Take Back Your Health - with Dr. Robert H. Lustig | The Empowering Neurologist EP. 122

People think that a sugar is a sugar. Now, why do they think that? Because the food industry says so. Are there any data anywhere in the literature that says a sugar is a sugar? No, nowhere. They only say that because the food industry says so. When you actually look at the data, it's very clear that this is not the case.

Well, hello everyone. Welcome back to The Empowering Neurologist. I'm Dr. David Perlmutter. We have a very exciting show for you today. Our guest is Dr. Robert Lustig. He's the author of a book called Fat Chance. We interviewed him in the past about that book. His new book is called Metabolical. It is an amazing, amazing book. It really is a deep dive into asking the question, what's wrong with our healthcare system? And I'll start off by simply saying that we spend 97.5% of our healthcare dollars dealing with the treatment of diseases, much of which can be prevented. Only about 2.5% of healthcare expenditure in the United States goes to actual disease prevention. And Dr. Lustig calls it out. He calls out what are the fundamentals leading to chronic degenerative conditions and why these are the things that really need to be addressed. I'm really very excited about our interview today. Let me tell you a little bit more about Dr. Lustig. Dr. Lustig is Emeritus Professor of Pediatrics in the Division of Endocrinology and member of the Institute for Health Policy Studies at the University of California, San Francisco. He has authored 130 peer-reviewed articles, 80 academic chapters and reviews, and dozens of op-eds for the public. His 2009 YouTube lecture, Sugar: The Bitter Truth, Has accrued 12 million views. He's the former chairman of the Obesity Task Force of the Pediatric Endocrine Society, a member of the Obesity Task Force of the Endocrine Society, and a member of the Pediatric Obesity Devices Committee of the US FDA, Food and Drug Administration. He's also the chief science officer of the nonprofit group Eat Real, which is dedicated to reversing childhood obesity and type 2 diabetes by bringing real food into schools. Dr. Lustig has never taken money from the food industry, so he has no issues with respect to conflicts of interest that he needs to declare. Very excited about our interview, and here we go. Well, hello, Dr. Robert Lustig. How in the world are you?

Well, given that it's COVID and given that, you know, I've been looking at the same 4 walls for the past 13 months. I'm terrific.

That's good. I don't say this lightly and I don't say it often. This is a groundbreaking book. I mean—

Thank you.

You called it out in any way you could imagine. You called it out, what's going on. And it's sobering, it's empowering for many of us, and it's very enlightening. I think what you've shown us, I mean, we're gonna jump right in. I did in the intro talked about what book is about. But I'd like to start, if we could, by— you talked early in the book about how you were kind of challenged early on when you were dealing with childhood obesity, dealing with patients with childhood obesity. You were called that because you're an endocrinologist. So what was— why was that an issue?

So first of all, at one point in time, endocrinologists didn't even own obesity patients. They actually Dispatched them from clinic, basically saying, you know, this is a calorie problem, this is not a hormone problem, we have nothing to do with this. I had a colleague in the University of Tennessee Memphis when I was there who had a form letter that he sent to referring pediatricians, basically saying, you know, get these kids out of my clinic, don't bother. And I always felt very uncomfortable with that. They're looking for help, they didn't know what was going on. And then we discovered leptin, and all of a sudden leptin made obesity an endocrine disease. And so there I was as a neuroendocrinologist, you know, saying, all right, let's, you know, let's take it on. And it's not that I had any affinity for obesity per se until that point. But that really started my obesity career, was the discovery of leptin in 1994.

So for our viewers, leptin being a hormone that basically says it's time to— secreted by fat cells— it's time to push away from the table, you've eaten enough, and kind of runs in tandem with something that is in the purview of an endocrinologist, which is insulin. Therefore, this still, because of leptin, allowed the calories in versus calories out mentality to continue, but can take it into the world of the endocrinologist.

That's right. So, the big breakthrough, if you will, in my career was taking care of patients at St. Jude Children's Research Hospital who had a disorder known as hypothalamic obesity. These are kids who survived their brain tumor. They were not going to die of their brain tumor, But after their— the tumor or the surgery or the radiotherapy, one of the 3, they would become massively obese and they would do it extremely rapidly. They would gain upwards of 100 pounds in a year. Kids who were previously thin, wiry, active now had become enormous, rotund, and more importantly, They were absolutely docile. They did nothing. They were lumps on a log. And the parents would even say to me, this is double jeopardy. You know, my kids survived the tumor really only to succumb to the therapy. And it was up to me to try to do something about it. Now, the good news was that there was a literature on this in animals, lesioning, you know, different areas of the brain. And so lesioning the hypothalamus led to this obesity syndrome in rats called hypothalamic obesity. And what was determined was that the reason that those rats gained so much weight was because the connection between the brain and the pancreas to release insulin was in hyperdrive. And now that we knew that leptin was the problem, we postulated, well, they're not seeing their leptin. Well, these kids were not seeing their leptin. And so we said, all right, if they're not seeing their leptin and their insulin is in overdrive, what can we do to stop the insulin? And that we had a drug for. It was called octreotide, and it suppressed insulin release at the level of the pancreas. So, in a clinical research protocol, we gave kids with this disorder this drug, octreotide, to suppress insulin. And lo and behold, not only did they lose weight, which was remarkable enough because these kids only gained weight, and fast, so that was remarkable on its own, but they started exercising spontaneously. One kid started competitive swimming. 2 kids started lifting weights at home. One kid became the manager of his high school basketball team, you know, running around collecting all the basketballs. I mean, these were kids who sat on the couch, ate Doritos, and slept. And the parents would come to me even before the weight loss and say, something's happened to my kid, that, you know, they're back, that somehow this Medicine was bringing their interest in life back, and their quality of life improved. And it turned out that we measured that in the next study, and it turned out the degree of quality of life improvement correlated with the degree of insulin suppression. The lower we got the insulin, the better these kids felt.

Well, now let's generalize that to, to kids today and people today that are challenging their insulin levels day in and day out. based upon the— let's make the connection, we may as well jump right in with both feet— based upon the influences of big food industry indicating really having a huge role to play in influencing what our dietary choices are. That's right. I'm super comfortable in the time we have together that we jump right into that because I think what we're going to develop here, what your book talks about, is this relationship between the influences on our food choices our illnesses that we then develop and how our medical system responds to that in the form of giving us drugs to treat the very problems that were induced by the choices that we thought we made that were actually not— that were made for us. So the segue is probably going to be insulin and also leptin and loss of leptin sensitivity.

