The Joe Rogan Experience - Joe Rogan Experience #1267 - Gary Taubes & Stephan Guyenet

00:00:00.000 Four.

00:00:01.000 Three.

00:00:02.000 Two.

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00:00:08.000 And we're live.

00:00:09.000 Alright, so to set this up, when Gary was on last, Gary Taubes?

00:00:15.000 Stefan, how do I say your last name?

00:00:16.000 Stefan Guillenet.

00:00:17.000 Guillenet.

00:00:18.000 Yeah.

00:00:18.000 Guillenet.

00:00:19.000 It's like DNA. Like DNA, but with a G. Right.

00:00:22.000 Got it.

00:00:23.000 Okay.

00:00:24.000 When you were on last, Stefan had some opposition to some of the things that you were saying.

00:00:31.000 We talked about getting him on and you on together.

00:00:35.000 We finally pulled it off.

00:00:36.000 There was a lot of wrangling, there was a lot of back and forth and cat wrangling, but we got it.

00:00:41.000 We're here.

00:00:43.000 Give me your position on, this is all for folks listening, this is all about obesity and the mechanism for obesity, is that fair to say?

00:00:54.000 Yeah, yeah.

00:00:54.000 So essentially, the main points that we want to talk about today are...

00:00:59.000 Try to keep this a fist from your face.

00:01:00.000 Okay, sure.

00:01:01.000 Just pull it, you can move it around.

00:01:03.000 What causes obesity and what causes insulin resistance, which is behind a lot of our chronic diseases that are common in society.

00:01:11.000 And please give us your background.

00:01:14.000 Yeah, so I have a BS in biochemistry, a PhD in neuroscience.

00:01:21.000 After 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.

00:01:31.000 Hopefully we'll get a chance to talk about those today.

00:01:33.000 And 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.

00:01:50.000 And yeah, so that's my background.

00:01:53.000 Now, what is your disagreement with Gary's position?

00:01:57.000 Everything.

00:01:58.000 Yeah, so how about I just, can I start by explaining what I believe causes obesity?

00:02:05.000 I'm going to be long-winded here, is that okay?

00:02:07.000 It's okay, go right ahead.

00:02:08.000 We have hours.

00:02:09.000 Okay, cool.

00:02:10.000 So first, a little bit of housekeeping.

00:02:12.000 I'm going to be citing a lot of evidence today.

00:02:15.000 Just please bring this up to your face.

00:02:16.000 Okay, sure.

00:02:17.000 Just move it around, because you want to sit back.

00:02:19.000 How's that?

00:02:20.000 Perfect.

00:02:20.000 Beautiful.

00:02:21.000 I'm going to be citing a lot of evidence today, and I want people to be able to follow along at home.

00:02:25.000 And so I've put many of the references that I'm going to be citing on...

00:02:29.000 Just do that so it doesn't cover your face.

00:02:31.000 Okay.

00:02:32.000 There we go.

00:02:32.000 All right.

00:02:33.000 I'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.

00:02:42.000 And I have a numbered list of topics there.

00:02:46.000 And I'm going to be calling out numbers.

00:02:49.000 Just scroll down to the number that I referred to and the references are all there.

00:02:54.000 Second 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.

00:03:02.000 I think low carb diets are a valid tool for controlling body fatness and controlling blood sugar.

00:03:08.000 I'm not here to talk anybody out of being on a low carb diet.

00:03:12.000 What I am here to try to talk people out of is some of the mythology that has accumulated around the low-carb diet.

00:03:19.000 Okay, so I want to get started with an analogy to help people understand why the brain is important in obesity.

00:03:27.000 So imagine you're an alien coming down from outer space, and you want to understand what's going on on Earth.

00:03:34.000 And you notice that on the highway, some cars are traveling faster than others.

00:03:37.000 Some cars go faster, some cars go slower, and you want to figure out why.

00:03:41.000 And so you go and you start studying the tires of the cars.

00:03:46.000 Because obviously the amount of force that is exerted by the tire onto the asphalt is the thing that determines the speed of the car.

00:03:54.000 We know this.

00:03:54.000 This is just physics.

00:03:55.000 And so you study the tires and you study the tires and you study them and you never figure out why some cars go faster than others.

00:04:04.000 Now why is that?

00:04:05.000 The reason is that you're studying the wrong part of the system.

00:04:08.000 If 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.

00:04:20.000 And so in this analogy, the tires are fat cells, and the person behind the wheel is the brain.

00:04:30.000 We're good to go.

00:04:49.000 That's because it's the wrong part of the system to study.

00:04:51.000 Fat cells do not regulate the size of fat cells any more than the tires on a car regulate the speed of the car.

00:04:59.000 The thing that regulates the size of fat cells is the brain.

00:05:03.000 So let's talk about, first I'll give you a little framework for thinking about this.

00:05:08.000 The brain evolved over about 600 million years to promote the survival and reproduction of our ancestors.

00:05:14.000 And over the course of that time, we evolved all these different brain circuits that have specialized functions.

00:05:20.000 They generate our hunger and our cravings and our fullness feelings.

00:05:24.000 They generate our eating behavior, what and how much we eat.

00:05:28.000 And they actively regulate the amount of fat on our bodies.

00:05:31.000 And that's one of the things I want to talk about.

00:05:34.000 And all of these circuits evolved.

00:05:36.000 And these are non-conscious, by the way.

00:05:38.000 So you don't decide you want to be hungry.

00:05:39.000 You don't decide that you want to have a craving.

00:05:42.000 These are things that bubble up from non-conscious parts of your brain that you don't control.

00:05:54.000 We're good to go.

00:06:07.000 So 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.

00:06:23.000 And then what you see as a result is the three hallmarks of obesity.

00:06:28.000 First of all, the obvious, you see elevated body fat mass.

00:06:32.000 Second of all, you see elevated calorie intake.

00:06:35.000 People with obesity consume more calories than people who do not have obesity after correcting for height and sex and physical activity level.

00:06:44.000 And third, you see that people with obesity defend their higher level of body fatness against changes.

00:06:51.000 And so there's actually a regulatory change that happens.

00:06:55.000 It's not conscious defense.

00:06:57.000 They're not trying...

00:06:59.000 To remain obese, it's these body fat regulatory circuits.

00:07:04.000 And this is where Gary gets it right, is that people with obesity are not just lean people who eat more calories.

00:07:10.000 There's actually a change in the regulatory activity that regulates body fat in the body.

00:07:15.000 And we can get back to how that happens, but I'll just leave it there for now.

00:07:20.000 So up until this point, I've basically just been telling a plausible story, right?

00:07:25.000 I mean, I haven't actually cited any evidence yet to support that my story is correct.

00:07:31.000 And so let's get into that.

00:07:32.000 Let's talk about what some of the evidence is that supports this idea that I've just laid out.

00:07:37.000 So I want to start with the genetics of obesity.

00:07:41.000 Can I interrupt for one second?

00:07:44.000 As long as it's very brief.

00:07:46.000 It's just a question.

00:07:47.000 I still don't quite understand what the model is.

00:07:49.000 I understand the dysregulation of the brain with the environment.

00:07:53.000 If you don't understand the model, how about I finish laying it out and then you can ask a question?

00:07:59.000 Because I may answer your question over the course of continuing.

00:08:02.000 So let me just finish.

00:08:04.000 Okay, 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.

00:08:16.000 So you get these studies, like the most interesting studies are the genome-wide association studies.

00:08:22.000 They get hundreds of thousands of people together, and they We're good to go.

00:08:50.000 That tells you what the mechanisms are that underlie everyday differences in body fatness in the general population.

00:08:56.000 And so to kind of warm ourselves up, let's start by talking about height genes.

00:09:01.000 So height has a strong genetic component, so does body fatness.

00:09:06.000 And researchers have figured out a lot of the genes that underlie differences in height between people.

00:09:12.000 And 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?

00:09:21.000 Because growth of the skeleton determines your height.

00:09:23.000 So 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.

00:09:42.000 So these studies are really good at getting at the underlying biological mechanisms that are driving these phenomena.

00:09:48.000 So what do these studies have to say about obesity?

00:09:52.000 If Gary's model is correct, we should see a bunch of genes popping up related to fat cells and insulin.

00:09:59.000 If my model is correct, we should see a bunch of genes popping up related to the brain.

00:10:04.000 And in fact, that's exactly what we see.

00:10:06.000 The genetics of obesity are overwhelmingly related to differences in brain activity between individuals.

00:10:15.000 Okay, so that's one piece of evidence.

00:10:17.000 Another piece of evidence, there are five FDA-approved weight loss drugs.

00:10:23.000 Four of those act in the brain.

00:10:25.000 One of them reduces dietary fat absorption in the digestive tract.

00:10:30.000 There are no effective fat loss drugs that I'm aware of that target insulin or fat cells.

00:10:36.000 Third 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.

00:10:46.000 Some of these People end up with extreme obesity.

00:10:51.000 People and also animals, we see this in mice and rats, just occasionally you get unlucky and you get really, really fat.

00:10:57.000 And researchers have been cataloging what are these mutations.

00:11:01.000 When we find people who are genetically really obese, what are these mutations that are making them fat?

00:11:07.000 What is the biological mechanism that's getting screwed up that's making them fat?

00:11:11.000 And 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.

00:11:21.000 And this is the leptin...

00:11:25.000 is the primary fat-regulating hormone in the body.

00:11:29.000 Gary 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.

00:11:45.000 So that's the third piece of evidence.

00:11:49.000 So 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.

00:12:02.000 We've established that the brain is central to obesity, but we haven't really established what it is exactly about that interaction.

00:12:08.000 Why does our modern food, why does our modern environment promote obesity, right?

00:12:17.000 Basically, there are three different ways that I'm going to look at this from.

00:12:24.000 But 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?

00:12:34.000 What is the diet that is more fattening than any others?

00:12:36.000 The answer to that is it's human junk food.

00:12:39.000 In a variety of non-human species and humans, it's human junk food that is more fattening than any others.

00:12:46.000 I'm going to skip over some of the research here that demonstrates this.

00:12:51.000 By the way, I haven't been calling out numbers here.

00:12:54.000 Okay, let me call out some numbers.

00:12:57.000 Reference number two on my website is those genetic studies.

00:13:04.000 Reference number one is the obesity drugs.

00:13:08.000 Reference number six is those spontaneously occurring genetic mutations.

00:13:13.000 And 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.

00:13:21.000 Essentially, what you find is that this stuff is really fattening in animals, many different species.

00:13:28.000 It's super fattening in humans, calorie-dense.

00:13:31.000 When you create an environment with abundant, easy, calorie-dense, tasty foods, rich carbs and fat, you see this dramatic overconsumption and fat gain.

00:13:43.000 Across many species, including humans.

00:13:45.000 And what you find in the research is that the sugar and the carbohydrate cannot explain that.

00:13:53.000 They're part of the effect.

00:13:55.000 Yes, they explain part of it, but you cannot replicate that effect by only feeding sugar and carbohydrate.

00:14:01.000 You can't replicate it in animals.

00:14:03.000 You can't replicate it in humans.

00:14:05.000 When you say you can't replicate it, you mean you can't replicate obesity?

00:14:08.000 What do you mean?

00:14:24.000 A variety of calorie-dense, palatable human foods.

00:14:27.000 You can't fully replicate it with sugar and carbs.

00:14:30.000 You cannot fully replicate it with fat alone either.

00:14:34.000 We can get deeper in this if you want.

00:14:37.000 But I'm confused.

00:14:38.000 So you're saying that the diet that causes the most obesity is what we think, right? 0.99

00:14:44.000 This human junk food diet, rich in sugar, simple carbs, bullshit diet, right? 0.99

00:14:51.000 You're saying that you can't replicate that with just sugar and carbs? 1.00

00:14:56.000 You cannot fully replicate it.

00:14:57.000 Fully in what sense?

00:14:58.000 What 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,

00:15:14.000 palatable foods rich in carbohydrate and fat.

00:15:19.000 That's very confusing.

00:15:21.000 How's that?

00:15:22.000 Because I'm not sure exactly what you're saying.

00:15:24.000 You'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?

00:15:39.000 So, 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.

00:15:58.000 And 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.

00:16:07.000 See, this is where I'm confused.

00:16:08.000 No, I don't see what you're saying.

00:16:09.000 Because 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?

00:16:22.000 Correct.

00:16:22.000 Is that what you're saying?

00:16:22.000 Yep.

00:16:23.000 But what are you giving them when you're giving them the diet of junk food?

00:16:26.000 You're giving them sugar and carbs. 1.00

00:16:27.000 Well, for example, in animals, no, it's different.

00:16:29.000 Because if you think about human junk foods, generally those foods contain fat and carbohydrate and salt and all kinds of other things.

00:16:37.000 So it's more than just carbs, right?

00:16:39.000 It's a lot of soda too, right?

00:16:41.000 There's no sugar.

00:16:42.000 It's just sugar in that.

00:16:44.000 So I'll get in more detail.

00:16:45.000 So the ways that you can do this, you can add sugar, just sugar, table sugar, to the feed of animals.

00:16:52.000 That's one way to do it.

00:16:53.000 Or you can add it to their drinking water.

00:16:55.000 Sometimes it's a little bit fattening, sometimes it's not.

00:16:58.000 It's not that fattening in animals.

00:17:00.000 In humans, you can ask them to drink sugar-sweetened beverages that are just sugar, and you can see what happens.

00:17:07.000 And people will gain weight.

00:17:08.000 Or you can tell them to stop drinking sugar-sweetened beverages and you can see what happens.

00:17:12.000 People 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.

00:17:27.000 So you're saying, well, obviously there's more calories, right?

00:17:30.000 If there's carbs and fat and all these other things?

00:17:33.000 Correct.

00:17:33.000 If you think that calories matter, then we agree.

00:17:36.000 Well, for sure it matters, right?

00:17:38.000 Gary doesn't think it matters.

00:17:39.000 You don't think it matters?

00:17:40.000 I think it's the wrong way to think about it.

00:17:42.000 What do you disagree, if anything, with what he's said so far?

00:17:46.000 Well, so far what he's said hasn't been particularly revelatory.

00:17:55.000 I 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.

00:18:11.000 Fundamentally, 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.

00:18:26.000 And the way it does it is by controlling or miscontrolling our intake and our expenditure, and the difference ends up in fat tissue.

00:18:37.000 Is that fair to say for the most part?

00:18:39.000 Primarily intake, but yeah.

00:18:40.000 Yeah, so Stefan has a brain-centric view of the universe and the community at large does as well.

00:18:46.000 So 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.

00:19:02.000 And it's been stored in their fat tissue.

00:19:04.000 And Stefan says, I think would say that the problem is in their brain's ability to regulate intake to expenditure.

00:19:14.000 Is that correct?

00:19:15.000 Yeah.

00:19:16.000 Okay.

00:19:18.000 And let me, I have to fix my headphones.

00:19:20.000 So how are we going to do this?

00:19:21.000 I'm getting feedback when I talk.

00:19:24.000 You're getting feedback?

00:19:25.000 Yeah, it's just weird.

00:19:26.000 Could be the, hold on one sec.

00:19:30.000 For those who don't know, I'm hearing impaired, as they say kindly.

00:19:34.000 My kids would say deaf is a post. 0.81

00:19:36.000 Is that better?

00:19:37.000 So I took off my hearing aids.

00:19:39.000 That's a little better.

00:19:40.000 Okay.

00:19:43.000 What I've been arguing, so I come along, my background, I'm a journalist.

00:19:46.000 I'm an investigative journalist with a science background.

00:19:50.000 Okay, that's what I do, and I'm curious.

00:19:53.000 And 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.

00:20:04.000 So I'm very sensitive to this.

00:20:07.000 And 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. 0.96

00:20:23.000 They just assumed that fat people are gluttons.

00:20:25.000 And I'm going to use some socially unacceptable language because in part that's how they thought about it. 0.98

00:20:31.000 In 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.

00:20:47.000 And 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.

00:20:54.000 And my favorite example is one team that was trying to get...

00:20:58.000 They got the wives to stop having sex with the husbands if they didn't lose weight every week. 1.00

00:21:03.000 And that would motivate them.

00:21:05.000 I think even you point out that sex is a greater motivator in your book than tasty foods.

00:21:11.000 It didn't work.

00:21:12.000 I didn't say it was greater, but I said it was on par.

00:21:14.000 On par.

00:21:16.000 So...

00:21:16.000 And I'm going to just read you...

00:21:21.000 I won't read you that.

00:21:23.000 While the obesity research community is focusing on the brain, there were people studying fat metabolism.

00:21:32.000 Endocrinologists, 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.

00:21:50.000 And our body does a very careful job of basically orchestrating how we use fuels after we eat.

