Insulin Resistance, Fasting, Ketones and “Why We Get Sick” – Dr. Ben Bikman with Dave Asprey : 804

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You're listening to Bulletproof Radio with Dave Asprey. Today we're going to talk about something that affects, well, at least half of the adults in the United States and a lot of kids and probably more than half. We're talking about insulin resistance. And it's something that has been a focus for me for more than 10 years. It's part of the bulletproof diet. It's part of fast this way. In fact, fasting is very impactful for this. And I've asked Ben Beekman, who's a PhD on the show today, to talk about why insulin resistance is happening. And the reason you care if you're not worried about diabetes is that insulin resistance makes you less powerful every day until you get diabetes. So it's about, can you use food and air to make energy? There's a core biohacking thing, and you've gotta nail this one thing. And everything else you do is easier when you have more electrons. So this is like ground zero of biohacking. Ben's a biomedical scientist and a pathophysiology professor at byu, and he's looked at elevated insulin and how it makes you fat and the relevance of ketones in how your mitochondria work. So I'm kind of an early keto guy. Bulletproof coffee has that brain octane that makes ketones. So these are really, really core bulletproof lifestyle issues. But we've got a professor who's gone really deep on them, and he's got new thoughts about insulin resistance and why you have to pay attention to it. This interview is based on his new book, why we get the Hidden Epidemic at the Root of Most Chronic Disease and How to Fight It. And I think you're really going to get a lot of information, a lot of knowledge out of this interview. I'm super excited to do it for you. Ben. Welcome to the show.

Hey, Dave, thanks so much for the invitation. I'm looking forward to it.

You could have studied a lot of things at byu. And getting really deep into metabolic function and cellular energy generation requires a. A certain kind of mindset. Why did this, of all the things you study, I mean, I. I want to know why octopus suction cups are so cool. I mean, you're a curious guy. Why did you go here instead of to the Octopus?

Yeah, yeah, right. For me, it started with one single manuscript. I can really point to one moment where during the course of my master's degree, which was in exercise physiology, and that itself was me just Sort of scrambling to know what area I wanted to focus on as I moved through academia. One paper I found the. The manuscript had been published in the late 90s and it detailed how fat cells released pro inflammatory proteins. That fat cells themselves could be a source of something that we thought was only coming from immune cells and was only relevant to immune function. That to me connected dots that, that at the time were very novel in the late 90s. I saw this manuscript in the early 2000s, so it had already been out a few years. I didn't know about it, but it started to explain the connection between fat tissue and disease. We knew having more fat increases the risk of numerous diseases and diabetes was the most obvious one that this manuscript was connecting it to, namely through insulin resistance. But the fact that the fat cell was producing these pro inflammatory proteins to me really revealed two interesting details. One, that fat cells are endocrine organs, just like the thyroid, just like the gonads, just like the adrenal glands, they release hormones into the body and we're learning more and more hormones like estrogen. Yes, that's right, yeah. Even sex hormones. So the fat cells are wildly relevant to the endocrine system. That was a revelation to me. And two, it, it pointed at a mechanism connecting the fat cell, as I already alluded to a moment ago, to disease throughout the entire body. That fat tissue itself is more than just an inert storage organ waiting to be fed or in a fasted state, waiting to give up its energy there it played a more, much more fundamental role in, in health and disease. And then insulin resistance, as I mentioned it really at the time, I saw it as only a mediator between fat tissue or obesity and diabetes. But the more I've scratched beneath the surface and this really started, it really accelerated as a professor rather than just a scientist when I wanted to start teaching some of these concepts of disease to my future. You know, these students who are pre med and nursing students. And then it was realizing that insulin resistance was far more relevant to just type 2 diabetes, but pivotal to Alzheimer's disease, heart disease, infertility, fatty liver disease, hypertension. And I could go on and on.

All the bad stuff and do it book length.

Of course.

Yeah. It's funny how teaching forces you to organize your thoughts and so does writing a book. It's one of the reasons, of course I write. It's also why I just launched the Upgrade collective where I said I'm going to teach all of my books over the course of one year, like almost university level courses. But not quite the hard, because teaching is going to make me even better at, at the nooks and crannies of the knowledge. I, I love it. Like I started teaching and then I had to go even deeper because a lot of people haven't taught, would never know that. That's the secret of learning is teaching.

That's for sure. That was certainly the case for me. In fact, at the time when I got my primary teaching assignment from the university, it was a class called pathophysiology. And I thought, well, I've taken a lot of physiology, but I've never taken pathophysiology. And I was so desperate to play to my strengths whenever I could in this course. You know, the secret of a first year professor is he barely knows more than, or she barely knows more than the students do, you know? Yeah, exactly. Yeah. But it really is true. And I thought I just need to, I need to lean into my strengths. And my strengths were insulin resistance, the background, and then, you know, even at a cell biology, a cell level. And so I thought, well, I know of insulin resistance and its connection to diabetes, so I can talk about that in that particular lecture and really speak with authority. And, and then when I worked on the hypertension lecture, I would think, yeah, I know there's a connection there. I may as well play it up a little bit just so I can speak with some authority and not be really just sort of faking it. And then the more concepts, the more, the more topics that we were covering. I kept asking, well, I wonder if it's relevant here as well. And I would, I would, I was always able to devote a little bit of time within a lecture and just highlight once again this, this relevance to, to one common disorder and, and beyond. I mean, someone listening may think, well, that's just the, the efforts of a selfish professor who wants to play to his strengths. But the more I looked into this and thought about it, the more I believed there was a genuine value to these future medical practitioners. If I can convince these future nurses and doctors that some of the most common health disorders, these plagues of prosperity, as I like to call them, have to at least some degree a common core. Rather than continuing to trim the branches only for them to grow back, let's just chop the damn tree down. We go right to the trunk of the problem and we address the insulin resistance. And then in my mind, I've convinced myself that these students, having seen the data that I show them, will know if insulin resistance is relevant to this disorder in my patient. Or the people you and I are talking to now, what's the best way to address it? And it is never a medication. But I get, I'm getting ahead of myself. But it's this idea I've convinced myself or this hope I have that these, my academic offspring, as they go into the clinic, they won't think. They won't think drug first. They'll think diet.

That is such a profound gift. So people can learn that. And there is a sea change happening in medicine now. As you go back 20 years and you talk about diet, they'd laugh at you and say eat less. And it's really shifted, at least in most doctor's offices. But when we get to insulin resistance, for me, every degenerative disease that I've found is tied to mitochondrial dysfunction. And so the mitochondria making energy, you make enough energy, your body will take care of itself. Don't have enough energy, it starts turning off repair processes that doesn't have energy to do. And one of the things is if you have problems inside the mitochondria making energy, well, you'll have insulin resistance because sugar can't go into the cell because it won't turn. Or you can have membrane issues. But the end of the day, I don't really know much of a difference between a mitochondrial inefficiency or insufficiency and insulin resistance. Because a bad mitochondria causes insulin resistance and insulin resistance that's membrane based causes mitochondrial dysfunction. It's like both sides of a coin. Is that a good way of thinking.

About for sure is there is. So mitochondrial dysfunction is a very broad term that will have an effect, a pathological or a pathogenic effect in countless ways. And without a doubt, there is there no doubt beyond any doubt, faulty or, or mitochondrial with. With a less. I hate to use the word dysfunction because sometimes there's a purpose to the mitochondria not working the way they are. But let's just go with dysfunction. If the mitochondria are dysfunctional, there's no doubt that the production of reactive oxygen species will directly antagonize the insulin cascade. You know, when insulin binds to its receptor on a cell, and it would be literally any cell in the body, it wants to initiate a series of biochemical events. These new. This change in redox status because of the production of reactive oxygen species, it will directly antagonize a portion or some aspects of that process. It'll in other words, stopping insulin from doing what it wants to do. And then to your point, this this can go. This is a bidirectional phenomenon where, where mitochondrial dysfunction certainly is a contributor to, to insulin resistance, although there are other inputs that are certainly worth noting. But, but insulin resistance itself will start to affect the degree to which the mitochondria work. And that's because insulin is a necessary hormone for any cell to maintain homeostasis. It, it provides a tone, if you will, letting a cell know signaling to a cell whether it is okay, whether it has the green light to repair itself. You know, like as a mitochondria, a mitochondrion starts to age each individual, in fact, even the mitochondria themselves are highly dynamic organs. We published a manuscript just a couple years ago finding that we could force the mitochondria within a cell to pull apart and be individual organelles. And then what has to happen in the life cycle of a cell? The mitochondria pull apart and then the cells can divide and then the mitochondria will fuse together again to facilitate optimal catabolism of nutrients. You know, if you are trying to burn fat or burn ketones or burn lactate, an oft overlooked fuel, you need the mitochondria to do that. And they, it works better when the mitochondria are reticular or stringy. In fact, the word mitochondria comes from the Greek word mitos, which means thread when you look at mitochondria under cells first. I will never forget the first time I did this. We had cells, we stained them to visualize the mitochondria, and it was just these little strings. And I'd never known that. I'd only ever been taught the kind of textbook example circle with a squiggle in the middle. Yeah, that's right. Yeah. So. So anyway, my point is, insulin will most certainly feed into that process and to a very real degree, prevention the mitochondria from being dynamic from fusing, undergoing fission and fusion, which is absolutely essential to mitochondria performing their jobs, which a primary one is of course, the catabolism of nutrients.

Given that we know excess white fatty tissue creates huge amounts of inflammation and creates insulin resistance, probably in part because of or in conjunction with that inflammation.

Yep.

A morbidly obese person walks into you, walks into the bar where you're sitting there now, it sounds like a joke and says, look, I know you know, you're not a treating doctor or anything like that. You're a PhD, but tomorrow I'm either getting liposuction or gastric bypass.

