The dominant energy balance theory of obesity—that weight gain results from consuming more calories than expended—may be fundamentally flawed as a tautology rather than an explanation; historical evidence from early 20th-century researchers like Julius Bauer and Solomon Silver suggests obesity may instead be a constitutional or fuel partitioning disorder where certain individuals' bodies preferentially store energy as fat regardless of caloric intake, as demonstrated by experiments showing that hypothalamic-lesioned rats and genetically obese mice can become obese even when food intake is strictly controlled.
Why the Calorie Is a Bad Idea: Gary Taubes on Obesity Science
Added:The First Law of Thermodynamics and the traditional 'Calories In, Calories Out' (CICO) model of weight management.
Basic endocrine system function, particularly the role of insulin in promoting fat storage (lipogenesis) and inhibiting fat breakdown.
The biochemical differences between macronutrients (carbohydrates, proteins, and fats) and their distinct metabolic pathways.
The concept of metabolic homeostasis and how the body dynamically adjusts basal metabolic rate in response to energy intake.
The academic debate between the Carbohydrate-Insulin Model (CIM) and the Energy Balance Model, including critical counter-perspectives and clinical trials (e.g., research by Kevin Hall).
Therapeutic applications of carbohydrate restriction and ketogenic diets in managing metabolic syndrome, insulin resistance, and Type 2 diabetes.
The endocrine functions of adipose (fat) tissue, specifically the roles of satiety hormones like leptin and hunger hormones like ghrelin.
An analysis of how evolving nutritional paradigms impact public health guidelines, food labeling, and systemic approaches to combating the global obesity epidemic.
101.7K views2.3Klikes1:59:04Original Release: 2022-06-12
[Music] okay my talk today is going to be very similar to the talk i gave on zoom last year for which i apologize for those of you watch the zoom but i don't know how many of you did it um as you guys know or maybe you know my interest originally as a journalist is good science and bad science or why it's so easy to make mistakes in science and so hard to get the right answer i just stumbled into nutrition by accident where the science happened to be so bad that it turns out i've never been able to get out um this is one of my favorite quotes about science okay because we have certain expectations about science being correcting that's what we always hear science is self-correcting this is karl popper the sort of godfather of the philosopher of science the history of science like the history of all human ideas is a history of irresponsible dreams of obstinacy of error but science is one of the very few human activities perhaps the only one in which errors are systematically criticized and fairly often in time corrected and the key word there the key words are fairly often in time corrected not always and a lot of you guys as physicians you've always heard that line when you have one med school professor right who says you know half of what we teach you is wrong and we don't know which half and we still don't know which half so i'm going to talk about sort of the primary there's fairly odd that's supposed to be a white side okay this is the quad i used the beginning of good calories bad calories and i always come back to it men and women this claude bernard okay the father of the study of experimental medicine the probably the greatest physiologist who ever lived if any of you have time i recommend you read this book an introduction to the study of experimental medicine published in 1865 the first third is fantastic then it gets slow men who have men who have excessive faith in their theories or ideas are not only ill prepared for making discoveries they also make very poor observations of necessity they observe with a preconceived idea and when they devise an experiment they can see in its results only a confirmation of their theory in this way they distort observation and often neglect very important facts because they do not further their aim you can think of all of science all of the rigor and the skepticism and the method that involved is trying to fight the lure of the preconceived idea or the fixed idea okay and in obesity theory there was always a preconceived idea and it's now sort of the this is like newton's laws of obesity okay the fundamental cause of obesity and ovoid is an energy imbalance between calories consumed and calories expended okay and when i've talked i've interviewed hundreds and hundreds and hundreds of researchers in the community in public health and obesity research none of them know where this come from except they think that it derives from the theory of thermodynamics this is the five dollar vocabulary version of the same preconceived ideas from a obesity pathogenesis scientific statement put out by the endocrine society from a thermodynamic perspective it's clear that obesity is generally the consequence of small cumulative imbalances of energy intake and expenditure if you go back in time 1954 johns hopkins has a meeting on fat metabolism and lawrence lesson wilkins is a professor at hopkins says i am sure that we all agree that every case of obesity is due to a caloric intake in excess of the energy and growth requirements of the individual even though they're actually talking about the metabolism of fat storage at the meeting go back even further to 1942 frank evans one of the problems in obesity science by the way is you can be somebody like frank evans who might have been a smart guy he was a doctor in pittsburgh in the 1930s he started using 400 calorie diets to treat his obese patients and lo and behold they lost weight so he became an authority on obesity he says the degree of obesity is a measure of the amount of overeating in which the patient has indulged the material thus converted into fat has not been inhaled it's not been absorbed through the skin it cannot be blamed on any gland endocrine or otherwise for there is none with an aperture through which it could have been inserted this material got under the skin by one portal of entry the mouth it was eaten okay attempted compromises with this indisputable fact have seriously clouded thinking as to the nature and causes of obesity this is the first edition of duncan's diseases of metabolism which became one of the seminal textbooks in the field okay and what i'm going to argue is it's because of this indisputable fact quote unquote that they seriously clouded the thinking as the nature and causes of obesity so it's worth going back prior to the say the calorie revolution just to see how people thought at the time and this is thomas hawk's tanner who had one of the seminal textbooks in medicine and this is the 1870 edition and you can see when they were talking about obesity back then doctors didn't really know what was happening so the cause of obesity are numerous it's often hereditary or constitutional overfeeding will induce fat they think that's true but the obese are not always great eaters so maybe they're not over feeding and then of course farinaceans and vegetable foods are fattening which are carbohydrates and saccharine matters sugar are especially so but we're not going there today constitutional what did they mean by didn't a constitutional cause of obesity and this was the alternative hypothesis the opposite way to think about this disorder and the best way i ever saw it described was actually by a character in a george bernard shaw fellaini tarleton who says no matter how little you eat you put on flesh if you're made that way okay that's the alternative hypothesis you might be able to stop it by starving yourself but what your body wants to do is put on flesh so we always have to keep that in mind one of the keys to doing good science is being able to keep two ideas in your head simultaneously so whenever you look at the data you can ask yourself not whether it supports your preconceived idea but whether it also supports all the other working hypotheses you could come up with so this constitutional idea is obesity as a fuel partitioning disorder not how much you eat and exercise and i didn't take and expenditure not overeating but feel partitioning what your body does with what you eat to quote eric westman thank you eric let's see where are william osler okay father of modern medicine in the united states johns hopkins university the first edition of the principles and practice of medicine a seminal textbook a very important factor is overeating but some of the aggravated cases of obesity over this plays no part and the unfortunate victim may be a notoriously small leader you still have both hypotheses here's a 1914 edition now his language is getting fancy the ideology primarily it results from inadequate oxidation of the foodstuffs associated with with or with exercise absorption of the materials which produce fire or with incomplete combustion both factors probably take part it is not always due to excess intake of food though many stout persons are light eaters on the other hand there are cases in which the increases in weight is directly due to an excess consumption you know they're confusing association right and causality they see some patients who eat a lot and get fat and they assume eating a lot causes of getting fat and they see some people who don't eat a lot and then they say it must be constitutional what's interesting is osler in 1914 is getting into fat metabolism it's beginning to be studied okay there's a marked hereditary tendency certain races are prone to obesity fat metabolism is yet imperfectly understood it's under the control of the internal secretions that's what they called hormones prior well actually by 1905 the word hormone had already been introduced but prior to that it was called internal secretions the whole science of endocrinology only began in the 1860s okay one of the things we forget or we tend if we think about science back then we don't really have any conception of what it was but what science was at the turn of the century particularly in a field like obesity was a few people thinking about the cause and there were a few people studying endocrinology and internal secretions mostly because they hoped that they could you know um purify testosterone and inject it and you know find eternal youth um meanwhile while this is going on there's a nutrition revolution so this is happening on the sidelines this starts in germany in 1860s with the creation of this device which is a calorimeter that allows biochemists for the first time ever to measure the energy expended by large animals or humans in this case there's a dog in the calorimetric device from the late 1860s onward to the 1920s all of nutrition science was about vitamins and minerals and protein and energy energy expended energy consumed you could measure those things so that's what they discussed and by 1903 1907 they finally had a theory that took this idea of calories in and calories out and transmuted it into obesity and it was uh carl von norden who was a leading diabetologist in germany at the time and he actually had three theories of obesity the first one was fascinating it was a diabetogenous obesity he called it and it was dead on it's really bizarre the above conception brings us to the following clinical schema there are cases in which the combustion of sugar and its conversion into fat are simultaneously defective glycosyria that's sugar in the urine of various degrees with wasting ordinary diabetes that's type one okay there are cases in which the combustion of sugar but not its synthesis into fat is defective obesity without glycosyria mass diabetes he called it and these cases that's obesity and syndrome and then cases develop at a later date into case in which the combustion of sugar is defective and the heaping up of carbohydrates in the form of excessive fat also begins to fail obesity with subsequent glycosyria that's type 2 diabetes okay and then he says by going step further case of group 3 become cases of group 1 which writes because the pancreas gets exhausted and he worsens through and he says this is a connection between diabetes and obesity completely dead on without any understanding of insulin insulin resistance or anything else he's just making a hypothesis based on his clinical observations but then he decides that he's going to get into this nutrition physics thing and he gives two more theories and he talks about the energy exchange this is later in the same volume in the book he said obesity is a result of a long continued disproportion between the fat consumed and that metabolized okay from this it follows that obesity may occur as a result of increased food supply too much food or enormous food supply with diminished energy expenditure so from this he comes up with two theories one he calls endogenous obesity which is obesity associated with normal expenditure and you eat too much that's most people and the other he calls exogenous excuse me that was exogenous because it's caused by bringing in too much food and then the second is due