00:21:56.000 And 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.

00:22:08.000 So today, when you read the literature, the articles will often say obesity is a sort of energy imbalance.

00:22:13.000 You take in more calories than they expend.

00:22:16.000 There were still the best scientists in the field, the best physician scientists would say, look, obesity is a sort of excess fat accumulation.

00:22:24.000 Let's look at what regulates fat accumulation in the human body.

00:22:28.000 Some people are programmed or dysregulated to store more fat.

00:22:32.000 And if they store more fat, their behavior is going to respond. 0.97

00:22:37.000 They'll be hungrier, they'll eat more, they'll be gluttons, all these things. 0.53

00:22:40.000 So it was switching the causality.

00:22:43.000 Instead 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.

00:22:56.000 If 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.

00:23:03.000 I'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.

00:23:18.000 You're going to worry that he's over secreting growth hormone.

00:23:21.000 So 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,

00:23:39.000 the obesity people were convinced that the problem was in the brain.

00:23:43.000 And 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.

00:24:03.000 And 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.

00:24:13.000 So for example, When I was in high school, senior year in high school, I weighed 195 pounds and I played football.

00:24:22.000 And my brother, two years older, weighed 195 pounds his senior year and played football.

00:24:28.000 My brother never got more than 195 pounds.

00:24:32.000 And I went up to 240. We both ate as much as humanly possible, you know, as you could imagine.

00:24:38.000 That's what high school athletes do. 0.81

00:24:40.000 My brother was always lean.

00:24:42.000 I was always chubby.

00:24:44.000 My brother stayed lean and became an endurance athlete.

00:24:47.000 I became a football player and I lifted weights.

00:24:49.000 I put on muscle easily and I fatten easily.

00:24:53.000 He didn't.

00:24:55.000 The conventional wisdom would be the reason I went to 240 and he never got to 195 was that my brain was different than his.

00:25:04.000 My argument is our bodies were fundamentally different.

00:25:07.000 So 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. 0.98

00:25:15.000 I think about why is her body driving her to be 300 pounds. 1.00

00:25:20.000 So that's, I think, kind of the fundamental difference.

00:25:24.000 And 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?

00:25:33.000 Is this a reductionist perspective?

00:25:35.000 Because, I mean, isn't it a holistic...

00:25:37.000 I 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...

00:25:45.000 I'm not saying it's separate.

00:25:46.000 The question is, is the brain driving what's happening in the body, or is it responding to what's happening?

00:25:51.000 Yeah, so...

00:25:52.000 And, you know, the brain, of course, does respond a lot to what's happening in the body, and we can talk about that and how that works.

00:25:59.000 But, you know, I think it's...

00:26:02.000 We can tell stories, but the thing that differentiates a story that's true from a story that is not true is evidence.

00:26:10.000 And so you talk about the difference between your brother and you.

00:26:13.000 This is where that genetics evidence comes back in that I was talking about.

00:26:17.000 Your brother and you only share half of your genes.

00:26:20.000 We 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.

00:26:33.000 I'm not done, Gary.

00:26:34.000 Let me finish.

00:26:35.000 I just want to read something from your book.

00:26:36.000 Can I read something from you?

00:26:38.000 Nope, nope.

00:26:38.000 Not right now.

00:26:39.000 I'm in the middle of saying something.

00:26:41.000 Those genes are primarily related to differences in brain function.

00:26:46.000 That is what the genetics say.

00:26:48.000 And 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.

00:27:00.000 That is what the research says.

00:27:02.000 Okay.

00:27:02.000 It's very difficult to parse out when you're talking about two 17-year-olds that weigh exactly the same amount.

00:27:07.000 Like, how do we know how much they consumed in calories?

00:27:10.000 I mean, we don't have any studies.

00:27:11.000 We don't have any tests.

00:27:12.000 I mean, I can guarantee you we both ate as much as humanly possible.

00:27:16.000 Actually, 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.

00:27:25.000 He just gets bored of eating after a couple of hours.

00:27:28.000 Okay, but maybe even though, like maybe if you looked at it scientifically, you ate more than him.

00:27:35.000 Or maybe you ate more sugar.

00:27:36.000 Or maybe you ate more carbs.

00:27:38.000 Well, so that's the difference.

00:27:39.000 So those are the two hypotheses.

00:27:41.000 One hypothesis is...

00:27:44.000 My body – and this is what Stefan is talking about.

00:27:47.000 So I want to – just the thing I wanted to read.

00:27:49.000 How much – I'll ask you the question.

00:27:51.000 How much of the variation in human obesity do those genes explain?

00:27:56.000 So if you look at the genetics of – No, I didn't ask how much – Gary, I'm answering your question.

00:28:02.000 Once he starts talking, yeah, you've got to let him talk.

00:28:04.000 Yeah, please, Gary.

00:28:06.000 So 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.

00:28:24.000 So, 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.

00:28:35.000 Now, we've only identified a small proportion of the specific genes that underlie the propensity to obesity.

00:28:43.000 And 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.

00:28:51.000 How much?

00:28:52.000 Right now, I think it's up to about 10%.

00:28:55.000 It was 3% when your book was published.

00:28:57.000 Yeah, that's correct.

00:28:58.000 So you're saying they did 7%?

00:28:59.000 Absolutely, yeah.

00:29:01.000 Actually, let me cite the study there.

00:29:04.000 No, just a second.

00:29:05.000 I'm going to cite the study.

00:29:06.000 Just a second.

00:29:06.000 I'm going to cite the study.

00:29:08.000 The study is under reference number two.

00:29:13.000 So you can go check that out.

00:29:15.000 It's about 10%.

00:29:15.000 And 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.

00:29:25.000 And 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.

00:29:34.000 And so that tells us That primarily the differences between individuals that determine differences in body fatness is about differences in brain activity.

00:29:43.000 No one should be shocked about this.

00:29:45.000 The brain generates all of our eating behavior, it generates all of our physical activity behavior, and it actually regulates body fatness.

00:29:53.000 No one should be surprised by this.

00:29:56.000 I am.

00:29:57.000 And I was.

00:29:59.000 And how are you surprised?

00:30:00.000 And what do you disagree with?

00:30:01.000 Well, virtually everything.

00:30:03.000 But let's begin with...

00:30:08.000 Let's track back now.

00:30:11.000 Okay, so drugs that explain obesity, 10%.

00:30:14.000 With 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.

00:30:24.000 You say Stefan, right?

00:30:25.000 Stefan.

00:30:25.000 It's okay.

00:30:25.000 I'm not offended.

00:30:26.000 It's okay.

00:30:26.000 But I mean, just so people don't get confused.

00:30:29.000 Thank you.

00:30:30.000 If 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.

00:30:48.000 So now they're trying to solve the problem.

00:30:51.000 Without the humans involved, why do some cars drive faster than others?

00:30:55.000 And they come up with all kinds of hypotheses, and some of them can explain it.

00:30:59.000 Even when they interpret the hypotheses, one of the common problems in science is called intellectual phase lock.

00:31:06.000 So 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.

00:31:23.000 And 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.

00:31:36.000 And leptin is a good example.

00:31:38.000 So leptin is discovered in 1993, and when leptin is discovered, obesity becomes sort of a legitimate field of science.

00:31:45.000 Until 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.

00:31:59.000 It 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.

00:32:15.000 Now, 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,

00:32:30.000 in the body.

00:32:31.000 And what leptin does is a hormone that sort of is secreted in response to how much fat you've accumulated.

00:32:39.000 And 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.

00:32:54.000 So it makes perfect sense.

00:32:55.000 If there's fat available in the fat cells, now you've got a signal telling, sort of influencing the other cells of the body to burn fat.

00:33:03.000 So now you've got a hormone that could work in the periphery, below that neck. 0.93

00:33:08.000 Or it could work above the neck, but you've got a community that's almost exclusively studying in the head. 0.87

00:33:14.000 They don't know there are human drivers down here.

00:33:16.000 So that's what they do.

00:33:18.000 So even in this world, I think I know the genome paper, Stefan is...

00:33:28.000 There have been a number of them, but yeah, that's the most recent.

00:33:31.000 The Harvard Group?

00:33:32.000 I don't remember.

00:33:34.000 So they had two papers, because this is what you cited in the article you co-authored with Rudy Leibel.

00:33:40.000 So they have two papers.

00:33:41.000 One is genes associated with obesity, and one is genes associated with body type.

00:33:48.000 So with body type, they're all below the neck.

00:33:51.000 They're all, you know, fat metabolism, basically.

00:33:55.000 And 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.

00:34:05.000 I don't think your brain is regulating how much muscle you're building other than your drive to go to the gym.

00:34:11.000 Basically, your body is responding to the stress on the muscle, all the things you do, and the weight lifting.

00:34:17.000 It's all below the neck.

00:34:18.000 So the argument here is, again, simple.

00:34:21.000 When these people looked at body type, it was insulin-regulated genes, for the most part, growth hormone, all these things.

00:34:31.000 When they looked at excess body fat, they decided they were in the head.

00:34:35.000 But 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.

00:34:42.000 Did they do the same kind?

00:34:44.000 And I was going to call the researcher involved.

00:34:45.000 I 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?

00:35:01.000 And did you do the same kind of searches?

00:35:03.000 I don't actually know how they determine where the genes work.

00:35:06.000 It's the same kind of searches.

00:35:07.000 They just came up with different sets of genes.

00:35:10.000 So they didn't start with any assumptions.

00:35:12.000 They were just finding whatever was there.

00:35:13.000 No, but the question is where the genes work.

00:35:15.000 So there's a common phenomenon in all this.

00:35:17.000 Like with leptin, a gene that everybody thinks about working in the hypothalamus seems to work in every cell in the body.

00:35:23.000 Can I respond to that?

00:35:24.000 Wait, let me finish talking.

00:35:25.000 Because you say this in your book.

00:35:26.000 Yeah, go ahead.

00:35:28.000 I'm prepared to respond whenever you're done.

00:35:30.000 Okay.

00:35:31.000 In your book, you say that genes work.

00:35:33.000 The body basically puts different mechanisms to work in many places as it can, and there are these homeostatic feedback loops.

00:35:43.000 Something happens, your whole body has to respond.

00:35:46.000 So a gene that might work primarily on one cell is scattered all over the body, and it'll do different jobs on different cells.

00:35:54.000 But if you think that the problem's in the brain, That's where you look.

00:35:58.000 So you get this kind of intellectual phase lock, where that's what we do, that's what we study.

00:36:05.000 A neurobiologist studies the brain.

00:36:10.000 Daniel 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.

00:36:21.000 Okay?

00:36:22.000 And basically, if you're studying the brain, that's what you look at.

00:36:26.000 If you're studying the gut, and so we all get trapped into that on some extent.

00:36:31.000 And 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.

00:36:47.000 It's just not there.

00:36:49.000 And I would argue It has to be there, even if it's wrong.

00:36:55.000 If it's not there, the absence of it, like you can't talk about leptin without talking about what it might be doing in the body.

00:37:02.000 You can't talk, you know, so there's a, and it's put me in a very odd position.

00:37:07.000 So Stephan is kind of the defender of the orthodoxy, and I'm the one who comes along and says, look, you guys just, you missed it.

00:37:14.000 You screwed up.

00:37:15.000 You had psychologists and psychiatrists running the field when the endocrinologist solved it, and then you discovered leptin and it became a molecular biology problem. 0.86

00:37:23.000 And you're now divorced from the very simplest observations about obesity.

00:37:29.000 So we can do huge genome-wide association studies.

00:37:32.000 They sound remarkable.

00:37:35.000 But if I were to ask a simple question like, why is it I get fat here?

00:37:41.000 You know, the love handle thing?

00:37:42.000 It's in the back with me.

00:37:43.000 It's not in the front, but it's here and not here.

00:37:48.000 I don't see what the brain has to say about that.

00:37:51.000 Okay, so as you mentioned, there have been different genetic studies that have looked at body fat distribution versus total body fatness.

00:38:01.000 So total body fatness is what we're talking about when we're talking about obesity.

00:38:05.000 Body fat distribution is what we're talking about when we're talking about the fat being on your hips versus on your wrist.

00:38:12.000 Now what we see is different sets of genes that come up.

00:38:15.000 So body fat distribution, we actually see insulin-related genes.

00:38:20.000 So 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.

00:38:29.000 But when you look at total body fatness, The thing that causes obesity, what you see is that those genes are dominated by the brain.

00:38:37.000 And the really cool point I want to make about the genetics research...

00:38:40.000 10% of those genes might be dominated by the brain, if they looked.

00:38:45.000 Come on, Gary.

00:38:46.000 It is unbiased.

00:38:48.000 That's the really cool thing about it.

00:38:51.000 This is whatever genes are popping up.

00:38:53.000 These studies do not care about what you believe about what causes obesity.

00:38:57.000 This is just whatever genes are popping up.

00:38:59.000 So it's unbiased.

00:39:01.000 And that's what they're saying.

00:39:02.000 And I'm not done here, Gary.

00:39:04.000 Now, I want to talk about...

00:39:05.000 You mentioned, Gary, that maybe leptin is having important actions, not just in the brain, but in the body.

00:39:14.000 First of all, I'm glad...

00:39:15.000 I'm flattered that you read my book, and I'm glad that you acknowledge the existence of leptin now.

00:39:20.000 This is good.

00:39:22.000 But now, you say that researchers...

00:39:26.000 Focus 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.

00:39:39.000 The 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.

00:39:48.000 There are actual experiments demonstrating this and I'll explain how these experiments work.

00:39:52.000 This is all in the scientific literature.

00:39:54.000 So if you knock out the leptin receptor Only in the brain, or only in the hypothalamus, you get obesity.

00:40:05.000 So that is what tells us that actually the brain is the key site of action, and particularly this part of the brain.

00:40:12.000 It tells you the brain is a key site of action.

00:40:16.000 Please let him talk.

00:40:17.000 He let you talk.

00:40:18.000 Yeah, and that's it.

00:40:19.000 So, 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.

00:40:27.000 So that shows that the brain is the site of action that is causing this to happen.

00:40:32.000 And this is no surprise.

00:40:33.000 We have these mechanisms worked out.

00:40:35.000 We know Specific groups of neurons that are receiving the leptin, that are controlling our appetite, that are controlling our metabolic rate.

00:40:44.000 We have many of these neural populations worked out.

00:40:46.000 In mice, we understand these systems so well.

00:40:49.000 We 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.

00:41:02.000 I mean, that's the level of understanding we have right now of how these systems work.

00:41:06.000 So, 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.

00:41:17.000 I 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.

00:41:33.000 Can I pause here?

00:41:34.000 Yeah.

00:41:35.000 Leptin is produced where?

00:41:36.000 Yeah, leptin is produced...

00:41:37.000 Yeah, let's talk about leptin a little bit.

00:41:39.000 It's produced in fat cells, and it's produced in proportion to the size of fat tissue.

00:41:45.000 So the amount of body fat you have, the more fat you have, the more leptin you have in the circulation.

00:41:50.000 And 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.

00:41:59.000 So with your thermostat, if you set your thermostat to 70...

00:42:18.000 We have many negative feedback loops in the human body To regulate body temperature, to regulate blood pressure, to regulate all sorts of things.

00:42:28.000 One of the negative feedback loops we have regulates body fatness. 0.62

00:42:33.000 And the hormone, so your thermostat measures temperature by using a thermostat.

00:42:39.000 Sorry, a thermometer.

00:42:40.000 Your brain measures body fatness using this hormone leptin that's in the circulation.

00:42:45.000 And then particularly when your body fat level drops, your leptin levels drop and your brain hears that and it kicks in a starvation response basically.

00:42:56.000 And this is the main reason why weight loss is so difficult because your brain is like, no, I don't want to be losing fat.

00:43:02.000 And it makes you hungrier.

00:43:04.000 It increases your cravings.

00:43:05.000 Is that a certain level of body fat?

00:43:08.000 Is this just when you're losing body fat in general?

00:43:11.000 Like even if you're a large person that's overweight, when you're losing body fat in general, your body exacerbates your hunger?

00:43:18.000 And this is the thing that's really important to understand about obesity.

00:43:22.000 Is that people with obesity have a higher set point.

00:43:26.000 So it's like turning your thermostat from 70 to 80 and then your thermostat's regulating around 80. People with obesity, they're not regulating around 170 anymore.

00:43:35.000 They're regulating around 250. And so when you cause a lean person to lose weight, you see the same thing as when you cause a person with obesity to lose weight.

00:43:44.000 You see this reaction change.

00:43:46.000 In their brain circuits that regulate body fatness that drives them to increase their cravings and their hunger, their metabolic rate drops.

00:43:55.000 So it would be an evolutionary mechanism to force you to seek food.

