The Dr. Hyman Show - How You've Been Lied To About Calories, Dieting, Exercise, & Losing Weight

Episode Date: March 20, 2024

View the Show Notes For This Episode Get Free Weekly Health Tips from Dr. Hyman Sign Up for Dr. Hyman’s Weekly Longevity Journal There are several different schools of thought behind obesity and metabolic dysfunction, for example, the energy balance model or “calories-in, calories-out” perspective that many people have felt fooled by. While calories certainly are one piece, there is much more to the puzzle of weight management and metabolic health, like hormonal cascades and oxidative stress. My guest today is Dr. Robert Lustig, an author and neuroendocrinologist with expertise in metabolism, obesity, and nutrition. He has dedicated his retirement from clinical medicine to help fix the food supply in any way he can, to reduce human suffering, and to promote a collective vision of metabolic health: protect the liver, feed the gut, support the brain.  In this episode we discuss: Is a calorie really just a calorie? (7:24) The surprising truth: All models of energy intake are a little right and a little wrong (9:20) Proven methods for reducing insulin to support weight loss (29:39) What are obesogens and how are they hijacking our metabolic health? (32:00) Reactive oxygen species and aging (and how to reduce them) (38:05) Why glucose and insulin monitoring are powerful levers for metabolic health (42:15) Summing up the facts and our beliefs around calories and weight (47:00) The cellular impact of oxidative stress and chronic stress (54:00) Monch Monch: a new fiber solution for absorbing simple sugars and preventing glucose spikes as well as increasing satiety and boosting microbial diversity (1:02:20) Food addiction in adults and children and addressing the root cause (1:10:45) What actions can we take based on scientific advances to make our lives better? (1:24:15) Why any food that feeds the gut, protects the liver, and supports the brain is a healthy food (1:33:35) Perfact and how to use it to understand what is metabolically healthy at your exact grocery store (1:40:20) This episode is brought to you by Rupa Health, Pendulum, ARMRA Colostrum, and Wonderfeel.  Streamline your lab orders with Rupa Health. Access more than 3,000 specialty lab tests and register for a FREE live demo at RupaHealth.com. Pendulum is offering listeners 20% off their first month’s subscription of Akkermansia for gut health. Visit PendulumLife.com and use code HYMAN. Save 15% on your first order of ARMRA Colostrum and unlock the power of 400+ functional nutrients. Just visit TryARMRA.com/Mark or use code MARK. Youngr™ NMN works by increasing your levels of NAD, a critical molecule our bodies produce that we literally need to survive. Feel the wonder of innovation at getwonderfeel.com. If you’re interested in checking out Levels, you can head over to levels.link/HYMAN to learn more and get a special offer if you decide to sign up.

Coming up on this episode of The Doctor's Pharmacy. Most everybody has this insulin resistance problem that, you know, is called metabolic syndrome. But insulin's the bad guy no matter how you look at it. There is no weight gain without insulin. You gotta get the insulin down. Bottom line is, anything that gets the insulin down ultimately leads to weight loss. Hey everyone, it's Dr. Mark. We all know that as functional medicine practitioners,

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and Access Medical Laboratories. And the best part? It's completely free. No more juggling multiple invoices or dealing with administrative headaches. Rupa Health simplifies the lab ordering process so you can get the data you need without the hassle. So sign up for free today. I love it, and I know you will too. You can find out more information by going to rupahealth.com. That's R-U-P-A health.com. Hey everyone, it's Dr. Mark. Have you ever heard of the blue zones? In short, these are areas around the globe where people tend to live the longest. Now, there are a number of characteristics people in blue zones share, many of which have to do with their gut microbiome. For instance, people in these regions have some of the highest levels of acromantia in their guts,

which is a really beneficial strain of bacteria known for strengthening and regulating the gut lining. Acromantia is also one of the most important determinants of maintaining your long-term health and metabolism. Now, it can be hard for those of us who don't live in a blue zone to get enough of this beneficial bacteria by our diets. But now, thanks to Pendulum, it's easy. They've done something nobody else could do. They're the first and only company to offer products that directly contain live acromantia mucinophilia. Right now, Pendulum is offering my listeners 20% off their first month of an acromantia subscription with the code HYMAN. Just head over to PendulumLife.com to check it out. That's P-E-N-D-U-L-U-M-L-I-F-E.com and use the code HYMAN to get 20% off. Welcome to Doctors Pharmacy.

I'm Dr. Mark Hyman and that's pharmacy with an F, a place for conversations that matter. And today's conversation is going to matter to all of you because it's about the number one thing you should all be paying attention about, which is your metabolism and how it's messed up by sugar, fructose, how our weight is controlled, how our weight is regulated. We are in a very sticky situation today in America and around the world because of the increasing rates of obesity. And we're going to be speaking today with a world expert in this. It'll help us sift through all the science and the confusion, Dr. Robert Lustig.

He's a neuroendocrinologist with expertise in metabolism, obesity, and nutrition. He's an emeritus professor of pediatrics in the Division of Endocrinology and a member of the Institute for Health Policy Studies at UCSF. He's also one of the leaders of the current anti-sugar movement that is changing the food industry. He's dedicated his retirement from clinical practice to help fix the food supply in any way he can to reduce human suffering and to salvage the environment by interacting with all the stakeholders to bring them together around a common vision for metabolic health, protect the liver, feed the gut, and support the brain. We're

getting into all that today. Dr. Lustig graduated from MIT in 1976. He received his MD from Cornell University Medical College in 1980. He also received his Master's of Studies in Law, which is amazing, at the University of California California Hastings College of Law in 2013. He is also the author of popular books called Fat Chance, The Hacking of the American Mind, and Metabolical, which is like diabolical, but your metabolism. He's the Chief Science Officer at the nonprofit Eat Real. He's on the advisory boards of the UC Davis Innovation Institute for Food and Health, the Center for Humane Technology, many other companies. He's also the chief medical officer at BioLumen Technologies, Perfect, and Kalen Health. I hope you enjoy this conversation with Dr. Lustig coming up on The Doctor's Pharmacy.

Welcome back to The Doctor's Pharmacy, Robert. It's so good to have you back. Oh, listen, you know, you and I are like Thelma and Louise. Yeah. Are we going to drive off the cliff in a convertible? We're going to do our best. You know, sometimes you have to sacrifice yourself to get to the truth.

But, you know, I think we met first as part of this film called The Fed Up. Right. We're essentially fed up with the food industry making all of our children sick and fat and killing them and needing liver transplants as teenagers and and bariatric surgery as teenagers and this movie did quite well and it oh yeah theatrical release yeah i mean you know you and i were the two talking heads you know that sort of you know but we didn't get to meet until the uh the la premiere that's right

we met at the premiere. And it was a really impactful movie for me because I realized in that scene that I was working in the movie where I was working with this family of five that lived in a trailer on food stamps and disability. The father was 42 and had dialysis from diabetes. The mother was 100 plus pounds overweight. The 16 year old kid was almost diabetic with a body composition. We did DEXA scans of 50% fat, 50% at 60 years old. And they lost 200 pounds in the first year.

The father lost 45, was able to get a new kidney. The son lost ultimately 132 pounds and went to medical school. And they- Amazing what good food will do. Well, it just taught me that people don't know the impact of all the ultra-processed food they're eating. They were trying to do the right things. And it really sort of set me to understand that it's really not that hard if people understand the biology of how their body works. Well,

the fact of the matter is they've been fed a myth. And the myth is that ultra-processed food is food. Yeah. Well, it was interesting because they had all this stuff in their kitchen that they thought was low-fat, diet this, healthy that. And it was all processed junk that had high sugar, even the Cool Whip, which they thought was a healthy dessert topping, said zero trans fat on the label. And in the container, if you read the ingredient list, forget the front of the package labeling, which is so misleading. I always say if it has a health claim on the label, it's dangerous for you, like gluten-free potato chips.

And it said zero trans fat, but it was only because it's mostly air and the FDA, through a loophole that the food industry forced them to do, because they basically have captured these agencies, said if it's less than half a gram per serving of trans fat, you don't have to say trans fat. But when you read the ingredients, it was high fructose corn syrup and partially hydrogenated soybean oil. That was it. And I was like, whoa.

So it was so powerful. And it kind of made me realize that we really have a problem of awareness and education and how our bodies work. And so your work has been so important because it unpacks the biology of how food interacts with our hormones, our gut microbiome, our immune system, our metabolism in ways that it's really information. So food food instructions. And there's a huge debate out there, which drives me crazy, which is this debate that

I want to get into today around the idea of, is a calorie a calorie? Because this is what we've been taught. And I'm just going to set this up and I'm going to let you roll. So I'm going to set this up and let you roll because I know you can roll for hours. The whole debate is, is a calorie a calorie? And is weight loss just about eating less and exercising more? Which has an implicit bias toward blaming the person for not exercising more and eating enough. So it blames the victim, in my view.

It doesn't understand the real root causes. It's great for the food industry because it's like, oh, it doesn't matter what calories you eat. It could be a Coca-Cola calorie or a Twinkie calorie, and it's the same as a broccoli calorie, as long as you don't go over your calorie count. And then there's the other extreme of the model, which is the carbohydrate insulin hypothesis, which essentially states that it's not what you eat, it's not how much you eat, it's what you eat, and that the quality of the calories matter, and that different macronutrients has different effects on your body, on your hormones, and your metabolism, and your gut microbiome,

and your immune system, all of which impact your weight. And there's other schools of thought around obesogens, which are environmental toxins that screw up your biochemistry and make you gain weight, and there's oxidative stress theories. There's a lot of theories out there. And, you know, we, you know, it's on nutrition is one of those really, you know, poor black sheep of the family in medicine

where it doesn't get funding for real research. And we need to be studying these things. But we do know enough, I think. And you and my friend David Ludwig have really helped us understand a lot about the role of sugar and fructose and how carbohydrates, refined carbohydrates affect our metabolism. So can you help us kind of navigate this whole story and tell us, you know, lay out, you know, the insulin hypothesis versus the energy balance

hypothesis versus the obesogen hypothesis and how they all interconnect and and are they all sort of right they are all sort of all sort of right and they're all sort of wrong and they're all sort of wrong so help us understand what you know whether we should be just do calorie counting or we should just be focusing on quality or we should be detoxing our bodies or we should be like i don't know what so tell us because we're all lost the short answer is they're all right and they're all wrong all together last month uh a group of four authors of which i was one the first author is hindel jerry hindel who was the head of the environmental endocrine disruptors uh group at the National Institute of Environmental Health Sciences. And myself and Tara Howard, who runs HEADS, which is Healthy Environment Endocrine Disruptors. And also Barbara Corky, who is the named professor at Boston U, won the Banting Award for the American Diabetes Association.

So not exactly lightweights. We came out with a paper in International Journal of Obesity, which we're very proud of. And it's called Obesogens, a Unifying Hypothesis for the Pathogenesis of Obesity. Now, how does this work? There are four prevailing models right now on weight gain and how it works. You've mentioned all four, but let's put some meat on those bones. Energy balance, calories. You eat too much, you exercise too little. And there is absolutely no question that people who

are obese have been shown to eat more and exercise less. And I don't argue that. The question is, is that cause or effect? Right, right. Okay. Is it a causative phenomenon? Is it a resultative phenomenon? Or is it an epiphenomenon? Okay. And they can't tell us which.

