WHOOP Podcast - What You’re Getting Wrong About Metabolism (And How to Fix It) with Dr. Nick Norwitz

Episode Date: August 19, 2026

Metabolic health is far more nuanced than conventional nutrition advice suggests. On this week’s episode of the WHOOP Podcast, WHOOP Global Head of Human Performance and Principal Scientist Dr. Kristen Holmes sits down with Metabolic Health Expert Dr. Nick Norwitz MD PhD to discuss why curiosity is one of the most powerful tools for improving long-term health. Dr. Nick Norwitz shares how a ketogenic diet unexpectedly put his inflammatory bowel disease into remission after numerous conventional treatments had failed. This experimentation sparked a career dedicated to challenging assumptions with rigorous science and thoughtful self-experimentation. Together, Dr. Nick Norwitz and Dr. Kristen Holmes unpack the difference between "evidence-based" and truly individualized care. This episode continues to explore why muscle, sleep, and visceral fat play central roles in brain, heart, and metabolic health. From discussions on protein, the microbiome, and emerging therapies to Nick's famous Oreo-versus-statin experiment, the conversation encourages listeners to move beyond one-size-fits-all health advice, and partner with their healthcare providers to embrace safe, data-informed experimentation for a better understanding of their biology. Shownotes:(00:00) Trailer Intro(00:43) Who Is Dr. Nick Norwitz?(03:07) Nick’s Personal Health Journey(08:29) Nutrition as a Medical Intervention(12:41) What Does “Evidence-Based” Care Really Mean?(16:42) The Key to Optimizing Your Health(19:17) Debunking Metabolic Health Myths(20:46) The Benefits of Training and Exercise(26:29) How Metabolism Affects Strength, Cardio, and Brain Health(30:03) How Does Sleep Impact Inflammation?(32:35) GLP-1s and Your Metabolism: What’s Really Happening?(34:47) Nick’s Take on Self-Experimentation(35:43) The Oreo vs. Statin Study(45:19) How to Burn Fat(49:43) Do We Really Need to Focus on Protein?(51:25) What Is Visceral Fat—and How Do You Lose It?(56:08) Why You Should Stay Curious About Your HealthResources:Fitness and aging (Nature Aging 2026); https://www.nature.com/articles/s43587-026-01150-x  Visceral fat and resistant starch: (Nature Metabolism 2024): https://www.nature.com/articles/s42255-024-00988-y Visceral fat and resistant starch, **YouTube Breakdown: https://youtu.be/wnEApLnKDRI   Visceral fat and brain volume: (Nature Comm 2026): https://www.nature.com/articles/s41467-026-71141-4 Leg power and longevity (twin study): https://pubmed.ncbi.nlm.nih.gov/26551663/ 600-calorie exercise burn study (Nature Metabolism 2025): https://www.nature.com/articles/s42255-025-01236-7 Microbiome and beige fat study (Nature 2026): https://www.nature.com/articles/s41586-026-10205-3 Oreo versus statin study: https://pubmed.ncbi.nlm.nih.gov/38276308/Follow Nick Norwitz:WebsiteYouTubeInstagramXLinkedInSubstackSupport the showFollow WHOOP:Sign up for WHOOP Advanced LabsTrial WHOOP for Freewww.whoop.comInstagramTikTokYouTubeXFacebookLinkedInFollow Will Ahmed:InstagramXLinkedInFollow Kristen Holmes:InstagramLinkedInFollow Emily Capodilupo:LinkedIn 

The term nutrition carries a lot of baggage. If you were to ask me 10 years ago what I thought about quote unquote nutrition science, I would have thought, oh, we haven't figured out as life would have it. My own medical journey kind of humbled me to that respect. And I was forced to really look in to how much potential there is to truly heal the body. I was in a very desperate place. I tried all the standard diets I tell you for gut issues. The most remarkable thing about my story was that it is not at all unique.

that there's this motif of people struggling with conventional approaches, getting desperate, bordering on hopelessness, trying things because they have nothing to lose, and then something works. And you're caught in a little bit of a catch of a 22, like, why was I never told about that? And answering that question has become a little bit of a passion of mine. Dr. Nick Norwitz, welcome. Thank you for having me. I am so pumped. We were talking offline about your academic pedigree, and I was kind of joking around, but the list is long. I mean, you're a valedictorian at Dartmouth for your undergrad, which is pretty impressive.

PhD from Oxford in metabolism and nutrition, I believe. Brain metabolism. Brain metabolism and nutrition. And MD from Harvard University. I think what's so cool, Nick, is just how you have emerged as quite the voice of reason as it relates to translating nutrition. And I hope I can use the word nutrition. Metabolic science. Or, yeah, I mean, I just think, I feel like nutrition, just the word kind of comes with a lot of baggage.

And, yeah, metabolic science might be. a better way to describe the work that you do. But I think you're providing, I think, a very interesting discourse among academia that is super helpful. And maybe if we can kind of start there, why have you felt the need to create this kind of public persona? Yeah. There's a lot of places to start answering that question.

But I actually want to unpack something that you just nailed, which is the term nutrition carries a lot of baggage. And if you were to ask me 10 years ago what I thought about quote unquote nutrition science, I would have thought, oh, we have figured out, you know, eat your five a day, my plate, balanced diet, and there's a lot of platitudes. So if you were to ask me if this was something, this world, be it you call it nutrition or metabolic health sciences that I would have gotten into, I would have said, heck no. That wasn't really of interest to me. As life would have it, my own medical journey kind of humbled me to that respect. And I was forced to really look in to the depths of what.

what I would call, I guess, metabolic health science, use another term, realizing how much potential there is to truly heal the body. And I say that without hyperbole. That then framed how I finished my PhD and then how I looked at medicine and healthcare as I was going through medical school, because I was kind of beset with this uncomfortable tension, which was, you know, you mentioned my academic pedicry. I also had. I came from a family of MD PhDs. So my mom and dad are both MD PhDs. The idea of going into medicine was like the default path. I like science. I don't want to help people.

Of course I'm going to go into medicine. And I hold in highest esteem, like physicians who commit their lives to helping people. So I had this very glorified ideal of what medicine was. And then when I got really sick myself, a few things happened to me, but the worst of it was inflammatory bowel disease when I was finishing up college and then starting grad school. Finishing up college. Yeah, actually. we can get into my back story a little bit. I don't want to go too down that rabbit hole,

but you mentioned I was valedictorian. One of the worst days of my life was commencement. I was giving the valedictory address, and I had just gotten diagnosed, but people didn't know how bad it was. So I was like most days having pretty bad bloody diarrhea 12 times a day. Oh my God.

It was horrible. And the worst part about that, it's not the pain, it's not like the uncontrollable blood diarrhea. it's like the confusion and the shame and they're not knowing how to handle it. It's like the psychological torture of like, well, of course I'm not going to date anybody because imagine having that person over and being like, excuse me, I'm going to go violently pooped blood for a minute. Oh my gosh.

