>>presenter: 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. [applause] >>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. 'Cause 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. [laughter] 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. This is just background. You know there's
an obesity epidemic in the works. I'm not gonna go over it because, as usual, I'm probably
gonna 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. [pause] 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 gonna
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 gonna 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 officials 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? 'Cause 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 wanna do when we talk about this, one of the key things you wanna
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,[audience chuckles] 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 wanna 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 wanna know is, is this true? 'Cause 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 wanna 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 [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 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 gonna 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 cause 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 to 60 thousand
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 Rosso, 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 [pause] it
was Rosso 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? 'Cause 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 'cause 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 percent of the women, 25
percent of the men, and 10 percent of the children were distinctly fat. And 20 percent
of 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 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 gonna come back to shortly
— many times, in fact.

OK, 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. OK, 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 wanna 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, 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? OK. How many of you would do that? [laughter] 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 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 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 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 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. 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
'cause 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. 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 [clears throat] 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 gonna 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 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 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 wanna
guarantee that you get hungry and eat more. And we're gonna 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 wanna 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 'cause 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 wanna 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 is 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 .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.

[pause] 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 gonna 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 gonna
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 gotta 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? Why do they
have the same body type? 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 'cause 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 gonna 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 'cause 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 they often get this lower body, localized obesity below
the waist. So the way these Europeans asked it, they said, "Are we gonna blame the top
half on under eating and bottom half on overeating?" [laughter] 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 cause 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. [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 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. [laughter] 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 lemme 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 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 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 wanna know, why is there so much energy accumulated in the fat mass? And I
wanna 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." [pause] Right? Have I told you anything meaningful
at all about why this? [laughter] 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 gotta 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 'cause 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 'cause I just told you to work out.

What's gonna happen to energy
consumed? It has to go up. You're gonna 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,
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 regulates
growth, right. So we wanna 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 'cause 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. [laughter] 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 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.

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 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 to
test what's driving it, like a genetic model, a surgical model. You could lesion the ventromedial
hypothalamus for rat and it'll get obese and eat voraciously. So you'll see voracious eating
and obesity. And you wanna know which causes which. Did this regulation of fat tissue cause what's
called hyperphasia? Or did the hyperphasia 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 M.R.C.
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 gonna 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 man? An animal's model of obesity,
when you break the gene, you intervene surgically. There are even dietary models. What you're
doing is disregulating the fat tissue. You're not making the animals eat too much. 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. [pause] 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 gonna 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.
Its 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 wanna 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
wanna 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, 'cause 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
wanna get insulin, if you wanna 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 'cause 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,