Breast Cancer Favors

>>presenter: this talk is part of the authors@googleof the health@google series. we'll have a lot of time at the end for questions and there'sa mic here. so, i'm very pleased to welcome today, garytaubes, who is a contributing correspondent for science magazine. his work has appearedin the new york times, the atlantic, the esquire. his work has also been included in the bestof the best american science writing and also has received three science in the societyjournalism awards from the national association of science writers. he's the author, also, of 'good calories,bad calories' that i'm sure many of you know about. and currently, he is the robert woodjohnson foundation investigator in health

policy research at the university of berkeley. so, with this, we'll have gary taubes talkabout his latest book. [applause] >>gary taubes: thank you very much. this bookis basically -- 'good calories, bad calories' took me about five years to write and was500 pages long. this is the screen i used to use for thistalk and i had written that book hoping to get both the lay readers and to the publichealth authorities around the country and the medical research community. 'cause thegoal of these books are to convince people that--i mean, it's almost a clichã©--but thatour fundamental understanding of why we get

fat, of obesity, is completely incorrect andthat a new paradigm is in order. and that google should change the foods thatthey're serving at their wonderful, healthy, low-fat cafes. so, after 'good calories, badcalories' came out, i wrote 'why we get fat', in effect, to make it the kind of airplane-readingversion of 'good calories, bad calories' for people who don't have the time. i got a lot of emails from people, from doctors,who asked me if i could write a book that their patients could read, from patients whoasked me if i could write a book that their doctors would read. [laughter]

so, in this lecture, 'why we get fat' is actuallybased on the lecture. so, once you've seen this, you don't actually have to read thebook. let me see if this works a little. that's better. this is just background. you know there'san obesity epidemic in the works. i'm not gonna go over it because, as usual, i'm probablygonna run a little long on this talk. the obesity epidemic goes along with the diabetesepidemic. diabetes diagnoses have tripled in the past 30 years in the united states. and let's see if this. [pause] diabetes, obesityare associated with a host of chronic diseases that are known as metabolic diseases, whichinclude fatty liver disease, atherosclerosis,

hypertension, stroke, cancer, asthma, sleepapnea, osteoarthritis, neural degeneration. actually, alzheimer's disease is a diseasethat's now associated with what's called insulin resistance in obesity. and one of the subtexts of the talk i'm gonnagive today is that the conventional wisdom is that as we get fatter, that increases therisk of all these diseases and the fundamental problem is us getting fatter. and i'm gonna suggest that the same foods,the same thing that makes us fat, also causes these diseases. so, it's a fundamentally differentcausality. so the question we want is why do we get fat?obvious question. and the officials answers

are, "obesity occurs when a person consumesmore calories from food than he or she burns." "overweight is the result of a caloric imbalanceand is mediated by genetics and health." that's what the old surgeon general and the nih tellsus. so how many people in this room actually believethis and think it's meaningful? that's not bad. you know, i gave this talk at tufts a coupleweeks ago to the nutrition department. and the tufts people have been behind every dietaryguidelines for the past 20 years. and i asked how many people believe this and nobody--literally,nobody--raised their hand. and then i said, "are you kidding? 'cause if you don't, i canleave." and then everybody raised their hand.

and then after the talk, they said, "well,we don't really believe it." so here's a conventional wisdom: "energy inis greater than energy out." and that's why we get fat. we take in more energy than weconsume. we overeat and the excess calories go to our fat tissue. you hear about thisin a lot of different ways. in the medical literature, they'll refer to"over nutrition". "positive energy balance" is another way to phrase it. and often, virtuallyevery article you read on obesity, they'll say, "obesity is a disorder of energy balance." and when they say that, what they mean iswe take in more calories than we consume and that's why we get fat.

so here's the general image of what's goingon here. and what you wanna do when we talk about this, one of the key things you wannado in any science is explain the observations. so we have this observation of an obesityepidemic and we want to explain it by our hypothesis, which is that we take in morecalories than we expend. and the way it's been done over the yearsis that the idea is "increased prosperity." this is what marion nestle, a new york universitynutritionist, wrote in 'science', "as we get richer, more food becomes available. we haveless reason to become physically active." that food's on every street corner. you don'thave to work to get it. and so we get fatter and fatter. kelly brownell,a yale university psychologist, used, coined

the term "toxic environment," which is anenvironment that promotes overeating and sedentary behavior. and so physical activity, and askelly put it, he said, "cheese curls and french fries,[audience chuckles] fast food jointsare as much a part of our environment as trees and clouds. mothers keep their kids home fromschool. we sit in front of computer screens all day long and video games and television." so a lot of reasons to eat too much, not enoughreason to burn it off. and the question we wanna know -- here's the hypothesis: increasedprosperity leads to overeating--energy in is greater than energy out-- and that leadsto obesity and the obesity epidemic. and what we wanna know is, is this true? 'cause thisis a science and in science, this is a hypothesis.

so you just ask a question. is this true?does it explain the observations? when i'm lecturing to nutrition departmentsand obesity research departments, i often wanna piss them off in the beginning. it'spart of my nature. and i'll say, "let's pretend this is a science for a second [audience chuckles]and see if this can actually explain the observations." there are a lot of observations out there,but they're less than obvious. they're not -- right now, we know we've got mcdonaldson every street corner. we know a lot of people watch television. and we know a lot of peopleare getting heavier. so we put them all together, these associations,and we say. "that's the cause". but we could find populations that didn't have all these,this toxic environment as we define it, and

we could look to see if the obesity existedthere. and one of the underlying contexts here, oneof my underlying hypothesis, and also of any science, the underlying principles is occam'srazor. so we should find the simplest possible hypothesis. so we're gonna work from the hypothesis ofwhatever makes any population fat is what makes our population fat, until we have tochange it. so, here we have a photo. this young woman,or middle-aged woman, was known as 'fat louisa'. this photo was taken in 1902. and fat louisawas a pima indian. and the pima live on the gila river reservation. now, it's the gilariver reservation, south of phoenix, arizona.

what's little-known about the pima is today,they are the poster children for obesity and diabetes in the united states cause they have,conceivably, the highest risk of any population. in the 17th, 18th, 19th century, they werethe most affluent native american tribe. they were hunters and gatherers. they hunted inthe nearby mountains. they fished in the gila river. they raised sheep--not sheep--cattle,pigs. they had warehouses full of food available in the 1840s. when the first us army battalion moved tothe pima territory on the san jose trail, they reported that the pima had this incredibleamount of food available. and they were all lean and sprightly. and by 1849, gold wasdiscovered in california.

and over the next 20 years, 20 to 60 thousand49ers went west to the pima territory and the us government asked the pima to feed them,which they did, and protect them from the hostile tribes farther west. and then by the1870s, 1880s, mexican americans and anglo americans started moving into the pima territoryand they overhunted the nearby mountains. they diverted the gila river water to irrigatetheir own fields, and the pima went into what they called the years of famine, which lastedfor 20 or 30 years. and by 1902, when frank rosso, a harvard anthropologistcame to live with the pima and wrote the seminole text on the pima indians, they were livingon a reservation. they were struggling as farmers to survive, and it was [pause] itwas rosso who took the photo of fat louisa

on the right. and he said many old peoplein the tribe, unlike the classical image of the strong, buff native american, many oldpeople in the tribe were actually obese and overweight. and this was an observation that was secondeda few years later by alex hrdlicka, who was the physician-anthropologist who went on tobecome the curator of the smithsonian, department of physical anthropology. so, the point aboutthe pima was that they went from being affluent in the 1840s -- that drawing was actuallymade in 1851 -- to poor in 1902. and they went through 30 years of famine in the middle.and 30 years of famine, you could think of as 30 years of being on a diet. and they shouldhave been leaner, right? 'cause our hypothesis

says if poverty leading to prosperity causesobesity, not prosperity leading to poverty. and yet, in the early 19th century, we havea high level of obesity observed by two separate anthropologists living with the tribe. ifthis was the only example, we could probably toss it and assume something else was goingon. but there are a lot of examples of obesity in what we would call "non-toxic environments." and one of the things that sort of pissedme off doing my research for 'good calories, bad calories', which took five years, is youonly had to go to look for them to find them. and yet, the obesity research community hadn'tbothered 'cause they had settled on their hypothesis. it's all about overeating. it'sall about taking in too many calories. it's

all about fast food joints. and so they neverlooked. if you go look, you'll find a lot of different populations. the sioux on thesouth dakota crow creek reservation, in 1928 -- this was a study done by two universityof chicago economists. and this, this population was so poor thatyou could use it. you could put it in the dictionary next to the definition of "dirtpoor." they lived four to eight people per room. something like 15 families with 32 childrenon the reservation were living only on bread and coffee. there were no bathrooms. there'sno plumbing. they had to get water from the river. and yet, 40 percent of the women, 25percent of the men, and 10 percent of the children were distinctly fat. and 20 percentof the women, 25 percent of the men, and 25

percent of the children were distinctly thin.and there were definite signs of malnutrition. the economists documented all kinds of deficiencydiseases among these native americans. and this combination of obesity and malnutrition,or under nutrition, existing in the same population is an observation i'm gonna come back to shortly-- many times, in fact. ok, african americans in charleston, south carolina in 1959. thirtypercent of the women are obese and 18 percent of the men. family incomes are nine to 53dollars a week. that's less than 400 dollars a week in 2011 dollars. zulus in durban, south africa in 1960. fortypercent of the women are obese. women in their 40s averaged 175 pounds. today in the unitedstates, the average weight for adult women

is around 165 pounds. trinidad, early 60s,trinidad's having a malnutrition, a famine crisis. the us government sends a team ofnutritionists down to help out and they come back reporting that a third of women over25 are obese. they report obesity as a "potentially serious medical problem in women." the percapita data. the next year, an mit nutritionist goes downto trinidad to figure out what's going on. she studies the diet of the obese women, comparesit to the diets of the lean women in trinidad and concludes that the per capita daily dietwas less than 2000 calories a day, 21 percent fat. fewer calories than were recommendedat the time by the food and agricultural organization for a healthy diet.

