Dhru Purohit Show - This Study Shocks Cardiologists: LDL and ApoB May Not Predict Heart Disease Risk in Healthy People with Dr. Nick Norwitz

Episode Date: April 7, 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 His journey has fueled a deep commitment to challenging outdated thinking around health, and he’s known for his infectious curiosity and dedication to teaching.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

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 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 a 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 and Sotomota, have been expending blood, sweat, and tears on for a few years, and I really have to give most of the credit that Dave Feldman, this started with him. He's, if you don't know, I'm an outsider or an engineer

who had this provocative question, we'll get into it, delved into lipidology, became obsessed with it, they 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 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 goes 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-calsified plaque to see. Does plaque progress in this population that conventional wisdom would say it is at super, super high

risk? Their LDL levels are 200, 300, 400, sometimes as close to 600. We had one person in this trial with an LDL of 591. So do they have plaque progression, like commensual 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, some nickel percent atheroma

volume increased by 0.8 percent, 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 LVL cholesterol that we always hear about or the associated marker APOB? And the answer was no. Actually, there was no predictive value, no association between Appleby and plaque regression or between LVL and PLAC progression. LVL and AppleB did not predict plaque progression. What predicted plaque progression was whether or not somebody had plaque at baseline. So you can get functional tests of your heart. These are becoming more and more mainstream to help people individualize their risk and their treatment decisions, something called

coronary artery calcium scan is one. And the CAC score, this functional test looking at the heart, did actually predict progression. So basically, if you have plaque to start with, you were more likely to have that plaque progress. If you didn't have plaque to start with, then you were unlikely to have progression. And LDL and Apple B were pretty much irrelevant in determining or predicting whether or not plaque would progress, which is really astonishing given the levels of LDL in this population. Again, 200, 300, 400, 500, LZL. It's quite remarkable, and I just want to emphasize one more thing, and then I'll get off my monologue.

The really interesting thing about this population, lean mass hyper responders, is they're the first and only human population we have ever studied that has high LVL as an isolated variable apart from metabolic dysfunction, because a lot of people are metabolic, metabolic, and that changes in metabolic context, and apart from genetic drivers like familial hypergolesterol lemia. So it's true if you have a broken lip metabolism. There are some people that are unlucky enough to be born with this. If you have broken lip metabolism, you can have very high LZL and also typically have

advanced heart disease at an early age. Something called homozygous familial hypolytraeclitealemia. Kids will get heart attacks at like, you know, age 10. This is different because it's not that these people have broken lipid metabolism, it's that in cutting out carbs, sometimes even irrespective of saturated fat intake, in cutting out carbs, there appears to be a metabolic response, whereby there, the cholesterol trafficking, fat trafficking system gets upregulated, and as a result, an epiphenomenon, you could say, the L, the L goes through the root. 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 with the 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 audiences 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? Yeah. 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. 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. And even people have seen very well-respected individuals on podcast talk about how they should be paying attention to these individual biomarkers that you've mentioned, LDL, APABETH. be 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 B and LDL being causative or 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 Apple B 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 Apple B or LVL particles or they're 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 apobie, 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 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, be on 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 life style 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, 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. Well, it's important to know what's the

absolute risk because what you might be trading by reintroducing carbs is an increased risk of flares and ending up in the hospital or, you know, trying a medication that might have a side effects promote insulin resistance or other, you know, negative health effects that you don't otherwise want. So I'm not here to say that LZL or Apple B is irrelevant. I'm here to say it's context dependent and that in assessing an individual's risk, you need to take a look at the whole picture. So, you know, TLDR is going over your head. Don't get your medical information, your health recommendations off of podcasts and YouTube. I'm here to provide information by the end of the day. Key thing is to assess your own risk profile. But with that caveat,

place. A question that I think we should ask is, why does LDL go up? We talk all the time about LDL, but not so much about the physiology behind what drives it. And people then tend to oversimplify and think, oh, it's just saturated fat. They're just, quote, butter guzzlers. Or it's just some quirk of genetics, right? Those are kind of hand-wavy statements, and in some cases, are true. Saturated fat can increase LDL, at least a little bit. Genetics can play a role. but when you have a really interesting phenomenon, like someone going low carbon, their LDL going for like 300, 400, 500, saturated fat almost certainly isn't the only thing at play.

And in some people, it's very weird because they even go like plant-based low-carbon. They'll still see this response. I can actually get to my LDL for like 300, 400 on a vegan keto diet. So you get to ask the question, well, what's going on here and what can we learn from it? That's where this population that we've been studying comes into play. Because what appears to happen when, When lean insulin sensitive people go low carb is when they're no longer relying on carbs as much for fuel, specifically what happens is the carb stores in the liver, which defend blood glucose stores when they drop.

It triggers this cycle whereby you're burning fat and some of the fat that kind of, if you could say, spills over, gets taken back up into the liver and then recycled through the body through a trafficking system that depends on cholesterol. So specifically you have these big, you could say fat carrying boats. they're called VLZL particles, very low density light-prudene particles. You need them because fat, stored fat, doesn't mix with aqueous solution. So water. You know that if you take oil, you put it in water, it doesn't mix. So it's the same way with fat in your body.

It doesn't really mix well with blood. So you need a way to carry it around the body, and it gets packaged the fat into these shipment containers that contain cholesterol. And in circulating around the body and dropping off fat back at fat tissue and muscle tissue, the result of that can be very, very high. which can actually be reversed in these people by just adding back carbs, which is why I can lower my cholesterol with Oreo cookies, which I've done and published on. You're laughing now and it seems like a joke, and to some extent it is. Like, you have to ask a question. Like, well, why would I do

a stunt where I publish a study where I lower my cholesterol with Oreo cookies? It's because, not because I think Oreo cookies are health food or I want people to eat them, but I want to get attention to this fascinating physiology. Like, yeah, of course. It's clickbait for me to eat Oreo cookies and lower my cholesterol. It's also legitimate in science. And if it opens up a conversation about what's going on here? What can we learn about this population? And, you know, 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 studies is basically the modern era of weight loss drugs, OZempic, Wagovi, GLP1 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 now in the modern era with social media, people get to see it happening, the science happening in real time. I was 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 know, 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 were 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 they're LDL is high in most cases. 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. You know, what are some of the, what is your understanding of the reasons that people might have plaque build up to begin with, right? 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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Head over to drinkelement.com slash Drew. That's Drink, D-R-I-N-K. element l mn t.com slash d hr u to claim this offer from my community today what i would say is why do they have flack a baseline well you know 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 keto drink 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 seed pre-existed as they were going on to 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

lack progression. It's far more likely blaming it on a few years of a ketogenic diet. And then just because that's very debated before you go further, what was that like? that they were living because you'll see a lot of our audience will see the arguments from people saying, hey, if you're eating meat, that's a lifestyle that's going to be, you know, leading to plaque buildup. Some people will say, hey, if you don't have a healthy workout routine and nitric oxide and endothelial protection, these are things that are going to be building. So what was that combination of lifestyle habits that you think were contributing to their plaque buildup for them or for anybody else? What I would say is, you know, we have 100 people in this study.

Actually, 100 people that enrolled in 100% retention. So no dropouts, which is actually pretty stunning. Just, you know, props to the participants. That's remarkable. But we didn't do a deep dive into every single lifestyle factor that every participant had. That was beyond the scope of the study. So I'll just talk in generalities about, like, you know, what could contribute to heart disease progression?

