Mind & Matter
Mind & Matter
Obesogens, Oxidative Stress, Dietary Sugars & Fats, Statins, Diabetes & the True Causes of Metabolic Dysfunction & Chronic Disease | Robert Lustig

Obesogens, Oxidative Stress, Dietary Sugars & Fats, Statins, Diabetes & the True Causes of Metabolic Dysfunction & Chronic Disease | Robert Lustig

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About the Guest: Robert Lustig, MD is a physician-researcher and expert of metabolic health. He is Professor emeritus of Pediatrics, Division of Endocrinology at the University of California, San Francisco (UCSF), specializing in neuroendocrinology with an emphasis on the regulation of energy balance by the central nervous system. His research and clinical practice has focused on childhood obesity and diabetes.

Episode Summary: Nick and Dr. Lustig discuss the true causes of obesity and metabolic discussion; how the in utero environment during pregnancy leads to multigenerational effects on health; different forms of sugar like fructose vs. glucose; different dietary fats like omega-6 and omega-3 PUFAs, and saturated fat; oxidative stress & mitochondria biology; how temperature, altitude & oxygen affect obesity; processed foods and how industry influences public perception; body positivity & public education; insulin, diabetes & fatty liver disease; statins & cardiovascular health; and more.

*My content is never meant to serve as medical advice.


Full AI-generated transcript below. Beware of typos & mistranslations!

Robert Lustig 5:20

loaded question, Nick, to say the least, we've learned in the last 30 years about a new aspect of medicine. And it's called the developmental origins of health and disease or DOHaD. The first person to notice this was a epidemiologist working in Southampton, England, by the name of David Barker. And he was basically going through records of people who were born during the war during World War Two. And notice that these people were dying early. And he didn't know why. And, you know, it was years later that he noticed this. And he did an enormous amount of exculpatory work that to this day is, you know, kind of classic epidemiology. And he came to the realization that something was going on in utero, that was actually changing these fetuses physiology, that was ultimately leading to the ultimate development of chronic disease, cardiovascular disease, type two diabetes, etc. And he presented that and people started, you know, looking at this question, and they found, you know, similar stories elsewhere, and they started doing animal experiments. And sure enough, it looked like, what the mother was exposed to, ultimately is visited upon the baby, later on. Now, we had always thought that the placenta was this great barrier that kept the mother from the baby. And we had lots of reasons to think that because after all, you know, mom's immune system does not become the baby's immune system. And, you know, we thought that these various transporters that live in the placenta help, you know, determine, you know, the stuff that needs to get in and keep the stuff out that doesn't need to get in. And there are enzymes in the placenta, that keep, for instance, cortisol from getting to the baby. You know, unless, of course, the mother takes something that the enzyme can't work on, like, for instance, dexamethasone, and then it does go to the baby. So we had this notion that the placenta was all seeing and all knowing, and the ultimate, you know, suit of armor for for the baby. And that mother's diet didn't matter, and that mother's medicines didn't matter. And ultimately, when we learned about microbiome, that mother's microbiome didn't matter. That turns out all of that is hogwash. The placenta is not that great. It's, it'll let a lot of stuff across, and it doesn't do what we think it does. And so in fact, the fetus ends up swimming in the same cesspool of contaminants and environmental exposures that the rest of us do. And so it shouldn't be too surprising that those contaminants when they have effects on us, that they would also have effects on the fetus. Now, one of those that I happen to be particularly interested in so I've done a lot of work on obesity, are these chemicals which we now term obesogens. That is, they are chemicals that drive adiposity drive, weight gain, drive chronic disease in humans, both, you know, adults, and as it turns out, also fetuses having nothing to do with their potential inherent calories. So there are a lot of substances that have calories, but generate more adiposity than their calories like my favorite fructose. And there are plenty of chemicals that generate adiposity having nothing to do with calories, like for instance, polyflor alkylated substances pee fast like Teflon, okay, or BPA, Bisphenol A, which turns out to be an estrogen. And, you know, there's a whole host of compounds satellites plasticizers PBDE, is flame retardants. Parabens are things that are in cosmetics, things that are in vinyl flooring things that are in. Oh, and by the way, air pollution to boot. All right. And so you'd think the placenta would be a great way to keep the fetus away from all of these things. Because after all, fetuses don't use cosmetics. And fetuses don't breathe our air. But you know, what? They're still getting damaged. And that's what we've learned. And the obesogens hypothesis brings this question of what's really at the, at the notice of this obesity pandemic, that is really only about 50 years old, you know, before, you know, 1970, only 5% of the population was above the 95th percentile for body mass index. You know, this has all occurred in the last 50 years. And something has to explain it. And you know, our DNA hasn't changed. But our environment Sure has. And, you know, people want to say, Well, it's because of the food, you know, because people are gluttons and slots. No, it turns out that there are chemicals driving this. And that's, you know, part of, you know, what my research has been about for the last 25 years.

Nick Jikomes 11:18

So there are both food and non food obesogens substances that we're exposed to that promote obesity, and and promote metabolic dysfunction probably in other ways. Starting with some of the food obesogens you mentioned fructose. Yeah, that's the big one. How now how is it no BS a general how is it punching above its weight compared to say glucose or some other comparable food?

Robert Lustig 11:41

Right? Absolutely. This this is what I've spent my entire, you know, obesity career. I have two careers. One was working on why boys are boys and girls with girls from the neck up. That was what I did for the first 20 years of my career and then for the second 20 Zhan obesity. But why is fructose a an obese surgeon unrelated to its calories, because glucose has calories, and glucose stimulates insulin and insulin drives weight gain. So glucose should be just as big a problem for obesity as fructose. It turns out that the reason is because of the way it is metabolized, and also what it does to the brain. So there are three reasons that fructose is worse than glucose in terms of obesity, and also metabolic disease like diabetes. And those three things are number one. Fructose is not metabolized in all the organs in the body like glucose is fructose is metabolized in the liver. So an entire fructose bolus, like a 20 ounce coke. You drink it, that fructose all goes to the liver, the glucose will go anywhere, but the fructose all goes to the left. So

Nick Jikomes 13:02

pound for pound, you're putting more stress basically on the liver on that one organ, gram

Robert Lustig 13:07

for gram right gram for gram. You're putting more stress on the liver, because it's all going to deliver because only the liver has the glute five transporter for fructose. So what does the liver do with the fructose once it's in there? Well, for glucose, what it does is it tries to turn it into glycogen, which is a storage form of glucose, which is non toxic and which basically, every liver has some and you know, marathon runners have more because they're running marathons. So they load up with pasta, very specifically to drive their liver glycogen stores. And that's where you want to put extra energy because glycogen is for lack of a better word non toxic, but fructose does not go to glycogen. Okay, there is no direct pathway from fructose to glycogen. It goes instead down to the mitochondria through the Indian Meyerhof or glycolytic pathway, which takes you from fructose to ask to Koay and then as to co a then enters the mitochondria and the mitochondria would then burn the gas to co a through the Krebs cycle to generate carbon dioxide and water and ATP. And the whole goal of this is ATP. So fructose overwhelms the mitochondria because the mitochondria are fixed, they have V max, maximum velocity, they can only they cycle can only turn so fast. The only way to make the cycle turn faster is to have more mitochondria. By the way, that's why exercise is good. You make more mitochondria. Yeah, that's a good thing. I'm not saying exercise is bad. But you know ultimately mitochondria and is a mitochondria and then you know, it's not like You can, you know, sort of pressure test the mitochondria. And if you overwhelm a mitochondrion, okay, it's not going to work better or faster. And so what happens is you overwhelm it, it can't deal with the load, it ends up sending out a compound called citrate. And the citrate leaves the mitochondria and through a process called the citrate shuttle. And then now that citrate is in the cytosol of the cell, and now the cell has to do something with that citrate, and what it does is it takes the citrate down to sto Co A the sto Co A gets bound to another sto Co A to make millennial Co A, and then the cell starts adding to carbon fragments on to that millennial Co A, and so builds from a two carbon string to a 16 carbons string, which we call Paul metate. And the liver only makes Paul metate and this process is known as de novo lipogenesis new fat making, this is how your liver turns sugar, fructose, in particular, into fat, Paul metate fructose deposited through this de novo lipogenesis. Now, once the palmitate is made, the goal is to package it in a form that can be exported out of the liver. And so it gets added to a glycerol molecule to make a triacylglycerol or serum triglyceride. And then that triglyceride gets packaged with a bo B 100 lipo protein, and now you've got this little molecule, which we call VLDL. Very low density lipoprotein. That's, and that's a bad one. And then that gets exported out of the liver. And now that your serum triglycerides have risen, because you have consumed to sugar to an excess amount of sugar, and then that VLDL can either be a substrate for adiposity because insulin will work on that VLDL to deposit in your peripheral subcutaneous tissue and now that grows or it can be potentially a driver of cardiovascular disease if it unloads in the arterial wall, okay, but but some of the triglyceride will be manufactured and we'll never make it out. It won't be packaged, in which case now you have a lipid droplet. Now you have fatty liver disease. When you have fatty liver disease, now your insulin signaling in your liver cell doesn't work anymore. Now you have liver insulin resistance, and that makes the pancreas have to make more insulin to make the liver do its job. And that has its own negative side effects. Because insulin is a mitogenic factor. It is a growth factor. It causes vascular smooth muscle growth, it causes glandular growth, therefore leading to cancer. So it actually increases cardiovascular disease, and it increases cancer risk. And it basically is the library driver of chronic metabolic disease Plus, you're putting so much extra stress on the pancreatic beta cell to make that insulin that you will ultimately burn out now you have type two diabetes. But there's only one problem. There are three okay, we have no we have now described one. Now let's describe problem number two. Right? You like barbecue? Oh, yeah. Yeah, me too. Yeah, why do we paint our ribs with barbecue sauce to get that nice caramel color and the caramel flavoring right that you know. So good right. White of bananas Brown. point is this is a reaction which is known as the my yard or the browning reaction. The browning reaction is the caramelization reaction. This is why if you take sweetened condensed milk and you put it in a pressure cooker, you will get putting that that's a way to make a very cheap dessert. But it turns white substance into a brown substance. Well, we are all Browning all the time as we speak. Okay, if I went in, if I was a cardiovascular surgeon and I opened up your sternum kick your, the cartilage ends of your sternum would be brown today. Okay, you're a young guy. Okay. Mine are even browner. Okay, they started out white. Now they're brown. And the reason is because of this mired reaction. It's occurring all over your body. It's a current one all of the time. It is a, you know, byproduct of life. There is no life without the mired reaction. But the goal is to make that mired reaction run as slow as possible. And the reason is because every time that mired reaction occurs, you are taking that protein and you're making it less flexible, you're making it less functional. Because there are these glucose or fructose molecules hanging off of it, which change its conformation. And every time that reaction occurs, you are releasing a reactive oxygen species.