Indeed. So insulin is the bad guy in the story. You know, there's just no way to make it the good guy. Now, it is true you need insulin. You know, if you don't have insulin, you have type 1 diabetes, and you will die early, you know, from ketoacidosis or from, you know, various other, you know, retinopathy, nephropathy, neuropathy, all bad things. But you don't need a lot of insulin. You need just enough. And The problem is if you have too much, you activate a whole set of other pathways in the cell, all of which lead to vascular smooth muscle proliferation, reduced autophagy, and increased risk for cancer.

Let me stop you right there because you brought up something very important. That is higher levels of insulin that we bring onto ourselves by eating A diet that's higher in refined carbohydrates stimulates the growth of these muscle cells within the blood vessels. We really need— let's unpack that for just a moment because it's so important as it relates to blood pressure, the kidney, et cetera.

That's right. So insulin is a growth factor. It's the ultimate growth factor. It is the growth factor in the fetus. It is the growth factor in the adult. It is a growth factor There is— the insulin receptor is coupled to a pathway in the cell that basically makes cells grow and divide. It's called MAP kinase, mitogen-associated protein kinase, and that pathway is very important when you are growing, like, for instance, a fetus, but once you've stopped growing, you don't really want a whole lot of that. And the problem is that the more insulin, the more growth. And so we should be trying to keep our insulin secretion down and our insulin sensitivity up in order to get our cells to burn. And one of the things I talk about in the book is the difference between growing and burning. Those are the 2 stereotypical paradigms of cellular physiology. A cell can grow or a cell can burn, but they can't do both at the same time. Okay, they cannot walk and chew gum at the same time. So if they're growing, then you want insulin to be high, and you want cells to not have much oxygen because oxygen actually stimulates the mitochondria to burn. And you want the glucose not to be burned. You want the glucose to be turned into structural elements for the cell. You want it to be turned into lipids for membranes. You want it to be turned into amino acids for proteins. You want it to be turned into nucleic acids and ribose, you know, for DNA in order to be able to divide. So that— switch in the cell that switches you from burning to growing or back again is insulin-dependent. And so when the insulin's high, you are going to grow, you're not going to burn. And that is good when you're a fetus, it's bad when you're an adult. We, we've basically engineered our food to basically take advantage of This pathway to growth, which we don't want to be doing.

So for our viewers, if you want to learn more about this, there's an interview we did recently with James Clement, who is the author of the book The Switch, and it talks about these things like AMP kinase and the mTOR pathway. So if you want to learn more, that would be a place to go. In your very last sentence, Dr. Lustig, you just said that the foods that we are eating are really very relevant as it relates to Our ability to get rid of things versus continuing to build and having cells divide like we might not want in the world where we're at risk for cancer, for example. There's certainly a place for that, but I think you've really hit upon something that I think maybe our viewers are not so aware of. You'll learn that insulin's involved with packing sugar away after a high glucose or carbohydrate meal. End of story. But you're letting us know that it's a powerful growth factor. It's a powerful stimulator or trophic hormone in the body and in the brain. Not that the brain's not part of the body, that insulin plays a really critical role in the brain as well, acting again as a trophic hormone. So when we become less able to respond to insulin, we become insulin resistant because it gets— the level gets higher and higher because we continue to challenge it. Then we see manifestations across the board throughout the body. You talked about this notion of, you know, the tenet of your book is protect the liver and feed the gut, that if we could adhere to those principles, we'd go a long way towards staying healthy. So why don't we start first with protect the liver?

Sure. So protect the liver means a bunch of things. Your liver is your detoxification organ. It's supposed to, you know, get rid of Toxins of various sorts. It metabolizes virtually all drugs, you know, through various cytochromes. But ultimately, the liver has a limit. It has a capacity, and if you exceed that capacity, the liver gets sick. Turns out the liver has a capacity to metabolize alcohol. We know that. I mean, all you have to do is show up at your local bar and you can see the guy who walks out and you can see the guy who gets dragged out. Okay, and what was the difference? The number of drinks. And you know that, and the bartender knows it too, and now they go to jail if they let the guy, you know, have 5 drinks and then get in his car. There's a limit to how well your liver can metabolize alcohol. If you exceed that, bad things happen. Well, it turns out sugar, the molecule fructose, the sweet molecule in sugar, and alcohol are metabolized by the liver virtually identically. And if you look at the biochemistry of the 2 molecules, it makes sense that that would be the case, because after all, where do you get alcohol from? Fermentation of sugar. It's called wine. We do it in Napa and Sonoma every day. The big difference between sugar and alcohol is that for alcohol, the yeast does the first step of metabolism called glycolysis. Okay. For sugar, we do our own first step, but after that, the liver can't tell the difference as to where it came from. So then it shouldn't be surprising to us that kids today get the diseases of alcohol without alcohol. Type 2 diabetes, fatty liver disease— these were diseases of alcohol until 1980. When you saw these, you said, oh, this is an alcoholic. But now kids get them. And in fact, 25% of the entire pediatric population of the United States have fatty liver. Now, they don't drink alcohol. Where'd the fat come from? Turns out that fat in that liver is now causing their liver to not work so well. And their pancreas, which makes the insulin, has to make extra to make the liver do its job. that's raising insulin levels all over the body, and that's meaning there's more insulin pressing on every organ, especially fat cells, and that's driving the weight gain, and it's also driving the chronic disease, and it's also, unfortunately, driving cognitive dysfunction, and will ultimately drive— it's driving dementia as well. So this phenomenon of hyperinsulinemia due to dysfunctional liver has been ignored by the medical establishment for the last 40 years since we first realized that we had this thing called non-alcoholic fatty liver disease. You have to protect the liver. The liver can't handle it in the same way it can't handle excess alcohol. It can't handle excess sugar.

You mentioned in your book that you had 2 pediatric patients, each of whom weighed in excess of 400 pounds, who developed actual cirrhosis. And did they need transplant? Right.

Just—

and I think you said just from drinking sugary beverages.

That's right. Just from drinking sugary beverages. And unfortunately, one of them didn't stop and ended up coming back and needing a second one. So this is a huge problem.

So this assault upon the liver by sugar is very, very widespread.

It is 45% of American adults and 25% of American children today, having nothing to do with obesity. So everyone says, well, only in fat people. Wrong. Thin people too. Yeah, less in thin people than fat people, but in everybody. And actually, it turns out there are more thin sick people in America than there are fat-sick people. And 88% of Americans have insulin resistance, have metabolic dysfunction because their liver is overwhelmed. So this is the main problem. This is the driver of chronic metabolic disease, and it's because of our food.

