Fat Chance: Fructose 2.0
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Good evenening every one. Welcome again to our penultimate class in this semesters’ course on nutrition
a reminder that next week we will be talking about vitamins and minerals and vitamin and mineral supplements so please join us for that last class
Dr Jeffrey Thais 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 but also in this room at a course very similar to this that I also chaired
and it’s really… I think changed his life more than anything else but I think the hope is, that… it’s also
changed the field and the topic and the policies and the politics that we are going to talk about tonight
many of you know Dr. Lustig is an internationally known neuroendicronologist in pediatrics
he trained for part of his time at UCSF then went back east to do a clinical neuroendicronology 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, ghrelin,
and appetite control and 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
the relationship of the dietary fiber and the 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 5 o’clock this evening
we think he had dinner, we know he hasn’t had sleep, it’s 4 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 he’s here tonight, ’cause I didn’t wanna 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 his ? school of law
getting a Master of studies in Law
and 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 so
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 and thank all of you for coming, you know, to some extent this is sort of like déjà vu all over again
you know having done this 4 years ago and it really did change my life and hopefully changed a few peoples’ lifes
in the audience and certainly around the world
I still get emails from that video today, ah, you know, people who’ve seen it for the first time
that video we are gonna refer back to it in some, to some extent tonight
’cause I am not gonna redo the biochemestry, there’s no point in doing it twice
what we’re gonna talk tonight about is primarily the physiology
so, in essence, the two videos will end up being complementary on youtube
and hopefully people who watch it will end up watching both, so keep that in mind
so, in essence, the two videos will end up being complementary on youtube
and hopefully people who watch it will end up watching both, so keep that in mind
all right, well, a lot’s happened in four years, and the data just keeps rolling in, and unfortunately for us all the data is pretty awful
so you’ll see why as we go and I will try to delineate that as we go
so first of all I have no disclosures, no food industry is putting me up to this
you be sure of that
so here’s the past, this is 2001
6 million kids are seriously overwheight, 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% more obese people on the planet than undernourished people
and this has happened only within 15 years because 15 years ago was exactly the opposite
and it’s occurring in countries that still have under nutrition
so how do you explain that, other than to say
that can’t be behaviour, that’s gotta be an exposure
this looks like any standard pandemic
influenza, typhoid, etc
this looks like a microbial phenomenon rather than a behavioral phenomenon, we’re gonna go there
366 million diabetics walking the earth, that’s 5% of the worlds’ population
and they are chewing through all the health-care resources
this was just three months ago, diabetics cost the US 24 billion dollars
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
ok, 41% rise in 5 years, this is going up so fast it makes your head spin
and here’s the future if we do nothing
experts predict 165 million Americans, 42% would be obese by the year 2030
100 million Americans, that’ll be 33%, will have diabetes by 2050
but fear not, because it won’t really matter because Medicare will be broke by 2026
so, as the Soup Nazi once said: “No health-care for you”
well, the fact of the matter is, I’m gonna be 69 in 2026 and I want my fricking Medicare
and… so should you all
the point is, we have to do something different, and you know the old’s adage, right?
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’ve done the same thing over and over and over again
and there has been no change in the result
so we have to rethink this, we have to reframe the argument and that’s what we are gonna try to do tonight
and I’m’a do it right now
so here’s the way people view this issue
this is a Venn diagram of all the adults in America
30% obese over here, and 70% normal weight over here
and everybody assumes that the problem is this group over here because
80% 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, etc
so, if you do the math on this, that’s 80% of 30% of 240 million, that’s 57 million sick
and it’s those 57 million that are bankrupting the country
and 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 is not correct
here’s the real story, in fact, 20% 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% of the normal weight population have the exact same metabolic dysfunction
that the obese do, they are just normal weight, and so they don’t even know they are 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, etc
and so when you do the math on that, that’s another 67 million, so that’s actually outclassing the obese, and so 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?