So then imagine I don't know how to control this. I've recently been diagnosed and I'm given the opportunity to give my commencement address. Like, what do you do in that situation? Because I'm like, I don't want this illness to take that opportunity away from me. However, there's a legitimate chance. I walk up on stage and shit blood. And so I have watched that video back. You can actually see in the video if you look,

my face is almost a little cushingoid because I was on steroids, which kind of makes your face bloat. So, well, my body was kind of lead. I had this bloaty face. And the interesting thing about that is you can't tell I'm like dying with anxiety. And the day ended up going fine.

But the reason I raised that, and I guess answer your question, with that tangent is that was the framework of my life for several years while I was going through conventional care, and it continued to fail me, and it continued to fail me. And ultimately, something worked that I would call fringe. We can talk about what that is later. I'll guess, spoiler, it was a ketogenic diet. And when that worked so potently for me, I was caught in this tension, which is I hold, quote-unquote, evidence-based medicine in the highest esteem, but it didn't help me. So then I got desperate and had to try something that wasn't quote-unquote evidence-based.

Right. And it worked. So that is not a traditional therapeutic intervention for IBD? Traditionally, no, there are some exceptions like fiber-free diets and pediatric resistance Crohn's disease, which they don't really teach you in med school, but there are reasons to believe it would work. Your doctor wasn't prescribing a ketogenic diet is what you're saying. No, and you can't hold that against them because it's never been proven, quote-unquote, evidence-based. But the point I'm getting to, and what I really struggled with going into med school, is this distinction between what is evidence-based and what is actually effective. Because evidence-based sounds nice, right?

It does, yeah. It sounds good. But you need to understand it in the context of the business models and the incentive structures we've built around medicine. Evidence-based really just means what have we asked and where have we checked the boxes. And so if there's something that is incredibly effective, let's say for the sake of, you know, argument, it helps 100% of people and it cures them 100%, biologically speaking. If nobody's invested the money to do the $10 million defendant of trial, it's not standard of care. So it's not evidence-based.

So there's this discrepancy between what is evidence-based and what can truly help people. And you kind of have to grapple with that uncomfortable tension, especially now when we're living in an age with so much metabolic disease that the conventional system hasn't properly addressed. Right. And so I think the way to thread that needle, and this is what we'll talk about, is exploring health and metabolic health through your own and equals one personal journey, given the tools that are available, even if Western medicine hasn't sanctioned them yet. We've already said metabolic health, I don't even know, a dozen times. How do you define that? That's a good question.

I feel like it's one of those things like ultra-processed food. You know it when you see it, but it doesn't have a fantastic operationalized definition. The simplest way to look at it is, and this is going to be like a definition by contradiction, is the absence of any signs of metabolic dysfunctional metabolic syndrome. So things like high blood sugar, high waist recarference, so excess visceral fat, high triglycerides, low HDL. They kind of make a metabolic fingerprint collectively in terms of how well your body's hormonal and energy-generating pathways are operating, is how I would define it. So if those markers are all aligned, it kind of gives you a good signature that the fundamental things, like your body's mitochondria, hormones, circadian rhythm are probably operating better.

You mentioned that you explored, I guess, the keto diet and that really worked as a therapy could end up intervention. I guess how did that even come into your mind as something to try? And what was the progression? How did it impact the disease progression, I suppose? Yeah. before I answer that question, I just want a caveat. Anytime certain buzz terms come up, like keto, I think there's a tendency to think that one is beset in the way that that is the way.

And I will tell you, when I tried keto, I was incredibly skeptical. And the impact it had on how I thought about nutrition might not be what people think. So we'll get to that in a minute. But I was in a very desperate place. So having tried a lot of different conventional medications that weren't working, I just started throwing spaghetti at the wall out of desperation. No expectation. So I tried all the standard diets I tell you for gut issues like low fob maps, specific carbohydrate diet,

and then things like vegetarian, vegan, paleo, Mediterranean, and kind of at the bottom of my list, I'm like, all right, I heard about this keto thing. Right. Somebody said it's going to be anti-inflammatory. I have nothing to lose. So high fat. High fat, very low carbohydrates. It's about 80% of my calories were coming from fat, about 15% from protein, and then the residual from carbs.

It really had a dramatic impact. as in my symptoms went away within days. Bloody diarrhea stopped. My inflammation markers dropped. And then eventually I had another biopsy. So they do a colonoscopy. They take tissue from your colon to see, is there inflamed disease activity? There was nothing.

So the disease went into full biopsy proven remission. I'm now not on any medications and I've been kind of healthy for, I guess it was June 1st, 2019 when I started. So it's been over seven years. That's incredible. So you have been on. the keto diet for... Yeah. With only a couple exceptions where I try to reintroduce carbs

and every time I've gotten flares, but not every time. Every time it's been longer than a two-week stint, I should say. It's been a flare. So there's something going on in me. And we could delve into why this work mechanistically. So, for example, ketones, they don't just fuel your brain. They fuel the regeneration of stem cells in the gut.

They're anti-inflammatory in the gut. It can change the microbiome in ways that could be protective in inflammatory bowel disease. And again, one of those situations where post hoc, after the fact, I can rationalize why this works and why this makes sense biologically, but at the same time, I cannot tell you there is the randomized control trial proving this works inflammatory bowel disease patients because it's never been done. Not because it's been done, it didn't work. And what I find most compelling about my story is as I waded in to the world of, call it nutrition, call it metabolic health, what have you, the most unique thing about my story, sorry, the most remarkable thing about my story was that it is. It's a world of, call it nutrition, is not at all unique. That there's this motif of people struggling with conventional approaches, getting desperate, bordering on hopelessness, trying things

because they have nothing to lose, and then something works. And you're caught in a little bit of a catch-22, like why was I never told about that? And answering that question has become a little bit of a passion of mine, because it's like only certain things get investigated because of what there's a business model for. So how can we empower people with the knowledge and tools to safely explore the options available to them,

even if they're not quote-unquote evidence-based in ways that can really transform lives. And the transformations I've seen, like, when I think about them too hard, they bring tears to my eyes. The first person I ever worked with, this was a patient with Parkinson's disease. When I was in Oxford doing my PhD, I was working in Parkinson's patients. And there was a woman from my clinical trials. She was in her 60s, and I used to be a dancer. So it took a lot of pride in body movement. And then Parkinson's disease, obviously, is a disease of severe immobility.

She also had rheumatoid arthritis. So she ended up being, like, confined, basically very sedentary. In fact, when we went to work on her nutrition for the first time, I had to put her in a shopping cart and push her around, like a little kid because she couldn't move. We had a lot of fun. Anyway, she got her nutrition locked in, and then everything started to change in her life. Her inflammation went down. Her hip got better. And I got this text that I will never forget from her.

