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Nick Norwitz MD PhD

@nicknorwitz • 130,539 subscribers

MD-PhD. Harvard-Oxford. 1.3M YouTube Best-Selling Metabolism Newsletter https://t.co/YoPdkV6tkd Educational content only. Not medical advice.

Shorts

The Lion Diet Experiment (A Primer 🧵👇) 1/7) For a 30 days I ran the strictest version of carnivore: the Lion Diet. No dairy. No eggs. No seafood. No coffee. Just ruminant muscle meat, salt, and water. I didn't do it as an intended permanent lifestyle shift, but as a personal exploration of what remains the most controversial diets of my lifetime, and a "fad" that won't die. Or, maybe it's more than that? ⚠️Trigger warning for later in the thread

The Lion Diet Experiment (A Primer 🧵👇) 1/7) For a 30 days I ran the strictest version of carnivore: the Lion Diet. No dairy. No eggs. No seafood. No coffee. Just ruminant muscle meat, salt, and water. I didn't do it as an intended permanent lifestyle shift, but as a personal exploration of what remains the most controversial diets of my lifetime, and a "fad" that won't die. Or, maybe it's more than that? ⚠️Trigger warning for later in the thread

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🥓I Ate 600 Strips of Bacon 🥓 🫀Here’s What Happened to My Cholesterol🫀 1/4) In an N =1 experiment modeled on the #720Eggs Eggperiment, I dropped my LDL by 22% while eating 600 strips of bacon over 20 days. That’s 21,000 Calories from bacon while eating ~300 grams of fat per day, and buckets of saturated fat, and I was able to drop my cholesterol. Here’s what you need to know…

🥓I Ate 600 Strips of Bacon 🥓 🫀Here’s What Happened to My Cholesterol🫀 1/4) In an N =1 experiment modeled on the #720Eggs Eggperiment, I dropped my LDL by 22% while eating 600 strips of bacon over 20 days. That’s 21,000 Calories from bacon while eating ~300 grams of fat per day, and buckets of saturated fat, and I was able to drop my cholesterol. Here’s what you need to know…