And I think living a lifestyle that leads to insulin resistance, having overweight or obesity, pre-diabetes or diabetes at any point in your lifetime, smoking, obviously, various genetic factors, all could contribute to heart disease progression. So, you know, the boilerplate stuff, sedentary, not sleeping well, smoking, eating poorly. It's kind of boring, but the fact of the matter is those are the things that probably increase your risk for heart disease, particularly things having to do with insulin resistance. So if you look at large-scale population studies, like having type 2 diabetes, pre-diabetes, high insulin resistance score, like an L-P-I-R or a home-I-R,

is a very strong predictor for poor cardiovascular health. So let's go back to the second part of the question. Before I interrupted you, you were kind of getting there anyway. Why would people who already have plaque see that they would see further progression of plaque, stickiness of plaque, I guess you could say, when they're going on largely what would be the diet that you follow, which would be a low-car, ketogenic diet. So I think you can kind of cluster into two possibilities. One is that there are just underlying susceptibility factors that we didn't identify in this study. So the people with placate

baseline are probably, let's say there are like genetic factors that make one more susceptible to heart disease. Even irrespective of LDL, Appleby, there are other factors that genetically could pre-imposed somebody to heart disease. The people that have plaque at baseline are more likely to have those factors. So it could just be these are the folks that have other risk factors for heart disease, you know, in their genetic code, in their microbiome, in their epigenetics, whatever. The other possibility, which I think is more interesting, is that the plaque itself, which is kind of like an inflammatory microenvironment, could propagate, self-propagate, that plaque gets plaque, that the inflammation there locally, the activated

immune cells could perpetuate more plaque growth. So think of it as like, if a seed was planted, and you see the sproutling growing, it's going to keep growing, right, versus that the seed was never planted in the first place. You know, this study didn't answer those particular questions, but they're great questions to ask because they are the frontier of, you know, what we need to study next, because this is all about individual risk assessment. And so, you know, trying to identify that why does person X have progression or person Y not, partitioning those groups and then also looking at the outliers, like, that's where we learn so

much. To double down on that point, you know, some people, they, they see someone with it. We have one person, actually not even a person of this study, but a person that's in a movie related to some of the research we're doing. You know, they're, you know, I'm about to turn 60. Their LDLs around 700, and they have no plaque on coronary CT in geography, none that can be measured. That's remarkable. That's jaw dropping. And some people may say, it's just n equals one. It's just an anecdote. I 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's 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.

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 health care 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, you know, my interpretation of the data. At the end of the day, talk to your physician, you know, 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 CTN geography, 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. they can go to, 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 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 to the different tests. But key point, you can look in your heart and see if you have plaque direction. and if you're, you know, middle-aged or above and you have no plaque, that's a really good sign. If you have some, then, you know, you have a little bit less buffer room to wiggle with. In addition to that, we can talk about biomarkers. I think everybody should know some form of insulin resistance score. So there's like a lycoprotein insulin resistance score, an L-PIRI-R or a Homa-I-R. You can also just get a fasting insulin and see if it's elevated.

But generally, you want low insulin-resistance. scores and low fasting insulin. If you have that, that's a pretty good sign. In addition to that, you can learn a lot just from a standard lipid panel. So LDL-HGLostrides. Generally, you want higher HDL, they say above like 40 for men, above 50 for women, and lower triglycerides. Normal's below 150, I think below 100 or even below 80 is better. It's a bit of a noisy variable.

It's really important to get the test fasted, about 12 hours water-owned. fast it is best. And that'll give you a lot of information. If you want a little bit more resolution, you can get more advanced lipid testing with, you know, LVL profiles, NMR spectroscopy. But I would say knowing your insulin resistance score, probably a blood sugar metric, like an HB1C, some marker of inflammation, like an HSCRP, and then a lipid panel, you can derive a lot from that. So a quick question or clarification on my end. I've heard from folks that sometimes if somebody goes to get traditional CT scan, which was one of the tests that you mentioned, which often people go to as a first line because it's very cheap and it's easy to do, they'll come back and they might have a very

low score, but it could give them a false sense of security because the CT scan is only looking for hard plaque, whereas some of the more functional tests that are out there, a CCTV is going to be looking at soft plaque. And I don't know if this is true or not, but that soft plaque is a bigger risk factor for heart disease. Is that make any sense? And what did I get wrong as part of that? Are you looking for one of the most effective ways to naturally boost cellular and mitochondrial health? Let's talk about red light therapy. With over 1,000 scientific studies backing its benefits, red light therapy has been shown to strengthen mitochondria, reduce pain and inflammation, improve circulation, enhanced performance, speed up muscle recovery, and so much more. I've even been

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slash Drew to start your red light therapy today. More or less makes sense, yes. I mean, soft plaques can rupture and then you can get basically a local clot and that can clob off your arteries. What I would say is the literature shows that the coronary artery calcium scan is a pretty good predictor of your heart disease risk. Like, if you have a CAC of zero, it's very unlikely you're going to have a heart attack in the near term.

And we can direct people to more resources on actual literature around that because it's pretty well studied that, you know, the CAC score does trump things like LZL as risk variables. The caveat that I'd lean into with respect to what you said about false sense of security is you want to interpret the results in the context of your current lifestyle and if anything changed drastically. So I'll be more concrete with an example. If your CAC is zero and you're 50 years old and you started a ketogenic diet, you know, six months ago.

After you started a ketogenic diet, your LZL went from 70 to 500. And then you get that scan, the CAC is zero. What does that actually tell you? Well, I'll tell you what it doesn't tell you. It doesn't actually tell you much about the impact of that super high LVL on your risk profile

because there just hasn't been enough time, presumably, for it to result in any change on a coronary artery calcium scan. So that will be a circumstance where I would say somebody might, might have a full set of security because they're interpreting or they could be interpreting the results of their functional scan within the context of a current marker that has changed in the near term. And the functional scans will take time to change. So a question,

I think people should ask themselves if they're looking at their lipid panel and something's changed is, you know, how high is the risk marker in question? So how high is your say L, the L or Apple B? And how long has it been there? I'll give another example because I think examples help people. My mom, she's about to turn 60. She has had high LDL her entire life. Generally, her LDL is run between like 160, 200 plus for the majority of her life until she went keto, and she's a lean mass hyperrespondener.

So then her LDL jumped like 400 and has been there for several years. So her lifetime exposure to LDL is high, many thousands of milligram per deciliter years. So she was trying to decide does she want to go on any lipid lipid? lowering medications. There are various drugs you can take to lower your cholesterol. What she did was get a scan of her heart, a coronary CT in geography, the one that looks not just for calcified but also non-calcified plaque, and she had zero plaque. So from that, she decided, just for context, she's an MD PhD, she can make her own decisions. I'm not persuading her to do anything. She decided she wasn't going to take lipid lowering medication. And to me, that's a sensible

choice for her because she knows she's had a lot of exposure and there's no measurable plaque. It will be different if, say, she had really low LDL her whole life, say she was 40, and then she changed her diet, and then her LDL went to 400. Then the calculus changes, if, you know, for the reasons I kind of, I just explained, does that make sense? So how high for how long you need to interpret the functional test score, the calcium score, or the coronary CTN geography score, in the context of your prior. exposure and whether anything has changed. So I'll just share my own personal anecdote that I've shared with my audience previously. But I, right around the age of 40 and having some history of heart disease in the family, and also knowing that South Asians, who generally are very metabolically unhealthy in America,

they work desk jobs, computer scientists, many of them are doctors, et cetera. There's not a lot of exercise and fitness, although a lot of that's changing. they're at the highest risk of heart disease of any ethnic minority in the United States. And so me being Indian and part of that community and having a history of high LDL and APOB, right as I turned 40, I sought out a more open-minded precision medicine cardiologist who would help me dig into all this. And I've done many podcasts with him, Michael Twyman. He's a great guy. I think you might even have maybe had some interaction with him at some point in time. And one of the tests that we did was a CCTV test.

I have no affiliation with them, but it was a brand name called Clearly. And why I wanted to seek that out, even though it is a lot of radiation, I've heard estimates that it's a thousand x-rays or something like that. I don't know if you have any insight on CCTV, how much radiation it is compared to normal x-ray that's there, but I've heard it's a lot of radiation. I don't think it's too much. Okay, okay. So maybe a thousand is overblown.

Well, I mean, it depends like what, I mean, like, because, I mean, that's all in relative terms, right? So if you said, you know, something has 10 times the calories of a stick of celery, it's not that many calories. So, you know, what x-ray? Some modern x-rays don't have a lot of radiation that say, like the dental x-ray. So I'm not sure. I think if you quantified it in terms of, I'm not 100% sure about this, but I think you've quantified it in terms of like background radiation, like exposure just from living in the free world. it's something like a few months. It's not eligible.

I wouldn't get one every six months. I've gotten one and I thought it was for friends that have gotten a few. I don't think it's catastrophically high. So I sought out one of these CCTV tests. Clearly was the brand, again, not affiliated with them. And when I got back the results, it gave me, and I break them down on my YouTube channel

with Dr. Twyman, along with all my metabolic labs that I got through Boston Health. And I thought it would be a good experiment for me to share that I'm just like my audience. I'm not an expert in this category. I'm just interviewing and getting a chance to ask people like you questions. And I'm trying to make my own mind up of do I want to live for the next 10, 20, 30, 40 years? And beyond that, of course, on the diet that I'm currently on that has my LDL being an elevated LDL,

where a traditional cardiologist would say, hey, you're at a super high risk of getting, based on family history, ethnicity, etc. you're at a super high risk of getting a cardiac event in the future. And that test gave me a deep peace of mind along with all my labs that I got done, that I had the cleanest test that he had ever seen for any man in his practice that was there. Granted, I'm 40 years old. I haven't had a cardiac event before. But I found a deep sense of peace of mind. And I was sharing with you before we started recording is that I still balancing everything

was asking myself, do I want to live the rest of my life? hopefully to 100 and beyond, with a super high APOB and LDL. And I ended up deciding, because I'm a hyper-reabsorber of cholesterol, I ended up deciding to go on the prescription medication, a Zetamide. And so I take that. I think it's the standard dosing is like 10 milligrams. And I take that every single day. And I saw a pretty big drop in my APOB, and I'm still eating the way that I'm eating.

