Bad News for Science: America’s Lab Rats May Be Mutants

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Eric Weinstein

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Eric Weinstein holds a PhD in mathematical physics from Harvard University and is a member of the Galileo Project research team. www.ericweinstein.org www.geometricunity.org

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What are the episodes of my of my podcast? Because I launched it off of this one. Yes, I listened to Werner Herzog. Yeah, I thought that was interesting, although he's a little bit self-congratulatory, which is a little shocking. But he is the most interesting man in the universe. He's a very interesting guy. He's also been in some really terrible movies, like he was in that Jack Reacher movie with Tom Cruise. The best part about that movie is that he drives a Chevelle, 1970 Chevelle. Don't know about this. You don't know about 70 Chevelle's. Did you listen to the Brett up, Brett episode? Brett Weinstein. Oh, your brother. No, I did not listen to that one. OK, I've only listened to five or six. If you listen to to episode 19, which is the Brett episode, I think that's been the most important one, except for the one released today. That sounds like you gear me up for the one released today. Well, I would start with the Brett one. And what's so important about the Brett one? The Brett one is a story about his prediction that all the laboratory mice that we use from the major supplier, which is the Jackson Laboratory in Bar Harbor, Maine, may have been compromised by their breeding protocols, which allowed the telomeres to radically elongate. And that we thought that these mice were representative of all mice and that they had radically elongated telomeres at the end of their chromosomes, which appear to mediate the level of mitosis that can happen during histological repair. So if you imagine that your cells can divide a certain number of times, if if there isn't a counter that stops the number of divisions, everything can become tumors. And since you have like 30 trillion or 100 trillion cells in your body, it means every cell almost can kill you. So it appears that the reason we may die from senescence, that is aging, is that that's our anti-cancer mechanism. So if you eliminate like infectious disease, like viruses and insult from, you know, being hit by a car, the two things that you have in the end is either you die from immortality, which is cancer, which where cells can divide an infinite number of times, or you die from the recursion limit, which is how many times the cell can divide called in biology the Hayflick limit. And Brett predicted from first principles that what we thought about mice, which is that they have radically elongated telomeres, was only true for laboratory animals because all the laboratory animals in which we test things like drugs have been broken. They've been broken because of selective breeding? Yep, because the breeding rotations privileged much younger mice and removed all sort of threats from the environment. And so because telomeres are not protein coding, there are sequences of nucleotides that repeat as a counter rather than coding for a translation in the ribosome into amino acid sequences. What you have is that the body can mutate, if you will, to use the Jackson Laboratories concept of this very rapidly, because it's not building something structural. It's just a question of do we have 17 on the end or 170 on the end? Because it's acting nucleic acid has multiple ways in which it can participate in regulating the body's responses. So in fact, the breeding protocols constituted a novel system of selective pressures that destroy the efficacy of all of our laboratory animals potentially. Holy shit. So that means... So he predicted from first principles, he said, I bet if you test wild type mice rather than laboratory mice, you'll find that their telomeres are not long as you believe. And this was actually carried out by Carol Greider, who did not acknowledge the prediction. She didn't acknowledge the prediction. You should listen to the show. Why did she not acknowledge the prediction? You should listen to the show. OK. It's OK. It's no, because it's it's this is serious. It's complicated. And it's a Nobel laureate on the other side of this. So we're taking some risk over there, over there at the portal. That's really interesting. So the consequences of this could be grave, could be that so much of the studies that are predicated on these mice tests are they're useless. Well, I've called up the Jackson Laboratory and asked them, when have you had any changes in your breeding protocol? Are you they say we don't even count the number of telomere, the telomere length. And I say, do you have a history of when you've changed the breeding protocols? Are you aware of these articles? And she said, like what? I said, you know, these articles of Carol Greider. And they said, how do you spell glider like the plane? I said, Greider, like the Nobel laureate. And how do you spell that? G R E I D E R. And so and then I then they said to me, well, we don't remember if we've changed the protocols. I said, you're producing laboratory animals. I would imagine you would have a documented history of every change in the time series of how these animals were prepared. Well, I don't know if there's anyone around from that time. It's like, are you kidding? Were you absent the day they taught science? Who are you? You know, this is like a single point of failure, if true. I can't even we've been at for 20 years. We've been trying to get an answer as 20 years. No one will break the story. I mean, this episode, which is almost impossible to listen to, because at the beginning of the episode, I'm absolutely insufferable to Brett because he won't tell the story. He's afraid to tell his own life story. Why