Carbs, Insulin, and Fat Storage | JRE Obesity Debate

take around, fat and carbon take around. And then we can throw all that garbage into a meta-analysis. And the one thing I'm pretty confident is they did a poor job because of one study I looked up, the one with the biggest effect. They mistook kilojoules for kilocalories. So they reported that 400 kilocalorie decrease in energy expenditure on the low-fat diet when it was a 400 kilojoule, which is, what's that factor? You know these numbers. .8, .18 or something? Several of the other studies were Jim Hill studies. We've talked about Jim Hill. The biggest studies were Jim Hill. And the way we approached it at the not-for-profit is say, you've got to understand what the question is and you've got to design an experiment to get the right answer. So when Stephen dismissed this Harvard. We've got three names for him now. What's that? Stephan, Stephan, and now Stephen. DNA, I think I've got DNA right. Dr. DNA, can I do that? His name's Stephan, it's really easy. Stephan, I can't do it, dude, I just don't get names. My name's Joe. Hi Gary. That I know, hi Joe. Stephan ultimately rejected this study, it's about a $12 million study that was done at Harvard based on Kevin Hall. So these are two names. It's about three people out there who are convinced that everything people like me are saying is wrong. Not everything, but most of it. And they keep coming up over and over again. So Kevin Hall claims that he has refuted the carbohydrate insulin model in his studies. So when a study comes out supporting it, he works to find out why that study's wrong. We all did the same thing. I did the same thing right here with the Kunis study, explaining why I don't find it meaningful. But anyway, that's the thing. The goal was to do the right study because ultimately you've got to remember what's on the line here. We have obesity and diabetes epidemics. I mean tragic shit is going on out there. I mean people, these are ruining lives. They're overwhelming the healthcare system. And the argument I made is that for the past 50 years, basically people have thought a lot like Stephan is thinking now, Dr. Guinet, and that there appears to be another story that could be true. And what we have to do is find out if it is true because people are dying out there. So, okay, the first thing I want to say is that this alternative explanation that Gary is talking about has already been investigated intensively, including studies that were funded by his own organization, NUSI. Two out of the three studies that have been published on that were clear refutations of the hypothesis. And no, no, no, I'm responded here. I know, I know, but you've got to represent the studies correctly. Gary, Gary, Gary, Gary. Representing them according to your beliefs is not representing them correctly, okay? Now, I've noticed a remarkable correlation between studies undermining your beliefs and you thinking those studies are garbage. And we should talk about Jim Hill and his studies a little bit. Because, you know, to me, just saying this guy has a conflict of interest and then insinuating that that makes the study bad, if you can't actually find a problem with the study itself, these were very rigorous studies. If you cannot point out- I gave you the problem with the study. It was designed with an assumption. It was designed based on the assumption it was supposed to test. It wasn't designed how Gary wanted it to be designed. If you cannot find a problem with that study, then you can't just dismiss it by making these insinuations that the person had a conflict of interest, okay? I explained to you the problem with the study. That's great, Gary. Now, let's go back to the- I didn't realize Jim Hill had done it at the time. All right, you're gonna be able to respond to this in a moment. Now, the Kuna, I think we should really get back to this issue, this non-industrial culture, because the primary basis for Gary's book, The Case Against Sugar, the primary observation that underlies Gary's belief on this is this observational correlational thing that cultures, when sugar gets into these cultures, they become fat and that is the common thread in obesity and so what I'm doing is I'm pointing out a culture where sugar came in and it did not make them fat and that's one of three cultures. I haven't even looked that hard, okay? These are just three cultures that I came across. There's probably a bunch more that are eating high levels of sugar but they're eating high levels. And are not becoming obese. And I think- Funny is the same. And again, Joe, explanation is right on point. There's a lot of other things going on in these cultures and it's more complicated than just sugar. That's exactly my point. Now I wanna talk about the Cuban economic crisis. This is reference number 22. From 1989 through 1995, the Cuban economy collapsed and the price of food went way up. The price of gasoline went way up. And so people started focusing on these really cheap foods. Cuba was a major sugar producer at the time. I don't know if they still are. And so the intake of sugar went way up. Intake of refined carbohydrate went way up. The diet became a 