Oh, that's Clever. That's a clever. What would you do? That's a clever boy. That is clever. So. Oh man, I hate both of them, for the record.

Agreed, agreed. But I think the lipo might have an advantage.

Yeah. So in fact, it's a wonderful question. Much of the metabolic. This is going to be a very provocative way of saying this, but I do mean it. Much of the metabolic damage that comes from fat tissue is that we can't get fat enough. There's this threshold that when the fat cells are unable to continue to store fat, they become insulin resistant, they become pro inflammatory. It's as the fat cells have become too hypertrophied. Now there are, and this is the vast majority of people, the vast majority of people get fat through a process of hypertrophy. The fat number, the fat cell number doesn't change. Each individual fat cell is getting bigger. There's a small portion of the population that has an almost limitless capacity for fat storage. It's because the, the moment the fat cell grows, they recruit, they recruit new fat cells. They force these pre adipocytes to differentiate into functioning fat cells. And that's a process called hyperplasia. So if someone can get fat through hyperplastic fat cells, they will have almost no metabolic disruption. They will be potentially obese, morbidly obese, they will not be healthy, but they will have a surprisingly good looking metabolic profile.

What percentage of people is that?

Yeah, so of obese people that is anywhere, it's a range of 10 to 20% of people that are obese have that potential. And these are the individuals that can get to 500 pounds. Most people could under no circumstances get that big. It wouldn't matter what they did, they could not have that much.

The fat cell can only get so big, then it forms ceramides on the outside to keep it from exploding, which cause insulin resistance. And then you're done and you're as fat as you're going to get and you're miserable.

Yep. And that's back to my original point in answering your question. It's. We get sick because we can't get fatter. And I know that sounds crazy, but it's because the person reaches their threshold, they reach their fat limit and beyond which the body, the fat cell itself, the hypertrophic fat cell, actually, it's, it's. We have to almost forgive it for causing the problem. But as the fat cell gets hypertrophied, it knows it can't get any bigger. If it gets any bigger, it will, it will die. And then we have necrosis, and that's an ugly, messy, dangerous process. And so in order to prevent itself from growing any bigger, it becomes insulin resistant and it starts to leak out fats when it shouldn't, because insulin would want to inhibit that process. And at the same time, adding insult to injury, this really. These really big fat cells have pushed each other too far from, from capillaries, from blood. And a cell must be right up against capillary. You get hypoxia, gas and that exactly right, yep. So the hypertrophic fat cell becomes insulin resistant to prevent itself from exploding. It becomes, in the process of becoming hypoxic, it starts releasing pro inflammatory cytokines, some of which will increase blood flow. It's trying to stimulate angiogenesis in order to save itself. But in the process of trying to save itself, you, and we are the ones who put it in that position because of our diet and lifestyle, it ends up leaking free fatty acids and pro inflammatory cytokines throughout the rest of the body. And this is all, of course, white adipocytes, which you'd mentioned at the beginning. This is the white form of the pure kind of fat storage form of fat cells. It starts leaking this stuff, this toxic cocktail throughout the body. And then we have other tissues becoming insulin resistant, like muscle, like brain, blood vessels, et cetera.

One of my favorite nootropic things to do that I don't do very often because of Dale Bredesen's work on insulin resistance in the brain as part of Alzheimer's. He's a friend who's been on the show a couple times, is to snort insulin or intranasal insulin. You take a very small amount of that, and it's like your super brain for a few hours. Is that bad for you?

Oh, what a great question. So, so the, the, the thought behind this, although your audience probably knows, right, the idea is you get the insulin yet. So you get the insulin directly up through the nasal passage, and it absorbs up and gets into the body, gets into the brain that direct that way. Um, and in that sense, it allows you to circumvent potential problems with insulin resistance, because that is. And your audience would know if Dale's been on there, that is a fundamental part of, of cognitive decline. This, this insulin resistance of the brain and a compromised glucose uptake. In fact, we're, we just had accepted for publication an article where we outline this broad reduction in glycolytic enzymes, glucose uptake, and glucose catabolism in the brains and of people with Alzheimer's disease. But you'll get a kick out of this. No deficits in ketone or ketolytic enzymes in these demented brains, but nevertheless, the idea of inhaling insulin, it does appear to facilitate insulin action in the brain. Now, a note of caution. I do, I confess I worry those epithelial cells of the nasal passage, it is a totally novel thing that insulin will would be coming to those epithelial cells. There's a little part of me that worries that if that were done chronically, that the insulin, which is very much a growth signal, might facilitate the growth of the epithelium on the upper aspect of the nasal cavity and either just thicken it and that would be where it ends, or in the worst case scenario, stimulating some degree of dysplasia, which would be a hop skipping, a jump away from cancer.

That's really interesting. I don't do it regularly because I don't think high insulin levels in the brain are a good thing. But on an occasional basis when you want to go into, you know, power up mode, it's kind of epic the way it feels.

Yeah, I know. I'm interested to hear that. Actually. I look forward. I'm really looking forward to more data coming out on that because I'd love to get my head wrapped around it.

Definitely. Dale probably has some stuff on that I can connect you guys if you're not already connected.

And I love it.

I look at that. And the other thing that comes to mind is we recently had a work or an episode with James Nestor who wrote Breath. And there's a substantial number of people who get the Roto Rooter sinus surgery who just have chronically dry sinuses forever. They probably should be hitting that insulin hard to cause some growth.

Yeah, yeah. I don't. Yeah, I wonder what it would do. I don't know.

I love the way you think about this stuff. And now, you didn't answer the question about liposuction versus bypass.

Oh, I didn't. Yeah. Yeah. So actually I wasn't trying to dodge it.

No, you didn't.

But that was a huge tangent, though, that I lost myself on.

It was great.

So part of illness, part of illness comes from metabolic illness, from you can't store more fat. And so the concern with liposuction, liposuction, you have physically removed fat cells and now if someone doesn't change their eating habits, the body is still going to want to be storing fat. And so people could look up the work by a scientist with the last name Klein K L E. I N. And he finds. This could be why. He finds that people don't experience improvements in metabolic health with liposuction, because what all you've done is remove fat cells, and now your ability to get fat and store that fat where it's supposed to be stored is compromised. So I would say this. I guess if someone has liposuction and they. They. That is accompanied by dramatic changes in diet that maybe eventually would have had them lose all that weight anyway, then I don't imagine there will be any negative consequences. If, however, someone has liposuction and they don't change the habits that caused them to get that fat in the first place, that the body is not going to be beat and in its efforts in it to store energy. And so two things would happen. One of two things or both. The remaining fat. And there is case studies for. For both of these. The. The remaining fat cells that aren't taken out will hypertrophy. Their growth will get exaggerated. And this can even happen. There's a case study of a man who had cold therapy, or whatever it's called, on his lower.

Oh, cool. Sculpting.

Yeah, that's it. Coolsculpting. Yeah. On his fat cells. On his fat around the lower part of his abdomen. And he ended up having this very odd pattern of fat regrowth. Right where they'd killed the fat cells. There's no fat, because you can't. Those fat cells are dead. But the other fat cells around it got exaggeratedly big. They hypertrophied significantly.

Same thing with liposuction. People oftentimes get fat, arms and legs. Because I was like, I got to put it somewhere. So you got to change what you eat.

Yep. So that was one of the two consequences. The second would be that you store it in what's called ectopic fat storage. Now you're storing more fat in your liver, you're storing more fat in your muscles, in your. In your. Around your heart. That's not a good trade off. So all of that is me saying I'm. I'm not an advocate of liposuction. Now, I'm also not an advocate of people perfectly mutilating perfectly healthy intestines, which is what gastric bypass is. There's nothing wrong with the intestines in those people. It's. And yet, to me, it's the only surgery I'm aware of. Maybe liposuction is actually the only other example where you're removing tissue that's perfectly healthy. There's nothing wrong with those Fat cells. There's nothing wrong with that gut. Now, having said all that, liposuction is one hell of a surgery. I mean, not liposuction, gastric bypass. You are messing around with a very dirty part of the body. If there weren't the potential for serious consequences from gastric bypass, I would probably be more of an advocate of bypass. But when you start cutting and sewing and moving around the intestines, you are. That, that is some messy stuff you're doing. But, but when it, when it works, the metabolic shift, the metabolic improvements are incredible. They are incredibly dramatic.

Almost the same as fasting. Right.

In fact, I was just going to say that's what happens when you take someone who could eat this much and you force them to only eat this much because otherwise they vomit because their stomach can't hold anything more. But the problem with the stomach in the intestines is it's a very plastic, dynamic tissue. If you continually eat to push that stomach, it will get big and then you eat more and all the weight you'd lost, you'll gain it all back and then some, and then you have no other recourse. So the metabolic improvements with gastric bypass are profound. I would argue if you could just have the mental fortitude. And I'm not saying it's easy to just eat as if you would, as if you'd had the gastric bypass. That's the sweet spot anyway. So, Dave, you're going to force me to decide. I, I actually may decide. I may would depend on how sick the person is. Dave. I'm not going to answer. I can't answer. It would just depend on how sick they were. If they're, if they were both very diabetic and heart disease, then I would say gastric bypass done hands down, because the liposuction will not fix those metabolic problems. It, it just won't. All the liposuction will do is let you look better in whatever you want to wear. But if they were too. Yeah, if they're healthy people, well, then maybe I'd say, well then definitely healthy. But overweight, I'd say, well then in that case, maybe the liposuction, I would.

Lean towards lipo because the gut's the second brain. And messing with the gut removal in the microbiome, all the nerves down there that we don't really know what they do, it's just too major of a surgery. And hey, if you have less fat cells and you change your diet, you will have less inflammatory cytokines, less estrogen generated by the fat tissues. There might be advantages, but you better not go back to, you know, the coke and donuts diet, because it's not, it's not going to serve you if you do that.

I agree, I agree. You have to have that little caveat at the end. Assuming they can change things, then that might change my answer.

