Fat Chance: Fructose 2.0

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the latest UCTV programs. Good evening, everyone. Welcome again to our
penultimate class in this semester's
course on nutrition. Reminder that next
week, we'll be talking about vitamins and minerals and vitamin mineral supplements, so please join us
for that last class. Dr. Jeffrey Tice will be the professor joining
us that evening. Tonight, we have, what I
guess for some of you has been the lecture
you've been waiting for since the beginning. Dr. Lustig gave a
similar lecture in 2009. Little did we know at the
time that it would have 3.5 million downloads since then.

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But it was in this
room, and a course very similar to this that
I also chaired, and it's really, I think, changed his life more
than anything else. I think the hope is that it's also changed the
field and the topic, and the policies and the politics of what we're going to
talk about tonight. Many of you know, Dr. Lustig is an internationally known neuroendocrinologist
in pediatrics. He trained for part
of his time at UCSF, then went back East to do clinical neuroendocrinology
and came back to UCSF in 2001, where he's continued to do his clinical science on
factors that control appetite, particularly the
interaction between the hormones of insulin, leptin and ghrelin and appetite control and the
metabolic syndrome and obesity. More recently, in part, around the time of the video and certainly in the
four years since, Rob has become an international leader in the efforts to improve
our nutrition, not only in the United
States but around the world. He's focused a larger part
by putting a real microscope on the issues of fructose and sugar in general and
refined foods in general.

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The relationship to dietary fiber and many of the other topics that we've been
talking about over the course of the course. Rob just returned from
Europe this morning. In fact, arrived here at
five o'clock this evening. We think he had dinner. We know he hasn't had sleep. It's four o'clock
Europe time for him. So this was really
a heroic effort. Our fingers were crossed that all the flights would be on time, and I'm very pleased, more
than you can imagine, that is here tonight
because I didn't want to give this lecture as well. But in addition to his work, Rob recently took a
sabbatical in order to further this work and spend a large part of that time
at Hastings School of Law, getting a master
of studies in law. Part of his aspiration
I think is really to add his legal training now to his science and
medical training to continue to advocate for good
nutrition around the world.

We're very anxious to hear about his newest thoughts
on this topic. We've entitled the talk the same title as his
best-selling book, Fat Chance, and
added the subtitle, Fructose 2.0. Rob? Thank you, Bobby. Thank
all of you for coming. To some extent, this is like
deja vu all over again. Having done this four years ago and it really did change my life, and hopefully it changed a few people's lives in the audience and certainly
around the world. I still get emails
from that video today. People who have seen
it for the first time. That video, we're
going to refer back to it to some extent tonight because I am not going
to redo the biochemistry. There's no point
in doing it twice. What we're going to
talk tonight about is primarily the physiology. In a sense, the two videos will end up being
complementary on YouTube, and hopefully people who watch it will end up watching both.

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So keep that in mind. Well, a lot's happened
in four years, and the data just
keeps rolling in. Unfortunately, for us, all
the data is pretty awful. You'll see why as we go and I will try to delineate
that as we go. First of all, I have
no disclosures. No food industry is
putting me up to this, you can be sure of that. Here's the past. This is 2001. Six million kids are
seriously overweight.

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Well, with all of
the media attention, with all of the NIH money, with all of the
clinical programs, and with Michelle Obama's
vegetable gardens, we are now up to 20 million. Here's the present.
Currently, there are 30 percent more obese people on the planet than
undernourished people. This has happened only within 15 years because 15 years ago, it was exactly the opposite, and it's occurring in countries that still have under-nutrition.

How do you explain that
other than to say, that can't be behavior, that's got to be an exposure? This looks like any
standard pandemic; influenza, typhoid, etc. This looks like a microbial phenomenon rather than a behavior phenomenon.
We're going to go there. Three hundred and
sixty six million diabetics walking the Earth, that's five percent of
the world's population. They are chewing through all
the health care resources. This was just three months ago, diabetes costs the
US $245 billion. Now, if we could recoup
even a fraction of that, we wouldn't even need
health care reform. In fact, it's been
suggested that we wouldn't even need financial reform.

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Forty one percent
rise in five years. This is going up so fast,
it makes your head spin. Here's the future
if we do nothing. Experts predict 165
million Americans, 42 percent will be
obese by the year 2030, 100 million Americans that'll be 33 percent will have
diabetes by 2050. But fear not, because it won't really matter because Medicare
will be broke by 2026. As the Soup Nazi once said, "No health care for you." Well, the fact of the matter is, I'm going to be 69 in 2026, and I want my frigging Medicare.

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So should you all. The point is, we have to do
something different than. You know the old adage, or the definition of
insanity is doing the same thing over and over again and expecting
a different result. Well, I'm here to tell you
for the last 30 years, we have done the same
thing over and over again, and there has been no
change in the result. So we have to rethink this, we have to re-frame the argument, and that's what we're going
to try to do tonight. I'm going to do it right now. Here's the way people
view this issue. This is a Venn diagram of
all the adults in America. Thirty percent
obese over here and 70 percent normal
weight over here. Everybody assumes
that the problem is this group over here, because 80 percent of the obese population is sick in some fashion with
type 2 diabetes, lipid problems, hypertension, cardiovascular disease, cancer, dementia, non-alcoholic
fatty liver disease, polycystic ovarian disease, etc.

If you do the math on this, that's 80 percent of 30
percent of 240 million, that's 57 million sick, and it's those 57 million that are bankrupting the country. So it's the obese
person's fault only, and that's the way
everyone views this. This is wrong. This is a mistake. This is a disaster actually,
because it's not correct. Here's the real story. In fact, 20 percent of the obese population is
completely metabolically normal. They have normal
insulin dynamics, they don't get sick, they will live a
completely normal life, die at a completely normal age, cost the taxpayer nothing. They're just fat. Conversely,
up to 40 percent of the normal weight population have the exact same metabolic
dysfunction that the obese do. They're just normal weight. They don't even know they're
sick until it's too late, because normal weight people get type-2 diabetes,
they get hypertension, they get dyslipidemia, they
get cardiovascular disease, they get cancer, they
get dementia, etc.

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When you do the math on that, that's another 67 million, so that's actually out
classing the obese. The total is 124 million. That's more than half
of all of America. Now, you may remember HIV. Remember HIV? When did HIV
become a public health crisis? In the '80s. No, not in the '80s. In 1991. 1979, patient zero. We first learned
about the diagnosis. Throughout the entire '80s, it was all about the
gays and the addicts. It was always, well,
it's their problem, their personal responsibility, their behavior, their fault. Then something happened in 1991. Anybody know what it was? Magic Johnson. Magic Johnson got HIV. All of a sudden everybody
went, "Holy, Mother." You know what. Everybody realized,
you know what? Everyone's at risk
and all of a sudden, it became a public health crisis. When does a personal
responsibility issue become a public health crisis? That's what we're going to
talk about tonight because this is a public health crisis.

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Here's the slide that
demonstrates the phenomenon. Here are two equally
weighted adult men, which one's healthy and which
one's sick? Anybody know? The one on the bottom is
sick. Right, he's sick. Why? All that visceral fat, all that fat
surrounding the organs. See, this guy over here, he's got big love handles. So what? In fact, this is
perfectly healthy, there's no problem
because subcutaneous fat is actually good for you. There are actually
studies that show more subcutaneous
fat, more longevity. Whereas this stuff,
this is the bad stuff, this is the poison
stuff over here. The fact is standing on a scale doesn't tell
you where your fat is. What does? Well, your waist circumference
is a good start, and then there's some lab
tests you can do as well. The bottom line is, there are a lot of normal way people who have this phenomenon called
TOFI, thin on the outside, fat on the inside,
probably some right here in the audience and
they get type 2 diabetes, they get dyslipidemia, they
get hypertension, etc.

