Episode 217: Nick Norwitz (Part 1)

Welcome to the Food Junkies Podcast. Here we aim to bring you the experience, strength, and hope of professionals working on the front lines in the field of food addiction. Our mission is to educate you, the listener, and increase overall awareness about food addiction as a recognized disorder. Here we discuss all things recovery, exploring the many pathways people take towards abstinence in order to achieve a health-forward lifestyle. We hope to inspire you to thrive rather than just survive. So stay positive, make a change for yourself, and share your journey with others. And hopefully the message will spread.

Hey there, Food Junkies listeners. Today we have an incredible guest with us, Dr. Nick Norwitz. If you don't know Nick yet, you're in for a real treat. He's a researcher, educator, and metabolic health advocate whose mission is to, quote, make metabolic health mainstream. Nick's academic journey is nothing short of impressive. He graduated valedictorian from Dartmouth College in 2018 with a degree in cell biology and biochemistry. He then went on to complete a PhD in metabolism at the University of Oxford before pursuing his MD at Harvard Medical School. But his passion for metabolic health isn't just academic, it's deeply personal. After struggling with severe inflammatory bowel disease, an illness that left him physically emaciated, mentally drained, and desperate for answers, Nick discovered that a ketogenic diet put his condition into remission when conventional treatments had failed. That moment of transformation ignited his relentless curiosity, and ever since, he's been on a mission to challenge outdated paradigms and bring metabolic science to the forefront of medicine. Nick is now in the final stretch of his dual doctorate, determined to disrupt the intellectual and social landscape of metabolic health. His mantra: stay curious. And today, we're diving deep into some of those most cutting-edge topics in nutrition and metabolism, from the link between food addiction and viruses to the science behind lean mass hyperresponders. This conversation was so fascinating that we decided to turn it into a two-part episode. So buckle up because today's discussion is going to challenge what you think you know about food, health, and metabolism. Nick, welcome to Food Junkies. Let's get into it.

We are so excited to have Nick Norwitz here today to discuss with us all things metabolic function, food addiction viruses, lean mass hyperresponders. We're so excited, we decided to do a 2-part episode with you. So thank you so much for being here.

Thank you for having me. I'm excited to be here.

Awesome. So we love our listeners to really get to know our guests so that they can connect with them. Would you mind sharing a bit of your personal story and how maybe it professionally influenced you and how it would, you know, essentially you are the kind of the person now that makes research findings make sense?

Yeah. I'll start with the very vanilla boring angle of it, which is on my academic trajectory, and then I'll fold in my personal narrative, which is maybe the kind of spicier person that I am. But I grew up in a family of doctors. I always wanted to be a doctor. I always loved science. So that's where my mind was at from the youngest age I can imagine. And in the environment I grew up in, that meant the standard, quote, success. For those just listening, I'm being heavy air quotes. Trajectory. Like, you want to get into the best college, you want to perform the best, you want to go to the best graduate school. So I went to Dartmouth, I graduated valedictorian, cell bio, biochem. I went to Oxford University to do a PhD in metabolism. Then I came back across the pond to do an MD at Harvard. So on paper, I was hitting all the marks. And if you would've told me at 18 that was going to be what your resume looked like, I would've been like, fantastic. That makes me so happy. I became a little disillusioned. That's kind of the spoiler alert there because I started dealing with my own health issues. So at the end of college, I started to develop gastrointestinal issues, which was really new for me. Like, I was always known as the person who, like, could eat anything, not gain weight, kind of like got away with it. Again, heavy air quotes for those listening. But, and I had no food aversions, but then I went to being like very food restrictive because anything I ate caused GI upset. And when I say GI upset, I don't mean just bloating, I mean bloody diarrhea. It was bad. And for those who haven't experienced that, there's the urge and then there's the urge when there's blood accumulating in your rectum. Sorry to be graphic, but it is something entirely different. And the reason I bring this up is because we all deal with our— come on, let's say shit. I like puns. We all deal with our stuff. In my case, it was shit. And we deal with it privately. A lot of the time, and for a lot of time I really suffered. And I know poop sounds funny, like it's a joke, but for someone struggling with this, it really is a lot more than physical pain. It is psychological torture. Imagine trying to date or socialize or even just take an exam when you don't know if you're going to have a flare. I actually did not have any anxiety around tests. I was kind of a unicorn there. I'd go into tests all confident, jamming out to I loved my pump-up song was "Let's Get Down to Business" from Mulan. That was always my pump-up song. So I'd go into biochem exams beforehand, you see, and everybody would be stressed and I'd just be jamming there and I'd do great. But it got to a point where like, I got a lot of anxiety going into tests, but because I thought, what if I have a flare mid-test? And the idea of dating, which is something a young man does in college, went out the window because again, sorry to have, you know, TMI, but like, you don't want someone over at your place in the evening having a romantic moment and it's like, by the way, let me take a break I'm going to go bleed in the toilet for a minute. Not very romantic. So things got worse and worse, especially after graduation. I ended up doing my PhD at Oxford, but I was spending a lot of time in the hospital, like in intensive care, even palliative level of care at one point. And very quickly, in the period of a couple of years, I went from being a high-performing academician and athlete. I had won a couple of push-up competitions, ran sub-3 marathons. I was a pretty high performer to being someone who had brain fog, was physically just very fragile, socially withdrawn, mentally not all there. So it's like you had this juxtaposition of like on paper, everything looks great for me. In real life, I was a shell of a human being. And when you're in that place, as anybody who's struggled with something similar or seen somebody like a loved one struggle with something similar, you get desperate. So, you start trying things not because it's evidence-based, not because you expect success, but because you have nothing left to lose and you're just throwing spaghetti at the wall, which is an ironic turn of phrase because the spaghetti at the wall that stuck for me was a ketogenic diet. So, what really got me interested in the area of metabolic health is I had a lot of negative ideas about keto, but I tried it because I had nothing to lose. And for me, it really worked. Like, my symptoms disappeared within a week. In conjunction with the drop in my inflammatory markers to normal levels. And the next time I got a colonoscopy with a biopsy, I was in biopsy-proven remission. And that really struck me. It didn't make me like a keto zealot or an evangelical about it. I thought, this is weird. And as a scientist and somebody interested in medicine, I had to grapple with the fact that this was my lived experience and it was so palpable. And at the same time, I can't go to literature, I still can't, and say, "Here's the randomized controlled trial that shows this should be standard of care." So, you're left scratching your chin and thinking a little bit about where we are with respect to research on metabolic health and where we need to go to help people like I was helped. And so, long story short, my personal experience is what drew me into the area of metabolic health, made me interested in it. And now, I'll wrap up my story with saying the most unique thing about my story is that it's not at all unique. That now I see this motif everywhere where somebody struggles with a chronic health condition, could be diabetes, could be obesity, whatever, and conventional approaches don't help them enough. And they just experiment with something in the quote metabolic health sphere. Sometimes it's considered fringe and it works remarkably. And they're left doing a double take like, why did nobody tell me about this? I'm in a very particular position because I have patient experience, but I also have a little bit of clinical training as a fourth-year Harvard medical student, and a scientific background. So I can kind of step back at the nexus of all this and say, like, okay, here's the low-hanging fruit, and here's how we're going to change medicine going forward, quote, make metabolic health mainstream, empowering people and also inspiring and funding the kind of research that needs to happen to change healthcare so people don't suffer like I did.