Nick Jikomes 20:35

So this is all like an oxygen dependent thing. Absolutely. Completely oxygen.

Robert Lustig 20:39

Okay. So bottom line is, you don't want that mired reaction to occur fast. You can't stop it, but you want it to occur as slow as possible. Well, turns out because of the nature of the stereochemistry of the fructose molecule, fructose engages in that mired reaction seven times faster than glucose. And it generates 100 times the number of reactive oxygen species. So that is the aging reaction. That is the reaction that causes wrinkles. That is the reaction that closes cataracts. That is actually the reaction that causes cardiovascular disease. So more fructose, more sugar, more cardiovascular disease, having nothing to do with insulin, and having nothing to do with energy, just because of the stereochemistry of this molecule. So unrelated to calories. And finally, number three, remember I said there were three fructose stimulates the reward center in the brain. So there's an area of the brain called the nucleus accumbens is the reward center. It's where cocaine, heroin, nicotine, alcohol, shopping, gambling, social media, internet, gaming, pornography all work. Okay, they all generated dopamine signal. So the question is fructose does that does glucose? And the answer is glucose does not do that. Glucose activates other places in the brain, mostly the basal ganglia and the cortex. But it actually does not stimulate the reward center, only fructose stimulates the reward center. So a little sugar means you're going to have a lot more sugar because of that reward.

Nick Jikomes 22:26

So this is what's fructose specifically, that is the sort of addictive sugar among the sugars. Exactly.

Robert Lustig 22:32

Fructose is addictive. And in fact, on February 15, so just three days from today, Dr. Nicola Vina, who is a neuroscientist at Mount Sinai, and who actually discovered sugar addiction. I mean, she's the one who basically put it on the map and I are going to be at the Commonwealth Club in San Francisco, discussing sugar addiction, both from a biochemical and from a public health standpoint. And

Nick Jikomes 22:59

when when you say fructose is addictive, it's it's not a metaphor, it's literally tapping into the same mechanisms that a drug of abuse would tap into. Exactly

Robert Lustig 23:06

right. So people who say, Oh, I have a horrible sweet tooth. That's sugar addiction till proven otherwise. It's not euphemistic that is hardcore biochemical. So

Nick Jikomes 23:19

fructose, so So tell me if this is a fair summary of what you've told us. So far, fructose is more obesogenic than glucose because the body metabolizes it differently. Right. And among other things, that tells us the body doesn't treat a calorie from over here the same way it does a calorie over there. I see that. That's why it's a problem to think about the whole weight loss thing as simply calories in calories out. Exactly. Right.

Robert Lustig 23:44

So everyone thinks it's about calories. Now, why do we think it's about calories? Because 100 years ago, this guy named Wilbur Atwater took a bomb calorimeter and threw some fat in it and exploded it and threw some protein in and exploded it and threw some carbohydrate in and exploded it. And he came to the calculation, that fat burn that nine calories per gram, and protein, burn that four calories per gram, and carbohydrate burned at four calories per gram also. And so he said, Well, fat, obviously, is more energy dense, which is true, but that is absolutely true. That is more energy dense. That's why there is fat because it's an easier way to put more calories in storage. And take up less room. Yeah, that's a good thing, I guess. Right. But from the standpoint of utilization that has nothing to do with anything All right. And it turns out that, that fat, just because it's nine calories per gram doesn't mean it doesn't have value or that it has, you know, too much value for it. And it's the target for trying to fix obesity, because you need certain fats, and you don't need other fats. And when you basically go fat free, which we all did for 50 years, okay, we actually got sicker, because we actually needed the fats. And what we did was we loaded up on the carbohydrate. Remember all the pasta bars from the 1980s, you know, as everybody tried to go fat free. That was the worst thing that we could have ever done. Because all we did was we took something that was actually good for us in our diet, and substitute something that was bad for us in our diet. Another example, which I love is, you know, as a pediatrician, chocolate milk, you know, they took the fat out of the milk. And then the kids wouldn't drink it because it tasted like dishwater. And what they do, they added the chocolate, right? They took the fat out, which was good. And they put in instead the sugar, which was bad. Because this has nothing to do with calories. And so I that is my mantra, kill the calorie, you know, hashtag kill the calorie. And we have shown 50 ways from Sunday, why obesity is not about calories.

Nick Jikomes 26:28

So you've told us about a carbohydrate. obesogen? That was the whole fructose discussion, we talked about how fructose affects the body differently than glucose. And because it's processed differently, and it's because of the way it's processed. It's more obesogenic Are there any obesogenic fats and what I'm thinking of here, based on what you just said, and some other things that that I've discussed on the podcast recently, there's two types of fats I would like to get your take on. So one are the basically the seed oils, the Omega six polyunsaturated fatty acids, and the extent to which there will be some genic. Then maybe after that, I want to ask you about you know, you were just talking about milk and other things. Saturated fat, because we've I've been told my whole life that saturated fat is, is the really problematic one that will drive cardiovascular disease and, and other bad things. Right.

Robert Lustig 27:18

So let's start with the Omega sixes. Okay. And I do believe you had Chris cannot be on your show. Ready? Yes. You know, major proponent of getting rid of omega sixes, and I love Chris, you know, great guy. I'm not sure that omega sixes are obesogenic. Specifically. However, they are pro-inflammatory. And when you are pro-inflammatory, you generate insulin resistance. And if you generate insulin resistance, then that is obesogenic. So, in that respect, they may be obesogenic indirectly as opposed to directly because they are pro-inflammatory. Now, omega sixes you need them. It's not like you can do without them. If you didn't have any Omega sixes, you would be eaten by the maggots. Right. They are part of your defense system against foreign invaders. And the reason is because omega six fatty acids which are in seed oils in canola oil, soybean oil is famous for it. So they are the precursors to arachidonic acid. arachidonic acid is the precursor to virtually all of the pro-inflammatory cytokines: thromboxanes, eicosanoids. missing one production of prostaglandins, the gland is prostaglandins, right? Sorry. So you need them. But you don't need too many of them. And it is estimated that what we need is an Omega six to Omega three, which is anti inflammatory Omega six Omega three ratio of about one to one would be optimal. But you can only really achieve that if you live on a coast. And worth, you know, three to one, four to one maybe tops. Our current Omega six Omega three ratio is 20 to 25. To one based on how many processed foods you eat.

Nick Jikomes 29:25

And when that little that little comment you made about living near the coast was that alluding to seafood?

Robert Lustig 29:31

Yeah, basically, seafood has omega threes and the reason is not because the seafood makes omega threes. The seafood eats the Omega threes. The Omega threes are made by algae. Algae make omega threes. The fish eat the algae, we eat the fish. So we get our omega threes thirdhand and they are anti inflammatory. We're talking about three omega threes. Ala alpha linoleic NIC acid ALA and that you can find in vegetables. But alpha linolenic acid ALA is been shown to have cardiovascular protection but not neural protection doesn't get to the brain. The next one is EPA I cosa Penta II Noack acid that gets to the brain. And that improves neural transmission, and is absolutely essential for brain health. The problem is that EPA is the one that smells fishy. So not a lot of processed foods. And they're so

Nick Jikomes 30:38

fresh EPA smells fishy. It's not just oxidized up. Well,

Robert Lustig 30:42

more oxidized EPA will smell fishy or got it without question. I mean, there's a little bit of a smell but not not nearly as much. And then finally, the last one is DHA, docosahexaenoic acid. The DHA is necessary for neuronal structure. Now, the problem is that ala does not really get converted to EPA or DHA, the percent conversion of that in the body is extremely low, like less than 1%.

Nick Jikomes 31:16

So if you tried to get all of your omega threes through a purely plant based diet, would that be problematic for that reason?

Robert Lustig 31:23

Yes, yes. And so people who are on plant based diets really do need to take some form of Omega three supplementation, because ala alone is not enough. So they can take fish oil, but then they're not vegan anymore. Because it came from fish, they can take algal oil and stay vegan, and that's okay. But algal oil is primarily DHA, not EPA. So it still becomes a little bit of a problem. So personally, I think the right, the best diet, if someone asked me what the best diet was, I would say pescatarian. Because you can basically have the best of both worlds in terms of what's your you're eating and effects on the on the environment. That would be my my personal choice. But you know, it is what it is I still like barbecue. So anyway, Omega sixes are highly inflammatory, because they are the precursors to these inflammatory cytokines. We need to get those down. And Chris Kenobi has basically argued, I think, effectively that those Omega sixes are driving multiple different diseases as well, including, in his case, acute macular degeneration are in and you know, for good reason. So, omega sixes are an issue. And

Nick Jikomes 32:54

probably if we just had to put put it in one sentence, the best way to reduce Omega six intake is probably just to reduce processed foods generally.