You get the picture?
Everyone's at risk because everyone's exposed. The question is, what is
it you're exposed to? Because obesity is not the
problem, it never was. They want you to think
it's the problem, but it ain't the problem.
What is the problem? Metabolic syndrome
is the problem. The cluster of diseases that I've just described to
you because that's where all the money goes. Obesity costs almost nothing. Metabolic syndrome is 75 percent of all healthcare costs today, and there's the list right there. Everybody with me now? Do
I have your attention? How does this work? This actually is
a redundancy from the previous YouTube video, so I apologize for that. It has to do with how you view the question of obesity
and what does it mean.

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Of course, obesity
obeys the first law of thermodynamics and
I don't argue that. The total energy inside a
closed system remains constant. It's a law. If I didn't believe in the
first law of thermodynamics, you'd have me written
out on a rail. I would be the ultimate heretic and zealot and I
would be discredited. Of course, I believe
in the first law of thermodynamics. It's a law. The question is, as
I've learned from my legal training, whose truth? Which interpretation? The Supreme Court always comes down five, four on everything. True. Because there are
two interpretations. I mean, basically, that's
what the Supreme Court's for, is interpreting the law.

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The law is the law, but the interpretation
is something else. Here are the two interpretations. If you eat it, you better burn it or you're
going to store it. If that's true, then this is
a matter of energy balance. That's what everyone
will tell you, and it's the result of
two aberrant behaviors, calories in, gluttony,
calories out, sloth, and that's what everybody assumes is,
if you're obese, well, you must eat too much or
exercise too little or both, and therefore, it's your fault. That's what we believe
and to this day, we still don't have insurance for obesity, although just today,
you know that the AMA finally said
obesity is a disease. This is funny because
actually in 2004, HHS said obesity was a disease. It took the AMA nine years to catch up with HHS.
Figure that out. It's based on this dogma. The dogma is that if you eat more than you burn,
you'll gain weight. If you eat less than you burn, you'll lose weight because
all calories are the same.

A calorie is a calorie. This is the biggest pile of, you know what? There is. This is absolutely not true. But if you believe it, then the corollaries of a calorie are, that this is free will, you get to choose what you
put in your mouth. It's personal responsibility
because if you're obese, you chose to be. Gluttony and sloth, that's your problem and diet and
exercise will fix it. That's what everyone believes from a calorie is a calorie. Who says that a
calorie is a calorie? Well, the food industry says a calorie is a calorie and that's because it serves them well.

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This is the fiction, this is Coca-Cola's
coming together video on YouTube released just before the Super
Bowl that says, "Beating obesity will take
action by all of us based on one simple common sense fact. All calories count, no
matter where they come from, including Coca-Cola and
everything else with calories." A calorie is a calorie.
Why pick on Coca-Cola? Why pick on Burger King? Why pick on any individual
because it serves them well, because it diffuses the issue?
Is that what we've got? We've just got a
caloric bacchanalia. Sorry, wait, this is
wrong. That's better. Indeed, we are all eating more, I don't argue that; 187
calories per day more for men, 335 calories per
day more for women, 275 calories more per day for teen boys than 25 years ago. We are all eating more, I don't argue that,
of course, we are.

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The question is why? So you'd
say, well, this is why. This is the evolution
of fast food over here. 1957, we have the original
White Castle hamburger, 210 calories right
there, one ounce. Over here, we have today's
Bob's Big Boy over here at 618 calories, and of course, in the midst of the
obesity epidemic, Hardee's had the
temerity to offer us the thickburger at
1,420 calories.

Of course, you can
go to Carl's Jr. and get the six dollar burger, which is 2,000 calories. That's the entire caloric
allotment for the day, and people are proud to go do it. Anybody here had a
Trenta? Yes, no? So that's this guy over here, so it's not hot coffee, it's a cold coffee drink
flavored with, you know what? It is 916 cc's. Well, your stomach is 900 cc's, it's bigger than your stomach. You'd say, well, there's your answer,
QED, it's all over. How about this? I love this. This came in the
mail, free chicken sandwich from KFC with the
purchase of a 30 ounce drink.

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The food's gotten so
cheap, we're giving it away, that's where we are. Or is it the opposite
side of the equation? Is it an activity famine? This is a study that was done looking at physical activity here on the y-axis against age, nine-years-old to
19-years-old for white girls and black girls, and you can see that by
the time they hit age 15, the black girls are just
lying prostrate on the floor because there is no physical activity whatsoever.

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So you say, well,
there's your answer, that's why everyone's
obese because they're eating too much and they're exercising too little; gluttony and sloth,
diet and exercise, just like common sense tells you. Well, you know what? I don't
believe in common sense. I believe in data, and
that's why we do research, because education consists mainly of what we have unlearned. In fact, if everything
that we knew were true, there would be no reason
for research, would there? I would never have to
do any research because everything we knew
was already right. In fact, everything we learned 10 years ago
is already wrong, and everything we know today will be wrong 10 years from now, and that's why you do research, and the fact is
the research tells us something very different.

Is this behavior? Is it personal responsibility?
What do you think? There are six reasons
to doubt this. Number one, no child
chooses to be obese. The quality of life of
an obese child is the same as a patient on
cancer chemotherapy. Why would anyone choose this? In fact, children are ostracized. Second, does diet work? Now, everybody knows
somebody who lost weight on a diet and then of course,
they gained it all back, and that's what all
the data shows. The number of people
who can actually maintain their weight loss for any length of time is
vanishingly small. If that weren't true, you wouldn't be sitting here listening to me
because you'd say, "Well, why do I have
to listen to him?" Does exercise work? Here are studies of exercise, and this is the
identity line here, and you can see when
compared with no treatment, exercise resulted in very small weight loss
across the board, one BMI point, vigorous
exercise, 1.5 BMI points.

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Considering we are all 78 BMI points more
than we should be, that ain't going
to cut it because exercise does not
cause weight loss. What does exercise do?
It causes muscle gain, and that's good because
muscle have mitochondria. Mitochondria burn energy, so
you stay insulin sensitive because you have a place
to put your energy instead of in your liver
where it causes problems. Exercise is the
single best thing you can do for yourself but if you think it's going to show
on the scale, think again. When you stand on the
scale, what do you measure? You're measuring four
compartments at once; bone, more is better, muscle, more is better, subcutaneous fat, more is better, I just showed you, and finally, visceral fat, more is worse. Now, the visceral fat
usually encompasses about 46 percent of
your total body weight. When you stand on the scale,
what are you measuring? You don't know. You
can't possibly know. We have all these doctors
telling their patients, well, if you'd only exercise,
you'd lose weight, and then of course, they don't because they've built
muscle, which is good, but it doesn't show
up on the scale, and then they get
depressed because, "Oh, I was doing this to lose
weight and it didn't work, and so I might as well stop because obviously, it
doesn't work for me." This is the single most
egregious thing doctors do to their patients today,
and as far as I'm concerned, that's almost malpractice
because the data say otherwise.

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Number three, this isn't
just about America, and it's not just about the UK, it's not just about Australia. Yes, we are the three
fattest countries and we spend the least amount
of our GDP on food, that's true, but it's going
on everywhere, every country. Every single country
on the planet has shown an uptick in obesity. Some have shown an uptick in diabetes and some have
shown a downtick, but for obesity,
everybody's gone up. It doesn't matter where you look. Every country has
shown an increase. Number four, the poor are
disproportionately affected. They don't have
access to choices. They can't even leave their
house for fear of crime. How are they going to exercise? How are they going to leave
the kids out to go play in the yard when they might
face a stray bullet? They don't have supermarkets. They live in food deserts. If you don't have a choice, how can you call it
personal responsibility? This is one of the most egregious pejorative statements
that there is.

Number 5, the prevalence
of obesity is going up in the group that you can least ascribe personal
responsibility to. The toddler, the
2-5 year-old group is going up the fastest. You want to say that that's
personal responsibility, or you say it's the
personal responsibility of the parent for letting them have the sugar pops and the sodas and the fruit juices and everything else,
it's the parent's fault. Except for one thing, we've
been having epidemic of obese six-month-olds and they
don't diet and exercise.

