Does Overeating Lead to Obesity? | JRE Obesity Debate

Can I pause here? Leptin is produced where? Yeah, leptin is produced, yeah, let's talk about leptin a little bit. It's produced in fat cells and it's produced in proportion to the size of fat tissue. So the amount of body fat you have, the more fat you have, the more leptin you have in the circulation. And basically what this is, it's what's called the negative feedback loop, which is a really simple engineering term that works like a thermostat. So with your thermostat, if you set your thermostat to 70, if it starts getting a little bit hotter, your AC turns on to bring it back down, it starts getting lower, the heat comes on to bring it up. That's called the negative feedback system and it maintains the stability of the temperature of your house. We have many negative feedback loops in the human body to regulate body temperature, to regulate blood pressure, to regulate all sorts of things. One of the negative feedback loops we have regulates body fatness. And the hormone, so your thermostat measures temperature by using a thermostat, sorry, a thermometer. Your brain measures body fatness using this hormone leptin that's in the circulation. And then particularly when your body fat level drops, your leptin levels drop and your brain hears that and it kicks in a starvation response basically. And this is the main reason why weight loss is so difficult because your brain is like, no, I don't want to be losing fat. And it makes you hungrier, it increases your cravings. Can I pause there? Yeah. Is that at a certain level of body fat? Is this just when you're losing body fat in general? Like even if you're a large person that's overweight? Correct. When you're losing body fat in general, your body exacerbates your hunger. And this is a thing that's really important to understand about obesity is that people with obesity have a higher set point. So it's like turning your thermostat from 70 to 80 and then your thermostat's regulating around 80. People with obesity, they're not regulating around 170 anymore, they're regulating around 250. And so when you cause a lean person to lose weight, you see the same thing as when you cause a person with obesity to lose weight, you see this reaction in their brain circuits that regulate body fatness that drives them to increase their cravings and their hunger, their metabolic rate drops. So it'd be an evolutionary mechanism to force you to seek food? Correct. And not just to force you to seek food, that's the main thing, but it also slows your metabolic rate, does everything it can to get more energy in your body and have less leaving. And it keeps doing that until the fat comes back. Can I pause here? Yeah. So when you're eating a sugary diet, a high calorie diet, you will produce more fat. Your body will get fatter, right? It depends on how many calories you're eating. If you're overeating, you're consuming a lot of sugar, a lot of carbohydrates, your body will get fatter. So your body will produce more leptin. Correct. So it comes from the diet? Yeah, indirectly, definitely. Can I pause? Please. So the leptin is produced not just in response to the size of the fat cell, but in response actually to glucose-mediated uptake into the fat cell, which is mediated in part by insulin. So you come back to insulin even with the leptin, you raise blood sugar and that's the carbs you eat, the carbs you raise. Blood sugar, you raise insulin, you raise fat storage, the glucose, and then you get more leptin. Again, one of the things you have to understand about this is everything that's said has two interpretations depending on which paradigm you're looking at. And these are fundamentally different paradigms. So in Stefan's world, and again, correct me if I'm wrong, the leptin is signaling fuel availability in the fat cells the way I would think of it in my very small world. Leptin is responding to fuel availability in the rest of the cells. So it's basically a molecule that can tell other cells that there's fat available and you could burn that fat for fuel and then you don't have to go eat. Or it can tell that there isn't fuel available. And depending on how much leptin there is, the cells, and then that will respond by a signal to eat or not to disinhibit eating behavior. Everything we're talking about, Stefan and I first sort of fell out, I don't know, eight years ago at the ancestral health symposium when I acted improperly, inappropriately. But one of the problems I had, so the way I think you should think about this, you have a hypothesis. And this is the fundamental thing, is obesity caused by overeating. Because we know if you're getting fatter, you're storing more calories than you're expend. That's just the, you know, that's like if a room is getting more crowded, more people are entering than leaving. That is the simplest, but it doesn't tell you why the room's getting crowded, it doesn't tell you why you're getting fatter. And again, what I've been arguing is the why you're getting fatter part has been left out and people decided that overeating was somehow an explanation. Then they went to the brain to look at why people might overeat. So what I, one of the questions I asked Stefan eight years ago, and it keeps coming up, is if we're going to blame obesity on the modern food environment, epidemics of obesity, you know, simple question to ask is can we find epidemics of obesity