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A case of two coronary scans: Nick Norwitz (high-fat, keto 🍳); Simon Hill (plant-based 🌱) First, for context, this post is largely in response to an incredibly nuanced and non-dogmatic podcast conversation between Dave Feldman and Darius Sharpe, one that had me scratching my chin and holding my ribs throughout. I definitely recommend giving it a listen. 12/10 Episode! They spend a substantial amount of time discussing cardiovascular risk and, in particular, the contrast between my coronary CT scan, showing 0 calcified and 0 soft plaque (total plaque 0mm3) despite astronomical LDL levels in the high 500s for seven years vs that of plant-based nutrition influencer Simon Hill, which showed 61.3 mm3 of plaque despite his never having had high LDL and, for the last decade or so, targeting exceptionally low LDL and ApoB, including by taking a PCSK9 inhibitor and eating a low-saturated-fat, plant-forward diet. First and foremost, there’s only so much you can conclude from a comparison of two cases. That’s obvious, so let me state that clearly. However, considering the broader context and expressed public interested, it’s still an interesting thought puzzle: What is “protecting” me from atherosclerosis, or what is leading Simon to develop plaque despite his low LDL and ApoB? I’ll address the common hand-wavy answer up front: “Well, maybe Nick has some special protective genetics.” What I’d say to this is that, although I can’t rule it out definitively since we haven’t annotated the entire human genome, my father had 99% occlusion of his left anterior descending artery at 44, and I also inherited his high Lp(a), which sits between 150 and 200. That is in addition to my historically exceptionally high LDL and a history of inflammatory bowel disease, which should further increase my risk of progression. Yet despite all of that, I have no measurable plaque, even though, as the patient, I can tell you that many cardiologists assured me I would. Additionally, the excuse that “he’s just young” doesn’t fly, since Simon is also young. We’re both in our 30s. And, as a historical comparator, children with homozygous familial hypercholesterolemia can develop plaque within a few years of being born. So, puzzle me this: Why am I not developing plaque if the relationship between LDL/ApoB exposure and plaque progression is so "remarkably consistent?" Hand-wave if you want, but I’d like something more specific please. (And I’d like anybody to tell me why they think I was confident enough to spend seven years on a self-experiment, risking my heart on the bet that this would effectively be the outcome. Was I just cocky and lucky?) That’s mostly what I want to post: a thought question to consider based on two individuals who have chosen to make their data publicly available. However, since this field is so wrapped in controversy, let me elaborate on a few more points that are related. 1. KETO-CTA. To anyone who wants to pivot and try to point the finger at KETO-CTA, I will remind you that, in 4 separate analyses, there was no relationship between LDL or ApoB and plaque progression. That remains true to this day. In fact, it's a result that remains more robust for having had our hands forced to run the additional analyses. With respect to our retraction of the April 7th Cleerly paper, which continues to be misrepresented (at this point, I have to assume willfully) I will remind you: i) we the authors, pushed forward the retraction of the April 7 paper; it was not forced upon us ii) we did so because of the Cleerly anomalies that came to light after publication – nb: Dave and I were blinded to elements of data willfully to protect the integrity of the project (there’s an irony for you) iii) we sought retraction only after company’s refusal to repeat a properly blinded rescan and quality assessment, and subsequent analyses that made the only reasonable interpretation that Cleerly systematically overestimated plaque progression iv) in none of the analyses did ApoB or LDL predict plaque progression, which was the main novel finding and remains robust. 2. Ezetimibe I am now taking ezetimibe. Critics have tried to cast this - incorrectly - as some form of me hedging, but I intentionally did not start it until after my 7-year scan, and I am not withholding any information from or about that scan. The reason I’m taking ezetimibe, which I have very clearly disclosed, including in my newsletter and in a video, is 2024 Aging Biology research suggesting cholesterol-independent effects on neuroprotection, which is something that’s important to me. The fact that I am taking it, I would cast as a testament that I’m not dogmatic on this issue, and I’m not trying to “LDL-maxx” for some aware. Rather, I’m being open, honest and transparent in my journey as a person and patient trying to make the best decision for myself at ever step of the journey. Also, on the topic of ezetimibe, see recent work by Adrian Soto-Mota DoctorTro et al., which adds another layer of nuance to LDL and ApoB management in the context of low-carbohydrate diets. TL;DR, if someone sees their LDL and ApoB rise on a low-carbohydrate / ketogenic diet, ezetimibe is likely to punch above its weight for LDL and ApoB reduction. Setting aside dogma, understanding individual biology and how to manipulate it can often be very useful in a clinical setting. I will always put data first. Acknowledging this fact is not contradictory to anything I’ve said, but completely consistent with it. It is all about individual context. Now, everyone should go listen to episode 43 of TFP_ with Dave Feldman and Darius Sharpe (Spotify, Apple and YouTube). It’s stupendous! P.S. I want to thank Dave for sharing on the podcast that, before each of my cardiac scans, I said a priori that I would release the results, whatever they were. You all know Dave to be impeccably honest. That is not in dispute, and it has always been my intent to share my data openly, as I have.