For the sake of anonymity, let's call her husband Peter. Yeah. She sends me this text. She's like, Peter just came home from work, and he caught me dancing in the kitchen. and we started dancing together and crying because we never thought I'd be able to dance again. And I've heard stories like that again and again. And again, I can't tell you it's quote evidence-based, but it worked for her. It worked for me.

It's worked for thousands of other people. I'm not even saying keto diet. I'm saying the things that conventional medicine considers unproven infringe. So how do you make what some might call outlier stories the norm? Because there's a lot of sick people that could use that level of recovery. Right. So that's my path, so to speak. And not to get into policy, but when you look at, you know, when you think about a primary care provider, you know, they are not, they don't have any latitude to experiment.

No. So it's just, it's so hard to recommend what feels like fringe but could actually maybe transform their life, you know, and how to help an individual. and that's why I think like what you're doing is so powerful. It's just this idea of you don't want to do harm, but because there's so much individual variability, we have to do some type of experimentation to figure out what works, even as a healthy person, right? I'm better with lower carbs.

I just am. But my best friend is better with higher carbohydrate. You know, like it just seems there's so much, you know, individual variability, right? Well, let's dig into that a little bit. We'll go back to the doctors not being able to experiment with their patients thing in a moment because I think there's a nuance there. But think about how we've built medicine. On this idea of a hierarchy of evidence, the pinnacle of which is the human randomized control trial.

You hear it all the time. Like it's golden in the beacon of truth. But the fact of the matter is, what is a randomized control trial, but looking for signals between large heterogeneous groups of people? Right. What that means in effect is you can have something that's evidence-based, proven in a randomized control trial, that when actually implemented in the real world, helps a minority of patients. In fact, by far, I think this is a statistic, it's a little out of dates, 2015 from a nature article, but one statistic was the top 10 grossing drugs actually help between 1 and 4 and 1 25 people who take them. Only help 1 in 4 and between 1.25. So, again, how you define quote-unquote help, I think there could be distinctions.

Obviously, say, GLP-1s probably work on a large proportion of people to cause weight loss. But the point is, just because something's evidence-based actually doesn't mean it's helping people to a large extent or helping most people. Right. So then the patient that gets prescribed the evidence-based medicine but has no improvement or even is harmed, how does medicine deal with that person? So you really do need the individualized approach. Which brings me back to the other thing you said about doctors not being able to, experiment with their patients. You can't treat a patient like a guinea pig.

Right. But I think where another place medicine has gone wrong, and this is more on us as a society, is putting the doctor on a pedestal is some like omniscient source of knowledge and truth, when in reality what the role should be is a support, a partner, and a guide, which also means a lot of responsibility falls on the patient, which is why what we're doing here in general with the transformation of access to scientific information is so important because if you can give people the tools to go to their doctor and say, I would want to try this thing and I want your support. Ask better questions. Yeah.

How can you support me with this exploratory journey and the tools at my disposal? That is a different conversation. And doctors can help with that. Right, right. I think that's such an important framework for folks to, because I do think we immediately, I think, assume a doctor is not really the person to guide us, you know, in a way. And I think we don't even give them the chance, maybe, is what you're saying, you know. But if we were to come to them with some ideas, they can maybe support us in ways that. Yeah. It's like having a conversation just with mutual respect and humility. They're going to have insights that you don't have, and you're going to have insights that they don't have. Right. Because they don't have your context and your constraints. Yeah.

Or the time you probably spent researching a topic that they weren't taught about in med school and they don't have time to learn about now because they're busy clinical load. So it really can be a partnership. We don't need to go into the rabbit hole of skills to approach your doctor. But the point is, I realize there's a lot of mistrust in conventional medicine right now. I dislike that because I think it has a lot strengths. However, I understand it. I understand the frustration because given the way the medical system is built, sometimes you find yourself budding heads, let's just say. And I'll pause it there. I don't want to deal this conversation with that. I want to get some more practicals. But I'm sure a lot of people listening to know what I'm talking about. I think there's a lot of distrust. I mean, I see it

even just in my kids. You know, I think the information that they're getting, you know, maybe online makes them feel as though their doctor wouldn't be the person to help them optimize their health. You know, like, and clearly a medical doctor is generally trained to treat disease, right? They're not actually there to help you optimize your health, which maybe we can talk about that just for a second before we get into some myths. I just feel like this is a trend, and it's misplaced in many ways. And I, but I'm not sure the best way to talk about it, but I bet you have a good idea. At a broad level, I'd frame it as, like, what are we taught to do in medical school? We're taught to treat disease because, I mean, that's basically.

Basically the job description as we think about it, not to optimize. Also, there are not a lot of studies on optimizing health and healthy people. It's can you reduce major adverse cardiovascular events and people with metabolic syndrome by giving them this lipid lowering a drug? That is the study on which our entire medical education system is based on what we learn to do. When you go to a doctor and ask them to help you with something that they were never trained to do, it doesn't mean they don't have the mental capability or the desire to help you in that. It just means it's a little bit out of the wheelhouse. Totally.

And I think that's going to change. And I think it's going to change in a bottom-up process. I think there are enough people that feel empowered that it's going to kind of force medicine to shift the spotlight a little bit, which is awesome. Yeah, agreed. But I think that's where we are now with this, like, uncomfortable, let's call it, like, puberty of medicine 3.0, where medicine is looking like, okay, patients want things. They're demanding things. They also want to learn to optimize. And honestly, at the end of the day, medicine is a business, and it's going to need to serve the population.

to patients. The power starts with the patience, truly. Agreed. Yeah. And I think having the right expectations going in, knowing what, to your point, what they're trained to do, what they're not trained to do, you know. Yeah, don't go in there looking for silver bullets. Try to find a partner and realize that it's a journey.

I think the superpower is if you can find the fun in that journey. If you're a healthy individual, do you think kind of functional medicine is a better way to go than kind of traditional medicine? I wouldn't necessarily create like a, I guess there's like a Venn diagram, but I wouldn't create a full distinction. I mean, let's say you're a healthy person. Do I think you should still get like a routine colonoscopy to, you know, as a prophylaxis to make sure you don't get colon cancer?