Yeah, and there's also something around, I guess you mentioned the cold therapy one, which, guys, if you're listening, I don't think I've ever talked about that. There's a technique where they suck your skin with all the fat under it between two metal plates and then freeze the fat, but not the skin by using antifreeze against the skin. And then the fat cells die with a huge inflammatory cascade. But that probably resets your leptin sensitivity better than taking cold showers. So there might be a side benefit from that, but I don't think that's probably the highest and best way to lose weight when there's so many other tools. Like your book talks about a bunch. You know, we talk about fasting and fastest way and like we know how to solve this problem without any surgery. But it's an interesting thought experiment, right?

Oh, for sure. Yeah. But I am, I just. There's a little part of me that as much as I appreciate the pathogenicity of the fat cell, I also appreciate the relevance and the necessity of the fat cells. And so I'm generally, you know, I'm not a fan of cutting out, killing those fat cells, shrinking them. Well, that's another story. Let's shrink them.

All right, I like that idea. If you can just develop the shrink ray, it's going to be a big thing. Well, before we go into insulin resistance, can you tell me all of the good stuff that insulin does in our bodies? Like why is insulin important?

Yeah, right. And what a great way to start that topic because we'll be speaking about insulin in its role of. As being a villain, but it's also very much a hero. It is absolutely essential to survival. You must have insulin in order to survive. Now, the obvious effect of insulin is that it controls blood glucose. It does, it does that very well. And that is an essential job. But to only. And this is much of the problem why I'm such an. An advocate, a zealous missionary in favor of. Of people being more aware of insulin. Insulin and insulin resistance. Insulin does far more than just control glucose. It only controls glucose by its actions mostly on fat cells and muscle cells. All the other tissues of the body can pull in Glucose to varying degrees. Without insulin, even the brain has insulin independent mechanisms. It's just that insulin facilitates insulin, this extra bit of glucose coming in. But insulin, the theme of insulin, and this is a bit of a challenge because insulin will literally affect every cell in the body. That's how essential it is. It. Every single cell has insulin receptors, little doors that only insulin can come and knock on. The theme of insulin is that insulin tells the cell what to do with energy, and by extension, it tells the body what to do with energy. And there's some nuance. There's because within that idea of telling the cell what to do with energy is encompassed this idea of telling a cell when it can grow and when it can shrink, when it can build and when it needs to break. Both of those processes are absolutely essential to healthy function and certainly longevity. Insulin's role in longevity is not nearly appreciated enough. Like everyone who's invoking MTOR as a fear of longevity, all the more reason to look at insulin. But that's a bit of a tangent. But nevertheless, the theme of insulin is to tell a cell what to do with energy. And that is in an obvious way reflected in what it does to glucose. In a less obvious way, it's reflected. It's reflected in what it does to fats in the blood, ketones in the blood, the production of lactate, so relevant to all of the nutrients.

It also builds muscle, right?

Oh, for sure, that's right. And that was reflected in what I mentioned with telling cells to grow or shrink insulin. In fact, Dave, it's an. There's a little nuance there. Insulin likely doesn't stimulate muscle protein synthesis. In fact, there's evidence in single muscle cell experiments to suggest that that isn't the case. But, but it does defend the muscle once, once the protein has been made. So insulin appears to be more anabolic, not in the sense that it's stimulating the growth, but rather protecting the breakdown, inhibiting the breakdown. Because insulin abhors breaking. Insulin only ever wants to build. Now, that's not always good. If a muscle is constantly in building, if MTOR is constantly activated, you actually start to lose the effect of mtor. MTOR stops working. In order for any tissue to be healthy and even muscle to grow, and this might seem odd, you have to grow, you have to build and break, build and break, build and break. And insulin only wants to build. It never wants to allow breaking.

That's why cancer cells have 28 times more insulin receptors on average than normal cells, because they like to grow. Like, who would have thought.

That's right. Yeah, that's right. Yeah. So, yeah. One of the key mutations in many cancers is to enhance their sensitivity to insulin and thus kind of hijack that growth signal.

Now, for people listening, if you're thinking about this and your mind was blown about that insulin cancer thing, I want you to Google insulin potentiated therapy. And I know many people who've had chemo in conjunction with an insulin injection who got better way faster than they were supposed to. So there's some interesting science there, but we're not going to go too deep on that. I don't think on this episode unless you have a lot of knowledge and experience there. Have you played around with that a lot?

No.

Okay. I didn't think you would. But just for people listening like that little thing, if I set off an alarm bell, just go research that. The reason I asked you about the good parts of insulin is that I'm getting a little bit tired of a basic human thing that we do. If something is good, more of it is better. And if something is bad, you shouldn't have any of it. And I've seen this with, you know, different macronutrients. You see it all over the place with carbs, you know, maybe you can go low carb instead of keto some of the time and you'll be all right, you know, so we demonize. And some of the studies that I reference in Superhuman, my big anti aging book, look, low insulin, chronically low insulin is correlated with a much, much higher all cause mortality than high insulin. Why would that be?

Oh, I would think if it's genuine states of low insulin, it must be encompassing people with diabetes, type 1 diabetes that are, that's poorly managed people on.

Long term, unending, non cyclical keto, the way I tell you not to do it for the last 10 years, you tend to get lower and lower and lower chronically low insulin levels, which probably isn't a good thing. Every now and then have some carbs. No, it's okay. Turn off corn syrup.

Yeah. In fact, what's so interesting about the ketogenic diet on insulin? There is, and I don't want to change the topic too dramatically, so pull me back if I start going down that route. Um, there's no question a ketogenic diet will lower insulin dramatically. That's the very nature of ketogenesis. There's no ketone. Unless insulin has basically taken a back seat there. That, that has, that does change the metabolic milieu in an individual with long term ketogenic diet adherence Some people will say it causes a physiological insulin resistance. That isn't a term I like because you don't have insulin resistance in the body. This global insulin resistance, unless insulin is elevated. There is to my knowledge, truly no exception to this. There are states of physiological insulin resistance, but even in those states, which is puberty and pregnancy, insulin is elevated significantly compared to where it was before the state started and where it will be after that period of rapid, explosive growth has ended. Now, however, there is a metabolic alteration in long term adherence to ketogenic diet. And the best way I think to describe it is to put it in context of metabolic flexibility. Anyone? Everyone knows metabolic flexibility. Is this a state where you eat a mixed macronutrient meal and in the ensuing hours following that meal you are in sugar burning or glucose burning mode. After a few hours, the glucose burning starts to turn off or taper off. Fat burning starts to predominate as the key metabolic fuel. So the human metabolism is that hybrid engine in overall, overall human metabolism and it really is a shift of glucose to fats. Now I'm not saying there aren't other nutrients, there are like there's amino acids.

And lactate and all that.

Yeah. But overall metabolic fuel is a mix of glucose or fats and that that switch is entirely dependent on insulin. If insulin is elevated, the body is obligatory, obligatory in sugar burning mode. When insulin is down, the body must shift and go to fat burning mode. And in fact it's fat burning so much that it starts making ketones. Now most of the population has a metabolic inflexibility and they're stuck in sugar burning mode. So even hours after they've stopped eating, they're still burning sugar and they just can't make that shift to fat burning. So good luck losing weight because if you can't tap your own fat for fuel, it's never going to go anywhere. And that's because the average person is insulin resistant and hyperinsulinemia. Now with long term adherence to a ketogenic diet. This is a bit of speculation now, but based on actual data, in fact, we're going to do some of these studies in rodents in just the coming weeks actually. But what happens is the body becomes metabolically inflexible in the opposite end of the spectrum, where the body now with long term ketogenic diet is stuck in fat burning mode. And so when you load the body with a bolus of glucose, you go on a binge and eat a bunch of cereal or something, which is what I would binge on then. Now Your glucose levels rise higher than they would have before and they stay much higher than before. And some people say, well, that's an insulin resistance. It isn't, it's a glucose intolerance because you are in fat burning mode and you're in. My theory, and we're testing this by taking out the islets from the pancreas is that actual insulin secretion has been altered. Insulin secretion has two phases. Very, very briefly. Some of that depends on preformed insulin, insulin that you've made and it's waiting just ready for the pancreatic beta cells to release it. And then you have a second phase, which is now you're making insulin from scratch. I predict that we have altered one or both of those phases of insulin with long term ketogenic diet adherence. And why not? The beta cells are thinking, I've been making this, this protein insulin, this peptide, this polypeptide, but what for? I'm just going to stop making it because it never does anything. It's wasteful. And so that is what I predict explains this metabolic inflexibility in the other direction. Now, whether someone uses that as justification for cyclical keto or not, I think that could be part of the justification to stay metabolically, truly metabolically flexible.

I'm going to predict something else in your study and I totally want to hear the results when we're done. I think you are probably partially right on that. The other thing that we know is that mitochondria are very effective at editing themselves. They'll change their shape, they'll change the component of their, their membranes. You know, we know cold showers, which, or cryotherapy in its various forms, not the, the fat reduction we talked about earlier, but you know, liquid nitrogen, the stuff that I do at upgrade labs and all that. We know that three days of just cold showers changes the level of cardiolipin in the mitochondrial membrane. And that's why if you can do three days, the fourth day you're like, oh, this cold shower doesn't bother me because it just took a short period of time. And I believe that the mitochondria are likely. I don't want you to tell me if I'm wrong here because you probably know more than I do, but that they're likely optimizing their pathways. So they're saying, well, okay, I never need to burn much glucose, so I turn down the parts of the Krebs cycle. And it is just a Krebs cycle, but there's a whole lot of little parts in it, the ones that are really looking for sugar, they're looking for ketones and so they over time just are better equipped to do that which will create insulin resistance. So it could be the pancreas is like, why would I spit out insulin? It's useless. But the cells are also like, why would I keep all the systems in place and highly polished, ready to get some sugar when it only comes once every six months in meaningful amounts? So it's probably both. Because there's no way mitochondria, a quadrillion of them are going to sit there, sugar, sugar, sugar, and never get it and not just stop picking, paying attention. Sound like it might be possible.

