Why does Peter Attia hate The Cholesterol Code?

Welcome everybody to Tuesday Live. I have a very special guest with me today, Nick Norwitz, who stars in the movie The Cholesterol Code. His, uh, participation and his, uh, his discussion and education in that movie is doing awesome on Amazon thanks to you and leaving the comments, reviewing that movie, and then sharing this information with other people. Today we are going to get into some of the nitty-gritty about what happens when conventional algorithmic medicine meets the rebels, which might be us. Those people who are challenging, this doesn't make sense with the patients I'm seeing. This doesn't make sense with some of our own assessments of health. There is no better star to the N of One than Dave Feldman and Nick Norwitz, who are both stars in this movie. The Cholesterol Code. First of all, Nick, thank you for coming onto my channel. Thanks for, uh, you know, bringing your curiosity my way.

I appreciate it, Annette, and you're being overly generous with me. I was, I was happy to be in the movie, but it's all, um, Dave and Jen. I was just filmed for a few days, but it ended up being a pretty spectacular film. So thank you to everybody that's watched it and that will watch it because it is doing tremendously, and that just, it brings joy to my heart. If I may sidebar for a quick moment, if anybody knows Dave or doesn't know Dave, like, I'm probably one of the few people in the world who knows how much he sacrificed for the sake of a question, for the sake of an honest scientific question. And to see, like, the global response to what is, I would say, not the culmination of a journey, but climax one of many climaxes to come. Is really heartening for me as his colleague and his friend. It's just really tremendous, so thank you, everybody.

Right, well, and he is— I have done the premiere with him here locally, but also just recently been in Vegas and watching how much, again, he derailed the life he had planned to answer this question about his own health, that his LDL cholesterol went off the charts when he did this ketogenic diet. And that wasn't just what most of us do or what most of my patients do, which is run to me saying, "Fix it," right? 'Cause that's what everybody says you should do. And that started many years ago as he used his experiment, his N-of-1, open and willing to share that with all of us. Well, there's a couple of things I want to tee up because I think most of my audience is probably not in the weeds of what's going on between the LDL cholesterol debate that is between scientists. And I'm going to ask you to give a brief history of a few stepping stones or stepping spots in this story. Let's go back to 2018. When Dave Feldman was on the Peter Attia Show, and he was there doing his thing, being transparent, saying, "I'm an engineer, but there's something up about the way my cholesterol responded." Why don't you just share with the audience what happened in that video, and then we'll move on to point 2, which is just as strange.

Sure. Before I directly answer that question, I was— we were offlining before we got on, and I was thinking about how to pose this in a way that doesn't come across as overly adversarial, because the fact of the matter is you're calling us like rebels, and to some degree we are, but like science requires the rebels. It requires people that challenge convention. Otherwise there isn't science, right? Because you're not trying to break the model. So Dave's coming with an authentic question. And I guess what I want your audience to keep in mind as we go through this discussion is not who is right and who is wrong, but what parties are actually looking to have an authentic engagement about new ideas as they're evolving. Who really believes in the idea of curiosity and just exploring and having conversations with people that aren't necessarily of like mind?

And there are many places where I have learned so much from Peter Attia, his team, his researchers, the gathering of information that would take me I mean, I don't think I would ever reach the level of scrutiny and organized information that he and his team have delivered to the medical community abroad. But there were places where things stood out as out of character, or that it was incongruent. And one of them was this interview with, you know, Dave Feldman is this, he wouldn't hurt a fly. He's there being truly curious, having this conversation, trying to put forth this model that we're going to talk about in a minute. Yeah, but something happened at the beginning of that interview that is weird.

I want to parse two things, which is the person and how they interact. And yes, I do think Peter's been overly adversarial towards Dave and the legitimacy of the ideas.

Right.

Like, and excuse me for this, but I want to address this up front because I know what the comments are going to show given some of the recent controversy around Attiya. Put aside his personal life, right? Because the fact of the matter is, even if he was Adolf Hitler, if he's making good points, they're good points. Doesn't matter who's saying them. So the question is, is he actually making accurate and good points? Now, to go to that podcast, Peter had a conversation with Dave around the lipid energy model. He ended up doing like a preface afterwards trying to debunk it. I will say his debunks haven't been that good and his assessments really haven't been balanced. For example, there was a fact check that he did post-talk of the interview, and he's only fact-checking Dave and not himself, even though he made multiple errors. In fact, There's a funny part in the interview. If you listen back, I talked to Dave about it after the fact where Dave says something about LDL receptors. They're talking about LDL cholesterol on the endothelium. And Peter's like, what are you talking about? There are no LDL receptors on the endothelium.

Yes, sir.

Turns out there absolutely are. If you watch, if you listen to the conversation through again, it's interesting how that completely then derails the conversation down like another tangent. What he just— Peter just made a factually wrong claim. That he's still never owned up to.

And we all do this. I mean, we're in medicine. You're not going to get it all right. There's no way we can put all that in our heads.

So then confidence, the confidence with which she made the error and the imbalanced nature with which you're willing to fact-check others and not look in the mirror. And then what happens? That's the real question. So that was 2018. That was way before I'm engaged in this process. The cool thing about that interview, I mean, to Dave's credit, is basically at the end, Peter throws down the gauntlet. He's like, well, go study it. Like, go, go, go study, go study the data.

Go Padres, go Mets, right?

And there's no way on earth he ever thought Dave would. Turns out Dave did. And now Dave has— I think I'm correct in this, people can fact-check me— more lipid and heart health papers published than Peter does.

I also just think that the part of The Cholesterol Code that's super endearing is the, you know, David versus Goliath part, where Dave is not Literally Dave. Right, I know, right? But he really takes on this giant of cholesterol and cardiology dogma and just says, "What if?" And boy, the kinds of places that he's run into suppression, you kind of cringe as saying, "Is he gonna make it to the other side?

Is he gonna live through this?" You'd be surprised how bad it gets.

Oh yeah, oh, I've heard.

Bear in mind what I was doing while we were doing this.