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Any hypothesis you
want to proffer, you have to explain this as well. It's even worse than
that because we have obesity in newborns. Birth weight's gone up
by 200 grams all over the world over the last 25 years. When you do DEXA scans
to figure out what the body composition
is, it's all fat. These babies are
laying down more fat before they're ever born and fat cells want to get filled. That's why we have
obese six-month-olds because everybody's
laying down more fat. The question is, how? Why? Why they're laying
down more fat today? Most clearly mother's diet. But you want to blame the
newborn for that problem? Is that their problem? Is that their fault? You want to blame
the pregnant mother. Well, then, it just goes
backwards like that. You basically blame
everybody or blame nobody. I blame nobody. Actually,
I do blame somebody. We're going to get
there at the end.

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We're talking about behavior. This is the definition
of behavior, this is all from
the original video, a stereotyped motor response to a physiological stimulus.
Let's take that apart. Stereotyped, same every time, so yes, eating is a behavior. Motor, muscles have to move. A thought is not a behavior. Finally, physiological, and
that's where I come in. What's the physiology behind
the obesity epidemic? Why do you eat too much
and exercise too little? All behaviors have a
biochemical basis. Now sometimes we're smart
enough to know what it is and sometimes we're not smart
enough to know what it is. Give me an example.
Schizophrenia.

For a 100 years, schizophrenia was
behavioral disorder. Now, we know it's a defect in dopamine neurotransmission and probably actually a defect in glucose transport
across the brain. These are biochemical
problems that ultimately manifest themselves as
a behavioral disorder. This is no different. What are the biochemical
underpinnings behind gluttony and sloth?
That's the question. That's what we're going
to try to answer now. In order to answer
that, you actually have to know some science. I'm gong to make this very
brief and very quick. We're going to talk
about these two hormones right over here called
leptin and insulin. Leptin is a hormone that
comes from your fat cell, goes to your brain,
and tells your brain, "You have enough energy
on board to engage in normal, expensive
metabolic processes.

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You can burn energy at a normal rate and
feel good doing it." It tells your brain, "You've
got enough energy on board." If your leptin goes down or if your brain doesn't
see your leptin, then your brain sees that as starvation. Everybody got that? Insulin is equally interesting because insulin tells your
fat cell one thing it says, "Store energy" and it tells
your brain something else. It tells your brain, "Stop. I'm in the middle of metabolizing a meal I don't need anymore. Let me deal with what I got." It's part of the satiety signal.

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It tells your fat cell, "Get bigger" and it
tells your brain, "Stop feeding your fat cell." It's got a dichotomous role and it's that dichotomous role, that is the linchpin in
terms of understanding the physiology of obesity. I'm going to go there. Here's how it works. We have to explain a paradox.
Here's the paradox. Who has children? Enough of you? What happens if you give a
five-year-old kid a cookie? They eat it. Yeah, they eat it. Yeah,
I know they eat it, yeah. What happens after that? They bounce off walls
is what they do. Ask any kindergarten
teacher what happens when the cupcakes roll out
for the birthday party. That's the end of the lesson.

They're bouncing off walls. It's known as the sugar high. What's going on? The fat cell gets filled because
of the cookie. The leptin goes up,
tells the brain, "Hey, I've got extra
energy on board." It tells the sympathetic
nervous system, the fight or flight part
of the nervous system that innervates your muscles and innervates your fat cells, "Hey, I got too much
energy." What happens? You burn it off. The
sympathetic nervous system tone to the muscles give
you the fidgeting, and the sympathetic nervous
system tone to the fat cells releases the extra fat and that gets used
for energy later. This is a nice negative feedback pathway
that keeps you in energy balance as long as your
brain can see its leptin. So far so good.
Here's the paradox. What happens if
you give an obese, five-year-old kid
a cookie instead? They're in the pantry
looking for more cookies.

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Anybody ever see a sugar high in an obese kid? It doesn't exist. That's why they're obese is because they don't
get the sugar high, because they can't
see their leptin. If they could see their
leptin, they'd have a sugar high, but they don't. That's the point.
Something's blocking that leptin signal.
That's the paradox. The question is, what is it? We learned about leptin from
this patient over here.

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This is the OB/OB mouse, the leptin-deficient
mouse who has a gene defect in the leptin gene. This animal's leptin is zero. His brain thinks he's
starving all the time. He'll eat anything in sight. Not only will he eat
anything in sight, but this animal is the
ultimate couch potato because his brain
can't see his leptin, so he thinks he's starving, so he doesn't want to burn energy, he wants to store it. The only reason this animal ever gets off his high knee is you put the food on
the other side of the cage and they'll
waddle over to that, sit down, eat it there, and stay there instead.
Everybody got it? Now the reason? Because leptin tells
the hypothalamus that, "You've got the energy to burn." If the hypothalamus
sees the leptin signal, then this diamond over
here gets activated.

Anorexigenesis, that
is, "I'm not hungry, I don't need anymore and I
can burn energy effectively." It tells the sympathetic
nervous system, "Turn on to fidget" and to
release fat from the fat cell, and it tells the vagus nerve, the energy storage nerve, "Hey, I'm not hungry. Appetite down and stop releasing insulin."
Everybody with me? Conversely, if the
leptin doesn't reach the hypothalamus because there's a gene deletion or because
there's something blocking it, then you get this diamond
instead, which is orexigenesis. "I'm hungry. I need more food
because I'm starving, and because I'm starving, I'm going to try to conserve." That means your
sympathetic nervous system tone goes down, which means you
sit on the log and your vagus nerve goes up
to increase your appetite so that you'll generate more
calories in order to put more into the fat cells to try to get more of a leptin signal.

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Everybody with me? This is that same negative
feedback pathway I showed you before, now schematized. There are
leptin-deficient people. Fourteen at last count, and they're all of consanguineous
marriages and they're all of Pakistani or
Turkish ancestry. When they're born, they're
perfectly normal weight, and by age six months, they are already
massively obese because their brain is
constantly starving. It doesn't matter how
much weight they gain, their brain can't see it
because it ain't there, because they have a
leptin gene defect. Here's a patient, 220
pounds by age nine. You start giving them shots of leptin every day and
look what happens. They lose weight
on a dime and it's all fat mass that
they're losing too. Hormone replacement
therapy because now their brain can see leptin because we're giving
it to them from a bottle instead of from
their own fat cell. Hormone replacement therapy, that's what I do as
an endocrinologist.

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That's my job. Here's an example. Here's the patient at three-and-a-half years of
age looking pretty awful, and here's after shot of leptin
every day for four years. Indistinguishable from normal because we
fixed the problem. Great for those 14 people. The problem is the rest of
us are not leptin-deficient. The rest of us are
leptin resistant. We got boatloads of leptin and the leptin correlates with
how much body fat we have. If our brain could
see that leptin, we wouldn't be obese. We'd burn it off in the sugar
high. Everybody got it? There's something blocking that signaling right there, that X. That's the holy grail
of obesity right there. What is blocking
leptin from working? If your hypothalamus
can't see it, then you are in this box
over here and you can see things just go in
the wrong direction. There's your gluttony
and there's your sloth. This is all biochemical. What role does insulin play in this leptin debacle?
That's the question. Remember I told you,
insulin tells your fat cell one thing and your brain
the exact opposite.

It tells your fat cell store
and it tells your brain, stop. That's the problem. This is the patient that got me started in obesity research, now 18 years ago, when I worked at
St. Jude Children's Research Hospital in Memphis. This was a 15-year-old
boy who weighs 364 pounds in this photo. At age of seven, this kid was perfectly
normal weight for height. Then he developed this
brain tumor sitting in the middle of his
energy balance pathway, and he required surgery and
he required radiation to kill this astrocytoma,
tumor of the brain. He started gaining weight at the rate of 30 pounds per year, nonstop for eight years until he was 364 pounds when I saw
him. Everybody with me? Now, this form of
intractable obesity due to a brain lesion, now, that area of the brain that controls this energy
balance is dead.

