yada.
Anyway, that was a long explanation to get to the fact that, as far as I know, nobody has corrected the problem that causes mice to have their telomeres elongate in the breeding colonies.
What I believe the problem is, in fact, I believe it is the only hypothesis that remains standing.
Carol herself tested the question of whether or not it was inbreeding that caused the elongation of captive mouse telomeres.
It is not.
What appears to be causal, the only hypothesis that remains standing that I'm aware of, is that it is the cutoff in the duration over which mice in these colonies are bred.
Because aging reduces the rate at which animals can reproduce, in order for this business which makes these mice to be economically efficient, they throw out the breeding mice after eight months.
So they're always breeding young animals.
And by always breeding young animals, they don't give the animals in the colony enough time to die of cancer.
So they remove that selective pressure for the cancer protection that comes from telomeres.
At the same time, the mice that come to evolutionarily dominate the colony are the mice that breed fastest.
You take a trade-off where selection is balancing cancer resistance and longevity and you take the cancer resistance out and you prioritize rapid breeding, so youthfulness, and you create hyper cancer-prone mice that don't really age.
Their tissues do not appear to age under a microscope.
In any case, The crazy thing to me, when I realized that this was the likely thing that was going on, and I knew for sure that the laboratory mice that were being supplied were broken in that they had these abnormally long telomeres, my thought was That's going to be a huge scandal.
These animals are a hazard from the point of view of science because they're a bad model.
You're taking a mammal and you're using this as your primary mammal model and it doesn't work like a normal mammal because you've created a hyper cancer-prone animal for one thing.
So this is bad for studies of cancer.
It's bad for studies of wound repair.
It's bad for basic mammal physiology.
And somebody's going to have to go through the entire literature that used these animals and figure out which of the results that we think are true actually are and which of them are the result of these labs from these broken colonies.
Well, that was me being naive.
That reckoning never came.
In fact, it's very strange when I try to talk to people about it, because I get one of a number of reactions that are not responsive.
Everybody knows the mice are broken.
Okay, but they don't have to be broken in this way.
There's a perfectly good way to solve this problem, and yet we don't.
So, we already knew that.
It isn't important.
Everybody knows the mice lie.
These are the excuses that are delivered.
But here's the punchline of the story.
Not only are these things bad models that are still used in science today, despite their elongated telomeres, but they are also used in drug safety testing.
And when I ultimately published my paper on this, I was very clear about the hazard of using them for drug safety testing because a mouse with ultra long telomeres has No limit on the number of times it can replace a broken cell, which means if you give it a toxin that doesn't outright kill it, it has the capacity to repair the damage where the human that you gave the same toxin would not have that capacity.
So, not only is it true that these mice are basically tailor-made to make you think that toxic drugs are safe, because the mice don't die until the dose is incredibly high, but You get a paradoxical result sometimes result which is that because these animals are effectively hyper prone to cancer
And because the reason that chemotherapy works for cancer is that cancer cells, because they're in the state of dividing very frequently, whereas most of your cells are in a state of quiescence, cancer cells are vulnerable.
If they're dividing, then they can't repair damage because the two halves of the DNA are not sitting next to each other, creating an error check.
So, the trick with chemotherapy is kill the cancer faster than you kill the patient.
You give a toxic drug and it kills the cancer.
Well, if you're doing drug safety testing on mice that have this high propensity for cancer, you may actually extend their lives if you give them a toxin because it's effectively chemotherapy.
And so, you know, okay, so now imagine The pharmaceutical industry is now testing their drugs with mice that are prone to give the answer that this drug is very safe.
And in fact, you get a weird paradoxical result.
Hey, this stuff is so safe, it actually makes the mice live longer sometimes, right?
That makes it sound like it's really benign, when really the message is, oh, that's highly toxic.
These mice are short-lived and cancer-prone.
They're not good models for drug safety testing.
And yet somehow, more than two decades later, we are apparently still using them.
So yeah, I don't know what to say about that other than in the the examples that you are pointing to, plus this example, plus who knows how many other examples that we don't know about, raise major questions about how science can be done.
And we haven't even talking about fraud.
I mean, that exists.
Nobody's checking, right?
If the numbers you gave on a chart in your paper, if they're not just made up, it's just the honor system.
There's fraud and then there's a million things in a gray area.
Yeah, yeah.
You know, the JAX lab hired somebody who's a mouse telomere expert.
I can't get a straight answer about what the state of the telomeres in their mice is.
So, okay, my paper got published.
Does deliberately ignoring the implication of my paper constitute fraud?
Presumably not, right?
How many people are ignoring some paper that says something inconvenient to what, I mean, how do you even manage a system, right?
So until you get to the point where you get rewarded for being right and therefore have an incentive to find everything that's wrong with the experiments you're running and the papers you're publishing, I think this is hopeless.
Which raises another question.
And I'm sorry.
I don't have the data on this, but am I correct that the period of time in between a discovery and the awarding of a Nobel Prize has gone down?
I don't know.
I haven't kept track.
But if your reason why you're asking about this is because of the last Nobel Prize, it seems a little premature that they gave it.
Well, that one, it took almost 25 minutes.
Before they awarded the prize for the pseudo-uridine enrichment of the mRNA and the... This is the same organization, the Nobel Prize Committee, that awarded lobotomies, right?
The inventor of lobotomies won the Nobel Prize.
Well, I'm going to steelman the case for lobot... I can't actually steelman the case for lobotomies, but... So, the reason I raise it is this.
It used to be presumably very frustrating to people who had made a Nobel Prize worthy discovery to have to wait a very long time to get a prize because of course the resources and acclaim that come from the prize, they're supposed to enable you.
We take the best of our scientists and we enable them to do more by giving them the special honor.
