Metabolic Health Experimentation with Nick Norwitz
14 Oct 2024 · 79 min
In this hour‑long interview, host Robert Sykes (ketosavage.com) talks with researcher‑clinician Nick Norwitz about his personal health journey, academic background, and a series of self‑experiments that explore metabolic health on low‑carbohydrate diets. Norwitz describes how ulcerative colitis drove him to adopt a ketogenic diet, which sparked a lifelong curiosity about metabolism. He explains the "lean‑mass hyperresponder" (LMHR) phenotype—lean individuals on keto who experience marked LDL‑C elevations alongside high HDL and low triglycerides—and introduces the lipid‑energy model that predicts LDL changes based on fat‑cell demand and carbohydrate intake. The conversation walks through several n=1 studies: the ORION crossover trial where Oreo cookies lowered LDL more than high‑dose rosuvastatin; a hyper‑caloric over‑feeding experiment with keto bricks that unexpectedly raised LDL; an egg‑consumption experiment (≈1 egg per hour for a month) that showed no cholesterol rise; and a planned bacon‑consumption experiment as a social‑media test. They discuss clinical implications, including the limited relevance of LDL alone, the use of coronary CT angiography and CAC scans to assess plaque, and the need for nuanced patient‑doctor conversations. The dialogue also touches on the tension between anecdotal evidence and scientific literature, the challenges of nutrition communication, and critiques of the "satiety‑per‑calorie" (Societal Calorie) model. Throughout, both speakers emphasize transparency, data‑driven curiosity, and the role of social media in disseminating metabolic research.
Chapters
Well, hello ladies and gents, Robert Sykes, ketosavage.com. Today I've got special guest Nick Norwitz on the line and we dive deep into all the experiments he has been conducting, such as the Oreo cookie experiment, in which case he ate Oreos and hydrostatins and the Oreos outperformed the statins for dropping LDL. We talked quite a bit about the lipid energy model, lean mass hyperresponders, all that good stuff. We talked about his high calorie experiment and what that did to his LDL markers. We talked about the satiety per calorie model and what his thoughts are towards it. And we talked about how he scored a lifetime or a year's supply of eggs, rather, because of his recent egg experiment, which he was pretty much eating the equivalent of one egg every single hour, every single day. So very interesting stuff. I got a lot of respect for Nick. He is an academic. He is a researcher. He is a scientist at heart. He's got a ton of curiosity and that drives all kinds of awesome experiments. A lot of respect for him, a lot of respect for what he's doing and the attention he is bringing to metabolic health and therapies within the ketogenic sphere, the low-carb sphere, the carnivore sphere. So happy to get him on the podcast, happy to dive deeper. Without further ado, sit back, relax, enjoy the conversation with Nick Norwitz. We are live. Nick, how are you, brother?
Great. Happy to be here.
Happy to have you, man. I met you. I don't even know if we actually physically met, but I heard of you, saw you speak on stage at the metabolic health summit back in whatever that was, January or February. And you were— you were just tearing up the stage alongside Dave Feldman with regard to your Oreo cookie study. And since then, we've been in contact and you've just been having one amazing experiment after the other, and I'm all for self-experimentation. So I definitely want to peel the curtain back and dive deep into all of those and some of your findings. But I love a little intro as to who— what even led to the person you are now, as far as you're incredibly witty, incredibly intelligent. You are very polarizing online, which I admire because you do so in a very respectful, tactful way, which is hard to do with social media. So I kind of want to get a little backstory on who you are, man. What got you into the fitness, nutrition, health space to begin with?
Yeah, for sure. Well, thanks for a lovely intro. I mean, I fancy myself first, you know, an academician. My background is undergrad. I studied cell bio and biochem at Dartmouth College. Then I went to Oxford in the UK for my PhD in human metabolism before coming back to the States to do my MD at Harvard, which I'm finishing up in the last months of that. So, you know, along this journey, I've done a lot of conventional training, a lot of normal academics, publishing papers, doing research. But along the way, I got drawn into the metabolic health community, I'll call it that, based on a personal journey with, with ulcerative colitis, where I was in a really dark place at the end of college and beginning of grad school with some severe inflammatory bowel disease. Symptomology, ulcerative colitis symptomology, in palliative care, ICU-level care. I mean, my life really had gone downhill quickly. I had gone from being a competitive athlete and top academician to, you know, being so physically depleted that getting up and walking to the bathroom took the literal effort running marathons used to. And I mentally wasn't there. I socially wasn't there. I was like a shell of the person I was. But, you know, through desperation, you're willing to try some crazy things, quote, crazy. And I found that a ketogenic diet was pretty effective for me at helping me put my colitis into remission and helping me regain my life and putting it back on course, finishing up my, my PhD and then going off to medical school. So a ketogenic diet really changed my life and I'm not someone to, you know, get super evangelical after just an N=1 experience, but it did pique my curiosity enough to get me to engage with more of the literature around metabolic health. And one thing led to another and now we're having this conversation.
And you started doing the ketogenic diets, was it like 7 years ago or something like that?
Um, a little over 5 years ago.
5 years ago. And so at that point, I mean, the keto diet— it's interesting because I've like watched the trends. I've been doing keto for almost 10 years now, and when I started doing it, there wasn't really much literature on— there wasn't really any books or the popularity that surrounds it now. I think it peaked in 2019 according to Google Trends at least, and now carnivore is kind of a subsidiary of that that's taken the limelight. But I always enjoy talking with people that have been doing the ketogenic diet for several years because it's obvious they're in it for the right reasons as opposed to just following the trends. And especially when it comes from a place of their own personal desire or desperation to improve health and well-being in some sort of an— or another. So hearing that makes me respect you all the more.
Yeah, I appreciate it. It's been It's been quite a journey, an eye-opening journey in many ways. I mean, it's funny looking back from where I am now, I realize there are a lot of stereotypes built around keto and carnivore, I guess, as one extreme therein that, you know, you have these caricatures and stereotypes propagated by mainstream points of view, which if I'm being totally honest with myself, given the ecosystem in which I've grown up and the training that I've been exposed to, I would probably hold those negative stereotypes if I didn't have my own, you know, n 1 experience. So it's a funny thing for me because my whole life mission now is to make metabolic health mainstream, including advancing research on ketogenic diets, even carnivore diets for that matter. We've had a couple papers on carnivore diets and potentially some more planned because I do find it metabolically interesting. With physiological plausibility, even though that butts up against, you know, conventional narratives and how to diplomatically walk the line so that I can introduce metabolic health therapy, ketogenic diet therapy, these fringe ideas to the mainstream who I know will be susceptible to them because they're based on, you know, rigorous science and physiology. And we're asking some provocative questions like, there's no reason people should be closed off to these approaches. However, you put them through the social media filter and you end up with these— I've used the word, but I'll use it again— like stereotypes and caricatures that are just really hard to kill and get propagated by the fact that, you know, things like keto bashing are just effective ways to get social media points from the mainstream, be it mainstream calorie-defending influencers. I know we both know a few. Or, you know, legacy media outlets who will tear into these concepts of like, there were recently a couple papers on red meat and diabetes. And it's like, it's a good clickbait title, but then you start to delve into the literature and it's like, you know, I almost am embarrassed to say I'm in the nutrition space. In fact, my parents, when they tell people what I do, they're like, oh, he is in nutrition science. And I'm always like, no, don't tell them that because nutrition science understandably has this like fluffy halo of a fluff science because it is such a— it's a field filled with so much crappy research that to dig through it and find the diamonds in the rough is something that it's intimidating. I understand it's intimidating for the average person to understand what to do. So My mission now is to try to, you know, make learning about metabolism, which I see is like a broader umbrella under which nutrition and diet fall, fun to learn about so people can actually engage with hardcore metabolic science and not just get the platitudes of what I used to think was healthy. And I think what a lot of people still think is healthy.