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You can have all the
leptin in the world, but if those neurons are dead, your brain thinks
you're starving because it can't transduce that signal. This is called
hypothalamic obesity, and this is how I got started in obesity research
many, many years ago. The question is, how
does this happen? Well, here are two
different hypotheses. This hypothesis says, when
you damage the hypothalamus, you get obesity because it
releases a satiety center, so now you become hyperphagia, except the data actually
doesn't support that. Data does not support
that there's hyperphagia, that there's too
much food intake. Actually, it supports that
there's too little burning is what it shows, and that the obesity
occurs, and then, because of the obesity, you have to secrete more
insulin to attend all that fat, and so that the insulin here
is a result of the obesity.

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But there's this
other hypothesis over here that says the damage
to the hypothalamus, yes, it leads to obesity, because it turns on that vagus nerve, because you can't
see your leptin. When you turn on the
vagus nerve, that tells your pancreas to
release more insulin, and that extra insulin
drives energy into fat, energy deposition, not
energy balance because of the high insulin
and the insulin is driving the obesity,
which is true. If this is true, nothing I can do about it because I
can't fix a brain. If this is true, it gives me a place I could
potentially intervene, right between the vagus
nerve and the pancreas. We have a drug that does that, and it's called octreotide. It's an endocrine drug
that I know how to use.

We asked the question, if we take these kids who have this
intractable obesity due to brain tumors and we
give them this drug to suppress their
insulin, might it help? That was the question.
Here's that same patient I showed you, 364 pounds, and here he is a
year later at 326, first time he took a
picture with his shirt off. It did pretty well. I'm going to show you the
piece de resistance over here, this isn't even my patient. This is a beautiful
13-year-old girl from Hawaii, notice the flower, who, a month after this
picture was taken, was in a very severe car
accident on a Honolulu Road. She was in the intensive
care unit for about a month. She survived, but she
stroked her hypothalamus, and so this is her a year later. Now, does anybody want to tell me that this is
gluttony and sloth? This kid now can't see her leptin because
those neurons are dead. Now, it just so happens
I happened to be giving grand rounds at Kaiser
Honolulu in 2008. They invited the patient than her mother to come to the
talk because they were thinking about putting this kid on octreotide even
though she didn't have a brain tumor because she
might have the same disorder, and so there I am with her, and here she is a year
and a half later on the drug at her high
school graduation.

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Now, who here wants to tell me that this is
gluttony and sloth? Do I have your attention? It's never gluttony and sloth. It's always biochemical.
The question is, are you smart enough
to figure out what the biochemistry is? We said, maybe this
could be true in adult obesity
without brain tumors or without hypothalamic damage. We did two studies, double-blind,
placebo-controlled. This is a patient, adult, Christmas 1998 holding up food, and here she is 35
pounds later in her jogging tags showing me
that she wanted to exercise. She actually wanted
to exercise and the reason was because
she wasn't storing it. Because her insulin went down because the drug
suppressed her insulin. When her insulin went down, she had the energy to burn and she wanted
to, and she did, and she's showing
you right here that the change in the biochemistry
changed her behavior. The biochemistry
drives the behavior. The cause of leptin resistance, that X up here, it's insulin. There's actually numerous studies now, biochemical,
molecular, genetic, that show that insulin blocks leptin-signaling by acting on the same neurons in the
brain as leptin does, and that's the point: insulin
blocks leptin-signaling.

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Now, why? What's in it for us? Why would God do this to us? The answer is because there are two times in your
life you actually have to gain weight.
What are they? Pregnancies. Pregnancy is one,
and the other is? Puberty. Puberty and pregnancy, both necessary for survival
of the species. If your leptin worked
right all the time, you could never gain the weight because you'd be
in the sugar high, you'd be burning
it off before you ever had a chance to
actually gain the weight. You'd be the 97-pound weakling
on the beach who couldn't bulk up and the
species would die out. There are two times in your life you actually have to gain weight, and both puberty
and pregnancy are insulin-resistant states
where your insulin goes high very specifically
to cause the weight gain, then you cut the
cord, baby's out, sex hormones go back down, the insulin resistance goes away, you'll lose the weight and
you can start all over again.

It actually makes
perfect Darwinian sense that insulin should block leptin, twice in your life. Twice in your life, insulin should block leptin. Problem is, now it blocks
leptin all the time because our insulins
are high 24/7, 365. The question is, how come? Where did the increased
insulin come from? That's the question, that
64 zillion dollar question, why are we all
hyperinsulinemic today? If you look at glucose
tolerance test done today versus ones that
were done 35 years ago, we're releasing double to
triple the amount of insulin today that we were 35 years,
and the question is why? I'm not going to tell you. I'm going to let
Will Smith tell you. What? Guess I owe you
some answers, hoss. What, you're feeling
chatty all of a sudden? Sorry, I can't talk right now.

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I got some secret cases
of my own I'm working on. I hate to tear you away
from your video game. All right, I'm hanging up. You know the most destructive
force in the universe? Sugar? If Hollywood knows
this, why don't you? Indeed, he's got it right. We know that there are
substances out there that are addictive and
hazardous to our health. Here's a perfect example, and we regulate it.
Well, guess what? It's not the only one. This is too, and I'll show you why. These are the two papers,
popular press items. This was from the New York
Times magazine in 2011. Is Sugar Toxic? from Gary Taubes based on
our work here at UCSF. This is a comment that
we had in nature, last year that got quite a
bit of heat more than light, unfortunately, called
the Toxic Truth About Sugar that I wrote
with my colleagues here, Laura Schmidt and
Claire Brindis at the Institute for
Health Policy Studies. Hazardous to your health. The reason is because
that common sense notion, a calorie is a calorie, it ain't true, because, a
calorie is not a calorie.

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What are we talking
about? Here we're talking about this stuff called
high fructose corn syrup. Fifty percent
fructose, so they say, there are actually some
studies that suggest that dispenser sugar, like from McDonald's or
Burger King or 7-Eleven might actually have 65
percent fructose sometimes. That would be a problem. But most of the time,
it's 55 percent, one glucose, one fructose, six-membered ring,
five-membered ring. Now, this stuff is
essential for life. Every cell on the planet utilizes
glucose for energy. It's so important that if you don't eat it, your body makes it. That's how important it is. This guy over here is
completely vestigial. There's not one
biochemical reaction in the body that requires it, but it's very sweet
and we like it a lot. The question is, what
do we do with it if we don't need it for any
biochemical reaction? That's one of the key questions.

But over here is sucrose,
this is table sugar, cane sugar, bee sugar,
the stuff you put in coffee, one glucose, one fructose, or
glycocidic linkage, linking the two, the enzyme in your intestine sucrose that cleaves this in
about a nanosecond. When you absorb the two moieties, they are exactly the same and that's what all the data say, is that they're exactly the same. High fructose corn syrup and sucrose are metabolically equal. Metabolically bad. Metabolically equally bad. This is what our
consumption of fructose, so double it for sugar, has done over the last 100 years.

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Our ancestors getting fruits and vegetables
out of the ground with the occasional honey
got about 15 grams of fructose per day
prior to World War II, with the nascent
candy and soft drink in the streets in the country, we got up to about
20 grams per day. By 1977, we got up
to 37 grams per day. This is just before high
fructose corn syrup invaded our shores at eight percent
of total caloric intake. By 1994, we were up
to 55 grams a day. That was 10 percent of
total caloric intake. Adolescents currently
consume 75 grams per day. That's 12 percent
of caloric intake. Twenty-five percent of
adolescents consume 100 grams of fructose per
day. Double that for sugar. That's 200 grams of sugar, multiplied by 4.1
calories per gram, that's 840 calories in sugar.

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For a 2,000 calorie allotment, that's 40 percent of
calories of sugar. The question is,
can you handle it? Can your liver handle it? Can you metabolize all that sugar before something bad happens? Remember what Paracelsus told us. The dose determines the poison. Could this be an overdose? Could that be hazardous
to your health? Indeed. As far as I'm concerned, our entire food supply has been adulterated,
fructose related. Because of the addition of
fructose for palatability, especially with decrease fat, and also sensibly as
a browning agent. Because food browns
better, right? You painted on your barbecue
ribs to brown it better. The caramelization
actually, we like that. The removal of fiber for
shelf-life and freezing. We also have substituted
trans-fats but those coming down because we
know those are poison, although they're still legal
and they're still on the generally recognized as
safe list at the FDA. Figure that out. Because
we know they're poison. Now, does sugar cause
obesity? Yes, no? Food industry will tell you
everything causes obesity and you know what they're
right.

