Joe Rogan Experience #1267 - Gary Taubes & Stephan Guyenet

Joe Rogan 0:00 Four, three, two, one. (clearing throat) And we're live. All right, so to set this up, um, when Gary was on last, Gary Taubes? S- Stephan, how do I say your last name?

Stephan Guyenet 0:16 Stephan Guyenet.

Joe Rogan 0:17 Guyenet.

Stephan Guyenet 0:18 Yeah.

Joe Rogan 0:19 Guyenet.

Stephan Guyenet 0:19 It's like D-N-A.

Joe Rogan 0:20 Like D-N-A, but with a G.

Stephan Guyenet 0:22 Right.

Joe Rogan 0:22 Got it. Okay. Um, when you were on last, Stephan had, uh, some opposition to some of the things that you were saying. We talked about getting him on and you on together. We finally pulled it off. Took... There was a lot of wrangling, there was a lot of back and forth, and cat wrangling-

Stephan Guyenet 0:40 (laughs)

Joe Rogan 0:40 ... but we got it. We're here. Um, give me your position on... This is all for, for folks listening, this is all about obesity and the m- the mechanism for obesity. Is that fair to say?

Stephan Guyenet 0:54 Yeah, yeah. So essentially, uh, the main points that we wanna talk about today are-

Joe Rogan 0:59 Try to keep this a fist from your face.

Stephan Guyenet 1:00 Okay, sure.

Joe Rogan 1:01 Just pull-

Stephan Guyenet 1:01 So-

Joe Rogan 1:01 Just pull... You can move it around.

Stephan Guyenet 1:02 Um, what causes obesity and what causes insulin resistance, which is behind a lot of our, um, chronic diseases that are common in society.

Joe Rogan 1:11 And please, uh, give us your background.

Stephan Guyenet 1:14 Yeah, so I have a, a BS in biochemistry, a PhD in neuroscience. 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. Hopefully, we'll get a chance to talk about those today. And then I went on, um, to become a science consultant, science communicator, and write a book called The Hungry Brain that is, um, my attempt to explain for a non-specialist audience what, uh, what causes obesity. And, uh, yeah, so that's my background.

Joe Rogan 1:53 Now, what is your disagreement with Gary's position?

Stephan Guyenet 1:57 Everything. (laughs)

Joe Rogan 1:57 Everything?

Stephan Guyenet 1:58 Yeah, so, uh-

Joe Rogan 1:59 (laughs)

Stephan Guyenet 1:59 How about-

Joe Rogan 2:00 Ask Gary.

Stephan Guyenet 2:00 ... how about I just-

Joe Rogan 2:02 Mm-hmm, sure.

Stephan Guyenet 2:02 Can I start by explaining-

Joe Rogan 2:03 As... Please do.

Stephan Guyenet 2:04 ... what I believe-

Joe Rogan 2:05 Yeah.

Stephan Guyenet 2:05 ... cause obesity?

Joe Rogan 2:05 Yeah.

Stephan Guyenet 2:05 Okay, I'm gonna be long-winded here. Is that okay?

Joe Rogan 2:07 It's okay.

Stephan Guyenet 2:07 Okay.

Joe Rogan 2:07 Go right ahead.

Stephan Guyenet 2:08 All right.

Joe Rogan 2:08 We have hours.

Stephan Guyenet 2:09 (laughs) Okay, cool. So first, uh, a little bit of housekeeping. I'm gonna be citing a lot of evidence today, and so I want-

Joe Rogan 2:15 Just please bring this up to your face.

Stephan Guyenet 2:16 Okay, sure, sure.

Joe Rogan 2:17 Just move it around.

Stephan Guyenet 2:18 Sure, sure.

Joe Rogan 2:18 If you wanna sit back, just r-

Stephan Guyenet 2:19 How's that?

Joe Rogan 2:19 Yeah, you're perfect.

Stephan Guyenet 2:20 Okay.

Joe Rogan 2:20 Beautiful.

Stephan Guyenet 2:21 I'm gonna be citing a lot of evidence today, and I want people to be able to follow along at home, and so I've put many of the references that I'm gonna be citing on-

Joe Rogan 2:29 Just wanna do that, so it doesn't cover your face.

Stephan Guyenet 2:31 Okay.

Joe Rogan 2:32 There we go.

Stephan Guyenet 2:32 All right. I've put a lot of the references that I'm gonna be citing on my website, stefanguyenet.com, or if you don't feel like spelling my name, you can go to wholehealthsource.org, and I have a numbered list of topics there. And I'm gonna be calling out numbers. Just scroll down to the number that I referred to, and the references are all there. Second thing I wanna say, uh, that I wanna be really clear about today is that I'm not here to be the anti-low-carb guy.

Joe Rogan 3:01 Okay.

Stephan Guyenet 3:01 Um, I think low-carb diets are a valid tool for, uh, controlling body fatness and controlling blood sugar. I'm not here to talk anybody out of being on a low-carb diet. Um, what I am here to try to talk people out of is some of the mythology that has accumulated around the low-carb diet. Okay, so I wanna get started with an analogy to help people understand-

Joe Rogan 3:24 (clears throat)

Stephan Guyenet 3:24 ... um, why the brain is important in obesity. So imagine you're an alien coming down from outer space, and you wanna understand what's going on on Earth. And you notice that on the highway, some cars are traveling faster than others. Some cars go faster, some cars go slower, and you wanna figure out why. And so you go, and you start studying the tires of the cars, 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. We know this. This is just physics. 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.

Joe Rogan 4:03 (clears throat)

Stephan Guyenet 4:04 Now, why is that? The reason is that you're studying the wrong part of the system. If you wanna understand the, uh, 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. And so in this analogy, the tires are fat cells, and the person behind the wheel is the brain. There has been tons of research on fat cell biology, on what factors put fat in fat cells, what take it out. There's been tons and tons of research on that, and it's intuitively obvious that we should be studying that to understand obesity, right? But in fact, all of that research has yielded very little insight into why some people are fatter than others. That's because it's the wrong part of the system to study. Fat cells do not regulate the size of fat cells any more than the tires on a car regulate the s- the speed of the car. The thing that regulates the size of fat cells is the brain. So let's talk about, um... First, I'll give you a little framework for thinking about this. The brain evolved over about 600 million years to promote the survival and reproduction of our ancestors. And over the course of that time, we evolved all these different brain circuits that have specialized functions. They generate our hunger, and our cravings, and our fullness feelings. They generate our eating behavior, what and how much we eat, and they actively regulate the amount of fat on our bodies. And that's one of the things I wanna talk about. And all these circuits evolved, and these are non-conscious, by the way. So you don't decide you wanna be hungry. You don't decide that you wanna have a craving. These are things that bubble up from non-conscious parts of your brain that you don't control. So, um, these circuits are calibrated to an environment of our ancestors, not the environment we're li- we're living in right now. So these circuits all evolved to function optimally in the environment of our ancestors, prov- promote the survival and reproduction of our ancestors-So, um, 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 onto fat. And then what you see as a result is the three hallmarks of obesity. First of all, the obvious, you see elevated body fat mass. Second of all, you see elevated calorie intake. People with obesity consume more calories than people who do not have obesity after correcting for height and sex and physical activity level. And third, you see that people with obesity defend their higher level of body fatness against changes, and so there's actually a regulatory change that happens. It's not conscious defense, you know? They're not trying to remain obese. It's these body fat regulatory circuits, and this is where Gary gets it right, is that people with obesity are not just lean people who eat more calories. There's actually a change in the regulatory activity that regulates body fat in the body. And we can get back to how that happens, but I'll just leave it there for now. So up until this point, I've basically just been telling a plausible story, right? I mean, I haven't actually cited any evidence yet to support that my story is correct, um, and so let's get into that. Let's talk about what some of the evidence is that

Stephan Guyenet 7:34 supports this idea that I've just laid out. So I wanna start with, um, the genetics of obesity, and I think this offers some-

Gary Taubes 7:42 But can we... (clears throat) Can I interrupt for one second?

Stephan Guyenet 7:44 Uh, as long as it's very brief.

Gary Taubes 7:46 Just a question. I don't, I still don't quite understand what the model is.

Stephan Guyenet 7:50 Okay, how about, how about this?

Gary Taubes 7:51 I mean, I understand the dysregulation-

Stephan Guyenet 7:52 How about, how about-

Gary Taubes 7:52 ... of the brain with environment, but-

Stephan Guyenet 7:53 If, if you don't understand the model, how about I lay out... How about I finish laying it out, and then you can ask a question? Because I may answer your question over the course of, uh, continuing.

Gary Taubes 8:02 Okay.