Robert Lustig 33:02

In general. Yes, absolutely. Because that's where they're headed. And then finally, you asked about saturated fat. Yep. Now, we have been told, for time immemorial, that saturated fat is the bad guy. I am here to say that saturated fat is not the bad guy. Saturated fat is cardiovascularly. Neutral. It's neither good nor bad, but it is necessary. You need saturated fat in order to be able to make a decent membrane, decent cell membrane.

Nick Jikomes 33:38

So there's actually an analogy here, maybe with the Omega sixes, which is you don't want too many Omega sixes. But they are essential. Can we think a similar way with the saturated fats?

Robert Lustig 33:48

Yeah, pretty much. You know, saturated fat has certain advantages. Number one, because it's saturated. You can heat it to any level you want. Right, and it won't cause the isomerization at the double bond to turn sis fatty acids into trans fatty acids. And trans fats are the devil incarnate. Trans fats are the single most poisonous thing you can put in your body that we call food. I see.

Nick Jikomes 34:20

So trans fats are very, very bad. And is telling me if this is a fair statement. Anytime you heat an unsaturated fat to high enough temperature, you're running the risk of creating some transfer, correct?

Robert Lustig 34:33

That's exactly right. So we want unsaturated fats we have demonstrated the benefit and value of unsaturated fats like for instance, olive oil, olive oils, oleic acid. oleic acid is the endogenous ligand of a transcription factor in the liver called PPA our alpha bruxism proliferation activated receptor Alpha. It's one of the things that runs the liver. It's fuel gauge on the liver cell. It's a good thing. And you know, I'm for olive oil, and I got a lot of it upstairs. But But olive oil has a relatively low smoking point of 310 degrees Fahrenheit. So cooking with it could be a problem. So depending on how you cook, cooking with olive oil, especially if you put it in a frying pan and you heat it something up, you know to fry something in olive oil could potentially be a problem because you could be making trans fats at home. And the more double bonds that any given fat has, the more risk you run of creating trans fats at home. So

Nick Jikomes 35:43

this is why this is like deep frying and Omega six polyunsaturated fats is so problematic. Exactly,

Robert Lustig 35:51

exactly. But of course, that's what every State Fair has. So what what are you going to do? So so saturated fat gets away from that saturated fat will not I summarize, because there's nothing to summarize. And the smoking point of saturated fat is much higher, so you will not get into any trouble. Now saturated fat got a bad rap. Because of all of this very bad epidemiology that was done back in the 1950s and 1960s. Right. Like guy named Ancel Keys, who was sort of famous in the literature. He was a hero even appeared on the cover of Time Magazine. Okay, and now he is a villain, and has been appropriately vilified. He was the one who basically correlated saturated fat consumption with mortality due to cardiovascular disease back in the 1950s. However, when you look at the data to cherry pick that he cherry picked it. Okay, he published a volume of a very long volume that an 800 Page volume called The Seven Countries Study.

Nick Jikomes 37:13

Geez, I don't know is that big? Yeah, it's pretty big. And

Robert Lustig 37:17

onto page 262 of that volume. And I know because I took it out. And I made, you know, like a slide of it. He basically said that the reason that sucrose sugar consumption was associated with cardiovascular disease, was because of the Association of sucrose with saturated fat. In other words, doughnuts. And all the countries that he picked in his seven countries, even though they're 22, he picked the seven that made his case, the seven that showed the highest incidence of mortality from cardiovascular disease world donut eaters. And the countries that we're not, we're not donut eaters.

Nick Jikomes 38:03

So it was obscuring the story. You told us earlier about milk dose?

Robert Lustig 38:07

Exactly. Exactly. Those people were not just eating high saturated fat, they were also eating high sugar. And what he did was he basically dropped it out.

Nick Jikomes 38:17

Is it made it? I don't, I don't want to spend too much more time on Ancel Keys because everyone's to death about him. Is it established fairly well, that he intentionally cherry pick this data?

Robert Lustig 38:30

Well, intent is complicated, as we have learned in the last two years. I'm not sure I never asked him. I don't know that anyone ever asked him if he intended. But there were 22 countries. And when he published it, there were only seven. We have the data on the other 15 and they don't fit. So I don't know. You tell me. Did he or didn't he?

Nick Jikomes 39:00

Got it? Okay, one more question about saturated fat, I think is important. Can we were talking about saturated fat. But are there multiple types of saturated fat that we should be distinguishing and thinking about analogous to the way that we talked about Omega sixes versus omega threes?

Robert Lustig 39:18

Well, in fact, that's right. So you know, we've learned the calories not a calorie and by the way, a an amino acids not an amino acid. And we've learned to carbohydrates, not a carbohydrate. We've even learned a fiber is not a fiber. And of course, a fat is not a fat. So there are two types of saturated fats. Not one, two, there's red meat saturated fats. And then there's dairy saturated fats, and they are not the same either. Even though dairy comes from a animal that also provides red meat So like, why is that, but it's true. So it turns out red meat is filled with even chain, saturated fatty acids, C 16, and C 18 palmitate. And stearic. And those, as I've said, are cardiovascularly, neutral.

Nick Jikomes 40:17

Got it? Red meat, saturated fats, even chained, those are cardiovascularly, neutral,

Robert Lustig 40:22

neutral, neutral, not not good or bad. Not good or bad. Neither good nor bad. Dairy saturated fat, so like in milk turns out to be odd chain, saturated fatty acids, C 15, and C 17. And those are chain saturated fatty acids have a specific phospholipid signature on their tail end, which is why they stay in solution. Because after all, that, you know, is in milk, right? I mean, yes, the cream rises to the top of distal fat and milk, even after the cream rises to the top that the phospholipid you know, allows both the you know, the oil and the water if you will to mix. And so they turn out to actually be protective against cardiovascular disease

Nick Jikomes 41:14


Robert Lustig 41:15

protective, dairy saturated fat is protective. So cardiovascular disease.

Nick Jikomes 41:21

So are you telling us that there's no saturated fats that are clearly negative across?

Robert Lustig 41:27

All right? That's right. There are no saturated fats that are clearly negative.

Nick Jikomes 41:32

They're neutral if they're even changed, like red meat. And they're actually protective if they're are chained, like from dairy.

Robert Lustig 41:38

Exactly right. So you also have to know that, you know, the reason everybody made a brouhaha over saturated fats was this molecule that came out of your liver called LDL. Now we've already talked about VLDL. Well, LDL and VLDL are not the same either. Okay, what makes VLDL sugar? What makes LDL, dietary fat? Dietary saturated fat? Okay, so there's no question that dietary saturated fat increases your LDL. And there's also no question that in large population studies, LDL levels correlate with cardiovascular disease. That is also true. Okay, the hazard risk ratio for high LDL, and coronary heart disease is 1.3. So if you have a high LDL, high LDL, you're a 30% more likely to die of a heart attack than if you don't have a high LDL. Okay, that's real. And I'm not even saying it's not I totally subscribe to that 1.3. Turns out the public health community has identified 1.3 as sort of what's necessary for a public health effort. So if it was 1.29, we wouldn't even be having this discussion. Because it'd be we'd be below the threshold. But we're at 1.3. That VLDL that I told you about before, the hazard risk ratio for high triglyceride and coronary heart disease is 1.8. So if you have a high triglyceride, you're 80% more likely to have a heart die of a heart attack than if you have a low triglyceride. So which one is worse? The LDL or the triglyceride? will clearly the triglyceride. So why are we spending all this time worried about the LDL when we're not even focused on the triglyceride? And the answer is because we had a medicine for it.

Nick Jikomes 43:46

So that's why that's why when my mother, my late middle aged mother recently went to the doctor, and her LDL was high, but her triglycerides, let's find the doctor was immediately like you should be on a statin.

Robert Lustig 43:59

Well, that's what the guidelines say. And the guidelines suck. Because they're not taking into account this whole issue. In addition, there's not one LDL,

Nick Jikomes 44:16

there's two, and we don't normally measure the VLDLs. When you go to the doctor, is that accurate? Number

Robert Lustig 44:22

one, you don't well, you measure serum triglyceride when you go to the duct, but there are two LDLs. So the LDL is its own thing, that there are two LDLs. There's one called large buoyant or type A and there's another one called small, denser type B. And it's been shown that the large buoyant is the one that dietary fat raises, but the large buoyant and that by the alleged board is 80% of your LDL concentration in your blood. But turns out the large points are cardiovascularly neutral. That's why I said you know, for the most part that cardiovascular neutral, because the large buoyant LDL do not contribute to Number one, they're large. They're so large, they don't fit under the surface of the endothelial cell to start the foam cell formation process to actually drive the plaque. And they're buoyant, they float. So they take, they go through laminar flow in your arteries and arterioles. And they basically don't set up a chance for those particles to be able to actually get into the end of psyllium to cause problems. So large buoyant, are cardiovascularly neutral, because they're not contributing to the pathogenetic process of heart disease. Conversely, small dents, they're small. Okay, they're, you know, I mean, from an angstrom standpoint, they're about 10 angstroms, smaller than the large Boyens. You know, 273 versus 283 microns or so, or angstroms, or entrance, they are small enough to get under the surface of the endothelial cell. And they're dense, they don't flood. So they fall out of laminar flow, so that they can approach the endothelial cell surface, so they can get underneath, and then they oxidize, and now you've got oxidized, small, dense LDL, and now you've got a pathogenetic substrate for heart disease, no ifs, ands, or buts. So the bottom line is a facet of fat. And LDL is not an LDL. Okay, and, you know, this whole concept that we should go fat free to solve the problem, actually only created two more, it created both obesity and type two diabetes,

Nick Jikomes 46:52

yeah, created those problems, and it did not solve the one that we thought it would. Right. So,

Robert Lustig 46:57

you know, we need to rethink how we did this and where we came from. And basically, you know, when you when you make a mistake, you admit the mistake and you're right, the ship, you know, we have not admitted the mistake, and we have not righted the ship. And so that's what I spend all of my time, basically trying to, you know, get the medical community to, you know, you know, sort of get get with the Get with the program.

