Realfoodology - Weight Loss, Cholesterol, + Quieting Food Noise | Dr. Nick Norwitz Part 2

Episode Date: September 17, 2024

EP. 213 Hello friends, and welcome back to Realfoodology! In part two of our conversation with Dr. Nick Norwitz, we cover effective weight loss strategies, intuitive eating, and the impact of GLP1 deficits on food noise. We also explore hunger cue hormones, the calories in versus calories out model, and the provocative idea that “calories are irrelevant.” Additionally, we discuss the Oreo vs. statin study, its long-term implications, and Dr. Norwitz’s views on cholesterol levels and bio-individuality.  Timestamps:  04:37 - Effective weight loss strategies  08:08 - Intuitive eating  10:30 - GLP1 deficit and food noise 14:59 - Hunger cue hormones  18:45 - Calming food noise  23:55 - Filling meals & fuel partitioning  32:22 - The calories in calories out model  35:36 - “Calories are irrelevant” 39:52 - Oreo vs statin study  50:29 - Understanding the physiology  55:03 - Long term impacts of the study  56:16 - Cholesterol levels  59:57 - Bio individuality  01:03:35 - The cholesterol myth book  01:09:49 - Oreo vs statin study conclusions  01:14:23 - Nick’s health non negotiables  Show Links:  212: Artificial Sweeteners, Insulin Resistance + Understanding Health Studies | Dr. Nick Norwitz Part 1 Oreo Vs Statin Study  The Cholesterol Myth Book Sponsored By: Wellnesse Go to wellnesse.com/realfoodology and discover the benefits of hydroxyapatite today  Organifi Go to www.organifi.com/realfoodology and use code REALFOODOLOGY for 20% Off, get a free Gold Chocolate bar with orders over $100 for a limited time  Seed Go to https://seed.com/realfoodology and save 25% your first month with code 25REALFOODOLOGY Puori Go to Puori.com/realfoodology and use code realfoodology to get 20% off BIOptimizers MagBreakthrough Get your free bottle of magnesium breakthrough while supplies last at magbreakthrough.com/realfoodologyfree ARMRA Collostrum  Get 15% off your first order at tryarmra.com/realfoodology Check Out Dr. Nick: Website Youtube Instagram Check Out Courtney  LEAVE US A VOICE MESSAGE Check Out My new FREE Grocery Guide! @realfoodology www.realfoodology.com My Immune Supplement by 2x4 Air Dr Air Purifier AquaTru Water Filter EWG Tap Water Database  Produced By: Drake Peterson

On today's episode of the Real Foodology Podcast. Bad intervention, good outcome. There's a paradox there, which means there's something we don't understand. So there's different ways you can respond to that. You can express curiosity or you can get defensive and try to superimpose a value judgment. There are things that people are inevitably gonna layer on

because they don't want to take the moment to actually try to understand what's being said and what was shown. What's up, everybody? This is Drake Peterson, the producer here at the Real Foodology podcast. I just wanted to let you know that this is part two of the episode with Dr. Nick Norwitz. If you have not listened to part one, it was released last week. So just go back and listen to that and then come back to part two. Hope you enjoy. Let's talk about oral health. This is incredibly important for your overall health. And if you've been looking for

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This is really exciting. Organifi now has kid stuff. They just released two kid products. One is called Easy Greens, and it's a refreshing green apple juice where kids will never know that it's packed with veggies. And the other one is called Protect. It's a delicious wild berry punch like the Kool-Aid that we used to have as a kid but without any sugar. This is really exciting and if you've listened to the podcast for a while, you know that I'm a huge fan of Organifi

and most specifically because every single product that they make is glyphosate residue free. So you know that you're gonna be able to give these powders to your kids and know that they will be able to consume them safely without any glyphosate in it. So let's break down each one.

The Easy Greens is a nourishing and delicious blend of superfoods and veggies that provides essential nutrients, probiotics, and digestive enzymes to bring balance to kids' growing bodies without fillers, additives, or junk. It helps to fill in nutritional gaps, aids in growth and development, supports digestive health, has a rich micronutrient profile, and includes digestive enzymes. This would be a great way to sneak in greens for your little one without them actually knowing that it's healthy for them. And the second one, which is the wild berry punch similar to Kool-Aid, is called Protect, and it is to support your child's daily immune health with food-derived nutrients that work to strengthen their body's first line of defense. I know just through girlfriends of mine that have

children that when your kids are going to school, to daycare they're coming home sick a lot more often just because they're getting exposed to different kids and different viruses when they're out in the world playing with kids so this would be a great way to help to support your little one's immune health it's organic and it's also made with real whole food ingredients it has a delicious berry taste and it's low sugar and it's gentle enough for kids to take every single day. And I really love the ingredients in this one. It's orange and acerol cherry, which is a powerful source of vitamin C and antioxidants.

Astragalus, elderberry and propolis. These are all really great for overall immune health. If you wanna try the products that I talked about today or any of the Organifi products, go to organifi.com slash realfoodology and use code realfoodology for 20% off. Again, go to Organifi.com slash RealFoodology and use code RealFoodology for 20% off. Again, that's Organifi. It's O-R-G-A-N-I-F-I.com slash RealFoodology. If somebody wanted to lose weight, how could they do this effectively knowing what we know about biology, genes, and the current food landscape?

Yeah. I mean, I think there's no one way to skin a cat. Like high level, we kind of hit the points, and these are like the boring but obvious fundamentals I think you need to hit. One is generally eating whole foods. Like if you eat, if you cook your own meals and base things on a single ingredient, you're probably going to do pretty well from the starting point of most people. And then the secret to success, it's a secret, a fundamental for success is really planning and building a community around you that

will be supportive. I really think the hardest part about sticking to a diet is not the diet itself, but the environment and the social community. So who's going to be your accountability buddy? Do you have people around you who are going to be the tempters or the supporters? Are you going to be able to build your environment in a way that removes temptation? Like, do you live by yourself? And so you can get certain foods out of the house? If not, let's say you're a parent and you live with kids and there's like, you know, breakfast cereal sitting around. How are you going to protect yourself against that when temptation comes knocking? We can talk about food noise in a moment. But conceiving of all those obstacles and figuring out how you're going to overcome them. You can join online communities and support groups. You can get a coach. I think just really being prepared and then committing to a journey and trying to stick

with it, acknowledging that it's not going to be easy at first, but there is a grass is greener on the other side element. You do adapt to these things at every level. Of course, I'm going to go on a tangent now because I can't help myself, but take intermittent fasting for an example. There's a mouse study, again, better to do with mice because you're looking at changes in brain activity with respect to, say, intermittent fasting. And the way they do it is actually decapitating the mice, staying in the brains, yada, yada, yada.

