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Home » Gary Taubes Presents at Authors@Google Transcript

Gary Taubes Presents at Authors@Google Transcript

Opening Speaker: This talk is part of the Authors@Google of the Health@Google series. We’ll have a lot of time at the end for questions and there’s a mic here.

So, I’m very pleased to welcome today, Gary Taubes, who is a contributing correspondent for Science Magazine. His work has appeared in the New York Times, the Atlantic, the Esquire. His work has also been included in The Best of The Best American Science Writing and also has received three Science in the Society Journalism 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 Wood Johnson Foundation investigator in health policy research at the University of Berkeley.

So, with this, we’ll have Gary Taubes talk about his latest book.

Gary Taubes

Thank you very much. This book is basically — Good Calories, Bad Calories took me about five years to write and was 500 pages long.

This is the screen I used to use for this talk and I had written that book hoping to get both the lay readers and to the public health authorities around the country and the medical research community. Because the goal of these books are to convince people that–I mean, it’s almost a cliché–but that our fundamental understanding of why we get fat, of obesity, is completely incorrect and that a new paradigm is in order.

And that Google should change the foods that they’re serving at their wonderful, healthy, low-fat cafes. So, after Good Calories, Bad Calories came out, I wrote Why We Get Fat, in effect, to make it the kind of airplane-reading version 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 who asked me if I could write a book that their doctors would read. So, in this lecture, Why We Get Fat is actually based on the lecture. So, once you’ve seen this, you don’t actually have to read the book. Let me see if this works a little. That’s better.

Obesity epidemic in the works

This is just background. You know there’s an obesity epidemic in the works. I’m not going to go over it because, as usual, I’m probably going to run a little long on this talk. The obesity epidemic goes along with the diabetes epidemic. Diabetes diagnoses have tripled in the past 30 years in the United States.

And let’s see if this — Diabetes, obesity are associated with a host of chronic diseases that are known as metabolic diseases, which include fatty liver disease, atherosclerosis, hypertension, stroke, cancer, asthma, sleep apnea, osteoarthritis, neural degeneration.

Actually, Alzheimer’s disease is a disease that’s now associated with what’s called insulin resistance in obesity. And one of the subtexts of the talk I’m going to give today is that the conventional wisdom is that as we get fatter, that increases the risk of all these diseases and the fundamental problem is us getting fatter.

And I’m going to suggest that the same foods, the same thing that makes us fat, also causes these diseases. So, it’s a fundamentally different causality.

So the question we want is why do we get fat? Obvious question. And the official answers are, “Obesity occurs when a person consumes more calories from food than he or she burns.”

Overweight is the result of a caloric imbalance and is mediated by genetics and health.” That’s what the old Surgeon General and the NIH tells us.

So how many people in this room actually believe this and think it’s meaningful? That’s not bad.

You know, I gave this talk at Tufts a couple weeks ago to the nutrition department. And the Tufts people have been behind every dietary guidelines 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? Because if you don’t, I can leave.” 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 in is greater than energy out.” And that’s why we get fat. We take in more energy than we consume. We overeat and the excess calories go to our fat tissue. You hear about this in 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, virtually every article you read on obesity, they’ll say, “Obesity is a disorder of energy balance.”

And when they say that, what they mean is we take in more calories than we consume and that’s why we get fat.

So here’s the general image of what’s going on here. And what you want to do when we talk about this, one of the key things you want to do in any science is explain the observations.

So we have this observation of an obesity epidemic and we want to explain it by our hypothesis, which is that we take in more calories than we expend.

And the way it’s been done over the years is that the idea is “increased prosperity.” This is what Marion Nestle, a New York University nutritionist, wrote in ‘Science’, “As we get richer, more food becomes available. We have less reason to become physically active.”

That food’s on every street corner. You don’t have 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 an environment that promotes overeating and sedentary behavior. And so physical activity, and as Kelly put it, he said, “Cheese curls and French fries, fast food joints are as much a part of our environment as trees and clouds. Mothers keep their kids home from school. 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 enough reason to burn it off. And the question we want to know — here’s the hypothesis: increased prosperity leads to overeating–energy in is greater than energy out– and that leads to obesity and the obesity epidemic. And what we want to know is, is this true? Because this is 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 departments and obesity research departments, I often want to piss them off in the beginning. It’s part of my nature. And I’ll say, “Let’s pretend this is a science for a second 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 McDonalds on every street corner. We know a lot of people watch television. And we know a lot of people are 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 existed there.

And one of the underlying contexts here, one of my underlying hypothesis, and also of any science, the underlying principles is Occam’s Razor. So we should find the simplest possible hypothesis.

So we’re going to work from the hypothesis of whatever makes any population fat is what makes our population fat, until we have to change 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 Louisa was a Pima Indian. And the Pima live on the Gila River reservation. Now, it’s the Gila River 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 because they have conceivably the highest risk of any population.

In the 17th, 18th, 19th Century, they were the most affluent Native American tribe. They were hunters and gatherers. They hunted in the 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 to the Pima territory on the San Jose Trail, they reported that the Pima had this incredible amount of food available. And they were all lean and sprightly. And by 1849, gold was discovered in California.

And over the next 20 years, 20,000 to 60,000 49ers 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 the 1870s, 1880s, Mexican Americans and Anglo Americans started moving into the Pima territory and they overhunted the nearby mountains.

They diverted the Gila River water to irrigate their own fields, and the Pima went into what they called the Years of Famine, which lasted for 20 or 30 years.

And by 1902, when Frank Russell, a Harvard anthropologist came to live with the Pima and wrote the Seminole text on the Pima Indians, they were living on a reservation. They were struggling as farmers to survive, and it was Russell who took the photo of Fat Louisa on the right. And he said many old people in the tribe, unlike the classical image of the strong, buff Native American, many old people in the tribe were actually obese and overweight.

And this was an observation that was seconded a few years later by Alex Hrdlicka, who was the physician-anthropologist who went on to become the curator of the Smithsonian, Department of Physical Anthropology. So, the point about the Pima was that they went from being affluent in the 1840s — that drawing was actually made 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 should have been leaner, right? Because our hypothesis says if poverty leading to prosperity causes obesity, not prosperity leading to poverty. And yet, in the early 19th Century, we have a high level of obesity observed by two separate anthropologists living with the tribe. If this was the only example, we could probably toss it and assume something else was going on. 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 pissed me off doing my research for Good Calories, Bad Calories, which took five years, is you only had to go to look for them to find them. And yet, the obesity research community hadn’t bothered because they had settled on their hypothesis. It’s all about overeating. It’s all about taking in too many calories. It’s all about fast food joints. And so they never looked. If you go look, you’ll find a lot of different populations.

The Sioux on the South Dakota Crow Creek Reservation, in 1928 — this was a study done by two University of Chicago economists. And this, this population was so poor that you could use it. You could put it in the dictionary next to the definition of “dirt poor.” They lived four to eight people per room. Something like 15 families with 32 children on the reservation were living only on bread and coffee. There were no bathrooms. There’s no plumbing. They had to get water from the river. And yet, 40% of the women, 25% of the men, and 10% of the children were distinctly fat. And 20% of the women, 25% of the men, and 25% of the children were distinctly thin. And there were definite signs of malnutrition.

