All language subtitles for Sugar: The Bitter Truth.eng

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- I'm going to tell you, tonight, a story.

And this story dates back about 30 years.

This story has a little bit
of something for everybody.

It has a little bit of biochemistry,

a little bit of clinical research,

a little bit of public health,

a little bit of politics, a
little bit of racial innuendo.

The only thing it's missing is sex.

(audience laughs)

But, well, we can see what
we can do about that, too.

By the end of the story I hope I will

have debunked the last 30 years

of nutrition information in America.

And I would very much appreciate it

if at the end of the
talk, you would tell me

whether or not I was successful or not.

Okay?

So, in order to get you in the mood,

as it were, let's start
with a little quiz.

What do the Atkins Diet

and the Japanese Diet have in common?

Anybody?

Hm?

Oh, you have the answers
right, never mind.

That's right, you have
the answer right there.

So the Atkins diet, of
course, is all fat no carb.

The Japanese diet's all carb, not fat.

They both work, right?

So what do they share in common?

They both eliminate the sugar, fructose.

So, with that, think about
what it means to be on a diet,

and what macro-nutrients you're eating

and which ones your not.

And then we'll go from there, and I'll try

to explain how this all works.

So, you've all heard about
the obesity epidemic.

Here are the numbers.

These are the NHANES
database Body Mass Index.

Everybody knows what that is now.

Histograms marching ever
rightward as time has gone on.

This was what was
projected for 2008 in blue.

We had so far exceeded and surpassed,

this is not even funny.

This was from 2003.

The reason I show this is not just to show

that the obese are getting obeser,

of course, that's true, but in fact

the entire curve has shifted.

We all weigh 25 pounds more today

than we did 25 years ago, all of us.

Now, it is often said that obesity

is the ultimate interaction between

genetics and environment.

And Doctor Christian Vaisse, who's sitting

in the back of the room, will be talking

to you next week about
the genetic component,

which I am also very interested in.

But, having said that, our genetic pool

did not change in the last 30 years,

but, boy oh boy, has our
environment sure changed.

So, tonight, we're gonna talk about

the environment rather than genes.

Now, in order to talk
about the environment,

we need to talk about what is obesity.

And, of course, you're all familiar with

the basic concept with the
first law of thermodynamics,

which states that the total energy

inside a closed system remains constant.

Now, in human terms, the
standard interpretation

of this law is the following.

If you eat it, you better burn
it, or you're gonna store it.

Now, who here believes that?

Oh, come on, you all do.

(audience laughs)

I used to believe that.

I don't anymore.

I think that's a mistake.

I think that is the biggest mistake.

And that is the phenomenon
I'm going to try to debunk

over the course over the next hour.

Because I think there's
another way to state the law

which is much more relevant,
and much more to the point.

Before I get there, of
course, if you believe that,

these are the two problems,
calories in, calories out.

Two behaviors, gluttony and sloth.

After all, you see anybody on the street,

"Oh, he's a gluttonous sloth,
that's all there is to it."

Tommy Thompson said it on the TV show.

"We just eat too damn much."

Well, you know, if that were the case,

how did the Japanese do this?

Why are they doing bariatric surgery

on children at Tokyo
Children's Hospital today?

Why are the Chinese, why are the Koreans,

why are the Australians?

I mean, all these countries
who've adopted our diet

all suffer now from the same problem.

And we're gonna get even
further in a minute.

There's another way to
state this first law.

And that is, if you're gonna store it,

that is biochemical forces
that drive energy storage,

and we'll talk about what
they are in a few minutes,

and you expect to burn it, that is normal

energy expenditure for
normal quality of life.

Because energy expenditure
and quality of life

are the same thing.

Things that make your
energy expenditure go up,

make you feel good.

Like ephedrine, it's off the market,

coffee for two yours, then
you need another hit, like me.

Things that make your
energy expenditure go down,

like starvation, hypothyroidism,
make you feel lousy.

And how many calories you burn

and how good you feel are synonymous.

So, if you're gonna store it,

that is an obligate weight gain

set up by a biochemical process,

and you expect to burn it, that is normal

energy expenditure for
normal quality of life,

then you're gonna have to eat it.

And now, all of the sudden,
these two behaviors,

the gluttony and the sloth,
are actually secondary

to a biochemical process,
which is primary.

And it's a different way
to think about the process.

And it also alleviates the obese person

from being the perpetrator,
but rather the victim.

Which is how obese people really feel.

'Cause no one chooses to be obese.

Certainly, no child chooses to be obese.

Oh, you say, "Oh, yeah, sure,

"I know some adults who don't care."

You know, Rossini, the famous composer,

you know La gazza ladra,
Figaro, and all that.

He retired at age 37

to a lifetime of gastronomic debauchery.

Maybe he chose to be obese.

But the kids I take care
of in obesity clinic

do not choose to be obese.

In fact, this is the exception
that proves the rule.

We have an epidemic of
obese six month olds.

Now, if you wanna say that it's all about

diet and exercise, then you
have to explain this to me.

So, any hypothesis that you wanna proffer

that explains the obesity epidemic,

you've got to explain this one too.

And this is not just in America,

these six month old obese kids,

but these are around the world now.

So, open your minds?, and let's go

and figure out what the real story is.

Let's talk about calorie intake,

because that's what today is about.

We're gonna talk about the

energy intake side of the equation.

Sure enough, we are all eating more now

than we did 20 year ago.

Teen boys are eating 275 calories more.

American adult males are eating
187 calories more per day.

American adult females are
eating 335 calories more per day.

No question, we're all eating more.

Question is why, how come?

'Cause it's all there?

You know what, it was there before.

We're all eating more, there's a system

in our body, which you've heard about

over the last couple
of weeks called leptin.

Everybody heard of leptin?

It's this hormone that
comes from your fat cell,

tells your brain, "You
know what, I've had enough.

"I don't need to eat anymore.

"I'm done, and I can
burn energy properly."

Well, you know what?

If you're eating 187 or
335 calories more today

than you were 20 years ago,
your leptin ain't working.

'Cause if it were, you
wouldn't be doing it.

Whether the food was there or not.

So, there's something wrong with our

biochemical negative feedback system

that normally controls energy balance.

And we have to figure out what caused it,

and how to reverse it.

And that's what tonight is about.

But, nonetheless, there are 275 calories

we have to account for.

So where are they?

Are they in the fat?

No, they're not in the fat.

Five grams, 45 calories
out of the 275, nothing.

In fact, it's all in the carbohydrates.

57 grams 228 calories.

We're all eating more carbohydrate.

Now, you all know, back int 1982,

The American Heart Association,

The American Medical Association,

and the US Department of Agriculture

admonished us to reduce our total

fat consumption from 40% to 30%.

Everybody remember that?

That how Entenmann's fat
free cakes came into being.

Remember that?

So what happened?

We did it, we've done it.

40% down to 30%, and look what's happened

to the obesity, metabolic syndrome,

non-alcoholic fatty liver
disease, cardiovascular disease,

stroke prevalence, all jacked way up,

as our total fat consumption
as a percent has gone down.

It ain't the fat,
people, it ain't the fat.

So what is it?

Well, it's the carbohydrate.

Specifically, which carbohydrate?

Well, beverage intake, right?

41% increase in soft drinks,
35% increase in fruit drinks,

fruitades, whatever you wanna call them.

Just remember, down here,

one can of soda a day, is 150 calories.

Multiply that by 365 days a year,

and then divide that by the magic number

of 3500 calories per pound,

if you eat or drink 3500 calories

more than you burn, you
will gain one pound of fat.

That's the first law of
thermodynamics, no argument there.

That's worth 15 1/2
pounds of fat per year.

One soda a day is 15 1/2 pounds per year.

Now, you've all heard that before.

That's not news to you.

The question is how come we don't respond?

How come leptin doesn't work?

How come we can't stay energy stable.

That's what we're gonna get to.

So, I call this slide, very specifically,

the Coca Cola Conspiracy.

Anybody here work for Coke, Pepsi?

Okay, good.

All right, so, this over here, 1915,

the first standardized bottle
of Coca Cola out of Atlanta.

Anybody remember this bottle?

Sure, a lot of you do.

I remember this bottle,
because my grandfather

in Brooklyn, took me on Saturday afternoon

down to the local soda shop
on Avenue M and Ocean Avenue,

and every Saturday afternoon
I had one of these.

I remember it very well.

Now, if you drank one of those every day,

assuming of course that
the recipe hasn't changed,

'cause after all, only
two people in the word

know the recipe, and they're not allowed

to fly on the plane at the same time.

You know that, okay.

Assuming the recipe hasn't changed,

if you drank one of those
every day for a year,

6 1/2 ounces, that would be worth

eight pounds of fat per year.

Now, in 1955, after World War II,

when sugar became plentiful again,

and wasn't being rationed,

we have the appearance
of the 10 ounce bottle,

the first one that was
found in vending machines.

You probably remember that one, as well.

Then in 1960, the ever ubiquitous,

12 ounce can, worth 16
pounds of fat per year.