That's why you don't do it on humans but if you food deprive mice for 24 hours when they're used to eating just all the time they have a huge anxiety response as measured by amygdala activity the fight or flight center of the brain about a three-fold increase in activity but if you just spend several weeks habituating mice to intermittent fasting, then if you give them the same exposure, there's no increase in activity in that fight or flight region of the brain. The reason I bring up this example is just like what might seem unpleasant at first, you, your physiology, your brain can adapt, rewire to actually find pleasurable in a way

that you never thought possible. So I've seen lots of people that are like, I could never like go a full eight hour waking hours without food to the point they were like, I can't believe some people eat three meals a day. Like I just, it's so liberating that I just only have to eat two and I can eat when I'm hungry. And you actually start to get like, you know, that intuition. People say like intuitive eating. It's a term I love and hate. I hate it because I think it's one of those like freebies where like YOLO, I'm gonna have an ice cream, because you can't eat intuitively. If your hunger, your true hunger for nutrition is being obscured by hormonal

fluctuations. But once you adapt properly, then you can get to a place where you actually are eating for your body's needs eating intuitively, like we evolved to do, that is the ideal. And that's what you get to. So like, you know, it's something that I think people can hold in their mind is something that every single human being can achieve, even if it seems like a myth. But planning on the difficult road to that point in time is something that is important. That's point two. I just wanted to say one thing really fast before you kept going. The thing about intuitive eating that a lot of people forget and is discounted, if you are eating a diet of mostly hyper-processed, ultra-processed foods and fast foods, there's no way that you can eat intuitively and live intuitively because your brain and your body is being hijacked by these food-like substances that were designed to be

overeaten. Yeah. So that's what I'm saying. That's where it's like the discrepancy between like, what do you, if you have one Oreo and you want a second, that's not eating intuitively. Yes, exactly. If you give into food noise because of the chocolate cake in your fridge at midnight, that's not eating intuitively. Yeah. So I would say the reason I sequence them like that is like the eating intuitively basically only applies to real foods. Yeah, exactly.

Yeah. So let's, yeah, I think that's a good way to frame it. Thanks for the clarification. Yeah. And then I would say, you know, the last thing is while your journey should be iterative, which means you start somewhere and you notice what works, what doesn't work and you tweak and you notice what works and doesn't work and you tweak again and you continue that. That's how metabolic health journeys work.

You know, your journey is individual. Think about what the best starting point is for you. And I'll reveal my bias here. I think the literature does suggest if you have an insulin resistance disorder, carbohydrate restriction probably is beneficial for several reasons. We can go into those, including benefits on energy absorption, energy expenditure, et cetera, et cetera, and effects that are just beyond weight loss. But if you have obesity, metabolic syndrome, or an insulin resistance disorder,

carbohydrate restriction probably is a good place to start. It doesn't mean you have to go carnivore or keto. It could be reducing the glycemic load of your diet, cutting out the starches and the high glycemic load fruits. So less papaya and mango, more blueberries, less pasta, more large roasted cauliflower heads or something like that. And if you want some steel-coated oats, I'm not poo-pooing these things. I'm just saying overall glycemic load reduction does have metabolic benefits, particularly for those who are insulin resistant. So that's my high level.

Okay. Well, and I was going to say, and where did GLP-1s come into this? And the reason I bring that up is because I think the reason why GLP-1s are so popular right now is because they reduce those hunger cues. And there's a lot of conversation, and you brought this up earlier, of the body's ability to create a semaglutide, ozempic type, what's the word, mechanism in the body. Yeah, so I mean, we produce, GLP-1 is produced by L cells in the gastrointestinal tract. It's an endogenously produced hormone.

These GLP-1 receptor agonists mimic that. So Ozempic, Wagovi, usually injectable. There's some more on that. But they mimic that. They're also super physiological doses, so not just equivalent to, you know, your body's endogenous production. Something to recognize though, which all people might not know, is that in insulin resistance disorders, PCOS, metabolic syndrome, diabetes, obesity, there's a GLP, on a population level I should say, a GLP-1 deficit. GLP-1 levels are lower.

Why do you think that is? Ah, good question. So my understanding is the field did not know, did not know. There are hand wavy things like there were literature in 2019 showing that inflammation could one, damage L cells in the gut directly. And two could promote the migration of certain T cells, IELs, I believe that have GLP receptors. So they gobbled up and swept up the GLP in the gut so there's less bioavailability. But even that's a little bit hand wavy because it doesn't necessarily get to the root cause.

Like, is there a causal cascade leading to a GLP-1 deficit? Actually, there are brand new data just came out. I have a video in the final stages of edit on it on at least one cascade by which it may work it was looking at just this is to give you a picture of how this could work mechanistically i'm not saying it's the whole picture but what they found is that um in a diet induced obesity so a westernized diet in mice that this westernized diet expanded levels of a particular gut bacteria, disulfavibrio.

And disulfavibrio has a hydrogen sulfide-based metabolism, and so much hydrogen sulfide was produced that it overwhelmed the detoxification systems of the gut, damaged mitochondria in L cells, which produce GLP-1. So the L cells then have an energy deficit and can't produce enough GLP-1. And actually if you block the hydrogen sulfide production, you could prevent diet-induced obesity in this model. The reason I was laughing just then is you can block it with the bismuth subsalicylate, which is Pepto-Bismol.

So they effectively take Pepto peptobismol to these mice and were able to rescue GLP-1 levels. And also I should note, yes, there's a mouse model because you need to do certain mechanistic studies in mice to demonstrate a causal cascade, things like fecal matter transplants, all that to germ-free mice. But in humans with metabolic syndrome, disulfovibrio levels are expanded and GLP-1 levels are reduced. So what you do in these sorts of studies, you'll see often in papers like Nature, is like you have the mechanistic mouse model, you use that to dissect it, and then you say, does this line up with the correlations we see in humans since you can't do the, you know,

dissection in humans? And what we see is, yes, we developed this model in mice. It proves to be causal in mice. And then we look at humans, is the same association true? And indeed, yes. With interventions that also tend to decrease the sulfavibrio levels, also improving obesity. There are some things that remain to be discovered, but high level here, we're beginning to unpack how diet, the root cause, can cause metabolic and microbiome dysfunction leading to a GLP-1 deficit, which can cause all range of metabolic dysfunction. And then you end up with this vicious cycle, right? Because let's say you have a GLP-1 deficit and you have more of that food noise, which we can get into in a minute. What are you going to snack on?

Hard-boiled eggs or the cake? You're going to snack on the cake. And what's going to skew you more in the direction of this metabolic deficit. So you end up in this vicious cycle, which is quite scary. And I was going to ask you, is there a connection with leptin and ghrelin,

the hunger Q hormones and GLP-1s? Because I would imagine there would be some sort of connection there. I would assume so. The thing is, there's gonna be a correlation, for example. So like if there's a GLP-1 deficit in obesity, if somebody has obesity, they're probably gonna have higher leptin

and leptin resistance. That's another mechanism we just discovered in 2024. It has to do with HDAC6, histamines acetylase 6 in the brain affecting leptin receptors. Whole different topic. I'll avoid that tangent, although I do have a video on that too. And ghrelin, hunger hormone. So again, it's like there's going to be higher ghrelin if you're having these insulin highs and lows with obesity and a GLP-1 deficit.

I don't know if there is a causal action of GLP-1. Like leptin, for example, is mostly in adipocyte. Now I'm just thinking on the fly. So it's mostly really from fat cells. GLP-1 receptor agonists at least don't really act that potently on fat cells. Another encrypted hormone, GIP, does. It's part of the action of manjaro to zepatide. But it's a good question. I don't know the exact answer. Okay. Well, I was just curious if that had been explored at all just because of – It might have been.

Because we're talking about with the food noise, and if you have – hold on, let me think about this for a second. If you have higher levels of leptin, you're probably most likely going to have lower amounts of food noise, I would assume. No, because if you have higher levels of leptin, you're probably most likely going to have lower amounts of food noise, I would assume. No, because if you have higher levels of leptin, you're probably leptin resistant. If you have very high levels, it's like insulin. If you have high fasting insulin, you're probably insulin resistant, right? Yeah. So there's a parallel thing with leptin resistance. I was alluding to that where, so people with obesity tend to have high leptin. So you're probably going to be the person who also has high food noise.