Sure. But is it also potentially worth exploring other avenues that your primary care physician might not be expert in to help get you to the next level? I think also sure. Yeah. One of the things that we hear a ton is, is that your metabolism all of a sudden is going to crash, you know, at the age of 30 or 40. 50. You know, we hear this a lot in the female physiology or kind of female health space where,

you know, as soon as you hit paramedopause, your metabolism like drops in some, you know, meaningful way. We actually, in our Woop data, um, across, you know, millions of members, we estimated daily energy expenditure declines gradually with age, but when we normalize for body weight and matched day strain, which is essentially how much load you're putting on your body. And we kind of have a metric called strain that quantifies that. We see that it's roughly 3 to 4% per decade. And there are no dramatic cliffs across any age group. So what's your kind of overall take on this myth that we hear that your metabolism crashes? I would say it's a myth with the grain of truth. The grain of truth is that quote unquote metabolism, and we're going to define

what that means, but let's call it broadly energy expenditure can decline with age. Let's say if you let it. So there's obviously habitual factors. Like what happens in your 30s? You have kids. You might have a sedentary job. Things get away from you. You're not sleeping well, so you're not exercising well, your muscle mass declines, your energy expenditure goes down. So there's the one bucket of, at the population level, probably some truth to it due to habitual factors. And then there's the, when we look under the metabolic hood, are there things that are changing purely as a function of age? There's a lot of directions I could take this, but I want to talk about a paper that came out this week, we're recording this July, 2026, this paper came out, Nature Aging July 2026. And I can

give you the reference to put in the notes. And this is the one that you just sent this morning. Oh, yeah, no, I sent it to you this morning unfairly because I was reading it this morning. No, it's amazing. I'm like, oh, this seems like it would be a good point of conversation. Absolutely. Coincidence, it was in the question deck you want to talk about. But what they did was they took, I think it was 47 adults, young adults and older adults,

but the older adults were split into three groups, trained, so fit, normal, so like, you know, intermediate, and then largely sedentary or remote. And what they did was advanced testing to look at metabolites in the blood, fat levels in the blood, so different lipids, and over 24,000 different transcriptomics, basically. So you have your DNA, the DNA gets turned into blueprints for making proteins. Those blueprints are called the transcriptome. So they looked at a huge swath of basically the metabolic blueprints of what makes you function, what determines your metabolism.

And then, like I said, there was the young adults and the older adults split into groups. They said, what declines with age? And then what things that generally decline with age at a population level are stable and resistant if you're well trained? And it turned out that over 55% of the changes that tended to decline with age, the signature of aging in muscles. I should add, this isn't muscles. They took muscle biopsies. Wow. Over 55% were completely stable.

if you were trained. So you could maintain the metabolism of youth, effectively, at least 55% of it, let's say, if you continue to exercise. Wow. I will also add... Can you define trained? Because there's just a lot of ways to skin that cat. I forget.

I should remember because I was reading this as morning. I'm just wondering proportion of... It wasn't like number of steps per day. That was a little bit more controlled. It was, let's just say, degrees of physical fitness. Okay. So you can measure this more objectively, you know, with something like... Did they have a VO2 match?

Max or, okay. I don't know if they use that to operationalize. Like strength tests or, okay. I forget the whole. I'm excited to read this paper. Yeah, paper the way they operationalize strength. I was literally reading it before I jumped from my car this morning. Yeah, yeah.

Elements of the methodology that I didn't dig into yet. But the punchline was a lot of the signature of aging could be prevented if you were, you know, fit and well trained. This 55% wasn't randomly distributed across the transcriptome. It was enriched in things that are essential to material. metabolism. So literally gene transcripts that are related to complexes in mitochondrial electron transport. So complex is one and four, which you wouldn't know what those are. Those tend to decline with age. They didn't if you were trained. Things like that. Or NAD. Another thing really important in aging, it's depleted in muscles and the brain as we age. Yeah. Your levels decline. Your level is significantly. There was a controversial paper about declining levels showing no decline recently if people are really into it. But it was looking at blood level specifically.

So in the muscle and the brain and other critical organs, it declines, and it's a signature of chronic disease. So if you look in the brains of patients with Alzheimer's, in the brains, NAD levels are depleted, and if NAD levels are normal, typically people's brain function is fine, even if they have a ton of amyloids. So like these are the core currencies of metabolic function in the body. And basically, what this study is saying, in agreement with other studies is if you exercise regularly, you can stave off these elements of aging. Not every element, but these elements.

And if you actually look at things like, you mentioned VO2 Max, or muscle mass, and correlate it with levels of enzymes that produce things like NAD in energy molecules, they say they're like, they're directly correlated. So the fitter you are, the higher these levels of core metabolic enzymes, proteins, molecules, and I know I'm throwing a lot of jargon out there. I want to boil it down with this image, which is, if I said exercise is good for aging, I think everybody would be like, all right, sure, I buy. But the conception might be, well, if you build up muscle, it's kind of like a reservoir. Maybe you're going to decay a little bit with age, but like you have more of a muscle reservoir to bank from. This is different. This isn't just, oh, look, you worked out so you've

a bigger muscle. This is, if I take the same little tiny cubic millimeter of muscle from a trained person, and an untrained person, then look inside the cells, down to the mitochondria level to say, are these mitochondria different? They're different. So the metabolic operating system itself is different, not just muscle mass. That is what is so cool.

And so that's where I would say the myth is busted that metabolism slows as you age. Aging's hard. I'm not necessarily speaking from experience. I understand the irony of a 30-year-old saying this. But that aside, the data suggests you can stave off. a lot of the metabolic signs of aging if you take care of yourself.

Yeah. Yeah, I think it's so encouraging that lifestyle can move you in such a powerful direction. You know, I mean, it's really empowering. It is. And it's one of those things that becomes super empowering when it, like, really gets internalized and hits you because it's not sexy. You don't feel it like the day of. You still have to go out there and do the work.

But in terms of, like, the gains you can get over the decades, I mean, if you imagine two different 80-year-olds, you could have somebody who's completely, like, immobile, their mind isn't there and somebody else who's like can go on jogs. Walk around Disney all day with their kid and that isn't luck. That is something that isn't within people's control to a large extent. What would you, do you have a hierarchy in terms of what you, from my, I guess like a muscle, when you think about it from a metabolic perspective, strength training versus cardiovascular work versus it all kind of matters, I think, but do you have like a hierarchy that you subscribe to

personally? I think it all matters. I think, you know, identify your weak point and work on that and also do things that you enjoy. Like I, I used to be a runner and I just loved running. Running is good for you. Do it to an extent. Don't injure yourself like I did. A whole other kettle of fish. Yeah. You want functional muscle mass. So resistance train, I think, at least two days per week, at least hitting all the major muscle groups and do some sort of cardiovascular training that doesn't need to be, if you don't like steady state cardio, like you're going to sit on a rower or go on a run, doesn't need to be that. You can work it in to full-body workouts.

So I personally really like full-body circuits. So it's like do jumping alternating lunges for a minute, then do 50 push-ups, then do some chin-ups, take a beat. Like that will give you a cardiovascular workout. So you can work strength training in cardiovascular fitness together, but I think all of it's important. Actually, one other sidebar, totally random fact. Sometimes I just go on, I call them Stay Curious SideQuest is the way I'm branding it. I just read a study about twins in cognitive aging where they took 24. twins, and they actually looked at cognitive function and brain atrophy, so much the brain shrunk.

Wow. And including in identical and fraternal twins, and you know what one of the best predictors for healthy brain aging in the twins was? Leg power. Oh, I have seen this. Yes, yes. And then I'm like, that's cool. Yeah.