That's amazing. To be honest, I haven't— I've never heard your story, Nick. So thank you so much for being willing to share that. And, you know, the thing is, is like you said, it's, it's a really personal topic. You said like we, we suffer in silence often or behind closed doors. You know, we don't share this kind of information. It is so important for us to share our stories no matter how gruesome they might be, because it might be the thing somebody might be listening to this and go, I'm experiencing similar symptoms., "And I need to go look into this." And so thank you so much for being willing to share that with us and then taking that and doing what you do. And this is what we really want to get into. So recently there was an article released on— so the reason why you're here on Food Junkies, obviously, is because we're interested in food addiction and we know that you have a really interesting and unique and important perspective on all of these things that we're going to try to talk about over the next couple episodes and the first one that we wanted to dive into is this idea of food addiction and a virus. There was recent literature published on it that you dissected. So can we get into that? Like, can you just, like, explain some of the roles that, like, our gut microbiome might play in food addiction?

Yeah, I think that first the thing to acknowledge is that with any mental health disorder or psychiatric diagnosis, the reason there's so much stigma around it and misunderstanding is because the brain is really a black box. Like, yes, the mind is rooted in the brain, the brain's material organ, But when you start to understand the methodologies people need to actually study brain biochemistry, it becomes immensely difficult. So, I'll often get— sorry for this tangent, but I think it's relevant— a comment on some mouse paper, right? Because I love the basic science. I'm like, "Oh, it's just a mouse paper." I'm like, "Well, yeah, but to do this methodology and understand the mechanism, they did need to cut the head off the mice and stain their brains. So, you're not going to do this study on humans." Because right now, at least, I think it's reasonable that ethic boards frown on decapitation. And I don't know about the listener, but I think they probably wouldn't want to volunteer for that study. So point being, science is limited by the tools we have. And studying mental health conditions can be very difficult. So things like food addiction, they can be classified based on clinical reporting. And so we generate criteria that allows us to classify them, but it remains biologically a black box. Food addiction now, it's not actually a DSM criteria, so it's not in the Diagnostic Statistics Manual, Edition 5. However, it's becoming more widely accepted as a genuine phenomenon, and you can measure it by different questionnaires that are just built on what are criteria for addiction. And you just switch out, say, alcohol use for sugar use or whatever. So, one scale is called the Yale Food Addiction Scale. Or YFAS or YFAS 2.0 is the updated. So, you can measure this clinically. Then the question is, why does this arise as a legitimate phenomenon? Is it just something "psychological" or what is the biology behind this? So, what I really love to do when it comes to mental health is say, "Look, there is hardcore biology behind this." We can talk about how bile acids actually go— they don't just digest fat, they literally go and bind to receptors in your brain, can alter depression, yada, yada, yada. With respect to food addiction, there was data published in Nature Metabolism by a group out of Spain looking at how a virus can promote features of food addiction. And at a very high level, what they did was they identified what in the virome, which is the virus component of the microbiome, stood out about people with food addiction. And they characterized this one virus or group of viruses called microviridae. And specifically, they're in— term's not important, but I'll just throw it out there. It was like a Goku Show virus, something like WZ2015A or something. I think that was it. It's been a little while since I read the paper, but basically they found this virus which infects bacteria in the gut. So it didn't affect directly human cells, but it affects the bacteria in your microbiome, changes microbiome metabolism, and in particular, it changes the processing pathways of tyrosine and tryptophan, which are the precursors for dopamine and serotonin. So to step back and simplify for a minute, there's a virus that infects bacteria in the human microbiome. It can change pathways related to dopamine and serotonin metabolism, and it's correlated with food addiction symptoms, and it's also correlated with changes on brain activity in fMRI. So, in terms of human data, that's about as good as you can do. Now, if you want to prove causation, you can come up with complementary mouse data. And so, what you do in these types of studies is generally do a transplant of the virus. So in this case, what they did is they took human samples, human poop samples, microbiome samples with and without the microviridae virus, and they can give it to mice and see if you can transmit the phenotype. So if you take the microviridae from humans and you give it to mice, can you make the mice food addicts? In this case, they were using chocolate pellets, and indeed you could. So that's kind of how you do the methodology to say, look, there's something going on in here in humans. So we have really interesting associations, virus with food addiction and changes in brain activity. Let's see if it's causal. And then you use the mouse model for that. And what they found was indeed it does appear that this virus almost certainly contributes to food addiction in humans. I'll pause for questions and then I'll add some caveats.

