In this episode, Dr. Gary Taubes and Dr. Stefan Guillenet debate whether or not the brain plays a role in obesity and insulin resistance, which is the root cause of many chronic diseases like diabetes, heart disease, and obesity. Dr. Taubes argues that the brain controls fat cells, which regulate body fatness, while the brain also controls the speed of the car, which determines the tire on the car. In other words, the tires are fat cells and the brain regulates fat cells. Why does the brain regulate fat cells? Why do fat cells regulate fatness? And why does the car go faster than the other cars on the road? Today's episode is a mashup of a debate between two people who disagree with each other on the cause of obesity and the role of the brain in obesity, and why the brain is more important than other parts of the body in regulating fatness and glucose production. This episode is sponsored by Whole Healthsource.org. To find a list of our sponsors and show-related promo codes, go to gimlet.media/OurAdvertisers and use coupon code: "WEBSITE" at checkout to receive 10% off your purchase of $10 or more! We're giving away a free copy of The Hungry Brain book, "The Hungry Brain: How to Eat Healthier and Live a Better Life" at the end of the episode! We'll be giving away $10, $20, $25, $50, $60, and $75, $100, and there's a year-long membership gets you get an ad discount when you sign up for the book is reviewed and reviewed, and a discount of $150, and I'll get a copy of the book review, too! I'll be shipping it to you get the book and you'll get $5, and they'll get 5 of your choice, and it'll get you an ad-free version of the entire book that's also receive $10% off the book, plus I'll also get a VIP membership, and you get 5 VIP access to the book will be shipping that gets you'll receive $5/place that's all-place pricing starts starting to receive $4/place you get a chance to review the deal starts shipping it starts shipping an ad will get a $24/place I'm also get $4 or 5MBMBOTION PRICING $5 or VIP access gets $4 VIP access?
00:01:14.000Yeah, so I have a BS in biochemistry, a PhD in neuroscience.
00:01:21.000After getting my PhD in neuroscience, I went on to study the neuroscience of obesity at the University of Washington and particularly the brain circuits that regulate body fatness.
00:01:31.000Hopefully we'll get a chance to talk about those today.
00:01:33.000And then I went on to become a science consultant, science communicator, and write a book called The Hungry Brain that is my attempt to explain for a non-specialist audience what causes obesity.
00:02:33.000I've put a lot of the references that I'm going to be citing on my website, stephanguena.com, or if you don't feel like spelling my name, you can go to wholehealthsource.org.
00:02:42.000And I have a numbered list of topics there.
00:02:46.000And I'm going to be calling out numbers.
00:02:49.000Just scroll down to the number that I referred to and the references are all there.
00:02:54.000Second thing I want to say that I want to be really clear about today is that I'm not here to be the anti-low carb guy.
00:03:02.000I think low carb diets are a valid tool for controlling body fatness and controlling blood sugar.
00:03:08.000I'm not here to talk anybody out of being on a low carb diet.
00:03:12.000What I am here to try to talk people out of is some of the mythology that has accumulated around the low-carb diet.
00:03:19.000Okay, so I want to get started with an analogy to help people understand why the brain is important in obesity.
00:03:27.000So imagine you're an alien coming down from outer space, and you want to understand what's going on on Earth.
00:03:34.000And you notice that on the highway, some cars are traveling faster than others.
00:03:37.000Some cars go faster, some cars go slower, and you want to figure out why.
00:03:41.000And so you go and you start studying the tires of the cars.
00:03:46.000Because obviously the amount of force that is exerted by the tire onto the asphalt is the thing that determines the speed of the car.
00:04:05.000The reason is that you're studying the wrong part of the system.
00:04:08.000If you want to understand why some cars go faster than others, you have to understand the part of the system that regulates speed, and that is the person behind the wheel.
00:04:20.000And so in this analogy, the tires are fat cells, and the person behind the wheel is the brain.
00:06:07.000So what happens when you put these brain circuits in the modern environment where you have abundant, calorie-dense, tasty foods rich in carbohydrate and fat is these same brain circuits push us to overconsume and they push our bodies to accumulate and hold on to fat.
00:06:23.000And then what you see as a result is the three hallmarks of obesity.
00:06:28.000First of all, the obvious, you see elevated body fat mass.
00:06:32.000Second of all, you see elevated calorie intake.
00:06:35.000People with obesity consume more calories than people who do not have obesity after correcting for height and sex and physical activity level.
00:06:44.000And third, you see that people with obesity defend their higher level of body fatness against changes.
00:06:51.000And so there's actually a regulatory change that happens.
00:08:04.000Okay, so now, the genetics of obesity offers us a lot of insight into the biological mechanisms that drive differences in body fatness in the general population.
00:08:16.000So you get these studies, like the most interesting studies are the genome-wide association studies.
00:08:22.000They get hundreds of thousands of people together, and they We're good to go.
00:08:50.000That tells you what the mechanisms are that underlie everyday differences in body fatness in the general population.
00:08:56.000And so to kind of warm ourselves up, let's start by talking about height genes.
00:09:01.000So height has a strong genetic component, so does body fatness.
00:09:06.000And researchers have figured out a lot of the genes that underlie differences in height between people.
00:09:12.000And when you look at what those genes do, they tend to be involved in the growth and development of the skeleton and the connective tissue, which is what you would expect, right?
00:09:21.000Because growth of the skeleton determines your height.
00:09:23.000So genes that determine diabetes risk, type 2 diabetes, are all about insulin sensitivity, all about insulin secretion, and the function of the Insulin secreting pancreas, which is what you expect because diabetes is a disease that is all about insulin.
00:09:42.000So these studies are really good at getting at the underlying biological mechanisms that are driving these phenomena.
00:09:48.000So what do these studies have to say about obesity?
00:09:52.000If Gary's model is correct, we should see a bunch of genes popping up related to fat cells and insulin.
00:09:59.000If my model is correct, we should see a bunch of genes popping up related to the brain.
00:10:04.000And in fact, that's exactly what we see.
00:10:06.000The genetics of obesity are overwhelmingly related to differences in brain activity between individuals.
00:10:15.000Okay, so that's one piece of evidence.
00:10:17.000Another piece of evidence, there are five FDA-approved weight loss drugs.
00:10:25.000One of them reduces dietary fat absorption in the digestive tract.
00:10:30.000There are no effective fat loss drugs that I'm aware of that target insulin or fat cells.
00:10:36.000Third piece of evidence, if you look at, some people get really unlucky in life and they end up with these horrible genetic mutations that, you know, knock out some biological pathways.
00:10:46.000Some of these People end up with extreme obesity.
00:10:51.000People and also animals, we see this in mice and rats, just occasionally you get unlucky and you get really, really fat.
00:10:57.000And researchers have been cataloging what are these mutations.
00:11:01.000When we find people who are genetically really obese, what are these mutations that are making them fat?
00:11:07.000What is the biological mechanism that's getting screwed up that's making them fat?
00:11:11.000And what they've found is that all of these mutations that they've identified to date, a number of them, are occurring in the leptin signaling pathway.
00:11:25.000is the primary fat-regulating hormone in the body.
00:11:29.000Gary avoids this, never talks about this in his writing, but leptin is the primary fat-regulating hormone in the body, and these mutations either knock out leptin, they knock out leptin receptors, or they knock out the leptin response pathway in the brain.
00:11:45.000So that's the third piece of evidence.
00:11:49.000So now, we haven't really gotten around to talking about what it is exactly about the bad interaction that happens between our ancient brains and the modern food environment that causes us to become fat.
00:12:02.000We've established that the brain is central to obesity, but we haven't really established what it is exactly about that interaction.
00:12:08.000Why does our modern food, why does our modern environment promote obesity, right?
00:12:17.000Basically, there are three different ways that I'm going to look at this from.
00:12:24.000But first, I want to say that probably the best way to answer this question is to start with the question, what is the most fattening diet in the world?
00:12:34.000What is the diet that is more fattening than any others?
00:12:36.000The answer to that is it's human junk food.
00:12:39.000In a variety of non-human species and humans, it's human junk food that is more fattening than any others.
00:12:46.000I'm going to skip over some of the research here that demonstrates this.
00:12:51.000By the way, I haven't been calling out numbers here.
00:12:57.000Reference number two on my website is those genetic studies.
00:13:04.000Reference number one is the obesity drugs.
00:13:08.000Reference number six is those spontaneously occurring genetic mutations.
00:13:13.000And now I'm talking about reference number 52. I'm going to gloss over some of the individual research because I'm being long-winded here.
00:13:21.000Essentially, what you find is that this stuff is really fattening in animals, many different species.
00:13:28.000It's super fattening in humans, calorie-dense.
00:13:31.000When you create an environment with abundant, easy, calorie-dense, tasty foods, rich carbs and fat, you see this dramatic overconsumption and fat gain.
00:13:43.000Across many species, including humans.
00:13:45.000And what you find in the research is that the sugar and the carbohydrate cannot explain that.
00:14:58.000What I mean is that if you just increase sugar intake in animals or in humans, you do get weight gain, but it is modest compared to what you get when you put people around a variety of calorie-dense,
00:15:14.000palatable foods rich in carbohydrate and fat.
00:15:22.000Because I'm not sure exactly what you're saying.
