Gary Taubes & Stephan Guyenet

00:00four three two one and we're live all right so to set this up um when gary was on last gary tobbs stefan how do i say your last name stefan dna dna yeah dna it's like dna like dna but with a g right got it okay um when you were on lass stefan had uh some opposition to some of the things that you were saying we talked about getting him on and yuan together we finally pulled it off took there was a lot of wrangling there's a lot of back and forth and cat wrangling 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 the mechanism for obesity is that fair to say yeah yeah so essentially uh the main points that we want to talk about today are try to keep this a fist from your face okay sure just move it around um what causes obesity and what causes insulin resistance which is behind a lot of our

01:09chronic diseases that are common in society and please uh give us your background yeah so i have 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 to become a science consultant science communicator and write a book called the hungry brain that is my attempt to explain for a non-specialist audience what uh what causes obesity and uh yeah so that's my background now what is your disagreement with gary's position everything everything yeah so uh how about how about i just can i start by explaining please do what i believe cause obesity yeah i'm gonna be long-winded here is that okay go right ahead all right we have hours okay cool

02:10so first uh a little bit of housekeeping i'm going to be citing a lot of evidence today and so i just please bring this up to your friends okay sure just move it around sure because you want to sit back how's that perfect i'm going to 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 going to be citing on do that so it doesn't cover your face okay there we go all right i put a lot of the references that i'm going to be citing on my website stefanie.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 going to be calling out numbers just scroll down to the number that i referred to and the references are all there second thing i want to say that i want to be really clear about today is that i'm not here to be the

02:59anti-low-carb guy okay i think low-carb diets are a valid tool for controlling body fat and controlling blood sugar i'm not here to talk anybody out of being on a low-carb diet 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 want to get started with an analogy to help people understand why the brain is important in obesity so imagine you're an alien coming down from outer space and you want to 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 want to 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

03:54just 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 now why is that the reason is that you're studying the wrong part of the system if you want to understand the 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 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

04:50the system study fat cells do not regulate the size of fat cells any more than the tires on a car regulate this 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 want to talk about and all of these circuits evolved and these are non-conscious by the way so you don't decide you want to be hungry you don't decide that you want to have a

05:41craving these are things that bubble up from non-conscious parts of your brain that you don't control so these circuits are calibrated to an environment of our ancestors not the environment we're living in right now so these circuits all evolved to function optimally in the environment of our ancestors promote the survival and reproduction of our ancestors so what happens when you put these brain circuits in the modern environment where you have abundant calorie dense tasty foods rich in carbohydrate and fat is these same brain circuits push us to over consume and they push our bodies to accumulate and hold on to 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

06:41height 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 supports this idea that i've just laid out

07:37so i want to start with um the genetics of obesity i think this offers some weight can i interrupt for one second uh as long as it's very brief just a question i don't i still don't quite understand what the model is okay i understand that this regulation environment 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 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 most interesting studies are the genome-wide association studies they get hundreds of thousands of people together and they sequence or they they measure all these markers in their genomes and they figure

08:32out 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 by talking about height genes so height has a strong genetic component so just body fatness and researchers have 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 because growth of the

09:21skeleton determines your height so genes that determine diabetes risk type 2 diabetes are all about insulin sensitivity all about insulin secretion and the function of the insulin secreting pancreas which is what you expect because diabetes is a disease that is all about insulin 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 okay so that's one piece of evidence another piece of evidence there are five fda approved weight loss drugs

10:23four 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 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

11:16are occurring in the leptin signaling pathway and this is the leptin 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 left and response pathway in the brain and 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 we've established that the brain is central to obesity but we haven't really established what it is exactly about that interaction why those are modern food why does our modern environment promote obesity right so um basically there are three different ways

12:21that i'm gonna look at this from but first i want to 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 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 going to skip over some of the research here 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 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 i'm going to gloss over some of the individual research because i'm being long-winded here but

13:22essentially what you find is that this 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 carbs and fat you see this dramatic over consumption and 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 you can't replicate it in animals you can't replicate it in humans when you say you can't replicate it you mean you can't replicate obesity what do you mean 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 over consumption using only sugar and carbohydrate that

14:22you 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 but i'm confused so you're saying that the the diet that causes the most obesity is what we think right this uh human junk food diet friction sugar simple carbs diet right what are you you're saying that you can't replicate that with just you fully replicated fully what i mean is that if you just feed if you just increase sugar intake in animals or in humans you do get weight gain but it is modest compared to what you get when you put people around a variety of calorie dense palatable foods rich in carbohydrate and fat similarly if you're that's very confusing how's that because i'm not sure exactly what you're saying you're

15:24saying 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 um so what i'm saying is that if you if you give people or animals the the actual human junk food with all the carbs and fat and everything they gain a lot more weight and a lot faster than if you just give them a diet that's high in sugar and high in refined carbohydrate and what that shows is that the sugar and the refined carbohydrate cannot fully explain the effect can't fully explain why those foods are fattening see this is where i'm confused no i don't see what you're saying because you're saying if you give people the diet of american junk food you you'd get not as much of an effect if you give them just the sugar in the carbohydrates yep so but what are you giving them when you're giving them the diet of junk food you give them you can

16:27for example in animals no it's different because if you think about human junk foods generally those foods contain fat and carbohydrate and salt and all kinds of other things so it's more it's more than just it's a lot of soda carbs right there's no sugar yeah so it's just okay just sugar so i'll get in more detail so 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 in humans you can ask them to drink sugar sweetened beverages that are just sugar and you can see what happens and people will gain weight or you can tell them to stop drinking sugar or sweetened beverages and you can see what happens okay people will gain weight they will lose weight suggesting that that is part

17:17of the explanation but it's a much smaller effect than you see with the this full palette of these foods that contain carbs and fat and all this other stuff does that you're saying carb well obviously there's more calories right if there's carbs and fat and all these other things correct if you think that calories matter then we agree well for sure it matters right gary doesn't think it matters you don't think it matters well 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 because you know while the low-carb community might have a better understanding of where we disagree um i think the greater community that joe reaches might not so fundamentally what stefan saying and what the research community is saying

18:14and the conventional thinking in this field is that the brain and correct me any point i get this wrong but the brain regulates does the fundamental job of controlling how fat we are yes and the way it does it is by controlling or miss controlling our intake and our expenditure and the difference ends up in fat tissue is that fair to say for the most primarily intake but yep yeah so stefan has a brain-centric view of the universe and the 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 yeah okay and let me i have to fix my headphones

19:20how are we going to do this i'm getting feedback when i talk you getting feedback yeah it's just weird could be the hold on one sec for those who don't know i'm hearing impaired as they say kindly my kids would say deaf as a so post took off my hearing aids that'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 i my first two books were studying what's called pathological science which is about people who got the wrong results in science because a lot of times scientists do so by 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

20:23they just assumed that fat people are gluttons and i'm going to use some socially unacceptable uh language because in part that's how they thought about it in fact when you read the 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 was all brain-centric 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 was one team that was trying to get they they got the wives to stop having sex with the husbands if they didn't lose weight every week and that would motivate them i think even you point out that sex is a greater motivator in your book than tasty foods it didn't say it was greater but i said

21:13it was on par on par so and i'm going to just read you uh i won't read you that the so there was this while the obesity research community was focusing on the brain there were people studying fat metabolism endocrinologists they study hormones and hormone-related disorders saying that the 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 well and our body does a very careful job of desi 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 it a sort of excess fat accumulation so today when you read the literature the articles of office obesity is a sort of energy imbalance you take in more calories and they expand

22:16they were still the best scientists in the field the best physician scientists would say look obesity is a sort of excess fat accumulation let's look at what regulates fat accumulation the human body some people are programmed or dysregulated to store more fat and if they store more fat they're going to their behavior is going to respond they'll be hungrier they'll eat more there'll be glutens 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 the 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 going to worry about how much heats and exercises i'm going to worry about what's going on with fat accumulation and this young girl that her body is just as if you give a

23:12you know if you have a child who's six foot eight when he's six years old you're not going to worry about how much he eats and exercises you're going to 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 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 that stored and when you look at that you find a whole world of places in which people can be predetermined you know be driven to be fat

24:13so 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 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 fatten 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 i don't think about what the problem is

25:12with 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 yeah is this a reductionist perspective because i mean isn't it a holist i mean holistically you look at the entire machine of the human body the idea that the brain is somehow another separate from the body is i'm not saying it's separate the question is is the brain driving what's happening in the body or is it responding to it yeah so 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

26:06true 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 not than others and we also know what the genes do that underlie those differences and they are primary i'm not done gary let me finish i just want to read things from your book those jeans nope nope not right now i'm in the middle of saying something those genes are 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

27:00the research says it's very difficult to parse out when you're talking about 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 questions i mean i can guarantee you we both ate as much as humanly possible right actually my brother who never got over 195 and i apologize for bringing you up on the air i know you don't like that used to say that he never gets stuffed he just gets bored of eating after a couple of hours okay okay but maybe even though like maybe if you looked at it scientifically you ate more than him or maybe you ate more sugar no i mean you ate more carbs well so that's the difference so the those are the two hypotheses one hypothesis is my body and this is what stefan is talking about so i want to just the thing i wanted to read how much

27:50i'll ask you the question how much of the the variation in human obesity do those genes explain so if you look at the genetics of no i didn't ask how much is gary i'm answering your questions you need to start talking yeah you gotta love it 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 percent 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 percent 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

28:49small and that's what i refer to in my book how much it's like uh right now i think it's up to about ten percent it was three percent when your book was published yes you were saying they did seven percent absolutely yeah the latest yeah actually let me cite the uh so while the study there 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 ten percent 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 relates to brain activity and so that tells us that primarily the differences between individuals that determine differences

29:40in body fatness is about differences in brain activity 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 i am and i was and how are you surprised well again what do you disagree with well virtually everything but um let's begin with i have to track back now the um okay so drugs that explain obesity 10 with the argument that i was making and the argument i continue to make imagine if you know take stefan's uh car he sees stefan he says stephanie you say stefan right it's okay i'm not that's okay but i mean just so people don't get confused thank you the uh if you take stefan's car analogy and somewhere in the 1970s i've used the car analogy for this too but i i don't think this is appropriate but one would

30:39think 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 do some cars drive faster than others and they come up with all kinds of hypotheses and some of them can explain it 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 car problem if they never noticed the humans so um and leptin is a good example so leptin is discovered in 1993 and when leptin is discovered obesity becomes

