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episode #135

Interview with Dr. Robert Lustig: Is Sugar Killing You, Fibers Role in the Diet and Over Prescribed Statins

March 28, 2022 in Podcast


This week I interviewed Best Selling Author and Neuroendocrinologist Dr. Robert Lustig! Dr. Lustig has fostered a global discussion of metabolic health and nutrition, exposing some of the leading myths that underlie the current pandemic of diet-related disease. In this episode, we discussed: - his new book Metabolical - how to protect the liver and feed the gut - fibers role in health - should fructose be blamed for obesity - dietary fats, statins and much, much more!

0 (1s): Coming up on the get lean, eat, clean podcast. 1 (4s): What are the two diseases that children now get that they never got before? And the answer was well type two diabetes and fatty liver disease. These were the diseases of adults before these were the diseases of aging before I said, all right, well, but kids now get them and they're not, you know, adults, and they're not aging, you know, the kids, but they're getting it. And so what I did was I said, all right, these are also these two diseases type two diabetes and fatty liver disease. They are the diseases of alcohol alcoholics, get these diseases, but kids don't drink alcohol. 1 (46s): Are they exposed to something that might be like alcohol or that might act like alcohol in their body. And so I opened up my biochemistry text. I turned to the alcohol page and there it was right next door. It was sugar. Yeah. Specifically the sweet molecule and sugar fructose fructose is metabolized in the liver, just like alcohol. And it turns out fructose is metabolized in the brain, just like alcohol. So I went to this meeting at the NIH and I S I, this is what I said. I said, I think sugar's the bad guy in the story because it's basically doubling as alcohol and it's causing the same diseases. 0 (1m 27s): Hello, and welcome to the get lean, eat clean podcast. I'm Brian grin. And I'm here to give you actionable tips to get your body back to what it once was in five, 10, even 15 years ago, each week. I'll give you an in-depth interview with a health expert from around the world to cut through the fluff and get you long-term sustainable results. This week I interviewed best-selling author and neuroendocrinologist Dr. Robert Lustig, Dr. Lustig has fostered a global discussion of metabolic health and nutrition exposing some of the leading miss that underlie the current pandemic of diet related disease. We discussed his new book, metabolically, how to protect the liver and feed the gut fiber's role in health should fructose be blamed for obesity, dietary fats, statins, and much, much more. 0 (2m 17s): This was a hard hitting interview with Dr. Lustig. I loved his new book metabolically, so definitely check out the book and enjoy the interview. All right. Welcome to the, get lean eat clean podcast. My name is Brian grin, and I have Dr. Robert Lustig on. Thanks for coming to the show. 1 (2m 34s): Thanks for having me, Brian. 0 (2m 36s): Yeah, I was Tanya, before we got on, I read your book and I don't read a lot of books and this is what I read all the way through. So I think that's, it shows how good the book was. Yeah. So I wanted to get you on, I know you've written a few other books, fat chance hacking of American mind. And then now metabolically, I guess maybe let the audience know you're a neuroendocrinologist I worked on practicing saying that. 1 (3m 6s): Yeah, it's a mouthful. 0 (3m 7s): Yeah. 1 (3m 8s): The door. 0 (3m 10s): Yeah. Is there a short way to put that out? 1 (3m 14s): Not really. No. Basically I study how the brain controls hormones and how hormones control the brain. 0 (3m 25s): And you work mainly with kids. 1 (3m 27s): Yeah. I'm a pediatric neuroendocrinologist so yes, I'm a pediatrician. However, you know, it's not like the systems change in adulthood. So, you know, I've done a lot of research on adults over the years, but yeah, it was boarded to practice pediatrics. 0 (3m 44s): And what made you write metabolic? Well, obviously your other books I have not read, but I'm curious. Did your, did your stance on any of this change? I know what 12 years ago, you, you did that YouTube. Well, you, you were on YouTube for the sugar talking about sugar. That was like that that's gone. I, I wanted to see how many views you're up to 17 million views on that. 1 (4m 6s): Something like that. Yeah. It's pretty ridiculous. Yeah. I didn't think anybody would watch that. I didn't say my mother would want that. In fact, she did not watch that, but 17 million people did. So I wrote fat chance back in 2013. 0 (4m 25s): And 1 (4m 26s): The reason I wrote it was because I knew that the standard mantra that everybody and his brother was following was exactly what was wrong. And that mantra was you are what you eat. And I knew that was not true. In fact, what I said in fat chance was you are what you do with what you eat. That metabolism is more important than calories because not every calorie is metabolized the same way and some calories cause more disease than others. And people needed to understand that in order to be able to switch what they were doing, and basically not believe the food industry party line, But the last eight years from the time of fat chance till now I have come to realize there is an entire literature and an entire dark underbelly of the food industry actually propagandizing their products and what they do. 1 (5m 37s): And we now have the paper trail to demonstrate how the food industry has actually provided a, you know, 40 year disinformation campaign about, you know, what they were offering the public and how we have succumbed and gotten sick. So in metabolically, which is half science, half expos, a, you know, what I did was I said, you know, I got it wrong. I got it wrong back in 2013, really the mantra should be, you are what they did with what you eat. And that is the politics and understanding, you know, what happened? What, what did they know? 1 (6m 18s): And when did they know it? And when you understand all that, you realize that in fact, we need an incomplete, an entire overhaul of our food system. 