00:15:24.000You're saying if you give people this calorie-rich sugar diet of junk food, you will make them gain weight, but not as much weight as what?
00:15:39.000So, what I'm saying is that if you give people or animals the actual human junk food with all the carbs and fat and everything, they gain a lot more weight and a lot faster than if you just give them a diet that's high in sugar and high in refined carbohydrate.
00:15:58.000And what that shows is that the sugar and the refined carbohydrate cannot fully explain the effect, can't fully explain why those foods are fattening.
00:16:09.000Because you're saying if you give people the diet of American junk food, You get not as much of an effect if you give them just the sugar and the carbohydrates?
00:17:08.000Or you can tell them to stop drinking sugar-sweetened beverages and you can see what happens.
00:17:12.000People will gain weight, they will lose weight, suggesting that that is part of the explanation, but it's a much smaller effect than you see with this full pallet of these foods that contain carbs and fat and all this other stuff.
00:17:27.000So you're saying, well, obviously there's more calories, right?
00:17:30.000If there's carbs and fat and all these other things?
00:17:40.000I think it's the wrong way to think about it.
00:17:42.000What do you disagree, if anything, with what he's said so far?
00:17:46.000Well, so far what he's said hasn't been particularly revelatory.
00:17:55.000I think we have to step back for a second, because while the low-carb community might have a better understanding of where we disagree, I think the greater community that Joe reaches might not.
00:18:11.000Fundamentally, what Stefan's saying and what the research community is saying and the conventional thinking in this field is that the brain, and correct me any point, I get this wrong, but the brain regulates, does the fundamental job of controlling how fat we are.
00:18:26.000And the way it does it is by controlling or miscontrolling our intake and our expenditure, and the difference ends up in fat tissue.
00:18:37.000Is that fair to say for the most part?
00:18:40.000Yeah, so Stefan has a brain-centric view of the universe and the community at large does as well.
00:18:46.000So if we go outside and we walk down Ventura Boulevard and we see someone who weighs 400 pounds, They've clearly taken in more calories than they should have over the course of their life.
00:19:02.000And it's been stored in their fat tissue.
00:19:04.000And Stefan says, I think would say that the problem is in their brain's ability to regulate intake to expenditure.
00:19:43.000What I've been arguing, so I come along, my background, I'm a journalist.
00:19:46.000I'm an investigative journalist with a science background.
00:19:50.000Okay, that's what I do, and I'm curious.
00:19:53.000And I've got a lot of, you know, my first two books were studying what's called pathological science, which is about people who got the wrong results in science, because a lot of times scientists do.
00:20:07.000And as I was doing the research for my first book, which took five years, what I noticed when you take a historical perspective is that the research community studying obesity was very focused on the brain.
00:20:23.000They just assumed that fat people are gluttons.
00:20:25.000And I'm going to use some socially unacceptable language because in part that's how they thought about it.
00:20:31.000In fact, when you read the It's shocking the way these people talked about people with obesity and the assumption was that they're gluttons or they're neurotic or they're anxious or they're just – but it was all brain-centric.
00:20:47.000And when they got to the 1960s, the field was being run by psychologists and psychiatrists who were trying to get – People with obesity eat less.
00:20:54.000And my favorite example is one team that was trying to get...
00:20:58.000They got the wives to stop having sex with the husbands if they didn't lose weight every week.
00:21:23.000While the obesity research community is focusing on the brain, there were people studying fat metabolism.
00:21:32.000Endocrinologists, they study hormones and hormone-related disorders, saying that fat storage and fat mobilization, the burning of fat in the human body is We're controlled by this very diverse set of hormones and enzymes and the nervous system is involved and well.
00:21:50.000And our body does a very careful job of basically orchestrating how we use fuels after we eat.
00:21:56.000And the implication was, and I think Stefan kind of stepped into this with the very first thing you said, so the assumption was obesity is a disorder of excess fat accumulation.
00:22:08.000So today, when you read the literature, the articles will often say obesity is a sort of energy imbalance.
00:22:13.000You take in more calories than they expend.
00:22:16.000There were still the best scientists in the field, the best physician scientists would say, look, obesity is a sort of excess fat accumulation.
00:22:24.000Let's look at what regulates fat accumulation in the human body.
00:22:28.000Some people are programmed or dysregulated to store more fat.
00:22:32.000And if they store more fat, their behavior is going to respond.
00:22:37.000They'll be hungrier, they'll eat more, they'll be gluttons, all these things.
00:22:43.000Instead of the brain determining energy balance and that determining fat accumulation, the idea was sort of, let's see what regulates fat accumulation if that's dysregulated.
00:22:56.000If I give birth to a daughter who weighs 100 pounds at age 4, I'm not going to worry about how much she eats and exercises.
00:23:03.000I'm going to worry about What's going on with fat accumulation in this young girl that her body is, just as if you give a, you know, if you have a child who's six foot eight when he's six years old, you're not going to worry about how much he eats and exercises.
00:23:18.000You're going to worry that he's over secreting growth hormone.
00:23:21.000So the idea, basically what I've done, my role in this is to say, look, In this vitally important period in the 1960s and 1970s, when obesity researchers came to understand, fat metabolism researchers came to understand the regulation of fat cells,
00:23:39.000the obesity people were convinced that the problem was in the brain.
00:23:43.000And those obesity people eventually grew into the world that Stefan got his PhD in, this neurobiological world where you study what's happening in the brain and you ignore What's happening in the fat cells and fat mobilization and fatty acid oxidation and fat stored.
00:24:03.000And when you look at that, you find a whole world of places in which people can be predetermined, you know, be driven to be fat.
00:24:13.000So for example, When I was in high school, senior year in high school, I weighed 195 pounds and I played football.
00:24:22.000And my brother, two years older, weighed 195 pounds his senior year and played football.
00:24:28.000My brother never got more than 195 pounds.
00:24:32.000And I went up to 240. We both ate as much as humanly possible, you know, as you could imagine.
00:24:55.000The conventional wisdom would be the reason I went to 240 and he never got to 195 was that my brain was different than his.
00:25:04.000My argument is our bodies were fundamentally different.
00:25:07.000So if I see somebody walking down the street that weighs 300 pounds, I don't worry about, I don't think about what the problem is with her brain regulating intake and expenditure.
00:25:15.000I think about why is her body driving her to be 300 pounds.
00:25:20.000So that's, I think, kind of the fundamental difference.
00:25:24.000And is it the brain that can't do the job or is it the body that can't do the job and the brain is responding to what's happening in the body?
00:25:35.000Because, I mean, isn't it a holistic...
00:25:37.000I mean, holistically, you're looking at the entire machine of the human body, the idea that the brain is somehow or another separate from the body is...
00:26:02.000We can tell stories, but the thing that differentiates a story that's true from a story that is not true is evidence.
00:26:10.000And so you talk about the difference between your brother and you.
00:26:13.000This is where that genetics evidence comes back in that I was talking about.
00:26:17.000Your brother and you only share half of your genes.
00:26:20.000We know that genetics has a strong impact on who has a greater susceptibility to body fatness than others, and we also know what the genes do that underlie those differences.
00:26:48.000And so that suggests that the reason why you had a greater propensity than your brother to become fat probably has to do with differences in genetics that relate to brain function.
00:27:12.000I mean, I can guarantee you we both ate as much as humanly possible.
00:27:16.000Actually, my brother, who never got over 195, and I apologize for bringing you up on the air, I know you don't like that, used to say that he never gets stuffed.
00:27:25.000He just gets bored of eating after a couple of hours.
00:27:28.000Okay, but maybe even though, like maybe if you looked at it scientifically, you ate more than him.
00:28:06.000So if you look at the genetics of obesity, what you find is that from twin studies and family studies that measure the overall contribution of genetics, about 75% of the differences in body fatness between individuals is due to genetic differences between those individuals.
00:28:24.000So, you know, 1995 America, if you just take a cross-section of people and you measure how much is genes, how much is environment, about 75% is genetic.
00:28:35.000Now, we've only identified a small proportion of the specific genes that underlie the propensity to obesity.
00:28:43.000And so, if you look at the percentage that we have specifically identified, it's very small, and that's what I refer to in my book.
00:29:15.000And these genetic studies are advancing very quickly, and that's why in the three years since I wrote that, we have explained a lot more than we did at the time that I wrote that.
00:29:25.000And so we have a portion of these genes identified, and what we're seeing is that most of that portion that we have identified relate to brain activity.
00:29:34.000And so that tells us That primarily the differences between individuals that determine differences in body fatness is about differences in brain activity.
00:29:45.000The brain generates all of our eating behavior, it generates all of our physical activity behavior, and it actually regulates body fatness.
00:30:11.000Okay, so drugs that explain obesity, 10%.
00:30:14.000With the argument that I was making and the argument I continue to make, imagine if, you know, take Stefan's car medical… You see Stefan, he says Stefan.
00:30:30.000If you take Stefan's car analogy… And somewhere in the 1970s, I've used the car analogy for this too, but I don't think it's as appropriate, but one way to think is somewhere in the 1970s, the aliens didn't notice that there were humans driving the car.
00:30:48.000So now they're trying to solve the problem.
00:30:51.000Without the humans involved, why do some cars drive faster than others?
00:30:55.000And they come up with all kinds of hypotheses, and some of them can explain it.