Wait, with high leptin? Yeah, let's talk about that. Okay, so ghrelin is grr, which is what we learned in school, which means it tells you when you're hungry. And leptin tells you when you're full. Yes, yes. Okay. Okay, so let's draw the analogy of insulin resistance again. So if you have high insulin levels,

does that equate to high activity in insulin signaling cascades? No, because it means it's not getting cold. Yeah. Well, if you're resistant, so what your body's trying to do an insulin resistance you know why you get hyperinsulinic in part is your body's trying to compensate your pancreas your beta cells are shouting louder and louder hear me tissues you're not

getting the insulin signal yeah please right so it's similar with leptin where levels go up when you have more fat tissue, but it doesn't actually mean there's more leptin signaling. What ends up happening is there's, um, a protein histone deacetylase six in the brain. It's one of these proteins that modifies the proteins by putting tags on them and it can modify the leptin receptor so that leptin signaling, um, you know, is less efficient. So higher leptin doesn't equate to more leptin signaling per se. Okay. Interesting. The hormone endogenously, its function is to reduce hunger. But if you take a cross-section of the population, those with high leptin probably will have high leptin resistance.

So they might not have as much or even less leptin signaling in the place that it counts. Okay. Yeah, that makes sense. Okay. And so we keep talking about this notion of food noise. Let's talk about what that means and then how can people calm it down? Yeah. I mean, it's a subjective term to describe that experience of like the chatter in your mind thinking about food where it just bugs you and bugs you and bugs you until you eventually give up. So, you know, if there's your favorite cake in the fridge and you know it's there and you're walking around the house and you're hungry and you know it's there and it bugs you and it bugs you and it

bugs you you can't stop thinking about it until you actually have it that's food noise there are neurons in the hypothalamus region of the brain which there are pre-ingestion satiety neurons so neurons that might signal when you're full while you're eating and the neurons that are pre-ingestion satiety neurons. So neurons that might signal when you're full while you're eating. And the neurons that are pre-ingestion satiety, so before you're eating, these are the ones that if they're more active than if you're cued to a food, if you know it's around, but they're more active than you have the pre-ingestion satiety, you can actually go like look at it and like, nah, I don't need that.

So that's the person who like, you know, they're sitting at the dinner party and there's finger food. Let's make it, what's the best finger food? What at the dinner party and there's finger food let's make it now what's the best finger food uh what's the best like hyper palatable finger food i don't know yeah i mean like i think like doritos doritos okay doritos doritos so let's say you love doritos and they're in front of you some people like they're gonna have the doritos there's no way they're not other people that can look at them and just be like, meh, I don't need them. Those meh people have the high active pre-ingestion satiety neurons. At least that's a way to think about it. And GLP-1 acts on these neurons. Actually,

it was found that this is one of the main mechanisms of action by which GLP-1 agonists act, by shutting off the pre-ingestion satiety neurons and calming food noise so that you get that liberation so that when the food queue is around you, you aren't driven, you aren't pulled to feel like you need to have it. But, you know, can calm that food noise and allow people to make better choices. And that I think is quite powerful. Now the question, how can people treat their food noise? Well, I mean, there's the hand wavy answer of, you know, get your metabolic health in check. Yeah. I'm not going to measure the social vibrational levels, yada, yada, yada. But I do think food noise will reduce as you become more metabolically healthy. Things

tend to fall into place and you, you know, gain that intuition that we were talking about, right? Again, kind of hand wavy. Now, of course, there's the pharmacotherapy route. I won't poo-poo that. Beyond that, I would just think this is, again, about constructing your environment in an adaptive way. I did say food noise arises when you're cued to X, Y, and Z. Can you remove the cues? Can you reconstruct your environment? You know, if you have lucky charms, getting them out of the house or getting them otherwise inaccessible or creating barriers to access that, you know, reduce the stimulus for the food noise. And this is all very individual because, you know, while we do these studies in controlled settings, we all have our Achilles heel, and that can be a particular food.

It can be a particular food in a particular context. It can be, you know, impacted by our emotional status. All these things which are just, you know, very individual and something to be aware of. Me, I'm a dork, and I just like that we're understanding the physiology of food noise so when people throw out these terms i'm like yes pre-ingestion satiety neurons in this region of the brain and these hormones act on them and i can see the curves in my mind so i like that as an academic exercise some people you might be this person i know a lot of people that aren't understanding the physiology gives them a handle to control the behavior so they they're like, I understand now what food noise is. So then when they have the food noise,

they actually think this is what's going on in my material brain. And that gives them the power to conquer that moment. That's one subset of people. It's not everybody. I find that's the case. I remember when I was a teenager, you know, and I was like first driving for was a teenager um you know and i was like first driving for the first time you know your prefrontal cortex is underdeveloped as

a young male like your 20s so i always have this urge especially relative about a sports car and sometimes i drive it like i want to just floor it but the reason i wouldn't is not because i didn't want to but i'm like i'm also aware at my age my prefrontal cortex isn't developed enough to properly weigh the risks. And that was actually what allowed me to make the smart choice and not go a hundred on the highway because I realized that my physiology and my neurobiology wasn't equipped to handle the moment. And that weirdly gave me the ability to handle the moment. I don't know. Which is amazing. It's interesting. I think I'm crazy. You know what?

You and I are very similar in that way. I like to nerd out over this kind of stuff. And so my brain works very similarly. And if I know the mechanism of the why behind it, I have way more power to want to stop it because I don't want to give in to that. Like knowing that that's how my brain is doing that in the moment, I'm like, oh, okay, well then I'm just not going to give into that. I will say though, personally, as someone who went through a phase where I felt like I was extra particularly really struggling with food noise was during a

time when I realized that my body was not metabolically healthy. And what really helped me the most was making sure that I was really prioritizing satiety-inducing meals. And what I mean by that, I was really making sure that I was getting enough good, healthy fats, salmon, nut butters. I love almond butter, avocado, olives, olive oil, and things like that that really bring satiety. It helped me cancel out a lot of that food noise and to really good high quality proteins. And over time, what I noticed was that as I was doing more of that and I was prioritizing more of these high-fat, higher-protein, lower-carbohydrate meals and snacks too, I would make these little fat balls that I would have for snacks.

And I realized that as I calmed down that satiety and made sure that I felt full and satisfied for longer, I had less food noise. Yeah, no, for sure. I think, especially on diets where people tend to restrict, if you're over-restricting, you're going to end up hungry. So I think including healthy fats, prioritizing proteins and packaging fats around that,

not packaged fats, packaging fats around that, is I think a generally good approach. One thing I'd add to that, because we talk about mere exposure effect and internalization of these messages, is a different way I want people to think about obesity and calories, because I think that's a very confusing concept. Because when you think about olive oil and nuts, my favorite, or macadamia, which are known to be super high calories, we're like, oh, but they're going to cause weight gain because of the calories. And this is, we alluded to it earlier, an area of controversy and gross misunderstanding

where I can simultaneously say calories do not cause obesity while saying thermodynamics applies. And as I say that, I would say most people, including most nutritional influencers, their mind kind of just like goes into like, you know, spinny wheel of death mode where they're like, wait, what are you saying? This is a logical inconsistency. It's not. It's just that people don't think deeply enough about what calorie balance is. And all it is an arithmetic equation, which is really a post-hoc description of what has happened, you know, to your energy balance after some intervention. Put otherwise, it's a consequence and it holds true, but it's not a cause. Cause is etiology,