And, you know, the player here is the difference between how we metabolize glucose versus fructose. And table sugar is immediately broken down 50 50% glucose, 50% fructose into free available fructose. And that makes the story of high fructose corn syrup even more compelling, doesn't it?

It does. So people think that a sugar is a sugar. Now, why do they think that? Because the food industry says so. Is there any— are there any data anywhere in the literature that says a sugar is a sugar? No, nowhere. Okay, they only say that because the food industry says so. When you actually look at the data, It's very clear that this is not the case. Glucose is the energy of life. Every cell on the planet burns glucose for energy. Glucose is so friggin' goddamn important that if you don't consume it, your body makes it, right? The Inuit, they don't have any carbohydrate. They don't have any fields to grow any carbohydrate. They don't have any wheat. They don't have any rice. They don't have any corn. They don't have any pasta. They don't have nothing. They got whale blubber. All right, but, but they still have a glucose level, a serum glucose level. And the reason is because it's so important that your liver will take amino acids or fatty acids, the glycerol and fatty acids, and will turn it into glucose. It's a process called gluconeogenesis. We learned it in medical school. Unfortunately, the food industry did not, because they say you need sugar to live. No, you don't. You do not need sugar to live. No one needs sugar to live. No cell on the planet needs sugar to live. But they say it because that's how they sell their products. So we have to get rid of the subterfuge, and we have to get rid of the propaganda, and the only way to do it is with science.

Well, that's the central theme of your book, is getting— is calling out the subterfuge. I mean, uh, you didn't— you pulled no punches in that regard.

This is a no-holds-barred, uh, you know, I like to— I like to say, you know, this is a kiss and tell, but really, because it's about diabetes, it's really more a piss and tell.

Well, well, you are, uh, you were practicing what's, I think, in writing the book, medical disobedience. So you are countercultural.

Well, you know, I'm, I'm now retired, and so I don't have to satisfy my university and, you know, have to— I don't have to stay in the ivory tower. So I think it's, you know, time to call a spade a spade, make it clear what the real problem is.

You mentioned that, uh, glucose is so fundamentally important, but in that it produces energy. And yet the metabolism of fructose actually consumes energy by reducing ATP down to ADP and AMP. That's right. So it's actually a situation where the body senses a reduction of energy and as such puts into play various types of things like the production of glucose, gluconeogenesis. To allow the body to keep glucose available and keep energy stores available.

That's right. So, first of all, fructose is phosphorylated in the liver to fructose-1-phosphate. That reduces ATP to ADP, and then that goes to AMP, that goes to uric acid. And that's the reason why sugar causes gout, is because it raises uric acid. I mean, Benjamin Franklin knew that. And wrote a poem about it, in fact. The fact is that fructose also inhibits AMP kinase, and AMP kinase is the enzyme that is the fuel gauge of the cell, knows when the fuel is starting to run out, and then gooses the mitochondria to burn more. Remember the growth versus burning? So when that AMP kinase is activated, It tells mitochondria, all right, you're in burning mode because we need more energy, but fructose blocks it, and so fructose actually makes the cell go into growth phase when it shouldn't be. So fructose does a lot of things that are not so good. Ron Kahn, the head of— the CEO of Joslin Diabetes Center at Harvard, published a paper. The first author was Sofdik, SOFTIC, in 2019, where he showed that glucose stimulates mitochondrial function through activation of both AMP kinase and HADH, which is hydroxyacyl-CoA dehydrogenase, which is the 3rd step on fatty acid oxidation. So, basically, burn, burn, burn. Glucose makes cells burn, burn, burn, which is good. Fructose Not only does it inhibit AMP kinase, but it also inhibits another enzyme called ACADL, acyl-CoA dehydrogenase long chain. And so what happens is the fats build up, and so now you got fatty liver. So every single thing about a sugar is a sugar or a calorie is a calorie is absolute total nonsense. Complete garbage. But of course, the food industry, this is their juggernaut. This is their gravy train. They're not giving it up even today.

At the risk of getting too far into the weeds, though, I love this stuff, and I think many of our viewers kind of fancy that they enjoy it as well. I want to just get to this fructose inhibiting AMP kinase and then, of course, stimulating an alternate pathway, AMP deaminase. too. And that's another very important switch that goes on because the inhibition of AMP kinase is basically telling the body that winter is coming. We need to make fat, we need to store fat. You talked about this, the lipoprotein lipase, et cetera, hormone-sensitive lipase back in Fat Chance. Right. But it's basically a signal. In fact, you talk quite a bit in this book about these sensors. these that are at play. But what you're telling your body when you're exposing it to fructose is that winter is coming, or at least a time of caloric scarcity is coming. Better pack on the fat, better augment insulin resistance, and better start making more glucose, enhancing gluconeogenesis. The drug metformin acts, which is given, used for diabetes, acts to stimulate this AMP kinase Guess what? We have another powerful drug to enhance AMP kinase activity. It's called exercise. Who knew? But in this regard, those are things that we would employ to counteract what fructose is doing. So you're calling it out exactly how it works. It's telling your body, get ready for winter, make a lot of fat and store a lot of fat and don't burn it. Reduce fatty acid oxidation. You know, in that context, it really answers a lot of questions for people who are just saying, I don't get it. I'm taking in X number of calories and I can't lose weight. My body is still storing the fat. And it gets back to this absolute nonsense. You called it out in your book about the battles going on between being a vegan versus being on a ketogenic diet. And what you say is that, you know, these types of diets should be on the same side and that the real enemy here are the producers and marketers of these ultra-processed foods.