I love that. I'll pause for questions. Yes. And I'm so glad you said all those bacteria words because when I was thinking about the questions for the podcast, I was like, maybe I'm going to have to get them to pronounce these viruses. Questions first before we start the podcast. So I was interested in two things. First, we know where this virus comes from or originates. And the second is, I know that in your video there was an acid supplementation that they've been beneficial for the mice in reducing food addiction. Could that be applied to humans?

Right. So to your first question, where does it come from? They didn't specify that in the paper, nor if it's, say, transmissible. There's other data on social habits being transmissible, but I don't necessarily think it's from a virus. So I can't comment on where this comes from the environment, nor do I think people need to be cautious about— this isn't a matter of washing your food or avoiding people with food addiction. People don't have cooties as far as I'm aware. I mean, I can't rule out human-to-human transmissibility, but I'm not trying to fearmonger over this. I'll get into the caveats in a minute. So unfortunately, I can't answer that question. The data just aren't there yet. In terms of the— it was, I think, anthranilic acid. And again, I can't recommend any sort of supplementation at this point in time. The difficult thing about communicating the basic science— and I'll just be like, often scientific communicators don't express this candidly, but I will— is something you really struggle with as a scientific communicator is being like, I want to be as nuanced and carefully caveated and not hyperbolic as possible. But I also know that the only way people are going to engage with the message is if I try to give them a practical takeaway. And so sometimes you're driven to be like, you should try to supplement with this X, Y, and Z. In this case, I don't think we know if it'll make a big difference for humans. And so the actionable takeaways from this research, I actually would say, well, I think it has relevance, but in terms of like you should do this protocol, you should do this supplement, I'm not going to suggest any of that. I don't think the research is there yet. What I think is valuable about it, and this is true about a lot of basic science, is that in uncovering the mechanisms, this is the first step in science in innovating solutions. And the thing about science is often you can't anticipate the innovation and the result that will transpire from something you're studying in the moment. So a great example that people— that will resonate with people is that of the weight loss drugs, Ozempic, GLP-1s. That research originated by studying Gila monster venom in the '90s. People like, this lizard has a weird venom and it kind of screws up its prey's metabolism. Let's study this venom. And now we're living in the age of GLP-1s. I'm not making an advert for or arguing against GLP-1. I'm just saying, in studying the basic science, we find some really interesting things. Now, kilo monsters were studied in the 1990s. The paper I'm sharing, the papers I tend to share are like 2024, now 2025 papers. So in sharing them, I want my audience to be aware what I'm trying to do is bring you along the journey of breaking-edge science, which means there's not going to necessarily be a supplement. Sometimes there is, And sometimes there really is a really actionable takeaway. We can get into that, or just a deeper understanding about why some of the things we do, like having olive oil, might be good for something we didn't think it was before, like muscle health. Again, something we can get into that I'll tease. But in terms of these data, what I would say is the reason I think they're so important is because of what you said about people struggling silently and things being misunderstood. Like, if somebody doesn't have food addiction, they don't understand. They're just like, eh, just don't eat. Food addiction isn't a real thing. People have to eat. But when we start to uncover these biological mechanisms, we can say, look, this is just like heart disease or diabetes. Mental health is based in biology. And in understanding that, it's the first step to destigmatize and also innovate, innovate solutions. So that's why I, I like to talk about things like that, even if I can't say, and here's the protocols to solve it.