00:30:59.000Even when they interpret the hypotheses, one of the common problems in science is called intellectual phase lock.
00:31:06.000So what I've been arguing is, in effect, the obesity research community left out of its research 1960s-era endocrinology, the hormonal metabolic regulation of fatty acid metabolism oxidation burning.
00:31:23.000And as such, when they did it, pretty much everything they've done since has been interpreted incorrectly, just like the aliens would interpret the car problem if they never noticed the humans.
00:31:38.000So leptin is discovered in 1993, and when leptin is discovered, obesity becomes sort of a legitimate field of science.
00:31:45.000Until then, it's a bunch of actually mostly psychologists studying it, and now it becomes a sub-discipline in molecular biology, and all the molecular biologists jump into the field, and they assume that what leptin does is control the brain.
00:31:59.000It signals how much fat is available to some kind of satiety or fuel deficiency hormone, and as such, they study the brain, and they study the action of leptin in the brain.
00:32:15.000Now, in 2002, Jeff Friedman, who gets credit for discovering leptin, perhaps incorrectly, publishes a paper in the journal Science that's saying perhaps as much as two-thirds or more of what leptin does is done in the periphery,
00:32:31.000And what leptin does is a hormone that sort of is secreted in response to how much fat you've accumulated.
00:32:39.000And then does it stimulate the brain to tell you to eat more or less, depending on how much fat, or it also works in liver cells, which were the cells they were studying, and the assumption is it probably does in all cells, to tell your cells to burn fat.
00:33:41.000One is genes associated with obesity, and one is genes associated with body type.
00:33:48.000So with body type, they're all below the neck.
00:33:51.000They're all, you know, fat metabolism, basically.
00:33:55.000And the genes, aspects of your body that you would expect to be controlled, like when you build up muscle and you have to take in excess energy to do it, it makes you hungry.
00:34:05.000I don't think your brain is regulating how much muscle you're building other than your drive to go to the gym.
00:34:11.000Basically, your body is responding to the stress on the muscle, all the things you do, and the weight lifting.
00:34:18.000So the argument here is, again, simple.
00:34:21.000When these people looked at body type, it was insulin-regulated genes, for the most part, growth hormone, all these things.
00:34:31.000When they looked at excess body fat, they decided they were in the head.
00:34:35.000But the question is, when they looked, They're programmed to think that excess body fat is caused by overeating, so they look in the brain.
00:34:44.000And I was going to call the researcher involved.
00:34:45.000I never got around to doing it, saying if body type, body shape, is determined by these genes, then doesn't it make sense that excess variations of body shape are going to be determined by the same genes?
00:35:01.000And did you do the same kind of searches?
00:35:03.000I don't actually know how they determine where the genes work.
00:36:10.000Daniel Kahneman, Stephan likes to cite Daniel Kahneman as well, had this concept, what you see is all, he's a Nobel laureate, cognitive psychologist, what you see is all there is.
00:36:22.000And basically, if you're studying the brain, that's what you look at.
00:36:26.000If you're studying the gut, and so we all get trapped into that on some extent.
00:36:31.000And what I'm saying is even in these studies, so Stephan wrote a book about the hungry brain that is supposed to be about obesity, but in fact you never mentioned anything about the metabolic regulation of fat accumulation.
00:37:15.000You had psychologists and psychiatrists running the field when the endocrinologist solved it, and then you discovered leptin and it became a molecular biology problem.
00:37:23.000And you're now divorced from the very simplest observations about obesity.
00:37:29.000So we can do huge genome-wide association studies.
00:37:43.000It's not in the front, but it's here and not here.
00:37:48.000I don't see what the brain has to say about that.
00:37:51.000Okay, so as you mentioned, there have been different genetic studies that have looked at body fat distribution versus total body fatness.
00:38:01.000So total body fatness is what we're talking about when we're talking about obesity.
00:38:05.000Body fat distribution is what we're talking about when we're talking about the fat being on your hips versus on your wrist.
00:38:12.000Now what we see is different sets of genes that come up.
00:38:15.000So body fat distribution, we actually see insulin-related genes.
00:38:20.000So people that have a central body fat distribution, so body fat around their waist, tend to have these insulin-related genes that are driving that.
00:38:29.000But when you look at total body fatness, The thing that causes obesity, what you see is that those genes are dominated by the brain.
00:38:37.000And the really cool point I want to make about the genetics research...
00:38:40.00010% of those genes might be dominated by the brain, if they looked.
00:39:26.000Focus on leptin actions in the brain because we're phase locked and we can't get out of our, you know, blinders of thinking about it in terms of the brain and that that's why we focus on leptin action in the brain.
00:39:39.000The real reason we focus on leptin action in the brain is because it has been demonstrated that its effect on body fatness are via the brain.
00:39:48.000There are actual experiments demonstrating this and I'll explain how these experiments work.
00:39:52.000This is all in the scientific literature.
00:39:54.000So if you knock out the leptin receptor Only in the brain, or only in the hypothalamus, you get obesity.
00:40:05.000So that is what tells us that actually the brain is the key site of action, and particularly this part of the brain.
00:40:12.000It tells you the brain is a key site of action.
00:40:19.000So, I mean, you get the same obesity if you knock leptin out of the brain, and particularly out of the hypothalamus, that you get if you knock it out of the whole body.
00:40:27.000So that shows that the brain is the site of action that is causing this to happen.
00:40:35.000We know Specific groups of neurons that are receiving the leptin, that are controlling our appetite, that are controlling our metabolic rate.
00:40:44.000We have many of these neural populations worked out.
00:40:46.000In mice, we understand these systems so well.
00:40:49.000We can control specific tiny populations of neurons very precisely, cause them to eat a ton, to stop eating, to gain fat, to lose fat, like the animals are marionettes.
00:41:02.000I mean, that's the level of understanding we have right now of how these systems work.
00:41:06.000So, I mean, all of this evidence is converging on the same thing, that the brain is central and that fat cell metabolism, I'm just not seeing the evidence for that.
00:41:17.000I mean, Gary, if you want to cite specific evidence demonstrating that that is an actual cause of differences in body fatness between individuals and the general population, I'm awaiting that evidence and I'm happy to sit here and listen to you cite the evidence that demonstrates that.
00:41:37.000Yeah, let's talk about leptin a little bit.
00:41:39.000It's produced in fat cells, and it's produced in proportion to the size of fat tissue.
00:41:45.000So the amount of body fat you have, the more fat you have, the more leptin you have in the circulation.
00:41:50.000And basically what this is, it's what's called a negative feedback loop, which is a really simple engineering term that works like a thermostat.
00:41:59.000So with your thermostat, if you set your thermostat to 70...
00:42:18.000We have many negative feedback loops in the human body To regulate body temperature, to regulate blood pressure, to regulate all sorts of things.
00:42:28.000One of the negative feedback loops we have regulates body fatness.
00:42:33.000And the hormone, so your thermostat measures temperature by using a thermostat.
00:42:40.000Your brain measures body fatness using this hormone leptin that's in the circulation.
00:42:45.000And 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.
00:42:56.000And 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.
00:43:08.000Is this just when you're losing body fat in general?
00:43:11.000Like even if you're a large person that's overweight, when you're losing body fat in general, your body exacerbates your hunger?
00:43:18.000And this is the thing that's really important to understand about obesity.
00:43:22.000Is that people with obesity have a higher set point.
00:43:26.000So 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.
00:43:35.000They'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.
00:43:46.000In their brain circuits that regulate body fatness that drives them to increase their cravings and their hunger, their metabolic rate drops.
00:43:55.000So it would be an evolutionary mechanism to force you to seek food.
00:43:59.000And 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.
00:44:35.000So 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.
00:44:46.000So you come back to insulin, even with the leptin, you raise blood sugar, and that's the carbs.
00:44:52.000You eat the carbs, you raise blood sugar, you raise insulin, you raise fat storage, the glucose, and then you get more leptin.
00:44:59.000Again, 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.
00:45:10.000So in Stefan's world, and again, correct me if I'm wrong, though, leptin is signaling Fuel availability in the fat cells the way I would think of it in my very small world.
00:45:24.000Leptin is responding to fuel availability in the rest of the cells.
00:45:29.000So 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.
00:45:37.000Or it can tell that there isn't fuel available.
00:45:42.000And 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.
00:45:51.000Everything we're talking about, Stefan and I first sort of fell out, I don't know, eight years ago at Ancestral Health Symposium when I acted improperly, inappropriately.
00:46:06.000But 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.
00:46:28.000But it doesn't tell you why the room's getting crowded.
00:46:30.000It doesn't tell you why you're getting fatter.
00:46:33.000And 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.
00:46:42.000And then they went to the brain to look at why people might overeat.
00:46:46.000So 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.
00:46:56.000You know, a simple question to ask is, can we find epidemics of obesity without this modern food environment?
00:47:04.000I mean, that's a sort of science 101, right?
00:47:07.000And it turns out that the world is full.
00:47:09.000And the first one I found in the literature was in 1902, in a population of the Pima, Native American tribe Pima, living in Arizona.
00:47:18.000And observers saying these people are poor, they're malnourished, they're suffering through famines.
00:47:25.000They've been suffering through a famine for 40 years, and famines, it's hard to overeat during a famine.