without this modern food environment? I mean, that's a sort of science 101, right? And it turns out that the world is full. And the first one I found in the literature was in 1902 in a population of the Pima Native American tribes, Pima living in Arizona. And observers saying these people are poor, they're malnourished, they're suffering through famines. They've been suffering through a famine for 40 years and famines, it's hard to overeat during a famine. And yet the women of the tribe who do virtually all the work, they were treated as pack animals in effect, were obese. So now we can disassociate obesity from the modern food environment. And we could disassociate it from this ultra-processed foods we eat and start to ask the question, what is it about? Can we find what might have driven obesity in that population despite the existence of famine? So it's from very simple observation. Once we get into these kinds of studies, say this and human genome studies say that, I actually rarely do that in my books because you can find studies that will say anything. And you'll see in the studies people misinterpreting them. What was the cause of the population of women to be obese? Well, so one of the things that happened during the beginning in the 1860s, the Pima were put on a reservation. They were reservationized, whatever the verb form would be. And they began eating Western foods. And back then it was sugar, flour, and lard for the most part, and sugary beverages probably. So that's a reasonable hypothesis. And you could find the same thing in the Sioux, Native American Sioux population living on a reservation in 1928 where you had both obese men and women living with malnourished, stunted children who clearly weren't getting enough diet, but they were on a reservation. They were getting Western foods. So ultimately, the question you ask in science determines the answer you get. So the question I was asking is we have this observation that any population that transitions to a Western diet or a Western diet and lifestyle gets obese and diabetic. They develop what's called metabolic syndrome, which is insulin resistance and all these issues. And we know that's true all over the world, from the Inuit to the Pima to South Pacific Islanders to Africans to Europeans. So the genetics aren't that important. The question is what's triggering it in the environment? And again, Stefan would say, well, there's too much food available. And it's too palatable. And we can't say no. And I have a lot of problems with the we can't say no part because if we're lean, it means they can't say no, and they being the people with obesity. And I don't believe that's true. And then, or is it some specific item or some specific group in this, these foods that travel with Western populations? And so the exists, the ability, and today, if you look up dual burden of obesity and malnutrition, I have a Dropbox folder I could share with you. There's probably 50 studies all over the world. You see the same observation, incredibly poor populations, malnourished, the children are stunted, which means they're protein deficient and they're calorie deficient. And often the mothers or the aunts or obesity, obesity tends to run in the females, which suggests it has a female sex hormone related effect that I don't believe works in the brain because we're dealing with populations that could not have overeaten. If they could have overeaten, why are the kids starving? That's sort of the question. And this was the first thing that I think we thought about back then. And it's still, if you can find populations with obesity epidemics, but without the modern food system, without snack wells and without Lay's potato chips. And if you know that they're going through a famine or you know that the kids at least aren't getting enough food, how do you explain obesity in the mothers without assuming that the mothers are overeat? Let's pause right there. Stefan is there a population of people that are obese, that are not eating a Western diet, that are not eating sugary foods? That are obese and that are not eating sugary foods. Probably not, because generally once you have an industrialized food system, that's going to include sugar. But there are populations that eat a lot of sugar and are not obese. And we should talk about some of these. Actually, let's talk about the Pima first. Can you go back to the... Yeah, sure. Let's talk about the Pima first. Now Gary has told a story. He's told his version of the Pima story. Let me tell the story, the version of the story that appears in the scientific literature. Now the Pima, originally they were agriculturalists. They were eating traditionally a very high carbohydrate diet based on unrefined carbohydrates. It was corn, beans, and squash, primarily. They were hunter-gatherers and agriculturalists. They were primarily... They were hunters. Gary, okay. They were primarily eating agricultural foods. They were also collecting some wild foods, that's correct. They were fishing and eating the skeet pods, primarily agricultural. And data are very clear on that, Gary. So... No, no, no, no. Yes, they are. Look, we have data. Things like that, Stefan, because we're going to disagree on what the data say. Let's move on. You think they ate mostly fish. That's incorrect, okay, according to the data. I remember you saying that in your book, something to that effect. Stefan, read what you've got in