How You've Been Lied To About Calories, Dieting, Exercise & Losing Weight | Dr. Robert Lustig

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.

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 gonna drive off the cliff in a convertible?

We 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, which 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 bariatric surgery as teenagers. And this movie did quite well.

Oh, yeah. Theatrical release. Yeah. I mean, you and I were the two talking heads, that sort of, you know, but we didn't get to meet until the LA premiere.

That's right. We met at the premiere and it was, you know, it was a really impactful movie for me because I realized, you know, in that scene that I was working in in the movie where I was working with this family of five that lived in a trailer on food stamps and disability that had, you know, the father was 42 and had dialysis from diabetes. The mother was 100 plus pounds overweight that 16-year-old kid was almost diabetic with a body composition. We did DEXA scans of 50% fat, 50% at 16 years old. And they lost 200 pounds in the first year. The father lost 45, so able to get a new kidney. The son lost 132 pounds and went to medical school.

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 set me to understand that it's really not that hard. 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, they, you know, 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, you will be the opposite. 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. Exactly. But when you read the ingredients, it was high fructose corn syrup and partially hydrogenated soybean oil. That was it. I was like, whoa. So, you know, it was so powerful and it kind of made me realize that, you know, we really have a problem of awareness and education and how our bodies work. And so, your work's 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 is 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 I'll let you roll because I know you can roll for hours. The whole debate 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. Absolutely. 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 the different macronutrients have 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 then 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 theory. There are. And that, you know, 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 the insulin hypothesis versus the energy balance hypothesis versus the obesigen hypothesis and how they all interconnect and are they all sort of right?

They are all sort of right.

They're all sort of right.

And they're all sort of wrong.

And they're all sort of wrong. So help us understand whether we should be just 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 altogether. Last month, a group of four authors, of which I was one, the first author is Heindel, Jerry Heindel, who was the head of the Environmental Endocrine Disruptors group at the National Institute of Environmental Health Sciences, and myself and Sarah Howard, who runs Heeds, which is Healthy Environment Endocrine Disruptors. and also Barbara Corkey, 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. Yeah. And I don't argue that. The question is, is that cause or effect?

Right.

Is it a causative phenomenon? Is it a resultant phenomenon? Or is it an epi-phenomenon? And they can't tell us which. So keep that in mind. There is nobody in the energy balance model camp who can actually say that that's the reason for weight gain. 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. 175 calories per day more for adult men, 335 calories per day more for adult women, 275 calories per day more for teen boys. Everyone's eating more.

And I 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, you know, 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's 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, you know.

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, okay, 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. Yeah, but 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 work. Fair enough. I know when I go in those.

Places it kicks in. Energy expenditure. And remember, there are three kinds of energy expenditure. There's resting energy expenditure, 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 generates heat.

It takes work to digest food.

It takes work to digest food.

So energy.

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 & 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, 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 obese.

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 before they even had a chance to eat Mother's Milk, never mind Ben and Jerry's. Okay? So whatever phenomenon, whatever model you want to proffer to me about what the cause of obesity is, you have to explain that. And you can't. Not with the energy balance model.

It's right. And I think just to kind of double down on this, calories do matter, obviously, but and 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 calorie eaten is not a calorie eaten. You say that a hundred 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 1 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 Harvard professor. Basically, he does what I do, except at Boston Children's.

And he's one of the few people who do randomized clinical trials. Yeah. And cross-sectional. He does the most rigorous kind of.

Research, not just population data. Right. And 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. Yeah, I have zero zero concerns about his accuracy, the quality or the veracity of his data or of his thinking. He's solid, across the board, and he's a friend. Full disclosure.

Me too, yeah, he's a good friend, yeah.

Now, I was a proponent of that model too, and the reason 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 servo mechanism, 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.

Yeah.

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. 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. 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 about something called the VMH lesioned rat, the ventromedial hypothalamus lesioned rat. So you put an electrode in the hypothalamus, you go bzzzz, 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.

Mm.

So that's interesting. We assumed at that point in time, this was 1995 now, so dark ages ago. 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 thought it was starving. And even though there was plenty of food without leptin saying stop, the body's like, I'm hungry, so let's store fat, let's get everything stored because I don't know when I'm gonna get my next meal. Exactly.

And insulin is that fat storage hormone. Right. 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 Urticetide. It happens to be used usually for acromegaly, for growth hormone secreting 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.

They lost weight.