00:47:30.000And yet, the women of the tribe, who do virtually all the work, they were treated as pack animals, in effect, were obese.
00:47:39.000So 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?
00:47:54.000Can we find what might have driven obesity in that population, despite the existence of famine?
00:48:01.000Once we get into these kind 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.
00:48:13.000And you'll see in the studies people misinterpreting them.
00:48:19.000What was the cause of the population of women to be obese?
00:48:23.000Well, so one of the things that happened beginning in the 1860s, the PIMA were Well, they moved on to a reservation.
00:48:29.000They were reservationized, whatever the verb form would be.
00:48:44.000And 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,
00:49:01.000So ultimately, You know, the question you ask in science determines the answer you get.
00:49:08.000So 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.
00:49:20.000They develop what's called metabolic syndrome, which is insulin resistance and all these issues.
00:49:26.000And 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.
00:49:37.000The question is, what's triggering it in the environment?
00:49:40.000And again, Stefan would say, well, there's too much food available, and it's too palatable, and we can't say no.
00:49:49.000And 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.
00:49:59.000And then, or is it some specific item?
00:50:03.000Or some specific group in these foods that travel with Western populations.
00:50:09.000And so the ability, and today if you look up Dual burden of obesity and malnutrition.
00:50:16.000I have a Dropbox folder I could share with you.
00:50:19.000There's probably 50 studies all over the world.
00:50:25.000The children are stunted, which means they're protein deficient and they're calorie deficient.
00:50:30.000And often the mothers or the aunts are obese.
00:50:33.000The 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.
00:50:47.000If they could have overeaten, why are the kids starving?
00:50:52.000This was the first thing that I think we fought about back then.
00:50:57.000If 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,
00:51:17.000how do you explain obesity in the mothers without assuming that the mothers are overeating?
00:53:08.000And 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.
00:53:21.000And 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.
00:53:31.000And these were calorie-dense refined foods.
00:53:34.000They were, like Gary said, flour, lard, and sugar.
00:53:42.000Now, 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 Not surprisingly,
00:54:05.000than the ones eating lard, flour, and sugar, okay?
00:54:08.000But Gary, you seem to believe that people can gain weight.
00:54:12.000You kept referring to famines and things.
00:54:14.000You seem to believe that people can gain weight even if they are eating very few calories.
00:54:20.000And you refer to this many times in your writing.
00:54:23.000And, you know, these are very casual observations that you're making, kind of these casual correlations and storytelling.
00:54:31.000But if you actually look at the data...
00:54:34.000On 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 physical activity level.
00:55:59.000They lose weight when you restrict their calorie intake down to that of a lean person.
00:56:03.000So this is the argument, what you're saying, that consuming low amounts of calories but high amounts of sugar doesn't make sense that you can get obese that way.
00:56:33.000Often 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.
00:56:45.000To 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?
00:56:58.000Okay, you could say that the obese expend a lot of energy and they eat a lot of calories.
00:57:02.000The question is, can they get obese without a lot of food?
00:57:06.000Like U.S., can you find a population that gets obese without sugar?
00:57:09.000Which was exactly the question to ask.
00:57:11.000So in Trinidad in the 1960s, there's a malnutrition crisis.
00:57:15.000The U.S. 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.
00:57:28.000And 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.
00:57:40.000And this is a population where it's not like, I mean, this is a very poor Trinidad population.
00:57:45.000And reports that they, I think it was 1,800 calories a day, what the obese women were eating was actually a little less than what the lean people seemed to be eating.
00:57:53.000And that it was lower than what the Food and Agriculture Organization considered for a healthy diet.
00:57:58.000So again, my role in this is to point out when you have populations like that, I don't see how the overeating hypothesis tells me.
00:58:06.000The brain is in control of how much they eat.
00:58:08.000It tells me anything about why the women were obese, especially when their kids are starving.
00:58:13.000This is the paradox of the stool burden, an obese mother with a starving child.
00:58:18.000If the obese mother has to eat superfluous calories to get fat, Why isn't she giving those calories to her kids?
00:58:32.000If 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.
00:58:42.000I mean, there are plenty of animal models.
00:58:44.000A famous quote I use in my books from Jean Maier, it was like the leading Harvard nutritionist who studied an obese strain of animals in the 50s.
00:58:53.000He said, my animals will get fat even when half starved.
00:58:57.000They will make fat out of their food even when half starved.
00:59:01.000These are generally animals with mutations in the leptin pathway, by the way.
00:59:07.000The question is, if I can make fat out of my food, At caloric levels that, for instance, a lean person can't, then I'm going to get fat eating the same amount.
00:59:22.000And that fat accumulation means I'm taking in more calories than I expend, but the point is, for some metabolic hormonal reason, I'm taking the fuel I eat and turning it into fat and storing it in the fat tissue.
01:00:09.000Just 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.
01:01:42.000What 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 Yeah,
01:02:07.000I don't know if there's malaria in Trinidad or not, but 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.
01:02:18.00030% of kids didn't even make it past childhood.
01:02:21.000And so, there's a lot of things that could have caused that, Gary.
01:02:25.000It's not necessarily because, you know, it's not necessarily the reason that you attribute it to.
01:02:47.000So 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.
01:02:59.000And furthermore, I want to get to another type of study that's really going to differentiate between this metabolic effect and Driven by insulin and the effect of calories.
01:03:12.000So we have a lot of studies that compared diets in which calories were the same, but carbohydrate and fat intake differed.
01:03:20.000And 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.
01:03:53.000Now, if we want to understand why people get fat, we can look at studies that overfed people on fat or carbohydrate exclusively.
01:04:02.000So this one study, the first one that I want to talk about, first they figured out people's baseline calorie intake.
01:04:10.000Figure 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.
01:04:29.000So, 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, etc.
01:05:55.000So 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.
01:06:05.000So there was no cheating, no inaccuracy, and they were measuring changes in body fatness using a gold standard method called underwater weighing, okay?
01:06:14.000And 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.
01:06:58.000The paradigm you work in determines the question you ask.
01:07:01.000And this experiment is a classic example because they assume that people get fat by overfeeding.
01:07:07.000So then they say if we overfeed them...
01:07:11.000We're just doing what happens naturally.
01:07:13.000Everything about the experiment is based on the assumption that they're supposed to be testing, which is, can people get fat by overfeeding?
01:07:21.000And so from the very conception of the experiment, they've built in the paradigm that we want to test, the hypothesis.
01:07:29.000On top of it, if it's a typical SIMS experiment, I actually wasn't familiar with this one.
01:07:34.000Oh, it wasn't SIMS. James Hill was funded from about 1998 to about 2008 by Procter& Gamble because he was an Alestra shill.
01:08:13.000But the whole idea of Alestra was to replace fat in the diet.
01:08:19.000So every study Hill and Peters did implicated dietary fat as a cause of obesity.
01:08:24.000I don't think we could ever use, I hate to say it, typically I don't think funding influences results, but I wouldn't use a James Hill study to make that point.
01:08:36.000Because you think it's a bio-study that was influenced by it?
01:08:41.000I mean, I talked about this in Good Calories, Bad Calories.
01:08:44.000When they reported their results, actually I did a FOIA on James Hill, because he works for the University of Colorado.
01:08:50.000I got all his documents back and forth between him and Alester.
01:08:54.000I'd be happy to share them with you if you'd like.
01:08:57.000I mean, him and Procter& Gamble, but he basically held Procter& Gamble for ransom.
01:09:01.000He would get a $500,000 unrestricted gift, and then he would do a study, and then he would conclude that fat is bad and carbs are good, and therefore Alestra is a viable product.
01:09:15.000Then he would ask for Procter& Gamble for more money before he then published the study.
01:09:21.000So, it's a particularly egregious example of someone who's, I suspect it was just his belief system.
01:09:28.000He believed dietary fat was bad, fat caused obesity, Lester 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.
01:09:39.000The point that we keep getting away from that I haven't had an opportunity to And Stephan knows this as well as I do.
01:09:49.000If you're gaining, say, four pounds a year of fat, or let's say between 20 and 40, you've put on 40 extra pounds.
01:09:57.000You're a nice, lean, healthy young guy.
01:09:59.000And 20, like many of us were, and by the time you're 40, you've got 40 pounds of excess fat.
01:10:04.000That's the equivalent of putting in about...
01:10:10.000It's storing about 10 calories a day into your fat tissue that you don't burn or metabolize.
01:10:16.000So you eat, say, 2,700 calories a day, half carbs, 35% fat, 15% protein, and 10 calories a day get trapped in your fat tissue.
01:10:28.000Less than a bite's worth of food, less than a sip's worth of beer.
01:10:34.000So the question we're actually trying to ask is, or answer, and this is, again, just my approach as a curious journalist with a science background, is how do we explain those 10 calories?
01:10:45.000Because when we talk about those obese women with starving children, all those obese women were doing was storing 10 or 20 calories a day, depending on how quickly they became obese in those populations.
01:10:56.000It tends to happen quickly in their 20s.
01:10:59.000So we're asking this question, you've got a situation where we have to end up with 10 calories stuck in the fat cells every day.
01:11:08.000That's 20, 30, 40 billion fat cells, so it's divided up very small.
01:11:13.000And is the brain somehow regulating that?