to metabolism so you eat normally but your metabolism is somehow slow okay these theories come on to dominate medicine for the next well will see what happens but again what happens is you have one textbook discussing it you have one expert one authority who comes up with an idea and the whole field says to themselves this must be this is what we got right i mean who knows maybe in physics if somebody else had come up with a different theory of relativity we'd have somebody to argue with you know einstein against but okay so there are obvious problems with the energy balance idea which are fascinating okay the first one is how does anyone knock that fat okay because the goal right is you're balancing your intake to your expenditure perfectly and eugene dubois who is the leading authority on metabolism the united states in the 1920s in his seminal basal metabolism and health and disease textbook addresses this problem he says look 165 pound man who weighs exactly the same amount 20 years ago had to balance his intake to expenditure perfectly okay this means that the total intake of food must have been adapted to the total expenditure with an error he says of only.005 or one percent if he only gains a kilogram in 20 years okay this is an extraordinary exactness which is equaled by few mechanical devices and almost no other biological processes there's no stranger phenomenon than the maintenance of a constant body weight under marked variation in bodily activity and food consumption this is a problem okay nowadays when i deal with people who are convinced it's all about calories and intake and expenditure i often say to them why is it you stay then what differentiates you from the rest of us and you're not allowed to say that it's because you're virtuous and you can balance your intake to your expenditure okay here's the other issue when you say that intake and expenditure cause fat accumulation cause the growth of your fat tissue you're going against every other physiological process i think dr uh bob sebas made this point earlier okay and gustavo bergman who is a leading german authority on internal medicine said this in 1927 it seems just as illogical to say child you shoot up in height because you eat too much or you exercise too little or you have remained small because you play too much sport that which the body needs to grow it always finds and that which it needs to become fat even if it's 10 times as much the body will save for itself from the annual balance okay that's the alternative hypothesis again 1930 comes along and the field gets experimental confirmation of the energy balance hypothesis this is really exciting okay if von norden was einstein lewis newberg was eddington you know the guy went to africa that measured the light being bent during the solar eclipse okay newberg and his lab assist in margaret woodwall johnson newburgh gives a talk in washington april 20 april 12 1929 it's a very boston excuse me american association physicians meeting and he says the medical profession in general believes there are two kinds of obese persons those who become fat because they overeat are under exercise and those composing a second group is adiposity is not closely related to diet but it's caused by an endocrine or constitutional abnormality and then when he presents this is the experiment newberg was very proud of the fact he thought that at university of michigan he had created a mechanism to measure the evaporation of perspiration from the skin and his expertise was water retention or not and like every other 3-bit scientist in the world if he had an expertise that defined everything he believed about what he was studying in this case he measured he put a thin person the normal subject during undernutrition so he semi starves a normal subject he measures how much weight they lose and he plots it against how much they should lose the laws of thermodynamics hold true and then he does the same with six or seven he's not precise obese people and he notices with the obese people the idea was if they didn't lose weight with calorie restriction that was evidence that they suffered this endocrine disorder but he says look they don't lose weight because they retain a lot of water and then when the water finally you know flushes there's the weight loss and you end up with the same weight loss and therefore in conclusion we can commit ourselves to the statement that obesity is never directly caused by abnormal metabolism okay this is a comparison of one normal weight subject versus six or seven obese subjects the one thing i have to add by the way when you cut calories to about 800 calories which he did you also cut carbohydrates significantly so one of the traps these people always fell into because they weren't thinking in terms of carbohydrates and insulin they knew nothing about that so they always fell into the trap of manipulating both variables simultaneously but only thinking of one frank evans who i mentioned was famous for giving people 300 400 calorie diets like 300 pounders and when he discusses the nutrient composition they have seven grams of carbohydrates in them but he thinks of them as very low calorie diets seven grams of carbs no fat okay it is always due to the food habits not adjusted to the metabolic requirement either the ingestion of food more than is normally needed or the failure to reduce the intake in response to a lowered requirement okay there are unavoidable implications to the energy balance perspective which is as as dubai pointed out you know a tiny difference in intake and expenditure leads up to an enormous amount of weight over time and so not only do lean people um balance their energy expenditure intake to expenditure perfectly better than any machine but people who get fat are gaining you know if you're gaining two or three pounds a year you're storing 10 or 15 excess calories a day as fat now excuse me 20 or 30 excess calories a day is fat so the question is why don't people adjust if that's how small the imbalance is you've got to answer this question why don't they adjust and as newberg put it well through long training they or you could say we have come to require stimuli of greater intensity before they feel satisfied or else they deliberately disregard the warning in order to continue a little longer the pleasures that come with eating in other words a combination of weak wound a pleasure seeking outlook upon life lays the background for the condition the mental makeup of these people resembles that of chronic alcoholics okay this is where the fat shaming comes in as soon as you accept that obesity is in a sort of energy balance you have to explain why people are overweight or obese do not adjust because it's a tiny imbalance that lead can lead to massive amounts of obesity i have a friend who used to weigh 400 pounds he got that he was 400 pounds at age 18 that's about 100 calories a day that he stored in his fat tissue that his lean friends didn't so why didn't he adjust what the hell was the matter with them and you're left with fat shame there's no way to get around it there's clearly something wrong with somebody who doesn't think enough to eat left what's interesting is even in 1930 as soon as newberg published that article julius bauer who was one of the pioneers of the science of endocrinology and and the relationship between endocrinology and genetics and in europe was horrified that americans would take this stuff seriously i don't know how else to put it and i use the word stuff as a euphemism so some bauer co-authors an article with solomon silver who was a young endocrinologist at mount sinai he became a very well-known endocrinologist he says one of us has for many years emphasized the importance of the constitutional nature of obesity however the exact limitations of this concept may not have been understood and then the many minds of many constitutions of scraphead and which are thrown all speculative medical concepts and he wants to set it right and one of the things he points out is that you've got to explain not why people who get fatter in positive energy balance because that's what the laws of thermodynamics tell you right getting fat is gaining weight adding mass that's you know intake greater than expenditure you've got to explain why they stay in positive energy balance for long enough to get fat why they don't adjust and the understanding of the problem obesity requires an answer to these questions rather than experiments to prove the obvious fact that obesity patients eat more than they expand they're being obese as proof of that and then he says if we locate the genesis of obesity and a constitutional destiny of the tissues of certain people to store fat then we can understand a disturbed balance between intake and expenditure is a necessary sequel of this almost irresistible tendency we're back to the alternative hypothesis of tarleton some people you know put on weight no matter how little they ate so the constitutional hypothesis made progress once bower and silva wrote about it and then uh it was uh published in a textbook on metabolic diseases written by the leading german expert eric graf that was then translated into english in 1933 suddenly the american community had access to this idea that obesity is a constitutional disorder and by 1938 russell wilder who was a leading obesity and diabetes specialist at the mayo clinic was saying look we got to take this seriously you know it deserves a tentative consideration the idea that people who get fat store a little bit of excess fat and they can't mobilize it after every meal is an important conception and it would explain he said a slight tendency in this direction would have a profound effect so what's some more on the console 1941.
bauer has moved to the united states he's fled europe he's a jew working in austria when the nazis uh the germans invaded austria in 1938 bauer flees comes first he settles in new orleans he works at lsu for a year uh not surprised that he then heads out to los angeles where he ends up working for the hospital of medical evangelist so this is one of the great endocrinologists in europe if you know anyone from the university of vienna and you ask them about julius bauer and they're in biology or medicine they're likely to know his name okay but now he's working in hollywood california and he's horrified to learn that the united states people take this energy balance idea seriously so he writes a 30 page article in annals of internal medicine in which he basically attacks the energy balance theory says the cons conception of obesity has been substantiated chiefly by newberg and johnson and almost universally accepted on account of its promulgation by leading authorities yet it's not satisfactory for the following reasons and he lists how many nine of them and i won't go through them all but they're interesting well maybe i will let's go backwards okay first of all it's a tautology not an explanation if someone gains weight they're in positive energy balance it doesn't tell you why they gained weight you just it's like if this room gets crowded more people have entered than left okay you probably can't produce obesity in a lean individual by overfeeding and those experiments were later done in every other system growth causes hunger not vice versa okay elephants eat more than basid hounds because elephants are bigger than basset hounds they don't get bigger because they eat more and this is true of every growth phenomena and then same for decreased output how would you know a decreased output is not the consequence of growth rather than the cause and disorders that result in reduced metabolism i.e hypothyroidism do not cause obesity and then he says if energy imbalance caused obesity then it would be necessary to discriminate between the different food stuffs only as far as their calorie value is concerned for the purpose of transformation of energy a calorie is a calorie for the purpose of treating obese persons it is not okay and then he goes on um is the distribution of the energy in the body to which counts not alone the rough imbalance between its intake and expenditure it's a fuel partitioning disorder it's what your body does with what you eat quoting eric westman again who's going to take seriously somebody's writing from hollywood california if you don't know anything about what's been going on in medicine in europe for the past 40 years which american physicians in general did not when i interviewed one of the leading endocrinologists in the country when i was writing good calories bad calories this was like 2003.
he did his work in the 1960s and i said why didn't anyone take your work seriously and he said what we used to say in medicine is the mississippi river runs long and deep so if you were to the west of the mississippi you could do anything you want nobody would pay attention the only thing that mattered was like you know from boston south to philadelphia okay energy balance carries a day bower writes his article attacking newberg a year later newberg responds with a 60-page article in the same journal showing the exact same data he showed in 1930.