—in medical school.

—a vulnerable position at Harvard Medical School. I was in a pretty vulnerable position. Let's say people came down on my head once or twice.

You're like, no, no, no. You keep in line. You're the medical student. We have so much power over you. That was true. Anyway. Yeah. Anyway.

Well, the cat's out of the bag now. So that was 2018. Right. You know, after a lot of— I would say we'll jump forward to present day. But I just want to give a little bit of insider knowledge on the back end, which is as this is developing, Peter and his colleagues have had many opportunities to engage. So for example, I think it was 2021, I was writing an editorial for the Journal of Clinical Epidemiology on lean mass hyperresponders. I reached out to Peter via his head of research at the time, and Peter deferred to collaborate. He actually cited that he himself was not expert enough in this domain.

And that's true of a lot of parts of medicine when you say, okay, do I still—

okay, okay. Oh, but like, just, just a little— put a little framework as we move up. And for people who have read some of his recent articles, he's stating he's not the expert. He's referring me to people who he considers the experts, like Ronald Krauss, William Cromwell. Those people have worked with us. In fact, as we will get into the lipid energy model discussion, fun fact, Peter's ex-head of research, Bob Kaplan, is an author on that paper. Yeah, the guy— so there are overlapping spheres here. The people who— the person who's helping Peter do his research is an author on the lipid energy model paper. Right. So— That'll become relevant in a moment, but like— He does surround himself by smart people.

And, you know, Kaplan's one of those to say, "No, he does think through it very well." But he also is really got some blinders on. So go fast forward to the Cell Metabolism article that you again can see Peter wrote on. This is a, you know, January 2026 where he— this is a really important statin review. I give you credit. Credit for saying in the depths of your stress of medical school, you missed it. So did all of us that this, um, that this article came out that statins are associated with— oh yeah, so total cholesterol, it lowers it, LDL cholesterol, A1C, insulin. And this is in Peter's blog, and you'll notice that that's where the image ends. But if you click on the paper and look inside, uh, here is what the image looks like. So And the point of the paper was to put, to say, guess what happened at 16 weeks when they took this very small dose of a statin? And sure, sure, yep, the LDL cholesterol did this, the A1C did this, but oopsie, let's see if I can make that go smaller. But the, it was the GLP-1 that dropped by 50%, and it just conveniently got clipped off of the way that blog post article was done inside Peter's, but he never mentions it. He doesn't just, Like brush it off.

He mentioned the whole article is about it. That is what's conspicuous is that. So, so some backstory. First of all, just a small correction point. It wasn't a low dose of a statin. It was a high dose. But my bad. Either way, it's— it also isn't just associated with— this is a human controlled trial. This is statins cause GLP-1 to plummet. Now, the date you mentioned, 2026, on Peter's article. So this is relevant because the article itself, the paper came out in 2024, 2 years before. So what? So what happens in 2025, 2026? I caught onto it and I covered it. And then I had a few pieces of content. It took this paper from obscurity and then it became Cell Metabolism's most read. So when this article came out, people were commenting on it.

I just want everybody to hear that. Cell Metabolism's most read article. That is a huge power of saying to use your influence for this kind of information to be on the table of discussion.

That's the point. And we'll get to that in a minute. Thank you. But the point being, like, so this is— when I read this, I was like, wait a minute, human controlled trial in top science journal on one of the most prescribed drugs of all time crushing GLP-1 levels. Like, how is this one, not making headlines, and two, not discussed at all in academia? But I am like walking around Harvard Medical School, like hospitals, asking cardiologists, have you heard of these data? And they're all universally like, no, no. And I'm like, what does that say about the data we choose to surface and those we don't? But anyway, so the timeline goes, I surface this, people are talking about it. Peter then responds. People are in the comments section saying, hey, Peter's responding to you, Nick. I'm like, does he mention me? I'm like, everybody knows it's you. Like, there's no other situation. But the point here is he then goes through point by point and tries to discredit this study. His points are weak. So for example, like, he's like, well, you know, the relative reduction looks big, but the absolute reduction is small because if you eat carbs, GLP-1s go up more. I'm like, you can't compare a fasting GLP-1, right, to like a postprandial. These are weird comparisons. But the conspicuous thing is you put so many words into trying to rebut this study, and then you show the figure— this is all about rebutting the GLP-1 effect— you show Figure 1, and then you crop out the only primarily relevant panel. That is effortful. And I will let people make their own conclusions on why he chose to do this. I think it's because the graph is too damning. An 8-year-old can tell you what's going on. I mean, I want to be clear, though, about one additional thing. It's, it's incredibly powerful. But what Peter and maybe some people in his community would say is, is two of the following things. One, this is a biochemical effect and we don't know the clinical relevance. And two, it was a small study. And to both of these things I say exactly. And here's why I say exactly. This is a signal that I think anybody with a modicum of biological background can be like, well, this is potentially hugely relevant given the drug in question and the hormone in question. So when these data come out, controlled trial in a top science journal, what should happen immediately is stop the presses, here are the headlines, here's millions of dollars to research this, to amplify this, to improve patient care. And actually, there are tidbits in this paper showing how you can do so using tools today. And these don't get surfaced if we don't talk about this. Right. But set that aside. The real story here is it's not being talked about and not being pursued. So yeah, it's a small study. You shouldn't judge a study based on its end value. And yes, we don't know the clinical consequences because nobody cares to ask the question, which is a huge disservice to medicine. And so really my thing here with Peter is with that article and then the one he came out with on the Cholesterol Code documentary is—

Right, so let's just do that timeline. So Cholesterol Code documentary, are we 10 days out?

Remember the release date on Amazon? It came out on— I think it was supposed to come out on the 17th, and it came out a day early, so April 16th.