Well, in fact, let me, I, I like it now. I would. Well, I'm, I'm gonna maybe tweak it a bit. So I don't think the, the problem would arise within the mitochondria because all, any nutrient that gets to the mitochondria converges on one single molecule called acetyl coa, and whether it's keto, ketolis, ketone catabolism, lactate catabolism, fatty acid catabolism and glucose catabolism. So I don't think it would be a citrate cycle or Krebs cycle problem, I would suspect. Exactly. It would be in the cytosolic glycolytic enzymes. It would be that process, that eight step or whatever the process.

You convince me. You're totally right. I buy that.

Yeah. So we could. Yeah, that's right. We couldn't afford to compromise the citrate cycle because every other nutrient is demanding it.

It has to be above it. I look at the picture in my head and it's kind of obvious now that you say it.

Yep, that's it. Yeah. Because glucose is the only molecule that will invol cytosolic enzymes. Every other nutrient that we're breaking down must exclusively rely on the citrate cycle.

And we know the body downregulates enzyme production when it doesn't need it. For instance, if you go on a low fat diet for a long time and then you eat a whole bunch of fat, you can't make enough lipase. It takes the pancreas a while to switch its gears to make more lipase to break down fat.

All right, so, you know, that's a. You know what, I've just made a note, Dave, and I'm going to credit you in this publication. I'm going to acknowledge you here. We're gonna, I'm gonna measure these glycolytic enzymes in the muscles.

Please do. It's gonna educate us. And I would bet 50 bucks that it's both. I think you're totally right on what you're saying. And I think this system, it just, it makes sense the way the body has to work even if we don't have a study. When you have enough of a picture, you could say, it must work that way. And you're right 70% of the time. Other times there's something no one knew about. But. And that, that's the, the beauty of biohacking, saying, well, if it probably works that way using this old fashioned thing called logic, let's try it. And if you get profound results, you were probably right. Or maybe there's another mechanism, but you were still right that it worked. And I'm one of those guys. I don't want to wait till the lab studies are out there. If it's safe to do. And is it safe to skip carbs for a while? Yeah, it's pretty safe. So you got to look at risk return. But this is fascinating. I cannot wait to see the results of the study. I'm very excited about this. Well, let's talk about your book. I mean, Gary Taubes wrote a really foundational thing a while back, Good Calories, Bad Calories, which is to date one of the best written science books I've read because there was not one wasted comma, like the writing is perfect and every sentence is a new science thing. And it's just mind blowing. And he's been on the show a couple times to talk about that, I believe, at least twice. And he was on recently to talk about fasting in his new book. But he's all about, you know, insulin is the devil, kind of in that book. Right. And in your book you're talking about, you know, why we get sick. And insulin is a major star in the show. Who are the co stars with insulin about why we get sick.

Yeah, yeah, yeah. I love that you mentioned Gary. Invoking Gary is appropriate and I'm delighted. So Gary's, Gary's toned down version of Good Calories, Bad Calories, you might remember, was called why We Get Fat.

Yeah.

And I actually asked him ahead of time, I said, hey, look, Gary, I'm thinking of, here's this book about insulin resistance. I think I wrote him, I think I'm going to call it why We Get Sick. I don't want it to feel too derivative of your work. And of course he was, he was.

Very high integrity for you. I did the same with Robert Greene. When I wrote Game Changers, I'm like, I have like 40 something laws that came out of the data I'm calling laws. I'm crediting you in the book, but I don't want like, you know, you're the master here. And he's like, yeah, go for it. It's so kudos. There are a lot of knockoff artists, so I appreciate your integrity.

Yeah, yeah. So Gary looked at insulin in those books. He looked at insulin almost strictly. And this was very much his purpose through the lens of obesity. That was the context. I wanted very much to make sure that wasn't just my context. As much as I am an adipocyte biologist, as a scientist, that would certainly be an accurate term for me. I'm fascinated in fat cells, but I wanted to go beyond the fat cell and look at it, look at insulin resistance role beyond adipose. Because I think, well, not, I think that was definitely necessary in order to appreciate just how insulin resistance is connected to all of these modern diseases. So I wanted to go beyond the fat in that case. But of course I had to talk about the fat in the sense that that's where insulin resistance starts. I'm utterly convinced other many tissues become insulin resistant. But I'm, I'm convinced based on data that it is the fat cell that falls first. It's the insulin resistant domino that tips and then it tips the rest down.

So you look at insulin first. What are some of the common things that people can read more details about in the why we get Sick book that you just released. What are some of the other common things? So if you know fat falls first, for instance, if you're getting xenoestrogens, you're going to put a lot more fat on than you're supposed to. It's one of the reasons I weigh 300 pounds. Live in a house with toxic mold that's a thousand times more estrogenic than estrogen. Yeah. So what are some of the things you know? It's not just insulin. There's, there's triggers in there. What are the ones you worry about the most? Your phone screen is aging your skin and wrecking your sleep at the same time. Artificial blue light goes from your phone screen straight into your eyes and deep into your skin. That light messes with your melatonin levels, interrupts your deep sleep and speeds up skin aging by breaking down collagen. The bodyguard's red light converter fixes this at the source. It's a first of its kind screen protector with real Tech that converts blue light into beneficial red light before it hits your face. It turns your scrolling into a slight skincare routine. It supports healthier skin, reduced eye strain, improved sleep quality and fewer screen related headaches. Third party testing showed a 50% plus increase in red light exposure within the optimal range of 620-770nm. And this comes with zero compromise on your screen. The red light converter preserves your screen's true colors and full touch touch sensitivity. Beyond its wellness benefits, the red light converter provides ultra thin edge to edge protection for your device and bodyguard stands by their quality. Enjoy peace of mind with lifetime replacements ensuring your red light converter continues to protect and support your biology for the long haul. Visit bodyguards.com and use code Dave for 25% off. That's bodyguards with a Z.com for 25% off.

Foreign. Yeah, yeah, thanks. So, so insulin, when it comes to insulin resistance, I believe there are three. I call that, I say that there are three primary causes of insulin resistance. And by primary, I use the term primary to touch on the fact that in all three key biochemical or biomedical models of research, insulin, these are, these are causes of insulin resistance. So the three that I'll mention, they can cause insulin resistance in isolated cell cultures like in petri dishes, they can cause insulin resistance in lab rodents and in humans. So we have all three of these, these levels of a bio biomedical model. And to me the three primary causes. One is chronically elevated insulin itself. Now that we've already been beating that one to death. But too much insulin will cause insulin resistance. Some people want to debate that. I don't think that's, I think it's beyond debate. There truly is evidence in all three models to establish that as a cause. Now the second I would say is the stress hormones cortisol and epinephrine, those in all models can stimulate insulin resistance very rapidly. And that of course is a problem because we live in an environment that promotes stress. And nowadays, Dave, not to, not to I guess step outside my lane here, but people want to be angry. For lack of a better way of saying it. People want to be anxious and they want to be upset, they want to be offended. And I mean that is going to ramp up your de. Stress hormones. You are almost always looking for the attack to happen even emotionally or intellectually. And, and so these stress hormones, cortisol and epinephrine, they are going to be elevated and in addition to their numerous other effects and cortisol has disastrous effects on the body long term. But what they share is that they are insulin antagonists. Those two hormones are constantly trying to push up glucose. Insulin now constantly trying to push it down must work ever harder than it did before. That is insulin resistance.

Well, in your study, one of the other reasons that unending the keto, bro, you know, if it's not a carb, I'll eat it crowd forever. They routinely and predictably get elevated cortisol that never goes down because they're just not getting enough carbs. So if you look at the average cortisol, if someone's, you know, I'm going to be keto all the time. And it's one reason that Atkins diet and unending keto people like, I lost 50 of my £100. The other 50 won't budge. And you look at their cortisol labs and they're off the charts. And this is one of the things that happened to me back in 1998 or 7 or whenever the heck I did before that. 95. When I read the first Atkins book, I'm like, this is awesome. Lost 50 pounds. The other 50 takes 10 years to lose. Cause you gotta learn about cortisol and all this other more complex stuff. So look at cortisol as an, as another driver in the little study that you're doing there. Because if you see that is elevated, given that it also causes ir, it could be a confounding factor.

Yeah. And yeah, if there's no question, if cortisol is elevated in individual with adherence to a ketogenic diet, that would definitely, I would definitely then suggest there's reason to cycle with. With carbs. Cortisol has a fascinating effect on fat cells.

Independent Google's news algorithm causes insulin resistance.

Yeah. Yeah. Well, yeah. I mean, that's what I'm talking about, though. I mean, it's an industry to keep people enraged or stressed.

Cortisol feels good. It's energizing. It really does. There's no doubt about it. Insulin feels good too. It's also energizing. But man, you pound yourself over the head with those things after a while and it wrecks your body. And then you're not really good at either one of them. Okay, so you had two things we had. So the third one, too much insulin, too much cortisol and adrenaline. What's the third?

Yep, inflammation. Now, to a degree, inflammation is also influenced by the hypertrophic adipocyte. But even independent of that, we know that even acute inflammation or, or the chronic inflammation that comes with autoimmune diseases, there's a fascinating report detailing the ebb and flow of insulin resistance, matching the ebb and flow of rheumatoid arthritis. When the, when the autoimmunity is active, inflammation is up. When the autoimmunity subsides, as autoimmunities so often do, insulin sensitivity improves. So inflammation itself is. And you touched on a molecule, you mentioned a molecule called ceramides earlier. That's a molecule close to my heart simply because of my postdoctoral work detailed the precise pathway whereby the initiation of an inflammatory event. One of the reasons, if not, I would say a main reason, is because it causes the cell to start accumulating this type of very active lipid called ceramides. Then ceramides directly antagonize the insulin signaling cascade, stopping it from realizing what it wants to do.