00:43:58.000 Correct.

00:43:59.000 And not just to force you to seek food, that's the main thing, but it also slows your metabolic rate, does everything it can to get more energy in your body and have less leaving, and it keeps doing that until the fat comes back.

00:44:10.000 Can I pause here?

00:44:11.000 So when you're eating a sugary diet, a high-calorie diet, you will produce more fat.

00:44:17.000 Your body will get fatter, right?

00:44:19.000 Is this correct?

00:44:20.000 It depends on how many calories you're eating.

00:44:22.000 Okay.

00:44:22.000 If you're overeating, you're consuming a lot of sugar, a lot of carbohydrates, your body will get fatter.

00:44:27.000 Correct.

00:44:27.000 So your body will produce more leptin.

00:44:29.000 Correct.

00:44:29.000 So it comes from the diet.

00:44:32.000 Yeah, indirectly, definitely.

00:44:33.000 Can I pause?

00:44:35.000 Please.

00:44:35.000 So the leptin is produced not just in response to the size of the fat cell, but in response actually to glucose-mediated uptake into the fat cell, which is mediated in part by insulin.

00:44:46.000 So you come back to insulin, even with the leptin, you raise blood sugar, and that's the carbs.

00:44:52.000 You eat the carbs, you raise blood sugar, you raise insulin, you raise fat storage, the glucose, and then you get more leptin.

00:44:59.000 Again, one of the things you have to understand about this is everything that's said has two interpretations depending on which paradigm you're looking at, and these are fundamentally different paradigms.

00:45:10.000 So 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.

00:45:24.000 Leptin is responding to fuel availability in the rest of the cells.

00:45:29.000 So it's basically a molecule that can tell other cells that there's fat available, and you could burn that fat for fuel, and then you don't have to go eat.

00:45:37.000 Or it can tell that there isn't fuel available.

00:45:42.000 And depending on how much leptin there is, the cells, and then that will respond by a signal to eat or not, to disinhibit eating behavior.

00:45:51.000 Everything 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.

00:46:06.000 But one of the problems I had, so the way I think you should think about this, you have a hypothesis And this is the fundamental thing.

00:46:13.000 Is obesity caused by overeating?

00:46:16.000 Because we know if you're getting fatter, you're storing more calories than you expend.

00:46:21.000 That's just the...

00:46:22.000 That's like if a room is getting more crowded, more people are entering than leaving.

00:46:26.000 That is the simplest...

00:46:28.000 But it doesn't tell you why the room's getting crowded.

00:46:30.000 It doesn't tell you why you're getting fatter.

00:46:33.000 And again, what I've been arguing is the why you're getting fatter part has been left out and people decided that overeating was somehow an explanation.

00:46:42.000 And then they went to the brain to look at why people might overeat.

00:46:46.000 So 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.

00:46:56.000 You know, a simple question to ask is, can we find epidemics of obesity without this modern food environment?

00:47:04.000 I mean, that's a sort of science 101, right?

00:47:07.000 And it turns out that the world is full.

00:47:09.000 And the first one I found in the literature was in 1902, in a population of the Pima, Native American tribe Pima, living in Arizona.

00:47:18.000 And observers saying these people are poor, they're malnourished, they're suffering through famines.

00:47:25.000 They've been suffering through a famine for 40 years, and famines, it's hard to overeat during a famine.

00:47:30.000 And yet, the women of the tribe, who do virtually all the work, they were treated as pack animals, in effect, were obese. 0.99

00:47:39.000 So now we can disassociate obesity from the modern food environment, and we could disassociate it from this ultra-processed foods we eat and start to ask the question, what is it about?

00:47:54.000 Can we find what might have driven obesity in that population, despite the existence of famine?

00:47:59.000 So it's from very simple observation.

00:48:01.000 Once 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.

00:48:13.000 And you'll see in the studies people misinterpreting them.

00:48:19.000 What was the cause of the population of women to be obese? 1.00

00:48:23.000 Well, so one of the things that happened beginning in the 1860s, the PIMA were Well, they moved on to a reservation.

00:48:29.000 They were reservationized, whatever the verb form would be.

00:48:33.000 And they began eating Western foods.

00:48:35.000 And back then, it was sugar, flour, and lard for the most part, and sugary beverages probably.

00:48:40.000 So that's a reasonable hypothesis.

00:48:44.000 And you could find the same thing in the Sioux, Native American Sioux population living on a reservation in 1928, where you had both obese men and women living with malnourished, stunted children who clearly weren't getting enough diet, but they were on a reservation, 0.62

00:49:00.000 they were getting Western foods.

00:49:01.000 So ultimately, You know, the question you ask in science determines the answer you get.

00:49:08.000 So the question I was asking is we have this observation that any population that transitions to a Western diet or a Western diet and lifestyle gets obese and diabetic.

00:49:20.000 They develop what's called metabolic syndrome, which is insulin resistance and all these issues.

00:49:26.000 And we know that's true all over the world, from the Inuit to the Pima to South Pacific Islanders to Africans to Europeans, so the genetics aren't that important.

00:49:37.000 The question is, what's triggering it in the environment?

00:49:40.000 And again, Stefan would say, well, there's too much food available, and it's too palatable, and we can't say no.

00:49:49.000 And I have a lot of problems with the we can't say no part, because if we're lean, it means they can't say no, and they being the people with obesity, and I don't believe that's true.

00:49:59.000 And then, or is it some specific item?

00:50:03.000 Or some specific group in these foods that travel with Western populations.

00:50:09.000 And so the ability, and today if you look up Dual burden of obesity and malnutrition.

00:50:16.000 I have a Dropbox folder I could share with you.

00:50:19.000 There's probably 50 studies all over the world.

00:50:21.000 You see the same observation.

00:50:22.000 Incredibly poor populations, malnourished.

00:50:25.000 The children are stunted, which means they're protein deficient and they're calorie deficient.

00:50:30.000 And often the mothers or the aunts are obese. 1.00

00:50:33.000 The 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. 0.97

00:50:47.000 If they could have overeaten, why are the kids starving?

00:50:50.000 That's sort of the question.

00:50:52.000 This was the first thing that I think we fought about back then.

00:50:57.000 If you can find populations with obesity epidemics but without the modern food system, without snack wells and without Lay's potato chips, And if you know that they're going through a famine or you know that the kids at least aren't getting enough food,

00:51:17.000 how do you explain obesity in the mothers without assuming that the mothers are overeating? 0.55

00:51:22.000 Let's pause right there.

00:51:24.000 Stephan, is there a population of people that are obese, that are not eating a Western diet, that are not eating sugary foods?

00:51:34.000 That are obese and that are not eating sugary foods.

00:51:37.000 Probably not, because generally, once you have an industrialized food system, that's going to include sugar.

00:51:44.000 But there are populations that eat a lot of sugar and are not obese.

00:51:49.000 And we should talk about some of these.

00:51:50.000 Actually, let's talk about the Pima first.

00:51:53.000 Yeah, sure.

00:51:53.000 Let's talk about the Pima first.

00:51:55.000 Now, Gary has told a story, he's told his version of the Pima story.

00:52:00.000 Let me tell the story, the version of the story that appears in the scientific literature.

00:52:05.000 Now, the Pima, originally they were agriculturalists.

00:52:10.000 They were eating traditionally a very high carbohydrate diet based on unrefined carbohydrates.

00:52:15.000 Originally it was corn, beans, and squash, primarily.

00:52:19.000 They were hunter-gatherers and agriculturalists.

00:52:21.000 They were primarily eating agricultural foods.

00:52:27.000 They were also collecting some wild foods.

00:52:29.000 That's correct.

00:52:30.000 They were fishing and eating mesquite pods, primarily agricultural.

00:52:36.000 And data are very clear on that, Gary.

00:52:40.000 Yeah.

00:52:40.000 No, no, no.

00:52:41.000 Yes, they are.

00:52:42.000 Look, we have data.

00:52:43.000 We can't say things like that, Stephan, because we're going to disagree on what the data say.

00:52:47.000 Let's move on.

00:52:48.000 You think they mostly fish.

00:52:49.000 That's incorrect, okay, according to the data.

00:52:52.000 I remember you saying that in your book, something to that effect.

00:52:55.000 Stephan, read what you've got in my book.

00:52:57.000 Read what I say.

00:52:57.000 Just read what I say.

00:52:59.000 Let's go on.

00:52:59.000 We don't have to argue about it.

00:53:00.000 Read what I say.

00:53:01.000 I'm going to move on here.

00:53:04.000 Now, the Pima...

00:53:06.000 Traditionally, we're agriculturalists.

00:53:08.000 And what happened, basically, is you had all these farmers moving into their area, settlers of European descent, and they diverted the water from their river, the Gila or Gila River.

00:53:20.000 Gila.

00:53:21.000 And so they were no longer able to grow their crops, their agricultural crops that they were primarily dependent on, and therefore the government started providing them with foods to eat.

00:53:31.000 And these were calorie-dense refined foods.

00:53:34.000 They were, like Gary said, flour, lard, and sugar.

00:53:39.000 And then they became very obese.

00:53:42.000 Now, there was a population of Pima right across the border from them in Mexico, also very similar culturally and all that, that maintained their traditional high-carbohydrate lifestyle and agricultural lifestyle, and there have been studies comparing those two populations, and the ones across the border with their traditional lifestyle are a Not surprisingly,

00:54:05.000 than the ones eating lard, flour, and sugar, okay?

00:54:08.000 But Gary, you seem to believe that people can gain weight.

00:54:12.000 You kept referring to famines and things.

00:54:14.000 You seem to believe that people can gain weight even if they are eating very few calories.

00:54:20.000 And you refer to this many times in your writing.

00:54:23.000 And, you know, these are very casual observations that you're making, kind of these casual correlations and storytelling.

00:54:31.000 But if you actually look at the data...

00:54:34.000 On this, what you see is that if you just measure calorie intake in people who have obesity, it is 20% to 35% higher than people who are lean after correcting for physical activity level.

00:54:50.000 I've got the references there.

00:54:53.000 We're getting a little bit into the weeds here.

00:54:56.000 Let me give you an example.

00:54:57.000 Can I pause you guys right here?

00:54:59.000 So these people, they have essentially the same lineage.

00:55:04.000 One group lives in Mexico.

00:55:05.000 They're not eating these sugary foods in this Western diet.

00:55:10.000 The ones that live in America are. 0.67

00:55:12.000 The ones that live in America are becoming obese.

00:55:14.000 The ones that live in Mexico are not. 1.00

00:55:15.000 Is that correct?

00:55:16.000 Correct.

00:55:16.000 Yeah.

00:55:16.000 And so now if you have someone with obesity...

00:55:20.000 Like I've said, the most accurate measures that we have suggest that they habitually consume and expend more calories.

00:55:29.000 And now, Gary's model says that that is downstream of the fattening effect.

00:55:33.000 It's not causing the fattening effect.

00:55:35.000 It is a result of the fattening effect, whereas my model says that that is actually required for the fattening effect to occur.

00:55:43.000 It is upstream.

00:55:44.000 So how did those people get fat?

00:55:46.000 What happens if you reduce their calorie intake by that same amount, 20 to 35 percent?

00:55:53.000 It doesn't matter if you do it by restricting carbs or fat.

00:55:57.000 These experiments have been done.

00:55:59.000 They lose weight when you restrict their calorie intake down to that of a lean person.

00:56:03.000 So 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.

00:56:13.000 Right.

00:56:13.000 So you're saying it's a calorie...

00:56:15.000 Yeah, correct.

00:56:15.000 And that's reference number 9 and 10 to support what I just said.

00:56:19.000 And I want to talk about another one that really...

00:56:21.000 Wait, wait.

00:56:21.000 Can we hold on, Stephen?

00:56:22.000 Yeah, yeah.

00:56:22.000 Let's keep going.

00:56:23.000 The reason I was using the dual burden example...

00:56:26.000 It's because we have to explain how those women are eating all those calories. 1.00

00:56:31.000 Usually women, again. 1.00

00:56:33.000 Often these studies were done by diabetes researchers who were studying diabetes in these populations and the men had high levels of diabetes and the women had high levels of obesity.

00:56:45.000 To give you an example where that measurement was done, in Trinidad in the 1960s, and again, all I'm doing, this is the role I played, is I asked the question, can you find populations that don't have a lot of food?

00:56:58.000 Okay, you could say that the obese expend a lot of energy and they eat a lot of calories.

00:57:02.000 The question is, can they get obese without a lot of food?

00:57:04.000 And so can we find populations.

00:57:06.000 Like U.S., can you find a population that gets obese without sugar?

00:57:09.000 Which was exactly the question to ask.

00:57:11.000 So in Trinidad in the 1960s, there's a malnutrition crisis.

00:57:15.000 The 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.

00:57:27.000 And this is a medical problem.

00:57:28.000 And the next year, an MIT nutritionist goes down to do exactly what Stephan asks for and to actually measure the diets in obese women and lean women and to study it.

00:57:40.000 And this is a population where it's not like, I mean, this is a very poor Trinidad population.

00:57:45.000 And 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. 1.00

00:57:53.000 And that it was lower than what the Food and Agriculture Organization considered for a healthy diet.

00:57:58.000 So 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.

00:58:06.000 The brain is in control of how much they eat.

00:58:08.000 It tells me anything about why the women were obese, especially when their kids are starving. 1.00

00:58:13.000 This is the paradox of the stool burden, an obese mother with a starving child. 0.58

00:58:18.000 If the obese mother has to eat superfluous calories to get fat, Why isn't she giving those calories to her kids? 1.00

00:58:27.000 Because she doesn't need them.

00:58:29.000 She clearly doesn't need them.

00:58:30.000 She's got fuel. 1.00

00:58:31.000 So what's going on there?

00:58:32.000 If you posit a hypothesis, as I did, which says that the obesity is triggered by the macronutrient content of the diet, Then you can explain.

00:58:42.000 I mean, there are plenty of animal models.

00:58:44.000 A 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.

00:58:53.000 He said, my animals will get fat even when half starved.

00:58:57.000 They will make fat out of their food even when half starved.

00:59:01.000 These are generally animals with mutations in the leptin pathway, by the way.

00:59:06.000 Whatever gene it is.

00:59:07.000 The 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.

00:59:22.000 And 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.

00:59:37.000 What is your response to this?

00:59:38.000 My response is that if you want the best answers, you have to use the best methods to answer the questions.

00:59:46.000 If you want a question answered properly, you have to use accurate methods to answer that question.

00:59:52.000 Now, as you know, Gary, it's very difficult to measure food intake in free-living individuals.

00:59:58.000 Particularly, you're traveling to a country you've never been to before.

01:00:01.000 It's very difficult to get accurate measures.

01:00:04.000 So just because some guy went to Trinidad and claimed...

01:00:07.000 It was a woman, actually.

01:00:08.000 Okay, fine.

01:00:09.000 Just because some woman went to Trinidad and claimed that people were eating 1,800 calories and becoming obese does not mean that that's what actually happened.

01:00:18.000 No, no, no, Gary, I'm responding.

01:00:20.000 Now, we have studies where researchers used accurate measures to measure calorie intake in people who had obesity.

01:00:30.000 Many of these people were saying we're only eating 1,200 calories a day.

01:00:36.000 When they actually measured their calorie intake, what they found was that they were consistently eating more calories than lean people.

01:00:44.000 So this phenomenon that Gary describes is something that is only observed when inferior methods are used to measure calorie intake.

01:00:53.000 Wait, wait.

01:00:56.000 Like I said, I'm just giving you an observation.

01:00:58.000 Obese mother with a starving child. 0.95

01:01:00.000 The dual burden of malnutrition and obesity.

01:01:02.000 This isn't one observation.

01:01:04.000 It's not one nutritionist.

01:01:06.000 The existence of the starving children strongly suggests That there's not a lot of food available.

01:01:15.000 And we have to explain obesity in the mother. 0.99

01:01:18.000 That's what I would like you to respond to.

01:01:19.000 Okay, fine.

01:01:20.000 I will respond to that.

01:01:21.000 Now, look, I haven't looked at these studies in particular.

01:01:24.000 I brought them up eight years ago.

01:01:25.000 We got in a fight about it.

01:01:26.000 We fell out eight years ago.

01:01:28.000 It ruined our, you know, it's like we used to be bites.

01:01:31.000 So now...

01:01:32.000 Look, there are many reasons why a child could be malnourished in a non-industrial situation.

01:01:40.000 I do a lot of work related to this.

01:01:42.000 What you see in non-industrial situations, you see a lot of infectious disease, you see a lot of malnutrition, so people not getting enough essential minerals and vitamins, not getting enough protein, and you see a lot of children who are just barely hanging on because of this collection of Yeah,

01:02:05.000 parasites, malaria.