I couldn't have said it better. Thank you, David. The vegans and the ketos are in a war with each other. And to be honest with you, it's a false war. It's a false flag war. And they don't get it. They don't understand it. I partly wrote the book in order to get them to get it. But, you know, what can I say? Look, I'm not against a vegan diet per se. I think that there are some things missing from a standard vegan diet, but they are potentially replenishable, you know, through either supplements or through, you know, being careful about the foods chosen. So I have no bone to pick. It's not that I'm anti-vegan. I'm also not anti-keto. In some ways, I'm pro-keto. We certainly used very low carbohydrate diets in our patients at UCSF, you know, from pediatric obesity clinic who would not respond to standard dietary manipulations, you know, if we couldn't get their insulin down far enough. So we would resort to that as well. And I've used it with great success. So I'm not against that either. You know, the reason both work is because they get insulin down. But the reason both work is 'cause they're both real food. Now, unfortunately, you can do vegan wrong 'cause Coca-Cola, Doritos, and Oreos are vegan. And you can also do keto wrong. And one of the ways to do keto wrong is if you're not measuring your ketone levels. And so a lot of people say they're eating keto, but they're not. And so a poorly done keto diet is really a moderate carbohydrate, high-fat diet, which is the worst diet. So if you're really keto, that is, you are checking your urine or checking your breath to make sure that you remain in nutritional ketosis, you are getting the benefits of keeping your insulin very low, and you're also getting the benefit of the beta-hydroxybutyrate, which is in itself a signaling molecule. It signals sirtuins, which signal mitochondrial function, which signal burning, which is good. Again, that's a good thing. So I am certainly not against keto. I am for it, in fact. All right, but I'm not for it against vegan. I am for both because both mean real food. The point is you can choose which one's best for you.

Yeah, and, and why pigeonhole yourself? I mean, uh, why? Yeah, we, we looked at the book Ketotarian indicating that, you know, these are not mutually exclusive. But the battle line is drawn against the influences on our dietary choices that would have us believe that that bag of Doritos is a good choice because, or the corn chips are a good idea because they're organic and gluten-free.

Yeah. Garbage. I mean, not that gluten-free is garbage per se. I talk about the gluten-free thing and obviously I know this is a big issue for you and I'm not against, I'm not pro-gluten-free, against gluten-free per se. What I've learned, and I learned it myself because I have it, is that it's not gluten, it's wheat. Turns out wheat is a very complex organism. It's a hexaploid, not diploid, and there are 700 different antigens. 2 of them are gluten, so gliadin and glutenin, and those are the famous ones, and those are the ones we have tests for. The other 698 we don't have tests for, and different people are, shall we say, intolerant of different ones. So you can be non-celiac. So if you have— if you have allergy or, you know, intolerance to either of those 2 proteins, you have celiac disease. There are a lot of people who don't have celiac but are still intolerant to wheat because they're intolerant to one of the other 698. So they need wheat out of their diet, and that is what I do, and that is what I have done, and my sister has. it too, and it turns out my kids have it. So I understand this and I am for that. And obviously if you're gluten-free, it means you're wheat-free. But you know what? I can have a beer because that's not— that's not wheat, that's barley. Now if it's a wheat beer, it's another story. So I am for, you know, being careful about what you eat, and I am for having all of these gluten-free options. But people should understand that it's probably more likely that they're— the problem is wheat rather than gluten per se.

One of the main pillars you talked about in Metabolical is the notion that mainstream medicine is pretty much focused on symptom management and not really treating the underlying disease. And I wonder if you could relate that back to our discussion a few minutes ago that much of these noncommunicable chronic diseases that are basically crippling the planet are related back to this mechanism of insulin, of de novo lipogenesis, the creation of fat in the liver, and how that is a reflection of the change in the diet that is really very, very new, at least in terms of what humans have been consuming.

Right, so completely on board. Um, okay, so let's take high LDL. Is high LDL the problem? High LDL is a symptom of the problem. Turns out that the real problem underneath that is the insulin resistance. High blood glucose— is the high blood glucose the problem, or is the real problem the pancreatic dysfunction and the insulin resistance? High blood pressure. Is the high blood pressure the problem, or is the problem the actual AMP deaminase 1 that we talked about in the uric acid, etc.? In every case, what we have is we have medicines in our medical armamentarium that you use, I use, that treat the symptoms of the underlying pathology but not the actual pathology itself. I liken it to giving an aspirin to a patient with a brain tumor because they have a headache. It'll fix the symptom.

No, I think you also said something about going into a room where there's a bunch of wasps or hornets and you kill one,

right? So you see a— you see a wasp in your attic, you know, what are you gonna do?

Yeah,

yeah, you know, what are you gonna do? You're gonna kill the wasp or you're gonna find the wasp's nest? Okay, that wasp ain't alone. Okay, you have to work upstream of the problem, and we doctors have never been trained to do that. You know, we've been trained to look at medicine as this big game of Clue. All right, you know, Colonel Mustard in the conservatory with the candlestick, you know, and, you know, you basically— you— I remember when I was a, a, an intern, there was a game called Intern. I don't know if you ever played it. Um, it, uh—

I'm sure I did in one way or another.

You got symptom cards, then you got disease cards, then you got treatment cards, and when you matched them all up and you laid them down on the And the goal was to discharge all your patients. Whoever did that first won the game. We used to play that in the call room. And, you know, that's the way we looked at medicine was, you know, match the symptom with the diagnosis with the treatment. Turns out that was missing the point, you know, and I didn't know it at the time. It took me, you know, 40 years, you know, to figure this out. And what I realized is that in order to treat disease, you have to prevent it, especially when we're talking about chronic disease. And the reason is because we're not touching the pathologies that are really causing the chronic disease. There are 8, you know, and I can't— I, I lay them out in the book, and they're important, and they actually go to the question of why doesn't exercise work, you know, to fix these. Here are the 8, and I'll just mention them for your audience: glycation, oxidative stress, Mitochondrial dysfunction, insulin resistance, membrane instability, inflammation, methylation, autophagy. These eight subcellular pathologies belie all the chronic diseases that we know of, and it turns out that all of our drugs none of them touch any of those. They touch the symptoms that come from them. But they don't actually fix those pathologies, which is why no one ever gets better. They could get better.

Which is why you talk about druggable versus foodable.

That's right. None of these are druggable. They're all foodable. If you ate right, you could fix all 8 of those. So then the question is, what about exercise? And I am for exercise. I mean, we're all for exercise. Exercise is the Single best thing you could do for yourself. But when you actually look at the molecular mechanisms of each of those 8, turns out exercise only affects 4 of them, maybe 5 if you push it. So it does not affect glycation, it actually makes glycation worse. It does not affect oxidative stress, exercise actually makes oxidative stress worse. It does not affect membrane stability because, as you know, that's about omega-3s, and exercise don't do a thing for omega-3s. Okay. And it sometimes will help methylation, but not always. It depends on, you know, how you do it. So the others will be affected, you know, it will help mitochondrial function because it builds new mitochondria, it will help insulin resistance because it lowers insulin secretion, it will help autophagy, it will help inflammation. So there are a lot of really good things about exercise. But you cannot outrun a bad diet. Ultimately, you know, people think, well, if I just, you know, get on the trainer or that Peloton and I pedal away, you know, I can basically eat whatever I want. And that is just not true.