the root driver. And so in a chronic sense, obesity is primarily driven by poor fuel partitioning. So when your body consumes food, that food contains chemical bonds that are broken up to liberate energy, which can be measured as calories. That's all true. Now your body has to decide what to do with that energy. It can be expended as heat. It can be expended as non-exercise activity, thermogenesis, little jittery movements, it can be used to build lean tissue, or it can be stored as fat. And your hormonal milieu determines your fuel partitioning. And then if you fuel partition well, great. If you fuel partition but with a preference towards fat storage, what ends up happening is you then need compensatory mechanisms to make up for the fat that has now been shoved into fat tissue and downstream of that what you end up getting is more hunger and a decrease in energy

expenditure and this has been shown in the literature and in human studies but also animal models again actually the animal models have the edge here because it provides those controlled in rigorous setting to demonstrate principles of physiology that undermine the standard calories approach. So for example, in pair feeding experiments where you have two groups of animals and you manipulate one such that even if you control their calories tightly or feed them less calories, you could feed the certain group calories, and they end up with more fat mass and weighing more. Well, you can uncouple these things. And it doesn't say calories don't matter. What it says is obesity is primarily a dysfunction of fuel partitioning. Calorie balance is a downstream consequence of that. So the takeaway from this, the functional takeaway is don't focus on the things that are

going to impact the scale tomorrow morning, because those behaviors can tend to also promote adverse fuel partitioning. So you get led down a dysfunctional path. Rather, focus on things that are going to keep you metabolically healthy and promote functional, healthy fuel partitioning, which can be very high-fat, high-calorie foods in some instances. And guess what? When you look at the literature, even things like macadamia nuts, I know of one macadamia nut interventional trial, and BMI went down. They weren't controlling calories in the subject. They said, eat more macadamia nuts, and BMI dropped significantly, actually, in just four weeks. And that does grate against what appears to be the calories in calories out model.

Now you could say, oh, but will they compensate it by eating less? Well, that's the point. That's the whole point. That's exactly. This summer, I have been all about embracing every moment, whether it's traveling to new places or simply enjoying the little things closer to home. And through it all, taking care of my health remains a top priority. That's why I've been relying on Seeds DS01 Daily Symbiotic to support my gut health every step of the way.

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I don't know if people know who he is apparently he's a big name he looks like a bodybuilder he definitely looks like a bodybuilder um he looks like john cena ate arnold schwarzenegger's big dude anyway he was coming after me like in a recent comment on a podcast about how dishonest i was and how inconsistent that like i said calories aren't relative i I think he meant relevant. And that at the same time, I did this experiment where I said I had an increase in non-exercisability thermogenesis. I'm like, you're proving my point.

You're not contradicting me. You're presenting these things that you see as logically inconsistent. What I'm saying is they're perfectly logically consistent because I'm not saying calories are not relevant. I'm saying that they are the consequence, not the cause. And that whole thing with non-exercise activity thermogenesis that you mentioned in me, well, yeah, my body is really good at compensating for several reasons. Part of it might be congenital, but part of it might be that my

body knows how to fuel partition at a high level. So if I overfeed, my body tends not to shove it into fat tissue, but it expends it. Calories, the consequence, not the cause. So this helps explain why if you feed, let's say you feed some people, you know, in the experiments that we've done, you overfeed people by a thousand calories, you know, of their calculated, you know, needs. With that acute change, will they gain weight? Most people will. Not all people. Most people will. But there's a massive heterogeneity, tenfold differences in fat accumulation based on non-exercise activity thermogenesis alone as a factor. And so what does that tell you? It tells you that the calories in

calories out model is, even over the acute time frame, such a crude metric has to be basically clinically useless. And chronically, I would say it's entirely useless to the point that it's misleading because sure, you can shove, you know, 10,000 calories down someone's throat for a short period of time. But that's actually like not super relevant to the longterm physiology that's causing obesity chronically, on top of the fact that in order to feed somebody 10,000 calories, you have to change other dietary variables as well. And again, there's so much heterogeneity that what we want is a physiologic understanding, the biological basis of obesity, not some lazy ass arithmetic, like calories in, calories out. So if people actually want to have this conversation

about where calories fit into the picture, we can, because I'm not saying they're irrelevant. I'm not saying they don't matter. I'm just saying there's physiology here. That's a priority, more important, more functional to understand. And we need to understand that. So yeah, I, but people, again, they get defensive, like this Stan guy. Again, they probably sound disrespectful. I don't know who he is, to be perfectly honest, but he's been pretty aggressive. So yeah, Stan, if you're listening, buddy, and you want to have a chat, I'm here. Please stop misrepresenting me.

Take a moment to actually try to understand what I'm saying. The words that are coming out of my mouth to quote, who was it from Rush Hour? Yeah, where was that from? I think that was Rush Hour, yeah. It was Rush Hour. Do you understand the words that are coming out of my mouth? Yeah. I love that movie. So anyway.

There's a couple things that were, yeah, yeah. No, there's a couple things that were going through my brain as you were saying that. First of all, I think about, you know, oftentimes with obesity, there's this conversation around we're having this epidemic of overfed but undernourished. And what's happening there from my understanding is that, yeah, you're eating a lot of calories, but there's not a lot of nutrients behind that, which is why we often see these children that are dealing with obesity, but then all their deficients,

all their vitamin and nutrients are super deficient. Now, on top of that, and I'm curious to hear what your thoughts are about that. And then also I think about, I use this example often. If you have a choice between getting a bag of mini Oreos for a hundred calories, those little hundred calorie Oreos, I don't even know if they still make them, but I remember like years ago they used to, or you get a little bag, a handful of a hundred calories worth of almonds. Now, if you're going to go for those a hundred calorie mini Oreos, you're going to eat those. And then you're probably not going to feel full and satisfied. And then you're going to reach for more snacks. Now, if you were to have that a hundred calorie almonds, you're getting a good amount of fat in there that's going to keep you full and satisfied.

Maybe the minerals and vitamins that are in the almonds are negligent, but your body is going to recognize that as actually food and you're getting a good amount of fat that's going to keep you full and satisfied. So I would argue, or even let's say, let's take this further. If you were to choose between a hundred calorie mini Oreos or 200 calories worth of almonds, I would- I was just about to say that exactly. I'm like, let's take that. You break my mind. Yeah. So- Almonds. Exactly. So, sorry. So that was my point. And that's what I misspoke when I said a hundred calorie almonds. I would always choose the 200 calories, the almonds, because guess what's going

to happen? You're going to feel full and satisfied. Okay. The 200 calories is negligent. Let's say 300, whatever it is. You're going to feel full and satisfied with that higher amount of calories, but a higher quality amount of food versus the 100 calorie Oreos, which then you're probably going to be reaching for another snack 20 minutes later. But I would go even one step further, which is to say it's not just about how you feel subjectively, but think about where are those 100 calories going? Now I'm just making up numbers entirely. But let's say if you eat the Oreos, your personal body responds by preferentially shuttling 80% of whatever Oreo calories you ate. Again, this is just a mental exercise,

into fat tissue. Versus if you eat the almonds, only 10% is shuttled into fat tissue, right? So you eat 100 calories in Oreos, then 80 calories goes into fat tissue. If you eat 200 calories in almonds, then 20 goes in. Interesting.