What was the initial goal like with you taking the academic path that you have before you were plagued with, with the IBS? Like what, what was the, the end goal for going the academic route that you, that you chose? Like, what were you planning to do with that as you went into your career?
I mean, imagine me as like a kid, 5, 6, 7, 8. Like, I was always super, super curious. Like, I'd go out into the yard and there'd be a dead snake with a, you know, lump in its belly. And even at like 5 or 6, I'm like, I need to do a dissection. I'd bring it in and it's like, is it pregnant? Do snakes get pregnant like that? How do snakes get pregnant? Because I've never seen a snake penis. Like, that was thoughts that went through my mind at 5 years old. And then you combine that with being, you know, in a medical household. So both my parents are MD-PhDs. It's like the default. You match up my love of science with living with medical parents. And, you know, when you have parents that are in a certain career field, be it medicine or the military, it's like you just, you take that on as, you know, something to aspire to, something that's noble. And so I have had in my mind my entire life I wanted to be a doctor and I wanted to be a doctor who did science. And the deeper you delve on that path, the more you get a clarified picture of what respectable looks like. You know, the professor who's gone through the, you know, top trainings in terms of college, medical school, residency, fellowship. You get the right grants, you get the right, you know, research partners, publications in the right journals. There's a very clear picture of what to do this the, quote, right way looks like. So that was always the aspiration because I thought it's how I could bring good to the world. And even after I had my, my own health experiences, you know, I had this lofty idea of, well, maybe there's something wrong with Western medicine, but to change the system, you need to work from within the system. And I have these privileges. Training at some of the oldest and most highly regarded by the public institutions, although some of them are doing some not great things for their legacies, maybe. But nevertheless, like things like Oxford and Harvard brands, they carry weight. So I'm in a pretty particular position, but I won't get into the details. But what I've realized is that now, especially in the 2020s, there's a lot more impact you can have directly through a bottom-up grassroots approach than, you know, working from within the— within the mainstream, with, you know, within the system. I can work from without, outside the system, and get people information now, get them enthused about metabolism, metabolic health, and empower them to take control of their own metabolic health journey, even separate from changing the system from within, which is a separate goal and one that It's a difficult thing to communicate because there's just so much wrapped up into it— familial, personal, and academic. But like, the idea now of actually changing the system is— it didn't sound Herculean before, you know, it, it's next to impossible to truly do if you don't have some sort of muscle from another angle. So I have really loved getting into the public space really over the last year or so and finding ways to reach out to people, empower people, teach people, and learn along the way. It's been a lot of fun.
Yeah, no, it's awesome. It's funny because I too came from a family that was, you know, steeped in conventional medicine. My mom has always been in healthcare and she's a nurse practitioner manager, went up the ladder within the hospital setting. My dad's a PhD biologist. And, you know, my, my upbringing at 5 or 6 years old was doing full-blown necropsies on different wildlife he harvested for students at a farm to, you know, see the entire digestive passage, everything. So like, that was what I was subjected to as a kid, which brought with it a ton of curiosity and insight and just perspective. But it is interesting because like their knowledge of nutrition is so predicated on what they went through. I mean, it may in part be from a generational standpoint. Like they didn't grow up with social media. They didn't grow up with people questioning the conventional norms like we are with the advent of social media, the internet, and just the ease of information flow. But it's funny because I started doing ketogenic diet long before they were accepting of it. They kind of discredited it. And then my mom started doing it. She had a ton of benefits that came as a result. My dad's still pretty skeptical, um, but I feel like this anecdotal evidence can't be ignored. And then once enough people have done it, most definitely can't be ignored. So I think bringing or bridging the gap between what you're able to do and how you're able to impact people at scale through social media and just the stories you're able to share is going to make a much more profound impact than one could ever hope to from within the conventional system.
You said some things that definitely resonated with my own background, especially with regards to your parents, because as I mentioned, like, both my parents were very conventionally trained and I think have an idea of science that a lot of people have, which is like, you know, it's about the data, which it is, truly is. But when it comes to personal decision-making, it is really about the stories, right? That's not something that can be discounted. We as humans resonate with stories. So it sounds like your mom really responded to your story. And actually the same with my mom. She's now keto and she adopted the ketogenic diet after me because, you know, she saw how well it worked for me and she's reaped her own benefits, although they're distinct. So it really is the stories that change people's minds. And, you know, that's something that if you were to talk to me 3 years ago, I would have discounted a little bit. I think the idea of anecdotes has a— well, I know the term anecdotes has negative connotation. But when we think about just raw data, like, that doesn't— or just datasets, p-values, statistics, whatever, it doesn't resonate with people the same way that stories do. And so I think what you need to do when you're telling or you're teaching science, talking about data, is you need to find a way to tell a story around the data. Anybody who's ever written a paper and gotten it published even knows this. Like, you need to tell a story around the data. Now, that's a tricky thing because, of course, in telling the story around the data, you're always going to introduce biases, you know, your interpretations based on your framing. That's the nature of things. So I think, practically speaking, we just need to acknowledge that science, while the scientific method itself is you know, cold and direct and emotionless. The body of science that results is a function of humans telling stories about what the data are showing.
Yeah. Um, and humans are so—
it's not bad. It's something we need to acknowledge in order to deal with the practicalities that arise, including the narratives that get propagated around things like nutrition.
Yeah, 100%. And nutrition is tricky, man, because humans are so— we're so— we're so fickle.
Like, we—
with any other animal, there's no debate as to what you know, types of foods they should consume. But there's such a, you know, societal standpoint, such an emotional standpoint tied with food and human consumption that is very triggering for people for whatever reason. And it— like, I'm trying to bridge the gap, as I know you are as well, because I, you know, having been brought up in the scientific community, I do place a lot of emphasis on quality data, but I'm also trying to take stock in the anecdotal evidence and what is sustainable and what is optimal from a health and well-being and vitality standpoint. And oftentimes those don't sync up. So I'll bring people on the podcast like the Layne Nortons of the world, as I respect their opinion, their viewpoints, and some of the value they bring to the table, but not at the complete exclusion of this anecdotal evidence. And I feel like there has to be a way to mesh that together as as it pertains to human consumption because we aren't lab rats in a controlled feeding study. We have all these other variables at play and we have to be realistic.
Yeah, I think we can talk through now a framework of kind of how to do that, reconcile the anecdotes with the data. And part of that is just considering what data we have and what data we don't. So for example, there are interventions that have clearly worked for people, or let's say people report that they clearly work for people. People. I'll use myself as an example. There's no doubt in my mind a ketogenic diet was highly effective for putting my disease into remission. That is my story. It's the narrative I tell myself, but it's also backed with my medical history. I suffered and I suffered and nothing was working. I tried a bunch of different diets, nothing worked. Then I tried this and it worked. It improved my symptoms. My inflammatory markers went down, and on biopsy there was no disease. So that's my narrative. But if you look at the literature, Can I say that there are human randomized trials showing that my intervention works for my use case, a ketogenic diet for inflammatory bowel disease? The answer is no. It doesn't mean it doesn't work. It just means we haven't properly asked the questions and investigated it. So I think sometimes people confuse absence of evidence with evidence of absence and say this isn't true because we don't have data to say it's true when it's never really been investigated. And on top of that, there are questions we just can't ask with certain forms of investigation, say the human randomized controlled trial, which is something that I think a lot of people point to as the, quote, gold standard, right? But not all investigations lend themselves to human RCTs. So we really just have to cobble together the data we have access to, be that human RCTs and Cochrane reviews or just biological plausibility. In animal studies, and then I think use those to frame the stories we, we are hearing and we are telling each other. And if anecdotes are arising that cut against the data where there are conflict, I think then it's appropriate to ask, are there other things contributing to this story where, you know, the biological reality could be divergent from the narrative that the person is telling themselves? Or is there something new and unique to learn here? And at the end of the day, I think we can have evolved discussions about what the published literature say while also acknowledging and celebrating individuals and their own healthcare journeys. I mean, like, personally, one of the reasons I love metabolic health is the proof is in the pudding. Your biomarkers, how you're doing in terms of your health, like, if you're doing great, I do not give a crap how you got there. I don't care if it was carnivore, I don't care if it was vegan, I don't care if it was eating McDonald's patties and Wendy's Frosties. I think Wendy's makes Frosties, one of those ice cream milkshake things. Point being, I mean, I think that's unlikely, but if you are doing well, that's all that really matters. And all we can do is look at the literature and kind of inform best practices and come up with ideas about how to get people there. And it's a fun academic exercise, but for the individual, at the end of the day, all that matters is their story, their n 1.