discusses von bergman and bowers theory in a single well two sentences the suggestion of von bergman so valuably defended by bower that the fat cells of obese persons possess an abnormally great ability for fat and exaggerated capacity for tainting it finds no support in experiments designed to test its validity body build is inherited obesity is not summary it's hoped that the foregoing discussion has convinced the reader that obesity is never directly produced by increased or diminished activity of an endocrine gland never in other words no internal secretion is capable of so changing the metabolism that the total amount of fat in the body will increase unless the inflow of calories is greater than the alpha that indeed is true but it's another tautology the implications again are clear you have to understand why you know why is it people get fat if this is the problem energy balance so the prime proximate causes to which some persons respond by overeating over emphasis by a parent to the importance of food a lot of you in this audience result as i am grew up with that kind of belief system gratification obtained from the flavors of food the feeling of reposing comfort produced by a full stomach temporary respite from anguish caused by intellectual social or sexual failure the food habits of youth disabling disease with its lessened energy requirement okay the last one may not be shaming the rest all are and then what happens is these articles are published for whatever reason maybe because nobody knew who bower was or he wasn't reproducing the conventional wisdom this is a chart of total citations his citations went nowhere okay 10 total citations by 1959 and then he's not cited again until good calories bad calories comes out and it starts trickling out newberg's articles are consistently published into the 1970s where this idea that obesity is caused by energy and balance has become so ingrained it's like you don't have to cite him any more than you have to reference darwin when you talk about evolution so testing the hypotheses one of the things that's fascinating so science is right hypothesis and test until you have an animal model you cannot test the hypotheses so it's all speculation and the kind of observational speculation that newberg did but now beginning in 1938 you finally have an animal model of obesity it's the lesioning the ventral medial hypothalamus of rats it's pioneered at northwestern university center there for the study of brain analogy run by a guy named stephen ranson who's a leading brain anatomist of the time and the work is pioneered by a graduate student named heatherington and there's another graduate student in the laboratory named brobeck actually they're both post-docs broback decides with the war looming to go back to medical school so he goes to yale and at yale he gets a job to pay for medical school and the job is to do research and they have the kind of stereotactic instrument in this laboratory necessary to do these venture medial lesions that he learned from hetherington at ransom's lab i'm going to get to this in a second i'm getting ahead of myself but i love this story so brobeck decides he's going to do vmh lesion animal experiments at yale after it's been pioneered by his buddy hetherington and northwestern so the questions to keep in mind when we look at those experiments if a laboratory animal eats voraciously as it grows obese does that mean the animal gets obese because it eats voraciously okay sorry maybe it is voraciously because of or for the same reasons it's getting obese that's always a possibility and if the animal develops obesity even when eating less than a lean animal no matter how little it eats says tarlington put it can we still say it got fat because it ate too much can we blame its appetite for the obesity these questions are going to come back for the next 70 years and i hope i have time to cover them because i have a gazillion slides and as i start telling the story i get into the details and the thing blows up competing hypotheses of hypothalamic lesions just as they were competing hypotheses of human obesity there were competing hypotheses of hypothalamic obesity so here's hetherington and rats first hetherington and ransom's first paper on the study in 1940 and then brobeck does his work and he says the present study was undertaken to investigate the pathogenesis of hypothalamic obesity in the rat by measuring the energy exchange of animals subjected to hypothalamic operations so he's already got that preconceived idea that it's about energy and it can learn something by looking at intake and expenditure and he says hypothalamic lesions which eventually induced adiposity were found to produce an increase in the amount of food eaten by the rats an increase which was usually evident even before the animal had completely recovered from the operation and he's fascinated by how much these animals eat i've interviewed people who did these experiments in the 1960s 1970s the animals wake up from surgery gasping for food the way they might have been gasping for breath if they had been suffocated all this time it's fascinating phenomena they do this in ravenous eating they voraciously eat and research has very quickly learned that they have to not let the animal eat until the anesthesia wears off or they'll choke to death eating that quickly so brobeck sees the rabbit of seeding he sees the animals getting obese he assumes the ravenous eating causes obesity because he's read newberg and he knows that obesity is caused by overeating that's his theory in fact he considers his discovery hypothalamic hyperphagia the idea is the fact that these animals get obese is not interesting to him he believes he's discovered the reason for the obesity which is the hyperphagia which means eating too much so now heatherington and ranson come along and heatherington rants and say something interesting in their lab they also saw animals that got obese without hyperphagia they were incredibly sedentary so what broback thought is that hetherington and ranson were arguing that the animals got obese because they were sedentary because brobeck couldn't get the energy balance idea out of his head but hetherington and ranson said something very different they said in the first place the two factors overeating and sedentary behavior hyperphagia and sedentary behavior are complementary in their effect upon body weight both would tend to increase it a very sedentary life combined with a high caloric intake would seem to be an ideal combination for building up a thick piniculus adiposes a layer of fat secondly these two factors may be only symptomatic okay not fundamental it's not difficult to imagine for example condition of hidden cellular semi starvation caused by a lack of easily utilizable energy producing material which would soon tend to force the body either to increase its food intake or to cut down its energy expenditure of both and this connection would be of great interest to determine whether these examined animals exhibit a preference for any particular class of foods ransom and hetherington have read bower they sight bower so they think look if you're making the animal obese and maybe you're shutting off its supply of fat to access to a fat supply that would explain why it wakes up so hungry and why it's sedentary because you've cut off its energy supply you've changed how it partitions fuel okay so they have the opposite hypothesis brobeck says it's because they eat too much the hyperphagia the energy balance hypothesis wins out for a very easy reason there's a famous expression that science precedes funeral by funeral in this case three months after heatherington and ransom published that paper ransom died of a heart attack literally a funeral and hetherington it's 1943 the postdoc joins the air force it's the middle of the war and brobeck is left in the field all alone the only one interpreting this data and he continues to interpret it as energy balance the greatly augmented food intake appears to be a consequence of a highly abnormal attitude towards food an attitude which is most noticeable blah blah blah you know the animals ate hardly this is all he sees okay and a careful search of the data i love this because people will say this today on twitter about our ideas a careful search of the data published from various laboratories however yields almost no evidence to justify the opinion that the lesions directly set up any type of metabolic disorder rather the data appear to support the interpretation that hypothalamic obesity arises from certain specific deficiencies in the regulation of intake and output okay almost and what's interesting about this is brobeck's own research provided evidence because brobec too had rats that got obese without increasing their intake so they ate just as much as the lean control animals and they got obese anyway at three of the 12 animals he studied and he decided there must have been something wrong with the experiment so he threw him out a common thing when you have a preconceived idea it gives you a license to throw out all the data you don't like we all do it by the way i do it also but i like to think i'm justified brobeck to attempt to explain the pathogenesis of the obesity therefore is to attempt to identify the source of the surplus energy and to determine why the animal spends less energy than it takes in this is the first major article written on obesity after world war ii and one of the things that happens after world war ii is people flood into the field they go back to their lives they go back to being doctors doctors become researchers and this is what programs them this and the fact that newberg is the only one left in the field also and newberg's still saying the same thing so the question is why do they eat so much that's what it comes down to by the post-world war ii because of the way brobeck interpreted these studies and because of branson's death and the fact that hetherington was a patriot and joined the war and denver went back to obesity research i can't say i blame him this is what happens so basic science 101 the importance of control experiments when you're studying pathological science one of the things you learn is that people who do bad science pathological science don't like to do control experiments because when you're doing a control experiment you're testing your hypothesis okay so if i think obesity is caused by eating too much let me do an experiment where i don't let the animal eat any more than any other animal i control for overeating and see if the animal gets fat anyway and it said brobeck did this and his animals did some of them so he threw him out okay mccuskey brooks and lambert at johns hopkins did this with their vmh lesioned rats using albino rats it was found that when potentially obese animals rats with lesions properly placed to produce obesity were limited to an amount of food which they habitually ate in the pre-op period they eventually became definitively obese anyway okay doesn't that tell you that this is not about overeating remember the power of a preconceived idea not to mccluskey brooks and lambert the major cause of this experimentally reduced obesity was a breakdown of the balance between intake and energy utilization inappropriate augmentation of the appetite was presumably accompanied by a significant decrease in caloric requirement even though when they controlled for the inappropriate augmentation of the appetite the animal got obese anyway so what happens is by 1948 you've got two entirely different theories while this has been going on there's also been a revolution going on in studying fat metabolism okay one of the things that's necessary was you needed a mechanism to follow where foods went in the body so you could see whether or not animals are building fat and what they're doing with the fat and the carbs they're eating and in the 1930s researchers at columbia university led by a german immigrant named rudolf shangham i pioneered the use of you know using a radioactive isotopes of hydrogen to to tag food so you could follow it from the diet to its end point in the animals and by 1948 research done enormous amount learning about what regulates fat metabolism so we have to keep these questions in mind again or maybe we don't um the laboratory we don't at the moment grow back 1948 the regulation of the energy exchange okay regulation of fat storage now appears to be a passive process subject only indirectly to control presumably the fatty depots increase in size whenever energy intake exceeds total output a decrease when the situation is reversed if this is true the quantity of fat in the body is determined by mechanisms which regulate food intake work or activity and body temperature very same year ernst weierheimer and bruce shapiro wertheimer was another german immigrant biochemist who fled nazi germany and went to israel shapiro was his graduate student they do the seminal work on the physiology of adipose tissue this is literally the first review article ever written so when you're studying obesity obesity is a passive fat accumulation is a passive process okay determined by how much you eat wernheimer and shapiro are saying the classical theory that fat is deposited in the adipose tissue only when given an excess of the caloric requirement has been finally disproved in fact it was disproved very easily and in conditions like think about diabetic lipemia uncontrolled diabetes these people or animals will have a high level of fat in the blood but their fat tissue is becoming emaciated so clearly the fat level in the blood isn't flowing into the fat tissue just because it's in excess there must be something directly controlling the accumulation of fat on the fat tissue that's on the fat cell as well as whatever hormonal factors