01:02:07.000 I 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.

01:02:18.000 30% of kids didn't even make it past childhood.

01:02:21.000 And so, there's a lot of things that could have caused that, Gary.

01:02:25.000 It's not necessarily because, you know, it's not necessarily the reason that you attribute it to.

01:02:32.000 I'm not attributing it to a reason.

01:02:34.000 I'm just asking for explanations.

01:02:35.000 Well, I don't have the explanation, but I'm throwing out possibilities that are alternative to the one that you're implying.

01:02:43.000 And that's quite possible, too.

01:02:44.000 Okay.

01:02:45.000 So, now...

01:02:47.000 So again, when you use accurate measures of calorie intake, you find that these people with magical metabolisms who have obesity and don't eat very much seem to not exist anymore.

01:02:59.000 And 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.

01:03:12.000 So we have a lot of studies that compared diets in which calories were the same, but carbohydrate and fat intake differed.

01:03:20.000 And the ones that I really want to focus on right now that I think are key here are the studies where they increased calorie intake.

01:03:27.000 So they fed people.

01:03:30.000 One study in particular, and let's see, I'm going to give you a number here.

01:03:38.000 Let me see if I can give you a number here, sorry.

01:03:41.000 While you look at that, can we bring up another issue?

01:03:45.000 Because what we're talking about ultimately is why people get fat.

01:03:48.000 Okay, I don't want to divert here.

01:03:49.000 I'm in the middle of something.

01:03:53.000 Now, if we want to understand why people get fat, we can look at studies that overfed people on fat or carbohydrate exclusively.

01:04:02.000 So this one study, the first one that I want to talk about, first they figured out people's baseline calorie intake.

01:04:10.000 Figure out how many calories they needed just to maintain, and then they increased that by 50% by exclusively giving them fat or exclusively giving them carbohydrate.

01:04:20.000 Which study was this?

01:04:22.000 This is Horton.

01:04:23.000 Okay.

01:04:24.000 Give me a second when you're done.

01:04:29.000 So, now, if Gary's hypothesis is correct, these people should have gained body fat on the carbohydrate overfeeding but not the fat overfeeding because that increases your insulin and has these effects on your fat cells, etc.

01:04:43.000 Okay?

01:04:43.000 Now, these were very rigorous studies.

01:04:45.000 I want to emphasize that.

01:04:46.000 Can I pause here?

01:04:47.000 Did they monitor the actual calories they got?

01:04:50.000 Correct, yes.

01:04:51.000 So, they had a baseline?

01:04:54.000 They used prisoners in the Vermont State Prison.

01:04:57.000 No, that's incorrect.

01:04:58.000 This is a different study.

01:04:59.000 So they had a baseline, and did they require them to maintain the same diet and then add additional fat or additional carbohydrates?

01:05:07.000 Yes.

01:05:08.000 So, same diet.

01:05:10.000 And then they just bump it up with fat or bump it up with carbohydrate.

01:05:13.000 Wait, wait, wait.

01:05:13.000 Which study did Horton do?

01:05:14.000 It wasn't Sims.

01:05:15.000 It was Ethan Sims.

01:05:16.000 Talk to the mic, please.

01:05:18.000 Which study did he do that was not prisoners?

01:05:21.000 He didn't have a metabolic war.

01:05:23.000 You know what?

01:05:23.000 Let me just finish describing this study.

01:05:25.000 Gary, that's an irrelevant detail, okay?

01:05:27.000 What's relevant is that you just didn't...

01:05:30.000 It's implied that I don't know what I'm talking about.

01:05:32.000 Gary, you know what?

01:05:34.000 I don't actually know.

01:05:35.000 Maybe it was in prisoners, okay?

01:05:37.000 Thank you.

01:05:37.000 All right.

01:05:37.000 You're welcome.

01:05:39.000 Now, but it was not the Sims overfeeding study that was done in prisoners.

01:05:44.000 That's what I know, okay?

01:05:45.000 Okay.

01:05:46.000 The reference, what's the reference?

01:05:47.000 Yeah, it's on my website.

01:05:49.000 You can go to my website, stephanguiennet.com, and it's reference number 16, and they're both there.

01:05:55.000 Okay.

01:05:55.000 So this was what's called a metabolic ward study where these people were in a research facility where the researchers could monitor and control every morsel of food.

01:06:05.000 So there was no cheating, no inaccuracy, and they were measuring changes in body fatness using a gold standard method called underwater weighing, okay?

01:06:14.000 And so what they found was that at the end of a two-week period of overfeeding, the carb and the fat groups gained the exact same amount of body fat.

01:06:25.000 Exact same amount of body fat.

01:06:27.000 There was another second study that did the same thing and found the same result.

01:06:32.000 Independent lab group, very similar experiment, three-week long instead of two weeks.

01:06:36.000 They found the exact same thing.

01:06:38.000 Same amount of fat gain, different insulin responses.

01:06:41.000 Different amounts of carbohydrate and fat, exact same amount of fat gain.

01:06:45.000 So this demonstrates that insulin and carbs are not what controls what gets fat into fat tissue.

01:06:53.000 Calorie intake is what controls that.

01:06:55.000 So let me explain again.

01:06:57.000 Remember I talked about everything.

01:06:58.000 The paradigm you work in determines the question you ask.

01:07:01.000 And this experiment is a classic example because they assume that people get fat by overfeeding.

01:07:07.000 So then they say if we overfeed them...

01:07:11.000 We're just doing what happens naturally.

01:07:13.000 Everything about the experiment is based on the assumption that they're supposed to be testing, which is, can people get fat by overfeeding?

01:07:21.000 And so from the very conception of the experiment, they've built in the paradigm that we want to test, the hypothesis.

01:07:29.000 On top of it, if it's a typical SIMS experiment, I actually wasn't familiar with this one.

01:07:34.000 Oh, it wasn't SIMS. James Hill was funded from about 1998 to about 2008 by Procter& Gamble because he was an Alestra shill.

01:07:51.000 I hate to say that, Jim.

01:07:52.000 I apologize, but I think it's a fair assessment.

01:07:55.000 And then when he stopped being funded by Procter& Gamble, he was funded by the sugar industry.

01:07:59.000 And J.C. Peters was the head of the Procter& Gamble Alestra.

01:08:05.000 Alestra, which is now something that no one eats.

01:08:08.000 Yeah, Alestra was a fat substitute. 1.00

01:08:10.000 The problem was you got like run out.

01:08:13.000 But the whole idea of Alestra was to replace fat in the diet.

01:08:19.000 So every study Hill and Peters did implicated dietary fat as a cause of obesity.

01:08:24.000 I 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.

01:08:36.000 Because you think it's a bio-study that was influenced by it?

01:08:39.000 Everything Hill and Peters did.

01:08:41.000 I mean, I talked about this in Good Calories, Bad Calories.

01:08:44.000 When they reported their results, actually I did a FOIA on James Hill, because he works for the University of Colorado.

01:08:50.000 I got all his documents back and forth between him and Alester.

01:08:54.000 I'd be happy to share them with you if you'd like.

01:08:57.000 I mean, him and Procter& Gamble, but he basically held Procter& Gamble for ransom.

01:09:01.000 He 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.

01:09:15.000 Then he would ask for Procter& Gamble for more money before he then published the study.

01:09:21.000 So, it's a particularly egregious example of someone who's, I suspect it was just his belief system.

01:09:28.000 He 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.

01:09:39.000 The point that we keep getting away from that I haven't had an opportunity to And Stephan knows this as well as I do.

01:09:49.000 If 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.

01:09:56.000 So now you're obese.

01:09:57.000 You're a nice, lean, healthy young guy.

01:09:59.000 And 20, like many of us were, and by the time you're 40, you've got 40 pounds of excess fat.

01:10:04.000 That's the equivalent of putting in about...

01:10:10.000 It's storing about 10 calories a day into your fat tissue that you don't burn or metabolize.

01:10:16.000 So 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.

01:10:28.000 Less than a bite's worth of food, less than a sip's worth of beer.

01:10:34.000 So 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?

01:10:45.000 Because 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. 1.00

01:10:56.000 It tends to happen quickly in their 20s.

01:10:59.000 So 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.

01:11:08.000 That's 20, 30, 40 billion fat cells, so it's divided up very small.

01:11:13.000 And is the brain somehow regulating that?

01:11:17.000 Or 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?

01:11:36.000 And so if you think about it that way, like you let yourself go to seed, today Joe Rogan decides I'm done.

01:11:42.000 I'm gonna do nothing but drink beer.

01:11:44.000 And you might start drinking five beers a day, and over the course of 10 years you get 20 pounds and it's all here.

01:11:51.000 That 20 pounds over the course of 10 years is still only about 20 calories.

01:11:55.000 You might have added 800 calories of beer to your diet and stored 20 calories as fat.

01:12:02.000 How does that happen and why does it go here?

01:12:06.000 And not elsewhere.

01:12:07.000 And as Stephan said, this is insulin-dependent fat tissue.

01:12:12.000 So when we're talking about this, like this question, can somebody get fat during a famine?

01:12:18.000 Or can they stay fat during a famine?

01:12:20.000 All they have to do is hold on to 10 calories a day extra.

01:12:23.000 If they're only eating 1,200, 10 get stuck in their fat cells.

01:12:30.000 1190 is excreted or expended.

01:12:33.000 It's not that hard to imagine.

01:12:35.000 And there's nothing in the laws of physics that says it.

01:12:38.000 So what could be dysregulated about their fat cells, even during a relative famine, not a complete famine, but a relative famine that might be...

01:12:47.000 And 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.

01:12:59.000 Can I pause you for a second?

01:13:01.000 Essentially 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.

01:13:22.000 Whereas if you were taking in just protein and vegetables and things along those lines, your body would not do that.

01:13:29.000 Well, so this gets to the mechanism question and the evidence question.

01:13:34.000 But you're saying that, right?

01:13:36.000 So 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,

01:13:52.000 that that person is going to gain a certain amount of calories and just put them to fat regardless.

01:13:58.000 Right.

01:13:59.000 That's, yeah, that's the hypothesis.

01:14:01.000 Same activity.

01:14:02.000 This being a science, that hypothesis can be tested.

01:14:05.000 Yes.

01:14:06.000 And Stephan thinks it's been tested 80 times.

01:14:09.000 So Stephan, you're...

01:14:10.000 I think they've done a bad job of testing it and...

01:14:14.000 But 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.

01:14:22.000 Your perspective is that this is not the case.

01:14:23.000 Your 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.

01:14:36.000 Yeah, that's right.

01:14:36.000 I mean, if Gary's hypothesis is correct, you have to see different levels of fat gain.

01:14:41.000 Was this a short-term statistic?

01:14:42.000 Yeah, it was short-term.

01:14:43.000 How short-term was it?

01:14:44.000 Two and three weeks.

01:14:46.000 Well, that's very short-term.

01:14:47.000 Yeah, it is very short-term.

01:14:48.000 But still, Gary says that insulin is the thing that gets fat in fat cells and that, I mean, you would see some kind of difference.

01:14:56.000 If insulin made any difference, you should have seen some kind of effect, right?

01:15:00.000 Some kind of difference in fat gain.

01:15:01.000 Well, actually, I don't want to start taking out charts, but this gets into insulin dynamics that was worked out.

01:15:08.000 So over a...

01:15:13.000 I promised I wasn't going to say oy on the show, but thanks to my Brooklyn-born mother, it's my program then.

01:15:24.000 And the same is true. 0.93

01:15:26.000 A lot of these overfeeding experiments do the same thing.

01:15:28.000 So when they talk about overfeeding, they literally overfeed.

01:15:32.000 So they kind of do a reasonable way of figuring out which reading is.

01:15:36.000 Stefan said they calculated how much energy they needed to stay in energy and balance.

01:15:43.000 And again, right there, that's a problem.

01:15:46.000 Because one of the hypotheses says that energy balance is dependent on the macronutrient content of the food.

01:15:53.000 So you're going to get a different level depending on what the macronutrient content is.

01:16:00.000 A different level of?

01:16:02.000 Of what's necessary for energy balance.

01:16:06.000 So 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,

01:16:24.000 and 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,

01:16:39.000 and 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.

01:16:52.000 And in that study, which was published a year ago, They saw different levels of energy expenditure depending on the carbohydrate content of the diet.

01:17:03.000 So the higher level of carbohydrates, this is trying to keep them in energy balance.

01:17:08.000 The higher the carbohydrate, the lower the energy expenditure.

01:17:12.000 The lower the carbohydrate, the higher the energy expenditure.

01:17:16.000 So again, it's just whether or not they did the study right.

01:17:18.000 Who knows?

01:17:19.000 Science is a compilation of a lot of studies and we're trying to, you know, address exactly this point.

01:17:26.000 But Merely building that into the experiment.

01:17:31.000 We know what their energy expenditure should be.

01:17:33.000 And then the point is when you increase.

01:17:36.000 And again, part of the trick of doing science is to say, look, we have competing hypotheses, multiple hypotheses.

01:17:43.000 And it's vitally important that you always keep the multiple hypotheses in.

01:17:49.000 In mind when you're interpreting the study.

01:17:51.000 So 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.

01:18:01.000 And when you do these experiments, like the experiment that Stephen is talking about, Stefan, I'm completely confused.

01:18:13.000 If you overfeed them, you start out with a 50% carb diet, now you overfeed them.

01:18:19.000 If there's a threshold effect on insulin, which it turns out there is, then you're just moving them.

01:18:24.000 And 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.

01:18:33.000 And above that point, you get pretty much flat.

01:18:36.000 So 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.

01:18:48.000 You wouldn't necessarily expect to see any difference.

01:18:51.000 The 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.

01:19:03.000 You want to set up the experiment so the hypothesis predicts, the two hypotheses predict something entirely different.

01:19:10.000 This experiment, arguably the two hypotheses predict the same thing.

01:19:14.000 You'll get fat gain because insulin is elevated regardless.

01:19:17.000 And when insulin is elevated, you're going to get fat gain.

01:19:21.000 The 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?

01:19:31.000 I have a friend who was 400 pounds when he was 18. He was a tall kid, about 6'5".

01:19:37.000 He was, say, 200 pounds overweight.

01:19:41.000 200 pounds overweight is roughly 100 excess calories over 18 years stored in your fat cells.

01:19:49.000 Even 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.

01:20:08.000 And the question would be, why can't he just stop doing that?

01:20:11.000 And again, Stefan would say, because his brain won't let him.

01:20:15.000 And I would say because his insulin is elevated, it doesn't matter whether he stops it or not.

01:20:21.000 Can I respond here?

01:20:22.000 He's got to address the underlying mechanism.

01:20:23.000 Okay.

01:20:25.000 All right.

01:20:26.000 So now, again, it's easy to tell stories.

01:20:30.000 It's not easy to tell stories that are supported by scientific evidence.

01:20:34.000 Now, I want to bring people's attention to reference number 11 on my site.

01:20:40.000 There have been 29 studies now that have measured differences in energy expenditure, metabolic rate.

01:20:47.000 Is this the Kevin Hall study?

01:20:49.000 Meta-analysis, correct.

01:20:50.000 There have been 29 studies to date that have measured calorie expenditure, metabolic rate, on diets differing in carbohydrate and fat content.

01:21:00.000 And 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.

01:21:13.000 And in fact, the very small difference that it does make Actually favors high carbohydrate diets.

01:21:19.000 So you get a slightly higher metabolic rate when the diet is predominantly carbohydrate.

01:21:25.000 Now 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.

01:21:36.000 So this study reported an effect bigger than any of these other 28. And the difference, we would say, is this.

01:21:43.000 Gary, I'm not done.

01:21:45.000 Gary, please.

01:21:45.000 Thank you.

01:21:47.000 And interestingly, if you actually look at the data, and these data have been reanalyzed by a researcher named Kevin Hall, and I think?

01:22:20.000 From 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,

01:22:37.000 and it's consistent with the previous 28 studies that were done.

01:22:41.000 So that's my perspective on that.

01:22:43.000 But I want to go back to this energy.

01:22:44.000 No, no, no.

01:22:45.000 Gary, you talked for a long time, and I'm going to talk for as long as I want now.

01:22:50.000 I want to talk about human energy metabolism and this idea of the 10 extra calories a day.

01:22:57.000 Gary, I really continue to get the feeling that you do not understand human energetics because that's not how it works.

01:23:04.000 Well, no, I'm just saying 10 calories stored in the fat tissue.

01:23:07.000 That's just mathematics.

01:23:09.000 I didn't say anything about how much you have to eat.

01:23:11.000 I'm not done.

01:23:12.000 Okay, no, but you're insulting me, Stephen.