I think it's a way to think about it based on the fuel partitioning concept. Again, those are totally fabricated numbers. It depends on many more things than that. But if we do think about obesity as primarily a dysfunction and where your body is putting the energy and how it's using it,

then it's not, if we could, we can't to be clear, but if we could come up with like a fraction of the calories from any particular food that are shuttled into fat tissue, I think that's a way to think about it. We can't, but like it, maybe that's useful to some people.

Yeah, I mean, I think, yeah, what you just said makes it easier to understand and more digestible for people. Because it really does, it comes down to the quality and what your body is going to actually do with that food and also how your hormones are going to respond. Like we forget there's a whole cascade of mechanisms that happen in the body after you eat whatever food you eat.

And depending on where those calories are coming from, it's going to trigger a different cascade in your body. Yeah, in your body, that's the point. Like, not everybody's equal. So I'm not even going to, I mean, I wouldn't, I would never endorse Oreos for health. But like, let's take a whole food, you know, something like a banana. If you're insulin resistant, that might not be the best choice for you. If you're a young, healthy athlete going to sports practice, have a freaking banana. I don't care. So it's what happens in your body. Yes, that's such a great point. So the Oreos, this is a great, great bridge to, which I know where you know where I'm going with this. You recently conducted a study on yourself with Oreos. And it has become famously quoted as the Oreo

versus statin, I guess, like personal study that you did. Can we talk about that? And can you explain to the listener what you did and what you found? Sure. So our colleagues and I, including Dave Feldman and Adrian Sotomota, a professor down in Mexico, have been studying this thing called lean mass hyper-responders for a while. Some listeners may have heard of it. High level, some people who go low-carb have massive increases in LDL cholesterol, which is kind of the boogeyman of low-carb diets. Now, these increases are astronomical and understandably scary to lots of patients and physicians.

In order to implement ketogenic diets for the broad use cases for which they're now being explored, in order to implement them clinically, we need to kind of understand this boogeyman and address it with better physiological understanding. So we asked the question, well, what's a driver of LDL change in low-carb diets, because most people actually don't see LDL go up, and generally have a broad improvement in all cardiovascular risk factors, generally. But a subset do see increases in LDL and ApoB, and to crazy high levels. So, you know, some people could wave their hands and say, oh, it's just an X, or oh, it's just saturated fat. Let's be clear, none of, neither of those actually explain all the phenomena we're seeing.

I've dug into this so many times, you can see my other content for that. But what we've discovered is lean insulin-sensitive people tend to be the ones that have larger increases in LDL. And the leaner you are, the higher your LDL tends to go, all things being equal, which is interesting. The model we have to explain that, called the lipid energy model, basically says if you're lean and insulin sensitive, and you go low carb, and your liver glycogen stores start to drop, your body shifts to trafficking fat very, very quickly and through this systemic system that relies on cholesterol-containing particles. And you end up with this triad of very, very high LDL,

high HDL, and low triglycerides, which defines a lean mass hyper-responder. Now, I won't get into the nitty-gritty of the lipid energy model here, in part for the sake of time, and part for the sake of just tired of hearing myself talk about it probably 700 times, but it makes certain predictions.

And one of the base predictions is that, oh, you add back carbs and you stop the driving force for energy needs through this cholesterol particle like lipid trafficking system. So this has been done well before the Oreo versus statin study where we've had interventional trials with fruits and starches and people generally swapping them and reducing their LDL levels by massive amounts of the lean mass hypersponders. We had one case series with one patient who dropped their LDL by 480. That's the LDL and the LDL dropped by 480 from 665 to 185. You can see that in our 2021 paper in current developments in nutrition. It's table

four, if I can remember correctly. And anyway, so this has been done before, but in my opinion, it was not being talked about enough, this physiology and this phenotype. So I envisioned a study to provoke attention to this broad body of literature. We now have 10 papers on the topic. And I thought, what is the most provocative way I can do this? And I said, I'm going to choose the most well-branded unhealthy carb source I can, Oreo cookies. And I'm going to choose an appropriate comparator, statins. In particular, high-dose resuvastatin, Crestor. I actually had a lipidologist consultant and co-author, William Cromwell, highly respected lipidologist. He trained Thomas Dayspring in lipids, if people know who Thomas Dayspring is,

who's closely associated with Peter Attia. But William Cromwell came on as consultant and co-author. My PCP was ordering all the labs, and I did this crossover trial where I did a run-in diet, my standard ketogenic diet, locked that in, then did about two weeks of Oreo cookie treatment, then a three-month washout period before going on Crestor at 20 milligrams for six weeks. And what we found, what I found, was that the Oreo cookies lowered my LDL by 71% in 16 days, which was twice as potent as high intensity statin therapy achieved in six weeks. So the Oreo cookies were twice as potent in one third of the timeframe. Evidently it's provocative. Harvard medical student uses Oreo cookies to lower cholesterol by more than any drug is expected to ever, you know, like it was meant to be provocative.

That was the point to provoke conversation that I think needs to happen. Overall, it's had a very positive impact in promoting relationship building so we can acquire resources and teams to do more research and get the millions of dollars we need to do to do the studies we want to do. And it's exposed clinicians to the lipid energy model, to our body of literature, which gives them the tools to use physiology-focused approaches in their patients. So now, literally because of the Oreo versus statin study, there are patients that are getting sweet potato therapy instead of statins and getting better effects. I know this because their clinicians email me. So, you know, this isn't actually dangerous. Some people are like, oh, you're going to convince people like Oreos are healthy. I've literally met zero people that legitimately

have been believing Oreos are healthy after this. That aside, that was the experiment and the purpose was provocation. And I think where people get in trouble is falling into the trap that I admittedly set, and which was what we have here is what we can probably agree is a quote, bad intervention, Oreo cookies, and quote, what will be presumed to be a good outcome, the LDL lowering. For most people, that would be presumed to be a good outcome.

Bad intervention, good outcome. There's a paradox there, which means there's something we don't understand. So there's different ways you can respond to that. You can express curiosity. Like I think most people shouldn't say, wow, this is weird. How did you predict this was going to happen? Let's understand the physiology because it's consistent with all the other literature and you were able to actually predict this would happen. Or can get defensive and and try to superimpose a value judgment like saying oh nick must be saying that statins are bad i didn't say that or that el hayal the all safe i didn't say that or that aria is healthy i didn't say that there are things that people are inevitably going to layer on because they don't want to take the moment to actually try

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how? What's the mechanism behind that? Because I think from what I understand with cholesterol, high processed, hyper processed, ultra processed, sugary carbohydrates, in my opinion, would make our LDL go up. So how did you lower it with that? So again, context, context, context, what metabolic context do you have? If you have metabolic syndrome and insulin resistance, then in general, eating highly processed, high sugar foods is just going to exacerbate that and probably lead to a decrease in LDL clearance. So you're going to have some particles floating around and you're going to end up with less clearance. So they accumulate in the bloodstream along with a lot of other

things that are, you know, building up like inflammation, oxidative stress, all bad. In this particular context, what we think is happening is my body was running a lot on fat. It runs a lot on fat in a ketogenic context. And because of my body habitus and activity levels and everything, the free fatty acids that are liberated from my fat tissue, some of them get gobbled up by muscle locally, but a lot of them circulate to the liver and they need to get recirculated around the body. So they hop aboard these large spherical VLDL particles, because remember, these are fats. They don't mix well with water. So they need little cargos or little boats to carry them. And then these VLDLs get turned over at the fat tissue to replenish the fat and then feed the