31:43sort of a legitimate field of science until then it's a bunch of actually mostly psychologists studying and now it becomes a sub-discipline of molecular biology and all the molecular biologists jump into the field and they assume that what leptin does is control the brain it signals how much fat is available to some kind of satiety or fuel deficiency hormone and as such they study the brain and they study the action of leptin in the brain now in 2002 jeff friedman who gets credit for discovering leptin perhaps incorrectly publishes the paper in the journal science 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 is the 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

32:46liver 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 and the you know below their 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 i don't i think i know the genome paper um stefan is probably referenced on is there have been a number of them but yeah that's the hardest group is it the i i don't remember the so they had two papers because it's what you cited in the article you co-authored with rudy libel so i have two papers

33:41one 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 musk you know some genes and 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 in the weight lifting 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

34:37they'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 going to 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 variations of body shape are going to be determined by the same genes and did you just do the same kind of searches i don't actually know how they determine where the genes work 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 no but the question is where the genes work so there's a common phenomenon all this like with leptin a gene that everybody thinks about working in the hypothalamus seems to work in everything can i respond to that wait let me finish talking because you say

35:25this in your book you say this in your book go ahead i'm prepared to respond whenever you're done okay in your book you say that genes work yeah the body is very basically puts different mechanisms to work in many places as it 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 because every cell and it'll do different jobs on different cells but if you think that the problems 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 the daniel kahneman i stephan likes to say daniel kahneman as well had this concept what you see is all he's a nobel laureate cognitive psychologist what you see is all there is okay and basically if you're studying

36:24the 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 stefan stefan wrote a book about the hungry brain that is supposed to be about obesity but in fact you never mentioned anything about the metabolic regulation of fat accumulation 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 and it's put me in a very odd position so stefan 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 endocrinologist solved it then you discovered leptin and it became a

37:21molecular 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 you know the love handle thing 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 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 fat and this is what we're talking about when we're talking about obesity body fat distribution is what we're talking about when we're talking about the fat being on your hips versus on your wrist now what we see is different sets of genes that come up so body fat distribution we actually see insulin related genes so people that have

38:21essential 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 at the point i want to make about the genetics research ten percent is that of those genes might be dominant by the brain if they looked 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 and that's what they're saying and i'm not done here gary now i want to talk about um you mentioned gary that maybe leptin is having important actions not just in the brain but in the

39:13body first of all i'm glad i'm flattered that you read my book and i'm glad that you acknowledged 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 left an action in the brain the real reason we focus on left an 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 side of action and particularly this brain it tells you guys

40:16please let him talk he let you talk 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 we can control specific popular 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

41:10on 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 want to cite specific evidence demonstrating that that is an actual cause of differences in body fatness between individuals and the general population i'm awaiting that evidence and i'm happy to sit here and listen to you cite the evidence that demonstrates that can i pause here leptin is produced where yeah leptin is produced yeah let's talk about leptin a little bit it's produced in fat cells 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 which is a really simple engineering term that works like a thermostat so with your thermostat you if you set your thermostat to 70

42:05if it starts getting a little bit hotter your ac turns on to bring it back down it starts getting lower ac comes on or the heat comes on to bring it up that's called the negative feedback system and it maintains the stability of the temperature of your house we have many negative feedback loops in the human body to regulate body temperature to regulate blood pressure to regulate all sorts of things one of the negative feedback loops we have regulates body fatness and the hormone so your thermostat measures temperature by using a thermostat sorry a thermometer your brain measures body fatness using this hormone leptin that's in the circulation and then particularly when your body fat level drops your leptin levels drop and your brain hears that and it kicks in a starvation response basically and this is the main reason why weight loss is so difficult because your brain is like no i don't

43:00want to be losing fat and it makes you hungrier it increases your cravings is that at a certain level of body fat is this um so here's just when you're losing body fat in general like even if you're a large person that's overweight correct when you're losing body fat in general your body exacerbates your hunger and this is 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. 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

43:51increase their cravings and their hunger metabolic rate drops so it would be an evolutionary mechanism to force you to seek food correct and not just to force you to seek food that's the main thing but it also slows your metabolic rate does everything it can to get more energy in your body and have less leaving and it keeps doing that until the fat comes back can i pause here yeah so when you're eating a sugary diet a high high calorie diet you will produce more fat your body will get fatter right it depends on how many calories you're eating okay if you're overeating yeah you're consuming a lot of sugar a lot of carbohydrates your body will get fatter correct so your body will produce more leptin correct so it comes from the diet um yeah indirectly definitely can i pause please uh so the leptin is produced not just in response to the size of the fat cell but in response

44:40actually to glucose mediated uptake into the fat cell which is mediated in part by insulin so you come back to insulin even with the leptin you raise blood sugar and that's the carbs you eat the carbs you raise blood sugar you raise insulin you raise fat storage the glucose and then you get more leptin 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 though the leptin is signaling fuel availability in the fat cells the way i would think of it and 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

45:36eat 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 stefan and i first sort of fell out i don't know eight years ago at um ancestral health symposium when i acted improperly inappropriately but one of the problems i so the way i think you should think about this you have a hypothesis and this is a fundamental thing is obesity caused by overeating because we know if you're getting fatter you're storing more calories than you expend that's just the you know that's like if a room is getting more crowded more people are entering than leaving that is the simplest but it doesn't tell you why the room's getting crowded it doesn't tell you why you're getting fatter and again what i've been arguing is the why you're

46:36getting 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 if on eight years ago and it keeps coming up is if we're going to blame obesity on the modern food environment epidemics of obesity you know simple question to ask is can we find epidemics of obesity without this modern food environment i mean that's a sort of science 101 right and it turns out that the world is full and the first one i found in the literature was in 1902 in a population of the pima native american tribe of pima living in arizona and observers saying these people are poor they're malnourished they're suffering through famines they've been suffering through a famine for 40 years and famines it's hard to overeat during a famine and yet

47:31the women of the tribe who do virtually all the work they were treated as pack animals in effect were obese so now we can disassociate obesity from the modern food environment and we could disassociate it from this ultra processed foods weed 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 i actually rarely do that in my books because you can find studies that will say anything and you'll see in the studies people misinterpreting them what was the cause of the population of women to be obese well so one thing that happened during the beginning in the 1860s the pima were put on the reserve well they moved on to resident they were reservationized whatever the verb form would be

48:33and 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 both obese men and women living with malnourished stunted children who clearly weren't getting enough diet they were on a reservation they were getting western foods so ultimately 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 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

49:33africans 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 that we can't say no part because if we're lean it means they can't say no and they being the people with obesity and i don't believe that's true and then or is it some specific item or some specific group in this these foods that travel with western populations and so there exists the ability and today if you look up the 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

50:30and often the mothers or the ants are obese the obesity tends to run in the females which suggests it has a female sex hormone related effect that i don't believe works in the brain because we're dealing with populations that could not have overeaten if they could have overeaten why are the kids starving that's sort of the question and you know this was the first thing that i think we thought about back then and it's still if you can find populations with obesity epidemics but without the modern food system without snack wells and without lay's potato chips and if you know that they're going through a famine or you know that the kids at least aren't getting enough food how do you explain obesity and the mothers without assuming that the mothers are overheated let's pause right there stefan is there a population of people that are obese that are not eating a western

51:29diet that are not eating sugary foods um that are obese and that are not eating sugary foods probably not because generally once you have an industrialized food system that's going to include sugar but there are populations that eat a lot of sugar and are not obese and we should talk about some of these actually let's go back to the 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 originally they were agriculturalists they were eating traditionally a very high carbohydrate diet based on unrefined carbohydrates originally it was corn beans and squash primarily they were hunter-gatherers and agricultural they were primarily beers gary okay they were primarily eating agricultural foods they were also collecting some wild

52:28foods that's correct they were fishing and eating mosquito pods primarily agricultural and um data are very clear on that gary so no no no no yes they are oh look we have david we can't say things like that because we're going to disagree on let's say let's let's move on you think they ate mostly fish that's incorrect okay according to the data that's i remember you saying that in your book something to that effect stephan read what you've got my book read wrong okay anyway just read what i said i'm going to move on here um now the pima traditionally were agriculturalists and what what happened basically is you had all these farmers moving into their area settlers of european descent and they diverted the water from their river the gila or gila river if you're going to gila and so they were no longer able to grow their crops their agricultural crops that they were primarily dependent on

53:28and therefore the government started providing them with foods to eat and these were calorie dense refined foods they were like gary said flour lard and sugar and then they became very obese now there was a population of pima right across the border from them in mexico also very similar culturally and all that that maintained their traditional high carbohydrate lifestyle and agricultural lifestyle and there have been studies comparing those two populations and the um ones across the border with their traditional lifestyle are a lot leaner and healthier 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 eating very few calories and you refer to this many times in your writing and you know these are

54:25very 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 percent higher than people who are lean after correcting for height physical activity level um and that i've got the references we're getting we're getting a little bit into the weeds here let me give you a reference number seven can i pause you guys right here so these people they they have essentially um the same lineage one group lives in mexico they they're not eating these sugary foods in this western diet the ones that live in america are the ones that live in america are becoming obese the ones that live in mexico are not is that correct correct yeah and so now if you have someone with obesity like i've said the most accurate

55:23measures that we have suggest that they habitually consume and expend more calories and now gary's model says that that is downstream of the fattening effect it's not causing the fattening effect it is a result of the fattening effect whereas my model says that that is actually required for the fattening effect to occur it is upstream so now what happens what happens 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 this is the argument what you're saying that you consuming low amounts of calories but high amounts of sugar does it doesn't make sense you can get obese that way um so you're saying it's a calorie yeah correct and that's reference number nine and ten um to support what i just said

56:19and i want to talk about another one that wait can we hold on the reason i was using the dual burden example is because we have to explain how those women are eating all those calories usually women again it's just often it was often these studies were done by diabetes researchers who were studying diabetes in these populations and the men had high levels of diabetes and the women had high levels of obesity to give you an example where that measurement was done um in trinidad in the 1960s and again all i'm doing this is the role i played as i asked the question can you find populations that don't have a lot of food okay you could say that the obesity spend 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 u.s can you find a population that gets obese without sugar

57:09which was exactly the question to ask so in trinidad in the 1960s there's a malnutrition crisis the u.s government sends a team of researchers down to study this and the researchers come back and say yeah there's malnutrition there's stunting there's deficiency diseases and two-thirds of the adult women are obese and this is a medical problem and the next year an mit nutritionist goes down to do exactly what stefan asks for and to actually measure the diets and obese women and lean women and to study it and this is a population where it's it's not like 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