And, you know, to have to wait till late in your career, even if you discover the thing early in your career, is frustrating.
On the other hand, it does tend to prevent embarrassing mistakes.
Right?
This Nobel Prize for Pseudouridine Enrichment of the mRNA in the COVID vaccines.
I mean, that, that couldn't be a more disastrous choice.
Yeah.
And there's just so they're going to be stuck with that.
It's going to be like lobotomies.
Hopefully I see that within my lifetime.
I don't know.
I don't know.
Yeah.
But then again, these things get sort of buried.
It could be decades.
It could be longer.
I mean, I hate to think of that, but.
Yeah, well, it also creates a just a series of perverse incentives because, you know, That something like that could get rewarded and... Right.
Yeah.
Nobody checks and...
Yes and you know I mean and in fact yeah I've told the story before but there's a scene in Catch-22 where um the bomber pilots have been given an assignment that's extremely dangerous and they're freaked out about it so they panic themselves and dump their bombs over the water rather than do the thing that they've been assigned to do and their uh the their commanding officers
I mean, I think that they actually believe that it's good work though.
That's my guess.
Oh my goodness.
cover it up, they give them medals for their bravery, right?
And it's like, okay, that's ridiculous.
But then we see this stuff, it happens.
And this is that sort of thing.
I mean, I think that they actually believe that it's good work though.
That's my guess.
Oh my goodness.
How could they?
So, I mean, for people who aren't aware, there are published papers and actually very prestigious journals showing all kinds of problems, you know, with this using N1 methyl pseudouridine and the mRNA vaccines.
So, just so people know, the mRNA vaccines are not like normal natural mRNA, because the uridines have been replaced by this other type of pseudouridine.
But that's causing all kinds of problems, like One might be that it might be leading to an issue where the cell can't get rid of this mRNA, you know?
Because we have RNAses that are supposed to break down natural mRNA, but it seems like this synthetic mRNA just could last for months, you know?
I think the longest we found was... I forget how many months.
A couple months.
Yeah, several months.
But a couple months and it's not like it petered out at that point.
That's where they stopped measuring.
Right, we're right.
Yeah, exactly.
Yeah.
So that's just like, we don't know what's going on there.
It's immature technology, you know, at best.
Yes, of all... This technology was absolutely immature.
The as well as the LNP technology.
But yeah, the emergency that supposedly justified us taking the risk of using this technology was not what it was represented to be.
So you have an immature technology brought to market under false pretenses and quality control was absolutely crappy.
But of all the design failures in this vaccine, and there are many, The pseudo-Uridine enrichment strikes me as top of the list.
Maybe it's not the absolute top, but it's certainly among the biggest design failures here.
Does that seem overblown to you?
It's hard to say because there are so many, but, um...
I think, well, at least just on a personal level, like if I had known about that, I wouldn't have gotten the shots.
I mean, just so people I know, I got the shots.
This was before I did any research on them.
I got two shots of the Moderna, which I now regret.
But if I had known that, oh, this is not like natural mRNA, which normally only lasts for hours to days in the body, but in fact can last for months, then it's like, whoa, that's a very new type of thing.
You don't know the implications of that.
And you could just be making spike protein during that time.
Maybe it is the worst.
Yeah, maybe it is the worst.
It's really bad.
Well, that and the fact that it's not targeted, too, I guess.
That's bad, too.
Failure of the targeting of the lipid nanoparticles.
But as I understand it, the Pseudouridine enrichment.
So, Pseudouridine is something that happens in nature.
It's a trick that nature uses, but very, very sparsely.
Yeah, in other types of RNA.
Not mRNA, I'm pretty sure.
Oh, I didn't know.
Okay, so it uses it in other types.
Well, that actually makes sense then, because... But N1 methyl Pseudouridine, I'm not sure if it is.
Maybe it's nowhere.
Nowhere natural.
Maybe.
I'm not sure.
But Pseudouridine is another...
But in any case, so they replaced every single uracil with this synthetic product that stabilizes these things.
So that's completely unnatural.
And then these things apparently cause the ribosome, which is what takes the mRNA message and turns it into protein, Stumbles on them.
It's not built to handle them, and it's certainly not built to handle a molecule in which every uracil has been replaced.
So what that means is that the brochure says, oh, we're going to inject you with this mRNA message.
They told us mRNA is short-lived.
And you're going to produce some spike protein, you'll get your immunity, it will clear from the body, blah, blah, blah, blah, blah.
Total bullshit.
The stuff persists indefinitely, and we have to say indefinitely because we don't know, we know that it's to the end of anybody's measurement, it's still present.
But it's also causing the production of who knows what.
Just like the quality control issue with the plasmids, When you put a message that even if the message itself was well written, if the ribosome that does the translating is tripping over it, then it's producing things that it's not even random stuff.
It's spike protein adjacent stuff.
Yeah, and fragments, yeah.
Yeah, which you don't want because the spike protein is interacting with the ACE2 receptor.
So what you don't want is a lot of molecular fragments that are somewhat biologically active Floating around the body.
That's just a disaster.
Yeah, actually there's some evidence to support that.
So do you know Bruce Patterson?
His research group was looking at patients who had long COVID-like symptoms but It didn't seem like they had actually gotten COVID, but they had gotten the vaccine.
So they hadn't actually tested positive, never had symptoms, but got the vaccine.
So it seems like their symptoms were from the vaccine.
Turns out that a subset of their monocytes, which is a part of the immune system, were carrying spike protein or fragments of spike protein, you know, similar, but not always spike protein.
Sometimes for many months, you know, they could detect it in their monocytes.
Wow.
And this paper, by the way, it's been in preprint for a very long time.
I mean, I got to speculate whether they're having a hard time getting it published because it's, you know, it's kind of embarrassing.
Yeah.