01:23:14.000 You've got to stop doing that, dude. 1.00

01:23:16.000 You keep acting like you think I'm an idiot. 1.00

01:23:18.000 All right, are you done now? 1.00

01:23:19.000 Are you done?

01:23:20.000 Can we be clear that we're talking about...

01:23:22.000 Are you done now?

01:23:23.000 Can I just finish this?

01:23:24.000 No, you can't until I am done.

01:23:26.000 You can't attack me without...

01:23:27.000 Gary, you have time to respond.

01:23:29.000 You can respond, write down notes on what you want to respond to, and after he's done, you can...

01:23:33.000 Yeah, but we're going to get into a long discourse on something that's not the point.

01:23:38.000 Well, let's find out if it is the point.

01:23:39.000 Yeah, it is the point.

01:23:40.000 Thank you.

01:23:41.000 Okay.

01:23:43.000 What you see, there's basically two things you need to pay attention to here in terms of energetics.

01:23:48.000 One is the imbalance between intake and expenditure, and that is very small.

01:23:53.000 So it only takes a little bit of extra calories to cause somebody to start gaining fat.

01:24:00.000 Their bodies get bigger.

01:24:02.000 They're gaining fat and lean mass.

01:24:04.000 People with obesity have more fat, more lean mass, and their calorie needs go up and up and up and up the larger their bodies get.

01:24:12.000 And so even though the imbalance between energy intake and expenditure is small, their calorie needs end up being quite a bit higher.

01:24:21.000 Can I pause for a second?

01:24:21.000 Yeah.

01:24:22.000 So you're saying that someone just gaining calories, eating additional calories, their body gains lean mass as well?

01:24:28.000 Yeah, that's correct.

01:24:30.000 How does the brain regulate that?

01:24:31.000 I didn't say it regulated.

01:24:33.000 Hold on, Gary, Gary, Gary, hold on.

01:24:34.000 That's fascinating.

01:24:35.000 How does the brain do that? 0.76

01:24:37.000 They're gaining muscle tissue?

01:24:38.000 Some of it's muscle, some of it's liver and organs.

01:24:42.000 Is 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?

01:24:52.000 Presumably, I'm actually not sure what the mechanism is.

01:24:55.000 But it doesn't have anything to do with the brain?

01:24:57.000 It's just a coincidence?

01:24:59.000 I don't know what causes it.

01:25:00.000 That's what I'm saying, Gary.

01:25:02.000 Okay.

01:25:02.000 Now, 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.

01:25:17.000 So it's not just one or two Cokes a day that is...

01:25:21.000 Allowing them to remain obese.

01:25:23.000 They are consuming 20 to 35% more calories.

01:25:26.000 That is what the most accurate studies are saying.

01:25:29.000 And so it's not just 10 extra calories or maybe just one or two Cokes.

01:25:34.000 We're talking about a substantial amount of extra calories.

01:25:37.000 But isn't this a generalization?

01:25:39.000 Because we don't know.

01:25:40.000 I mean, what's the ratio of how much weight people are gaining?

01:25:44.000 Everybody gains a different amount of weight.

01:25:46.000 Like when you're saying they're eating 20 to 30% more calories.

01:25:49.000 Like who is?

01:25:50.000 Yeah.

01:25:50.000 Like, how much are they gaining?

01:25:52.000 Like, people get fat, they get 20 pounds overweight.

01:25:54.000 People get fat, they get 100 pounds overweight.

01:25:56.000 I mean, it varies widely.

01:25:57.000 Yeah, 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.

01:26:08.000 People who have a little bit of obesity eat about 20% extra calories.

01:26:12.000 People who have very, very great obesity eat more like 35%.

01:26:17.000 Is it possible?

01:26:18.000 So it tracks with the amount.

01:26:19.000 I'm sorry, is it possible what he was saying, that if you do consume 10 extra calories over long periods of time, that will accumulate?

01:26:26.000 No, it's not 10 extra calories.

01:26:28.000 You're accumulating 10 extra calories.

01:26:30.000 It's like a dime is going into the bank.

01:26:33.000 How much do you have to deposit to get the dime?

01:26:36.000 It is correct that if every day you eat 10 calories more than what you need, Then yes.

01:26:43.000 Or your body stores.

01:26:44.000 Or your body stores.

01:26:45.000 Yeah, we'll say that.

01:26:46.000 That's correct.

01:26:46.000 If your body is storing 10 extra calories over top of what you need.

01:26:52.000 But the thing is that as you get bigger, what you need goes up and up and up.

01:26:56.000 Because you're carrying around more weight.

01:26:57.000 Correct.

01:26:58.000 And so it's 10 extra calories on top of...

01:27:04.000 The elevated amount that you're already eating.

01:27:07.000 So you end up with these big differences in calorie intake.

01:27:11.000 So that's how it really works.

01:27:13.000 But 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.

01:27:25.000 I want to talk about the fact that Sugar intake in the United States has been declining for the last 20 years.

01:27:33.000 So 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.

01:27:47.000 This is number 17. We're good to go.

01:28:06.000 I don't believe that.

01:28:08.000 Okay, well, you can argue with the data.

01:28:09.000 They're number 17 on my blog.

01:28:12.000 They're about 22% lower.

01:28:14.000 And this is what we see across a number of different industrialized countries.

01:28:18.000 You see a stagnation or decline in sugar intake in recent decades as obesity rates are continuing to increase.

01:28:27.000 And, of course, that 50-year period that covers the decline in the UK covers the entire UK obesity and diabetes epidemics.

01:28:36.000 But there's another one I want to talk about.

01:28:38.000 Can I respond to that?

01:28:39.000 Yeah, we should probably respond to that.

01:28:41.000 Stephen, actually, I'll let you respond for me, because we had this debate with the Cato Foundation, so you know my counterargument.

01:28:47.000 You want to give it?

01:28:48.000 Yeah, sure, absolutely.

01:28:50.000 I mean, are you sure you want to let me give it, though?

01:28:52.000 I might correct it.

01:28:53.000 Okay, all right.

01:28:55.000 So, 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,

01:29:13.000 and not necessarily about the sugar we eat today.

01:29:16.000 Well, it's not exactly right.

01:29:18.000 Okay, so the argument I made was – because he brought this up when we had to do a written debate on the Cato Foundation website.

01:29:25.000 And it's interesting, if you think about – use tobacco as an example.

01:29:29.000 So 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.

01:29:40.000 Okay, and I think we both agree that cigarettes are a major cause of lung cancer, smoking.

01:29:45.000 So 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.

01:29:57.000 So if sugar goes up, obesity and diabetes goes up, and if sugar turns over, they don't.

01:30:02.000 So here's the thought experiment I used in Cato, which is 1965 we're smoking per capita about 20 cigarettes a day.

01:30:12.000 As it starts to come down, imagine we only cut that to 17 cigarettes, or 16 cigarettes, a 20% reduction in smoking.

01:30:21.000 Would you expect to see a reduction in the lung cancer rates?

01:30:25.000 Again, this is the point I made about what you would expect to see, rather than using simplistic metaphors.

01:30:31.000 So the question is, would you, like, Joe, we go from 20 to 16, do you expect to see the lung cancer rates turn over?

01:30:38.000 No.

01:30:39.000 No.

01:30:39.000 And in sugar, we went from— No, the derivative might drop.

01:30:44.000 You might expect it to slow a tiny bit.

01:30:48.000 Still, it's a weird comparison because one of them is poison and the other one is food, right?

01:30:53.000 Well, but in this case, the food, the question is how toxic is the food?

01:30:57.000 So in sugar, we have a variety.

01:30:59.000 In 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.

01:31:10.000 And in fact, if you actually look at the rates, the rate of increase, the prevalence appeared to plateau around six or seven years later.

01:31:19.000 Who knows whether that's relevant?

01:31:21.000 But to get a small decrease in sugar, even if it's 20%, that's 20 to 16 cigarettes.

01:31:30.000 And 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.

01:31:41.000 So there's a generational effect.

01:31:43.000 And 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.

01:31:58.000 So 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.

01:32:10.000 So 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.

01:32:17.000 But 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,

01:32:33.000 will give birth to children who are at higher risk of becoming obese and diabetic when they get older.

01:32:38.000 And at younger ages, and those children will pass it on.

01:32:42.000 So 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.

01:32:51.000 But 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.

01:33:01.000 The sugar hypothesis is a little different than what we've been talking about, and it's pretty simple.

01:33:06.000 We have obesity and diabetes epidemics worldwide, as we talked about.

01:33:10.000 It doesn't matter the genetics of the population.

01:33:12.000 You add something about a Western diet to those populations, Western diet and lifestyle, you get these explosions of epidemics of obesity and diabetes.

01:33:24.000 And what I'm hypothesizing in this book is that sugar is the something that has to be added.

01:33:30.000 Maybe it's sugary beverages, for all I know.

01:33:33.000 Or it could be, you know, a more complex hypothesis.

01:33:37.000 A 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,

01:33:52.000 Caucasians 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. 0.92

01:34:07.000 Stephen, you want to respond to that?

01:34:09.000 Sure.

01:34:10.000 I mean, Gary, you called it, man.

01:34:13.000 It's always possible to tell a story to salvage your hypothesis, but that doesn't necessarily make the story correct.

01:34:19.000 I mean, I can come up with a story that cosmic rays cause obesity by hitting my fat cells and making them fat.

01:34:26.000 You can't disprove that.

01:34:28.000 Nobody here can disprove that.

01:34:30.000 We could do an experiment to protect you from cosmic rays.

01:34:34.000 We don't have the data right now.

01:34:37.000 You don't have data supporting your hypothesis.

01:34:40.000 No, we do.

01:34:40.000 You just dismissed it.

01:34:41.000 No, no, no, no, no.

01:34:42.000 Can I get back to the Kevin Hall study?

01:34:44.000 No, I am responding right now.

01:34:45.000 Let's let him respond, then we'll go to Kevin Hall later.

01:34:48.000 Yeah, so...

01:34:49.000 What do you think about what he's saying about sugar and increased rates of diabetes and that this is the cause?

01:34:55.000 Yeah, I mean, so let me put it this way.

01:34:58.000 We don't have any evidence supporting what he just said.

01:35:00.000 So that is a story that is not supported by evidence.

01:35:04.000 Now, does that mean that it's definitely incorrect?

01:35:08.000 No, I cannot say that that's definitely incorrect.

01:35:10.000 Same way I can't say it's definitely incorrect that cosmic rays cause obesity.

01:35:16.000 I'm going to use a Christopher Hitchens quote here.

01:35:19.000 That which is asserted without evidence does not require evidence to refute.

01:35:24.000 And that's the way I feel about this particular story.

01:35:27.000 But, you know, there are cultures that...

01:35:31.000 Consume large amounts of sugar and do not develop obesity.

01:35:35.000 We've talked about this also.

01:35:37.000 We're going to talk about it again right now.

01:35:39.000 So this is reference number 21 on my blog.

01:35:46.000 I'm going to talk about three different cultures, one of which we have not talked about, Gary.

01:35:50.000 The first one is the Hadza, hunter-gatherers of Tanzania. 1.00

01:35:55.000 This is a really interesting non-industrial culture.

01:35:58.000 They, as part of their hunter-gatherer diet, eat a lot of honey.

01:36:02.000 Honey is a very common food among hunter-gatherers living similarly to how our ancestors used to live.

01:36:08.000 And if you measure their year-round honey intake, it's about 15% of their calories.

01:36:14.000 So this is a major calorie source for them.

01:36:15.000 That's about as much sugar as the average American eats.

01:36:19.000 And they eat fruit sugar on top of this.

01:36:21.000 They eat a lot of fruit on top of that.

01:36:23.000 And so they're eating quite a bit of sugar.

01:36:26.000 And the Hadza, men have about 12% body fat, women have about 18, so they correspond pretty closely to our Western ideals. 0.59

01:36:35.000 But isn't that high for hunter-gatherers?

01:36:37.000 No, not really.

01:36:38.000 That's higher than me.

01:36:41.000 Let me ask you this.

01:36:42.000 How have you had your body fatness measured?

01:36:45.000 I've had it measured a bunch of ways.

01:36:47.000 Electricity.

01:36:47.000 I've had this machine where you hold on to these things.

01:36:51.000 You stand on this platform.

01:36:54.000 I've done it in a physician's office.

01:36:57.000 I've done it with calipers.

01:36:59.000 Okay, so all the methods that you mentioned are not gold standard methods.

01:37:04.000 So the gold standard methods are underwater weighing and DEXA. Are they underwater weighing these people on this island?

01:37:11.000 Actually, I'm not sure.

01:37:12.000 I highly doubt that they bring that equipment to this island.

01:37:15.000 Correct.

01:37:15.000 But, okay.

01:37:16.000 Look, I can tell you that you can look up photos.

01:37:19.000 I don't remember how they measured their body fat.

01:37:22.000 But you can look.

01:37:23.000 I am 12% as measured by DEXA. So I'll just tell you that.

01:37:26.000 Okay.

01:37:27.000 So 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,

01:37:46.000 that they seem to have a higher percentage of body fat than the average hunter-gatherer.

01:37:49.000 If 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. 0.82

01:37:58.000 Okay, so the pygmies, that's the second culture I was going to cite that eats a ton of honey.

01:38:04.000 Do they?

01:38:04.000 Yeah, 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.

01:38:15.000 So they also eat a lot of honey and are lean.

01:38:17.000 Not just lean.

01:38:18.000 Part of the year.

01:38:19.000 Correct, yeah.

01:38:20.000 For them, it's part of the year.

01:38:21.000 The Hadza eat it more consistently. 0.76

01:38:23.000 And the Hadza have low levels of body fat.

01:38:26.000 Their cardiovascular risk markers are excellent.

01:38:29.000 They don't have diabetes.

01:38:31.000 But this is absolutely not like a controlled study in the consumption of their calories.

01:38:36.000 Absolutely not.

01:38:36.000 I absolutely agree with you.

01:38:38.000 That'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.

01:38:47.000 They're doing everything else right.

01:38:48.000 The sugar is not enough to make them fat.

01:38:50.000 It's not single-handedly enough.

01:38:52.000 I'm not saying it doesn't contribute.

01:38:54.000 I 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.

01:39:06.000 So the third culture is pretty interesting, the Kuna of Panama. 0.72

01:39:11.000 And the reason they're interesting is that they actually aren't eating honey, they're actually eating white sugar.

01:39:17.000 So they're a culture that they live primarily a non-industrial lifestyle.

01:39:22.000 They're farmers and hunter-gatherers.

01:39:27.000 But they do a little bit of trade.

01:39:30.000 And one of the things they trade for is sugar, and they eat sugar-sweetened foods as well.

01:39:35.000 So like donuts and pastries, and they drink soda and Kool-Aid.

01:39:39.000 What is their lifestyle?

01:39:40.000 They have a natural lifestyle.

01:39:43.000 They are hunter-gatherers and subsistence farmers.

01:39:46.000 So they're living a physically active, natural lifestyle.

01:39:50.000 So this is the problem in comparison with any westernized civilization. 0.98

01:39:54.000 You burn off so many more cowards.

01:39:58.000 I 100% agree with you, and I think that is exactly the point I'm trying to make, is that it's more complicated than just sugar.

01:40:06.000 It is more complicated than just sugar, but with a normal lifestyle, it may not be.

01:40:13.000 The thing about burning of the calories is also the glucose demands, the glycogen demands on the muscle.

01:40:30.000 We're good to go.

01:40:41.000 I 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.

01:40:54.000 I 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...

01:41:03.000 There's a much more significant load on your body.

01:41:07.000 Like, when I... I did this sober October fitness challenge with my friends during October, and I was working out four hours a day.

01:41:14.000 And I was fucking eating everything that moved. 0.97

01:41:17.000 I was drinking soda. 0.99

01:41:18.000 I never drink soda.

01:41:19.000 I was eating cookies.

01:41:21.000 I didn't gain any weight other than muscle.

01:41:23.000 I didn't gain any fat at all.

01:41:25.000 Yeah. 0.99

01:41:26.000 And I was eating a terrible fucking diet, but I was going crazy. 0.99

01:41:30.000 When 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. 0.99

01:41:42.000 Just the hiking that's required, the amount of exercise that's required.

01:41:46.000 It's off the charts in comparison to a standard Western We are on the same wavelength here.

01:41:52.000 I mean, I completely agree with you that it is more complicated than just sugar.

01:41:56.000 But 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.

01:42:10.000 Do you think that physical activity doesn't matter?

01:42:13.000 I think it's a...

01:42:15.000 No, I don't think it makes a hell of a lot of difference.

01:42:18.000 When we're talking about the cause of obesity, I don't believe obese people get obese because they're sedentary.