bantu "pensioners" in south africa in themid-60s. these are the poorest of a disenfranchised population. 30 percent of the women are severelyoverweight and the mean weight of women over 60 is 165 pounds. raratonga in the south pacific.forty percent of the women are obese, 25 percent are greatly obese, grossly obese. that's in1971. and then, factory workers in chile in 1974.thirty percent are obese. nearly 50 percent of the women over 54 are obese. ten percentsuffer undernourishment. ok, so here's that combination again of obesity and malnutritionin the same population and most are engaged in heavy labor. so, these are factory workers. they probablydon't belong to a gym. they probably don't

have gyms in their factory in chile in the70s. they're not working out regularly. they're not training for marathons. they're probablynot doing triathlons. but they're engaged in heavy labor, heavy,manual, physical labor. so we can assume on a day-to-day basis they are more physicallyactive than we are. and yet, 30 percent are obese and nearly 50 percent--half of them--over54. and here's the last study i'll show you. thisis mexican americans in starr county, texas in 1981. fifty percent of the women in their50s are obese, 40 percent of the men in their 40s. and the living conditions, most inhabitantsare employed in agricultural labor and who work in the oil fields. so again, very physicallyactive population, but high levels of obesity.

and there was one restaurant in starr county,texas in 1981. starr county is on the border of mexico, about 200 miles due south of sanantonio. and that was a mexican restaurant. so again, this definition, there's no increasedprosperity for many of these populations. there's no prosperity at all. there's no toxicenvironment as we would define it today. but something's making them fat and we wanna knowwhat. why were these populations fat? so if we can figure out why these populations werefat, we can probably figure out why our populations are getting fat. so here's how this question was phrased in1973. ralph richards was a university – he was a british-trained diabetes specialistwho went to jamaica in the early 1960s, founded

a diabetes clinic at the university of thewest indies, and in the early 70s reported that a third of the women over 25 were obeseand that obesity reached what he called "monstrous proportions" in this age group. and he said,"it's difficult to explain the high frequency of obesity seen in a relatively impecunioussociety such as exists in the west indies, when compared to the standard of living enjoyedin the more developed countries." he's asking the same question i'm asking andwe all should be asking. if poor people are so fat, our theory says it’s the rich oneswho should be fat. "malnutrition and sub nutrition are common disorders in the first two yearsof life in these areas and account for almost 25 percent of all admissions to pediatricwards in jamaica." so, by "sub nutrition",

he means not enough food. "sub nutrition continuesin early childhood to the early teens." so the children are stunted and show signsof emaciation and then "obesity begins to manifest itself in the female population andreaches enormous proportions from 30 onwards." so here's that question asked again. exactlythe same observation, exactly the same question 30 years later, this time by benjamin caballeroof johns hopkins. and now, within this paradigm of caloriesin, calories out, of overeating. when, when richards asked in 1973, he had an open mind.he didn't know what the answer was. but now benjamin caballero thinks he knows the answer,which is the answer we all think we know. and he says, a few years ago, this was inthe new england journal of medicine in 2005,

an article called 'obesity and malnutrition:a nutrition paradox'. he says, "a few years ago, i was visitinga primary care clinic in the slums of sã£o paulo, brazil. the waiting room was full ofmothers with thin, stunted young children, exhibiting the typical signs of chronic undernutrition. their appearance, sadly, would surprise few who visit poor urban areas inthe developing world. what might come as a surprise is that many of the mothers holdingthose under-nourished infants were themselves overweight." and then he says, "the coexistence of underweightand overweight poses a challenge to public health programs, since the aims of programsto reduce under nutrition" --which is get

people to eat more, make more food available—"areobviously in conflict with those for obesity prevention" --which is make less food available.so we have a problem. and i put this "poses a challenge to publichealth programs" in italics because the coexistence of underweight and overweight poses a challengeto your paradigm, your belief system. if you believe that the mothers got fat because theytook in more calories than they expended, they took in superfluous calories that theydidn't need, and the children aren't getting enough food, then you believe that the mothersare willing to starve their children to death so that they can sneak outside and eat a snickersbar, in effect. and i don't know how many, this is a youngaudience, how many mothers are there in this

audience? ok. how many of you would do that? let your children starve so you can get fat,as opposed to, perhaps, the other way around, right? so you've got two paradigms colliding.we've got our paradigm maternal behavior that says population, species don't survive unlessthe mothers make sacrifices for their children. and we have the paradigm of obesity that saysthese mothers are just happily guzzling excess calories while they're watching their kidsstarve to death. and this is an anomalous observation. i usedto, started my career writing about high-energy physics, and high-energy physics, they justbuilt the large hadron collidor at cern that costs i forget how many billions of dollars,all designed to just create an observation

that their theory can't explain so they canproceed onward. here, we've had this observation going backprobably to 1928 at least, and nobody cares. and my point is you have to throw out oneof the two paradigms. and i'm gonna throw out the obesity paradigm 'cause my mother--may she rest in peace-- would have killed me if i threw out the maternal behavior paradigm. let's look at some other inconvenient observations,okay? "eating less doesn't work." our hypothesisis that if we eat more, if we take in more calories than we expend, we will gain weight.so the idea is if we take in less calories than you expend, you'll lose weight. all youhave to do is create what's called "negative

energy balance." so you go on a semi-restrictedcalorie diet and there are a lot of meta-analysis over the years, systematic reviews, showinghow poorly these work. the cochrane collaboration a few years agowhen they looked at this. the cochrane collaboration is a collaboration created just to do unbiasedreviews of the data. their assumption being every other review of the data is biased.so we have to create the methodology that doesn't allow bias to enter into it. and withthis, they put it back in--i think it was 2002, i can't see my notes, unfortunately,because we're not in notes mode, here--the weight loss achieved, that was 2002. it'sso small as to be clinically insignificant. and what you see in the literature is fascinating'cause people, they try to deal with this

when they write about obesity; the fact thateating less doesn’t work. but they believe that a calorie-restricted diet is crucial. so you'll see these chapters in obesity textbooks,like the 'task force of obesity', task force textbook, where the researchers will writethat restricting calories is the fundamental approach, the -- i forget the word they usebecause i don't have my notes-- to curing obesity, yet it rarely, if ever, works. exercising more also doesn't work. one ofthe problems here, i could also show you meta-analyses that talk about how clinically insignificantthis effect is. but there's, the best evidence i found so far for this is the american heartassociation and the american college of sports

medicine in 2007, put out their physical activityguidelines. and the physical activity guidelines--these are people, two organizations, that want usto engage in healthy lifestyles, that believe that physical activity should make a difference. and you would expect them to spin the datain favor of physical activity for exercise, for weight loss--and the way they put it isthis. they said, "it is reasonable to assume that persons with relatively high daily energyexpenditures would be less likely to gain weight over time, compared to those who havelow energy expenditures." that's logically equivalent to saying, "it'sreasonable to assume that if you're a couch potato and you increase your energy expenditure,you will be less likely to gain weight than

if you remain a couch potato." and then they say, "so far, data to supportthis hypothesis are not particularly compelling." and the point of this is this hypothesis isin the neighborhood of 100 to 150 years old. there, you could find obesity texts in the1860s in which somebody like william banting talks about his doctor telling him to go fora row every morning to burn off calories. he also talks about how it didn't help. youcould find in, by the 1890s, when the laws of thermodynamics [clears throat] had beenshown to hold with animate objects as well as inanimate objects, with living beings aswell as inanimate objects, researchers said, "hey, maybe if we just get people to expendmore energy, they'll gain weight. i mean they'll

lose weight and over the course of a hundredyears, 150 years, this is the best we could say about it. "the data to support this hypothesisare not particularly compelling." and that's a bad sign. when i was writingabout high-energy physics, it was an unwritten rule of high-energy physics by pief panofsky,who's a founder of the stanford linear accelerator center here. and pief said, "if you throwmoney at an effect and it doesn't get bigger, it means it's not really there." okay? and the corollary here is if you've been studyingan effect, for a century and the best you could say about it is "the data to supportthis hypothesis are not particularly compelling", there's a very good chance that your hypothesisis wrong; that increasing energy expenditure

and physical activity will have no effecton how much you weigh, or how much weight you've gained. and one way to think about this and to thisi owe a british blogger. imagine that i'm having, i'm hosting a dinner party tonightand i've got the ten last finalists from top chef cooking. and they're making this amazingfeast and i send you all invitations and i say, "i've got this feast. it's gonna be aton of the best tasting food you've ever eaten in your life. come hungry." what would youdo to make sure you came hungry? and here i'll take questions. anyone wanna answer?what would you do during the day? >>male audience member #1: skip snacks.