Nick Jikomes 47:25

So, given what you told us about statins and LDL and all that, in your opinion, what are the what, What characteristics does someone have that justify a statin prescription?

Robert Lustig 47:38

So, statins stop you from making your own LDL. Okay, that that is true. And by the way, full disclosure, I have been on a statin for 33 years. Okay, I went on my Sasha takeback, sir. 31 years, 31 years. I've been on a statin since 1993. And the reason is because every one of my family has heart disease. My grandfather died at age 44 have a heart attack. My father had his first heart attack at age 61. Okay, everyone in my family has rampid heart disease. My sister when the 40 years ago, when I worked at Rockefeller, she was a research subject in Jim Breslow, his lab, and my colleague, and good friend Elliot Britton did heparin test on her to demonstrate that she had familial hypercholesterolemia. So I am a heterozygote. Oh,

Nick Jikomes 48:34

really? Yeah. So, I already know you have a specific genetic reason for this. I have

Robert Lustig 48:39

a specific genetic reason. So I have been on a statin for 31 years. And I've also tried myself off the statin more recently, and my LDL popped up from 70 to 300. Again,

Nick Jikomes 48:53

and how common is this condition? How common are one of like, you got one and

Robert Lustig 48:57

500 500? Okay. Okay. So I'm not against that. And they probably, you know, the reason I'm still sitting here talking to, okay, for the right patient. And if you have familial hypercholesterolemia, either homozygous or heterozygous, you need them. Okay, so I'm glad they're here. I'm not anti statin. I want to make that very clear. However, having said that, okay. of the people who are on statins today, which is a whole lot of people turns out, probably four out of every four out of five people who are on him don't need him. They were put on him for what we call primary prevention. That is, they went to the doctor, they got their labs drawn, doctor said, Oh, your LDL is a little high. Let's put you on a statin. And the reason is because the guidelines say so. So if you don't put somebody on a stand, you're not following the guidelines. And the guidelines are based on this hazard risk ratio. 1.3 So the question is for primary prevention, do statins work? We've been using statins for over 40 years. for primary prevention, do statins work? The answer is many meta analyses have been done. And they all show up for primary prevention that is not having had a heart attack yet, just having a high LDL, no event. The mean increase in lifespan for being on a statin is four days. Four days. Now, when you think about the fact that 20% of people who go on statins, end up with some level of rhabdomyolysis, you know, that muscle breaks down, they end up with severe inflammation, and 20% have high blood glucose, they have hyperglycemia. Because statins interfere with mitochondrial function, that's why they work to get your cholesterol done. Okay. You know, that's not a good thing. So you're putting people at risk for four days of increased longevity? And, you know, incurring this huge side effect profile.

Nick Jikomes 51:27

So let's just restate this explicitly, as you when you say you're putting people at risk with a step at risk for what's the

Robert Lustig 51:34

the rhabdomyolysis and hyperglycemia

Nick Jikomes 51:37

hyperglycemia. And muscle loss Basically, yes.

Robert Lustig 51:41

So, you know, bottom line, if you have said, if you've already had a heart attack, if you've already declared yourself, okay? Or if you have familial hypercholesterolemia, like I do, then you absolutely need a statin. And then the data on statin use and longevity is very, very strong and very robust. So for secondary prevention, totally, absolutely. Sign up. You need it. And if you're, if it's primary prevention, and you don't have FH, I think this is, you know, real travesty.

Nick Jikomes 52:19

If you have type, let's say you have type two diabetes, no personal history of heart attacks, and you know, no family history that's abnormal. Its average family history with respect to cardiovascular disease. What would what would your general position be if statins are a good idea for a diabetic? No.

Robert Lustig 52:37

So if you have type two diabetes, the first thing to do is get rid of the type two diabetes. Everyone assumes that type two diabetes is this chronic, unrelenting, progressive, destructive degenerative process that will never get better. And you know, you're going to be on medicine, whether it's insulin or oral hypoglycemics for the rest of your life. That's the general Gestalt amongst the cognoscenti in, in medicine, garbage. absolutely not true. absolutely not true. Numerous studies now show that a ketogenic diet can actually reverse type two diabetes verta Health 77% of people who go on a ketogenic diet, reverse not ameliorate reverse their type two diabetes, just by getting rid of the offending agent and what is the offending agent? Well, what is type two diabetes, it is extreme carbohydrate intolerance. So if you're intolerant to something, what's the best way to deal with it? Get it out of your diet. That's how you deal with an intolerance. If you are lactose intolerant, get the lactose out of your diet, okay, if you have you know, if you have peanut allergy, get the peanuts diet, whatever it is that you have an intolerance to, you know, get it out of your diet. So, but yeah, so carbohydrate out of your diet, you are on a ketogenic diet. And it turns out a ketogenic diet will reverse reverse type two diabetes now, there are other ways to do it, too. It's not like you have to be on a ketogenic diet, but that is one way and what it does is it is the you know, the the the test case, it is the, it is the you know, theory of the of the argument, okay? That if you fix the diet, you can fix your type two diabetes

Nick Jikomes 54:48

so, you know, I have family members who are type two diabetic, they're on statins. They're not, they're not given clear dietary guidelines by their physician except to cut out basically junk food which Which by that they mean like candy and things like that, but they're told for example, eat as much fruit as you want. Does that make sense to you?

Robert Lustig 55:11

It's complicated but let me let me try to explain fruit. Okay, so yes get rid of candy but there's a whole bunch of other things you have to get rid of too in order to you know make that right. I guess the you know, the question is okay, get rid of candy shirt shirt. Is Cheetos food is Cheetos food yes or no? Oh, not calories calories is Cheetos food. So what is the definition of food? That's, that's what we need to know. So, go to the dictionary, man got one up here if you want, I'll read it to you. Okay, I've learned I've memorized the definition of food is a substrate that contributes to either the growth or burning of an organism that is food growth or burned. So, the question is, does Ultra processed food contribute to growth? My colleague Dr. Front months and ego or non at Hebrew University, Jerusalem, has now looked at this and has shown actually that ultra processed food inhibits growth. It inhibits skeletal bone growth inhibits trabecular bone growth inhibits long bone growth, it actually reduces calcium in cortical bone, okay. It changes it difficile function. Okay, so it is inhibiting growth. And we also know it hijacks growth for cancer. You know, because it basically fructose in particular does not need to be burned in the mitochondria. Right? So it

Nick Jikomes 56:55

sounds like you're saying there's an inhibition of natural or good growth. And there's actually it's actually stimulating pathological forms of growth, correct.

Robert Lustig 57:05

About burning. So mitochondria burn, right. Fructose, which is in virtually all Ultra processed foods, I mean, it's been added to 73% of the items in the American grocery store, on purpose. Any of its three separate enzymes necessary for mitochondria to do their job. It inhibits MP kinase, which is the enzyme that drives mitochondrial biogenesis. So you get make more mitochondria and fresher mitochondria. It inhibits a CAD L, A soakaway dehydrogenase long chain which is necessary to cleave the two carbon fragments to engage in beta oxidation in the mitochondria so that you can burn in the first place. And finally inhibit CPT one a carnitine palmitoyltransferase. One A, which is the enzyme which regenerates carnitine carnitine is the shuttle mechanism by which the fatty acids get from outside the mitochondria to inside the mitochondria. So basically, you can't even import the fatty acids to burn. So Ultra processed food does not contribute to growth and does not contribute to burning. So is ultra processed food. Food is Cheetos food. What do you think what I was asking when I asked him? Yeah, bottom line is we think it's food because it has calories. Can you name something else that has calories? That's not food? alcohol, alcohol. Alcohol is not food. There's no dietician on the planet who will say that alcohol is food. But alcohol is calories. It's got seven calories per gram about trans fats. Trans fats are nine calories per gram, or trans fats, food, trans fats, it used to be food. And in 2013, the FDA said no, actually, they're poison. So just because something has calories doesn't make it food. And that's the key. That's, that's what we have to impress upon the population. And that's a different message than they have been getting for the last 50 years.

Nick Jikomes 59:21

So, you know, I originally wanted to ask you about obesogens and in my mind, I had food and non food obesogens. But it sounds like the way you would frame it is actually none of them are foods really, we there's just some that we normally think of as foods, and then the ones that we already don't think of as foods. That's right. Because these are all you would just call all of these obesogens or contaminants or even poisons.

Robert Lustig 59:44

Absolutely. They happen to be in our food but that doesn't make them fruit. That's exactly right. So so then that let's go back to the question you asked me at the beginning that started this diatribe fruit What about fruit, because fruit has fruit sugar fruit has fructose. So is it not food? The answer is, fruit is okay. And the reason it's okay, is because not only does it have the poison, but it also has the antidote, which is a fiber antidote is the fiber. No,

Nick Jikomes 1:00:22

I fully recognize this. And and I accept the argument here. I think it makes sense for a healthy person. But let's say you've you've you're talking about someone with type two diabetes whose goal should be to reverse that. My inclination would be to say, Well, why don't you just cut out all of the fructose? So yes, the fiber will prevent you from absorbing it as quickly. But wouldn't a better strategy would be to just cut it out completely until you reverse the diabetes?