Yeah.
But that's beside the point.
But no, it's not.
I mean, I think this is kind of the point is The difference between what the textbook says and the actual process in nature is often an immense difference.
Yeah.
The difference between what the brochure about how science works suggests and the way science actually works can be equally as off.
It could be the opposite.
It can be the exact opposite, right.
So you've got people not only... Look, let's say we didn't have science.
Well, now you've got a lot of people running around based on mysticism, OK?
That's bad.
But how much worse is it if your mysticism is dressed scientifically, is awarding scientific prizes, is ordering scientific stuff with federal grants from suppliers, but it's really just as mystical, right?
Because that's kind of what it feels like.
And, you know, all right, I'm in an unusual position.
I had a run in with this, you know, decades ago with the mice.
Right?
Okay.
That could just be a super weird encounter, right?
One in a million.
It just happened to me But now you start looking technique after technique and what you find is they've all got bodies buried Somewhere and nobody knows or nobody's talking about where they are.
So the degree to which the whole system is spitting out Sanitize scientifically sanitized conclusions that aren't based on science is Completely alarming And that you would ever trust your health to it.
Oh, yeah.
I mean, in medicine, it's just so much worse.
I mean, you know, you were talking about niches earlier.
Is this something I've been thinking about?
Because we now have a new kind of niche in the system.
I don't mean like the biological system, I mean like ways to make a living.
Because now it's not just pharmaceutical companies, but pharmaceutical companies that are so large, have so much money, that they could put money into everything, you know?
The media, the FDA, the CDC, doctors, organizations, medical schools, how they are taught in medical schools, very much just focused on giving up pharmaceutical products, I'm not saying there aren't any good doctors, but they are very biased towards this pharmaceutical model.
And then the journals themselves, you know, the trials that they run, the people running the trials.
The people run, the contractors running the trials who know which side of the bread is buttered.
The whole thing is a racket.
In medicine, I think it's even worse.
I mean, it's bad enough in just biology and maybe it's the same in chemistry.
I don't know.
But medicine, I think it's even worse.
Well, I mean, back when I was wrapping my mind around this mouse thing, the conclusion was I had strayed from evolutionary biology where, yeah, there was bad stuff, but basically what people were struggling over was Credit, jobs, you know, earthly stuff.
They weren't struggling over fortunes.
Yeah.
Billions of dollars.
The closer you get to medicine, the more fucked up it is because of the amount that is at stake.
Yeah.
And that only gets worse when you're talking about governmental coordination of a, you know, massive pandemic response that resulted in a huge number of injuries and deaths.
Right.
The incentive for pure lives to be dressed up as unassailable facts is immense.
Which, yeah, so, you know, astrophysics?
Here's my guess.
It's probably not that bad.
Well, you still have the, you know, people who need to publish papers, you know.
Yeah, you've got the academic stuff.
Yeah, the academic stuff.
Yep, you've got the academic stuff, which is of a whole different scale than the fortunes won and lost liability.
But yeah, probably not as bad as medicine.
Yeah, it can't be.
Yeah.
So this brings me to another thing that I was hoping to discuss with you.
It's kind of a very it's a very different style of topic but There is a lot of fractiousness amongst the COVID dissidents.
I don't think the public really has any idea what they're looking at in terms of schools of thought, right?
I think at best they have a sort of sense that there's a mainstream version.
It got some stuff wrong.
There's some dissident world.
They got some stuff right.
You know, that's about as far as most people have gotten.
I don't see it like this at all.
I see the mainstream as having gotten the story upside down.
And then I see a weird, in some cases I feel like it's inorganic, the landscape of disagreement over in dissident space.
So the question I wanted to have you address is Maybe we need to build out a taxonomy of the various different beliefs, but there are people who disagree.
Let's take ourselves out of dissident space for a second.
There are people who argue viruses are not real.
There are people who believe in viruses who believe that SARS-CoV-2 is not real.
That's not to say it never existed, but their argument is It didn't have anything to do with the phenomenology that we experienced in the COVID years.
Then there are people who believe that it did exist, circulated, continues to circulate, who come in a different couple different stripes.
Then there are people, you know, you could divide Those who believe it did exist, but it came from the wild, did exist, came from a lab, which lab it came from, if it came from a lab.
So how do you see this set of disagreements?
How do you make sense of it?
You mean like which do I believe or?
Let's start with where you where you fall out and where I fall out.
We'll see if those are the same.
Um, well, I believe there was a virus that was novel, probably from a lab.
Okay.
But all these things, like, I mean, you know, whether it's from a lab or which lab, I wouldn't say I have super high confidence just because, like, unless I I've done experiments myself.
Even then, it's like, where did these samples come from, right?
I can't be 100% sure about any of it, you know.
What I can say is that the side who argue for natural origins, I've cut them in a lot of lies, so that doesn't look good on their side.
That and we know that there have been lab leaks in the past that were just uncontroversial.
Many, it turns out.
Yeah, yeah.
Many, yeah.
And this was reported all over the place, not just in like some kind of fringy places, but like science, the journal Science, you know.
So it's certainly possible that it was from a lab.
So you believe there was a virus that was novel.
Do you believe it's still out there?
Still circulating?
Yeah, I mean, probably evolved, but yeah.
And the main reason I think that it was novel was that the symptoms seemed different from just flu, for example.
It's a little strange that flu disappeared for a while there.
I don't understand what was going on there.
I really don't.
But it seemed novel.
Okay, so you believe there was a novel pathogen, probably from a lab, that it circulated, continues to circulate, and some modified descendants of it continue to circulate in some meaningful way.
You don't No, which lab?
Okay, good.
So for my part, I will say I believe, I certainly believe viruses exist.
In fact, I believe we know that viruses exist.
I mean, you know, we see them.