the balance between deposition and mobilization must thus be controlled by a factor acting directly on the fat cell so theories of obesity post neubring and brew back this is fascinating to me they become theories of eating behavior from 19 post-war on when researchers are talking about obesity and they're coming up with theories they're not trying to explain why people who get fat easily get fat easily they're trying to explain why fat people eat too much because they believe that's the cause okay so jean my ear who became famous he was a leading nutritionist one of the first nutritionists to go to work at the harvard school of nutrition has a glucose static mechanism of regulation of food intake the idea is somehow your brain's responding to blood sugar and determining whether to eat or not and fat people must be defective alteration of the regulation of energy intake in particular hypothalamic obesity and he's experienced citing brobec and then the kennedy in the uk the role of depot fat and the hypothalamic-controlled food intake this idea was that somehow the fat stores and the fat in the blood signal the brain when to eat and when not this became fed into the theory of leptin which the longer you guys let me speak the more i might get into by the 1960s psychologists and psychiatrists were in charge of the field of obesity okay that's where all the progress was made joan myer is still writing about it but he says when for some reason this balance is upset in such a way that energy intake consistently exceeds energy expenditure the inevitable result is obesity so it's regulation of food intake that's what we're studying we're not studying regulation of fat accumulation that's going on in a different field by the 1960s they've focused in on insulin which is dominating that but this talk isn't about that here's stanley schachter whose work was considered sort of the seminal work in the field in the late 1960s these persistent findings that the obese are relatively insensitive to variations in the physiological correlates of food deprivation but highly sensitive to environmental food-related cues is perhaps one key to understanding the notorious long-running effectiveness of virtually all attempts to treat obesity this is a fancy way of saying that obese people have no willpower and it's back to fat shaming but this was one of the great advances of posts in the late 1960s perhaps the only advance and then by the 1970s one of shakhtar's collaborators judith rhoden who went on to run the rockefeller foundation actually published a paper explaining how they screwed this up so it wasn't even true so what are they missing and again it's the pair feeding experiments the controls if you think obesity is caused by eating too much control for eating too much and see what happens okay independence of food intake and obesity following ventumato hypothalamic lesions in the rats by the 1970s these experiments have been dozens and dozens and dozens of times you could fix the food intake and experimental obesity consistently results from ventral medial hypothalamic lesions independently of the development of hyperphagia this was a review in 2005 by bruce king it was at the university of new orleans about a hundred page review and this sentence shows up over and over and over again in the article okay vmh lesions could not have been called the obesity could not have been caused by hypervasia because the obesity happens even without it okay now we'll get to leptin most obesity researchers don't go into obesity research because they want to elucidate the fundamental cause of the problem because they think it's been elucidated right people who suffer from obesity eat too much okay they stumble into the field from some side like they're studying some signaling molecule and some signaling pathway that ends up being linked to obesity and a mouse model and suddenly they're obesity researchers this is one reason why they know nothing about the history of the field you now know more about the history of obesity research than 99.99 of everyone in the field okay jeff friedman rockefeller university is one of the few people who went into this field determined to make a great discovery about obesity and he wanted to understand why obese animals might eat too much and he had read kennedy articles on his lipostatic theory what's the signal from the fat tissue to the brain so that as the fat tissue starts to grow the brain knows to eat less there must be a signal and then he had been talking to people at cornell university in the 1973 discover that cholecystokinin was a signal that went from the gut to the brain and animals and was a influenced how much the animals ate depending on the cholecystokinin cornell people didn't say anything about obesity they didn't consider it relevant to obesity but it was another idea that there's a signal from the gut or the fat tissue telling the brain how much to eat okay or when to stop eating so that's what left in his target animal was the obob mouse which showed up in a laboratory in uh you know the the jackson labs in maine i think it was 1947 or 57. the fat mouse grows up the fascinating experiments done where you do peribiosis where you link the rats together there was also there's an obob mouse that was obese and a dbdb mouse and a different strain that got obese and diabetic and then this fellow george harvey in the uk also did peribiosis experiments where you'd link the circulatory systems together and he said the obesity is due mainly if not entirely to an increase in the amount of food eaten and what's interesting here is he says not entirely but he's quoting both heatherington and ranson and brobeck so one of the things that happens is people believe that obesity is caused by overeating can read hetherington and grandson and not actually realize they're saying something different and then they start referencing as you'll see friedman does the same so in 1993 1994 friedman identifies the gene that's defective in this obob mouse and he calls it leptin and he says the mechanisms that balance food intake and expenditure determine who will be obese and who will be lean that's the first line because that's what friedman grew up believing and that's what he went to study okay that's what he was looking for it was a preconceived idea remember claude bernard if you start off with the preconceived idea you're going to observe your expanding the results of your experiments incorrectly you're going to observe the results of experiments through the prism of that preconceived ideas the increase in body weight associated with vmh lesions as a result of both increased food intake and decreased energy expenditure he's citing brobeck okay because he's an energy balance guy and when the new york times reports this they report leptin as a you know as friedman was thinking about as a hormone that's the fat tissue secretes that tells the brain whether to eat or not that way the fat stores of the body tell the brain how big or small they are and the brain can regulate food intake accordingly okay this is leptin's uh friedman's review article in nature it has been proposed that signals reflecting nutritional state are sensed by the hypothalamus which in turn modulates intake and energy expenditure he too was citing hetherington and ransom even though that's not what they said or that's not what they proposed is the explanation and then you come up with the theory this is my no there there theory when you look at it um all the signals are going from the fat tissue to the hypothalamus of the brain and then they're determining food intake energy expenditure when you look at the fat tissue itself which is on the upper left here and down here there's no intake okay the idea is that's completely regulated by food intake energy expenditure and then he does have fat and glucose metabolism but he doesn't point out that that could dramatically increase so by this time the constitutional hypothesis has gone away even though they've now found a gene the first gene ever that's definitively linked to obesity the interesting thing is that while this is happening they start publishing articles linking obesity leptin itself and demonstrating its effect in the periphery as a fuel partitioning hormone you can kind of think of leptin as doing for fat and fatty acids what insulin does for glucose so it tells the body the cells to burn fat because it's also it's being secreted in response to glucose uptake of fatty acids in the fat cells and then it's signaling the rest of the body look we got fat go ahead and burn it it's actually upregulating fatty metabolism and other cells in the same way that insulin upregulates glucose metabolism so it's like the fat version of insulin these data demonstrate that leptin has direct acute effects on skeletal muscle these are like three of a few hundred articles leptin may have a stimulating effect on fat oxidation and obese subjects this is a seminal article in science these findings suggest that down regulation of scd-1 in the liver is an important component of leptin's metabolic actions that a significant proportion of leptin's metabolic effects may result from inhibition of this enzyme so in this article published in science friedman who believes that leptin is an appetite hormone is saying that a significant effect of its action could be the down regulation of this enzyme in the liver having nothing to do directly with food intake and this enzyme happens to be in the malonyl coa pathway that leads to the krebs cycle and it works opposite insulin so insulin up regulates this enzyme and leptin inhibits it okay the data suggests that insulin up regulates and leptin down regulates adipocyte fatty acid uptake leading to alterations in fatty acid partitioning that affect obesity adiposity a likely participating mechanism for these effects has leptin induced partitioning of triglycerides into oxidative pathways that's the same concept i mean these are there are i don't know if there are hundreds there are dozens of these articles there's thousands and thousands of articles on left and most of them are interpreted through the conventional wisdom when people went to look for effects in the periphery they found profound effects several studies have suggested that leptin's effects on metabolism are mediated by the liver skeletal muscle and heart or other highly metabolic organs and have been suggested to play a role in the increased energy expenditure associated with leptin treatment however leptin's effects on metabolism or mitochondrial function in these tissues have not been directly studied this is friedman himself in 2008 okay so they've been so focused on appetite that they could say all the effects in the periphery determining fuel partition the up regulation or down regulation of fatty acid oxidation the sort of insulin-like effect of leptin on fat haven't been studied so energy balance wins out again because it's perceived idea by the time friedman writes is left in a 20 an overview leptin functions is an afferent signal and a negative feedback loop that regulates food intake okay metabolism to maintain homeostatic control so perhaps the biggest question is how do we decide to eat or not to eat perhaps the answer to this timeless question will be part of future volumes on less than biology so you would think right they're studying obesity jeff friedman thinks of himself as studying obesity the question is why are these people accumulating fat right who cares how much they eat we'll figure that out down the road it's probably related if hetherington and ranson were right leptin modulates food intake and body weight largely although not exclusively by stimulating neurons in the rq8 nucleus of the hypothalamus again there's no there there there's just no nothing's going into the fat tissue except the excess left over from intake and expenditure so what did they not do actually they did it they did the control experiment season control experiments were actually done by doug coleman okay doug coleman was at jackson labs he did the original parabiosis experiments on the obi db mouse that led friedman to discovering leptin and coleman shared most of the awards with friedman coleman passed away a few years ago i wish he was still alive okay so what he did in 1985 is fascinating what he published in 1985 this is the second time he'd done this experiment second time he published it he measured how much food lean animals ate cut it in half and fed it to obob mice okay so he is literally semi-starving the obob mice and they get obese anyway okay i asked jeff friedman about this a couple years ago and he said you know it's an interesting observation i haven't really thought about it that much i'm direct quote and i'm i hate to sorry jeff um even when maintained on 50 of normal food intake mutants still become obese how can this possibly be disorder an appetite food intake disorder if you can cut the food they're eating in half and they get fat anyway and everyone who struggles with obesity understands precisely what's happening to these mice sometimes i think the problem with this research is that the people who study obesity aren't struggling with obesity themselves okay recent signs of a constitutional hypothesis a few more slides and then with irony and the preconceived idea okay adipose lipid turnover a group of researchers in the carolinsk institute in stockholm have actually believed for 20 years that obesity is this order of adipose tissue not overeating oh they don't like to say it pete arner is ahead of that lab and they published this article in 2019 in which they demonstrated using uh the same techniques that are used to uh carbon date basically using the radioactive isotopes in the atmosphere from the nuclear bombs that went off both in japan in 1945 and then during the tests