Yeah, I completely agree. And I feel like as more time passes, we'll have more solid data to lean on. And I feel like there's so much that is left, there's so much lacking in that department, especially as it pertains to performance athletes. I mean, I never— I didn't get into keto because of some ailment or disease or anything like that. I came to it honestly because I had a negative relationship with food, eating high carbohydrate diets. But I love the sport of bodybuilding. Which is what led to the high carbohydrate diet. So I wanted to find a way to compete at a competitive level in the complete absence of carbs. And I got a ton of negative pushback there. And everybody was just suggesting that that was not even feasible in the context of a ketogenic diet. So I was— I love, as you do, proving people wrong. So that's what I set out to do. And lo and behold, it worked beautifully. And I've kind of staked my, you know, flag in the ground and that's the hill that I'm dying on that performance not can only maintain, but honestly outperform those with carbohydrate-dependent approach, especially in the long-term play. 'Cause you're looking at people now that are taking in performance-enhancing drugs, obviously that's a whole nother world in and of itself. But you see all these athletes that just really start to dwindle as time goes on. I'm excited to see what I'm performing like when I'm 73 years old following this way of eating., you know, indefinitely until then.
No, no, no, your, your journey is amazing. And actually, I, I need to ask, and other people have asked me to ask, um, one thing I really like about you is, um, you, you post pictures very like authentically and transparently, both in like the extreme cutting and bulking phases, um, which if people look at your socials, like there's a huge discrepancy there. Yeah. The, the reason I like that is one, anybody who's been like a physique athlete or even recreationally understands that like, you know, those optimal or, you know, based on societal standards, optimal male physique photos are a function of like pristine timing, hydration status, lighting, all these things. And it's phasic. So first I want to applaud you for, you know, posting at both sides of the spectrum, but also just ask out of my own curiosity, what is the time lag between, say, like if you post a bulking photo and then your most cut photo, is that like months apart, weeks apart? Is that a function of actual body fat loss or hydration status? Like what does the transition from like that bulk photo to that cut photo really look like?
Yeah, great question. So I honestly do not cut water like a lot of competitors do. I think that's one of the beauties of following a ketogenic prep protocol is I don't have to dehydrate. Um, so I'm fully hydrated in both an off-season photo and a competition photo. So that's not a variable at play there. As far as the time, my last prep was 33 weeks. I probably looked my best at 27 weeks, which is when I earned the pro card on my third of 5 shows this past season. Um, so 27 weeks from peak bulk to peak cut. I could have done it faster, but by going more slowly, I preserved more lean tissue and overall health and well-being. So that's about 27 weeks roughly.
Yeah. Do you ever get your lipids tested when you're at, um, a cut versus bulk?
Yeah, I get all my markers tested. Um, I do that usually about every 3 months as I'm going through a building phase, a peak cut, and then back to reverse dieting and finding that, you know, slight surplus to operate at for extended periods of time. So I'm getting my lipids tested through, I'm getting my hormones tested through all. Now when you take, like, naturally, when you get that lean, testosterone, for instance, is, is very correlated to overall body fat levels. So when you drop below 5% body fat as a male, your testosterone plummets. I mean, I think at my leanest of 3.9%, my testosterone was like 89 or something crazy scary low. Now that's obviously not healthy or optimal. So as I put on a healthy amount of body fat in the building phase, that returns to a healthy normal baseline. But yeah, all these— I try to be very transparent with both the build and the cut because I don't want to glorify just the cut because being that lean for that long is not healthy.
No. And I think it really affects young men. Like, I'm really— I'm 28. Romy, how old are you?
Uh, 32. I'll be 33 next month.
Right. So we're like, we're both on the younger end where we, I mean, maybe just missed the access of social media to like, you know, preteens. Mm-hmm. I just think about how it would've affected my psyche when I was going through like puberty and like the 5th and 6th grade. I hit puberty a little bit early to have access to what kids have access to now. I mean, people talk a lot about societal standards for women, but I think, you know, there's an effect on men too. So I think transparency around that, especially if people use like— there are some, you know, people, especially people like actors, they're prepping for a role, be like Chris Hemsworth for Thor or something like that, clearly use PEDs. I think that's fine. It's part of the journey. He's preparing for his job. You're preparing for your sport. I don't know if you use anything, but there just doesn't seem to be a lot of transparency in discussion about like what a natural male physique is or what actually feels good because people see you at that level or like I've been super lean. I don't know if I've ever on Dexa at least been 3.9%, but like I also know that at my leanest I feel like shit.
Yeah.
And usually I'm there incidentally, not necessarily like willingly for various reasons. And discussion around that I just think is valuable. But that was sidetracked from the question I wanted to ask about the labs. Lean versus bulk. What do your lipids look like, if I may ask? I would assume your LDL jumps when you're cutting and drops when you're bulking. Is that accurate?
What was that last part?
You assume your LDL cholesterol— I mean, I mean, we'll probably talk a little bit about cholesterol. You know, a lot of my research around lean mass hyperresponders, I never asked you about your lipids. Yeah, I mean, I should jump when you're cutting.
Uh, actually, there's like a— it's like a weird, um, bell curve. So like when I am in peak bulk and I'm really trying to be aggressive with the surplus, it is higher. And then when I'm in a, you know, deficit— it's basically on the extremes. So like as I'm dieting down, LDL drops typically. But you know, when I'm at that, you know, peaking moment, it can be all over the place, man. It's very highly dependent upon what I'm eating then as well, because like I'll have refeed meals in at that point which are predominantly higher in fat. So it just depends on when I get the labs drawn based off of where I'm at in the prep cycle. But my, my standard lipid panels are typically around— shooting from memory here— like my trigs will get around 30 or 40, HDL is like 120, I believe. LDL is typically between 120 and 200, give or take.
Okay, so you can approach— sounds like lean mass hyper-responder physiology. Yeah, especially with the HDL that high. I mean, do you remember what it was on a mixed diet? I assume it was much lower.
Yeah, the HDL was much lower. I didn't get labs drawn that frequently when I was on a mixed diet. I mean, it was a long time ago when I was eating carbohydrates, um, but this is honestly the best my lipids have been, um, honestly the best all of my markers have been since doing a ketogenic diet. I think it gets better the longer you're doing it. I'm kind of Like, a lot of people talk about metabolic flexibility and cycling carbs in, but I've kind of fallen to the belief that your body is very adaptable. It's going to make the most of whatever you give it. And if you're staying strictly ketogenic, your body's metabolic pathways upregulate to optimize around fat metabolism. And if you do that for long enough, everything improves for that function. So I have no plans to deviate because my health has never been better.
Awesome, awesome, awesome.
So 100%, man. Um, I've got like a million different, uh, questions upon the different experiments you've done because you've done so many of them I've lost track of them all. But my introduction to you, like I said in the beginning, was that Oreo cookie versus statin study. But since then you've also— I mean, you sent me a post on Instagram the other day about you getting a year's supply of eggs, so we could talk about that. Uh, you also made a post that I saw about the satiety per calorie model, which I've, I've got some thoughts on as well. Okay. Whatever you want to talk about, man. Like, I want the floor to be yours because I want to talk about whatever is exciting you at the moment and where you think you want to take the conversation. Sure.