77% carbohydrate, primarily white rice and sugar, 28% sugar of their total calorie intake. So that's like double what Americans eat. Now their calorie intake went down and because of the lack of gasoline, people got really physically active because they had to walk everywhere. So now, again, this is a situation where we can test Gary's hypothesis. If Gary is right and calories don't matter only refined carbohydrate and sugar matter, obesity should have gone through the roof in this population over that period of time. What you actually see is that the prevalence of obesity declined by half. So there was a 50% decline. It went from 14% to 7% over the period of this increase in sugar intake, increase in refined carbohydrate intake. And you might think, well, these people are just starving like crazy and that's why obesity rate went down. Well, we actually have evidence on the rate of underweight as well. And so we can check on that. The rate of underweight increased only slightly. It went from 8% to 10%. And so we know these people weren't just totally starving. And what happened then was as the diet rebounded, as the economy rebounded and the diet rebounded and their diet shifted away from these refined carbohydrates and sugar and back to the normal diet that was higher in fats and lower in carbohydrate, lower in sugar, the obesity rate went right back up as soon as they went back to their normal diet. And so I find this- Because they were not walking as much. Yeah, it was the exercise and also just their diet became richer again. I mean, if you're eating a diet, that's a very poor diet, eating like white rice and sugar. I mean, it's not like, if that's most of what, if you're sitting there and on your plate is a white rice and sugar, you're not gonna be eating a ton of that and getting fat as opposed to eating a richer diet with more varied foods. And so this is a case where you have an entire country testing Gary's hypothesis and finding that basically the opposite of what his hypothesis predicts. Gary, let's go with the, when he was refuting the studies and you wanted to- But this was a level of discourse that I didn't really wanna get into because that's a study that I'm gonna have to read. He's right, I'm gonna read it to try and figure out what the problem is. I remember looking at that study and thinking there wasn't the kind of data you're citing. Maybe there's multiple studies put together, but the one study I looked at, the kind of data you're citing wasn't in there. This is again a problem. References are on my website, so have at it. No, I will, but we'll be off the air by then. The beginning of his, when he started talking, he was referencing some studies and you had a problem with that? Well, this whole, it's a game people plan. Again, it's why basically in my book I try not to get into the he said, she said studies because you never know how well they did. I think we both agree that there's a reproducibility crisis in science and some huge proportion of the studies are just wrong. Whether they're experiments or observations, people sometimes aren't very good at what they do. And so anyone in either business, Stephen likes to say I have no evidence. Stephen, damn it. But simultaneously people excuse me of writing a 600 page book with 150 pages of references that was too long to read. So there's clearly evidence for this observation and this hypothesis. My issue with Stephen is that he speaks as though he knows with this authority. And so again, I would like to just read a little bit from your book because as I was prepping for this, before you do that though, he was referencing studies. The Cuban situation, I don't know what the reality is. Before that, when he first started talking, he was referencing things that you were stating that he was saying, what were you saying that the organization that supports him actually refuted some of these? Oh, that was the Jim Hell studies. No, no, no, no, no, the Newsy studies. Now we're talking about the Newsy studies, the first two of which, and we can get into detail on this on how those refuted Gary's beliefs. And I would say Gary is about the only person who thinks they did not refute his beliefs. The scientific community is pretty unanimous. You can respond, but could you please say what would the study state? Well, let me do it before he, so the first study is a pilot study that depends what you look at to depend whether or not it refuted your beliefs. So there, again, you have to understand this world. There are researchers who believe one thing, Kevin Hall and NIH tends to believe that obesity is an energy balance problem and people get fat because they eat too much. I hope I'm doing Kevin justice. And then there's David Ludwig and his colleagues at Harvard who tend to believe what I believe. And we funded them both to do studies, and Kevin Hall's study. If you believe what Kevin, if you believe Kevin interpreted it correctly, was not supportive of this model that carbohydrates are ultimately driving insulin, and insulin is driving up fat accumulation. And then the David Ludwig study reported the opposite, and David has criticized Kevin's study and Kevin has