01:11:17.000Or again, is there a dysregulation in the body involving pick your hormones, pick your enzymes that somehow traps fat in the fat cells or prevents the fat from being used for fuel when it's released from the fat cells?
01:11:36.000And so if you think about it that way, like you let yourself go to seed, today Joe Rogan decides I'm done.
01:12:35.000And there's nothing in the laws of physics that says it.
01:12:38.000So what could be dysregulated about their fat cells, even during a relative famine, not a complete famine, but a relative famine that might be...
01:12:47.000And again, animal experiments, of which there are probably hundreds by now, different animal models, you can Disassociate obesity from eating too much in the animals.
01:13:01.000Essentially you're saying that even if someone is taking in a good amount of calories, a smart amount of calories, 2,000 calories a day, If you're taking in these calories in the form of sugar, your body is going to take a certain percentage of them even if you're getting enough food and store it as fat.
01:13:22.000Whereas if you were taking in just protein and vegetables and things along those lines, your body would not do that.
01:13:29.000Well, so this gets to the mechanism question and the evidence question.
01:13:36.000So you're saying that if two people are on the same diet, one of them is on 2,000 calories of chicken and fish and vegetables, and the other one is on 2,000 calories of milkshakes and sugary drinks and pasta and bullshit,
01:13:52.000that that person is going to gain a certain amount of calories and just put them to fat regardless.
01:14:10.000I think they've done a bad job of testing it and...
01:14:14.000But we will both tend to reject the studies that we don't like when we define don't like by whether or not they got the answer we think is correct.
01:14:22.000Your perspective is that this is not the case.
01:14:23.000Your perspective is that, like, as you were saying in the study where they closely monitored these people's diets and they added additional fat and additional carbohydrates, that they both gained the same additional amount of weight.
01:16:02.000Of what's necessary for energy balance.
01:16:06.000So the classic example is a study that's my not-for-profit funded that's been very controversial where they Got their subjects, this is David Ludwig and Kara Ebeling and their colleagues at Harvard and Boston Children's Hospital,
01:16:24.000and they did this study in Framingham, and they basically got subjects to lose 10 or 12% of their body weight, and then they randomized them to three different diets of three different macronutrient compositions,
01:16:39.000and they basically calculated their energy expenditure on the three different diets, which is kind of exactly what we're talking about, If you want to be in energy balance, you know you feed people exactly what they're expending.
01:16:52.000And in that study, which was published a year ago, They saw different levels of energy expenditure depending on the carbohydrate content of the diet.
01:17:03.000So the higher level of carbohydrates, this is trying to keep them in energy balance.
01:17:08.000The higher the carbohydrate, the lower the energy expenditure.
01:17:12.000The lower the carbohydrate, the higher the energy expenditure.
01:17:16.000So again, it's just whether or not they did the study right.
01:17:19.000Science is a compilation of a lot of studies and we're trying to, you know, address exactly this point.
01:17:26.000But Merely building that into the experiment.
01:17:31.000We know what their energy expenditure should be.
01:17:33.000And then the point is when you increase.
01:17:36.000And again, part of the trick of doing science is to say, look, we have competing hypotheses, multiple hypotheses.
01:17:43.000And it's vitally important that you always keep the multiple hypotheses in.
01:17:49.000In mind when you're interpreting the study.
01:17:51.000So one hypothesis says it's how much they eat, and another hypothesis says it's what they eat, and that what they eat is moderated primarily through insulin.
01:18:01.000And when you do these experiments, like the experiment that Stephen is talking about, Stefan, I'm completely confused.
01:18:13.000If you overfeed them, you start out with a 50% carb diet, now you overfeed them.
01:18:19.000If there's a threshold effect on insulin, which it turns out there is, then you're just moving them.
01:18:24.000And when you look at insulin dynamics, when insulin is below a very low point, the fat cells will mobilize fat and the lean tissue will burn it for fuel.
01:18:33.000And above that point, you get pretty much flat.
01:18:36.000So if you start people who are eating 1500 calories from carbs, And you add them, bump them up to 2500 calories from carbs, you're still in the plateau side of the insulin.
01:18:48.000You wouldn't necessarily expect to see any difference.
01:18:51.000The only way you expect to see a difference, and that's why it helps to really interrogate both hypotheses so that you know when you're doing the experiment whether or not you're actually testing something.
01:19:03.000You want to set up the experiment so the hypothesis predicts, the two hypotheses predict something entirely different.
01:19:10.000This experiment, arguably the two hypotheses predict the same thing.
01:19:14.000You'll get fat gain because insulin is elevated regardless.
01:19:17.000And when insulin is elevated, you're going to get fat gain.
01:19:21.000The question comes back to, again, always vital to keep this in mind, what could possibly cause a 10 or 20 calorie excess that causes fat storage?
01:19:31.000I have a friend who was 400 pounds when he was 18. He was a tall kid, about 6'5".
01:19:41.000200 pounds overweight is roughly 100 excess calories over 18 years stored in your fat cells.
01:19:49.000Even if you assume that you have to consume 300 calories To have 100 excess stored in your fat cells, that's, you know, one, two Coca-Colas a day that he was drinking, or one half a quarter pounder a day that he was eating that his lean friends weren't.
01:20:08.000And the question would be, why can't he just stop doing that?
01:20:11.000And again, Stefan would say, because his brain won't let him.
01:20:15.000And I would say because his insulin is elevated, it doesn't matter whether he stops it or not.
01:20:50.000There have been 29 studies to date that have measured calorie expenditure, metabolic rate, on diets differing in carbohydrate and fat content.
01:21:00.000And when you put all those studies together, or at least the first 28 together, and you look at what the overall literature says, it makes almost no difference to metabolic rate whether people are eating carbohydrate or fat.
01:21:13.000And in fact, the very small difference that it does make Actually favors high carbohydrate diets.
01:21:19.000So you get a slightly higher metabolic rate when the diet is predominantly carbohydrate.
01:21:25.000Now this study that Gary cited is the one study out of these 29 that has reported a larger effect than any others of carbohydrate restriction on energy expenditure.
01:21:36.000So this study reported an effect bigger than any of these other 28. And the difference, we would say, is this.
01:21:47.000And interestingly, if you actually look at the data, and these data have been reanalyzed by a researcher named Kevin Hall, and I think?
01:22:20.000From the pool of subjects, this big effect size starts to shrink and shrink and shrink and shrink until after you've gotten rid of all of it, this study no longer reports a higher energy expenditure on a very low-carbohydrate diet,
01:22:37.000and it's consistent with the previous 28 studies that were done.
01:24:38.000Some of it's muscle, some of it's liver and organs.
01:24:42.000Is this because they're carrying around this extra weight, and so the extra calories, and then on top of that, carrying around the extra weight forces their body to grow larger?
01:24:52.000Presumably, I'm actually not sure what the mechanism is.
01:24:55.000But it doesn't have anything to do with the brain?
01:25:02.000Now, so, but the point is, by the time the person has obesity, they are consuming 20 to 35% more calories than they were when they were lean.
01:25:17.000So it's not just one or two Cokes a day that is...
01:25:57.000Yeah, and that's why I give a range, because what you see is that people who are overweight, so they're in the overweight range and just have some extra fat, they eat about 10% extra calories.
01:26:08.000People who have a little bit of obesity eat about 20% extra calories.
01:26:12.000People who have very, very great obesity eat more like 35%.
01:27:13.000But I want to talk about some interesting observations, because Gary, you like to talk about what's going on in different dietary trends and different cultures, and I find that pretty interesting too.
01:27:25.000I want to talk about the fact that Sugar intake in the United States has been declining for the last 20 years.
01:27:33.000So it peaked in 1999, and it is currently, depending on which source of evidence you believe, 15 to 23% lower than it was in 1999. This has been corroborated by a number of different sources of evidence.
01:28:55.000So, your counter-argument is that the amount of sugar that we consumed 20 years ago, or even maybe 50 years ago, may be continuing to fatten us today, and it's about the sugar that we used to eat 20 or 50 years ago,
01:29:13.000and not necessarily about the sugar we eat today.
01:29:18.000Okay, so the argument I made was – because he brought this up when we had to do a written debate on the Cato Foundation website.
01:29:25.000And it's interesting, if you think about – use tobacco as an example.
01:29:29.000So tobacco smoking, per capita smoking in America peaked in 1965 right after the Surgeon General's report, and it took 30 years before lung cancer rates turned over.
01:29:40.000Okay, and I think we both agree that cigarettes are a major cause of lung cancer, smoking.
01:29:45.000So what you basically have is a system in which if there are any, there's the assumption that Stefan is making when he quotes this kind of data is that the relationship between sugar and obesity is linear.
01:29:57.000So if sugar goes up, obesity and diabetes goes up, and if sugar turns over, they don't.
01:30:02.000So here's the thought experiment I used in Cato, which is 1965 we're smoking per capita about 20 cigarettes a day.
01:30:12.000As it starts to come down, imagine we only cut that to 17 cigarettes, or 16 cigarettes, a 20% reduction in smoking.
01:30:21.000Would you expect to see a reduction in the lung cancer rates?
01:30:25.000Again, this is the point I made about what you would expect to see, rather than using simplistic metaphors.
01:30:31.000So the question is, would you, like, Joe, we go from 20 to 16, do you expect to see the lung cancer rates turn over?