Stephan Guyenet 8:02 So let me, let me just finish. Um, 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. So you get these studies, like, the, the, the most interesting studies are the genome-wide association studies. They get hundreds of thousands of people together, and they, um, sequence or they, they measure all these markers in their genomes, and they figure out what parts of the genome make some people fatter than others. So if you have version A in this particular location, you end up a little fatter than if you have version B. And when you look at all the places where this is happening, you can see the genes where it's happening in, and that tells you, if you look at what those genes are doing, that tells you what the mechanisms are that underlie everyday differences in body fatness in the general population. And so to kind of warm ourselves up, let's start talk, by talking about height genes. So height has a strong genetic component, so does body fatness. Um, and researchers has figured out a lot of the genes that underlie differences in height between people, 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? 'Cause growth of the skeleton determines your height. So genes that determine diabetes risk, type two diabetes, are all about insulin sensitivity, all about insulin secretion and the function of the, uh, insulin-secreting pancreas, which is what you expect because diabetes is a disease that is all about insulin. So these studies are really good at getting at the underlying biological mechanisms that are driving these phenomena. So what do these studies have to say about obesity? If Gary's model is correct, we should see a bunch of genes popping up related to fat cells and insulin. If my model is correct, we should see a bunch of genes popping up related to the brain. And in fact, that's exactly what we see. The genetics of obesity are overwhelmingly related to differences in brain activity between individuals. And, um, okay, so that's one piece of evidence. Another piece of evidence, there are five FDA-approved weight loss drugs. Four of those act in the brain. One of them reduces dietary fat absorption in the digestive tract. There are no effective fat loss drugs that I'm aware of that target insulin or fat cells. Third piece of evidence, um, 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. Some of these people end up with extreme obesity. People and also animals, we see this in mice and rats, just occasionally, you get unlucky, and you get really, really fat. And researchers have been cataloging, what are these mutations? When we find people who are genetically really obese, what are these mutations that are making them fat? What is the biological mechanism that's getting screwed up that's making them fat? 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, and this is... Leptin, um, is the primary fat-regulating hormone in the body. 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. And, um, so that's the third piece of evidence. Okay, 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. Um, we've

Stephan Guyenet 12:03 established that the brain is central to obesity, but we haven't really established what it is exactly about that interaction. Why does our modern food, why does our modern environment promote obesity, right? So, um...... basically, there are three different ways that I'm gonna look at this from. Um, but first I wanna say that the... Probably the best way to answer this question is to start with the question, what is the most fattening diet in the world? What is the diet that is more fattening than any others? And the answer to that is-

Joe Rogan 12:38 (clears throat)

Stephan Guyenet 12:38 ... it's human junk food. In a variety of non-human species and humans, it's human junk food that is more fattening than any others. And I'm gonna skip over some of the research here-

Joe Rogan 12:49 (clears throat)

Stephan Guyenet 12:49 ... um, that demonstrates this. By the way, I haven't been calling out numbers here. Okay, let me call out some numbers. Um, reference number two on my website is, um, those genetic studies, reference number one is the obesity drugs, reference number six is those spontaneously occurring genetic mutations, and now I'm talking about reference number 52. So, um, I'm gonna, I'm gonna gloss over some of the individual research 'cause I'm being long-winded here. But, um, essentially what you find is that this s- stuff is really fattening in animals, many different species, it's super fattening in humans, calorie dense. When you put, create an environment with abundant, easy, calorie-dense, tasty foods rich i- carbs and fat, you see this dramatic overconsumption in fat gain across many species, including humans. And what you find in the research is that the sugar and the carbohydrate cannot explain that. They're part of the effect. Yes, they explain part of it, but you cannot replicate that effect by only feeding sugar and carbohydrate.

Joe Rogan 14:01 (clears throat)

Stephan Guyenet 14:01 You can't replicate it in animals. You can't replicate it in humans.

Joe Rogan 14:05 Well, when you say you can't replicate it, you mean you can't replicate obesity? What do you mean?

Stephan Guyenet 14:09 Yeah, um, that's right. You cannot, you cannot cause the same degree of fat gain, the same extent of fat gain, the same extent of overconsumption using only sugar and carbohydrate that you can cause with a variety of calorie-dense, palatable human foods. You can't fully replicate it with sugar and carbs. You cannot fully replicate it with fat alone either. If you put those... And we can, we can get deeper in this if you want.

Joe Rogan 14:37 But I, I'm confused.

Stephan Guyenet 14:38 Yeah.

Joe Rogan 14:38 So, you're, you're saying that the, the diet that causes the most obesity is what we think, right? This, uh, human junk food diet-

Stephan Guyenet 14:46 Correct.

Joe Rogan 14:46 ... rich in sugar, simple carbs, bullshit, bullshit diet, right? Y- what are you... You're saying that you can't replicate that with just sugar and carbs?

Stephan Guyenet 14:56 You cannot fully replicate it.

Joe Rogan 14:57 Fully, in what sense?

Stephan Guyenet 14:57 So, it's... What I mean is that if you just feed... if you just increase sugar intake-

Joe Rogan 15:04 Right.

Stephan Guyenet 15:04 ... 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, palatable foods rich in carbohydrate and fat. Similarly, if you-

Joe Rogan 15:19 Tha- that's very confusing. So-

Stephan Guyenet 15:21 How's that?

Joe Rogan 15:22 Because I'm, I'm not sure exactly what you're saying. You're saying you... 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?

Stephan Guyenet 15:38 Um, so (clears throat) what I'm saying is that if you, if you give people or animals the, uh, the actual human junk food-

Joe Rogan 15:47 Right.

Stephan Guyenet 15:47 ... with all the carbs and fat and everything-

Joe Rogan 15:50 Mm-hmm.

Stephan Guyenet 15:50 ... 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. And what that shows is that the sugar and the refined carbohydrate cannot fully explain the effect, can't, like, fully explain why those foods are fattening.

Joe Rogan 16:07 See, this is where I'm confused.

Stephan Guyenet 16:08 You see what I'm saying?

Joe Rogan 16:08 No, I don't see what you're saying.

Stephan Guyenet 16:09 Okay.

Joe Rogan 16:09 'Cause you're, you're saying if you give people the diet of American junk food, you, you get not as much of a, an effect if you give them just the sugar and the carbohydrates?

Stephan Guyenet 16:22 Correct.

Joe Rogan 16:22 Is that what you're saying?

Stephan Guyenet 16:22 Yep.

Joe Rogan 16:23 So, but what are you giving them when you're giving them the ju- the diet of junk food? You're giving them sugar and carbs.

Stephan Guyenet 16:26 You can... Well, for example, in animals... No, it's different 'cause if you think about human junk foods, generally those foods contain fat and carbohydrate and salt-

Joe Rogan 16:36 Right.

Stephan Guyenet 16:36 ... and all kinds of other things. So it's more, it's more than just-

Joe Rogan 16:39 Well, it's a lot of soda, too, right?

Stephan Guyenet 16:41 ... carbs, right?

Joe Rogan 16:41 There's no sugar.

Stephan Guyenet 16:41 Yeah, so this-

Joe Rogan 16:42 It's just, uh-

Stephan Guyenet 16:42 And... Okay, so-

Joe Rogan 16:43 ... just sugar and that.

Stephan Guyenet 16:44 So I'll get in more detail. So the, the ways that you can do this, you can add sugar, just sugar, table sugar, to the feed of animals. That's one way to do it. Or you can add it to their drinking water. Sometimes it's a little bit fattening, sometimes it's not. It's not that fattening in animals. Um, in humans, you can ask them to drink sugar-sweetened beverages that are just sugar-

Joe Rogan 17:05 Mm-hmm.

Stephan Guyenet 17:06 ... and you can see what happens, and people will gain weight. Or you can tell them to stop drinking sugar-sweetened beverages and you can see what happens.

Joe Rogan 17:12 Okay.

Stephan Guyenet 17:12 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 the, this full palate of these foods that contain carbs and fat and all this other stuff. The-

Joe Rogan 17:27 So are you saying carb... Well, obviously there's more calories, right? If there's carbs and fat and all these other things?

Stephan Guyenet 17:32 Correct.

Joe Rogan 17:33 Right.

Stephan Guyenet 17:33 If you think that calories matter, then we agree.

Joe Rogan 17:36 Well, for sure it matters, right?

Stephan Guyenet 17:38 Uh, Gary doesn't think it matters.

Joe Rogan 17:39 (clears throat) You don't think it matters? Well, let, let's- I think it's the wrong way to think about it. What, what do you disagree, if anything, with what he said so far? Well, so far, what he said hasn't been particularly revelatory. Um, the, uh... I think we have to step back for a second 'cause, you know, while the low-carb community might have a more better understanding of where we disagree, um, I think the greater community (clears throat) that Joe Reaches might not. So fundamentally, what Stefan's saying and what the research community's saying and the conventional thinking in this field is that the brain... And correct me any point, I-

Gary Taubes 18:20 ... get this wrong, but the brain regulates- does the fundamental job of controlling how fat we are.

Stephan Guyenet 18:26 Yes.

Gary Taubes 18:26 And the way it does it is by controlling or miscontrolling our intake and our expenditure and the difference ends up in fat tissue. Is that fair to say?

Stephan Guyenet 18:38 Yep, for the most part.

Gary Taubes 18:39 Primarily intake, but yep. Yeah. So Stefan has a brain-centric view of the universe and the commu- community at large does as well. So if we go outside and we walk down, you know, Ventura Boulevard and we see someone who weighs 400 pounds, um, they've clearly taken in more calories than they should have over the course of their life and it's been stored in their fat tissue. And Stefan says... I think would say that the problem is in their brain's ability to regulate intake to expenditure. Is that correct?

Stephan Guyenet 19:15 Yeah.

Gary Taubes 19:16 Okay. And let me... I have to fix my headphones, so how are we gonna do this? I'm getting feedback when I talk.

Stephan Guyenet 19:24 You're getting feedback?

Gary Taubes 19:25 Yeah. It's just weird. Could be the... Hold on one sec. Ah, for those who don't know, I'm hearing impaired, as they say kindly. My kids would say deaf as a post.

Stephan Guyenet 19:36 (laughs) So better?

Gary Taubes 19:37 So I took off my hearing aids, and it's a little better. Okay, so what I've been arguing... So I come along... My background, I'm a journalist. I'm an investigative journalist with a science background, okay? That's what I do. And I'm curious, and I've got a lot of, you know, and I, I... My first two books were studying what's called pathological science, which is about people who got the wrong results in science, 'cause a lot of times scientists do. So my- I'm very sensitive to this, and as I was doing the research for my first book, which took five years, what I noticed in- when you take a historical perspective, is that the research community studying obesity was very focused on the brain. They just assumed that fat people are gluttons. And I'm gonna use some socially unacceptable, uh, language, 'cause in part that's how they thought about it. In fact, when you read the, uh, obesity literature from the '40s and '50s, 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, you know, they're... But it- but it was all brain centric.