The economists documented all kinds of deficiency diseases among these Native Americans. And this combination of obesity and malnutrition, or under nutrition, existing in the same population is an observation I’m going to come back to shortly — many times, in fact.

Okay, African Americans in Charleston, South Carolina in 1959. Thirty percent of the women are obese and 18 percent of the men. Family incomes are nine to 53 dollars a week. That’s less than 400 dollars a week in 2011 dollars.

Zulus in Durban, South Africa in 1960. Forty percent of the women are obese. Women in their 40s averaged 175 pounds. Today in the United States, 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 of nutritionists down to help out and they come back reporting that a third of women over 25 are obese. They report obesity as a “potentially serious medical problem in women.”

The per capita data

The next year, an MIT nutritionist goes down to Trinidad to figure out what’s going on. She studies the diet of the obese women, compares it to the diets of the lean women in Trinidad and concludes that the per capita daily diet was less than 2000 calories a day, 21 percent fat. Fewer calories than were recommended at the time by the Food and Agricultural Organization for a healthy diet.

Bantu “pensioners” in South Africa in the mid-60s. These are the poorest of a disenfranchised population. 30 percent of the women are severely overweight 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 in 1971.

And then, factory workers in Chile in 1974. Thirty percent are obese. Nearly 50 percent of the women over 54 are obese. Ten percent suffer undernourishment. Okay, so here’s that combination again of obesity and malnutrition in the same population and most are engaged in heavy labor.

So, these are factory workers. They probably don’t belong to a gym. They probably don’t have gyms in their factory in Chile in the 70s. They’re not working out regularly. They’re not training for marathons. They’re probably not 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 physically active than we are. And yet, 30 percent are obese and nearly 50 percent–half of them–over 54.

And here’s the last study I’ll show you. This is Mexican Americans in Starr County, Texas in 1981. Fifty percent of the women in their 50s are obese, 40 percent of the men in their 40s. And the living conditions, most inhabitants are employed in agricultural labor and who work in the oil fields. So again, very physically active 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 San Antonio. And that was a Mexican restaurant.

So again, this definition, there’s no increased prosperity for many of these populations.

There’s no prosperity at all. There’s no toxic environment as we would define it today. But something’s making them fat and we want to know what.

Why were these populations fat?

So if we can figure out why these populations were fat, we can probably figure out why our populations are getting fat. So here’s how this question was phrased in 1973. Ralph Richards was a university – he was a British-trained diabetes specialist who went to Jamaica in the early 1960s, founded a diabetes clinic at the University of the West Indies, and in the early 70s reported that a third of the women over 25 were obese and 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 impecunious society such as exists in the West Indies, when compared to the standard of living enjoyed in the more developed countries.”

He’s asking the same question I’m asking and we all should be asking. If poor people are so fat, our theory says it’s the rich ones who should be fat. “Malnutrition and sub nutrition are common disorders in the first two years of life in these areas and account for almost 25 percent of all admissions to pediatric wards in Jamaica.” So, by “sub nutrition”, he means not enough food. “Sub nutrition continues in early childhood to the early teens.”

So the children are stunted and show signs of emaciation and then “obesity begins to manifest itself in the female population and reaches enormous proportions from 30 onwards.”

So here’s that question asked again. Exactly the same observation, exactly the same question 30 years later, this time by Benjamin Caballero of Johns Hopkins.

And now, within this paradigm of calories in, calories out, of overeating. 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 in the New England Journal of Medicine in 2005, an article called ‘Obesity and Malnutrition: A Nutrition Paradox’. He says, “A few years ago, I was visiting a primary care clinic in the slums of São Paulo, Brazil. The waiting room was full of mothers with thin, stunted young children, exhibiting the typical signs of chronic under nutrition. Their appearance, sadly, would surprise few who visit poor urban areas in the developing world. What might come as a surprise is that many of the mothers holding those under-nourished infants were themselves overweight.”

And then he says, “The coexistence of underweight and overweight poses a challenge to public health programs, since the aims of programs to reduce under nutrition” –which is get people to eat more, make more food available—”are obviously 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 public health programs” in italics because the coexistence of underweight and overweight poses a challenge to your paradigm, your belief system. If you believe that the mothers got fat because they took in more calories than they expended, they took in superfluous calories that they didn’t need, and the children aren’t getting enough food, then you believe that the mothers are willing to starve their children to death so that they can sneak outside and eat a Snickers bar, in effect.

And I don’t know how many, this is a young audience, how many mothers are there in this audience? Okay. 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 unless the mothers make sacrifices for their children.

And we have the paradigm of obesity that says these mothers are just happily guzzling excess calories while they’re watching their kids starve to death.

And this is an anomalous observation. I used to, started my career writing about high-energy physics, and high-energy physics, they just built the Large Hadron Collider 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 can proceed onward.

Here, we’ve had this observation going back probably to 1928 at least, and nobody cares. And my point is you have to throw out one of the two paradigms. And I’m going to throw out the obesity paradigm because 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 hypothesis is 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 you have to do is create what’s called “negative energy balance.” So you go on a semi-restricted calorie diet and there are a lot of meta-analysis over the years, systematic reviews, showing how poorly these work.

Cochrane Collaboration

The Cochrane Collaboration a few years ago when they looked at this. The Cochrane Collaboration is a collaboration created just to do unbiased reviews 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 with this, 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’s so small as to be clinically insignificant.

And what you see in the literature is fascinating because people, they try to deal with this when they write about obesity; the fact that eating 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 write that restricting calories is the fundamental approach, the — I forget the word they use because I don’t have my notes– to curing obesity, yet it rarely, if ever, works.

Exercising more also doesn’t work?

Exercising more also doesn’t work. One of the problems here, I could also show you meta-analyses that talk about how clinically insignificant this effect is. But there’s, the best evidence I found so far for this is the American Heart Association and the American College of Sports Medicine in 2007, put out their physical activity guidelines. And the physical activity guidelines—these are people, two organizations, that want us to engage in healthy lifestyles, that believe that physical activity should make a difference.

And you would expect them to spin the data in favor of physical activity for exercise, for weight loss–and the way they put it is this. They said, “It is reasonable to assume that persons with relatively high daily energy expenditures would be less likely to gain weight over time, compared to those who have low energy expenditures.”

That’s logically equivalent to saying, “It’s reasonable 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 support this hypothesis are not particularly compelling.” And the point of this is this hypothesis is in the neighborhood of 100 to 150 years old. There, you could find obesity texts in the 1860s in which somebody like William Banting talks about his doctor telling him to go for a row every morning to burn off calories.