So keep that in mind. There's nobody in the energy balance model camp who can actually say that that's the reason for weight gain. All right. Could it be the cause? Could it be the result? So keep that in mind. Now, there is no question we are eating more as a society. Okay. 175 calories per day, more for adult men, 335 calories per day, more for adult women. Yeah. 275 calories per day, for adult women, 275 calories per day more for teen boys. Okay. Everyone's eating more. And I just want to make a point on this before you dive into that.

Yes, we're eating more calories per person. But if you look at the data from 2000, and this is from the NHANES data, the National Health Nutrition Examination Survey, which is a national survey of tens and tens, 100,000 people. And what they found was from 2000 until now, calorie counts have gone down as obesity rates have gone up, which is kind of a paradox that's hard to explain with the energy balance hypothesis. Well, in fact, the food industry actually argues that sugar consumption has gone down as obesity rates have gone up in that same 20-year period. So they say, well, it can't be the calories and it can't be the sugar.

Well, wait a second. It depends how you define sugar. There are a lot of- If it's cane sugar, yeah, maybe, but that's some other reasons. There are a lot of whys and wherefores to that. And we'll get there. Now, all of that is true. In addition, people say, well, we're exercising less. And we are exercising less, except not in the last 20 years. In fact, the exercise rates have actually stabilized out. Yeah, it's crazy.

I see like gyms on every corner, Orange Theory, Solid Core, all these businesses popping up. That doesn't really work because you don't know what they're doing in those gyms. They're paying their money in for initiation, and then you don't know if they're actually being used. So gym memberships does not equate into energy expenditure. And remember, there are three kinds of energy expenditure. There's a resting energy expenditure, just living, which is 65% of energy expenditure. There's a resting energy expenditure, you know, just living, which is 65% of energy burning. There is the thermic effect of food, which is 10% of energy burning. That is just the metabolism of food itself that, you know, generates heat.

Yeah, it takes work to digest your food. It takes work to digest food. So energy, yeah. And that gives you body heat. And then finally, there's voluntary energy expenditure, which runs between 25% and 35% of total energy expenditure. So if energy expenditure is going down, which it's not, but if it was going down, which of those three buckets actually explain it?

Well, in fact, none of them do. So there are a whole bunch of issues with regards the energy balance model to start with. In addition, it doesn't explain why when people lose weight, they plateau. Because if they eat less and they lose weight, you'd expect them to continue to lose weight, but they don't. They plateau. And of course, that gets everybody crazy. And then they say, oh, I'm a failure. And then they go eat the Ben and Jerry's, you know, and it's all over. And they've, you know, yo-yoed back up to where they belong in the first place, right? So if energy balance were the only issue okay it that would that phenomenon would not occur so there are a whole bunch of things wrong with energy balance in addition energy balance does

not explain why we have newborn obesity yeah why little kids come out why babies come out obese now four separate studies one in israel one in south Africa, one in Russia, one in the United States. Over the last 25 years, newborns weigh 200 grams more than they did 25 years ago. And when you stick them in DEXA scanners to figure out what the 200 grams is, it's all fat. Almost half a pound of what you're saying. Half a pound of extra fat. Wow. Before they even had a chance to eat mother's milk, never mind Ben and Jerry's.

Right. Okay. So whatever phenomenon, whatever model you want to proffer to me about what the cause of obesity is, you have to explain that. Yeah. And you can't. Not with the energy balance model. It's right. And I think just to kind with the energy balance model. That's right. And I think just to kind of double down on this, calories do matter, obviously.

But it's really about the quality of those calories and what they do to your body. You always have this saying that a calorie burned is a calorie burned, but a calorie eaten is not a calorie eaten. Exactly. I've heard you say that 100 times. And what that means is when you eat food, it interacts with your microbiome, it interacts with your immune system, it interacts with your hormones. So it's not the same. And when people say it's all about calories, then I say, well, how do you explain the fact that a type one

diabetic can eat 10,000 calories a day and lose weight at the same time because they have no insulin. Because they have no insulin. And so that's where the second model comes in, the carbohydrate insulin model. Now, I will tell you, until about two years ago, three years ago, I was a proponent of the carbohydrate insulin model because I had done research in it myself. So this is a model that has been particularly proffered by David Ludwig, and, you know, appropriately so. And I was a support of it. Basically, he does what I do, except at Boston Schultz.

And he's one of the few people who do randomized clinical trials. Yeah, absolutely. He does the most rigorous kind of research, not just population data. He does it on humans, and it's a lot of money, but he does it. Perspective clinical trials done with appropriate controls. David's a top-notch scientist. I have zero,

zero concerns about his accuracy, the quality, or the veracity of his data or of his thinking. He's solid. Yeah, absolutely. Okay, across the board. And he's a friend. You know, full disclosure. Me too, yeah. He's a. Yeah, absolutely. Okay, across the board. And he's a friend, full disclosure. Me too, yeah. He's a good friend, yeah. All right. Now, I was a proponent of that

model too. And the reason that I was a proponent of that model was because I did a similar experiment when I worked at St. Jude Children's Research Hospital in Memphis, Tennessee. So you're probably familiar with this phenomenon called hypothalamic obesity. So these are kids, for the most part, adults too, but mostly kids who get tumors of the posterior fossa, the hypothalamus mostly, and they require surgery, they require radiation. They end up with hypothalamic damage, and now they can't see their

leptin. So leptin is a hormone that your fat cells make that feeds back on the brain and tells your brain, hey, I've eaten enough, I don't need to eat anymore, and I can burn energy at a normal rate because I have enough energy stored in the body. Okay. So it's a servomechanism, just like the thermostat on your house. Okay. So leptin is basically telling you the heat's high enough. Okay. We don't need any more heat. So you don't have to eat anymore. Okay. Well, these kids lost their ability to see their leptin because those neurons were dead. And so, number one, they ate like crazy. And number two, their energy expenditure was in the sewer. And the catecholamine levels in their urine were zero

because their sympathetic nervous system was basically shut down because they're trying to conserve. Because the sympathetic nervous system is what innervates the muscles to work. The sympathetic nervous system is what innervates the fat cells to give up their fat. Yeah. Okay. So they can't give up their fat and they can't burn. So they're eating like crazy and they're burning like zero.

Right. Okay. And so they're gaining weight out of sight, 30 pounds, 40 pounds a year ad infinitum, and there's nothing that anyone could do about it. Yeah, like the governor is off. Like the thing that tells you, oh, I'm full is just off. Yeah, the thermostat's broken. Right. So I inherited a cadre of about 40 of these kids at St. Jude who had survived their brain tumors but became massively obese because of the therapy. And the parents would scream at me, this is double jeopardy. My kids survived the tumor

only to succumb to the therapy. And that was unfair to say the least. And it was up to me to do something about it. Now, as a neuroendocrinologist, I did know that there was this literature, okay, about something called the VMH lesioned rat, the ventromedial hypothalamus lesioned rat. So you put an electrode in the hypothalamus, you go, and those animals become massively obese also. But what was interesting was you could cut the vagus nerve, the nerve that connected the brain to the pancreas, and then they wouldn't. So we assumed at that point in time, this was 1995 now, so almost 30 years ago. Dark ages. Dark ages, yeah. The days of the giants. Remember them? I was there. I graduated medical school in 87. So yeah, I was there.

So we assumed that these kids couldn't see their leptin, so their brains thought they were starving. So their sympathetic nervous system was in the sewer and their vagus nerve was telling their pancreas to release more insulin in order to drive whatever they did eat into fat to raise the leptin but they still couldn't see it because the body thought it was starving because the body and even though there was plenty of food without leptin saying stop the body's like I'm hungry so all the store fat let's get everything stored because I don't know what I'm gonna get my next meal exactly and insulin is that fast storage hormone

and right so exactly so insulin was the business end of the equation. So I'm not a neurosurgeon, I can't cut a vagus nerve, but could I do something similar? So we gave them a drug that suppressed beta cell insulin release. So that drug is called octreotide. It happens to be used usually for acromegaly, for growth hormones to create tumors. But we repurposed it because it also suppresses pancreatic insulin release. Because there are somatostatin receptors on the pancreas, on the beta cell. And we gave these patients octreotide. And lo and behold, they lost weight.

But something even more remarkable occurred. They started exercising spontaneously. Yeah, yeah. One kid became a competitive swimmer. Two kids started lifting weights at home. One kid became the manager of his high school basketball team. These were kids who sat on the couch, ate Doritos, and slept. They had lost all touch with the world around them because they felt awful.

They felt like crap all the time. And all of a sudden, they woke up and the parents would, like within a week, they would say, before there's any weight loss, they say, I got my kid back. And the kids were active

and they were saying, this is the first time my head hasn't been in the clouds since the tumor. So what did that teach you? So we did a double-blind placebo-controlled trial, proved it again, then what we did was we did a study in adults.

Taking this trial, taking the drug, and then blocking the effect. Blocking the effect of insulin. So then we asked the question, are there adults without brain tumors who might manifest the same problem? That is leptin resistance, not being able to see their leptin, high insulin release, driving their weight gain and driving their sloth.

And by the way, with leptin resistance, just like insulin resistance, you see high levels of leptin in the blood so you can measure it. Dr. Oh yeah, super high because their fat was so large levels of leptin in the blood so you can measure it. Oh, yeah, super high. Yeah, yeah. Because their fat was so large that their leptins were in the stratosphere. Yeah, and the company I co-founded, Function Health, where people can ask their labs, their basic lab panel includes leptin, insulin, and adiponectin, three things you need to know that are really important

for understanding insulin and carbohydrate metabolism. Without question. Yeah. Explain that to the American Diabetes Association. I know. So we said, are there adults who might have the same pathophysiology, that is leptin resistance, insulin release, driving their weight gain? And if we gave them octreotide, would they lose weight? And sure enough, they did. Not every patient, only 20% of the total, eight out of 44. But what was interesting about the eight was that their insulin response to glucose was markedly different from the patients who did not respond, number one. Yeah. Meaning they had higher levels of insulin, they had higher spiking levels after eating sugar. Right. Yeah. And what we did in that study was we measured resting energy expenditure with a metabolic

cart. Yeah. Before and six months. Your basic metabolic rate, your basal metabolic rate. And what we saw was that the patients who lost the weight, the responders who had the high insulin response, their energy expenditure did not go down, even though they lost weight. You expect it to go down because once you lose weight, you conserve. Their energy expenditure went up. Really? Because we got the insulin down. So there is a subset of patients with obesity that are just like these kids. And so insulin is a linchpin in driving weight gain in everyone,

but not everybody has this insulin release problem that the kids did. Most everybody has this insulin resistance problem that is called metabolic syndrome. To some degree or another. Some degree or another. And what is it? But insulin's the bad guy no matter how you look at it. There is no weight gain without insulin.