0 (6m 31s): Yeah. And I love in the book, you know, towards the end, you start going into reasons and things that, that we should do to try to change the food system, which has a lot, has to do with subsidies and where the money's going. And we can touch on that maybe towards, maybe towards the, the end. But I, I wanted to read the, this was right in the beginning and you don't, you don't mess around in this book. This is this, 1 (6m 56s): Alrighty, this book calls the calls. It like it is it's, it's, it's as hard hitting as I can possibly be. You know, if it were, if it were a Hollywood book, we'd call it a kiss and tell, but because it's about diabetes really, it's more like a piss Intel. 0 (7m 14s): Yeah. And I just, a few days ago, I interviewed Dr. William Davis and he doesn't hold back either and on the food system and what's going on in healthcare. But I, one of the quote, one of the things you said, you said U S the U S has the best doctors, hospitals, and medical technologies, the most innovative surgeries, the best, the newest drugs, and spends the most per capita on healthcare of all the countries on the globe. And are we healthier? Do we enjoy better healthcare? Do we live longer? And the answer is an empathetic. No, 1 (7m 44s): That's exactly right. Yeah. Ultimately none of those things have impacted our health. One iota, the medical system has basically failed us when it comes to chronic disease. And, you know, I don't feel good saying that, you know, cause I was part of that system for a very long time. And I would say for the first 20 years of practice, you know, I basically towed the party line. I did what everybody else did, you know, eat less exercise more, you know, if you're fat, it's your fault, et cetera, et cetera, you know? But then I started doing the research and I realized that the research actually didn't fit the party line. And you know, really made me realize that this was not what was going on. 1 (8m 30s): And you know, the more science I elaborated, the more, you know, shall we say it on the other side, I seem to find myself. So I have become in my old age and iconoclast, you know, trying to break down, you know, and, and, and destroy the sacred cows because they need to be, 0 (8m 50s): Was there like a moment where you're like, I just gotta start. W was it a, was it over, or was it a moment that hits you maybe with a patient or with something that you read or that sort of made you want to sort of go the other way? 1 (9m 2s): Right. So there were three aha moments for me. Three, let me take them in order. The very first aha moment was back in 1995, right? I had just moved to St. Jude children's research hospital in Memphis, Tennessee is cancer hospital. And I was presented with about 40 patients who had survived their brain tumors only to become massively obese because of either the surgery or the radiation or the chemotherapy. 1 (9m 42s): So these people had damage to the area of the brain that controls energy balance. It's called the hypothalamus. And so we call this form of obesity. It's an intractable form of obesity called hypothalamic obesity because the hypothalamus is damaged and these kids cannot lose weight. They only gain it no matter what you do, they gain weight. And the question of course is, you know, like why, and what do you do about it? Cause I had 40 of them. I had to figure out how to help them. Right? Well, the, the hormone leptin had just been discovered the year before 1994. 1 (10m 23s): And so I postulated at the time that these kids, before the tumor, they could see their left and they were normal, but now they couldn't see their leptin. And because they couldn't see their leptin because that area of the brain was dead, that these kids had brains starvation, that their brain could not tell that the leptin levels in their blood were high because they were, you know, because they, because fat makes let them so more fat, more leptin, but then the leptin's supposed to tell your brain don't eat so much, but if you can't see it, then you're going to eat like crazy. So I postulated that these kids had what we would call anatomic leptin resistance. 1 (11m 5s): That is they couldn't see their leptin because the brain was damaged. So then the question is, all right, if that's the case, what are you going to do about it? Well, I then went to the literature and look downstream of what went on in the hypothalamus. And I knew that these kids released an enormous amount of insulin. Insulin of course, is the energy storage hormone. So when you eat something, your insulin goes up and that forces it into energy stores in your body, particularly fat insulin makes fat. And I knew that. So I figured, well, there must be a connection between that hypothalamus and the pancreas to release insulin. 1 (11m 53s): Could I block that? And there was a drug at my disposal called Octreotide, which inhibits insulin release at the level of the pancreas. So I said, what if we give these very unfortunate kids, this drug, that blocks insulin. And so we did a study and lo and behold kids started losing weight, but something even more remarkable happened. These kids used to sit on the couch, eat Doritos and asleep. They had lost all interest in the world and anything that was going on around them. We put them on the medicine and all of a sudden people start calling up. I got my kid back and the kids would say things like, well, this is the first time my head hasn't been in the cloud since the tumor. 