57:57diet so again my role in this is to point out when you have populations like that i don't see how the overeating hypothesis tells me the brain is in control of how much they eat tells me anything about why the women were obese especially when their kids are starving this is the paradox of the student 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 books from jean my year was like the famed leading harvard nutritionist who studied an obese strain

58:52of animals in the 50s he said my animals will get fat even when half starved they will make fat out of their food even when half starved these are generally animals with mutations in the leptin um it doesn't whatever by the way whatever gene it is and 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 going to 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 what is your response 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

59:49accurate 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 a woman actually okay fine 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 no no no gary i'm responding now we have studies where researchers used accurate measures to measure calorie intake in people who had obesity many of these people were saying were only eating 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

60:47something that is only observed when inferior methods are used to measure calories stefan the reason i'm using these populations like i said i'm just giving you an observation obese mother with a starving child the dual burden of malnutrition obesity this isn't one observation it's not one nutritionist the existence of the starving children strongly suggests that there's not a lot of food available and we have to explain obesity in the mother you know that's what i would like you to respond okay fine i will respond to that now look i haven't looked at these studies in particular i brought them up eight years ago when i got in the fight about it we fell out eight years ago it ruined our you know it's like ours we used to be biting um so now 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

61:42what you see in non-industrial situations you see a lot of infectious disease you see a lot of malnutrition so people not getting enough essential minerals and vitamins not getting enough protein and you see a lot of children who are just barely hanging on because of this collection of really bad stuff that's happening in their lives and so parasites things yeah yeah parasites malaria i don't know if there's malaria in trinidad or not but i mean all the diarrhea pneumonia these are the things that we all had before we had modern medicine and great sanitation in a country like the united states 30 of kids didn't even make it past childhood and so there's a lot of things that could have caused that gary it's not necessarily because you know it's not necessarily the reason that you attribute it to now i'm not attributing it to a reason i'm just asking okay

62:36well i i don't have the explanation but i'm throwing out possibilities that are alternative to the one that you're implying that's quite possible 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 want to i want to get this to another type of study that's really going to differentiate between this metabolic effect driven by insulin and the effect of calories so we have a lot of studies that compared diets in which calories were the same but carbohydrate and fat intake differed and the ones that i really want to focus on right now that i think are key here are the studies where they increased calorie intake so they fed people they one study in particular and um let's see i'm going to give you a number here um

63:38let me see if i can give you a number here sorry while you look at that um can we uh bring up another issue because what we're talking about ultimately is why people get fat okay i don't i don't want to divert here i'm in the middle of something so um now if we want to understand why people get fat we can look at studies that overfed people on fat or carbohydrate exclusively so this one study the first one that i want to talk about first they figured out people's baseline calorie intake figure out how many calories they needed just to maintain and then they increase that by 50 percent by exclusively giving them fat or exclusively giving them carbohydrate okay let's study what's this is horton okay um give me a second 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 over feeding but not

64:37the fat over feeding because that increases your insulin it has these effects on your fat cells etc okay now these were very rigorous studies i want to emphasize that can i pause here did they monitor the the actual calories they got correct yes they were they were they had a baseline they used prisoners in the vermont state prison no that's incorrect this is a different study so they had a baseline and did they require them to maintain the same diet and then add additional fat or additional carbohydrates yes yeah so so they say the same foods and then they just bump it up with fat with carbohydrates horton there wasn't sims it was ethan sims which study did he do that was not prisoners what was the uh he didn't have a metabolic you know what let me just finish describing this stuff no it's just it not gary that's an irrelevant detail okay what's relevant is that you just

65:30implied that i don't know what i'm talking about gary all right you know what i i don't actually know maybe it was in prisoners thank you all right you're welcome now um but it was not the sims overfeeding study that was done in prisoners that's what i know okay okay so friends what's the reference um yeah it's on my website you can go to my website uh stefanie.com and it's reference number 16 and they're both there okay so this was what's called a metabolic ward study where these people were in a research facility where the researchers could monitor and control every morsel of food so there was no cheating no inaccuracy and they were measuring changes in body fatness using a gold standard method called underwater weighing okay and so what they found was that at the end of a two-week period of overfeeding the carb and the fat groups gained the exact same amount of body fat exact same

66:26amount of body fat there was another second study that did the same thing and found the same result independent lab group very similar experiment three week long instead of two weeks they found the exact same thing same amount of fat gain different insulin responses different amounts of carbohydrate and fat exact same amount of fat gain so this demonstrates that insulin is not and carbs are not what controls what gets fat into fat tissue calorie intake is what controls that so let me explain again remember i talked about everything the paradigm you work and determines the question you ask and this experiment is a classic example because they assume that people get fat by over feeding so then they say if we over feed 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

67:19fat by overfeeding and so that from the very conception of the experiment they've built in the paradigm that we want to test the hypothesis on top of it if it's a typical sims experiment i actually wasn't familiar with this one oh it was uh it wasn't sims was a or james hill and jc peter james hill was funded for the the from about 1998 to about 2008 by procter gamble because 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 industry and j.c peters was the head of the procter gamble olestra a lester which is now something that no one eats yeah lester was a fat substitute and the problem was you got like run out of diarrheas and like that but the whole idea of illustra was to replace fat in the diet so every study helen peters did implicated

68:22dietary fat as a cause of obesity i don't think we could ever use i hate to say it typically i don't think funding influences results but i wouldn't use a james hill study to make that point that because you think it's a biased study that was influenced everything hell everything helen peters did okay 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 hilks he works for the university of colorado so he could actually again i got all his documents back and forth between him and lester i'd be happy to share them with you if you'd like their revelation i mean him and procter and gamble but he basically held proctor and gamble for ransom he would get a 500 000 unrestricted gift and then he would do a study and then he would ask it and it would conclude that fat is bad

69:12and carbs are good and therefore lester is a viable product then he would ask for procter gamble for more money before he then published the study so it's a particularly egregious example of someone who's i suspect it was just his belief system he believed dietary fat was bad fat caused obesity lester is a good thing because you eat that instead of fat you don't absorb it and then every study he did confirm that the point that we keep getting away from that i haven't had an opportunity to 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 the 10 calories i said storing about 10

70:11calories a day into your fat tissue that you don't burn and metabolize so you eat say 2700 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 sips 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 because when we talk about those obese women with starving children all those obese women were doing was storing 10 or 20 calories a day depending on how quickly they became obese in those populations it tends to happen quickly in their 20s so we're asking this question how do we if you've got a situation where we have to end up with 10 calories stuck in the fat cells every day that's a 20 30 40 billion fat cells so it's divided up

71:12very small and is the brain somehow regulating that or again is there dysregulation in the body involving pick your hormones pick your enzymes when 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 going to 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

72:15can somebody get fat during a famine or can they stay fat during a famine all they have to do is hold on to 10 calories a day extra if they're only eating 1200 10 get stuck in their fat cells 1190 is excreted or expended it's not that hard to imagine and there's nothing 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 be and again 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 can i pause you for a second so essentially you're saying that even if someone is taking in a a good amount of calories a smart amount of calories 2 000 calories a day if you're taking in these calories in the form of sugar your body is going to take a certain

73:18percentage of them even if you're getting enough food and stored as fat whereas if you were taking in just protein and vegetables and things along those lines your body would not do that well so this is uh gets to the mechanism question and the evidence question so but you're saying that right so you're saying that if two people are on the same diet one of them's on 2 000 calories of chicken and fish and vegetables and the other one is on 2 000 calories of milkshakes and you know sugary drinks and pasta and that that person is going to gain a certain amount of calories and just put them to fat right regardless that's yeah that's the hypothesis this being a science that hypothesis can be tested yes and there's stefan thinks it's been tested 80 times so stephanie i think it's they've done a bad job of testing it and we will both tend to reject the studies

74:17that we don't like when we define don't like by whether or not they got the answer we think is correct your perspective that this is not the case your perspective is that like as you were saying in the study with a closely monitored these people's diets and they added additional fat and an additional carbohydrates that they both gained the same additional amount of weight that's right i mean if carriers is correct you have to see different levels of fat gain i mean this is a short-term study yeah it was how short-term was it uh two and three weeks well that's very short yeah it is very short-term but still well gary says that insulin is the thing that gets fat in fat cells and that i mean you would see some kind of difference if insulin made any difference you should have seen some kind of effect right some kind of difference in fat gain well actually um

75:03i don't want to start taking out charts but this gets into insulin dynamics that was worked out so over a hey um i promised i wasn't going to say oy boy on the show but it's my thanks to my brooklyn-born mother it's my program dan um and the same is true a lot of these over feeding experiments do the same thing so when they talk about overfeeding they they literally overfeed so they kind of do a reasonable way of figuring out which reading is stefan said they measured they calculated how much energy they needed to stay in energy and balance and again right there that's a problem because one of the hypotheses says that the energy balance is dependent on the macronutrient content of the food so you're going to get a different different level depending on what the macronutrient content is and then a different level of of what what's necessary for energy balance so

76:06the 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 kare ebeling and their their colleagues at that harvard and boston children's hospital they did the study in framingham and they they basically got the subjects to lose uh 10 or 12 percent 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 because if you want to 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

77:05trying 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 again part of the trick of doing science is to say look we have competing hypotheses 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

78:03the experiment that that uh stephen is talking about stefan um i'm completely confused uh if you over feed them you start out with a 50 carb diet now you over feed them if there's a threshold effect on insulin which 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 the only way you expect to see a difference and that's why it helps to really interrogate both hypotheses so that you know when you're doing the experiment whether or not you're actually testing

79:01something you one hypothesis you want to 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 going to get fat gain the question comes back to it this again always vital to keep this in mind we want to what could possibly cause a 10 or 20 calorie excess that causes fat storage i have a friend who was for 400 pounds when he was 18. he was a tall kid about six foot five um he was 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

80:04half 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 because his brain won't let him and i would say because his insulin is elevated it doesn't matter whether he stops it or not addressing the underlying mechanism 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 i want to bring people's attention to reference number 11 on my site there have been 29 studies now that have measured differences in energy expenditure metabolism study meta-analysis correct there have been 29 studies to date that have measured calorie expenditure metabolic rate on diets differing in carbohydrate and fat content when you put all those studies together when you are at least the first 28 together

81:05and 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 expenditures so this study reported an effect bigger than any of these other 28 and um difference we would say gary please thank you um and and interestingly if you actually look at the data and these data have been re-analyzed by a researcher named kevin hall and if you look at the data you find that some of the participants some of the data that represent some of these participants are literally physically