No, not in the 80s
In the, in 1991
1991, 1979 patient zero, so we first learned about the, you know
the diagnosis, throughout the entire 80s it was all about the gays and the addicts
and it was always, it’s their problem, their personal responsibility, their behavior, their fault
and then something happened in 1991, anybody remember what it was?
Magic Johnson, Magic Johnson got HIV
and all of a sudden everyone went “Holly Mother…” you know what
and everybody realized, you know what? everyone’s at risk, and all of a sudden it became a public health crisis
so when does a personal responsibility issue become a public health crisis? and that’s what we’re gonna talk about tonight
because this is a public health crisis
here’s the slide that demonstrates the phenomenon
so here are two equally weighted adult men
which one’s healthy and which one’s sick
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, but you know, so what?
in fact, this is perfectly healthy, it’s no problem, because subcutaneous fat is actually kinda 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
so, the fact is, standing on a scale doesn’t tell you where your fat is
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 weight people who have this phenomenon called TOFI
Thin in the outside fat on the inside
ok? Probably some right here in the audience
and they get type-2 diabetes, they get dyslipidemia, they get hypertension, etc, etc, you get the picture?
everyone’s at risk, because everyone’s exposed, the question is, what it is 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 you, ’cause that’s where all the money goes
obesity cost almost nothing, metabolic syndrome is 75% of all health-care cost today
and there’s the list right there, everyone with me now? Ok, do I have your attention? Ok
So how does this work? So 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, so
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
ok, if I didn’t believe in the first law of thermodynamics you’d have me written out on the rail, I’d 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, who’s truth, which interpretation
you know the Supreme Court always comes down 5-4 on everything, right, right?
True, ok, because there are two interpretations, I mean, basically that’s what the Supreme Court is for, interpreting the law
the law is the law, but the interpretation is something else, so here are the two interpretations
If you eat it, you better burn it, or you gonna store it
if that’s true, then this is a matter of energy balance
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
and 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”
so it’s funny, because actually in 2004 HHS said obesity is a disease
it took the AMA 9 years to catch up with HHS, figure that out
so the do… 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 absolute not true
but if you believe it then the corollaries of a calorie is a calorie are
that this is free will, you get to choose what you get to put in your mouth, it’s personal responsibility because if you are obese you chose to be
gluttony and sloth that is your problem and diet and exercise will fix it
that’s what everyone believes from a calorie is a calorie
and who says that a calorie is a calorie, well?
the food industry says a calorie is a calorie, and that’s ’cause it serves them well, so this is the fiction
this is Coca-Cola’s coming together video on Youtube
released just before the Superbowl, that says: “Beating obesity will take action by all of us based on one simple common sense fact”
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
so, is that what we’ve got? We’ve just gut a caloric bachanalia? Oh, sorry, wait, this is wrong, that’s better, ok
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, question is why
so you’d say, well this is why, this is the evolution of fast food over here, 1957 we had the original White Castle hamburger, 210 calories right there, 1 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 hardies had the temerity to offer us the Thickburger at 1420 calories
and of course you can go to Carls’ Junior and get the 6$ burger, which is 2000 calories, that’s the entire caloric allotment for the day
and people are proud to go do it, right?
How? Anybody here had a Trenta?
A Trenta, yes, no? Ok, so that’s this guy over here
so it’s not hot coffee, it’s a cold coffee drink
flavored with you-know-what, and it is 916 cc
well, your stomach is 900cc, it’s bigger than your stomach
so you’d say, well there’s your answer, Q.E.D, it’s all over right?
How about this? I love this, it’s came in the mail
“Free chicken sandwich from KFC with the purchase of a 30 ounce drink”
the food’s gotten so cheap we’re are giving it away? That’s where we are, ok
Or is it the opposite side of the equation? Is it an activity famine?