1 (12m 39s): And they started physically exercising on their own spontaneously. One kid became a competitive swimmer. Two kids started lifting weights at home. One kid became the manager of his high school basketball team running around, collecting all the basketballs. These kids had zero energy and all of a sudden, because they're on this medicine, they are now physically active. And the parents and the teachers and everyone around them sees it knows it. It's like amazing. Wow. So I said, wow, this is really cool. So then we did a double blind placebo controlled trial and showed the exact same thing. 1 (13m 20s): Then we determined that their energy expenditure had actually gone up. They were actually burning energy better. And the reason was because we'd gotten their insulin down and we showed that the improvement in their physical activity was because we suppressed their insulin. And so this was the first aha, because everyone says, you know, that obesity is because of two behaviors, gluttony and sloth, and the gluttony and sloth is what drives the weight gain. And what we showed was that no, in fact, obesity is due to too high and insulin level. 1 (14m 1s): And the insulin was causing the gluttony and sloth that the biochemistry drives the behavior. And that obesity was really not being able to see your leptin and excess insulin. And so we completely changed our obesity paradigm and we changed what we did for our patients. And instead of running an obesity clinic, I ran an insulin reduction clinic. And guess what? We helped a lot of kids. Okay. Better than any other program in the country, because we focused on the real problem. So that was aha. Moment. 1 (14m 41s): Number one, aha. Moment. Number two was okay. There are a whole bunch of people who don't have brain tumors who have brain damage, who are massively obese and they have high insulin too. How come I was asked by the NIH to come give a talk at a symposium back in 2007 on what I thought was the most important environmental insult that led to obesity. And I'm thinking, what am I going to say? What am I going to say? What am I saying? And I said, well, all right, let me look at it this way. 1 (15m 23s): What are the two diseases that children now get that they never got before? And the answer was well type two diabetes and fatty liver disease. These were the diseases of adults before. These were the diseases of aging before I said, all right, well, but kids now get them and they're not, you know, adults, and they're not aging, you know, the kids, but they're getting it. And so what I did was I said, all right, these are also these two diseases type two diabetes and fatty liver disease. They are the diseases of alcohol alcoholics, get these diseases, but kids don't drink alcohol. 1 (16m 5s): Are they exposed to something that might be like alcohol or that might act like alcohol in their body. And so I opened up my biochemistry text. I turned to the alcohol page and there it was right next door. It was sugar. Yeah. Specifically the sweet molecule and sugar fructose fructose is metabolized in the liver, just like alcohol. And it turns out fructose is metabolized in the brain, just like alcohol. So I went to this meeting at the NIH and I S w I, this is what I said. I said, I think sugar is the bad guy in the story because it's basically doubling as alcohol and is causing the same diseases. 1 (16m 47s): And, you know, after I spoke, they applauded and then there was a bathroom break and they didn't come back for the rest of the symposium really had to go to the bathroom. So I left and I went to the bathroom and they, they captured me. They actually sat on me in the bathroom. These are toxicologists scientists screaming at me. Oh my God. Oh my God. Oh my God. You're right. Sugar is just like alcohol sugars, a toxin sugars. What's driving. I think this, you have to tell everyone. I said, boy, I mean, toxicologists, you know, like got, so worked up over this. 1 (17m 32s): They cornered you in the bathroom. Yeah. The bathroom wouldn't let me go back to the symposium. It was like crazy. So that was the second ha and then the third, aha. Wasn't even my aha. It was my colleague's. Aha. So I remember I mentioned the dark underbelly of the industry, my colleagues at UCF, Kristin Karnes, Laura Schmidt, and Stan glance in 2016, published a paper where they had actually found the paper trail between the sugar association and two par Harvard school of public health scientists, the head of the department of nutrition, Fred stair, and his associate mark Hegsted who became head of the USDA, where they actually paid these guys off to write two review articles saying saturated fats, the bad guy, and leave sugar alone. 1 (18m 27s): And you know, this was not disclosed. And they made 50,000 in today's dollars from writing this and basically, you know, it's propaganda. And so I came to realize, you know, through that, that, you know, this was a put up job. This was, this was destined because of dark forces. And so that was the third. Aha. And that's really the moment when I realized I had to write this book, metabolically, you know, to basically clear the air and make it very clear to the public, you know, what's really going on. 0 (19m 5s): Yeah. Wow. Those are, those are some good stories. I mean, good and bad. Right? 1 (19m 9s): Well, a lot of bad, a 0 (19m 11s): Lot of bad. Yeah. It 1 (19m 12s): Is what it is. 0 (19m 14s): There was another part in the book that I liked this quote was we spend 97.5% of our healthcare budget on individual treatment and only 2.5% on prevention. 