criticized David's study, and this is the nature of science. This is what you do in science. You do an experiment, people critique it. Ideally, you do another one. Kevin has decided, well, Kevin is doing another one. I think he's asking the wrong questions, but what I just saw the other day that he's doing another experiment. To me, the middle study was a free living diet study where done by Christopher Gardner at Stanford University. And the idea was, original idea was 600 people randomized to either a very low carbohydrate diet or a very low fat diet. And we funded it in part because we hoped that Christopher would be able to get people to almost a ketogenic diet on the low carb side. And Dean Ornish, who promotes a low fat diet, always complained that the low fat diet wasn't fat enough, so hopefully they'd be able to separate out these two. At the end of the trial, they got pretty lousy adherence. Low carb was about 25 to 28% carb, which is by no means a low meaningful low carb diet. Pretty typical. In free living studies, and the low fat was about equal. What they did, which it's funny, we realized this on one side, but not the other, they told the low carb group not to eat sugars and refined grains, which are, by my hypothesis, the most fattening carbohydrates. And they also told the low fat group to not eat refined sugars and refined grains. So they basically removed the most fattening parts of the diet from both arms of the study. It's funny, we knew that we were gonna do it with the low carb group, because you have to. And my colleagues actually knew they were gonna do it with the low fat group. I didn't know that when I found out I was stunned, because now you're testing two diets, neither one of them have sugar or white bread. So now you see similar weight loss with relatively poor compliance. Why would they do that? That doesn't make any sense with the low fat diet. Well, they're argument, and we talked to Chris Furlotta. His argument, he was afraid, there were two things. He wanted the diet to be healthy. So a healthy diet in 2015 has become a diet that doesn't have sugar and white bread in it. So he wasn't going to promote sugar and white bread to one diet or another. I take some- How long was the period of time where they were studying these people? They were on the diet. They were supposed to be on the diet for a year. Okay, that makes sense then, right? Yeah, so the question is, again, would you expect to see a difference? I can send you an email I wrote to my NUSI colleagues in 2015, I could read it. When I found out about the slow fat thing, saying this is insane. He's removed the, both groups are carbohydrate restricted. So you could think of it as a low fat, carbohydrate restricted diet, and a high fat carbohydrate restricted diet. And then he kind of got the same answer, which could be for any reason whatsoever. There's a paper, I don't know if I can, well, I'm not going to talk about it. It's bad enough talking about ambiguous studies that have been published without getting into unpublished research. But, so people see this, the New York Times, for instance, did two stories on it. One of them said, it's not about calories, it's about the quality, the sugar and the refined grain, because both groups restricted sugar and refined grains and lost weight. The other, and that was written by a reporter who tends to believe what we believe. And the other article said, it's all about the calories, because both groups ended up on average eating 500 calories each. It ends up, from a scientific perspective, being a poorly done study, even though we funded it. I'm not, it just didn't answer the question. You said 500 calories each. 500 calories less. On average, they restrict their calories. And that's actually self-reported, so it's not accurate. So it's not particularly meaningful. So again, these are, I don't like using, it's whether or not. That's a complicated study because it's low in sugar. Well, and it's also free living, yeah. So both sides are low in sugar, both sides are not eating processed foods. There were two full differences in total carbohydrate intake, okay. So even though they were both not eating as much refined carbohydrate, there were still two full differences or greater over the period of that study in total carbohydrate intake. If you believe the food frequency questionnaires that you just said, we don't know whether we have. And you could be talking about vegetables, you could be talking about fruits. Well, these are healthy carbohydrates that they had primarily in this study. Can we agree that that study can be interpreted from virtually any way you want it? Especially because it was a free living study. I definitely don't agree with that. Now, what we will agree on, I'll agree with you on this, is that refined carbohydrates and sugar are the most fattening type of carbohydrate that we can agree on. Oh my God, we came to an agreement? No, but the question is why? Is it because people eat too much of them? Here's the thing. If you believe Gary's hypothesis, now any kind of carbohydrate increases insulin levels. Some do it more than others. Refined carbohydrates do it more. Any kind