We can actually look at some viruses on an electron micrograph.
I do believe they cause disease.
I believe SARS-CoV-2 did exist.
That it emerged from a lab.
I also have no way of knowing what lab, right?
For one thing, all of the evidence that suggests that it came from the Wuhan Institute, if you were going to try to pin it on somebody else, you might deliver it in such a way that it would appear to emerge from the Wuhan Institute.
So I have always left open the possibility that the appearance in Wuhan is not what it seems to be.
On the other hand, the behavior of the Chinese Sure looked like they were hiding something, right?
And if they hadn't been, I guess I could tell a story in which they had other things to hide.
And so they couldn't afford to be transparent or, you know, the authoritarian nature of the CCP caused them, you know, to look guilty when in fact they were just being controlling about information.
But my instinct is probably came out of the Wuhan Institute, especially with what we know they were working on with the story.
We know about them having gone to Yunnan and pursued viruses after the six miners became sick with something from the cave.
So I believe SARS-CoV-2 existed, probably came from the Wuhan Institute.
Certainly what came out of the Wuhan Institute is not independent of Ralph Baric.
What have I left off the table?
doing in North Carolina, not independent of Anthony Fauci and the gain of function weapons program.
It turns out that he was managing.
What have I left off the table?
Oh, but I will say, and you tell me how you fall out on this.
I believe there was a pathogen.
I'm not sure I'm a little bit agnostic on what pathogen.
I agree with you.
There's something weird about flu disappearing.
There are, you could imagine, that the pandemic measures that were taken.
Had little impact on COVID, but that flu was evolved to our normal style of interacting as humans and that it disrupted that.
It's possible.
I don't think it's likely, but it's possible.
It's possible that there was vast misreporting of normal flu because there was pressure to encode everything that went wrong with everybody as COVID for the purpose of selling a plan.
Hospitals were incentivized to have more COVID cases.
Totally.
So I believe, could be, that there was a lot of flu buried inside of what we called COVID.
It's possible that COVID largely went extinct or wasn't highly dangerous and that most of the pathology that we're talking about, the novel pathology, was the result of flu.
But What do you mean COVID went extinct?
Like when?
After it emerged?
I don't mean, so you've got a lot of coronaviruses.
So there's a question, and we may end up getting to talk about abuse of PCR as a mechanism for making it seem like there was a lot more COVID circulating than was because you could take contamination and turn it into a positive test.
So I'm a little bit agnostic about what was circulating.
My guess is it was At least one and maybe more than one novel pathogen.
The reason I say novel is...
I believe my family came down with cases of things that did not match a normal pattern.
Right?
Did not match a normal pattern in several different regards.
It's not just the symptoms.
To me, the primary indicator is season.
That too, yeah.
Right?
Not flu season.
Yeah.
So what the hell?
Something had to be circulating that caused people to get sick, not in flu season.
And it could be a lab leak flu.
It could be...
Who knows?
But anyway, I don't know that it was COVID.
I do know that there was an annoying pattern where you would get sick, you'd be told you had COVID, and you couldn't get a test to trigger, right?
You'd be in the middle of the worst of it, and the test would come back negative.
So that suggests something else was circulating too.
The place I I'm frustrated is there's this very aggressive cluster of people who believe that all of us folks who believe there was a novel pathogen are just idiots because what they see in the data is no evidence of, you know, a wave of death.
My feeling is to say there is a novel pathogen is not to say there was a pandemic.
A rational discussion of pandemic would involve something about the severity.
And COVID, there were variants that were more severe and less severe.
But it was not a deadly disease.
It was a disease that was actually highly manageable.
So I believe it was turned into an emergency artificially by propaganda.
I also think I can imagine them doing this as a pure PSYOP with no pathogen.
I don't think that's what happened, but I'm absolutely willing to say I don't think a pathogen was required for the shenanigans that unfolded to have done so.
But anyway, you've got this group of people who go around punishing, demonizing, and slandering those of us who believe there was an actual circulating novel virus, even if we're ready to acknowledge that a virus was not a requirement.
It was present, as far as we can tell.
So anyway, how does that sit with you?
Are you in a similar place?
It's possible.
Um, I just don't know of what technology could do that or, you know, to create that kind of symptomology in people.
Like doctors were seeing something, right?
Oh yeah.
Yeah.
No, I'm not, I'm not arguing you could arrange that.
I'm arguing that you could get people The public to respond to a pandemic that did not involve a pathogen.
You could probably get- But then how would we explain like what doctors were seeing in the hospitals?
Well, again, I think what doctors were seeing, and we know a number of doctors, they were definitely seeing something.
Yeah.
Something novel.
Am I in a position to say it was SARS-CoV-2?
No.
But I do believe they were seeing something novel.
So I'm not arguing that.
But what would happen if all of the public stuff had panicked the citizenry?
And doctors have been incentivized to see COVID or see whatever the pathogen was everywhere.
And so doctors face a lot of people who have illnesses, you know, idiopathic illness.
Yeah.
Illnesses of no known cause.
And so all I'm saying is that now that I've seen a mass panic, I believe it is within the realm of possibility to get a population to behave in a crazy fashion without there actually needing to be a circulating bug.
And the fact that COVID is not terribly dangerous Right?
It's bad.
I think it's going to shorten our lives, and the fact that we're going to apparently get it multiple times is not good for you.
But in terms of any individual case and how lethal it is to the patient, not very, unless you're pretty infirm.
So what that suggests, if that was the novel pathogen, It suggests that you could get a population to shut down the world and collaborate with, you know, monsters with a not very dangerous illness circulating.
Yeah.
Yeah.
So do you want to, somehow it belongs in that conversation to talk about PCR abuses.
Yeah, and actually it's appropriate because tomorrow happens to be the anniversary of Carey Mullis' death.