But something even more remarkable occurred. They started exercising spontaneously. One kid became a competitive swimmer, two kids started lifting weights at home, one kid became the manager of his high school basketball team. These were kids who sat on the couch, ate Doritos and slept. okay? They had lost all touch with, you know, 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, you know, like within a week, they would say before there was any weight loss, they say, I got my kid back. And the kids were active and they were saying, yeah, my head 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- I mean taking this.

Trial, taking the drug and then blocking.

The effect- Blocking the effect of insulin, right. 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.

Oh, yeah, super high. 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 for 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.

Meaning they had higher levels of insulin, they had higher spiking levels after eating sugar.

And what we did in that study was we measured resting energy expenditure with a metabolic cart 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.

Down, yeah.

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 is the bad guy, no matter how you look at it. There is no weight gain without insulin. you've 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. 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- We've been doing this in.

The Ultra Wellness Center for 25 years. so absolutely, you know, 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 big round belly. I was convinced she was gonna have a high blood sugar, high A1C, she was gonna 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 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. Her insulin fasting was like, I think, 50, and it went up to 200 or 300.

Two or 300? Two or 300. My kids went up to 1200.

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, 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, you know, that's why you did this to 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. Right, you don't make energy, you're dead.

In a couple minutes. That's what cyanide does for.

Right, exactly.

Exactly.

All right. And why? Because it affects the mitochondria. So we're going to go back to the mitochondria again. That's your little energy factory, right? Because that's our systems biology, you know, 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. Now, 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 San Joaquin Valley. Farm workers.

I know about that study. 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 they, 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. striking to me.

And of course, we looked at puberty, we looked at obesity. And so we know that mothers, 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. 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, PPAR gamma 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. 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.

Okay.

So clearly we needed some more. 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 part of how it's controlled.

Like your blood pressure, your blood sugar, 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 are, there's an energy metabolism pathway in every cell to teach that cell whether it's gonna burn or grow. And there are three enzymes. One is PI3 kinase, phosphatidylinositol 3 kinase. This is the enzyme that Lou Cantley, first at Harvard, 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 for diabetes.

Exactly. And so what it does is it tells the cell to make more mitochondria.

Because the 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 is good, but it can also be overdone. Well, it tells the cell to divide. It's the division signal. So if you're dividing, you're growing. But if you're burning, you're not growing. You're doing one or the other. No cell does both at the same time. So there are 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 has been associated with weight gain or environmental obesogens like phthalates or BPA and parabens, whether.

They generally- All the petrochemical things 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 tributyltin 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, 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 quenchers. Yeah, so ROS is reactive oxygen.

It's basically like rusting. So we talk about is like when you get wrinkles on your face, your car rusts, or 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. 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?

100%.

And we are now in the process of designing the study to do that. Yeah.

So, it's interesting, Robert, in 2007, I wrote an article. It was titled Systems Biology: Toxins, Obesity, and Functional Medicine. And, I literally wrote and that was almost 20 years ago, writing about my observations that there were certain patients that were struggling with weight. They 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 what we can check? We checked heavy metals 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 down to normal. Yeah, 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. One of the interesting things is as 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 youe 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. And it turns out stress does it too.

Yeah, for sure.

So pretty much everything that drives weight gain and drives these chronic metabolic diseases, can be basically bundled into one of these four, one of these three bins. The food, the environmental exposures, or the stress. None of this has anything to do with genetics.

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.

So, it's not that... And actually, I noticed this one second, I just interrupt because I was just thinking all these things. But, I had this meal in Martha's Vineyard once on a summer with a friend and we ordered from this organic regenerative thing. We ordered so much food and it was so delicious and both of us are basically fed healthy guys who have no metabolic issues and we ate an enormous amount of healthy food and we had our continuous glucose monitors on and we call 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. I believe that insulin is the bad guy. I wish that we had a method for monitoring- Continuous insulin monitoring.

When are we getting that? I've been asking that for 20 years. Five years.

Five years.

Serious? Like in patch?

Five years. That's going to 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.

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 it.

They don't pay for it, but it's not that expensive. And I've been doing it for 25 years, so you can get it done.

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 gonna wake up? You know, when we have the continuous insulin monitor, that's when. Yeah, yeah. 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, and also generates uric acid, which also increases blood pressure. And 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.

No, you don't measure it.

It's a different family.

You can measure like HbA1c, we used to measure fructosamine.

Well, you can, yeah, but fructosamine is a measure of glucose, it's not a measure of fructose. 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. Glucose is, in my estimation, about 10% of the equation on metabolic health. Interesting. But that's a 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 company 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 in non-diabetics, in normal weight people. And we also have data that shows that if you know your glucose, you lose weight.