He also talks about how it didn’t help. You could find in, by the 1890s, when the laws of thermodynamics had been shown to hold with animate objects as well as inanimate objects, with living beings as well as inanimate objects, researchers said, “Hey, maybe if we just get people to expend more energy, they’ll gain weight. I mean they’ll lose weight and over the course of a hundred years, 150 years, this is the best we could say about it. “The data to support this hypothesis are not particularly compelling.”

And that’s a bad sign. When I was writing about 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 throw money 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 studying an effect, for a century and the best you could say about it is “the data to support this hypothesis are not particularly compelling”, there’s a very good chance that your hypothesis is wrong; that increasing energy expenditure and physical activity will have no effect on how much you weigh, or how much weight you’ve gained.

And one way to think about this and to this I owe a British blogger. Imagine that I’m having, I’m hosting a dinner party tonight and I’ve got the ten last finalists from Top Chef cooking. And they’re making this amazing feast and I send you all invitations and I say, “I’ve got this feast. It’s going to be a ton of the best tasting food you’ve ever eaten in your life. Come hungry.” What would you do to make sure you came hungry?

And here I’ll take questions. Anyone want to answer? What would you do during the day?

Audience Member: Skip snacks.

Gary Taubes: Skip snacks, eat less.

Audience Member: I would take a long walk.

Gary Taubes: And take a long walk. Exercise more. You’d work out.

So the exact same things that we prescribe overweight people to lose weight are the two things that you’re going to do if you want to guarantee that you get hungry and eat more.

And we’re going to explain that in a while. But you can see already that there’s something wrong here. Here’s another problem with our energy balance idea. Practicing energy balance is impossible. This is a new phrase you hear.

The past two or three years, the idea there are now industry programs developed in collaboration with the government to help you practice energy balance, to make sure you match calories in to calories out so you don’t gain weight.

And the industry loves the idea. The food industry loves the idea of obesity being all about calories, because you can’t demonize anything. It’s all about just it’s your fault if you’re overweight. You just have to eat less and exercise more and if you want to build a gym in your neighborhood, or a track or a park, go to Coke or Pepsi and ask them for money. They’ll give it to you because they would 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 practice energy 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 a decade, 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 want to ask the question, “How well do I have to maintain energy balance? How well do I have to practice energy balance so that I don’t gain 20 pounds in a decade, 40 pounds in 20 years, so by the time I’m in my mid-40s I’m obese?” What does that entail, because that’s what the government is trying to get us to do.

And the answer is you have to maintain your energy 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 gain 40 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 is the number of calories, roughly, in a pound of fat. And you end up with 21 pounds in a decade. 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 you only 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 0.8 percent accuracy. Nobody can do that. Nobody, even I will bet my life’s income–it’s not that big–that the world champion calorie counter in the world, Guinness — if there is such an entry in Guinness, cannot gauge within 20 calories how much food they were eating per day and then you have no idea how much you’re expending.

You’re just guessing, even when you go in to do research sessions. They just do calculations. So the point here is I got this calculation from a 1937 Nutrition and Metabolism textbook, written by a fellow named Eugene Dubois, who’s a leading expert on metabolism in the United States, pre-World War II. And Dubois uses calculations. He said what’s interesting about it is since nobody can do that, how do we maintain our weight? The question isn’t why are some of us fat? The question should be why aren’t all of us fat? Okay?

Because if you overshoot by even 20 calories a day on average, you’re going to end up getting obese. And you could say, “Okay. Maybe one way 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 going to eat 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’re not looking in the mirror. They don’t have clothes they’re putting on. So how do they maintain their weight and virtually all animals do? They don’t get chronically obese. So the idea that Dubois says it’s obviously something else is going on here, other than consciously matching 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 got to apologize now. 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, as well as just whether they do or not.

And one of the things I’m doing now is just channeling these pre-World War II researchers. And in fact, all I’m saying in my books is I’m taking the theory that German and Austrian researchers developed pre-World War II, back when the Germans and Austrians did the best medical research in the world and there was virtually no meaningful medical research being done in the United States.

And I’m taking that theory and I’m updating it. 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 overeating hypothesis might explain why these women are fatter than these women. These took in too many calories and these practiced perfect energy balance.

But what about this combination? And why do they have the same body type? It’s been known since the 1930s that obesity has a strong genetic component. Identical twins – it’s not that their faces look alike. Their body types are the same, too. So what’s going on here? What do these genes determine? Do they determine exactly how much these women, how many forkfuls of food these women overate over 20, 30, 40 years? And exactly how long they sat on a couch versus going for a walk?

Or, did they determine something else about how much and where they accumulated fat because they have the identical body?

Here’s a different variation of an animal husbandry and it’s even easier to see here what I’m talking about. Farmers, livestock breeders, 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’s the meat. I should say it’s stocky, but you can see all the subcutaneous fat, the intramuscular fat, here. And here’s a lean species, a lean breed of cattle, the Jersey Cow. And you can see the ribs showing, you can see the swollen udder. It’s definitely a dairy cow.

And you can ask yourself simply, there are different breeds. Obviously, different genes are determining how much they get fat. What exactly is going on here? What are these genes determining? Do they determine how much these animals eat and exercise? Do they determine how many calories per graze, or per bite of grass, this cow takes? The Aberdeen Angus grazes for 12 hours. The Jersey only grazes for ten a day. Does the Jersey want to go to work out? So, on the Far Side cartoon when it gets dark at night, the Jersey goes for a jog. The Aberdeen Angus goes in and watches television. And it’s obviously absurd, Okay?

Whatever determines how much these animals get fat, we can be confident that how much they eat and exercise has nothing to do with it. 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 go here.

So you could assume that it just partitions the 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 going to go to the udders to produce milk. And you don’t want it wasting energy, in effect, bulking up. So maybe what these genes determine is not 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 below the waist. Both these people would have had to overeat, take in more calories than they expend to get fat. This has doubled his risk of heart disease. This has not doubled her risk. If the weight’s below the waist, it doesn’t double your risk. What do the calories have to do with it? Okay?

And what do the calories have to do with where they get fat, because obviously, that’s a huge component of it. And another way to look at it is puberty. Men and women, when they go through puberty, boys, they begin puberty with roughly the same amount of body fat. When boys go through puberty, they lose fat and gain muscle. When girls go through puberty, they gain fat and breasts and hips and buttocks.

And by the time they’re out of puberty, the girls have about 50 percent more fat on their bodies than the men. Both boys and girls got bigger. So they both overate. They both took in more calories than they expend, but the boys lost fat and gained muscle. The girls gained fat in specific places.

So you just ask the question, what do the calories have to do with it? What did the fact of their overeating have to do with whether or not they gained muscle or fat? And this is obviously controlled by sex and growth hormones and that’s an issue we’ll get to.


Now, lipidystrophies. This is again, from the same 1940 textbook, which took it from a 1933 German text book. This is a lipidystrophy called a progressive lipidystrophy. In the 1950s, there were about 200 of these on record. Most of them were in women. It’s called progressive because these cases, they begin losing all subcutaneous fat in the face, in their forehead, and it moves downward with time.