my book. Read what I say. Okay, anyway. Just read what I say. Let's go on. We don't know you better read what I say. I'm going to move on here. Now the Pima, traditionally we're agriculturalists. And what happened basically is you had all these farmers moving into their area, settlers, of European descent, and they diverted the water from their river, the Gila or Gila River. Gila, not Gila. And so they were no longer able to grow their crops, their agricultural crops that they were primarily dependent on. And therefore the government started providing them with foods to eat. And these were calorie dense refined foods. They were, like Gary said, flour, lard, and sugar. And then they became very obese. Now there was a population of Pima right across the border from them in Mexico, also very similar culturally and all that, that maintained their traditional high carbohydrate lifestyle and agricultural lifestyle. And there have been studies comparing those two populations. And the ones across the border with their traditional lifestyle are a lot leaner and healthier, not surprisingly, than the ones eating lard, flour, and sugar. But Gary, you seem to believe that people can gain weight. You kept referring to famines and things. You seem to believe that people can gain weight even if they are eating very few calories. And you refer to this many times in your writing. And these are very casual observations that you're making, kind of these casual correlations and storytelling. But if you actually look at the data on this, what you see is that if you just measure calorie intake in people who have obesity, it is 20 to 35% higher than people who are lean after correcting for height, physical activity level. And I've got the references here. Can I, can I, no, no. This is, we're getting a little bit into the weeds here. Let me give you an example. Reference number seven. Can I pause you guys right here? So these people, they have essentially the same lineage. One group lives in Mexico. They're not eating these sugary foods in this Western diet. The ones that live in America are, the ones that live in America are becoming obese, the ones that live in Mexico are not. Is that correct? Correct. Yeah. And so now if you have someone with obesity, like I've said, the most accurate measures that we have suggest that they habitually consume and expend more calories. And now Gary's model says that that is downstream of the fattening effect. It's not causing the fattening effect. It is a result of the fattening effect. Whereas my model says that that is actually required for the fattening effect to occur. It is upstream. So how did those people get trapped? Now what happens, what happens, Gary? What happens if you reduce their calorie intake by that same amount, 20 to 35%? Doesn't matter if you do it by restricting carbs or fat. These experiments have been done. They lose weight when you restrict their calorie intake down to that. This is the argument, what you're saying, that consuming low amounts of calories but high amounts of sugar doesn't make sense. You can get obese that way. Right. So you're saying it's a calorie dependent? Yeah, correct. And that's reference number nine and 10 to support what I just said. And I want to talk about another one that really- Wait, wait. Can we hold on, Stefan? You didn't- Yeah, let's- What I, the reason I was using the dual burden example is because we have to explain how those women are eating all those calories. They're usually women again. It's just often it was, often these studies were done by diabetes researchers who were studying diabetes in these populations and the men had high levels of diabetes and the women had high levels of obesity. To give you an example where that measurement was done, in Trinidad in the 1960s, and again, all I'm doing, this is the role I played, is I asked the question, can you find populations that don't have a lot of food? Okay. And I would say that the obese expend a lot of energy and they eat a lot of calories. The question is, can they get obese without a lot of food? And so can we find populations? Like you asked, can you find a population that gets obese without sugar? Which was exactly the question to ask. So in Trinidad in the 1960s, there's a malnutrition crisis. The US government sends a team of researchers down to study this and the researchers come back and say, yeah, there's malnutrition, there's stunting, there's deficiency diseases, and two-thirds of the adult women are obese. And this is a medical problem. And the next year, an MIT nutritionist goes down to do exactly what Stephan asks for and to actually measure the diets in obese women and lean women and to study it. And this is a population where it's unlike, I mean, this is a very poor Trinidad population. And reports that they, I think it was 1800 calories a day, what the obese women were eating was actually a little less than what the lean people seemed to be eating. And that it was lower than what the Food and Agriculture Organization considered for a healthy diet. So again, what my role in this is to point out when you have populations like that, I don't see how the overeating hypothesis tells me the brain is in control of how much they eat, tells me anything about why the women were obese, especially when their kids were starving. This is the paradox of this duper, an obese mother with a starving child. If the obese mother has to eat superfluous