82:05impossible they break the first law of thermodynamics this is a 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 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 with the previous 28 studies that were done so that's my perspective on that but i want to go back to this gary you've talked for a long time and i'm going to talk for as long as i want now um i want to i want to talk about human energy metabolism and this idea of the 10 extra calories a day gary i i really continue to get the feeling that you do not understand human energetics um because that's not how it

83:04works well no i'm just saying 10 calories stored in the fat tissue that's in calories 10 calories i didn't say anything about how much you have to eat i'm not done okay no but you're insulting me you got to stop doing that dude you keep acting like you think i'm an idiot all right are you done now are you done can we be clear that we're talking about are you done now can i just finish this no you can't you until i am done without no you have time to respond you you can respond write down notes on what you want to respond to and after he's done you can yeah but we're going to get a little discourse on something that's not the point well yeah thank you okay now what you see there's basically two things you need to pay attention to here in terms of energetics one is the imbalance between intake and expenditure and that is very small so it only takes a little bit of extra calories to cause

83:57somebody to start gaining fat however as they gain fat their bodies get bigger they're gaining fat and lean mass people with obesity have more fat more lean mass and their calorie needs go up and up and up and up the larger their bodies get and so even though the imbalance between energy and taking expenditure is small their calorie needs end up being quite a bit higher can i pause for a second yeah so you're saying that someone just gaining calories eating additional calories their body gains lean mass as well that's as fast how does the brain regulate that i didn't say it regulated hold on that's so fascinating but how does it bring muscle muscle they're gaining muscle tissue some of its muscles some of it's okay is this because they're carrying around this extra weight and so the extra calories and then on top of that carrying around the extra weight forces their body to grow larger

84:52presumably i'm actually not sure what the mechanism is but it doesn't have anything to do with the brain it's just a coincidence i don't know what it causes it that's what i'm saying gary okay now um so so but the point is by the time the person has obesity they are consuming 20 to 35 percent more calories than they were when they were lean so that's not just one or two cokes a day that is allowing them to remain obese they are consuming 20 to 35 percent more calories that is what the most accurate studies are saying and so it's not just 10 extra calories or maybe just one or two cokes we're talking about a substantial amount of extra calories but isn't this a generalization because we don't know what i mean what's the ratio of how much fat people get how much weight people are gaining everybody gains a different amount of weight like you're saying they're eating 20 to 30

85:48percent more calories like who is like how many people how much are they gaining like people get fat they get 20 pounds overweight people get fat they get 100 pounds overweight they made a video that's right yeah and that's why i give a range because what you see is that people who are overweight so they're in the overweight range and just have some extra fat they eat about 10 extra calories people who have a little bit of obesity eat about 20 extra calories people who have who are very have very very great obesity eat more like 35 percent so it tracks with the amount i'm sorry is it possible what he was saying that if you do consume 10 extra calories over long periods of time that will accumulate no it's not 10 extra calories you're accumulating calories that's it like 10 a dime is going into it so how much do you have to deposit this is correct right it is correct that if

86:38every day you eat 10 calories more than what you need then yes or your body's your body stores yeah we'll say that that's correct if your body is storing 10 10 10 extra calories over top of what you need but the thing is that as you get bigger what you need goes up and up and up because you're carrying around more correct and so it's 10 and 10 extra sorry not percent is 10 extra calories on top of the elevated amount that you're already eating so you end up with these big differences in calories intake so that's how that's how it really works but i want to talk about some interesting observations because gary you like to talk about um you know what's going on in different dietary trends and different cultures and i find that pretty interesting too i want to talk about the fact that sugar intake in the united states has been declining for the last 20 years

87:34so it peaked in 1999 and it is currently depending on which source of evidence you believe 15 to 23 percent lower than it was in 1999 this has been corroborated by a number of different sources of evidence this is number 17 on my blog and of course we know that obesity has increased diabetes has increased substantially over the last 20 years in the percentage of the population or actual numbers percentage yeah and uh in the uk sugar intake has been declining for 50 years i don't believe that okay well you can argue with the data they're uh number 17 on my blog they're about 22 percent lower and this is what we see across a number of different uh industrialized countries you see a stagnation or decline in sugar intake in recent decades as obesity rates are continuing to increase um and of course that 50-year period that covers the decline in the uk covers the entire uk obesity and

88:33diabetes epidemics um but there's another one i want to talk about that can i respond to that yeah we should probably respond to yeah stefan actually i'll let you respond for me because we had this debate with the cato foundation so you know my art counter argument you want to give it yeah sure absolutely i mean are you sure you want to let me give it though i might correct it okay all right so your counter argument is that the amount of sugar that we consumed 20 years ago or even maybe 50 years ago may be continuing to fatten us today and it's about the sugar that we used to eat 20 or 50 years ago and not necessarily about the sugar we eat today well it's not exactly right okay so the argument i made was staff because he brought this up when we had to do a written debate on the cato foundation website and it's interesting if you think about use tobacco as an

89:28example so tobacco smoking per capita smoking in america peaked in 1965 right after the surgeon general's report and it took 30 years before lung cancer rates turned over okay and i think we both agree that cigarettes are a major cause of lung cancer smoking so what you basically have is a system in which if there are any there's the assumption that stefan is making when he quotes this kind of data is that the relationship between sugar and obesity is linear so as sugar goes up obesity and diabetes goes up and if sugar turns over they don't so here's the thought experiment they used in cato which is 1965 we're smoking per capita about 20 cigarettes a day as it starts to come down imagine we only cut that to 17 cigarettes or 16 cigarettes a 20 reduction in smoking would you expect to see a reduction in the lung cancer rates again this is the point i made about what you would expect

90:27to see rather than using simplistic uh metaphors so the question is would you like joe we go from 20 to 16 do you expect to see the lung cancer rates turn over no no and in sugar we see them drop no you might the derivative might drop you might expect it to slow a tiny bit still you it's there's a but it's a weird comparison because one of them is poison the other one's food right well but in this case the food the question is how toxic is the food so in sugar we have a variety in sugar what happened is the equivalent of going from 20 cigarettes to 16 beginning in 1999 and stefan is saying i would expect to see an immediate change in obesity in fact if you actually look at the rates the the rate of increase the the prevalence appeared to plateau around six or seven years later who knows whether that's relevant but to get a small decrease in sugar 20 even if it's 20 percent that's

91:2820 to 16 cigarettes and i'm saying the other factor that i talk about my book and stephan knows this is you very clearly have maternal transmission of the propensity to obesity and diabetes so there's a generational effect this and this is studies that were done in the same on the same pima the same native american tribe where each generation if gets more and more uh susceptible to whatever it is in the diet that's triggering an obesity and diabetes so if that's been happening in the united states and around the world you've got a generational effect that could last far longer might even keep going indefinitely even if the sugar levels drop so you have the sugar kicking off the obesity epidemic and yeah stefan's about to say this is a story and it is a story but it's clearly the case that mothers who are obese during pregnancy or diabetic or gestationally diabetic

92:25they become diabetic during pregnancy or they have metabolic syndrome they're just insulin resistant or they gain a lot of weight in pregnancy will give birth to children who are at higher risk of becoming an obese and diabetic when they get older and at younger ages and those children will pass it on so again we have you know i would be nice i would love it if sugar consumption came down and with it obesity and diabetes plummeted but it's not in any way a refutation of this hypothesis which i just want to state what it is because people get confused about it we never got to it the sugar hypothesis is a little different than what we've been talking about and it's pretty simple we have obesity and diabetes epidemics worldwide as we talked to it doesn't matter the genetics of the population you add something about a western diet to those populations western diet and lifestyle you

93:20get these explosions the epidemics of obesity and diabetes and what i'm hypothesizing in this book is that sugar is the something that has to be added maybe it's sugary beverages for all i know maybe or it could be you know a more complex hypothesis the same possible one is you add sugar to any population's diet insufficient whether it's southeast asians living on rice or the inuit living on reindeer and whatever or the native americans of the great plains or you know caucasians living in the upper east side of manhattan add enough sugar and eventually through the metabolic effects of the sugar and the generational effects you will get explosions of obesity and diabetes and metabolic system you want to respond to that sure i mean gary you called it man um it's always possible to tell a story to salvage your hypothesis but that doesn't necessarily make the story correct i

94:19mean i can come up with a story that cosmic rays cause obesity by hitting my fat cells and making them fat you can't disprove that nobody here can disprove that but there's no way we could do an experiment to protect you from okay make sure but we don't science we don't have the data right now you don't have data supporting your hypothesis no we do you just dismiss it no no no no no but can i get back to the kevin all-stars yeah so um what do you think about what he's saying about sugar and increased rates of diabetes and that this is the cause yeah i mean so let me put it this way we don't have any evidence supporting what he just said so that is a story that is not supported by evidence now does it does that mean that it's definitely incorrect no i cannot say that that's definitely incorrect same way i can't say it's definitely incorrect that cosmic rays cause obesity

95:15but you know i'm gonna i'm gonna use a christopher hitchens quote here that which is asserted without evidence does not require evidence to refute and that's the way i feel about this particular story um but you know there are cultures that consume large amounts of sugar and do not develop obesity we've we've talked about this yeah and we're going to talk about it again right now um so this is reference number 21 um on my blog i'm going to talk about three different cultures one of which we have not talked about gary the first one is the the hadza hunter gatherers of tanzania this is a really interesting non-industrial culture they as part of their hunter-gatherer diet eat a lot of honey honey is a very common food among hunter-gatherers living similarly to how our ancestors used to live and if you measure their year-round honey intake it's about 15 of their calories so this

96:14is a major calorie source for them that's about as much sugar as as the average american eats and they eat fruit sugar on top of this they eat a lot of fruit on top of that and so they're eating quite a bit of sugar and the hadza men have about 12 body fat women have about 18 so they correspond pretty closely to our western ideals but isn't that high for hunter gatherers no not really i mean that's higher than me they're running around let me ask you this how have you had your body fatness measured well i've had it measured a bunch of ways electricity i've had this machine where you hold on to these things you stand on this platform and then okay it's done in physicians office of okay so um with calipers the most okay so all the methods that you measure that you mentioned are not gold standard methods so the gold standard methods are underwater weighing and are they