Stephan Guyenet 20:46 Mm-hmm.

Gary Taubes 20:47 And when they got to the 1960s, the field was being run by psychologists and psychiatrists who were trying to get people with obesity to eat less. And my favorite example is one team that was trying to get the- they got the wives to stop having sex with the husbands if they didn't lose weight every week-

Stephan Guyenet 21:03 Hmm.

Gary Taubes 21:04 ... and that would motivate them. I think even you point out that sex is a greater motivator in your book than tasty foods.

Stephan Guyenet 21:11 (laughs) I didn't say-

Gary Taubes 21:12 It didn't work.

Stephan Guyenet 21:12 ... it was greater, but I said it was on par, yeah.

Gary Taubes 21:15 On par. So a- and I'm gonna just read you, uh... I won't read you that. The- so there was this... While the obesity research community is focusing on the brain, there were people studying fat metabolism. Uh, endocrinologists, they study hormones and hormone-related disorders, saying that the o- you know, fat storage and fat mobilization, the burning of fat in the human body is controlled by this very diverse set of hormones and enzymes, and the nervous system is involved in it well. And our body does a very careful job of deci- of basically orchestrating how we use fuels after we eat. 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. So today when you read the literature, the articles will often say obesity is a sort of energy imbalance. You take in more calories than they expend. There were still... The best scientists in the field, the best physician scientists, would say, "Look, obesity is a disorder of excess fat accumulation. Let's look at what regulates fat accumulation in the human body." Some people are programmed or dysregulated to store more fat and if they store more fat, they're gonna... their behavior is gonna respond. They'll be hungrier, they'll eat more, they'll be gluttons, all these things. So it was a switching the, the causality. Instead of the brain determining energy balance and that determining fat accumulation, the idea was, uh, sort of, "Let's see what regulates fat accumulation." If that's dysregulated, if I have a- if I give birth to a daughter who weighs 100 pounds at age four, I'm not gonna worry about how much she eats and exercises, I'm gonna worry about what's going on with fat accumulation and this young girl, that her body is... Just as if you give a- you know, if you have a, a child who's six foot eight when he's six years old, you're not gonna worry about how much he eats and exercises, you're gonna worry that he's over secreting growth hormone. 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, uh, fat metabolism researchers came to understand the regulation of fat cells, the obesity people were convinced that the problem was in the brain. 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. And when you look at that, you find a whole world of places in which people can pre- be predetermined, you know, be driven to be fat.

Stephan Guyenet 24:13 Mm-hmm.

Gary Taubes 24:14 So for example, when I was in high school, senior year in high school, I weighed 195 pounds and I played football.... and my brother, two years older, weighed 195 pounds his senior year and played football. My brother never got more than 195 pounds, and I went up to 240. We both ate as much as humanly possible, you know, as you could imagine.

Joe Rogan 24:38 Mm-hmm.

Gary Taubes 24:38 That's what high school athletes do. My brother was always lean. I was always chubby. My brother stayed lean and became an endurance athlete. I became a football player, and I lifted weights. I put on muscle easily, and I fattened easily. He didn't. Um, 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. My argument is our bodies were fundamentally different. So if I see somebody walking down the street who weighs 300 pounds, I don't worry about that. I don't think about what the problem is with her brain regulating intake and expenditure. I think about what's, why is her body driving her to be 300 pounds? So that's, I think, kind of the fundamental difference. Um, and is it, 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?

Joe Rogan 25:33 Yeah, is this a reductionist perspective? 'Cause I mean, i- i- isn't it a holis- 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 l- is seems-

Gary Taubes 25:45 I'm not saying it's separate.

Joe Rogan 25:46 Right.

Gary Taubes 25:46 The question is, is the brain driving what's happening in the body or is it responding to what's happening in the body?

Stephan Guyenet 25:51 Yeah, so-

Joe Rogan 25:51 Mm-hmm.

Stephan Guyenet 25:52 Um, 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. Um, but you know, I think it's... We can tell stories, but the things, the thing that differentiates a story that's true from a story that is not true is evidence. And so, you know, you talk about the difference between your brother and you, this is where that genetics evidence comes back in that I was talking about. Your brother and you only share half of your genes. We know that genetics has a strong impact on who has a greater susceptibility to body fatness than o- than others, and we also know what the genes do that underlie those differences.

Gary Taubes 26:32 No, no, w- wait, wait. Let me-

Stephan Guyenet 26:33 And they are primar- I'm not done, Gary. Let me finish.

Gary Taubes 26:35 I just wanna read something-

Stephan Guyenet 26:35 Those genes-

Gary Taubes 26:36 ... from your book.

Stephan Guyenet 26:36 Those genes-

Gary Taubes 26:37 Can I read something from it?

Stephan Guyenet 26:38 No, nope.

Gary Taubes 26:38 Okay.

Stephan Guyenet 26:38 Not right now. I'm, I'm in the middle of saying something. Those genes are, um, primarily related to differences in brain function. That is what the genetics say 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. That is what the research says.

Joe Rogan 27:01 But isn't that very difficult-

Stephan Guyenet 27:03 Okay. When you actually look at the research.

Joe Rogan 27:03 ... to parse out when you're talking about-

Gary Taubes 27:04 But-

Joe Rogan 27:04 ... two 17-year-olds that weigh exactly the same amount? Like how do we know how much they consumed in calories? I mean, we don't have any studies. We don't have any tests.

Gary Taubes 27:12 No, of course we don't, but I-

Stephan Guyenet 27:12 No, of course we don't, but-

Gary Taubes 27:12 ... I mean, I could guarantee you we both ate as much as humanly possible.

Joe Rogan 27:16 Right, but maybe you ate more.

Gary Taubes 27:16 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. He used to say that he never gets stuffed. He just gets bored of eating after a couple of hours. Okay?

Joe Rogan 27:29 Okay, but maybe-

Gary Taubes 27:30 I mean, that's s-

Joe Rogan 27:31 ... e- even though, like maybe if you looked at it scientifically, you ate more than him or maybe you ate more sugar-

Gary Taubes 27:36 Well, no, I clearly-

Joe Rogan 27:37 ... or maybe you ate more carbs.

Gary Taubes 27:38 Well, so that's the difference. So the, th- those are the two hypothesis.

Joe Rogan 27:41 Right.

Gary Taubes 27:41 One hypothesis is my body... And this is what Stephan has talked about. So I wanna... Just the thing I wanted to read, how much... I'll ask you the question. How much of the, the variation in human obesity do those genes explain?

Stephan Guyenet 27:56 So if you look at the genetics of-

Gary Taubes 27:59 No, I didn't ask how much g- is genetic.

Joe Rogan 28:01 Gary, I'm answering your question.

Stephan Guyenet 28:02 Look, once he starts talking-

Joe Rogan 28:03 You need to let me-

Stephan Guyenet 28:04 Yeah, please, Gary. Um, 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. 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. Now, we've only identified a small proportion of the specific genes that underlie the propensity to obesity. 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.

Gary Taubes 28:50 How much?

Stephan Guyenet 28:52 It's like, uh, right now, I think it's up to about 10%.

Gary Taubes 28:55 It was 3% when your book was published.

Stephan Guyenet 28:57 Yeah, that's correct.

Gary Taubes 28:58 So you're saying they did 7%?

Stephan Guyenet 28:59 Absolutely, yeah. The latest... Yeah, actually let me cite the, uh, the study there.

Gary Taubes 29:04 S- so, while, while Stephan s-

Stephan Guyenet 29:04 No, just a second. I'm gonna cite the study. Just a second. I'm gonna cite the study. Uh, the study is under reference number two. So you can, you can go check that out. It's about 10%. 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. 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. And so that tells us that primarily the differences between individuals that determine differences in body fatness is about differences in brain activity, and no one should be shocked about this. The brain generates all of our eating behavior. It generates all of our physical activity behavior, and it actually regulates body fatness. No one should be surprised by this.

Joe Rogan 29:57 I am.

Gary Taubes 29:58 And I was.

Joe Rogan 29:59 And how are you surprised? Do you-

Gary Taubes 30:00 Well, again, I-

Joe Rogan 30:00 What do you disagree with?

Gary Taubes 30:02 Well, virtually everything, but, um, let's begin with... I have to track back now. The, um, okay, so drugs that explain obesity, 10%. Well, the argument that I was making and the argument I continue to make, i- imagine if, you know, take Stephan's, uh, car metaphor.

Joe Rogan 30:22 You see Stephan, he says Stefan.

Gary Taubes 30:24 Okay, sorry.

Joe Rogan 30:24 You say Stefan, right?

Stephan Guyenet 30:25 It's okay.

Joe Rogan 30:25 Stefan.

Stephan Guyenet 30:25 I'm not offended.

Joe Rogan 30:26 That's okay.

Gary Taubes 30:26 But I mean-

Stephan Guyenet 30:27 I apologize.

Joe Rogan 30:27 Just so people-

Stephan Guyenet 30:28 Stefan.

Joe Rogan 30:28 ... don't get confused.

Stephan Guyenet 30:29 Thank you.