And, of course, today, this, over here

is the single unit of measure, 20 ounces.

Anybody know how many
servings are in that bottle?

- [Audience Member] 2.5.

- 2.5 eight ounce servings, that's right.

Anybody know, anybody gets 2.5 eight ounce

servings out of that bottle?

That's a single serving, right?

So that would be worth
26 pounds of fat per year

if you did that every day.

And then, of course, over here,

we have the 7/11 Big K, Thirst Buster,

Big Gulp, whatever you wanna call it,

44 ounces, worth 57
pounds of fat per year.

And if that wasn't bad
enough, my colleague,

Dr. Dan Hale, at the University
of Texas San Antonio,

tells me that down there they
got a Texas size Big Gulp.

60 ounces of Coca Cola, a Snickers bar,

and a bag of Doritos, all for 99 cents.

- [Audience] Oh.

- So if you did that every day for a year

that would be worth 112
pounds of fat per year.

So why do I call it the
Coca Cola conspiracy?

Well, what's in Coke?

Caffeine, good, good, so what's caffeine?

It's a mild stimulant, right?

It's also a diuretic, right?

It makes you pee free water.

What else is in Coke?

We'll get to the sugar
in a minute, what else?

Salt, salt.

55 milligrams of sodium per can.

It's like drinking a pizza.

So what happens if you take on sodium

and lose free water, you get...

- [Audience] Thirsty.

- Thirstier, right.

So, why's there so much sugar in Coke?

To hide the salt.

When was the last time you
went to a Chinese restaurant,

had sweet and sour pork?

That's half soy sauce,
you wouldn't eat that.

Except the sugar plays
a trick on your tongue,

you can't even tell it's there.

Everybody remember New Coke, 1985?

More salt, more caffeine.

They knew what they were doing.

That's the smoking gun.

They know, they know.

All right, so, that's why
it's the Coca Cola conspiracy.

So, are soft drinks the cause of obesity?

Well, depends on who you ask.

If you ask the scientists for the

National Soft Drink Association,

they'll tell you there's absolutely

no association between sugar
consumption and obesity.

If you ask my colleague,
Doctor David Ludwig,

remember, I'm Lustig he's Ludwig,

he does what I do at
Boston Children's Hospital.

Some day we're gonna open up a law firm.

(audience laughs)

Each additional sugar
sweetened drink increase

over a 19 month follow up period in kids

increased their BMI by this much

in their odds risk ratio
for obesity by 60%.

That's a prospective study
on soft drinks and obesity.

The real deal.

If you look at meta-analysis,

everybody know what a meta-analysis is?

It's a conglomeration of numerous studies

subjected to rigorous
statistical analysis.

88 cross sectional and
longitudinal studies

regressing soft drink consumption against

energy intake, body weight,
milk and calcium intake,

adequate nutrition, all showing
significant associations.

And some of these being longitudinal,

this came from Kelly
Brownell's group at Yale.

I should comment, a
disclaimer, those studies

that were funded by the beverage industry

showed consistently smaller effects

than those that were independent.

Wonder why.

Now, how 'bout the converse?

What if you take the soft drinks away?

So this was the fizzy drink study

from Christ Church England James et al,

British Medical Journal, where they went

into schools and they took
the soda machines out.

Just like we did here in California.

We haven't seen the data yet,

but they went and did it for a year.

So the prevalence of obesity in

the intervention schools stayed

absolutely constant, no change.

Whereas the prevalence of obesity

in the control schools
where nothing changed

continued to rise over the year.

So that's pretty good.

So, how 'bout type two diabetes?

Are soft drinks the cause
of type two diabetes?

Well, this study from JAMA in 2004

looked at the relative risk ratio

of all soft drinks, cola, fruit punch,

and found a very statistically significant

trend of sugared soft drinks, fruitades,

et cetera, causing type two diabetes.

And you know we've got
just as big a problem

with type two diabetes as we do

with obesity for the same reasons.

And this was a sugared
sweetened beverage against

risk for type two diabetes
in African American women.

Looking here at sugar
sweetened soft drinks,

just the downward arrow shows that

there was a significant rise

as the number of drinks went up.

You can see that here.

Whereas orange and grapefruit
juice, interestingly, did not.

So, two different studies,
two different increases

in type two diabetes, relative
to soft drink consumption.

So, what's in soft drinks?

Well, in America, it's this stuff, right?

High fructose corn syrup.

Everybody's heard of it, right?

It's been demonized something awful.

So much so that the corn refiners industry

has launched a mega-campaign to try

to absolve high fructose
corn syrup of any problems,

which we'll talk about in a moment.

But the bottom line is, this is something

we were never exposed to before 1975.

And currently we are consuming

63 pounds per person per
year, every one of us,

63 pounds of high fructose corn syrup.

- [Audience Member] That's America?

- That's America, yes.

Now, what is high fructose corn syrup?

Well, you'll see in a minute.

It's one glucose, one fructose,

we'll talk about those at great length.

One of the reasons we use
high fructose corn syrup

is because it's sweeter.

So here's sucrose, this
is cane or beet sugar,

standard table sugar, you
know, the white stuff,

and we give that an index
in sweetness of 100.

So here's high fructose corn syrup,

it's actually sweeter, it's about 120.

So, you should be able to use less, right?

Wrong, we use just as
much, in fact, we use more.

So, here's lab fructose over
here, crystalline fructose.

And they're starting to
put crystalline fructose

into some of the soft drinks.

They're actually advertising
it as a good thing.

Phew.

And that's got a sweetness of 173,

so you should be able to
cut that way back, right?

They're not.

Lactose, down here, milk
sugar, it's not sweet at all.

And glucose, I should
point out over here, 74.

It's not particularly
sweet, and we're gonna

get to that at the end, and
what goes on with glucose.

But anyway, there's why
we use it, it's sweeter,

it's also cheaper as I'll show you.

So, here's high fructose corn syrup.

One glucose, one fructose.

Notice the glucose is a six membered ring,

the fructose is a five membered ring.

They are not the same.

Believe me, they're not the same.

That's what this whole talk is about

is how their not the same.

And here's sucrose, and they're just

bound together by this ether linkage.

We have this enzyme in
our gut called sucrose,

it kills that bond in two seconds flat,

and you absorb it and, basically,
high fructose corn syrup,

sucrose, it's a non issue, it's a wash.

They're the same.

And they know that they're the same,

the soft drink companies
and the corn refiners.

Because here are their missives.

This comes from the Corn
Refiners Association.

Obesity research shows
high fructose corn syrup

metabolizes and impacts
satiety similar to sugar.

Indeed it does, I agree.

Decent meetings, academic
meetings around the country.

Hunger and satiety profiles energy intakes

following ingestion of soft drinks,

bottom line, research supported by

the American Beverage Institute

and the Corn Refiner's Association.

They are correct, there is absolutely

no difference between high
fructose corn syrup and sucrose.

So much so that the Corn
Refiner's Association,

in attempt to capture market share,

came out with this entire ad campaign.

You probably saw it on the back page

of the New York Times, it
was on TV, it's everywhere.

"My hairdresser says
that sugar's healthier

"than high fructose corn syrup.

"Wow, you get your hair done by a doctor?"

I didn't know I could cut hair.

If you all wanna see all of them,

there are a whole bunch of them.

You can go to www.sweetsurprise.com

and see how you're being hoodwinked.

But indeed, this is true.

High fructose corn syrup and
sucrose are exactly the same.

They're both equally bad.

They're both dangerous,
they're both poison.

Okay, I said it, poison.

My charge before the end of tonight

is to demonstrate fructose is a poison,

and I will do it, and you will tell me

if I was successful.

None the less, here's
Center for the Science

and Public Interest and the
Corn Refiners Association.

Everybody remember last
year, when Gavin Newsom

floated his soda tax, last February?

Governor Patterson of New
York has since floated one.

And other people are
starting to talk about it.

So, why are they saying this?

Well, they're saying obesity's a problem,

kids are drinking soda, let's tax it.

So they're talking about soda
like it's empty calories.

I'm here to tell you that it
goes way beyond empty calories.

The reason why this is
a problem is because

fructose is a poison, it's
not about the calories.

It has nothing to do with the calories.

It's a poison by itself,
and I'm gonna show you that.

Nonetheless, I just wanna read you

this paragraph here in yellow.

"We respectfully urge that the proposal

"be revised as soon as possible to reflect

"the scientific evidence that demonstrates

"no material differences
in the health effects

"of high fructose corn syrup and sugar."

I agree.

Here's the important sentence.

"The real issue is that
excessive consumption

"of any sugars may lead
to health problems."

I agree, that's exactly right.

Not may, does, does.

So, here's the secular trend in

fructose consumption
over the past 100 years.

Before we had food processing, we used to

get our fructose from
fruits and vegetables,

and if we did that today, we would consume

about 15 grams per day of fructose.

Not sugar, fructose.

So sugar would be 30
grams, it'd be double.

We're just talking about fructose, today.