That's a cool study. Yeah. And there are a lot of ways we can... Don't neglect your squats, people. No. As I was saying, squat for your synapsing, my bumper sticker. I love that. But if you think, I mean, there's now, like, you know, that degree of human evidence, but, like, mechanistically, it makes so much sense.

It does. Because your muscles aren't just, your muscles are, and I say this with the full weight of what this means, endocrine organs. Right. So you're adrenal. Glucos uptake. They're synchre. But, like, they secrete hormones like, you know, a recent that go to the brain, increase BDNF levels. They're, the whole class of molecules and hormones secreted from the muscles has a term.

It's called myokines. Mio-a-Muselis for hormones. And brain-derived neurotropic factors. brain-derived neurotrogen factor is like miracle growth for neurons. So your bottom line is your muscle communicates directly to your brain to help it grow and stay healthy. So, yes, things like a run or doing some squats actually do help your brain. Yeah, amazing. Yeah.

I mean, that definitely tracks with kind of what we see in our data. We definitely see people who just only lift have worse cardiovascular profiles. You know, not surprising, right? I think you need both. I think your heart rate. your resting physiology matters, you know, in terms of long-term health. And so, yeah, getting the heart rate up, whether it's via circuits or, you know, some dedicated sprinting or something like that is important.

Yeah, you need to put the work in. It doesn't need to be long and arduous, though. No, I agreed. I've gotten into, if you've used those vertical skiergs, the ones where you, like, pulled. I have this, if I have no time, I'll do a high-intensity workout where I do, full-out sprints for two minutes on that, two-minute rests, and then repeat for, like, five to seven, if you really go hard, it's like you're done. You're, you're, you're, you're, you are smoked. I mean, two minutes. That's, you are smoked. That's a long time.

But the end you're gas. Have you seen those ropes too that you? Yeah. I mean, things like that. It's a whole, it doesn't need to be boring. You can change it up. It can actually be a lot of fun. You need to find something. Just get yourself out of breath. Yeah. Yeah. No. Um, and find a way to, to have that be satisfactory. I love it. Okay. Myth. Oh, myth two. Myth number two. Pore sleep directly causes cardiovascular inflammation. Is this a myth? Or am I'm supposed to say this is true. This is, uh, this is, this is, this is, this is a This is... I'm going to call it true.

So, okay. Yeah. Let's start with... You're the sleep expert, so if I say anything wrong, you can fact check me, but... I will, I will.

Okay, I think... Let's start with what we agree on in terms of the correlational evidence. And I will say, we do have some whoop data here, which is interesting. So 1.45 million members. Okay.

Okay. HRV, so hearty variability was approximately five milliseconds lower on poor sleep nights, okay, which is clinically significant. Resting heart rate was approximately 3.5 beats per minute, higher on poor sleep nights.

88.6% of members showed lower HRV after their worst sleep nights. Yeah. So there's HRV and resting heart rate. The question's about inflammation. So we'll tackle that first. Then we can switch back to the heart rate metrics, which is, okay, we agree, I'm sure, that like sleep deprivation and shift work is associated with worst cardiovascular outcomes. I think it's something like 20% increased risk of a cardiovascular event if you're a shift

worker. Yes. It's correlation. You could have like, you know, donuts at the nurse to stage, maybe. Are there mechanisms? I can think of a few, and I can send you this paper. The one that jumps to mind has to do with the hypocretin hematopoises axis, so I'll unpack that jargon. Hypercretin's a hormone release from your brain.

It's kind of like a Swiss Army knife. It's involved in sleep, also called a rexin, but it also is a signaling molecule. So it communicates with different parts of your body, including the hub of where blood cells are produced, bone marrow. hematopoises is a generation of new blood cells. So there are at least pre-clinical evidence, so animal models, because you can't do these experiments easily in humans, but showing that sleep deprivation causes changes in signaling of this hormone from the brain to the bone marrow, causing inflammatory cells to be produced

and then go into arteries and actually promote inflammation, which is a core feature of heart disease. So does sleep deprivation associate with poor cardiovascular outcomes in humans? yes, are there mechanisms to describe directly how sleep deprivation can cause inflammation in blood vessels? Also, yes. I'm going to call that not a myth. Yeah. I don't know if you agree. You're right.

All right, sleep does cause inflammation. It does. You know, and we obviously can't measure inflammation directly, but yeah, I mean, you know. You can't almost ERP. Right, exactly. Funny story for you. With resting physiology, we can't directly measure inflammation. But through this mechanism, through this very plausible scenario you just outlined.

I have a funny story for you, actually. I, you know I do a lot of experiments. One of them I did recently was with this new drug Gratatututide, the GLP3. It was an intense month. We can get into that experiment later, but one of the things that happened when I, it was just for one month and it was at a low dose, but my biological age went up. Now, that's weird. And I looked at that signal.

I'm like, that's weird. Why would one month of taking this GLP increase my biological age? This is probably what happened. So biological age, there's a different ways to calculate it. One of the ways involves incorporating inflammation as one of the metrics. One way you measure inflammation is something called HSCRP. And sleep deprivation can bump it short term. So one of the things that was happening when I took this medication is my heart rate went up a lot.

And I was jittery. I've published papers on this. Yeah, yeah. We see this in our data with GLP users. Yeah. Their cardiovascular profiles take a huge hit on GLP ones. My resting heart rate went from low 40s to mid-70s. It was a huge jump.

But as a function of that, I was like jittery. Like my energy expenditure went through the roof. You just couldn't drop in a deeper stages of sleep. So the night before the follow-up test, I had five hours of sleep. And so what I think happened is my HCRP bumped acutely. So my inflammation marker went up acutely. And so then when it calculated my biological age, it's like, well, you're older. Anyway, that's an anecdote.

I'm like, wow. So. I mean, we definitely see, you know, exercise attenuates that negative impact on cardiovascular profile, but not that much, only slightly. but that is a really interesting interaction. Right. And the downstream effects could be problematic for some folks. It emphasis on for some people.

I mean, to be clear, probably somebody's asking if they're looking at me is like, why is this person with a BMI of like 21 taking the rents? I'm like, I did not do this for my health. I did this at the risk of my health. I like to guinea pig myself if people know me because, you know, I like to understand how things work in part through personal experience. I think some of the effects of these medications are incredible, well beyond weight loss.

Well, I think it's like the tip of the iceberg that said, sometimes you try something and something weird happens in an individual like it did to me, and then you want to troubleshoot. So I'm not putting any value judgments on this or any other GLP. It was just like, well, that was interesting. Yeah. Well, I think what's important about the way you experiment is that you're looking at all sorts of different markers, right? You're not just blindly going on how you feel. You're looking at very objective things that you wouldn't be able to assess without,

a blood test. I think that's an important caveat, right? I got 127 biomarkers for that experiment. And again, the purpose was, like, I want to guide people through their health journey at the same time. Everybody has a different risk tolerance

and things that matter in life. Right. So some people might be like, I know it's not great for my health, but I'm going to go out and party and drink. I won't judge that, you know it's not good for your health. They're going to do it anyway.