of carbohydrate increases insulin levels relative to fat, okay. And so if that is true and these groups, and that matters for fat loss, these groups had two full differences in carbohydrate intake. Even though it was predominantly healthy carbs, you should have seen something. You shouldn't have seen the exact same amount of weight loss in these two groups, right? Right, but they're not high in sugar. Correct. Like isn't your argument as always that sugar. That's the other part of the argument, which is you take away the sugar and that was the problem with, one of the problems with the energy. Yeah, the argument I make, and Stefan's completely right, I'm defending my hypothesis, okay. I see a study that, he does the same thing. He did it here. We all do it. You see a study that disagrees with you. You find the reason why they're not believe it, and every study ever done has plenty of reasons not to do it, not to believe it. That's why independent replication is something you always wanted. You get another group to do the study, ideally a third group, people come in, they criticize the study, then you do it again, and again and again. And so, you know what I was trying, even when we started the nutrition science initiative, that was a nonprofit, the choice of the word initiative was to get nutrition researchers to, in effect, stop using these garbage poorly designed studies to come to conclusions because they like or dislike the interpretation, but try to get them to think the way harder scientists would. In developing studies, it asks precisely the right question. And then, so even the pilot study that was interpreted is not supporting this hypothesis, and again, you could argue that for an hour and nobody's gonna care. That study was not randomized. So a non-randomized study, you can't infer causality. That's why it was a pilot study, one of the many reasons it was a pilot study. The people who think this carbohydrate model. So when we talk about the carbohydrate insulin model, it means carbohydrates are fattening. That's the basis of it, bread, pasta, potato, and sugar may be the thing that's necessary to add to the diet to make all these carbs fattening because sugar, as we talked about this a year and a half ago, the fructose molecule is metabolized in the liver. It's linked to fat accumulation in the liver, which is linked to insulin. I don't know the way you're squeezing your stomach while we're talking about this. I gotta work out, dude. I'm just bored. For these experiments to be done right, they have to be tested right. I think you can't use poorly designed experiments, and every experiment ever done. What we've tried to do is keep working towards better experiments. There's now a new version of the Ludwig experiment being done at the Arnold Foundation. Lauren John Arnold funded to the tune of, I think, 13 million dollars. And whatever that study finds, Kevin Hall will probably find a reason, look in it and find a reason to question it. Ideally, they would be working together so that you've come up with the criticisms before you've spent 13 million dollars, but this is how science works. My job was to tell a good story, as Stefan would say, and I believe people who read the books can judge whether it's a good, you know. Am I convincing in arguing that you add sugar, counter evidence to everything? There wasn't counter evidence. I wouldn't require a journalist to come along in 20, whatever it is, 19, to make these arguments. Let me ask you this, because this is something that you've admitted to, something you said, rather. Why are sugary carbohydrates the most fattening? Well, if this hypothesis is correct, I think you would say that they trigger a food reward, or they are a food reward. Yeah, absolutely. Wait, wait, wait, let me just finish. I would say the counter argument is that they create a hormonal milieu in the body that over responds to insulin. And insulin, what we haven't said is, if you look in a textbook for fat metabolism and fatty, you know, what causes fat storage, insulin is the hormone that primarily regulates fat storage in your fat cells. So the idea is you raise insulin, and the sugar, because of this half of it being fructose, and that mostly being metabolized in the small intestine and the liver, seems, may indeed cause insulin resistance, and if it does, you over respond insulin. So one is a peripheral explanation, not that people don't love it, and they don't wanna over consume it, whatever that means, and the other is a central explanation. Yeah, so I mean, sugar is a factor that makes us wanna eat foods, right? I mean, this is one of the many food properties, and I would love to talk about this more, that cause dopamine release in the brain. And dopamine is a chemical that sets our motivational levels to do certain behaviors. So the reason we become addicted to drugs is that they go in the brain, and they stimulate dopamine release, and that reinforces drug seeking behaviors. Right, but this is just causing you to consume more. Correct. But you're saying that the actual amount, let's say if you have the same amount of carbohydrates that are sugary carbohydrates, versus the same amount