You got to get the insulin down. And so once I learned this, I changed my clinic practice completely. And instead of being a weight loss program, it was an insulin reduction program. Yes. Get the insulin down any way you can. And I have been trying to promulgate this as a modality, as a model for other obesity programs. And only my former fellows do it that way. It's been remarkable. We've been doing this for an ultra wellness center for 25 years.

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G-E-T-W-O-N-D-E-R-F-E-E-L.com. It's more than wonderful. It's Wonderfeel. And now let's get back to this week's episode of The Doctor's Pharmacy. I just want to sort of highlight this point because just to go back to this diabetes, type 1 diabetes, if you have no insulin like a type 1 diabetic, you can eat 10,000 calories and you'll lose weight. Absolutely. But if you eat very little and you have high insulin, you're going to store all that fat. Exactly. And I had a patient once that just was one of those teaching patients. You know how you think you learn medical school and you learn shit? No, it's actually the patients that teach you. Of course. And this patient, she looked like an apple. She had a big round belly. I was convinced she was going to have a high blood sugar, high A1C. She was going to be having diabetes.

Checked her blood sugar. It was perfect. So I said, let's do a glucose tolerance test, but measure insulin also. Right. Fasting and after one hour and two hours. Her blood sugar never changed. Like it was at 90 and then it went to like 110 and then 105 in two hours. It was like perfect blood sugar. You never would have thought she had any issues. And that's what doctors do, but they don't measure insulin.

Insulin, right. Her insulin fasting was like, I think 50 and it went up to two or 300. Two or 300? Two or 300. My kids went up to 1,200. Oh, yeah. I never saw that. Well, you're a pediatric endocrinologist.

You're a pediatric endocrinologist. You see the worst of the worst. But I was like, oh, wow. Okay. Insulin is the problem here for her. She's spiking so much insulin she can't lose weight, and she's storing all around her belly. Bottom line is anything that gets the insulin down ultimately leads to weight loss. And there are different ways to be able to do that.

Obviously, caloric restriction will get insulin down. Carbohydrate restriction will get insulin down. The ketogenic diet, which is the extreme of carbohydrate restriction, will get insulin down. Metformin will get insulin down. And all of those are clear. Having lots of fiber. Metformin will get insulin down. And all of those are clear, you know. Having lots of fiber. Yeah, high fiber diet will get insulin down.

Thank you. Exactly right. All of these are modalities that basically impact insulin response, the insulin kinetics. And so there is absolutely no doubt that insulin is the linchpin in weight gain. So the carbohydrate insulin model that David helped promulgate and which I subscribed to because of the work I had done, I was in that camp until about two to three years ago. Ah, okay. Interesting. When I learned a little more.

Yeah. Okay, that's why you do see me. The thing about everything is that we polarize everything. And there's truth in everything. Like, it's not one thing. And in functional medicine, we understand the network effect in biology. It's basically an ecosystem, a set of biological networks that all interplay with each other. And there are many variables that can create the same outcome, right?

Agreed. So the bottom line is if you think it's a nutritional issue, you'll stick with nutrition. If you think it's an endocrinologic issue, you'll stick with the endocrinology. If you think it's a GI issue, you'll stick with the GI. We have siloed medicine so severely. The fact is, this is a systems biology issue.

Yeah, exactly. I mean, you can do a fecal transplant and make someone less insulin resistant by changing their microbiome. Exactly. So if you just do a poop transplant, you can lose weight and improve your diabetes. Well, how does that make sense, even not changing your diet? It's because there's so many variables, right? Well, and because there are so many different nodes, because energy is so integral to survival of the species that there's redundancy built into the system. That's right.

You don't make energy, you're dead in a couple minutes. That's what cyanide does. Yeah, about four. Right. Exactly. Exactly. All right. And why?

Because it affects the mitochondria. So we're going to go back to the mitochondria again and again and again. That's your little energy factory, right? Because that's our systems biology 101 for today is the mitochondria. You're going to hear this a lot, people. All right. So about three years ago, Jerry Heindel put together a meeting on environmental obesogens. I've done some of this work as well because I worked along with my colleagues at UC Berkeley on a study called the Chamaco study, which is the children and

mothers of the Salinas Valley. Farm workers. I know about this. I wrote about it in my book. And these kids, you know, these were the offspring of mothers who were exposed to high doses of pesticides through their pregnancy. And so they measured the, you know, pesticides in the pregnant mother's urine and then watched the outcome of the babies after the babies as they grew up.

So, you know, and we looked at several different phenomena. We looked at growth. We looked at reproductive capacity. We looked at neurologic. IQ. I mean, there were 41 million IQ points lost in that cohort. That was striking to me. And of course, we looked at puberty.

We looked at obesity. And so we know that pregnant mothers' DDE levels, which is a metabolite of DDT, which hasn't been around since 1972. But it's still everywhere. It's still everywhere. It's a forever chemical. Predicted obesity in their five-year-olds. Mm-hmm, mm-hmm.

So this clearly means that there's something going on even before birth. Like, for instance, those newborn obese kids we just talked about. So trying to understand how obesogens, that is environmental factors that can lead to weight gain, what might be the reason for that? Well, we wrote three papers back in

2022 about this, 44 authors. I was lead author on one of the three papers. And there are a lot of different ways that you can make a fat cell. Estrogen will make a fat cell. Androgen will make a fat cell. PPR-GAM will make a fat cell. The aryl hydrocarbon receptor will make a fat cell. You mean make a fat cell bigger or make a new fat cell? Both. You know, different ones at different times. And there are windows of critical periods. So the question is, does the energy balance model explain this?

No. Does the carbohydrate insulin model explain this? No. No. So clearly, we needed some more. Yeah. And so the question is what ties all of this together? In walks Barbara Corky, who has done a lot of this work. And she had done work on reactive oxygen species, both in the dish and in the animal.

And it turns out reactive oxygen species, which are things you can't get away from if you're alive, you've got ROSs, okay? Because mitochondria make ROSs. It's a part of normal biology. It's out of control, like anything, like your blood pressure, your blood sugar, or whatever. It's normal, but you don't want it too much. ROSs change the phosphorylation status

of the enzymes in the cell. In English, please. Every cell in its lifetime has to grow or burn. Make energy. Utilize energy. Yeah. Okay. But not both.

They do one or the other. And there's an energy metabolism pathway in every cell to teach that cell whether it's going to burn or grow. And there are three enzymes. One is PI3 kinase, phosphatidyl inositol 3 kinase. This is the enzyme that Lou Cantley, first at Harvard and then Cornell, found is basically predictive of cancer, right? Because what it does is it opens the spigot for glucose to enter the cell in high concentration. The second one is AMP kinase. That is the fuel gauge on the liver cell, on pretty much every cell. That's regulated by metformin, which is a drug used for diabetes, yeah.

Exactly, and so what it does is it tells the cell to make more mitochondria because the cell- Energy is low. When energy is low, that goes up. I call that one of the longevity switches. It's part of our hallmarks of aging, yeah. Correct, and then finally, the third enzyme is mTOR, mammalian target of rapamycin.

That's a kinase also. All three of these are kinases. Again, I call that one of the longevity switches, which makes protein and it's good, butian target of rapamycin. That's a kinase also. All three of these are kinases. Again, I call that one of the longevity switches, which makes protein and it's good, but it can also be overdone. Well, it tells the cell to divide. Yeah. Okay. It's the division signal. So if you're dividing, you're growing. Okay. But if you're burning, you're not growing. Yeah. Okay. You're doing one or the other. No cell does both at the same time. So there is two pathways and the switches are these three enzymes. Well, these three enzymes are kinases, which means their phosphorylation status dictates whether they're on or off. That's just a chemical reaction that kind of regulates whether

they're working or not working, right? That's right. And guess what makes that phosphorylation occur? Reactive oxygen species. So we started looking with Barbara at the question of whether or not all of the things that we know cause weight gain, whether it be inflammatory things like, for instance, air pollution, which has been associated with weight gain, or environmental obesogens like phthalates or BPA and parabens, whether they generate- All the petrochemical things that are everywhere from pesticides to plastics and everything in between. And whether they cause reactive oxygen species to drive the weight gain.

And Bruce Blumberg at UC Irvine has shown that tributyl 10 is a great model for this because not only does it cause reactive oxygen species, but it changes the genome, the epigenome, I should say, so that it carries forward for at least four generations because of reactive oxygen species. and then we looked at the diet. And sure enough, everything in our Western diet generates more reactive oxygen species. Just the inflammatory processed food in general. Exactly. Not necessarily containing toxins, but just pulverized science-like, science food projects. As soon as you generate more ROSs than you can quench, you know, and antioxidants are the quencher.

Yeah, so ROS is a reactive oxygen. It's basically like rusting. So we talk about it as like when you get wrinkles on your face or car rust. Or cataracts. Cataracts. That's going on in your body inside, not just outside. And that's normal, but if you have too much of it, it causes damage to your cells. Faster.

You die faster. Yeah. Basically, it is the aging reaction sped up yeah okay and it turns out ultra processed food does all of that and so the question is can we use this paradigm of reactive oxygen species generation and lack of quenching as the model for being able to actually do something about obesity and we are now in the process of designing the study you know to do that yeah so it's interesting you know uh robert in 2007 i wrote an article it was titled systems biology toxins obesity and functional medicine I literally wrote, and that was like almost 20 years ago,

writing about my observations that there were certain patients that were struggling with weight that weren't because of what they were eating or not exercising. There was something else. I had one woman, she was a fitness trainer. She ate perfectly and she couldn't lose the 40 pounds that were hanging on her body. I'm like, geez, you know, I don't know,

but I think there's some data that shows that environmental toxins may be an issue. Why don't we check? Well, we can check. We checked heavy metal and she had high mercury. And we got the mercury out of her system. We detoxified her. She lost 40 pounds like that.

And her blood pressure probably came back down to normal. And I started looking at the data and there was data on how environmental toxins are interfering with every cellular process, including metabolism and drive insulin resistance and also affect thyroid. And one of the interesting things is people lose weight. You mentioned the plateau. But when you lose weight, where are the toxins stored? They're stored in your fat tissue.

So they get released and then they start to interrupt your metabolism. So they interrupt the conversion of T4 to T3, which is the active thyroid hormone, which is your metabolic rate. So it's sort of the science then was in its infancy, but I saw it. And I actually had a chapter in my book in 2005 called Love Your Liver and Ultrametallism to kind of help people understand that detoxification and getting rid of these chemicals from their environment and lifestyle and also from their bodies by a scientific detoxification approach really works.

So there are a whole bunch of different things that we are exposed to that affect different aspects of our energy burning pathway. The one that we are now most interested in and most concerned about is the mitochondria because after all that's where ATP generation occurs. That's where your metabolism is essentially isn't your mitochondria right? Right so we can talk about environmental obesogens we can talk about food or we can talk about stress. Yeah. That turns

out stress does it too. Yeah for sure. So pretty much everything that drives weight gain, drives these chronic metabolic diseases, can be basically bundled into one of these three bins. The food, the environmental exposures, or the stress. None of this has anything to do with genetics. Right. And I would say the calorie quality and the amount matter. So it's not like it's an either or. You need to pay attention to it.