One British physician reported that his patient lost fat at about one inch a year. That’s why it’s progressive. And then it usually stops above the hips. And then often get this lower body, localized obesity below the waist. So the way these Europeans asked it, they said, “Are we going to blame the top half 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 upper body, maybe even five pounds, just to smooth out her curves, her BMI was about 32 already just because of her lower body obesity. And she went into the doctor then. The doctor wouldn’t recognize the lipidystrophy. And he would just say, “Look, eat less and exercise more.”

And the point that the Europeans are making is if you can’t explain the localized conditions by under eating and overeating, why would you 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 they were looking at cases that today we would call anorexia and assuming that that also wasn’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 look at a little physics here, Okay? And this is the reason.

We believe it because of the first law of thermodynamics. Every time somebody like me makes this point for the past 50, 60 years, you get accused of not believing that thermodynamics holds for human beings.

I had one of the high points of my life. I was on the Larry King Show after ‘Good Calories, Bad Calories’ came out. And they had Jillian Michaels, the trainer from ‘The Biggest Loser’, come on. And she gave me a lecture on the laws of thermodynamics on national television.

And I have a physics degree from Harvard.

I mean, I was a — I was a lousy student, but it was definitely, I literally, I’m sitting next to. I just, I didn’t respond. If you watch the show, it’s on, you can Google it. I didn’t know what to say. I mean, how do I respond to this?

So let me give you a little, thermodynamics is pretty simple. The first law of thermodynamics — it’s the law of energy conservation. It says a change in energy in a system—this is the simplest possible way to put it– is equal to the energy in minus energy out. All it’s saying is you can’t create energy from thin air.

So, if a system gets bigger, delta E goes up. And it’s got to 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 fat mass E-in is energy consumed, E-out energy expended. So change in fat mass equals energy consumed 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 by that I mean it doesn’t say in any way if energy, energy consumed greater than energy expended causes change of fat mass. It just says this is the way the universe is.

If a system gets bigger, it takes in more energy than it expends. And if a system gets smaller, it takes in less. It says nothing about what causes it. And to understand that, a metaphor I could use. Like, let’s assume I was asking the question why is this room crowded right now? Okay?

And it’s as similar when we’re talking about fat mass. We want to know, why is there so much energy accumulated in the fat mass? And I want to ask the question, why is there so much energy accumulated in this room in the form of people? So you ask me, “Gary, why is it crowded?” And I say, “Well, because more people entered than left.”

Right? Have I told you anything meaningful at all about why this? I mean, of course more people entered than left. But why is it crowded? And then I say, “Well, look. If more people enter than leave, it’s got to get crowded, right?” And I still haven’t told you anything meaningful.

This is what magicians would call–I forget the word–vacuous? It’s the equivalent as saying, why did you get fat? Because you took in 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 you take in more energy than you expend,” there’s no arrow of causality. There’s nothing meaningful here.

This is a mistake that was made occasionally prior to the Second World War. It became ubiquitous after the Second World War. Whenever we tell someone, “You got fat because you overate,” you are misinterpreting the laws of thermodynamics on an eighth grade mathematics level.

And the more I talk about it, the more it’s almost unbelievable that this ever happened. And yet, it did. And so there’s another way you could play with this thermodynamics. And for this I owe University of Washington grad student named Sonya Trejo, who said, “What happens if you start transposing elements?”

So how about this. Instead of, we had delta E over here and E out over here. How about if we say energy out is equal to energy in minus delta E? And so now, the energy expended is equal to energy consumed minus change in fat mass, Okay?

So if fat mass gets bigger — for we don’t know why, we’re working on that — and the person doesn’t eat anymore, then energy expenditure has to go down. Okay? So you look at it this way and an increase in fat mass causes sedentary behavior. If fat mass gets smaller, energy expended has to go up.

So if somebody’s losing weight, they have to get more physically active. Or how about this one? We just do a little more transposing and we end up with energy-in equals delta E plus energy-out. So the energy we eat is equal to change in fat mass plus energy expended.

Let’s assume change in fat mass is fixed by biology. And if you read the New York Times today there was an article about that. And energy expenditure goes up because I just told you to work out. What’s going to happen to energy consumed? It has to go up. You’re going to get hungry. You will work up an appetite.

This used to be something that everyone believed in the 1960s and beyond. There used to be this term, “working up an appetite.” So it used to be, if you worked out, you worked up an appetite. Now if you work out, you’re supposed to lose weight and energy consumed is supposed to stay fixed. But there’s no guarantee this’ll happen.

So here’s the alternative hypothesis. This is the way that the pre-World War II Europeans thought about it. They said, started from first principles, obesity is a disorder of excess fat accumulation. So today, you read obesity is a positive energy balance, or obesity is an energy balance problem and those are assumptions. They just started at the beginning. Having too much fat is a disorder of having too much fat. So it’s not energy balance. It’s not overeating. It’s not sedentary behavior.

And if you ask it this way, the next question you’re likely to ask, which we’ll get to, is what regulates fat accumulation? Because what we know is there’s too much fat.

Like, if I was standing in here with Yao Ming, who’s 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 regulates growth, right. So we want to know what regulates growth. So, by this hypothesis, overeating and inactivity are compensatory effects. They’re not causes.

And the way it was put to me by several different individuals doing animal research, so we don’t get fat because we overeat. We overeat because our 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 energy balance 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 these photos because he’s so cute. He was. Here he was one year old, 20 pounds. Okay? 2006. Here he is 2009, 45 pounds. He’s gained 25 pounds in three years, right? He’s been in positive energy 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 because he was secreting growth hormone. And the growth hormone sparked his tissues to grow muscle, organs, fat, bone. And he had to take in more calories than he expended to fuel that growth. And if he wasn’t growing fast enough, we might have even given him more growth hormone to speed his growth, at which point that would have created even more positive energy balance.

Here’s a gruesome analogy: cancer. Here’s a 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 we want to starve it to death, but that’s a given.

Like, just if we don’t want this room to get crowded, 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 balance is in effect.

And in every other example in nature, positive energy balance is always an effect of growth, not the other way around.

Lipophilia hypothesis

So, this was a German-Austrian hypothesis prior to World War II. It was known as the lipophilia hypothesis. I’ll explain that in a second. The primary proponents where Gustav von Bergmann, who was a German specialist in internal medicine. Today the highest award in the German Association of Internal Medicine is the Gustav von Bergmann Award.

And then Julius Bauer, who was a geneticist and endocrinologist at the University of Vienna, Bauer was very famous in Austria. If you have any molecular biology or genetics friends in Austria, email them and say, “Have you ever heard of Julius Bauer?” And they’ll probably say, “Oh, yeah. Absolutely.”

And the theory was more or less fully accepted in Europe by 1940. This comes from the 1940 textbook. And the problem was 1940 was a bad year for Europe. So, the German and Austrian medical research communities evaporate. Unlike in physics, where we, we embraced all the European physicists who got chased out of Europe 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, “Julius Bauer, Hollywood, California,” and nobody took his work seriously, although his son became Dean of the USC Medical School.