>>gary taubes: skip snacks, eat less. >>female audience member #1: i would takea long walk. >>gary taubes: and take a long walk. exercisemore. you'd work out. so the exact same things that we prescribeoverweight people to lose weight are the two things that you're going to do if you wannaguarantee that you get hungry and eat more. and we're gonna explain that in a while. but you can see already that there's somethingwrong here. here's another problem with our energy balance idea. practicing energy balanceis impossible. this is a new phrase you hear. the past two or three years, the idea thereare now industry programs developed in collaboration

with the government to help you practice energybalance, to make sure you match calories in to calories out so you don't gain weight. and the industry loves the idea. the foodindustry loves the idea of obesity being all about calories, because you can't demonizeanything. it's all about just it's your fault if you're overweight. you just have to eatless and exercise more and if you wanna build a gym in your neighborhood, or a track ora park, go to coke or pepsi and ask them for money. they'll give it to you 'cause theywould like you to exercise more so that way, they can't be blamed for your obesity epidemic. so, let's see what it takes actually to practiceenergy balance. a typical american's food

intake is about 2700 calories a day. okay?that's men and women. so that's a million calories a year. ten million calories in adecade, okay? it's about ten to twelve tons of food per decade. now, all you'd have to do is ask the question.let's say, right now, i'm a 25 year old and i'm lean and i wanna ask the question, "howwell do i have to maintain energy balance? how well do i have to practice energy balanceso that i don't gain 20 pounds in a decade, 40 pounds in 20 years, so by the time i'min my mid-40s i'm obese?" what is that entail, because that's what the government is tryingto get us to do. and the answer is you have to maintain yourenergy balance to 20 calories per day. if

over 20 -- this is actually a trick answer,because if 20 calories per day goes into your fat tissue that you don't burn, you will gain40 pounds in 20 years. here's the calculation. it's pretty simple. very simple. even i could do this and i don't work at google.twenty calories times 365 days a year times ten years, divided by 35 hundred, which isthe number of calories, roughly, in a pound of fat. and you end up with 21 pounds in adecade. okay? so if you go over that, if you can match your energy in to your energy out,to 20 calories a day and not exceed that on average, you'll only gain 40 pounds. if youonly want to gain 20 pounds, it's ten calories. if you don't want to gain any weight, of course,the idea is you have to do it perfectly.

twenty calories a day is .8 percent accuracy.nobody can do that. nobody, even i will bet my life's income--it's not that big--thatthe world champion calorie counter in the world, guinness -- if there is such an entryin guinness, cannot gauge within 20 calories how much food they were eating per day andthen you have no idea how much you're expending. you're just guessing, even when you go into do research sessions. they just do calculations. so the point here is i got this calculationfrom a 1937 nutrition and metabolism textbook, written by a fellow named eugene dubois, who'sa leading expert on metabolism in the united states, pre-world war ii. [pause] and duboisuses calculations. he said what's interesting about it is since nobody can do that, howdo we maintain our weight? the question isn't

why are some of us fat? the question shouldbe why aren't all of us fat? okay? because if you overshoot by even 20 caloriesa day on average, you're gonna end up getting obese. and you could say, "okay. maybe oneway to do it is i just watch my weight. i look in the mirror. i see i'm getting fatter.my belt's getting snug, or my pants, or my skirt doesn't fit. so therefore, i'm gonnaeat less for a while until i get my weight back." so you oscillate around perfect energy balance,but then you have to ask the question, how do animals do it? because they don't. they'renot looking in the mirror. they don't have clothes they're putting on. so how do theymaintain their weight and virtually all animals

do? they don't get chronically obese. so theidea that dubois says it's obviously something else is going on here, other than consciouslymatching calories in to calories out, which none of us can do. so let's look at some other inconvenient observations. genetics is one of them. i gotta apologizenow. if you go to an obesity textbook today, you will not see photos of naked human beings.but if you go to an obesity textbook pre- world war ii, you would. because those researchers,those clinicians, thought you could learn a lot about watching how people fatten, aswell as just whether they do or not. and one of the things i'm doing now is justchanneling these pre-world war ii researchers.

and in fact, all i'm saying in my books isi'm taking the theory that german and austrian researchers developed pre-world war ii, backwhen the germans and austrians did the best medical research in the world and there wasvirtually no meaningful medical research being done in the united states. and i'm taking that theory and i'm updatingit. okay? because they didn't survive the war. that community didn't survive the war.so, for starters, here's genetics. and there's a pair -- and this comes from a 1940 textbook.here's a pair of lean identical twins. here's a pair of obese identical twins. our overeatinghypothesis might explain why these women are fatter than these women. these took in toomany calories and these practiced perfect

energy balance. but what about this combination? why do theyhave the same body type? and why do they have the same body type? it's been known sincethe 1930s that obesity has a strong genetic component. identical twins – it's not thattheir faces look alike. their body types are the same, too. so what's going on here? what do these genes determine? do they determineexactly how much these women, how many forkfuls of food these women overate over 20, 30, 40years? and exactly how long they sat on a couch versus going for a walk? or, did they determine something else abouthow much and where they accumulated fat 'cause

they have the identical body? here's a different variation of an animalhusbandry and it's even easier to see here what i'm talking about. farmers, livestockbreeders, have been breeding more or less fatty cows, pigs, sheep, for centuries, probably.and here's a particularly fat breed of beef cattle. this is an aberdeen angus. here'sthe meat. i should say it's stocky, but you can see all the subcutaneous fat, the intramuscularfat, here. and here's a lean species, a lean breed of cattle, the jersey cow. and you cansee the ribs showing, you can see the swollen udder. it's definitely a dairy cow. and you can ask yourself simply, there aredifferent breeds. obviously, different genes

are determining how much they get fat. whatexactly is going on here? what are these genes determining? do they determine how much theseanimals eat and exercise? do they determine how many calories per graze, or per bite ofgrass, this cow takes? the aberdeen angus grazes for 12 hours. the jersey only grazesfor ten a day. does the jersey want to go to work out? so, on the far side cartoon whenit gets dark at night, the jersey goes for a jog. the aberdeen angus goes in and watchestelevision. and it's obviously absurd, okay? whatever determines how much these animalsget fat, we can be confident that how much they eat and exercise has nothing to do withit. more likely, and again, this is a beef cow. so what you want is it's an effectively,brutally speaking and i apologize for the

vegetarians here, to the vegetarians here.it's a machine that takes in fuel here and deposits it here and you want it all to gohere. so you could assume that it just partitionsthe calories it eats into fat and protein. and the jersey cow, you want to create milk.so you take in the fuel and it's all gonna go to the udders to produce milk. and youdon't want it wasting energy, in effect, bulking up. so maybe what these genes determine isnot how many calories we take in, but how we partition the fuel we take in. that's a technical term. sexual variations.men and women fatten differently, okay? men fatten above the waist. women fatten belowthe waist. both these people would have had

to overeat, take in more calories than theyexpend to get fat. this has doubled his risk of heart disease. this has not doubled herrisk. if the weight's below the waist, it doesn't double your risk. what do the calorieshave to do with it? okay? and what do the calories have to dowith where they get fat, because obviously, that's a huge component of it. and anotherway to look at it is puberty. men and women, when they go through puberty, boys, they beginpuberty with roughly the same amount of body fat. when boys go through puberty, they losefat and gain muscle. when girls go through puberty, they gain fat and breasts and hipsand buttocks. and by the time they're out of puberty, thegirls have about 50 percent more fat on their

bodies than the men. both boys and girls gotbigger. so they both overate. they both took in more calories than they expend, but theboys lost fat and gained muscle. the girls gained fat in specific places. so you just ask the question, what do thecalories have to do with it? what did the fact of their overeating have to do with whetheror not they gained muscle or fat? and this is obviously controlled by sex and growthhormones and that's an issue we'll get to. now, lipidystrophies. this is again, fromthe same 1940 textbook, which took it from a 1933 german text book. this is a lipidystrophycalled a progressive lipidystrophy. in the 1950s, there were about 200 of these on record.most of them were in women. it's called progressive