And I chose that because largely as I was weighing all the pros and cons, it was generally as recommended to me from my cardiologist. Again, everybody needs to go see their own medical doctor and get their own prescription for what's right for them, lifestyle, medication, etc. It was the one that had the least potential side effect. That would be there. So do you have any commentary about my situation

and how I approached it? I love how you approached it. I think, you know, you got functional testing on yourself that informed your decision, and nevertheless, you went about doing a risk-benefit analysis that was right for you. You thought this medication had a low side-effect profile, which I think generally it does, and also fit your physiology. You know, the azetamibas I know you know, and your audience might know, it blocks cholesterol absorption at the level of the gut.

So as a response, your liver increases the LDL receptors and pulse them out of the blood. You know, more or less, it's acting locally at the intestines and then signaling to the liver. So if the side effect profile is pretty low and the risk profile is pretty low and they're not, you know, having any symptomatic side effects. and all that's happening is a number on your lab report is going down that might reduce your risk or might, but it might, then why not? And the rest benefit analysis, the way I see you think through it is like, you know, I am reassured by this functional test. Nevertheless, the cost of me taking this prescription is basically nothing, and there might be benefit.

So why not? It seems pretty reasonable to me. I'll add one more layer, and I'd love to get your thoughts on this. There was a pretty wild study that came out last year. from a group of researchers from Italy. I'm sure you came across this, where they did autopsies, and they saw that the individuals had the highest level of plaque,

also had a large amount of microplastic accumulation inside of that plaque. And do you have any thoughts on this? And why I'm asking is because I'm also, you know, knowing that we have an increased toxic burden and that all of us are being exposed to microplastics in the air, in the water, from our clothing, in our foods, I don't know if you saw on Twitter, the plastics list by Nate. I forgot his last name, Nate, it'll come back to me.

We'll link to the show notes. But they basically found that everything from like Whole Foods ground beef to, you know, many places like are filled with extraordinary levels of plastics in the food. So did you come across a study? And what are your thoughts about that when it comes to heart health, even for healthy individuals like you and me who have pretty clear, levels of hard plaque and soft plaque. It's an interesting point.

I did. There were a lot of studies, actually, that came out last year, I think starting with one in the New England Journal about, yeah, plaque in, sorry, microplastics in black. And it was pretty shocking. I think I did a video a while back on, like, ways to avoid microplastics. And I was doing the research for it. And I was just like the most depressing thing.

They're like, they're everywhere. They're literally everywhere. How can you avoid it? And, you know, I think it's one of those things where, I'm not sure what the absolute risk exposure is and how we need to reevaluate what our modern risk profile might be, you know, as we age, you and me being generally younger men versus, say, our grandfathers. I think it's something to take into consideration independently and then do your best to try to, you know, avoid. I think my impression is, yes, they're everywhere, but there is still the big, like, heavy hitting items you can avoid. void. So like don't get plastic, takeout containers and microwave plastic. Do not microwave your

food in plastic. Don't have plastic water bottles, things like that. You know, maybe if you get some like grass-fed regenerative beef, there might be a little microplastic in there. I think that's probably a lower absolute exposure than the things that people typically do. So if you, you know, carry around like a water canteen and use pure, you know, purified filtered water, you're not microwaving in plastics. I think that probably should bring most people a decent piece of mind. other than that, it's just like, what can you do in your, you know, your lifestyle from, for example, like, I live in downtown Boston. You know, next to a couple hospitals. We live there because my girlfriend works at one.

She's just to get up like 4 a.m. for her surgical residency. So, like, it makes sense to live in a city. In the city, is the air quality that great? No. As there probably a lot of plastic exposure, yes, but it's where I am in my life. So I think everybody just kind of needs to make the reasonable decision for themselves and realize that might not be perfect. So yeah, microplastics, probably a problem. Do what you can.

That's where I stand. You know, to drive this idea home, I want to ask you a question. If I came to you and I said, Nick, I want to design the absolute worst diet and lifestyle regimen that is guaranteed to create an environment in somebody's body where they end up not only having a heart attack, but have it early, right? Walk us through this person's daily routine. You want to create insulin resistance and crazy blood sugar levels and lots of stress. So I would say this person would probably be a shift worker working at night, but not just

at night. Like their schedule will be changing. So maybe, you know, they, you know, work, you know, the eight-hour shifts. So they're like constantly cycling with a change in their circadian pattern. You know, they're probably a smoker. You know, that's definitely going to promote heart disease. Snacking on sugar all the time. So like always with some M&Ms or Oreos and their.

pocket. This is a very high-stressed lifestyle. So, you know, always worked up, always raging at things, probably a little social connection, not a lot of time for de-stressing, very little exercise. So they're getting 2,000 steps per day. And that's only when they're walking to the vending machine to get more Oreo cookies. Not exercising, sleep-deprived, smoking, junkie diet. And yeah, I think that will probably manifest in heart disease pretty quickly. And just, you know, I know it sounds silly, but I think that sometimes. Sometimes the audience really responds to this. Like, what is this person eating for breakfast, lunch, and dinner?

You talked about them snacking on sugar a lot. But what does their diet look like, breakfast, lunch, and dinner? Let's put it in the context of something that, like, people would realistically eat. Because, of course, you'd say, oh, they're just eating Oreos for every meal. But I would say, imagine this person's going to Starbucks. And they're getting a coffee. But they're getting it with, like, you know, multiple pumps of, like, syrup and sugar. I mean, you can go to Starbucks and get some of these, what, like, like, white mocha,

lattes with two times more or more the sugar of like a regular 12 ounce coke, something like 79 grams of sugar. So something that, you know, might seem like, all right, it's not the healthiest, but might not be too bad. It can actually be really bad. So let's say they're going to be a sugary frappuccino or like a mocha, you know, white chocolate latte at Starbucks with some sort of breakfast pastry. So they're loading up in the carbs of sugar, but something that people realistically eat.

And just because of the culture and, you know, maybe they work in a hospital setting and there's like donuts at the nurse station, they pop a couple donuts at 10 a.m. For lunch, what's in the cafeteria? Let's say there's like pizza and fries and a salad. But the salad has, you know, pretty low quality oil. Maybe it's made with like old soybean oil. So having this like salad with pizza and maybe a chop of milk just because it's available. So a little carbon has 40 cents.

So more sugar, more processed food, all of that. Maybe they have a snack later. Maybe they have an energy bar. Let's say it's a cliff bar. again, lots more sugar. Something that people generally eat, they think, oh, there's some protein in here, does micronutrients? Because it's been fortified, but it's just sugar on sugar on sugar. You know, they're spiking their blood sugar all the time.

They're dropping their blood sugar because it's spiking. So they're probably going to be hungry again for dinner at around like six, seven, or eight. So, you know, what do they get for dinner? Well, let's just get some Uber eats. What's good? Oh, let's get, you know, a burrito and a soda. And then they're hungry later. so, you know, Yolo, let's treat myself as out of stressful day.

Let me have, you know, some potato chips and maybe an ice cream bar from the vending machine. And, you know, that sounds kind of, you know, actually what I would say is the person listening should pause. How did that sound to them? Because I actually think you're probably going to have like a bifurcation of listeners. Some people are going to be like, oh, my God, that's disgusting. I can't believe anybody eats like that. And other people are going to be like, yeah, I can see it. So I think that's actually interesting for an interesting exercise for the listener to pause and do a reflection on what their response was as I was describing it because it's so interesting how we can calibrate and recalibrate to what is normal.

Like when I was a teenager, that would have been like, yeah, it's a reasonable day of eating. It's not the healthiest, but like, okay. Now I cannot imagine eating like that. I just truly can't imagine it. or, you know, my recalibration for sweet is totally changed. I used to be like, oh, yeah, ice cream daily. That's pretty normal. You know, if you're healthy, you know, you probably can outrun that, quote, bad diet.