01:42:23.000 But let me put it this way.

01:42:24.000 So if you take someone who's an elite athlete, and they start consuming a lot of sugar, but they ramp up their exercise accordingly.

01:42:34.000 Like, say if someone does what I did during the Sober October, they're working out three, four hours a day, every day.

01:42:40.000 You don't think that they have higher sugar demands and that their body would just burn that off?

01:42:45.000 Yeah, no, absolutely.

01:42:46.000 I think that if there's a real benefit to exercise, it's burning off the carbohydrates you consume and you need less insulin to do it.

01:42:53.000 Can I respond to the Kuna?

01:42:55.000 Get back to them for a second.

01:42:57.000 I mean, one of the issues I have with Stephan is he writes off my stories as stories, which they are.

01:43:04.000 All science begins as stories.

01:43:08.000 Hypotheses.

01:43:08.000 And then what you do is go look for the evidence.

01:43:10.000 And then he quotes studies and refers to it as evidence as though this is...

01:43:17.000 We had this discussion a year and a half ago, and you didn't disagree with me at the time, and it had no influence.

01:43:23.000 I'm just going to read from the email I wrote to Stephen.

01:43:27.000 Oh, boy.

01:43:29.000 We're reading emails.

01:43:31.000 It's gotten to that point in the conversation.

01:43:33.000 I'm not only going to read from the email.

01:43:36.000 If I have time, I'm going to read from your book.

01:43:38.000 Read the Kuna.

01:43:39.000 The study you cited is interesting.

01:43:40.000 Okay, 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.

01:43:54.000 And 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.

01:44:07.000 I 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.

01:44:12.000 One way or the other, it's not processed sugar.

01:44:15.000 So it's roughly 274 grams of sugar per week, or about 32 pounds per year.

01:44:21.000 Now, 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.

01:44:27.000 So 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.

01:44:36.000 And then I said, wait, hold on.

01:44:38.000 I thought you did.

01:44:39.000 That's what I heard.

01:44:41.000 If 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.

01:44:49.000 Do you really think these urbanized Kuhn are consuming only three 8-ounce sodas per week?

01:44:54.000 So 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. 0.78

01:45:08.000 So five glasses of Kool-Aid, no candy, no ice cream, nothing.

01:45:12.000 I'd like to know more about the Urban Kuna before I accept such an analysis as valid.

01:45:16.000 On 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.

01:45:24.000 So 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?

01:45:34.000 So this is what science is.

01:45:36.000 You have studies, you have evidence, and the question always is, you've got competing hypothesis.

01:45:41.000 Does this evidence really speak to the hypothesis?

01:45:44.000 And 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.

01:46:00.000 So 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,

01:46:18.000 and you get epidemics of obesity and diabetes.

01:46:21.000 So here's a population that's been eating honey for maybe thousands of years.

01:46:25.000 In 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.

01:46:37.000 Population is a death sentence for the child and for the mother who gives birth. 1.00

01:46:41.000 So you're going to very quickly weed out anyone.

01:46:44.000 So 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?

01:46:55.000 And the answer is, I don't think so.

01:46:57.000 Stephen thinks it does.

01:46:58.000 You could flip a coin.

01:46:59.000 All of this can be settled with experiments.

01:47:02.000 One 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.

01:47:14.000 It's endemic.

01:47:15.000 It used to be 20 years ago, if you had fatty liver disease, and you told the doctor you didn't smoke, they would assume you were lying.

01:47:24.000 Now, it's so common and so common in children, and particularly common in Hispanic children, that it's clear it's not caused by alcohol.

01:47:33.000 And the question is, what causes it?

01:47:35.000 Because 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.

01:47:46.000 So my not-for-profit funded a pilot study Well, we just took 40 kids.

01:47:51.000 Well, 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.

01:48:02.000 In 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.

01:48:13.000 And this study was published in JAMA four months ago, and it just Get rid of the sugar in the diet.

01:48:20.000 The fatty liver disease resolves.

01:48:22.000 It was pretty simple.

01:48:24.000 It tells you nothing about mechanism.

01:48:26.000 The kids lost a little bit of weight.

01:48:29.000 Maybe it was a weight loss.

01:48:30.000 The 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.

01:48:38.000 But 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.

01:48:47.000 There's two ways you could do science.

01:48:49.000 You could say let's look at all the junk that was done for 30, 40, 50 years.

01:48:54.000 Let's find everything we can that even vaguely speaks To the experiment and ignore any quality of the study.

01:49:01.000 So 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.

01:49:14.000 And then we can throw all that garbage into a meta-analysis.

01:49:18.000 And 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.

01:49:28.000 So 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?

01:49:38.000 You know these numbers.

01:49:39.000 Yeah.

01:49:41.000 0.8, 0.18 or something?

01:49:43.000 Several of the other studies were Jim Hill studies.

01:49:45.000 We've talked about Jim Hill.

01:49:47.000 The biggest studies were Jim Hill.

01:49:48.000 And 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.

01:49:56.000 So when Stephen dismissed this Harvard… You've got three names for him now.

01:50:02.000 Stephen, Stephon, and now Stephen.

01:50:04.000 Guy and A. I can't get Guy and A right.

01:50:07.000 Dr. Guy and A. Can I just do that?

01:50:08.000 Stephen.

01:50:08.000 His name's Stephen.

01:50:09.000 It's really easy.

01:50:10.000 Stephen.

01:50:10.000 I can't do it, dude.

01:50:11.000 I just don't get names.

01:50:13.000 My name's Joe.

01:50:15.000 Hi, Gary.

01:50:15.000 That I know.

01:50:16.000 Hi, Joe.

01:50:20.000 Stephen ultimately I've rejected this study.

01:50:25.000 It's about a $12 million study that was done at Harvard based on Kevin Hall.

01:50:31.000 So these are two names.

01:50:32.000 It's about three people out there who are convinced that everything people like me are saying is wrong.

01:50:38.000 Or not everything, but most of it.

01:50:40.000 And they keep coming up over and over again.

01:50:42.000 So Kevin Hall claims that he has refuted The carbohydrate insulin model in his studies, so when a study comes out supporting it, he works to find out why that study's wrong.

01:50:55.000 We all did the same thing.

01:50:56.000 I did the same thing right here with the Kuna study, explaining why I don't find it meaningful.

01:51:01.000 But anyway, that's the thing.

01:51:02.000 The goal is to do the right study, because ultimately, you've got to remember what's on the line here.

01:51:06.000 We have obesity and diabetes epidemics. 0.99

01:51:09.000 I mean, tragic shit is going on out there. 0.99

01:51:12.000 I mean, people, you know, these are ruining lives. 0.99

01:51:14.000 They're overwhelming the healthcare system.

01:51:17.000 And 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.

01:51:31.000 And what we have to do is find out if it is true, because people are dying out there.

01:51:35.000 Stephen?

01:51:36.000 Okay.

01:51:36.000 The first thing I want to say is that this alternative explanation that Gary is talking about has already been investigated intensively, including studies that were funded by his own organization, NUSI. Two out of the three studies that have been published on that were clear refutations of the hypothesis.

01:51:57.000 No, no, no.

01:51:57.000 I'm responding here.

01:51:58.000 I know, but you've got to represent the studies correctly.

01:52:02.000 Gary, Gary, Gary.

01:52:03.000 Representing them according to your beliefs is not representing them correctly, okay? 0.96

01:52:07.000 Now, I've noticed a remarkable correlation between studies undermining your beliefs and you thinking those studies are garbage.

01:52:15.000 And we should talk about...

01:52:18.000 Jim Hill and his studies a little bit.

01:52:20.000 Because, you know, to me, just saying this guy has a conflict of interest and then insinuating that that makes the study bad, if you can't actually find a problem with the study itself, these were very rigorous studies.

01:52:31.000 If you cannot point out a specific problem with the study, it was designed with an assumption.

01:52:37.000 It was designed based on the assumption it was supposed to test.

01:52:39.000 It wasn't designed how Gary wanted it to be designed.

01:52:42.000 If you cannot find a problem with that study, Then you can't just dismiss it by making these insinuations that the person had a conflict of interest, okay?

01:52:53.000 I explained to you the problem with the study.

01:52:56.000 Okay, that's great, Gary.

01:52:57.000 I didn't realize Jim Hill had done it at the time.

01:53:00.000 All right, you're going to be able to respond in a moment.

01:53:03.000 Now, the Kuna, I think we should really get back to this issue, this non-industrial culture, because the primary basis... 0.97

01:53:11.000 For Gary's book, The Case Against Sugar, the primary observation that underlies Gary's belief on this is this observational correlational thing that cultures, when sugar gets into these cultures,

01:53:28.000 they become fat and that is the common thread in obesity.

01:53:32.000 And so what I'm doing is I'm pointing out a culture Where sugar came in and it did not make them fat.

01:53:39.000 And that's one of three cultures.

01:53:40.000 I haven't even looked that hard, okay?

01:53:42.000 These are just three cultures that I came across.

01:53:44.000 There's probably a bunch more that are eating high levels of sugar and are not becoming obese.

01:53:51.000 We don't know if honey is the same.

01:53:53.000 And again, Joe...

01:53:55.000 The explanation is right on point.

01:53:57.000 There's a lot of other things going on in these cultures, and it's more complicated than just sugar.

01:54:01.000 That's exactly my point.

01:54:02.000 Now, I want to talk about the Cuban economic crisis.

01:54:06.000 This is reference number 22. From 1989 through 1995, the Cuban economy collapsed, and the price of food went way up, the price of gasoline went way up, and so people started focusing on these really cheap foods.

01:54:24.000 Cuba was a major sugar producer at the time.

01:54:28.000 I don't know if they still are.

01:54:29.000 And so the intake of sugar went way up.

01:54:31.000 Intake of refined carbohydrate went way up.

01:54:34.000 The diet became 77% carbohydrate, primarily white rice and sugar, 28% sugar of their total calorie intake.

01:54:44.000 So that's like double what Americans eat.

01:54:47.000 Now, their calorie intake went down and because of the lack of gasoline, people got really physically active because they had to walk everywhere.

01:54:56.000 So now, again, this is a situation where we can test Gary's hypothesis.

01:55:03.000 If Gary is right and calories don't matter, only refined carbohydrate and sugar matter, Obesity should have gone through the roof in this population over that period of time.

01:55:13.000 What you actually see is that the prevalence of obesity declined by half.

01:55:17.000 So there was a 50% decline.

01:55:20.000 It went from 14% to 7% over the period of this...

01:55:26.000 We're good to go.

01:55:41.000 The rate of underweight increased only slightly.

01:55:45.000 It went from 8% to 10%.

01:55:46.000 And so we know these people weren't just totally starving.

01:55:51.000 And 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,

01:56:07.000 The obesity rate went right back up as soon as they went back to their normal diet.

01:56:12.000 Because they were not walking as much.

01:56:15.000 Yeah, it was the exercise and also just their diet became richer again.

01:56:18.000 I mean, if you're eating a diet, that's a very poor diet, eating like white rice and sugar.

01:56:24.000 I 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.

01:56:38.000 And so this is a case where you have an entire country testing Gary's hypothesis and finding that basically the opposite of what his hypothesis predicts.

01:56:49.000 Gary?

01:56:50.000 Let's go with when he was refuting the studies and you wanted to oppose that.

01:56:54.000 But this is a level of discourse that I didn't really want to get into because that's a study that I'm going to have to read.

01:56:59.000 He's right.

01:56:59.000 I'm going to read it to try and figure out what the problem is.

01:57:01.000 I remember looking at that study and thinking...

01:57:04.000 There wasn't the kind of data you're citing.

01:57:06.000 Maybe there's multiple studies put together, but the one study I looked at, the kind of data you're citing wasn't in there.

01:57:12.000 This is, again, a problem.

01:57:14.000 References are on my website, so have at it.

01:57:16.000 No, I will, but we'll be off the air by then.

01:57:20.000 The beginning of his, when he started talking, he was referencing some studies, and you had a problem with that?

01:57:27.000 Well, it's a game people play.

01:57:30.000 And again, it's why basically in my book I try not to get into the he said, she said studies, because you never know how well they did.

01:57:36.000 I think we both agree that there's a reproducibility crisis in science and some huge proportion of the studies are just wrong.

01:57:44.000 Whether they're experiments or observations, people sometimes aren't very good at what they do.

01:57:50.000 And so anyone in either business, you have to, Stephen likes to say, I have no evidence. 0.98

01:57:55.000 Stephen, damn it. 0.64

01:57:57.000 But simultaneously, people accuse me of writing a 600-page book with 150 pages of references that was too long to read. 0.99

01:58:04.000 So there's clearly evidence for this observation and this hypothesis.

01:58:09.000 My issue with Stephan...

01:58:12.000 Is that he speaks as though he knows, with this authority.

01:58:16.000 And so, again, I would like to just read a little bit from your book, because as I was prepping for this...

01:58:21.000 Before you do that, though, he was referencing studies...

01:58:25.000 The Cuban situation.

01:58:26.000 I don't know what the reality is.

01:58:28.000 Before that, when he first started talking, he was referencing things that you were stating...

01:58:33.000 That he was saying, what were you saying, that the organization that supports him actually refuted some of these?

01:58:40.000 Oh, that was the Jim Hill studies.

01:58:42.000 No, no, no, no.

01:58:43.000 The NUSI studies.

01:58:45.000 No, we're talking about the NUSI studies.

01:58:46.000 The first two of which, and we can get into detail on this, on how those refuted Gary's beliefs.

01:58:53.000 And I would say Gary's about the only person who thinks they did not refute his beliefs.

01:58:57.000 The scientific community is pretty unanimous.

01:59:00.000 You can respond, but...

01:59:01.000 But could you please say what the study stated?

01:59:05.000 Let me do it before he...

01:59:07.000 So the first study is a pilot study that depends what you look at to depend whether or not it refuted your belief.

01:59:18.000 So again, you have to understand this world.

01:59:20.000 There 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.

01:59:30.000 I hope I'm doing Kevin justice.

01:59:33.000 And then there's David Ludwig and his colleagues at Harvard who tend to believe what I believe.

01:59:38.000 And we funded them both to do studies.

01:59:41.000 And 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.

02:00:11.000 This is what you do in science.

02:00:13.000 You do an experiment, people critique it, ideally you do another one.

02:00:17.000 Kevin has decided Well, Kevin is doing another one.

02:00:20.000 I think he's asking the wrong questions, but I just saw the other day that he's doing another experiment.

02:00:26.000 The 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

02:00:56.000 complained that the low fat diet wasn't fat enough so hopefully they'd be able to separate out these two.

02:01:06.000 At the end of the trial, they got pretty lousy adherence.

02:01:11.000 Low carb was about 25 to 28 percent carb, which is by no means a low, meaningful low carb diet.

02:01:17.000 Pretty typical.

02:01:18.000 In free living studies, and the low fat was about equal.

02:01:22.000 What they did, which it's funny, we realize this on one side, but not the other.

02:01:28.000 They told the low-carb group not to eat sugars and refined grains, which are, by my hypothesis, the most fattening carbohydrates.

02:01:38.000 And they also told the low-fat group to not eat refined sugars and refined grains.

02:01:44.000 So they basically removed the most fattening parts of the diet from both arms of the study.

02:01:50.000 It's funny, we knew that we were going to do it with the low-carb group, because you have to.

02:01:54.000 And my colleagues actually knew they were going to do it with a low-fat group.

02:01:57.000 I didn't know that when I found out.

02:01:58.000 I was stunned because now you're testing two diets.

02:02:01.000 Neither one of them have sugar or white bread.

02:02:04.000 So now you see similar weight loss with relatively poor compliance.

02:02:09.000 Why would they do that?

02:02:10.000 That doesn't make any sense with the low-fat diet.

02:02:12.000 Well, their argument, and we talked to Chris for a lot of his argument, he was afraid.

02:02:16.000 There were two things.

02:02:18.000 He wanted the diet to be healthy.

02:02:20.000 So a healthy diet in 2015 has become a diet that doesn't have sugar and white bread in it.

02:02:27.000 So he wasn't going to promote sugar and white bread to one diet or another.

02:02:32.000 How long was the period of time when they were studying these people?

02:02:35.000 They were on the diet.

02:02:36.000 They were supposed to be on the diet for a year.

02:02:38.000 Okay, that makes sense then.

02:02:39.000 So the question is again, would you expect to see a difference?

02:02:42.000 I can send you an email I wrote to my NUSI colleagues in 2015. I could read it.

02:02:48.000 When I found out about this low-fat thing, saying this is insane.

02:02:53.000 Both groups are carbohydrate-restricted, so you could think of it as a low-fat carbohydrate-restricted diet and a high-fat carbohydrate-restricted diet, and then he kind of got the same answer, which could be for any reason whatsoever.