So here’s lipophilia in a nutshell. The idea is lipophilia means ‘love of fat’. Okay. The way these people saw it, is that some tissues are more or less predisposed to accumulate fat, in the same way that, you can think of it, 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 fat on 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’t accuse them of under eating because they’re losing weight. We know that there’s a lot of different issues involved.

So Bauer put it like this. He said, “Like a malignant tumor or like the fetus, the uterus or the breasts of a pregnant woman, the abnormal lipophilic tissue seizes on foodstuffs, even in the case of under nutrition. It maintains its stock, and may increase it independent of the requirements of the organism. A sort of anarchy exists; the adipose tissue lives for itself and does not fit into the precisely regulated management of the whole organism.”

And this phrase, “even in the case of under nutrition,” begins to tell us why these women could get obese in a population where their children are starving because it didn’t matter how little food there was. If there was something driving their accumulation of fat, they were going to 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 to test what’s driving it, like a genetic model, a surgical model. You could lessen the ventromedial hypothalamus for rat and it’ll get obese and eat voraciously. So you’ll see voracious eating and obesity. And you want to know which causes which.

Did this regulation of fat tissue cause what’s called hyperphagia? Or did the hyperphagia cause the accumulation of fat? So what you do, is you just do the experiment and then you put the animals on a diet and see whether they get fat anyway. Okay?

And what you’ll find for every animal model of obesity is they will get obese anyway, even if you put them on a diet. You can, in some cases, starve them. There’s a genetic strain of mice that MRC Greenwood studied in the early 1980s, when she put these animals on a diet from the moment they were weaned and they became more obese.

They became fatter than their lean control than their genetic controls. Even though they were on a diet their whole life, they actually weighed less. Their organs were smaller. Their muscle tissue was smaller and they had more fat. And in effect, their drive to accumulate fat was, in order to do that they cannibalized their organs and their brain.

And Jean Meyer, a Tufts nutritionist who played a large role in this, usually to the detriment of society. The way he put it, he studied a genetic strain of mice. He said, “These mice will make fat out of their food under the most unlikely circumstances, even when half-starved.” Okay? So it’s not that these mice got fat because they ate too much. They got fat if you let them eat anything basically.

And we’re going to propose, again, that the same thing’s happening in humans. So here’s some obvious questions. Why vertical growth but not horizontal? When we look at children, we know that overeating is the effect. Growth is the cause. Why animals but not men? An animal’s model of obesity, when you break the gene, you intervene surgically.

There are even dietary models. What you’re doing is dis-regulating the fat tissue. You’re not making the animals eat too much.

Adiposity 101

And then the question, if obesity is sort of excess fat accumulation, what regulates fat accumulation? So here’s a regulation of fat. Adiposity 101. If you learn this, you’ll know more than your doctors do.

By the way, what gets me is that again, it’s 2011. I lecture in medical schools. I lecture to obesity research centers. And I’m telling them, it’s like I’m telling them 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 fat tissue 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 growth problem, like I said, from cancer to height to anything, all you’re going to care about is what hormones, what enzymes, are driving growth.

So let’s care about it here, too. And what you learn is fat is stored as triglycerides in your fat tissue. Here’s a triglyceride. It’s three fatty acids bound together by a glycerol molecule. Fatty acids are burned for fuel and the fat enters and exits the cell as these fatty acids. And the reason that is, is because the triglycerides themselves are too big to fit in and out of the cell to 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 want to get it out, you have to break it down into its component parts again. So the fatty acids can get out. So, it’s a very simple mechanism for storing fat. Here it is in a, in a diagram. Here’s fatty acids outside the cell. They pass through the fat cell membrane. Inside the cell, there’s this triglyceride fatty acid cycle. So the fatty acids are bound to an activated glycerol molecule and you’ll have a triglyceride. And as a triglyceride, they’re fixed in the fat cell. And then they break down.

There’s a hormone, several hormones; a primary one called hormone sensitive lipase, which breaks down the triglycerides into the fatty acids and then they can escape again.

So, here’s where we care about energy-in minus energy-out. You will get fatter if more fat enters your fat tissue than leaves. And you will get leaner if more fatty acids leave your fat tissue than enter it. And what we want to know is what determines this balance of fatty acids going in versus fatty acids going out. It’s that simple.

So here it is, circa 2010. I could’ve used the same diagram from the mid-1960s, because this was figured out by the mid-1960s. Unfortunately the 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, the hormone insulin, is a principle regulator of fat metabolism. This is Rosalyn Yalow and Solomon Berson who invented the radioimmunoassay for measuring hormones. Yalow won the Nobel Prize for it. Berson had died by then.

And you could see when it comes to white fat tissue, 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 author is interested in in metabolic regulation is insulin. It up regulates here. It up regulates there. It up regulates here, it up regulates here. It down, it suppresses fat mobilization and then there’s some role from other hormones in increasing fat mobilization. But it’s basically insulin that puts fat in the fat tissue and it’s insulin that suppresses fat mobilization.

Here, it’s putting fat in. Here, it’s putting fat 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 you want to get insulin, if you want to get fat out of your fat tissue, you have to lower your insulin levels.

That’s the fundamental thing that the Adiposity 101 tells you. So, and what’s funny is we’ve known for like, 50 years that insulin is a fat-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 first emaciated daughter diabetic patient demonstrated a fine pad of fat tissue, made as a result of 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 she was something like 17 years old. And for the next 47 years, she injected herself with her insulin in two spots on her thighs. And she ended up with these huge fat masses. In this picture 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 injected insulin on the accumulation of fat into fat cells are graphically illustrated here. That’s what happens when you raise insulin levels.

So here’s the bottom line. When insulin is secreted 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 primarily in response to the carbohydrates in our diet.

This is how George Cahill, he was a Harvard diabetes 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 take this science of fat metabolism and make it available to the people who didn’t read biochemistry and physiology textbooks.

And as Cahill put it to me, “Carbohydrate is driving insulin is driving fat.” That is basically the message in that textbook. And the interesting thing is you can take out “is driving insulin” and get “carbohydrate is driving fat.” It’s logically equivalent.

So, and when I give this lecture at medical schools, it’s really funny because I could watch the audience and I see, “Oh, wait a minute. Geez, He used that word ‘carbohydrate’. That means this is that Atkins crap.” And the 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 glycemic index 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 the bloodstream. 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 wrote in the New York Times magazine article a few weeks ago, are the fundamental cause of this condition 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’t up until 1960. In the 1820s, when a Frenchman named Anthelme Brillat-Savarin wrote what was 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 with stout, exceedingly stout people, it was fairly clear that the cause of obesity was a genetic predisposition to fatten. Plus, starches, what he called farinaceous foods, and sugar made everything worse. And for the next 140 years, the conventional wisdom in this country and elsewhere was that carbohydrates make you fat. This was the first line of a British Journal of Nutrition article in 1963, written by the two, one of two most prominent British dieticians, “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 was the Bible of child-raising in our country from the 1946, the first edition, to the end of the century. This one sentence was in every single edition. “The amount of plain, starchy food, cereals, breads, potatoes taken is what determines, in the case of most people, how much weight they gain or lose.”