1 (19m 25s): Right. I 0 (19m 25s): Thought that, yeah. 1 (19m 26s): Well, the problem is when you understand the molecular mechanisms, we understand how this actually works. When you understand what causes type two diabetes and hypertension and dyslipidemia and cardiovascular disease and cancer and dementia, the fatty liver disease and polycystic ovarian disease, all these chronic metabolic diseases that are basically chewing through our entire healthcare budget. Okay. 75% of all healthcare dollars go into those eight diseases. Okay. When you look at the molecular mechanisms, you realize that none of them have a drug target. These are not druggable. And the reason is because these are mitochondrial diseases and we don't have any medicines that make it to the mitochondria. 1 (20m 17s): The only thing that makes it to the mitochondria is food. These diseases are not druggable, but they are food bubble. 0 (20m 27s): Right? I was to say 1 (20m 28s): That hasn't stopped big pharma from coming up with all sorts of, you know, medicines to try to ameliorate or placate or smooth over, you know, paper over, you know, the problem. Ultimately, we cannot solve chronic disease with medicine. It has to be solved with food. And that's the reason why I had to write metabolically because you know, health is going down the tubes and you know, we gotta, we got to salvage it. We gotta rescue it somehow. And we can't do it with our current process. Food diet. 0 (21m 6s): Yeah. I know a chapter you mentioned it's not druggable. I think it's right. It's suitable. It's it's right. And, and on that point, you talk about two things. Two points you mentioned was protecting the liver and feeding the gut. And perhaps you can elaborate a little bit on that. 1 (21m 23s): Sure. So protect the liver. So protect the liver from what? Well, you know, the liver is your primary detoxification organ. Okay. It chews up a lot of poisons, but any poison can overwhelm the liver's capacity, right? Some overwhelming easily, some overwhelming, a little harder. But ultimately if you overwhelm your liver's capacity to be able to be toxified something, then you're going to get sick from it. That's the way it works. Right? So the liver has several toxins that affected, you know, cyanide affects the liver. 1 (22m 3s): Okay. Causes ATP, not to be able to be, you know, used because it's a mitochondrial toxin. That's what cyanide is. It's you know what an acute, you know, very potent mitochondrial toxin, Seren Ryson VX gas. You know, I mean, there are whole hosts of acute toxins that work in parts per billion keel over and die. But there are also chronic toxins that don't necessarily kill you with one exposure. But with serial exposure, they will no doubt kill you. Like for instance, arsenic, carbon, tetrachloride benzene, tobacco smoke, right? 1 (22m 45s): Where one exposure may not kill you, but multiple exposures will well and alcohol, another one, you know, you know, you can ha you can go on one binge. You can go into a binges. You can even go on maybe a hundred binges, but you know what, once you get to about a hundred binges, you're gonna have a problem. And it might just kill you. Well, turns out sugar is just like alcohol. And so it's the same concept. It's not one high sugar meal. It's, you know, when every meal is a high sugar meal and that's what we have in America today, breakfast, lunch, dinner snacks, okay. 1 (23m 28s): They're all high sugar meals example, the national school breakfast program, 29% of all children today eat their breakfast in the national school breakfast program. And what is the national school breakfast program? It's a bowl fruit loops and a glass of orange juice. That's what it is. Now. The American heart association says that children should get no more than three teaspoons of added sugar per day. That's 12 grams for the day. So what's a bowl of fruit loops in a glass of orange juice. 1 (24m 9s): That's 41 grams. That's more than triple and it's just breakfast. So they are consuming more than triple their limit. And they've just started. So this is going to have negative consequences, and that is what we're seeing across the board. So that's, and that's just kids. I mean, you know, it's really no different for adults when you consider the fact that 62% of the added sugar in our diet is an ultra processed foods. Okay. And ultra processed foods now account for 56% of all the food sold in America and 67% of what kids eat. 1 (24m 56s): You know, then you shouldn't be surprised that we're in this mess. So that's what has to be fixed. So protect the liver, protect the liver from sugar, protect, deliver from branch chain, amino acids, leucine ice solution veiling, which is high in corn, fed beef, chicken, and fish protect the liver from glyphosate Roundup because it has its own negative effects. Protect the liver from other heavy metals like cadmium, which is high in cocoa, protect the liver from other toxins that are in our environment as well. Okay. Feed the gut, feed the gut. What well, what the bacteria in your gut like to feed on is fiber that's food for bacteria. 1 (25m 44s): The reason there's fiber in your diet is because now you're feeding your gut and your gut will take the fiber cause you can't metabolize the fiber, but the gut can, and they will metabolize it into various components that they need to grow such as short chain, fatty acids. Okay. And they have, and they will also extract, you know, flavonoids and other things that come with the fiber fraction bottom line. If you don't feed your gut, your gut will feed on you. We will actually strip those materials, strip the mucin layer right off your intestinal epithelial cells, exposing them and de nuding them and putting you at risk for things like leaky gut, inflammatory bowel disease, irritable bowel syndrome, et cetera, all of which lead to systemic inflammation, insulin resistance, and then chronic disease as well. 1 (26m 37s): So protect the liver, feed the gut, protect the liver from sugar, feed the gut with fiber. You need a low sugar, high fiber diet. That's called real food. Unfortunately, the Western diet is the opposite. And so that's why we need to change our food supply. 