Well, yeah, of course. Because calorie amount means more ROSs. Yeah. So it's not that. And actually, I noticed this one thing. I just interrupted because I'm just thinking all these things. But I had this meal in Martha's Vineyard once in the summer with a friend. And we ordered from this like organic, regenerative thing.

We ordered so much food, and it was so delicious. And both of us are basically fit, healthy guys who have no metabolic issues, and we ate an enormous amount of food, of healthy food, and we had our continuous glucose monitors on, and we called each other at 10 o'clock, and I'm like, hey, Michael, what is going on? Your blood sugar high. Yeah, my blood sugar's high.

So it was like my blood sugar went to like 150 because it was the amount of food also had this effect. Well, of course. I mean, there's no question you can overwhelm your body's ability to handle or to clear glucose. And so that brings us to the question of should we be monitoring this phenomenon, glucose and insulin. So I believe that insulin is the bad guy. I wish that we had a method for monitoring insulin monitoring. When are we getting that? I've been asking that for 20 years. Five years.

Five years? Five years. Serious? Like a patch? Five years. That's going gonna be a game changer because glucose is sort of fine but it's the last thing to go up it's coming yeah okay everybody's interested and everybody knows that's where the action is going to be

but we don't have insulin right now but we do have glucose but you can measure your blood test for insulin yeah fasting and you can also do postprandial insulins if you know how and if your doctor actually understands what they're doing. And if you can find a lab that will actually stick you for glucose and insulin and send all of them. For the most part, the insurance company won't pay for that. But it's not that expensive. And I've been doing it for 25 years. So you can get it done easily.

I did oral glucose tolerance tests with simultaneous insulin levels on all of my obese patients. That's how I, you know, came to the realization insulin was the bad guy. Yeah, me too. Me too. Exactly right. So, you know, when is the rest of medicine going to wake up? You know, when we have the continuous insulin monitor, that's when. Yes. But it's coming. It's just not here yet. Point is, we can use glucose as a proxy for insulin. Now, glucose is bad by itself because high glucose leads to endothelial dysfunction. It changes the cells inside your arteries.

It's one of the reasons for high blood pressure. It's one of the reasons, you know, and also generates uric acid, which also increases blood pressure. And, you know, there's neuropathy, nephropathy, retinopathy, all small vessel disease related to severe fluctuations in glucose. So glucose is a bad guy in the story, but there are two worse guys in the story. One of them is insulin, and the other one is fructose which is not measured

in the serum glucose it's a different phenomenon you can measure like we used to measure fructosamine yeah but fructosamine is a measure of glucose it's not a measure of fructose I wish it were true I would be measuring it on everybody but it's not true

I wish it were so anyway bottom line is there are other things to know other than glucose. Yeah. Glucose is, in my estimation, about 10% of the equation on metabolic health. Okay. Interesting. But that's the 10% we have now. And we can glean the information on both insulin release, which is its own problem phenomenon, and insulin

resistance, which is its own problem phenomenon, and be able to figure out which is which, and then be able to address our therapies to the appropriate pathology by understanding what's going on with glucose. So I am for continuous glucose monitoring, even in non-diabetics. And of course that's one reason why both you and I, full disclosure, are advisors to companies called Levels Health. And that's exactly what they do. And I have to say that we have data that shows that exercise affects that glucose response, that we have data that shows sleep affects that glucose response, that we have data that shows sleep affects

that glucose response in non-diabetics, in normal weight people. And we also have data that shows that if you know your glucose, you lose weight. Yeah, yeah, it's a feedback mechanism. It is. It's like a little shock. I'm like, oh, my blood sugar's high when I ate that,

whatever, cookie, I'm not gonna eat that again so so there are there's data to be had that we can access today is it perfect no of course not do we need more information absolutely but you know to to you know ignore this possibility i think is, is not serving our patients properly. I will tell you, I recently, just within the last week, had dinner with two of my former trainees, and they didn't know a thing about this. I mean, they're pediatric endocrinologists. Yeah. And they didn't know a thing about this.

Tell me about my daughter's third year medical student, Rachel. Learned about insulin resistance? Not really. So there is this big hole. About nutrition? Nope, no, no, no medical school. Yeah, there's a big hole in medical education. And the reason, I think, is because, you know,

what we learn in medical school, and we've talked about this, you know, there's a pill for that. Yeah. Well, there is no pill for this. That's what we've learned. There is no pill for chronic metabolic disease. Well, was is no pill for this. That's what we've learned. There is no pill for chronic metabolic disease. Well, ozempic? No. Okay. Let me just unpack what you said because

it's so important. I want to make sure people got all the things we talked about. So there's basically three to four hypotheses that are needed to explain all the facts. So science is designed to try to explain the facts that are observed. However, a lot of times in science, we misinterpret the facts and we create meaning in ways that actually aren't true. For example, I'm reading this book called Rethinking Diabetes by our friend Gary Taubes. It's this fascinating history of diabetes. And he talks about how in the early days with type 1 diabetics, you had to give them a high fat keto diet or they would die.

So Elliot Joslin knew this. Joslin, right. Glucose is of no use to the body. That's a direct quote from Elliot Joslin before he knew what insulin was. Right, right. In 1893. Right, right.

He said this, right. And Fred Allen, who took over for Joslin in 1919, published a treatise basically saying the way to treat type 1 diabetics was a 70% fat, 8% carbohydrate diet. So they said that, but then what happened was years later when they started getting insulin, they saw that all these people were dying of premature heart disease and atherosclerosis. So they made the observation that the fat in the arteries was happening in these patients

and they hypothesized based on that set of facts that it was the high fat diet that they ate when they were younger that caused clogged arteries. They just misinterpreted those facts. So why I brought that up is we have to agree that we have a whole set of facts that don't meet all the theories. So we need multiple theories to actually understand it. So is the energy hypothesis wrong? Not completely. Is the carbohydrate insulin model wrong? No, it's actually mostly right, but this doesn't explain everything. Is the obesogen model the entire

story? No, not exactly. Because like stress plays a role. For example, stress, I found out when I was researching one of my books that your vagus nerve and your sympathetic nervous system innervates every one of your fat cells. That's right. So when you're stressed, it literally sends a nervous signal to your fat cells to say, stop burning calories. So these are the four things we talked about that all play a role and have to be encountered. And you have to personalize the approach to each person. It's not like, oh, this is going to work for this person, that doesn't work for that person. There is no one

size fits all. So to that point, and I'm glad you brought that up, you know, people think that the sympathetic nervous system results in lipolysis because you exercise- That's burning fat. Burn fat, right? And that is true in the acute situation. In the acute situation, you release norepinephrine from your sympathetic nervous system. The norepinephrine via the intermedial lateral cell column and the peripheral sympathetic nerves go to each fat cell, bind to the beta-3 adrenergic receptor, activate hormone-sensitive lipase, ultimately leads to dissolution of the triacylglycerol into free fatty acids and glycerol, which then

circulate back in the bloodstream to the liver, which then turns them into ketones for the rest of the body to use. That's lipolysis. And that's what acute sympathetic nervous system activation via exercise does. Acute. And by the way, everybody should know that insulin blocks lipolysis. So basically insulin prevents the fat breakdown. So as long as your insulin is high, it's hard to lose weight. Yeah, that's exactly right. Insulin blocks your ability to be able to lose weight. That's why getting insulin down is job one. Yeah. For just that reason. Exactly right. Now, here's the problem with that. Yeah. yeah chronic activation of the sympathetic nervous system

does the opposite now how come so every sympathetic neuron in your body whether it's in your in your spinal cord or in your brain doesn't matter releases norepinephrine, but also releases a neuropeptide called neuropeptide Y, NPY. They are co-released. It turns out NPY binds to its receptor. In the case of the fat cell, it's the Y2 receptor. And what it does is it shuts off that hormone-sensitive lipase. So the lack of insulin and the sympathetic nervous system, now instead of generating lipolysis, you are actually generating lipogenesis.

You mean you build fat instead of burn fat. Yes, exactly. And so chronic stress because- I'm sorry, I'm the, you know how Obama had his anger translator? I'm the Robert Lustig translator. Absolutely. The point is chronic stress does the opposite. And we all know that chronic stress is the bad guy in the story. Acute stress is, for the most part, adaptive. But chronic stress is clearly maladaptive. And it's not just because when you're stressed, you eat that pint of Ben and Jerry's. It's another mechanism, right? It's another mechanism. If you eat that pint of Ben and Jerry's on top of it,

it makes it even worse. but it's, yeah. Well, the pine and ben and jerrys is because of what's happening at the amygdala. In the brain. At the fear center of the brain, okay? Because dopamine is one of the ways to basically put, you know, placate that amygdala, you know, at least short term, you know?

And so that's, you know, what stress eating's about. And, you know, I'm, you know-carrying member of the stress eating club. Yeah, me too. Until I did the research and understood it better, and now I'm a whole lot more appropriate. I know last night I was really tired. I had a very stressful weekend, and I flew from New York to LA, and I was really— You looked pretty good.

I was really tired, and I went shopping, and I was really hungry. I went shopping at Air One, and literally this voice in my head was, buy the ice cream, buy the ice cream, buy the ice cream, and I literally had to override that, because I knew if I brought it home, I would eat the whole thing. Of course. Right? But I was able to manage. My higher self kind of kicked in and told that guy to shut the F up. And I was able to sort of manage the store.

It was very tough, but I got out of the store safe and didn't bring it home. But I would have eaten it, even though I know everything I know. I've written 19 books about this. It's not something you can willfully control. Right. So the bottom line is we have to, number one, get the insulin down and number two, we have to get the amygdala working properly. Those are our two most important things. Now, how do you get the insulin down? Well, number one, don't let it go up.

Well, but can I just interrupt for a sec? Because you're basically laying out these different hypotheses, but I hear you going back to insulin. Are you leaning more towards the carbohydrate-insulin hypothesis? Well, I'm leaning more to the ROS hypothesis. So the question is, what does ROS do to your beta cell? Turns out it makes more insulin release. ROSs in the beta cell actually generate a bigger insulin response. So basically oxidative stress from anything, environmental toxins, sugar, ultra-processed

food, our microbiome being messed up. Chronic stress. Chronic stress. All these variables have to be looked at. So it's not just a... I mean, obesity is not an ozempic deficiency, is it? And we'll talk about that in a minute. That's right.