Prior to World War II,
before it got rationed again,

we were up to about 16
to 24, about 20 grams.

So, a small increase from the beginning

of the century to World War II.

Then, in 1977, just as
high fructose corn syrup

was hitting the market,
we had increased that,

we had, basically, doubled
up to 37 grams per day,

or 8% of total caloric intake.

By 1994 we were up to 55
grams of the stuff per day.

Remember, if you wanna do
sugar, then double the number.

So, that's 10.2, so you
can see that more and more

of our caloric intake, a higher percentage

is being accounted for by
sugar every single year.

So, it's not just that we're eating more.

We're eating more sugar.

And for adolescents today,
up to almost 75 grams,

12% of total caloric intake.

25% of the adolescents today consume

at least 15% of their
calories from fructose alone.

This is a disaster, an
absolute unmitigated disaster.

The fat's going down,
the sugar's going up,

and we're all getting sick.

Now let me show you why.

How'd this happen?

Why'd it happen?

So, this is where the politics comes in.

This is the perfect storm,

and it was created from
three political winds

that swirled around all at the same time

to create this perfect storm.

So, the first political wind,

everything bad that ever happened

in this country started with one man.

(audience laughs)

And it's still being felt today.

So, Richard Nixon, in his
paranoia back in 1972,

food prices were going up
and down, and up and down.

I'm gonna show you that on the next slide.

And he was worried that this was

actually gonna cost him the election.

So, he admonished his
Secretary of Agriculture,

Earl Rusty Butz, I love that name,

to basically take food
off the political table,

to make food a non-issue
in presidential elections.

Well, the only way to do
that was to make food cheap.

So, he was out to find all methods

to be able to decrease the price of food.

Remember Nixon's war on poverty?

We're suffering from it today.

That's what this is.

Second political wind, the advent

of high fructose corn syrup.

So, this was invented in
1966 at Saga Medical School

in Japan, by a guy named
Takasaki, who's still alive.

As far as I'm concerned, this stuff

is Japan's revenge for World War II,

except, of course, that they're suffering

from it now, themselves.

Like everything, it always
comes back to haunt you.

And it was introduced to
the American Market in 1975.

So, what do you think happened

to the price of sugar when
this thing hit the market?

Here's what happened.

So, here's the US producer
price index of sugar

going up and down, and up and down.

This is not good.

Stability is at 100%, if
it stays nice and stable

at 100%, that's what you
want if you're a politician.

Up and down, here's where corn sweeteners

entered the market, 1975, 1980.

And you can see that since then the price

of sugar has remained remarkably constant.

And it did so, not just in the US,

but also on the international stage.

Here's the London price
doing the same thing.

And when you look at
the difference in price

between sugar and high
fructose corn syrup,

you can see that high
fructose corn syrup's

about half the price.

So, in other words, it's cheap.

So, high fructose corn syrup is evil.

But it's not evil because
it's metabolically evil.

It's evil because it's economically evil.

Because it's so cheap that it's

found it's way into everything.

It's found it's way into hamburger buns,

pretzels, barbecue sauce, and
ketchup, almost everything.

Somebody emailed me the other day

and told me they went into
their local grocery store

and went through every
single loaf of bread

on the shelf, and out of 32 types of bread

on the shelf, only one of them did not

have high fructose corn syrup in it.

So, we are being poisoned by this stuff,

and it's been added surreptitiously

to all of our food, every processed food.

The question is why?

Well, you'll see why in a minute.

So, the corn refiners like to point out,

"Well, you know, it's
just been a substitution.

"As the high fructose
corn syrup's gone up,

:the sugar's gone down.

"You know, we're just
replacing, like gram for gram."

Well, not exactly, because here's

73 pounds of sugar per year.

This is from the Economic Research Service

of the US Department of Agriculture.

So disappearance data.

73 pounds, up to 95 pounds by 2000.

And there's something
missing from this slide.

Anybody wanna tell me what it is?

What's missing?

Juice, juice is missing.

'Cause juice is sucrose, right, sugar.

And juice causes obesity.

So this is a study done by Myles Faith,

a prospective study in
inner city Harlem toddlers.

And the number of juice servings per day

predicts the change in BMI score per month

in these inner city Harlem toddlers.

Now, where do these inner city

Harlem toddlers get their juice?

From what, from where, from whom?

From WIC.

Anybody heard of WIC?

You know what WIC is?

Women Infants Children, right?

A government entitlement
program set up under who?

Nixon, to prevent failure to thrive.

They did.

This is the equal and opposite reaction.

So, let's add juice in, here it is.

So, most fructose items
when you put it together,

now we're up to 113 pounds on this graph,

and I just heard from Brian Williams,

of NBC News, after the
most recent study came out,

that was in the Journal
of Clinical Investigation,

that we are actually up to
141 pounds of sugar per year.

Each of us.

That's what we're up to.

141 pounds of sugar per year.

Now, do you think that this might

have some detrimental effects on you?

Hasn't stopped you, has it?

That's the point, it hasn't stopped you.

That's why we need to talk about this.

So, juice consumption increases

the risk for Type 2 diabetes.

So this is the relative risk ratio

as juice intake goes up, and
this is in the Nurse's Study.

Showing again, juice consumption,

sucrose, obesity, diabetes.

Okay, the third political
storm, that's swirling around

to create this disaster,
this mega-typhoon,

that thing that happened in 1982,

the USDA, the American Hearth Association,

the American Medical Association,

all telling us we had to
reduce our consumption of fat.

Now, why did they tell us that?

To stop what?

To stop hear disease.

Did we?

No, we didn't, did we?

In fact, it's worked the exact opposite.

We've only created more.

So, now how did this come to be?

Why did they tell us to stop eating fat?

Well, in the early 1970s we discovered

something in our blood called LDL,

low-density lipoproteins.

You've heard of that, right?

Is it good or bad?

- [Audience Member] Bad.

- Not so bad, we'll talk about it.

In the mid 1970s we learned that

dietary fat raised your LDL.

So, if dietary fat is A, and LDL is B,

we learned that A lead to B.

Dietary fat definitely increases your LDL,

no argument, it's true.

And then, finally, in
the late 1970s we learned

that LDL correlated with
cardiovascular disease.

So let's call cardiovascular disease C.

So we learned that B lead to C.

So, the thought process by some

very smart nutritionists, et cetera,

the USDA et cetera, said,

"Well if A leads to B, and B leads to C

"then A must lead to C,
therefore, no A, no C."

This was the logic.

Now, any logicians in the room?

Anybody see any problems with that logic?

Go ahead.

(speaking away from microphone)

- That's right, the premise is incorrect.

And I'll tell you why
the premise is incorrect.

Because this suggests that
this is all transitive.

But, in fact, only the
contrapositive is transitive.

So, it's not no A, no C, it's no C, no A.

So, the logic isn't even right.

There's faulty logic here.

So, this doesn't work on any level.

So, I'm gonna show you
why this doesn't work.

But, before I how you why it doesn't work,

I'm gonna show you that this was

a battle royal back in the 1970s.

This was not a simple thing.

There were people lined up
on both sides of this story.

So, this, over here, is
a book, 1972 it came out,

and it was called Pure White and Deadly.

It's all about sugar.

Written by a British physiologist,

nutritionist, endocrinologist,

by the name of John Yudkin.

Now, I never knew John
Yudkin he's passed away.

But, I read this book about a year ago.

And without even knowing
it, I was a Yudkin acolyte.

I was a Yudkin disciple.

Every single thing that this man said

in 1972 is the God's honest truth.

And if you wanna read a true
prophecy, you find this book.

It's not easy to find,
but you go find this book.

And I'm telling you, every single thing

this guy said has come to pass.

It's astounding, I am in awe of this guy.

But on the other side we
had this guy over here.

His name was Ancel Keys.

Anybody heard of him?

So, Ancel Keys was a
Minnesota epidemiologist,

very interested in the cause
of cardiovascular disease.

And he performed the first multivariate

regression analysis without computers.

Now, anybody know what that means?

Multivariate regression analysis?

So, this is where you
take a whole lot of data,

and normally you would just
run a few computer programs,

but basically, the object is to try

to figure out what causes what,

and to try to factor out other things

and determine what the contribution

of various things all at once are

to an outcome that you're looking for.

So, he was interested in
cardiovascular disease.

So, what he did was he did this study,

along with other people around the world,

called the Seven Countries Study.

Very famous, front page
of Time Magazine in 1980.

So, here's the data on
the Seven Country Study.

So, we have the US, Canada, Australia,

England and Wales, Italy, Japan.

And here's percent calories
from fat on the x axis,

and here we have coronary
disease death rate on the y axis.

And so you'd say, "Oh, look at that."

I mean, it's very obvious, isn't it.

Sure, percent calories from fat

correlates very nicely with
coronary disease, right?

Except for one little problem.

Anybody see it?

Japan and Italy?

So, how much sugar do they eat?

Didn't I tell you the Japanese
diet eliminates fructose?

They never even had it 'til

we brought it to them after World War II.

