Dhru Purohit Show
This Study Shocks Cardiologists: LDL and ApoB May Not Predict Heart Disease Risk in Healthy People with Dr. Nick Norwitz
Mon, 07 Apr 2025
This episode is brought to you by LMNT and Lumebox. The mainstream narrative around LDL cholesterol has long claimed that high LDL is always harmful—no matter the individual or their overall health status. The traditional view holds that elevated LDL levels directly increase the risk of cardiovascular disease, regardless of metabolic health. Today’s guest, Dr. Nick Norwitz, shares groundbreaking research that further explains why plaque buildup progresses and how it can lead to heart disease. Today on The Dhru Purohit Show, Dhru sits down with Dr. Nick Norwitz to explore a groundbreaking study on LDL cholesterol and its implications for cardiovascular health. Dr. Norwitz dives into the role of diet, individual risk factors, and the significance of plaque progression while also addressing lifestyle influences and practical strategies for heart health. He also shares insights on the limitations of current testing methods, the impact of microplastics on cardiovascular health, and the growing gut health crisis. Dhru and Dr. Norwtiz emphasized the need for personalized nutrition, informed decision-making, and a balanced perspective between scientific research and real-world experience. Dr. Nick Norwitz is a researcher, educator, and passionate advocate for metabolic health whose mission is to “Make Metabolic Health Mainstream.” He earned a PhD in Metabolism from the University of Oxford and is now completing his MD at Harvard Medical School. Nick’s drive in this field stems from his personal battle with severe Inflammatory Bowel Disease, which he overcame through a ketogenic diet after conventional treatments failed. His journey has fueled a deep commitment to challenging outdated thinking around health, and he’s known for his infectious curiosity and dedication to teaching. In this episode, Dhru and Dr. Norwitz dive into: Dr. Norwitz’s landmark study (00:41) How the study fits into people’s diets and lifestyles (06:04) Plaque progression in individuals with existing buildup (14:45) Lifestyle factors that contribute to continued plaque progression (16:30) How to assess your personal risk (20:55) Dhru’s personal story and testing journey (30:00) The worst diet and lifestyle habits for heart health (38:27) The impact of carnivore and ketogenic diets on gut health (45:01) Vegetables, fiber, and insights on the omnivore diet (1:02:40) The aspartame study and what it means for humans (1:07:58) Seed oils and their effects on the body (1:23:00) Final thoughts and where to follow Dr. Norwitz (1:34:52) Also mentioned in this episode: Plaque Begets Plaque, Not ApoB, JACC Journals Metabolic Mind YouTube Study from Italy on Microplastics in Cardiovascular Events For more on Dr. Norwitz, follow him on Facebook, Instagram, X/Twitter, YouTube, LinkedIn, Threads, and his Website, and subscribe to his Newsletter. This episode is brought to you by LMNT and Lumebox. Right now, LMNT is offering my listeners a free sample pack with any purchase. Head over to drinkLMNT.com/dhru today. Lumebox is offering my community $260 off their FDA-registered portable Red Light device! That's over 40% off! Go to thelumebox.com/dhru and get your Red Light device. Learn more about your ad choices. Visit megaphone.fm/adchoices
Chapter 1: What groundbreaking study is discussed in this episode?
Dr. Nick Norwitz, a pleasure to have you on the podcast. I'm a huge fan of your work. I've been trying to get you on for a little while, so I'm grateful that you're here today. And we have some exciting news for our audience. Today, you're here to talk about a first of its kind, groundbreaking study that will give us massive insights into into a few areas that have all come together.
The carnivore diet, the low carb diet, high LDL, ApoB, and whether or not certain risk factors lead to poor cardiovascular health and even increase our risk of heart attack. So let's talk about this study, who you did it with and why it matters.
We had a bunch of other things we were going to talk about. We decided we actually found out this morning our paper got accepted. So we're kind of pivoting. You had a lot of enthusiasm in that opening. I hope I can deliver. But this is truly an exciting moment with this paper getting accepted because it is a first of its kind study.