0 (26m 56s): And I'm sure people think, well, what about, I'm sure you get this question a lot about fruit. 1 (27m 2s): Everyone wants to buy. 0 (27m 4s): And I get this question too. I think I know what you're gonna say, but go ahead. Yeah. 1 (27m 10s): So fruit has sugar. Sure. That's why it's sweet. And it's the same fructose molecule. As in, you know, ice cream and cake and soda. There's no difference in the molecule. There is a difference in the amount because the amount of sugar in fruit is actually kind of low. It's not high, it's low, but the thing that makes fruit okay, is the amount of fiber, right? So there are two kinds of fiber there's soluble and insoluble. They are not the same sizeable. Fiber is like pectins or inulin. Like what holds jelly together. Insoluble fiber is cellulose or tightened things like the stringy stuff in celery. 1 (27m 53s): Now fruit has both. You need both, 0 (27m 57s): You know, 1 (27m 58s): Now why do you need both? So imagine you had a spaghetti colander metal bowl with holes. You run the water, water runs right through. Okay. Now take a blob of petroleum jelly, throw it into the center of the colander. Now run the water still runs right through. Maybe bounces off the jelly. Now take your finger and rub it all the way around the inside of the colander. Now we're on the water. Now the water does not run right through. Now the water is blocked. Now there's a barrier, right? The jelly used the colander as a scaffolding to be able to create a, an impenetrable secondary barrier. 1 (28m 47s): Well, this is exactly what happens in your intestine. You can actually see it on electromicroscopy the cellulose, the insoluble fiber acts like the colander, the soluble fiber, like the pectins plug, the holes in that lattice work. And together they form a gel on the inside of the intestine, a secondary barrier that actually keeps sugars from making it to the liver, thus protecting the liver. And guess what? If you're not, if you're not absorbing it early, they go further down the intestine where the bacteria can chew them up. You're feeding the gut. 1 (29m 28s): So fruit is okay because the fiber is the antidote and it's in the form that your body can use. Now. Unfortunately, once you smoothie it, throw it in the Vitamix or the Breville. What you've done is the blades of the Vitamix will have a sheared, the insoluble fiber to smithereens. And now you can't set up that gel because you don't have the lattice work. It'd be like taking a fish net and taking a, you know, a bunch of scissors to it and then expecting it to be able to catch fish. 0 (30m 6s): Got it. Yeah. It's so it's the drinking of the juices. That's, that's more of an issue than actually eating it. 1 (30m 14s): That's right. So eat your fruit. Don't drink it. 0 (30m 18s): And as far as feeding the gut fiber's role is that essentially you want to have natural sources of fiber, obviously. Like, you know, you see a lot of this, like Metamucil and there's Metamucil, I think. Yeah, but you're talking more whole foods, obviously 1 (30m 35s): Metamucil is soluble. Fiber Metamucil is psyllium. It's a soluble fiber. Now it's not a soluble. Fiber has no use. It has used, there are six things that fiber does when you have soluble and insoluble together. Metamucil does to cardboard does too. Cause that's straight cellulose. What you want is you want a combination of the Metamucil and the cardboard. All right. Now I dare you to be able to find that in any food other than real food 0 (31m 8s): Right 1 (31m 8s): Now, I will tell you just off topic, we are working on a fix for that. It's not ready yet. We're in clinical trials, but we're hoping to be able to introduce a fiber that can be basically baked into food that would double as soluble and insoluble fiber that would then make processed food healthier. But you know, that's for another day, 0 (31m 34s): One other topic I wanted to chat about as well was, you know, cholesterol is role and statins are everywhere. As you know, and you mentioned in the book perhaps maybe just give an overview of how ineffective they can really be and, and sort of how it's just become over abundant and unnecessary. 1 (31m 54s): Right. Well, I wouldn't say unnecessary. That's not quite right. So let me, let me explain the fat story. 0 (32m 5s): Okay. 1 (32m 5s): All right. Once upon a time we used to eat a lot of fat. Okay. We ate relatively little carbohydrate and we pretty much only fat. Okay. Those were the days of, you know, the hunters, you know, in the, in the evolutionary scheme, right. Then of course the 0 (32m 29s): Saturated fats for the most 1 (32m 31s): Part, mostly saturated fats. The gatherers came along and we introduced agriculture and we started eating a lot more carbohydrate. Right? What we saw was that when we started adding sugar to our diet, which was basically in the late 18 hundreds, early 19 hundreds, when, you know, CNH and domino and Texas, Louisiana, Hawaii, and the potstill and everything really sort of got going, we started seeing a marked increase in cardiovascular disease. And the question of course is, you know, what was the cause of that at the time we didn't know. 1 (33m 11s): And then in 1955, president Eisenhower had a heart attack. And so then this question came straight to the, for what's causing all the heart disease. And there were two camps. One camp was saturated. Fat was the bad guy. And that was led by a Minnesota epidemiologist named ancil keys. But there was another camp that said sugar was the problem. And that was led by a British physiologist nutritionist physician by the name of John Yudkin. And they both wrote books and they do it out throughout the sixties and seventies. What caused heart disease? 