Robert Lustig 1:00:47

I agree with that. If you have diabetes, if you have type two diabetes, almost assuredly, you also have fatty liver disease. Okay, the correlation between fatty liver disease and type two diabetes is extremely tight. Okay, it's almost for sure that the reason for your diabetes is because your livers not working right. And because your livers not working right, your pancreas had to make extra insulin to make your liver work, right. And now your pancreas is burned out. And so you got to give your pancreas a chance to regenerate. And you know, and work properly, the only way to do that is to make your liver work properly. So you got to burn off that liver fat, you got to get rid of that liver fat in order to fix the problem. And ketogenic diet, we'll do that. And the reason is because the LDLs that the liver makes out of your dietary fat don't get clogged, only the VLDL that comes from sugar gets clogged, the LDL is get exported right out the VLDLs sometimes don't. So if you're clearing LDL, and you're not making VLDL, your liver has a chance to be able to heal itself. And so that, to me, is where it starts. So if you have type two diabetes, and you have fatty liver disease, which if you don't know it, I'm telling you, odds are you do best thing to do is give your liver arrest. And the best way to give your liver arrest is don't challenge it. And fructose is a primary challenge. And so if you're asking me if you have type two diabetes already best not to eat fruit until the diabetes is resolved. And then you can probably add it back in reasonable amounts.

Nick Jikomes 1:02:48

What are some other? So the caveat of everything we just talked about with the definition of food? I want to talk about non food obesogens. You mentioned some earlier, what are one, two big examples, things that are all over the place that people are using commonly. And what do we know about the mechanisms here?

Robert Lustig 1:03:07

Well, there are a lot there are a lot of obesogens there are a lot of mechanisms. Bottom line is they're all they're all around us. And to me, for the most part, we put them there. They're all for the most part part of our Anthropocene. They're part of you know, the manmade environment that we have created for ourselves. They can act through multiple different pathways. There are multiple receptors in the body that can transduce these obesogen signals, but they're all basically receptor mediated signals. So it can be the estrogen receptor. It can be the androgen receptor can be the glucocorticoid receptor. It can be the Aryl hydrocarbon receptor, it can be LA, LX or FX or in the in the liver. K can be the PPR gamma receptor. There are a bunch of different compounds and there are a bunch of different receptors, all of those receptors that I just listed all are part of the evolutionary process of a fat cell. They will create out of oh I got thyroid hormone receptor that's in there. They will create adiposity when stimulated, and so different obesogens will stimulate different receptors. So the Aryl hydrocarbon receptor, grilling your food will activate the Aryl hydrocarbon receptor. So remember, I said I love barbecue. Well, you want to get rid of you might have to get rid of the barbecue. Well, that's the problem.

Nick Jikomes 1:04:54

Is it about the barbecue? Is it is it the like the chart? The chart? Yeah, the charge part.

Robert Lustig 1:04:59

Yes. I don't know how to make barbecue without charring. It's part of the part of the process. Unfortunately, that's one of the reasons why everybody says eat raw to number one, the fiber is still there, and you haven't created any of these dietary advanced glycation end products. That's another thing that drives this phenomenon. So the glycation that we talked about before the mild reaction, it can occur in the body or can occur in the, in the cam, before you even eat it. If it occurs in the body, it generates the reactive oxygen species directly. If it occurs in the can before you eat it, then what happens is that dietary advanced glycation end product will bind to a receptor for advanced glycation end products on your cells called rage, or a GE receptor for advanced glycation end products and activate the NADPH oxidase generating reactive oxygen species also. So it's, you know, they're everywhere, including in the cans, or, you know, packaged foods to start with that, you know, if they, if the food's been heated before you got it, there's a good chance there dietary AG is in the food before you even put it in your mouth. Air pollution, as I mentioned, is an inflammatory reactance, which has been shown to increase adiposity. And that has nothing to do with calories. It has to do with the air, right? pm 2.5 particulate matter a 2.5 microns or smaller so that it gets into your bloodstream and drives an inflammatory response, BPA Bisphenol A, which activates the estrogen receptor, because it needs just need. The estrogen receptor just needs two hydroxyl groups 22 angstroms apart, and you're in estrogen. So you know, there are a lot of estrogens are in our in an in our environment. And BPA is everywhere. If you've ever opened up a can, and there's a whitish lining to it, that's BPA. So

Nick Jikomes 1:07:08

it just it just happens to be the the estrogen receptor has a structure that is sensitive to things that many components of modernity are made out of. Yes,

Robert Lustig 1:07:18

exactly. Exactly. You know, years ago, many, many, many, many years ago, I was taking care of a kid in Wisconsin, a five year old girl with breast development. So everybody thought she had precocious puberty. And we looked at her we assessed her we did every exam, you know, every lab test, you know, under the sun, and everything came back negative. And then I sent her urine for a tox screen, thinking maybe she was getting into mom's birth control pills, but Mom swore she didn't have any birth control pills. So where would she be getting from but I sent the urine for the tox screen anyway. And what came back was Genesis Stein. What is Genesis Stein? genestein is a plant estrogen. It's plant estrogen. And that was what was driving her breast development. Where does that come from? So I asked them I said, you've already told me about her diet. What do you bathe her in? And she actually she looked at it. She was on the phone at home. And she said, Well, I use this Victoria's Secret bath gel. And I said, What are the ingredients and then she looked at it she says Not for use in children. And the reason is because the reason it's Victoria's Secret bath gels because it's loaded with plant estrogens to make your skin silky smooth, so this kid was absorbing the estrogen through her skin from her bath.

Nick Jikomes 1:08:59

Got him her mom was inadvertently giving her a sex hormone therapy.

Robert Lustig 1:09:03

Yeah, without knowing it. So environmental estrogen can also be an environmental obesogens because after all, estrogen lays down subcutaneous fat as an example, right. Parabens are things that are in cosmetics like lipstick. Okay and haircare products

Nick Jikomes 1:09:27

you know it the list is you know, it's it's the basically your grill tribunal

Robert Lustig 1:09:31


Nick Jikomes 1:09:32

I'm not gonna say everything but lots and lots of things.

Robert Lustig 1:09:35

tribunal tin is what they use to paint the bottoms of boats to keep the barnacles from attaching to the hall. Okay, so all our water supply is filled with tribunal 10 And my colleague Dr. Bruce Blumberg at University of California, Irvine has shown that this particular compound is so egregious and also has As epigenetic effects going forward, so you can expose an animal to try butyl 10. And their great, great, great grandchild will be obese because of what you did to the great, great, great grandmother.

Nick Jikomes 1:10:16

If we're using it on boats. Is it in the tap water? Yeah, it's in the tap water. And we're in the tap water at, you know, levels that are that concern us?

Robert Lustig 1:10:26

Yeah, yes, absolutely. So, you know, you're never gonna get away from these pee fast, you know, polyfluorinated alkylated substances, you know, the whole Teflon thing. If anybody wants to watch the movie dark waters came out in 2019 with more Gruffalo, it's all about DuPont and how they hid the Teflon story from you know, the from the populace for 20 years, okay, this is this is and these are forever chemicals, they are not going away. Another example DDT. So, DDT is a plant as far as is an insect estrogen. Okay, it is an insecticide gates, what we sprayed on all of the crops during World War Two, you know, to basically get rid of the, you know, insects and malaria and what have you, okay, but turns out DDT is a, an estrogen, you know, two hydroxyl groups 22 angstroms apart, that's why it was a good insecticide, you know, was basically contraceptive, you know, for the insects. But we can measure dde levels in in pregnant women's urine today, and it predicts obesity in the child at age five. Okay, it's been gone for 50 years, but we can still measure it. So,

Nick Jikomes 1:11:48

you know, given everything that you're telling us, it's, you know, the question is simply going to be, you know, how does an ordinary person react to learning all of these things, and, you know, I can think of a number of reactions, but none of them seems particularly palatable. You know, reaction, one could just be you become Ted Kaczynski, and you move to a shack in Montana and try to destroy civilization. Let's assume we don't want to go down that path, you know, reaction to could just be to say, Fuck it, like, whatever, I don't care, I'm just gonna, this is what we live in. And that's basically do Yep. You know, reaction three could be to just become completely neurotic about all this stuff. And, you know, become an Uber health, not for lack of better term. But most people probably aren't willing to do that don't want to have the anxiety and the stress that come with that as well. Is there another path? What is the path? Yeah. So,

Robert Lustig 1:12:41

Nick, you're absolutely right. And you've identified three of the four paths. There's a fourth. Okay, so you're no question we've got people who, you know, are lunatics. In part because of, you know, what society has wrought upon them. We have the people who have basically chosen to ignore it, because it's just too hard. That's a lot most of the population, I would say, we have orthorexia six, you know, who basically now, you know, question every single thing they put in their mouth and, you know, are dysfunctional because of it, it basically feeds into OCD, you know, to to, you know, make them very miserable. Or there's a fourth, which is actually do something about, Okay, number one, vote. You know, this is a voting issue, this whole obesity thing, the whole food thing, the whole environment thing, is a voting issue. Now, a lot of people think that there are other reasons to vote, but this is one of them. And, you know, you should, you should actually, you know, want to do something about this. Another is explain this to your doctor, because your doctor doesn't understand any of this. And they need to, and the reason is because doctors went to medical school to learn two things, the two P's prescriptions and procedures. And I know because I'm one and I, that's what I learned. There's a third P prevention. Does doctors learn prevention? law currently? Why is that? Because 80% of the medical school costs are underwritten by big pharma.