It's been one that my colleagues and I, Dave Feldman and Adrian Sotomayor, have been expending blood, sweat and tears on for a few years. And I really have to give most of the credit to Dave Feldman. This started with him. He's, if you don't know him, an outsider, an engineer who had this provocative question. We'll get into it.
Delved into lipidology, became obsessed with it, crowdfunded a clinical trial and executed on it. And we've been working on this area of research. We've had like 10 papers on it over the past couple of years.
But this is really the landmark study because what we did, what the team did was take this group of people that turned lean mass hyper responders, these people who go low carb and see their LDL go through the roof, like sky high levels and followed them
over the course of one year with high resolution CT angiography to look not just for calcified plaques, but also non calcified plaque to see does plaque progress in this population that conventional wisdom would say is that super, super high risk their LDL levels are 200, 300, 400, 500. Sometimes it's close to 600. We had one person in this trial with an LDL of 591.
So do they have plaque progression like conventional wisdom would predict? And if there is plaque progression at a population level, what actually is the major risk factor? What drives the progression? And I'll just give you the headline. There was no or minimal progression in the majority of people.
On a population level, there was a tiny bit of progression, something called percent atheroma volume increased by 0.8%, which is pretty modest at a population scale. And the really critical thing is in addition to most people having no or minimal progression, you had to ask what predicts progression? Is it this LDL cholesterol that we always hear about or the associated marker ApoB?
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Chapter 2: How does LDL cholesterol relate to heart disease risk?
Chapter 3: What are the lifestyle factors contributing to plaque progression?
So this is really a complex story that I'd love to get into with you about novel corners of physiology. resulting in pretty dramatic cholesterol lipid profiles that give most cardiologists heart attack by proxy. By that, I mean it's very shocking. And then examining, well, what's the mechanism behind this? And also, what does it mean for risk?
And these new data say the risk profile might not be what we would otherwise think if we weren't studying this population.
So a lot of our audience is listening today and they're asking themselves this question on a regular basis, which is, is the diet that I'm eating leading to a healthier heart or a not as healthy heart? And in the context of everything you shared and this journal, this paper that was just published in the journal, we'll have the link below in the show notes.
Um, the question that I'd like to ask you is how can you help our audience understand the body of work that's out there and where this study fits into it? Many people have seen the headlines that, Hey, red meat. is going to increase your risk of developing a heart attack.
Chapter 4: How can individuals assess their personal heart disease risk?
And even people have seen very well-respected individuals on podcasts talk about how they should be paying attention to these individual biomarkers that you've mentioned, LDL, APOB, such to the degree that some experts even have said that those things are causative for atherosclerosis.
So the person who's just trying to make sense of this all today and understand what this paper may mean for them, what do you want to share for them?
Right. So I think we're going to have to step back and go through some of the framing literature, but also make the critical point that some of the things you said that might sound at odds with what I said, like Apple being LDL being causative, are actually consistent with what I said.
And I think the challenge I want to present your listeners with is really grapple with the ideas and the words I'm saying and hear how these ideas are actually consistent, not conflicting, and how context is really important. Let me first actually attack that idea of LVL and Applebee being causative in heart disease, because indeed they are. And by that, I mean they're part of the causal cascade.
So if you didn't have ApoB or LDL particles or they were at the floor, you really can't develop heart disease progression. That's true. But it's also true that context, metabolic context really matters. If two different people have the same exposure to LDL or ApoB. So the same level, how high it is for the same duration of time. Will those two people develop heart disease at the same rate?
And the answer is no. There are other factors that influence what the absolute risk or absolute progression rate is. Some person might have really rapid progression. Other person might have such minimal progression that it's basically negligible. You can think about it as kind of if you like, you're mathematically inclined, a little graph.
And on the x-axis is exposure to LDL, exposure to LDL, cholesterol exposure to aqua B. And the y-axis is how much plaque actually accumulates in your heart. Some person can have a very steep slope, meaning with a little exposure, they get a lot of plaque.
And other person could have a very shallow slope, meaning for a ton of exposure, they actually develop very little or maybe even no plaque, not even a measurable amount. That difference is really, really important because people are trying to decide what to do with lifestyle or whether or not to take medications that do have side effects.