1 (33m 51s): Was it the fat or was it the sugar in the mid 1970s three? We learned three things that basically sealed yet fate. They threw him under the bus. Okay. And we went saturated fat as the problem whole-hog and you know, for the next 40 years, no one was allowed to question it. So here's what we learned in the early 1970s, we learned about a molecule in our bloodstream called LDL, low density lipoproteins and at one brown and Goldstein, a Nobel prize for discovering this. And the reason they discovered this was because there are patients who are missing the receptor for LDL off their liver. 1 (34m 39s): They can't clear the LDL, their LDL levels are in the hundreds and they get heart attacks at age 18 and die, which is true and still true. Yeah. And it's not that brown and Goldstein were wrong. Everything they said was right. So LDL was then fingered by others to be the bad guy right now, as it turns out there's another bad guy, which is actually even worse than LDL is called triglyceride. And we ignored that. And then secondly, we learned that dietary fat and increasing your dietary fat increases your LDL level in your blood. 1 (35m 25s): We learned that in the seventies also. And then finally in the late seventies, we learned that in large populations, LDL levels correlated with risk for heart disease. So if dietary fat is a, an LDL is B and heart diseases C well, what we learned was if a led to B and B correlates with C, then aimlessly to C, therefore dietary fat raises your LDL, which causes heart disease. And that was it. And they threw yet going under the bus, never to be heard from again, they took his office away at the university of London. 1 (36m 6s): They gave him room closet. Okay. And they took all his grants away and he died ignominiously in 1995. Never to be heard from again, but you know, relegated to the dustbin of history. Well, because of this, you know, shall we say perverted notion now it is true that indeed dietary fat raises your LDL a does lead to B. I don't argue that. And it is true that B correlates with C, but that doesn't mean because of C, B could lead to D E F G H and I, and not come back to C and actually the contrapositive of an argument does not know a no-see it's really no C no, a, this doesn't even make sense on logistical grounds. 1 (36m 54s): So the bottom line was, you know, we bought this concept lock, stock and barrel, and we didn't test it, but we basically turned our food supply over to make Entenmann's fat-free cakes. 0 (37m 11s): I remember 1 (37m 13s): My father has Infamous fat-free cakes, so I was there and I saw it. So the question is, was it true? The answer is now we know that. In fact, there's not one LDL. There's two, One is called large buoyant, and one's called small dense. When you measure LDL, you're measuring both. It turns out the large buoyant is driven by dietary fat. That's true. It turns out the large point is kind of cardiovascularly neutral. Doesn't matter. The one that matters is the small vents, this other species, which is about 20% of your LDL. And it turns out that's responsive to carbohydrate. 1 (37m 55s): And it turns out that's the bad guy when it comes to heart disease. So when we went low fat, we went high carbohydrate and high sugar. And so our LDL went down, but we got more heart disease because we had more small, dense LDL, even though our total LDL went down. And so this didn't make any sense to anybody until we pieced out these two different species of LDL. And now it's starting to make more sense. And now we realize that that small dense LDL is actually the remnant of triglyceride after triglycerides offloaded, it's lipid in the adipose tissue. 1 (38m 38s): So now we've got the evolution of the different bad particles and how they relate to each other. So now it's very clear that fat wasn't the problem, but Hey, the drug industry made a fortune on Statens and still do. So the question is, does this work? And the answer is for secondary prevention. If you've already had a heart attack, if you already declared yourself, as at risk statins do seem to help, but for primary prevention. So like, if you go to your doctor, your doctor says, Hey, your LDL is high. You should go on a stat. Okay. The increase in survival from taking a Staton for primary prevention of heart disease is a total of four days. 0 (39m 28s): And I remember reading that in the book and four days. Yeah. 1 (39m 33s): And the reason is because you're not effecting the bad particle, you're not affecting the small dense LDL. All you're doing is bringing down the large buoyant that who cares about that. So we've gotten this entire thing completely wrong. We have basically stood modern medicine on its head in the hope that somehow we could do something good. And all we did was make things worse. So that is my job is to basically fix that good luck to me. 0 (40m 6s): And you mentioned the markers that you should look at, like triglycerides to HDL ratio, correct? 1 (40m 14s): That's a much better marker because what that is a marker of is how well your insulin is working. It's a marker of insulin sensitivity. So a triglyceride to HDL ratio has much more information in it. That's valuable than any cholesterol level. So, you know, we have to rethink this. The question is, does your doctor know this? Well, I wrote metabolically to try to train them because you know, they don't get nutrition, you know, in, in medical school. So like, how are they going to learn this? 0 (40m 47s): I got to get your book. 1 (40m 50s): Okay. So I'm doing your podcast. 