Gary Taubes 30:30 So the, uh-If you take Stefan's car analogy and somewhere in the 1970s ... I, I've used a car analogy for this too, but I, I don't think it's as appropriate. But one would think that somewhere in the 1970s, the aliens didn't notice that there were humans driving the car. So now they're trying to solve the problem without the humans involved. Why is it some cars drive faster than others? And they come up with all kinds of hypotheses, and some of them can explain that even when they interpret the hypotheses, one of the common problems in science is called intellectual phase lock. 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. 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 c- car problem if they never notice the humans. So, um, and leptin is a good example. So leptin is discovered in 1993, and when leptin is discovered, obesity becomes sort of a legitimate field of science. Until then, it's a bunch of actually mostly psychologists studying. And then now it becomes a subdiscipline in molecular biology, and all the molecular biologists jump into the field. And they assume that what leptin does is control the brain. Uh, it signals how much fat is available. It's, uh, some kind of satiety or fuel efficiency, um, hormone. And as such, they study the brain, and they study the action of leptin in the brain. Now in 2002, Jeff Friedman, who gets credit for discovering leptin, perhaps incorrectly (laughs) , um, publishes a paper in the journal Science. It's saying perhaps as much as two thirds or more of what leptin does is done in the periphery, in the body. And what leptin does, it's a hormone that sort of is, is secreted in response to how much fat you've accumulated. 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. So it makes perfect sense 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. So now you've got a hormone that could work in the periphery, in the br- in the, you know, below the neck, or it could work above the neck, but you've got a community that's almost exclusively studying in the head. They don't know there are human drivers down here, so that's what they do. So even in this world, the, the, I, I don't ... I think I know the genome paper, um, Stefan is probably referenced on his website.

Stephan Guyenet 33:28 There have been a number of them-

Gary Taubes 33:29 Stefan, excuse me.

Stephan Guyenet 33:29 ... but yeah. That's the most recent.

Gary Taubes 33:31 The Harvard group? Is it the-

Stephan Guyenet 33:33 I, I don't remember.

Gary Taubes 33:34 The ... So they had two papers 'cause it's what you cited in the article you co-authored with Rudy Leibel. So they have two papers. One is genes associated with obesity, and one is genes associated with body type. So with body type, they're all below the neck. They're all, you know, fat metabolism basically, and the musc- you know, the genes that ... 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. I don't think your brain is regulating how much muscle you're building other than your drive to go to the gym. Basically, your body is responding to the stress on the muscle, all the things you do and the weightlifting, it's all below the neck. So the argument here is again, simple. When these people looked at body type, it was insulin regulated genes for the most part, growth hormone, all these things. When they looked at excess body fat, they decided they were in the head. 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. Did they do the same kind ... And I was gonna call the researcher involved, 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 f- variations of body shape are gonna be determined by the same genes? And did you d- do the same kind of searches? I don't actually know how they determine where the genes work.

Stephan Guyenet 35:06 It's the same kind of searches, they just came up with different sets of genes. So they didn't start with any assumptions, they were just finding whatever was there.

Gary Taubes 35:13 No, but the question is where the genes work. So there's a common phenomenon on all this, like with leptin, a gene that everybody thinks about working in the hypothalamus-

Stephan Guyenet 35:21 Yeah.

Gary Taubes 35:21 ... seems to work in every cell in the body.

Stephan Guyenet 35:23 Can I, can I respond to that and since you get to-

Gary Taubes 35:24 Wait, let me finish talking.

Stephan Guyenet 35:25 Okay, fine. No, go ahead.

Gary Taubes 35:25 'Cause you say this in your book. You say this in your book.

Stephan Guyenet 35:27 Yeah, go ahead. I'm prepared to respond whenever you're done.

Gary Taubes 35:30 Okay. In your book you say that genes work ... You know, the body is very ... Basically it puts, uh, different mechanisms to work as many places as they can, and there are these homeostatic feedback loops, you know. Something happens, your whole body has to respond. So a gene that might work primarily on one cell is scattered all over the body 'cause every cell ... And it'll do different jobs on different cells. But if you think that the problem's in the brain, that's where you look. So you get this kind of intellectual phase lock where that's what we do, that's what we study. A neurobiologist studies the brain. Uh, uh, Daniel Kahneman, I ... Ste- Stefan likes to cite Daniel Kahneman as well, had this concept, what you see is all ... He's a Nobel Laureate, uh, cognitive psychologist. What you see is all there is, okay? And basically if you're studying the brain, that's what you look at. If you're studying the gut ... And so we all get trapped into that on some extent, and what I'm saying is even in these studies ... So-... Stephon-- Stephan wrote a book about the hungry brain that is supposed to be about obesity, but in fact you never mention anything about the metabolic regulation of fat accumulation.

Stephan Guyenet 36:47 (laughs)

Gary Taubes 36:47 It's just not there. And I would argue it has to be there, even if it's wrong. 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. You can't talk, you know, so there's a, a... And it's put me in a very odd position. 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. You screwed up. You had psychologists and psychiatrists running the field when the endocrinologists solved it, and then you discovered leptin and it became a molecular biology problem. And you're now divorced from the very simplest observations about obesity." You know? So we can do huge genome-wide association studies. They sound remarkable. But if I were to ask a simple question like, "Why is it I get fat here?"

Stephan Guyenet 37:41 (laughs)

Gary Taubes 37:41 You know, the love handle thing?

Stephan Guyenet 37:42 Mm-hmm.

Gary Taubes 37:42 It's in the back with me. I don't... It's not in the front. But it's here, and not here. I don't see what the brain has to say about that.

Stephan Guyenet 37:51 Yeah. Um, okay, so as you mentioned, there have been different genetic studies that have looked at body fat distribution versus total body fatness. So total body fatness is what we're talking about when we're talking about obesity. Uh, body fat distribution is what we're talking about when we're talking about the fat being on your hips versus on your wrists. Now, what we see is different sets of genes that come up. So body fat distribution, we actually see insulin res- uh, related genes. 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. 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. And the really cool thing out... point I wanna make about the genetics research is that-

Gary Taubes 38:41 10% of those genes might be dominated-

Stephan Guyenet 38:43 It's, it's-

Gary Taubes 38:43 ... by the brain. If they looked.

Stephan Guyenet 38:45 Uh, come on, Gary. It, it is unbiased. That's the really cool thing about it, is that they're just... This is whatever genes are popping up. These studies do not care about what you believe about what causes obesity. This is just whatever genes are popping up, so it's unbiased.

Gary Taubes 39:01 Okay.

Stephan Guyenet 39:01 And that's what they're saying. And, and I'm not done here, Gary. Now, I wanna talk about, um, you mentioned, Gary, that maybe leptin is having important actions not just in the brain, but in the body. First of all, I'm glad... I'm flattered that you read my book, and I'm glad that you acknowledge the existence of leptin now. This is good. Um, but now, you say that researchers 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. The real reason (laughs) we focus on leptin action in the brain is because it has been demonstrated that its effect on body fatness are via the brain. There are actual experiments demonstrating this, and I'll explain how these experiments work. This is all in the scientific literature. So if you knock out the leptin receptor only in the brain or only in the hypothalamus, you get obesity. So that is what tells us that actually the brain is the key site of action, particularly this part of the brain-

Gary Taubes 40:12 It, it tells you, it tells you the brain has any-

Stephan Guyenet 40:13 called hypothalamus- Any, any-

Joe Rogan 40:13 Gary, Gary, Gary, Gary, Gary, Gary, let-

Gary Taubes 40:15 ... any key site of action.

Joe Rogan 40:16 Please let him talk. He let you talk.

Stephan Guyenet 40:18 Yeah, and that's it. 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. So that shows that the brain is the site of action that is causing this to happen. And this is no surprise. We have these mechanisms worked out. We know specific groups of neurons that are receiving the leptin, that are controlling our appetite, that are controlling our metabolic rate. We have many of these neural populations worked out. In mice, we understand these systems so well y- we can control specific populat- 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. I mean, that's the level of understanding we have right now of how these systems work. 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. I mean, Gary, if you wanna cite specific evidence demonstrating that that is an actual cause of differences in body fatness between individuals in 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.

Joe Rogan 41:33 Can I, can I pause here?

Stephan Guyenet 41:34 Yeah.

Joe Rogan 41:34 Um, leptin is produced where?

Stephan Guyenet 41:36 Yeah, leptin is produced... Yeah, let's talk about leptin a little bit. It's produced in fat cells, um, and it's produced in proportion to the size of fat tissue. So the amount of body fat you have, the more fat you have, the more leptin you have in the circulation. And basically what this is, it's what's called a negative feedback loop, um, which is a really simple engineering term that works like a thermostat. So with your thermostat, you, uh, if you set your thermostat to 70, if it starts getting a little bit hotter, your AC turns on to bring it back down. If it starts getting lower, AC comes on, or the heat comes on to bring it up. That's called a negative feedback system, and it maintains the stability of the temperature of your house. We have many negative feedback loops in the human body to regulate body temperature, to regulate blood pressure, to regulate all sorts of things. One of the negative feedback loops we have regulates body fatness. And the hormone... So your, your thermostat measures temperature by using a thermostat, uh, sorry, a thermometer.... your brain measures body fatness using this hormone leptin that's in the circulation. And then, particularly when your body fat level drops, your leptin levels drop, and your brain hears that and it kicks in a starvation response basically. And this is the main reason why weight loss is so difficult, 'cause your brain is like, "No, I don't wanna be losing fat." And it makes you hungrier. It increases your cravings-

Joe Rogan 43:05 Can I pause there?

Stephan Guyenet 43:05 Yeah. Sure.

Joe Rogan 43:05 Is that, is that at a certain level of body fat? Is that at a s-

Stephan Guyenet 43:08 Um, so here's the-

Joe Rogan 43:09 Is this just when you're losing body fat in general, like even if you're-

Stephan Guyenet 43:11 Yeah.

Joe Rogan 43:11 ... a large person that's overweight?

Stephan Guyenet 43:13 Correct.

Joe Rogan 43:13 When you're losing body fat in general, your body, it- it exacerbates-

Stephan Guyenet 43:17 Yeah.