He was the one who invented PCR, won the Nobel Prize for it.
By the way, it's really funny because when he first submitted his PCR work to both Nature and Science journals, the most prestigious journals, they rejected it.
But anyway, Nice.
But he has also... Where was it ultimately?
Did they eventually publish it?
Yes, some other journal.
It's not as famous.
They're not as famous.
Well, that's... I can't remember.
That's interesting.
Yeah.
Yeah.
Really goes to show you.
But anyway, he's actually talked about, you know, things related to this, but obviously not related to COVID because he wasn't alive during that time.
He died in 2019.
Right, shortly before COVID started.
But PCR is basically just a way to amplify.
So it looks for a specific sequence of DNA.
And then you can amplify, make many, many copies, you know, that's what PCR does.
But it can't tell you whether that The DNA that you've amplified, it comes from a virus that is actually living or not.
And I'm not saying the virus is a living thing.
You know, it's not exactly a living thing, but whether it's something that is capable of replicating in a cell or not, it could just be from quote, dead virus.
So fragments of nucleotides.
And Fauci has also said this.
Yeah, back when he was a sane person.
Right, yeah.
I believe he said that.
I could be wrong.
So, just because you test PCR doesn't mean that it's coming from active virus that could actually kill cells and replicate, let alone transmit.
So that's one problem with PCR.
And that's talked about sometimes, you know.
So I want to add one thing that people don't know.
The PCR technology, which basically, again, trades on biological enzymes that naturally copy DNA or RNA, it functions in an exponential fashion.
So effectively you're making a soup that contains the right biological stuff to take tiny amounts of something that you could never see, that you would never find, needle in a haystack, and amplify the needles exponentially, right?
And if you've ever looked at exponential growth, You know that it defies the mind's intuition, right?
I've forgotten what the math is, but if you put one grain of rice on the first space of a chessboard and then you double it.
Two and then four.
Right.
You end up getting Absolutely beyond astronomical numbers of rice grains 64 spaces later, right?
So anyway, the point about PCR is that it amplifies these things, but in a way that is exponential, right?
You're taking something that is so rare in your sample that you literally wouldn't be able to find it, and you're making it do that trick.
So anyway, what happens here with the way PCR was done?
Yeah, so I mean, like I said, Mullis himself has also said it's not going to tell you whether.
So just to clarify, in the case of PCR tests for checking for SARS-CoV-2, SARS-CoV-2 has RNA, and you take the RNA, you make a complementary DNA, and then you use PCR to amplify it.
Okay.
And Mullis has said, The PCR test is just going to tell you whether that sequence that you're looking for is there or not.
It's present.
Yeah.
It's not going to tell you whether you get sick because you have that.
So that's one problem.
So if you had an infection and your immune system defeated it and it was just clearing out the junk, you could still, if you use PCR as a test, you could still test positive even though actually there is no virus there anymore.
There are fragments.
Yeah, yeah, could be fragmented, quote dead virus.
Now, one way that they try to validate PCR is that so this is this is not really a new thing, right, that people are aware of this, but there's another deeper layer.
So one way you try to validate like whether so you can use PCR, but If you're trying to answer the question of does it mean you actually have infectious virus, right?
One way you could try to answer that is you culture cells that can be hosts to the virus, right?
There are all kinds of cells you can use, but what often gets used are Vero cells.
They are from the African green monkey kidney cells, and they happen to be very, very susceptible to SARS-CoV-2, even more than human lung epithelial cells, you know, so very, very vulnerable to this.
So, what you do is you take in like a Petri dish, you make like a lawn of the Vero cells, those are the hosts, then you You add the virus on there and then let the virus do its thing.
It's going to infect some of the cells.
Every time there's like an infection, it makes sort of like an empty spot, right?
It's a plaque.
So then you know, okay, there was killing off the cells.
There was one cell that was killed there.
So that means, hey, we've got active live virus here.
But the problem is that you might be overestimating How infectious this virus is because the host cells are highly susceptible.
It might be that lung cells wouldn't have been susceptible to this virus.
Even if you were using lung cells though, right?
Lung cells are not a good model for like living lung cells within a lung system.
Lung cells aren't a lung.
Right, which lungs have more than just lung cells.
They have immune cells there.
There's mucus, which helps to clear out microbes and proteins.
There's cilia that is moving the mucus.
It's a whole system designed to keep you from getting infected.
All kinds of proteins that are like, you know, antiviral in nature and stuff like that.
So in reality, That live virus would just be like cleared out immediately, like, you know, or even if your lung cell got infected, you know, our cells have mechanisms to make sure it doesn't spread and become an active infection, like apoptosis, like killing oneself.
They'll kill itself so that like stops the virus dead in the tracks.
But we're using this assay, Vero cells, right?
To say whether, oh, okay, so the PCR test is positive and it shows that, you know, these are infectious, you know, so good to go.
So the Vero test is being used to validate that the PCR test is in fact finding live virus.
Yeah.
Okay.
Yeah.
But it may be that those cells are so susceptible that they are also biased in the direction of a positive result.
Yeah, overestimating, you know, just how infectious SARS-CoV-2 is.
The only way really you can know how infectious somebody is, you know, is if you were to put them in a room with another person and see if they make the other person get it, right?
You'd have to actually do human experiments.
Yep, which are unethical.
Yeah, well, now we can do it.
In the beginning, it was unethical because like, you know, they were claiming like, it could be too dangerous.
But now, they've had some studies, you know, with like younger people, you know, they're not going to die from COVID.
And so they do that.
And it's, you know, it's not As infectious as you think.
Yeah.
And you're telling me they actually run that experiment?
Yeah, it exists.
Yeah.
Okay.
Yeah.
All right.