muscle tissue. So the triglycerides in their core gets sucked out and go to the fat and the muscle. And as they're sucked out by this protein lipoprotein lipase these large spherical vldls they shrink and become ldls the ldl particles with ldl cholesterol but also as you shrink a sphere surface area is lost and some of that surface area includes cholesterol that gets picked up by acceptor hdl particles so what you end up with the ldl and the htl goes up and the triglycerides go down because the core of this VLDL that has the triglycerides, the stored fat is getting sucked out so much. But if you just remove the driving force for this circuit to be running, which is, you know, partial liver glycogen depletion, because I'm low carb, then it removes the need for this trafficking system and the LDL goes down so what we when you take a level you only have like a moment in time of this the standing levels in the blood it's

actually not telling you how things circulate so on me I might have a very rapid circulation of these particles with higher steady state levels but if you remove the driving force then I have less production and less export by a lot so my levels drop massively versus if you remove the driving force, then I have less production and less export by a lot. So my levels drop massively versus if you take somebody with a BMI of 37 in metabolic syndrome and you give them Oreos, presumably over a longer period of time, then what happens is, first of all, they were on a mixed diet anyway. They don't have the driving force to cause the lipid energy molecule that's kicked into full clinically relevant gear, metabolically relevant gear. And then you have damage, glycation, inflammation,

all these hand-wavy terms you throw around. Basically, though, they're going to have less clearance. So they end up with the same production, less clearance at the liver, so particles build up. So again, context, context, context, the sucralose in the context, you know, of the other carbs, it matters. Oreo in the context of our heliolimus hyper-responder or low carb diet or a person on a standard American diet with obesity and metabolic syndrome, it matters. All these contexts matters. And the, you know, the consequence of high LDL, you know, etiology, cause, what is driving it up does matter. It doesn't, again, it doesn't mean this is safe. All these things people like to entangle and jump from one thing to another.

So even if I say this lipid energy model is normal physiology, it's adaptive. That doesn't mean, I mean, it's safe. I think it's safe and healthy. Those can be separable because it could be an acute adaptive response. Like if you're being chased by a lion and you have an adrenaline rush, but if you're like constantly having that stress response, it's harmful. So for me, it's a metabolic demonstration because I want to understand the physiology. I'm not putting value judgments on this. I'm just saying this is something curious. And if anybody listening is a real scientist, they'll be curious too. And my question is, what are your thoughts around, do you think that eventually if you continue to eat these Oreos every single day, that there would be a turning point and it would

start going back up again? Because at some point your metabolic health would most likely, I would assume, suffer. Yes. I would say yes, if eaten indefinitely. However, it would never get as high as it would be on keto. Again, order of magnitude here. My peak LDL was in the 500s. So you take somebody on a standard American diet, you can feed them all the saturated fat you want, all the Oreos you want, don't actually do this, but their LDL will never even get to half of that. It'll go up, but it won't go up to the magnitude. So if you think of the inverted J, it's like if I started way up here and I dropped to here, if I continued Oreos, it might creep up as I develop metabolic syndrome and obesity. It's never going to skyrocket to that level. But again, it's going to go up for a different reason. It's not going to refer to its original physiology.

Yeah, this is fascinating. Another truth about diet is acute results do not equal chronic results, as you're pointing out. Yeah. And what are your overall thoughts on LDL, HDL? Because there's been a lot of conversations lately that are going against the mainstream grain. And do you tend to lean on the side of you think a higher LDL is not necessarily of concern, depending on other factors? For example, I'll give myself as an example. My LDL is just barely a little bit higher than what mainstream health would consider to be healthy. Mine's just a little bit higher. And my integrative doctor told me recently, I'm not worried about that in the least bit.

Where do you lie on that? First thing first, I'm a PhD scientist and a fourth-year medical student, which means I'm not a licensed clinician. And of course, you should never give medical advice off of social media. So nothing I say in medical advice. Yeah, this is all opinion.

All opinion. That said. All opinion, yeah. I think it's fair to say that context always matters. So I really dislike phrases. This happens all the time. Like lower is better. Lower LDL is better.

Lower APOB is better. I'm like, with respect to what? With respect to your independent risk of cardiovascular disease? And also, how are you lowering it? You know, because all interventions have trade-offs. So what I would say is, I think the data suggests that LDL particles are part of the causal pathway of cardiovascular disease, that they're necessary, although not sufficient. So on that logic, you know, it makes sense to undermine something that's necessary in a process for a disease development. So I won't say LDL isn't causal, that it's not a cause, that it's not an independent risk factor. However, it requires greater context.

So if you asked me the question, do I think everybody with any increased LDL needs pharmacotherapy, my answer would be no. And again, I don't think that's controversial. It's reasonable. And actually the data are trending towards that way now. When you look at getting functional tests, CACs and CCTAs of arteries to see is there plaque, the data show that if people don't have plaque, it's kind of makes sense, right?

Functional tests, it's a biomarker. You know, then there might not be benefit to intervening with medications that have side effects known and unknown. Statins have side effects. We can quantify them. I'm not going to say they're rat poison. I'm not going to say they have no place in medicine. I think they do, but we can just admit, but they also have side effects. So in any individual, it's always about weighing the pros and the cons, what is known and also what is unknown, because some of these medications have plausible concerns that have just never been investigated. So you need to weigh the knowns and the unknowns and also

acknowledge where, so you need to weigh the pros and the cons and acknowledge where there are unknown risks and then make an individual choice that's best for you based on your personal history, including things like your personal history of cardiovascular disease, do you have plaque on scans, and family history. It's very different if like you have a scan with plaque on it, and you had two parents that both died of 50 of a heart attack, and you have genetic risk factors, oh, and you smoked and have obesity. That's different than somebody who's had, oh, somebody who's had, you know, an LDL of 200 their entire life, they're 60, they have a CCTA with zero plaque score, and they have no family history of cardiovascular disease. Those two people, even if they had the same cholesterol, should not be treated the same. So I can say, I think it's

fair to say LDL particles are part of the causal pathway and necessary, but they need to be taken in context. And not everybody with high LDL requires pharmacotherapy. And I think it's a pretty reasonable stance. 100%. I completely agree with you. And what I love so much about this is that a lot of our conversation today has come back to this notion of bio-individuality, which is there's always going to be nuance and we can't just put a blanket statement on every single human and just say, this applies to every human that lives and eats and breathes on this planet. There's a lot of other things that we need to take into account. And what you just so beautifully laid out, I think is incredibly important for people to understand

because it all depends on the context. And the terrain, the terrain of the body. My LDL is going to be very different compared to somebody who is overweight and eats the standard American diet and smokes. If they have a higher LDL, even if I have a higher LDL than them, I probably would be more concerned about them.