Joe Rogan 43:17 ... your hunger?

Stephan Guyenet 43:18 And this is, this is the thing that's really important to understand about obesity, um, is that people with obesity have a higher set point. So it's like turning your thermostat from 70 to 80, and then your thermostat's regulating around 80. People with obesity, they're not regulating around 170 anymore. They're regulating around 250.

Joe Rogan 43:37 Mm.

Stephan Guyenet 43:37 And so when you cause a lean person to lose weight, you see the same thing as when you cause a person with obesity to lose weight. You see this reaction in their brain circuits that regulate body fatness that drives them to increase their cravings and their hunger-

Joe Rogan 43:53 So it'd be-

Stephan Guyenet 43:53 ... and their metabolic rate drops.

Joe Rogan 43:55 So it'd be an evolutionary mechanism to force you to seek food.

Stephan Guyenet 43:58 Correct. And not just to force you to seek food. That's the main thing, but it also slows your metabolic rate.

Joe Rogan 44:03 Mm.

Stephan Guyenet 44:04 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.

Joe Rogan 44:10 Can I pause here?

Stephan Guyenet 44:11 Yeah.

Joe Rogan 44:11 So when you're eating a sugary diet, a high, a high-calorie diet, you will produce more fat. Your body will get fatter, right? Is this correct?

Stephan Guyenet 44:20 Um, it depends on how many calories you're eating.

Joe Rogan 44:22 Okay. If you're overeating, you're-

Stephan Guyenet 44:23 Yeah.

Joe Rogan 44:24 ... you're consuming a lot of sugar, a lot of carbohydrates, your body will get fatter.

Stephan Guyenet 44:27 Correct.

Joe Rogan 44:27 So your body will produce more leptin.

Stephan Guyenet 44:29 Correct.

Joe Rogan 44:29 So it comes from the diet.

Stephan Guyenet 44:32 Um, yeah, indirectly. Definitely, yeah.

Gary Taubes 44:33 Can I-

Joe Rogan 44:34 Yeah.

Gary Taubes 44:34 ... pause?

Joe Rogan 44:35 Please.

Gary Taubes 44:35 Uh, so the leptin is produced not just in response to the size of the fat cell, but in response to actually glucose (clears throat) mediated uptake into the fat cell, which is mediated in part by insulin. So you come back to insulin even with the leptin. You raise blood sugar, and that's the carbs. You eat the carbs, you raise blood sugar, you raise insulin, you raise fat storage, the glucose, and then you get more leptin. Um, again, one of the things you have to understand about this is everything that's said has two interpretations depending on which paradigm you're looking at. And these are fundamentally different paradigms. So in Stefan's world, and again correct me if I'm wrong, the leptin is signaling fuel availability in the fat cells the way I would think of it in, in my very small world. Leptin is responding to fuel availability in the rest of the cells. So it's basically a molecule that can tell other cells that there's fat available, and you could burn that fat for fuel and then you don't have to go eat. Or it can tell that there isn't fuel available, and if, 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. Um, everything we're talking about... When Stefan and I first sort of fell out, I don't know, eight years ago, at, um, uh, Ancestral Health Symposium when I acted improperly, inappropriately.

Gary Taubes 46:06 But one of the problems I... So the way I think you should think about this, you have a hypothesis, and, and this is the fundamental thing. Is obesity caused by overeating? 'Cause we know if you're getting fatter, you're storing more calories in your expend. That's just the, you know, that's like if a room is getting more crowded, more people are entering than leaving. That is the simplest... But it doesn't tell you why the room's getting crowded. It doesn't tell you why the f- you're getting fatter. And again, what I've been arguing is the why you're getting fatter part has been left out, and people decided that overeating was somehow an explanation. And then they went to the brain to look at why people might overeat. So what I... One of the questions I asked Stefan eight years ago, and it keeps coming up, is if we're gonna blame obesity on the modern food environment, epidemics of obesity, you know, a simple question to ask is, can we find epidemics of obesity without this modern food environment? I mean, that's a sort of Science 101, right?

Joe Rogan 47:07 Mm-hmm.

Gary Taubes 47:08 And it turns out that the world is full. And the first one I found in the literature was in 1902 in a population of the Pima, Native American tribe the Pima living in Arizona. And observers saying these people are poor, they're malnourished, they're suffering through famines. They'd been suffering through a famine for 40 years. And famines, it's hard to overeat during a famine. And yet, the women of the tribe, who do virtually all the work, uh, they were treated as pack animals in effect, were obese. So now we can disassociate obesity from the modern food environment, and we could disassociate it from, uh, this ultra-processed foods we eat and start to ask the question, what is it about... Can we find what might have driven obesity in that population despite the existence of famine? So it's from very simple observation. Once we get into these kind of studies say this and human genome studies say that, um, I actually rarely do that in my books because you can find studies that will say anything.

Joe Rogan 48:13 (laughs)

Gary Taubes 48:14 And you'll see in the studies, um, people misinterpreting them.

Joe Rogan 48:20 What was the cause of the population of women to be o- obese in this?

Gary Taubes 48:23 Well, so one thing that happened during the fa- beginning in the 1860s, the Pima were put on a reserv- well, they moved onto a reserv- they were reservationized, whatever the verb form would be, and they began eating Western foods. And back then, it was sugar, flour, and lard for the most part and sugary beverages probably. So that's a reasonable hypothesis-And you could find the same thing in the Sioux, Native American Sioux population living on a reservation in 1928, where you had, uh, o- both obese men and women living with malnourished, stunted children who clearly weren't getting enough diet, but they were on a reservation, they were getting Western foods. So ultimately, y- you know, the question you ask in science determines the answer you get. So, the question I was asking is we have this observation that any population that transitions to Western diet or Western diet and lifestyle gets obese and diabetic. They, they develop what's called metabolic syndrome, which is insulin resistance and all these issues. And we know that's true all over the world, from the Inuit to the Pima to South Pacific Islanders to Africans to Europeans. So, the genetics aren't that important. The question is, what's triggering it in the environment? And again, Stefan would say, "Well, there's too much food available, and it's too palatable, and we can't say no." And I have a lot of problems with the "we can't say no" part, 'cause if we're lean, it means they can't say no, and they being the people with obesity, and I don't believe that's true. And then, or is it some specific item or some specific group in this, these foods that travel with Western populations? And so, the exist- the ability ... And today, if you look up, uh, dual burden of obesity and malnutrition, I have a Dropbox folder I could share with you, there's probably 50 studies all over the world you see the same observation. Incredibly poor populations, malnourished, the children are stunted, which means they're protein deficient and they're calorie deficient. And often, the mothers or the aunts are obese. See, 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 'cause we're dealing with populations that could not have overeaten. If they could have overeaten, why are the kids starving? That's sort of the question. And, you know, and this was the first thing that I think we thought about back then, and it's still, if you can find populations with, uh, obesity epidemics, but without the modern food system, without Snackwell's and without Lay's potato chips-

Joe Rogan 51:09 Mm-hmm.

Gary Taubes 51:11 ... um, and if you know that they're going through a famine or you know that the kids at least aren't getting enough food,-

Joe Rogan 51:17 Mm-hmm.

Gary Taubes 51:17 ... how do you explain obesity in the mothers without assuming that the mothers are overeating?

Joe Rogan 51:22 L- let's pause right there. Y- Stefan, is there a population of people that are obese that are not eating a Western diet, that are not eating sugary foods?

Stephan Guyenet 51:33 Um, that are obese and that are not eating sugary foods, probably not, because generally, once you have an industrialized food system, that's gonna include sugar. But there are populations that eat a lot of sugar and are not obese, and we should talk about some of these. Actually, let's-

Gary Taubes 51:51 Oh, can you-

Joe Rogan 51:51 ... let's talk about the Pima first.

Gary Taubes 51:51 ... can you go back to the ... Yeah, okay.

Stephan Guyenet 51:53 Yeah, sure. Let's talk about the Pima first. Um, now, Gary has told a story. He's told his version of the Pima story. Let me tell the story, the version of the story that appears in the scientific literature. Now, the Pima, um, originally the, they were agriculturalists. They were eating traditionally a very high carbohydrate diet based on unrefined carbohydrates. Originally, it was corn, beans, and squash primarily.

Gary Taubes 52:19 They were hunter-gatherers-

Stephan Guyenet 52:20 Um-

Gary Taubes 52:20 ... and agriculturalists.

Joe Rogan 52:21 They were hunters-

Stephan Guyenet 52:21 They were primarily ... Gary, okay.

Gary Taubes 52:24 Go ahead.

Stephan Guyenet 52:24 They were primarily eating agricultural foods. They were also collecting some wild foods. That's correct. Um, they were fishing and eating mesquite pods, primarily agricultural. And, um, data are very clear on that, Gary. So-

Gary Taubes 52:40 No, no, no, n- yeah.

Joe Rogan 52:41 (laughs)

Stephan Guyenet 52:41 Yes, they are. Uh, look, we have data-

Gary Taubes 52:43 We, we can't say things like that, Stefan-

Stephan Guyenet 52:45 (laughs)

Gary Taubes 52:45 ... 'cause we're gonna disagree-

Stephan Guyenet 52:46 All right, well, let's-

Gary Taubes 52:47 ... on what the data say, okay?

Stephan Guyenet 52:47 ... let's, let's move on. You think they ate mostly fish. That's incorrect, okay?

Gary Taubes 52:50 I didn't s-

Stephan Guyenet 52:50 According to the data. That's, I, I remember you saying that in your book, something to that effect.

Gary Taubes 52:55 S- Stefan, read what ... You've got my book. Read what I say.

Stephan Guyenet 52:57 Okay. Anyway-

Gary Taubes 52:58 Just, just read what I say.