0 (40m 53s): And then uric acid is something that has been coming up lately. And I know uric acid, a lot of people believe that, you know, meat, alcohol are reasons for people getting gout. What are your thoughts around getting of uric acid levels tested? 1 (41m 12s): So two of my good colleagues and friends, Rick Johnson and David Perlmutter have both written books in the last month. 0 (41m 19s): Yeah. I noticed they 1 (41m 20s): That have basically sort of, you know, fingered uric acid as a bad guy in the story. Rick wrote a book called why nature wants us to be fat. Nature wants us to be fat. 0 (41m 32s): Yeah. I have that one. 1 (41m 33s): And David Perlmutter road drop acid, great name. So they're not wrong. They think that uric acid is a bad guy. And I do too. I don't know if it's the only bad guy, a bad guy, one of many. So I'm on board with that. And we found uric acid to be a problem in our studies of adolescents with metabolic syndrome, they had higher ORIC acid. So, you know, we have reason to suspect. It's about problem to what we've learned about uric acid is that it inhibits mitochondria from being able to burn fat, inhibits an enzyme necessary to shuttle fats into the mitochondria for burning. 1 (42m 30s): And so when your acid levels go up, you end up making more fat instead of burning more fat. And that's a bad thing when you're trying to stay healthy. So there is definitely a role for uric acid and uric acid inhibition in terms of disease and disease prevention. And so, you know, what makes uric acid go up? Two things, meat, red meat pairings, because that's what makes the uric acid, that's where it comes from and the other sugar. And the reason is because sugar causes a depletion of phosphate in the liver when it's metabolized and that depletion of phosphate then takes ATP down to uric acid and you ended up screening it. 1 (43m 20s): So Ben Franklin knew this. He actually wrote an ode to his gout way back in the late 17 hundreds. And he knew he had to stay away from red meat and sugar. So w 0 (43m 34s): I'm curious your thoughts on, on red meat quality red meat. Let's just say you're having grass fed grass finished meat, you know, almost every day, but your all your metabolic markers seem, seem in line. What, what are your thoughts around pro protein too? I'm curious. 1 (43m 52s): So, so let's take two countries that eat more meat than us Argentina and New Zealand. Both of them eat more meat than us. We eat 23 kilos of meat per year. Argentina eats 44 kilos of meat per year. They double what we do, and they don't have gout and they don't have heart disease or cancer at the rates that we do much lower. Despite the fact that they double the meat. The reason is because they don't need as much sugar either. Right now, it is true that meat can do this. 1 (44m 35s): And it is true that there is, you know, uric acid to be made from pure greens in meat on not arguing. That point is we didn't have a problem with this until we became insulin resistant. So in the face of insulin resistance, then U S meat becomes a problem. 0 (44m 59s): That's it? That thing fed to the animals, 1 (45m 1s): Corn fed branch chain, amino acids, more insulin resistance, more higher Piering content also, and you know, sugar as well. So if you eat Argentinian beef, doesn't seem to be a problem. If you eat American beef, that's another story. So meat is not good for you. It's question is how bad for you is it? And the answer is depends on whose meat it is, 0 (45m 32s): Where it's being sourced 1 (45m 33s): And where it's being sourced. That's right. What those cows are eating. So that's one of the issues. Now having said that there's not, it's not like red meat is great for you. Okay. It does have all of the amino acids you need. It has more trips to feign, which is absolutely essential. And, you know, vegans are to some extent, trip to feign deficient. 0 (45m 57s): What about like creatine and the B vitamins and things like that. 1 (46m 0s): And th those are much higher in, in red meat. So there are things to be had, but there's another thing that's in red meat. Also, that's a potential problem. And that's called Coleen. Now you need Coleen. Coleen B is either sort of turned into as tail Coleen and your brain, which is a neurotransmitter, and you need it, or phosphatidylcholine, which is necessary for lipid transport around the body. It's used in the liver to make those lipoproteins like, you know, triglyceride, all right. So you need Coleen. Coleen is essential. You must have coli. Here's the problem. 1 (46m 40s): Excess Coleen will be metabolized by your gut into a compound called trimethylamine or TMA, which then goes to your liver, gets oxidized to something called TMAO trimethylamine oxide, which Stanley Hazen at Cleveland clinic has shown is the stickiest substance that our body makes. And it lines our arteries and is probably one of the primary drivers of heart disease and TMA levels correlate with heart disease. Very, very tightly. And since Coleen is the source of the TMAO, that makes it a question mark, as to whether eating a lot of meat is a great idea. 1 (47m 21s): So I'm not telling you red meat is bad. I'm not telling you red meat is good. All right. But it depends on where it's from and depends on how much and depends on whether or not it's being turned into TMAO or not. The point is that all of these scientists and I put that in quotes because they haven't looked at the science. They say red meat's bad because of the saturated fat. It's not red meat might not be great. Red meat might have problems, but it's more because of the iron, which is an oxidative stress or the branch chain amino acids, which can cause insulin resistance or the TMAO. So, got to know what, what the real problem is 0 (48m 2s): And where do you recommend people get their protein from their protein