You're probably the right guy to ask this question. For the last, oh, six or seven years, I've been aware of supplements that contain ceramides and they're marketed for anti aging. And certainly if you have higher levels of ceramide in the skin, the skin is. It's healthier, it holds fat better, which is something your skin needs to do as you age. So I've been hesitant. In fact, I don't take ceramide supplements because of what you just spoke about. Do you think it's metabolically advisable or not advisable to take extraceramides nutritionally?

Yeah. Yeah. I love that you asked that question. This is, in fact an exact conversation. My postdoc mentor in the lab that we had in Duke, in the medical school in Singapore where I was doing my fellowship, we talked about that exact thing because one of the gals, one of the gals in the lab asked, she said, well, my, my lotion, my skin lotion, my moisturizer has ceramides. And someone else said, one of the guys, like, yeah, my shampoo has it. And it is for the reasons you mentioned. If you can kind of create this lipid wall, then you can just retain water because water isn't going to want to pass through that lipid wall. Now the. Now, unfortunately, Dave, to disappoint you, there is no evidence either way that that topical ceramides will come into the body and exacerbate or influence insulin.

I don't worry. I'd put it on my skin, it wouldn't bother me. But these are capsules, like swallowing ceramides to be digested.

That is. You know what? I still don't know because I'm trying to wonder. Ceramides are such a unique molecule that I don't know whether there is going to be. No, there are transporters for ceramides, but whether we have them on the epithelium of the intestines, I don't know. We probably would. So yeah, I would say, but you.

Don'T want more ceramides inside the body, but you might want more on the skin. So I never took them because I was like, there's something's not right about this. But you, I mean, if anyone on earth could answer that question, it's probably you.

So, yeah, so there is no data on it, I can say that definitively, but I would speculate that. Don't put it in your mouth, keep it on your skin.

There you go, guys. If you were thinking about taking ceramides orally, maybe you shouldn't. And I'm talking to exactly four people who are as geeky as me, but still. Well, let's talk continuous glucose monitoring. Because you and I met because we are both advisors to, and I'm an investor in Levels, the Levels Health, the continuous glucose monitor. And we've had a whole episode with the founder of Levels recently. Um, but I, I've been blown away by just looking throughout the day at what the, my blood sugar levels do and seeing how high do they go after a meal, after a different meal, whether you slept, whether you exercise, all these things, you realize how much control you have over your blood sugar, which then drives your insulin response. Um, so let's talk about continuous glucose monitoring for a minute. And, and what, what that has to do with all of this.

Oh yeah. In fact, I am utterly convinced that the sooner the average individual can use a cgm, the sooner they will begin to self impose their own dietary changes.

Such good feedback. Even me, I'm pretty good, right? I'm like, you know what, I'm going to tweak that meal a little bit because I don't want to see this bike afterwards. It's very motivating. By the way, guys, Levels Link Dave puts you at the front of the line. They've got almost 100,000 people trying to get one. And there's limited numbers, but I asked them for a code for bulletproof radio listeners. There's no discount, but hey, at least you get to get it first. Levels Dot link slash Dave.

Yep. Yeah, so that's what I think the true value is. The, the main value is you can tell someone all day long, including a diabetic, which is the obvious user of a cgm. Don't eat those Carbs, it's just gonna. Especially in the case of a diabetic, a type one, who's treating insulin. The excessive we tell them, take as many, eat as many carbs as you want and just cover it with your insulin. That is the asinine clinical advice we give to someone. And remember, the very nature of their disease is that they don't metabolize glucose very well. So why on earth are we telling them to eat glucose anyway? What is. Even in an average, non diabetic individual, a high carb diet means that your glucose is swinging like this all day long. There are real consequences to that, independent of potential damages to nerves and blood vessels, which glucose elevated glucose can cause. If you are among the majority of people whose brain is yoked to insulin to glucose, if because your insulin is always high, your glucose is always high, your brain is adapted to only using glucose, you feel that drop in glucose, you will feel the symptoms of hypoglycemia, that carb crash. You will get jittery, you'll get shaky, you'll get anxious, you'll get hungry again, even though you just ate 90 minutes ago. It's because your brain is so addicted to glucose that when it starts to drop, and in the absence of ketones, which aren't there in that situation, you have no alternative, the brain starts to starve or to sense this panic because it is so yoked to glucose that the drop in glucose is panic to the brain.

And the panic equals cortisol and adrenaline equals more insulin resistance. It's a pretty nasty situation.

Yeah. Vicious cycle. Yeah. So to me, a CGM is mostly the value in my mind lies in the, in the, in the utility of helping someone change their behavior. Now, Dave, you'll get a kick out of this. Levels is funding a very cool project in my lab where we are attempting to profile individuals who have paradoxical rise, a paradoxical rise in glucose, even though they're adhering to a low carb diet. You know, there's that segment of the population that goes low carb and they're doing great, they're feeling fine, they're losing weight, and yet their glucose levels, which maybe had been in the 90s, are now creeping up into the hundreds every morning. Even though they're being super strict. We're going to identify this, you know, that subset of a low carb population and then do a full endocrine profile on these individuals, because I suspect the problem lies in hormones, even potentially cortisol, potentially glucagon, potentially catecholamines, like epinephrine. And we're going to do. We're not only going to do fasting conditions, we're going to do macronutrient challenges. Have them do a load of protein and get blood for a couple hours, a load of glucose, a load of fat, and just see the response.

I want to see the answers. Are you going to pull cortisol as well? I'm sorry, not cortisol. Thyroid. And you'll do thyroid?

I don't know. That's a different panel. Let me take a note.

It's worth thinking about because thyroid's the energy thermostat there. And I find a lot of people with low thyroid get high blood sugar because they just, like, they can't get the.

I don't.

I should know the mechanism other than just what?

No, no, but the engine idle. If, if thyroid is down, then the, the rate at which a cell is doing its work, including glycolysis, is compromised. That's a universal phenomenon in the body.

When, when people don't lose weight with the fastest way stuff or the bulletproof diet, I'm like, just get a thyroid panel. And then after that, get your C reactive protein and homocysteine, which are inflammation markers. So they have inflammation, they'll have insulin resistance. If they, they have thyroid, they just aren't going to use the energy that's in their body. And generally, I mean, yeah, they might need testosterone, and it's an infinite number of things, but those seem to be like, the really high, interesting ones. And it might be worth considering in the context of what you're doing with levels. That's. I'm. I'm excited to see the results of these. You're doing some really groundbreaking stuff in the labs. That's why I want to have you on the show. But I had no idea you were doing something.

Yeah, it's fun. It's fun. Dave, There's. There's something kind of noble about getting paid to be curious. It's a pretty cool job.

It's. It's awesome. It's why I write and it's why I'm just always. It's amazing. This is such an elegant machine that is far more elegant than the Internet or any of the bigger machines we've created on the planet so far. And it's also small.

Well said. Well said. I agree.

What's a maximum blood sugar level that people should have after a meal? Because we get a transient spike where it just goes up for a little while and then it comes back down. Even if we eat some protein. Usually if you have pure fat, it shouldn't change at all if you're like most people. But what's a number that you really ought not to exceed?

Yeah, that's. It's hard to answer in a living, free, living individual because I would say if this was someone drinking a 75 gram oral, like glucose tolerance test, then you never really want to see that get above 200.

Yeah, that's a pretty crazy test, right?

That is, yeah, yeah, that it is. But what the problem with the average individual though, who's going to maybe try to do this, they're looking at their glucose levels and they may be eating like, you know, three bowls of cereal, four pieces of toast, you know, they, they may just go crazy. But if someone were to control and just say, all right, this many slices of bread, it's a slice and a half or, or whatever it is. So I'm getting 75 grams of glucose and they want to watch their CGM to kind of do that diagnostic work at home, which is one of the values of a CGM. I would say if that has gone above 200 or maybe even the high hundreds, that's be, be careful.

I like to see my blood sugar not go above 130 when I have carbs, protein and fat in a meal. But not sugar.

Oh yeah, right. But you mix the three macros. Yeah. When you mix the three macros, you do depression, the, the glucose, the glycemic response.

So I think we're going to find a lot more over the next five years when we get millions of people's data from levels and we can really see. And because you take a picture, you type, what did I eat? So then we are going to be able to do machine learning on that and learn something about the human condition we never have learned before. Which that's why biohacking is so cool. We get to use data instead of just guessing.

Yeah, I agree 100%.

Now there was a recent study that drove me nuts, like, wow, this, don't do this. Harmful, dangerous. Back to our news headlines. Habit with your coffee, it's the end of the world. And in a small study, they gave people an enormous amount of sugar as breakfast and said, if you have coffee after the sugar, your blood sugar goes up less than if you have coffee before the sugar, therefore don't have coffee before breakfast. And I'm like, that wasn't breakfast, man, that was candy. If it was a normal breakfast, I think they would have seen different results. But that leads us to the question Coffee and insulin resistance. What do you know?

Yeah, well, there's no evidence to suggest that coffee is going to drive insulin resistance alone. I would say so much depends on if there's any relevance to that story in a. In a general sense, it would be, what are you adding to the coffee? The coffee itself is going to do nothing. It's how much cream and sugar. Those two together are not an optimal mix. Cream, no problem. Butter, no problem. That's right. The moment you've started sweetening this and you're spiking your insulin because of that, then that's a problem. But the coffee alone is not.

That was my assessment when I read the study. I'm like, guys, come on, don't have candy is what I learned from the study.

Oh, that's right. Yeah. Yeah. That's clickbait.