'cause these cases, they begin losing allsubcutaneous fat in the face, in their forehead, and it moves downward with time. one british physician reported that his patientlost fat at about one inch a year. that's why it's progressive. and then it usuallystops above the hips. and then they often get this lower body, localized obesity belowthe waist. so the way these europeans asked it, they said, "are we gonna blame the tophalf on under eating and bottom half on overeating?" right? and this is again, obviously absurd.it's like a gedanken experiment. but if this woman had ten pounds more fat on her upperbody, maybe even five pounds, just to smooth out her curves, her bmi was about 32 alreadyjust cause of her lower body obesity. and

she went into the doctor then. the doctorwouldn't recognize the lipidystrophy. and he would just say, "look, eat less and exercisemore." and the point that the europeans are makingis if you can't explain the localized conditions by under eating and overeating, why wouldyou even think to explain the generalized obesity by overeating? or, in those cases,often these textbooks, pre-world war ii were titled 'obesity and leanness' because theywere looking at cases that today we would call anorexia and assuming that that alsowasn't an under eating problem. it was some problem of how the fat tissue was regulated. so why do we believe this? and let's lookat a little physics here, okay? and this is

the reason. [pause] we believe it 'cause of the first law of thermodynamics.every time somebody like me makes this point for the past 50, 60 years, you get accusedof not believing that thermodynamics holds for human beings. i had one of the high points of my life. iwas on the larry king show after 'good calories, bad calories' came out. and they had jillianmichaels, the trainer from 'the biggest loser', come on. and she gave me a lecture on thelaws of thermodynamics on national television. and i have a physics degree from harvard.

i mean, i was a, i was a lousy student, butit was definitely, i literally, i'm sitting next to. i just, i didn't respond. if youwatch the show, it's on, you can google it. i didn't know what to say. i mean, how doi respond to this? so lemme give you a little, thermodynamicsis pretty simple. the first law of thermodynamics -- it's the law of energy conservation. itsays a change in energy in a system--this is the simplest possible way to put it-- isequal to the energy in minus energy out. all it's saying is you can't create energy fromthin air. so, if a system gets bigger, delta e goesup. and it's gotta take in more energy than it expends. and if a system gets smaller,it's got to expend more energy than it takes

in. for our sake, we'll make delta e the fatmass e in is energy consumed, e out energy expended. so change in fat mass equals energyconsumed minus energy expended. and the problem, the fundamental problem,and it's almost unbelievable to me, is that there's no arrow of causality here. and bythat i mean it doesn't say in any way if energy, energy consumed greater than energy expendedcauses change of fat mass. it just says this is the way the universe is. if a system gets bigger, it takes in moreenergy than it expends. and if a system gets smaller, it takes in less. it says nothingabout what causes it. and to understand that, a metaphor i could use. like, let's assumei was asking the question why is this room

crowded right now? okay? and it's as similar when we're talking aboutfat mass. we wanna know, why is there so much energy accumulated in the fat mass? and iwanna ask the question, why is there so much energy accumulated in this room in the formof people? so you ask me, "gary, why is it crowded?" and i say, "well, because more peopleentered than left." right? have i told you anything meaningfulat all about why this? i mean, of course more people entered thanleft. but why is it crowded? and then i say, "well, look. if more people enter than leave,it's gotta get crowded, right?" and i still haven't told you anything meaningful.

this is what magicians would call--i forgetthe word--vacuous? it's the equivalent as saying, why did you get fat? because you tookin more energy than you expended. well, of course i took in more energy than i expended.i got fat. but why did i get fat? and then you just turn around and say, "well, if youtake in more energy than you expend," there's no arrow of causality. there's nothing meaningfulhere. this is a mistake that was made occasionallyprior to the second world war. it became ubiquitous after the second world war. whenever we tellsomeone, "you got fat 'cause you overate," you are misinterpreting the laws of thermodynamicson an eighth grade mathematics level. and the more i talk about it, the more it'salmost unbelievable that this ever happened.

and yet, it did. and so there's another wayyou could play with this thermodynamics. and for this i owe university of washington gradstudent named sonya trejo, who said, "what happens if you start transposing elements?" so how about this. instead of, we had deltae over here and e out over here. how about if we say energy out is equal to energy inminus delta e? and so now, the energy expended is equal to energy consumed minus change infat mass, okay? so if fat mass gets bigger -- for we don'tknow why, we're working on that -- and the person doesn't eat anymore, then energy expenditurehas to go down. okay? so you look at it this way and an increase in fat mass causes sedentarybehavior. if fat mass gets smaller, energy

expended has to go up. so if somebody's losing weight, they haveto get more physically active. or how about this one? we just do a little more transposingand we end up with energy in equals delta e plus energy out. so the energy we eat isequal to change in fat mass plus energy expended. let's assume change in fat mass is fixed bybiology. and if you read the new york times today there was an article about that. andenergy expenditure goes up 'cause i just told you to work out. what's gonna happen to energyconsumed? it has to go up. you're gonna get hungry. you will work up an appetite. this used to be something that everyone believedin the 1960s and beyond. there used to be

this term, "working up an appetite." so itused to be, if you worked out, you worked up an appetite. now if you work out, you'resupposed to lose weight and energy consumed is supposed to stay fixed. but there's noguarantee this'll happen. so here's the alternative hypothesis. thisis the way that the pre-world war ii europeans thought about it. they said, started fromfirst principles, obesity is a disorder of excess fat accumulation. so today, you read obesity is a positive energybalance, or obesity is an energy balance problem and those are assumptions. they just startedat the beginning. having too much fat is a disorder of having too much fat. so it's notenergy balance. it's not overeating. it's

not sedentary behavior. and if you ask itthis way, the next question you're likely to ask, which we'll get to, is what regulatesfat accumulation? because what we know is there's too much fat. like, if i was standing in here with yao ming,whose seven feet six inches tall, and we wanted to know why he grew to be seven foot six,we wouldn't care that he was in positive energy balance. we would want to know what regulatesgrowth, right. so we wanna know what regulates growth. so, by this hypothesis, overeatingand inactivity are compensatory effects. they're not causes. and the way it was put to me by several differentindividuals doing animal research, so we don't

get fat because we overeat. we overeat becauseour fat tissue is accumulating excess fat. overeating is a given. if you're getting fatter,you have to take in more calories than you consume. but we're saying the positive energybalance is in effect. here's a way to see it. this comes from the,again, straight out of the pre world war ii text. although the child is mine, i use thesephotos 'cause he's so cute. he was. here he was one year old, 20 pounds. okay? 2006. herehe is 2009, 45 pounds. he's gained 25 pounds in three years, right? he's been in positiveenergy balance. he has overeaten. he's taken in more calories than expended.but he did not take in, he did not grow because he overate. he overate because he was growing.he grew cause he was secreting growth hormone.

and the growth hormone sparked his tissuesto grow muscle, organs, fat, bone. and he had to take in more calories than he expendedto fuel that growth. and if he wasn't growing fast enough, we might have even given himmore growth hormone to speed his growth, at which point that would have created even morepositive energy balance. here's a gruesome analogy: cancer. here'sa tumor. you can barely see it. then it's growing at day 10. it's growing at day 20.it's bigger and bigger. this tumor is in positive energy balance; nobody cares. we care if wewant to starve it to death, but that's a given. like, just if we don't want this room to getcrowded, we'll shut the doors before anyone comes in. but what we care about is what genes,what hormones are disruptive that drive the

growth because the positive energy balanceis in effect. and in every other example in nature, positiveenergy balance is always an effect of growth, not the other way around. so, this was a german-austrian hypothesisprior to world war ii. it was known as the lipophilia hypothesis. i'll explain that ina second. the primary proponents where gustav von bergmann, who was a german specialistin internal medicine. today the highest award in the german association of internal medicineis the gustav von bergmann award. and then julius bauer, who was a geneticistand endocrinologist at the university of vienna, bauer was very famous in austria. if you haveany molecular biology or genetics friends

in austria, email them and say, "have youever heard of julius bauer?" and they'll probably say, "oh, yeah. absolutely." and the theory was more or less fully acceptedin europe by 1940. this comes from the 1940 textbook. and the problem was 1940 was a badyear for europe. so, the german and austrian medical research communities evaporate. unlikein physics, where we, we embraced all the european physicists who got chased out ofeurope because we had atomic bombs to build and hydrogen bombs and a cold war to fight.in medicine and public health, we didn't. so julius bauer ended up working in hollywood,california for the hospital of medical evangelists and publishing articles that just said, "juliusbauer, hollywood, california," and nobody

took his work seriously, although his sonbecame dean of the usc medical school. so here's lipophilia in a nutshell. the ideais lipophilia means 'love of fat'. okay. the way these people saw it, is that some tissuesare more or less predisposed to accumulate fat, in the same way that, you can think ofit, we grow hair in some places and not in others. and we get fat in some place and not in others.so we don't tend to get fat on our foreheads or the back of our hands, but we put in faton our guts, under our chins. and so they said maybe fat is just like hair. and so,some people are hairier than others, just like some people are fatter than others.