The point is everybody who's got metabolic disease, which is 93% of America, has a problem with one or more of the five things you just mentioned. That's staggering, Robert. 93% of Americans have some degree of this problem, even though 75% are overweight. So you don't have to be overweight to have this problem. You can be what we call skinny fat or metabolic, obese, normal weight, or, you know, toffee, thin on the outside, fat on the inside. And what we know is that those patients have liver fat. So just because you don't have

subcutaneous fat doesn't mean you don't have liver fat. So just because you're healthy doesn't mean you're well. And just because you're fat doesn't mean you're well, and just because you're fat doesn't mean you're sick. The overlap is huge. So this is a problem for everybody. And so the question is, what do you do about it? How do you figure it out? Are you at risk? Does your doctor know it? Will they help you? And if not, how are you going to figure it out for yourself? Well, that's what you and I are doing this friggin podcast for her yes it's to try to help people understand that yeah exactly right okay point is insulin is one of the drivers promote metabolism get insulin down the other one is suppress inflammation because inflammation drives

insulin resistance. From anything, an infection. Viruses have been linked to obesity, right? Absolutely, adenovirus 36, for one, and others too, but mostly AD36. Point is, inflammation drives ROSs, because inflammation drives NADPH oxidase at the level of the liver driving those RSS

that's that's what our NADPH oxidase makes yeah as our OS's okay now there's part of your mitochondrial processing of the food you eat and oxygen you breathe in it sort of has these little pathways and when it goes kind of awry it's like going on the wrong pinball thing and it goes doesn't go where you want it to go exactly it ends up causing more damage exactly right our OS's have to be quenched. Now, the quenching occurs in the paroxysm, and that's where the antioxidants live. So in the liver, it's glutathione or maybe vitamin E.

In other cells, it might be, you know, other... SOD, catalase, glutathione, peroxides. These are all antioxidants that your body makes, and they're so powerful. And often they're overwhelmed, and often we don't support their function with the right nutrients. Right, exactly. So, for instance, glutathione needs methionine. Well, methionine is the second rarest amino acid after tryptophan. That's the rarest.

And you need tryptophan in order to be able to turn that amygdala off, all right? But methionine is necessary to be able to make S-adenosylmethionine, which then contributes the methyl group for glutathione. Well, if you're methionine deficient to be able to make S-adenosylmethionine, which then contributes the methyl group for glutathione. Well, if you're methionine deficient, you got a problem. Yeah. And glutathione is like the King Kong of antioxidants, essentially. Exactly. Yeah.

Your body makes it. My colleague, Jackie Marr at San Francisco General, studies the methionine choline deficient rat, the MCD rat. Poor rat. Okay. Not the McDonald's rat, but it might as well be. Okay. This is the fastest way to fatty liver disease there is.

And the reason is because without methionine, you can't generate glutathione, so you're going to get NAFLD, non-alcoholic fatty liver disease. And also choline. Choline makes phosphatidylcholine, which is part of ApoB, which helps export the fat out of the liver so it can go to the adipocyte instead. So without choline,

you can't get the fat out of the liver. So you make too much and you can't clear it. And so these animals have fatty liver like crazy. Like about almost 100 million Americans. Point is, point is, methionine and choline are things that you don't find much in processed food. No, no. Where are they found? Well, they're found in real food.

I mean, methionine is found in, you know, basically good protein. When I say good protein, fish, poultry, eggs. Meat? Oh, sure. Red meat. Absolutely. Absolutely. You know, and also Red meat. Absolutely. Absolutely. You know, and also you need iron for this too.

And choline is where? And choline is in red meat as well. Eggs? Eggs and eggs. Sardines. Sardines, yes. Which I have a can of sardines here with me now for lunch. The problem with choline is that choline can be acted on by the intestinal microbiome to

form trimethylamine. Dr. TMIO, right. And then that gets oxidized. You know, Stanley Hayes in a Cleveland Clinic where you, by the way, are, you know... Dr. Working, yeah. Working as well, you know, with Michael Roysen in their wellness program. So you know, even though sometimes things are good, sometimes too much of a good thing is not so good.

And so we have this problem in nutrition also is that we have inverted U-shaped curves for certain things like choline. You know, choline used to be called vitamin B4. You know, so it's essential. It's essential, right. It's essential. So it's, these are the things that are wrong that we have to fix. With our diet.

You were going about inflammation. You were going inflammation is driving this. So where inflammation is coming from, if it's coming from stress, if it's coming from toxins, coming from sugar, coming from microbiome. It's coming from our diet. That's where it's coming from. So if you have an autoimmune disease,

it's coming from your immune system. But if you don't have an autoimmune disease, which is 90% of us, 10% do, but 90% of us don't, it's coming from your immune system. But if you don't have an autoimmune disease, which is 90% of us, 10% do, but 90% of us don't, it's coming from your gut. Now, your gut is a sewer. What's the definition of a sewer? A pipe with you know what in it. Yes.

Okay, that's what the gut is, it's a sewer. Well, all that junk in there is bad for you. You don't want it in your bloodstream. It stays in your gut. So there are three barriers in your intestine to keep the junk out of your blood. The first is the physical barrier, the mucin layer. The mucus. Right.

And it lines the intestinal epithelium all the way through. The second is the biochemical barrier, which is the zonulins, the tight junctions that hold the intestinal epithelial cells together. Like Lego blocks stuck together. Yes, kind of, sort of like Lego blocks. And when they become dysfunctional, then they get permeable and that leads to what we call leaky gut. Yeah.

And the third is the immunologic barrier. And those are called TH17 cells, and they make a cytokine called IL-17. So those are white blood cells, and they're making inflammatory compounds, right? Exactly. To get rid of foreign invaders. Yeah. Okay. So three separate... It's like the front line of the military on the front lines, right? Yeah. Well, you've got the guys at the front, the pawns, then you got the knights, and then you got the bishops, all right, before you get to the king, right?

I mean, you have all of these things in defense of your bloodstream. The point is all three of those are failing today because of ultra-processed food. The mucin layer, because of the lack of fiber, the microbiome will actually chew up the mucin layer, because of the lack of fiber, the microbiome will actually chew up the mucin layer for its own purposes because it otherwise is starving. Fiber is the food for your microbiome. Fiber is the food for your bacteria. Fiber is the nutrient you don't absorb because it's not for you, it's for your bacteria. But our is fiber you know fiberless on purpose yeah because you can't freeze fiber exactly so the food industry took it out yeah well we got to put it back in and that's

what this yeah what is this so this packet so you know full disclosure i am the chief medical officer and co-founder of a fiber company and it's called biolumen, and the product is called Monch Monch. And we just released it end of November. It's doing very well. And what's in it? What is in it, these are microcellulose sponges, seven microns in diameter, so the size of a red blood cell.

So it flows like a powder. It's colorless, odorless, tasteless, textureless, because your tongue can't tell six microns. Yeah. It's got to be 12 microns or greater for your tongue to be able to discern that it's there. So it can go into bean dip. It can go into chocolate. It can go into ice cream and smoothies, yogurt, anything that's non-aqueous.

Not water. Well, you can put it in water and then drink it right away. Right. If you leave it, it'll swell. It's like gel. And you can put a spoon in and it stands straight up, right? Right. We don't want to do that because then no one will drink it.

Yeah. You swallow it in the food or otherwise. In the stomach, it'll start expanding. It expands 70-fold over its original size. Incredible. So that'll give you a feeling of fullness, which helps. And when it expands, it exhibits the nooks and the crannies in the sponge, right? Like the kitchen sponge, you know, has the holes in it. Yeah.

Impregnated in all of those are a set of proprietary hydrogels, soluble fiber, which sequester, absorb, soak up glucose, fructose, sucrose, simple starches. And fat too. No, not fat. Not fat? Not fat. It doesn't limit cholesterol?

Because a lot of the fibers will, like metamucilins, will reduce cholesterol absorption. Yeah, but this one won't. Interesting. So that's one of the geniuses of this, is it only works on carbohydrate. Interesting. Because you don't want to absorb fat because if you absorb fat number one you get bad gi side effects that's what happened you don't if you want a calorie you know you don't want to prevent the absorption of fat right exactly

with oralist that and that fat blocker that was having disaster pants with right so this is basically what's in regular food and everything that's in this packet is food yeah all the components are food they're food grade we get them on amazon we just assemble them in a specific proprietary you take it before you eat essentially you take it with you with the food i just came back from tanzania and i met with the honey hunters the i mean the uh the uh hadza which are are this incredible tribe, the last hunter-gatherer tribe. And they hunt and they gather. And 20% of their diet is honey. Honey. And the other part of their diet is an enormous amount of fiber. They eat 150 grams of fiber a day. We literally dug a root out of the bottom of a tree. It was kind of a wild yam.

And they eat that. And so we all ate about 100 to 150 grams of fiber per person a day. We literally dug a root out of the bottom of a tree. It was kind of a wild yam. And they eat that. And so, you know, we all ate about 100 to 150 grams of fiber per person a day. Now we eat about eight or less. And it's destroying our microbiome. It's making us metabolically unhealthy. And it's hard to get that much unless you're eating... Unless you're a hosda. Yeah, unless you're a hosda or you're like eating tons of fiber all the time. And it's hard. And I think the data is really clear on other studies too, like from Metamucil and even things like polyglycol plex from glucomannan helps in this, some of that in there. Right. So the concept is right. I mean, so this

is both insoluble fiber cellulose and soluble fiber, these hydrogels. Okay. And so it's unusual because it's a combination of both. So it gonna do a couple things tell us the things that it does so number multiple actions in terms of its effect six separate effects so the first thing is it gives you feeling of fullness second it absorbs carbohydrate and you know especially simple sugars in the duodenum preventing their ability to cross into the bloodstream. Thus, you reduce the glucose response, you reduce the insulin response. We just said that's the most important thing.

So you take a slow absorption of sugar into your blood and it prevents this glucose spike and the insulin spike that makes you gain weight. Correct. In addition, it moves the food through the intestine faster because fiber, you know, is a lot. Transit time, we call, is a lot. Transit time, we call it. Transit time. Transit time decreases.

That means that you get your satiety signal sooner because it's at the end of the intestine, the peptide YY signal in the ileum at the end of the intestine. In addition... So what you just said there was you feel full, the satiety signal, which is PYY and others that get released in the lower part of the intestine and get activated from the fiber. So that makes you actually shut your brain down from wanting food. Correct.

Which, by the way, is what GLP-1 does. Yeah. Okay. And we'll get to that. Number four, it feeds the microbiome. So it increases microbial diversity, which is a way to prevent inflammation. Yeah. And there's bugs that are good bugs in your gut and bad bugs.

And when you eat processed food, you grow bad bugs. When you eat fiber, you grow good bugs. Exactly. Okay. And the good bugs are anti-inflammatory and the bad bugs are inflammatory. So it doesn't matter what you eat. If you have inflammatory bugs, you get something called metabolic endotoxemia, which means your inflammation from your bugs causes insulin resistance independent of your diet.

And do you know what does that? Sugar. Because sugar nitrates those tight junctions and makes them non-functional. And so transiently increases leaky gut. Yeah, and gluten. And gluten. Well, of course gluten.

And all the food additives, the emulsifiers, which destroy the lining of the gut. That's destroying that mucus layer. That's right. Number five, the soluble fiber acts as food for the colonic bacteria generating short-chain fatty acids, which have been shown to be anti-inflammatory, anti-Alzheimer's. Anti-cancer.

Anti-cancer. Yeah. And finally, the insoluble fiber helps clear cancer cells from sloughing from the colon. So basically... I think there's one more. What's the one more? Well, you secrete extra toxins from your liver into your bile and it goes in your gut and so you have environmental toxins that get pushed out as well faster.