Just like a little bit of empty calories, no biggie. Now I can have, like, a few frozen cherries, and it tastes like an ice cream Sunday used to. So I think the interesting part about that exercise is for people to reflect it, like, where is your baseline of expectation for what a healthy, reasonable diet is? Which you can kind of, you know, test by what was your emotional reaction to me to that unhealthy lifestyle or that on healthy diet, so to speak. Well said. Nick, I want to move on from heart health, unless if there's any other commentary that you

have on that, and I want to ask you a bigger picture question about gut health, which is something that has been a big part of your journey and inspiration around your journey. Today, more than ever, when we look around, we're seeing individuals that have poor gut health, autoimmune diseases that are related to gut health are on the rise. And generally, a lot of people feel that their digestion is just completely out of whack. As I mentioned, you have your own personal relationship to this. But before we get into your story, I want to hear from your perspective, why do we see so many people in our modern society with such bad gut health? Westernized diets. I mean, if you look globally at like, where,

inflammatory bowel disease and also irritable bowel syndrome is like on the rise it's everywhere that there's you know a westernized diet so the more processed junky food we eat with the more added chemicals in the more like we are we are to develop gut dysfunction that shouldn't really be surprising i mean when you just think about the scale of the things that are adding to our food that we were not designed to be exposed to evolutionarily speaking it's no surprise that things are getting screwed up. And the fact of the matter is the burden of proof is not on the food industry that's introducing these foods to demonstrate no long-term harm. They can, you know, show no, like, acute toxicity. But in terms of just like this scale of exposure and, you know,

the inadequacy of long-term safety testing for the things that get introduced to the diet, it really should be no surprise that eating a more processed Westernized diet contributes to an increase in, let's just say, gastrointestinal upset on the spectrum of I get some bloating to I have bloody diarrhea 20 times a day. I need to get my colon removed. So that's not uncommon that other individuals haven't said, but where I think you have a unique perspective that I'd love to have you expand on is many people like yourself, because of gut health issues and challenges and diagnoses have found themselves in a place where they've had to seek out things like a ketogenic or a carnivore diet as the means to help them reach some sort

of level of health. Why has that been a huge driver for so many individuals getting into the space, the carnivore and the ketogenic diet for gut health? We need to first acknowledge that this is a population that is, I would say, suboptimally served by Western medicine. That is not to say doctors aren't doing their due diligence with their patients. It is not to say some patients don't do remarkably well with surgeries or immunomodulating medications or other medications. That is to say that there is a population of people, and I was in this group, who despite trying all, quote, evidence-based medicine has to offer, still find themselves suffering terribly. And if you have ever been in that sort of situation or known someone in that sort of situation,

you know that desperation can lead people to try crazy things. things that aren't necessarily proven with the most rare risk research. So I think that's what's driving people to try things like a carnivore diet, which from the mainstream sounds crazy. But when you're desperate, you'll do anything. And if you hear stories of people saying, well, I suffered like you, and I tried this thing and it worked remarkably, then what goes through that person's mind, the person's suffering is,

well, what do I have to lose? Like, sincerely, you could be in the ICU. you could have no, you know, social life or engagement because you just have to, like, find a toilet every, you know, 30 minutes to, like, crap out your ass and you're in an incredible pain and you're losing weight. What do you have to lose by trying a dietary tweet? So people try things like carnivore or ketogenic diet, and then a lot of them actually have incredible responses. So it's spreading from grass from its experimentation, word of mouth.

Now, just to give a little bit more literature context, we have done. a case series on people using carnivore diets for inflammatory bowel disease. I interviewed these patients. Ten patients, we did in-depth medical histories, dietary histories. We had lab reports, colonoscopy reports. And to hear these patient's stories and look at their medical histories, I mean, the things I've seen and heard, I can't unsee in here. To hear people say, like, I suffered with this for 20 years, medications didn't help, surgery didn't help. Now I'm living a life that I never thought I could have again. I feel like a new person.

Why can somebody tell me about this earlier? Like, that gets you really interested and curious. And there's physiological reason to think this would work. It's already actually known that fiber elimination, now top in carnivore, can be therapeutic and treatment resistant cases of Crohn's disease. It's actually sometimes prescribed for kids with Crohn's disease who aren't responding to treatment. They put them on fiber-free liquid diets. And in about 60 to 85 percent of cases, they go into remission.

this is published on. And we also know that ketones are anti-inflammatory. They help feed the gut lining cells. They reduce inflammation. And there's actually an inverse association between ketone levels and inflammatory bowel disease activity in patients. So higher ketones, lower inflammatory bowel disease activity. So we have some data to say, this makes sense. And then a building mountain of clinical cases saying, this works.

The next step is going to be to do the randomized lymphomaeal. trials needed to make this mainstream. The fact of the matter is, they're hard to get funded and organized. I mean, you need millions of dollars for these studies. Big pharma isn't paying for it. The NIH isn't giving me that money. So you need to get a little bit more creative. So the stage we're at now is getting the word out about, look, this appears to be helping people. We need more research so it can help more people. You know, I hinted at your story, and I think I have the details right. Correct me where I have them wrong. But in your late teens, you faced devastating health issues, first severe osteoporosis, then ulcerative colitis.

And that even ended up with you, I believe, ending up in palliative care? Is that accurate? Yes, it was the John Radcliffe Hospital in the NHS when I was at Oxford. I spent some time in palliative care ward in ICU. And yeah, no, I was quite poorly off. I was a dangerously low weight. So malnourished that my heart rate was like dropping into the 20s, very weak. And I had, you know, over the course of a couple of years gone from being like, you know, a high-performing athlete and academician to being just completely broken. I mean, the psychological trauma of being like a social person who's breaking push-up records and running sub-three marathons to being like, I'm in a bed, 20-something-year-old guy, not dating, not engaging with my friends, can't even keep up with my studies, you know, wasting away physically, knowing that right now it takes me more energy to be. get up and go to the bathroom, then running a marathon used to take and not having an answer, like that's where I was. So when you talk about desperation and trying something, quote,

crazy, you have to understand, like, that is the mindset that people are in when they start experimenting with these things that society still stigmatizes. And I think when you start to appreciate that, you can understand the decisions some people make with respect to their health. Give our audience some context. What were the unique combination of circumstances that you, now looking back from everything that you know of being a researcher in the space, and your lived experience, what were the unique combination of circumstances that led to your health issues? And then how did you end up finding the carnivore diet and the ketogenic diet and how quickly did it take before you noticed a difference? So with respect to the osteoporosis, I'll get to that

first. I actually do have a very weird genetic mutation, a very, very rare one. And basically the way it probably manifested is when I got to marathon running. Generally, when you load bones mechanically, they should respond and get stronger, just like when you load a muscle. When you lift up heavy weights, your muscles should get stronger. But these programs are dependent on certain genes and certain genes getting activated. And I have a mutation in one gene pathway. LRP5 went signaling. So basically, when I started running more, my bones didn't get stronger or fast enough.

So they got weak really quickly. And that's how I developed osteoporosis. That sits improved. I just can't run anymore. But otherwise, I'm perfectly healthy there. no longer have osteoporosis. In thumb for a bowel disease, it's hard to say. I mean, I did eat a pretty standard westernized diet, quote, balanced diet.

I ate a lot of fruits and vegetables, but I did eat, you know, a fair amount of junk food as a kid too. Normal kid growing up in the 2000s. You can imagine what I ate. And also unique to me is I did get intravenous antibiotics very early on in life as a neonate. And we actually do know that can screw up your microbiome, basically. for life. So we know that early life antibiotics, you know, when you're a neonate, can increase inflammatory bowel disease risk, say, in your 20s by about 500 percent. So I did have that

insult behind me in addition to eating a pretty standardized Western diet and then developed ulcerative colitis at a pretty typical time, my early 20s for a young guy. So, you know, maybe I would have developed it anyway if I didn't get the IV antibiotics or even if I ate perfectly, I think that's unlikely. But those were the contribution to factors that led. to my health issues. Now, how I found a ketogenic diet was it just existed in the zeitgeist, and it was something that I didn't know much about, and I tried prior to having any true interest in education in it, I was just desperate.

I had tried everything else. I tried, you know, specific carbohydrate, low phob mat, you know, paleo, Mediterranean, pescatarian, vegan, vegetarian, whatever. And eventually I tried a ketogenic diet. And the results were that my inflammatory markers dropped to the lowest they'd been in a long, long time, into the normal range. I just started feeling much, much better. And then eventually, years later, when I got another colonoscopy, I was in biopsy-proofing remission. So, you know, everything went my way.