I mean, Oreo versus statins is always a fun thing to start with and we can roll from there. But so this was a project I did. A lot of people listening probably already know about it, so I'll go through it quickly. But I wanted to bring attention, the purpose was to bring attention to a lot of work we've been doing. We have now 10 published papers on this lean mass hyper-responder phenotype, which is, to cut the jargon, when lean people tend to go low-carb, they tend to see these increases in LDL cholesterol, which some people call the bad cholesterol, along with increases in HDL cholesterol and low triglycerides, which is a pattern that appears in, and sounds like in you as well, especially when you're lean, the high LDL, the high HDL, and the low triglycerides. This is really important to study because ketogenic diets are gaining popularity for a whole host of conditions, inflammatory conditions, mental health conditions, neurological disorders. But when it comes to clinical medicine, a major sticking point and obstacle remains cholesterol, where some people will see increases in LDL. And that scares patients, it scares doctors because of what we've been told around LDL cholesterol and markers like ApoB for those those who are a little bit more cholesterol-versed. Mm-hmm. So it's become important for my colleagues and I to kind of figure out why lean people see the increases in LDL when they go low-carb. And indeed it does appear particularly in lean people. So we, for example, did one meta-analysis of human randomized controlled trials. This was led by my friend Adrian and published in the American Journal of Clinical Nutrition. And what we found was an inverse association between LDL and BMI such that when people went low carb, the leaner you were, the higher your BMI went. Sorry, the leaner you were, the higher your LDL went. Lean, low BMI. The leaner you were, the higher your LDL went. And actually, if you broke up and did meta-analyses by each of the BMI categories, only lean people with BMIs below 25, only that group saw increases in LDL. Who had overweight or obesity, those groups did not see increases. Class 2 obesity actually saw decreases. So, this is starting to explain a source of heterogeneity in the data where it's like, okay, this is interesting. For the people that have the big jumps in LDL, it doesn't appear to be things like even genetics or saturated fat as much as it is being lean. And that's odd. So, we have a model to explain why that is. It's called a lipid energy model. We can get into the nitty-gritty around it, but the lipid energy model makes certain predictions.. And one of the most rudimentary predictions of our model is, um, because it appears that when lean people go low carb, they really shift over to fat burning well. And the fat, um, trafficking system depends on these particles. LDL goes up, but if you reintroduce carbs, then you remove the need for this lipid energy model flywheel to spin and the phenotype reverts. Another way to say that is add back carbs, LDL goes down. If you're a lean mass hyper-responder, mm-hmm, this is interesting physiology, but I wanted to get people to engage with it who might not otherwise have been aware of it. And so I kind of had to envision what was the most provocative way I could demonstrate a principle of this model. And one way to do that would be to lower my LDL with an unhealthy food. An unhealthy food with carbs. And I chose Oreo cookies because simply I could not come up with a better branded unhealthy food that everybody would know. And I predicted that it would lower my cholesterol, my LDL cholesterol. And because I know how to dot my i's and cross my t's as a researcher, I did it as a rigorous crossover trial, which means I did the Oreo intervention, but I also had a washout period where I reverted and got back to my like you know, set point for cholesterol when I'm on keto. And then I tried a statin, a high-dose, high-intensity statin, which was 20 milligrams of rosuvastatin, which is Crestor, for 6 weeks. And the experiment was, let's see what does better at lowering my cholesterol, Oreo cookies or standard of care high-dose statin therapy. I went to Harvard's Institutional Review Board, Their IRB got an exemption. I collaborated with lipidologists and cardiologists and my primary care provider who was ordering all my labs. And the results were that the Oreo cookies, the Oreo cookie intervention, which was a pure addition, I was not reducing my fat. In fact, since Oreos have fat and saturated fat, I was actually increasing my fat, but I was adding in carbs. And what happened was the Oreos reduced my LDL by 71%., which is dramatic, more than you could expect from any medication. And the statins reduced my LDL by 32.5% over actually 3 times longer a time period. So in the end, the Oreos were twice as potent at dropping my LDL as the statin in 1/3 the time, which was a metabolic demonstration that was effective in its purpose, getting people to have discussions with us about the broader literature around lean mass hyperresponders.
I'm assuming the pharma companies were probably not ecstatic about this study.
I mean, they didn't reply. I, I think it made waves. It did not make waves so big that Pfizer is coming after me.
Yeah.
Um, so no, I have not gotten any emails from Pfizer or anything. I mean, I'm humble in what this is. I mean, it was an n=1. It's not going to change guidelines or anything, and they know that.
Yeah.
But, uh, it did stimulate conversation, got word of our work out there, helped us build more collaborations and gain more resources to future studies that are underway.
Out of curiosity, what were some or any— were there any symptoms that you had while you were doing the high-dose statin?
Yeah, I had— I mean, myalgias are very common, so like muscle pains and cramps in my lower legs. This was a high dose. Generally, people would not start on 20mg of Crestor. It's pretty high. And that occurred with some increase in my CPK. So a marker of muscle damage. So there might have been a little bit of cramps and, you know, increase in this marker of muscle damage. It wasn't very high. It was low enough that actually we noticed this early on in the study. And I talked to a lipidologist colleague. He's like, look, this is uncomfortable, but actually had a patient on this. I don't know that I keep them on it for life at these levels, but it was safe. Like, it wasn't at risk of going into rhabdomyolysis or anything like that. But I had some, I had some muscle pains. It was pretty moderate. Quite honestly, the Oreos had worse side effects. Like, my stomach was just not happy with me. Yeah, but Yeah, you know, I think to kind of put this in a clinical context, if this were to happen, a patient were to start on this high dose of statin therapy and have these symptoms, what will probably happen is their clinician would just decrease the dose, um, because you can get most of the effect for LDL lowering for a statin at lower doses. I just started with a high dose because I wanted the highest intensity protocol I possibly could have because I'm a hardo like you.
Totally. So a lot of people, like, speaking from a layperson standpoint, they're concerned about going keto for fear of what the mainstream media has inundated them with over the years as to, you know, high fat clogging their arteries, the need for a statin. They'll oftentimes notice an increase in LDL or cholesterol, total cholesterol, you know, early on, and then they'll go to a doctor, primary care, and they'll automatically always push them towards a statin. So this study just basically forces them to question the rationale behind all of this.