Yeah, I just had this conversation with my mother, which I have permission to talk about. You tell me if this is a good idea because I'm considering doing a video on it. But she is about to turn 60. And we were looking through her old medical records. Her LDL has not been, even going back to like 30 years ago, has not been below 170. It's currently over 300. So she's had a huge exposure. And it's been a hard conversation because she has concerns about, you know,

treatment, and so we decided together, I mean, she likes my input on these topics because I've read a lot, like to get functional testing. CCTA, not a CAC, her coronary CT angiography shows zero plaque anywhere. Wow. And it's like, what do you do with that? Because it's not just like, okay, it's not about just how high, but how high for how long. So if you go keto and your LDL goes to even, let's say it goes to 500, but it's there for a year, I'm not going to say you can gather much from a ccta one year later but if you've had levels averaging like 250

for 30 years and then you have no plaque then i mean i think yeah there's less cause for concern you take a medic this is a i bring this up because i don't mean to make it like it's a very obvious answer i bring it up as you know authentically and transparently like i don't gamble with my own health i definitely don't gamble with my mother's health these are conversations we have and never say do this don't do that but it's like a conversation that we you know i'm about to be an mdphd she is an mdphd we still struggle over it's like a dunning kruger thing it's like we like we acknowledge all the unknowns and what we don't know that these are hard decisions that people have to make in an informed manner,

not a dogmatic one, because these are real people, real hearts, real lives. But it does deserve a conversation, and every case is different. I was going to say, I was going to ask, do you think I should do a video? My mom's given me permission to do a YouTube video. I think you should. I think you should, and I think a YouTube video would be best because it will give you enough time to really lay out all of it because nuance really matters a lot in this particular situation. And I would be curious, and I'm not asking you to divulge this now, or even if you want to divulge it publicly, period. I would be

curious to know if there's been any sort of dietary changes, changes to A1C, metabolic health. I would just get curious around those areas. She's been low carb since probably for three years. I went keto five years ago, and my whole family just kind of followed for individual reasons. Hers were for more cognitive longevity. That's a whole different topic. But yeah, no, it's tough. Yeah, that is tough. And that's a hard one. But you know,

and then I go into, I had, do you know Johnny Bowden? He wrote The Cholesterol Myth. No. Okay. I would love to hear your take on his book. He wrote a book called The Cholesterol Myth, and I had him on the podcast a couple of years ago. And I know you're not going to be able to respond to it now, but maybe something to look into. And he came on the podcast and said that we have gotten cholesterol all wrong. And without going into the full details of it, essentially, he's pushing back on this mainstream notion of that we, and I think you and I are of the same mind in this sense, is that he thinks that it's damaging for us to put a blanket statement on everything needs to be lowered, we need to lower the cholesterol,

it needs to be as low as possible. And he talked about how the medical community over the years has continued to lower what the average cholesterol should be. And this has been a fight to get more people on the statins essentially. And his argument is that this is really damaging because we forget when we have this certain conversation of continually lowering cholesterol that cholesterol actually plays a really important role in our body and especially in our brain. And so there is this fine line of making sure that we're not lowering it to the point where we are seeing cognitive decline and we're seeing other issues in our health.

Yeah, it's complicated because I can play devil's advocate for either side. I mean, each tissue does generate its own cholesterol and all it needs to survive um and also like peripheral cholesterol like the ldl particles aren't really crossing into the brain so if you have uh you know like a tropopidoic acid which you know inhibits an enzyme in the liver that's gonna like inhibit cholesterol synthesis specifically there could it really affect the brain is it really gonna affect the brain like i it really going to affect the brain? Like, I don't know. But again, it's a matter of like, these medications all come with side effects and possibilities, concerns. So even independent of the effects on cholesterol, it's like, what is the absolute benefit you're deriving, presumably from the lowering? Let's even say

that lowering does reduce your cardiovascular risk, everybody by some extent, however much. If the absolute benefit's really small, what other risks are you incurring by taking these medications? Again, known and unknown. There are things like the PCSK9 inhibitors, which are very potent at lowering LDL. Why do people with PCSK9 loss of function not tend to live longer? In fact, if you go into the Mendelian randomization studies, which people love to point to, I don't love them, but people love to point to for LDL and apobyling. I remember reading this one paper on Mendelian randomization for PCSK9 loss of function. They didn't even really comment on it in the text or emphasize

it at least, but there was this one graph, I can text it to you later or DM it to you, where they were looking at hazards ratios for increased risks of different diseases. And then it was like, basically the way it's designed, the particular graph is if it's more to the right, there's an increased risk. If it's more to the left, there's a decreased risk. And I remember I was reading it on my phone, and I was like, okay, PCSK9 loss of function, decreased risk of stroke, decreased risk or ischemic stroke, decreased risk of heart attack, decreased risk of this, that, and the other. And I was scrolling down, and then I got to one that said Alzheimer's disease. But there was no, the way the plot works is there's like a little dot.

And there was no dot. I'm like, where is this dot for Alzheimer's disease? And what I realized was I was reading it on my phone, so it was a vertical screen. The dot was so far to the right for increased risk, this study, that it wasn't even on my screen. So I had to look at it in a different format to see that it was actually the biggest effect, but it wasn't really emphasized. Now, to be clear, I'm not saying these drugs will increase your risk of Alzheimer's disease. I'm just saying we can't have double standards. So if you're pointing at the MR to make a case, and there's another MR that says, well, there actually might be this risk based on this study,

but then you don't have the long-term data to rule out the risk or confirm it's there. Then you have to keep it open as a possibility. So then we just don't say, oh, you're going to take this drug and we know it's not going to have this effect because we don't know. There's a possibility that it could affect your cognition long-term. A possibility could increase your Alzheimer's risk. So yeah, maybe it's going to reduce your cardiovascular risk by some extent. But if your LDL baseline is not that high, let's say like people say, oh, you want it like below 50 for whatever reason, that'll prevent cardiovascular disease. If it's 100, do you want a PCSK9 inhibitor?

I think most people at this point would say probably not. And again, it's like, is there a benefit potentially? Is there a risk? Potentially. So let's weigh them and make an informed choice. And it's just like, I feel like a lot of academicians struggle with interacting with the general public because they feel if they give an inch a mile is going to be taken. And so they try to brush side effects under the rug rather than trying to have an evolved conversation and just try to communicate the nuance and the caveats. And then if there are risks, say there are risks, then quantify them. And people aren't stupid. So then they pick up on this and they get frustrated because they feel like they've been lied to or deceived, or that's the attempt. And so you get

this chasm of mistrust. And that is just problematic, but that's kind of where we are right now. Yeah. And when you build up that much mistrust, it can be incredibly damaging because, you know, then information that could potentially really be life-changing and life-saving, people dismiss it because they're like,

oh, well, they lied to us about this. They're probably lying about this. And it leaves a lot of room for conspiracies. So I think people are undermining their ability to treat the patients who need treatment by brushing under the rug potential concerns, which are fair to acknowledge while acknowledging the utility of the interventions, including the innovations of pharmacotherapy that we do have. Yeah. Yeah. You bring up a really good point of informed consent, which is basically the entire premise of my platform, which is at the end of the day, I really don't care what you do and what you do with your life and what choices you make as long as you have informed consent and you know you have the ability to go in and weigh the risks versus what benefits you're going to get out of it. And I think that's incredibly important. And I wanted to ask you one more thing

in the essence of time because I've taken up a lot of your time. What have you concluded thus far with your Oreo versus statin study in the sense of I was thinking as we were talking about this just now, what is the listener going to take away from this? What did you learn that you're excited to continue to dive into further down the path? And what did it mean to you when you found that out as far as what people could apply

to their day-to-day life? Yeah. Well, I kind of knew how, I had a very strong prediction how the results would roll out because of our understanding of the physiology and the fact that people like Dave, my friend Dave Feldman had done very similar things before. So the actual results themselves didn't really surprise me. Maybe the magnitude of the Oreo result did. What I learned, I think what's applicable to the viewer, and especially in including those who aren't lean mass hyper responders, is, I mean, I didn't know, I talked about this in my interview with Walter Willett. Like, I didn't know how people would respond to this, because admittedly, I was