that are vegetable carbohydrates, the sugary carbohydrates are gonna be more fattening. No, no, I didn't say it was independently of calories. It's entirely dependent on calories. Yeah, correct. And we have randomized controlled trials demonstrating this. So if you look at the randomized, by the way, we're not operating in an evidence vacuum. There's tons of randomized controlled trials on sugar. Can I ask you this? Yeah. These randomized controlled studies, are they short term? Well, it depends on how you define short term. They're not lasting years and years and years. Isn't the issue though, long term chronic effects? Like that seems to be- Possibly, but let me put it this way. If you believe that insulin is the cause, the effect of insulin on fat cells happens almost immediately. So insulin, I'm not aware of any mechanism of insulin on fat cells that takes more than a few hours to occur. And so if you believe that insulin causes obesity, this should be happening immediately. You shouldn't have to wait months and months for this to occur. Oh, no, that doesn't make any sense at all. No, it does make sense. Why doesn't it make sense? No, no, no, it doesn't make sense to me. You eat carbohydrate. Why doesn't it make sense to you? Well, because again, he's kind of making this up as he goes along. So the idea is- Oh, Jesus. Well, explain why it doesn't make sense without insulting him, if that's possible. Has he not been insulting me? Or am I just biased? I realize that everything is perspective. I don't necessarily think he's insulting your stories, not you personally. But why doesn't it make sense to you? Okay, so the idea is when your insulin is elevated, you're storing fat, right? It depends on what you mean by that. That's not, see, you do a little bit of bait in the switch here. No, no, no, no, that's an intel. Just answer the question. If it's not true, clarify. Well, it depends, what do you mean by store? I mean, your fat cells are accumulating fat when insulin is elevated. Do you mean accumulate like next day you'll have- I called on to fat. Like it inhibits- Yeah, that's incorrect. It stimulates lipoprotein lipase and it inhibits hormone- We should really talk about this because that's incorrect. It's in the textbooks. No, yeah, we'll talk about what's in the textbook. Don't worry, Gary. They, Jesus. Okay, so you don't believe insulin. Well, just give me your position and I'll let him refute it. It's here. But just say it. No, no, we'll just show it, okay? Okay. Because again, you're gonna say it's not in here, so I have the same textbook. And then we'll let Joe hear, suppression of fat mobilization by insulin. And there's another graph that is stimulation of fat mobilization. Congratulations to all of you people that are listening to this. Yeah, we're all- They're still hanging in there. I know we're in the weeds scientifically. Let me just say, this is gonna take a long time. So we agree on the molecular mechanisms. We agree on the molecular mechanisms, the impact of insulin on enzymes and fat cells. What we disagree about is the implications of that. And I think that's what we should talk about. Because nowhere in that textbook does it say that insulin regulates the total size of body fat stores. Absolutely, absolutely. That is something that you have added onto that mechanism. Would you like to know the conversation I had with the author of that textbook? Not right now, actually. So the- Now the- Let me tell you about the conversation I had with Gary. Let me explain this. I was actually in Oxford. We talked about this for three hours. Can you stop interrupting me, please? Okay. Now, let me explain. So insulin essentially does have effects on enzymes that cause fat cells to take up more fat and to release less fat. So that's the part that you're right about. That's what that textbook talks about. Now, that does not mean, that does not imply that insulin causes fat storage as in the accumulation of fat from day to day. And let me explain why that is. So insulin is basically a traffic cop that allows your body to burn the fuel that you just consumed. So when you eat a diet that's high in carbohydrate and low in fat, your insulin goes up, your body restricts the fat from going out of fat cells. It turns that down, not off, but down. It causes less fat to come out of your fat cells and then your body's burning carbs. That's what you just ate, right? Now, if you eat a diet that's high in fat and lower in carbohydrate, you secrete less insulin. Those effects don't occur on your fat cells and that allows your body to burn the fat that you just ate. But at the end of the day, the amount of fat that you have in your body is the amount that you ate minus the amount that you burned. That's what determines the amount, this is just arithmetic, right? Amount that you ate minus the amount that you burned. And if you eat a low-fat diet, you're not eating much and you're not burning much, you're in the same place as if you're eating a diet where you're eating a lot of fat and burning a lot of fat. And the way we know that's true is because varying the amount of carbohydrate and fat in the diet makes no difference to body.