Well, it really takes us to a place of food as information. You know, it really is the— it's instructing us at a metabolic level and certainly instructing us at an epigenetic level. multiple levels that we've had this relationship to some degree mediated by our microbiome, which turned out to be a big player in your book. It's step 2 in Feed the Gut, talking about how we're basically starving our microbial friends and we're paying the price for that.

Indeed. Basically, you're not eating for one. We always say you're pregnant. When you're pregnant, you're eating for 2. Well, actually, we're always eating for 100 trillion. Always. And the bottom line is you got to feed your bacteria. And if you don't feed your bacteria, guess what? They feed on you. Okay, they are only commensal if you feed them. If you don't feed them, they become parasitic and they will eat you instead. They will eat the mucin layer right off your intestinal epithelial cells. in order to stay alive. They'll do whatever they have to to stay alive. They're not going to die. You're going to die is what's going to happen. And if you eat that mucin layer off your intestinal epithelial cells, now the bacteria are apposed right on your intestinal epithelial cells, and that has been shown to reduce the integrity of the tight junctions that basically keep your intestine a barrier. And so now you've got lipopolysaccharides and cytokines and bacteria themselves making their way through to your bloodstream, and now you've got systemic inflammation, not just in your liver but all over your body, including your brain, and now you've got, you know, cognitive deficits, etc., and you are basically promoting all of those other chronic diseases, especially insulin— chronic pathologies, especially insulin resistance. making things much worse. So you must feed your bacteria. Now, the question is, all right, what do you feed them? What do they like? Well, it turns out they like fiber. That's what they like the best. Yes, they'll eat the glucose, they'll eat the fructose too, but they really like fiber, especially your colon. Your colonic bacteria love soluble fiber, and they do you a favor because what— not only do they chew it up, but they The waste product of their chewing up that fiber is short-chain fatty acids, propionate and butyrate, which turn out to be anti-inflammatory and anti-insulin for you. So you are— if you're depriving them of that soluble fiber, you are actually making yourself worse. So you gotta protect the liver. Don't let it get overwhelmed by not just sugar but by other, you know, problems like polycyclic aromatic hydrocarbons, like, you know, from grilling and what have you, but— and also heavy metals and things like that that affect energy metabolism. But you also have to feed your gut, and if you feed your gut, then your gut will not eat you. And if that hap— and if you do both of those, then you're healthy. And if you don't do both of those, then you're going to be in a wheelchair, you know, sucking on a tube and, you know, waiting for your next amputation.

That doesn't sound like fun. You use the term commensal or commensal bacteria, and I think it's a great word. Co means with, mensa, eat. So they're eating with us, they're not eating us. And I think that the description of starving our bacteria, then they're eating the mucin off of our protective lining of the gut epithelium leading to increased permeability, which is a powerful player as it relates to inflammation throughout the body, including the brain, is really something I think our viewers can— we've talked about it time and time again. We've gotta do everything we can. So I think the part of the story that may be a little unfamiliar, getting back to the liver and this creation of fat and the increased insulin resistance and how that is just pervasive throughout the body in terms of the opening the door to degeneration. I use the metaphor of treating our medicine, standard medicine today treats, focuses on the smoke but not the fire. No. And you, as you say, we wanna try to get upstream. That's right. So, what are we up against? I mean, These chronic degenerative conditions are, according to the World Health Organization, the number one cause of death on the planet. We know that America, your book calls it out, ranks number one in terms of type 2 diabetes on the planet, and probably somewhere around number 3 with respect to senile dementia of the Alzheimer's type, which is, you know, directly related to what we've been talking about. What I think is very clear is that if things could go a different direction in terms of our nutrition, That we could have a huge impact on our healthcare expenditures and certainly on the prevalence of these and other diseases.

Right. So this gets to the whole economics question. Um, the food industry today in America— we'll just talk America, we'll leave the rest of the world out for the moment— food industry today in America grosses $1.5 trillion a year. Big business. Of that, $660 billion is gross profit. So that is a gross profit margin of 45%. That's pretty good. The next highest industry after food is pharma at 21%. So 45%, 21%. Okay, and we call Big Pharma drug whores. So what does that make Big Food? Drug whores. I don't know what that makes them, but they're making money hand over fist— $660 billion a year. Now here's the problem: medical care in this country costs $3.6 trillion a year, and of that, 75% are all these chronic metabolic diseases that we've been talking about. And of that, 75% of those could be mitigated If we could just go back to levels of 1970 before the processed food glut. So we wouldn't get rid of them entirely, but just get back down to where we were before we went off the rails. So 75% of 75% of $3.6 trillion is $1.9 trillion. So we are wasting triple what the food industry makes every single year cleaning up their mess. This is unsustainable. We can't keep doing this.

You indicated that 12% of adults in America don't have 1, 2, 3, 4— have 5. 12% of American adults have 5 chronic diseases. That's a scary proposition, especially when you think about that these are probably each going to require their specific drug cocktail. So the expenditure for the Americans, as you just indicated, is understandable from that perspective. What are you seeing now in terms of, you know, we used to call these adult diseases, but what's happening with these diseases in the pediatric population?

Well, we now have 2 diseases that we never had before, you know, Type 2 diabetes and fatty liver disease. These are 2 diseases we never saw in children, and the most important thing is these are the diseases of alcohol. Type 2 diabetes and fatty liver disease were the diseases of alcohol before 1980, and now kids get them, and lots of kids get them. It's not a few kids. 1 out of every 3 new diabetes diagnoses is type 2 in kids, and 25% of kids, if you stick them in an MRI scanner, have fatty liver disease. Now, they don't have cirrhosis yet, but, you know, it'll get there. It'll get there. It's a slow process. It'll get there. To me, that's telling me what's going on. You know,

it was called adult-onset diabetes,

right?

And that didn't work.

That didn't work, right? Because now kids get it. So, and we've got 5-year-olds with

it. In the later parts of your book, you talk about how we can, uh, screen ourselves looking at our own metabolic panels. to determine where we are in terms of the harbingers for future disease. So maybe we can just unpack that a little bit and look at some of the key players in terms of laboratory studies.