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It's true. Because if you look
at this study from Mozaffarian and at Harvard
School Public Health, looking at what foods cause
the most weight gain, potato chips and french fries. Indeed, I agree with that. Those are the bad guys
in terms of weight gain. Sugar, distant third. When a meta-analysis was done earlier this year from
the University of Otago, you'll notice the diamond doesn't cross the identity line. That means that it's significant. There is a significant
increase in weight. But when you actually
do the math, it's only 0.8 BMI points. Remember I told you, we got seven or eight BMI
points to deal with. Does sugar cause weight gain? Yes. Does sugar cause
obesity? A factor. Is sugar the cause of obesity? Not even remotely close. The problem is, it's
not about obesity. Remember it's about
metabolic syndrome, and that's where the money goes.

I don't even care about obesity. What I care about is people getting sick because
I'm a doctor. Here's the problem. Common
wisdom says that sugar is just empty calories
and you can get your discretionary
calories from anywhere. The problem is that hepatic
fructose metabolism is completely different
from that of glucose. This is what the first
YouTube video went into in exhausting detail and
I will not repeat it.

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But I'm going to show
you very quickly that chronic fructose exposure alone promotes the metabolic syndrome. This again is from
that first video. When you consume glucose, say rice, white bread, starch, 80 percent of the glucose goes to all
the organs of the body. Only 20 percent hits the liver. Where does it go? It goes to this guy over here, glycogen. Glycogen is liver starch. Liver starch, for lack of
a better word, is good. Because that's your energy
store for a rainy day. That's the first energy
that's used when you fast. That's why marathoners carb-load
before a marathon race, is to try to build up their glycogen stores because
glycogen is non-toxic.

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If you can up your
glycogen stores, your liver has more energy in reserve, and
that's a good thing. Now, a little of it will
sneak down here and get metabolized by the
mitochondria and throw off a little of this
stuff called citrate, and that will then get
turned into liver fat. This process here
in orange is called De novo lipogenesis,
new fat-making. This is how your liver turns
carbohydrate into fat, is through this process here. But you're not dealing with very much carbohydrate here
because it all went to glycogen and most of it actually got metabolized elsewhere anyway. Your liver is protected. Everybody see that? Your
liver is protected. This is for lack of a
better word, is normal. Let's talk about something
that's not normal. This guy, alcohol,
that's not normal. Carbon, hydrogen, oxygen. But alcohol is a toxin, right? It's two toxins in one. You wrap your Lamborghini
around the tree, acute alcohol toxicity,
and you fry your liver.

Chronic alcohol toxicity. We keep it out of the
hands of children. Here's acute alcohol exposure. Here's acute sugar
exposure, none. Why? Because the brain doesn't
use fructose for energy. It does use alcohol, but it doesn't use
fructose for energy. You don't get any of those CNS symptoms because it
doesn't get there. Let's consume the same number
of calories of alcohol. Now, most of them go to the liver instead of going
to the periphery. What happens to it? You see glycogen anywhere? No glycogen. It by-passes glycogen and goes
down to the mitochondria, and since there's so much of it, you get big-time fat-making and some of it won't make it out. Now, you get that lipid droplet, that's alcoholic steatohepatitis. You're going to make
lots of triglycerides, and so you're going to
have hypertriglyceridemia and that's going to
end up in the muscle. Now, I've got muscle insulin
resistance and it serves as a substrate for
weight gain as well. We also know that alcohol has this inhibiting
effect on your brain, which causes you to drink more. Oh, I'm just going
to have one drink and you end up with five.

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Of course, if you
do that too often, maybe you'll even
become an alcoholic. That's addiction right there. Positive feedback effect. Here's a problem because
this is toxic and abused. We regulate it. Now
let's do fructose. We're going to consume sugar now, we going to consume orange juice. Same number of calories. The glucose does the same 20-80 split it did
before 12 and 48, but all the calories from fructose are going to
go to the liver because only the liver has the transporter for
fructose called GLUT5. You see glycogen anywhere? No glycogen. Go straight
down to the mitochondria, just like alcohol did. Because there's so much of it, your mitochondria
have no choice but to turn the excess into liver fat. There's your lipid droplets. Now you've got nonalcoholic
steatohepatitis. You've got high triglycerides, just like you did with alcohol. You get the muscle
insulin resistance, substrate for obesity, and it tells your insulin
receptor not to work. Now you've got liver
insulin resistance, which makes your
pancreas have to make more insulin in order to
make delivered to its job.

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Now the high insulin
goes to the brain, blocks leptin, and now you
can't see your leptin. What does it do? It makes
you think you're starving. What does it make you do?
Consume more fructose. Now, you've got a
positive feedback effect between a compound
that's toxic and abused, causing damage to the liver, damage to the
pancreas eventually, and damage to the brain. But we don't do
anything about that. You would never think about
giving your kid a beer, but you don't think twice
about giving your kid at Coke and they do the same thing. That's one problem. Now,
there's a second problem. Here are five photographs. What do they all have in common? There's one thing they
have all hung come, they're all brown.
Good, thank you. They're all brown. This
is the browning reaction, for the maillard reaction. Anybody you know what
hemoglobin A1c is? That's the lab test they do for diabetics to see how the
blood sugar control is. That's glucose binding to
proteins in the blood. Well, that's what this is. This is the maillard
reaction: glucose binding to proteins
in the actual food.

The common link is
this browning or maillard reaction or
non-enzymatic glycation. Here's the deal. You can
think of it this way. You can roast your meat at
375 degrees for an hour, or you can roast your
meat at 98.6 degrees for 75 years, the
answer is the same. We all brown. It's part of aging, it's normal aging,
and everyone does it. The question is, how
fast do you do it, and if you don't believe
me, here's just an example. Here's newborn rib cartilage
nice and white and here's 88 year old rib
cartilage nice and brown, and if you had orange juice this morning, you
are browning faster. That's the deal.
That's what we know and we know it, and
we know it's true, because every time
this reaction occurs, you release a hydrogen peroxide, and that hydrogen
peroxide does damage inside the cell unless it's
quenched by an antioxidant, and if you don't take
enough antioxidants, you're going to do
damage and that's what nonalcoholic
steatohepatitis is. Here's that reaction. Here's the aldehyde of
glucose and it binds to the amino group of lysine
off the hemoglobin molecule.

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It forms what's known
as a shift base which then decomposes and develops this amid linkage here
and bottom line is, it's non-enzymatic and
it happens all the time. The question is how much, and this shows that it's very, very specific to fructose
in terms of amount. This is an animal model of non-alcoholic fatty
liver disease called methionine-choline
deficient rat, the MCD rat. Not the McDonald's rat
but it might as well be because what happens is when you give
the animal sugar or starch with normal amounts
of methionine-choline, no problem, the
liver can handle it, but if you're deficient which happens when you have a bad diet, then only sugar causes the
problem, starch doesn't, and you can see here in a nonalcoholic fatty liver disease clinic at
Duke University. This is Doctor Manal
Abdelmalek's work showing that the greatest steatosis
or fatty liver is dependent on how much
fructose consumption, whether it's daily or not and the stage of
fibrosis, same thing.

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So two problems; fatty
liver and cell aging. So far, so good? All right, so now we're going to
get into the weeds. Here are the 10 most obese states in the nation. Anybody surprised? Anybody from any of them?
I used to live in Memphis, you know what I'm
talking about, right? North Carolina. North Carolina, you know what
I'm talking about, right? I'm turning to those
ribs. Yeah, I know. Ten most of these states. Here are the 10 laziest
states in the nation. What's going on over
there in Nevada? I guess you can only burn so much
energy going like this. Here are the 10 most unhappy
states in the nation. Here's the adult diabetes rate, here's the adult
heart disease rate, and finally, here's soda per capita consumption.
Now, what do you see? Coke. Pretty significant
overlap, wouldn't you say? Yeah. Well, now this
is correlation, not causation and I'm very
clear on the difference. We're going to talk
about the difference. The question is, which
direction does it go? Is it that soda causes
heart disease and diabetes or is it
that people with heart disease and diabetes
like to drink soda? You can't tell, because
it's one snapshot in time, you can't tell which
way the data went.