I love that. And you know what's so interesting is As a clinician, I try really hard to be nuanced because there is research literature, no matter what it is that I'm looking up. Is eggs— are eggs good for me? Is bacon good for me? Is there such a thing as global warming? No matter what it is, there will be research literature that backs up all sides of the argument. And so I love hearing you say, as a scientist, as a researcher, you know, that that population should also try to be nuanced. In how that information is presented so as not to be definitive. Unless, right, like with facts, facts are facts. But as far as like how that impacts people as a whole population or n 1, it's really important that you not necessarily do that. And I think that's an important aspect when I think about, you know, thinking about like knowing this research exists now about this virus and kind of answering some of these, you know, questions that maybe come to mind, you know, when we think about would that or could that lead to human treatments and how that could work, like thinking about, you know, what's going on with this idea of virus and bacteria and what— and talking about GLP-1s and Gila monster stuff, you know. So, so can you kind of get into that?

Yeah, I think the thing I would want to highlight, it's, it's more of a word of caution for people about incentive structures and me trying to be transparent, using myself as a case study about like Look, to be frank, go to my YouTube page, look at the thumbnails. You will see things that look sensational. The Food Addiction Virus, it has like a virus sitting over a pizza and the title is something about food addiction virus. I don't say I can solve it for you, but the point is there's this idea of clickbait and people like to say this is bad. The fact of the matter is it's a practical tool. I think it can be misused if it's just completely shallow and there's no value add. But if I, as a scientist, I'm trying to, you know, compete in a space where engagement is the currency, and I actually want people to get the nuanced information, then I have to wrap it in something enticing so they will click because I'm competing with all the just influencers that are using clickbait out there. So the reason I say this is because the way the incentive structure is, the information that's going to be presented to you on the surface, the headlines, the thumbnails, is going to be incredibly simplistic. I think it's something people just need to acknowledge at face value and then understand and find the resources you trust to go like, well, but who's using this as like legit bait wrapping paper on a package that actually has some depth? And that's something, I mean, like your audience is smart. They can kind of feel when somebody's being authentic and nuanced and when somebody's trying to sell them a product, you know, just for the sake of making a buck or just for the pure sake of getting clicks. That's something that like The reason this space, the podcast space we're in now, is rising so much is because people develop trust. They develop trust with you. They're listening to this because they trust you. And so it's not something that I can say, here are the criteria to find a trusted resource. It's something that, that is built over time. And I'm sorry, the incentive structures are the way they are. It makes it difficult for me to compete in this space. I'd love to be just like, here is the nuanced takeaway without any hyperbole, but If I were doing that, and that's how I started, you know, your video gets 50 views and you don't end up having any discussions. So you have to figure out a way as a scientific communicator to make it enticing. Sometimes that comes off more clickbaity and it truly is an art. The reason I say all of this is because I struggle with it and I think anybody who's thoughtful in the space will be struggling with it. It's not an easy thing. So I just like to talk about it because I'm not perfect at it. I want to talk about the nuance, but like, How do you get the nuance out there? Because as soon as you say, let me talk to you about Gokusho virus and microviridae and anthranilic acid, you'll lose people. So like, you gotta get people to the table.

Definitely. And that's, and I think, you know, everything that you just said is so validating for us too, as far as because we do try to be nuanced and nuance isn't sensational, it's not sexy, it doesn't sell. Yet here we are trying to have a nuanced conversation thinking about, okay, this virus has been discovered, or several viruses have been discovered. There's correlated links to food addiction. How could we take that relationship, understanding of that relationship, and potentially then treat humans? And I think you're the person maybe to talk about that. Yeah. So could we talk about that?

Yeah. Well, I would say another thing to acknowledge here is Whenever you're studying a basic science causal mechanism, if you just were to read that one paper, it might give the impression that this is the answer. So the impression that like, oh, somebody has food addiction, it's because of this virus. That's not the case. You can have causal pathways, but the degree to which any one pathway actually contributes to a disorder in a given person, like this could be absolute. Say you have a patient with food addiction and they have this microviridae virus. It could be contributing to their food addiction. It could be causally contributing and it could be causally contributing 1% of the symptomology, if you get my point. So, in these mechanistic studies, as much as I love them, they're my favorite to cover, they're never the whole picture, especially when something as complex as food and food addiction, which is largely behavioral. So, I think the value here is to say, okay, I have my clinician hat on and talking to someone, I'm like, look, I believe what you're struggling with. I truly do. I think it's a real clinical phenomenon and I think there's a solid biological basis behind it that is beyond a matter of just will. Here's an example. Not your fault. Good luck with your day. It's not your fault or whatever. This is a biological phenomenon that you are tasked with dealing with. Now, how are we going to find a solution to this? So, I think that in one way is destigmatizing. Like, look, this isn't a matter of will. I'm not just saying fix it, don't eat. I'm saying you're dealing with something. We're going to have to find innovative solutions. Right now, a lot of those solutions will be behavioral. So, constructing your food environment in a way that is less tempting. To be clear, you're not getting addicted to hard-boiled eggs. Food addiction, you're getting addicted more to junk food. It could be sugar addiction, ultra-processed food addiction, whatever you want to call it. So, setting up barriers, changing behavioral loops, engaging in cognitive behavioral therapy if that helps, finding substitutes, finding supportive communities, things like that. So, it can still circle back to the kind of interventions that you would've implemented anyway, but I think backed by a deeper understanding of the biology and the fact that it's not someone's fault, but it is still their responsibility to deal with the biological problems that plague them. For me, it was inflammatory bowel disease. It's not my fault I got it, but I do have to deal with it.