So like 11, 12 days out. Okay, so, and a week later, uh, you— we get, we get this, uh, on Peter's, uh, again, in conjunction with Thomas Dayspring, a very, uh, well-respected, uh, lipidologist. And it is again the— why is The Cholesterol Code wrong, essentially. Why is that movie that's getting all this fanfare wrong? And, you know, 16 pages later, there's plenty of things in here that kind of take you through the history lesson. He does a good job of some basic sciences, and then there are some problems. There are some problems. So just in brief, do you want to like walk through what, you know, what— sure, I mean, I, I can point out the things that I want you to talk about, but I I think he does a nice job of saying, guess what? Cholesterol is complicated. You shouldn't just look at the total cholesterol. You know, you've got your lipoproteins, the different sizes. I think he skipped a couple of things that my team might— He's just peacocking. Right, right, right.

Here's the thing is, this is all— it's posturing. So I want to first dissect, if you start reading the article, how Peter goes about framing this. First of all, he conspicuously never mentions anybody's name. I think that's a way to kind of circumvent this, only attributes it to the Citizen Science Foundation, which is Dave's, you know, charity that funded it. And then the way it's cast, and you can read this for yourself, but my takeaway, and I'm interested in yours, Annette, is he does try to frame it as this is like a group of like, like know-nothing rebels who are doing this study in this movie. But let's return to the fact that there are a host of highly esteemed lipidologists and cardiologists that have been associated not with the film but with the research as well, including people Peter has recommended to me, including people that have been on Peter's team, including his past head of research. Right. He brushes all that under the rug because it's frankly inconvenient. Mm-hmm. Peter and his team, including Tom Dayspring, have every opportunity to authentically engage with these ideas and they avoid again and again. And then they pretend like they're trying to engage with these ideas authentically, see the other side, when they've never truly given it the chance. My challenge to them, honestly, as we go through some of the things, is like, Dave and I are ready to like live anytime, have these discussions. If you think you have an upper hand on the literature, make us look like fools. You can't. I'm confident you can't. If you think otherwise, prove us wrong. Right. Otherwise, I have no other option but to rebut what are incredibly weak points. And you can be an incredibly intelligent person. Tom, Peter, they're intelligent, but that doesn't excuse them from being ignorant in certain domains, overly arrogant, and then just making blatant mistakes. They make mistakes left and right that people don't catch. Remember, Tom Dayspring once had a tweet about how ketosis lowers LDL receptor expression. And everybody just gobbled it up like, oh, this is so insightful. I'm like, you made that up. Show me one reference. I have references showing the opposite. Just where did this come from?

And you get— hold on, say the statement again. Tell me that again.

He stated that ketosis lowers LDL receptor expression. Hmm, news to me. There's no evidence that it does. There are studies in rats using exogenous ketones showing ketosis increases LDL receptor expression. And there are studies in humans looking at peripheral cells showing that ketogenic diets, including those high in saturated fat, don't lower LDL receptor expression. As far as I'm concerned, these are claims that he's just making up and pulling out his butt. And if— again, I'm saying this on a live with you, being very ready to have— be made the fool if he can come up with a reference, but I'm pretty confident he can't.

Yes. Well, and I think, you know, looking at some of the, the powerful things within the article are— I mean, if you're new to ketogenic diet and you're saying, what, what should I care about my cholesterol? I think, well, I'll end with what I think people should care about, but these are the kinds of questions that many of my, my patients have, uh, quite the struggles with. And when you look inside these articles, uh, you say, well, if you look at several of the things that he brings contempt with, like, okay, here are the hypothesis that, uh, what happens inside a lean mass hyper-responsive patient, what's that hypothesis? So I'm going to read this out loud so you can then just lift off and say, yep, that's true, or that's not true. So first of all, uh, what does it mean? It's a characteristic triad where the LDL rises dramatically, often exceeding 200 milligrams per deciliter, even as high as 400. And your example is— is it your total cholesterol at 700 or your LDL?

My total is 705, my LDL is 574, or has been. We can get into that in a moment. But yeah, right. And I mean, my— like, people don't even believe it, right, when I say how high it is.

Well, and I've had both patients show up in my, in my, um, you know, practice and say, what do I do now? I'm like, you calm down, because the next thing that we look at is what is their HDL. Um, the HDL often rises, and they make a— they bring this up in a minute. While typically the third thing that happens is those triglycerides are lower. In fact, sometimes, and I think I've seen your data out there, your triglycerides are lower than your HDL cholesterol. While that LDL, that bad cholesterol, is, it's like familial hypercholesterolemia. It's like something's wrong. They can't get rid of it. They're gonna die. And that is the reflex that I see over and over again with, newbies into the ketogenic space, and, and maybe they didn't check their cholesterol at first, but if they are like you or like Dave, where they are lean, and then they, they— you don't do anything halfway— they really lean into an advanced ketogenic diet for medical reasons, this mess happens in their cholesterol. And like what got Dave curious in the first place is, well, I feel amazing. I feel so much better than I did. Is this gonna kill me? And that was his first, you know, first question.