before the test ban era and they showed that lipid removal rate decreases during aging with the failure to reciprocally adjust the rate of lipid uptake resulting in weight gain so they actually measured how old the fat was in the fat tissue the triglycerides stored in the fat tissue and they determined then people are obese the fat tissue is holding on to the fat much longer than it is in lean people they seem to be trapping the fat and keeping it there they say the imbalance corresponds to an average weight gain of 20 over 13 years which is enormous that's like 40 pounds for a 200 pounder right that's a lot of weight gain that could just come from this inhibition of fatty acid mobilization by the way insulin inhibits fatty acid mobilization and then they say previous population based studies have shown that the main driver for obesity is calorie intake not energy expenditure our results had a dynamic dimension to this suggesting that a failure to reduce calorie intake and aging leads to weight increase so they've now demonstrated that people who struggle with obesity are trapping fat in their fat tissue in a physiological phenomena that could be explained a dozen ways that we already know very well and then they conclude that the problem is that they're not eating less to make up for it okay here's a conclusion hildebrook leading authority on childhood obesity in the 1930s and 40s and 50s and 60s in 1957 she wrote a book called the importance of overweight she was at columbia university said looking at obesity without preconceived ideas one would assume that the main trend of research should be directed towards an examination of abnormalities of the fat metabolism since by definition excessive accumulation of fat is the underlying abnormality okay it's in fat accumulation disorder study the regulation of fat accumulation not how much people eat and then she said in 1957 none of this work is being done and in 1973 she wrote another book actually on anorexia more than obesity where she said now we've done this work and still nobody cares to make progress in obesity research and treatment researchers have to stop studying why and how much we eat and instead study why our bodies seem determined to accumulate excess fat okay it's not what they've been studying for the past 70 80 years and until they start thinking of it that way they're never going to make progress and i say that despite the existence of you know gop-1 agonists that probably do wonders if you don't mind taking a drug for the rest of your life to treat obesity anyway thank you very much for your extraordinary patience thank you so much now i realize you're not a clinician but based on what you're seeing in all of these patterns do you feel like we as providers should be looking at adiponectin and leptin to get a bigger picture of what's happening in our patients especially now the prices are coming down no i mean unless you have some freak patients who are doing freak things and you want a scientific puzzle to unravel and you think this will do it but otherwise you know you know what the problem is it's insulin and insulin resistance and you know the sequelae that come with it and on some level actually this is an interesting question because there's a no home movement now towards personalized nutrition to go with personalized medicine and it just it kind of mystifies me but i think the research community believes that they can you know do a genomic analysis on patients and then they'll be able to tell them based on what they learned from their genome precisely what diet works and i can't actually imagine somebody coming in who struggles with obesity who's probably spent their whole life trying to diet and trying in effect virtually every diet one of the reasons we're all here is because we eventually got to low carb ketogenic diets and they work for us and i just i wonder if there's anything they can learn from doing that that'll help them any better than telling their patients don't eat carbohydrates replace it with either fat or protein depending on who you believe and let's see what happens to you anyway yes i thought it was amusing that she said unless there's a or i think you were saying unless there's a freak uh experimenter tilt the mic up a little thank you as it happens i've actually gotten quite a lot of uh testing with leptin in particular with a lot of my experiments and actually ironically one of the most robust ones i've done which i've now replicated twice it's 15 days long in three phases which is maintenance level hypochloric and then hypercaloric i was getting fasting insulin leptin and a few other hormones including glucagon and i continue to see at least within my own blood work that leptin very tightly correlates with insulin levels it's the lower my insulin the more my my leptin and it's a very very tight regression and that doesn't surprise me but knowing that how do you change treatment well that's and that's where it gets interesting because i can't seem to translate that into my dad's side of the family that's very severely type 2 diabetic where the numbers are all over the place yeah and it's not as clear yeah one of the interesting things is you know researchers they don't actually get funding to treat obesity either they get funding to do the kind of stuff ideally they would do the kind of stuff dave does but they don't even do that so they get funded everybody gets an r01 if they're lucky which is you know five hundred thousand dollars a year for five years it doesn't get it's not a lot of money when you're also funding a laboratory and you get to look for molecules and signaling pathways and all these things and then once you find something that's linked to obesity you have to talk it up to continue getting funding so you have to make it seem like it's important and what you end up doing is basically generating noise and advertising for yourself and your molecule your ped molecule your your theory about your pet molecule and no progress gets made towards treating the disorder because nobody really wants to fund research and to treat disorder unless it's this idea of you know let's find a gene that might determine that you have a 17 percent higher chance of losing weight on a mediterranean diet than a keto diet which i don't believe yeah so just to clarify what is your leading hypothesis for why fat gets trapped in fat cells right abnormally put the mic down a little i have to say i'm hearing impaired so just to clarify what is what is your leading hypothesis right now in terms of why fat gets trapped in the fat cell pathologically why it gets trapped i think it's just postprandial insulin that is i don't think it's just postpander i think it's insulin resistance but and remember i'm a journalist who's become a historian so insulin inhibits fatty in the pollicis of fat from the fat cells so as long as insulin is elevated the fat is trying to hold on to fat okay and if you're insulin resistant you're hyperinsulinemic by definition and your fat basically your fat cells are going to be singling for most of the day to hold on to fat not to mobilize on and the same insulin is also telling the fat the lean tissue not to oxidize just leptins telling it to oxidize fat insulin is telling it not to and so you've got the signal that's basically putting you know the cliche the diet book dr lingo is fat storage mode and if you look at the evidence here that metabolism researchers who study fatty acid metabolism refer to adipose tissue as the phrase that always comes up is exquisitely sensitive to insulin okay so if there's any insulin in the bloodstream at all the fat tissue is trying to it senses it and is trying to hold on to fat so all of this again my journalistic way of thinking it well you've got a signal in your body most of the day longer than anyone who's lean to hold on to fat that's what your body's doing so fat is coming in it's not going out if it's getting out it's not being mobilized um there would be one other issue if i could remember what it is but the specter of being asked what question by eric westman has wiped it from my mind eric westman durham north carolina so i think it's required reading for medical students residents and especially obesity medicine specialists your first book on obesity which is good calories bad calories it was pivotal for me influential to try to figure out how we got into the mess that we're in and it's not quite as tedious as your talk right today although it's almost i mean yeah so the the first half of the book best i can tell no one has refuted the first half of good calories bad calories i mean it's history it's the the weak science that got us where we were or where we are were and um the second half about insulin and cancer and all that well yeah i was a little push but that's okay so anyway good calories bad calories i must read uh then you're um audience said how about doing something a little more readable or no publisher said why would we get fat why would we get no right but the good calories bad calories has the largest reference section i've seen in a book on obesity ever you know it's very well referenced thank you it's a dubious accomplishment if i'm getting it wrong though um because i don't think you got it wrong is there a question well so again i i find myself using my collegiate translation skills throughout my life you have some taobisms that are just stick with me like you know the restaurant why is it crowded and and why is bill gates rich i mean yeah well this is what i just i spoke to eric's class here by the way i got invited to speak to a uh a freshman at duke invited me to come speak to their public health class this year and it didn't seem related to you guys which is a good sign it's a good place it is the um yeah it's just you know how do we it's surprisingly difficult to get across to people this idea that the energy balance models of obesity are taught illogical that they don't tell you anything but what's a totality what does tautological mean i'm sorry i oh sorry yeah you're from north carolina okay this is like we're like a comedy routine he's he's eric's my straight man um tautology is something that says the same thing in two different ways so the energy balance equation which i think i just happened to have is another slide i wasn't going to use delta e zn minus e out okay when the the scientific committee of the endocrine society published their uh you know scientific statement on etiology of obesity they said it's a thermodynamic issue and this is what they mean the first law of thermodynamics delta e is equal to e and minus e out and so people think that obviously if you increase e in and you don't increase the out then delta e which is the energy stored in the body goes up and this tells you that if you eat too much you get fat and if you decrease energy expenditure but don't compensate by decreasing energy in this tells you that decreasing energy expenditure being sedentary can also make you fat so you take a conservation law of physics that says this is how the universe works energy cannot be created or destroyed okay so if the energy in the system changes that's the equivalent of saying that more energy went in and went out like if the number of people in this room changes it's the equivalent of saying that more people entered than left or more people left than entered because you cannot create people from nothing just like you can't create energy from nothing for somebody to get rich that means they made more money than they spent doesn't mean they got rich because they made more money than they spend so often when i talk about this when i'm talking to you know audiences don't know me i say imagine i came up here and instead of talking about obesity and weight regulation i'm talking about financial you know issues and we want to understand how to make more money how to get rich and i say well bill gates got rich because he took in more money than he made than he expect and i'm like laughed out of the room right because of course bill gates took in more money than he spent in fact we know exactly how much money balance he was in over the course of his life right because it's like 65 billion dollars whatever his net worth is just like whatever my weight is can be converted into calories and we could determine exactly my and positive energy balance from whatever my birth weight was okay so we take my weight and subtract seven pounds six ounces and we convert it to calories that's my positive energy balance none of those things say anything about cause that's the point so somehow in this world people took this conservation law and they turned it into a law of causality and on some level it's crazy okay but it happens all the time it's finally crumbling by the way or at least it's crumbling on twitter finally people are beginning to understand they don't give up the idea that obesity is caused by eating too much or any of the implications of the energy balance law but they're finally beginning to accept that this says absolutely nothing about why people get fat any more than taking in more money than you spend says anything more about why somebody got wealthy or they didn't so that's one of the i just complicated what do you think is a very simple statement but that's that's the point and it's you know that my whole lecture could have come down to i mean it's interesting at what point in the history could this have been stopped you know like had ransom not died of a heart attack would he have explained had the germans not invaded austria and the european medical community hadn't been swallowed up by the war would there have been pushback from this idiot energy balance thinking and yet one of the interesting that happened if you read you know science a couple months ago published an article by two of my best friends