True. Here's what's
happening worldwide. This is global consumption
of sugar and sugar crops. Here we are at 629
calories availability here in blue and here's
the rest of the world. Now, the American
Heart Association says 150-200 calories in added sugar per day right here,
this color blue. How many countries
are above that? How about all of them?
In fact, that's why diabetes is skyrocketing
everywhere. Here's world sugar consumption tripling over the past 50 years. Per capita consumption,
notice Brazil. Brazil used to be a poor country. They were always
a sugar exporter, but they couldn't
afford their own sugar, but now they can because
they're a BRIC country.

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They sell Embraer
jets and biodiesel and World Cup, and
all that stuff, and the fact is that Brazil
now has the highest increase in rate of prevalence of type
2 diabetes in the world. It doesn't have the
highest prevalence. That's reserved for
Saudi Arabia, Kuwait, United Arab Emirates, Qatar,
and Malaysia. Why them? Why do they have the highest
diabetes rates in the world? No alcohol, but they got soft drinks like they're
going out of style. Why? Because it's hot
and the water supply is a question mark and no alcohol. This is their reward. Now the difference is alcohol, for lack of a better word, is self-limiting, because
you end up under the table, but soft drinks, you can drink them all day, and they do, and that's
why they have diabetes. Now, how do I know that the
sugar cause the diabetes? Because correlation
is not causation, but we have causation too
and this is our work.

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It just came out
three months ago. I'm very proud of it. Sanjay Basu, one of my colleagues at Stanford
Prevention students and I took four databases and
melded them together. We took the Food and
Agriculture Organization or FAO statistics database from the World
Health Organization which for the whole decade, 2000-2010 which has food
supply as total calories, fruits excluding
wine, oils, roots, tubers, pulses, nuts
and vegetables, meat, cereals and sugar,
sugar crops and sweeteners as separate items. We then link that to the International Diabetes
Federation statistics database for diabetes prevalence
worldwide for the decade, and then we linked
that to the World Bank gross national income database to control for GDP, urbanization and aging,
and then we linked that to a physical activity database to control for
physical inactivity, and we asked the question,
what about the world's diet? Predicts diabetes prevalence
change over time worldwide. That was our question.
Everybody with me? Here's what we did:
204 countries, we had complete data for 154, the 50 that we did not use
were no different from the 154 by a very fancy
set of statistics, and we did a lot of statistics.

This is called an
econometric analysis. Now a standard percent versus percent would be called
an ecological analysis. This is not an
ecological analysis, this is an econometric analysis. This actually won two economists Nobel Prizes for
being able to predict stock market crashes
based on what's happening before to predict
what happens after, because there's causational
inference in this. Generalized estimating
equations with a conservative
fixed-effects approach called the Hausman test, a hazard model to control for selection bias called
the Heckman test. This is the important one. Since we had the whole decade, we didn't have a snapshot. We had the movie and
you can learn a whole lot more from a movie than you can from a snapshot, can't you? That's called the
Granger causality test because we can determine
what came first. Because you can't
infer causation if something didn't come first. Proximate cause. You need proximate cause, and period effects to
control for secular trends. We did all this really, really neat statistical
analysis and Sanjay Basu was an
absolute genius. What we did was a control for GDP obesity, urbanization, aging and physical activity,
so the question was, is it the obesity or is it something specific
in the food supply? That was the question.
During the decade, diabetes prevalence rose from 5.5-7 percent
worldwide.

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Not good. Here's the effects model. Sugar, sugar plus controls
plus period, bottom line. Remember that diamond that
can't cross the identity line? Well, it doesn't. It's very significant. In fact, for every 100 calories, you increase your
diabetes prevalence worldwide by 0.8
percent and here's the adjusted association when you took all the
factors into account between sugar availability
and diabetes prevalence. Here's what you
need to take home. This is the take-home slide.

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Only changes in
sugar availability predicted those changes in diabetes prevalence
worldwide only. If you consumed 150 calories extra per day in total calories, diabetes prevalence
only went up by 0.1 percent. Nothing. But if those 150 calories
happen to be a can of soda, diabetes prevalence
went up 11-fold, 1.1 percent, and we're
not consuming one can of soda per day, we're
consuming two-and-half. So that's 2.4 percent. Given that American diabetes
rates are 8.3 percent, that means that 26 percent
of all diabetes in America today is due to
sugar and sugar alone. Not due to obesity, not
due to total calories, sugar, and sugar alone. You want to do something, you want something actionable, you want something
that's going to change how much money we spend so we can salvage
Medicare, here it is. Of course, our government is
doing absolutely nothing. Our data show that 25 percent of diabetes worldwide
is explained by sugar. More importantly, this is causation because these
data meet what's known as the Austin Bradford Hill criteria for what we call
causal medical inference.

Now, what does that mean? It means that you can
show dose effect, you can show duration
effect of sugar on diabetes and you can show most importantly
directionality. That is, those countries
where sugar went up showed an increase in diabetes
rates, those countries, the few of them where
sugar went down, showed decreased diabetes
rates and precedence. Three-year time differential. So every country when
their sugar went up, three years later you
saw the change in diabetes in either direction. That's causal medical inference. Now, it's not scientific proof. There are different
kinds of proof. There's anecdotal data which of course is absolute garbage, and you can't do
anything with that because an N of 1 means nothing. Then there's correlation but correlation suffers from this
directionality question, which came first because it's a snapshot and
you can't tell. Then there's this thing called
causal medical inference. We're going to talk
about that right now. Then there's this thing
called scientific proof that everybody keeps harping on. In medicine today, what
percentage of what we know is scientifically based, evidence-based, scientific proof, randomized controlled trials? That's the standard.

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How
much of what we know, what percent of what we know today is due to scientific proof? What do you think? You want to give
me a percentage? Five. Ten. Ten, good. Ten percent of what we know is due to
randomized control trials. That means 90 percent
of what we know is causal medical inference. So here's a question. What
level of proof do you need? You tell me. Who here
believes in global warming? Why? Got any proof? [inaudible] Causal inference? Can you a randomized controlled
trial and show me that that's what's going on? No. Who here believes that football trauma
causes Alzheimer's? How come? You got proof? No, [inaudible] Causal inference. Who here believes that
tobacco causes lung cancer? How come? You got proof? Who's done the randomized
control trial where you take naive people
and expose them to cigarette smoke for
the next 50 years and see what their
lung cancer rates are.

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Number one, it would
be too expensive. Number two, it would be damn
unethical, wouldn't it? In fact, most of these studies
would be damn unethical. You ever think we're going to get the actual scientific studies, the scientific proof for
sugar causing diabetes. Number one, nobody's got a
zero baseline, nobody's naive. Number two, this is
something that happens over 40, 50, 60 years. How are you going
to keep people on the same diet for that long? How are you going
to figure out what they actually ate when we can't even figure
it out after one day? Don't you think it'd be a little unethical to do that to people? You'll never get this data.

But of course, the
food industry says, well, we don't have the data, we need more research. We always need more research. Of course, we need more research. The question is, do we
have enough proof to act? Them saying we need more proof, is them moving the goalposts because we'll never get
enough proof for them. The question is, what do you think? Do you
think we have enough? We have causal
medical inference for sugar and diabetes.
Do we have enough? Yes. Is for you to decide. Addictive,
the last piece of this. Binging on high-calorie foods may be as addictive as cocaine or nicotine and could cause compulsive eating and obesity
according to a study. Here are all these
books that came out on obesity and addiction and reward.