Stephan Guyenet 52:59 Let's, let's go on.

Gary Taubes 52:59 That's ... We don't have to argue about it.

Stephan Guyenet 53:00 Let's go on.

Gary Taubes 53:00 Read what I say.

Stephan Guyenet 53:01 Nope, I'm gonna move on here. Um, now, the Pima traditionally were agriculturalists. And what ha- what happened basically is you had all these farmers moving into their area, settlers, uh, of European descent, and they diverted the water from their river, the Gila or Gila River. I forgot how you pronounce it.

Gary Taubes 53:21 Yeah.

Stephan Guyenet 53:21 Gila. And so, they were no longer able to grow their crops, their agricultural crops, that they were primarily dependent on, and therefore, the government started providing them with foods to eat. And these were calorie-dense, refined foods. They were, like Gary said, uh, flour, lard, and sugar. And then they became very obese.

Gary Taubes 53:42 They were.

Stephan Guyenet 53:43 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, um, ones across the border with their traditional lifestyle are a lot leaner and healthier, n- not surprisingly, than the ones eating lard, flour, and sugar, okay? But Gary, uh, you seem to believe that people can gain weight. You kept referring to famines and things. You seem to believe that people can gain weight even if they are (door creaks) eating very few calories.

Gary Taubes 54:20 Yeah.

Stephan Guyenet 54:20 And you refer to this many times in your writing. Um, and, you know, these are very casual observations that you're making, kind of these casual correlations and storytelling. But if you actually look at the data on this, what you see is that if you just measure calorie intake in people who have obesity, it is 20 to 35% higher than people who are lean.

Gary Taubes 54:46 Okay.

Stephan Guyenet 54:47 ... after correcting for height, physical activity level. Um, and that, I've got the references-

Gary Taubes 54:51 Can I-

Stephan Guyenet 54:52 ... there.

Gary Taubes 54:52 Can I... No, no.

Stephan Guyenet 54:52 No?

Gary Taubes 54:53 Just tell me-

Stephan Guyenet 54:53 This is what we're getting... We're getting a little bit into the weeds here.

54:56 Um, seven.

Gary Taubes 54:56 Let me give you an example.

Stephan Guyenet 54:57 Reference number seven.

54:58 Can I pa- Can I pause you guys right here?

54:59 Yeah.

54:59 So these people, they, they have e- essentially, um, the same lineage. One group lives in Mexico. They, they're not eating these sugary foods and this, uh, Western diet. The ones that live in America are. The ones that live in America are becoming obese. The ones that live in Mexico are not. Is that correct?

55:16 Correct, yeah. And so now, if you have someone with obesity, like I've said, the, the most accurate measures that we have suggest that they habitually consume and expend more calories, and now Gary's model says that that is downstream of the fattening effect. It's not causing the fattening effect, it is a result of the fattening effect. Whereas my model says that that is actually required for the fattening effect to occur, it is upstream. Now what happens-

Gary Taubes 55:45 So how did those people-

Stephan Guyenet 55:45 What happens, Gary-

Gary Taubes 55:46 ... get fat?

Stephan Guyenet 55:47 What happens if you reduce their calorie intake by that same amount, 20 to 35%? It doesn't matter if you do it by restricting carbs or fat, these experiments have been done. They lose weight when you restrict their calorie intake down to that-

56:03 So this is the argument-

56:04 ... of a lean person.

56:04 ... what you're saying, that you c- consuming low amounts of calories, but high amounts of sugar does- doesn't make sense, you can get obese that way.

56:13 Um, right.

56:13 So you're saying it's a calorie-dependent-

56:15 Yeah, correct, and that's reference number nine and 10, um, to support what I just said. And I wanna talk about another one that really-

Gary Taubes 56:20 Wait, wait. Can we... Hold on, Stefan.

Stephan Guyenet 56:22 Yeah, yeah. Let's, let's keep going.

56:22 You didn't...

Gary Taubes 56:23 But I, the reason I was using the dual-burden example is because we have to explain how those women were eating all those calories. Usually women, again, it's just ... Often it was, inter- 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. Um, to give you an example where that measurement was done, um, in Trinidad in the 1960s, and again all I'm doing, this is the role I played, is I asked the question, "Can you find populations that don't have a lot of food?" Okay, you could say that the obese expend a lot of energy and they eat a lot of calories. The question is can they get obese without a lot of food, and so can we find populations? Like you asked, can you find a population that gets obese without sugar? Which was exactly the question to ask. So in Trinidad in the 1960s there's a malnutrition crisis. The US government sends a team of researchers down to study this, and the researchers come back and say, "Yeah, there's malnutrition, there's stunting, there's deficiency diseases, and two-thirds of the adult women are obese." And this is a medical problem. And the next year an MIT nutritionist goes down to do exactly what Stefan asked for and to actually measure the diets in obese women and lean women, and to study it. And this is a population where there's... It's unlike... I mean this is a very poor Trinidadian population and reports that they, I think it was 1800 calories a day, what the obese women were eating was actually a little less than what the lean people seemed to be eating and that it was lower than what the Food and Agriculture Organization considered for a healthy diet. So again, what my role in this is to point out when you have populations like that, I don't see how the overeating hypothesis tells me the brain is in control of how much they eat, tells me anything about why the women were obese, especially when their kids were starving. Hmm.

Stephan Guyenet 58:14 This is the paradox of this dual burden, an obese mother with a starving child. If the obese mother has to eat superfluous calories to get fat, why isn't she giving those calories to her kids? Because she doesn't need them. She clearly doesn't need them. She's got fuel. So what's going on there? If you posit a hypothesis, as I did, which says that the obesity is triggered by the macronutrient content of the diet, then you can explain... I mean there are plenty of animal models. A famous quote I use in my book from Jean Mayer, it was like the fame- leading Harvard nutritionist who studied an obese strain of animals in the '50s. He said, "My animals will get fat even when half starved. They will make fat out of their food even when half starved."

59:01 These are generally animals with mutations in the leptin, um-

59:04 It doesn't... Whatever gene it is-

59:05 ... pathway, by the way.

59:06 Whatever gene it is, it's kind of-

59:08 Let's-

59:08 The question is, if, like, I can make fat out of my food at levels of... at caloric levels that, for instance, a lean person can't, then I'm gonna get fat eating the same amount. And that fat accumulation is going to be, you know, means I'm taking in more calories than I expend. But the point is, I'm, for some metabolic hormonal reason, I'm taking the fuel I eat and turning it into fat and storing it in the fat tissue.

59:37 What is your response to this?

59:38 Yeah. So my response is that if you want the best answers, you have to use the best methods to answer, to answer the questions. Okay? If you want a question answered properly, you have to use accurate methods to answer that question. Now, as you know, Gary, it's very difficult to measure food intake in free living individuals, particularly you're traveling to a country you've never been to before. It's very difficult to get accurate measures. So just because some guy went to Trinidad and claimed- It was a woman actually.

1:00:08 Okay, fine.

1:00:09 She didn't-

Gary Taubes 1:00:09 (laughs)

Stephan Guyenet 1:00:09 Just because some woman went to Trinidad and claimed that people were eating 1800 calories and becoming obese does not mean that that's what actually happened. Now-

Gary Taubes 1:00:18 But let me-

Stephan Guyenet 1:00:18 No, no, no, no. Gary, I'm responding. Now, we have studies where researchers used accurate measures to measure calorie intake in people who had obesity. Many of these people were saying, "We're only eating 1200 calories a day." When they actually measured their calorie intake, what they found was that they were consistently eating more calories than lean people. So this, this phenomenon that Gary describes is something that is only observed when inferior methods are used-

Gary Taubes 1:00:52 Well, wait, wait.

Stephan Guyenet 1:00:52 ... to measure calorie intake.

Gary Taubes 1:00:53 Wait. Stefan, the, the reason I'm using these populations-... like I said, I'm just giving you an observation. Obese mother with a starving child, the dual burden of malnutrition/obesity, this isn't one observation, it's not one nutritionist. The existence of the starving children strongly suggests that there's not a lot of food available, and we have to explain obesity in the mother.

Stephan Guyenet 1:01:17 You know, I-

Gary Taubes 1:01:18 That's what I would like you to respond to.

Stephan Guyenet 1:01:19 Okay, fine. I will respond to that. Now, look, I haven't looked at these studies in particular.

Gary Taubes 1:01:24 I brought them up eight years ago.

Stephan Guyenet 1:01:25 Oh. (laughs)

Gary Taubes 1:01:25 We got in a fight about it.

Stephan Guyenet 1:01:26 Wonderful. (laughs)

Gary Taubes 1:01:27 We fell out eight years ago.

Stephan Guyenet 1:01:28 Okay. (laughs)

Gary Taubes 1:01:28 It ruined our, you know, it's like our... we used to be buddies.

Stephan Guyenet 1:01:31 Um, so now, (laughs) look, um, there are many reasons why a child could be malnourished in a non-industrial situation. And this is... I do a lot of work related to this. What you see in non-industrial situations, you see a lot of infectious disease, you see a lot of, um, malnutrition, so people not getting enough essential minerals and vitamins, not getting enough protein. And you see a lot of children who are just barely hanging on because of this collection of really bad stuff that's happening in their lives. And so-

Joe Rogan 1:02:03 Parasites, things along those lines?

Stephan Guyenet 1:02:05 Yeah, yeah, parasites, malaria. I don't know if there's malaria in Trinidad or not, but I mean, all the... diarrhea, pneumonia. These are the things that we all had before we had modern medicine and great sanitation in a country like the United States. 30% of kids didn't even make it past childhood. And so there's a lot of things that could have caused that, Gary. It's not necessarily because, you know... it's not necessarily the reason that you attribute it to. Now-

Gary Taubes 1:02:32 I'm not attributing it to a reason, I'm just asking for explanations.