Right. But I love that you just emphasized that biology part of it. I think we forget about that. You know, as a clinician, I often say this is a biological cycle, right? It's biopsychosocial emotional. And we, we forget about the biological part of it so often because, you know, one, the type of clinician that I am, my lane is not necessarily the biology. I can educate about the biology to the best of my understanding as I read the research literature. But I'm not a medical professional. I'm not a scientist in a lab that's learning about the, the virus, you know, this potential causation or correlation here with the virus, you know, or any other biological aspect. And so I just really appreciate you emphasizing the biology part. So I just wanted to— sorry to interrupt. I just wanted to point that out, that we do need to remember that there is biology here that we literally have zero control of.

Yeah. I'm wondering if you can speak to even something like somewhat similar in saying, you know, you had this very positive ketogenic experience, it reversed all your symptoms and went really great for you. And then I have certain clients who have tried to switch to this way of living and they are these lean mass hyperresponders and now their doctors are freaking out. They're like, "Oh, keto is killing me." And so I'm hoping that you could potentially speak to first, like, just give us the basics of what a lean mass hyper-responder is, how it has affected— how it affects cholesterol in this certain population, and maybe the best information you have on it for individuals that are listeners that have been struggling with this and need support.

Yeah, to kind of cement, I see the bridge in your mind about how these things are related because this is all about understanding individual biology. And in the case of the food addiction virus, okay, the takeaway isn't very clear in terms of what pragmatically can you do understanding this biology. But there are other cases where you can have extreme presentations and even without the randomized controlled trials that have taken years and millions of dollars to do, In understanding the physiology, you can have solutions. So, an example that you just raised is this lean mass hyper-responder phenotype. People go keto and basically the people who tend to be lean and actually insulin sensitive have this bizarre response where their cholesterol goes through the roof. And anybody who's in the nutrition space has probably heard keto can increase your cholesterol. It's just like the tagline, the boogeyman of why not to do a ketogenic diet. Now, The fact of the matter is most people who go keto do not see an increase in cholesterol, and specifically don't see an increase in LDL cholesterol. In fact, their cardiovascular risk profile tends to improve on balance. However, there are a select few who see not just increases— increasing is not doing it justice. The increases are so massive that if you tell your average clinician how high some of these numbers get, they do not believe you. They don't even believe me as nearly a double doctorate at Harvard when I say these numbers like, "Nah, you're mistaken. This can't be." Because sometimes they get so high, it's equivalent to a 1 in 1 million genetic condition that a lot of clinicians haven't seen in their career. So to say that this is a common and reproducible phenotype, specifically in lean people who go low carb, and to just give you numbers for those who know the numbers, like I'm one of these phenotypes. And if I go low carb, even if I'm like eating vegan low-carb, my LDL can get over 300. It's been over 500. The highest it ever was was 545 for the LDL, meaning the, in this case, the total was near 700. That will give a clinician a heart attack seeing that number. So, these numbers are no joke. Now, the question is, well, why does this arise? Because again, I'll be clear, this is equivalent to homozygous familial hypercholesterolemia, in some cases a 1 in 1 million genetic condition. Study of which won a Nobel Prize. But that is a genetic dysfunction where kids are born with broken receptors in this pathway, LDL receptors, and they have from the start of their lives very, very high cholesterol. What we're seeing here is not that. What we're seeing here is normal people, normal lean insulin-sensitive people, albeit they might be struggling with inflammatory bowel disease or epilepsy or something. They have some reason to go on a ketogenic diet and they go keto and their cholesterol goes up from a normal baseline. So, Using myself as an example, when I was eating a standard American diet, I could eat fudge and ice cream and burgers and French fries, like trans fats, saturated fats, whatever, sugar, my LDL was like 80. Normal. I wasn't born with a broken LDL receptor. I wasn't born with familial hypercholesterolemia. But when I cut carbs out of my diet, my LDL skyrockets. That's kind of weird. And like I said, it's not saturated fat related, at least not in me. I can eat a very low saturated fat diet. In fact, the highest my LDL ever was when was when I was on a very low saturated fat diet, 85% unsaturated fat, only 15% saturated fat as percent of fat, and yet my LDL gets this high. And so you're like left wondering what's going on here. And what I'll boil it down to for your listeners is what we think is it has to do with energy trafficking. So when you're lean, insulin sensitive, and you go low carb and you have these little fat cells, you mobilize a lot of fat. In fact, weirdly enough, more than someone with obesity because you're more insulin sensitive. So, the free fatty acids in your blood, they spike. It sounds a little paradoxical because if you're on a mixed diet, if you have diabetes and insulin resistance, you actually have higher free fatty acids. You can say there's a reversal and you see this in the fasting literature. If you have somebody with diabetes and obesity and somebody who's a lean athlete and you have them fast, the person who is lean will have lower fatty acid to begin with, but then it'll spike much higher than the person with obesity. So, the fat gets liberated very quickly, and to traffic the fat around the body, you actually use the cholesterol system. So, the fatty acids get taken up by the liver and then repackaged into a storage form of fat called triglycerides, where you take 3 little fatty acids and you tack them on a backbone, so it kind of looks like an M. And this molecule doesn't mix well with water. You know, oil and water don't mix. This is a fat, it's kind of like an oil, so you need carrier particles. And long story short, the particles that carry the fat around the bloodstream use cholesterol or have cholesterol in their shell and in their core to some extent. And then these start off as very low-density lipoproteins, these big VLDL kind of shipping containers. And when they drop off the triglyceride fat at your fat tissue, the result is this phenomenon of very high LDL in conjunction with what's called high HDL cholesterol and low triglycerides. We don't need to dig into the methodology. You can link people to references on model papers on that. But the long story short is it's being lean, insulin sensitive, and going low carb that shoots the cholesterol through the roof, which is weird. But then what's the implication of that? The implication of that is in understanding the physiology, you can do some weird stuff to, quote, "solve the problem." Do you want to tell them about Oriokisu-shi?