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They're all popular books, based on no data. But what do you think? You think that science
could catch up to this? So here's neuroimaging studies, PET scanning of
dopamine receptors. Dopamine is the feel-good
neurotransmitter, the pleasure neurotransmitter
in the reward center here. Here's a control brain with nice hot dopamine
receptors, which is good. Here's a cocaine brain where
there had been damped down. This is the
neuroanatomic equivalent of the phenomenon of tolerance. Because dopamine down-regulates
its own receptor. So once this happens, you need more substrate
to get the same effect. That's called tolerance. Then of course,
when you withdraw, now you get withdrawal
and you get symptoms. Everybody with me? Well, here's a control brain, and here's an obese brain. What do you see? Same thing. Not quite as bad,
but same concept. So this is the reward system. Here's the ventral tegmental area here where the dopamine
neurons live and here's the nucleus
accumbens where the dopamine information
gets received. How fast this gets transduced
has everything to do with what level of reward you achieve with any given stimulus.

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Whether it'll be power
or gambling or shopping or cocaine or alcohol or
for that matter, sugar. This just shows what happens. So here's that dopamine neuron and you see it's going
bleep, bleep, bleep. So you add nicotine and
you get more reward. That's basically what
we're talking about that's why people start smoking
and then, of course, the dopamine receptors go down then they can't stop smoking. That's addiction. Food intake is a readout
of reward because here's injecting morphine
into the reward center and you can see that as
the morphine goes up, the food intake goes up because food intake is a
readout of reward. You can see that all the
reward centers are all linked together into the nucleus accumbens including
the hypothalamus, which is the starvation
area, the amygdala, which is the fear area, and of course the reward area.

So hunger, reward, and stress, all reasons to eat and they all conspire against us
all at the same time. When we see a patient
in our clinic, that's the question
we ask ourselves. Is this patient obese
because they are hungry? I know what to do about that. Or is this patient
obese because of the reward system is defective
and they're addicted? That's a lot harder to deal with, but we know how to do that too.

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Or is this person eating
because of stress? Which is enormous problem,
especially in America. That one's a really hard one
because it's not the stress, it's the response to stress. If you think you're stressed, you're stressed whether
you are or your not. Most kids today are
stressed like never before. You know what stresses
them the most? Facebook. This is going on in every animal. See here's humans right
there, big dopamines. There are receptors here. When obese, dopamine
receptors go down. Here are bonnet
macaques, same thing. Here are rats, same thing. Bottom line, obesity means down regulation of
dopamine receptors, which means you need more food to get the same level of reward, or you might as well
crawl in a hole and die. That's what it's all
about. These people are eating because their
brain says they have to. The question is, is fast food addictive?
What do you think? Yes. Yes, no, what do you think? Yes.

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We actually looked
at that question. Everybody would be
familiar with this book? Michael Moss put this out. Salt Sugar Fat: How The
Food Giants Hooked Us. This is wrong. This is a
mistake because there's one thing not on the
list. What's missing? Caffeine. Now, we've
got fast food; salt, sugar, fat, and caffeine. The question is, of these
four, which are addictive? Let's talk about salt.
Is salt addictive? No, it's not addictive. In humans, the threshold
is physiologically fixed.

Higher levels are
attributable to preference, but you can alter
that preference. Lots of people do, especially when they have to
go low salt for some reason. We know because we take
care of a disease in endocrinology called salt-losing congenital adrenal hyperplasia, where their kidneys are
losing salt non-stop. But when we give them
the salt retaining hormone that works in the
kidney called aldosterone, their salt intake goes way down. If they were addicted,
that wouldn't happen. When we fix their physiology, their preference
gets a lot better. Salt, not addictive.
Now let's take fat. Is fat addictive?
What do you think? No. No. Rodents binge but show
no signs of dependence. Humans, they always
binge on high fat, high carb or high sugar items
like pizza and ice cream.

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You don't binge on high
fat per se, otherwise, the Atkins diet
would have everybody addicted and they'll tell
you they're losing weight. How could they lose weight
if they were all addicted? Energy density actually has a stronger association with obesity metabolic
syndrome than fat does. Fat, not addictive. We're
left with these two. Caffeine? Caffeine's addictive. If you take my Starbucks away
from me, I will kill you. Model drug of dependence, gateway drug, in fact.

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Dependence shown in children,
adolescents, adults. Thirty percent who
consume it meet the DSM criteria for dependence, and the physiologic addiction is well-established
with the headache and the test performance
and everything else. Mega addictive. But do you see anybody
going out and regulating Starbucks or pizza or
anything like that? Why? Because it's not toxic. It's addictive but not toxic. Unless you mix it with alcohol and then you
got something called Four Loko and that we're
banning. Everybody got it? When it's toxic and addictive, we ban it or we regulate it.

Caffeine, alcohol together,
that's a bad deal. But caffeine alone, keep
your hands off my Starbucks. Caffeine; yes, addictive.
That leaves this one. Sugar; is sugar addictive? What do you think? You know, we've known this for a long time. Anybody know what this is? It's called Sweet-Ease. This is a super concentrated
sucrose, sugar, solution that you dip the
pacifier in and you put in the newborn baby boy's
mouth before you do the circumcision because it releases opioids and
It deadens the pain. This has been known forever. Then you mix it
with a little wine and then you got a
real good cocktail.

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Is there really such a
thing as sugar addiction or we have to look
for similarities to other drugs of dependence like nicotine, morphine,
amphetamine, cocaine? The one I think is most
appropriate is alcohol, because after all, alcohol and sugar basically
metabolize the same way. Because after all, where
do you get alcohol from? Fermentation of sugar.
It's called wine.

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We do it every day
up in Napa Sonoma. The big difference
between alcohol and sugar is that for alcohol, the yeast does the first step of metabolism called glycolysis, for sugar, we do
our own first step. But after that, when the
mitochondria see it, it doesn't matter
where it came from. That's the point. That's
why they both cause the same diseases and they do the same
thing to the brain. The criteria for addiction
in animals are binging, withdrawal, craving, and then this one down here
called cross sensitization with other drugs of abuse.

That means that if you expose an animal to one
drug of abuse like cocaine for three
weeks and addict them and then you expose them to a second drug
they've never seen before, like say amphetamine, they're addicted
to the amphetamine even though they'd
never seen it before. Because the dopamine
receptors are already downregulated because they're the same dopamine receptors. Everybody got it?
Does sugar do this? Absolutely, QED, slam dunk, sugar's addictive in animals. What about humans? Who saw
this movie? Did you like it? Yep. More or less? I have
big problem with this movie because if
you watch the movie, his doctor, Morgan's doctor keeps saying,"You got to get
off this high-fat diet." Not the high fat diet, it's the high sugar diet. That's what caused
all the problems. Can sugar be addictive? Watch. I was feeling bad in the car. I was feeling really
sick and unhappy. Started eating, I feel great, feel really good now.

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I feel so good, it's crazy.
Isn't that right baby? Yeah, you're crazy all right. This was on Day 18 of his 30-day sojourn
through McDonalds. He just described withdrawal.
That's withdrawal. He needed another heap
in order to feel good again. He just
described withdrawal. He was a vegan, because his
girlfriend was a vegan chef. In 18 days, he's a sugar addict. You tell me. This is
what we're dealing with. We are dealing with an industry that wants us to
consume its product. Every industry wants us to consume their product in
some fashion or another. The question is, what
if it hurts you? Here, this is an example, this is the Federal
Trade Commission versus Sugar Information back in 1972. This was an arm of the
Sugar Research Association. The fat time of day; you're really hungry and ready
to eat two of everything, Here's how sugar
can help. Any data? They can advertise
any way they want, they're allowed.
How about this one? The birth of the Uncola, why we have the
youngest customers in the business, from 7 Up.

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You're okay with that? This was going on. How about this one? This was in Publix, the supermarket chain in
Florida just a year ago. Drinks are on us; Publix is rewarding top grades with
free apple juice and sodas. Students, we salute your
thirst for knowledge. The American Heart
Association gets it. I'm a proud member of the American Heart Association
because they get it.

The fat hypothesis has been debunked and they've
taken it back. 2010, American Journal of Clinical
Nutrition carries it all. But this is dietary sugar intake and cardiovascular health. I was a coauthor of this and
very proud to have been so. We recommend a reduction in sugar consumption
from 22 teaspoons of added sugar per
day down to either nine for males or
six for females. That's a reduction by
two-thirds to three-quarters. How are we going to
do that? How are we going to ever accomplish that? Especially since we don't
even know we're consuming it. Because only one-third of
our total added sugar intake comes from sugar
sweetened beverages like soda juice, sports drinks.