Nick Jikomes 1:14:35

So I'm trying to put I'm gonna put this in a way that isn't gonna seem like defeatist. So let's take those in reverse order. So I like the idea of talking to your doctor about these things. But how does how does an ordinary person talk to their doctor about these things in a way that doesn't make their doctor just roll their eyes and say, you know, who are you to lecture me?

Robert Lustig 1:14:54

I went to medical school. Okay, so yes, but no Uh, I mean, it's true. Okay, some doctors are very provincial, and some doctors are very paternal. And I know a lot of them. And, you know, a lot of them live in the ivory tower, you know, where I used to practice as well. So I know what your I know what I know from whence that question comes. And I and I, and I, you know, I identify with it to a great extent. Having said that, no doctor actually wants to do harm. You have to basically show them how what they're doing is doing harm. The easiest way to do that is to show up at your doctor's office 50 pounds lighter,

having not taken their advice. And then when the doctor says, What would you do?

And then the patient says, Well, I actually got the carbohydrate out of my diet, I actually changed what I had in my pantry. And, you know, this is where we are. And then the doctor says, really, that's what happened. So they need to see the results. They you know, you can't you can't explain this to them, you have to show it to them. Let me give you another example. I am working right now with a food company. Okay, I take no money from them. But food company offshore in the Middle East. This company is the Nestle of the Middle East. They make all sorts of problem foods. They make flavored milks, frozen yogurt, ice cream, confectionery tomato sauce, biscuits, okay, like all Ultra processed food to the highest degree, all bad stuff. And their CEO at age 48, weighed 350 pounds, and had type two diabetes and back pain. And he went to his UK physicians. And they put them on insulin and oral hypoglycemics. And he got worse. And he said, this is not working. And so what'd he do? He went to Dr. Google. And he started researching it for himself. And he found two people online, he found Jason Fung, who is in a frolic just in Toronto, who is a great believer in intermittent fasting. And has written several books, the obesity code, the diabetes code, the if it's a code, cancer code, if it's a code says, Okay, that's his code, and meat. And so, CEO started doing what we said to do. And lo and behold, in nine months, he dropped 100 pounds as type two diabetes resolved, his back pain disappeared, and he thinks we're on the moon. Okay, great. And then he has his aha moment, his moment of epiphany, where he said, Wait a second, I did this to myself, eat my own crap, what am I doing to the rest of the Middle East? And so they came to me four years ago, this company. And they said, We want to move into the 21st century, we want to be a metabolically healthy company. We want to change the food to contribute to the health of our population, not heard it. Wow. How cool is that. And we've been doing that. And we actually published a paper last year in March of 2023, in frontiers in nutrition, called the metabolic matrix reengineering, ultra processed food, to protect the liver, feed the gut, and support the brain. And it turns out any food, if it does, all three of those things, protects the liver feeds the gut supports, the brain is healthy. And he foods that there's none of the three is poison. In any food that there's one or two, but not all three, it's gonna be somewhere in the middle. And so you can actually set precepts and you can set protocols for being able to actually determine what needs to be done and what needs to be in Ultra processed food to actually make them healthy. Now, can people do that at home? And the answer is absolutely yes. They can. Okay, well, they need some education. They needed tools to be able to help them do that. And we have developed one just for them. Okay, and your for your audience. It's called perfect, p e r f AC T is a recommendation engine, it is not AI, very specifically not AI. Because in nutrition, you know, the AI only knows what the internet knows and in with when it comes to nutrition. The internet is replete with garbage with just trash. And so you don't want AI to be making your decisions for you. But you want a scientist who actually We know something about metabolic health to be making your decisions for you. So go to http colon slash slash perfect with an a.co P er f ac t.co. And you will find a recommendation engine. And what you do is, you click on it, and it will show you all of the items at Walmart, Amazon and target all the food items. And you can apply different filters. Like for instance, no added sugar filter, or a Keto filter, or a peanut allergy filter or a oxalate filter, or, you know, oh, no, no Ultra processed food filter. And so it will only show you that which you can buy to make yourself metabolically healthy, so that the store becomes a store instead of an obstacle course. There's a way right there.

Nick Jikomes 1:21:00

So we talked about like these four different reactions that people can have to the whole situation, the obesogenic situation that we are in better than, you know, one of them. The second one that we talked about was the, you know, the one that just says, fuck it, like this is what we have. And that's probably where most people are. And I want to ask you about how difficult it's actually going to be to get people out of that, given the unholy alliance between different factions in our society. So you've got big pharma, who now has things like GLP, one drugs at their disposal, which you know, are, get get skinny for free cards. That's basically what they're being treated as, you know, you've got the big food, Big Ag side, which is, which makes the voting the voting thing difficult, because everyone we vote for is completely plugged into all these special interests. And then you've got I think, you know, both sides of that equation, they're promoting things like the so called body positivity movement, you know, saying, hey, it's, Hey, this is the way we are, and you should love yourself the way you are, and therefore, you can just keep consuming all of these things. Help. How do we break the the sort of alliance of forces out there that is seems quite strong? Right?

Robert Lustig 1:22:21

Nick, I couldn't agree with you more. Okay. There are many stakeholders in this, and they all have their own angle. Agreed. And, you know, you can't fix those until you give them a better answer. Okay, it's like the Arab Israeli conflict, you know, too many stakeholders, too difficult to come up with a single answer that fact that helps everybody, but you know, what, there actually is a way, there is a way to do this. And it requires everyone coming to the table at once. And that's what I'm trying to do. That's actually part of why I do what I do, is trying to bring the doctors and the nutritionists, the dietitians, and public health, and the food industry, and politicians, you know, and the public, you know, to the table all at the same time, but you have to be working off the same set of facts. And as you've learned, as we've learned, you know, people have their own facts. whether they're right or not, is a different story. And that's one of the reasons why I'm happy to do this podcast with you now is to try to deliver, you know, the, shall we say the truth, somebody will say, No, that's listings truth, but, you know, I can document virtually everything I say. So, nonetheless, how do you do this? Here's how I think about this problem. And I am Welcome to, you know, suggestions. In the last 30 years, we have had for counted for cultural tectonic shifts in America. And here they are. Number one, bicycle helmets and seatbelts. Smoking in public places. Number three, drunk driving. Number four, condoms and bathrooms. Now 30 years ago, if a legislator stood up in a state house or in Congress or in Parliament or the Duma or anywhere else in the world, and proposed any legislation for any one of those four, they'd have gotten laughed right out of nanny state, Liberty interest, get out of my kitchen, get out of my bathroom, get out of my car. Okay. Now none of those are problems today. We have solved Every one of those who can you don't hear anybody belly aching about this? Oh, you hear about other belly aching. I mean, vaccines. Perfect example of, you know how, you know, new things have come into this quote nanny state issue. Okay, but the bottom line is those four are solved. Now how to resolve. We taught the children, the children grew up, and they voted member voting, and the naysayers are dead. That's why this is a generational shift. That's but that's also why it takes 30 years. Now, the good news about this is we're about 10 years and all this started around 2013. So it's going it's we already see signs of it working. We already see documentation of the public being educated, and I can actually prove that the public is being educated. The food industry actually generated the data for me. There's a public relations arm of the food industry called ifac. I fic, the intimate international food information Council. Okay, it is just a PR arm of the food industry. But they publish a report every year. And every year, they asked the public a question. And in 2011, they asked the public the following question, what foods stuff is most likely to cause weight gain? And in 2011 11% of the population said, refined carbohydrate and sugar? And 42% said a calorie is a calorie or I don't know. They asked the exact same question seven years later, in 2018. The exact same way, no change. And now 33% of the public said, refined carbohydrate and sugar. And the exact same number reduced from a calorie is a calorie or I don't know. In other words, we taught those people the real story. So you can do it. But it's a generational shift. Because there are a lot of people who will never get it. And I'm given up on trying to get those people to get it, I gotta get the people who are receptive to be able to get it. Because they'll live longer, because they did the right thing. And then we'll actually see the change. I have no qualms about the fact that this problem is going to outlive me. You know, I'm just a cog in this wheel. This is gonna go way past my lifetime. Right. But the fact of the matter is, you got to do something. Yeah,

Nick Jikomes 1:27:53

I mean, the piece about this I that I think I like the best is whether we like it or not. These things are generational, they do take generational periods of time to change. And that means no matter what your position is, an effective strategy probably has to involve educating the young. That's what

Robert Lustig 1:28:14

and that's what we're trying to do. I am the Chief Science Officer and co founder of a nonprofit here in the Bay Area called the Eat Real. So you can find that on at eat real.org. And our function is to get real food into K to 12 around the country. Okay, well, these public schools right now, they don't even have food preparation facilities, they were taken out. Back in the late 70s, early 80s, they were taken out because the food industry started supplying, you know, all of these schools with Ultra processed food, calling it quote, nutritious, unquote, and I put that in air quotes for very specific reasons. Okay, because it wasn't nutritious. It was calories, but it wasn't nutritious, because it wasn't food. And that's when the grades started going down. And that's when the obesity start, you know, pandemic started, you know, rearing its ugly head. And, you know, it's only gotten worse than if you go to any standard school in America today. It's a disaster. So I have a question for you. I have a quiz for you, Nick. What is the largest fast food franchise in America?

