Gary Taubes | Talks at Google

Gary Taubes | Talks at Google

August 8, 2019 0 By William Morgan


>>presenter: This talk is part of the [email protected]
of the [email protected] 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, 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 cause 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 wanna 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 ’cause
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 gotta 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 ’cause 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’—’cause you don’t
have to restrict calories ’cause 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’
’cause 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 gonna 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 gonna tell an entire nation to
eat bread, cereal, rice, pasta. And sweets,
weirdly enough, get a free pass ’cause they’re
nonfattening.
So, Coke, Pepsi, SoBa ice tea, Snapple. 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. ‘Cause
if it didn’t have fat in it, you couldn’t
put fat on.
So, [pause] just to wrap up. I’ve already
gone too long cause 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 ’cause 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 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,
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.
[pause]
>>Male Audience Member #2: 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: Yeah.
[laughter]
>>Male Audience Member #2: And what is your
waist size in inches?
[laughter]
>>Gary Taubes: My waist size in inches? Well,
the question is, see this is always one of
the mistakes people make in life. I mean,
I’m OK. Okay? Basically, I have the same body
I had when I was in college. I was a 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 ’cause 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 Aitkin’s
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’s 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 gonna 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 Member #3: 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, OK. 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.
[pause]
>>Male Audience Member #4: 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 gotta put sugar in it. If you want to
buy meat, they’re gonna 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
gonna 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 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 cause 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 Member #4: 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 gonna [ ] and you are gonna 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 Member #5: 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, cause 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
group 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 wanna 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 the
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. ‘Cause 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
’cause 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 you’re
paradigm might be wrong. OK.
>>Female Audience Member #2: 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 ’cause 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.
>>Female Audience Member #2: 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 gonna 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.
>>Female Audience Member #2: 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 wanna 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 ’cause
diabetes was rampant. They said that it’s
actually worse among the vegetarians sects.
Probably ’cause they were also eating the
most sugar, which they suggested in 1907.
But you can improve the diet by removing 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 gonna 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, ’cause 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 gonna 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.
>>Female Audience Member #3: 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? [pause]
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, cause weight is
an issue there. Whereas marathoners, you might
wanna be as light as possible.
Or, actually, this is where I get confused.
The evidence suggests you can do just fine
without any carbs and I actually recommend
— email me. I’ll forward your email to Steve
Finney. He’ll write three thousand words back
in response cause 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.
>>Male Audience Member #6: 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 ten 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, the, and the point is first of
all, this is an observation.
Remember I said, if somebody gets heavier,
they gotta eat more, or exercise less because
they’re gonna be in positive energy balance.
So even if, and it’s pretty much assumed that
food availability went up, our food 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 gonna 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.
[applause]