when men start losing their hair, we don'taccuse them of under eating because they're losing weight. we know that there's a lotof different issues involved. so bauer put it like this. he said, "likea malignant tumor or like the fetus, the uterus or the breasts of a pregnant woman, the abnormallipophilic tissue seizes on foodstuffs, even in the case of under nutrition. it maintainsits stock, and may increase it independent of the requirements of the organism. a sortof anarchy exists; the adipose tissue lives for itself and does not fit into the preciselyregulated management of the whole organism." and this phrase, "even in the case of undernutrition," begins to tell us why these women could get obese in a population where theirchildren are starving because it didn't matter

how little food there was. if there was somethingdriving their accumulation of fat, they were gonna get fat anyway. so when you look at animal models of obesity,which you can, what you'll find--what i found--was they all fall into two categories. either,well, let me just explain. if you have an animal model of obesity, how do you want totest what's driving it, like a genetic model, a surgical model. you could lesion the ventromedialhypothalamus for rat and it'll get obese and eat voraciously. so you'll see voracious eatingand obesity. and you wanna know which causes which. did this regulation of fat tissue cause what'scalled hyperphasia? or did the hyperphasia

cause the accumulation of fat? so what youdo, is you just do the experiment and then you put the animals on a diet and see whetherthey get fat anyway. okay? and what you'll find for every animal modelof obesity is they will get obese anyway, even if you put them on a diet. you can, insome cases, starve them. there's a genetic strain of mice that m.r.c.greenwood studied in the early 1980s, when she put these animals on a diet from the momentthey were weaned and they became more obese. they became fatter than their lean controlthan their genetic controls, even though they were on a diet their whole life. they actuallyweighed less. their organs were smaller. their muscle tissue was smaller and they had morefat. and in effect, their drive to accumulate

fat was, in order to do that they cannibalizedtheir organs and their brain. and jean meyer, a tufts nutritionist who playeda large role in this, usually to the detriment of society. the way he put it, he studieda genetic strain of mice. he said, "these mice will make fat out of their food underthe most unlikely circumstances, even when half-starved." okay? so it's not that thesemice got fat because they ate too much. they got fat if you let them eat anything basically. and we're gonna propose, again, that the samething's happening in humans. so here's some obvious questions. why vertical growth butnot horizontal? when we look at children, we know that overeatingis the effect. growth is the cause. why animals

but not man? an animal's model of obesity,when you break the gene, you intervene surgically. there are even dietary models. what you'redoing is disregulating the fat tissue. you're not making the animals eat too much. and then the question, if obesity is sortof excess fat accumulation, what regulates fat accumulation? so here's a regulation offat. adiposity 101. if you learn this, you'll know more than your doctors do. [pause] bythe way, what gets me is that again, it's 2011. i lecture in medical schools. i lectureto obesity research centers. and i'm telling them, it's like i'm tellingthem something new. i mean, they don't learn this in medical school but they forgot it.but when it comes to the relevance of obesity,

or why we get fat, the idea that your fattissue is regulated and has anything to say about this, it's considered radical and quackish.okay? and the point i'm making is any other growthproblem, like i said, from cancer to height to anything, all you're gonna care about iswhat hormones, what enzymes, are driving growth. so let's care about it here, too. and whatyou learn is fat is stored as triglycerides in your fat tissue. here's a triglyceride.its three fatty acids bound together by a glycerol molecule. fatty acids are burnedfor fuel and the fat enters and exits the cell as these fatty acids. and the reasonthat is, is because the triglycerides themselves are too big to fit in and out of the cellto get through the cell membrane of the fat

tissue. so, the fatty acids enter the fat tissue.and then they're bound together inside the fat tissue into a triglyceride and as a triglyceride,it's fixed in the fat tissue. it's that simple. it's too big to get it out. and if you wanna get it out, you have to breakit down into its component parts again. so the fatty acids can get out. so, it's a verysimple mechanism for storing fat. here it is in a, in a diagram. here's fatty acidsoutside the cell. they pass through the fat cell membrane. inside the cell, there's thistriglyceride fatty acid cycle. so the fatty acids are bound to an activated glycerol moleculeand you'll have a triglyceride. and as a triglyceride,

they're fixed in the fat cell. and then theybreak down. there's a hormone, several hormones; a primaryone called hormone sensitive lipase, which breaks down the triglycerides into the fattyacids and then they can escape again. so, here's where we care about energy in minusenergy out. you will get fatter if more fat enters your fat tissue than leaves. and youwill get leaner if more fatty acids leave your fat tissue than enter it. and what wewanna know is what determines this balance of fatty acids going in versus fatty acidsgoing out. it's that simple. so here it is, circa 2010. i could've usedthe same diagram from the mid-1960s, 'cause this was figured out by the mid-1960s. unfortunatelythe germans and austrians weren't around by

then. we required two technologies to do it;a way to measure fatty acids in the bloodstream, a way to measure hormones accurately. by 1960,it was done. and by 1961, it was clear that insulin, thehormone insulin, is a principle regulator of fat metabolism. this is rosalyn yalow andsolomon berson who invented the radioimmunoassay for measuring hormones. yalow won the nobelprize for it. berson had died by then. and you could see when it comes to white fattissue, here's fat storage. here's fat mobilization. tag is triglycerides. and so you just ask,you know the little pluses show that it up regulates it. and the only hormone this particular authoris interested in in metabolic regulation is

insulin. it up regulates here. it up regulatesthere. it up regulates here, it up regulates here. it down, it suppresses fat mobilizationand then there's some role from other hormones in increasing fat mobilization. but it's basicallyinsulin that puts fat in the fat tissue and it's insulin that suppresses fat mobilization. here, it's putting fat in. here, it's puttingfat in. here, it's suppressing it. and release of fatty acids, as yalow and berson said,from fat cells requires only the negative stimulus of insulin deficiency. so, if youwanna get insulin, if you wanna get fat out of your fat tissue, you have to lower yourinsulin levels. that's the fundamental thing that the adiposity101 tells you. so, and what's funny is we've

known for like, 50 years that insulin is afat-producing hormone. this is best and best of the banting and best who discovered insulin.the fact that insulin increases the formation of fat has been obvious ever since the firstemaciated daughter diabetic patient demonstrated a fine pad of fat tissue, made as a resultof treatment with the hormone. this is insulin and fat stored. this is a 2001 textbook, endocrinology 101,and here's a young woman who basically, she was diagnosed with type 1 diabetes when shewas something like 17 years old. and for the next 47 years, she injected herself with herinsulin in two spots on her thighs. and she ended up with these huge fat masses. in thispicture in the textbook, the caption is "the

overall action of insulin on the adipocyte,the fat cell, was to stimulate fat storage and inhibit mobilization. that's the remarkable effects of locally injectedinsulin on the accumulation of fat into fat cells are graphically illustrated here." that'swhat happens when you raise insulin levels. so here's the bottom line. when insulin issecreted or chronically elevated, fat accumulates in the fat tissue. when insulin levels drop,fat escapes from the fat tissue and the fat depots shrink. and we secrete insulin primarilyin response to the carbohydrates in our diet. this is how george cahill, he was a harvarddiabetes specialist, who co-authored in 1965, a 500 page handbook of adipose tissue, metabolism;co-edited. it was put out by the american

physiological society. they wanted to takethis science of fat metabolism and make it available to the people who didn't read biochemistryand physiology textbooks. and as cahill put it to me, "carbohydrateis driving insulin is driving fat." that is basically the message in that textbook. andthe interesting thing is you can take out "is driving insulin" and get "carbohydrateis driving fat." it's logically equivalent. so, and when i give this lecture at medicalschools, it's really funny 'cause i could watch the audience and i see, "oh, wait aminute. geez, he used that word 'carbohydrate'. that means this is that atkins crap." andthe doctors immediately shut down. they've been with me up until then, up until now.and then they start thinking "fad diet alert!"

not all carbohydrates are equally fattening.if you care about the underlying science, the key words, you have the high glycemicindex carbs are fattening, the easily digestible carbs, the base of the food guide pyramid,bread, cereal, rice, and pasta. we break those carbs down easily. they get glucose into thebloodstream. you get insulin spikes from them. and then, sugar. sugar is a unique case. sucrose,high fructose corn syrup. it's half glucose, half fructose, for all intents and purposes.we metabolize the fructose in our livers. and it's quite likely that sugars, as i wrotein the new york times magazine article a few weeks ago, are the fundamental cause of thiscondition insulin resistance, which then makes all carbohydrates bad.