97:07underwater weighing these people on this island uh actually i'm not sure i'm not sure how they bring that equipment to this island correct but okay look um i can tell you that you can look up photos i i don't remember how they how they measured their body fat but you can look i am 12 as measured by dexa so i'll just tell you that okay just so you can get a sense of what 12 is by dexa um which is a gold standard method um so you can look at photos of these people they're very fit they're lean they're not like ripped you know they're not arnold schwarzenegger in peak form but they are no i understand that but it seems to correlate with a higher consumption of sugar that they seem to have a higher percentage of body fat than the average hunter gatherer no if you look at a lot of the average hunter gatherers like a friend of mine does a lot of work with uh the pygmies and uh

97:56the congo and they're very lean okay so you see six packs that's the second culture i was gonna say that eats a ton of honey do they yeah the if they're the same ones the mabuti pygmies of the congo um they eat up to 80 percent of their calories can come from honey during the rainy season so they also eat a lot of honey and are lean not just a year correct yeah for them it's part of the year the hodgson eat it more consistently and the hodza have low levels of body fat their cardiovascular risk markers are excellent they don't have diabetes same but this is absolutely not like a controlled study in the consultation absolutely not i absolutely agree with you that's exactly the point i'm trying to make is that when you have an a that is eating a lot of sugar but everything else is in place they're doing everything else right the sugar is not enough to make them fat it's not

98:51single-handedly enough i'm not saying it doesn't contribute i think sugar does contribute just to be very clear i think sugar does contribute to obesity and diabetes and cardiovascular disease but it's not single-handedly responsible as gary has argued so the third culture is pretty interesting the cuna of panama and the reason they're interesting is that they actually aren't eating honey they're actually eating white sugar so they're a culture that um they live primarily a non-industrial lifestyle they're farmers and hunter-gatherers and they but they do a little bit of trade and one of the things they trade for is sugar and they eat sugar-sweetened foods as well so like donuts and pastries and they drink soda and kool-aid what what is their lifestyle in terms of like what they have a natural lifestyle they are hunter-gatherers and subsistence farmers

99:46so they're you know living a physically active natural lifestyle so this is the problem in comparison with any westernized civilization that you you burn off so many more calories i 100 agree with you and i think that is exactly the point i'm trying to make is that it's more complicated than just sugar it is more complicated than just sugar but with a normal lifestyle it may not be this is you know like the consumption the thing about burning of the calories is also the the glucose demands the glycogen demands on the muscle you're you're not just existing like the one of the problems with western lifestyle is that many people are just existing they're sitting in a chair they're walking to a desk they're sitting in their car they're not doing anything to burn any of this off so even if you have like if you get a baseline of a minimal amount of calories that you require for the day

100:41i think what gary's getting at is that if you if you have this lifestyle the lifestyle that many of us have and then with that lifestyle consume sugar that you're going to get fat i don't think you can compare that to athletes and in that respect i don't think you can compare that to hunter-gatherers because you're requiring there's a much more significant load on your body you like when i i did this sober october fitness challenge with my friends during october and we i was working out four hours a day and i was eating everything that moved i was drinking soda i never drink soda yeah i was eating cookies i didn't gain any weight other than muscle i didn't get any fat at all yeah and i was eating a terrible diet yeah but i was going crazy when you're trying to stay alive and you're running around plowing and growing foods and hunting and gathering and fishing you're burning

101:40off insane amounts of calories just the hiking that's required the amount of exercise that's required it's off the charts in comparison to a standard western lifestyle we are on the same wavelength here i mean i completely agree with you that it is more complicated than just sugar yeah and but if you read what gary has written and please correct me if i'm wrong here gary argues that sugar is the primary cause of obesity and that physical activity does not matter calorie intake does not matter do you think that physical activity doesn't matter uh and i think it's a uh uh no i don't think it makes a lot of difference for fatigue when we're talking about the cause of obesity i don't believe obese people get obese because they're said but let me put it this way so if you take someone who's an elite athlete and they start consuming a lot of sugar but they they ramp up their

102:32exercise accordingly like say if someone does what i did during the sober october they're working out three four hours a day every day you don't think that they have higher sugar demands and their body would just burn that off no absolutely i think that if there's a real benefit to exercise it's burning off the carbohydrates you consumed and then you need less insulin to do it can i respond to the kuna get back to them for a second okay i mean one of the the issues i have with stefan is he writes off my stories as stories which they are all science begins as stories um hypotheses and then what you do is go look for the evidence and then he quotes studies and refers to it as evidences though this is somehow by calling it evidence that may and then we had this discussion a year and a half ago and you didn't disagree with me at the time and it had no influence so i'm just going to read from

103:24the email i wrote to you so oh boy no it's reading emails it's gotten to that point in the conversation indeed well because it's i'm not only going to read from the email if i have time i'm going to read from your book read the kuna the study you cited is interesting okay so this was a study that professed to measure sugar intake of this population on an island gandhi and compare it to the population in veracruz where they uh they had emigrated and i say but their added sugar intake on alagandi according to figure one is 25 teaspoons per week plus the equivalent of 24 ounces of sodas at 78 grams if it's coke 32 ounces of kool-aid that's 96 grams i said i'm leaving out the cup of a sugar cane because i don't know what that is meant or how they assess it one way the other it's not processed sugar so it's roughly 274 grams of sugar per week or about 32 pounds per year

104:21now that alone is very low intake and we don't know how it changed over the years so we have no idea if it's increasing recently or been low for years so you just use the as an example of a population that eats a lot of sugar and stated it dogmatically but that a lot of sugar is 32 pounds a year and then i said wait hold on i thought you did that's what i heard uh if we believe this study the and veracruz are consuming roughly the same amount but i'm not sure i believe this study when it comes to the veracruz population do you really think these urbanized are consuming only three eight-ounce sodas per week so the implication was as population of caribbean islanders immigrates to veracruz they move into the city and they consume more sugar back where they used to live because they trade for it than when they get into the city so five glasses of kool-aid no candy no

105:11ice cream nothing i'd like to know more about the urban cuna before i accept such an analysis is valid on top of this as they say the analysis is done mostly of women because quote the women were available to study because they were at home during the day unquote so what were the men consuming and what were the children consuming when they weren't at home and was there something magical about this freak food frequency questionnaire and these researchers that they captured it accurately so this is what science is you have studies you have evidence and the question always is you've got competing hypothesis does this evidence really speak to the hypothesis and one of my issues with stephen it's what provoked our initial discord is that he's constantly citing studies that don't actually either they only speak to one hypothesis like the overfeeding study or they're poorly constructed and

105:59poorly done so even this has the example with the honey is something we discussed in email very kindly and we went back and forth i said i don't actually think it's a refutation because the hypothesis i'm defending here the case against sugar is you add sugar to any population's native diet and you get epidemics of obesity and diabetes so here's a population that's been eating honey for maybe thousands of years in fact when they emigrated to this area they may have added honey to their diet and had obesity and diabetes then and stephen points out in the book obesity and diabetes in a hunter gathers population is a death sentence for the child and for the mother who gives birth so you're going to very quickly weed out anyone so again it just comes back to this question of does this actually is it a refutation the hypothesis that i found a hunter-gatherer population that

106:52eats a lot of honey and isn't fat and the answer is i don't think so stephen thinks it does you could flip a coin all of this can be settled with experiments one of the experiments we did at new city uh so one of the the metabolic problems that goes along with obesity and diabetes is non-alcoholic fatty liver disease it's endemic it used to be 20 years ago if you had alcoholic fatty if you had fatty liver disease the doctor would and you told the doctor you didn't smoke they would assume you were lying now it's so common and so common in children and particularly common in hispanic children that it's clear it's not caused by alcohol and the question is what causes it because if you could create a fatty liver with a macronutrient you could probably create insulin resistance as well and then this whole slew of disorders including obesity and diabetes so my

107:46not-for-profit funded a pilot study where we just took 40 kids by the researchers at uc san diego and emory university in atlanta took 40 kids who had non-alcoholic fatty liver disease and randomized them into two groups and one group we gave them the entire family all the food they needed so they could overeat to their heart's extent but no added sugars in their diet no sugary beverages and this study was published in jama four months ago and it's just it get rid of the sugar in the diet the fatty liver disease resolves you know it was pretty simple i could there tells you nothing about mechanism the kids lost a little bit of weight maybe it was a weight loss the conventional wisdom would be they just ate less which i wouldn't be at all surprised because they probably didn't like the food as much without sugar in it but these are the kinds of ways you could

108:41test these hypotheses and problems i have with like the meta-analysis getting back to kevin hall there's two ways you could do science you could say let's look at all the junk that was done for 30 40 50 years let's find everything we can that even vaguely speaks to the experiment and ignore any quality of the study so if it maybe asks it asks this question like we want to know what happens when people do this but in doing this we switch their you know fat intake around fat and carb intake around and then we can throw all that garbage into a meta-analysis and the one thing i'm pretty confident is they did a poor job because of one study i looked up the one with the biggest effect they mistook kilojoules for kilocalories so they reported that 400 kilocalorie decrease in energy expenditure on the low-fat diet when was a 400 kilojoule which is what's that factor you know these numbers uh

109:410.8.18 or something several of the other studies where jim hill studies we've talked about jim hill the biggest studies were jim hill and the way we approached it the not-for-profit is say you've got to understand what the question is and you've got to design an experiment to get the right answer so when stephen dismissed this heart three names for him now stefan stefan dna gets dna right doctor his name's stefan it's really easy stefan i can't do it dude i just don't get names um my name is joe hi gary that i know hi too the um stefan uh ultimately rejected this study it was about a 12 million dollar study that was done at harvard based on kevin hall so these are two names it's about three people out there who are convinced that everything people like me are saying is wrong or not everything but most of it and they keep coming up over and over again and they so kevin hall

110:43claims that he has refuted the carbohydrate insulin model in his studies so when a study comes out supporting it he works to find out why that studies wrong we all did the same thing i did the same thing right here with the kunis study explaining why i don't find it meaningful but anyway that's the thing the goal is to do the right study because ultimately you've got to remember what's on the line here we have obesity and diabetes epidemics i mean tragic is going on out there i mean people you know these are ruining lives they're overwhelming the health care system and the argument i made is that for the past 50 years basically people have thought a lot like stefan is thinking now dr dna and that there appears to be another story that could be true and what we have to do is find out if it is true because people are dying out there okay um the first thing i want to say is that this