01:30:59.000In sugar, what happened is the equivalent of going from 20 cigarettes to 16 beginning in 1999. And Stefan is saying, I would expect to see an immediate change in obesity.
01:31:10.000And in fact, if you actually look at the rates, the rate of increase, the prevalence appeared to plateau around six or seven years later.
01:31:21.000But to get a small decrease in sugar, even if it's 20%, that's 20 to 16 cigarettes.
01:31:30.000And the other factor that I talk about in my book, and Stefan knows this, is you very clearly have maternal transmission of the propensity to obesity and diabetes.
01:31:43.000And this is studies that were done on the same Pima, the same Native American tribe, where each generation gets more and more susceptible to whatever it is in the diet that's triggering an obesity and diabetes.
01:31:58.000So if that's been happening in the United States and around the world, you've got a generational effect that could last far longer, might even keep going indefinitely, even if the sugar levels drop.
01:32:10.000So you have the sugar kicking off the obesity epidemic, and yes, Stefan's about to say this is a story, and it is a story.
01:32:17.000But it's clearly the case that mothers who are obese during pregnancy or diabetic or gestationally diabetic, they become diabetic during pregnancy, or they have metabolic syndrome, they're just insulin resistant, or they gain a lot of weight in pregnancy,
01:32:33.000will give birth to children who are at higher risk of becoming obese and diabetic when they get older.
01:32:38.000And at younger ages, and those children will pass it on.
01:32:42.000So again, we have, you know, it would be nice, I would love it if sugar consumption came down, and with it, obesity and diabetes plummeted.
01:32:51.000But it's not in any way a refutation of this hypothesis, which I just want to state what it is, because people get confused about it, and we never got to it.
01:33:01.000The sugar hypothesis is a little different than what we've been talking about, and it's pretty simple.
01:33:06.000We have obesity and diabetes epidemics worldwide, as we talked about.
01:33:10.000It doesn't matter the genetics of the population.
01:33:12.000You add something about a Western diet to those populations, Western diet and lifestyle, you get these explosions of epidemics of obesity and diabetes.
01:33:24.000And what I'm hypothesizing in this book is that sugar is the something that has to be added.
01:33:30.000Maybe it's sugary beverages, for all I know.
01:33:33.000Or it could be, you know, a more complex hypothesis.
01:33:37.000A single possible one is you add sugar to any population's diet and sufficient, whether it's Southeast Asians living on rice or the Inuit living on reindeer and Whatever, or the Native Americans of the Great Plains, or, you know,
01:33:52.000Caucasians living in the Upper East Side of Manhattan, add enough sugar, and eventually, through the metabolic effects of the sugar and the generational effects, you will get explosions of obesity and diabetes and metabolic syndrome.
01:37:27.000So you can get a sense of what 12% is by DEXA. I understand that, but it seems to correlate with a higher consumption of sugar,
01:37:46.000that they seem to have a higher percentage of body fat than the average hunter-gatherer.
01:37:49.000If you look at a lot of the average hunter-gatherers, like a friend of mine does a lot of work with the pygmies in the Congo, and they're very lean.
01:37:58.000Okay, so the pygmies, that's the second culture I was going to cite that eats a ton of honey.
01:38:04.000Yeah, if they're the same ones, the Mubuti pygmies of the Congo, they eat up to 80% of their calories can come from honey during the rainy season.
01:38:15.000So they also eat a lot of honey and are lean.
01:38:38.000That's exactly the point I'm trying to make, is that when you have a culture that That is eating a lot of sugar, but everything else is in place.
01:38:54.000I think sugar does contribute, just to be very clear, I think sugar does contribute to obesity and diabetes and cardiovascular disease, but it's not single-handedly responsible, as Gary has argued.
01:39:06.000So the third culture is pretty interesting, the Kuna of Panama.
01:39:11.000And the reason they're interesting is that they actually aren't eating honey, they're actually eating white sugar.
01:39:17.000So they're a culture that they live primarily a non-industrial lifestyle.
01:40:41.000I think what Gary's getting at is that if you have this lifestyle, the lifestyle that many of us have, and then with that lifestyle, consume sugar, that you're going to get fat.
01:40:54.000I don't think you can compare that to athletes, and in that respect, I don't think you can compare that to hunter-gatherers, because you're requiring...
01:41:03.000There's a much more significant load on your body.
01:41:07.000Like, when I... I did this sober October fitness challenge with my friends during October, and I was working out four hours a day.
01:41:14.000And I was fucking eating everything that moved.
01:41:26.000And I was eating a terrible fucking diet, but I was going crazy.
01:41:30.000When you're trying to stay alive and you're running around plowing and growing foods and hunting and gathering and fishing, you're burning off insane amounts of calories.
01:41:42.000Just the hiking that's required, the amount of exercise that's required.
01:41:46.000It's off the charts in comparison to a standard Western We are on the same wavelength here.
01:41:52.000I mean, I completely agree with you that it is more complicated than just sugar.
01:41:56.000But if you read what Gary has written, and please correct me if I'm wrong here, Gary argues that sugar is the primary cause of obesity and that physical activity does not matter, calorie intake does not matter.
01:42:10.000Do you think that physical activity doesn't matter?
01:43:40.000Okay, so this was a study that professed to measure sugar intake of this population on an island, Ali Gandhi, and compare it to the population in Veracruz where they had emigrated.
01:43:54.000And I say, but their added sugar intake on Alagandhi, according to Figure 1, is 25 teaspoons per week, plus the equivalent of 24 ounces of sodas at 78 grams if it's Coke, 32 ounces of Kool-Aid, that's 96 grams.
01:44:07.000I said, I'm leaving out the cup of a sugar cane because I don't know what that has meant or how they assess it.
01:44:12.000One way or the other, it's not processed sugar.
01:44:15.000So it's roughly 274 grams of sugar per week, or about 32 pounds per year.
01:44:21.000Now, that alone is very low intake, and we don't know how it changed over the years, so we have no idea if it's increasing recently or been low for years.
01:44:27.000So you just use the Kuhn as an example of a population that eats a lot of sugar and stated it dogmatically, but that lot of sugar is 32 pounds a year.
01:44:41.000If we believe this study, the Kuhn and Veracruz are consuming roughly the same amount, but I'm not sure I believe this study when it comes to the Veracruz population.
01:44:49.000Do you really think these urbanized Kuhn are consuming only three 8-ounce sodas per week?
01:44:54.000So the implication was this population of Caribbean islanders emigrates to Veracruz, they move into the city, And they consume more sugar back where they used to live because they trade for it than when they get into the city.
01:45:08.000So five glasses of Kool-Aid, no candy, no ice cream, nothing.
01:45:12.000I'd like to know more about the Urban Kuna before I accept such an analysis as valid.
01:45:16.000On top of this, as they say, the analysis is done mostly of women because, quote, the women were available to study because they were at home during the day, unquote.
01:45:24.000So what were the men consuming, and what were the children consuming when they weren't at home, and was there something magical about this food frequency questionnaire and these researchers that they captured it accurately?
01:45:36.000You have studies, you have evidence, and the question always is, you've got competing hypothesis.
01:45:41.000Does this evidence really speak to the hypothesis?
01:45:44.000And one of my issues with Stephen, and it's what provoked our initial discord, is that he's constantly citing studies that don't actually either They only speak to one hypothesis, like the overfeeding study, or they're poorly constructed and poorly done.
01:46:00.000So even this Hasda example with the honey is something we discussed in email very kindly, and we went back and forth, and I said, I don't actually think it's a refutation, because the hypothesis I'm defending here, the case against sugar, is you add sugar, To any population's native diet,
01:46:18.000and you get epidemics of obesity and diabetes.
01:46:21.000So here's a population that's been eating honey for maybe thousands of years.
01:46:25.000In fact, when they emigrated to this area, they may have added honey to their diet and had obesity and diabetes then, and as Stephen points out in the book, obesity and diabetes in a hunter-gatherer.
01:46:37.000Population is a death sentence for the child and for the mother who gives birth.
01:46:41.000So you're going to very quickly weed out anyone.
01:46:44.000So again, it just comes back to this question of, is it a refutation of the hypothesis that I found a hunter-gatherer population that eats a lot of honey and isn't fat?
01:46:59.000All of this can be settled with experiments.
01:47:02.000One of the experiments we did at NUSI So one of the metabolic problems that goes along with obesity and diabetes is non-alcoholic fatty liver disease.
01:47:35.000Because if you could create a fatty liver with a macronutrient, you could probably create insulin resistance as well, and then this whole slew of disorders, including obesity and diabetes.
01:47:46.000So my not-for-profit funded a pilot study Well, we just took 40 kids.
01:47:51.000Well, the researchers at UC San Diego and at Emory University in Atlanta took 40 kids who had non-alcoholic fatty liver disease and randomized them into two groups.
01:48:02.000In one group, we gave them, the entire family, all the food they needed so they could overeat to their heart's extent, but no added sugars in their diet, no sugary beverages.
01:48:13.000And this study was published in JAMA four months ago, and it just Get rid of the sugar in the diet.
01:48:30.000The conventional wisdom would be they just ate less, which I wouldn't be at all surprised because they probably didn't like the food as much without sugar in it.