Italy, aside from gelato,
I mean what else they got?

They got a lot of pasta,

there's a lot of glucose, but no fructose.

There's no sugar in the Italian diet

other than the occasional
sweet, which they moderate.

They're very careful about
moderating, and they cost a lot.

But, here we got England,
Wales, Canada, Australia, US,

you know, we are sugarholics, aren't we?

We're also fataholics.

So, in fact, the fat
migrated with the sugar.

So, here's, this is from Keys's own work.

Page 262, if you wanna pick
up the 500 page volume.

And I'm just gonna read you the

one paragraph that talks about this.

The fact that the incidence rate

of coronary heart disease
was significantly correlated

with the average percentage of calories

from sucrose in the diet, is explained by

the intercorrelation of
sucrose with saturated fat.

In other words, donuts.

Where ever there was the
fat, there was sucrose too.

Because these guys here eat donuts.

(audience laughs)

Partial correlation analysis show

that with saturated fat constant,

there was no significant correlation

between dietary sucrose and the incidence

of coronary heart disease.

Okay, when you do a multivariate
linear regression analysis,

you have to do it both ways.

You have to do holding fat constant

showing the sucrose doesn't work,

and then you have to hold sucrose constant

and who that fat still works.

You see that anywhere?

He didn't do it, he didn't do it.

He didn't do the thing that you need to do

to do a multivariate
linear regression analysis.

Now, this was done before computers.

We can't check the work.

He's dead, he died in 2004.

So, we're left with a conundrum.

Do we believe this?

Do we believe this study, because we based

30 years of nutrition
education, and information,

and policy in this country on this study.

And, as far as I'm
concerned, it has a hole

as big as the one in the USS Cole,

all right, you got it?

Everybody, am I debunking, yes, no?

Let's keep going.

Remember, I told you
LDL may be not so bad?

Well, here's why.

Because there really isn't
one LDL, there are two.

There are two LDLs.

Here's one over here, it's called

pattern A or large buoyant LDL.

So, everybody knows that LDL correlates

with cardiovascular
disease, and that's true.

I'm not gonna argue that, that is true.

But, it's not this one, pattern A LDL.

These guys are so light,
they are buoyant, they float.

So, they get carried
through the bloodstream,

and they don't even have a chance,

because they're so big
and they're so buoyant,

they don't even get underneath the edge

of the endothelial
cells in the vasculature

to start the plaque formation process.

But, over here we have
this other guy, over here,

called pattern B or small dense LDL.

You see the difference?

These guys are dense.

These guys don't float.

These guys are small, they get underneath

the edge of the surface of the surface

of the endothelial cells,

and they start the plaque formation.

And it's been shown by
numerous investigators now,

the dense LDL is the bad guy.

Okay, now, when we measure
LDL in the bloodstream,

when you do a lipid profile,

you measure both of them together,

because it's too hard
to distinguish the two.

So, when you get an LDL,
you're getting both LDLs.

The neutral one and the bad one.

Now, how can you tell whether your LDL

is the neutral one or the bad one.

What you do is you look at
your triglycerides level

in association with it,
'cause your triglycerides

tell you which one it is.

So here, here's pattern A over here,

big large buoyant LDLs, and you'll notice

that the triglycerides are
low, and your HDL is high.

That's what you want, you
want a low triglyceride,

high HDL, 'cause that's
the good cholesterol.

You want high good cholesterol.

Over here, you have pattern B.

And here you have high
triglyceride, low HDL.

That's the bad guy, that's
the guy you don't wanna be.

'Cause you're gonna die of a heart attack.

No question about it.

Triglyceride to HDL
ratio actually predicts

cardiovascular disease way
better than LDL ever did.

Point is, when you measure
LDL, you measure both.

So, dietary fat raises your large buoyant.

What do you think raises your small dense?

Carbohydrate.

Okay, so here's percent carbohydrate,

and here's your pattern B going up.

Everybody got it?

So what did we do?

What did we do in 1982?

(speaking away from microphone)

What did we do?

We went on a high carb diet, which was

supposed to be a low fat diet, right?

So, here's the low fat craze.

Took America and the world by storm.

Because the content of low fat

home cooked food, that
you cook by yourself,

in your house, you can
control the content of fat.

But when you process it,
low fat processed food,

it tastes like cardboard.

It tastes like (bleep).

So the food companies knew
that, so what'd they do?

They had to make it palatable?

So, how do you make something

palatable that has no fat in it?

You add the, sugar.

So, everybody remember Snackwells?

Two grams of fat down, 13
grams of carbohydrate up,

four of them being sugar,
so that it was palatable.

Well, we've just shown you that

that's the worst thing you could do.

And that's what we've done.

And we're still doing it, today.

So when you find a
mistake, what do you do?

You admit the mistake
and you right the ship.

We haven't admitted the mistake,

and we haven't righted the ship.

So, we've our food supply adulterated,

contaminated, poisoned, tainted.

On purpose, and we've
allowed it, and we've let it,

thought the addition of fructose

for palatability, especially
because of the decreased fat,

and also as a ostensibly browning agent,

which actually has it's own issues.

Because why it browns so well

with the sugar in it, actually is

what's going on in your arteries.

Because that's causing what we call

protein glycation and cross linking,

which is actually contribution
to atherosclerosis.

So it works on your steak on the grill,

it works in your arteries the same way.

And removal of fiber also.

Now, why did we remove
fiber from our diet?

We, as human beings walking
the earth 50,000 years ago,

used to consume 100 to 300
grams of fiber per day.

We now consume 12.

Why? What did we do?

We took the fiber out.

So, why'd we take the fiber out?

It takes too long to cook,

takes too long to eat, and shelf life.

So, people ask me, "What's
the definition of fast food."

Fiberless food.

I dare you, other than a salad, I dare you

to go to any fast food restaurant

and find anything on their menu

that they actually have to cook,

that has more than one
gram of fiber in it.

'Cause there isn't any,
and that's on purpose.

Because they take the fiber out,

'cause that way they can freeze it,

ship it around the world,
and cook it up fast,

and not only is is fast cooking,

but it's fast eating, which also

causes it's own satiety issues.

Bottom line, we have a
typhoon on our hands.

And then, finally, the last issue

was the substitution of transfats,

which are clearly a disaster,

but those have been going down,

because we know that those are a problem.

So we've actually gotten
rid of most transfats,

not completely, but most.

So this is it, this is what we've done

over the last 30 years.

Now, to the biochemistry.

Now, how many of you here
have taken biochemistry?

About 25%.

I am going to show you a lot of reactions

in excruciating detail.

(audience laughs)

If you've studied biochemistry,

you will have an anaphylactic reaction.

(audience laughs)

If you haven't studied biochemistry,

you will fall asleep.

So, what I'm gonna suggest that you all do

is just let me do my
thing, to show you that,

at least it works, and
just count the arrows.

Okay?

You can do that, right?

Can you count the arrows,
it's not like counting sheep.

Okay, you can count the
arrows, and just stick with me.

Just let me do my thing,

and let me show you why
fructose is not glucose.

'Cause what the liver does to fructose

is really unique, and you've gotta

understand it to understand
everything I've just told you.

So, number one, fructose is seven times

more likely than glucose to
do that browning reaction.

The advanced glycation end-products.

The thing that happens on your grill,

happens in your arteries
for the same reason.

You can actually see the color too,

the color change too.

Fructose does not suppress
the hunger hormone.

There's a hormone that
comes form your stomach

called ghrelin you've
heard about, already.

So, if you preload a
kid with a can of soda,

and then you let him loose
at the fast food restaurant,

do they eat more, or do they eat less?

They eat more.

They just took on 150
calories, yet they eat more.

Reason?

'Cause fructose doesn't suppress

the hunger hormone
ghrelin, so they eat more.

Acute fructose ingestion
does not stimulate insulin,

because there's no receptor for fructose,

no transport for fructose on the beta cell

that makes insulin, so
the insulin doesn't go up.

Well, if the insulin doesn't go up,

then leptin doesn't go up, and if leptin

doesn't go up, you're brain doesn't

see that you ate something.

Therefor, you eat more.

And finally, I'm gonna show you

liver hepatic fructose metabolism

is completely different between

fructose and glucose,
completely different.

And I'm going to show you,
before the evening is out,

that chronic fructose exposure alone,

nothing else, causes this thing

we call the metabolic syndrome.

Everybody knows what the
metabolic syndrome is?

So, this is the conglomerate

of the following different phenomena,

obesity, Type 2 diabetes, lipid problems,

hypertension, and cardiovascular disease.

Those all cluster together,
called metabolic syndrome.

I'm gonna show you how fructose
does every one of those.

I wanna show you the difference between

glucose and fructose in a way that

will be glaringly apparent.

So, let's consume 120 calories in glucose.

Two slices of white bread.

What happens to that 120 calories?

You eat the 120 calories, 96 or 80%

of the total will be used by
all the organs in the body.

80% off the table.

Why?

Because every cell in
the body can use glucose.