Sure. So you have seven there. Yeah, seven. Seven is a lucky number. We haven't studied that one yet, but that's actually very true. The point is what this does is it recapitulates the effect of the fiber that was in the food to start with before the food industry got to it.

But it doesn't mean you can take that and eat ultra-processed food. You want to still eat healthy food, right? Well, ultimately, the question is, can you have your cake and eat it too? And that, by the way, that was just an article in The Guardian three days ago with that title. I'm not proposing we abandon trying to fix ultra process i just had one of those before my pint of ben and jerry's or what we need we need all the tools i bet that's what people are thinking well we need all the tools we can get yeah okay there are sugar addicts out there who you know no matter what information we give them you know they're going to continue you know

hitting the uh hitting the sodas, hitting the Ben and Jerry's. And we have to provide them with methods for dealing with their problem as well. Think of it this way. Okay. You got a heroin addict. Okay. Why is heroin bad? Because it's addictive.

Because it's addictive. Well, caffeine is addictive, but there's a Starbucks on every street corner. True. So why is heroin such a problem? Because during the withdrawal phase you go steal a car. That's why. All right. So what did society do?

We came up with this thing called methadone. And methadone basically is an oral opioid which basically takes the edge off the peaks and the valleys. Think of this as methadone for your sugar. That's incredible. Addiction. How do you like that? I like that. I mean, I would rather you know your sugar.

It doesn't fix the problem, but it helps mitigate the risk. But it's also not addictive. No, of course not. Methadone is addictive. So it's not quite methadone. But I think, you know, I just want to bring this up because there are a lot of criticisms about this whole food addiction theory. Yeah.

And there are a lot of people who are pushing back and saying it's not a problem, that it's really just people's gluttony and that it's not really a biological phenomenon and doesn't meet the criteria. Actually, it does meet the criteria. But if you look at, I mean, listen, Kelly Burnell has created a whole Yale food addiction score. It's a valid metric. Ashley Gearhart has done enormous work.

Nicola Vina has demonstrated sugar addiction in animals and now in humans. And I just met with her. We just did the Commonwealth Club last week. We're going to meet in New York next week as well. There's a food addiction symposium in London in May. There's different degrees of it. But there was a really interesting meta-analysis of a systematic review of 281 studies from 36 countries. And they found that overall, the prevalence of food addiction, according to the Yale Food Addiction Score, which is a validated metric, was 14% in adults and 12% in kids.

And 14% of the population is alcohol addicted. So it's like the same as alcoholism and tobacco is about 18%. So let's use alcohol as the template for this. Okay, let's take the American population. 40% of Americans are teetotalers, never touches stuff. 40% are social drinkers,

pick up a beer, put it down. I'm in that category. 10% are binge drinkers and 10% are chronic alcoholics. Yeah. Okay. So even though alcohol is available everywhere, 80% of the population does not seem to have a problem. But 20% do. And the question is, what are you going to do for that

20%? And why do they have it? And why do they have it? Well, it turns out they're probably the same people. So the idea that there's no sugar addiction doesn't make sense, just because not everyone's addicted doesn't mean it doesn't exist. In fact, sugar and alcohol are metabolized virtually identically. The fructose molecule and the ethanol molecule basically do the exact same thing

at the level of the mitochondria. So it shouldn't be surprising that children who don't drink alcohol have the same diseases as alcoholics, type 2 diabetes and fatty liver disease, even without alcohol, because they have a substitute. Yeah. They have sugar. Yeah. It's really interesting.

I mean, I think the food addiction thing is fascinating because even, you know, there's people say, where are the randomized controlled trials? Well, David Ludwig did one where he basically took, it was fascinating, I call it the milkshake study. Yeah, I know. You know about this study. Basically, a group of overweight guys. Yeah. And he gave them on different times different milkshakes.

But they were identical in terms of calories, carb, fiber. But they were different in sugar. Protein, fat. Right. And the speed of the absorption of the sugar was the only difference. So one had a rapidly spiking sugar, the other one didn't. And they measured their brain MRIs, and they measured their blood chemistries. And even though they were identical in calories, the group that had, and they tasted the same,

the group didn't know which one they were eating. The ones that had the high spiking sugar carbohydrate had higher levels of insulin, higher levels of glucose, higher triglycerides, more inflammation, and higher cortisol, higher adrenaline. And their brains in the area of addiction, the nucleus accumbens, lit up like a Christmas tree. And that's the same area that lights up with heroin and cocaine. And I think the- Anything that makes that nucleus accumbens activate in the extreme is addictive. And now we know there's genetics that play a role, right? So I don't know if you do this, but I...

We haven't found the genetic locus yet for alcohol or for nicotine or for sugar. Well, we may not know exactly, but we do know that there's difference in dopamine receptors. So we can measure genes for dopamine receptors and dopamine is the receptor that feels pleasure. So in these people with dopamine receptor problems, they end up needing more stimulation to feel the same goodness.

Because the dopamine receptor has been downregulated. It's the law of diminishing returns, basically. Well, it's both, right. Ligands downregulate their own receptor. Well, there's habituation, but there's genetics also, right? Well, yeah. So the TACA1 allele of the dopamine receptor, so it's in about 20% of people,

turns out they make 30% fewer dopamine receptors on their neurons. They gain more weight. And those are the people more likely to be addicted or gain weight or have sugar addiction. So you're right. It's not like people, oh, sugar addiction. Not everybody's alcohol addicted.

Not everybody's sugar addicted. But it's a thing, and it's as big a thing as alcoholism and it's causing societal devolution okay in the same way alcohol did and so then the question is all right if you know that something is both toxic and addictive like cocaine heroin nicotine alcohol you, alcohol. You have societal interventions that deal with it. We call it public health. What do we have for sugar? Nada. Not here.

I mean, I just came back from Chile and Argentina. And you're right. They have incredible laws that have really radically changed their food consumption patterns and to reduce the amount of refined sugars and carbohydrates and junk food because they put black box warnings on the front of the package. They have limited advertising. They got rid of Tony the Tiger. They have no junk food in schools. So there's a lot of ways that we actually can fix this. And Paul, you're working on policy. I'm working on policy stuff. So we have to get this done. Right. So to that point, we've got standards for sugar in California down to

5% of calories in schools. It's called SB 348. And my nonprofit, Eat Real, which you're very familiar with. Yeah, they help support. And my CEO, Nora Latorre is a force of nature. She's amazing. She is, yeah. Okay. Worked with Nancy Skinner of the California legislature to push this through, and we're trying to make this national. And just today, the White House announced that Eat Real is now one of its model programs for dealing with childhood obesity going into 2025. we are going to be taking 1 billion meals in out of in schools and making them low sugar and zero process that's god's work i mean because our kids are our future and we poison our kids i mean we 40 plus overweight 25 are obese we have uh decreased performance in school, decreased job performance, decreased earning capacity, shorter life expectancy, 13 years of your obese as a kid.

I mean, it's really a big deal. It is. So let's the audience understand how this occurred. Because ultimately, when you drive into a ditch, you have to know how you drove in in order to be able to back out. You can't just hit the accelerator and expect to be able to come out the other side of the ditch. You have to back yourself out. So you have to know how you drove in. Why did this happen? So when you and I were kids, and we're about the same age, we had school, and we had cafeterias, and we had lunch ladies.

My mom always made my lunch. Okay. Well, you know, my mom made me tuna fish sandwich every day, and I could kill her to this day. We didn't have school food when I was in the elementary. I don't remember that. Well, they had the blue hairs with the hairnets and the lunch ladies. Okay.

In 1971, the Department of Education passed an ordinance, you know, administrative law called Resolution 242, which basically said that all cafeterias in the United States in public schools had to make book. That is, they could not lose money for the school. They had to basically fend for themselves with their own budget. Yeah. for the school, they had to basically fend for themselves with their own budget. Now, that sent every food services director in every school in America running for cover. What are we gonna do? How are we gonna solve this?

Because the biggest issue was the personnel and the infrastructure, keeping it running to be able to make school food. So in walked Aramark and Cisco and Guggenheim and McDonald's and Pizza Hut. He says, hey, we'll do it for you. We'll provide every kid with an, air quote, nutritious, un-air quote, meal every single day, and you won't have to do anything.

We'll take care of it. And most importantly, because we'll take care of it, you can take your infrastructure, you can take your food preparation facilities- Yeah, get rid of the kitchens. And get rid of the kitchen and turn it into classrooms. And that was the goal. That was the plan.

No, you need a deep fryer and a microwave and you're fine. Right. And the point is that once you take the equipment out, now you're hostage to the food industry for the rest of your life. And 1971, you can track when grades in elementary school started. And the reverse is true. I don't know if you know about my friend Jill Shaw who created a program called My Way Cafe in Boston where she basically paid for, so philanthropists paid for the re-institution of a kitchen in a school. Showed how powerful it was. Got the entire Boston city

schools to do it and now the entire inner city of Boston a kitchen in a school. Showed how powerful it was. Got the entire Boston City Schools to do it. And now the entire inner city of Boston schools all have kitchens. The menus have all been designed by top chefs. The food's delicious. The kid eat it. They don't throw it out. It meets the school budget guidelines,

the federal guidelines for school lunches. And everybody's winning. And they're not getting food shipped in across state lines in packages with plastic, with who knows what kind of toxins that are infiltrating the food in addition to the junk that's in the food that's heated up in microwaves and deep fryers the point is there are a lot of business models that work so eat real is dedicated to finding

the business model that would work with it within any district so for instance we started out in Contra Costa County you know right across from San Francisco enterprising soup food services director, wonderful guy, Dominic Mackey, he purchased a dilapidated factory, repurposed it into a food preparation facility for the entire district, 27 schools, 27,000 kids. They made 27,000 lunches per day. And because they were buying at scale, they could buy cheaper and they could control what was in the food. And so they could get rid of, get this, 10 pounds of sugar per kid per year. They got rid of 100,000 pounds of sugar in the first year. We have now gotten rid of 5 million pounds of sugar from kids' diets.

Yeah, it was some great visual that Jamie Oliver did on a TED Talk where he took a bathtub full of sugar. Well, a school bus full of sugar. Oliver did on a TED Talk where he took a bathtub full of sugar. Well, a school bus full of sugar. And that's what an average kid eats in a year, right? Right. The point is Dominic was able to actually save money because they could buy a scale. And so they made it in the one central facility

and then shipped it out to the 27 schools each day. And so every kid got a real nutritious meal, a hot food meal, where we could control what was actually in it. And you saw performance get better. Everything got better. Attendance got better. Behavior issues got better. Exactly.

Weight got better. Another example, and this was not our example. This was in Israel. Yeah. 15 years ago the Ramallah school district in the West Bank had a 27% graduation rate. 27%. Oh yeah, that's not good. And if you don't graduate, what happens to you? There's a likelihood you're going to...