And with respect to carnivore, because my initial ketogenic diet did have more, it was kind of like more Mediterranean-esque spin, lots of like olive oil. you know, green vegetables, a salmon, et cetera. My interesting carnivore arose as, I mean, the carnivore diet movement just arose. I'm like, this is provocative and interesting. And I like curious, provocative, interesting things. So I started to delve into it and dabble with it myself and start to talk to people who had tried a carnivore diet. And I thought, you know, this is a remarkable frontier of a nutritional therapy that deserves further exploration. So to that extent, I've kind of become much to my.

in a way, dismay, like a bulldog of the carnivore diet. Like, I'm kind of like agnostic. I don't care. I'm not anti-intaturated fat. I don't really care. You know, I don't think oxalates are that big a deal or a lot of the things that people talk about in the carnivore diet community. But I do think the carnivore diet deserves more study and it's super poorly understood

and stigmatized. So you do see me standing up for it a lot of the time. Writing case reports on it, do myth doing myth-busting around it. Not because I think it's the one diet for everybody, but I think because it's just an underutilized and under-researched tool that could really help people. Sometimes I've seen that the criticism around the carnivore diet, when people pursue it for things like ulcerative colitis or autoimmune conditions, one phase of the criticism is, hey, why don't you just do some other more evidence population, public health-based study things

to improve that area that don't have as much downside? on things like your heart health or longevity. Now, we've already talked about the heart health piece of it, and that has many, many layers, and that was the first part of this podcast. The part that I want to understand to have you chime in on, the way I get it from listening to your story is I would say, hey, look, Nick went through a combination of things in his life,

but probably the antibiotics being a huge factor, that it's so permanently altered his microbiome that the idea of him eating, you know, some more fiber, which you've tried a lot of this stuff, the idea of putting in some probiotics, some more fiber, some fermented foods to fix it, and doing this general population level stuff that's there, the microbiome is so off and so sensitive that if he doesn't go to something that's a more seen as extreme, the level of flare-ups and the level of issues just prevents him from even living his normal life. So why even play in that category he has to try to do something else?

Is that an accurate way to think about it from my side? Accurate way to think about it in general, but not for me. So the fact of the matter is, like I said, I started a ketogenic diet that was very not carnivore. And it was sufficient to put me into remission. So the factor at play in me is probably has to do more with ketosis being protective. So I could eat, in theory, a plant-based low-carb diet and be an IBD remission. It doesn't mean my symptoms are perfect. So often people confuse inflammatory bowel disease with irritable bowel syndrome. Inflammatory bowel disease, either ulcer of clitis or Crohn's diseases,

like you look in the colon and there are histological signs. You have a disease pathology. We can see it. We can visibly see it if we look in your colon. Irritable bowel syndrome is a little bit more fluffy and symptomatic. It's like, you know, constipation, diarrhea, GI upset, real symptoms that people experience, but it's not exactly clear what's causing it. and you don't necessarily see signs on histology, say you look in the colon.

And so a lot of people have irritable bowel syndrome. And those symptoms matter too. People have bad constipation, diarrhea, bloating. Like, that's unpleasant. So for me, if I eat lower fiber and more animal base gearing towards more carnivore, my GI system is just happier. And my days are happier. I don't have to spend as much time in the bathroom in the morning.

It makes my life easier. And do I know for a fact that isn't affecting my long-term health negative? in some other ways. No, I don't. I absolutely don't. And I would say all things being equal, my personal opinion would be probably more diverse diet, you know, more fermented foods, more fiber, all things being equal, which is really important, you're probably hedging your bets on a healthier gut and healthier life overall. I don't know that for sure. There's actually literature suggesting maybe a carnivore diet and keto diet don't do things like decreased diversity or diversity isn't even that important. Actually, as a quick aside, there was just a paper that

was published on trying to restore the microbiome of people in industrialized society. I think with people in Canada, and they were using a non-industrialized diet designed from the diet of people in Papua New Guinea. And it was interesting. It's all the restore diets. People go into PubMed. I think it was a cell host in micro, but one of the cell journals. But what they found was that the diet improved, you know, cardio-metabolic risk factors.

It was a plant-based diet, plant-based restore diet that was not a diet. best realized, improved health. It was thought to, quote, improve the microbiome, but diversity actually went down, which is interesting because it kind of like cuts out a couple, let's say, like motifs, themes, common wisdoms. And one of them is that more microbiome diversity is better. I don't want to myth bust that right now. Like that is such a crude marker. Just having more diversity in your microbiome doesn't mean you have a healthier microbiome. All we really know about the microbiome of, you know, what is a healthy microbiome? It's a microbiome of healthy people. So it's really complicated to study. But that said, I would say on balance, if you can, eating more diverse

whole foods with different fiber types, including plant foods, fermented foods, I'm a big fan of fermented foods, in theory, at least, probably is good for your gut health. But again, it comes down to individual choice. So for that individual, if they're going to be happier and feel much better on a carnivore diet, for whatever reason, they're probably going to do that, even if it theoretically could affect their health of the long term. And then the question becomes, can you actually change your microbiome? Can you really adapt it? Like you said, I'm kind of behind the eight ball with these IV antibiotics that got us a neonate.

I would love a protocol. I truly would love a protocol where I'm like, I can make my microbiome super healthy and resilience to all sorts of, quote, stressors. Because quite honestly, roasted Brussels sprouts with like crumbled walmuts, maybe a little bit of cranberry on it. Sounds delicious. It sounds so good. I want to eat it.

It screws with me. Or like a cauliflower mash with a ton of ghee. Delicious. But I'd be tooting like a chimney. So I don't have it. It's not that I don't think they're not healthy. It's just that it doesn't suit me. And theoretically, people think, oh, you can shift a microbiome.

The protocols are not straightforward. It's things we need to design. I think maybe, like, you know, maybe a feature will have protocols for fecal matter transplants. That's super cool. But it's not as easy as you just take somebody else's poo and take a pill. Like, how do you process it? How do you prime your gut with antibiotics?

Because you kind of have to throw a grenade in there to wipe things out before you repugulate the microbiome. And then how often do you have to take, you know, the sample? Do you take it orally? Do you take it rectally? And how do you like keep the sample? It's actually kind of complicated when you get down to brass stacks. I've thought about it. I've thought it genuinely about having friends who I think of how healthy microbiome is

donate poop samples and trying to repopulate myself, but I just have not been able to come to to like, this is a protocol I feel comfortable with on executing. If your audience is a way of research that comes up anytime in the future or maybe even exists, I don't know about, and they have a protocol, like a genuine protocol for an FMT, they want me to test, I'll do it. I love the idea. It's just like a lot harder than you think. So for those people who are behind the eight ball with their gut health, like people do what they can. They just do. They do with can't to survive and feel good every day. And it's always how people are going to operate. I love it. So if you have a poop fecal transplant protocol, hit Nick up on X.

Oh, yeah, my next N equals one experiment. I don't know how my thumbnail is going to look on that one, but, well, like, N equals on experiments, it would be super interested, I think. You know, the thing I appreciate, I don't want to just dose myself with harsh antibiotics for no reason. The thing I appreciate you about you, Nick, is that you really dive into the nuance around a lot of these things. And I think that a lot of our audience members, even myself, included, and I've shared this in episodes that I've done with folks in the past on the topic of carnivore is that when you see some of the loudest voices in the space, it comes with such a level of demonization around certain topics that you have a hard time knowing what to take

seriously. Now, obviously, there's voices like yourself, Dave, other people that are out there, a lot of the metabolic mind folks, I've had some of them on my podcast, that can break things down and say, here's what we know, here's what we don't know, here's what people's experience is, here's where there's strong data, here's where there's weak data, here's where you have to make your own decision. But you know, you talked about a few of these areas that are the most controversial, that you have a little bit of a different take on. I just want to expand on those a little bit more, right? So you talked about vegetables and how the idea of if you could eat some Brussels sprouts, which I love Brussels sprouts and I do well with them, if you could

eat some Brussels sprouts that were roasted with a little olive oil, cranberries, maybe, you know, a side of avocado, some nuts on there. You would because it tastes great. And you generally think we have evolved. I've heard you talk about it in other podcasts. We've evolved as omnivores as human beings. We should have the ability to be able to eat a lot of things because that would adapt us to living into a lot of different climates

and being more resourceful as a species. Some individuals that are out there that are especially in the carnivore and keto side of things blanketly say that fiber overall is not just not recommended, but straight up a disservice to individuals because of lectins, oxalates, antinutrients, and other aspects that might be there. Can you extrapolate on your thoughts? I would say I'm going to paraphrase from a patient quote I heard recently, which was something to the effect of anywhere you go on the internet, you can find someone telling you that any food is bad for you. So I guess I should just not eat. Oh, but also fasting kills you

as well. But don't stress about it because that'll kill you as well. Like anywhere you go, you're going to have somebody saying something negative about some compound on the diet, be a 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, you know, 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, you know, inflammatory and bad for you. But the literature mostly shows that sesame and sesame products like the he and are anti-inflammatory. And so you think, oh, like, 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 the linoleic 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's 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 fearmonger 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 okay to be aware of that, but taken with a grain of salt.