01:48:38.000But these are the kinds of ways you could test these hypotheses and problems I have with like the meta-analysis getting back to Kevin and Hall.
01:48:47.000There's two ways you could do science.
01:48:49.000You could say let's look at all the junk that was done for 30, 40, 50 years.
01:48:54.000Let's find everything we can that even vaguely speaks To the experiment and ignore any quality of the study.
01:49:01.000So if it may be asked, it asks this question, like we want to know what happens when people do this, but in doing this we switch their, you know, fat intake around, fat and carb intake around.
01:49:14.000And then we can throw all that garbage into a meta-analysis.
01:49:18.000And the one thing I'm pretty confident is they did a poor job because the one study I looked up, the one with the biggest effect, they mistook kilojoules for kilocalories.
01:49:28.000So they reported a 400 kilocalorie decrease in energy expenditure on the low-fat diet when it was a 400 kilojoule, which is, what's that factor?
01:49:48.000And the way we approach it at the not-for-profit is to say, you've got to understand what the question is, and you've got to design an experiment to get the right answer.
01:49:56.000So when Stephen dismissed this Harvard… You've got three names for him now.
01:50:40.000And they keep coming up over and over again.
01:50:42.000So 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.
01:51:02.000The goal is to do the right study, because ultimately, you've got to remember what's on the line here.
01:51:06.000We have obesity and diabetes epidemics.
01:51:09.000I mean, tragic shit is going on out there.
01:51:12.000I mean, people, you know, these are ruining lives.
01:51:14.000They're overwhelming the healthcare system.
01:51:17.000And the argument I made is that for the past 50 years, basically, people have thought a lot like Stephan is thinking now, Dr. Guillenet, and that There appears to be another story that could be true.
01:51:31.000And what we have to do is find out if it is true, because people are dying out there.
01:51:36.000The 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.
01:52:18.000Jim Hill and his studies a little bit.
01:52:20.000Because, 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.
01:52:31.000If you cannot point out a specific problem with the study, it was designed with an assumption.
01:52:37.000It was designed based on the assumption it was supposed to test.
01:52:39.000It wasn't designed how Gary wanted it to be designed.
01:52:42.000If 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?
01:52:53.000I explained to you the problem with the study.
01:52:57.000I didn't realize Jim Hill had done it at the time.
01:53:00.000All right, you're going to be able to respond in a moment.
01:53:03.000Now, the Kuna, I think we should really get back to this issue, this non-industrial culture, because the primary basis...
01:53:11.000For 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,
01:53:28.000they become fat and that is the common thread in obesity.
01:53:32.000And so what I'm doing is I'm pointing out a culture Where sugar came in and it did not make them fat.
01:54:02.000Now, I want to talk about the Cuban economic crisis.
01:54:06.000This 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.
01:54:24.000Cuba was a major sugar producer at the time.
01:54:29.000And so the intake of sugar went way up.
01:54:31.000Intake of refined carbohydrate went way up.
01:54:34.000The diet became 77% carbohydrate, primarily white rice and sugar, 28% sugar of their total calorie intake.
01:54:44.000So that's like double what Americans eat.
01:54:47.000Now, their calorie intake went down and because of the lack of gasoline, people got really physically active because they had to walk everywhere.
01:54:56.000So now, again, this is a situation where we can test Gary's hypothesis.
01:55:03.000If 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.
01:55:13.000What you actually see is that the prevalence of obesity declined by half.
01:55:46.000And so we know these people weren't just totally starving.
01:55:51.000And what happened then was 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,
01:56:07.000The obesity rate went right back up as soon as they went back to their normal diet.
01:56:12.000Because they were not walking as much.
01:56:15.000Yeah, it was the exercise and also just their diet became richer again.
01:56:18.000I mean, if you're eating a diet, that's a very poor diet, eating like white rice and sugar.
01:56:24.000I mean, it's not like, if that's most of what, if you're sitting there and on your plate is white rice and sugar, you're not going to be eating a ton of that and getting fat as opposed to eating a richer diet with more varied foods.
01:56:38.000And 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.
01:59:07.000So the first study is a pilot study that depends what you look at to depend whether or not it refuted your belief.
01:59:18.000So again, you have to understand this world.
01:59:20.000There are researchers who believe one thing, Kevin Hall at NIH. Tends to believe that obesity is an energy balance problem and people get fat because they eat too much.
01:59:33.000And then there's David Ludwig and his colleagues at Harvard who tend to believe what I believe.
01:59:38.000And we funded them both to do studies.
01:59:41.000And Kevin Hall's study, if you believe Kevin interpreted it correctly, I 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.
02:00:13.000You do an experiment, people critique it, ideally you do another one.
02:00:17.000Kevin has decided Well, Kevin is doing another one.
02:00:20.000I think he's asking the wrong questions, but I just saw the other day that he's doing another experiment.
02:00:26.000The middle study was a free-living diet study done by Christopher Gardner at Stanford University, and the idea was The 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
02:00:56.000complained that the low fat diet wasn't fat enough so hopefully they'd be able to separate out these two.
02:01:06.000At the end of the trial, they got pretty lousy adherence.
02:01:11.000Low carb was about 25 to 28 percent carb, which is by no means a low, meaningful low carb diet.
02:02:39.000So the question is again, would you expect to see a difference?
02:02:42.000I can send you an email I wrote to my NUSI colleagues in 2015. I could read it.
02:02:48.000When I found out about this low-fat thing, saying this is insane.
02:02:53.000Both 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.
02:03:06.000There's a paper, I don't know if I can, well, I'm not going to talk about it.
02:03:11.000It's bad enough talking about the ambiguous studies that have been published without getting into unpublished research.
02:03:19.000The New York Times, for instance, did two stories on it.
02:03:21.000One 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.
02:03:31.000And that was written by a reporter who tends to believe what we believe.
02:03:35.000And the other article said it's all about the calories, because both groups ended up, on average, eating 500 calories each.
02:03:41.000It ends up, from a scientific perspective, being a poorly done study, even though we funded it.
02:03:46.000I'm not It just didn't answer the question.
02:04:07.000Both sides are not eating processed foods.
02:04:09.000There were two full differences in total carbohydrate intake.
02:04:13.000Okay, so even though they were both not eating as much refined carbohydrate, there were still two-fold differences or greater over the period of that study in total carbohydrate intake.
02:04:25.000If you believe the food frequency questionnaires that you just said we don't know whether we… You could be talking about vegetables.
02:04:34.000Well, these are healthy carbohydrates that they had primarily in this study.
02:04:38.000Can we agree that that study can be interpreted from virtually any way you want it, especially because it was a pre-living study?
02:04:45.000No, I definitely don't agree with that.
02:04:48.000Now, 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.
02:05:13.000Any kind of carbohydrate increases insulin levels relative to fat.
02:05:18.000And so, if that is true, and that matters for fat loss, these groups had two-fold differences in carbohydrate intake, even though it was predominantly healthy carbs, you should have seen something.
02:05:32.000You shouldn't have seen the exact same amount of weight loss in these two groups, right?
02:05:40.000That's the other part of the argument, which is you take away the sugar, and that was one of the problems with the energy.
02:05:46.000The argument I'm making, and Stephan's completely right, I'm defending my hypothesis.
02:05:52.000I see a study that, he does the same thing, he did it here, we all do it.
02:05:56.000You see a study that disagrees with you, you find the reason why to not believe it in every study ever done.
02:06:02.000has plenty of reasons not to believe it.
02:06:04.000That's why independent replication is something you always wanted.
02:06:07.000You 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.
02:06:15.000And so, you know, what I was trying, even when we started the Nutrition Science Initiative, the choice, that was a non-profit, the choice of the word initiative was to get nutrition researchers to an effect.
02:09:10.000I would say the counterargument is that they create a hormonal milieu in the body that over-responds to insulin.
02:09:18.000And insulin, what we haven't said is if you look in a textbook for fat metabolism and what causes fat storage, insulin is the hormone that primarily regulates fat storage in your fat cells.
02:09:34.000So 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, may indeed cause insulin resistance, and if it does, you over-respond insulin.
02:09:48.000So one is a peripheral explanation, not that people don't love it, and they don't want to over-consume it, whatever that means, and the other is a central explanation.
02:09:59.000So, I mean, sugar is a factor that makes us want to eat foods, right?
02:10:03.000I 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.
02:10:10.000And dopamine is a chemical that sets our motivational levels to do certain behaviors.
02:10:16.000So 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.
02:10:25.000Right, but this is just causing you to consume more.
02:10:28.000But you're saying that the actual amount, if you have the same amount of carbohydrates that are sugary carbohydrates versus the same amount that are vegetable carbohydrates, the sugary carbohydrates are going to be more fattening.
02:14:43.000So insulin is basically a traffic cop that allows your body to burn the fuel that you just consumed.
02:14:51.000So 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.
02:15:03.000It causes less fat to come out of your fat cells, and then your body's burning carbs.
02:15:09.000Now 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.
02:15:22.000But 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.
02:15:32.000The amount that you ate minus the amount that you burned.
02:15:34.000And if you eat a low-fat diet, you're not eating much and you're not burning much.
02:15:37.000You'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.
02:15:44.000And the way we know that's true is because varying the amount of carbohydrate and fat in the diet makes no difference to body fatness in randomized controlled trials.