If you went to a hospital in the 1940s and 1950s and were obese, this is the kind of diet they would put you on. I could’ve shown the same diet from Harvard Medical School, from Stanford Medical School, from Cornell Med School. This is actually from ‘The Practice of Endocrinology’, a British textbook written by Raymond Greene, who was the brother of Graham Greene and the most influential British endocrinologist of the mid-20th Century. Foods to be avoided: bread and everything made with flour, cereals, potatoes, foods containing much sugar, all sweets. 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 are fattening. You limit them. These foods you can eat as much as you like because they literally do not make you fat.

It’s not about calories. It’s about the effect of the food on the hormones that regulate fat accumulation, insulin. So here are the conclusions. Biology, not physics. This is a biological problem. The laws of thermodynamics have nothing to do with it, no more than the laws of relativity do. Obesity disorder, fat accumulation, not energy balanced, not overeating and sedentary behavior. Fat accumulation is regulated fundamentally by insulin and dietary carbohydrates. Carbohydrates driving insulin is driving fat.

And the only non-pharmaceutical remedy is to restrict or remove the causative agent, carbohydrates. Now, here’s the problem.

If you lower the carbohydrate content of the diet, but you keep calories high because it’s not about calories and you want to make sure the person has enough calories to fuel, to run their body and if you’re obese or you’re overweight, you need a lot of fuel because you have a big body.

If you lower the carb content and keep calories high, you raise the fat content. So, you end up with a high-fat diet. Fat, actually, happens to be the one nutrient that does not stimulate insulin secretion. Protein does. So, a healthy diet, if you’re overweight and obese, 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’ve been, what the cafeteria is here feeding.

It’s this low-fat dogma. It’s got to be about lowering the fat. And it’s not about the fat. It’s about the carbohydrates. So, you can 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 ‘Principles of Biochemistry’, Lenningers’. It’s sort of the seminal biochemistry textbook. This is the latest edition from a couple years ago. What makes fat tissue fat? High blood glucose–that’s carbs–elicits the release of insulin, which speeds the uptake of glucose by tissues, favors the storage of fuels as glycogen–it’s a good thing– and triglycerols–fat, a very bad thing–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’s energy-consuming activities. The point I’m making is that the same thing that makes your fat cells fat is what makes you fat. Because if you’re fat, for the most part, it’s because all your fat cells are too fat.

And this disconnect, I was interviewing this British Oxford University fat metabolism specialist, who took 15 minutes on the phone explaining to me all the ways that insulin makes fat cells fat. And then got around to people and evoked 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 to people, you brought in this vague overeating thing. And he literally said to me, “I never thought of that.” He’s like, in his mid- to late- 60s.

Here’s the other thing that happened. In the 1960s, we started to believe that dietary fat causes heart disease. So when dietary fat causes heart disease, you remember I just told you that a carb-restricted diet is a high-fat diet.

And so the same year that the American Physiological Society put out its high-fat diet, its handbook of adipose tissue metabolism saying carbohydrates drive 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 the low-carbohydrate reducing diet, which one of them calls ‘nonsense’—because you don’t have to restrict calories because it’s not about calories— and another compares to ‘mass murder.'”

This is Jean Meyer, who was the most influential nutritionist in the country; went on to become president of Tufts University. ‘Mass murder’ because you’re giving people high-fat diet.

So the science says carbohydrates is driving insulin is driving fat. Cut the carbs out.

And the nutritionists are saying, “You can’t do that. You’re going to kill people.”

And that’s how we’ve seen it ever since. And you get to the point by the 1980s when you end up with the food guide pyramid because we believe fats are fattening and we believe red meat causes colon cancer, or God knows what. We’re going to tell an entire nation to eat bread, cereal, rice, pasta. And sweets, weirdly enough, get a free pass because they’re non-fattening.

So, Coke, Pepsi, SoBa ice tea, Snapple. There was actually a theory in the 1980s, you could drink as much, you could eat as much any food you want if it didn’t have fat in it. Because if it didn’t have fat in it, you couldn’t put fat on.

So, just to wrap up. I’ve already gone too long because I always do.

I started off asking question, why were these populations fat? Rolf Richards, in 1973, “Most third world countries have a high carbohydrate intake as their economic dependence is predominantly agricultural, with a heavy dependence on non-dairy produces. It is conceivable that the ready availability of starch in preference to animal protein, 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 conventional wisdom that carbohydrates make you fat. And over the course of 20 years, from the 1960s to the 1980s, turned it into the conventional wisdom that you grew up with, that carbohydrates are heart healthy diet foods and it’s the fat that makes you fat. And that’s why there’s an obesity epidemic. I mean, surely the sugar and high fructose corn syrup didn’t help.

And that’s why we all have trouble struggling with our weight because the approach we use to cure it–eat less, exercise more and eat low fat diets–is exactly the wrong thing.

Basic question is, I’ll phrase it the way it’s usually phrased. What about those Southeast Asians who live on low-fat, high carb diets and don’t get fat? And one of the fundamental issues here, and actually, this is partially why I wrote the sugar story in the New York Times a couple weeks ago. Basically in the beginning I showed you populations that ate high carb diets that were very poor and were fat.

And then there are populations, the Japanese, the Koreans, the Chinese, elsewhere, the Kitavans who eat high carb diets and aren’t fat. And what’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 get fat, 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 Kitavans eat virtually no sugar. The way the research will talk about it is these nations don’t have sweet tooths. Sweet teeth?

So my answer would be, and this is one of the reasons why I believe it may be necessary, sugar may be necessary to trigger this. And that’s what the biochemistry, the science suggests today. And once sugar’s in the diet often.

One of the interesting things, one of the suggestions I made in the New York Times magazine article was that sugar could actually be the fundamental cause of cancer.

So remember, you want to explain observations and one observation is that Japanese women in Japan have relatively very little breast cancer. And then they come to the United States and within two generations, you have virtually the same breast cancer rates as any other population. And what could explain this? There’s something happening here that’s causing it, or there’s something that’s preventing it in Japan. It’s a common observation throughout the world. And one of the things I would suggest is they come here and more sugar gets into their diets. And the reason they don’t have it there is because there’s such little sugar.

They don’t have insulin resistance and they don’t have all these triggers. But so, the no hypothesis to me would be “it’s a sugar.”

You could evoke other hypotheses; the length of time that the refined carb, in this case, rice, or white rice or the grain, had been in the population. But the sugar is the thing that would seem the most obvious.

Question & Answer Session

Male Audience: Hi, I have a couple of personal questions. You’re free to not answer them. One is, do you follow this diet that you recommend?

Gary Taubes: Yes.