You know, I, I don't put in the ORION study any value on LDL or statins. Like, that is not the place of this study. Inevitably, people are going to try to tie that in. And the reason I think they do so is because what inevitably is, is, or what's being presented here is an inevitable an unavoidable tension where we have what we all agree, pretty much all agree, is an unhealthy intervention. Adding Oreo cookies onto your standard diet is not a healthy thing. I don't think anybody, anybody believes it is. But my LDL cholesterol went down, which a lot of people would presume to be a good thing. So very, very simply, you have a bad intervention and a good outcome, and that creates a paradox, a tension, a cognitive dissonance. That a lot of people are uncomfortable sitting with. And that's not to put any value on statins or any value on LDL. That's just to say, here's something curious. And if it's curious to you and appears paradoxical to you, that means there's something you or we don't understand. And I want people to sit with that curiosity, get inquisitive, and then go down the rabbit hole of our literature and start asking the right questions. To speak quickly on, you know, that, that patient scenario, the doctor-patient scenario, patient goes keto and their LDL goes up and it's all scary. What I would say is reassuringly, we now have multiple studies showing that if somebody is using a ketogenic diet for like type 2 diabetes, obesity, or overweight, they will tend not to see increases in LDL and actually tend to see improvements in overall cardiovascular risk markers, including markers like triglycerides and HDL and LDL. And ApoB. Sometimes there are transient blips up in LDL, but typically the LDL particle count and the ApoB will actually go down, and risk will overall be reduced in people who are starting from a place of metabolic dysfunction with overweight or obesity, which is actually most people, which is also probably why in general, if you look at all the studies, you don't see increases in LDL on keto diets because most people have overweight or obesity. But you do have this subset who are basically lean and metabolically healthy who see the increases. Now, these people can be adopting ketogenic diets for a variety of reasons. Focusing on those who are using them for medical purposes, ketogenic diet for medical purposes, it could be mental health conditions, neurological conditions, autoimmune or inflammatory disorders. And that does create a rock and a hard place scenario. If the LDL was up very high, like to 300, 400, 500, which we definitely see, but the ketogenic diet therapeutic for that person. At that point, they have to have a discussion with their doctor about what is their risk. And that is a question we are openly investigating because the fact of the matter is we don't know. And anybody who tells you we do know is lying through their teeth or speaking beyond the literature because this phenomenon, this phenotype is unlike anything we've ever seen before. So while you can say the, quote, preponderance of evidence, the body of literature existing suggests that LDL particles and ApoB have a causal role in cardiovascular disease, when you have an entirely new population with a new physiologic driver of this biomarker, they need to be studied uniquely in order to understand the absolute risk associated with this profile. So we're doing that at the present time We have preliminary evidence, some of which has been published, some of which we're still writing up. It looks very reassuring that this does not appear to be a population in which there's any rapid progression of plaque. It doesn't mean there's zero risk associated with the profile, but the data we have thus far have been reassuring. We can caveat them, we can say they're preliminary, but the fact of the matter is right now we're the only— well, I have a few teams, but our teams are the only ones that are actually investigating this question on this population. So you can call the evidence preliminary, but it's all we have at this point in time.
Yeah, I had, had Feldman on a couple months back, I guess after part 1 had been published but not part 2. And what, what was the average LDL reading from the participants in, in that study?
I mean, it was around 200 or 300, right? Yeah, the mean LDL was 272, um, milligrams per deciliter for the lean mass hyperresponders. 272 is very, very high compared to a matched control which had an LDL of 123. So the difference is 149 milligrams per deciliter between the groups. And the keto group have been keto for our average of 4.7 years. And we did not see any increase in plaque in the keto group as measured by coronary CT angiography. So high-resolution scans looks beyond just calcified plaque, including non-calcified plaque.. And we didn't see any increase in plaque. In fact, the lean mass hyperresponder group was trending towards lower increase, not significant, but trending towards, sorry, not lower increase, lower plaque levels than the matched control. And there was also no association between LDL and plaque amount in the lean mass hyperresponders. We've actually now had more data. We've also looked at correlations between ApoB, LDL particle count, even small dense LDL particle count. And none of these things appear to predict the amount of plaque in lean mass hyperresponders for reasons we are working to explain. And now we're working on writing up the prospective data, so where we actually monitor the individuals with multiple scans over the course of time to see what is the progression in lean mass hyperresponders of plaque and if it has any association with ApoB or if other things like preexisting plaque might be better predictors of plaque progression. So I can't pull the curtain back on the data quite yet as it's not published, but they're going to be provocative findings that turn a lot of heads. Actually, after this Zoom meeting, I'm getting on a call with Dave and Professor Adrian Sotomayor to discuss some of our preliminary analyses on this paper we're wrapping up in the meantime. You know, it's a, it's a cool space to watch. And I want to emphasize, I absolutely want people to be cautious and have open-minded discussions with their physicians, contemplate the potential pros and cons of various interventions, the risks involved, the risks involved with respect to maintaining high ApoB levels, even in lean mass hyperresponders, the risks of various interventions, and that includes trying your best to weigh the unknowns in these equations, because there are a lot of unknowns. For example, you know, we don't know what the effect of the lean mass hyper-responder phenotype is over 20 years because we just don't have those data. But correspondingly, we don't have great data on the long-term risks associated with, say, taking a PCSK9 inhibitor, which is one LDL-lowering drug. And we can talk about data there that I mean, are concerning enough that I am not on one of these medications. So it's like the art of medicine has to do with trying to make the best decision you can given an individual context, given what you know, acknowledging that there is a lot of unknowns, and it is a matter of best guesses and updating your individual choice at any one point in time. So I don't think there's a right and wrong answer. And all we're trying to do here is advance the science and have open-minded discussions and speak in a nuanced manner as best we can about the data as it's evolving so people can make their own informed choices.
Yeah, and I think the more data we have, the better we'll be able to put their minds at ease. But I mean, the, the common story I see unfold is that people will adopt ketogenic diet, they'll, you know, depending on how frequently they've checked their lipid panels in the past, they may be slightly alarmed by what their LDL is showing, but then they'll almost unanimously say they feel exponentially better. They've got more enhanced cognition. They don't have any GI distress. And to me, like, as not a scientist, that just— I mean, like, I, I like to let people lean into how they feel, like truly be observant in what their body's biofeedback is telling them. And if they are empowered enough to do so and they notice, you know, benefits across the board— better sleep quality, better performance, better recovery— Like that tells me all I need to know.
Yeah, I, I get that. I also get that people are going to make decisions with their gut and a lot of people have that mindset. I will caution that you do not feel progression of cardiovascular disease. It's not something that you can like, you know, just intuit in your gut. And, you know, the first sign could be a fatal heart attack. That's very possible. I just want to put that out there because I do not want to discount the fact that even if you feel great, there could be long-term consequences to a particular lifestyle pattern.
Yeah, I totally agree with that.
It's something to be cognizant of.
Yeah, 100%. And I'm a big advocate for collecting as much hard data as possible, which is why I do like, you know, 3-monthly— like I do the lipid test and the hormone test every 3 months when I'm going through my own self-experiments because I want to know the numbers. I want to be able to be objective with that data. But I want people to also, you know, be able to listen to their body because so many people seem to have failed to do that simple task, which is important.
A nice thing I'll just add is you're talking about collecting data, like you can collect functional data on yourself. So like you don't need— okay, we're trying to figure out at a population level the risk associated with lean mass hyperresponders, right? That is still going to be a population average. When it comes to you, What you should really care about is, is there plaque in your arteries? And you can get scans to look. Mm-hmm. So you can go get a coronary CT angiography and see, is there plaque? And if there is, I will be concerned. If there's not, I will be less concerned, especially if you've had high levels for a long period of time. I'll, um, use my mom as an example. She's given me permission to, to talk about her case in broad strokes. But, um, she, for example, Unlike me at baseline, her LDL is pretty high. I think it's always been above 160 and she's about to turn 60. So that exposure alone is pretty high exposure. But on top of that, she will manifest lean mass hyper-responder physiology when she goes low carb. She's very petite, probably about 105, 110 pounds, and her LDL will jump to close to 400. So she has had this massive exposure lifelong to LDL. And people tend to say, you know, it's about milligrams per deciliter a year exposure and LDL and ApoE. She's had this enormous exposure.. And it goes up when she's keto, which she's been now for several years. So we've had a lot of discussions. I mean, the last thing I want to do is gamble my mom's health. I'm like, what she should do, whether she should take a statin or ezetimibe or other medication, she should go off keto or low carb. In the end, we got her some scans, including a CIMT and a coronary CT angiography. And lo and behold, her total plaque score was a flat zero. Now, I'm not going to say that's going to generalize to all 60-year-old women on ketogenic diets, but for my mother, it does not appear she has any plaque, given— even given and despite very high LDL for a very long time, which is sufficient for her. This is her decision. She's medically informed. I'm not pulling the wool over her eyes. She's an MD to say she doesn't want to take a medication at this time because It's not clear that there would be any benefit. She's had a big exposure, she hasn't had any plaque accumulate that's measurable, so like why would she take therapy? Again, just going through an n=1 thought process and the kind of thing you can do for yourself, if you measure your plaque, I mean CAC for calcium score is a little bit more rudimentary but still pretty decent, and there isn't any plaque, like that should be reassuring. And the data shows that's reassuring even in people with familial hypercholesterolemia. You know, if a CAC score is zero, that is better at predicting, you know, future events than an ApoB or an LDL. So you can get a scan on yourself is the point. You don't have to guess about the plaque in your artery. You can go get it measured.