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One-sixth comes from things
that we call desserts; candy, ice cream,
things like that. That means one-half of
our sugar consumption is hidden in foods that we
didn't even know had sugar, like salad dressing,
yogurt is a big one. Anybody here think
yogurt is healthy? I got a bridge to sell you. Plain yogurt, sure. You want to take some
whole fruit and mix it with plain yogurt
like they do in Europe? No problem. Off you go. But processed yogurt, the stuff they're selling on the shelves in the supermarket, take a look, just take a
look at the amount of sugar. Now, that's total sugar. Some of it's lactose,
which is milk sugar.

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The question is,
how much of it is lactose and how much
of it is added sugar. You can't know. You're not allowed to know because the food industry
won't let you know. Because in 1989, the
food industry lobbied the Food and Drug Administration when they were coming out with the Nutrition Labeling
and Education Act of 1990. They said, if we told our
consumers, our customers, how much added sugar we put in each of our
processed foods, our competitors could
duplicate our recipes.

This is proprietary information and you're not
allowed to know it. You know what the FDA
said, okay, sure. Let's just show. Here's
what you need to know. Of the 600,000 items in the
American grocery store today, 80 percent of them are
spiked with added sugar. That's not for our purposes, that's for the industries because they know
when they add it, you buy more for all the reasons that
we've just discussed. Worse yet, there are
56 names for sugar and you don't know them and you're
not allowed to know them. Does anybody know what
Florida Crystals are? Sugar. Anybody know what
evaporated cane juice is? If you evaporate cane juice, what do you
get? You get sugar. That's what they use in yogurt because cane juice must be
healthy. Juice from cane. Here's how your food
dollars have been bastardized and
reallocated for you. Meats, this is 1982, 30 years ago, here's 2012. Meats down 10 percent because
of the low fat directive. Fruits and vegetables, the same. Survey says eat your
fruits and vegetables.

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You know what? We're eating just as
much as we were before. Grains and baked goods, 13-14 percent, so all the carbohydrate.
That's only up a little bit. Dairy products 13 down to 10 percent because now everyone
is lactose intolerant. Processed foods and sweets, 11.6, 22.9; a
doubling in 30 years. That's what's happened. That's the change, and that's what we're
talking about tonight. Because processed
food is high sugar, low fiber, and real food
is low sugar, high fiber. Every diet that
works is low sugar, high fiber because every diet
that works is real food. That's what this is about. This is a process food disaster. But the food industry
is making money off it. In fact, lots of it. Because here's the S&P 500
over the last five years. Here's the economic downturn
of 2008 right here, and here's the stock
price of McDonald's, Coke, and Pepsi.

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They're
doing very well. Thank you. Here's General Mills, Hormel Conagra, Kraft, Procter & Gamble,
Archer Daniels Midland. I said Hormel, I think already. Bottom line, they're all
doing better than the S&P. Want to make money, invest in a food company
because they have a winning formula for
getting you to eat more. Back to that first law. Remember, it's not
about common sense, it's about the science. Let's restate it. Let's re-frame the argument. If you're going to store it, that is an obligate weight
gain due to energy deposition. The most obvious of
which is high insulin, and you know where
that came from, and you expect to burn it. That is normal energy expenditure
for normal quality of life because energy
expenditure and quality of life are synonymous. Things that make your
energy expenditure go up make you feel good like ephedrine
off the market, caffeine for two hours, exercise.

Things that make your
energy expenditure go down make you feel lousy. Hypothyroidism, starvation. If you're going to store
it, energy deposition, and you expect to burn it,
then you have to eat it. Same first law, but now reinterpreted based
on the science, not the common sense. Because the aberrant behaviors are a result of our biochemistry, and our biochemistry is a result of our
changed environment. The only way we're
going to fix it is to change the environment back. Here's a list of diseases. Every one of these was a personal responsibility disease until the sheer weight,
magnitude and gravity, and the money that went into it, made it very clear that it was a public health crisis instead.

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Here are some more
newer ones and these are very clearly personal
responsibility diseases. Except they're not, they're
public health crises. How about this one down here? What do you think about guns? It's San Francisco, so I know
what you think about guns. John Howard, the
Australian Prime Minister, perhaps the most conservative politician in the last
100 years in any country, banned assault weapons in Australia back in the late '90s. He was on CNN about two months ago and they asked him, "How
could you do that? You're a conservative politician, libertarian, how
could you ban guns?" He said, "Look, this is
not a Democratic issue, this is not a Republican issue. This is not a liberal issue, this is not a conservative issue. This is a public safety issue." That's exactly right. Even he got it. But we don't get
it. Well, this is a public safety issue because
we will have no Medicare.

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The questions I'm going
to leave you with, I have two homework
assignments for you. Can our toxic food environment be changed without government
or societal intervention? Especially when there are potentially addictive
substances involved? Has education worked for any
substance of abuse? Not one. Did Nancy Reagan's
Just Say No work? Does the Surgeon
General's warning on a pack of cigarettes
stop people from smoking? No. The thing that stop people from smoking was secondhand smoke. When your smoking affected me, that's when we started
getting legislation. Then the tobacco
documents came out and we realized there was corporate
malfeasance involved. That's when things changed. But not one lick of education made any difference
in the amount of tobacco consumed and
Stan Glantz right here at UCSF showed
that very nicely. Second question; can
we afford to wait? The food industry will say, we need more research. Of course, they're going to
say we need more research, it's moving the goalpost. Can we afford to wait to enact these public health measures
when healthcare will be bankrupt due to chronic
metabolic disease in just 13 short years? That's your homework assignment.

This is my second to last slide. This is a paper that just
came out in Lancet in March. Profits and pandemics: prevention of harmful effects of tobacco, alcohol, and ultra-processed
food and drink industries. What it says is that what we used to practice was
called the old medicine, and we focused on
infections as the problem, and microbes as the vectors. Now, the new medicine
is all about chronic disease and the
vector has changed. It is now multinational
corporations instead. That's who we're battling. For further reading,
I refer you to a whole bunch of
academic articles, and more academic articles, and more academic articles, and more academic articles, and more academic articles, and finally, non-academic. If you should choose to
pick it up, Fat Chance, which is written for the public, but really to be honest with you, I wrote it for doctors. My publisher says,
"You cannot write a book for doctors,
we won't publish it." I said, "Okay, fine. I'll
write it for the public." But I really wrote it
for doctors because the whole medical
profession has to change.

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The problem is, they bought the bill of goods that
the food industry was selling and we got to fix it because a calorie
is not a calorie. It never was and never will be. Lastly, we have
started a non-profit very specifically to provide
medical, nutritional, and legal analysis and
consultation to promote personal and public
health against Big Food, called the Institute for
Responsible Nutrition. There is our website and contact me if you would like
any more information. I want to thank my
collaborators here at UCSF, the Weight Assessment for
Teen and Child Health clinic, where we do the actual
boots on the ground, changes in people's lives to
actually make kids better. Stanford Prevention Institute,
my colleague Sanjay Basu, who is an absolute genius.

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Touro University, my
colleague Jean-Marc Schwarz, who's a card carrying
fructose biochemist and vetted all the
biochemistry on this. Kathleen Mulligan at UCSF Clinical Translational
Sciences Institute, who is my right-hand. Berkeley Department of
Nutritional Sciences, and also my colleagues Claire Brindis and
Laura Schmidt at the Institute for
Health Policy Studies here at UCSF as well..

One Exotic Loophole Dissolves 59 lbs

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Fitnestor
Fitnestorhttps://fitnestor.com
Anyone who loves or pursues or desires to obtain pain of itself, but because occasionally circumstances occur in which toil and pain can procure him some great pleasure. Which of us ever undertakes laborious physical exercise, except to obtain some advantage from it? But who has any right to find fault with a man who chooses to enjoy a pleasure?

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