You're marginalized. You're going to be marginalized, terrorist, whatever. Not good. And the Israeli government did not know what to do with this. A entrepreneur who's done very well in the tech industry, Yossi Vardy, went to Netanyahu, said, give me the Ramallah school district. I will take care of it.

And they were only too happy to divest themselves of it. And Vardy did one thing. Change the food. He fed them. He didn't even change the food. He fed them. Yeah. He didn't even change the food. He fed them.

That's so right. And they went from a 27% graduation rate to a 95% graduation rate in two years. Yeah. Now, I see this. I just came back from Kenya, and I went to this school called Little Lions where it's in the worst slum, Kibera Slum, in Kenya.

It's the worst slum in Africa. I went and visited there, walked around. It was incredible. People live on $3 a day. There's garbage everywhere. I mean, it's awful. And this friend of mine started this whole school and his main thing was feed these kids three meals a day, real food. And these kids are thriving. They're performing academically. They're going to be doctors now and getting out of their poverty. Why are we surprised? Yeah, I'm not surprised. Your brain needs nutrients. Well, let's back up a little. Not just glucose.

It needs fatty acids. It needs protein. Yeah, it needs food. It needs, you know, anthocyanins. It needs selenium. It needs zinc. It needs, you know, omega-3s. Where are you going to get them except your food?

So I want to back up because clearly we need to fix our school system. We need to fix schools. Eat Real is an amazing nonprofit. I encourage you to check it out. I'm a huge fan of it. I'm a friend and a supporter of the whole program and Jordan Schlain and Nora and you. So it's great. Thank you.

But I want to back up because we spent a lot of the conversation talking about these four different, not opposing, but different models of thinking about the causation of obesity. And if we're going to address this obesity epidemic, I mean, yeah, we can all take Ozempic and spend $5 trillion a year and bankrupt the country and cause all these side effects and bowel obstruction and so forth. Or we can really address the cause. And so you talked about the energy balance hypothesis, which essentially is calories in, calories out. The carbohydrate-insulin hypothesis, which is too much sugar and carbs causes too much insulin,

which makes you gain weight and prevent fat loss and dysregulates your brain. You talked about environmental toxins or obesogens that disrupt things in many ways by destroying our mitochondria, by screwing up our microbiome, by causing inflammation, by causing active stress, by triggering our thyroid function, by so many different mechanisms, which I actually outlined in that paper

I should send it to you. You'll love it. It's like 20 years old, but I saw it coming. And then lastly, this whole redox hypothesis, which is all these things also cause too much oxidative stress. So for the average person listening, they're like, well, that's cool. Interesting science, but like, what the heck do I

do? So let's take the rest of the time to break down what are the action steps to address these things? And how do we create an integrated model? And what is the average person going to do who is struggling with weight gain, who's struggling trying to lose weight, who's trying to understand all this conflicting biology, who's hearing one Instagram influencer saying, you know, this is garbage. Another one saying, this is garbage. No, this is true.

No, that's true. Eat this. Be a carnivore. Be a vegan. No, this is true. No, that's true. Eat this. Be a carnivore. Be a vegan. No, don't eat fat. Eat fat. Eat carbs. Don't eat carbs.

It's like, you're going to go crazy. It's a mess. So it's a mess. It is. It's a total mess. So help us from a scientific perspective. How do we break down the action steps for the average person listening who wants to understand how do we take these scientific advances, which are really remarkable in our

understanding of obesity and metabolism, and turn those into action steps that people can do to help their lives get better and lose weight. So I'm on record. You can't fix health care until you fix health. You can't fix health until you fix diet. And you can't fix diet until you know what the hell is wrong. And for the last 50 years, we until you know what the hell is wrong. And for the last 50 years, we've been barking up the completely wrong tree.

We've been working on the idea that fat was the bad guy. Fat ain't the bad guy. Now, what is the bad guy? Well, it's a bunch of things. Basically, anything that makes ROSs. All right, well, what makes the most ROSs? Turns out trans fats make the makes ROSs all right well what makes the most ROSs okay turns out trans fats make the most ROSs shortening but we now know that and it's basically been banned from the American diet finally you know why they call it shortening right no it shortens

your life oh yeah fair enough but no this is like Crisco, right? Indeed. Back in the day. Indeed. But it's been regulated as non-grass, which means generally not recognized as safe. Correct. However, it's still in the food. Yes, it is. So you can go to the grocery store. It should not be there. It was almost 10 years ago, and you can still find that crap everywhere.

You are exactly right. And for the exact reason you said, because they round down. Yeah. So- Read the label, in other words. Scott Grundy, years ago, showed that two grams of trans fat per day is enough to lead to diabetes and cardiovascular disease. Two grams per day.

Okay. If a serving of ultra processed food in America has 0.49 grams. Less than 0.5. Less than 0.5, okay? They can say it's zero. Zero, right. Because of rounding down. Yeah.

So if you consume four servings of whatever that is. Yeah, which is not hard. Which is not hard, okay? You have achieved your two grams. That is all still a problem. So you are absolutely right. We have actually not completely solved the problem of trans fats. Okay, so trans fats are bad.

Next is... Okay, so the question is what to do about all of these issues. So anything that causes reactive oxygen species is a problem. Is a bad guy. So there's a lot of things. Well, what's the next thing? Fructose. Fructose causes the Maillard reaction, the glycation reaction,

the browning reaction, seven times faster than glucose. Crispy chicken skin. Crème brûlée. Bananas. Yeah. You know, anything that browns. Yeah.

Okay? You know, barbecue sauce on the grill. Okay? And that's an oxidative stress reaction. That's not... and generates 100 times the reactive oxygen species. It creates ages, right? We call it advanced glycation end products, otherwise known to age you.

It can happen in your cell or you can eat it. So dietary ages, okay? So basically, if you take a can of sweetened condensed milk and you put it in a pressure cooker for an hour, you get pudding, okay? It went from white to brown. Okay? That's the Maillard reaction.

Okay? It occurs in the food. The point is the sugar is what drives those advanced glycation end products. But it's not just fructose, right? Any kind of sugar will cause glycation. Well, glucose will do it, but fructose does it seven times faster and generates 100 times the ROSs because of the stereochemistry of the molecule. So fructose is particularly egregious. Yes, glucose does it too, but fructose does it way more.

Lactose, galactose much less. So lactose is not a big problem. People think dairy is a problem. It's not a problem. Okay. So don't quit your breast milk? Don't quit your breast milk. Don't quit the breast milk. And we can talk about neonatal nutrition maybe on another podcast. But the bottom line is the amount of sugar in our diet is a mess. The third thing is the inflammation because that's generating the ROSs. And there it's the emulsifiers's the emulsifiers, because the emulsifiers are leading to that leaky gut. So name some. Carboxymethylcellulose, polysorbate 80, carrageenan. By the way, which food has the most carrageenan?

Your almond milk. Ice cream. Ice cream, oh. Ice cream. And who introduced carrageenan to ice cream? This quiz i don't know the eskimos it's seaweed margaret thatcher margaret thatcher margaret she liked her ice cream thicker she was an ice cream chemist before she was an mp what that's a good little trivia yeah okay so there's there's other ones xanthan gum guar gum all these thickeners that you see in even health

foods well the thickeners don't necessarily mean they're emulsifiers. They, you know, emulsifiers very specifically hold fat and water together. So the thickeners are yet another issue. And they've been linked to autoimmune disease. Absolutely. Because they cause leaky gut. No question. Okay.

Another thing that's a big problem is monoglycidal acids. Okay. Three NCPD. It's a compound called E471. But you don't see it on the label of a food. Well, no, you do see it. It just doesn't call it, they don't call it E471. Monoglycidal esters, okay? So those are a problem as well. So bottom line is, here's what we need to do. And the food itself is inflammatory, inflammatory right so if you're eating trans fat sugar of course ultra processed food just by nature it's inflammatory exactly through a whole series of mechanisms so we have to promote

metabolism best way get rid of the sugar and we have to suppress you also mean flour you also mean yeah well refined carbohydrate and sugar. Refined sugar and carbohydrates. And we have to suppress inflammation. And how do we do that? Increase the fiber, get rid of the emulsifiers, increase the omega-3s. Okay, so get rid of the sugar, increase the fiber, increase the omega-3s, and decrease the emulsifiers.

All right. What food looks like that? Sardines? Eat the bones? I don't know. Well, real food. Real food, right. Real food. I mean, fish in particular, yes. I mean, I am a big proponent of fish because they got omega-3s. But remember, it's not the fish that make the omega-3s. The fish eat the omega-3s. The algae make the omega-3s. The fish eat the algae. We eat the fish. That's why small fish have more omega-3s than large fish. Large fish eat the small fish. Right?

Exactly. So how do we do that? So in 2020, I was contacted by a company in the Middle East. But I noticed you didn't say reduce calories. No, nothing about calories. You didn't say... It's not about didn't say reduce calories. No, nothing about calories. You didn't say... It's not about calories. Yeah, yeah.

Okay. Not about calories. In 2020, I was contacted by a company in the Middle East called Kuwaiti Danish Dairy. And they recognized that they wanted to be part of the solution, not part of the problem. Kuwait has an 18% diabetes rate and an 80% obesity rate. It's about 10% here. So it's almost double.

It's 11.4 right now. Okay. Jeez. I can't keep track. I know. I know. Every day, it keeps going up. They wanted to become a metabolically health company and they wanted to lead the way. And they're a privately held company so they could take the long view. They didn't have Wall Street quarterly reports to have to deal with so their business model was make better food and make it at a price point that they could still make a profit that was what they want to do so they contacted me to convene a scientific advisory team to help them re-engineer their entire food portfolio

180 items that's amazing and so do you know Tim Harlan who is the head of culinary medicine at George Washington University Rachel Gao who ran the omega-3 for ADD trial at the NIH Andres corn stout who is a computer scientist out of Stanford and Wolfram Alderson who's been in the food business longer than all of us we started the first farmer's market in Los Angeles back in 1979. We convened the scientific advisory team to basically deconstruct the entire portfolio of this company to determine what were they doing? What ingredients were they using? Did they actually meet criteria for healthfulness or not?

Were the vendors actually telling them the truth about what was in the things that they were selling them? And what could we do about the production and the packaging in order to actually improve the healthfulness of the food? And we came up with three precepts. And these are the precepts of metabolic health. And we call it the metabolic matrix. I love this. Here we go. Protect the liver, feed the gut, support the brain.

Any food that does all three of those is healthy, irrespective of if it's processed or ultra-processed. Any food that does none of the three is poison. So feed the gut, support your liver, help the brain. Protect the liver, support the brain. Yeah. Okay? Those are the three precepts. And you can actually determine- How do you do that?

How do you do that? Yeah. Well, it's easy when you know what each of the foods, what each of the ingredients do within the body. So you have to understand metabolic health to be able to do that. So nutrition does not answer those questions. So there's this thing called food science. There's this thing called nutrition.