calories to get fat, why isn't she giving those calories to her kids? Because she doesn't need them. She clearly doesn't need them. She's got fuel. So what's going on there? If you posit a hypothesis, as I did, which says that the obesity is triggered by the macronutrient content of the diet, then you can explain. I mean, there are plenty of animal models. A famous quote I use in my books from Jean Maier. It was like the same leading Harvard nutritionist who studied an obese strain of animals in the 50s. He said, my animals will get fat even when half starved. They will make fat out of their food even when half starved. These are generally animals with mutations in the leptin pathway, by the way. Whatever gene it is. The question is, if I can make fat out of my food at levels of – at caloric levels that, for instance, a lean person can't, then I'm going to get fat eating the same amount. That fat accumulation is going to be – means I'm taking in more calories than I expend, but the point is I'm – for some metabolic hormonal reason, I'm taking the fuel I eat and turning it into fat and storing it in the fat tissue. What is your response to this? Yeah. So, my response is that if you want the best answers, you have to use the best methods to answer the questions, okay? If you want a question answered properly, you have to use accurate methods to answer that question. Now, as you know, Gary, it's very difficult to measure food intake in free living individuals, particularly you're traveling to a country you've never been to before. It's very difficult to get accurate measures. So, just because some guy went to Trinidad and claimed – It was a woman, actually. Okay, fine. Just because some woman went to Trinidad and claimed that people were eating 1,800 calories and becoming obese does not mean that that's what actually happened. Now – Wait a minute. No, no, no, no, no. Gary, I'm responding. Now, we have studies where researchers used accurate measures to measure calorie intake in people who had obesity. Many of these people were saying were only eating 1,200 calories a day when they actually measured their calorie intake. What they found was that they were consistently eating more calories than lean people. So, this phenomenon that Gary describes is something that is only observed when inferior methods are used to measure calorie intake. Wait, wait, wait, wait, Stefan. The reason I'm using these populations, like I said, I'm just giving you an observation. Obese mother with a starving child, the dual burden of malnutrition and obesity. This isn't one observation. It's not one nutritionist. The existence of the starving children strongly suggests that there's not a lot of food available and we have to explain obesity in the mother. You know, I – That's what I would like you to respond to. Okay, fine. I will respond to that. Now, look, I haven't looked at these studies in particular. I brought them up eight years ago. We got in a fight about it. Wonderful. We fell out eight years ago. It's like we used to be biting. So now, look, there are many reasons why a child could be malnourished in a non-industrial situation and this is – I do a lot of work related to this. What you see in non-industrial situations, you see a lot of infectious disease, you see a lot of malnutrition, so people not getting enough essential minerals and vitamins, not getting enough protein and you see a lot of children who are just barely hanging on because of this collection of really bad stuff that's happening in their lives. And so – Parasites, things along those lines. Yeah, yeah, parasites, malaria. I don't know if there's malaria in Trinidad or not, but I mean all the diarrhea, pneumonia, these are the things that we all had before we had modern medicine and great sanitation in a country like the United States. 30% of kids didn't even make it past childhood. And so there's a lot of things that could have caused that, Gary. It's not necessarily because, you know, it's not necessarily the reason that you attribute it to. Now – I'm not attributing it to a reason. I'm just asking for explanations. Okay, well, great. Well, I don't have the explanation, but I'm throwing out possibilities that are alternative to the one that you're implying. And that's quite possible to me. So now, I – so again, when you use accurate measures of calorie intake, you find that these people with magical metabolisms who have obesity and don't eat very much seem to not exist anymore. And furthermore, I want to get to another type of study that's really going to differentiate between this metabolic effect driven by insulin and the effect of calories. So we have a lot of studies that compared diets in which calories were the same, but carbohydrate and fat intake differed. And the ones that I really want to focus on right now that I think are key here are the studies where they increased calorie intake. So they fed people. One study in particular, and let's see, I'm going to give you a number here. Let me see if I can give you a number here. Sorry. Let me look at that. Can we bring up another issue? Because what we're talking about ultimately is why people get fat. Okay. I don't want to divert here. I'm in the middle of something. So now, if we want to understand why people get fat, we can look at studies that overfed people on fat or carbohydrate exclusively. So this one study, the first one that I want to talk about, first