A case of two coronary scans: Nick Norwitz (high-fat, keto 🍳); Simon Hill (plant-based 🌱) First, for context, this post is largely in response to an incredibly nuanced and non-dogmatic podcast conversation between Dave Feldman and Darius Sharpe, one that had me scratching my chin and holding my ribs throughout. I definitely recommend giving it a listen. 12/10 Episode! They spend a substantial amount of time discussing cardiovascular risk and, in particular, the contrast between my coronary CT scan, showing 0 calcified and 0 soft plaque (total plaque 0mm3) despite astronomical LDL levels in the high 500s for seven years vs that of plant-based nutrition influencer Simon Hill, which showed 61.3 mm3 of plaque despite his never having had high LDL and, for the last decade or so, targeting exceptionally low LDL and ApoB, including by taking a PCSK9 inhibitor and eating a low-saturated-fat, plant-forward diet. First and foremost, there’s only so much you can conclude from a comparison of two cases. That’s obvious, so let me state that clearly. However, considering the broader context and expressed public interested, it’s still an interesting thought puzzle: What is “protecting” me from atherosclerosis, or what is leading Simon to develop plaque despite his low LDL and ApoB? I’ll address the common hand-wavy answer up front: “Well, maybe Nick has some special protective genetics.” What I’d say to this is that, although I can’t rule it out definitively since we haven’t annotated the entire human genome, my father had 99% occlusion of his left anterior descending artery at 44, and I also inherited his high Lp(a), which sits between 150 and 200. That is in addition to my historically exceptionally high LDL and a history of inflammatory bowel disease, which should further increase my risk of progression. Yet despite all of that, I have no measurable plaque, even though, as the patient, I can tell you that many cardiologists assured me I would. Additionally, the excuse that “he’s just young” doesn’t fly, since Simon is also young. We’re both in our 30s. And, as a historical comparator, children with homozygous familial hypercholesterolemia can develop plaque within a few years of being born. So, puzzle me this: Why am I not developing plaque if the relationship between LDL/ApoB exposure and plaque progression is so "remarkably consistent?" Hand-wave if you want, but I’d like something more specific please. (And I’d like anybody to tell me why they think I was confident enough to spend seven years on a self-experiment, risking my heart on the bet that this would effectively be the outcome. Was I just cocky and lucky?) That’s mostly what I want to post: a thought question to consider based on two individuals who have chosen to make their data publicly available. However, since this field is so wrapped in controversy, let me elaborate on a few more points that are related. 1. KETO-CTA. To anyone who wants to pivot and try to point the finger at KETO-CTA, I will remind you that, in 4 separate analyses, there was no relationship between LDL or ApoB and plaque progression. That remains true to this day. In fact, it's a result that remains more robust for having had our hands forced to run the additional analyses. With respect to our retraction of the April 7th Cleerly paper, which continues to be misrepresented (at this point, I have to assume willfully) I will remind you: i) we the authors, pushed forward the retraction of the April 7 paper; it was not forced upon us ii) we did so because of the Cleerly anomalies that came to light after publication – nb: Dave and I were blinded to elements of data willfully to protect the integrity of the project (there’s an irony for you) iii) we sought retraction only after company’s refusal to repeat a properly blinded rescan and quality assessment, and subsequent analyses that made the only reasonable interpretation that Cleerly systematically overestimated plaque progression iv) in none of the analyses did ApoB or LDL predict plaque progression, which was the main novel finding and remains robust. 2. Ezetimibe I am now taking ezetimibe. Critics have tried to cast this - incorrectly - as some form of me hedging, but I intentionally did not start it until after my 7-year scan, and I am not withholding any information from or about that scan. The reason I’m taking ezetimibe, which I have very clearly disclosed, including in my newsletter and in a video, is 2024 Aging Biology research suggesting cholesterol-independent effects on neuroprotection, which is something that’s important to me. The fact that I am taking it, I would cast as a testament that I’m not dogmatic on this issue, and I’m not trying to “LDL-maxx” for some aware. Rather, I’m being open, honest and transparent in my journey as a person and patient trying to make the best decision for myself at ever step of the journey. Also, on the topic of ezetimibe, see recent work by Adrian Soto-Mota DoctorTro et al., which adds another layer of nuance to LDL and ApoB management in the context of low-carbohydrate diets. TL;DR, if someone sees their LDL and ApoB rise on a low-carbohydrate / ketogenic diet, ezetimibe is likely to punch above its weight for LDL and ApoB reduction. Setting aside dogma, understanding individual biology and how to manipulate it can often be very useful in a clinical setting. I will always put data first. Acknowledging this fact is not contradictory to anything I’ve said, but completely consistent with it. It is all about individual context. Now, everyone should go listen to episode 43 of TFP_ with Dave Feldman and Darius Sharpe (Spotify, Apple and YouTube). It’s stupendous! P.S. I want to thank Dave for sharing on the podcast that, before each of my cardiac scans, I said a priori that I would release the results, whatever they were. You all know Dave to be impeccably honest. That is not in dispute, and it has always been my intent to share my data openly, as I have.

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“Definitely Do Not Stop Statins.” — Bryan Johnson “I’m not the best person to make these arguments [about statins].” — also Bryan Johnson Seems inconsistent 🤔 I’d politely suggest you walk back your stance or admit to overstepping on your blunt recommendation. I’d be happy to have a conversation with you or your team on the matter of precision and personal prescription of lipid-modifying medication. I think you’ll find my stance rather moderate & reasonable. 3000 word deep dive here: Cc More Plates More Dates

“Definitely Do Not Stop Statins.” — Bryan Johnson “I’m not the best person to make these arguments [about statins].” — also Bryan Johnson Seems inconsistent 🤔 I’d politely suggest you walk back your stance or admit to overstepping on your blunt recommendation. I’d be happy to have a conversation with you or your team on the matter of precision and personal prescription of lipid-modifying medication. I think you’ll find my stance rather moderate & reasonable. 3000 word deep dive here: Cc More Plates More Dates