There's this thing called metabolic health. They are not the same. Food science is what happens to food between the ground and the mouth. In the laboratory. In the laboratory. Not when you buy an apple in the grocery store. There's no food science there. Nutrition is what happens to food between the mouth and the cell. Metabolic health is what happens inside the cell. But all of these metabolic diseases are all happening inside the cell. So nutrition is only

valuable as it informs metabolic health. Food science is only valuable as it informs metabolic health. But they are one or two steps divorced from metabolic health. So if you use metabolic health as the North Star, as the watchword, as the goal, and the World Economic Forum has endorsed this. They came out with a white paper called The True Purpose of Nutrition. And the World Business Council for Sustainable Development is coming on board with that as well. If you use metabolic health as the North Star and gear your food re-engineering efforts to the vast concept of protect the liver, feed the gut, support the brain, you can actually make healthy food, even. Even if it's ultra processed. Yeah.

And that's what we have done in Kuwait. And they have turned 10% of their portfolio over in the last two years. That's amazing. Based on these processes. So if you're not eating Kuwaiti Danish food, what do you eat? Well, we need to impress upon the food industry here in America. Here, to do the same thing. To do the same thing.

100%. It is a uphill battle battle to say the least. I love this because everybody's looking for solutions. So this is really a well thought out solution. I am a scientific advisor to the Innovation Institute for Food and Health at UC Davis, who has lines to all of the food industry at different levels, startups and CPG companies. And the goal is to get companies to understand what it is that they are doing, basically ditching the idea of nutrition and focusing on metabolic health instead. Example, Unilever and Danone in the last two years

reduced their carbon, sorry, their sugar footprint, both of the companies, by 14%. Now, you think that's good or bad? I don't know. 14%. I think it sounds good, but there's a catch. Well, I mean, it's better than not. Yeah.

But 14%. When you are, you know, when you use triple your limit in the food, going down by 14% doesn't quite get you there. Yeah, it's like when they said they're going to take six trillion calories out of the food supply by making Oreo cookies 90 calories instead of 100 calories. Exactly. It's BS.

Exactly BS. That's exactly right. And they did that in 2014 and it was a piece of crap then and it's a piece of crap now. That's how you really feel crap now. Exactly right. That's how you really feel, Robert. Yeah. I will.

How about... So the point is 14% sounds good. It actually got Emanuel Faber fired at Danone because of it. At KDD, at this Kuwaiti Danish dairy, we have reduced the sugar footprint of that company by 78%. That's amazing. That's amazing. 78%. So again, what That's amazing. 78%.

So again, what do people eat for lunch? The last thing I want to say, this all sounds great, Mark. What the F do I eat for lunch? All right. So obviously the easy answer is real food. So what's real food? Food that came out of the ground or animals that ate what came out of the ground. That's real food.

All right. I make it simple. I say, eat the food that God made, leave the food that came out of the ground or animals that ate what came out of the ground. That's real food. All right. I make it simple. I say, eat the food that God made, leave the food that man made, right? Yeah, right. I mean, if you think Cheetos is food, I mean, you know, you're sunk. Right. It's just that simple. Yeah.

So we have to redefine food population. What is food? What is food? Okay. So what is food? What is the definition of food, Mark? It's something that provides nutrition to the cells. What is food? What is food? Okay. So what is food? What is the definition of food, Mark? It's something that provides nutrition to the cells.

No, that's not the dictionary definition of food. It's something you eat? I don't know. I should know. I read a book about this. Yes, you should. Substrate that contributes to either growth or burning of an organism. Growth or burning.

Yeah. Okay? Remember we said at the beginning every cell has to grow at one point in its life, every cell has to burn at one point in its life, but it can't do both at the same time. Okay. Remember we said at the beginning, every cell has to grow at one point in its life. Every cell has to burn at one point in its life, but it can't do both at the same time. Burning or growing. Okay. So does ultra processed food contribute to burning? Well, sugar inhibits three mitochondrial enzymes. We named them before. Sugar actually inhibits burning. Okay. And 73% of the items in the grocery store are you know overdose with sugar does sugar contribute to growth does ultra-prositive

food contribute to growth? Yeah kind of makes you grow. No my colleague Dr. Frant Monsonigo-Ornan who's the head of nutrition at Hebrew University Jerusalem has looked at this question it actually inhibits trabecular bone growth cortical bone growth skeletal bone growthbecular bone growth, cortical bone growth, skeletal bone growth, cancellous bone growth. But it makes belly growth bigger. It hijacks growth. Yeah. Actually drives cancer formation.

Yeah. Okay. Point is, it does not contribute to growth. Yeah. So if a food stuff, if a compound that passes your lips does not contribute to growth and does not contribute to burning, is it a food? Yeah. No. yeah no yeah well if it's not a food what is it it's a food like substance poison right there yeah and so we have to start redefining what we need so you are big in food as medicine yeah okay dari mozaffarian big in as medicine. I am here to say food can be medicine.

Or it can be poison. It can also be poison. Yeah. And when we start differentiating those two. I wrote an article called Food is Healer, Food is Slayer. It's like the both, right? As soon as we start teaching the public the difference, that's when things will start changing.

But not until. So education has to come first. Now, can we provide the public with tools to help them? My colleagues working with KDD, we have developed a tool that everyone right now online can use. This minute, you can look it up. It's called Perfect. P-E-R-F-A-C-T. Not perfect, perfect.

And you can find it at http colon slash slash perfect dot co and what it is is it's a recommendation engine with a set of filters that will filter your grocery store your grocery store not any grocery store your grocery store to basically only show you the things that are metabolically healthy for you. So if you have a gluten problem, it will only show you the gluten-free stuff. If you have a metabolic syndrome problem, it will show you all the things that don't have refined carbohydrate or sugar or trans fats, et cetera. If you have a problem with oxalate, it will show you the low oxalate items. If you have a problem with-

So it helps you navigate this confusing landscape of nutrition and figure out what's going to be good or bad for you because as soon as you walk in the store you're sunk yeah because all of those nutrition facts labels are staring you in the face there are 40 000 items what are you going to do read 40 000 uh nutrition facts even if you go to whole foods it's's still a disaster zone. It's still impossible. Point is, this does it for you. Yeah. Okay? And it does it based on what you want it to look for,

not what they want you to look for. So everyone can use this. And there are four filters right now. There is a metabolic matrix filter that does protect the liver, feed the gut, to support the brain. There's a Robert Lustig filter

that is no added sugar, no artificial sweeteners. There is a Nova filter, our colleague Carlos Montero, so basically takes all the Nova class four items off. That's 80% of the store. Right. Okay. So you can do that now. So it's a guide for people to shop and it's really helpful.

And where can they find that? Perfect.co. It's free. Okay. Okay, you know, so... So it's a guide for people to shop and it's really helpful. And where can they find that? Perfect.co, it's free. Okay, spell it again. P-E-R-F-A-C-T. Okay, we're going to put that in the show notes and we're also going to put the link to Levels because people want to know what their blood sugar is. It's levels.link forward slash hymen

if you want to get access to a special offer to sign up to get your own blood sugar looked at because that's really important to track things that are going on. So you know actually what's happening with your own biology exactly and and you have this whole framework of the metabolic matrix feed the gut protect the liver support the brain which you've written a lot about and we're going to link to all your articles all your ted talks all your videos uh and your books which are incredible and i think people need to take a look at them. I read most of them.

Fat Chance was the one I read all the way through, Hacking the American Mind and Metabolical. I want to say Metabolical, but like Diabolical. Well, it is. Yeah. And so your work is so important. I feel like we literally just scratched the surface. Oh, yeah. We just started. I mean, this has been a phenomenal conversation and a frustrating conversation because everything, I want to spend an hour or two just talking about that. And I got to have you back because we just touched on things like artificial sweeteners.

We touched on some of these high-level concentric toxins. But I think just to summarize for people as we close, you know, obesity is complex. Weight is complex. It's not one theory. It's understanding the full matrix of the science and all the data and trying to help understand where the data actually supports one idea or another and it's understanding how these all fit together.

So the energy balance hypothesis, calories do matter but maybe not in the way we think. Carbohydrate insulin is a real thing but it's more complicated. The gut microbiome plays a role. Absolutely. Environmental toxins play a role. Redox plays a role. Right. And I think all these things are really, really important in understanding how we deal with

our weight and our metabolism. And so the science now is better than ever before. And what we're trying to do, what you do, what I do, is trying to get this out there to people, to help them understand this, to talk about it. You slept all the way down here from San Francisco because you want to talk to me, and I'm grateful for that. Not a bit. And I think we're going to have to do this again, Robert, because I just have so-

I'm just up the road. It's only four or two miles. So thank you for your work. Thank you for being the advocate across policy, science, business. And you could be playing golf right now, but you're not. You're actually doing the right thing and helping us all understand this complexity. And I think anybody who kind of tries to reduce any of us,

me, you, any of who are talking about this to some simple soundbite, it's just unfortunate because we really have such a deep understanding of the biology from our clinical work, from our scientific work, from our understanding of all the literature. And we put it together in a way that I think is the right way. And I think all the things you came to are things that I've been thinking about for decades and it all makes sense, right? Right. Absolutely. And the point is, you know,

thank you for, you know, acknowledging my work, but, you know, vice versa, you know, I mean, we are, you know, I hate to say it to say it but you know we're two very lonely warriors you know i mean there are people coming on board there are a few but i got to tell you i have been very very disappointed in the uh standard medical um uh architecture yeah well you know only 28 of medical schools even have a nutrition curriculum. I wonder if it's because AMA gets $192 million from an industry and pharma. Exactly. And 80% of the medical curriculum is underwritten by big pharma. They don't want to know this. They don't want to know there's this thing called prevention. They don't want to know there's this thing called public health. They want the pill. They want the procedure because

that's where the money is. And I would say prevention is so important, but I would also say what we're talking about is treatment. It actually can reverse these conditions. It's not like you're one-way street. And so people should check out the Perfect. They should check out Biolumine, which you're a part of,

which helps create this fiber that you're talking about. Where can they find that? They can find it at munchmunch.shop. Spell that. So M-O-N-C-H, M-O-N-C-H.shop. .shop. Okay, great.

We'll put all that in the show notes. We'll put all your work. Thank you for coming. Let's do this again soon because I'm like... I told you, we got to hang out. I feel like I'm in a marathon and I'm in a hundred yard line and I still have another 26 plus miles to go with you to unpack all this stuff. So thanks again for being here and coming all the way down and being

on the podcast. My pleasure, Mark. All right. Thanks for listening today. If you love this podcast, please share it with your friends and family. Leave a comment on your own best practices on how you upgrade your health and subscribe wherever you get your podcasts. And follow me on all social media channels at DrMarkHyman. And we'll see you next time on The Doctor's Pharmacy. This podcast is separate from my clinical practice at the Ultra Wellness Center and my work at Cleveland Clinic and Function Health,

where I'm the chief medical officer. This podcast represents my opinions and my guests' opinions, and neither myself nor the podcast endorses the views or statements of my guests. This podcast is for educational purposes only. This podcast is not a substitute for professional care by a doctor or other qualified medical professional. This podcast is provided on the understanding that it does not constitute medical or other professional advice or services. Now, if you're looking for your help in your journey, seek out a qualified medical practitioner. You can come see us at the

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