I want to know more.

So, This is a good case endpoint for how to use social media to get a message across. We had done trials including case series, clinical published case series, and interventional trials where we said, look, if this is the model, then the simple thing is, you know, setting aside whether or not this is risky— there's actually reason to believe it might not be as risky as one might think— but in the absence of knowledge, if people want to be conservative and can have carbs, Then if this is the model, adding that carb should just reverse the phenotype. So instead of going on statin therapy, could just eat a sweet potato. And so we've done that and it works. We've seen LDLs drop as much as 480, a drop of 480 in LDL. So 665 to 185 in LDL as a drop just adding like a sweet potato and like a banana per day. So it's effective. Now, fruit lowers cholesterol isn't that sexy. So it wasn't catching headlines. I think this is very important science. So being a very impatient and very motivated young person wanting to get the word out, I thought to myself, how can I beat the drum on this? How could I test this model and do it in a provocative way that'll get the word out? So I designed a trial where I lowered my own cholesterol with Oreo cookies. I locked in my ketogenic diet, which would manifest in this lean mass hyper-responder phenotype. So my LDL was like 400. And then I didn't just go do it. I designed the protocol in consultation with lipidologists, with my primary care physician ordering all the labs. And because I know how to be a scientist, I got an IRB exemption from Harvard to then do the study so I could then publish it. I could have published it anyway, but this is how you dot your i's and cross your t's. There are more levels there, but it actually ended up being a crossover trial. This is how I designed it because I'm like, I'm not just going to do this, I'm going to do it with a control group. So, what you do is you have an intervention that you're going to do on yourself and then you have a washout period to reset and then you have another intervention as a comparison. What's a logical comparison? Statin therapy. First-line therapy for lowering LDL cholesterol. And I went for the gorilla dose of the gorilla statin, rosuvastatin, Crestor, at 20 mg for 6 weeks. So really, like, this is the thing to be like, using pharmacotherapy, if you're going to use one drug that's first line, this is what you're going to hit it with. And I compared it to the Oreos. And I said, I'm going to do this. I announced it before I did it. I did the experiment, and the finding was I could lower my cholesterol, my LDL cholesterol, more than twice as much in one-third of the time by eating Oreo cookies, by adding Oreo cookies in my diet. So taking my diet, locking it in, then adding a sleeve of Oreo cookies per day, and my LDL dropped from 393 to 111 in 16 days. So To be clear, I'm not recommending Oreos as a health food, but this was a metabolic demonstration to say, look, when we understand this physiology, you can get crazy results. They're legitimate. And I under— I, I, I, I— this was premeditated. I know what the headlines are going to run. I know what the thumbnail is going to be. Harvard scientist lowers his cholesterol with Oreo cookies. Harvard scientist proves Oreo cookies outperform statin. Yeah, it's clickbait. It's also true clickbait. And it speaks to genuine physiology, that is important to speak about. Why is it important to speak about? Because this is affecting other people. So, the irony is here, you know, in the weeks and months that followed, I would get emails and contacted by clinicians around the world being like, "Hey, because of your Oreo experiment, I understood this physiology, became aware of it, and I have these patients. So now, we didn't know what to do with them. They were statin intolerant. Now, their LDL is dropped because I'm treating them with sweet potatoes." So, you can see the levels here. Anyway, that was one of my stunts.

So, is it something specific about sweet potatoes or does it have to do with just increasing the carbohydrate amounts?

Just carbohydrates. So, that was the point of the Oreo study. I'm like, "It doesn't matter what carbs you eat for the outcome of cholesterol." I could do this with sweet potatoes, I could do it with bananas, I could do it with honey, I could do it with pure sugar, I could do it with milkshake. I did it with Oreos. Why did I choose Oreos? Because they were literally the most provocative branded agreed-upon unhealthy food that I can possibly imagine. That is why I chose them.