Nick Jikomes 1:29:26

I mean, my guess would be McDonald's. Our

Robert Lustig 1:29:28

nation's public schools owe if you add up McDonald's and Burger King and Wendy's and subway, that is only half of our nation's public schools. Jesus. Okay. And every school in America uses Ultra processed food to feed their kids. And the reason is because they don't have any place to make food because all of the food preparation facilities and all the blue Harrods you know, with the hair nets and stuff, you know that they used to make the food they're all fired and gone. So the question is how can you get real food into schools today, when there's no infrastructure to support it. That's our genius. That's what real does. So we have multiple different paradigms. We have multiple different ways to do it, depending on the district, depending on the infrastructure that's there, depending on the geographics, depending on the food procurement availability. So there's not one way to do it. But let me give you our first way, the way we started. We worked with the Mount Diablo Unified School District right across the bay, in Contra Costa County, over in east of San Francisco. And they had an enterprising food services director. And what we did was we helped him purchase a dilapidated factory, which he then repurposed into a food preparation facility hired all the people to work at that facility, they would create 27,000 meals per day. And because they were making so much food, they were able to buy at scale, and they were able to buy local, and they knew what was in the food. So they were able to keep all the bad stuff out of the food. And then they would use trucks to basically ship it to all of the different schools each day. And so we got every kid, not just a hot meal, but a truly nutritious meal, a metabolically healthy meal, we lost 100,000 pounds of sugar out of the kids diets in one year. And guess what? Their grades got better. And the kids ate the food.

Nick Jikomes 1:31:48

And we're not going to have time to love to, you know, we're not gonna have time to get into this. But do you think that the grades getting better part? Do you think that's basically because a better diet is literally going to help your brain function better,

Robert Lustig 1:32:01

better mitochondrial function? Absolutely. Da. This ain't rocket science.

Nick Jikomes 1:32:12

I want to shift gears a little bit. And I want to ask, I want to ask you about something that is very striking. Other people have pointed this out. I mostly don't hear good answers to this. And I think it might sort of tie back to things that we talked about earlier, but didn't necessarily explicitly put together. So before I asked the question, you know, this paper on obesogens you put out recently, it basically goes through the four main models of obesity that scientists and thinkers on this stuff have used to explain obesity in the past. And you basically come to the conclusion, if I read you right that we need that the model that you like, is an integration of the obesogens model and the oxidation reduction model. So contaminant, and stuff causing oxidative stress in the body. Right.

Robert Lustig 1:32:59

So this paper that you're referring to, which is an International Journal of Obesity, January of 2024, first author for those who want to look it up as hind Dell, Jerry hind Dell. So this is a conglomeration of four authors. Jerry Hein, Dell, who used to run the environment endocrine disrupters section of the National Institute of Environmental Health Sciences, myself on second author Sarah Howard, who runs heeds healthy eating and endocrine disruptors. And finally, Barbara Corky, who is the Banting, Professor of venting award winner, sorry, at the at Boston University School of Medicine, who's done more on hyperinsulinemia than anybody else. And we published this paper called obesogens, a unifying hypothesis on the pathogenesis of obesity. That sounds a little too, shall we say, you know, full of ourselves. But nonetheless, we think we've gotten there. So the standard model that everyone believes, which I hope I've already debunked, just from doing this podcast, is the calories in calories out model, or the energy balance model. If you eat more than you burn, you'll gain weight. If you eat less than you burn, you'll lose weight. And I

Nick Jikomes 1:34:19

should just emphasize to people even like I, I did my PhD in neurobiology in the department of Endocrinology, diabetes metabolism at Harvard Medical School, and even people studying the neurobiology of people with fancy degrees doing fancy experiments, we would often just default to the energy balance model without even thinking about it.

Robert Lustig 1:34:37

Absolutely. And I know that and I, and I cannot tell you how many arguments that I have had over my career with really smart scientists, who basically just say, Yeah, but a calorie is a calorie. Yeah, but it's it's calories in calories out. Okay, I can document who in my harir have basically, you know, thwarted this notion that there might be something else going on. So this is this is well, you know, ensconced, you know, it's calcified in the minds of most of the intelligencia. And the fact that it occurred in the Division of Endocrinology at Harvard Medical School is no surprise. And you know, I won't call out your your your bosses, but I know who they are. Anyway, bottom line, if the energy balance models, right, and how do you explain obesogens if the energy balance model is right, then how do you explain obese newborns? If the energy balance model is right, how come body temperature has gone down? 1.5 degrees centigrade over the last 150 years? If the energy balance model is right, why are animals in captivity, gaining weight over the last 25 years? All of those say that the energy bonds model is bullshit. Plain and simple. Now, there is no question that calories play a role. But just because calories play a role does not mean the energy balance model is correct. And I will give you four reasons right now that the energy balance model is bullshit. Okay, let's start with fiber. You like almonds? Yeah, I love almonds. Almonds are great. Okay, except for they take a lot of water. Okay, but you eat 160 calories and almonds. How many of those calories do you absorb 138 160 absorbed 130 were the other 30 Go. The fiber in the almonds, the soluble and insoluble fiber formed a gel on the inside of the intestine an impenetrable secondary barrier. So the insoluble fiber acted like a fishnet. And the soluble fiber, plug the holes in the fishnet. And you can actually see the whitish gel on the inside of the intestinal lumen on electron microscopy. And so what's happening is that it's preventing those 30 calories from being absorbed early. So they go down the intestine, where the microbiome is, and then they get chewed up by the microbiome for its own purposes. So even though you consumed it, even though pasture lips, you actually didn't get it because your microbiome did. You know, we always, you know, we always tell pregnant women you're eating for two, well, we're always eating 400 trillion, because we have to feed our microbiome, you know, they ended up consuming 25 to 30% of all the calories that we eat. Well, it's they consume 25%. But if you can change the microbiome, so that they consume 30% of what we eat, you've just gotten thin, just by changing the microbiome, from 25% to 30%, without changing anything that passed your lips. So this calories in thing is just bullshit from the beginning has been forever. Number two protein. So if you are using a, an amino acid to build muscle or build anything in the body, then the amino acid goes straight there, okay, fine. If you're using the amino acid to turn into energy, you have to take the amino group off. Okay, because you can't burn an amino acid. You can burn organic acid, but you can't burn an amino acid. So you have to deactivate the amino acid, you have to take the Amino, the NH two group off the amino acid, right? That ends up costing more energy. Then say phosphorylating a carbohydrate getting it ready for absorption. So there's a net loss in burning protein for energy then there isn't good burning carbohydrate for energy, even though they're both four calories per gram. So a calorie is not a calorie because if you're burning an amino acid versus burning a carbohydrate, you're losing energy. There's a net loss. So calories, not a calorie number three fatty acids. We've already talked about this. We have you know omega threes over here heart healthy save your life, anti Alzheimer's anti inflammatory best thing you can put your body over here we have trans fats you know devil incarnate. You know consumable poison will kill They're both nine calories per gram. Well, it'll save your life well, okay, because the calories not a calorie. And finally, fructose and glucose. And we've already done that. Fructose makes adiposity. Because of the three things it does that the noval epigenesis, the mired reaction and the activation of the reward center. Glucose doesn't. But they're both four calories per gram. So calories in calories out, never made sense. In addition, I did work that basically showed this to me back in the 90s. I took care of these kids at St. Jude Children's Research Hospital in Memphis, Tennessee, that became massively obese after their brain tumor. So this is a form of obesity called hypothalamic obesity, because your hypothalamus is damaged. And these kids gained weight, like crazy. As soon as the tumor was diagnosed and treated, they started gaining weight at a kilo a month nonstop, ad infinitum. Now, George Bray, the father of obesity research in America, at UCLA harbor years years earlier, 1975, took eight of these kids admitted them to his Clinical Research Unit at UCLA Harbor, locked him up, throw away the key and fed them 500 calories a day for a month, what do you think their weight

went up? How do you gain weight on 500 calories a day?

Nick Jikomes 1:41:36

Well, if you're basically if we're talking about an obesogen, if they're very obesogenic calories, then that would be the answer. It's

Robert Lustig 1:41:43

because these kids made enormous amounts of insulin. These kids would rather store it than burn it. These kids had catecholamine levels at zero in their urine, because their sympathetic nervous system was in absolute zero default mode, okay, the and their insulin was driving everything they ate into fat. And the reason was because they're fat made leptin. We didn't know about leptin back then. But their fat made leptin. But the leptin didn't work at the level of the brain that brains thought they were starving because those neurons were dead.

Nick Jikomes 1:42:21

I see. So the satiety signal wasn't getting through this

Robert Lustig 1:42:24

tiny signal, and the energy sufficiency signal wasn't getting through. And therefore, these kids released enormous amounts of insulin to try to store more energy to get an energy signal through but it would never go through because those neurons were debt from the tumor or the surgery of the radiation. So it was up to me to figure out what to do to help these kids. Now, I knew from my neuro endocrine training, that there was a connection between the hypothalamus and the pancreas that ran through the dorsal motor nucleus of the vagus nerve. So I knew that there was a vagal output that was driving that insulin. And you could show that in animals very easily. And if you cut the vagus nerve, the animal stopped gaining weight, even though they had a hypothalamic lesion. So I said, Well, I can't cut a vagus nerve. I'm not a surgeon. But can I do something as good? Can I give them a drug that will suppress insulin release. So we did a pilot trial in these kids, eight kids, where we gave them a drug that suppressed insulin release called octreotide. And lo and behold, they lost weight. And most importantly, not only they lose weight, but they started exercising spontaneously.

Nick Jikomes 1:43:47

And how obese were they were they extremely obese, 300 400

Robert Lustig 1:43:49

pounds a while. And they lost weight just as fast as they were gaining it. And they would say things like, this is the first time my head hasn't been in the cloud since the tumor. And the parents would say, I've got my kid back. Because these were kids who sat on the couch ate Doritos and slept. They chose not to engage with society because they felt like crap, because they had no energy to burn. And now because we blocked their insulin, they did have energy to burn. 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 are kids who were lumps on a log. We changed their behavior because we changed their biochemistry. We got the insulin down, and they started losing weight, and they started burning energy faster.