Yeah, it's a feedback mechanism.

It is.

It's like a shock. Like, oh, my blood sugar is high when I ate that whatever cookie. I'm not gonna eat that again.

So 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 ignore this possibility, I think, is, you know, 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 it. Tell me about my daughter's third year medical student.

My Rachel, learn about insulin resistance.

Not really. So there is this big hole. About nutrition.

Nope. No, no, none medical school. Yeah, there's a big hole in medical education. Okay. And the reason, I think, is because, you know, what we learn in medical school, and we've talked about this, you know, is 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.

Was that big?

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, you know, 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. 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. Joslin, right. Glucose is of no use to the body. That's a direct quote from Elliot Joslin before he knew what insulin was. 1893. 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 and 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 obesigen model the entire story? No, not exactly, because 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, a nerve signal to your fat cells to say, stop burning calories. Well, 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 gonna work for this person, that is gonna 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.

Burning fat.

Burn fat, right? And that is true in the acute situation. In the acute situation, you release norepinephrine from the sympathetic nervous system, norepinephrine, via the intermediolateral 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 should 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.

That's exactly right. Insulin blocks your ability to be able to lose weight. That's why getting insulin down is job one for just that reason. Exactly right. Now, here's the problem with that. 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 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 becomes-- I'm sorry, I'm the truth. You know, like 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.

It just makes, if you eat that pineal ben and jerry's on top of.

It, it makes it even worse, but it's, yeah. Well, the pineal ben and jerry's is because of what's happening at the amygdala. At 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 is about. And, you know, I'm, you know, card 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- look pretty good. I was really tired and I went shopping and I was really hungry. I went shopping at Erawan 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 like override that because I knew if I brought it home, I would eat the whole thing. Of course. Right? But I just, 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. And it, you know, 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, can I just interrupt for a sec? Because you're basically laying out these different hypothesis, but I hear you going back to insulin. Are you always 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. ROSes 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% of our weight. So you don't have to be overweight. you have this problem. You can call skinny fat or metabolically 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.

Yeah.

So just because you don't have subcutaneous fat doesn't mean you don't have liver fat. Yeah. So just because you're healthy doesn't mean you're well. And just because you're fat doesn't mean you're sick.

Yes. Okay.

The overlap is huge. Yeah. All right, 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, you know, that's what you and I are doing this friggin podcast for. 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.

And the virus 36. Right, 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 ROSs. That's what NADPH oxidase makes, those ROSs. Okay?

Now, they are- that'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 doesn't go where you.

Want it to go. Exactly. It ends up causing more damage. Exactly right. ROSs have to be quenched. Now, the quenching occurs in the peroxisome 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 peroxidase. 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, you got a problem. Yeah, and glutathione is like the King.

Kong of antioxidants essentially. Exactly, yeah. My colleague, Jackie Maher 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, 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. And also you need iron for this too.

And choline is where?

And choline is in red meat as well. 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.

TMAO.

And then that gets oxidized, you know, Stanley Hazen at the Cleveland Clinic where you, by the way, are working as well with Michael Roizen in their wellness program. So 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. 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.

You were saying inflammation is driving this. So wherever inflammation is coming from, if it's coming from stress, if it's coming.

From toxins, if it's coming from sugar, from your microbiome, it's coming from our diet. 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 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 cecus.

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. 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. Okay, so three- It's like the front.

Line of the military on the front lines, right?

Yeah, well, you've got the guys the front, the pawns, then you got the knights, then you got the bishops, before you get to the king. 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. 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 food is fiber, you know, fiberless on purpose because you can't freeze fiber. So the food industry took it out. Well, we got to put it back in and that's what this.

Yeah, what is this? You got 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 Munch Munch, 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. 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. Well, you can put it in water and then drink it right away. If you leave it, it'll swell.

It turns into gel and you can put a spoon in it and it stands straight up, right?

Right, we don't want to do that. because then no one will drink it. You swallow it in the food or otherwise, in the stomach it'll start expanding and 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, it has the holes in it. Impregnated in all of those are a set of proprietary hydrogels. souble fiber which sequesters, absorbs, soak up glucose, fructose, sucrose, simple starches. In fat too? No, not fat.

Not fat. Not fat. It doesn't limit cholesterol because a lot of the fibers will, like Metamucil, sometimes.

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 happens. You don't want to see a calorie.

You don't want to prevent the absorption of fat.

Right, exactly.