So we've got two problems that you've identified.
One is that PCR does not distinguish between active virus and fragments of Just so the audience understands, you and I are gonna trip over the idea of live virus because there's some question as to whether a virus is ever properly considered alive.
We should have no trouble saying dead.
Right?
So PCR can take a dead virus and it will still trigger the test to be positive because the fragment of the molecule is still still present.
So...
Dead viruses triggering a PCR positive.
The assay cells being oversensitive to a very weak virus, maybe a virus that's on the way out at the end of an infection or something.
So that would suggest, it would suggest that a PCR test that shouldn't have been positive, that does not actually indicate active virus, it would mislead us into thinking it was.
What else?
Even if that virus, like I said, could infect one of your cells, it doesn't mean it's going to lead to an infection.
And even if you had an infection, it doesn't mean... I mean, from a public policy standpoint, right?
The reason we're taking the test is like, do I need to isolate or not?
But even if you have an infection, is that virus transmissible?
How transmissible is it?
It's not the same thing.
Infectiousness is not the same thing as transmissible.
On top of that, co-infections are a very common thing.
When you have SARS-CoV-2, you could have all kinds of other things that could be causing symptoms, and it turns out the virocells are susceptible to those as well, and sometimes when they're running the tests, you could be infecting them with not just SARS-CoV-2, but other
viruses and so if you're seeing that plaque that dead what looks like dead uh cells in your assay it could have been that it was killed by some other virus some other virus sure and actually uh that i've never heard this before but that seems very plausible to me because if the uh The Vero cells, did you say?
Vero, yeah.
Vero cells are very susceptible to SARS-CoV-2.
Then they presumably have an ACE2 receptor, which means that if you put dead spike junk on them, it could very well render them vulnerable because it would interact with the surface receptor on those cells.
And so it could create a vulnerability to something that was still alive.
to a live pathogen.
Maybe that's not plausible, but to me it's superficially plausible.
You haven't mentioned cycle thresholds yet.
I mean, first of all, it's so hard to find out what is actually going on with PCR tests.
In cities, you still sometimes see these kiosks where people will do a test.
I go on their website, and then it doesn't tell you anything about the protocols or what they're doing.
But presumably you shouldn't.
So every time you amplify the DNA, right, like it's called the threshold.
If you're doing it too many times, you know, your test could be too sensitive because you're You might be just looking at one molecule that was originally there, and you don't care about something like that, right?
Every cycle, you would get a doubling, right?
So if every cycle is a doubling, it's exactly like the chessboard with the grains of rice.
And if you're unconvinced of what an astronomical number that is.
Try calculating it yourself.
You'll be shocked.
But what that means is that the PCR test, the number of doublings, is going to go from a very low number of copies to an astronomical number very quickly.
And if you imagine how these tests were done, Okay, you're doing the test in a hospital where people are being hospitalized for all kinds of things.
Some of them have COVID and are hospitalized for something else.
Some of them are hospitalized for COVID.
There's contamination all over the place.
And with a process as powerful as PCR, this was really one of one of Kerry Mullis's points, with a process as powerful as PCR, it's going to pick up Any stray molecule, and if you run enough cycle thresholds, you're going to amplify it, so you're going to say, oh yeah, for sure, this sample came in, I ran it through the PCR machine, and there's definitely SARS-CoV-2 in evidence.
Present, yeah, but it could have just been one virus.
Yeah, you might have picked up one molecule from somebody who coughed down the hallway, you know, however it got in there, and the point is, the amplification process is so powerful, it can literally turn that into a positive result.
So, What happened with the cycle thresholds during the so-called pandemic?
You know, I'm actually not even sure, but what I heard was that they were just way too high in the beginning, so they were just amplifying something that might have been contamination.
What I heard was that they lowered it at some point.
I'm not actually sure.
It's not like I've looked at the protocols of all that.
I mean, do you know?
I don't know.
I know that they were suspiciously high.
Yeah.
I know that the environment was one in which Every trick in the book was used to increase the apparent commonality of COVID and the lethality of it, right?
So people were literally dying with COVID from being hit by a bus and it would show up as a COVID death.
So the environment was primed to make COVID look as dangerous as possible and as common as possible.
And in such an environment, having a suspiciously high cycle threshold had an obvious interpretation, which is this is one more trick, It's being used to make the public think that this thing is everywhere and to be terrified.
And I also, because of the financial incentives, which I'm not an expert on, but the financial incentives that existed for diagnosing COVID and then treating it in particular ways and not other ways, the, you know, what did happen to the cycle threshold?
What actually happened?
You know, in a hospital where, just like everything else, if you're being rewarded for finding COVID, you know, did that apply to the people running these things?
And even if they were supposed to lower the thresholds, did they?
Right?
The way to find COVID is to turn the thresholds way up so that any molecule is enough.
And so anyway, I don't know what happened, but... I mean, even after they lowered it, though, I mean, it's unclear to me That the methods they were using could tell you that, okay, this lower threshold is okay now, because they were using Vero cells, right?
So they could say, okay, 40 is a number where we find, you know, consistently, it kills the Vero cells, but that's not the same as the number that means you have active infection, right, in a human, in a normal human being.
So when you say 40 is, you know, it's a hypothetical, but 40 is the number of cycles in which a positive test means active infection.
What you're saying is, not that you can take anything from the PCR and infect the vero cells, but that You could take a sample from a patient and you could do PCR on it and see whether 40 cycles gets you a positive result and then take a sample from that patient and use it to infect the cells.
But there's a lot of weakness is your point in that chain of evidence because you don't know what they got, right?
You don't know what the cells actually contracted and You don't know, you know, you don't know that it's transmissible to another person, which is really what you're trying to figure out with the test you're doing in the first place.
Exactly.
Yeah.