Every bacteria can use glucose,

every living thing on
the face of the earth

can use glucose, because
glucose is the energy of life.

That's what we were supposed to eat.

24 of those calories, or
20% will hit the liver.

So let's watch what happens
to those 24 calories.

Here they go.

So, the glucose comes in
through this transporter

called Glut2, out here, the glucose

is gonna stimulate the
pancreas to make insulin,

the insulin's gonna bind to it's receptor,

and it's gonna take
this substrate over here

called IRS-1, insulin
receptor substrate 1.

That's not important
right now, don't worry.

And it's gonna tyrosine phosphorylate it.

And it's going to be tyrosine IRS-1,

which is now active, that's active.

And it's gonna stimulate the second

messenger here called AKT.

Now what AKT does is, it
stimulates this guy down here.

SRABP1, sterol receptor
binding protein number 1.

Don't worry about it.

But this is the thing that, ultimately,

gets fat mechanics going.

So, you 'll see in a minute.

So, one of the things that SRABP1 does,

is it activates this enzyme
here called glucokinase,

which takes glucose to
glucose 6 phosphate.

Now, glucose 6-phosphate
can't get out of the liver.

The only way to get glucose 6-phosphate

out of the liver is with hormones.

Glucagon or epinephrine, that's
the way it can get it out.

So now, the glucose is fixed in the cell,

but it's only 24 calories worth,

so it's not a big bolus of it.

Now, the glucose 6-phosphate

almost all of it, is gonna end up

going over here to
something called glycagen.

Now, glycagen is the storage
form of glucose in the liver.

Because glycagen's easy
to fish the glucose out

with glucagon and epinephrine.

So, my question to you, and granted,

this is a physiology question,

is how much glycogen can your liver store

before it gets sick?

The answer's any amount.

It's unlimited.

We have carb loaders who
run marathons, right?

Does it hurt them at all?

We have kids with a
disease where they can't

get the glucose out of the glycagen,

called glycagen storage disease type 1A,

or von Gierke disease.

They got livers down to
their knees their so big.

They're hypoglycemic like all get out

'cause they can't lift the
glucose out of their liver.

But, they don't go into liver failure.

Because glycagen is a non-toxic storage

form of glucose in the liver.

So, the whole goal of glucose

is to replete your glycagen.

So, this is good, this
is not bad, this is good.

Now, a little of that glucose
is gonna fall down here,

it's gonna get metabolized down

to this stuff here, called pyruvate.

And the pyruvate is gonna

enter your mitochondria, over here.

Remember, your mitochondria are

the parts of your cell that
actually burn the energy.

They're your little factories.

They make the stuff that lets you live.

Called ATP, ATP, adenosine triphosphate,

that's the energy of life, right there.

So, the pyruvate comes in, gets converted

to something called acetyl-CoA,

gets metabolized by this thing called

the Krebs cycle, TCA
cycle, and you throw off

ATP and carbon dioxide
which you breath off.

So far, so good?

Have I snowed anybody yet?

You're with me?

I snowed one guy back there.

(audience laughs)

I'm doin' my best, I swear to God,

I'm doing my best.

Anyway, so this stuff over here,

this acetyl-CoA, gets
burned off in the TCA cycle.

Maybe you won't burn all of it off,

and so, some of it may exit as citrate.

And the citrate then
leaves the mitochondria

through a process known
as the citrate shuttle.

And then that citrate
can then be broken down

by these three enzymes, which are all

subservient into this SRABP1.

This is ATP citrate lyase acetyl-CoA

carboxylase fatty acid synthase.

They're not important.

The only thing to know is these three

enzymes together turn sugar into fat.

This is called denovo, meaning new,

lipogenesis, fat making.

This is denovo lipogenesis.

So you take the citrate
which came form the glucose,

and you end up with
something called acetyl-CoA,

which then gets packaged
with this protein here,

and you end up with something called VLDL,

very low density lipoprotein.

Now, anybody heard of that before?

Is it good or bad?

It's bad, that's bad.

VLDL is bad because that's one of

the things that causes heart disease.

It's also a substrate for obesity.

So, you don't wanna make much of this.

But the point is, you
started with 24 calories,

maybe a half a calorie
will end up as VLDL.

So, that little Japanese
guy with the little hat,

you know, working out in the field,

eating rice for the next 90 years,

can he die of a heart attack at age 90?

Sure.

But that's not so bad.

If you make it to 90,
you're doing alright.

Because that VLDL coming from glucose.

Glucose made a little bitty VLDL.

And that serves as a substrate
for adipose deposition

into your fat cell, here triglyceride.

In addition, because of the insulin

went up in response to the glucose,

your brain sees that signal.

And it knows that that is supposed

to shut off further eating.

In other words, hey, I'm busy
metabolizing my breakfast.

I don't need lunch.

And so, you have a nice
negative feedback loop

between glucose consumption, the liver,

the pancreas, and the brain, to keep you

in normal negative, yin
yang energy balance.

This is good, this is not dangerous.

This is what's supposed to happen.

So now, let's talk about
a different carbohydrate.

Let's talk about my favorite
carbohydrate, maybe yours too.

(crowd murmuring)

Ethanol.

Ethanol is a carbohydrate, isn't it?

Here's the structure,
carbon hydrogen oxygen,

it' a carbohydrate.

But, we all know that
ethanol is a toxin, right?

A poison, right.

You can wrap your
Lamborghini around a tree,

or you can fry your liver, your choice.

Depends on how much you
drink and how often.

Right? Okay.

So, we know that ethanol
is not good for you,

except, of course, a
little bit is good for you.

So, we can talk about that
too, later, if you want.

But, let's talk about
how it's bad for you.

So, here's acute ethanol exposure.

CNS depression,
vasodilatation, hypothermia,

tachycardia, myocardial depression,

pupillary responses,
respiratory depression,

diuresis, hypoglycemia,
loss of fine motor control,

you all went to college.

(audience laughs)

Here's fructose, nothing.

It doesn't do any of those.

Because the brain doesn't
metabolize fructose.

Alcohol gets metabolized in the brain,

to cause all of those
things, but fructose doesn't.

So, fructose is not an
acute toxin, ethanol is.

We control ethanol, don't we?

We have something called

the Bureau of Alcohol
Tobacco and Firearms.

We have all sorts of
things, we tax ethanol.

We do all sorts of things to
limit consumption of ethanol.

The Nordic countries, all the
liquor stores are state run

in attempt to try to set the
price of ethanol high enough

so as to discourage consumption
for public health reasons.

We have 1500 years of alcohol
control policy in this world

to draw on, in terms of
how to limit consumption.

Got it?

Because ethanol is a
toxin, and we know it.

So, let's consume 120 calories in ethanol.

Shot of Makers Mark.

Anybody taste it?

Yeah, good, okay.

So, 24 calories right off the top.

The stomach and the
intestine have something

called the first pass
effect, so 10% off the top,

and kidney, muscle, brain
will consume the other 10%.

So there goes 20% or 24
calories right off the top.

96 calories of the 120
are gonna hit the liver.

Now, how many was it for glucose?

It was 24.

So, four times the substrate
is gonna hit the liver,

and there's the rub.

This is a volume issue.

We're gonna show you how.

So, the ethanol comes
in, passive diffusion,

there's not receptor
for it, not transporter.

First thing that happens is ethanol

gets converted to this guy,
over here, called acetaldehyde.

Anybody know anything about aldehydes?

Like formaldehyde? Right?

Are aldehydes good for you or bad for you?

They're bad, right?

'Cause what do they do?

They can cause cancer, they cross link

proteins is what they do.

So, if you cross link enough
proteins in your liver,

what do you think happens to it?

You get something called...

Cirrhosis, right exactly.

So this guy, over here, is bad.

And it generates something
called reactive oxygen species.

Reactive oxygen species
damage proteins in the liver.

And the more alcohol you drink,

the more of this stuff you get.

So far, so good?

So, this is one of the
reasons why alcohol's bad.

Now the acetaldehyde will come down here

to something called acetate.

The acetate will enter the mitochondria,

just like the pyruvate did before.

Will get converted to acetyl-CoA

and participate in the TCA cycle,

just like before, to generate energy.

So that alcoholics don't
die form lack of energy,

they got energy, it's
everything else they don't have.

They're gonna have a whole lot of citrate.

Because they have 96 calories that

have to get metabolized.

How many calories made it to
the mitochondria with glucose?

About half, right?

Because most of it went to glycogen.

So, we've got a big
citrate, so it's in big font

to show you that we're
talking about big citrate now.

And so, the big citrate
is gonna get metabolized

all the way to VLDL by the CRABP1.

And so you're gonna get a lot of the LDL.

And this is the dyslipodemia
of alcoholism, right here.

Everybody see that?

So, the liver's gonna try to export

this VLDL out so that it doesn't get sick,

because when fat builds up in the liver,

that's not good for it.

Some of it's gonna exit
as free fatty acids,

and those free fatty acids,
will take up residence

in the muscle, and you get something

called muscle insulin resistance.