Stephan Guyenet 1:02:36 Okay. Well, great. Well, I, I don't have an... the explanation, but I'm throwing out possibilities that are alternative to the one that you're implying.

Gary Taubes 1:02:43 And that's quite possible, too.

Stephan Guyenet 1:02:44 Okay. So now, um, I... so again, when you use accurate measures of calorie intake, you find that these people with magical metabolisms who have obesity and don't eat very much seem to not exist anymore. Um, and furthermore, I wanna, I wanna get this to another type of study that's really gonna differentiate between this metabolic effect driven by insulin and the effect of calories. So, we have a lot of studies that compared

Stephan Guyenet 1:03:14 diets in which calories were the same, but carbohydrate and fat intake differed. And the ones that I really wanna focus on right now that I think are key here are the studies where they increased calorie intake. So they fed people, they, they f... one study in particular, and, um, let's see, I'm gonna give you a number here. Um, let me see if I can give you a number here. Sorry.

Gary Taubes 1:03:41 While you look at that, um, can we, uh, bring up another issue? 'Cause what we're talking about ultimately is why people get fat.

Stephan Guyenet 1:03:48 Okay, I, I don't, I don't wanna divert here. I'm in the middle of something. So, um, now if we wanna understand why people get fat, we can look at studies that overfed people on fat or carbohydrate exclusively. So there's one study, um, the first one that I wanna talk about, first they figured out peoples' baseline calorie intake, figure out wh- how many calories they needed just to maintain, and then they increased that by 50% by exclusively giving them fat or exclusively giving them carbohydrate, okay?

Gary Taubes 1:04:21 Which study was this?

Stephan Guyenet 1:04:22 This is Horton.

Gary Taubes 1:04:23 Okay.

Stephan Guyenet 1:04:24 Um, and-

Gary Taubes 1:04:25 Give me a sec, and when you're done-

Stephan Guyenet 1:04:25 Yeah, so number 16, number 16. So, um, now if Gary's hypothesis is correct, these people should have gained body fat on the carbohydrate overfeeding, but not the fat overfeeding, because that increases your insulin and has these effects on your fat cells, et cetera. Okay? Now, these were very rigorous studies. I wanna emphasize that.

Joe Rogan 1:04:46 Can I pause here?

Stephan Guyenet 1:04:47 Yeah.

Joe Rogan 1:04:47 Did they monitor the, the actual calories they got?

Stephan Guyenet 1:04:51 Correct, yeah. So they were-

Joe Rogan 1:04:52 So, they-

Stephan Guyenet 1:04:52 They were... go ahead.

Joe Rogan 1:04:53 They, they had a baseline?

Stephan Guyenet 1:04:54 Yeah.

Gary Taubes 1:04:54 They used prisoners-

Joe Rogan 1:04:55 But they-

Gary Taubes 1:04:55 ... in the Vermont State Prison.

Stephan Guyenet 1:04:57 Uh, no that's incorrect.

Joe Rogan 1:04:58 But hold on sec-

Stephan Guyenet 1:04:58 This is a different study.

Joe Rogan 1:04:59 So they, they had a baseline, and did they require them to maintain the same diet and then add additional fat or additional carbohydrates?

Stephan Guyenet 1:05:07 Yes.

Joe Rogan 1:05:08 Yeah.

Stephan Guyenet 1:05:08 So same diet-

Joe Rogan 1:05:09 So they studied the same foods?

Stephan Guyenet 1:05:10 ... and then they just bumped it up with fat or bumped it-

Gary Taubes 1:05:12 Wait, wait, wait.

Stephan Guyenet 1:05:12 ... up with carbohydrate.

Gary Taubes 1:05:13 Which study did Horton ... It wasn't Sims. It was Ethan Sims. Well, which study did he do?

Joe Rogan 1:05:17 You talking to my, please?

Gary Taubes 1:05:18 Which study did he do that was not prisoners? What was the, uh... he didn't have a metabolic war.

Stephan Guyenet 1:05:22 You know what? Let me just finish describing this study. We can-

Gary Taubes 1:05:24 No, I'm just saying-

Stephan Guyenet 1:05:25 No. Gary, that's an irrelevant detail, okay?

Gary Taubes 1:05:27 But, uh, what's relevant is that you just in- implied that I don't know-

Stephan Guyenet 1:05:31 Gary.

Gary Taubes 1:05:31 ... what I'm talking about.

Stephan Guyenet 1:05:32 Gary, I... you know what? I, I don't actually know. Maybe it was in prisons, okay?

Gary Taubes 1:05:37 Thank you.

Stephan Guyenet 1:05:37 All right. You're welcome. Now, um, but it was not the Sims overfeeding study that was done in prisons. That's what I know, okay?

Gary Taubes 1:05:45 Okay. The reference-

Stephan Guyenet 1:05:47 So-

Gary Taubes 1:05:47 What's the reference?

Stephan Guyenet 1:05:47 Um, yeah, it's on my website. You can go to my website, uh, stephanguenet.com, and it's reference number 16, and they're both there. Okay, so this was a, what's called a metabolic ward study where these people were in a research facility where the researchers could monitor and control every morsel of food. So there was no cheating, no inaccuracy, and they were measuring changes in body fatness using a gold standard method called underwater weighing, okay? And so what they found was that at the end of a two-week period of overfeeding, the carb and the fat groups gained the exact same amount of body fat, exact same amount of body fat. There was another second study that did the same thing and found the same result. Independent lab group, very similar experiment, three-week long instead of two weeks, they found the exact same thing. Same amount of fat gain, different insulin responses, different amounts of carbohydrate and fat, exact same amount of fat gain. So this demonstrates that insulin is not... and carbs are not what controls what gets fat into fat tissue. Calorie intake is what controls that.

Gary Taubes 1:06:55 Okay. So let me explain again. Remember I talked about every... the, the paradigm you work in determines the question you ask. And this experiment is a classic example 'cause they assume that people get fat by overfeeding. So then they say, "If we overfeed them..."... we're just doing what happens naturally. Everything about the experiment is based on the assumption that they're supposed to be testing, which is, can people get fat by overfeeding? And so they'd ... From the very conception of the experiment, they've built in the paradigm that we wanna test, the hypothesis. Um, on top of it, uh, if it's a typical Sims experiment, I actually wasn't familiar with this one. Oh, it was, uh ... It wasn't Sims, it was, uh-

Joe Rogan 1:07:37 Hork.

Gary Taubes 1:07:38 ... James Hill. Oh, and J.C. Peters. James Hill was funded for the (laughs) the ... from about 1998 to about 2008 by Procter & Gamble 'cause he was an Olestra shill. I hate to say that, Jim. I apologize, but I think it's a fair assessment. And then when he stopped being funded by Procter & Gamble, he was funded by the sugar industries. And J.C. Peters was the head of the Procter & Gamble Olestra, uh-

Joe Rogan 1:08:05 Olestra, which is now-

Gary Taubes 1:08:06 Oli-

Joe Rogan 1:08:06 ... something that no one eats.

Gary Taubes 1:08:08 Yeah. Olestra was a fat substitute. Uh, the problem was that you'd got, like, run out.

Joe Rogan 1:08:12 Ruthless diarrhea.

Gary Taubes 1:08:13 Of the, you know. Yeah, yes, and shit like that.

Joe Rogan 1:08:14 Yeah.

Gary Taubes 1:08:14 But the whole idea of Olestra was to replace fat in the diet. So every study Hill and Peters did implicated dietary fat as a cause of obesity. I don't think we could ever use ... I hate to say it, I'm ... Typically, I, I don't think funding influences results, but I wouldn't use a James Hill study to make that point. The ...

Joe Rogan 1:08:36 Because you think it's a biased study that was influenced by-

Gary Taubes 1:08:38 Everything Hill, everything Hill and Peters did ... And when it was ... I mean, I talked about this in Good Calories Bad Calories. When they reported their results, I actually, I did a FOIA on James Hill 'cause he works for the University of Colorado, so you could actually ... And I got all of his documents back and forth between him and Olestra. I'd be happy to share them with you if you'd like. They're revelat- ... I mean, him and Procter & Gamble, but he basically held Procter & Gamble for ransom. He would get a $500,000 unrestricted gift, and then he would do a study, and then he would ask a ... And he would conclude that fat is bad and carbs are good, and therefore Olestra is a viable product. Then he would ask for Procter & Gamble for more money before he then published the study. So it ... a particularly egregious example of someone who's ... I, I suspect it was just his belief system. He believed dietary fat was bad, fat caused obesity. Olestra 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.

Gary Taubes 1:09:39 Um, the point that we keep getting away from that I haven't had an opportunity to, um ... And Stefan knows this as well as I do. 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, so now you're obese. You're a nice, lean, healthy young guy in 20, like many of us were, and by the time you're 40, you've got 40 pounds of excess fat. That's the equivalent of putting in about, uh, f- 10 calories a day, storing about 10 calories a day into your fat tissue that you don't burn or metabolize. So you eat, say, 2,700 calories a day, half carbs, you know, 35% fat, 15% protein, and 10 calories a day get trapped in your fat tissue. Less than a bite's worth of food, less than a sip's worth of beer. 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? 'Cause 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, it tends to happen quickly in their 20s. Um, so we're asking this question. How do we ... If f- you've got a situation where we have to end up with 10 calories stuck in the fat cells every day, that's, uh, 20, 30, 40 billion fat cells, so it's divided up very small, and is the brain somehow regulating that? Or again, is there a dysregulation in the body involving pick your hormones, pick your enzymes, when they'll en- ... Um, 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? And so if you think about it that way, like you let yourself go to seed. Today, Joe Rogan decides, "I'm done. I'm gonna do nothing but drink beer." 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. That 20 pounds over the course of 10 years is still only about 20 calories. You might have added 800 calories of beer to your diet and stored 20 calories as fat. How does that happen, and why does it go here and not elsewhere? And as Stefan said, this is insulin-dependent fat tissue. Um, so those are ... That's ... When we're talking about this, like this question, could somebody get fat during a famine? Or can they stay fat during a famine? All they have to do is hold onto 10 calories a day extra. If they're only eating 1,200, 10 get stuck in their fat cells, 1,190 is excreted or expended. It's not that hard to imagine, and there's nothing th- in the laws of physics that says it, so what could be dysregulated about their fat cells even during a relative famine, not a complete famine, but a relative famine that might le- ... And again, uh, animal experiments of which there are probably hundreds by now, different animal models, you can disassociate obesity from hype- from eating too much in the animals.