Just making sure, just clarifying for the listener. So, if you are a person who's listening to this—

If you're going to do this, I would say have a bowl of fruit instead. And again, to be clear, most of your listeners are not lean mass hyperresponders. Some might be. So, why should the non-lean mass hyperresponders care? The reason, and this is the drum I beat all the time, is we are all exceptional in some way, shape, or form. And nevertheless, we get handed these boilerplate guidelines that are presented as kind of one-size-fits-all, like fiber is good, fruit is good, eat your 5 a day, meat is bad, yada, yada, yada. All these things have deeper nuances. And by actually questioning and understanding what's going on in yourself as an individual, you can get results beyond your wildest dreams. It's all about presenting, like being curious about yourself and then investigating your own health through an n=1 science approach, which means identify something you want to change. Come up with a hypothesis about what might change it, then implement it and non-judgmentally assess what are your results, and then live your life like that. And when you do that, you can have remarkable transformations, be it dropping your cholesterol, be it dropping, you know, 200 pounds and going from being, you know, depressed to being married in good financial status, 200 pounds down, partying with Arnold Schwarzenegger on Venice Beach. That is a real case of my friend Dave who I met at over 400 pounds. I always bring up him as an example because he's such a great example. No medical background, no science background, engaged in this just n=1 approach. I could see it in his eyes where he's like, "I am motivated and I'm going to take this n=1 science approach to my own life. I'm going to live this life." And literally, he's now dropped way more weight than I weigh as a fully grown man, finished an MBA, gotten married. And you can see him literally with Arnold Schwarzenegger at his house and then on Muscle Beach in Venice. Because it's just such an inspirational story. And it's not because he's a biogenius or has the secret that somebody sold him for $10 million. It's because he said, I'm going to try something, see if it works. Oh, and then I'm going to try the next thing and try the next thing. And I engage in this process. And I genuinely believe— genuinely believe— sorry, my tongue is twisted up now— that is achievable for anyone. I realize it's not the standard, but the question that we as scientists and clinicians need to ask ourselves is how can we make that outlier the average? And I think we can.

Agreed. And you know what's so funny that you say that is my husband has always said, you know, like when we're trying something new that we've never tried before with our children, you know, or even he used to say, we're high school sweethearts, so we have a long history. He just always used to say, ah, it's for science. And I've really taken that on as a clinician. And I like to share it with listeners. I like to share it with our clients too, you know, like give it a try. It's for science. Like, literally do a thing and, like you said, non-judgmentally observe the results. Did you get what it is that you're looking for? And if not, you know, was there some sort of confounding factor? Is there something that you need to go back and change up and try the thing again? Or do you need to scrap the whole thing and try something completely different? Do you need to go back to something that was working and give it another shot? You know, so I love exactly what you're saying. What it does is it's just very empowering for anybody listening to take— it's empowering. Take back your power. Ask these questions. Get curious. Make decisions for yourself regardless of what an influencer is saying, regardless of what— like, even like you were saying, like, there's a medical professional telling you, a Harvard scientist, almost double doctorate, you know, program kind of thing going on here where they're like, that doesn't exist. You must be joking. You're wrong. You know, whatever it is they're telling you, you're like, no, literally, I'm seeing it. So I just love your message of like, Don't be afraid to have some critical thinking. Don't be afraid to just try these things out and prove other people wrong.

That's okay.

It's okay for other people to be wrong and you to be right about you.

One thing I'll say is a word of caution because I'm very careful about not, like, say, doctor bashing, and I know that's none of our intents, is there's a lot of breaches of trust, I feel, or like lack of trust between the general public that I see now in modern medicine. I have a lot of thoughts on that. What I would say is most clinicians I've met really want the best for their patients. But in any given clinician-patient relationship, you need to find the right person that fits for you. It doesn't mean somebody, a doctor is a good doctor or a bad doctor, but if somebody isn't working for you, it's fine to go get another opinion and you deserve to be listened to. So find someone who can respect and listen to your point of view and be a collaborator on this n=1 journey because —people might be asking themselves, "Well, yeah, you talked about Dave, but you, Nick Norwitz, you have scientific background that gives you an unfair advantage." That's true, but you don't have to do this alone. That's the point. So you should be able to do this where you're starting from and then seek support. And I would hope that everybody has a clinician in their life who can be that support.

Absolutely. Absolutely. So that makes me curious then what you were saying about ways of eating, different ways of eating. We've been talking about lean mass, hyper- hyperresponders, this protocol, whatever. You don't know. You don't know if the protocol is going to work for everybody who's a lean mass hyperresponder either. So curiosity from me is, does that mean that keto or low carb— because if you're saying add the carbs back, that changes things for people. So if we're adding carbs back, does that mean that keto, low carb wouldn't be sustainable for somebody who might be meeting criteria for lean mass hyperresponder? Or is there another way to manage it?