they figured out people's baseline calorie intake, figure out how many calories they needed just to maintain, and then they increased that by 50% by exclusively giving them fat or exclusively giving them carbohydrate. Okay. Which study was this? This is Horton. Okay. Give me a second what you're doing. Yeah, so number 16. So now, if Gary's hypothesis is correct, these people should have gained body fat on the carbohydrate overfeeding, but not the fat overfeeding because that increases your insulin and has these effects on your fat cells, et cetera. Okay. Now, these were very rigorous studies. I want to emphasize that. Can I pause here? Yeah. Did they monitor the actual calories they got? Correct. Yes. They were... Go ahead. They had a baseline. They used prisoners, but they were months. No, that's incorrect. This is a different study. So they had a baseline, and did they require them to maintain the same diet and then add additional fat or additional carbohydrates? Yes. Yes. So same diet. So they had the same foods? And then they just bump it up with fat or bump it up with carbohydrate. Wait, wait, wait. What study did Horton... There wasn't Sims. It was Ethan Sims. What study did he do that was not prisoners? What was the... He didn't have a metabolic board. You know what? Let me just finish describing this study. No, it's just that... Gary, that's an irrelevant detail, okay? What's relevant is that you just implied that I don't know what I'm talking about. Gary, you know what? I don't actually know. Maybe it was in prisoners, okay? Thank you. All right. You're welcome. Now, but it was not the Sims overfeeding study that was done in prisoners. That's what I know, okay? Okay. The reference. What's the reference? Yeah, it's on my website. You can go to my website, stephangeana.com, and it's reference number 16, and they're both there. Okay. So this was what's called a metabolic ward study where these people were in a research facility where the researchers could monitor and control every morsel of food. So there was no cheating, no inaccuracy, and they were measuring changes in body fatness using a gold standard method called underwater weighing, okay? And so what they found was that at the end of a two-week period of overfeeding, the carb and the fat groups gained the exact same amount of body fat, exact same amount of body fat. There was another second study that did the same thing and found the same result. Independent lab group, very similar experiment, three-week long instead of two weeks, they found the exact same thing, same amount of fat gain, different insulin responses, different amounts of carbohydrate and fat, exact same amount of fat gain. So this demonstrates that insulin is not, and carbs are not what controls what gets fat into fat tissue. Calorie intake is what controls that. So let me explain again, remember I talked about the paradigm you work in determines the question you ask. And this experiment is a classic example because they assume that people get fat by overfeeding. So then they say if we overfeed them, we're just doing what happens naturally. Everything about the experiment is based on the assumption that they're supposed to be testing, which is can people get fat by overfeeding? And so from the very conception of the experiment, they've built in the paradigm that we want to test, the hypothesis. On top of it, if it's a typical Sims experiment, I actually wasn't familiar with this one. Oh, it wasn't Sims. It was James Hill, JC Peter. James Hill was funded from about 1998 to about 2008 by Procter and Gamble because he was an Alestra shill. I hate to say that, Jim. I apologize, but I think it's a fair assessment. And then when he stopped being funded by Procter and Gamble, he was funded by the sugar industry. And JC Peters was the head of the Procter and Gamble Alestra. Alestra, which is now something that no one eats. Yeah, Alestra was a fat substitute. The problem was you got like run out. Oof, less diarrhea. I hope the anal gas and shit like that. But the whole idea of Alestra was to replace fat in the diet. So every study, Helen Peters did implicated dietary fat as a cause of obesity. I don't think we could ever use, I hate to say it. I mean, typically, I don't think funding influences results, but I wouldn't use a James Hill study to make that point. Because you think it's a biased study that was influenced by it? Everything Helen Peters did. And when it was, I mean, I talked about this in good calories, bad calories. And they reported their results. Actually I did a FOIA on James Hill because he works for the University of Colorado. So you could actually, and I got all those documents back and forth between him and Alestra. I'd be happy to share them with you if you'd like. They're rebel, I mean, him and Procter and Gamble. But he basically held Procter and Gamble for ransom. He would get a $500,000 unrestricted gift. And then he would do a study and then he would ask it, and it would conclude that fat is bad and carbs are good and therefore Alestra is a viable product. Then he would ask for Procter and Gamble for more money before he then published the study. So it's a particularly egregious example of someone who's, I suspect it was just his belief system. He believed dietary fat was bad, fat caused obesity, Alestra is a good thing because you eat that instead of fat and you don't absorb it. And then every study he did confirmed that.