31,332 görüntüleme

700 Cholesterol 0 mm3 Plaque (CCTA + Heartflow) The scan we review in today’s video (🔗 below) is not your average CAC scan. It quantifies both calcified and soft plaque throughout the arteries. And importantly, “he’s young” is not a sufficient explanation. 👉People in their 20s and 30s commonly show measurable plaque on these scans. 👉There are even well-known plant-based influencers in their 30s with a decent amount of plaque 👉Children with homozygous familial hypercholesterolemia as young as a year or two can already demonstrate advanced plaque burden with LDL levels similar to mine. The irrefutable reality is that elevated LDL and ApoB do not translate into identical plaque progression in every individual. That is 100% a fact. Understanding the biological differences that make some people dramatically more or less susceptible than others is absolutely critical to precision medicine. Anyone pretending these individual differences do not matter is ignoring reality. Anyone who protests again asking questions that need to be answered is a problem.

700 Cholesterol 0 mm3 Plaque (CCTA + Heartflow) The scan we review in today’s video (🔗 below) is not your average CAC scan. It quantifies both calcified and soft plaque throughout the arteries. And importantly, “he’s young” is not a sufficient explanation. 👉People in their 20s and 30s commonly show measurable plaque on these scans. 👉There are even well-known plant-based influencers in their 30s with a decent amount of plaque 👉Children with homozygous familial hypercholesterolemia as young as a year or two can already demonstrate advanced plaque burden with LDL levels similar to mine. The irrefutable reality is that elevated LDL and ApoB do not translate into identical plaque progression in every individual. That is 100% a fact. Understanding the biological differences that make some people dramatically more or less susceptible than others is absolutely critical to precision medicine. Anyone pretending these individual differences do not matter is ignoring reality. Anyone who protests again asking questions that need to be answered is a problem.

14,145 görüntüleme

Videos

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🚨#OreoVsStatin - PUBLISHED!🚨 OREO Cookie cookies were 💥2X as potent💥 at lowering my LDL cholesterol (LDL-C) compared to high-intensity statin therapy! What you NEED to know... 👉This was a metabolic demonstration, a 'do not do this at home' experiment that makes no 'health' claims about cookies or cholesterol. 👉The purpose was to BOLDLY test a prediction of the Lipid Energy Model #LEM, i.e. that adding in carbs, including in the from of an Oreo cookies 'addition' (not carb-fat swap) would lower LDL-C in an LMHR on a #keto diet Why Oreos? ... It's (productively) provocative! 😱 Research on #cholesterol on #keto diets and the #LEM and #LMHR phenotype has so much to teach us about human lipid metabolism! ... But how do I (we) communicate the scientific 'awe' that we feel to the greatest number of people (as well as force a conversation about #LMHR and #LEM that needs to happen)? ... A dramatic demonstration designed to turn heads might work! It's not 'just click bait' ... it's 'legit-bait' I want YOU to feel the 'shock and awe' I feel every day studying this topic. And I want you to engage in the research journey. What you need to do... or should do... 🙏PRETTY PLEASE 🙏! 👉PLEASE WATCH 👀 VIDEO ABSTRACT here (<8 min): 👉 SHARE THIS LINK to the paper itself in a quote RT or original Tweet of your own: ... doing so helps promote the work and provoke the discussion ... and feel free to tag in your favorite influencers (or least favorite 😉)... A HUGE thanks to the senior author and expert lipidologist William Cromwell, MD for his guiding wisdom, insightful thoughts, and always open and curious mind. And to Dave Feldman, my friend, research wife, and the '#LEM daddy' Finally... there will be a LOT of coverage of this experiment. Keep in mind, we are not making any health claims, but through a dramatic demonstration, highlighting an uncomfortable tension that arises from a prediction of the Lipid Energy Model, and that is consistent with prior data (7+ papers, including 'highest tier' data like our recent meta-analysis of 41 RCTs). Science is supposed to embrace such uncomfortable questions... so, join us in being curious and advocating for much needed research on #LEM and #LMHR so we can make sense of what observations like this really mean... STAY CURIOUS 🤔

Nick Norwitz MD PhD

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