So insulin resistance, that's a bad thing.

That makes your muscles and
your liver now work so well.

And can cause all sorts of
other problems like diabetes.

Some of the acetyl-CoA
won't even make it out,

and will precipitate as a lipid droplet,

so there's your alcoholic steatohepatitis.

This acetyl-CoA, and this ethanol,

and these reactive oxygen species

can start this enzyme activated.

It's called c-jun n-terminal kinase 1,

or JNK1, and it really is JNK1

because it is the bridge between

metabolism and inflammation.

So, when you generate JNK1, you
do bad things to your liver,

which I will show you when
we talk about fructose.

So let's talk about fructose.

Fructose is sweet, we like it a lot.

We like it in everything,
we like it in our bread,

we like it in our pretzels,
we like it everywhere we look.

So, let's consume 120 calories in sucrose.

A glass of orange juice.

Everybody got it?

So, two slices of white
bread, a shot of makers mark,

a glass of orange juice,
all the same 120 calories.

But, three different substrates.

Let's see what happens to the fructose.

So, number one, the glucose, remember,

'cause sucrose is half
glucose half fructose,

so 60 of the calories
of the 120 are glucose.

12 are gonna make it into the liver,

48 out here for the rest of the body.

The same 20/80 split we
had before with glucose.

So far, so good.

But all 60 calories of fructose are

gonna be metabolized by the liver.

Why?

Because only the liver
can metabolize fructose.

So, what do we call it, where when you

take in a compound that's
foreign to your body,

and only the liver can metabolize it,

and in the process,
generates various problems?

What do we call that?

We call that a...

Poison.

So, let me show you how it's a poison.

So, let's watch the fructose.

So, the fructose comes in
through this transporter, now.

Before it was Glut2, now it's Glut5

No insulin, remember, 'cause fructose

does not stimulate insulin.

Fructose, then, gets metabolized
by this guy, over here,

called fructokinase, to form something

called fructose 1-phosphate.

In the process, ATP has to give up

one phosphate to ADP 'cause the phosphate

had to come from somewhere,
so it comes from here.

Now, before we had 24 calories

that had to be phosphorylated.

Now we have 72 calories that
have to be phosphorylated.

So, we have three times the substrate,

and there's the rub.

It's a volume issue, for right now.

So, we're gonna lose a lot
of phosphate, aren't we?

So there's a scavenger
enzyme in your liver

called AMP deaminase 1 to rescue

the phosphates off the
rest of the ATP molecule,

and it takes ADP down to
AMP, adenosine monophosphate,

down to IMP, Inositol monophosphatase,

and finally, to the
waste product uric acid.

Anybody every heard of uric acid?

What is it?

It's a waste product.

Goes out in your urine.

'Causes what disease?

Gout, right.

Also causes another disease
called hypertension.

Let me show you how.

Because uric acid, turns out, blocks

the enzyme in your blood vessels

called endothelial nitric oxide synthase.

And that's the enzyme that makes

the stuff called nitric oxide, NO.

And that is your endogenous
blood pressure lowerer.

That keeps your blood pressure low.

So, when you can't make it,
your blood pressure goes up.

So, this just shows that
fructose consumption

increases gout in adults.

So, this is a study
that came out last year

showing that fructose consumption

increases the risk for gout,

showing that uric acid's going up.

And this is a study done
by pediatric renal fellow,

Stephanie Winn, just published in

Journal of Pediatrics,

it's not submitted any
more, it's long in press,

showing that this is
in the NHANES database

in the adolescents, showing
that sugar sweetened beverages,

as it goes up, your uric acid goes up.

And, not only does your uric acid go up,

but here's your sugar sweetened beverages,

and here's your systolic
blood pressure going up.

And here's a study done by Dan Fige,

at the University of Texas San Antonio,

where he took obese
adolescents with hypertension,

and he gave them the drug Allopurinol.

And Allopurinol is the drug
that you treat gout with,

to lower the uric acid.

And look what happened
to the blood pressure.

Systolic, diastolic, went down.

Showing that, in fact, uric acid

is an important part of hypertension.

We have a hypertension
epidemic in this country.

Here it is.

It's the sugar.

Okay, so, so far we have
high blood pressure.

Let's keep going.

The fructose will get metabolized

down to pyruvate, the pyruvate

will enter the mitochondria
just like before,

throwing off a lot of citrate.

And here's a little trick that fructose

does that glucose doesn't.

'Cause these to can reform this stuff

over here called fructose
1 6 bisphosphatase,

which can then reform with glyceraldehyde

to form this guy, over here,
called xylulose-5-phosphate.

And I get to
xylulose-5-phosphate in a moment.

But I wanna point out this asterisk.

That's there to remind
me to tell you something.

That's there to remind me to tell you

that this is why the
sports drink companies

put high fructose corn
syrup in the sports drinks.

Because if you are glycogen depleted,

in other words, if you just ran a marthon,

and you have no glycogen
left in your liver

because you burned it all, and you take in

a sports drink with high
fructose corn syrup,

you can replete your glycogen faster

than with glucose alone.

That's true.

So, for elite athletes, a
high fructose corn syrup

containing sports drink
actually makes sense.

And so, indeed, sports drinks

have high fructose corn syrup.

The question is who
drinking the sports drinks?

Any elite athletes you know?

Who's drinking the sports drinks?

The kids, right?

Why are they drinking it?

Because it's cool, right?

'Cause it's cool and it tastes good.

So, before we go on, I just wanna,

now, digress for a moment.

1967, University of
Florida patents Gatorade.

Everybody remember Gatorade?

Okay, 1970, the Florida Gators win

the NCAA Championship in football.

Gatorade makes a big splash.

Okay, big deal.

Anybody ever taste the original Gatorade?

Yeah?

What'd it taste like?

Tasted horrible.

It tasted like something
that you might find

coming out of you instead
of going into you.

(audience laughs)

It tasted awful.

1992, Pepsi buys Gatorade, and they say,

"How are we gonna market this swill?"

So, what did they do?

They added the high fructose corn syrup.

So, now who drinks it?

Fat kids, right?

Not even skinny kids, fat kids drink it.

Okay, so there's a problem here.

Okay, and we're gonna
show you how that works.

Okay, so xylulose-5-phosphate,
just to show you,

if you take a rat, and
you glycogen deplete him

by making him run on an exercise wheel,

and then you re-feed them with starch

or with sucrose, the xylulose-5-phosphate

goes way up with the sucrose.

So you get more xylulose-5-phosphate

through this pathway
here, going over here.

So why do we care about
xylulose-5-phosphate?

Well, here's why.

Because it stimulates this guy, over here,

called PP2A, which then activates

this transcription factor here,

carbohydrate response
element binding protein,

which then activates what three enzymes?

New fat making right,
the novo lipogenesis.

So here's the citrate,
we got lot's of that.

And here we've got acetyl-CoA,
which is the way into fat,

which then gets packaged to the VLDL,

and now you've got the dyslipidemia

of obesity of fructose consumption,

which has, been known for many years.

So, here's normal medical students,

if you can call them normal,

taking in a glucose load.

Notice, almost none of it ends up as fat.

Taking in a fructose load,
same number of calories,

30% of it ends up as fat.

So when you consume fructose,

you're not consuming a
carbohydrate, you're consuming fat.

So everybody talks about a high fat diet.

Well, high sugar diet is a high fat diet.

That's the point.

That's exactly the point.

This is a study where they gave

acute administration of fructose,

and you can see the triglycerides

going up compared to the control.

Serum triglyceride, right there.

Here's normal medical students, again,

six days of high fructose feeding.

Triglycerides doubled, de novo lipogenesis

went up five times higher,
and here's free fatty acids,

which then cause insulin
resistance, doubled.

Six days.

So, here's the dyslipidemia
of fructose consumption.

We're not done.

Some of the fat won't
make it out of the liver,

just like with ethanol.

And now you've got a lipid droplet,

so now you've got this
nonalcoholic steatohepatitis.

So, this is work that we did in our clinic

looking at sugar sweetened
beverage consumption

against the liver enzyme marker ALT,

alanine aminotransferase, which
tells you about fatty liver.

And sure enough, here's
sugar sweetened beverages

against ALT, and you can see a nice

linear relationship in Caucasians.

African Americans, it's
a different relationship,

and that' a' whole 'nother
story all by itself.

So, there's the lipid droplet

of nonalcoholic steatohepatitis.

Some of it will come
out as free fatty acids

and populate the muscle, will also tell

the insulin to go up higher.

Remember that JNK1?

So, here's what JNK1 does.

So, the acetyl-CoA and the
fructose can all activate JNK1.

And what JNK1 does is, remember when we

used glucose, this IRS
became tyrosine IRS-1

and that was good?

Remember that?

Well, JNK1, what it does, is it's

serine phosphorylated IRS-1.

And serine IRS-1 is inactive.

So now, the insulin can't
even do it's job in the liver.

So, now you have liver
insulin resistance as well.