Well, what I would say is, you know, any intervention is affecting multiple things. So my role in communicating, you'll find, like, I, I will give you information. I will tell you how to lower your cholesterol if you're a lean mass hyperresponder. That's not a 'you should do this.' It's not actually even me cautioning, cautioning against cholesterol. I'm talking about mechanism. The risk question is another question. We have studies now, well, one published, another on the way, saying, you know, this might not be that high-risk profile. That's not for my— it's not my place as a public communicator and a scientist. That is between you and your doctor to figure out what your risk assessment is. I don't know your medical history. I don't know your family history. I'm just saying, here's the information. It becomes complicated because you can imagine, for me, for example, inflammatory bowel disease keto works. I'll take the high cholesterol. I don't want the bloody diarrhea back, thank you very much. And I'll assess my plaque progression via functional imaging. I'm aware of my own history and I can make my own individual decision. So, it's one variable among many. So, for a lean mass hyper-responder, maybe they have a good reason to be keto. Maybe they don't want to take medications. It's their right to choose whatever they want. It's just about options and then assessing honestly what are the pros and cons. Like, I can't tell you with confidence what the risk profile of this phenotype is. Some people might be more confident than me. I'm not confident it's a high-risk phenotype, but I also can't tell you I know for a fact it's low risk. So, what do you do with that? Well, it depends on what other factors are in your life. If you are just a young, healthy athlete and eating a sweet potato is nothing for you and you're just kind of doing ketosis on a whim, fine. If I were you, I'd probably just eat the freaking sweet potato because I like them. If you're someone with epilepsy or a mental health disorder, say like schizophrenia or depression, and this is therapeutic for you, I would totally understand if you're like, "I'll take the high cholesterol. It's fine." Or, "I'll take the high cholesterol with the medication, whatever." Individual health is really hard and there's not always this— There rarely is a silver bullet. So, you're playing variables off against each other. It's just a fact.

Yeah, I love that so much because I also had similar clients who were like, "Well, you know, the cholesterol, it is what it is. I'll watch it, but my mental health has never been so good and I'm going to stay in ketosis." And I get it, right? Again, I also feel like you don't necessarily need to do all of these tests all the time. Like, even with me, I tried because I knew all the benefits of a ketogenic way of eating and I was already lower carb. I switched to keto and Like, I started to be like, my skin felt greasy. I actually gained weight. I stopped sleeping. It's like, this doesn't make me feel good in my body. And so that's not for me. And that's— so I switched back to eating more carbohydrates and just more whole foods. But that's why I'm saying, like, you have to— there's so many factors, right? Just because a ketogenic way of eating has all these great benefits, If it feels that uncomfortable for you, then don't do it.

Yeah, there's no reason to be tribal about it. It's complicated because I like to just be transparent about my story. And so as soon as you say, "I had a keto transformation," people immediately be like, "Oh, so you must be selling this as your thing." I'm like, "I don't care." My story isn't delegitimized by you having a negative reaction to keto. And I just want you to be happy and I want me to be happy and I want to learn about science. So it's like, It does work for me. If it doesn't work for you, it doesn't offend me. But people get that way, which is the funny thing, especially influencers where they're like, "Keto is terrible." They might have tried it once and they're like, "Do this balanced diet approach," or whatever. I won't put words in an individual's mouth, but like, yeah, there's no reason to be defensive that your way needs to be the way. And if it doesn't work for somebody else, that it's some sort of commentary on you.

It's not. Yes. This is what we love so much because we want to just encourage our listeners to say, like, do what feels good for you, like if that's vegan, if that's keto, if that's carnivore, which we'll get into more later, that we are— and it's keeping you in recovery from your food addiction symptoms, then go you.

Yeah, I'm happy for anybody. Like, if somebody's healthy, I'm happy for them. It does— we'll speak about carnivore. Actually, I'll just— I'll pause on the carnivore. We'll tease that. I know that's going to be in our part 2, so people can listen to that because I have a lot of thoughts on that.

Okay. I have one final thing before we go. Is there any other cholesterol myth that you want to kind of debunk before we move on to episode 2?

Dietary cholesterol, for most people, does not increase your blood cholesterol levels. I would say that. So no reason to avoid eggs. Eggs are a health food. Again, n 1. There's variability here. Some people eat eggs and it does affect their cholesterol. You did the egg thing, too. I did the egg thing. We can even save that. It's probably what I'm most famous for now.— it is insane, hundreds of millions of views cross-platform. I've literally been flown around the world for this egg thing. I ate a bunch of eggs, 720 in the month, and my cholesterol didn't go up. It was again a metabolic demonstration. A paper came out and I think it was Cell Metabolism of this hormone called cholecin that binds to a G-protein coupled receptor. I'm like, this is interesting. Let me do a demonstration of how this works. And then it just went viral. But bottom line, yeah, dietary cholesterol tends not to increase your cholesterol. So, shrimp, shellfish, eggs. You can monitor it, but it won't affect most people unless you're starting from like a vegan baseline, then maybe. But yeah, no reason to fear eggs. I think eggs are a good food if you like them. If you don't like them, don't eat them.

I send that video to every client who comes in with that antiquated thinking of like, "Eggs are, you know, my doctor told me not too many eggs." So just for information's sake, I always think, you know, and then they're like, "Oh, okay." I mean, I eat 3 eggs a day. A day, every day. I'm okay. Anyway, so I am so excited to talk more about, you know, we're going to talk about dairy, we're going to talk about olive oil and carnivore. So we will be back next week with Nick Norwitz again, part 2. Thanks for joining us this week on Food Junkies: Recovery from Food Addiction. Make sure to join our Facebook group, Sugar Free for Life Support Group. I'm sweet enough. Molly and Clarissa are food addiction professionals who offer one-to-one counseling and group coaching through Sweet Sobriety. Please subscribe to our show so you never miss an episode. While you're at it, if you found value in today's episode, we'd appreciate you leaving us a review on your favorite platform. Your feedback helps grow our show and allows us to reach other others who need to hear this message of recovery. Don't forget to pick up a copy of Dr. Tarman's book, Food Junkies. And as Vera always says, the power is ours.