Yeah, it— so I think one thing that often gets misunderstood, including by Peter— he, he's made missteps on this before— is it is not the case that we believe, or we're postulating, that high triglycerides and low— sorry, high HDL and low triglycerides, which are markers of good metabolic health, are somehow magically protective and a shield against high LDL and ApoB. That is not the case. What is very interesting is the pattern. So just how this emerges as a triad, when it emerges, the pattern itself is a fingerprint, a signature of something going on underlying that is different than anything that's been described before. So to dumb it down When we take any measure in biology, it's always wrapped in a context. So let's put aside cholesterol and say height. This is an analogy I use commonly, but I think it's a decent one, which is you can be really, really tall for multiple reasons. You can be Shaq, and guess what? You got great DNA, you're tall, you have an excellent NBA career, you're famous, and you make millions of dollars. Or you can be tall because you have a growth hormone-secreting brain tumor. You're also 7'1" like Shaq, but for a different reason, and the outcome is different. And it's the same for cholesterol. There are many different reasons your LDL can be high. Because you have a genetic disorder, familial hypercholesterolemia, because you're metabolically unhealthy, or ironically, you're healthy, you're low-carb, and your body is trafficking fat fuel. So the context in which that LDL arises matters. There's no reason to think it wouldn't impact outcome. It seems stupid to assume it wouldn't. So that's the question. The fact of the matter is When Dave stumbled upon this, nobody knew the answer because nobody had bothered to study it. So there's just this presumption that it aligns with the risk we see in familial hypercholesterolemia. I bet my life, and when I say that, I'm not just like using a turn of phrase, I literally mean I have bet my life on the fact that is wrong. Right. Yeah. So, you know, that's one thing Peter and his colleagues are missing. And I want to then— I realize we're getting nuanced here and you can pause me, but this is a really important point again that Peter grossly misunderstands. If you go listen to him on any podcast, like when he was on Huberman Lab, he just espouses, "I am obsessed." I'm quoting him. Yeah, I saw this. He's like, "I'm obsessed with causality." Mm-hmm. Causality, I think, is the most abused term in cardiology because all it means is something is part of a causal cascade. And importantly, what it does not mean is something is important or that something needs to be treated. So we can say LDL and ApoB are causal. They're part of the domino chain of cardiovascular disease and they're necessary. It doesn't mean that it's that important a variable, and it doesn't mean it needs to be treated when high. In fact, going back to the 2018 podcast, I think it's hilarious because Peter's own analogy for explaining this idea of necessary, sufficient, and causal. Yeah, he talks about oxygen and fire where he analogizes LDL to oxygen and atherosclerosis to fire. And I'm like, I love your analogy, Peter, because, okay, oxygen is causal to fire. Oxygen is necessary for fire.

Take away the oxygen and you won't have a fire.

Yeah, if I take away the oxygen, I have a lower risk of my lungs spontaneously combusting into flames. That is true. I will also suffocate and die.

I mean, it's just like— and I mean, you look back at, um, some of the other parts that, uh, just to watch this unfold again. The first time I heard Lean Mass Hyperresponder, I'm like, huh, I got nothing. What are you talking about? Meaning, I see patients come into my practice, they have chronic medical problems, they have insulin resistance for decades, and the, the first thing that usually happens to somebody with severe insulin resistance— this is not you, this is not Dave, this is my audience of patients, is their cholesterol does get better. That LDL cholesterol gets better for a season. I mean, for a pretty good measurement. As you watch that insulin resistance get better, better, better, better, as the fat mass decreases, as their waistline decreases, as their BMI gets south of 25, so in a healthy range, there is a shift in what happens for your body's ability to shuffle fat through that subcutaneous fat cells, through, you know, not parking them in visceral fat, and then watching how quickly you can respond to the need for energy. And it doesn't happen to everybody. Well, this is actually one of the theories that had a light bulb moment when I was watching the movie was, could I say that as I watch people progress through a ketogenic diet, they come in very insulin resistant And they got 100 pounds to lose. So I'm not actually looking at cholesterol till I get the insulin down and the, you know, the C-reactive protein and, you know, all the other markers of get them out of the diabetic range. And then, only then do I start to see when they're very lean that there's a health marker of when they've got a lean body mass, when they've reached the goal of being healthy, then they start to do this thing. Like, could it be this spectrum, this continuum of when you come in that sick, your cholesterol is gonna get better, but the healthier you get, there are people that when they get that lean, when they look like you and Dave, their cholesterols are in the 400s, 500s.

Yeah, so I wanna reiterate what I think I hear you saying because we see this clinically as well where somebody starts off, let's say their BMI, we have these cases are like 40, right? They have obesity, they go keto, they're presumably eating basically the same diet, their BMI is dropping, dropping, 35, 30, their LDL dips a little bit, maybe it started at 120 and it's now gone down to 100, 90, then they get leaner, leaner, leaner, they hit a BMI of like 25, and then it goes like, oh, it went from 120 to 90, whoa, now it's 300. Yes. It's that hairpin turn. And where do I want to go with this? I think what I want to go with this is The lipid energy model, we'll discuss it and some of the errors Peter made on it, is a hypothesis. Mm-hmm. But it's a hypothesis that can explain this and associated phenomena in a way that no alternative hypothesis posed ever has. So my challenge to people like Peter is, if you pride yourself on being a thoughtful clinician, what do you charge, like a quarter million dollars per patient? This is a clinical case. Explain it. Explain it. If you think this hypothesis is wrong, what is yours? Because this hypothesis has predicted pretty accurately all these clinical outcomes and tests. So it's kind of cheap to throw stones at it, which actually miss on several marks, and provide no alternative. What is your alternative hypothesis? Let's get back to what we were saying before. It's not about who's right, who's wrong. It's about who is actually willing to stand up and have a conversation. And thus far, with the exception of 2018, that has not been people like Peter. And I think that is putting a brick wall in front of scientific progress, one that we will climb. But nevertheless, I don't think he's accelerating progress. I don't think he's helping science.

I think he's hindering it. Right. So looking at this, this is the next part of his article, is like, okay, he tries to explain the lipid energy model. He does a few things that I think are really naughty. He says things like, um, it supposedly leads to decreased insulin and leptin levels. Well, as a clinician teaching the ketogenic diet, I will tell you, you cannot make ketones if the insulin's going up and the leptin is— the only way you're in a ketogenic state is your insulin's better than it used to be. Now, what that absolute number is changes, but it's not supposedly shift, it absolutely has to shift to be in a ketogenic state. The next thing he talks about is that there is a, um, there has a hepatic, uh, triglyceride synthesis rises, meaning the, the liver makes, uh, triglycerides the triglycerides rise and it puts them in these VLDL particles. This VLDL particle supposedly rises as well. And the third one that's in there is that as the triglycerides are removed from the VLDL particles and they become LDL particles, I'm just gonna do a quick flash here of saying this is the, where the VLDL up here is, can you see that? Maybe you can't see that. The VLDL right there next to the chylomicron, that's filled with triglycerides as it circulates into the body and becomes an LDL cholesterol particle. Cholesterol. He's saying there's more of these VLDLs being made in the lipid— this model, and it ultimately results in an elevated LDL cholesterol model. So as you look at this diagram, do you think there's anything as we are trying to teach this that we should—

so basically what he's describing is you see like, okay, Okay, number step 1, glycogen going down in the liver. That's because you're going low carb, and that can be a signal along with low leptin and low insulin, which is point 2, to fat cells to release fatty acids. And then what he gets to is you get around the circle and he's talking about VLDL secretion. So step 4.