Sure, sure. So the first thing you have to understand is your doctor doesn't know how to read your labs. Okay? And, you know, it took me a while to figure it out and I had nobody to ask. I had to do it basically, you know, empirically, you know, with, with the data, you know, that of my patients. But, you know, I've, I've ultimately, you know, figured out how to look at 'em. So there's no one test. It's a pattern of tests. It's a profile of tests. So you have to know what the tests are. And never, and one of the things I say in the book, never, ever, ever take the word normal as an answer. If you basically let your doctor say to you, oh, your labs are normal, okay, then you're as big an idiot as he is. It's just that simple. Never accept normal for an answer. Get the—

or in the normal range, or their reference range.

Yeah, in the reference range. Who made that reference range? And that's actually to the point. One of the tests that I find most helpful is a fasting insulin. If you go to the American Diabetes Association website right now, this minute, it will say do not draw fasting insulins. Fasting insulins are useless. Yet I think they are the most important test that you can possibly have. How can that be? How can the ADA say one thing and me say another? They must be right because I have to be an idiot, right? Well, here's why they say what they say. They say it for 2 reasons. Number one, insulin assays are not standardized across different labs. That is true. And one of the reasons is because The insulin assay also, in most cheap labs, I mean, you have to have a really good lab to do it, the insulin assay also picks up the precursor proinsulin. So proinsulin gets measured in the insulin assay. When your pancreas is working overtime, it's got to push all the vesicles out, and sometimes it doesn't have enough time or enough prohormone convertase 1, which is the enzyme that Cleaves the C-peptide out of the proinsulin molecule to make a mature functional insulin. So it's pushing out proinsulin in order to try to get that blood glucose down. So it will get measured in the insulin assay, but it's not insulin, it's proinsulin. That is true, they are right. And a lot of cheap assays that don't distinguish those will not give you the answer you want. I don't argue that. But that's not a reason not to do it. That's actually more of a reason to do it because you need to know. Because if your insulin level is up, whether it's insulin or proinsulin, you got a problem and you need to do something about it.

Even if your glucose level is normal?

Even if— especially if your glucose level is normal.

Right. That'll take you off the trail

because that's

the first thing that changes. You just focus on the insulin.

Right.

Yeah. You know, I wanna tell you, 9 years ago I wrote a book called Grain Brain. And in that book, at the end of the book, featured 8 laboratory studies. One of them was a fasting insulin level. And the amount of grief I got from my colleagues was, why would we want— you think people are walking around with insulinomas? I said, no, this is how we will know if people are now requiring higher levels of insulin to keep their blood sugars normal. If you just focus on the A1C or the fasting glucose, you have no sense as to what's going on. And to this day, people still call me out on that and I think it's fundamentally important. I'm glad you went to that as lab, lab test number one.

Yeah, well, the second reason that they say don't draw it is because fasting insulin levels do not correlate with obesity. That's true. They correlate with metabolic health. And the reason is because subcutaneous fat, which is what you measure on the scale, has nothing to do with your fasting insulin. What does have to do with your fasting insulin is your ectopic fat. The fat in your liver and in your muscles that's not supposed to be there. That's what your fasting insulin is looking at, is your ectopic fat. But you don't measure that on the scale. That does not show up when you stand on the scale. So it has nothing to do with obesity, has to do with metabolic health. So the 2 reasons that the ADA says don't draw fasting insulin are both bogus and garbage. Okay. So that's my first and biggest important test that people need to get and understand, and their doctor needs to understand what to do. And if the doctor reads the book, then they'll understand it. Second question.

Okay, I gotta just have to stay with the first one still. Why do you suppose— and I know where this is going— why do you suppose the ADA wouldn't want people to check their fasting insulin levels?

Well,

I had to do it.

All right. So, I think the ADA is very co-opted. I, you know, I've been to ADA meetings, and they don't really talk about prevention very much. They're about treatment, and they're about the fact that, you know, diabetes is a chronic progressive disease that doesn't get better, and you have to measure your blood glucose, and you have to do this, you have to do that, and you're going to be on these medicines for the next 30, 40 years. And you know, they get a lot of money from pharma. In fact, they are number 100 of all charities in the world for getting money, and 60% of their money comes from big pharma. So like, why would an association dedicated to eradicating a disease want the disease eradicated? That's the question. Because if they got it eradicated, maybe they would go out of business. Hmm. So I'm— I've got a— I've got a bone to pick with the ADA.

Let's just stick for a moment with fatty liver. Not everybody's going to be able to have a CT, but ultrasound is available. But what about lab work? What about liver function studies? How might they relate?

Okay, so that's my second one, and thank you for that because that's where I was going.

I don't know, these aren't listed, so I think our minds are We're doing the Vulcan mind thing here.

Indeed, indeed. So the second test that I think is extraordinarily important is an ALT, alanine aminotransferase. Used to be known as an SGPT, um, they changed the name about 25 years ago. It doesn't matter, same test. Um, this is a test that tells you about liver fat. Now, it's not perfect. It's sensitive but not specific. So that means that if it's high, it means something. If it's low, it doesn't. Okay, but if it's high, that means something, so you should take a look. Um, if you have fatty liver, that's the first thing that you will see go up. Now, the problem with the test is the reference range. When I entered medical school— David, when did you start medical school?

'81.

'81. I started in '76. And when I started, the upper limit for ALT was 25. Now today, if you pull out the lab slip and, you know, gives you the reference range, it tells you that the upper limit for ALT is 40. Same test was 25, now it's 40. Why is that?

It's a reference range.

Yeah, it's a reference range 'cause everyone's got fatty liver.

And there was no, no manifestation, there was no clinical manifestation at higher levels. So they skewed the reference range to the right.

Exactly. The reference range is skewed to the right. So now everyone's over here instead of over here. And so everyone thinks 40 is okay. 40 is not okay. 40 is very not okay. 25 is really, you know, sort of not okay. You know, it should really be lower than that. And African Americans, it should be 20 for that matter, because they actually don't even make as much fat in the liver. They have a mutation in their APOC3 gene, so they actually don't accumulate as much fat. So if you— if they have fat in their liver, then their ALT will be above 20. So you have to be able to know what the appropriate reference range for you is, and it ain't on the lab slip. So an ALT is extraordinarily useful if you know how to read it. And if it's above 25, that's probably an indicator of a metabolic problem. So I find that very, very helpful, and we used it in pediatric obesity clinic all the time.

All right, number 3.