On balance, my opinion is not that fiber oxalase, leptins, plant, antinutrients 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 think the time to separate 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 future, but no, I don't hold those perspectives, which some people in the carnivore community might hold, and that's fine. I think it's ridiculous. actually, I was criticized recently by somebody on Instagram who said they were upset that I was affiliating with people in the carnivore community. They said something to the effect of, why would you affiliate with these people who you don't share this perspective with? And I was so taken aback. I was like, really? Your expectations that I'd only collaborate and communicate with people who have a carbon copy of my perspective of the nutrition world? Isn't that a little

is functional? So we can differ on these things. I'm sharing my opinions. You know, they're evidence-based insofar as I'm reading the literature. But interpreting science is subjective. These are my two cents. You're free to hear other people's two cents and come to your own conclusion. Let's talk about one that is a hot topic right now. And this goes beyond just the carnivore community. And it's the idea of diet Coke and some of the ingredients in it. And you recently made a video on this topic, and that led to a lot of debate, chatter, maybe some criticism that are there. So for followers that are listening of my podcast that have no idea what we're talking about, set the stage, and then let's talk about it.

So there was a study that just came out in cell metabolism on how the sweetener aspirin can cause heart disease. I did use the word cause very intentionally. And that's because this was a mechanistic study. It was looking at how aspiratame can promote heart disease progression. It was done in mice and monkeys, which, you know, comes with the caveats of animal studies. But bear in mind, like, you can't do this study in humans. You can't do a randomized control trial where you say, here, you people, you're going to randomize you to a three-di-coup-per-day protocol for 30 years and then check back in.

Like, you feasibly can't do this study. So you do need to turn to animal models to, you know, delve into mechanism and see how that lines with the human population data. And human population data do suggest that artificial sweeteners associate with. with cardiovascular disease. So this gives mechanistic insight. Now, what they did in this study is use different doses of aspartame, starting in mice, who were vulnerable to cardiac disease, and showed that even at low doses, equivalent of about three diacokes per day, we'll get back into that in a minute because it's been

controversy over the dosing, but I'm going to say three diacokes per day, cause plaque progression. And what they found was that it contributed to insulin resistance, increased insulin levels and what that led to was an increase in an adhesion molecule, CX3, CL1, the name's not really important, but basically a molecular baseball glove for circulating immune cells, which then grabs the immune cells, brings them in to the artery wall, and that promotes plaque progression. So they showed this happen in mice, and then monkeys had a similar response, at least with respect to the insulin response to aspartame, and it starts to build a case for, yeah, well, if we have an association between artificial sweetener intake, including aspartame and

cardiovascular disease, and we have this mechanism which generalizes to primates, at least in some case, then what does this mean for cardiovascular health and humans? The data have their limitations. All studies do. You will never have the RCT that some people are asking for. It's implausible. I present these data as food for thought so people can decide whether or not they want to have a Diet Coke. And, you know, Diet Coke contained it being a common aspirational. containing food. And one thing I'll say is like, you know, my perspective is that the risk of eliminating a Diet Coke is negligible. Zero with respect to metabolic health. Like, if you don't have Diet Coke, nothing negative happens metabolically. It is totally a leisure item. And I also don't like

the binary of people like, but is it worse than a Coke? I'm like, probably not. But why set up that binary? People don't have a choice between just Coke and Diet Coke. You can have a war. You can have a sparkling water. You can have a stevia sweetened beverage. So I'm not a fan of that binary. These are what the data said. And yes, people got very up in arms, very defensive. I mean, it's not really surprising.

One guy did a hit piece on it that was kind of misleading, but he was being paid by the American Beverage Association. So that's not really surprising. They definitely have their tentacles everywhere. At the end of the day, people make their own decisions, but those are what the data say. But I think it's socially fascinating. to see how people tried to slice and undermine it.

So going back to that three Diet Coke's per day thing, they don't say exactly how much fluid the mice consumed per day, but it was 0.15% aspartame. So there's different ways you can do the calculation. In medical news today, the New York Post, were both reporting three Diet Coke per day based on their calculations, but they didn't show their math. So I showed my math, how do I got to that number,

and came to a three Diet Coke's per day, dose. Now, ironically, I actually made two math errors, but they balanced each other so that I redid the math. It comes out to about three diacogues per day. Or, I mean, there's many different ways to do the math. One person was saying, oh, but you should do it based on body surface area, not adjustment for weight, because you want to adjust the mouse weight to the human weight, and they came to 11 diacogues per day. I'm like, okay, fine. Three, 11. It's besides the point. And in fact, even at the lower dose of 0.5%, which would chop that 11 to a 3.66% dose, a 3.66 diacotose, there was still a biological effect. So the point here is, if you do try to dose adjust,

there may be a physiologic response in humans. It's complicated by the fact that the human literature isn't really clear. Acute feeding studies in humans of Asperdame don't necessarily show insulin spikes, but the literature's a little bit murky. Chronic feeding with artificial sweeteners does show an insulin resistance response in some people and not in others. So yeah, the human data is murky. I'm not saying this is a closed and shut deal. But the new interesting mechanistic data, I think, and people can watch my video and see if it's reasonable, should make people think twice about having a Diet Coke. And at the end of the day, if they say, I really love Diet Coke and a possible health, negative consequence, risk is worth it to me, then have a Diet Coke. You made an

informed decision. Congratulations, you're an adult. That's where I stand. I'm not saying the data are conclusive, be all, end all. I'm just saying. these are cool data. Think about them. I think they're compelling. I don't know if you read the paper, but what you thought, but that's where my stance is. I didn't read the paper, not even that I have the background or knowledge to be able to dissect it. That's where I'm using Chad GPT deep research these days to at least find some, you know, human level speak because I have no training in that area. Part of there seems to be a diet coat tribe separation in the health space. And this is just what I've seen in the outside is that I have many friends that are largely individuals that would

agree that like, hey, we want even practitioners, medical doctors, naturopathic doctors, DOs, who are like, look, I want me and all my patients to be metabolically healthy. And as the evidence-based landscape of what works and doesn't work is out there, I think that they see it a lot of people were fearmongering about the impact around Diet Coke and Aspartame on gut bacteria and how we didn't really know really a lot of what, as you've shared before, what does good gut bacteria look like across the board? And is it relevant for other people? Comparatively to the studies that are out there for individuals who, let's say, rely on Diet Coke as a way to get off of sugar and reduce their overall caloric load, which could be helping.

So I've seen this uptick in people sort of proudly signaling that they are healthy individuals that might even be eating all their meat from grass fed and other things, but they're still a champion of Diet Coke. And that's besides the fact that they probably like Diet Coke and it's one of their sources of caffeine, it's also what I see as like a public signal of like, hey, listen, I just want you to know what sort of where I stand in the landscape of things. So that's just something that I've noticed from the outside. So what I'm hearing from you is like, look, this study is something worth paying attention

to. It's not by all means a conclusive study on all aspects related to human beings. If you like Diet Coke, continue to have Diet Coke. If you're somebody who's largely is healthy and you're having a few Diet Coke's a day and that's your risk assessment, great, continue to do it. And if you're somebody who's unhealthy, who's using Diet Coke to get off regular Coke, great. It doesn't have to be a binary thing. You could have water.

You could have other stuff that are out there. Basically, I'm hearing you say, if it works for you, keep doing it. I'm just talking about what I found interesting in this study. 100%. I stand by that as like a general rule of thumb. I don't care if people like have, you know, ice cream and grilled cheese for every meal and they're happy and healthy. Like, at the end of the day, you do you. And I will not judge you.

I'm genuinely not like a judgmental person. You just have to make your own decision, but you should make your own informed decision. And also acknowledge there's no such thing as perfection. So, for example, you were talking earlier about microplastics in red meat, like in ground beef. Does that mean I'm not going to eat red meat? No. Like, I'll have the ground beef. Maybe there's some microplastics in it.

Boo-hoo. It sucks. It's not ideal. But, you know, I'd rather have that than go, you know, let's, you know, create the binary and say, go get like a pizza at dominoes. So know where Diet Coke fits in as a tool or maybe the lesser of two evils in your own life. If the truthful decision for you is really between a Coke and a Diet Coke, and that's how you see things, and you have the Diet Coke, and you feel better than great, fine.