With oral of stat and that fat blocker that everybody was having disaster pants with, right?

So, this is basically what's in regular food and everything that's in this packet is food. All the components are food. They're food grade. We get them on Amazon. We just assemble them in a specific proprietary.

So, you take it before you eat, essentially.

You take it with you.

I just came back from Tanzania and I met with the honey hunters. I mean, the Hadza, which are this incredible tribe, the last hunter-gatherer tribe. And they hunt and they gather and 20% of their diet is 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 a bottom of a tree. It was kind of 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.

Right.

And, and it's, 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 host. Yeah. Unless your hosts are eating tons of fiber all the time. And it, and it's hard. And I think the data is really clear on other studies, too, like from Metamucil and, and weight, even things like. Polyglycoplex from glucomannan helps in 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's going to do a couple things. Tell us the things that it does. So number one- Multiple actions in terms of its effects.

Six separate effects. So the first thing is it gives you a feeling of fullness. second, it absorbs carbohydrate, 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.

It's 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 of time.

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 at the end in the ileum, at.

The end of the intestine. In addition, so you just said there was you feel full the satiety signal, which is a PYY and others that get released in the lower part of the intestine and 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, there's bugs that are good bugs in your gut and bad bugs. But you eat food, you grow bad bugs. When you eat fiber, you grow good bugs. Exactly. 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, glucose, 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.

And gluten. And 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. It goes in your gut, and so you have environmental toxins. they get pushed out as well, faster. So you have seven there.

Yeah, seven.

Seven is a lucky number.

We haven't studied that one yet, but yeah, 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 have one of those before my pine to 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, hitting the sodas, hitting the 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. 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 would rather be addicted to methadone.

It doesn't fix the problem, but it.

Helps mitigate the withdrawal. But it's also not addictive. Methadone is addictive. Of course. Methadone is addictive. So 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. 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 then it's not really a biological phenomenon and doesn't meet the criteria.

Actually, it does meet.

But if you look at, I mean, listen, Kelly Brownell has created a whole Yale food addiction score.

It's a validated. Ashley Gearhart has done enormous work. Nicole Avina 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 gonna meet in New York next week as well.

There's a food addiction symposium in London in May. There's different degrees of it, you know, like there's different degrees. But there was a really interesting meta-analysis of 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 touch the stuff. 40% are social drinkers. Pick up a beer, put it down. I'm in that category. Yeah. 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. Yeah. But 20% do.

Do, right.

And the question is, what are you gonna do for that 20%? 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. they have sugar.

Yeah, it's really interesting. I mean, I think that the food addiction thing is fascinating because even, you know, there's people say, where are the randomized control trials? Well, David Ludwig did one where he basically took, it was fasting, I call it the milkshake study. Yep. You know about this study? Basically, a group of overweight guys. Yep. And he gave them on different times different milkshakes, but they were identical in terms of calories, carb, fiber, protein, fat. 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.

Exactly. And that's the same area that lights up with heroin or 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- I haven't found the genetic locus yet. Right. For alcohol, or for nicotine, or for- 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 down regulated. It's the law diminishing returns basically. Well, it's both right. It's ligands down regulated.

There's habituation, but there's genetics also, right?

Well, yeah. So the TAKA1 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 it's not like, 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 problems. 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 have societal interventions that deal with it. We call it public health. What do we have for sugar? Not here.

I mean, I just came back from Chile and Argentina. And 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 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 non-profit Eat Real, which you're very familiar with.

Yeah, I help support it.

And my CEO, Nora Latorre, is, you know, good friend. She's amazing. Okay. You know, worked with Nancy Skinner of the California legislature to push this through. 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 schools and making them low sugar and zero processed.

That's God's work. I mean, because our kids are our future and we poison our kids. I mean, we have 40% plus overweight, 25% are obese. We have decreased performance in school, decreased job performance, decreased earning capacity, shorter life expectancy, 13 years of your obesity as a kid. I mean, it's really a big deal.

It is. Well, 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. Okay? 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, okay? 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 killer to this day.

They didn't have school food when I was in the islands. 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, 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. 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, you know, keeping it running to be able to make school food. So in walks Aramark and Cisco and Guggenheim and McDonald's and Pizza Hut and says, Hey, we'll do it for you. Wills provide every kid with an air quote, nutritious, unair 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, and get rid of the kitchen and turn it into classrooms. And that was the goal.

All that needs is a deep fryer in the 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 reinstitution 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 Boston schools all have kitchens. The menus would all be 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 and in packages with.