I'm the person that's like, I'm going to experiment on myself. I'm not saying this is good for my health, but I really want to figure out what's going on. So I've done some crazy experiments, and so this is just part parcel for me. I'm not advocating for any particular way of doing things. It's just

a way I explore the world and I enjoy it. Before we get to the next myth. Yes. What is the craziest experiment you've ever done? The first one that was kind of my launch into social media was the Oreo versus statin study. Oh, this is so good. Yes. So, okay, so for a little bit of background.

Wild. People might want to pause the podcast now and go to PubMed. Yeah. This is published. Because you're not going to believe me until it is a paper. So for background. Yeah, talk about why you did this because I think that this is like, this is just you in a nutshell. It is me in a nutshell.

So we were studying a group of people with very interesting cholesterol metabolisms where, you know, people think, oh, you have high cholesterol, you have low cholesterol, it's kind of static, maybe diet affects it a little bit, this is something different. We were seeing people, and let's just say I'm one of those people who can change my cholesterol levels 500% basically overnight. This does not happen. This does not exist in medicine in the medical textbooks.

And the levels can get so high, including in me, that the only other circumstance in which they're known is a very deadly one in a million genetic disease called familial hypercholomelemia, study of which ended up snowballing

into a Nobel Prize and kind of kicked off the modern era of heart health, cholesterol, understanding. So now we're seeing this group of people, like, it's so weird that it's like

if you saw someone who could snap their fingers and change from being five foot to eight foot back to five foot. Like it's metabolically like that, but people can do it. And when we started studying it, we were publishing some papers, but like nobody cared. And I'm like, how does nobody care about this? This is medically incredible. And I don't have a lot of, you know, I didn't have resources. Second year medical students.

I don't have an ad money. I don't have money for like the, you know, $10 million I want to do the Defender Study. So I'm like, okay, how can I make people pay attention? and I just kind of got a naughty thought. I'm like, well, what if I devised the most diabolical, click-worthy but legitimate experiment where, in this case, I can lower my cholesterol by understanding my own physiology with Oreos. Let me unpack how I think this works. So I mentioned earlier in the podcast I went on a ketogenic diet.

That helped with my ulcerob colitis, but something weird happened, my cholesterol went sky high. It first tripled and then over quintuples. went from sitting in the 80s and 90s to peaking LDL, just the LDL, near 600, which anybody medically listening might have just had a heart attack of their own. Doctors don't believe me until they see the test. So it is astronomical, but the weird thing was, when I started a ketogenic diet, it wasn't like I was guzzling butter and bacon and had no fiber. I was like avocados, salmon, olive oil, nuts.

Long story short, it probably happens to me and people like me, is if you're metabolically flexible and lean, when you switch from carb-burning mode, because you run on carbs for fuel if you're eating carbs, to fat-burning mode and you're ketogenic, your body starts trafficking fat fuel throughout the body, and it needs a carrier delivery trucks, let's just say, to do this, and those delivery trucks have incorporated within them, cholesterol. So you can have a system that fluxes fat throughout the body, is fuel that gets revved up. And this, as a phenomenon, creates a certain signature in the blood,

including an increase in LDL cholesterol, along with very high HDL and low triglycerides. So we talk about like the lipid markers for metabolic health. Very, very high HDL. My HDL is like 125. Triglisorides, very low, like 30. It's an extreme profile. But the punchline here is if our hypotheses were correct and I say R because the team of people working with me, it's not a solo effort, are right, then if the problem, quote unquote problem is I don't have carb fuel. if you just add carb fuel back, shouldn't the quote-unquote problem of high cholesterol go away?

If the hypothesis is correct, it doesn't need to be a healthy carb, it doesn't need to be a carb swap. It can be a pure addition of any carb, which means I can take my normal diet and binge Oreo cookies on top of that, which is what I did. But I like to dot my eyes and cross my teas, so I decided I would go to Harvard's institutional review board and say, I'm going to do this. Can you give me permission? They're like, sure, go ahead. You can experiment on yourself. And then I also did it as a crossover experiment, which means I have two faces. And the comparator was high-dose statins.

So front-of-the-line medications grows hundreds of billions of dollars for pharma. And I'm like, I'm going to take Oreos and compare them to statins in this experiment on myself. So I did this experiment. You can look up the exact methodology. But bottom line is eating a sleeve of... Oreos outperformed statins. Yeah, that's the punchline was Oreos were twice as powerful as statins at lowering cholesterol and worked three times as fast.

And it's legitimate. It doesn't mean, again, what am I trying to say with this? Am I trying to put a value on LDL or Oreos or statins? None of that. It's being like, whoa, you can do this with a human body, and you can do it in a predictive manner. It wasn't a fluke. It was like, I think this is going to happen.

I broadcast before I did it. This is my hypothesis, like a good scientist. Then I did it. You pre-registered. You did the whole. I mean, it was an N-equals one that got exemption, so I didn't need like an actual pre-redge. But I literally went on a very popular veg podcast,

who's also like a friend. And I'm like, hey, I want to do this thing. like the world's I might be a fool it might be wrong but I'm going to do the thing the thing worked so that was the craziest experiment I ever did and honestly this is the funniest part it's been replicated a lot because people like me there's a lot of them and increasing number because more more people play with diet so more lean people are trying ketogenic diets and developing metabolism is like mine what cholesterol goes up including doctors at Harvard so there's people that were like my senior residence during med school and you're like I can't believe this work by the way I have this profile will over

work on me. I'm like, I can't tell you to do this. You are a licensed clinician. I can't tell you not to do it, and they would come back later. And they're like, it worked. The one time I told somebody not to do it was a resident who was pregnant. And I'm like, please finish your pregnancy. Before trying this, she came back later and said it worked. So there's a story for you. Yeah, I've done a lot of experiments like that. And the point is never to proselytize for one approach. The point is to be like, let's get excited about what you can do with your body because the outcome of changing cholesterol like whatever nonsense doesn't really impact my health as far as I'm aware but if I can do that think about what you can do with an outcome you actually care about if you understand your individual

physiology and I trust me people can have unbelievable transformation stories so this was kind of just you can call it clickbait that's what it was it was still legitimate science but it was clickbait to start a conversation around this niche area of cholesterol metabolism, which is one of my nerdy passions. So more than anything for me, it was a social experiment to see, can I use the tools at my disposal to get people excited and interested in some nerdy, esoteric, scientific topic? And I've been devoting the last couple years of my life to figure out how to do that, how to get people excited about science and metabolism because at the top of, you know, the surface, as you opened with,

it's not, it doesn't sound sexy. Right. You know, you know, eat your rainbow, five a day, balance, fiber, gut health, like all the platitudes. And there's so many platitudes that need to be deconstructed because there's so much nuance and just like a scientific awe that is at our fingertips under our noses, things that you can do. And the data are there. There's like human trials showing how you can change your macro-neutral.

in distributions to get a 600 calorie per day increase in energy expenditure without changing activity at all. Like those human trials exist. Nobody talks about them. And to surface those things and talk about them is just, it's an absolute pleasure, which is why I love doing this. I want to apologize to everybody in advance for talking fast because we're getting close to time, but we have a lot of topics we want to cover.