Yeah.
All right.
And I guess I would add one other thing, which unfortunately comes from the people who I believe are behaving very badly by demonizing everybody who thinks there was a novel pathogen, which includes both you and me, apparently.
But Because there are a lot of other coronaviruses around, because this is a common family of viruses, you know, colds, for example, contain coronaviruses, or the group of things that we call colds do, there's a question about how specific the test actually is.
Right, if you're amplifying circulating cold viruses and getting a positive test and then doing your Vero cell test and the patient had something else that the Vero cells will contract, that would look like, oh there's definitely SARS-CoV-2 and it's still infectious and the cycle threshold at 40 was what it took to find it, but you could get there and it could be a totally false connection between those things.
All right, well that was fun.
What else?
So we've talked about PCR abuse and broken models.
Was there more you wanted to say about Carey Mullis?
There's always more to say about Carey Mullis, but I'm blanking out.
Yeah, he's a fascinating, fascinating character.
His autobiography is really great.
Yeah, it is really great.
And I'm, you know, a little bit heartbroken that he didn't live to say his piece about what took place.
Oh, I'm sure he would have had a lot to say.
And he was not a fan of Fauci.
No, he was not.
But the whole medical system is very aware of all of that.
Yeah.
Okay.
I have written myself two notes.
One of which is... But you can't read your own handwriting, can you?
Oh, I figured it out!
You're right, I can't.
And I have that problem frequently.
It's very frustrating to find a note that I've written to myself.
Sometimes I even type notes to myself and then I can't figure out what I was talking about.
I don't want to spook you, but that happens.
Often I write cryptically.
Okay, the question about a conflict in style between the do-your-own-research folks and the stay-in-your-lane folks.
I know you have a great many thoughts about this.
You want to... Yeah, well, I... Okay, I'll first talk about how biology is done.
I think biologists should go out of their lane.
Cary Mullis actually used to say this about it.
Cary Mullis was not even a biologist, but he was a chemist.
Yeah.
A lot of people who were outside of one field made contributions in another field.
Between Watson and Crick, I never remember which one was the physicist, but one of them was a physicist.
But they both won the Nobel Prize for elucidating the structure of DNA.
Yeah.
Many examples of people sort of outside of a field contributing to another field.
My PhD advisor actually was another example.
He kind of was all over the place.
And he had always, we sometimes, you know, butted heads.
But I agree with him on this that, you know, If you go on to academia, you should do something in your postdoc that's totally different from your PhD, you know, that's going to help you grow.
You know, I, in my sub stack, I write about vaccines and viruses, immunology, which is not what I did in my PhD.
I mean, I worked on a microbe, you know, diatoms.
And I've sometimes gotten pushback from people like, well, that's not your area of expertise.
And no, it's not.
But the way that I became an expert in my PhD research is the same thing as what I'm doing now, which is reading a lot of papers in the field.
That's all it was.
It wasn't anything special.
And there were no classes that I took in my PhD for the subject of my PhD.
It's just reading a lot, you know, and of course it's self-educating.
Once you've proven that you can do it, you can self-educate on a topic.
Yeah, that's all it is.
Of course, it's helpful to have some background.
If you know absolutely no biology, it's hard, you know, but you don't necessarily need a PhD to like make sense of some of the things that you see in papers, you know.
There's ways that you can train for that.
And the number of people, the number of contributions that have been made by somebody from some other field is disproportionate.
It's not even like those people sometimes succeed.
The chances that somebody who comes from outside is going to see what insiders can't see is high.
So, you know, is there a cost to not having, you know, gotten your degree on this particular thing?
Maybe.
But if you're, you know...
To cite a mutual friend of ours, Alexandros Marinos, who talks about epistemic humility, if you have the epistemic humility to know when you've gotten away from what you actually do know about, there's no risk in It doesn't matter how far afield.
Yeah.
Well, plus you could always ask people who know more about that topic, right?
And that's what happens in academia as well.
I mean, right.
The reason why biology papers often have so many authors is that there are different groups who work on different things because, you know, they, they're the experts in like a certain thing.
That's why you end up, you know, collaborating, you know, it's, it's no different whether you're outside of academia or not.
Yeah, I strongly believe in doing your own research.
Yeah, of course it's helpful if you have, like, a formal background, you know?
On the other hand, a formal background can sometimes, you know, push you into groupthink, you know?
Because, like, if everyone around you, they're academics, like, if certain views are just no-go zones because you'll be called an anti-vaxxer or something like that, then certain options will be closed to you, right?
I think it's the biggest danger is that, you know, Everything I have managed to figure out in science that was new.
was the result of being free from the assumptions that you acquire as you formally study a new field and the problem is you come in the process of formal study you inherently come in as a powerless underling so you're not in a good position to question a bad assumption so if you take that assumption in when you're young and vulnerable
By the time you're not young and vulnerable, you've just simply... it's become part of you.
So you're not in a good position to spot it.
So, you know, for me, spotting bad assumptions is the whole game, right?
You spot a bad assumption, then you can figure out what people are doing wrong.
They're not going to figure it out if they're taking it as an assumption and unwilling to question it because it was gospel when they were taught it.
So anyway, yeah.
So coming from the outside, educating yourself.
These are They don't really need a defense, as long as you're not going to misrepresent what you know, you know?
Yeah.
We also have some examples of very accomplished people who did their own research and had very, like, almost no formal training, like Thomas Edison, the Wright Brothers, apparently.
I think they, like, were dropouts or something.
Yeah, they certainly didn't study aviation.
Benjamin Franklin?
Yeah.
Oh, sure.
All the best people are outsiders.
Oh, and okay, when it comes to medicine, you really got to do your own research because if you're going to medical doctors, most medical doctors, there are some that are exceptions.