111:40alternative explanation that gary is talking about has already been investigated intensively including studies that were funded by his own organization nuci two out of the three studies that had been published on that were clear refutations of the hypothesis and no no no no no i responded here i know i know you've got to represent the studies correctly gary gary i representing them according to your beliefs is not representing them correctly okay now i've noticed a remarkable correlation between studies undermining your beliefs and you thinking those studies are garbage and we should talk about uh jim hill and his studies a little bit because you know to me just saying this guy has a conflict of interest and then insinuating that that makes the study bad if you can't actually find a problem with the study itself these were very rigorous studies if you cannot point out

112:33a specific problem with the study it was designed with an assumption it was designed based on the assumption it wasn't designed how gary wanted it to be designed um you cannot find a problem with that study then you can't just dismiss it by making these insinuations that the person had a conflict of interest okay i it's now into the problem okay so that's great gary now okay all right you're gonna be able to respond in a moment now um the kuna i think we should really get back to this issue this non-industrial culture because the primary basis for gary's book the case against sugar the primary observation that underlies gary's belief on this is this observational correlational thing that cultures when sugar gets into these cultures they become fat and that is the common thread and in obesity and so what i'm doing is i'm pointing out a culture where sugar came in and it did not make

113:38them fat and that's one of three cultures i haven't even looked that hard okay these are just three cultures that i came across there's probably a bunch more that are eating high levels of sugar but they're eating and they're not both the other two are hobies and again joe explanation is right on point there's a lot of other things going on in these cultures and it's more complicated than just sugar that's exactly my point now i want to talk about um the cuban economic crisis this is reference number 22. from 1989 through 1995 the cuban economy collapsed and the price of food went way up the price of gasoline went way up and so people started focusing on these really cheap foods cuba was a major sugar producer at the time i don't know if they still are and so the intake of sugar went way up intake of refined carbohydrate went way up the diet became

114:3677 carbohydrate primarily white rice and sugar 28 sugar of their total calorie intake so that's like double what americans eat now their calorie intake went down and because of the lack of gasoline people got really physically active because they had to walk everywhere so now again if this is this is a situation where we can test gary's hypothesis if gary is right and calories don't matter only refined carbohydrate and sugar matter obesity should have gone through the roof in this population over that period of time what you actually see is that the prevalence of obesity declined by half so there was a fifty percent decline it went from fourteen percent to seven percent over the period of this um increase in sugar intake increase in refined carbohydrate intake and you might think well these people are just starving like crazy and that's why obesity rate went down well we

115:35actually have evidence on the rate of underweight as well and so we can check on that the rate of underweight increased only slightly it went from eight percent to ten percent and so we know these people weren't just totally starving um and what happened then was as the diet rebounded as the economy rebounded and the diet rebounded and their diet shifted away from these refined carbohydrates and sugar and back to the normal diet that was higher in uh in fats and lower in carbohydrate lower in sugar the obesity rate went right back up as soon as they went back to their normal diet and so i find this because there were they were not walking as much yeah i was the exercise and also just their diet became richer again i mean if you're eating a diet that's a very poor diet eating like white rice and sugar i mean it it's not like if that's most of what if you're

116:28sitting there and on your plate is white rice and sugar you're not going to be eating a ton of that and getting fat as opposed to eating a richer diet with more varied foods and so this is a case where you have an entire country testing gary's hypothesis and finding that basically the opposite of what his hypothesis predicts gary uh let's go with the the the when he was refuting the studies and you wanted to this was the level of discourse i didn't really want to get into because that's a study that i'm going to have to read he's right i'm going to read it to try and figure out what the problem is i remember looking at that study and thinking there wasn't the kind of data you're citing maybe there's multiple studies put together but the one study i looked at the kind of data you're citing wasn't in there that this is again a preferences are on my website so have at

117:16it no i will but we'll be off the air by then um the beginning of his when he started talking he was referencing some studies and you had a problem with that well this whole it's a game people playing again it's why basically in my book i try not to get into he said she said studies because you never know how well they did i think we both agree that there's a reproducibility crisis in science and some huge proportion of the studies are just wrong whether they're experiments or observations people sometimes aren't very good at what they do right and so anyone in either business you have to stephen likes to say i have no evidence stefan damn it but simultaneously people accuse me of writing a 600 page book with 150 pages of references that was too long to read so there's clearly evidence for this observation and this hypothesis my issue with stefan is that he speaks as though he knows

118:15with this authority and so again i would like to just read a little bit from your book because as i was prepping for this before you do that though he was referencing the cuban situation i don't know what the reality is before that when when he first started talking he was referencing things that you were stating that he was saying what were you saying that uh the the the the organization that supports him actually refused oh that was the jim health studies yes no no no no the uh the nucia studies yeah we're talking about the news the first two of which and we can get we can get into detail on this on how those refuted gary's uh beliefs and i would say gary is about the only person who thinks they did not refute his beliefs the scientific community is uh pretty unanimous you can respond but but but could you please say what was what would the study stated well let me let me let

119:06me do it before he so the first study is a is a pilot study that it would uh depends what you look at to depend whether or not it refuted your belief so there's again you have to understand this world so there are researchers who believe one thing kevin hall and nih tends to believe that obesity is an energy balance problem and you people get fat because they ate too much i hope i'm doing kevin justice um and then there's david ludwig and his colleagues at harvard who tend to believe what i believe and we funded them both to do studies and kevin hall study if you believe what kevin if you believe kevin interpreted it correctly was not supportive of this model that carbohydrates are ultimately driving insulin and insulin is driving up that accumulation and then the david ludwig study was reported the opposite and then david has criticized kevin's study and kevin

120:08has criticized david's study and this is the nature of science this is what you do in science you do an experiment people critique it ideally you do another one kevin has decided well kevin is doing another one i think he's asking the wrong questions but i just saw the other day that he's doing another experiment um tony the the middle study was a free living diet study where uh done by christopher gardner at stanford university and the idea was uh original idea was 600 people randomized to either a very low carbohydrate diet or a very low fat diet and we funded it in part because we hoped that christopher would be able to get people to almost a ketogenic diet on the low carb side and dean ornish who promotes a low fat diet always complained that the low fat diet wasn't fat enough so hopefully they'd be able to separate out these two at the end of the trial they

121:08got pretty lousy adherence uh low carb was about 25 to 28 percent carb which is by no means a low meaning pretty typical in free living studies and the low fat was about equal what they did which it's funny we realized this on one side but not the other they told the low carb group not to eat sugars and refined grains which are by my hypothesis the most fattening carbohydrates and they also told the low-fat group to not eat refined sugars and refined grains so they basically removed the most fattening parts of the diet from both arms of the study it's funny we knew they were going to do with the low carb group because you have to and my colleagues actually knew they were going to do with the low fat group i didn't know that when i found out i was stunned because now you're testing two diets neither one of them have sugar or white bread so now you see similar weight loss with

122:08relatively poor compliance why would they do that that doesn't make any sense with the uh well there are arguments we talked to chris for a lot of his argument he was afraid there were two things um he wanted the diet to be healthy okay so a healthy diet in 2015 has become a diet that doesn't have sugar and white bread in it so he wasn't going to promote sugar and white bread to one diet or another um i take how long was the period of time where they were studying these people uh they were on the diet they were supposed to be on the diet for a year okay that makes sense yeah so that's the question is again would you expect to see a difference i can send you an email i wrote to my newsy colleagues in 2015. i could read it when i found out about this low-fat thing saying this is insane he's removed the the both groups are carbohydrate restricted right so you could think of it as a

122:57low-fat carbohydrate-restricted diet and a high-fat carbohydrate-restricted diet and then he kind of got the same answer which could be for any reason whatsoever there's a paper uh i don't know if i can well i'm not going to talk about it's bad enough talking about the ambiguous studies that have been published without getting into unpublished research but so people see this the new york times for instance did two stories on it one of them said it's not about calories it's about the quality the sugar and the refined grain because both groups restricted sugar and refined grains and lost weight the other and that was written by a reporter who tends to believe what we believe and the other article said it's all about the calories because both groups ended up on average eating 500 calories each it ends up from a scientific perspective being a poorly done study

123:45even though we funded it i'm not it's just it didn't answer the question you said 500 calories each five years on an average daily restricted their calories and that's actually self-reported so it's not so it's not particularly meaningful so again these are i don't like using it's complicated study because it's low in sugar well it's also free living yeah so both sides are low in sugar both sides are not eating processes they were twofold differences in total carbohydrate intake okay so even though they were both not eating as much refined carbohydrate they were still twofold differences or greater over the period of that study in total carbohydrate intake if you believe the food frequency questionnaires that you just said we don't know whether we can and you could be talking about vegetables you could be talking about fruits um well these are healthy

124:36carbohydrates that they had primarily in this study can we now can we agree that that study can be interpreted from virtually any way you want it especially because it was a free living i definitely don't agree with that um now now what we will agree on i'll agree with you on this is that refined carbohydrates and sugar are the most fattening type of carbohydrate that we can agree on oh my god we came to an agreement no no but the question is then the question is why is it because people eat so here's the thing if you if you believe gary's hypothesis now any kind of carbohydrate increases insulin levels some do it more than others refined carbohydrates do it more any kind of carbohydrate increases insulin levels relative to fat okay and so if that is true and these groups and that matters for fat loss these groups had twofold differences in carbohydrate intake even though it was

125:28predominantly healthy carbs you would have should have seen something you shouldn't have seen the exact same amount of weight loss in these two groups right right but they're not high in sugar like right isn't your argument is always that's the other part of the argument which is you take away the sugar and that was the problem with one of the problems with the energy yeah the argument i'm making and stefan's completely right i'm defending my hypothesis okay i see a study that he does the same thing he did it here we we all do it you see a study that disagrees with you you find the reason why not believe it in every study ever done has plenty of reasons not to do not to believe that's why independent replication is something you always wanted right you get another group to do the study ideally a third group people come in they criticize the study then you do it again yes and again

126:15and again and so you know what i was trying when we even when we started the nutrition science initiative the choice that was a non-profit the choice of the word initiative was to get nutrition researchers to in effect stop using these garbage poorly designed studies to come to conclusions because they like or dislike the interpretation but try to get them to think the way harder scientists would in developing studies that ask precisely the right question and then so even the pilot study that was interpreted as not supporting this hypothesis and again you could argue that for an hour and nobody's going to care that study was not randomized so non-randomized study you can't infer causality it's that's why it was a pilot study one of the many reasons it was a pilot study the people who think this carbohydrate model so that when we talk about the carbohydrate insulin model it