I know. So just like put it on 0.75 speed for what follows. Perfect. Yeah. So that thing I just kind of tease, which I'm glad you're biting the hook there. I bet, yeah. It was, so this, okay, it's going to start in the weirdest of places. Did you hear about the sugar diet trend last year?

No. This was a thing. Google it. There were like influencers like, I'm doing the sugar diet. And when I say the sugar diet, I mean like candy, fruit juice, skittles, raisins. And they were like, and I'm losing body fat. And I'm like, this is nonsense. This can't possibly work.

But I knew some people who were trying it and I'm like, all right, it's interesting enough that I'm going to dig into it. Coincidentally, around that time, a paper dropped in nature metabolism. Nature metabolism is a highly regarded journal, and I had things. three human control trials in it where they did something that's going to sound very counterintuitive, but I will unpack it, they gave lean, healthy men, that was population, a low protein diet. Low protein, not high protein. They cut their protein down to 9% of calories from protein, and their energy expenditure went up by about 20%. They did three separate studies, and every time energy expenditure went up by 20%.

And there was no loss significant loss of lean mass over that study period. How long was the study period? Five-week intervention. So it was admittedly short time frame. And I'm not recommending this. But again, metabolic fascination. What was going on with their metabolism? Probably what was happening is a couple things.

One was a change in a hormone called FGF21, which the liver can make, and it can affect fat cells and cause an increase in energy expenditure. And there are probably some other things going on with the microbiome. So this is where the story takes a nibone. new turn, where it came out in a paper, it was in nature or cell, one of the big two, I guess big three, if you include science, where they started to look at brown fat. So just to catch people up, there's different types of fat in the human body. There's a white fat, which is like your storage fat, and different types of white fat. We could talk about, you know, visceral fat. And then there's very metabolically active fat. So brown fat and another type called beige fat, which is like its cousin,

that produces a lot of energy. It burns off calories like gangbusters. But the funny thing is And that declines significantly after birth, right? Typically, the brown fat does, the beige fat you can produce. Okay. Anyway. Yeah. Their lineages are a little bit different. But that aside, if you put humans in a scanner and basically look at brown fat activity across adults, massive variation.

Some people have a lot of really active beige fat that's burning off energy. And other people have, like, none. It's a metabolic injustice. But then what they did was they, tried to figure out, what is the signature of these really metabolically active fat people, humans? And they looked in their microbiomes. Long story short, the microbiome is secreting molecules that can collectively activate brown fat.

And different people have different microbiome profile. So here's where things get cool. They tried to identify the minimal consortium, team of microbes that collectively produce a cocktail that can activate thermogenesis, fat metabolizers. fat metabolism, burning off energy. They ended up with four, which they combined into a probiotic they called HU4. I don't know if it stood for human four, for four bugs, but that's what I think. And then this hasn't been trialed in humans yet, but they give it to mice.

The reason you do it with mice first is you need to wipe out the microbiome, so that's heavy antibiotic treatment. But they were effectively able to show they could massively boost the mice's energy expenditure. Wow. So I'm kind of cobbling the story together here, and I can send you those two papers, but what probably is happening to some extent is the protein restriction. is changing the microbiome to change metabolism in a way that downstream activates energy

expenditure. It's still being sussed out. I know the original team is doing more work in women, older people and people with obesity, to see if they affect replicates. But, like, I'm not saying go do a low protein diet now, although I've tried this and it does work. I did not try it with a 4 to 1 ketogenic diet. It was crazy.

I could not stop from losing weight, and I just kept on eating your own intake. Is that just because, I mean, how, what's the choleric profile? Is it how? A ketogenic diet? No, no, no, for this low protein. So 9% kilo calories from protein was what they did in this study. Okay. So you can kind of break that down depending on your overall intake.

But, and I will be clear. People say, like, don't mix fat and carbs. One of the studies was high fat, high carb, low protein. I think it was 41% carb, 50% fat, low protein, and it still worked. What? So they had to increase the people's energy intake to prevent them from losing weight. They just kept on increasing the calories, like 5, 600 calories. They still lost weight.

And again, it wasn't necessarily. necessarily lean mass. There wasn't a significant negative nitrogen balance that normalized. Did they look at visceral fat? They didn't. I would love to have them look at visceral fat. But again, not advocating for this, but like think about how cool that is. And also then think, what if you could hack this and make that probiotic work in humans? Yeah. Could you make a probiotic that burns 600 calories per day? Sure. You could. In theory, you could if you can get it to stick. Because then you could modulate people's beige and brown fat activity, which is like wild.

So we are on the cusp of doing these things. That's just insane. Which is cool. I can send you the PubMed references like the DOIs. And that would be a natural therapy. Effectively the way I think about it is you're giving a meta, like, think about the people with certain like advantages genetically. Maybe they're tall.

Maybe they have like great musketure. Yeah. Or they have active brown fat. Yeah, just take that benefit and give it to someone who's quote unquote less fortunate metabolically. People call things cheap. Just like take your advantages, take your wins where you can. Also, if it's improving your overall health.

Yeah. Which in this case, I see no reason to think that it would be harming you. In fact, there are animal model literature showing FGF21. Certain pathways can increase longevity in animals, but I'm saying the net benefits probably good to health. Would you imagine if this continued beyond the five weeks, and let's say we get into 10, 15 weeks, do you think there would be a shift in lean mass, given that there's a decrease in protein? Or as long as you're still stimulating the muscle, you should be fine. Honestly, it's hard for me to speculate.

I would say I would be careful, especially if you're an older adult. Yeah. A lean, healthy person probably has a little bit of buffer room to wiggle with. Right, right. I still will be careful. Yeah. I will say that I think right now we're a little bit in the protein maxing era and it's overhypes. More is not necessarily better and probably people need less than they think they need.

And metabolism adjusts to different circumstances. Let's go there. How much protein do you think? As someone who just spends their life studying this, how much protein does the average adult healthy adult need. This is such a hard question to answer because when people are giving the advice of the RDA is too low, which is like 0.8 grams per kilogram, which is 0.3.6 grams per pound. I'm like, at a population average, I think it is harmful to give that advice.

I much rather use go for one. We're quadrupling that. I much rather see a person for one gram per pound. Right. I do not think that, to be clear, I do not think that it's harmful. and in terms of like even just satiety signaling, if you're going to be eating a decent amount of protein, I think that is a good place to start for your average person. Right.