won't he tell the story? Because in academics, the idea of some punk kid alleging that they predicted in a telephone call to a Nobel laureate that if they would test wild type mice, the telomeres would be radically along radically shorter than the elongated telomeres of the laboratory test. And then the person refuses to acknowledge that such a prediction was made, even though we have emails from the lab that. So she refuses to acknowledge it or she doesn't. I cannot find a single I've been over the literature. There is no mention anywhere of and I live this with bread in real time. So I know the events were happening. We have communications with that lab since. There is I cannot find any acknowledgment from the Johns Hopkins University laboratory that this interaction ever took place and that because he called and wrote and did not write an email, he did not have a paper trail of that prediction. Now, there's consequential, consequential emails that show the interaction between the labs. But how many times have you ever heard anyone predict a molecular result from first principles in evolutionary theory? This is what Brett was supposed to be famous for. And then, you know, he became like this obscure professor at some ridiculous college. And then this thing happened to him. But that's not his origin story. His origin story is that he is the badass of biology who was able to make this prediction from first principles and may have advanced the theory of why we have to die balanced between deaths from immortality, that is tumors and deaths from recursion limits. That is telomere mediated Hayflix, Hayflick limits. So what, if anything, has been done since this information has gotten out? The world went crazy for the episode and there was silence everywhere inside of what I've called the gated institutional narrative. Because to acknowledge it, they really have to throw out how much research we don't know. I don't know. But it puts the question out how much research is compromised by the laboratory breeding protocols and breeding rotations. From a single point of failure at the Jackson Laboratories in Bar Harbor, Maine. Wow. Episode 19. And you will hear me in a way where you will just say, Eric is the biggest dick I've ever heard in my life, but it's all to push Brett to actually talk. You should have him back on the show to talk about it. It's killing. I would love to. Yeah. So he just wants to. He kind of wants a soft dancing. Is that what it is? Soft step step? He's just wrong. I mean, here's the problem. There's a point after which I'm not Mr. Nice Guy and I'm just like adamant. Mm hmm. And Brett is simply wrong. It's a it's a result and a story that needs to be told. If there is another side to the story, we need to hear the other side of the story. And my goal is to have Carol Greider say, you know what? This interaction did happen and I probably could have handled this better because she has work that she's done, which is beyond question. Some of the most important work that has nothing to do with anything Brett has done. But it does not give that laboratory the scientific right to deny the existence of this interaction, the importance of the interaction. And because there are potential downstream consequences in pharmaceuticals, we need to have an answer. And every answer is interesting. Like if the laboratory mice having radical radical, radically elongated telomeres is not a problem in some way, that's fascinating. How could you have an animal that has this huge adaptation to the laboratory not affect things? That would be interesting. If it does affect things, that's fascinating. Well, especially if you're if you're running tests on it that have anything to do with telomere. Right. Well, no, but if it doesn't have to do like, for example, if you're trying to do a test, like, for example, let's say you have a really toxic substance, right? And it causes a lot of cell death that requires histological repair. Well, if you have huge long telomeres, you're going to have an ability to metabolize that toxicity very much better. Right. Right. You'll be able to take the insult that comes from this. And so these mice are probably preternaturally disposed towards radical histological repair. That's why they remain youthful and young. And if you test something that might be, you know, if you're doing toxicology studies, it could be that the telomeres, even though you're not testing the telomeres, what you're actually doing is picking up that these broken mice are like the world champs of repair, but they suck at cancer. They all die of cancer. All of them. Yeah, almost. Essentially, all the mice with radically elongated telomeres let go long enough, all die of cancer, because they're tricked out for one special thing, which is we are the best at repair. Oh, wow. Right. So the thing about it is the theory of death and the clear way, all of the noise, there are two ways that nature can't figure out and escape from. Either you die of immortality, which is that you think all your cells want to live forever, you know, and that's a huge death, a huge danger. Or we call it a resource leak in computers, or they die because the only thing nature can figure out to do is to say you only get a finite number of cell divisions up front. Now, there's some adjustments to the theory, but if you only get it, like if you look at the moles on my face, which people love to comment on in the comment section, they probably started as a runaway replicative process that arrested at the border of the mole in order to keep it from killing me. All right. So we have cells that go rogue all the time. But then what happens is, is that there's some means of making sure that the process doesn't take down the entire organism. But think about 30 trillion assassins as the cells in your body, all of which might kill you at any moment. It's like terrifying.