It is clickbait. There's another kind of metabolic candy, the omega 6 seed oils that I've been minimizing for in my own life, 14 years now, so people call linoleic acid. But there's other Omega 6s that seem to gum up the works of the insulin receptors. Can you talk about omega 6s particularly damaged or oxidized omega 6s and insulin resistance?

Yeah, yeah. In fact, Dave, we. You. We don't even have to add that little qualifier. Omega sixes are so readily oxidized that it's all. It's practically a guarantee.

Yeah. Once they're in the body some.

At some point. Yeah. At some point these are going to become oxidized. And that's why. That's one of the reasons I'm such an advocate of. Saturated fats are so stable. That's right. They're so stable that in order for those to become a reactive. A lipid peroxide, which is a very reactive, dangerous fat, you have to heat that bugger up to like 300 Celsius or something when it comes to saturated fats. But these. These polyunsaturated fats. And linoleic acid is a prime example. It is so readily oxidized that you don't have to do anything to it. And it's. So much of its damage comes in. The fact. Comes from that fact. It becomes a very, very reactive or radical lipid. And when you have a. When you have a lipid that is now an oxidative stress molecule, it's particularly damaging because lipids can go wherever they want. They can move through cell membranes, they can move through organelles, they can get into the nucleus, they can get into the mitochondria. And they can start bump, sharing or passing this oxidative stress onto any molecule, literally anything they bump into. So part of the problem with linoleic acid and one of the key lipid peroxides that it turns into, which is called 4HNE, is that 4HNE. Now, there are many, many consequences to this molecule. And because I'm an adipocyte biologist, I'll emphasize one. One of the consequences is that it, it forces fat cells to grow through hypertrophy. And at the very beginning of our conversation, I kind of described the healthy way to get fat and the sick way to get fat. Hypertrophy of fat cells is the sick way to get fat. So this would be a person who's, whose threshold of how much fat they can hold before they get sick is basic. It's depressed. We're pushing that threshold down. We are limiting how fat this, these fat cells can get and stay healthy. So that is one. And these, these people listen, although I'm sure your audience is more savvy than this.

People may think there's always new people, so don't assume everyone knows everything.

Yeah. So they may think, well, I'm not getting linoleic acid. Yeah, you are. If, if you're. If most of your food is coming from bags and boxes with barcodes, it is extremely likely. Yep, that's right. Yep. If it's fried at a restaurant, it's extremely likely that, that soybean oil and other oils that are rich in omega 6s are the. Not only a main source of fat, but the single main source of fat. Christopher Ramsden at the NIH in the United States. He has published work detailing that soybean oil is, is literally the number one source of fat in the American diet. Now, as much as people worry about beef, we're getting no more of our fat from beef than we were a hundred years ago, and maybe even more.

Because we don't fry anything in tallow anymore. So we're getting much less animal fat than we did.

Yep, that's right. Yep. The number two fats in the Western diet now is soybean oil and shortening. And those are both derived or they're both very enriched with omega 6 fats. And they, these omega 6 fats become part of cell membranes. They are precursors to inflammatory proteins, inflammatory molecules like the arachidonic acid pathway. There is, there's no good reason to, to have these. And the more someone eliminates them from the diet, without a doubt, the better off they're going to be now. And There are other consequences, Dave, with regards to genuine severe mitochondrial damage, including changes in cardiolipin that you mentioned already, fundamentally altering the function of the mitochondria. And that may be part of the very real data in rodents that shows that linoleic acid is a key driver of some cancers, insofar as cancer may be a mitochondrial disease more than a nuclear or a genome disease.

I've been saying for years that if I had a choice between eating a plate of french fries cooked in soy or canola or all the other seed oils and smoking a cigarette, I'll take the cigarette. Because the inflammation throughout the body lasts for a lot less longer. And nicotine at least is anti Alzheimer's. But I don't smoke and I don't eat french fries.

In fact, Dave, we could. No, I hear you. We could even present a more tempting scenario where you drink a cup of soybean oil or you eat an equal isocaloric amount of sugar. Someone would say, oh, Ben and Dave, you're such fat friendly individuals, you'll pick the soybean oil. I don't think I would. I would, because my body knows what to do with that sugar. As terrible as it is eating in, at no point in history have humans been consuming this level of omega 6 fats. These were only ever trace fats in the human diet. And they are abundant, they are ubiquitous. They're everywhere but in minuscule amounts. We have in our past consumed refined, not refined, but, you know, something like honey, which is nature's closest version of sugar. Our ancestors would have eaten honey. Our bodies know what to do with it. Not that I'm promoting honey at all, but we, we know what to do with it. Soybean oil, there's almost nothing. Or, or these refined omega 6 oils. There's. There's nothing good that comes from that. There's nothing. We don't know what to do with it. We're poorly adapted to this change in fats. And I believe the, the biggest shifts in our diet are, are what's. What we've done to carbohydrates. We've these refined carbohydrates and these refined oils that our ancestors would have never experienced. We were poorly adapted to those, these new sources of macronutrients.

If you look throughout history, we had the tobacco lobby that said, oh, you know, smoking is good for you. I have a white lab coat, trust me, right? And then we went from there, and now we've got glyphosate. There's a $10 billion judgment in the first of many against Monsanto, which is now owned by Bayer. So that's, that's the next one that's going to fall. And after that it's the seed oil industry. Those guys are just going to have to fess up because the evidence is overwhelming at this point and it's only going to be more overwhelming in 20 years. So they're going to tell you with billions of dollars of marketing it's good for you and eventually they're going to pay trillions of dollars in fines because we have inflation. So one of the, one of my investments that's still confidential is in a company that's solving that problem for mass available oil. That's not bad for you because we, it doesn't have to be bad for you. And speaking of not being bad for you, if someone eats a hundred grams of soybean oil or 100 grams of my favorite grass fed butter, will they actually get fatter from one versus the other?

Yeah, well, there's no evidence in humans that would be a difficult study. But in rodents, yes. There was a rodent study that ate, that fed these animals. And this is part of the problem that I have with people invoking the laws of thermodynamics. A calorie is a calorie. And I actually truly this is a tangent. I promise I'll come back. I believe invoking physics and thermodynamics in understanding food, giving foods calorie values I think is one of the greatest disservices we did that scientists did to diet and nutrition as we know it. I think it skewed our perception of what is healthy and what is not by, by trying to make it into a bean counting, calorie counting tedium. It's, I rage against it for many, many reasons. But in that aside, this rodent study fed these animals isocaloric diets that varied in the type of fat they were getting. One, one source of fat was coconut oil. There was a third, I can't remember, it might have been butter or ghee. And then the, the, that was the second. And the third was soybean oil. And guess who got much fatter than the rest? It was the soybean oil eating animals. They got fatter and sicker even though they were eating the exact same amount of calories.

If that study can exist and you're listening to this going calories are the thing, they aren't the thing. There's also industrial chemicals we treat cattle with so they get fat on one third less calories. They actually Measure the effect of hormones on cows. So, no, calories don't make you fat. It's what the calories are made of. So like you said, it's a great disservice to people. And it allows packaged food companies to stand up and say, hey, this is all the same and it can be a part of a balanced diet. No, there's good calories and there's bad calories. To quote a dear friend of both of ours, right?

This is real, Dave. It lets them Virtue signal. And they get stamps of approval from, from organizations that we would look to as authorities on health. They will, by, by cutting out all the fat and all the natural saturated fats. Then, then they get that little stamp from the American Heart association and they can say, this is heart healthy. They get a stamp from the American Diabetes association because even they say to, to, you know, cut your saturated fats and eat more carbs, which is ridiculous. But it lets them.

I love the American Diabetes Association. It's right in their name what they cause.

Well said. In fact, late 80s, someone, we're laughing, but Gerald Reaven, in the late 80s, he was a legendary diabetes scientist. He published a paper where he took type 2 diabetics and put them on the perfectly prescribed ADA diet, the American Diabetes association diet, and they got sicker. It didn't help them.

This is the guy who first discovered what he called syndrome X, which he was the discoverer of metabolic syndrome and a great early visionary in the field. In fact, he informs some of the thinking behind the very early bulletproof diet experiments. And my recommendation to people, and I want you to tell me whether it's directionally accurate or whether you like it or you don't like it, is that eat a substantial amount of fat, at least 50% of your calories from fat, but at least half your fat needs to be saturated and most of the rest of it monounsaturated.

Oh, I love that. I love it. In fact, I, I think in general that's generally going to be what's reflected in natural fats. If someone is eating fats from. By natural, I mean animal and fruit sources. Fruit fats tend to be a little more extreme like. But I don't mean that in a bad way. Coconut oil tends to be overwhelmingly saturated. Olive oil tends to be overwhelmingly monounsaturated. But those are natural fats are. Humans have been eating those for millennia. Those are not the same as seed or what's called vegetable oils. So the animal fats and the fruit fats and animal fats will tend to have a wonderfully broad spectrum and, and, and be closer to, to in some instances a one to one of saturated to monounsaturated. And so, so to me, if someone is focusing on natural fats from animals and fruits, they can't go wrong.

When I put together the bulletproof collagen bars, one of the big drivers for how I made it was what kind of fat and how much fat can I get in there. And grass fed beef has about 2% polyunsaturated fat and my bars have about 1.6%. I was targeting saturated and monounsaturated or I don't want it in there because it's so easy to just stuff a bunch of nuts and seeds into a bar, say it's good for you. But then people get hungry and they get fat when they eat a lot of that stuff. What percentage is the max percentage of omega 6 that you think people can handle?