Okay, okay, okay. Step 4 is right there.

Yeah, yeah. And the one below it as well. So you have the liver going out and putting out these little particles. Yep. And then the next step, which she's going to discuss, is this. It's called LPL-mediated VLDL turnover. A lot of letters. Basically, the enzyme lipoprotein lipase is taking that big fluffy VLDL, which is packed with fat, and it's pulling the fat out to give it to fat cells and muscle tissue. Right. As that gets turned over, what you're going to see is— see that big particle in the green circle? It's big because it's filled with fat. It shrinks down as you pull the fat fuel out the middle. It's like deflating a balloon, right? And then it becomes VLDL to LDL. But as you're shrinking the VLDL, you also— because you're shrinking a sphere, you lose surface area. Part of that surface area includes cholesterol. It goes to HDL, right? So you end up with is the pattern we see, right? Very low triglycerides because they've been pulled out of the VLDL. And then as a result of the turnover process, high LDL and high HDL. That is the lipid energy model and how it explains this pattern of the very high HDL, the very low triglycerides, and the very high LZL. That is the model which he attempts to explain and rebut, but makes, as we will get into, a few—

Right. So, you know, he goes— the next section he goes through examining the evidence, and I could stop on that and point that out, but I think there's some really important parts where he leans into the study that you and that Dave and his team and you talk about on that cholesterol code movie, why don't you just explain the study that's done, the 80 people who had the— their, um, who were— was it 80 or 100? Sorry if I don't remember.

So there were two studies. Um, there was originally design, right, was that you were going to follow a cohort of people like me, get a baseline scan and a follow-up scan looking at with advanced scanning, um, their heart for soft and calcified plaque. Now the original design was to follow the cohort over time It's very difficult to develop, like, and for expense reasons, but also practicality reasons, a control group. But what we did do is at the baseline, which wasn't when— to be clear, baseline is not when they started a ketogenic diet. Baseline is first scan. So on average, these people who were in their mid-50s on average had been on a ketogenic diet for 4.7 years at the baseline, which is about like, what, 5 years of exposure to very, very high LDL cholesterol. I think of the whole cohort, it was an average of 272 LDL. And then as best we can match it to another population, in this case a generally healthy population called Miami Heart, and see, you know, all else being equal, is there more plaque in the heart of the lean mass hyperresponders with high LDL versus those of the matched population? Was the baseline study. And then there was a follow-up study where we tracked plaque over time.

And I think one of the key things that's really been useful for me to reiterate to patients is they're not just saying, let me measure your cholesterol and predict the heart disease or the risk for cardiovascular disease. Let me look at the intimal development on one of the best ways we can look at that in humans through the CT angio. Like, don't play around by guessing what a marker might be predicting. Look for disease. And that's how they entered the study. That's the baseline was, okay, if you've got this lean mass hyper-responder— and they didn't just casually say, is that you? They had to show that your, your LDL cholesterol— was it higher than 200 to be entered in the study?

It was 190 as a study cut point. They had a little bit more liberal cut points than actual lean mass hyper-responders, and then 190 was the cut point.

Yeah. And their HDL and triglycerides, uh, you know, had to be the markers we just talked about that allowed— or less.

I think it was like 70 for— yeah, it was slightly more liberal than lean mass hyperresponders, which is 200 for LDL, 80 for HDL, and 70 for triglycerides. But roundabouts there. I— if it helps, I can basically summarize my qualms with some of Peter's points. Yes. I mean, I'm happy to go point by point in a 5-hour podcast with him if he's really ready to do that. But bottom line is His commentary is misinformed, is misguided, misdirected, distractionary, and not actually like hitting on the big questions or misrepresenting our claims. So for example, like on the lipid energy model study, I think he tries to cast doubt on it by saying, well, these pieces of evidence haven't been proven, which like certain things like, okay, we haven't proven the, you know, with tracer studies that the free fatty acids are getting taken up and putting on VLDL and shipped out. Yeah, true. We've never claimed otherwise. You know why? Because we don't have $2 million on hand to do that study. So what you do is you develop a hypothesis and see if it explains the phenomenon, and it does. You can't discredit the hypothesis by saying this definitive piece of evidence hasn't been collected when the team that's putting forth the hypothesis has never claimed it has. We're just saying this is what the model predicts, now let's test it together. Right. There are also things where he's talking about, you know, the clinical trial and imperfect matching where he just doesn't have insight. Into what are the practical domains of matching. If you look, the thing with lean mass hyperresponders is they're so unique, right? It's literally impossible to match them to another population along all dimensions but LDL. I mean, the part that irritated me— You can't do it, right?

It's like, well, if you're LDLs, you're going to match the LDLs. But hey, you guys are healthier, you're leaner, your C-reactive protein was less, your HDL was less. I'm like, exactly. So I'm saying you're asking me to throw this process out when the human in front of me is so much healthier than they were. And you want me to chase that number as a result of, I mean, restoring this vitality in patients that says, I might have been raised by hog farmers, but there is something healthy about that patient. Don't miss it. Don't look just at that one number, period. Yeah.

I don't know if I want to say this. Am I going to sound like an asshole? As you said, as I was raised by hog farmers, I was thinking, I mean, I don't know if people know my background, but—

You have more PhDs than MDs in the primary home, right?