kevin hall and john speakman and they said look the carbohydrate insulin thinking on obesity is completely wrong but insulin does indeed play an important role so we're going to take insulin and put it into the energy balance model of obesity and then they start complicating the energy balance amount of obesity so that soon you won't be able to tell what it says at all so instead of recognizing it as being wrong and a tautology you'll just scratch your head and then they can say it's all about insulin and they could take you know it's the whole thing is crazy and sometimes i feel that way when i'm talking about this it's like how did we get here where the newton's laws of obesity are you eat too much so can i can i paraphrase you can even ask a question if you want so is what you're saying that it's all about energy balance it's just that doesn't explain why you're taking in more calories than you're burning that's exactly what i'm not saying so it's just what you say it's not how much you eat now it's not what you what how much you eat is what your body does with what you eat okay does your body preferentially store calories as fat or does it preferentially shunt them to the lean tissue does it not want to store calories as fat people are lean are not people who expend more energy than you know who are not people whose lean tissue is eating up the energy before the fat tissue gets it they're people whose fat tissue does not want to store that energy so the only thing they can do with it is burn it off you have to completely shift your causality um the energy balance thing if we never thought about energy balance again we would be fine when you're talking about growth defects or growth genetic you know acromegaly or something like that you don't care how much the people eat and exercise that's what um von bergman was saying about children when you're looking at why your kid is growing or how fast he's going i have a 12 year old who's obsessed with basketball he's desperate to go into a growth spurt because at 12 it really matters and his best friend like shot up in six inches in the past year and suddenly his best friend is getting more playing time on the basketball team you know feeding them more isn't going to make a damn bit of difference right might make them you know i might be able to modulate igf levels or something if i give them enough sugar but but seriously we don't talk about how much people you know if he grows when he grows he'll be in positive energy balance but that's not why he's growing it doesn't tell you anything so let me talk about the nut issue is an interesting one okay because you think that one of the reasons your trigger foods are nuts right one of the trigger foods so you prohibit nuts which is probably a good idea in general because there's certainly a trigger food for me but if you think about it once you go keto not to your primary source of carbohydrates okay so are people do people overeat them and that's why they can't keep their weight under control once they're going keto or is it the carbs stimulating insulin now the pancreas is hypersensitive to any signal from the carbs and the carbs are coming primarily from nuts so that stimulates fat accumulation and if you stimulate fat accumulation you'll stimulate hunger just like when my 12 year old does start having a growth spurt he'll start eating more because he'll have to feel that growth so one of the things you have to do and i remember in the beginning when i said you have to keep multiple working hypotheses in your head at one time any observation you make you have to ask okay maybe this is explained by its calories and people just eat too much maybe it's explained by the absence of leptin or protein if you believe in the protein leverage hypothesis which i don't maybe it's explained by the fact that these foods have carbohydrates in them and then now they are the primary source of carbohydrates in a ketogenic diet or of easily digestible carbohydrates so how would you explain i have a question yes the have you seen this uh reality tv show naked and afraid it's kind of like survivor people go out with permit they want to go out to this forbidden you know a place florida everglades and ireland they take away the clothes that's the naked thing but it's all blurred out it's you know and then and then they're afraid because there's things that think can kill them i mean you know snakes and things like that alligators and you should watch the show sometime because they they lose they lose a pound a day and i bring this in in my clinical situation and if you haven't been one on one with me i do it in a very nice way it's only to say that they lose a pound a day wait because they're in negative energy balance of course they're a negative energy balance there's independent of the day it's like i know remember abbott and costello who's on first and they get to i don't know when he goes third base see i don't want people to be confused with the fact that if you take the energy to zero everyone will lose weight yes yes absolutely and that's one of the observations that people got confused about because you can starve animals or starve humans and they will lose weight they thought that tells you somehow that obesity is caused by overeating because you can make people thinner by under under feeding them okay you can make animals thinner by underfeeding but you can also stunt a child's growth right by starving them you put a kid on a desert island that kid's growth is going to be stunted but you still aren't going to say that this kid grows because he's in positive energy balance it just happens to be this is where you have to understand your observation as long as you're locked into energy balance you think and they literally did i mean you see these discussions going back to the 1930s that's basically what newberg did i starve these people they lose weight they lose weight at the same rate as you would expect more or less be based on energy balance therefore this is an energy balance problem people are eating too much well i i think there are elements that i have to as a diplomat among fields that i have to acknowledge that there are times when you can perturb the energy balance and you can have people lose weight and actually sam feltham and his n1 of one study recently published gained weight on a keto diet but he had to eat 5 800 calories of it per day in order to gain weight so clearly there were but even then the question would be are you changing the physiological regulation of the fat tissue and fatty acids can you overload the tissue with fat you're storing the fat you burn the fat you eat okay that's the gets stored primarily first so it's conceivable you can overload that or it's conceived there are a lot of hormones that drive weight gain or you know the sex hormones are you know related there's a lot of ways people can be dysregulated such that their fat tissue is going to take up fat even in a zero insulin environment there is one or they're secreting insulin to the protein it's one reason why high protein diets worry me why it wouldn't be you know do you see it with type 1 diabetics who go and people with type 1 diabetes who go on ketogenic diets they are very low carb diets they now have the dose for protein because the amino acids from the protein are the dominant carbohydrates in their diet whereas when they're eating what the ada wants them to eat that protein carb signal is being just you know buried by the carb carb signal so there are all kinds of ways to explain the fat accumulation more than just we gave them a lot of calories and that the job of the scientists is to plan experiments that can say let's you know there's a way like an interesting experiment would be to fix the carbohydrates so study take a stand you know people eating their standard american diet calculate exactly what they're eating how much sugar how much carbs how much fat how much protein and the amount of calories it takes to keep them weight stable on that diet and then control for the carb content so now feed them an identical caloric you know diet where now the carbs are fixed but you manipulate the calories maybe cut the calories the fat calories dramatically and see what happens that experiment was actually done on obese women 1970 72 somewhere around there by some researchers at i think case western and they said basically insulin is responding only to the carbs and their weight doesn't change i don't depending on how much you cut the fat you might be able to get some weight out but it would be an interesting experiment to do but because in any of these experiments you're changing more than one variable at a time so you can fix carbs cut calories and cut fat you don't know if the effect is how that translates to one of the questions we want to know the prominent question is why do people get fat to begin with okay thank you eric mark cucazella west virginia university and um we can't let this finish with a softball question from eric so again thanks to gary gary actually came to west virginia three years four years ago maybe so travel into appalachia and just help me review it uh review a chapter on epidemic of obesity and diabetes in appalachia but maybe a in your opinion a quick it could even be a yes no but you had healed a bunch about the children you know when it comes to metabolism and fat accumulation are kids just little adults just little adults um in medicine the pediatricians will say like if we say kids are just little adults you'll you'll get your head cut off but when it comes to fat accumulation is there a significant difference with children i mean in terms of the dietary that's a complicated question all right well we'll hold the question yeah thank you mark but that is try to address that i mean i think the cause of what we well again the kind of obesity you're seeing in appalachia so it's not a long a i've been mispronouncing it my whole life [Music] is probably mostly pre-programmed and then fed by the you know poor quality high carb high sugar diets so you know they're not little adults in the sense that they're manifesting the obesity much earlier than their parents probably did and there are other factors going on but the treatment if you want to reverse the obesity the idea still it's the carbs in the diet that are being triggered that you know that are triggering the insulin dysregulation that's causing the fat accumulation this question might be just a little bit weird but we you started talking about well everyone will starve everyone if you go to no calories they're going to lose weight and i seem to remember a reference and i in your extensive research have you read anything about um various rates of starvation for example in uh concentration camps there were people that were scrutinized because they were kind of resistant they thought that they were being fed uh or secretly eating because they seem to resist starvation compared to others have you heard anything i actually haven't but it's an interesting question um you know you look at the obob mice right you put them in a concentration camp they're obese anyway so um but i have not seen any studies that you know again in general the people doing this work weren't thinking on that level of except that's what newberg was trying to demonstrate because his belief was if people have some uh endocrinological or constitutional predisposition to get you know to be obese that means that they won't be they will resist semi-starvation and lo and behold i semi starve them and they don't that means they're no different than lean people what he should have asked is why is it i have to semi starve these people to make them lean where i don't have to semi starve lean people that's a different question and now you're either they because these people are you know just fat people look how much they eat or maybe there's some reason that they're they can't stay in energy balance at a low weight and then the reverse is also true there are some people you could feed ad nauseum and they don't gain weight right i have brother who couldn't get he was six foot five and road crew and couldn't get over 195 pounds if he tried when i could get up to 240. um he used to say he'd come to my breakfast my cafeteria at college he was doing a fellowship there when i was a senior and he'd come to the cafeteria and he'd eat for like an hour and a half and then he would walk out with six sandwiches that were peanut butter and jam and granola on toasted raisin bread and it happened and he'd just eat him on the way home and he used to say i never get stuffed i just get bored of eating after a couple of hours and there was i i i couldn't be as thin as him i mean i would you would have to starve me and i might weigh as little as he did but i would look like i'm starving to death and he was like so yeah i often wonder if like the people study obesity and i've wanted to do this as an experiment and sort of sit outside with them in a public place like go to new york and sit in union square and just pick people at different levels of because they believe that body now the assumption is that sort of body type is genetic but obesity is wired in the brain and i want to go what point is a body what does it go from being body type to obesity does it switch from being a genetic determination of body shape to basically you've got something wrong with your brain that you can't balance and take an expenditure and i'm wondering if there's a point in which they'll say no no that's definitely eating too much but that's just body shape even though they're like five pounds different than you know weight anyway me again so there are a couple of things that really helped me in my experience the seeing the emaciated type one child who couldn't store fat be given insulin you can look up these these