Oh my goodness. I, I'm afraid I don't know. I would, I would only say this just so I can answer that question with something because I don't know a percent. Now in defense of the polyunsaturated fats, they do appear to be essential. You need some and that's why they are ubiquitous in natural foods. They are there. I so rather than my being able to speak to a percent of calories, I would maybe speak to a ratio. When it comes to polyunsaturated fats, we are at a ratio of about 20 to 1 when it comes to omega 6s to omega 3s. Now someone would think, well, why bring in the omega 3s polyunsaturated fats? It's because they are both polished polyunsaturated fats and they do compete for the same metabolic pathways to be converted and used or just changed in the body. So they compete for metabolic pathways and we need omega 3s, of course, desperately. If you have a 20 to 1 imbalance in favor of omega 6s, good luck getting those omega 3s access to those metabolic pathways. So ancestrally, it appears that we ate more of a 3 to 1 omega 6 to omega 3. I would say the closer someone can get to that being balanced one to one, then the better than the better they're going to be. Now Dave, not to, I'll just mention this. That's what we did. I, I with a couple of my brothers, we made a low carb shake that is lower carb, higher fat, high protein and it was a one to one. It's, it's called Health Code. Anyone who wants to know, just go to get Health. H l t h gethealth.com Just two and two. Me and two of my older brothers trying to make a better low carb shake.

You're a teacher, you're a professor, you're working on doing good stuff. You find something that's cool, happy to share stuff that's made the right way.

Well, thanks.

I don't have to be the only guy selling anything. That's why I talk about all kinds of stuff that works that I don't make. Because I want to be a curator of awesome and a source of awesome, but not the only source of good stuff. So that's totally fine. Tell me the URL one more time.

Yeah, Get Health. H L T H, I didn't even.

Realize you were doing that. But awesome.

It's fun. Well, and Dave, just like you, there's something, there's something awesome about finding answers to questions. But when you think you have answers to questions, you can't help but want to then go into providing solutions to problems.

And so if you can't buy something, you go make it. If you care enough about it, like that's how it's supposed to be, Right? So good for you. In your book, in the third part of the book, you talk about the solution, like, what do you do about this stuff? And you have just some practical steps in the book. Can you walk listeners through the things you do that prevent or reverse insulin resistance?

Yeah. Yeah. And Dave, let's start with one that is close to your heart. I know. And that's fasting. So I will mention four what I believe are absolutely pivotal or fundamental steps to take with changing diet. And it must be diet. Any effort to improve insulin sensitivity. If it isn't including diet, you're just, you're just wasting your time. And I'm an advocate of exercise, I'm an advocate of good sleep. Those all matter. But if you haven't changed your diet, you're not really, you're just, you're just flirting with the change. It doesn't actually happen until you change the food you eat and when you eat. And so fasting is wildly effective to the point that you can take people on various intermittent fasting strategies or time restricted eating. And these are people with type 2 diabetes that are so insulin resistant, they've been given insulin as a therapy and within weeks they're off all their medications, They've become so insulin sensitive. So just stopping eating will lower the insulin very, very rapidly. And now you've started to improve the sensitivity to that insulin. So fasting is a good one to start with.

That's, that's why I wrote fast this way. Because most people think it's too miserable to ever try it. Like, it doesn't have to hurt to do it. And I want you to honestly criticize or support as you see fit, an approach that I wrote about in Fast this way. When people are getting started fasting, you know, they get cold, they get cranky, hypoglybitschy, et cetera, et cetera. And you know, 10 years ago when I first online, put up the bulletproof diet. Like, have a bulletproof coffee in the morning because there's no protein, it won't change mtor, it won't affect autophagy, and it doesn't have to have a lot of butter. People like, it's 400 calories. No, you can do 100 calorie bulletproof if you want. You dial the calories up and down as you see fit. It's got the MCT oil in it to provide a source of ketones so you don't get hunger and all that. And to do that at the beginning of intermittent fast where insulin doesn't go up. And that's been validated by a third party who looked at 300 breakfasts and this was the number one, doesn't move insulin at all. So if someone wants some of the benefits, maybe not the microbiome benefits, but the metabolic benefits of fasting, and they start out learning how to fast by saying, I'm going to have some fat in my coffee in the morning. Give me the pros and cons of that. Like, truly, honestly, you can tell me it's a terrible idea if you want, but I'm curious.

Yeah, yeah. In fact, Dave, I like to describe fast. I'm a man with a hammer, and everything's a nail to me. I see insulin everywhere, and not because I'm delusional, but it is relevant. Once upon a time, one of the legendary fasting starvation scientists, George Cahill, referred to the difference between the fasted state and the fed state is the hormone insulin. If insulin is up, it. Even if you've just infused insulin and didn't eat a thing, the cells of the body are in a fed state. They start storing and building. When insulin is down, the body's in a fasted state and it starts mobilizing the energy that had, that had stored and starts turning over pieces of itself within cells or autophagy. Now, because of that, because of the relevance of insulin. In defining the fed in the fasted state, you can keep insulin down through two ways. One is what I could call or, and I do call a true caloric fast. You are not eating or drinking any calories. A true fast. You're drinking water and electrolytes, and that is it. Well, that's, you know, a true water fast.

Yeah, you gotta dry fast too, right?

That's right. You can. Yep. Now, on the other side of this, you can of course, eat while keeping insulin low. And I refer to that as a nutritional fast. And this is when you've simply cut the carb, cut the carbs and to a large degree the protein. And now you're just focusing on the fat. Insulin doesn't move. So as far as your body's cells are concerned, it's like you're still fasting. Now, there are undoubtedly some other biochemical events within the cell that are sensing just the fat itself that might alter it, but. But I don't know that it does. So to me, you have either avenue. Now, I do think there's something to be said for sometimes just not eating and it's uncomfortable. And I think if someone can't fast for 16 hours, that's a problem. And you've just become addicted to feeling food in your stomach and you need to get off that addiction. So it's going to be uncomfortable and just grit your teeth and get through it. But, but there are other times where a person thinks, I had a very demanding workout the day before. This is a lean person or whatever. Not even. They just think, I need some energy. I need some literal energy in something I'm drinking so that I feel like that does promote satiety. You do feel fuller. And so put some oil or some butter. I'm a very big fan of butter because it has so many nutrients and such a wonderful range of fatty acids, long to even short chain fats. So nevertheless, my point being, I like to think of fasting as two different states, A caloric fast or a nutritional fast. I strongly, strongly contend even if you're in a nutritional fasted state, you are getting many of the benefits of the true fast, including autophagy, improved insulin sensitivity and heightened fat burning, which is evident in the production of ketones. If you're making ketones, that means you're burning fat like gangbusters.

I love it. It's definitely been my experience over the past 10 years that it works. And we see people, their insulin levels go down and insulin resistance reverses and people stop being type two on this approach, but they're also eating the right foods. It doesn't work well at least doesn't work as well if you're still eating a bunch of fried garbage at restaurants when you break your fast. So you got to talk.

In fact, Dave, I. One other thing I add about fasting is the most important thing about a fast is how you break it. The food that you eat when you're finishing your fast, I argue matters at least as much as the fast itself.

Do tell.

Because if you fasted. Well, my own, my view on this is admittedly less scientific because I don't know of evidence to support this. But I just imagine these situations and in some instances I've seen it. Someone says I'm just going to eat one meal a day. I'm fasting for 23 hours and I eat in one hour. But what they eat in that one hour is shocking. And so I think, I worry that in some people one meal a day form of fasting becomes just a sort of, is just a nicer version of a binge purge cycle. They fast all day, they eat themselves sick and they regret it. They have remorse, self hate, they double down, they recommit. Tomorrow I'm going to fast again and I'm not going to end my fast that way. Now I'm not at all opposed to one meal a day. Not at all. I'm not opposed to any prudent fasting strategy. But it matters. How you break your fast matters tremendously.

So what's your recommendation for breaking a fast?

Yeah, so I'll mention that. But I would just say have a plan. If a person knows they're going to fast, make sure you have that meal in place and it doesn't involve you going out and go grocery shopping. And you know, it doesn't have shopping.

When you're hungry is a bad idea.

No, it really is. And you, and make sure that your pantry, that you just don't have stuff. So for me, for example, I cannot have cereal in the house if I get really hungry. Cereal is like a drug to me and I'm sure it's a carryover from my college days. You know, when you're a college student undergrad, you eat cereal like every meal of the day. And so the culture in my home and with my little children and, and my wife, we, we just aren't a cereal family. We don't have cereal. I'm glad for that because I can't control myself. But I also just, that's not part of breakfast for my children. So to me, the perfect way to end the fast, drink a good amount and a good amount of electrolytes and then focus on. In my home, it's meat and vegetables. That's typically. That's typically the dinner meal. It's meat and vegetables. And now, Dave, to touch on our earlier topic, although I'll still get back to the solutions to insulin resistance. You mentioned cyclical ketogenic diets. I actually generally adhere to a cyclical kind of low carb diet because my rule as a family man, husband and father, which is absolute rule number one for me, I eat dinner with my family.

I do, too. That's every night when I'm home, anyway.

Lunch. Yep. Yep, that's it. Breakfast and lunch are meals that I can have perfect control over. Even though I'm breakfast with my kids. I may make them some different kind of crepes or something. I might not eat the crepe. I'll either have a cup of tea, sometimes with butter, or I'll just fast through it entirely. Lunch, I'm here at work. I can maintain my perfect integrity to low carb.

And you're not doing coffee because you're Mormon, I'm guessing That's it.

Yeah, yeah, I don't drink coffee. Yep.

There's lots of performances during tea. In fact, it's really popular in Utah.

It works. It works. So in. But it's dinner with the family. And, you know, and if my daughter, like one time, it hit home when I was trying to be really strict, my oldest daughter wanted to make grilled cheese sandwiches for dinner. And I was thinking to myself, how can I, Should I just pick the cheese off? And I caught myself and thought, ben, what are you. What have you become? What have you become? Dinner. I'm going to. If my daughter makes grilled cheese sandwiches, I'm going to eat those grilled cheese sandwiches. Now, if there's a way for me to make it low carb and not make it weird, okay, I'll do it. But in general, because my wife is so aligned with all this, the meals end up being generally good meat and vegetables. And, and, and it works.