And the cost of a CAC scan nowadays is, it's like less than $300 in most places, right?
Oh, it's cheap. Yeah, you can get it cheap. And I mean, insurance should cover it if you have you know, hypercholesterolemia, which if you're a lean mass hyperresponder, you will. Yeah. And also a coronary CT angiography could be covered by insurance. It was for me and I'm in my 20s.
Yeah.
So, you know, these are scans you can talk with your doctor and they should be tools you use to inform your decision. So I'll use myself again as an example. I got a coronary CT angiography years after I've been keto. With the stipulation that if there was plaque, I'd go on pharmacotherapy. I told my doctor, look, I want you to order this, and I'm telling you before the results come in that I'll take medications if I have a positive finding. Yes, I'm young, but my levels are exceptionally higher. They had been exceptionally high such that my overall exposure was above 5,000 milligrams per deciliter years. So it was plausible though there could have been plaque. Turns out there wasn't. I will continue to update my decisions as I collect more data on myself. But like you, I am very attuned to my own data, always getting lipid tests, and will follow up with further functional measures as I see fit. And then just update my decision. I'm not closed off to things like medication. It just, for me, it doesn't make sense. That's my—
As far as experiments go, I don't know the context of what all you were trying to decide or discover with the calorie experiment that you were doing. I know you were eating a ton of keto bricks and a ton of macadamia butter. Oh yeah. But what was the— What was the objective of that experiment?
So first of all, thank you for the Keto Bricks. They are incredibly delicious and they were what made this experiment feasible because for people who don't know me, I'm a pretty petite guy. BMI around like 21 at about 5'7", 5'8". So eating, I was eating like well over 6,000 calories a day is very, not very easy. Made possible by Keto Bricks, but The purpose of the experiment was actually to drop my LDL. So other people, including for example Siobhan Huggins, have been able to drop their LDL by just going, quote, hypercaloric, even while keto, which is another— I love my n=1s, right? Another way to demonstrate principles of lipid energy model and associated principles. So basically the idea, high level, is if you acutely gain a lot of fat, which if you eat crazy amount in a short period of time, you should still be able to gain a decent amount of body fat or your fat cells should grow. Then the, there are a few things that happen. One, your insulin will go up even if you're eating keto and that will help with fat storage. And also the expansion of the fat cells themselves acting as storage depots will have a structural demand, at least this is the thought. So they will have a structural demand for LDL particles, ApoB particles, and that will drop your ApoB. So For example, Siobhan has shown that when she went hypercaloric, I think it was, I think she did a 5-day protocol where part of the day she was eating 4,000 calories, then she went up to 6,000 and she was eating like tons of heavy cream. I think that was her main source of calories. Her LDL plummeted more than it ever had. I forget how much you can look up LDL drop experiment, Siobhan Huggins, if you want the detailed numbers, but she dropped hers well over, I think it was over 150 milligrams. Per deciliter with cream. And I wanted to replicate that. Other people have actually, over 20 other people have shown that if they go low carb, but they go like crazy high calorie for a short period of time, even eating tons of saturated fat, their LDL will go down for the reasons I explained. So I wanted to replicate that. I'd never done it. So that was the purpose of the experiment. The interesting thing was I was entirely wrong with that experiment. What ended up happening is my LDL didn't change much. It actually went up a tiny bit, which was fascinating to me because that was an n 1 that contradicted the findings of 20 other people. And what was even more fascinating is to think about why the results were what they were in my circumstance. And so I was measuring a lot of things along the way, and what happened in me quite uniquely is my body temperature when I was feeding at this level went up quite a bit. My heart rate jumped a lot. I graphed this out. You can see it in the video. And, you know, my subjective NEAT, non-exercise activity thermogenesis, went up a lot. So I was bouncing all around and actually didn't end up gaining much weight at all. And so the way I explained the results and the LDL not changing or even going up, which are totally consistent with our model, is Some people are hard gainers, some people are easy gainers. I'm a hard gainer, and when I overfeed— and this has been shown in the literature, different people have different responses to overfeeding— my body just wants to burn that energy off. So it increases my body temperature, it increases my heart rate, I'm bouncing around all the time. And as a result, my fat cells didn't end up growing that much, so there wasn't a structural demand. And in addition to that, my energy demands went up. And what happens when you're lean and low-carb and your energy demand goes up? All things being equal, the lipid energy model has to spin a little bit faster to get you the energy you need, and that predicts an increase in LDL, which is exactly what happened. So, it was a really cool experiment for me because it was one where I was— I'm not feigning humility here, I was actually wrong. But in being wrong, the results still perfectly fit the model. And not only that, but the model explained an idiosyncratic individual response in me while also explaining results in other people. So it was an individualized application of the model, which was really cool. People can see the video if that's going over their head. But, um, that was that experiment. And it was one of those moments where, yeah, did not turn out as I expected. And so I needed to look back at the data and explain or evolve the model and reinterpret, you know, the data and see what we could learn together. So I love my ankles one, and that was a fun one.
No, that's super interesting. So are you familiar with Brad Marshall?
He's the, fire in a bottle.
Yeah. Yeah. So I don't— I mean, this is definitely his wheelhouse and not mine, but he is hypothesized that the stearic acid is going to make the actual adipocyte themselves more insulin resistant. And with you consuming such a high percentage of your calories from Keto Bricks, which are primarily cacao butter, the highest source of stearic acid, I wonder if that could have been a reason as to why you didn't have any growth in the fat cells themselves.
I don't think the stearic acid was qu— I mean, I was eating other things. I was eating a ton of macadamia butter and macadamia oil, which is mostly monounsaturated fat. You know, I could replicate this with other fat sources to see if it would have a similar response. I have looked at some of Brad Marshall's stuff. I'm not so sold myself on that model. So I don't know if I have any further commentary.
I do not know. Like that, like I said, that's not my wheelhouse by any means, but I am curious to see how the different types of fats impact fat cells. So I'd be curious to learn more on that as well.
Yeah, I think a lot of those things might be a function of more chronic effects. This was a short-term study. Um, and so for things like, you know, saturated versus unsaturated, or let's even get more granular, different types of fatty acids in the diet, be it linoleic acid or stearic acid or omega-3s, omega-7s, in order to, I think, affect physiology long-term, it requires a more chronic timescale. Yeah, that would be my high-level suggestion.
Yeah, no, I agree. I agree. What about satiety per calorie? You wanna dabble into that conversation?
We, we can. I'm, I'm going to try to refrain. So there have been some, let's say, strong words exchanged between me and the proponents of Society vs. Calorie. I'm going to try to keep that in check because I think, let's say, we've both been aggressive towards each other. I definitely think I'm in the right. I'm sure they think they're in the right. But we can keep this high level and discuss it at an academic and intellectual perspective. I will start by letting you give your two cents.
I, I've had both on the podcast. Uh, you know, Ted Naiman obviously is a proponent of his PE formula, which a lot of the satiety per calorie is based on. And a lot of that is honestly very similar to what I started doing with my traditional bodybuilding, you know, dietary protocol. I mean, very high fiber, higher protein, relatively lower fat model. And from just my anecdotal experience, I did not experience more satiety with that. What I've noticed is that when I have higher— like, if calories are equated for them and I'm following a ketogenic approach with higher fat, moderate protein, very minimal carbohydrate, versus a calorie-equated model with higher fiber, higher protein, lower fat, lower carbs, I experience much more satiety with the ketogenic approach. Even with calories equated, I'll have fewer meals, I'll have less feeding frequency. Some of that may be psychological, some that may be cephalic phase of insulin response, not sure. But what I've noticed and what I've theorized is that if I'm consuming less fiber, that's not going to hinder absorption of the nutrition that I am consuming, especially in the context of a caloric deficit, as I'm in when I'm in a prep.. And if I consume fewer meal frequencies with really high quality, highly bioavailable food, that seems to be the most satiating form of consumption for me. And I've been able to replicate that amongst my clientele. So that is in stark contrast to the satiety per calorie model, but that's just been my personal experience.