02:03:06.000 There's a paper, I don't know if I can, well, I'm not going to talk about it.

02:03:11.000 It's bad enough talking about the ambiguous studies that have been published without getting into unpublished research.

02:03:17.000 So people see this.

02:03:19.000 The New York Times, for instance, did two stories on it.

02:03:21.000 One of them said it's not about calories, it's about the quality, the sugar and the refined grain, because both groups restricted sugar and refined grains and lost weight.

02:03:31.000 And that was written by a reporter who tends to believe what we believe.

02:03:35.000 And the other article said it's all about the calories, because both groups ended up, on average, eating 500 calories each.

02:03:41.000 It ends up, from a scientific perspective, being a poorly done study, even though we funded it.

02:03:46.000 I'm not It just didn't answer the question.

02:03:49.000 You said 500 calories each?

02:03:51.000 On average, they restricted their calories.

02:03:53.000 And that's actually self-reported, so it's not accurate.

02:03:56.000 So it's not particularly meaningful.

02:03:57.000 So again, these are...

02:03:59.000 I don't like using...

02:04:01.000 That's a complicated study because it's low in sugar.

02:04:04.000 Well, and it's also free living, yeah.

02:04:05.000 So both sides are low in sugar.

02:04:07.000 Both sides are not eating processed foods.

02:04:09.000 There were two full differences in total carbohydrate intake.

02:04:13.000 Okay, 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.

02:04:25.000 If you believe the food frequency questionnaires that you just said we don't know whether we… You could be talking about vegetables.

02:04:33.000 You could be talking about fruits.

02:04:34.000 Well, these are healthy carbohydrates that they had primarily in this study.

02:04:38.000 Can we agree that that study can be interpreted from virtually any way you want it, especially because it was a pre-living study?

02:04:45.000 No, I definitely don't agree with that.

02:04:48.000 Now, what we will agree on, I'll agree with you on this, is that refined carbohydrates and sugar are the most fattening type of carbohydrate.

02:04:56.000 That we can agree on.

02:04:57.000 Oh my God, we came to an agreement?

02:04:58.000 No, but the question is why?

02:05:01.000 Is it because people eat too much of them?

02:05:02.000 So, here's the thing.

02:05:03.000 If you believe Gary's hypothesis, now, any kind of carbohydrate increases insulin levels.

02:05:09.000 Some do it more than others.

02:05:11.000 Refined carbohydrates do it more.

02:05:13.000 Any kind of carbohydrate increases insulin levels relative to fat.

02:05:18.000 And 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.

02:05:32.000 You shouldn't have seen the exact same amount of weight loss in these two groups, right?

02:05:35.000 Right, but they're not high in sugar.

02:05:37.000 Correct.

02:05:38.000 Isn't your argument as always?

02:05:40.000 That's the other part of the argument, which is you take away the sugar, and that was one of the problems with the energy.

02:05:46.000 The argument I'm making, and Stephan's completely right, I'm defending my hypothesis.

02:05:52.000 I see a study that, he does the same thing, he did it here, we all do it.

02:05:56.000 You see a study that disagrees with you, you find the reason why to not believe it in every study ever done.

02:06:02.000 has plenty of reasons not to believe it.

02:06:04.000 That's why independent replication is something you always wanted.

02:06:07.000 You get another group to do the study, ideally a third group, people come in, they criticize the study, then you do it again, and again, and again.

02:06:15.000 And 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.

02:06:27.000 Stop We're good to go.

02:06:37.000 We're good to go.

02:06:46.000 It was interpreted as not supporting this hypothesis.

02:06:51.000 And again, you could argue that for an hour and nobody's going to care.

02:06:56.000 That study was not randomized.

02:06:58.000 So a non-randomized study, you can't infer causality.

02:07:01.000 That's why it was a pilot study, one of the many reasons it was a pilot study.

02:07:04.000 The people who think this carbohydrate model...

02:07:08.000 So when we talk about the carbohydrate-insulin model, it means carbohydrates are fattening.

02:07:13.000 That's the basis of it.

02:07:14.000 Bread, pasta, potato, and sugar may be the thing that's necessary to add to the diet to make all these carbs fattening.

02:07:23.000 Because sugar, as we talked about this a year and a half ago, the fructose molecule is metabolized in the liver.

02:07:29.000 It's linked to fat accumulation in the liver, which is linked to insulin.

02:07:34.000 I like the way you're squeezing your stomach fat while we're talking about that.

02:07:38.000 I gotta work out, dude.

02:07:42.000 I'm just bored.

02:07:44.000 For these experiments to be done right, they have to be tested right.

02:07:49.000 You can't use poorly designed experiments in every experiment ever done.

02:07:55.000 And so what we've tried to do is keep working towards better experiments.

02:07:59.000 There's now a new version of the Ludwig experiment being done at the Arnold Foundation.

02:08:03.000 Lauren John Arnold funded to the tune of, I think, $13 million.

02:08:10.000 Whatever that study finds, Kevin Hall will probably find a reason, look in it, and find a reason to question it.

02:08:18.000 And ideally, they would be working together so that you've come up with the criticisms before you've spent $13 million.

02:08:24.000 But this is how science works.

02:08:27.000 My job was to tell a good story, as Stephan would say, and I believe people who read the books can judge whether it's a good...

02:08:34.000 Am I convincing in arguing that You add sugar.

02:08:39.000 There's counter evidence to everything.

02:08:41.000 There wasn't counter evidence.

02:08:43.000 It wouldn't require a journalist to come along in 2019 to make these arguments.

02:08:48.000 Let me ask you this, because this is something that you've admitted to, something you said, rather.

02:08:53.000 Why are sugary carbohydrates the most fattening?

02:09:00.000 Well, if this hypothesis is correct, I think you would say that they trigger a food reward or they are a food reward.

02:09:08.000 Yeah, absolutely.

02:09:09.000 Wait, wait, wait.

02:09:09.000 Let me just finish.

02:09:10.000 I would say the counterargument is that they create a hormonal milieu in the body that over-responds to insulin.

02:09:18.000 And 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.

02:09:34.000 So the idea is you raise insulin and the sugar, because of this Half of it being fructose, and that mostly being metabolized in the small intestine and the liver, may indeed cause insulin resistance, and if it does, you over-respond insulin.

02:09:48.000 So 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.

02:09:59.000 Yeah.

02:09:59.000 So, I mean, sugar is a factor that makes us want to eat foods, right?

02:10:03.000 I mean, this is one of the many food properties, and I would love to talk about this more, that cause dopamine release in the brain.

02:10:10.000 And dopamine is a chemical that sets our motivational levels to do certain behaviors.

02:10:16.000 So the reason we become addicted to drugs is that they go in the brain and they stimulate dopamine release and that reinforces drug-seeking behaviors.

02:10:25.000 Right, but this is just causing you to consume more.

02:10:27.000 Correct.

02:10:28.000 But 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.

02:10:40.000 No, no.

02:10:40.000 I didn't say it was independently of calories.

02:10:43.000 It's entirely dependent on calories.

02:10:44.000 Yeah, correct.

02:10:45.000 And we have randomized controlled trials demonstrating this.

02:10:49.000 So if you look at the randomized – by the way, we're not operating in an evidence vacuum.

02:10:55.000 There's tons of randomized controlled trials on sugar.

02:10:57.000 Can I ask you this?

02:10:58.000 Yeah.

02:10:59.000 These randomized controlled studies, are they short-term?

02:11:02.000 Yeah.

02:11:04.000 Well, it depends on how you define short-term.

02:11:07.000 They're not lasting years and years and years.

02:11:09.000 Isn't the issue, though, long-term chronic effects?

02:11:11.000 That seems to be...

02:11:13.000 Possibly, but let me put it this way.

02:11:15.000 If you believe that insulin is the cause, the effect of insulin on fat cells happens almost immediately.

02:11:23.000 So insulin, I'm not aware of any mechanism of insulin on fat cells that takes more than a few hours to occur.

02:11:31.000 And so if you believe that insulin causes obesity, this should be happening immediately.

02:11:35.000 You shouldn't have to wait months and months for this to occur.

02:11:39.000 No, that doesn't make any sense at all.

02:11:41.000 No, it does make sense.

02:11:43.000 No, it doesn't make sense to me.

02:11:45.000 Why doesn't it make sense to you?

02:11:46.000 Well, because again, he's kind of making this up as he goes along.

02:11:51.000 So the idea is...

02:11:53.000 Well, explain why it doesn't make sense without insulting him, if that's possible.

02:11:58.000 Has he not been insulting me?

02:12:00.000 Or am I just biased?

02:12:01.000 I realize that everything is perspective.

02:12:04.000 Well, I don't necessarily think he's insulting your stories, not you personally.

02:12:08.000 But why doesn't it make sense to you what he's saying?

02:12:12.000 Okay, so the idea is when your insulin is elevated, you're storing fat, right?

02:12:20.000 It depends on what you mean by that.

02:12:23.000 See, you do a little bit of bait and switch here.

02:12:25.000 No, no, no.

02:12:26.000 That's an insult.

02:12:26.000 Just answer the question.

02:12:27.000 If it's not true, clarify.

02:12:29.000 Well, it depends.

02:12:30.000 What do you mean by store?

02:12:31.000 I mean, your fat cells are accumulating fat when insulin is elevated.

02:12:35.000 Do you mean accumulate like next day you'll have...

02:12:38.000 Like hold on to fat.

02:12:39.000 Like it inhibits...

02:12:41.000 Yeah, that's incorrect.

02:12:42.000 It stimulates lipoprotein lipase and it inhibits hormone synthesis.

02:12:47.000 We should really talk about this because that's incorrect.

02:12:50.000 It's in the textbooks.

02:12:51.000 Oh yeah, we'll talk about what's in the textbook.

02:12:53.000 Don't worry, Gary.

02:12:55.000 Okay, so you don't believe insulin...

02:12:59.000 Well, just give me your position and I'll let him refute it.

02:13:02.000 It's here.

02:13:03.000 But just say it.

02:13:04.000 No, no, we'll just show it, okay?

02:13:05.000 Because, again, you're going to say it's not in here, so I have the same textbook.

02:13:10.000 And then we'll let Joe hear.

02:13:12.000 Suppression of fat mobilization by insulin.

02:13:15.000 And there's another graph that is...

02:13:20.000 Stimulation of fat mobilization.

02:13:22.000 Congratulations to all of you people that are listening to this.

02:13:25.000 They're still hanging in there.

02:13:26.000 I know we're in the weeds scientifically.

02:13:28.000 Gary, let me just say, this is going to take a long time.

02:13:30.000 So we agree on the molecular mechanisms, okay?

02:13:33.000 We agree on the molecular mechanisms, the impact of insulin on enzymes and fat cells.

02:13:39.000 What we disagree about is the implications of that, and I think that's what we should talk about.

02:13:44.000 That's true.

02:13:45.000 Because nowhere in that textbook does it say that insulin regulates the total size of body fat stores.

02:13:52.000 Absolutely.

02:13:52.000 Can I guarantee you that?

02:13:53.000 Absolutely.

02:13:55.000 Something that you have added onto that mechanism.

02:13:59.000 Would you like to know the conversation I had with the author of the textbook?

02:14:02.000 No, not right now, actually.

02:14:06.000 Let me tell you about the conversation I had with Keith Frey.

02:14:10.000 I was actually in Oxford.

02:14:11.000 We talked about this for three hours.

02:14:13.000 Can you stop interrupting me, please?

02:14:15.000 Okay.

02:14:16.000 Now, let me explain.

02:14:19.000 So insulin essentially does have effects on enzymes that cause fat cells to take up more fat and to release less fat.

02:14:28.000 So that's the part that you're right about.

02:14:30.000 That's what that textbook talks about.

02:14:33.000 Right.

02:14:34.000 That does not imply that insulin causes fat storage as in the accumulation of fat from day to day.

02:14:42.000 And let me explain why that is.

02:14:43.000 So insulin is basically a traffic cop that allows your body to burn the fuel that you just consumed.

02:14:51.000 So when you eat a diet that's high in carbohydrate and low in fat, your insulin goes up, your body restricts the fat from going out of fat cells, it turns that down, not off, but down.

02:15:03.000 It causes less fat to come out of your fat cells, and then your body's burning carbs.

02:15:07.000 That's what you just ate, right?

02:15:09.000 Now if you eat a diet that's high in fat and lower in carbohydrate you secrete less insulin those effects don't occur on your fat cells and that allows your body to burn the fat that you just ate.

02:15:22.000 But at the end of the day the amount of fat that you have in your body is the amount that you ate Minus the amount that you burned.

02:15:29.000 This is just arithmetic, right?

02:15:32.000 The amount that you ate minus the amount that you burned.

02:15:34.000 And if you eat a low-fat diet, you're not eating much and you're not burning much.

02:15:37.000 You're in the same place as if you're eating a diet where you're eating a lot of fat And burning a lot of fat.

02:15:44.000 And the way we know that's true is because varying the amount of carbohydrate and fat in the diet makes no difference to body fatness in randomized controlled trials.

02:15:54.000 That's why we know that what I just said is correct.

02:15:57.000 So, first of all, it's one randomized controlled trial.

02:16:00.000 It's Kevin Hall again.

02:16:01.000 No, I'm talking about a meta-analysis of 20 randomized controlled trials.

02:16:06.000 We can't talk about the meta-analyses.

02:16:07.000 We decided that, I think, you know, that the...

02:16:11.000 What's wrong with meta-analysis?

02:16:13.000 You get every crappy study ever done.

02:16:15.000 He doesn't like who did it, basically.

02:16:17.000 No, no, no.

02:16:17.000 I don't care who does it.

02:16:18.000 I don't like meta-analyses.

02:16:20.000 I don't like the concept of them.

02:16:21.000 I 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.

02:16:31.000 And the answer is do better studies.

02:16:33.000 The answer is always do better studies.

02:16:34.000 You can't do meta-analyses exist for everything.

02:16:37.000 The issue is just a simple one.

02:16:40.000 Remember, we're talking about the 10 calories a day.

02:16:42.000 So 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.

02:16:50.000 That's what we're talking about.

02:16:51.000 10 calories in the fat tissue.

02:16:54.000 Okay?

02:16:55.000 So 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.

02:17:09.000 Can you cite evidence to support this thing you're saying right now?

02:17:11.000 Well, you could take, for instance, the Energy Balance Consortium study, the Kevin Hall study that we've talked about.

02:17:17.000 There are two things that happen when you put people on a ketogenic diet.

02:17:20.000 Among other things, you generate ketones, and you lose ketones in the breath and in the urine.

02:17:25.000 And one of the things you have to do in these energy balance experiments is measure calories lost through fecal material.

02:17:32.000 Who knows?

02:17:33.000 Maybe you jack up the fat consumption. 0.99

02:17:36.000 Maybe they lose more fat calories when they shit it out.

02:17:40.000 Or maybe you jack up the fiber. 0.58

02:17:42.000 So you think calories matter?

02:17:43.000 I think when you're measuring the fat balance, which you're talking about, you have to measure the amount of fat in and out.

02:17:51.000 And so I'm giving you an example in response to your question because you gave me an example.

02:17:55.000 In that study, they didn't do either of those measurements.

02:17:57.000 They modeled one and the other one, they couldn't get the assay to work after a year or two years and gave up on it.

02:18:05.000 And so you just don't know.

02:18:07.000 But getting back to this question, we're talking about somebody storing 10 calories of fat in their fat cells.

02:18:12.000 Let's never get away from that, or 20 calories.

02:18:14.000 And so the question is always, is this mechanism capable of explaining the 20 calories, or is the...

02:18:22.000 What did you find from looking in that book?

02:18:25.000 Well, it's essentially what he was saying.

02:18:27.000 And insulin inhibits fat mobilization from fat cells.

02:18:30.000 Well, I could read it if you want me to read it.

02:18:32.000 I mean, Gary and I both agree with what's in that textbook.

02:18:38.000 You can read it if you want, but I don't see the point.

02:18:39.000 Yeah, it says insulin restrains fat mobilization through two mechanisms.

02:18:42.000 Suppression of lipolysis.

02:18:44.000 Is that right?

02:18:45.000 Yeah, lipolysis.

02:18:47.000 Mechanisms are described in the text and the stimulation of the re-esterification of fatty acids within the adipocytes.

02:19:01.000 Adipocytes?

02:19:02.000 Adipocytes.

02:19:04.000 Note that the same process of esterification will also be simultaneously incorporated fatty acids from circulating triglycerides released by lipoprotein lipos That's enough,

02:19:27.000 Joe.