And in the context of a whole person, you always have to do this benefit analysis. It's not about snapping your fingers. You can't snap your fingers and change one biomarker in isolation. Say you're using a ketogenic diet to treat inflammatory bowel disease, but your LDL is really high.
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Chapter 5: What are the worst diet and lifestyle habits for heart health?
You have to ask questions like, well, why would I do a stunt where I publish a study where I lower my cholesterol with Oreo cookies? It's not because I think Oreo cookies are a health food or I want people to eat them, but I want to get attention to this fascinating physiology. Yeah, of course. It's clickbait for me to eat Oreo cookies and lower my cholesterol. It's also legitimate science.
And if it opens up a conversation about what's going on here, what can we learn about this population, and how can we rally to study this population, I think that's very worthwhile. I just want to make the point that in science, the greatest discoveries, let's say the most impactful discoveries, come out of just pursuing these curiosities. Why does my cholesterol go down when I eat Oreo cookies?
Why does Gila monster venom screw up the metabolism of its prey? People studying Gila monster venom in the 90s, they didn't know what would happen as a result of the studies. Guess what? The result of the studies is basically the modern era of weight loss drugs. Ozempic, Wigovi, GLP-1 receptor agonists are a result of studying Gila monster venom.
In the same vein, what we're doing now can have knock-on effects and knock-on discoveries that I think are generalizable to every single human being. If just then now in the modern era with social media, people get to see it happening, the science happening in real time.
I wasn't laughing. I was smiling because I love that you did that. And I was a huge fan of you putting out that work. So to follow up on that, you mentioned something really interesting earlier. You said in the study, you saw two groups of people. One group of people were individuals that didn't have a lot of plaque built up already and we're lean mass hyper-responders, right?
Individuals that are on a low carb diet whose LDL is very high and probably also their ApoB is probably high too, right? If their LDL is high in most cases. They basically go hand in hand in this.
case they go hand in hand so their apob is high and their ldl is high but they had no plaque that was there and so you saw with that group they didn't get any further plaque progression but the other group is where i want to ask the question individuals that already had some plaque build up did see further plaque progression let's talk about that group Two questions about them.
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Chapter 6: How do different diets affect gut health?
What is your understanding of the reasons that people might have plaque buildup to begin with, especially if they're eating very healthy right now? And then why do you think that these individuals, just a hypothesis on your end from what you know, why would these individuals see further plaque progression?
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What I would say is, why do they have a baseline? Well, these people, the average age at time of enrollment was about 55 years old. And at that point in time, average time on a keto diet was 4.7 years. So if you do the math, these people didn't start a ketogenic diet on average until they were over 50. So they had the first 50 years of their life when they were doing other things.
They might have been eating a standard American diet, might not have been living a healthy lifestyle during which they could have had plaque accumulation. You know, just because you adopt a healthy lifestyle doesn't erase decades of living another lifestyle. So it could just be a phenomenon of You know, their prior diet, their prior exposure, their prior lifestyle led to plaque being there.
And then the change of diet didn't just make the plaque suddenly vanish. So there was like a you could say a chink in the blood vessel armor, so to speak. And that, you know, seed preexisted as they were going on to this this trial. So I think that's probably the most likely phenomenon. There could be other phenomenon as well. I mean, there could be genetic contributions, for example.
I guess we'll never know for certain, but I would say the most likely explanation is that people spent 50 years living another way. Probably that contributed to life progression. It's far more likely than blaming it on a few years of a ketogenic diet.
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Chapter 7: What insights does the aspartame study provide?
It's just an anecdote. You can say that if you want. I prefer to say this really rubs up against the status quo. Yes, at a population level, this person is an outlier. Don't you want to know why they're an outlier? Don't you want to know what makes them resistant? Because once you figure that out, that's the seed of a solution that could generalize to more people. So I love studying the outliers.
This whole population is a population of outliers, but that's what makes them so cool to study and why we have so much to learn from them.
For somebody who's listening today who's like, I want to do individualized and personalized risk assessment when it comes to my cardiovascular health. Let's start off with somebody maybe that has a lot of resources and can go outside the scope of traditional medicine. What would you recommend for that individual?