That's gonna make the
pancreas work that much harder

generating higher insulin levels,

which raise your blood
pressure even further,

cause further fat
making, cause more energy

to go into your fat cell.

There's your obesity.

And finally, our research has shown

that the higher the insulin goes,

the less well your brain
can see it's leptin.

And so there you've got
continued consumption

because your brain thinks it's starving.

And it's been shown in many different ways

that fructose consumption changes

the way your brain recognizes energy.

All in a negative fashion, so that you,

basically, think you're starving.

Your brain gets the signal
that you're starving

even though your fat cells are generating

a signal that says, "Hey,
I'm full like all get out."

So, this just shows you how it goes.

So, the high insulin generates the obesity

because this is that, remember the first

law of thermodynamics,
the biochemical force

generating the energy storage

as the primary phenomenon, remember,

if you're gonna store it,
and you expect to burn it

then you're gonna have to eat it.

So, here's the store it.

Normally, that would make leptin,

and the leptin should feed back

and turn everything off, but it doesn't,

because the insulin gets in the way,

and the high fat diet gets in the way.

Also, the hyperinsulinemia
stops the leptin

from acting on that nucleus accumbens,

and so you get an increased reward signal.

So that continues your appetite,

continues more fructose,
more carbohydrate,

generating more insulin
resistance than you can see.

You generate a vicious
cycle of consumption

and disease, and no stopping.

So, here we are,
hypertension, inflammation,

hepatic insulin resistance,
hyperinsulinemia,

dyslipidemia, muscle insulin resistance,

obesity, and continued consumption.

Looks like metabolic syndrome to me.

So, here are the phenomena associated

with chronic ethanol exposure.

Hematologic disorders,
electrolyte abnormalities,

hypertension, cardiac
dilation, cardiomyopathy,

dyslipidemia, pancreatitis, malnutrition,

obesity, hepatic dysfunction,

that's alcoholic steatohepatitis,

fetal alcohol syndrome, and addiction.

Here's fructose.

Eight out of twelve.

Why?

'Cause they do the same thing.

'Cause they metabolize the same way.

Because they are the same.

They come from the same place, right.

How do you make ethanol?

Naturally.

Right, you ferment sugar.

Hasn't changed, 'cause it
has all the same properties.

Because it's basically
taken care of by the liver

in exactly the same way,
and for the same reason.

Because sugar and ethanol are the same,

every which way you turn.

So, here's our clinic intervention.

This is what we do in our clinic.

It's as simple as you can imagine.

We write this on the back of a matchbook.

It's just as simple as you can make it.

We have four things we teach

the kids to do, and the parents.

Get rid of every sugared
liquid in the house, bar none.

Only water and milk, there is no

such thing as a good
sugar beverage, period.

Eat your carbohydrate with fiber.

Why?

Because fiber is good.

Fiber is supposed to be
an essential nutrient.

And we can talk later, if you want,

after the cameras turn off,

as to why fiber is not
an essential nutrient.

Because the government
doesn't want it to be.

'Cause then they couldn't
sell food abroad.

Wait 20 minutes for second portions,

to get that satiety signal.

And finally, buy your screen time

minute-for-minute with physical activity.

That's the hardest one to do.

So, if you play for half an hour,

you can watch TV for half an hour.

You wanna watch TV for an
hour, play for an hour.

That one's a hard one, but anyway.

We follow our patients every three months.

So, here's my question.

Does it work?

What do you think?

Yeah, it works.

So, this is BMI z-score
time from initial visit.

It works.

But, we were interested
in what made it work,

and made it didn't work, so we did

a multivariate linear regression analysis.

The thing that made it not work,

sugared beverage consumption.

The more sugar beverages the
patient drank at baseline,

the less well lifestyle
intervention worked

for all the reasons I just showed you.

So, why is exercise important in obesity.

Because it burns calories?

Come on.

20 minutes of jogging's
one chocolate chip cookie.

You can't do it.
(audience laughs)

Are you joking me?

So, why is exercise important?

I'll tell you why, here's why.

Number one, it improves
that skeletal muscle

insulin sensitivity because you're insulin

actually works better at your muscle,

which then brings your
insulin levels down.

Which is good for you.

Number two, it's your
indigenous stress reducer.

It's the single thing that
actually stress reduces.

And if you stress reduce,

what do you think your appetite does?

Goes down, because stress
and obesity go hand in hand,

for all sorts of reasons which are beyond

the scope of this lecture today.

But, we can talk about it in

the question period, if you want.

And then finally, remember
that de novo lipogenesis?

Remember those three nasty enzymes?

What if you burned the stuff
off before you made the fat?

That's what exercise does, 'cause it makes

that TCA cycle run
faster, so you don't get

the citrate leaving the mitochondria,

so it doesn't get turned into fat,

so it doesn't precipitate and cause

all the problems you just saw.

(speaking away from microphone)

That's what they mean by
a higher metabolism, yes.

But it has nothing to do
with burning of calories.

That is the stupidest reason

that I've every heard of for exercise.

You gotta be joking me.

You can't do it.

I mean one Big Mac and you gotta

mountain bike for ten hours.

(audience laughs)

Are you joking?

So, why is fiber important in obesity?

So, this is my motto in clinic.

When God made the poison, he
packaged it with the antidote.

'Cause fructose is a poison.

I think I've, hopefully, shown you that.

But, wherever there's fructose in nature,

there's way more fiber.

You ever see a piece of sugar cane?

It's a stick, right?

(audience laughs)

You can't even chew the damn thing, right?

You gotta suck the stuff out.

(sucking)

Like that, right?

I mean, how many calories you think you're

gonna get out of a piece of sugar cane?

They actually did studies
on the sugar plantations

back in the early 1900s.

All of the workers were healthy

and lived longer than the sugar executives

who got the processed product.

How 'bout that, wonder why.

So, eat your carbohydrate with fiber,

that's why we say that.

That includes sugar,
that's why fruit's okay.

Because number one, it limits

how much fructose you're gonna take in,

and number two, it gives
you an essential nutrient

which you needed in the first place.

And you get some
micronutrients along with it

so that you actually, your
liver works healthier.

So, here's what fiber does.

Number one, it reduces the rate

of intestinal carbohydrate absorption.

Now, sometimes that's bad.

I'll tell you when that's bad.

Now when that's bad?

That's bad when you're
at a formal function.

'Cause what happens if you reduce

the rate of carbohydrate
absorption in your gut?

The bacteria get to it.

So, as far as I'm concerned,

in life you've got two choices.

It's either fat or fart.

(audience laughs)

It increases the speed of transit

of the intestinal contents to the ilium,

and that raises this hormone over here

called PYY, which goes to your brain

and tells you the meal's over.

That's your satiety signal.

So when you add fiber to your diet,

you actually get your
satiety signal sooner,

because the food moves through faster.

And then, finally, it also inhibits

the absorption of some free fatty acids

all the way to the colon, and then those

get chopped up into little
itty bitty fragments

called short chain fatty acids,

and those actually suppress insulin,

as apposed to long chain fatty acids

which stimulate insulin.

So there are a whole bunch
of reasons why fiber is good.

Anybody ever heard of
the Paleolithic Diet?

Go home and read up on it on the internet.

The Paleolithic Diet.

Basically, if you east everything as it

came out of the ground
raw, with no cooking,

you would cure diabetes on a dime.

Takes about a week.

Because you're getting that 100

to 300 grams of fiber I mentioned before.

That's why, 'cause fiber is good for you.

And the more, the better.

- [Audience Member] Type 2.

Type 2, right, Type 2, not Type 1.

I stand corrected, Type 2.

Now, for some fun.

That's the end of the biochemistry.

Phew, how'd I do?

(audience applauds)

I told you I'd get you through it.

So, now comes the fun part.

The racial innuendos, and
all the political stuff.

The fructosification of America,

and, of course, the world.

Ready?

Another quiz.

Can you name the seven foodstuffs

at McDonald's that don't have

high fructose corn syrup or sucrose?

- [Audience Member] Mustard?

- (laughs) No, mustard has it.

(audience chatter)

Oh, come on, come one, the big one.

French fries, but they
have salt, starch, and fat.

So, they're not so good either.

Okay, what else?

We'll get to coffee.

Hash browns, for the same reason,

salt starch and fat.

What else, chicken
McNuggets, I was shocked.

I was shocked.

No sucrose or high fructose
corn syrup in chicken McNuggets.

But, as the Circuit
Court Judge in New York

called them, they are still
a McFrankenstein creation.

(audience laughs)

But, nonetheless, no sucrose,
I was really shocked.

Sausage.

Oh, they're terrible,
they're just disastrous.

But, I mean, there's
nothing good in them at all,

but there's not fructose.

Sausage, Diet Coke, Coffee,
if you don't add the sugar,

and ice tea, if you don't add the sugar.

By the way, the chicken McNuggets,

we have a disclaimer, because no one

eats the chicken McNuggets
without a dipping sauce.

And there's a whole bunch
of high fructose corn syrup

in the dipping sauce, right?

Okay, good, all right.