throwing what is a social media grenade out there, creating a fire that I might not be able to control the narrative of. And to some extent, it's gotten away from me. That was always going to be the case in certain circles. However, I was auditing the response to say, on balance, is this helpful or harmful? Is it actually provoking people to be curious, which is my thing, stay curious, it's my mantra, and engage, including academicians, including clinicians, including the lay public, and bring us all together in a unified curiosity about physiology? And my unequivocal answer is yes, which is very heartening for me. And it's also, I think, the useful takeaway for the viewer, because again, I wasn't presenting a value judgment here or even necessarily providing

a tool. Although if you're a lemus hyper-responder, carbs will lower LDL. What I was doing is saying with this awkward finding, are you okay with sitting in curiosity and joining us on the journey of asking the questions? Because the cool thing about this day and age is there's so much access to information. You don't need to wait until the textbooks are written to gain access to it. You can see it happening in real time, which means I can present to you data

that provokes more questions than answers and present to you something that might not immediately seem actionable. I know people love when podcasters say like, do this to get that. Sometimes I'm like, this is curious. Isn't this cool to just think about? And then we engage on this journey of the questions and the discovery together. That's what I want to emphasize that I learned that I think I really hoped that I could get people curious and excited. And I found people

were, which means, you know, that a large proportion of those listening, actually probably a hundred percent by those listening at the two hour mark are in that population of people who are what I consider true scientists. A scientist is not something that comes with a degree, but it's something that is an attitude. If you're listening at two hours and if you're curious about Oreo versus statin, then you have that attitude, which makes you a scientist. Yeah. I love that. That's so cool. Well, I'm very excited to see what happens with this and what you continue to discover, because I think you're probably going to continue doing more studies

around this, I would assume? It's just getting warmed up. So, yeah, the end of... Yeah, well, I mean, I've been doing all this, I would assume? It's just getting warmed up. I've been doing all this through the roughest years of medical school. So now I'm going to be getting a little bit more bandwidth. I will say, one project we're designing now is a seven-figure project. The things we've done thus far, I had a budget to buy myself Oreos.

That's what I got. Things are scaling up now. And also it snowballs because people get interested and we attract more and more eyes, including the eyes of some very heavy hitting people. Harvard, Stanford, Oxford, elsewhere. The nice thing about my education path is people tend to honestly,

probably the most valuable thing about Harvard education is people respond to a.harvardedu email. Oh, for sure. It makes it easy to make connections. So I'll leverage that. I have no shame leveraging that. But yeah, no, we have a lot coming down the pipeline. Things are only going to accelerate.

I'm so excited. Well, I can't wait to continue to follow along. I want to ask you one more question. This is just a personal question that I ask all my guests at the end, which is what are your health non-negotiables? So as somebody who cares a lot about your health and you're very mindful about your diet, what are your health non-negotiables? Mine might not be generalizable to other people because I use a ketogen diet for inflammatory bowel disease therapeutically. So I will say right now a non-negotiable outside of experimentation is maintaining a ketogenic diet

for me. I would say I'm very strict with my eating windows. Again, that's specific to me. I'm not saying eating at 9 p.m. is going to kill everybody, but like I just find my gut gets wrecked if I eat dinner late. So I generally stop eating at 6.30pm. With very few exceptions. I guess it's not a complete non negotiable. But like, I even know if I eat dinner at like 745, like my I just will sleep terribly. So it just has a snowball effect on me. Beyond that, exercising, if I'm not injured, at least six days a week, it's just so good for my mental health. I don't do it. Do you know to hit performance metrics anymore? I used to be competitive. I'm not but it just like, it makes me more efficient. It makes me happier. It makes me nicer to people

around me. Those are my high level non negotiables Getting enough protein every day. I mean, always. I mean, my fat intake is pretty high, but even fat, like I don't measure fat or even really think about it. It's like, all right, if I ate 350 grams of fat today, fine. If I only ate 100, I'll eat more tomorrow. The protein is just like, it's always the staple.

So I don't, I mean, so yeah. Are you measuring your ketones? Are you just kind of, you know? Not anymore. I mean, I used to, and I can probably guess within 0.2 millimoles what they are at any given time. I developed a sixth sense when I was tracking it very early on, because I could just like tell based on how my gut was, like where my ketones were up to a certain point. And if they're above 2.0 millimoles, then I couldn't guess, or they're really high, I can't guess. but no, I mean, I'm in ketosis.

I used to measure a ton with my keto mojo via finger stick. At this point, I just have an intuition. Um, and do you find that your, does your, uh, protein intake sometimes throw you out of ketosis if you eat too high protein? Yeah, it can. It can. Um, I would say it's not usually, I've never had symptoms from, well, maybe like if I have like a 20 ounce steak, I'm a small guy, then the symptoms might not then be related to going

out of ketosis. Exactly. Yeah. Within reason. No, I mean, don't go like a rabbit star. Like, I'm not like saying don't eat like pounds of codfish and like lean chicken breast. But I wouldn't be afraid of protein. I usually eat around one to one point one grams per pound, which is a lot of protein. So like over like two point two grams per kilogram or more. That amounts to, though, like 20 percent or less of my my energy requirements. So I'm not scared of protein protein but i'm also not like high proteins become such a thing now that like people like think high protein and like are trying to eat

i've seen like 2.5 grams per pound and i'm like that is absurd yeah there's no benefit to that that's just like way over the top um i'm not saying it's gonna hurt your kidneys or anything i'm just thinking it's a little bit unnecessary so So if your goal is ketosis, don't do that. But I don't think you need to restrict protein either, unless for whatever reason you need like a three to one or a four to one ketogenic diet. But outside of some very specific conditions, I don't think that's necessary. So no, I'm not protein phobic. Amazing. Well, Nick, this has been absolutely fascinating. I am just so honored to have had two hours of your time. I love the work that you're doing.

I think what you're doing is groundbreaking, I think. It's really cool. I love the way that your brain works and the questions that you posed. I love the nuance and the way that you're able to speak to these nutrition concepts really from a different standpoint than I've heard anybody talk about, which is very cool. It's a gift that you have. Thanks. I think you pose a lot of really important questions and you really get the listener to think. I mean, you definitely made me think through all of these topics that we talked about today. And I think that's really

valuable. Thank you. I appreciate it. Yeah. So please let everybody know where they can find you and yeah, just plug anything that you want to plug. I'm at Nick Norwitz on basically all platforms. N-I-C-K-N-O-R-W-I-T-Z. That includes Instagram. That includes Twitter, YouTube. I'm now on Threads, LinkedIn, Facebook. So I've very recently expanded my socials historically I was on X and YouTube so follow me engage with me on your favorite platform I'm probably most active like looking at comments on YouTube where I produce videos so engagement there is appreciated oh I also have a state curious metabolism newsletter where i give kind of stream of consciousness often or

like commenting on hot topics so any of those would be great and um yeah engage with the research i always appreciate when we put out work we have a couple papers that have been accepted will be coming out two this month actually one on the-responders, another on inflammatory bowel disease, and a carnivore diet. I think it's such a skirt. But yeah, reading those, sharing those are really helpful. I will say we talk a little bit about incentive structure, quite honestly. Attention for papers makes journals happy. It helps us do more papers. So like reading the paper, talking about the paper, sharing the link to the paper in a unique tweet with the link kind of like near the beginning of the tweet. It literally helps boost paper metrics, which journals do look at. And so all those things help.

But really just express curiosity, engage with me authentically. That's all I want. I love that. Yeah. Thank you so much for your time. Thank you so much for listening to The Real Foodology Podcast. This is a Wellness Loud production produced by Drake Peterson and mixed by Mike Fry. Yeah. Thank you so See you next time.