Nick Jikomes 1:44:51

And so I guess the wider lesson there is, you know, these are kids who had, you know, tumors and you know, it required a physician to come in and fix the problem, which is to get the insulin lower. But for everyone else, our insulin is often high because of our diet. And we can take to you just that. Thank

Robert Lustig 1:45:08

you. Thank you. Exactly right. So, you know, people say, Well, you know, that was great for these kids. But what are you gonna do about everybody else? Well, everyone else has super high insulin, our insulin levels are two to four times higher than they were 50 years ago. And it's because of our diet. So if you fix our diet, you get the insulin down, and now you have it to burn. And that's why body temperature is gone down is because our insulin is high. Because if you're storing it, then you're not burning it, and therefore your body temperature goes down. So the second model is the carbohydrate insulin model. Okay, carbohydrate drives insulin, insulin drives weight gain, irrespective of total calories. So the energy balance model and the carbohydrate insulin model, they've been fighting it out. And by the way, they've been fighting it out right at Harvard Medical School. And I used to be a proponent of the carbohydrate insulin model. I was, you know, on that train as well. And the reason was because of this work I had done with the kids, because I knew that the insulin was the driver. But you know what that model doesn't explain the epigenetics. It doesn't explain the obese newborn. It doesn't explain the things that change in utero. So there was still something else that needed to be added. And so this paper that I have referred to behind Dell paper, what we've done is we've assembled all of the models that currently exist, the energy balance model, the carbohydrate insulin model, another model, a third model, which is very important called the redox model. So, oxidation reduction, so reactive oxygen species. So every cell has an energy pathway has to because you got to make ATP. Every cell has enzymes that regulate that energy pathway. And every energy pathway checkpoint is a kinase. In other words, it has to be phosphorylated. And so it is subject to reactive oxygen species, and it is also subject to pH to determine whether or not those kinases are phosphorylated to direct energy, one direction or direct energy and another direction. That turns out when you look at the data that's in the literature, okay? When cells become depleted of energy, the kinases change in order to re replete energy. And if you all if you block that, then it doesn't happen. So those and those are eat intracellular, so has nothing to do with hormones, it has to do with what's happening inside each cell. But it turns out that all the different organs have different responses. So the brain has a different response that causes more food intake and more insulin release, the liver has a response that causes more than ovulate biogenesis more fat making, okay, the pancreas has one that releases more insulin. So all of the different phenomena that occur in each of the different organs are all lined up, to promote adiposity together, or not, or the opposite or to burn the energy and not eat together. So it looks like the behaviors are all conglomerated. The gluttony and the sloth are conglomerated together, but they're actually all because of changes in Cellular Physiology that are occurring simultaneously due to the changes in these biochemical checkpoints, which are subjected to reactive oxygen species. And as long as the reactive oxygen species stay low, you can burn when they start getting high, that tells the cell it's got a store because it can't handle it. So it actually makes physiologic and teleological sense that this would be a control point. And then the obesogen model is the fourth model. And it turns out that almost all the obesogens generate reactive oxygen species.

Nick Jikomes 1:49:32

So that's when those two fit together. So well, they fit together

Robert Lustig 1:49:35

very well. And so they so the the, the redox obesogen together model, actually explained both the carbohydrate insulin model because it's driving the insulin. And that also explains the energy balance model too, because of the eating and burning. So in fact, it's really a unifying hypothesis that brings all the models together, but it actually identifies our OSS as the thing to do Target. And so now the question is, can we set up a research experiment? To answer that question, and we're in the process of doing that.

Nick Jikomes 1:50:09

I want to in the just the few minutes that we have left, I want to ask you about a striking relationship that I've heard people attempt to explain. But I'm wondering if you have a better explanation that might involve things like reactive oxygen species, mitochondria, and obesogens. And that is the striking correlation, at least in the continental US, between geography and in particular altitude, and obesity rates. Everyone looks at Colorado, which I believe has the lowest obesity rates are among the lowest and typically the default answer there is, well, you know, people move to Colorado because they love the outdoors and they go hiking a lot. Yep. What's going on? Right?

Robert Lustig 1:50:45

So everybody thinks Colorado is less obese because they have a great lifestyle. Garbage. Colorado is less obese, because it's cold and high. And every place that's cold and high has less obesity. The heat map on altitude and obesity are virtually identical. Another example is Switzerland versus Germany. Same, you know, sauce laden food, you know, you know, was it cubs cubs lace Miss Schlag? You know, but bottom line, Germany is obese, and Switzerland is not? It's not because of skin. It's because of altitude. Okay, because what sillens High in Germany's not. So what's happening? Well, because you are in a rarefied atmosphere, because you are mildly hypoxic. You have to push your mitochondria, harder to generate more ATP. Because the oxygen tension is lower. So you need more mitochondria. So in the same way, exercise generates mitochondria, which is true, it does. And I'm gonna saying it's just as bad. It's good. Okay. Altitude generates mitochondria. And exercise and altitude, well, that's great. Then then you're an alpine skier. Okay, and then that's fine. Okay, but for the rest of us mere mortals. Okay. Altitude, basically does what exercise does in terms of generating increased mitochondrial capacity. And that's why Colorado is less obese. Also, because it's colder, so you have to generate more body heat in the first place. So it's not that Colorado is not less obese. It is the question is, is the reason because of an active lifestyle? And the answer is no, it's not because of an active lifestyle is because of the geography, the altitude. Another

Nick Jikomes 1:52:47

way of saying that would be you could transport someone from somewhere else, you know, say Louisiana into Colorado, change nothing about their lifestyle, nothing about their exercise or eating habits, and you would expect them to actually lose weight. Yeah,

Robert Lustig 1:53:01

exactly. Expect them to lose weight. This concept of hypoxia reducing energy function, energy utilization, actually contributing to longevity has actually been shown in animals. So if you actually expose animals to hypoxic regimens, like instead of 20%, oxygen, 11% Oxygen, okay, they live three times longer. This is work done by colleague here at UCSF by the name of Isha Jain, you know, looking at the role of hypoxia, and longevity. And the reason is because of reduction in reactive oxygen species formation. So, you know, it's, it's all internally consistent. Ultimately, you got to make your mitochondria work better.

Nick Jikomes 1:53:49

Yeah, so much of it comes comes down to the mitochondria. I think, knowing everything I know, today, you know, if if I had to go back and go through school again, and go through the academic science track, I think I would probably study something about mitochondria, probably in the brain. Because I think that's just a fascinating area, and an important one right now, I

Robert Lustig 1:54:06

couldn't agree more and, you know, I, I've become a, you know, self taught mitochondrial adjust. And it's hard. It's, it's complex to be to be sure, but you know, the data are coming in from various, you know, directions and different places in science, demonstrating that mitochondrial function is perhaps, you know, the single most important nitrous for understanding the diseases that als you know that this is really where the, where the rubber hits the road. I refer you to a colleague at University of California, San Diego by the name of Robert NatGeo. And Avi a UX and he has done enormous work on reactive oxygen species, external ATP to the cell and the inflammatory response and how mitochondria fit into all of that. It's, you know, this is this is Shall we say, a hot topic?

Nick Jikomes 1:55:04

We've just got a couple of minutes left. So I'm gonna do a very simple question that is very practical for people. But given. So, health, and Nutrition and Metabolism, it's sort of inherently difficult area. And I don't just mean like the subject matter is complicated. But there's a lot of motivated reasoning, there's a lot of conflicting opinions, even among credentialed experts. And, you know, when you couple that to the proliferation of information that our technology has enabled, you know, you can go watch a podcast with any number of people, and there's going to be some level of mutually contradictory information out there. When it comes to when it comes to metabolic health. And, you know, the science of that general area, who are, I don't know, two or three or four names of people that are out there that are, you know, on podcasts, on the internet, writing books, or whatever, that you think are mostly right or directionally, that are worth following for people other than

Robert Lustig 1:56:01

yourself, aside from myself. So I think David Perlmutter, he's gotten a bad rap. And I think it's totally undeserved. He neurologist who wrote Grain Brain, but is totally on board with the snip notion and mitochondria being sort of the, at the at the focal point of Cellular Physiology. Rick Johnson, Richard Johnson, at University of Colorado, is also you know, totally on this and has written about the fructose and Alzheimer's and wrote a book called White nature wants us to be fat. And the last person that I would refer you to is Christopher Palmer, right there at Harvard. He's at McLean. He's a psychiatrist, and he is going to explode the field of metabolic psychiatry, there are other metabolic psychiatrists, Chobani, SETI at, at Stanford, and Georgia Eid at also at Harvard. There. So there are other people in that field, too, but Christopher's just done the most. And he's the one who has shown that basically, a ketogenic diet can reverse bipolar disorder, because it is a biochemical problem, not a behavioral one. And, you know, it's, it's, it's really quite remarkable when when you see the data and when you hear the stories, it's, it's it's so uplifting. Anything.

Nick Jikomes 1:57:27

Anything else you want to reiterate for people that we talked about, you can't

Robert Lustig 1:57:32

fix a problem if you don't know what the problem is. Okay, and we've been we've gotten the problem wrong for the last 50 years. Because we were told it was fat. Wrong. gotta fix it. But unfortunately, the food industry doesn't want to fix it. So we have a lot of work to do.

Nick Jikomes 1:57:51

All right, Robert Lustig Thank you very much for your time.

Robert Lustig 1:57:53

Oh, thank you for having me. Appreciate

Mind & Matter
Mind & Matter
Whether food, drugs or ideas, what you consume influences who you become. Learn directly from the best scientists & thinkers about how your body & mind react to what they're fed. New episodes weekly. Not medical advice.