Where to begin?
I'm not questioning the motives of most medical doctors.
I think a lot of them have the best motives, but they're just not taught to look for root causes.
They often know very little about nutrition.
They get very little training on nutrition in med school.
And like we talked about before, the med school is often very influenced by pharma, even if they don't realize it.
Just anecdotally, the people I know who have gotten chronic issues solved were people who did their own research.
Yeah.
If you go to a medical doctor, they'll give you some pill to manage the symptoms, but it won't cure them.
You know, someone I know who had psoriasis and has went to, I don't know how many dermatologists he went to, I think like six or seven, they all give him pills that are like, that inhibit your immune system basically, you know, and who knows what's that doing, that's doing in the long term.
Then we just looked at YouTube videos, things like that, asked around and UV treatment, UV light treatment apparently is helpful.
That's helped, you know?
No, it didn't.
Someone I knew who had insomnia, you know, actually he went to a sleep lab and they had bright lights on.
Were you trying to sleep?
Crazy.
Yeah.
And he's like, this is dumb.
The number of places where I've fixed my own life by just being willing.
I mean, you know, it's not like I read it on the internet and I know it's true.
Right.
Right?
But you might have a hypothesis based on something that you read and then you test the hypothesis.
Hey, just try it out.
Right.
And there's just a lot of stories out there of people, oh I tried this, dietary changes.
Wheat allergy.
I had a wheat allergy and I was poisoning myself with wheat.
I had no idea how many things that I just thought were part of life were actually symptoms of a chronic case of inflammation.
And, you know, I tested negative on the gluten allergy test.
I don't think I have a gluten allergy, but I can tell you for sure I have a wheat allergy.
I know that because every time I get a little bit of wheat, the stuff comes rushing back and it's like plain as day.
So yeah, you have a lot to gain by just even employing a crude scientific toolkit based on what you can discover.
You know, there are a lot of people in the world and a lot of them are talking about experiences they've had.
A lot of it's nonsense.
But, you know, how cheap is it to test, you know, just cutting wheat out?
Right?
When I first heard of gluten allergies, I rolled my eyes.
I thought this was nonsense.
I thought it was a fad, right?
I tested it because I had tried a dozen other things to get rid of a chronic cough that I got every winter.
Nothing worked.
And then I read some people have asthma from a gluten allergy and I thought, no way.
But you know, I had ripped the heating system out of my house.
We had forced air heat.
We put in hydronic floor heat.
I had lived without cats.
My cats had died and I had stayed without cats for a couple years.
Didn't matter.
I was told that it was dust mites and the bedding needed to have, you know, special hypoallergenic covers.
Didn't do a damn thing, right?
So I had been through all of those things and the answer is, well, okay, if some people do it, cure this with taking wheat out of their diet, let's at least check that one off the list.
It's easier than everything else I've done.
Lo and behold.
Shocking, right?
The pattern was very clear.
I had to take weed out for weeks, right, because the inflammation doesn't clear right away.
But having done that, it was amazing and I thought, ah, you must be imagining that.
Brought weed back and boom!
All the symptoms were right there.
It was just, you know, it's not... A lot of doctors will just like, they'll just kind of poo-poo that, right?
Right.
Yeah.
Doesn't fit their model.
Yeah, but the test is negative.
Right, the test is negative.
To his credit, the doctor I had at the time who tested me and it came back negative, I said, Doc, something's wrong.
I know I have an allergy because I have the evidence.
It's really clear.
Why is the test negative?
He says that happens a lot.
Test isn't very good.
So, you know, my guess is that test tests for gluten and there are a lot of other wheat allergies.
Yeah.
That'd be my guess.
Yeah.
And unfortunately, doctors often don't really understand the tests themselves either.
They don't have a deep understanding of how they work, the limitations of the tests.
Yeah, and they do not like, you know, there are two kinds of doctors in the world.
There are doctors who actually want to talk about the details, they want to tell you about their thinking and all of that, but most doctors don't.
Most doctors kind of enjoy The authority of their position.
They don't like the complexity of, okay, I'm going to prescribe this drug to you, but that's going to have a downside, right?
They want to tell you, oh, this one's safe.
It's worth it, you know, and it's, it's not reasonable.
I wanted to coin a term.
So the stay in your lane thing has always struck me as insane.
I'm, I'm, Constitutionally not capable of staying in my lane, right?
I don't even have a lane.
I don't admit to having a lane.
I'm not sure I know what lanes are.
But okay, so for people who either, as a matter of their particular character, or people who come to understand that they're going to have to get out of their lane just to even protect themselves and their family, I think we should be called lane splitters.
You know what lane splitting is?
Uh, I think so.
When a motorcyclist is riding between lanes.
Yeah.
Swerving between.
Okay.
Yeah.
Well, not necessarily swerving, but most motorcycles are now, uh, water cooled.
Um, but back in the day, a lot of motorcycles were air cooled, um, which meant that they had to keep moving or they would overheat.
And so it was sort of allowed that you could ride between lanes because that would keep you going.
Um, huh.
Yeah, so anyway, lame splitters.
I think that's what we are.
It sounds too close to hair splitters, though.
Which is not the most positive thing.
Hair splitters.
No, yeah, it's going to be hard to spin that.
I agree, hair splitters.
Alright, I'll come up with a better term and let you know.
Alright, anything else you were hoping to talk about?
I don't think so.
We've covered a lot.
We have covered a lot of ground.
Yeah.
Alright, well it's been great fun.
It has.
Jumi Kim, people can find you at Substack, at Let's Be Clear.
Where else?
I have a Twitter profile.
Jumi Kim one.
Jumi Kim 1, J-O-O-M-I-K-I-M 1 on Twitter.
All right.
Well, it's been a pleasure and great to have you here in person.