pictures on the internet internet not only stopped the glucose from going in the urine it let the babies plump up and become fat store fat so this is like an obvious aha moment insulin helps you store fat but the idea what they thought is the insulin stops the carbs from being peed away so you could still see that this is where everything has multiple explanations so we don't see it as well you've changed energy balance because they're no longer excreting calories they're now holding on to them so well we know now insulin facilitates fat storage yeah so well this is what just for a second it's fascinating because this phenomenon would happen almost immediately in fact it would happen before like their faces would plump up before their bodies started getting fat and so the diabetologist of the year the 1921 once insulin was discovered up john made insulin you know they created insulin they made it available to the leading diabetes specialists in the country so they could test it on their patients that's how you did you didn't have randomized controlled trials back then and they measured you know they consistently observing not only that they got fatter but that obesity was a problem in these patients within sometimes months of going on these drugs so they would go from these emaciated children to suddenly these obese children and of course the doctors thought well now they're just eating too much in there um but jocelyn this one you mentioned the 600 units of insulin was in when jocelyn first got jocelyn's the leading diabetologist in the united states and he's writing the textbooks he's had the only clinic the first clinic specializing in diabetes so he's like the god of diabetes in the u.s and in the 1920s he's trying to keep his patients with type 1 diabetes he doesn't with the acute child onset version to 15 units of insulin anything more than that he thinks is irresponsible um yeah my patient was on 600 yeah i mean it's that he would have that would have been the end of jocelyn right there if you didn't know the doctors who were recommending 40 or 45 he thought was irresponsible um the other time in life and any one who's had a child go through teenage years growth hormone makes you grow right and makes you [Music] eat more or less can you go through this equation it was really helpful for me if you can just point why doesn't a child get bigger in teenage years just because they eat more you know this is eventually our access to me he reminds me that he went to stanford and so yeah but it was years after you the um look give them growth hormone that's going to increase delta e right okay so they're getting bigger delta e goes up so that means en has to be bigger than e out and uh that awesome so either the energy so with the growth hormone they're either gonna eat more they're gonna expend less or some combination of the belt they might become lazy so my son wasn't just eating more and then he grew he was he grew was growing so that's why he ate more yes oh got it okay thank you it took me a while no really i hope that's helpful think of times when hormonally you eat more and this is what's happening with garden variety obesity but the hormone is insulin yeah yeah exactly and glucagon also but not as much hey gary how are you i would tell you that bill gates is extraordinarily wealthy because he can't stop making money he has no stopping point i i work really hard i make money but when i stop working i end i terminate my income so it's interesting you're saying his wife is actually not going to get all that wealthy because she's decided she can't stop giving it away so she's like a marathon runner and he's correct if she gets money from him it's a finite amount he has the capacity to make money so but i think what we what this whole equation is missing is the word purpose and the question is what is the purpose of your excessive energy consumption is it growth is it endurance athleticism is it muscular bulk or is it pleasure and what you're not or what a lot of people confuse is global energy consumption and uh energy output without considering purpose and the purpose drives the hormones so if you're consuming for pleasure there is that's the bill gates that doesn't stop there's no stopping point to that yeah i mean it's an interesting question because think about what determines purpose remember we could go back to um with von bergman he said that which the body needs to grow fat it'll take what it wants so the question is like when you're growing see excreting growth hormone that's telling the skeletal system to grow and you need muscles and fat tissue and vasculature and everything to go with it so that's signaling that's determining the purpose and the purpose is going to have to take the energy it needs you could think about i used to think about you know the thought experiment that i could run by my researchers we were working with back when i ran news to that i could get them to see the problem with their thinking because one of the problems with the overeating thinking is how does the body know that it's got excess energy but isn't that exact point every purpose outside of obesity has a negative feedback stopping signal obesity is positively reinforced by pleasure there is no stomach but even the pleasure again you know that if we change the hormonal regulation the fat tissue you could still do the pleasure but you can disassociate it from the obesity right but look at alcoholism alcoholism is never got to do with any other solution other than alcohol also let's rephrase let me go back you're assuming you're making the same assumption that they did when they said some people get fat because they overeat because they thought they get enormous pleasure from their food and that's why they eat or you and i we might we're in a bad mood when i'm depressed i still crave sugar okay my wife buys atkins bars god they're awful but if they're in the house i asked her to hide them from me okay so i but there's your negative feedback signal but the point is we know that the stress hormones are working on the fat tissue and we're getting you know there's a lot going on hormonally the point is the just the process of eating alone and bringing in those calories is not enough to make the fat tissue take it up and hold on to it and the rest of the body not to metabolize it and again you don't gain three pounds in one day it's not like your body has to adjust to 9 000 calories that you've overeaten i mean maybe at christmas time that is the case but you know it's sort of they're tiny amounts of fat we're trying fat accumulation we're trying to explain and a lot of children these people are pre so the other possibility is that the pleasure they get from the food determines this is what i talked about this in good calories bad calories because the point that the magma and this french brilliant french physiologist made he said look there's a famous french saying which is hunger is the best sauce right the hungrier you are the better that food will taste so maybe the pleasure and that if that hunger is determined by the availability of metabolic fuels so you're you know you get depressed or stressed your fat tissue decides to hold on to fat or whatever happens and now you've got a dearth of metabolic fuels i have a colleague who i think is probably right like your hepatocytes are not generating enough atp and now you perceive that as hunger and when you eat it foods taste better best meal i ever had was i'm not going to go into that why is it exclusively carbohydrates that make people fat people do not get i don't know if it is exclusively well i can tell you that i've never seen somebody get fat from fat and protein in a system can you just say that they get found on ketogenic you can get fat on occasion no there was that experiment that was done for a short period of time but 5800 calories a day how long can you sustain that well no and that's i and i agree 21 days i agree with you so that's why carbohydrates because they stimulate insulin why alcohol not water why alcohol not water why carbohydrates not protein and fat and the reason for that is signaling there's satiety endpoints for protein and fat there is no satiety endpoint for carbohydrates or alcohol first of all you have to start saying things like the reason for that is probably insulin okay because it's a speculation it's a hypothesis it's interesting back when i got into this business remember i told you i my obsession is good science and bad science and one thing i learned from the physicists i studied from is good science good scientists discuss their evidence and their conclusions and their interpretations tentatively and there's a famous sign line by richard feynman the first principal science is you must not fool yourself and you're the easiest person to fool so if you think you've discovered something you think you've understood something the history of science says you're wrong okay and only the very lucky person is right and so you have to discuss your results tentatively so you could back away from them when somebody finally does an experiment or you do it yourself ideally and prove that you're wrong so i it's a trigger for me when people speak declaratively even though i got to quote you speaking declaratively in my book and i'm grateful because i need other people to do it because i don't like to do it but anyway that's you know i the question then becomes why does food bring some people pleasure so much so that they overeat and get fat i mean i love a good steak i was disappointed at lunch i didn't look at the menu closely and i realized i missed what looked like a one pound rib eye at the restaurant here and had a salad much to my dismay you know but it's not going to make me fat right because there's no virtually carb free but if i had the same thing with pasta not only would it have inclined to make my body store these calories as fat and store whatever fat that came with it i'd have fallen asleep at three o'clock and i didn't miss my lecture so the question is always there was an entire field it's really interesting when i talked about the field of research into fat metabolism evolving independently of the study of obesity which is so fascinating there was also a field of physiological psychology that was studying fundamental human behaviors like hunger and thirst that also evolved independently of both of these fields although the physiological psychologists were reading the fat metabolism research because they had to so they developed theories of for instance hunger and appetite and satiety based on the availability of metabolic fuels and this idea that's what la magnan was famous for and this idea that hunger is the best source if you starve someone foods will taste better someone who's physiologically so if a person who's obese is predisposed i use this example in the case for keto you've got two people walking down the street one is lean and one is obese and the obese individual is insulin resistant and they pass they could be walking through the airport and they pass a cinnabon store right and i'm sure the cinnabon people have fans that blow the you know the aroma of freshly baked cinnabons out into the airport and the lean person who is insulin sensitive and lean smells and goes in but the obese person secretes insulin and response called the um cephalic phase insulin secretion so he secretes insulin response to the smell of the cinnabon and now that insulin tells his body to store fat and even to store carbohydrates as glycogen that empties the the the circulation of metabolic fuels so he's literally getting hungry smelling the cinnabon by the time he walks in not only do any observers go well that's why he's obese he's eating cinnabons they don't understand that his physiological state created both the hunger and then the pleasure he gets from eating the cinnabons what i want to figure out is why do i eat those damn atkins i mean there's no pleasure in it i mean not after the first bite anyway so when i focus just on chronic hyperinsulinemia causing kind of a fat part or fuel partitioning error causing fat to be trapped i have a hard time reconciling why people who do something like a potato diet would lose so much weight and be successful with it when they are allowed to eat as many potatoes as they want and they still seem to be doing pretty well yeah i i mean it's an interesting question there are few possibilities i suggest because i believe that they do i one of my best friends one of my oldest friends who lives in los angeles and has a lot of new age practitioners his father died of a heart attack ran a candy store in brooklyn and died of a heart attack in 1957 so he's very health conscious at one point he went on the blood type diet and got his blood type checked and they said look you can't eat fatty foods and he went on a very low fat diet and he lost 25 pounds in six weeks absolutely sorry thing i mean there i can imagine various scenarios to explain it even particularly zero fat or virtually zero fat diets like you could be starving your body of fat tissue because you need of fat supplies or organs that preferentially burn fat and if you're not eating fat i don't know it could be fat balance it could be hyper lipid has a theory about the zero low very low fat diets basically i forget making your liver insulin sensitive it could be that they go from eating standard american diets of some sort so they eat better quality carbs and no sugar and no sugary beverages and maybe even minimal fruit and that makes them more insulin sensitive they're lean tissue compared to your fat i mean there are a lot of ways to explain it i would love to see it studied but even then when you're studying these things it's hard to study mechanism you know you could study predictions of a theory like if you go on this diet