Both my parents are MD PhDs. My dad's a Rhodes Scholar. My mom's a Marshall Scholar. My sister's in medical school. My brother's in medical school. All our partners are in medical school. If you go to our partners and my parents, we're batting 8 for 8 MDs with most of us having PhDs. PhDs. You nerds. Point B, wait, but here's the point. I have been brought up since my earliest memories in this environment, in the environment of like, I know what the path is to be respected in academic medicine. Go to a great college, go to a good grad program, go to the best medical school, all of that. So I have every reason to have a bias towards the establishment, that establishment. But based on what I've seen, I can't in good conscience say they're right because they're wrong. Right. And this is where I'm saying I'm betting my life on this because I understand the audacity. Let's shine the spotlight on me for a minute. For the past 7 years, my, my total cholesterol has been about 700 and I've been unmedicated. Wow. The audacity of— at the time when this started to develop, I was 23, a 23-year-old who knows what goes into developing a career in academic medicine, saying, you know, there's a decent chance all of cardiology on this particular topic is wrong. Ideas that have been built up over, you know, 50, 70 years by people with probably collectively millions of years of experience. And I'm a 23-year-old PhD student at the time. Right. But the fact of the matter is the data judges— like, science judges the data, not the credentials, and this is a question and a corner of lipidology and cardiology that is grossly underexplored and people are misunderstanding and misrepresenting, which is why I don't see it even as that like awful a thing for me to be betting my literally own life on this concept because I'm like, it just— I'm asking a hard question. Yeah, if you're really knowledgeable, you should be able to come up with data to compel me to make a particular decision because I think I'm a pretty reasonable person and I can process the data with you. So like, that is the chall— I put this challenge forward to Peter and like Tom Baisman. Like, if we can get on a live call and you can like show me up with the data, I will go on lifelong lipid-lowering therapy on the spot. But you have to convince me. You have to actually put forth a compelling argument, not just hand wave about the preponderance of evidence, which means the body of evidence, when it doesn't apply. To this population. So let's talk about the emerging data and the questions, you know, that are arising from it. Um, I'm gonna have to split in a sec.

I do, I do want to though, I want you to tell it because what I do love about you is that yes, you are in the midst of a, a very— I mean, you live in Boston with all the ivory towers where all the best, uh, you know, teachers and collaboration is supposed to be happening, and yet you stand there saying, my cholesterol's 700.

105. Well, was. Oh, okay. Was. So this is where I want to be careful because I think there's a tendency— and you can tell me if you feel this pressure yourself because I'm much newer to being a public figure than you are— which is people create caricatures of you. They misrepresent you. They create cartoons and misrepresentations of your ideas. I think there then there is a compulsion, even if like subconscious, then to defend that caricature. Right. To defend that position and become ever more extreme. And I think this is how different sides then polarize is because they feel they need to continuously defend the more extreme position that is being thrust upon them rather than what their position actually is. Right. And I really try to be conscious of this and walk the walk, which is why, like, I'm not trying to be the poster child of live healthy with high LDL or don't take medications.

Like the gauntlet is there. I mean, I really do. That's what I love about this is, you know, he is standing still saying, show me, teach me what you think the difference is for that. And then to watch some of the experiments, like the one that you're— are you releasing it on Friday, what you're doing, or is it already released?

I released— so I released a letter today and there's gonna be a video Friday The plot twist, which isn't actually a plot twist, is I'm starting some cholesterol-lowering medications, ezetimibe and bempedoic acid, which is like, ooh, I've become so controversial on this topic that people are gonna be like, oh my God, pivot. The fact is it's not a pivot at all when you understand my rationale. And I'll point you to that content, the letter path of this thing.

I'll put the link to all these places that I've grabbed on this in the show notes.

And Friday I'll go over my rationale in the video. But basically the plot point and how this dovetails else I just said is I came across some really interesting literature on ezetimibe, which is one quote-unquote cholesterol-lowering drug, and another called bempedoic acid. And here's a truth: molecules in biology don't give a crap about the labels we append to them, right? So just because you call something a cholesterol-lowering drug, that doesn't dictate its actual scope of impact on the body.

Yeah, the marketing versus the science, right?

Right. So people say cholesterol-lowering drug because the idea is LDL is the important thing. I don't think is. Bottom line is, other data came out that's like, wow, ezetimibe might actually be good for the brain. And I'm really interested in Alzheimer's prevention, so I'm like, cool, I actually think this is generally a safe medication, and I think there might be brain benefits, so I'm going to take it for that purpose. Now, if my cholesterol goes down— and actually did, my cholesterol, my LDL and ApoB dropped by 56% on ezetimibe monotherapy— then fine. Again, I'm not trying to just dogmatically live with high LDL for no purpose. That is a coincidence. It's a side effect, but it takes up all the oxygen because of where medicine has shown the spotlight.

My brain just went weird. Like, you dropped your LDL cholesterol that much with ezetimibe? Yeah.

So that's the thing is I don't— I'm not even surprised by it when you understand. So let's go back to lipid energy model. High level, I am trafficking fat as fuel. I eat a lot of fat. If I eat a lot of fat, I need to put out bile and cholesterol into my intestines. So, if ezetimibe blocks that, that's gonna have a higher— Right, so, but that's what the thing is like, your average clinician is like, "Well, this is a huge impact. This is an outlier." I'm like, "But—" Not when you see the outcome. You can generate outliers in each patient if you understand their physiology. That is medicine. It is individualized. It's treating the person, not the population. That's what everybody here is missing. And so anyway, back on, and people can watch the video. It's gonna come out on my channel.

I'll make sure to link that.

Because it is a challenge. Yeah, but the challenge here is not just to be the rebels for being the rebels' sake, or not just saying LDL doesn't matter. It's saying let's continuously approach this with an open mind and refuse to dumb it down or adopt extreme positions just because detractors are willing to go low, right, and play those points. Let's go high and just continue to have like authentic, nuanced discussions. Like what we said at the beginning, my challenge here is to have the discussion. Who is stepping up to talk about it and who is throwing around platitudes like Atiyah and unwilling to actually defend their position or just making gross errors and not owning up to them?