Joe Rogan 1:12:59 Can I pause you for a second?

Gary Taubes 1:13:00 Yeah.

Joe Rogan 1:13:00 Y- so, uh, essentially you're saying that even if someone is taking in, uh, uh, uh, a good amount of calories, like, uh, a s- 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. Whereas if you were taking in just protein and, uh, vegetables and things along those lines, your body would not do that.

Gary Taubes 1:13:30 Well, so this is, uh, gets to the mechanism question-

Joe Rogan 1:13:33 Yes.

Gary Taubes 1:13:33 ... and the evidence question.

Joe Rogan 1:13:34 So but, but you're saying that, right?

Gary Taubes 1:13:36 Yeah.

Joe Rogan 1:13:36 So you're saying that if, 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, uh, you know, sugary drinks and p- pasta and bullshit, that that person is going to gain a certain amount of calories and just put them to fat-

Gary Taubes 1:13:58 Right.

Joe Rogan 1:13:58 ... regardless.

Gary Taubes 1:13:59 That's ... Yeah. That's the hypothesis.

Joe Rogan 1:14:01 Same-

Gary Taubes 1:14:01 And that hypothesis-

Joe Rogan 1:14:02 ... same activity?

Gary Taubes 1:14:02 This being a science, that hypothesis can be tested.

Joe Rogan 1:14:05 Yes.

Gary Taubes 1:14:05 And, uh, Stefan thinks it's been tested 80 times, a dozen times-

Joe Rogan 1:14:09 So, Stefan, your-

Gary Taubes 1:14:10 ... I think it's, they've done a bad job of testing it. And 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.

Joe Rogan 1:14:22 From your perspective, this is not the case. Your perspective is that, like, uh, as you were saying, in the study where they c- closely monitored these people's diets, and they added additional fat and a- a- additional carbohydrates, that they both gained-

Gary Taubes 1:14:34 Yeah.

Joe Rogan 1:14:34 ... the same additional amount of weight.

Gary Taubes 1:14:36 Yeah, that's right. I mean, if Gary's hypothesis-

Joe Rogan 1:14:38 But is this a short term?

Gary Taubes 1:14:38 ... is correct, you have to see different levels of fat gain. I mean, Gary's-

Joe Rogan 1:14:41 Was this a short term study that they did?

Gary Taubes 1:14:43 Yeah, it was short term.

Joe Rogan 1:14:43 How, how short term was it?

Gary Taubes 1:14:44 Uh, two and three weeks.

Joe Rogan 1:14:46 Two is very short term.

Gary Taubes 1:14:47 Yeah, it is very short term.

Joe Rogan 1:14:48 Yeah.

Gary Taubes 1:14:48 But still-

Joe Rogan 1:14:49 Well, and it-

Gary Taubes 1:14:49 ... Gary says that insulin is the thing that gets fat in fat cells and that ... I mean, you would see some kinda difference. If insulin made any difference-

Joe Rogan 1:14:58 Well-

Gary Taubes 1:14:58 ... you should've seen some kind of effect, right?

Joe Rogan 1:15:00 Okay.

Gary Taubes 1:15:00 Some kind of difference in fat gain. Well, actually, um, I don't wanna start taking out charts, but this gets into insulin dynamics that was worked out. So over a ... Um, I promised I wasn't gonna say oi-

Joe Rogan 1:15:15 Oi?

Gary Taubes 1:15:15 ... on the show, but it's my ... Thanks to my Brooklyn-born mother, it's my-

Joe Rogan 1:15:20 Mm-hmm.

Gary Taubes 1:15:21 ... programmed in. Um, and the same is true, a lot of these overfeeding experiments do the same thing. So when they talk about overfeeding, they, they, they literally overfeed. So they kinda do a reasonable way of figuring out what you're eating is, Stefan said they measured the ... They calculated how much energy they needed to stay in energy imbalance. And again, right there, that's a problem, because one of the hypotheses says that energy balance is dependent on the macronutrient content of the food. So you're gonna get a different, different level depending on what the macronutrient content is. And then ...

Joe Rogan 1:16:01 A different level of?

Gary Taubes 1:16:02 Of what, what's necessary for energy balance.

Joe Rogan 1:16:06 Okay.

Gary Taubes 1:16:06 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 Cara Ebeling and their, their colleagues at, at, at Harvard and Boston Children's Hospital, and they did this study in Framingham. And they, they basically got, uh, subjects to lose, uh, 10 or 12% of their body weight, and then they randomized them to three different diets of three different macronutrient compositions. And they basically calculated their energy expenditure on the three different diets, which is kind of exactly what we're talking about, 'cause if you wanna be in energy balance, you know you feed people exactly what they're expending. And in that study, which was published a year ago, and they saw different levels of energy expenditure depending on the carbohydrate content of the diet. So the higher level of carbohydrates, this is trying to keep them in energy balance. The, the higher the carbohydrate, the lower the energy expenditure. The lower the carbohydrate, the higher the energy expenditure. So again, it's just whether or not they did the study right. Who knows? Science is a compilation of a lot of studies, and we're trying to, you know, address exactly this point. But merely building that into the experiment, we know what their energy expenditure should be. And then the point is when you increase ... And par- again, part of the trick of doing science is to say, "Look, we have competing hypotheses, uh, multiple hypotheses," and it's vitally important that you always keep the multiple hypotheses in mind when you're interpreting the study. 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, is moderated primarily through insulin. And when you do these experiments, like the experiment that, that, uh, uh, St- S- (laughs) Stefan is talking about, Stefan, um ... Now I'm completely confused. Uh, if you overfeed them, you start out with a 50% carb diet, now you overfeed them, if there's a threshold effect on insulin, which it turns out there is, then you're just moving them ... 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. And above that point, you get pretty much flat. 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, you wouldn't necessarily expect to see any difference.

Joe Rogan 1:18:51 Mm-hmm.

Gary Taubes 1:18:51 The only way you expect to see a difference, and this is why it helps to really, um, interrogate both hypotheses so that you know when you're doing the experiment whether or not you're actually testing something you ... One hypothesis ... You wanna set up the experiment so the hypothesis predicts, the two hypotheses predict something entirely different. This experiment, arguably the two hypotheses predict the same thing. You'll get fat gain because insulin is elevated regardless. And when insulin is elevated, you're gonna get fat gain.... the question comes back to if, this again, always vital to keep this in mind, we wanna, what could possibly cause a 10 or 20-calorie excess that causes fat storage? I have a friend who was four- 400 pounds when he was 18. He was a tall kid, about six foot five, um, he was a, say, 200 pounds overweight. 200 pounds overweight is roughly 100 excess calories over 18 years stored in your fat cells. That's, you know, 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. And the question would be, why can't he just stop doing that? And again, Stefan would say, "'Cause his brain won't let him." (smacks lips) And I would say, "Because his insulin is elevated. It doesn't matter whether he stops it or not."

Stephan Guyenet 1:20:21 Can I respond here?

Gary Taubes 1:20:22 He's got to address the underlying mechanism.

Stephan Guyenet 1:20:23 Please. Okay. Um, all right, so now, again, it's easy to tell stories. It's not easy to tell stories that are supported by scientific evidence. Now, um, I wanna bring people's attention to reference number 11 on my site. There have been 29 studies now that have measured differences in energy expenditure, metabolic rate-

Gary Taubes 1:20:47 Is this the Kevin Hall study?

Stephan Guyenet 1:20:49 ... meta-analysis, correct.

Gary Taubes 1:20:50 Yeah.

Stephan Guyenet 1:20:50 There have been 29 studies to date that have measured calorie expenditure, metabolic rate on diets differing in carbohydrate and fat content, and when you put all those studies together, when you, 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. And in fact, this very small difference that it does make actually favors high-carbohydrate diets. So, you get a slightly higher metabolic rate when the diet is predominantly carbohydrate. 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. So this study (laughs) reported an effect bigger than any of these other 28, um-

Gary Taubes 1:21:41 And the difference we would say is, is this-

Stephan Guyenet 1:21:43 And, Gary, I'm not done. I'm not done.

Joe Rogan 1:21:45 Gary, Gary, Gary, please.

Stephan Guyenet 1:21:45 Thank you. Um, and, and interestingly, if you actually look at the data, and these data have been reanalyzed by a researcher named Kevin Hall, and if you look at the data, you find that some of the participants, some of the data th- that, uh, represent some of these participants are literally physically impossible. They break the first law of thermodynamics. This is the conservation of energy. Gary knows about this. He has a physics background. And they literally don't add up. And when you start subtracting the err- the clearly erroneous data 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 does no long- no longer reports a higher energy expenditure on a very low-carbohydrate diet, and it's consistent (laughs) with the previous 28 studies that were done. So, that's my perspective on that. But I wanna go back to this energy-

Gary Taubes 1:22:44 No, wait,