so the question is should this be surprising?this idea that carbohydrates are inherently fattening. and the answer is, well, it wasn'tup until 1960. in the 1820s, when a frenchman named anthelme brillat-savarin wrote whatwas then, has been for many years, the single most famous book ever written about food,'the physiology of taste'. brillat-savarin basically said after 500 conversations withstout, exceedingly stout people, it was fairly clear that the cause of obesity was a geneticpredisposition to fatten. plus, starches, what he called farinaceous foods, and sugarmade everything worse. and for the next 140 years, the conventional wisdom in this countryand elsewhere was that carbohydrates make you fat. this was the first line of a britishjournal of nutrition article in 1963, written

by the two, one of two most prominent britishdieticians, "every woman knows that carbohydrates are fattening, this is a piece of common knowledge,which a few nutritionists would dispute." dr. spock's 'baby and child care', which wasthe bible of child-raising in our country from the 1946, the first edition, to the endof the century. this one sentence was in every, single edition. "the amount of plain, starchyfood, cereals, breads, potatoes taken is what determines, in the case of most people, howmuch weight they gain or lose." if you went to a hospital in the 1940s and1950s and were obese, this is the kind of diet they would put you on. i could've shownthe same diet from harvard medical school, from stanford medical school, from cornellmed school.

this is actually from 'the practice of endocrinology',a british textbook written by raymond greene, who was the brother of graham greene and themost influential british endocrinologist of the mid-20th century. foods to be avoided:bread and everything made with flour, cereals, potatoes, foods containing much sugar, allsweets. and you can eat as much as you like of the following foods: meat, fish, birds,all green vegetables, eggs, cheese, fruit except bananas and grapes. these foods arefattening. you limit them. these foods you can eat as much as you like cause they literallydo not make you fat. it's not about calories. it's about the effectof the food on the hormones that regulate fat accumulation, insulin. so here are theconclusions. biology, not physics. this is

a biological problem. the laws of thermodynamicshave nothing to do with it, no more than the laws of relativity do. obesity disorder, fataccumulation, not energy balanced, not overeating and sedentary behavior. fat accumulation isregulated fundamentally by insulin and dietary carbohydrates. carbohydrates driving insulinis driving fat. and the only non-pharmaceutical remedy isto restrict or remove the causative agent, carbohydrates. now, here's the problem. if you lower the carbohydrate content of thediet, but you keep calories high because it's not about calories and you wanna make surethe person has enough calories to fuel, to run their body and if you're obese or you'reoverweight, you need a lot of fuel 'cause

you have a big body. if you lower the carb content and keep calorieshigh, you raise the fat content. so, you end up with a high-fat diet. fat, actually, happensto be the one nutrient that does not stimulate insulin secretion. protein does. so, a healthy diet, if you're overweight andobese, and i would argue in my books for everyone, is a high-fat carbohydrate restricted diet.okay. usually i just added that -- i don't go through that, but i've seen what you'vebeen, what the cafeteria is here feeding. it's this low-fat dogma. it's gotta be aboutlowering the fat. and it’s not about the fat. it’s about the carbohydrates. so, youcan just ask this question, "where did the

science go?" and there's two places. first,the calories in, calories out hypothesis just swept it away. so, you'll find textbooks today, like 'principlesof biochemistry', lenningers'. it's sort of the seminal biochemistry textbook. this isthe latest edition from a couple years ago. what makes fat tissue fat? high blood glucose--that'scarbs--elicits the release of insulin, which speeds the uptake of glucose by tissues, favorsthe storage of fuels as glycogen--it's a good thing-- and triglycerols--fat, a very badthing--while inhibiting fatty acid mobilization. what makes people fat? to a first approximation,obesity is the result of taking in more calories in the diet than are expended by the body'senergy-consuming activities. the point i'm

making is that the same thing that makes yourfat cells fat is what makes you fat. because if you're fat, for the most part,it's 'cause all your fat cells are too fat. and this disconnect, i was interviewing thisbritish oxford university fat metabolism specialist, who took 15 minutes on the phone explainingto me all the ways that insulin makes fat cells fat. and then got around to people andevoked this overeating, over nutrition mechanism. and the point i made was, why did you suddenly,you switched mechanisms? you had one mechanism for the fat cells and then when you got topeople, you brought in this vague overeating thing. and he literally said to me, "i neverthought of that." he's like, in his mid- to late- 60s.

here's the other thing that happened. in the1960s, we started to believe that dietary fat causes heart disease. so when dietaryfat causes heart disease, you remember i just told you that a carb-restricted diet is ahigh-fat diet. and so the same year that the american physiologicalsociety put out its high-fat diet, its handbook of adipose tissue metabolism saying carbohydratesdrive insulin, drive fat. that's the simplified eight-word version of a 500 page text. the new york times was already panning carbo-light,low-carb diets. "new diet decried by nutritionists. its dangers are seen in low carbohydrate intake.some of the nation's top nutrition experts are concerned at the new popularity of thelow-carbohydrate reducing diet, which one

of them calls 'nonsense'—'cause you don'thave to restrict calories 'cause it’s not about calories—"and another compares to'mass murder.'" this is jean meyer, who was the most influentialnutritionist in the country; went on to become president of tufts university. 'mass murder''cause you're giving people high-fat diet. so the science says carbohydrates is drivinginsulin is driving fat. cut the carbs out. and the nutritionists are saying, "you can'tdo that. you're gonna kill people." and that's how we've seen it ever since. andyou get to the point by the 1980s when you end up with the food guide pyramid becausewe believe fats are fattening and we believe red meat causes colon cancer, or god knowswhat. we're gonna tell an entire nation to

eat bread, cereal, rice, pasta. and sweets,weirdly enough, get a free pass 'cause they're nonfattening. so, coke, pepsi, soba ice tea, snapple. therewas actually a theory in the 1980s, you could drink as much, you could eat as much any foodyou want if it didn't have fat in it. 'cause if it didn't have fat in it, you couldn'tput fat on. so, [pause] just to wrap up. i've alreadygone too long cause i always do. i started off asking question, why were thesepopulations fat? rolf richards, in 1973, "most third world countries have a high carbohydrateintake as their economic dependence is predominantly agricultural, with a heavy dependence on non-dairyproduces. it is conceivable that the ready

availability of starch in preference to animalprotein, contributing as it must the main caloric requirements of these populations,leads to increased lipogenesis and the development of obesity." in this country, we took the conventionalwisdom that carbohydrates make you fat. and over the course of 20 years, from the1960s to the 1980s, turned it into the conventional wisdom that you grew up with, that carbohydratesare heart healthy diet foods and it’s the fat that makes you fat. and that's why there'san obesity epidemic. i mean, surely the sugar and high fructose corn syrup didn't help. and that's why we all have trouble strugglingwith our weight 'cause the approach we use

to cure it--eat less, exercise more and eatlow fat diets--is exactly the wrong thing. basic question is, i'll phrase it the wayit’s usually phrased. what about those southeast asians who live on low-fat, high carb dietsand don't get fat? and one of the fundamental issues here, and actually, this is partiallywhy i wrote the sugar story in the new york times a couple weeks ago. basically in thebeginning i showed you populations that ate high carb diets that were very poor and werefat. and then there are populations, the japanese,the koreans, the chinese, elsewhere, the kitavans who eat high carb diets and aren't fat. andwhat's the difference, or is it not the carbohydrates? and again, what i'm saying it's the high glycemic,high refined carbs and the sugars. and if

you look at the populations that don't getfat, they have, they eat effectively very little sugar. so, the japanese, for instance,in the 1960s were eating the amount of sugar that we were eating in the 1860s. the kitavanseat virtually no sugar. the way the research will talk about it is these nations don'thave sweet tooths. sweet teeth? so my answer would be, and this is one ofthe reasons why i believe it may be necessary, sugar may be necessary to trigger this. andthat's what the biochemistry, the science suggests today. and once sugar's in the dietoften. one of the interesting things, one of thesuggestions i made in the new york times magazine article was that sugar could actually be thefundamental cause of cancer.

so remember, you want to explain observationsand one observation is that japanese women in japan have relatively very little breastcancer. and then they come to the united states and within two generations, you have virtuallythe same breast cancer rates as any other population. and what could explain this? there'ssomething happening here that causing it, or there's something that's preventing itin japan. it's a common observation throughout the world. and one of the things i would suggestis they come here and more sugar gets into their diets. and the reason they don't haveit there is because there's such little sugar. they don't have insulin resistance and theydon't have all these triggers. but so, the, the, no hypothesis to me would be "it's asugar."