Male Audience: And what is your waist 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 okay. Okay? Basically, I have the same body I had when I was in college. I was a defensive tackle 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. It is actually not important how big I am on my diet. What would be important is how much bigger 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. My brother is a professor of mathematics at Harvard. A very smart guy. He was always lean and I was always thick. He was always, you could see when he was seven, you could see his muscles and his veins and you could see my pot belly.

And when we grew up, we both ate all the food we could. As a matter of fact, we ate as fast as we could because if I didn’t eat fast, he’d eat 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 lean as my brother is ’cause we are physiologically, we partition fuel differently. But the question is 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. So for 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 thing I don’t have time to do in this lecture, I do in another lecture. If you actually look at the clinical trials, which compare high fat diets to low fat diets, the way these have been done over the past decade is basically putting people, randomizing people to an Aitkins diet, which is high fat, high saturated fat.

Eat as much as you want. And a low fat, American Heart Association, low calorie, restricted diet. So one diet, you cut fat. You cut saturated fat. You cut calories. You’re eating like, skinless chicken breast and lettuce. And the other diet, you can eat as much as you want.

So, you’re eating eggs and bacon for breakfast and meat and double cheeseburgers without the bun in a sort of iconic Atkins thing. And nobody really sticks to these diets the way they should.

But when the trials are done, what you find is not only the people on the high fat diet, ad lib the eat as much as you want diet, weigh less. Even though they’re told they could eat as much as they want, their heart disease risk profile factors improve. And this is what actually got me into this subject.

When I was writing a story for the New York Times magazine in 2002, I found five of these trials that had been done and not been published yet. 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 is that if you eat more you’ll get fat.

So now, I’m going to put you on a diet that says you can 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 gain weight and get heart disease.

And instead, what happened in these trials is these people lose 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: You answered my question to some extent. You answered the last one, but clarify for personal happiness. In the beginning of your talk you spent a lot of time on genetics and you had the fat twins and the skinny twins, and the fat cow and the skinny cow, and the fat mouse. And you sort of abandoned that toward the end of the talk. So could I infer that everybody has their genetic predisposition, which they start with and their sugar intake regulates them around that? Or how would you describe it?

Gary Taubes: The question is what role does genetics play when it comes to — like there’s an obesity epidemic? The experts will tell you, obviously our genes haven’t changed.

What I’m arguing is again one of the fundamental observations 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 the deer to overeat. But you don’t get fatter deer. You get more deer. You don’t get obese deer. So the question is why do they get fat? Why do they stay lean, in effect, regardless of how much they eat. And actually, it’s interesting for 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 with us? And I would say they’re responding to basically how we process the carbs in the diet.

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’t have the carbs in the diet, we would all basically have, we would all be lean. And then, when you live, grow up, in a high carb environment, then the phenotype manifests itself of obesity. And what the genes are responding to are the carbs in the diet. It’s basically how you metabolize them, how much insulin you secrete, how sensitive your fat tissue is to that insulin, and things like that.

And what’s interesting again is I used to live 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 girls from NYU who were eating their low fat bagels and their low fat soy cream cheese and their low fat soy lattes.

And they were doing exactly what the government thinks they should do and what they’ve been told to do to live a healthy lifestyle. And I assumed they believed they were just doomed to be overweight because they were doing what they were told to do. And the argument I would make is that they’re doing it in a high carb environment. And if they didn’t live in a high carb environment, that they didn’t eat the carbs, they would be lean. Their phenotype wouldn’t manifest itself.

And the message I’m trying — this is the battle that I’m trying to fight, is to get these ideas across because there are a lot of people out there, like obese children, who are being tortured with starvation diets and 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’s over. And they count the 300 calories of Gatorade and they go, “Oh, Okay. This is good. I’m in negative energy balance.” And they’re still driving fat accumulation.

So we have to get the carbs out of their life and I sound like a quack diet book doctor when I say that. That’s what the research shows.

Male Audience: I have a very practical question. So, my question is how do you actually do it? How do you avoid carbs? You go into a store. You want to buy bacon. You look in the ingredients. There’s sugar in there. You come here in Google cafes. There is sugar everywhere. Like, every main dish, every stew, they got to put sugar in it. If you want to buy meat, they’re going to give you lean cuts of 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 kids off the sodas and the fruit juices and you don’t try to give them low fat foods, you don’t try to give them the low fat yoghurts.

I actually have this ongoing argument with my 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 exception I think, of Cheerios, weirdly enough, it’s going to have a high sugar content. So the best you can do is eat less. So again, my kids will go eat bacon that’s cured, apple-cured bacon, which I assume means it’s sweet and it tastes sweet and there’s sugar in it. But it’s still better than Frosted Flakes, or Coco Puffs, or getting apple juice with their — So you can always improve. And everyone, it sounds more difficult than, you made it sound difficult. But the reality is when you — when people try it without looking as closely as you do, at least the ones who succeed email me and tell me. I don’t know if there’s this huge background of people who fail on these diets. I don’t think they work for everybody because I think after a point, you can get.

And this is what the British physician wrote about 50 years ago, looking at his 1500 people he put on a low carb diet. And he said the ones 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 that are much more, that play a much greater role in their fattening.

And these people – it’s sort of — they may reach the point of no return. But again, the argument I’m making is that if you look at the heart disease risk factors and other profiles, I recently had to post on my blog, my own lipid profile, which I got measured because people wanted to know if I appeared to be killing myself. And I’m not by standard measures anyway. But if you look at that, it would still be a healthier diet. So you do better, but you don’t have to avoid sugar entirely. You might be healthier if you do, but we could certainly all cut back on it.

Male Audience: Okay. So maybe I should give a little bit of clarification. So, yes, I mean, if you want to go healthier than the average, you can certainly do it if you’re going to — and you are going to make lots of progress. Me personally, I made lots of progress. But if you want to go to the next 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 working in an office. See, I work at home. So I can control and I live in Berkeley. I’m sure you have it here. So we have these gourmet butchers from farms that raised their animals humanely and don’t put sugar in things.

Again, I’m just a journalist. I can’t solve every problem. I’m trying to fight this particular battle. And then I hope that if I make some progress and the other people out there fighting this battle make some progress, then maybe the whole society will move into a point where it will get easier.

I have a lot of fans at Microsoft, I hate to say, and they’ve been trying to get the Microsoft Wellness Group to put low carb lines in their café. So they have at least the effect of the Atkins like choices. And so far, as far as I know, they’ve had no luck. But give them time.

Male Audience: Hi. I was wondering, you mentioned five studies that were unpublished, and how many of them are now published, or do you think there’s a publication bias, where these studies that talk to the dogma don’t ever get published?

Gary Taubes: Actually, they virtually have all been published that I know of. Probably several dozen studies published. I mean, the results 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’s basically the metabolic syndrome in some resistance resolved. It goes away and should go away if I’m right, because it’s pretty obviously caused by the carbs in the diet. There are publications biases.

For instance, people who go in believing that it’s all about calories, will interpret their data to make it all about calories, even if they published that the Atkins’s 6group does better than the American Heart Association 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’s a great study done on Type 2 diabetes at Duke University where most of the subjects were able 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 want to deal with all the flack he would get trying to publish in the mainline journal.