I think it's a little bit of a weird binary, but fine. When I get criticism is about, quote, fear-mongering, covering this study, basically. If you watch the full content, you can see it's not very detrimental. But, yeah, it has a hooky thumb. That's what YouTube is about. You get some engagement bait. But I think they're kind of alluding to the fact that I could be doing harm by dissuading people from having Diet Coke and then they're going to go have a Coke?

It only seems like the implication. And I'm like, I've never met someone once who are like, oh, ex person on YouTube said Diet Coke is bad. I guess I'll just have regular soda. I have gotten comments by people like, wow, this is the motivation I needed to just kick the diet soda pattern and just have water. And I'm also at people say,

this was the motivation I needed to kick diet soda, come back and then say, oh, wow, my migraines went away. So the cost of a limiting diet soda, even as an experiment, is negligible to benefits. So I don't think it's a problem to be talking about these data, even in a sensational manner. And you can place the caveat at the end. Some people have problems with that. But I think, like, to see, wow, this is exciting. This is really interesting.

Let's talk about the data. Get people's emotions provoked and then just talk about the data and let people make decisions. I think it's totally fine. In the universe of, let's call it, health sensationalism, I don't think spreading the message that, Hey, diet soda might not be that good for you. Is that dangerous? I actually think it's probably in a hedge courts more beneficial. But again, at the end of the day, you do you.

And if a Diet Coke works for you and you want to flex that you have Diet Coke and you're super healthy and happy, guess what? I'm going to give you two thumbs up and say, I'm happy for you, sincerely. Yeah. Well, what I love that we have the ability to do in this day and age is we can have a discussion on a podcast. I think one of your thoughts, I think it was a tweet or maybe a post, you wrote that, felt that some people were taking you out of context in terms of your whole message around the topic and your video and what you were saying and what you weren't saying. And that's the nature of the internet. People do that all the time. I've probably taking people out of context on stuff that

we've covered over here. And we can at least have these follow-up discussions on Twitter, on X, on Instagram, on long-format podcast. And I appreciate that side. But I, you know, to steal man the other side, I do think that there's a group of people that are out there who are, maybe less pro. I'm in the camp of like, let's hear all the conversations that are there and let's have people talk about any kind of topics that they want to talk about. People have such a hard time already, especially when it comes in the category of dropping weight and liquid calorie seems to be a big part of that.

And if we dissuade this individual who tends to be the person who's not going to be listening to these longer format podcast or going into the nuances along with you on your journey, that actually one snippet or one person's amplification could be enough to dissuade them from choosing Diet Coke and now people go towards unhealthy options. I do think that that's what the other side, not to make it about sides, I think that's what the other side believes.

Now, I don't believe that personally, but I do think that that's what the other side believes. And again, everybody can have their own beliefs about stuff. It's possible. And I guess all I'd say to that is I agree with you. I don't believe that. actually happens, not at least at any scale. I've never heard of someone like being like, I saw a single Instagram flip that said Diet Coke is bad, and now I'm drinking regular Coke.

I just, it seems so hyperbolic and implausible to me that I don't think it happens. To the same extent, like when I do Oreo versus Staten, I was pretty sure that no adult human being will be like, oh good, Oreas are a health food. Let me get off my Staten and just start binge eating Oreo cookies and nutterbutters. I just don't think people give the general public enough credit for common sense. I think people want, with their engagement, nuance and depth and are willing to chase the rabbit hole a little bit before making health decisions. That's my perspective. Broadly, I think people are frustrated because the self-proclaimed intellectuals and gatekeepers of health information tend to patronize and be like, this is what you should do and here's the simplistic

way to think about it and here are the rules and guidelines without delving into the nuances. I don't think that's very compelling, nor do I think it's productive towards building trust. So I think it is okay to be like a little bit fun, engaging, provided you draw people in to then have the nuanced discussion and say, well, here the data. I'm going to show you the graphs from the paper. I'm going to link you to other resources where you can have a set of links to the human randomized control trials and meta-analyses and other studies and playlists where I delfts I delve into this topic. Go as deep as you want. Hear the data. Here's what I think about them. At the end of the day, you make your own decision. I think that's a much more productive approach than just saying,

we don't know that Diet Coke is bad, therefore you should have it, because we haven't conclusively proven in the 30-year human randomized control trial that aspirin doesn't have a negative effect in the human heart. It's ridiculous. And I said this in a recent clip, the one I was responding to somebody, they did take me out of context. They tried to make it seem like I was making a point that I wasn't. based on what are pretty weak data. And weak data are fine, provided you're drawing the appropriate conclusion based on the data, the claim needs to be commensurate with the data supporting it. So if data are early and you say, this is really interesting, and this shows X, Y, and Z, and then caveat and this is what it doesn't show, that's fine.

The precision of the words really matters. For me to say, Asprete may cause heart disease and use the word cause, is dead accurate. the animal model show it may cause heart disease. Here is the mechanism. And then I couch it in the human data saying, here's what we know about in some response with respect to aspirin and humans. Here's where we are now.

If you look at the full context, the story is told. And my perspective, be it right or wrong, is that people deserve the benefit of the doubt that you can serve them that nuance. Well, on the topic of nuance, Nick, I just have a couple more categories here that I want to touch on as we wind down today's interview. And one, you've already touched on.

it a little bit and it's the topic of seed oils that you have such a nuanced take on we've had people on this podcast that have written entire books about seed oils and will tell you that they're more dangerous than smoking we've had people that have come on this podcast that have talked about how the data largely shows that individuals that have seed oils in their diet and that remove saturated fat have a lower risk of heart disease that's there You start off the topic by first helping people understand that the topic of seed oils, before we can have any discussion around it, is first about what are we actually talking about? There's a huge difference between McDonald's friar oil that's out there and having some seed oil that might be from canola oil that's cold pressed. So let's talk about that.

I think, you know, first and foremost is, yeah, seed oil is refer to a lot of different things. It can refer to highly oxidized, industrialized, processed oils that are pre-oxidized, so really damaged fats that can be inflammatory. Okay, don't drink the fire oil at McDonald's. They can probably agree that's not a good idea. But there's kind of a logic creep because then people go to, oh, well, what's the harmful component? It's high levels of omega-6 fats.

One primary omega-6 is a little like acid. And then there ends up with this, I'd say, fearmongering about omega-6 fat-rich foods as a category. So then you end up lumping in things like raw nuts, walnuts, or sesame thing I brought up before, in that same category as like friar oil McDonald's and all the industrialized processed oils I could put into our junk food. And I don't think that's appropriate because literature does not show that it is necessarily harmful. It does become a nuanced and curious area when we entertain the fact that, yeah, like if you look at, say, the omega-6 to omega-3 balance in the body, it does matter. So, you know, having a higher omega-6 and lower omega-3 can lead to a pro-inflammatory state. Again, and this is where I might lose some people, but I think it's an important point to note what we can actually study in humans, because the fact of the matter is you can't shift omega-6-3 ratio in humans without shifting other components to the diet because they're essential fatty acids.

So, again, you need to turn to like animal models, and you can show by actually genetically manipulating them that, yeah, higher omega-6-to-3 ratio can be more pro-inflammatory. So it could lead one to speculate that in theory, you could get like an omega-6-3 imbalance by just like over-consuming omega-6 fat in theory. I just think it probably hard to do in practice. Like, I think it would be hard to be like, I'm going to binge eat raw walmuts and it'll lead to negative health effects. And we don't have data to say that. Whereas I don't see a negative effect of saying, you know, aspirin may cause problems. Because if you kick that I cope, what you do. I do see a negative potential effect of saying, like, you need to get rid of all omega-6.

in the diet because then people are cutting out whole foods that could be healthy, like walnuts, tahini, or even in some cases, this is going to sound crazy, but I hear it, fatty fish, because fatty fish is high in polyunsaturated fats, which are fragile. So you can get a creep there. I had one person telling me that sardines were unhealthy because they're high in polyunsaturated fat, because they're high in omega-3. And they were truly convinced that a quest bar was healthier and got very upset when I told them, no, I disagree with you. That aside, you can see where the logic creek goes. So at a very high level, because I realize we don't have two hours to into just one topic, I'd say define what you're talking about when you say seed oils.