you could evoke other hypotheses; the lengthof time that the refined carb, in this case, rice, or white rice or the grain, had beenin the population. but the sugar is the thing that would seem the most obvious. >>male audience member #2: hi, i have a coupleof personal questions. you're free to not answer them. one is, do you follow this dietthat you recommend? >>gary taubes: yeah. >>male audience member #2: and what is yourwaist size in inches? >>gary taubes: my waist size in inches? well,the question is, see this is always one of the mistakes people make in life. i mean,i'm ok. okay? basically, i have the same body

i had when i was in college. i was a defensivetackle at harvard. i was a bad one. actually, i'm 20 pounds less than i was then.but when you're trying to be a defensive lineman, you're trying to be as heavy as you can. itis actually not important how big i am on my diet. what would be important is how muchbigger i would be if i added carbohydrates back into the diet. that would be the relevant.like, i am never, i could starve myself. actually, my good example is my brother. mybrother is a professor of mathematics at harvard. a very smart guy. he was always lean and iwas always thick. he was always, you could see when he was seven, you could see his musclesand his veins and you could see my pot belly. and when we grew up, we both ate all the foodwe could. as a matter of fact, we ate as fast

as we could 'cause if i didn't eat fast, he'deat it first. he was more physically active. well, he wasn't. he could run longer distances.i could starve myself to death and never look like my brother. i will die of starvation before i am as leanas my brother is 'cause we are physiologically, we partition fuel differently. but the questionis what would happen if i added carbs back to my diet? would my waist size be bigger?right now, i'm six foot two, 220 pounds. my waist size is probably 35. when i was in college, i was six foot two,220 pounds. actually, and my waist size was 35. in between i was heavier. never had the,never likely to be obese. although because

i'm a big guy, my bmi could go over 30. sofor me, well, it might kill me. that's the question. the question is not whether i'm heavy or light.the question is am i going to die sooner because i ate a lot of saturated fat? and one thingi don't have time to do in this lecture, i do in another lecture. if you actually lookat the clinical trials, which compare high fat diets to low fat diets, the way thesehave been done over the past decade is basically putting people, randomizing people to an aitkin’sdiet, which is high fat, high saturated fat. eat as much as you want. and a low fat, americanheart association, low calorie, restricted diet. so one diet, you cut fat. you cut saturatedfat. you cut calories. you're eating like,

skinless chicken breast and lettuce. and theother diet, you can eat as much as you want. so, you're eating eggs and bacon for breakfastand meat and double cheeseburgers without the bun in a sort of iconic atkins’s thing.and nobody really sticks to these diets the way they should. but when the trials are done, what you findis not only the people on the high fat diet, ad lib the eat as much as you want diet, weighless. even though they're told they could eat as much as they want, their heart diseaserisk profile factors improve. and this is what actually got me into this subject. when i was writing a story for the new yorktimes magazine in 2002, i found five of these

trials that had been done and not been publishedyet. and again, if we say, "let's pretend this is a science," we have a hypothesis,we have two of them. one of them is that saturated fat causes heart disease and one of them isthat if you eat more you'll get fat. so now, i'm gonna put you on a diet that says youcan eat as much as you want and as much saturated fat as you want and i recommend you do it. our hypothesis predicts that you will gainweight and get heart disease. and instead, what happened in these trials is these peoplelose weight and their heart disease risk factors improve. across the board, everything improves.so the question then becomes, maybe our hypothesis is wrong.

>>male audience member #3: you answered myquestion to some extent. you answered the last one, but clarify for personal happiness. in the beginning of your talk you spent alot of time on genetics and you had the fat twins and the skinny twins, and the fat cowand the skinny cow, and the fat mouse. and you sort of abandoned that toward the endof the talk. so could i infer that everybody has theirgenetic predisposition, which they start with and their sugar intake regulates them aroundthat? or how would you describe it? >>gary taubes: the question is what role doesgenetics play when it comes to -- like there's an obesity epidemic? the experts will tellyou, obviously our genes haven't changed.

what i'm arguing is again one of the fundamentalobservations is that you don't see obesity in any animals in the wild. on the east coast,where i used to live, there's a deer epidemic. there's obviously enough food for all thedeer to overeat. but you don't get fatter deer. you get more deer. you don't get obesedeer. so the question is why do they get fat? whydo they stay lean, in effect, regardless of how much they eat. and actually, it's interestingfor hibernators, for instance. they'll get fat yearly, regardless of how much they eat.so their fat tissue's regulated. and what are the genes responding to withus? and i would say they're responding to basically how we process the carbs in thediet.

so if we all grew up in a carb free environment,if we were inuits or masai, or native plains indians of the great plains, and we didn'thave the carbs in the diet, we would all basically have, we would all be lean. and then, when you live, grow up, in a highcarb environment, then the phenotype manifests itself of obesity. and what the genes areresponding to are the carbs in the diet. it's basically how you metabolize them, how muchinsulin you secrete, how sensitive your fat tissue is to that insulin, and things likethat. and what's interesting again is i used tolive in new york, up until a year ago, and i'd get my coffee from a bagel shop downstairs.this was right around the corner from nyu.

and it was full of these heavy set young girlsfrom nyu who were eating their low fat bagels and their low fat soy cream cheese and theirlow fat soy lattes. and they were doing exactly what the governmentthinks they should do and what they've been told to do to live a healthy lifestyle. andi assumed they believed they were just doomed to be overweight because they were doing whatthey were told to do. and the argument i would make is that they're doing it in a high carbenvironment. and if they didn't live in a high carb environment, that they didn't eatthe carbs, they would be lean. their phenotype wouldn't manifest itself. and the message i'm trying -- this is thebattle that i'm trying to fight, is to get

these ideas across because there are a lotof people out there, like obese children, who are being tortured with starvation dietsand being made to run five miles a day, or whatever. and that's not why they're fat.and the problem is they're tortured like that and then they get their gatorade when it’sover. and they count the 300 calories of gatorade and they go, "oh, ok. this is good. i'm innegative energy balance." and they're still driving fat accumulation. so we have to get the carbs out of their lifeand i sound like a quack diet book doctor when i say that. that's what the researchshows. >>male audience member #4: i have a very practicalquestion. so, my question is how do you actually

do it? how do you avoid carbs? you go intoa store. you want to buy bacon. you look in the ingredients. there's sugar in there. youcome here in google cafes. there is sugar everywhere. like, every main dish, every stew,they gotta put sugar in it. if you want to buy meat, they're gonna give you lean cutsof meat. you can't get like nice fat cut of meat. so how do you get fat? >>gary taubes: well, you can but it's difficult.i mean, the idea is you can always eat less of it. so if you're not, if you get the kidsoff the sodas and the fruit juices and you don't try to give them low fat foods, youdon't try to give them the low fat yoghurts. i actually have this ongoing argument withmy wife where i say, "look, this michael pollan

kind of thing. if a food makes a health claim,look to see how much sugar is in it." there's almost invariably, with the exceptioni think, of cheerios, weirdly enough, it's gonna have a high sugar content. so the bestyou can do is eat less. so again, my kids will go eat bacon that's cured, apple-curedbacon, which i assume means it’s sweet and it tastes sweet and there's sugar in it. butit's still better than frosted flakes, or coco puffs, or getting apple juice with their. so you can always improve. and everyone, itsounds more difficult than, you made it sound difficult. but the reality is when you, whenpeople try it without looking as closely as you do, at least the ones who succeed emailme and tell me. i don't know if there's this

huge background of people who fail on thesediets. i don't think they work for everybody because i think after a point, you can get. and this is what the british physician wroteabout 50 years ago, looking at his 1500 people he put on a low carb diet. and he said theones who had been fat for a long time, who were very obese, who had been obese the longest,and women more so than men, because women have the sex hormones are much more, thatplay a much greater role in their fattening. and these people – it's sort of -- theymay reach the point of no return. but again, the argument i'm making is thatif you look at the heart disease risk factors and other profiles, i recently had to poston my blog, my own lipid profile, which i

got measured cause people wanted to know ifi appeared to be killing myself. and i'm not by standard measures anyway. but if you look at that, it would still bea healthier diet. so you do better, but you don't have to avoid sugar entirely. you mightbe healthier if you do, but we could certainly all cut back on it. >>male audience member #4: okay. so maybei should give a little bit of clarification. so, yes, i mean, if you want to go healthierthan the average, you can certainly do it if you're gonna [ ] and you are gonna makelots of progress. me personally, i made lots of progress. but if you want to go to thenext step, and if you want to really completely

cut the sugar out, and be really healthy,how do you practically do it? >>gary taubes: first of all, you stop workingin an office. see, i work at home. so i can control and i live in berkeley. i'm sure youhave it here. so we have these gourmet butchers from farms that raised their animals humanelyand don't put sugar in things. again, i'm just a journalist. i can't solveevery problem. i'm trying to fight this particular battle. and then i hope that if i make someprogress and the other people out there fighting this battle make some progress, then maybethe whole society will move into a point where it will get easier. i have a lot of fans at microsoft, i hateto say, and they've been trying to get the

microsoft wellness group to put low carb linesin their cafã©. so they have at least the effect of the atkins like choices. and sofar, as far as i know, they've had no luck. but give them time. >>male audience member #5: hi. i was wondering,you mentioned five studies that were unpublished, and how many of them are now published, ordo you think there's a publication bias, where these studies that talk to the dogma don'tever get published? >>gary taubes: actually, they virtually haveall been published that i know of. probably several dozen studies published. i mean, theresults are always the same. people on these diets, they lose more weight.their triglycerides go down more. their hdl

goes up more. everything gets better and it'sbasically the metabolic syndrome in some resistance resolved. it goes away and should go awayif i'm right, cause it’s pretty obviously caused by the carbs in the diet. there arepublications biases. for instance, people who go in believing thatit’s all about calories, will interpret their data to make it all about calories,even if they published that the atkins’s group does better than the american heartassociation group. there are people who own, there are now like,low carb journals out there, 'journal of nutrition and metabolism'. so some people will do, there'sa great study done on type 2 diabetes at duke university where most of the subjects wereable to get off their diabetes medications.