02:15:54.000That's why we know that what I just said is correct.
02:15:57.000So, first of all, it's one randomized controlled trial.
02:16:21.000I think it's one of the problems with modern nutritional and medical science is you do crappy studies, generate garbage, and then you sift through the garbage and say, I can find a truth in here.
02:16:40.000Remember, we're talking about the 10 calories a day.
02:16:42.000So when you said the difference between the fat burned and the fat stored or the fat consumed and the fat expended has to be 10 calories a day.
02:16:55.000So if it is true that if I consume 1500 calories a day and I Somehow metabolize or excrete 1490, and I guarantee that no such study was ever so carefully done.
02:17:09.000Can you cite evidence to support this thing you're saying right now?
02:17:11.000Well, you could take, for instance, the Energy Balance Consortium study, the Kevin Hall study that we've talked about.
02:17:17.000There are two things that happen when you put people on a ketogenic diet.
02:17:20.000Among other things, you generate ketones, and you lose ketones in the breath and in the urine.
02:17:25.000And one of the things you have to do in these energy balance experiments is measure calories lost through fecal material.
02:19:04.000Note that the same process of esterification will also be simultaneously incorporated fatty acids from circulating triglycerides released by lipoprotein lipos That's enough,
02:19:55.000This book, which we're talking about, Metabolic regulation, a human perspective.
02:20:00.000It's written by Keith Frane, who's a retired Oxford professor, who's a wonderful man, and he was the world's leading authority on metabolic regulation, how your body controls its use of fuel and orchestrates storage and oxidation.
02:20:13.000And in this book, Keith Frane Talks about how insulin determines fat accumulation and fat cells.
02:20:22.000Not accumulation, that's not the correct word.
02:21:20.000So my assumption is the same reason people get fat is the same reason their fat cells get fat, and you've got a whole lot of, you've got this disorder, metabolic syndrome we're talking about, which includes not just diabetes, Problem is with your blood lipids,
02:21:37.000but it includes getting fat at your waistline increasing, and it's an insulin resistance-related disorder, which means your insulin is elevated.
02:21:44.000And again, this is where we end up with two hypotheses about why insulin is elevated.
02:21:49.000But if, for instance, sugar can elevate insulin, you end up with metabolic syndrome, you're in fat storage mode.
02:21:55.000That's the terminology of diet book doctors.
02:21:58.000So now you're storing fat, and you only have to do 10 calories a day.
02:22:02.00020 calories a day, you're going to get obese.
02:22:05.000And it's insulin-mediated and insulin is responding to the carbohydrate content of the diet primarily.
02:22:11.000And when I said this to Keith, you know, you've got one mechanism for why fat cells get fat and a different mechanism for why humans get fat.
02:22:18.000And I'd like to talk about this overeating concept.
02:22:22.000He said, you know, I never thought of that.
02:22:24.000I mean, the guy had been in the field 40 years, and he lived maybe 50. And then I had a long conversation with him.
02:22:30.000I was back in Oxford when I did that insane Alan Aragon debate.
02:22:35.000I stopped off at Oxford on the way to Manchester, and we had a long conversation with Keith.
02:22:40.000And I said, look, what I want you to do is just...
02:22:43.000Come up with a hypothesis of obesity from the fat cells perspective, right?
02:22:49.000Shed your brain-centric, energy-balance-centric thing and ask yourself, what does the fat cells see?
02:22:56.000And if nothing else, ask the student to do it as an experiment.
02:22:59.000I mean, that would be a great thought experiment for a kid.
02:23:14.000He said, I can't put energy balance aside.
02:23:17.000You're telling me to not think in terms of intake and expenditure, and I can't do it.
02:23:23.000And I mean, wonderful man, he literally, and this is again what I've been arguing, is all these people are so, including Stephan, who was, you know, learned in this world, they're so locked into this thinking that obesity is this energy imbalance.
02:23:40.000So everything they do, everything they interpret, and when Stefan says there's study after study, and there's 20 randomized control studies, and it's sort of, I'm going to shovel the evidence on top of you, and I'm saying, look, I guarantee if we go through those 20 studies, it'll be just like the Jim Hill study.
02:23:54.000They assumed energy balance was the cause, and then they wanted to see what caused energy imbalance, and they started with the wrong hypothesis.
02:24:21.000I tore through it and I was so persuaded when I initially read this 10 years ago that I ate a low carbohydrate diet for six months because I thought the carbs were going to make me fat and give me diabetes.
02:24:34.000So I was fully immersed and convinced by your perspective when I read this book.
02:24:47.000And the thing that caused me to go away from that perspective was when I actually started investigating the evidence on my own underlying these ideas.
02:25:36.000Honestly, I'm going to try to say this in a non-insulting way, but I will simply say that others who have looked at the same historical evidence have come to different conclusions than you have.
02:25:48.000And that includes me in the places where I've looked at the historical evidence.
02:25:52.000And so, I think that, you know, this idea that I am, like, locked in some paradigm and can't see what you're talking about.
02:26:33.000Okay, and you didn't really have an explanation for it.
02:26:36.000I don't have a very, well, anyway, go ahead.
02:26:39.000Yeah, so again, the argument I've been making is there's two ways to look at everything.
02:26:45.000So one way is the low-carb diet somehow, because of, I don't know, food reward issues, affects your urge to eat low-carb foods, and because of that you don't Hunger for them as much.
02:27:05.000And when you're on a higher carb diet, I think the way you phrased on this other podcast was your body sort of tells you it's mealtime.
02:27:39.000She's probably telling me I'm getting shrill.
02:27:42.000There's a different way to look at everything.
02:27:44.000That's the point I'm trying to, with every study.
02:27:47.000I mean, can you tell me evidence that, can you give me actual evidence that the lower level of insulin is the cause of not needing to eat those meals?
02:28:51.000When you feed people, whether it's overfeeding or underfeeding and you're causing weight loss or weight maintenance, the carb to fat ratio of the diet makes almost no difference.
02:29:04.000The famous feeding study from the 60s, which I thought when you said Horton, I thought you meant Ed Horton, not TJ Horton.
02:29:10.000So Ed Horton and Ethan Sims did a prisoner study.
02:29:13.000They literally, they wanted to get overfeed.
02:29:16.000Again, they're using their thinking in terms of eating too much.
02:29:18.000They wanted to first get college kids to gain 25% of excess body weight.
02:29:24.000This was in the 60s, and they couldn't get the college kids to do it, which suggests that college kids were different in the 60s than they are today.
02:29:31.000So they used prisoners in the Vermont State Prison and they overfed them.
02:30:04.000If you looked at pounds gained per calorie added, they gained more per calorie of fat than they did per calorie of carbs.
02:30:14.000But if you looked at how much they could eat, They couldn't add that much fat and they could add 8,000, 7,000 extra calories of carbs.
02:30:24.000There's actually a line in one of the papers where they said they would eat 10,000 calories and then go to bed hungry, craving more carbs.
02:30:31.000So then the question becomes again, is it because the carbs are doing something in the brain to increase food reward, Or is it the carbs are doing something in the body so that their body has figured out a way it can orchestrate, deal with this massive influx of carbs versus fat?
02:30:46.000But there's always two ways to look at it.
02:30:49.000And every time Stephan says there's masses of evidence, my job as a journalist was to go through and say, does this refute that hypothesis?
02:30:57.000And if it doesn't, we have to hold on to it.
02:30:59.000Because remember, we have an obesity and diabetes epidemic.
02:31:01.000And the kind of advice where we tell people to sleep better And eat less or avoid foods that they love, don't have pizza and ice cream.
02:31:12.000It implies that the reason they get fat, even the overeating hypothesis...
02:31:17.000So you think they should be eating pizza and ice cream?
02:31:32.000We know, if nothing else, I think you would agree with this.
02:31:35.000So the whole low-carb movement, as you said it on this podcast, was that what I've done, if nothing else, is I've convinced people they could eat low-carb diets without killing themselves.
02:31:58.000Not entirely, because you're telling people that only carbohydrate matters.
02:32:03.000I'm not telling people only carbohydrate matters.
02:32:06.000You have argued at length that calorie intake and dietary fat intake and physical activity do not influence body fatness and are not important.
02:32:37.000In part, and again, it just requires...
02:32:39.000But what I'm saying is that there is harm in what you're saying because, yes, we all agree that these carbohydrates are fattening, but you're saying that these other important things are irrelevant, and that's the dangerous part of what you're saying.
02:33:40.000There just never seemed to be enough food to satiate Carl's growing body.
02:33:44.000After school, he would eat a foot-long sub before his mother's home-cooked dinners, even after having a hefty lunch of homemade chicken, rice, and vegetables and his favorite snacks, granola bars, and a bunch of crunch.
02:34:23.000You can measure their calorie intake and you can know.
02:34:26.000I don't know what you're talking about there, Gary.
02:34:28.000We would eat a foot-long sub before his mother's home food dinners, even after having a hefty lunch of homemade chicken, rice, and vegetables.
02:35:00.000Well, that depends on how you define that, but I could look at your body composition and I could tell you whether you were overeating relative to a lean person, yes.
02:35:15.000Yes, so without knowing if I have excess body fat, you cannot tell whether I'm overeating, which is the cause of the excess body fat, right?