Yep. Meat and vegetables with lots of fat is what you're going to find at my house and sometimes carbs, too, but not, not excessive and not a lot of sugar. And it seems to work for decades.

Yeah.

One more question before we get into the other few things. Recommendations from the book. Now, we talked about linoleic acid, the omega 6 acid that's bad for you from seed oils and a lot of the, the Logic twisting. Vegans will say, well, you can't eat butter because it has trans fats in it which are a different, a different form called conjugated linoleic acid, which is really good for you. My understanding is that CLA blocks the uptake of the bad linoleic acid. But can you talk a little bit more about cla, why it's good and how it interacts with the bad? L A?

I can't. I wish I could. I actually don't know. I know only that there are significant human clinical studies to show that increasing CLA consumption improves metabolic health. I don't know the mechanism.

Ooh, interesting.

Know the result.

I've got to find an expert who knows that because we, we know cla is good for you. It's, it's pretty well proven at this point. And you get it from grass fed butter and grass fed beef fat, or actually there's some of it in pastured pork if it is the right stuff as well. So, and lamb certainly is very high in it. But it's one of those strange things where, you know, you can simplify and say, well, that's linoleic acid, it's a trans fat, but it's just a different molecule. Okay, and you're not an expert.

Yeah. Well, let me speculate though, I will speculate. These polyunsaturated fats, including linoleic acid, when they are in the brain and they haven't been, I guess, for lack of a better word, bastardized into some lipid, reactive lipid. They are highly oxidized. The brain, the astrocytes in the brain actually can metabolize polyunsaturated fats very, very well. And for example, alpha linoleic acid, the kind of plant derived omega 3, we always will say, well, that's useless because it doesn't convert to DHA and epa, which are more of the structural fats in the brain, which is why they're so essential. ALA is actually the most, the most, the single most ketogenic of all the fats. And it is a polyunsaturated fat in the brain. And I would encourage anyone who wants to learn more about this, look up the work of a man named Stephen Cunane. And he's looked at the effects of ala even from, you know, I know it's, it's, it's plant derived. And so I'm not saying drink flaxseed or drink chia oil, but if it's, if you are getting some flak, powdered milled flax or milled Chia for those omega 3s. The informed person would say, well, it's not converting into DHA and epa. And you can say, yes, it's not. But the brain uses that as an energy source extremely readily. I wonder whether cla is maybe a better energy source for some cells.

That's a good thought. By the way, Dr. Kanane at UC San Diego is one of the major guys proving that keto works. He's the first guy to figure out that brain octane. He actually used our brain octane in the studies, but showed that it was four times more ketogenic than C12. And he's also the guy who showed that the amount of caffeine in two small cups of coffee doubles ketone production or caffeine from tea. If you drink enough tea, you know, it doesn't have to be coffee. And I've actually funded some of his research down there a few years ago at UC San Diego because he's like such a major keto guy. I love that you brought.

He's awesome. Yeah. Anyone after? Everyone? After you read Dave's book and read my book, get Stephen's book called Survival of the Fattest. It is so interesting looking at the. This idea, this paradigm or theory of human brain evolution and the reliance of dietary fat to fuel these big hungry brains that we've got. It's a fascinating view of human development and the necessity of why humans are born obese and we're the only land based mammals that are.

That is a fantastic book. I love that you brought that up. I actually haven't interviewed him yet. I think I'll have to do that. All right, we've got a couple more points from the book. I know this interview is running long, guys. I don't know. This has been full of knowledge and information for me. So I'm going to make this a long episode, probably another 10, 15 minutes. So tell me, tell me what else people can do. So we talked about fasting as a major thing and people. You definitely want to. You want to read his book for more details. And there's really cool stuff. If you couldn't tell from this interview. And it's why We Get Sick is the name of the book. If you haven't ordered Fastest Way get why We Get Sick and Fastest Way at the Same Time. So then the algorithms at the almighty Amazon will know that these books belong together because they, they really complement each other. So other ones in why We Get Sick.

Yeah, yeah. So the other three then start to go together, which is this theme of managing their macronutrients. And so it's control carbohydrates, prioritize protein and don't fear fat. And the control carbs, as people are gathering from our conversation, I am not saying carbs are evil. I'm not saying you can never eat them, but you do need to be smart about them. And to me, the simplest way of interpreting that or applying it is focus on fruits and vegetables and be generally very careful of everything else. That's the simplest way. Now we.

So I could eat just as many bananas, you know, 40 bananas.

Yeah, so that's what I was going to say. So that's. So first order thinking would be focus on fruits and vegetables. Next order is avoid the tropical fruits like pineapples, bananas, mangoes that are the most sugary and avoid vegetables that grow in the ground. That, that's kind of next level controlling carbs. But I would say even if someone went to that first level of focusing on fruits and vegetables, but eat them, don't drink them, don't turn them into juices, don't turn them into smoothies, you're, you're fundamentally altering the nature of that plant. That's, that's good enough. Just, I would say it's a first step. It's a first step. Control carbs and then prioritize protein and don't fear fat. Those two, I think I like to say they should come together because in nature the best proteins come with fats. There's no exception. The best proteins are animal source. That is just reality. And so eggs, dairy and meat are the best proteins. They have the highest net absorption and the best amino acid profiles when it comes to dietary proteins. And they always come with fat. We should eat them that way. Don't take out the fat. And there's even something beyond just nature, I guess, which is coming to physiology. A little known fact is that when we eat fat, the gallbladder will release bile acids to facilitate the digestion of that fat. Bile acids actually have a very primary role for protein digestion. And bile acids facilitate, they improve the actions of those proteolytic enzymes in the intestines that are trying to pull apart the proteins to the amino acids that we can then absorb. One of the reasons I think so many people will eat like a pure whey, protein based, you know, well, protein and it'll upset their stomach is because you're doing something that isn't natural. Now I don't mean that in a kind of hippie frou frou way, but we in nature we, as humans, we would have never eaten pure protein. It doesn't happen.

Yeah. In fact, one of the ones that really scares me is milk protein isolate. And a lot of companies, it's, it's basically a waste product at this point from dairy where we have these national stockpiles of powdered milk from the 1950s programs. And because we have these, these giant silos from the 1950s where we just say economically we need to have a lot of dried milk. So people are like putting it in coffee and saying, well, it's protein. But it seems like different proteins do different things. I tend to say, don't have a lot of casein because of the pro cancer stuff. Some is fine, but not much. And milk protein isolate is just like, it's better than soy protein, but it's such a low quality protein. Like, what are your top three favorite proteins from dairy? Or do you just always say just, you know, eat a piece of cheese and go for it?

Well, well, I, I do tend to err on the side of just get protein with fat. And that was very much part of the focus on the shake that we made that I made with my brothers. But even still, the best protein is, I think it's egg white. But even then someone would say, well, then I'm just going to have egg whites. But there was a study done in men. They exercised and they made. They pulled a muscle biopsy from these fellows and after exercise they measured, they could quantify a degree of protein synthesis in the muscle. In other words, albeit microscopically, the muscles grew. They had them eat egg whites, mussels grew a little more. Then they had them eat egg and yolk together. Mussels grew even beyond the protein alone. What we don't appreciate is that as much as we focus on protein as this anabolic macronutrient, there's no question fat is an essential part of that anabolic response. That's why people take a lot of omega 3s. That's why fat should come. So fat and protein together, one, help the protein digest better. And two, it's more anabolic at the muscle. So anyone focusing on protein, do it. I think it's wonderful. That's why I say prioritize it. Eat the fat. Yep.

Egg whites by themselves deplete biotin and the yolk is full of biotin, like they were meant to go together. And for people, eat egg white omelets, just pass your yolks over my way. And because there's also protein in the yolk.

And in fact, Dave, I think There's a bit of hubris in that sense when it comes to nutrition. I think we sometimes think we're more clever than we are. And when we have stripped, when we have done something unnatural like pulling the fat away from a protein, which is why I don't like whey protein isolate. And I'm more an advocate of protein concentrate because at least it still has fats in it. Keep the fats there. Who do we think we are that we know better than, than what the world is providing for us? Naturally, fat is supposed to come with protein and then to kind of round that out on the emphasize the, the don't fear fat aspect. I do think there is a genuine health and value to dietary fat. And so something like butter, which has little bits of proteins and it has rich, many, many nutrients in it. I am a big fan. When someone's eating protein like meat and they want to add butter to it, I don't have a problem with that.

Yeah. In fact, if you're eating muscle meat, which is low in fat, I think you should add butter to it. And you probably should add some collagen somewhere as well, because we normally didn't. We ate nose to tail. And that's, you know, a big part of the, the recommendations in the bulletproof diet is you take some liver capsules or eat the organs even though they don't taste good. And that's just how it works. And if you do, that changes how you feel. And you don't get hungry the next time you fast because you had fat and protein. And if you have just protein, you'll be really hungry. There's that.

Oh, for sure. That's right. So fasting control carbs prioritize protein. Don't fear fat. The power of those last two macronutrients. Protein can have an effect on insulin and glucose, although there's some context there, the degree to which it may affect it. And then fat essentially has no effect. And so those two macros, not only are they both the essential macronutrients, but they also have the least or no effect on insulin. That's why I'm a very big advocate of those two macros and putting carbs in their place, which is to say they should be in last place.

Ben, this has been a fascinating and fun and exploratory interview. Your book is excellent. Why We Get Sick Guys, you really want to read this book? I know I oftentimes suggest you read a good number of books. Get them on audible if you don't want to read it. But seriously having it playing while you're taking a shower or something. It's how you learn. And when you have the knowledge, it actually makes it easier for you to say, oh, I'm going to fast today or I'm going to make a better food choice. So constant learning is what it takes. I will see you guys on the next episode. Thank you.

Foreign.

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