this is supposedly an irreversible disease.and the author, the first author only sent to the 'journal of nutrition and metabolism',where it would basically be read by the converted, because he didn't wanna deal with all theflack he would get trying to publish in the mainline journal. so there are definitely biases, but if youdo these studies now, i think you almost have to. there's a clinical trials website whereyou have to register them and part of the reason for that is to make sure that peopledon't only publish positive results. so the pretty much all get published, but they doget spun. and often, the spin takes over. the biggest study ever done came out of -- itwas pennsylvania, upenn, colorado, and university

of cincinnati. and they put 300 subjects onan atkins diet in effect and an american heart association diet. and they referred to itas a low carb versus a low fat diet. this is a classic way to do it. but the low fat diet is calorie restricted.so when you're told to go on the low fat diet, you're told to eat 14, 15 hundred caloriesa day, basically semi-starve yourself. and when you go on the low carb diet, you're toldto eat as much as you want. just don't eat carbohydrates. and one of the lessons i learned writing aboutphysics is it's absolutely crucial to define your terms carefully, so people know whatthey've done and what you've done and can

replicate it. and so, you're not in effecttrying to fool people. and if i was writing that study, it wouldsay "low fat, low calorie versus low carb, ad libitum. 'ad libitum' means eat as muchas you want. and i would always use those terms because you never want them to forgetthat one group is low calorie and one group is ad libitum. 'cause that also suggests,and in this case they got essentially the same weight loss. the atkins group did betteron heart disease risk factors, but the weight loss was virtually the same. and you want people to remember that one groupis being semi-starved and one group isn't 'cause that evidence that it’s not aboutthe calories. and they just didn't do it.

they mentioned it in their methodology thatthe low fat group was calorie restricted and then they ignored it. and the title was 'lowfat versus low carb', and the papers picked it up: low fat versus low carb. and they leftout the crucial ingredient, which is one diet restricts calories and the other diet doesn't,which is the ingredient that tells you you're paradigm might be wrong. ok. >>female audience member #2: i'm just wonderingif any of your research, you came across any connections between people who drop the carbohydrates,but coincidentally, they're also dropping the trans fats, because most of the carbohydrateswe purchase commercially are covered with trans fats, which tend to be the worst fatsfor you in terms of heart disease risk.

>>gary taubes: it's funny 'cause i would alwaysargue it the other way. to me, the evidence that trans fats are bad comes from mostlyfrom observational studies where you compare people who eat a lot of trans fats to peoplewho eat very little. like the nurses health studies, what they're doing is there, whenyou think who eats a lot of trans fats and who doesn't, you're comparing in effect, peoplewho buy a lot of processed foods and fast foods, to people who cook most of their mealsfor themselves. >>female audience member #2: you can't separatethe carbohydrates. >>gary taubes: you can, but you're also, butthe point is, as you put it, the processed foods come with the carbs. the trans-fat datajust doesn't wow me.

i mean, it is true if you give up the carbs,you're gonna have to give up the trans fats. but remember all those populations i talkedabout in the beginning, like the trinidadians, the sioux -- native american sioux. they wouldnot have been getting trans fats. so we don't know what their heart disease risk was. butwe know that they weren't getting margarine. they weren't getting -- there wasn't foodindustry forcing trans fats on them. so it's quite likely, the obvious, again, the nullhypothesis would be the carb content of the diet. >>female audience member #2: and then my secondquestion is, that there are populations that tend not to eat meat, like india. there'sso many vegetarians and they get their proteins

mainly from legumes. so what is your takeon the glycemic index of legumes and other non-meat sources of proteins for people whoaren't really eating meat? >>gary taubes: well, i do think, again, theargument i make in the book. the book is called 'why we get fat'? not 'how to lose weight'.the reason why i call it 'why we get fat' is i wanna make this argument that it’sliterally about the carbs, high glycemic index carbs. it doesn't -- the -- legumes are lowerglycemic index. green vegetables are low glycemic index. and the sugars. and anyone can improve their diet if theyjust remove the sugars and the white flour and to some extent, what we call whole wheatflour in the united states. and actually,

even one of observations that i wrote aboutin 'good calories, bad calories'. as early as 1907 the british medical associationhad a meeting in which they had a discussion about the diabetes problem in india 'causediabetes was rampant. they said that it's actually worse among the vegetarians sects.probably 'cause they were also eating the most sugar, which they suggested in 1907. but you can improve the diet by removing thefat and the carbohydrates regardless, is the point. but if somebody’s very predisposedto get fat, if someone's 300 pounds, i would argue that you have to get basically, they'renot gonna get enough calories that they. the easiest, the way to maximize caloriesand minimize carbs is with animal products.

and so, that's the problem. so if these people,they could improve on a vegetarian diet. and i get emails all the day from people tellingme how much they lost, just giving up sugars. i don't think that's enough. in my experience,i can just ask myself, like, "what would happen if i added whole wheat pasta back to my diet?maybe three times a week." and i could pretty much bet that i'd gainten pounds. but the point is anyone can lose weight justby getting rid of, and improve their risk profiles, 'cause the argument i make is thesehigh glycemic index carbs and sugars are the cause of the chronic diseases that associatewith obesity and diabetes and insulin resistance. so, and then, if it's an all vegetarian orvegan diet, you're still gonna be better.

you may not be as lean as you could be ifyou threw your ethical considerations to the wind and switched to meat, but you will behealthier than if you keep these foods in your diet. >>female audience member #3: i was wonderingabout people who do a lot of athletics, especially like endurance stuff and talk about thingslike carbo loading, and other studies that have recently suggested that women typicallywill recover better when they eat carbs after a meal too. and how that fits into all this. >>gary taubes: the question is about how,what about athletics and endurance exercise. don't you need the carbohydrates? aren't theycrucial? [pause]

this is not my area of expertise and i wasnot an endurance athlete. but in the late 1970s, early 1980s, there was some researchdone at the university of vermont by a fellow named steve finney, who's now an emeritusprofessor of nutrition at uc davis. and he put professional bike racers on ketogenicdiets. and it takes about three weeks to what's called "ketoadopt," where you adopt completelyto the complete lack of carbs in the diet, in effect. and the bottom line was they didfine. they lost a little bit of their sprinting ability, but they lost a lot of – they lostnone of their endurance. the interesting thing, i get a lot of emailsfrom bike racers, long distance bike racers, and mountain bike racers, cause weight isan issue there. whereas marathoners, you might

wanna be as light as possible. or, actually, this is where i get confused.the evidence suggests you can do just fine without any carbs and i actually recommend-- email me. i'll forward your email to steve finney. he'll write three thousand words backin response cause that's what he does. but -- and that's a different issue than whetheror not if you carb load like two days before the race, you'll do better. although, i thinksteve would argue that it's not necessary. >>male audience member #6: this is a questionabout the data. so, in the 1970s, americans ate an average of 2200 calories a day. andas your slide says, now they eat 27 hundred calories per day. and in those days you hadless than ten percent obesity and now you

have like 30 percent or something. do youthink their genetics change over 30 years, or with the calories is there no correlationthere? >>gary taubes: i mean this is again, thesenumbers, by the way, are very iffy. but certainly the question was, if you lookat the food consumption numbers, in the 1970s we were eating around 2200 calories. thenit went up by 500 calories. so doesn't that prove that it’s about the calories? that's,in effect, the, and the point is first of all, this is an observation. remember i said, if somebody gets heavier,they gotta eat more, or exercise less because they're gonna be in positive energy balance.so even if, and it's pretty much assumed that

food availability went up, our food portionsizes got bigger, etc., etc. but did people get fatter because they consumedmore? did they get hungrier because they were getting fatter? and those numbers don't, associationslike that tell you nothing about causality. they only tell you that two things happenedsimultaneously. the price of tea in china probably also wentup since 1970, but we're not gonna blame obesity on that. why would we blame it on the availabilityof calories in the food supply? when you look at what those calories were, they were almostexclusively carbohydrates and most of it was high fructose corn syrup. if you actually look at the number in fat,it's something like three percent of the increase

is from fat. or actually fat -- the usda hasscrewed up the numbers and that's another story. but fat consumption, basically, wentdown a little bit. protein consumption went up a little bit and carbohydrate consumptionwent up a lot. and it reflected the public health advice. the shift to pasta, breads,potatoes and then this increase in sugar consumption that i believe was driven high fructose cornsyrup, by the fact that we first didn't know that high fructose corn syrup was sugar. andsecond, believed it wasn't a problem because the problem was all about fat. thank you.