Well, I really just want to say, I know you have to run, and I want to say thank you for taking the time to just unpack this. You know, looking at cholesterol and teaching cholesterol through the ketogenic diet has been, you know, probably the biggest learning curve for not just me as an internist, but as an internist who's trying to teach this to people that I never will meet. They are on a YouTube channel saying, "Talk to your doctor," but walk in with some of the science behind what a lipoprotein is, how it circulates around your body and brain. And, you know, Nick, it is great to have your footprint of education and influence in this space. You—

I appreciate that.

You bring lots of energy.

There's a lot of things to be energetic about. I do want to tap on something you just said though about teaching people you'll never meet, which is— I hope everybody like listening appreciates what a privilege it is to be living in this day and era with the democratization of information. What I'm trying to do, what Dr. Boz is doing, just trying to authentically communicate. We don't all have to agree, but that democratization of information is the single greatest threat to a paternalistic medical system. That is right. And I find it so funny, especially with content coming out in recent days with some of the remarks, to watch the death throes of a paternalistic medical system because people are rebelling against this arrogance and certainty, and the response by some of the people is just more paternalism, arrogance, and certainty. They're accelerating their own demise and they can't see it. It's kind of amusing to watch. Mm-hmm. I won't comment on particular individuals, but I'll just say there's some less than favorable and personal attacks on me. They don't hurt me because I'm like, this is reeking of desperation. It's so pathetic. Like, and I'm sorry, but these are the people that are becoming obsolete. If people are just like defending a paternalistic medical system with more arrogance, certainty, paternalism, You have made yourself obsolete. I don't know what to say. So democratization of information, it's an amazing time to live in this space and learn. And we'll keep the conversation going because it needs to be.

Well, thank you, thank you for joining the show. And I've got some questions from folks that I'll take on. I'll try to hold the team up without you here. And I just want to say thanks again. We will put a major plug that we looked today about the number of reviews that are on Cholesterol Code. And I think it was like in the 300s. So this is super important that you leave authentic review. Like, some people have written in saying my review did not get posted because it was too, I don't know, cheerleading. So be sure it's an authentic review on Amazon so that it gets posted. And that is how we can help support just the conversation to keep going.

I mean, don't be afraid of being too cheerleading. There's usually a lag time between when you post it. Maybe that's another one. Is one thing. Um, so yeah, no, everybody, we really appreciate it. It's been remarkable. It's like like 98% 5-star reviews. And these early responses really do help dictate the ultimate, um, algorithm fate of the film. Amazon, I, seems to have taken notice. They've expanded it to a few more countries. You'll notice, unfortunately, and this is out of our control, I want to be clear, they did jack up the price for a rental from $2.99 to $4.99 because I think they realized it's going to be a cash cow for them. So sorry about that. We don't control that. But it's a good mark that Amazon's taking notice. They're spreading it wide. And your contribution of $5 to watch a movie and leave a review, like, really makes a meaningful impact. Talking about democratization of information, like, this is your vote, right, to change the tide of these discussions. We're getting Peter's attention.