Uric acid. So uric acid is, again, a surrogate marker of purine metabolism because purines go to uric acid, but it's also a surrogate marker of glucose— of fructose metabolism. Sorry. And the reason is because when fructose enters the liver, ATP has to donate a phosphate. So ATP becomes ADP, and then it goes into AMP and to uric acid. There's no scavenger mechanism to return that, so it goes to uric acid. So the amount of uric acid your liver makes is proportional to the amount of sugar you're consuming. Now, Uric acid is not just a waste product. Uric acid has effects. It has effects on the mitochondria because it interferes with the enzyme carnitine palmitoyltransferase 1. So it means that you're not getting stuff into your mitochondria to be able to get things burned. And in addition, uric acid is the endogenous inhibitor of the enzyme in your Blood vessels, endothelial nitric oxide synthase, or eNOS, which is your endogenous blood pressure lowerer. And so when your uric acid is high, your blood pressure goes up. And so that is one of the causes of hypertension, and it is really an unheralded cause of hypertension. People always talk about salt being the cause of hypertension. Sugar is a much bigger cause. of hypertension than salt is. Think of it. Once upon a time, we had these whaling vessels out on the Atlantic catching fish, all right? And they didn't have freezers, they didn't have refrigerators. They were whaling vessels. They had sailboat, you know, sails to move, okay? But they would catch fish, and they'd bring it back to shore. How'd they keep the fish fresh? They packed them in— Salt. Salt. The average consumption of salt in, you know, prior to refrigeration was about 15 grams of salt per day. 15. And there was no hypertension. But today, the average consumption of salt is 6.9 grams per per day, half as much, and we have a 40% incidence of hypertension. How can we have less salt but more hypertension? And the answer to this, which is not immediately known to most doctors, is insulin is important at the level of the kidney. Insulin helps resorb sodium. And so in the face of a high insulin, that 6.9 grams ends up being enormous. But if you became insulin sensitive, that 6.9 grams would only be half of what your ancestors consumed, and it would go straight out your kidney and wouldn't be a problem. So that salt is only a problem in the face of a high insulin. And where'd you get the high insulin from? The sugar.

Yeah, let me just, if I can vet the, uh, Enos a little bit more, that, you know, the role of uric acid in terms of antagonizing nitric oxide at the level of the endothelium does actually compromise how insulin works, especially at the myocyte, by 2 levels, entry into the myocyte, but also the transgression through the endothelium, which is facilitated by nitric oxide, inhibited by uric acid. And also uric acid feeds back to enhance fructose metabolism, And further antagonizes the action of AMP kinase. So, it's a feed-forward cycle that Dr. Richard Johnson characterized as being a survival mechanism for our primate ancestors 14 to 18 million years ago when we developed the mutation, the uricase mutation.

Mutation, right.

Actually, there were several that led to humans our ancestors rather, having higher levels of uric acid as a key mediator of insulin resistance, of obesity, lipogenesis, and certainly hypertension, that those things were survival mechanisms, that hypertension was a survival mechanism in a time when we were risking dehydration and inability to reabsorb salt.

Right.

So now it's, we see that the environment has changed where we have fructose abundance, overabundance. And purine consumption is high as well. Foods, organ meats, anchovies, those types of foods. And therefore uric acid levels have increased quite dramatically in comparison to the 1920s. Right. And what you and I are talking about right now is the dangers of high uric acid above and beyond gout and kidney stones. that it's turning out, and I'm so glad to hear that it's on your list, to be a really central player, not just as a marker, but proving to have a powerful mechanistic role.

Yes, exactly. And I'm very familiar with Rick Johnson's work, and we're good friends. Been to several meetings together. We both, you know, have identified high fructose corn syrup as, you know, shall we say, a poison. And so I follow his work, you know, very carefully. Ultimately, uric acid is a problem even in children, and we never think of uric acid as being an issue in children. We use it all the time. You just have to know what the reference range is. And again, you can't use the adult reference range when you're looking at children. So these are, you know, on my lists of things that you need to know. That your doctor would look at the thing and say, ah, you're fine. And

you don't have gout, good to go.

Right, exactly. And so, you know, doctors need, you know, shall we say, to get their nutrition knowledge upgraded. And I have a whole chapter in the book, you know, dedicated to what, you know, why doctors know nothing about nutrition. And they truly are know-nothings when it comes to nutrition. And to be honest with you, that goes back 110 years to the Flexner Report, because neither Flexner, Abraham, nor Simon believed in nutrition.

Why is it taught in veterinary school, one wonders?

Well, because we— because, because—

Does it matter?

Dog— because it matters, because dogs eat food. I don't know. They don't get medicine.

You touched on homocysteine in the book too.

Yeah, so homocysteine is a driver of cardiovascular smooth muscle proliferation. It is one of the things that cause, you know, leads to heart attacks. It's been known for years that patients with homocystinuria that, you know, I take care of have problems with their blood vessels, you know, small and large. And the thing is that homocysteine is normally metabolized down to— down the urea cycle to succinate by the enzyme MTHFR, methyltetrahydrofolate reductase. And the problem is that folate is really important, but we have enzymes that get screwed up, and then you methylate proteins because you don't have the methyltetrahydrofolate reductase working. And now you've got an epigenetic problem that drives chronic disease. Again, if you have got an enzymatic abnormality, that's one thing, but you don't want to make yourself have an enzymatic abnormality by eating the wrong stuff.

And not eating the right stuff as well.

Right, and not eating the right stuff. Exactly. So all of this stuff is, you know, stuff that doctors don't learn. They're not taught about it. Dietitians, you know, they're still in calorie mode. And as far as I'm concerned, you know, that they're— you know, doctors' diplomas don't say nutrition, they say medicine. But dietitians' diplomas do say nutrition and dietetics. And the fact of the matter is, they're still in calorie mode, and my job is to kill the calorie mode. And that unfortunately means turning dietetics on its head.

Well, you also brought out that we generally don't get continuing medical education credit for nutritional type of symposia that we may attend even to this day.

Well, we're not, we're not, only 28% of medical schools even have a nutrition curriculum and there's no CMEs for nutrition except some rare things like integrated medicine at University of Arizona or my colleague Tim Harlan, Does Health Meets Food at George Washington University. There are some, there's a few of them, but they're not required. You know, in California, I had to take 12 hours of palliative care as an endocrinologist. I had to take 12 hours of palliative care. Now, like, why did I have to do that? Not that palliative care is not worth something, it is, but like, they made me do that to keep my license. But no one says a damn thing about nutrition. And that is killing people ever. And that's killing people. Yeah. And no one has to do that. So, you know, figure it out.