versus that diet i predict this will happen versus that but you can't say that it did happen because your theory is correct even if like it associates i would expect their insulin to go down i wonder how much i do believe people can live with hunger i did it when i was younger for months and months and months and then eventually you can't anymore or you slowly gain the weight back also so i'd like to see the long-term effects of those diets but the same is true of keto there are people who and this happened to me i'm on what i thought was a keto diet with a lot of nuts you know i lost 25 pounds and then i slowly put 15 on back and then i gave up the nuts and you know it's hard to this what i was going to say i'm going to forget again um oh when people do studies they measure insulin fasting insulin so often then when they do the dietary studies comparing different diets they measure fasting insulin insulin in the morning before you eat and that's the point in time when the two diets when insulin levels are going to be closest to being identical on any diets right because you've had eight hours of fasting and so one of the i think flaws in all those studies is you cannot measure fasting insulin and say well you know they're the same on these two diets because they're going to be the same on virtually any diets it's the wrong thing to measure and again it's one of the problems that makes this as a science extraordinarily difficult to do because there's a basically an infinite number of variety you know measurements you could do and times you could do the measurements and ways you can do the measurements and when you look at the history the measurements completely determined how people thought about what they had discovered one of the reasons they didn't think insulin had people studying insulin resistance didn't believe they would write paper seminal papers about the effect of insulin on high triglyceridedemonia and insulin and insulin resistance and they would ignore the fat tissue because they're measuring insulin resistance is glucose uptake only so if they were measuring insulin resistance as fat uptake by the fat tissue says remember fat is exquisitely sensitive to insulin it is the most sensitive tissue in the human body to insulin and yet they didn't think insulin resistance affected fat tissue because they were only measuring glucose uptake their choice of what to measure determined what they believed about virtually everything that followed and it confounds everything you do hello and thank you for your work i love it i refer my clients to your books all the time uh i i wanted to say first that i i work with a lot of people that are severely underweight from significant illness and we are able to gain the weight back on the ketogenic diet i i myself gained 50 pounds on the ketogenic diet so you can manipulate it and it's often done in a similar way that's used for children with epilepsy right much higher levels of fat but what i haven't seen and i'm sure exists but i haven't seen people get obese while eating it or go over a healthy weight right so um that said i spent a lot of my time in third world countries researching with traditional cultures and there's this interesting phenomenon that i see where as soon as like a little food comes in from the modern world it could just be corn and vegetable oil and often that is it they're not getting potato chips and cheetos and all sorts of other things but when that comes in then a huge expansion in weight of course there are other factors usually at this time they become more prone to infection so antibiotics anti-parasitics can come in as well and i think we've seen with the microbiome some interesting things that give us some puzzles for instance the chicken virus if you all have seen that that is tied so interestingly with very severe obesity in some cases or if you've seen the reuterized studies which are just fascinating to me they're animal models so you have to take them with a grain of salt but uh where the little mice become like supermodels despite the amount that they consume and i'm really interested on how this might be informing our fat storage and our our insulin and all of this and if if you've gone into this this area as well well there's a lot going on let me unpack your questions a little and i'll probably forget some the first observation is interesting by the way about you know malnutrition or anorexia being cured or reversed by ketogenic diet so one of the things i implied in my first two books is that if obesity is in a sort of overeating then anorexia is probably not a disorder of undereating and you could imagine that if somebody's so typically you your lean tissue get ins insulin resistant just what von norden described in his diabetes obesity and then your fat tissue remains sensitive to insulin so it could take up the continue to take up fat even in this hyperinsulinemic environment but you could imagine if the adipose tissue became insensitive to insulin first you could have a scenario where somebody would lose weight because they're losing weight their delta e is going down that means their en has to go down or their e out has to go out actually many people write who are anorexic are also you know will work out for hours and hours a day and it's explained on the basis that they have dysmorphic body you know and i have friends who have suffered with anorexia so i think that might be true but still you can have a scenario where you could explain malnutrition and then when researchers pre-world war ii wrote about this like the one of the seminal books on obesity was called obesity and leanness because the idea was still that maybe extreme leanness was also a fat accumulation disorder that went the other way and one of the pioneers in low diets wolf king cats what was his name huh blitz thank you in austria and his books on the subject showed sworn that he could put make people who suffer from under nutrition or anorexia look healthy eating ketogenic diet so it was always an interesting idea that if you remove if you have a diet that a person just like somebody with type 2 diabetes or type 1 diabetes can metabolize fat and protein you could feed them fat and protein and if they don't need insulin to metabolize it to take it up their bodies will work normally and this was shown in animals as well so um you know it's i can imagine that being true and i think i still to this day think that you know anorexia is not a nervous disorder so even the idea that one of the arguments for being a psychological disorder is so prevalent in women rather than men and young women but if you think of young women going through puberty massive hormonal changes going on and every young woman who goes through puberty i suspect tries to keep her weight under control right so you take a thousand young women you launch them into you know sexual maturity with massive doses of sex hormones and then you have a thousand of them try to starve themselves and maybe one out of every thousand successfully breaks their fat tissue so that it can no longer store fat now they eat less they're not getting they're not emaciated because they're not eating they're not eating because their body won't store fat they have no place to put it and you need some place to put calories in between meals i had a friend a woman who reached out to me because she read good calories bad calories who used to run the eating disorders clinic at the mayo clinic very good diet and she said they had a patient she thought the book was good calories bad calories terrific and we had it was wonderful feedback for me because she was so clearly thoughtful and intelligent she bought into my theory but she also said they put weight back on their anorexic patients by overfeeding them and she had one patient one young adolescent girl realized that she could eat atkins and be overfed and not gain weight back so that seemed to refute my hypothesis but i'm glad to hear that it's not necessarily dead it's only wounded it's not dead and i should say all the clients i work with are not anorexics actually they're from ulcerative colitis or malabsorption issues when they're underweight mine was also for malabsorption issues but in eating disorders i've seen some interesting things histamine disorders can mimic that if the histamines are very high it can give you clinical anorexia where you have no interest in food and the zinc deficiency models and animals too but yeah i would think it would work with the anorexia just as well well and it's interesting because there are animal models where you like knock out the insulin receptor on the fat tissue and those animals can't get fat no matter how much you feed them so um you know it's a science i don't know how the field years ago whenever i engaged with people who studied eating behaviors i tried to get them to think in terms of this being not necessarily an eating disorder but a fat accumulation disorder but i did not have much luck except for my mayo clinic friend very interesting yeah thank you thank you hi john hi i have a question couldn't we learn more from instead of looking at lab animals look at livestock and just think about that for a while yeah well i used to use livestock in my lectures you know jersey cattle versus whatever the beef cattle is i forget at the moment you know lean cattle versus fatty cattle um you know you start looking at livestock john you start making progress and could i recite a quick quote with a little um updated this is from the newer knowledge of nutrition the animal husbandryman knows more than the medical practitioner and i'll just get to the point because if they don't they're out of business i completely agree hi gary i'm tacla i have a keto snack not a keto crap company okay turn your mic down hi thank you and i actually credit gary with the reason why i am a keto person i'm a physicist and so is he and that's actually where my personal belief came from and actually the thing i'm gonna share is um do you know the metaphor you start with a spherical cow which is you make simplistic assumptions livestock one maybe a physics joke so in order to explain this the very simple model that i've come up with is think of a bath you know everyone's familiar with the turn the tap on and off and then water runs out of it and everyone's like you maintain an equal amount now imagine a bath where some of the the drain is really big on a bath where the drain is really small the drain that's really big is a lean person the drain whether with the small rain is an obese person so you can turn the taps off in both scenarios and everyone gets to zero ultimately so the size of the hole is your metabolic system and it works phenomenally as a way of explaining how those systems work i'm going to think about this just because i think the whole size of the hole responds to the it gets more complicated but i think we need a third we need the bathroom floor flooding we actually that's the fat tissue we need two taps ultimately and different types of holes for different metabolic systems but it works to start with interesting i'm going to think about that thank you thank you for staying longer i really appreciate that and i'm going to make this quick good calories bad calorie of course was very influential for me as well so thank you my question to you is this do you put any stake in the idea that neurological pathways can get worn in for binge eating and and eating disorders my the reason i asked that is because i've struggled with binge eating and bulimia most of my life and i absolutely can binge on steak and broccoli i can absolutely binge on keto foods it doesn't have to be carbohydrates and it doesn't have to be trigger foods but it's those it seems to me it's those neurological pathways that have been worn in so what have when you binge do you purge afterwards or do um in the past i have i don't now fortunately but i can still feel myself at times go i could just keep eating this steak and i could keep eating this broccoli and i just could keep eating and eating and eating well this is and this is and so is it more neurological or is it hormonal or do you have a idea about that i mean again it's probably both on some level interacting but i have one of the issues with overeating is you can't define overeating if you don't overeating is what the person is doing when they're getting fatter because overeating is positive energy balance which means you're getting fatter so if you're not getting fatter that's why i asked a few herbs then the question is are you overeating and so i have my own definition of overeating because i can keep going endlessly i mean i'm a big so and it's like when i've eaten you know say 1500 calories after i got stuffed that's for me overeating but simultaneously i'm confident that i'm going to you know the next day i'm not going to crave overeating again or the day after that at some point no matter how many you know i i'll get to the point i won't be able to look at a rib eye yeah no you are correct i mean i i'm the same way i'll it could be that i'll binge and then you know i'm fine for weeks or even months yeah which is an entirely different phenomena from when you know you're a i was a car beater and then you know you're basically you're hungry all the time but that seems to me again a neurological thing versus a hormonal thing yeah no it could be but i'm just saying the nerve again a good eye point at some point was that the neurological thing was not just an isolated behavior but was responding to the physiology of your body which included the hormonal thing and then you might be stuck with that link that doesn't go away um yeah i still two nicorettes 20 years after putting smoking so great thank you so much again my pleasure thank you [Music] you
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