Plastic with who knows what kind of toxins that 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 Eater is dedicated to finding the business model that would work within any district. So for instance, we started out in Contra Costa County, you know, right across from San Francisco. An enterprising food services director, a 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, that was some great visual that Jamie Oliver did on a TED Talk, where he took a bathtub Full of sugar and that's a school bus. 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 at 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, weight got better.

Another example, and this was not our example, this was in Israel. 15 years ago, the Ramala school district in the West Bank had a 27% graduation rate. 27%.

That's not good.

And if you don't graduate, what happens to you? You know, there's a likelihood you're going to marginalize, you're going to marginalize terrorists, whatever, you know, not good. And the Israeli government did not know what to do with this. An entrepreneur who's done very well in the tech industry, Yossi Vardi, went to Netanyahu and 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 Vardi did one thing.

Change the food.

He fed them. He didn't even change the food. He fed them.

So right.

And they went from a 27 graduation rate to a 95 graduation rate in two years. Yeah. Now, I've seen 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 three dollars a day. It's. 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? Your brain needs nutrients.

Let's back up a little bit.

Not just glucose. It needs fatty acids. It needs protein. It needs anthocyanins. It needs selenium. It needs zinc. It needs omega-3s. Where are you gonna 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 people 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 think go Zempick and spend $5 trillion a year and bank up the country and cause all these side effects and bowel structure 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 oxidative stress, by 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 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, 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, don't eat fat, eat fat, eat.

Carbs, don't eat carbs.

It's like you're gonna have- 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've been barking up the completely wrong tree. We've been working off 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 ROSSes. All right, well what makes the most ROSSes? Turns out, trans fats make the most ROSSes. 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, fair enough.

But no, this is like Crisco, right? Back in the day, But it's been regulated as non-grass, which means generally not recognized as safe. However, it's still in the food.

In the food, yes.

So you 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.

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.

Which is not hard.

Which is not hard, okay? You have achieved your two grams, that is still a problem. So you are absolutely right. We have actually not completely solved the problem.

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 a reactive oxygen species 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 crispy chicken glucose.

Creme brulee.

Bananas. Anything that browns. Barbecue Q sauce on the grill.

And that's an oxidative stress reaction.

That's enough and generates 100 times the reactive oxygen species.

It creates ages, right? We call it advanced location end products otherwise known as age you.

It can happen in your cell or you can eat it. So dietary ages. Yeah. 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. Yeah. The point is the sugar is what drives those advanced glycation products. But it's not just fructose, right?

Any kind of sugar will cause it.

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. Now, and we can talk about neonatal nutrition. Tricia, 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 because the emulsifiers are leading to that leaky gut.

So name some.

Carboxymethyl cellulose, polysorbate 80, carrageenan, By the way, which food has the most carrageenan? Almond milk.

Ice cream.

Ice cream.

Ice cream.

And who introduced carrageenan to ice cream? Is it a quiz? I don't know.

The Eskimos, it's seaweed. Margaret Thatcher. Margaret Thatcher. 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 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. 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. Another thing that's a big problem is monoglycyl acids, okay, 3-NCPD, it's a compound called E471. But you don't see it on the label of a fast food.

Well, no, you do see it.

It just doesn't call, they don't call it E471.

What do they call it?

Monoglyceral 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, right? So, if you're eating trans fat, you eat sugar, if you eat 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 say sugar, you also mean flour.

You also mean refined carbohydrate.

Refined sugar and refined carbohydrate. 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.

Because sardines.

Large fish eat small fish. Yeah. Right? Exactly. So how do we do that? So in 2020, I was contacted by a company that wanted to reduce calories.

But I noticed you didn't say reduce calories.

No, nothing about calories.

You didn't say- It's not about calories.

Yeah, 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.

That's 11.4 right now.

Okay, geez. 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 wanted 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, Andreas Koernstadt, 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 farmers 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? We came up with three precepts.

Yeah.

And these are the precepts of metabolic health.

I love that.

And we call it the metabolic Matrix.

I love this.

Here we go. Protect the liver. Yeah. Feed the gut. Support the brain. Any food that does all three of those is healthy, irrespective of its 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. Those are the three precepts. And you can actually determine.

How do you do that?

How do you do that? 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 a laboratory.

In a 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 forms 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 Gearing your food re-engineering efforts to vast concept of protect the liver, feed the gut, support the brain, you can actually make healthy food, even if it's ultra processed. 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 the-- so if you're not.

Eating Kuwaiti Danish food, what do you eat?