sources from because Yeah, 1 (48m 10s): Eggs next best place fish, neither of which are on the vegan menu. 0 (48m 18s): Got it. And as we finish up here, cause we're getting closer to the hour, we could go another hour. Maybe we'll do this down the road. I'd love to, towards the end of the book, you talk about ways to solution as to how we can maybe help the food industry and change this obesity epidemic you talk about instead of icing real food, perhaps maybe just touch on that as we close up. 1 (48m 43s): Sure. So the bottom line is our processed food diet is killing us, you know, and the book makes, hopefully makes that very apparent and clear. So the question of what do you do about it? Well, number one, everyone votes, you vote 21 times a week. The question is, what are you voting for? If everyone voted against something, 0 (49m 11s): You know, it wouldn't be there. 1 (49m 12s): You would hear it all right. Now that's hard. You know, boycotts don't work very well. I'm not calling for a boycott of processed food. We ultimately need process, but we just have to make it healthier. And we are actually doing that. I am part of a scientific group that has been working with an offshore processed food company in the middle east to actually improve the metabolic profile of their entire portfolio can be done Unilever and denote did this exercise for themselves. 1 (49m 52s): And they were able to get rid of 14% of the sugar in their portfolio. We think that's a drop in the bucket. We think we can get rid of 78% of the added sugar in this company's portfolio. 0 (50m 7s): Yeah. I mean, if the big food companies decide to make some changes in their formulations, I'm sure that obviously that can go a long way. 1 (50m 13s): It could. And that's what we're trying to prove to the rest of the world is that this can be done and it can be done, you know, would that, you know, still making a profit and sustainably. So, you know, working at the level of the industry, you know, it toward, toward a common goal is one, one thing that could be done. A second thing that could be done is get rid of the subsidies because the subsidies are all things that kill us, corn, wheat, soy, sugar, that's what the subsidies are for. And the reason is because those are all storable food commodities. Okay. So you can sell them on the commodities exchange. You can not sell an orange on the commodities exchange. 1 (50m 56s): You can sell frozen, concentrated orange juice on the commodities exchange. So once it's processed and it becomes storable food and that then reduces depreciation and increases shelf life and makes it cheaper and, you know, makes it a commodity problem is it's killing you. So is it a good idea to consume something that kills you, even if it's cheap? Not really. Right. So that's the, you know, the question is how do we get rid of subsidies food subsidies? There's not an economist on the planet who believes in food subsidies and the reasons cause they distort the market, let the market work, you know, whatever it is, come to whatever price it's supposed to be at. 1 (51m 45s): Even the libertarians should be able to get on board with that. You know, cause, you know, if, you know, ultimately subsidies distort the market and that's, you know, a major problem. So I think that that is the single most important, you know, 0 (52m 3s): Move 1 (52m 4s): Things, that thing that has to fall right in order to be able to make any headway in this. And that is something that government doesn't control control of. And that's why we need government to help us because if we changed the cost, okay, we would change people's diets, 0 (52m 23s): Right? Let me process food is so much cheaper than real food. But for the most part, although, you know, you mentioned eggs, 1 (52m 31s): Well, eggs are expensive and when the price of eggs go up, people stop eating eggs. And the reason is because there's nothing addictive in them, but you know, sugar is another story, but the most, the three most price, any Lastic items that is the, the items that don't reduce in sales, when the price goes up or fast food, soft drinks and juice. And the reason is because they have an addictive substance in them, 0 (53m 2s): People keep them 1 (53m 4s): And we keep buying them. And the food industry of course knows that, 0 (53m 7s): You know, well, this was great. This is just a quick, a quick hour, quick hour. So I really, yeah. I really 1 (53m 16s): Appreciate your time. 0 (53m 18s): Yeah. I appreciate the message that you're spreading through your book and through getting on podcasts. And this is definitely a book that I recommend or if watching on YouTube, there it is. And a metabolic panel Dr. Robert Lustig, thank you for coming on the podcast. 1 (53m 34s): And my pleasure, Brian, thanks for having me. 0 (53m 38s): Thanks for listening to the get lean, eat clean podcast. I understand there are millions of other podcasts out there and you've chosen to listen to mine. And I appreciate that. Check out the show notes@briangrin.com for everything that was mentioned in this episode, feel free to subscribe to the podcast and share it with a friend or family member. That's looking to get their body back to what it once was. Thanks again, and have a great day.

Dr. Robert Lustig

This week I interviewed Best Selling Author and Neuroendocrinologist Dr. Robert Lustig! Dr. Lustig has fostered a global discussion of metabolic health and nutrition, exposing some of the leading myths that underlie the current pandemic of diet-related disease. In this episode, we discussed: - his new book Metabolical - how to protect the liver and feed the gut - fibers role in health - should fructose be blamed for obesity - dietary fats, statins and much, much more!


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