Yeah. Um, what I'll say is first and foremost, As I said earlier, I'm for whatever tools and heuristics people want to use that serve them. That's fine. And I think the levers of the Societal Calorie Model, which are things like hedonic factor, a little pseudoscientific there, but you know, how much a food gives you pleasure, the hedonic factor, the percent protein and the fiber content, each can be like, you know, levers people can reflect on and, you know, toggle as they see fit and as is useful for them. That's fine. It's similar to— you mentioned Ted Neiman's PE model. PE is not a scientific model. It's just a ratio. But if it's a ratio that helps people make more intelligent choices for themselves, I'm totally cool with that. And I think there are people who have benefited from using a PE mindset. I've never said that wasn't the case. I take issue— and maybe this is just me being a snooty academic and overly intellectualizing things— but a lot of the claims that have been made around satiety per calorie are just speaking beyond the data, arrogant and pseudoscientific. And those sound like aggressive terms, but they're actually very accurate descriptors, which is why, I mean, this can be demonstrated by the results that are output from the satiety per calorie model, which the proponents themselves like to well, let's say, speak strongly about. And it's always a slew of ridiculous things like, you know, the claims. And these are claims that they will make about like things like, you know, what is the most metabolically healthy ice cream? And they'll give a score to like Halo Top ice cream and like the high 50s or the mid— actually it was like 53, so not high 50s, something like that, maybe 52 regardless, which scores better than like things like avocados, egg yolks. So They're making direct claims or very strongly implicit claims about the metabolic health value of something like junk food, Halo Top ice cream versus cheeses and egg yolks and avocado and higher fat foods that are actually more nutrient dense. And overall, I think the literature would show better for metabolic health and devaluing things based on their caloric density, wrapping it all around this calorie-centric mindset since calories are in the denominator. So foods like macadamia nuts, which they like to tease me about because I like macadamia nuts. So that's become a poking point for them, get downgraded. And yet when you look at the literature, there actually is at least one interventional trial where just adding macadamia nuts to the diet caused weight loss. And their model, their model is a tool, it's a toy, it's a heuristic. And that's fine if you present it as such. But what they try to do is pretend that it's solid science when it's not. It's not validated. It's not even sensible because when you accumulate all these factors, some of which don't even really have real science behind them, like hedonic factor, then you weight them arbitrarily, which they do. Ted has fully admitted the weighting is entirely arbitrary. You end up with a scoring system where you're trying to quantify different foods, directly compare them on a 1 to 100 scale, And the science behind it is completely shoddy, which is why you always end up getting some ridiculous results. And it's not even necessarily ridiculous results biased against low carb all the time. They've also had scores like, you know, protein berry ice cream is better than salmon, or pizza is better than watermelon for weight loss. And it's like, these things are ridiculous. And then what inevitably happens is they'll just go toggle the score because they can't, because it's arbitrary. So they can just behind their, you know, curtain change the algorithm and then have a new score that appeases people and sell the product. And honestly, if it was just that, it would be fine. It's just the arrogance of claims like satiety per calorie explains all dietary phenomena in the diet space, period, end of story, which Ted has said. And I'm like, man, This is a falsifiable statement, for one. He's asked me to falsify it. I falsified it multiple times. And it's just intellectually dishonest. And I have quite honestly been— and I'll speak directly to them if they're listening— like, I've just been profoundly disappointed in their lack of intellectual rigor, for one, and the dishonesty with which they market the product. I mean, like, the whole thing with me was, um, I was engaged with them very early on in helping them, or I offered to help them. They did not accept the help. It's kind of formulate this in a way that I thought would be marketing it in an intellectually honest manner because I thought it was an idea that initially had legs. But they chose not to validate it. They chose not to be transparent about their methodology or the studies they were citing as a conglomerate. They went on making these, you know, absurd, grandiose claims, cherry-picking data and. And then just honestly, like, I tried to disengage. They kept poking at me. So what happened is this response video, you can look it up on my channel if you want. It is strongly worded, something like satiety per calorie is a scam. And I go through the flaws. I systematically go through the flaws and also their marketing playbook because I think it is a great case study of where you actually had what was a potentially good idea that was poorly executed for business purposes at the expense of people. And quite honestly, since then, they've just been— it's been disappointing. I don't put most of it on Ted. I think he's just kind of following along. But one thing they did, for example, recently, I didn't even respond because it wasn't worth it. It was so pathetic and desperate. But they took a clip from me for a short about— I was talking about a randomized controlled trial on sucralose sweetener conducted out of Yale, and they took it out of context. And misrepresented it and the literature really around it. And to try to make some extreme point. And in fact, the tweet they put out was something about oatmeal. I hadn't talked about oatmeal. They were just trying to go for clickbait. And it was just like, I've offered them many opportunities to talk to me. I've debated Ted once. It was— did not go well for him. And, and they're at the point where, like, I've tried to disengage. Now they're poking me and misinterpreting randomized controlled trial literature. Either intentionally or because they just genuinely don't understand the data. It's become a little bit of a shit show, to be honest. And I don't really hold grudges. I just, I've just been really, really disappointed in that marketing model. Okay, heuristic, terribly, terribly executed with really weak scientific basis. And so I, I'm sad for the people that feel betrayed because It spun off of Diet Doctor, which a lot of people went to as a go-to source. And a lot of people were hurt by the pivot to kind of, you know, reach and pander to a new audience while giving up scientific integrity. And so I think that's why a lot of people flocked away, probably why Bret Scher left, who I thought was like the heart and soul of Diet Doctor. And ever since then, I think it's just been a down spiral of virtue signaling. And I've just been disappointed. I've tried to disengage because I honestly think it's killing itself. But they have a tendency— I don't know if you've noticed this on Twitter. I don't know if you're on Twitter much, but they love to tag me into things. I have them both muted, but like they will tag me incessantly to a point that it just appears desperate and kind of pitiful. So I don't know. I, I, I'm, I'm sad for people, to be perfectly honest. It's a community.
It's unfortunate. I haven't— I've seen Dr. E speak. We were at a conference together. I've had Ted on the podcast. I've had Brett Scher on the podcast. Um, and you know, my experience with, with Ted when I had him on was it was mostly— this was all pre-Satiety Pro-Calories. We're talking about his PE approach, and I, you know, appreciated the nuance he brought there. But I feel like as a coach, I see people, I see clientele, I see, you know, people that are wanting to just simply improve their health. Not all of my clients are competitors by any means, and people tend to flock to absolutes and absolutes are a very hard thing to convey in nutrition for humans. And when you're scoring foods with an absolute score and you have people justifying the consumption of, you know, X, Y, or Z because of its, you know, arbitrary score, like, that just never really tends to go over well. And I think that's been the model. I'm not sure of the marketing. I don't have the, the app. I don't even know app is called, but I see people gravitating to that and then being led astray, and then I've got to help them pick up the pieces. And that's my frustration.