So, who's really drinking this?

We talked about this before.

Gatorade AM.

So, this is an attempt by Pepsi

to capture market share
on the juice market.

Do you think there are any elite athletes

who actually drink this stuff?

You gotta be kidding me.

Okay, this is for kids, right?

So, this really blew my socks off.

This was my daughter, when she

was in second grade, two years ago,

Miriam Lustig, brought these two

cartons of milk home for me, and said,

"Dad, you're not gonna believe this."

Second grade.

So, here's the calories in Berkeley Farms

1% low fat milk, 130 calories,
15 of them are sugars,

'cause it's lactose, which is okay.

And here's Berkeley
Farms 1% chocolate milk,

190 calories, 29 grams of sugar,

all high fructose corn syrup.

It's like a glass of milk plus

a half a glass of orange juice.

And that's what we're giving to our kids.

And do you know what the

nutrition department at the SFUSD says?

"Well, we have to get our
kids to drink milk some how."

Is that brilliant, or what?

I don't know.

Now, what about WIC.

So, we talked about the 112 pounds

of orange juice that the kid
down in Salinas was drinking.

What bout WIC?

Remember what we started with?

We have an epidemic of
obese six month olds.

Remember?

So, could this be the reason?

So, here's a can of formula.

43.2% corn syrup solids, 10.3% sugar.

It's a baby milkshake.

Soda, Coca Cola, is 10.5% sucrose.

Formula is 10.3% sucrose.

Any difference?

And there's a huge literature that's

now coming of age that shows that

the earlier you expose kids to sweet,

the more they're gonna crave it later.

Plus, there's a new literature that shows

the more sugar the pregnant
woman drinks or eats

during the pregnancy, the more that gets

across the placenta, and actually causes

what we call developmental programming,

changing the kids adiposity
even before the kid is born,

and driving this whole
epidemic even further.

So, we'll close in a few minutes.

But, I just wanna point
out what's the difference.

Here, we got a can of Coke.

Here we got a can of beer.

And I'm not picking on
Schlitz, or anything.

It's any beer you want, okay.

So, 150 calories each, no difference

in terms of total calories.

Percent carbohydrate, so
10.5% from sucrose here,

except it's high fructose
corn syrup, but who cares.

3.6% alcohol, here's the breakdown.

75 fructose, 75 glucose for the Coke.

90 alcohol 60 maltose for the beer.

Remember, the first pass GI metabolism

takes 10% of the alcohol off the table.

So, when you actually compute

the number of calories hitting the liver,

which remember was the big difference

between glucose and fructose, remember?

72 versus 24 and started
the whole thing into motion

as term of what happens that's bad.

Bottom line, no difference.

So, we have something called beer belly.

Well, welcome to soda belly.

'Cause that's what
America's suffering from.

No ifs ands or buts.

That's what it is.

Now, you wouldn't think twice about

not giving your kid a Budweiser.

But, you don't think twice about

giving your kid a can of Coke.

But, they're the same,

in the same dosing, for the same reason,

through the same mechanism.

Fructose is ethanol without the buzz.

Fructose is a carbohydrate.

Yes, it is.

But fructose is metabolized like a fat.

And I've just shown you that 30%

of any ingested fructose
load ends up as fat.

So when people talk about high
fat diets doing bad things,

no, what they're really talking

about is high fructose diets,

and that's what Ancel Keys was looking at.

So, the corollary to that
is, in America at least,

and around the world too, a low fat diet

isn't really a low fat diet.

Because the fructose or
sucrose doubles as fat,

it's really a high fat diet.

That's why our diets don't work.

And fructose, just like ethanol,

for the same reason,
through the same mechanism,

and in the same dosing, is also as toxin.

Now, last, what can we do about it?

Can we do anything about it?

How 'bout the FDA?

You think they can do something about it.

After all, aren't they
supposed to regulate our food?

Aren't they supposed to regulate

what they can put in food?

Weren't they supposed to regulate tobacco?

Now they are, actually.

So, you know, weird things.

So, I wanna just show you what

the tobacco company thinks of all this.

This is actually from the UCSF Legacy

Tobacco Documents Library that

Stan Glantz runs right across the street.

Stan's a good guy, like Stan a lot.

And he showed me this.

"Under the regulations
governing food additives,"

so this came from an Altria
or Phillip Morris executive,

"it is required that additives be safe,

"defined as a reasonable certainty

"by competent scientists that no harm

"will result form the
intended use of the additive."

Now, does fructose meet that standard?

Well, the FDA says that fructose,

high fructose corn syrup,
has what's knows as GRAS,

G R A S status, generally
regarded as safe.

Now, where'd that come from?

No where.

It came from no where.

It came from the notion
that, "Well, fructose

"is natural, it's in
fruit, it must be okay."

Well, tobacco's natural too.

But it's not.

Ethanol's natural, but it's not.

A whole bunch of, you know,

Jamaican ackee fruit's
natural, but it's not either.

It kills you.

Keeping on going.

"A food shall be deemed to be adulterated

"if it bears or contains any poisonous

"or deleterious substance which may

"render it injurious to health."

Fructose fits that description, right?

Uh-uh, but now with the prevention

of chronic diseases, even though

it's own regulations explicitly

postulate the connection between

such products and such diseases.

In other words, the FDA will only regulate

acute toxins, not a chronic toxin.

Fructose is a chronic toxin.

Acute fructose exposure
did nothing, remember.

'Cause the brain doesn't
metabolize fructose.

The liver does.

And the liver doesn't get
sick after one fructose meal.

It get's sick after 1000 fructose meals.

But, that's how many we eat.

So, the FDA isn't touching this.

The USDA isn't touching this.

Because if the USDA touched
this, what would that mean?

That would mean an admission to the world

that our food is a problem.

So, what to you think that would do?

There are three things in this country

that we can still sell overseas.

Weapons, entertainment, and food.

Cars? (laughs) Computers?

I don't thinks so.

Can anybody think of anything else

that another country wants of ours?

What?

Tobacco, right, tobacco. (laughs)

All right, you get the picture.

So, the USDA doesn't
wanna know about this.

'Cause this is bad news.

And so, who runs the food pyramid?

The USDA.

It's the fox in charge of the hen house.

Because their job is to sell food.

And who's eating it?

We are.

So, in summary, fructose, and I don't care

what the vehicle is, it's irrelevant,

sucrose or high fructose corn syrup,

I don't care, fructose
consumption's increased

in the past 30 years, coinciding
with the obesity epidemic.

A calorie is not a calorie.

And the dietitians in the country

are actually perpetrating this on us.

Because the more you think
a calorie's a calorie,

the more you think, well than if you

ate less and exercise more, it would work.

It doesn't.

All of the studies show it doesn't work.

Here's why it doesn't work,

because a calorie is not a calorie.

Fructose is not glucose.

We know a calorie is not a calorie.

'Cause there are good fats and bad fats.

There's good protein and bad protein.

Okay, there's good carbohydrate
and bad carbohydrate.

And glucose is good carbohydrate.

Glucose is the energy of life.

Fructose is poison.

You are not what you eat.

You are what you do with what you eat.

And what you do with fructose

is particularly egregious and dangerous.

Hepatic fructose metabolism leads to all

the manifestations of
the metabolic syndrome.

Hypertension through
that uric acid pathway,

de novo lipogenesis, dyslipidemia,

hepatic steatosis
through that DNL pathway,

those three enzymes, the
new fat making pathway,

inflammation through JNK1,
hepatic insulin resistance

because of the serine phosphorylation

of IRS-1, obesity because
of the VLDL transport

to the adiposite, and leptin resistance

promoting continuous consumption,

basically starving your brain,

making you think you need more.

Fructose ingestion interferes
with obesity intervention,

as we showed in our clinic.

The more soft drinks, the less well

diet and exercise actually worked.

Fructose is a chronic hepatotoxin

for the same reason that alcohol is.

The only difference is alcohol is

metabolized by the brain,
so you get alcohol effects.

Fructose is not metabolized by the brain

so you don't get those effects.

But everything else it does is the same.

But the FDA can't and won't regulate it.

It's up to us.

I'm standing here today to recruit you.

That's a famous saying here
in San Francisco, right?

"I'm Harvey Milk, and
I'm here to recruit you."

I'm Robert Lustig, and
I'm here to recruit you

in the war against bad food.

And this is what's bad.

With that, I wanna thank my colleagues

at the UCSF Department of Pediatrics

in our Weight Assessment for
Teen and Child Health Clinic,

UCSF Department of
Epidemiology and Biostatistics,

and also Department of
Nutritional Sciences

at UC Berkeley, in particular
Doctor Jean-Marc Schwarz,

who is a card carrying
fructose biochemist,

PhD biochemist, who vetted all of these

pathways that I've shown you today,

and looked at this and said,
"Oh my God, it is a toxin."

He worked in the stuff for 15 years,

and he didn't even realize it
was a toxin until he saw this.

So, with that, I'll close.

Thanks you.

(audience applauds)

(upbeat techno music)