So there are definitely biases, but if you do these studies now, I think you almost have to. There’s a clinical trials website where you have to register them and part of the reason for that is to make sure that people don’t only publish positive results. So they pretty much all get published, but they do get spun. And often, the spin takes over.

The biggest study ever done came out of — it was Pennsylvania, UPENN, Colorado, and University of Cincinnati. And they put 300 subjects on an Atkins diet in effect and an American Heart Association diet. And they referred to it as 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 calories a day, basically semi-starve yourself. And when you go on the low carb diet, you’re told to eat as much as you want. Just don’t eat carbohydrates.

And one of the lessons I learned writing about physics is it’s absolutely crucial to define your terms carefully, so people know what they’ve done and what you’ve done and can replicate it. And so, you’re not in effect trying to fool people. And if I was writing that study, it would say “low fat, low calorie versus low carb, ad libitum. ‘Ad libitum’ means eat as much as you want. And I would always use those terms because you never want them to forget that one group is low calorie and one group is ad libitum. Because that also suggests, and in this case they got essentially the same weight loss. The Atkins group did better on heart disease risk factors, but the weight loss was virtually the same.

And you want people to remember that one group is being semi-starved and one group isn’t because that evidence that it’s not about the calories. And they just didn’t do it. They mentioned it in their methodology that the low fat group was calorie restricted and then they ignored it. And the title was ‘Low Fat Versus Low Carb’, and the papers picked it up: Low Fat versus Low Carb. And they left out the crucial ingredient, which is one diet restricts calories and the other diet doesn’t, which is the ingredient that tells you your paradigm might be wrong.

Audience Member: I’m just wondering if 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 carbohydrates we purchase commercially are covered with trans fats, which tend to be the worst fats for you in terms of heart disease risk.

Gary Taubes: It’s funny because I would always argue it the other way. To me, the evidence that trans fats are bad comes from mostly from observational studies where you compare people who eat a lot of trans fats to people who eat very little. Like the nurses health studies, what they’re doing is there, when you think who eats a lot of trans fats and who doesn’t, you’re comparing in effect, people who buy a lot of processed foods and fast foods, to people who cook most of their meals for themselves.

Audience Member: You can’t separate the carbohydrates.

Gary Taubes: You can, but you’re also — but the point is, as you put it, the processed foods come with the carbs. The trans-fat data just doesn’t wow me. I mean, it is true if you give up the carbs, you’re going to have to give up the trans fats.

But remember all those populations I talked about in the beginning, Like the Trinidadians, the Sioux — Native American Sioux. They would not have been getting trans fats. So we don’t know what their heart disease risk was. But we know that they weren’t getting margarine. They weren’t getting — there wasn’t food industry forcing trans fats on them. So it’s quite likely, the obvious, again, the null hypothesis would be the carb content of the diet.

Audience Member: And then my second question is, that there are populations that tend not to eat meat, like India. There’s so many vegetarians and they get their proteins mainly from legumes. So what is your take on the glycemic index of legumes and other non-meat sources of proteins for people who aren’t really eating meat?

Gary Taubes: Well, I do think, again, the argument 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 want to make this argument that it’s literally about the carbs, high glycemic index carbs. It doesn’t — the legumes are lower glycemic index. Green vegetables are low glycemic index. And the sugars. And anyone can improve their diet if they just remove the sugars and the white flour and to some extent, what we call whole wheat flour in the United States. And actually, even one of observations that I wrote about in ‘Good Calories, Bad Calories’.

As early as 1907 the British Medical Association had a meeting in which they had a discussion about the diabetes problem in India because diabetes was rampant. They said that it’s actually worse among the vegetarians sects. Probably because they were also eating the most sugar, which they suggested in 1907.

But you can improve the diet by removing the fat and the carbohydrates regardless, is the point. But if somebody’s very predisposed to get fat, if someone’s 300 pounds, I would argue that you have to get basically, they’re not going to get enough calories that they — the easiest, the way to maximize calories and 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 telling me 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 gain ten pounds. But the point is anyone can lose weight just by getting rid of, and improve their risk profiles, because the argument I make is these high glycemic index carbs and sugars are the cause of the chronic diseases that associate with obesity and diabetes and insulin resistance.

So, and then, if it’s an all vegetarian or vegan diet, you’re still going to be better. You may not be as lean as you could be if you threw your ethical considerations to the wind and switched to meat, but you will be healthier than if you keep these foods in your diet.

Audience Member: I was wondering about people who do a lot of athletics, especially like endurance stuff and talk about things like carbo loading, and other studies that have recently suggested that women typically will 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 they crucial? This is not my area of expertise and I was not an endurance athlete. But in the late 1970s, early 1980s, there was some research done at the University of Vermont by a fellow named Steve Finney, who’s now an emeritus professor of nutrition at UC Davis. And he put professional bike racers on ketogenic diets. And it takes about three weeks to what’s called “ketoadopt,” where you adopt completely to the complete lack of carbs in the diet, in effect. And the bottom line was they did fine. They lost a little bit of their sprinting ability, but they lost a lot of – they lost none of their endurance.

The interesting thing, I get a lot of emails from bike racers, long distance bike racers, and mountain bike racers, because weight is an issue there. Whereas marathoners, you might want to 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 back in response because that’s what he does.

But — and that’s a different issue than whether or not if you carb load like two days before the race, you’ll do better. Although, I think Steve would argue that it’s not necessary.

Audience Member: This is a question about the data. So, in the 1970s, Americans ate an average of 2200 calories a day. And as your slide says, now they eat 27 hundred calories per day. And in those days you had less than 10 percent obesity and now you have like 30 percent or something. Do you think their genetics change over 30 years, or with the calories is there no correlation there?

Gary Taubes: I mean this is again, these numbers, by the way, are very iffy. But certainly the question was, if you look at the food consumption numbers, in the 1970s we were eating around 2200 calories. Then it went up by 500 calories. So doesn’t that prove that it’s about the calories? That’s, in effect — and the point is first of all, this is an observation.

Remember I said, if somebody gets heavier, they got to eat more, or exercise less because they’re going to be in positive energy balance. So even if, and it’s pretty much assumed that food availability went up, our food portion sizes got bigger, etc., etc. But did people get fatter because they consumed more? Did they get hungrier because they were getting fatter? And those numbers don’t, associations like that tell you nothing about causality.

They only tell you that two things happened simultaneously. The price of tea in China probably also went up since 1970, but we’re not going to blame obesity on that. Why would we blame it on the availability of calories in the food supply? When you look at what those calories were, they were almost exclusively 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 has screwed up the numbers and that’s another story. But fat consumption, basically, went down a little bit. Protein consumption went up a little bit and carbohydrate consumption went 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 corn syrup, by the fact that we first didn’t know that high fructose corn syrup was sugar.

And second, believed it wasn’t a problem because the problem was all about fat.

Thank you.

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