127:10means carbohydrates are fattening that's the basis of bread pasta potato and and sugar may be the the thing that's necessary to add to the diet to make all these carbs fat and because sugar as we talked about this a year and a half ago the fructose molecule is metabolized in the liver it's linked to fat accumulation in the liver which is linked to insulin i like the way you're squeezing your stomach fat while we're talking about this i got to work out dude um the uh i'm just bored you know for these experiments to be done right there they have to be tested right like you can't use for poorly designed experiments are poorly you know in every experiment ever done and so what we've tried to do is keep working towards better experiments there's now a new version of the ludwig experiment being done that the arnold foundation lauren john arnold funded to the tune of

128:06i think 13 billion million dollars and whatever that study finds kevin hall will probably find a reason look in it and find a reason to question it and ideally they would be working together so that you've come up with the criticisms before you've spent 13 million dollars but this is how science works my job was to tell a good story as stefan would say and i believe people who read the books can judge whether they're it's a good you know am i convincing in arguing that you add sugar there's counter evidence to everything there wasn't counter evidence it wouldn't require a journalist to come along in 20 whatever it is 19 flip to make these arms let me ask you this because this is something that you've admitted to something you said rather why are sugary carbohydrates the most fattening well if this hypothesis is correct i think you would say that they

129:06they trigger food reward or they are yes but wait wait let me just finish i would say the counter argument is that they create a hormonal milieu in the body that that over responds to insulin and insulin what we haven't said is if you look in a textbook for fat metabolism and fatty you know what causes fat storage insulin is the hormone that primarily regulates fat storage in your fat cells so the idea is you raise insulin and the sugar because of this half of it being fructose and that mostly being metabolized in the small intestine in the liver seems may indeed cause insulin resistance and if it does you over respond insulin so one is a peripheral explanation not that people don't love it and they don't want to you know over consume it whatever that means and the other is essential explanation yeah so i mean sugar is a factor that makes us want to eat foods right i mean

130:03this is one of the many food properties i would love to talk about this more that cause dopamine release in the brain and dopamine is a chemical that sets our motivational levels to do certain behaviors so the reason we become addicted to drugs is that they go in the brain and they stimulate dopamine release and that reinforces drug seeking behaviors right but this is just causing you to consume more correct but you're saying that the actual amount this if you have the same amount of carbohydrates that are sugary carbohydrates versus the same amount that are vegetable carbohydrates the sugary carbohydrates are going to be more fattening no no i didn't say it was independently of calories it's entirely dependent on calories yeah correct and we have randomized controlled trials um demonstrating this so if you look at the randomized by the way we're not we're not operating

130:53in an evidence vacuum there's tons of randomized controlled trials these random these randomized controlled studies are they short-term um it depends well it depends on how you define short-term they're not lasting years and years and years isn't the issue though long-term chronic effects like that seems to be possibly but let me put it this way you know if you believe that insulin is the cause the effect of insulin on fat cells happens almost immediately so insulin i i'm not aware of any mechanism of insulin on fat cells that takes more than a few hours to occur and so if you believe that insulin causes obesity this should be happening immediately you shouldn't have to wait months and months for this to occur oh no that doesn't make any sense at all no it does make sense why because it doesn't make sense you eat carbohydrates to you well because again he's he's kind of making

131:49this up as he goes along so the idea is we'll explain why it doesn't make sense without insulting him that's possible has he not been insulting me ever am i just biased i realize that i it's everything but necessarily saying he's insulting your stories not you personally but what what what do you what why does it make sense to you okay so the idea is when your insulin is elevated you're storing fat right uh it depends on what you mean by that that's not see you do a little bit of bait and switch here no no no that's an intel just to answer the question if it's not true clarify well it depends what do you mean by store i mean your fat cells are accumulating fat when insulin is elevated do you mean accumulate like like what necessarily hold on to fat like it inhibits uh yeah that's incorrect it stimulates lipoprotein lipase and it inhibits hormone should we should really talk

132:48about this because that's important it's in the textbooks oh yeah we'll talk about what's in the textbook don't worry gary jesus um okay so you don't believe in well just give me your position and i'll let him refute it uh it's here but just say it no no we'll just show it okay because again you're going to say it's not in here so i have the same textbook and then we'll let joe here suppression of fat mobilization by insulin and there's another graph that is a stimulation of fat mobilization congratulations to all of you people that are listening to this yeah we're all still hanging in there i know we're in the wheelchair scientifically let me just say this is going to take a long time so we agree on the molecular mechanisms okay we agree on the molecular mechanisms the impact of insulin on enzymes and fat cells what we disagree about is the implications of

133:42that and i think that's what we should talk about that's true because nowhere in that textbook does it say that insulin regulates the total size of body fat absolutely absolutely that is so i'm just talking you have added on time absolutely that mechanism would you like to know the conversation i had with the author of no not right now actually so um the now the um let me tell you about the conference no actually gary can you stop interrupting me please okay now um let me explain so insulin essentially does have effects on enzymes that cause fat cells to take up more fat and to release less fat so that's the part that you're right about that's what that textbook talks about right now that does not mean that does not imply that insulin causes fat storage as in the accumulation of fat from day to day and let me explain why that is so insulin is basically a traffic cop

134:46that allows your body to burn the fuel that you just consumed so when you eat a diet that's high in carbohydrate and low in fat your insulin goes up your body restricts the fat from going out of fat cells it turns that down not off but down it causes less fat to come out of your fat cells and then your body's burning carbs that's what you just ate right now if you eat a diet that's high in fat and lower in carbohydrate you secrete less insulin those effects don't occur on your fat cells and that allows your body to burn the fat that you just ate but at the end of the day the amount of fat that you have in your body is the amount that you ate minus the amount that you burned that's what determines the amount this is just arithmetic right amount that you ate minus the amount that you burned and if you eat a low-fat diet you're not eating much and you're not burning much you're

135:37in the same place as if you're eating a diet where you're eating a lot of fat and burning a lot of fat and the way we know that's true is because varying the amount of carbohydrate and fat in the diet makes no difference to body fatness in randomized controlled trials okay that's why we know that what i just said is correct no so first of all it's one randomized controlled trial it's kevin hall again no i'm talking about a meta analysis of 20 randomized controlled drugs about the meta-analyses we decided i think you know that that um what's wrong with the meta-analysis he doesn't like crappy study ever done he doesn't like who did it basically no no no no i don't care who does that i don't like meta-analyses i don't like the concept of them i think it's one of the problems with modern nutritional and medical sciences you do crappy studies generate garbage and then you sift

136:28through the garbage and say i can find a truth in here and the answer is do better studies answers always do better studies you can't do you know meta-analyses exist for everything the issue is just is a simple one remember we're talking about the 10 calories a day so when you said the difference between the fat burned and the fat store or the fat consumed and the fat expended has to be 10 calories a day that's that's what we're talking about 10 calories in the fat tissue okay so if it is true that if i consume 1500 calories a day and i somehow metabolize or excrete 1490 and i guarantee that no such study was ever so carefully done evidence support this uh well you could say for instance the energy balance consortium study the kevin hall study that we've talked about one of the things there are two things that happen when you put people on a ketogenic diet among other things you

137:21generate ketones and you lose ketones in the breath and in the urine and one of the things you have to do in these energy balance experiments is measure calories lost through fecal material who knows maybe you jack up the fat consumption maybe they lose more fat calories when they it out or maybe you jack up the calories matter i think when you're measuring the fat balance which you're talking about you have to measure the amount of fat in and out and so i'm giving you an example in response to your question was can you give me an example in that study they didn't do either of those measurements they modeled one and the other one they couldn't get the the assay to work after a year or two years and gave up on it and so you just don't know but getting back to this question we're talking about somebody storing 10 calories of fat in their fat cells let's never get away

138:12from that or 20 calories and so the question is always is this mechanism uh capable of explaining the 20 calories or is the what did you find from looking in that book well it's essentially what he was saying and then sun inhibits fat mobilization from facebook i could read it if you want me to read it you know i mean but i mean gary and i both agree with what's in that textbook uh you can read it if you want yeah it's there's insulin restraints fat mobilization through two mechanisms so suppression of like lipolysis is that is that right yeah lipolysis so mechanisms are described in the text and the stimulation of the re-esterification of fatty acids within the adipo adipocytes adipocytes fat cells note that the same process of uh esterification will also be simultaneously incorporated fatty acids from circulating triglycerol triglycerides yeah uh triacylglycerol triacyl

139:21triacylglycerol right released by lipoprotein lipos lampase lymphoma that's enough joe we get lipase yeah l-i-p-a-s-e uh into stored triasso glycerol yeah so let me just explain this briefly the argument i've been making and others is that insulin inhibits fat loss like if you're a fat cell and you see insulin you hold on to your fat right kind of that simple it's stefan's absolutely right this book which is we're talking about is a metabolic regulation a human perspective it's written by keith frain who's retired oxford professor is a wonderful man and he was the world's leading authority on metabolic regulation how your body controls its use of fuel and orchestrates storage and oxidation and in this book keith frain talks about how insulin determines fat accumulation in fat cells and that's not accumulation whatever fat storage fat storage fat dynamic fatty acid trafficking in and

140:29out of fat cells okay thank you so the first time i ever interviewed keith was for a piece i was doing for the journal science on uh insulin resistance and we spent about an hour on the phone and he explained to me for 20 minutes all the way insulin traps determines fatty acid trafficking across the fat cell membrane and you raise insulin you accumulate more fat on the short term and then we got to obesity and they said obesity is you know caused by uh people eating too much and i said keith when we were talking about why fat cells get fat it was all insulin mediated and when we were talking about people get fat it was this eating too much thing okay and you switched mechanisms on me so my assumption is the same reason people get fat is the same reason their fat cells get fat and you've got a whole lot of you've got this disorder metabolic syndrome we're talking about

141:30which includes not just problems with your blood lipids but it includes getting fat at your waistline increasing and it's an insulin resistance related disorder which means your insulin is elevated and again this is where we end up with two hypotheses about why insulin is elevated but if the for instance sugar can elevate insulin you end up with metabolic syndrome you're in fat storage mode that's the terminology of diet book doctors so now you're storing fat you only have to do 10 calories a day 20 calories a day you're gonna get obese and it's insulin media and insulin's responding to the carbohydrate content of the diet primarily and that's it and when i said this to keith you know you've got one mechanism for why fat cells get fat and a different mechanism for why humans get fat and i'd like to talk about this overeating concept he said you know i never thought of that