Not discounting that. Do you need that metabolic in a preserve or build muscle? No. Right. It was actually a really fascinating study in 2024 where they took lean people and fasted them for seven days. Water only, completely water only fast and then did a refeed. And basically after the fast and the refeed, very little lean mass was lost. Interesting.

So your body like, is. is pretty smart about preserving critical infrastructure, so muscle. Right. So I do think we're right now over-hyping protein because it's a macronutrient that's very easy to love. I love it. Like, I'm not going to not eat a 16 ounce of ribeye if I get served it. It's easy to sell, too. It's easy to sell.

So, you know, I'm definitely not anti-protein. I'm not saying do a 9% kilo-calories from protein diet. I'm just saying there's another level here worth exploring. And we'll leave it of that. All right. Let's talk about visceral fat. We mentioned it. So it definitely plays obviously a super low.

large role in just overall metabolic health and functioning. I had my visceral fat done in November. I'm due to get it done again. I think it's 0.14 pounds. It's pretty good, right? Pretty good. Yeah. So why don't we just talk about what is visceral fat?

How is it different from other fat? Why do we need to kind of keep track of it? What are ranges that are helpful or good for us to think about in terms of age? Yeah. Yeah. So when you think about like general. fat. Well, set aside brown and beige fat. You have fat that is subcutaneous, so under your skin, think love handles, think muffin top. Maybe you don't like it. But honestly, if you, it jiggles and

you can pinch it, it's probably less harmful than visceral fat, which is the type that sits in your, you know, abdominal cavity wraps around your internal organs. And it is inflammatory, harmful. The analogy I come back to you guys, I think it's kind of funny and cute, and I love funny and cute analogies is like if an endocrine organ, which secrete's hormones, had a baby with a cancerous tumor, that's visceral fat. Oh, dang. Okay. It's a sticky one, right?

That's, it's spinning off inflammatory molecules. It's harming your heart. It's harming your brain. In fact, a recent study came out, 26 out of, I think collaborators at Harvard and in Israel and Germany looking at, this was drawn from, I believe, four different randomized control trials, but visceral fat and visceral fat and visceral fat change and changes in brain function and brain volume over time and specifically visceral fat,

not subcutaneous fat, was associated with quicker brain shrinkage. If you kept your visceral fat lower for longer, your brain was healthier, your cognition was healthier. And there are mechanisms to explain that. Also, visceral fat potently harms the heart. So long story short, you want to reduce it. The question that becomes how.

I'll give you my bullet point list, which is first and foremost, the most powerful things are the least sexy things. Sleep, exercise, general proper nutrition. If you're losing overall body fat, you're probably losing visceral fat. There are a few things that might potently reduce visceral fat specifically.

Two come to mind. Resistance starch. So there are double-blinded, calorie-controlled human RCT data showing resistant starch. In this type, I think it was type 2 resistant starch. We won't go into the four types, but was able to reduce visceral fat in humans. So it was 40 grams. I'm just going to give people the practicals and the protocol. 40 grams for eight weeks of type 2 resistant starch found from high.

my amylose maze is what they did. So if people look up, resistant starch, visceral fat, nature, one of the nature journals published it, they can find a paper. But that was able to reduce visceral fat, probably again, changing the microbiome. Right. Resistence starch, change microbiome,

microbiome makes hormones that affects visceral fat. The other thing that's very potent, and you can't get it without a prescription, is Tessimorella in the peptide. Okay. So there's a peptide out that is FDA approved for visceral fat reduction, specifically in patients with HIV.

Historically, that population was given drugs that caused visceral fat increase, so that's what it's studied in. But that through acting on the growth hormone pathway, can reduce visceral fat. So point being, it's important for brain health, heart health. You can reduce it through healthy lifestyle practices, some things that are readily available, resistant starch, and then there are new things coming out like these peptide.

So gut biome health is the thing to address first, if you want to improve your visceral fat. I would say a lot of your health. The resistance starch aspect is a very particular intervention. So what you're saying is you can't do it all with food or nutrition. You could. I mean, sure you could. Or you accelerate it with exercise food.

If you're doing all the things, you can accelerate. This is one of those things where I'm like, really what I'm trying to tell you is not, here's a magic bullet, even though resistant starch is very cool. It's more here's another really important outcome of all the boiling. plate things you're probably already told about. So when you're at the gym, let's like, I'll do an autopsy in this conversation. Yeah, yeah.

You're doing squats. What are you doing those squats for? Because you're not doing it just to build a muscle. You're doing it to change your transcriptone. So those 55 to 59% of Jane's stay healthy. To build your brain, because you're sending a BDNF there, and now we know about that twin study, to reduce your visceral fat.

Those are the reasons. Right. You're doing the boilerplate, fluffy, health, and, you know, nutrition things. Yeah. That is what's happening inside your body, even if you don't know it. So if you're taking nothing else,

maybe some extra motivation for hitting the gym or eating well because what it's doing to you is so profound and so beyond what means people appreciate. It's not just shrinking, you know, gut and aesthetics. It's not just building muscle. It is so much more. It's changing your body's operating system. Amazing. Which I find very cool.

So you have this really beautiful philosophy or framework about staying curious. What's your message for our listeners? And how do they think about curiosity as an entry point? Yeah. At the risk of seeming redundant, I'll kind of end where I started, which was with my health journey, because I really wanted a solution to be handed to me. And I got to a place where I was very desperate and hopeless. And just the little bit of curiosity that kept me afloat got me to try something that eventually saved my life. And I say that without exaggeration. And since then, I have found so much pleasure not only in exploring the natural world, but being on a

a quest to figure out how to get that light to go on in someone's eye where they realize taking care of yourself experimenting on your body in safe and responsible ways learning about your own like underlying biology isn't a chore but an immense privilege there was so much joy in that that like the journey and indulging in what i think is very a very basic human quality that we all have within us curiosity is like, it's such an immensely powerful tool. Because once you unlock that pleasure, you start on this lifelong journey of always experimenting and iterating on your health and applying the scientific process to you as like an organic being. And when you do that, like, that is, that is the only guarantee or as close as a guarantee you can have that your health will ascend

rather than decline. And most of ours are declining. It doesn't mean every experiment will work. That's not how science works. It means that everyone you're going to learn something from and you're going to iterate. You can do the next thing, and the next thing, and the next thing, forever. And it's not a chore. It's fun. So when you can excite that spirit in someone, that's what Stay Curious means to me. It unlocks pleasure.

It unlocks community. And it is as close to the secret of lasting health as you can get. I love that. It's perfect. Well, Nick, I could just talk to you all day long. I love the way you think about science. I love the way you communicate it. you're doing just exceptional work and deeply grateful for all of your contributions at just

still a young age. You've got your whole lifetime ahead of you. I appreciate it. So, yeah, so thank you so much. Thank you so much.