And then let's also talk about the person who may not have as much resources or is dependent on only the healthcare that they have through insurance.
Obviously, the caveat here is I'm not a medical doctor, at least not for a couple months. I'm a PhD researcher, and I'm talking about my interpretation of the data. At the end of the day, talk to your physician, think about this thoroughly. But with that said, I think I can say the data is showing more and more that the best thing you can do is look for plaque.
You can get a functional test, be that a coronary artery calcium scan, a CAC, which are pretty cheap and widely available. I know I've heard places you can get them for like 75 bucks or maybe 150 bucks. And it's a pretty good risk predictor. of whether or not you'll develop plaque later on in life.
If you want more details on the different tests available, so there's one coronary artery calcium scan that looks at calcium in the blood. Sorry, not calcium in the blood. Calcified plaques. And another one called coronary CT angiography, which looks at soft plaques as well as calcified plaques. That one's... more detailed, you could say, but a little bit more radiation.
If you want the pros and cons of those, I'll actually direct people to a video. There's a group, Metabolic Mind. They have a YouTube channel, and I'm sure you know the cardiologist, Dr. Brett Scher, a friend of mine. He did a dedicated video on CAC versus CCTA scanning. That is great.
He's a board-certified cardiologist, so if people want the details, I'd say you can get functional testing of your heart You can check out that video if you're actually interested in the pros and cons of the different tests. But, key point, you can look in your heart and see if you have plaque correction.
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Chapter 8: What role do microplastics play in cardiovascular health?
Like anywhere you go, you're going to have somebody saying something negative about some compound of the diet, be it cholesterol, saturated fat, salt, oxalates, lectins, what have you. Sometimes, actually, usually I'd say there's a grain of truth to that. So oxalates, for example, some people might have sensitivities.
Doesn't necessarily mean, though, that the whole food that has this component in it is actually bad for you. Because whole foods are complex ecosystems. And so it's not always clear what the biological result will be of having that food. And you can't reduce it down to a singular ingredient that may or may not be harmful in certain contexts and at certain doses.
things are always more complicated than that. One of my favorite examples is sesame. The reason I like this example is because it's super high in linoleic acid, omega-6. And people think about that as inflammatory and bad for you. But the literature mostly shows that sesame and sesame products like tahini are anti-inflammatory. And so you think, oh, how can we reconcile that?
And then you realize, oh, well, the whole food is packaged with things that help, say, protect against oxidation of the fat. So these things called lignin antioxidants in the sesame. And if you actually look at the oxidation profile of sesame fat with a little like acid, it's super low compared to just say like, you know, processed industrialized seed oil.
Again, like the whole food is different than the isolated component. Let's talk oxalates. What does the literature on dark chocolate say? On balance, is it healthy for you or unhealthy for you? On balance, dark chocolate is healthy for you. It's good for heart health, good for vascular health. It's good for brain health. On balance, that's what the literature says. Is it high in oxalates as well?
Yes. So, you know, people have their different sensitivities. You're always going to find somebody in the corner of the Internet that will, I don't want to say fear monger because that cheapens it. And I don't think that's the point. But let's say be particularly sensitive to potential pitfalls of certain ingredients. And I think it's OK. to be aware of that, but take them with a grain of salt.
On balance, my opinion is not that fiber, oxalates, leptins, plant anti-nutrients are a terror. I think most people can tolerate them just fine. I think on balance, vegetables are perfectly healthy for most people. And I say that with the context and the framing that, but I don't eat a lot of vegetables, fiber, or these foods because of my personal circumstance.
I don't think a lot of people try to take the time to separate like their narrative and what they do from maybe what the literature says. But my perspective now getting more philosophical is like what the literature says and what somebody else does that might work for them has no bearing. on my individual history and my individual narrative.
So if somebody eats a high oxalate, low fat vegan diet and does it tremendously well and is healthy and happy, that doesn't detract from the fact that I had a benefit on a ketogenic diet. It doesn't. I just want people to get to a place where they are healthy and happy. And I think just discussing the literature openly facilitates that. This is my current stance. It could change in the future.
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