Well, that's, that's getting to a bigger stage, truly, to look at, can we have this conversation? And it takes two sides. It takes that discussion. So, uh, let's hope we sparked that. Thank you so much, Annette. You bet. All right, folks, so that was, uh, again, my favorite treat is to have on somebody like Nick Norwitz sharing his expertise, sharing his, you know, his courage to talk about things that many people would just say, no thanks, I'm tapping out, don't need this attention. I have a couple, we're gonna get to your questions. I do have a couple of announcements. I am going to be in Tennessee this weekend and it is Meatstock in Gatlinburg. I will be signing books on Saturday. If you are in the area, bring your books, sign up or just show up and I'll sign your books. Book. I'll bring a few books, but they are— I'm actually heading— I was out last week, one of the first times I've missed one of my Tuesday Lives in a while. We ended up on a cruise with our friends, and I will tell you that I am really happy to be back in a ketogenic state. That is shocking to me, what happens when you get around normal people, non-ketogenic people, and how often they eat, how much that affects me. And I am— I, I checked my numbers before the show, but I didn't get a chance with Nick Norwitz's attendance. My blood sugar is still in the 90s, but I think my ketones are 5. Like, I maybe overshot those because of— I don't know why they're that high. Let's just show you. Yeah, those are my numbers for right before the show. Looking at a really big announcement for me as tomorrow, or actually after the show, I hop on a plane and head to Washington, D.C. with the privilege to talk with some folks at HHS on what is the policy for teaching about reversing medical problems with, with keto, with a ketogenic diet. And I just want to say thank you for everybody who has— I've had this opportunity in the past and I've said no thank you. And I am, I am a woman of faith, so say a prayer that everything goes in a place that the message can be heard and that the influence for reversing medical problems so they never end up in my clinic is what the conversation we will hopefully facilitate. That's what, that's what the goal um, so I will go over to your questions. Here we go. Um, all right, so Betty writes in and says, I'm 62, uh, years old, female, who has been doing keto for 5 years. My body mass index is 19.8. Again, that's pretty lean. So, um, her A1C 5.2, triglycerides 52, total cholesterol 293, up from 271 last year. HDL is almost, almost twice as high as her triglycerides, and her LDL is 194. "Should I ever expect my cholesterol to level off or should I just not worry about it?" So this is what I was trying to say to Nick is that when I see, so I think Peter brings some amazing things to the table, which is an incredible collection of smart people studying the literature, reporting on that, a blog that has taught more physicians than most medical schools will ever teach. He has, there is credit of what he's done. Nick brings to the table a young whippersnapper, innovative, from a dynasty of MD PhDs, and yet has some severe, like the worst luck when it comes to genetics for predicting Alzheimer's and having cardiovascular disease. And you can go to his blog, this is not a secret, he talks about having ApoE4 of 4, which is a predictor of Alzheimer's. Has the genetic unluckiness of having a high Lp, which makes your lipoproteins stickier, they're more atherosclerotic. So for him to have that genetic footprint and then have such a high total cholesterol, it is a unique place that he enters this, the space of what should you do? And I think what my approach— what's my place in all this? I have been seeing patients for over 25 years, chronic disease management. My peak brain performance has been what my clinic has been about, which is how I got to the ketogenic diet in the first place. But to watch how the pattern of health getting worse and then getting better, what does that continuum look like? And when I hear stories like Betty saying, boy, she's pretty lean. She has, you know, a much higher LDL than than what her, her traditional medical team would, would recommend. And I would say she has a badge of honor, meaning she has that, uh, those triglycerides low, she has that HDL high. And because she uses fat, she uses fat to fuel her body, she's in a constant ketogenic state, you are finding the movement of lipids at a much higher pace in her system so that when we draw the blood bed, 12 to 15 hours after she had her last bite of food, we are finding a much higher volume of those particles moving through her system. What I can say with confidence is I bet those particles were not in her circulation as long as some of the patients that come to my practice with severe insulin resistance. Uh, their particles will stay in the circulation for 4 or 5 days, whereas Betty, in the state that she's at, it would be my guess— and I would need to see a few labs— but it would be the profile that you see as you're that lean, you circulate cholesterol more efficiently. Now, the key thing that I would recommend to Betty is if you're trying to follow your cholesterol over time, please pay cash for an NMR. That's a nuclear magnetic resonance, which looks at the size, number, volume of lipoproteins. I think the— you can have it done by Quest or LabCorp. I think the one by LabCorp is a little easier for patients to read. You want to just make sure you're measuring the LPI-R Lipoprotein-Insulin Resistance score. So it takes the math of all those particles and it puts it together and says, what's the risk that she has insulin resistance? And I would contend from just looking at the numbers here that she has got a low risk for insulin resistance. So doing an LP-IR score with your yearly cholesterol, or maybe you do it every 6 months, but at least doing an NMR once a year. But then be careful that you check your cholesterol at the same time as, as far as He says, check it in the morning. That's when it's the easiest to do, but it's also the easiest to repeat and compare cholesterol checks over time. But there's two parts of that story that I, I really try to double-click and tell patients, be careful to do this. So the time of day is one thing, and I recommend the closer to 7:30 in the morning, early first lab draw of the day. That's the best one because it's reproducible. It's easy to predict what your cortisol was doing. Hopefully you slept well the night before. But the second part is, is if you draw your blood at 7:30, how many hours since the last bite of food. And it shouldn't be a 36-hour fast. That's gonna throw the numbers off. Like, wait, she hasn't eaten in 2 days or a day and a half? The volume of cholesterol that you're circulating because you're fasted is gonna be much higher than it would be typically. So it's— so check that cholesterol fasted about 14 hours fasted. And keep it as water and black coffee. Please don't play with that. That ability for you to be able to look at those cholesterol changes over time is really important on a ketogenic diet. Pay cash for checking your own NMR if your doctor won't do it. It's a, it's a really big part of the equation. All right, the last one, last question, and then we will call it. I gotta go get on a plane. So, um, so the next one is, what blood test should we do at a yearly wellness checkup? Uh, you would think with this I would say cholesterol, but I stopped doing cholesterol in patients a long time ago. I do do an NMR, and again, for this reason, I'm looking for insulin insulin resistance. I, I can best look at that when they are that 14 hours fasted, when it's first thing in the morning, and I'm looking at the particle size along that, along that, um, the spectrum of what it was in the past and what it is again this year. When I look at other blood tests, I've got a couple of PDFs that you can download off of the website that says here's what I do for my patients, here's the blood tests I um, there is also a— inside the workbook of Keto Continuum, I, I put that in. If you can't get an NMR done, it is things like C-reactive protein, uric acid, vitamin D. I am a big homocysteine measure— measure homocysteine. It's another independent factor for predicting cardiovascular disease. And then just like what happened with Nick Norwitz, Nick Norwitz. If you're trying to assess if you have cardiovascular disease, quit measuring the, the proxy markers, which are all these blood tests. Look for disease. Look at a coronary artery calcium score. Look at a CT angio if your insurance can afford to cover that. When I teach patients how do you get a healthier body, it's because you learn all of these things. One Tuesday live at a time. This is a really advanced lecture, and so any of you still around, I appreciate the praise for just sticking around and saying this is the kind of messiness that we get into in the lectures inside one of our classes. But for most lectures on this, on our Tuesday lives, we're trying to reach the audience that's new at this, that's trying to figure out what is the stumbling blocks for, uh, for the mistakes people make. This morning when I was kind of practicing this lecture to my Pinchasers, the, which is the bowling alley that we meet at every Tuesday morning at 8 o'clock. I said, this is why when you come on the ketogenic diet, I'm not gonna judge your cholesterol for 18 months. Now you'll hear me say, don't check your cholesterol till you're 6 months in. That's me hedging the bets because as people come into the ketogenic diet, they think it's like, okay, flip a switch and I'm gonna be there. But it's like any behavior change. You're gonna do well and then you're gonna fall off and then you're gonna say, wow, I felt better on the ketogenic diet. It might take you a hot minute to get back into a good ketogenic rhythm. And I need you in a consistent ketogenic state for like 9 months for me to be able to assess what is your body doing with these cholesterol changes. You can judge Nick Norwitz every 10 days. He's lean, his inflammation is low, he's young and healthy. He hasn't had 3 to 4 decades of elevated insulin. When people arrive into the ketogenic state and say, well, what am I worried about? I'm like, these are the steps we go through in the keto continuum. Don't look around and sure as heck do not look at that cholesterol for many months. And I contend, I won't judge your cholesterol if you're my patient for 18 months on a ketogenic diet because I'm gonna give you the space at the beginning of this story to mess it up. That's just human. You're learning a skill that you didn't, that you don't know, you don't know you're not good at it. Staying in a ketogenic state is, is baby steps of change till they finally get to this place where they can consistently be keto. And now we can talk cholesterol. All right, I appreciate everybody sticking around. Please pray for favor tomorrow as we have the audience of HHS to see if— can we get a few more people talking about why a ketogenic state is so good for your health? Signing off, we'll see you