If we're talking about industrialized processed oils, that's a different thing than saying anything rich in omega-6. And what I'd say is in theory, having a very high omega-6 diet can be bad for you, but I would not actually say one should avoid whole omega-6 food, the whole omega-6 rich foods, like walnuts, various nuts, cold-press canola oil, olive oil is like 14% or something, omega-6. because these foods are generally, I'd say on the whole, pretty healthy. And it's not a linear relationship. It's not like if you eat 10 grams of omega-6 and 1-grain of omega-3, the ratio in your body is 10 to 1.

It does not work like that. The processing is a lot more complicated. So I eat a decent amount of omega-6, far far more than omega-3, and I eat a lot of omega-3 too, but it's just way easier to get bulk load omega-6. And my ratio in my cells, if I measure it, a perfect one-to-one. And I do not avoid things like walnuts or sesame. I eat them to my heart's content, fiber permitting, and my blood ratios of mega-6-3 are actually perfect. One-to-one ratio

in mega-6-3 and a 17.2% EPA to DHA ratio, which, by the way, is way better than Brian Johnson. He has a table on all his biomarkers that it's like, I'm in the top echelon at 9.98% and I'm reading that. I'm like, well, I'm a 17.2. You know, I've had Brian Johnson on the podcast, and I want to just say from afar. I really love the experimentation that he's doing and putting all his labs out there. And I'm not saying you don't. I think you probably feel largely that you love the experimentation that's there. The point that I was going to make is actually going back to the beginning of this podcast where we're talking about getting functional test and especially these CCTVAs. My suspicion is somebody who grew up vegetarian has looked at a lot of, been very convinced by

my cardiologist about the multitude of factors. that play a role in plaque buildup. We talked about things like microplastics, but we didn't really dive deep into it, but I've done episodes on it, endothelial function, nitric oxide, the level of alcohol intake somebody might have stress factors that are there as well to,

in addition to potentially the role that certain oxidized fats and things might have in a diet if somebody's having a lot of those that are there, I think that if a lot of the individuals that are the most vocal voices on this, their approach to lowering people's risk of cardiovascular disease, if they actually got a clearly test done or a CCTV and published their results, I think a lot of them would be shocked to see that their level of plaque is not where they expected it to be. And I'm in particular,

I'm thinking about a lot of the vocal voices in the vegan, vegetarian, plant-based community. Well, Brian hasn't, and speaking of Brian, he hasn't gotten. a CCTA? To my knowledge. Yeah, I think I think Joel Khan, who was a cardiologist, who's a vegan cardiologist, who actually has a very clean, clearly, CCTA scan, we talked about his on my podcast. I think he said he's an advisor to Brian, but he just didn't want to risk the radiation that would come with it.

So, you know, again, that's up to Brian, but I'm not so worried about Brian. I feel like he's got everything sort of doubted in his sort of world that he's doing. but, you know, there's other voices that are out there, not to name any names. I think they'd be very shocked to see that their heart is maybe not as healthy as they thought it would be. Yeah. No, I mean, on Brian, I'm right now, honestly, I'm interested to see what, I don't know if you know what I've learned, Joseph Everett.

I don't. No. He's a big YouTube channel, but he's had like a little bit of a spicy confrontation with Brian. He asked me to be interviewed on his channel, so he's going to be dropping a criticism video, which I was interviewed for. I a high level Brian is one of my favorite characters in the longevity space like truly we definitely don't eat the same but I think he he has a very on the whole open uh you know authentic via humorous persona and I think he is pretty transparent about his methodology and doesn't mind making a little bit of a joke of himself I actually I think it's very endearing I do have if if you you know, if I were to, this is my kind of core criticism, to render it Brian.

I haven't found, I don't know how you feel, but I haven't found his optics around the scientific rigor have been very solid. Sometimes he gets on podcasts. And like, he is so thoughtful in long form. Some of my favorite podcasts were having with Trevor Noah and there was Diary of a CEO and I heard him on Derek on more plates more dates. Like all three, he was so well spoken about the philosophy of Do Not Die. But then my personal feeling was when it came to the, the logic behind the protocols, it was kind of opaque. And either he misspoke on some studies, which he admitted he did.

Like there was this olive oil study he misspoke on. Or he deferred to his team who were also pretty opaque. And I feel like the rationale behind their protocols is also opaque. So there are things that I've seen here and there that kind of like get me to draw a little bit of a question. So as much as I like Brian as a personality and I think he's thoughtful about his approach, what I would like to see more from him. Now I'm just taking my two cents in case he ends up listening to this or you poke him about it is I would like to see more rigorous science projected from him and or his team about the rationale behind the protocols. As far as they're allowed to do, you know, I know that a lot of their, you know, information is proprietary.

But in the interest of open science, I'd like to see more. And quite honestly, I see opportunities. not saying this is just to be a troll, but I see constructive opportunities. Like, I read literature on things related to olive oil that are like groundbreaking. And I'm like, why haven't you covered this literature? You're selling olive oil. Like you could do an enrichmental larapine. And like there's a new study showing that in aging, calcium import into mitochondria goes down. And this affects muscle metabolism negatively. And actually in animal models, if we supplement back this compound found in olive leaves, it increases endurance and even increases muscle mass in

aged mice. And you could tell a story around that that is so compelling with the relationship to like your olive oil. I mean, he's already doing marketing around olive oil. It's just very superficial stuff. And so in reading the physiology and literature myself, there's no expert in one particular area, but a broad interest, I actually, I'm bringing this up because I see an opportunity for Brian to expand his impact by, I think you could get more rigorous with the physiology. And quite honestly, I'd be happy to help. Pro bono. I'm not asking for anything in return. I just think what he's doing is interesting.

And we're all looking to grow and communicate as communicators in this space. I by no means think I am perfect at it. I think we're all growing and developing. And I just see this chink in his approach that I would just love the opportunity to finagle and fine tune because I think it could be scaled up. And I do love what he's doing, particularly around. And this is where I think we have a great unity of mind. challenging norms saying just because this is the way people understand it today, screw that. Like, how are people going to think about it in the future?

Like, we should evaluate the data, ask provocative questions, and push the boundaries of not only human knowledge, but human societal norms. And I do think he does that really well. So overall, I give him big props. I just, he's an interesting character. And he's an interesting person from a social perspective to kind of try to decode and analyze. Well, I think you said it well. You know, you said you appreciate him as somebody who push the bounds and questions the status quo.

And that's how I see him, but that's also how I see you and the work that you guys are doing in this space. And I think that that's important. You know, we have a society that is largely unhealthy and there is a movement that's been happening and it's going to continue to happen where people are sicker than ever. And it's created this perfect storm where people are actually. asking, what do we have to do to get myself healthy and what do we have to do to get other people healthy? And I appreciate that you are a key player in that space, first with your own journey and then also the studies that you guys are publishing, which we talked about in the beginning. So, Nick, I just want to say that this has been a fantastic conversation. I've been a big fan of yours.

I actually mentioned to you in the beginning, but I tried to interview you last year. You were too busy at the time with stuff that you had on your plate, legitimate stuff. And I want to give a shout out to a mutual friend of ours that actually, you know, suggested to have you back on or an acquaintance. I don't know if you guys are friends or acquaintances. But Dr. Joe Zendell was the one who said, hey, listen, if you haven't had Nick on, I really appreciate the way that he communicates. And I think you'd have a great conversation. I was like, this is the perfect reminder to reach back out to Nick because I'd love to have him on the podcast. Thank you so much.

I apologize. I'm at that stage where it's like you're, I mean, I'm sure you. you can, this resonates with you, but you're kind of like a one-man team and you don't have much support. Like I have one editor, but you're also like balancing everything else in life because it's not a full-time thing. So like, I'm doing research, medical student, and then I'm like trying to dabble with socials at the same time.

And with all the DM streams, I just get like, some things just get missed. But I'm so happy we circle back to have this conversation. And I look forward to hopefully future conversations because I think we both plan if a heart attack doesn't get us first to be in this space for the decades to come. Absolutely. Nick, we'll link to all your socials in the show notes below. Anything you want to plug while our audience is still listening? Just, yeah, if you want to, I mean, YouTube is where I'm most active.

I have a lot of fun breaking down the science there. And also my newsletter, Stay Curious Metabolism is where I kind of do my first digest. So often, like, paper comes out at like 4 a.m. and sell. And I'm up because I can't sleep. You could have like, you know, I digest the paper by like 7 a.m. Because I just like, that's how I operate. I'm like, this is exciting right now. I need to cover it.

And so, you know, I engage with me on whatever your preferred platform is and provided your input in comments are sincere and thoughtful, I really do appreciate constructive criticisms. I'm kind of, you know, I'm finishing my rookie year in this, so to speak. And I look forward to growing with everybody. So their feedback is my data. And thanks for having me. Thank you again.