02:19:28.000 Lipase, L-I-P-A-S-E, into stored triacylglycerol.

02:19:35.000 Yeah, so let me just explain this briefly.

02:19:38.000 A lot of big words.

02:19:41.000 The argument I've been making, and others, is that insulin inhibits fat loss.

02:19:47.000 Fat mobilization.

02:19:47.000 Like, if you're a fat cell, and you see insulin, you hold on to your fat.

02:19:51.000 Right.

02:19:52.000 Kind of that simple.

02:19:54.000 Stefan's absolutely right.

02:19:55.000 This book, which we're talking about, Metabolic regulation, a human perspective.

02:20:00.000 It'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.

02:20:13.000 And in this book, Keith Frane Talks about how insulin determines fat accumulation and fat cells.

02:20:22.000 Not accumulation, that's not the correct word.

02:20:23.000 Whatever, fat storage, fat storage. 0.92

02:20:26.000 Dynamic fatty acid trafficking in and out of fat cells.

02:20:30.000 Okay, thank you.

02:20:31.000 So the first time I ever interviewed Keith was for a piece I was doing for the Journal of Science on insulin resistance.

02:20:38.000 And we spent about an hour on the phone and he explained to me for 20 minutes all the ways insulin...

02:20:46.000 It traps, determines fatty acid trafficking across the fat cell membrane and you raise insulin, you accumulate more fat on the short term.

02:20:56.000 And then we got to obesity and he said, obesity is caused by people eating too much.

02:21:02.000 And I said, Keith, when we were talking about why fat cells get fat, it was all insulin mediated.

02:21:11.000 And when we were talking about people get fat, it was this eating too much thing, okay?

02:21:17.000 And you switched mechanisms on me.

02:21:20.000 So 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,

02:21:37.000 but it includes getting fat at your waistline increasing, and it's an insulin resistance-related disorder, which means your insulin is elevated.

02:21:44.000 And again, this is where we end up with two hypotheses about why insulin is elevated.

02:21:49.000 But if, for instance, sugar can elevate insulin, you end up with metabolic syndrome, you're in fat storage mode.

02:21:55.000 That's the terminology of diet book doctors.

02:21:58.000 So now you're storing fat, and you only have to do 10 calories a day.

02:22:02.000 20 calories a day, you're going to get obese.

02:22:05.000 And it's insulin-mediated and insulin is responding to the carbohydrate content of the diet primarily.

02:22:10.000 And that's it.

02:22:11.000 And 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.

02:22:18.000 And I'd like to talk about this overeating concept.

02:22:22.000 He said, you know, I never thought of that.

02:22:24.000 I mean, the guy had been in the field 40 years, and he lived maybe 50. And then I had a long conversation with him.

02:22:30.000 I was back in Oxford when I did that insane Alan Aragon debate.

02:22:35.000 I stopped off at Oxford on the way to Manchester, and we had a long conversation with Keith.

02:22:40.000 And I said, look, what I want you to do is just...

02:22:43.000 Come up with a hypothesis of obesity from the fat cells perspective, right?

02:22:49.000 Shed your brain-centric, energy-balance-centric thing and ask yourself, what does the fat cells see?

02:22:56.000 And if nothing else, ask the student to do it as an experiment.

02:22:59.000 I mean, that would be a great thought experiment for a kid.

02:23:01.000 What's going to make a fat cell fat?

02:23:03.000 And then our assumption is going to be that's what's going to make a human fat.

02:23:06.000 And Keith said, he literally said to me, he was retiring and he was going off to...

02:23:12.000 I kind of envied him.

02:23:14.000 He said, I can't put energy balance aside.

02:23:17.000 You're telling me to not think in terms of intake and expenditure, and I can't do it.

02:23:23.000 And 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.

02:23:38.000 And they can't get away from it.

02:23:40.000 So 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.

02:23:54.000 They assumed energy balance was the cause, and then they wanted to see what caused energy imbalance, and they started with the wrong hypothesis.

02:24:03.000 They're trapped in a paradigm.

02:24:04.000 We've all seen this.

02:24:06.000 Can I respond to this?

02:24:07.000 Please.

02:24:07.000 Okay.

02:24:08.000 So, Gary, I pre-ordered your book.

02:24:12.000 I have a copy of your book right here, Good Calories, Bad Calories.

02:24:15.000 I pre-ordered this in 2008 because I was so excited to read this book.

02:24:19.000 Yes.

02:24:20.000 You emailed me.

02:24:21.000 I 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.

02:24:34.000 So I was fully immersed and convinced by your perspective when I read this book.

02:24:41.000 And you signed this book.

02:24:43.000 I have your signature.

02:24:45.000 We had a very nice dinner together.

02:24:47.000 And 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.

02:24:59.000 I started doing my own research.

02:25:01.000 I didn't take your word for it.

02:25:03.000 I started doing my own research in the lab as well and actually doing real scientific studies.

02:25:08.000 And I found that it did not line up with what you were saying in your book.

02:25:13.000 And what I ended up realizing about good calories, bad calories...

02:25:18.000 Is essentially your arguments primarily rely on historical narratives and speculation.

02:25:24.000 And there's very little of actually saying, what is the most pertinent scientific evidence to answer this question?

02:25:31.000 And what does that evidence have to say?

02:25:33.000 It's mostly historical narratives.

02:25:36.000 Honestly, 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.

02:25:48.000 And that includes me in the places where I've looked at the historical evidence.

02:25:52.000 And 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.

02:26:00.000 I was there, Gary.

02:26:01.000 I am post-Taubes.

02:26:02.000 So, let me...

02:26:03.000 Okay, so let me just...

02:26:05.000 It was interesting, because you were...

02:26:06.000 I'm going to wrap this up soon, so let's...

02:26:09.000 Have we really gone here three hours almost?

02:26:12.000 Remember when you...

02:26:12.000 I drove up here from San Diego this morning, and I was listening to Stephan on a different podcast, and you were talking about how...

02:26:20.000 Your eating behavior differed on low-carb diets versus the higher-carb diet you eat now, and you talked about your resistance.

02:26:29.000 It was easier to fast on the low-carb diet.

02:26:32.000 Correct.

02:26:33.000 Okay, and you didn't really have an explanation for it.

02:26:36.000 I don't have a very, well, anyway, go ahead.

02:26:39.000 Yeah, so again, the argument I've been making is there's two ways to look at everything.

02:26:45.000 So 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.

02:27:05.000 And 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.

02:27:12.000 So it's conditioned to me better.

02:27:14.000 So the alternative hypothesis here, the other way to think about it is on the low carb diet is insulin levels are staying lower.

02:27:20.000 When they're staying lower, he's mobilizing fat, and he's oxidizing that fat.

02:27:24.000 And as you said on the podcast, even a 135-pound marathoner has enough fat in his body to run for a week.

02:27:32.000 So the reason you're able to skip meals is because insulin is low.

02:27:37.000 My wife is calling.

02:27:39.000 She's probably telling me I'm getting shrill.

02:27:42.000 There's a different way to look at everything.

02:27:44.000 That's the point I'm trying to, with every study.

02:27:47.000 I 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?

02:27:56.000 No.

02:27:58.000 I'm giving you a hypothesis.

02:27:59.000 I'm glad you're being honest.

02:28:00.000 When you're talking about fasting, right?

02:28:04.000 If you're fasting for a certain prolonged period of time, your body's going to go into a ketogenic state.

02:28:08.000 We all agree with that.

02:28:09.000 And that's the reason why it's easier to fast.

02:28:12.000 In ketogenic states, your body starts burning off fat, and this is a widely reported side effect.

02:28:17.000 Well, it's living on fat.

02:28:18.000 It's metabolically flexible.

02:28:20.000 You don't have to eat, but the idea that it's living on your fat is evidence that you're getting thinner on that low-carb diet.

02:28:28.000 No, because it's fat balance.

02:28:29.000 It's the amount you're eating minus the amount you're burning.

02:28:32.000 No, but the question is, it's also the amount you're trapping, and that's what you keep leaving out.

02:28:36.000 No, that has been tested and refuted, is what I'm saying.

02:28:41.000 It has not been tested.

02:28:42.000 That's what I'm saying.

02:28:43.000 That's why we founded NUSI. That's why we spent $30 million.

02:28:46.000 That's why David Ludwig is doing another $13 million study.

02:28:49.000 It has not been tested.

02:28:51.000 When 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.

02:29:02.000 Let me give you another example.

02:29:03.000 There are many studies on this.

02:29:04.000 The famous feeding study from the 60s, which I thought when you said Horton, I thought you meant Ed Horton, not TJ Horton.

02:29:10.000 So Ed Horton and Ethan Sims did a prisoner study.

02:29:13.000 They literally, they wanted to get overfeed.

02:29:16.000 Again, they're using their thinking in terms of eating too much.

02:29:18.000 They wanted to first get college kids to gain 25% of excess body weight.

02:29:24.000 This 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.

02:29:31.000 So they used prisoners in the Vermont State Prison and they overfed them.

02:29:35.000 And you discuss this in your book.

02:29:39.000 They could get these prisoners to eat 10,000 calories a day of excess carbohydrates.

02:29:48.000 It was calories, not carbohydrates.

02:29:52.000 It might have been calories.

02:29:53.000 They couldn't get them to add more than a thousand calories of fat.

02:29:57.000 Okay, and they talk about this.

02:29:59.000 The SIMS studies were crazy because they published in 15 different journals.

02:30:02.000 So they interpreted the study.

02:30:04.000 If you looked at pounds gained per calorie added, they gained more per calorie of fat than they did per calorie of carbs.

02:30:14.000 But 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.

02:30:24.000 There'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.

02:30:31.000 So 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?

02:30:46.000 But there's always two ways to look at it.

02:30:49.000 And 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?

02:30:57.000 And if it doesn't, we have to hold on to it.

02:30:59.000 Because remember, we have an obesity and diabetes epidemic.

02:31:01.000 And 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.

02:31:12.000 It implies that the reason they get fat, even the overeating hypothesis...

02:31:17.000 So you think they should be eating pizza and ice cream?

02:31:19.000 What do you think?

02:31:20.000 No, I think we would both say don't eat pizza and ice cream.

02:31:23.000 Okay, they don't ask questions like that.

02:31:25.000 Thank you.

02:31:26.000 The...

02:31:29.000 There's something wrong out there.

02:31:31.000 Tragically wrong.

02:31:32.000 We know, if nothing else, I think you would agree with this.

02:31:35.000 So 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.

02:31:45.000 So that's a good thing.

02:31:46.000 And I'm implying that, I assume with the sugar book, even if I'm wrong, That getting people to eat less sugar is a good thing.

02:31:53.000 So ultimately, these are good things that I've done.

02:31:56.000 Not entirely, Gary.

02:31:58.000 Not entirely, because you're telling people that only carbohydrate matters.

02:32:03.000 I'm not telling people only carbohydrate matters.

02:32:06.000 You have argued at length that calorie intake and dietary fat intake and physical activity do not influence body fatness and are not important.

02:32:15.000 You're explaining it the wrong way.

02:32:17.000 I'm arguing that Look at the model that we published that you contributed to and we signed off on.

02:32:22.000 It doesn't say anything about physical activity.

02:32:24.000 It says that physical activity, dietary fat intake, and calorie intake are not important contributors to obesity.

02:32:30.000 I refuse to believe that somebody who's obese got that way because they were sedentary.

02:32:36.000 Okay.

02:32:37.000 In part, and again, it just requires...

02:32:39.000 But 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.

02:32:53.000 No, no, [...

02:32:53.000 What I'm saying about calories is it's the wrong way to think about it.

02:32:57.000 So wait, you think they do matter?

02:32:59.000 I'm saying calories are the wrong.

02:33:00.000 Don't put words in my mouth.

02:33:01.000 Okay, do they matter or not?

02:33:03.000 Do calories matter or not?

02:33:04.000 Calories are a way to measure the quantity of food you're eating.

02:33:06.000 You could use grams.

02:33:08.000 You could use anything else you want.

02:33:09.000 The question is, is it the right way to think about it?

02:33:12.000 Can you solve an obesity problem?

02:33:14.000 Let me give you an example before we go.

02:33:16.000 Let me just read it.

02:33:16.000 So, excess calorie intake and physical inactivity are secondary to this process and not themselves determinants of body fatness.

02:33:25.000 That is what you said in our debate notes, okay?

02:33:31.000 I'm not putting words in your mouth here.

02:33:33.000 I just want to read.

02:33:34.000 Yeah, but that's different than what you just tried to get me to say.

02:33:36.000 Okay, sure it is.

02:33:38.000 Okay, let me read you something.

02:33:40.000 There just never seemed to be enough food to satiate Carl's growing body.

02:33:44.000 After 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.

02:33:55.000 Okay?

02:33:56.000 A lot of calories.

02:33:58.000 Okay.

02:33:59.000 We're talking about one person.

02:34:00.000 We are talking about one person.

02:34:02.000 We're getting in the weeds here.

02:34:02.000 How is this going to differentiate between our hypothesis?

02:34:06.000 One of my problems with the whole overeating hypothesis is it's tautological.

02:34:14.000 You don't know if someone's overeating unless they're fat, right?

02:34:20.000 Incorrect.

02:34:21.000 Well, this fellow, I just read you.

02:34:23.000 You can measure their calorie intake and you can know.

02:34:26.000 I don't know what you're talking about there, Gary.

02:34:28.000 We 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.

02:34:34.000 Yeah, yeah, yeah.

02:34:34.000 Again, that's one story.

02:34:35.000 I know, but the point is, my point is, it's like...

02:34:40.000 You cannot tell if someone's fat.

02:34:45.000 You have no idea how many calories I consume, right?

02:34:47.000 I could probably get a pretty decent estimate actually based on published formulas.

02:34:54.000 Okay, so and then how would you know whether I was overeating?

02:34:56.000 Remember, we're talking about 10 calories a day.

02:34:58.000 No.

02:34:59.000 It gets stored in the fat tissue.

02:35:00.000 Well, 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.

02:35:12.000 Because I have excess body fat.

02:35:14.000 Correct.

02:35:15.000 Yes, 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?

02:35:23.000 Doesn't that strike you as circular?

02:35:25.000 There's nothing circular about it.

02:35:27.000 Look, if you take somebody and you increase their calorie intake...

02:35:31.000 Carbs or fat, either way, they gain body fat.

02:35:34.000 There's nothing circular about saying that calories increase body fat.

02:35:37.000 We can be pretty confident that the fellow...

02:35:39.000 And if you take someone who currently has obesity and you reduce their calorie intake, carbs or fat doesn't make any difference.

02:35:47.000 They lose body fat.

02:35:48.000 So there's nothing circular about this calorie thing at all.

02:35:51.000 But it does make...

02:35:52.000 No, no.

02:35:53.000 I just...

02:35:54.000 I don't understand how you could possibly think that was circular.

02:35:58.000 It's so simple and direct.

02:35:59.000 Let me go through it one more time.

02:36:00.000 Listen, you're not going through anything one more time.

02:36:03.000 We're going to wrap this up because I don't think we're getting anything done here.

02:36:06.000 It was a lot of fun.

02:36:09.000 It wasn't that much fun.

02:36:11.000 It was.

02:36:11.000 It was interesting.

02:36:13.000 I don't know who to believe.

02:36:15.000 Quite honestly.

02:36:16.000 I think you both make some excellent points.

02:36:19.000 And I think there's definitely some real legitimate concern that you have about his position.

02:36:26.000 And I think that your position has some merit as well.

02:36:29.000 The position about insulin and about carbohydrates and sugar.

02:36:33.000 This is a really long conversation, and I think we could probably do this for another six days.

02:36:38.000 Forget about hours.

02:36:40.000 I think if I would recommend people, I think people have to really kind of figure this out for themselves.

02:36:46.000 I would recommend, Stephan, please recommend your book.

02:36:49.000 What is your book again?

02:36:50.000 Yeah, the book is called The Hungry Brain.

02:36:52.000 The Hungry Brain.

02:36:53.000 And it's available everywhere, Amazon, all that jazz.

02:36:55.000 Correct.

02:36:57.000 Gary?

02:36:58.000 Yeah, it's good calories, bad calories, or why we get fat, or the case against sugar.

02:37:04.000 I think we've just begun this debate.

02:37:06.000 I think legitimately.

02:37:07.000 It's been going on for 70 years.

02:37:09.000 I've got a lot of evidence here that I didn't have time to cite, unfortunately.

02:37:13.000 Yeah, well, it was a long one, but thank you, gentlemen.

02:37:15.000 Thank you.

02:37:16.000 All right, thank you, Joe.

The Joe Rogan Experience - March 19, 2019

Joe Rogan Experience #1267 - Gary Taubes & Stephan Guyenet

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