I wanna end our time together on a positive note, and I'm gonna leave that up to you to— let's, let's talk about the empowerment part. What do people do starting at the day they read your book or even the day they see this podcast? What's the good news here?

The good news is the food industry doesn't care. That's the good news. That's good news. That's the good news.

I can't wait to hear the bad news.

That is the good news. The good news is the food industry doesn't care. They don't care what they sell as long as they sell. They will respond to the consumer. They've told me this a zillion times directly to my face. We don't care what we sell, we just have to sell. You as a consumer get to vote. You get to vote 21 times a week. You get to vote with your fork. And if everyone started, you know, choosing real food over processed food, the food industry would say, whoa, everyone wants real food instead of processed food. Maybe we should do something about that. And the more we educate people, the more they will lean on their congressmen to do something about the food industry in the same way we did something about the tobacco industry. industry, and the same way we did something about the alcohol industry. But it can't happen until the public is educated. And that's why I wrote the book, is basically to get us there. Yeah. There's personal intervention, which for lack of a better word we can call rehab, and there's societal intervention, which for lack of a better word we can call laws. Rehab and laws, rehab and laws, personal and societal intervention. This is about food. It's not about medicine. Listen, it's about— it's not about drugs. There's no drug for this. There is no pill for this. And based on these subcellular pathologies, there never will be a pill for this. So we have to educate the public as to what the real problem is, because you cannot solve a problem if you do not know what the problem is. Having said that, once they do know what the problem is, like we found out with tobacco, remember when those tobacco company executives stood up in front of Congress. It was all over C-SPAN. I believe nicotine is not addictive. And we caught them in their own lie. And now we have the master settlement agreement and we have, you know, something at least, you know, to change cigarette consumption in America. And it did go down. You know, it got cut in more than half after that. So these things are cultural tectonic shifts. There have been 4 cultural shifts in America in the last 30 years, and here they are: bicycle helmets and seatbelts, smoking in public places, drunk driving, condoms in bathrooms. 30 years ago, if a legislator would stand up in a statehouse or in Congress and propose any legislation against any one of those 4, they'd have gotten laughed right out of town. Liberty interest, you know, nanny state, you know, get out of my kitchen, get out of my bathroom, get out of my car. Today, they're all facts of life. Okay? And if you get in your car today and you don't buckle your seatbelt, your kids will scream at you. So what happened? How did we do that?

There was one other thing I, I wanted to, to touch on because you, you talk about it in the book and very briefly, you meant, you correlate this type of diet that has the, the standard American diet with outcome risk as it relates to COVID infection.

Yep.

So if, in briefly, just walk us through what you perceive to be this relationship and perhaps more importantly, what people should be thinking about in terms of what they can do to improve their odds.

Absolutely. Really, really important. Thanks for bringing it up. There are 3 things wrong with processed food. Insulin. Turns out insulin drives ACE2, A-C-E-2, Angiotensin-converting enzyme 2. Now, that is normally a water channel in cells, especially lung, but it drives the production of ACE2. ACE2, because that COVID virus is so freaking goddamn smart, it uses ACE2 as its injector point, and so the more molecules of ACE2 you have on your surface of your cell, The more chance that that virus is going to infect you. So that's problem number 1. If you get your insulin down, your ACE2 level goes down in your cells, you know, you're going to protect yourself. Number 2, short-chain fatty acids. So remember we talked about the soluble fiber and the short-chain fatty acids? Turns out those short-chain fatty acids are immunosuppressive and keep the cytokine storm that the virus generates at a low ebb, and so that will keep you from succumbing, you know, to, you know, massive cytokine storm from, you know, being so sick with COVID So that will reduce mortality rates. And then number 3, diabetes itself. High blood glucose basically crystallizes around the edges of those ACE2 molecules and keeps them open so that the virus has an even easier chance of infecting you. So, 3 separate things about processed food that drive COVID morbidity and mortality. We have shown in our studies at UCSF that you can get your insulin down, and you can get your fatty liver down, and you can get your uric acid and your ALT down, in 9 days, 9 days by eating real food. So people are so worried. I mean, you know, everybody says, yes, people of color and obese and comorbid conditions, yes, all true. Those are all bad things for COVID. Those are all risk factors for dying from COVID You can turn— well, you can't change your color, but you can change your risk for dying from COVID in 9 days by eating properly.

And yet the average American is eating 7.5 servings of ultra-processed foods every day right now.

And Kraft can't keep up with the macaroni and cheese.

Well, Dr. Lessig, thanks for spending time with us. And again, my pleasure. I've said it earlier today, this is a landmark book, and I, I'm not sure what my comment was on the back of your book now, but I hope it was something to that degree because it's really— it's going to do a lot.

I was very appreciative. You know, I wrote this book because every stakeholder is only interested in their own stake. That's— and the thing is, we have to work together. So the doctors and the patients and the food industry and the pharma industry And the White House and Congress, you know, everyone's got their own vested interest, and I understand that. But ultimately, real food can solve all of these problems, and everyone can still make money, okay? But we have to do it basically talking together, but we have to talk over the same set of sciences and facts. And that's why I wrote the book, is to explain to each stakeholder what their contribution can and should be. Okay.

We put together an op-ed in MedPage Today last month for President Biden, really calling out, you know, what is happening in America with respect to sugar and how we need to rethink the guidelines that were just again put out for the next 5 years. And, you know, we do these things one day at a time and hope that we gain some traction. But, um, you know, we can't afford this any longer, right?

Yeah, it's, you know, I mean, unfortunately, unfortunately, when you're doing big things, it's baby steps. But, you know, as my colleagues often say, you know, how do you eat an elephant? One bite at a time,

right? Interesting thought. All right, well, listen, great to see you, and, uh, I wish you all the best. And, uh, I know that you're, you're doing anything but being retired, whatever that means.

I know what I'm, I'm, I'm just not seeing patients anymore, but I'm, you know, just as involved and I'm still doing research and policy and consulting and, you know, get— and writing books. So, yeah.

There you go. I, I'm right there with you. Thank you again and terrific to see you.

You too. You too. Always my pleasure. Thank you.

All I can say is, wow, what an interview that was. Dr. Lustig has done some incredible work. And, you know, this is, it's very disruptive, but it's certainly what we've needed to hear for a very long time. Again, the book is called Metabolical. Very, very glad that he's spent so much time doing so much research and really gifting us this incredible deep dive into what's really going on as it relates to healthcare here in America. Thank you for joining me on the program today. I'm Dr. David Perlmutter, and we'll be back soon. Bye for now. Bye for now.