142:24i mean the guy had been in the field 40 years and he lived maybe 50. and then i had a long conversation with him i was back in oxford when i did that insane allen aragon debate i stopped off at oxford on the way to manchester and we had a long conversation with keith i said look what i want you to do is just come up with a hypothesis of obesity from the fat cells perspective right shed your brain centric energy balance centric thing and ask yourself what does the fat cell see and if nothing else ask a student to do it as an experiment i mean that would be a great thought experiment for kid what's going to make a fat cell fat and then our assumption is going to be that's what's going to make a human fat okay and keith said he literally said to me he was retiring and he was going off to garden um i kind of envied him but he said i just can't i can't put energy

143:16balance aside you're telling me to not think in terms of intake and expenditure and i i can't do it and i mean wonderful man he literally and this is again what i've been arguing is all these people are so including stefan who was you know learned in this world they're so locked into this thinking that obesity is this energy and balance and they can't get away from it so everything they do everything they interpret and when stefan says there's study after study and there's 20 randomized control studies and it's sort of i'm going to shovel the evidence on top of you and i'm saying look i guarantee if we go through those 20 studies they'll be just like the jim hill study they assumed energy balance was the cause and then they wanted to see what caused energy imbalance and they started with the wrong hypothesis they're trapped in a paradigm we've all seen this can i

144:06respond to this please okay so uh gary i pre-ordered your book i have a copy of your book right here good calories bad calories i pre-ordered this in 2008 because i was so excited to read this book yes and emailed me i tore through it and i was so persuaded when i initially read this 10 years ago that i ate a low carbohydrate diet for six months because i thought i was good i thought the carbs were going to make me fat and give me diabetes so i was fully immersed and convinced by your perspective when i read yeah and you and you signed this book you i have your signature we had a very nice dinner together and the thing that caused me to go away from that perspective was when i actually started investigating the evidence on my own underlying these ideas i started doing my own research i didn't take your word for it i started doing my own research in the lab as well

145:05and actually doing real scientific studies but what you were saying that it did not line up with what you were saying in your book and what i ended up realizing about good calories bad calories is essentially your arguments primarily rely on historical narratives and speculation and there's very little of actually saying what is the most pertinent scientific evidence to answer this question and what does that evidence have to say it's mostly historical narratives and honestly you know i'm gonna try to say this in in a non-insulting way but i will simply say that others who have looked at the same historical evidence have come to different conclusions than you have um and that includes me in the places where i've looked at the historical evidence and so um i think that you know this idea that i am like locked in some paradigm and can't see what you're talking about i

146:00was there gary i am post let me okay so let me let me let me just it was interesting because we're going to wrap this up soon so we've really gone there three hours almost um remember when you i was drove up here from san diego this morning and i was listening to stefan on a different podcast and you were talking about how your eating behavior differed on low carb diets versus the higher carb diet you eat now and you talked about your resistance it was easier to fast on the low carb diet correct okay and you didn't really have an explanation for it i don't have a very well anyway go ahead yeah so again the argument i've been making is there's there's two ways to look at everything so one way is the low-carb diet somehow because of i don't know food reward issues uh affects your urge to eat car low carb foods and because of that you don't hunger for them as much and

147:06when you're on a higher carb diet i think the way you phrased on this other podcast was your body sort of tells you it's meal time so it's conditioned to me even better so the alternative hypothesis here the other way to think about is on the low-carb diet his insulin levels are staying lower when they're staying lower he's mobilizing fat and he's oxidizing that fat and as you said on the podcast and even a you know the 135 pound marathon or has enough fat in his body to run for a week so the reason you're able to skip meals is because insulin is low i feel my wife is calling she's probably telling me i'm getting shrill um there's a different way to look at everything that's the point i'm trying to with every study i mean can you tell me evidence that can you give me actual evidence that the lower level of insulin is the cause of not needing to eat those meals no

147:57okay i'm giving you a hypothetical i'm glad you're vegan again let's no let's say like we're talking about fasting right if you're fasting for a certain prolonged period of time your body is going to go into a ketogenic state we all agree yeah right and that's that's the reason why it's easier to fast once you're in ketogenic states your body starts burning off fat and this is a widely reported it's living on fat it's metabolically flexible you don't have to eat because so but it's the idea that it's living on your fat is evidence that you're getting thinner on that low-carb diet the temperature because it's fat balance it's the amount you're eating minus the amount you're burning no but it's the question is it's also the amount you're trapping and that's what you keep leaving out so if you have no that has been tested it has not been tested that's what i'm

148:42saying that's why we founded nuci that's why we spent 30 million dollars that's why david ludwig is doing another 13 million dollar study it has not been tested when you when you feed people whether it's over feeding or under feeding and you're causing weight loss or weight maintenance the carb to fat ratio of the diet makes almost no difference let me give you another there are many studies on this the famous feeding study from the 60s which i thought when you said horton i thought you meant ed horton not tj horton so ed horton and ethan sims did a prisoner study they literally they they wanted to get over feed again they're using their thinking in terms of eating too much they wanted to get first get college kids to gain 25 percent of excess body weight this was in the 60s and they couldn't get the college kids to do it which suggests that college kids were

149:29different in the 60s than they are today so they used prisoners in the vermont state prison and they overfed them and you discuss this in your book they could get these prisoners to eat 10 000 calories a day of excess carbohydrates and excess calories it was calories not carbohydrates might have been calories they couldn't get them to add more than a thousand calories of fat okay and they talk about this sim studies were crazy because they published in 15 different journals so they interpreted the study if you looked at pounds gained per calorie added they gained more per calorie of fat than they did per calorie of carbs but if you looked at how much they could eat they couldn't add that much fat and they could add like eight thousand seven thousand extras calories of carbs it's actually a line in one of the papers where they said they would eat ten thousand calories and then go to bed

150:28hungry craving more carbs so then the question becomes again is it because the carbs are doing something in the brain to increase food reward or is it the carbs are doing something in the body so that their body has figured out a way it can orchestrate deal with this massive influx of carbs versus fat but there's always two ways to look at it and every time stefan says there's masses of evidence my job as a journalist was to go through and say does this refute that hypothesis and if it doesn't we have to hold on to it because remember we have an obesity and diabetes epidemic and the kind of advice where we tell people to sleep better and eat less or avoid foods that they love don't have pizza and ice cream and it's implies that the reason they get fat even the overeating hypothesis do you think they should be eating pizza and ice cream what do you think

151:20uh no i think we would both say don't eat pizza don't ask questions like that thank you um the uh is something wrong out there tragically wrong we know if nothing else i think you would agree with this so the whole low carb movement as you said it on this podcast was that you know what i've done if nothing else is i've convinced people they could eat low-carb diets without killing themselves that's a good thing yeah and i'm implying that i assume with the sugar book even if i'm wrong that getting people eat less sugar is a good thing so ultimately these are good things that i've done my overall entirely gary not entirely because you're telling people that only carbohydrate matters i'm not telling calories you have argued at length calorie intake and dietary fat intake and physical activity do not influence body fatness and are not important for your experience the wrong way i'm arguing

152:17that no if you're gonna look look at the model that we published that you contributed to and we signed off it doesn't say anything about faith it says that physical activity dietary fat intake and calorie intake are not important i refuse to believe that somebody who's obese got that way because they were sedentary okay okay and again this requires but what i'm saying is that there is harm in what you're saying because yes we all agree that these carbohydrates are fattening but you're saying that these other important things are irrelevant and that's the dangerous part of what you're saying no no no no no what i'm saying about calories is it's the wrong way to think about it so wait you think they do matter are you saying calories are the one don't put words in okay do they matter do calories matter calories are a way to measure the quantity of food you're

153:06eating it could use grams you could use anything else okay the question is is it the right way to think about it can you solve an obesity problem let me give you an example before we go let me just read you so excess calorie intake and physical inactivity you're secondary to this process and not themselves determinants of body fat yes that is what you said in our uh can i read you something debate notes okay that's i'm not putting words to agree i just want to read that yeah but that's different than what you just tried okay sure it is they're just okay let me read you something there just never seemed to be enough food to say carl's growing body after school he would eat a foot long sub before his mother's home-cooked dinners even after having a hefty lunch of homemade chicken rice and vegetables and his favorite snacks granola bars and bunch of crunch okay

153:57a lot of calories okay we're talking about one person we are talking about one of the weeds here yeah how is this going to well i just want to know just one of my problems okay so one anecdotal one of my problems with the whole overeating hypothesis is it's tautological you don't know if someone's overeating unless they're fat right uh incorrect well this fellow i just read you you can measure their calorie intake and you can know well wait no we would eat a foot long sub before his mother's home cooked dinners even after having a hefty lunch of homemade chicken rice and vegetables yeah yeah yeah yeah yeah again that's one story i know but the point is my point is it's like you cannot tell if someone's fat i you have no idea how many calories i consume right i could probably get a pretty decent estimate actually based on published formulas okay so and then how

154:55would you know whether i was overeating remember we're talking about 10 calories a day no it gets stored in a fat tissue well that depends on whether you mean how you define that but um i i could look at your body composition and i could tell you whether you are overeating relative to a lean person yes because i have excess body fat correct yes so without knowing if i have excess body fat you cannot tell whether i'm overeating which is the cause of the excess body fat right doesn't that strike you with circular there's nothing circular about it look if you take somebody and you increase their calorie intake carbs are fat either way they gain body fat there's nothing circular about saying that calories increases pretty confident that the fellow and if you take someone who is cur currently has obesity and you reduce their calorie intake carbs are fat doesn't make any

155:46difference they lose body fat that so there's nothing circular about this calorie fight at all it does make it no no i just the i i don't understand how you could possibly think that was circular it's so simple so let me go through it one more time listen you're not going through anything one more time we're going to wrap this up because i don't think we're getting anything done here no no it was a lot of fun it wasn't that much fun it was it was interesting i mean there's i i don't know who to believe quite honestly i think uh you both make some excellent points and uh i think there's definitely some real legitimate concern that you have about his position and i think that your position has some merit as well the position about insulin and about carbohydrates and sugar this is a really long conversation and i think we could probably do this for another six days forget about hours

156:40i think if i would recommend people i think people have to really kind of figure this out for themselves i would recommend stefan please recommend your book what what is your book again yeah the book is called the hungry bird the hungry brain and it's available everywhere amazon all that jazz correct and uh gary yeah it's uh good calories bad calories or why we get fat or the case against sugar i think we've just begun this debate i don't know i think it's been going on yeah i've got a lot of evidence here that i didn't have time to cite unfortunately well it was a long one but thank you gentlemen thank you all right thank you you