Well, we need to impress upon the food food industry here in America.

To do the same thing.

To do the same thing. 100%. It is a uphill battle to say the least.

I love this because everybody's looking for solutions. So this is really a solution.

This is a solution. Yeah. I am a scientific advisor to the Innovation Institute for Food and Health at UC Davis, who is, you know, 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.

Yeah.

Example, Unilever and Danone in the last two years reduced their carbon, sorry, their sugar footprint, both of 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. But 14% 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 gonna 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. Exactly.

That's how you really feel, Robert.

I will. How about that? So the point is 14% sounds good. It actually got a manual favor fired at DenoM. Yeah. Because of it. At KDD, at the Sakaei Danish Dairy, we have reduced the sugar footprint of that company by 78%.

That's amazing.

That's amazing.

78%. So again, what are people- Without changing taste. What are people in for lunch? Listen, like, this all sounds great, Mark.

This all sounds great, Dr. Ludwig. 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 man made.

Right?

Yeah, right.

I mean, if you think Cheetos is.

Food, I mean, you know, you're sunk. It's just that simple. 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. No, that's not the dictionary definition of food. It's something you eat.

I don't know.

Substrate.

You should know, I read a book about that. Yes, you should.

Substrate that contributes to either growth or burning of an organism. Growth or burning. 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. And 73% of the items in the grocery store are overdose with sugar. Does sugar contribute to growth? Does ultra-processed food contribute to growth?

Yeah, it kind of makes you grow.

No, no. My colleague, Dr. Monseigneur Ornan, who's the head of nutrition at Hebrew University of Jerusalem, has looked at this question. It actually inhibits trabecular bone growth, cortical.

Bone growth, skeletal bone growth, cancerous bone growth.

But it makes belly growth bigger. It hijacks growth, actually drives cancer formation. Yeah. Okay. Point is it does not contribute to growth. 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.

Well, if it's not a food, what is it? It's A.

Food like substance. Poison. Poison, right.

And so we have to start redefining what we need. So you are big in food as medicine. Dariush Mozaffarian, Big in Food as Medicine. I am here to say food can be medicine.

Or it can be poison.

It can also be poison. And when we start talking about food.

Is healer, food is slayer, it's like they're 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://perfect.co. And what it is, is it's a recommendation engine with a set of filters that will filter your 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, etc. 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. Because all of those nutrition facts labels are staring you in the face. There are 40,000 items. What are you going to do, Loree?

40,000 nutrition facts labels.

How many if you go to Whole Foods? It's impossible. It's still impossible. Point is, this does it for you. 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. Okay? There is a Nova filter, you know, our colleague Carlos Monteiro, so basically takes all the Nova class four items off. That's 80% of the store. Right.

Right.

Okay. You know, 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 gonna put that in the show notes and we're also gonna put the link to Levels because people wanna know their blood sugar. It's levels.link/hymen. If you wanna get access to the 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 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 and your books, which are incredible. And I think people need to take a look at them. I've read most of them. Fat Chance was the one I read all the way through, Hacking the American Mind and Metabolic, Metabolical.

Metabolical.

I want to say Metabolical, but like Diabolical.

Well, it is. Yeah.

And so, you know, 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. I gotta have you back because we just touched on things like artificial sweeteners. We touched on some of these high level constant about 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 will 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. Environmental toxins play a role. Redox plays a role. 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.

Didn'T-- I'm just up the road.

It's only four hours. 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 tries to reduce any of us, me, you, who are talking about this to some simple sound bite, 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, thank you for acknowledging my work, but vice versa. I mean, I hate to say it, but we're two very lonely warriors. I mean, there are people coming on board. There are a few, but I gotta tell you, I have been very, very disappointed in the standard medical architecture. Yeah, well, you know, 28% of medical schools even have a nutrition curriculum.

I wonder if it's because AMA gets $192 million from the industry.

Exactly. And 80% of the medical curriculum is underwritten by Big Pharma. Yeah. 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. 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 BioLumen, which you're part of, which helps create this fiber that you're talking about. Where can they find that?

They can find it at monchmonch.shop.

Spell that.

So M-O-N-C-H, M-O-N-C-H.shop.

That's where they can put all that in the show notes. Put all your work. Thank you for coming. Let's do this again soon because I.

Told you we gotta hang out.

I feel like I'm in a marathon and I'm at 100-yard line and I still have another 26 plus miles to go with you to back all this stuff. Thanks again for being here and coming all the way down. All right, if you love that last video, you're gonna love the next one. Check it out here.