Yeah, it is just— I think, you know, Andreas is a very astute businessman, maybe Ted to some extent too. And so what I, what I saw in their, their marketing, which plays very well in short form, is very characteristic business tax that sell well in short form, things like changing the burden of proof from you onto the person who's taking the question, even when it's in a very pseudoscientific manner. So I go through, I think, 5 of their playbook approaches in my video, and people can look at it. I think it is, you know, it generalizes beyond Society for Calorie, where it was just an example of like, I see this pattern again and again. And media marketing around nutrition where people use these tacks for great engagement and probably great business results, but it's used to stand up a complete absence of science. And if they were serious, they would be transparent, fully transparent about their methodology, what literature, all of it, what they're citing, how they're determining how to weigh things. They would even go about trying to validate it or even just simply write a perspectives piece on their approach, citing literature, which they fail to do even when I've offered that opportunity to them. I don't think either of them has published any papers before, you know, not to per se knock on that. But if you are going to claim, for example, as Ted has, that he's the most unbiased scientific mind in the low-carb community who's read the studies, you probably should have some degree of scientific background and not continuously make claims that are directly falsifiable, which you're right, people love absolutes. I don't know if Ted was on your, when Ted was on your podcast, if he, you know, said anything like, like I mentioned earlier, where the PE model or society per calorie explains every phenomenon in the diet space. But like when you say that, when you're an MD and you say it with confidence, people take you seriously. It takes someone who's actually read the literature to be like, that's false. Here are data that contradict it. And he's done that several times, including in, in like we had a debate where he'd said something about the carbohydrate insulin model and said, well, here's why it's wrong and these data don't doesn't exist. And I'm like, you sure you want to double down on that? And he said yes. And I'm like, well, here the data are. Here's a human randomized controlled trial that you just didn't look at. You haven't read. You weren't aware of it. So you can make absolutes and people will believe you. But quite frankly, it's incorrect and dishonest. So my hangup is, again, not with the heuristic in the approach. It's about how it's being sold and the absolutism around it and what I think are some dishonest marketing tactics. But again, If people use the tool and it works for them, great. I just want people to be better. So there's the conflict between, you know, the, the coach in me and then the, the academic and intellectual, which, you know, in fairness to them, playing devil's advocate best I can, like, I don't think that they're trying to be academics. And I don't think everybody always wants an academic message. So sometimes maybe confidence in absolutism, even when it bucks the data, maybe it's functional for some people. It's the best argument I can make for them.
But anyway, I just think transparency is, you know, first and foremost. So like whichever path they're taking, as long as they're doing so with a transparent roadmap like that, at least give people a level playing field.
Yeah. Yeah. Anyway, we can move on. I'm trying not to become hung up on it. It's just something that's a sore point of disappointment. It's just because I like— it was one of these things, you know, when you like, you really want to give something the benefit of the doubt and then you really try to help and then it just like completely goes leftwards.
Yeah.
And, uh, that's how things feel now. So I think it's something to, as best I can, cut my losses on. And, you know, if I'm accurate in my read and their insistent poke— incessant poking at me at this point in time is just a sign of desperation, I think they're probably sinking themselves. Just let the sinking ship sink.
Makes total sense, man. I wanna be respectful of your time, but I do want to figure out what's going on with these year supply of eggs, man. What, what, what, what do you think?
Oh yeah, that was unexpected. So I've done a, I've done a lot of unequal ones and a recent one was, I ate 720 eggs in a month, which you probably could match, but it was on average 1 egg per hour, every hour for a month. And it was again, just lipid energy model type stuff, but really was meant to be a hook for some new data on how cholesterol metabolism is, is regulated or how cholesterol is regulated in the body when you intake more dietary cholesterol. So there's a new hormone that was discovered. You can see the video about that. It's called cholecin. But that aside, I basically showed that eating a lot of eggs didn't increase my cholesterol. And as a lean mass hyper-responder, if I added carbs to the mix while eating an absurd amount of cholesterol in the form of something like, you know, 133,200 milligrams of cholesterol in that month, my cholesterol actually went down. So it was a metabolic demonstration. It had a pretty juicy hook for a YouTube video. I had like all these eggs laid out on my queen bed, so the queen bed was literally like covered in egg cartons from Vital Farms. The video went off beautifully. It's been less than a week. It has on YouTube well over 110,000 views, and then on Instagram, the reel has something like 2 million.. And Vital Farms, the company that made the eggs, saw it and they're like, this is awesome and we're gonna award you a year's free supply of eggs. So that was unexpected. But yeah, now I'm gonna get free eggs for a year. So that probably will amount to something like 8,000 free eggs from Vital Farms. So people can say for the next year that I'm bought by Big Egg if they want. Although the video was created without a conflict of interest because I totally did not expect that. But somebody knocks on my door and says, I'm gonna give you free eggs for a year, man, I'm taking that.
Heck yeah, man. We've got chickens for that very reason. I routinely eat between a dozen or two dozen eggs a day, so I am glad to hear that I'm not the only one eating an absurd amount of eggs.
I love it. I love it.
Well, what's the next experiment you got cooking, man? What's on the pipeline for you?
Well, I had already replicated— I've done a few experiments on that were similar to the egg one. The one I have upcoming is 600 strips of bacon per day. I've already done it. And quite honestly, it's a social experiment. I'll just be very transparent. I was very intrigued by how well the egg video went off. And I, as someone that's new to social media and kind of finagling with the YouTube algorithm, I want to see what common factors, including with, you know, thumbnail, title, hooks, really play well. So it's almost like a carbon copy well, not carbon copy, but like a very similar replica to the egg video with some twists. And I just want to see as a social experiment if the audience response is the same. So, um, that one will be coming out in due time, and, um, I— we'll see if people have fun with it. But yeah, more of a social experiment to me. Um, in, in the, in the— I try to be transparent about what I'm doing at any given time, but like, you know, I love to communicate nuance and talk about data breakdown, cell science, Nature papers and videos, but like that has a cap. Yeah, it's a very niche area. So how to ex, you know, expand the audience to get people talking more about metabolic health, you know, maybe n=1 video might be part of the story. So playing with that in the meantime and we'll see how audience, audience replies. But yeah, hopefully I'll be, Well, actually, I'll just leave it at that and people can look and wait and see.
I love it, man. And if that goes viral and you score a year's supply of bacon, then you're really set. Bacon and eggs.
Then I just have figured it out, right? I just can get free food for life. I just need to do n=1 experiments with the right— so I just choose my favorite foods, do n=1 experiments, and I'm totally supplied and my grocery budget goes to zero.
I love it.
That is actually the total, uh, plan. Total plan for 2025.
Hey man, I could totally get behind that. I, I do love how how you've been able to just rock this content, man. Like the YouTube content, the Instagram content, like you're tapping into a whole new audience and it's awesome stuff, man. The level of detail you bring to the table as a scientist, as an academic, as a researcher is just unmatched. So by all means, keep doing it.
I appreciate it. It's been, uh, it's been a fun thing and not a lot of things medical students get to do, um, but it definitely is growing quickly. I think the YouTube's grown from like basically nil to 70,000 subs in, uh, 9 months or something. So it's a fun thing to play with, I have to be honest. And, uh, it's a good outlet, um, to talk and learn and, and, uh, develop myself as a communicator. So anyway, I appreciate your time. Always nice to have a discussion.
Always, man. Well, if there's anything I can do for you, Nick, you just let me know and I'm there. I hope to see you at a conference here soon. And where do you want to direct people to dive deeper into your world?
Yeah, sure. So look up Nick Norwitz, N-I-C-K-N-O-R-W-I-T-Z, on any of your favorite social platforms. My biggest right now are Twitter and YouTube. I'm now on Instagram as well, Threads, Facebook, LinkedIn. And you can go to nicknorwitz.com. Again, N-I-C-K-N-O-R-W-I-T-Z is a kind of a hub with links towards my papers and my various socials. But the nice thing about having my name is I don't think there are any other Nick Norwitzes in the world, so I'm super easy to find.
You're the only one I know, so keep killing it, man. I'm enjoying the conversation. Pleasure to know you, and I look forward to seeing you soon.
I appreciate it.
See you, brother. Bye.
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