So this is a study that was done looking at physical activity here on the Y axis
against age, 9-years old to 19-years old, for white girls and black girls
so you can see that by the time they hit age 15 the black girls are just lying prostrate on the floor
’cause there’s no physical activity whatsoever
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
Ok? 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 ’cause 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
so, is this behavior, is this personal responsibility? What do you think?
there are 6 reasons to doubt this
Number 1: no child chooses to be obese
the quality of an obese… life of an obese child is the same as a patient on cancer chemotherapy
why would anyone choose this, in fact, children are ostracized
Does, 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
and the number of people who can actually maintain their weight loss for any length of time is vanishingly small
and if it 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? So,
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, bigger exercise 1.5 BMI points
considering, we are all 7 to 8 BMI points more than we should be
you know, that ain’t gonna cut it, because exercise does not cause weight loss. Does not cause weight loss.
What does exercise do? It causes muscle gain, and that’s good
because muscles 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
so, exercise is the single best thing you can do for yourself, but if you think it’s gonna show up on the scale, think again
So when you stand on the scale, what are you measuring? You’re measuring 4 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 accompasses about 4 to 6 percent of your total body weight
so when you stand on the scale, what are you measuring? You don’t know, you can’t possibly know
So, 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
Number 3, this isn’t just about America
and it’s not just about UK, it’s not just about Australia, yes we are the 3 fattest countries
and we spent 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 going up, doesn’t matter where you look, every country has shown an increase
Number 4, the poor are disproportionately affected
and they don’t have access to choices, they can’t even leave their house for fear of crime
how they’gonna exercise, how they’re gonna let their kids out, to go play in the yard, when they might, you know, face a straight bullet
they don’t have a supermarkets, they live in food desserts, so if you don’t have a choice, how can you call it personal responsibility?
You know, 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 wanna say that that’s personal respons… oh you say
the personal responsibility of the parent, right, for letting them have the sugar pops and
and you know, and the sodas, and the fruit juices, and everything else is, parents’ fault
except for one thing, we’ve been having an epidemic of obese 6 months olds, and they don’t diet and exercise
so any hypothesis you wanna proffer, you have to explain this as well
and it’s even worse than that, because we have obesity in newborns
newborns, ok? Birth weights gone up by 200 grams all over the world
all over the world over the last 25 years, and when you look at, when you do dexa scans to figure out what the body composition is
it’s all fat, it’s all fat
so there, these babies are laying down more fat before they’re ever born and fat cells wanna get filled
that’s why we have obese 6 months old, because everybody is laying down more fat, so the question is how? Why?
Why they are laying down more fat today?
Most clearly, mother’s diet
But you wanna blame the newborn for that problem?
Is that their problem? Is that their fault?
So you wanna blame the pregnant mother? Well you know… then, just go backwards like that, so basically blame everybody
or blame nobody, I blame nobody. Actually I do blame somebody but you’re gonna get there by the end
So we are talking about behavior, right? Behavior, so this is the definition of behavior, this is all from the original video
A stereotyped motor response to a physiological stimulus, so 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
and 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?
Because all behaviors have a biochemical basis
Now sometimes we are smart enough to know what it is and sometimes we are not smart enough to know what it is
give you an example: schizophrenia
For a 100 years schizophrenia was behavioral disorder, now we know it’s a defect in dopamine neuro transmission, and probably actually a defect in glucose transport across the brain
Ok? These are biochemical problems, that ultimately manifest themselves as a behavioral disorder, this is no different
So what are the biochemical underpinnings behind gluttony and sloth? That’s the question, and that’s what we’re gonna try to answer now
So in order to answer that we have to know some science, and I’m gonna make this very brief and very quick
We’re gonna talk about these two hormones right over here, called leptin and insulin
so 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
you can burn energy at a normal rate and feel good doing it
ok? And 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 any more, let me deal with what I’ve got, and so it’s part of the satiety signal
so it tells you… fat cell, get bigger and it tells your brain, stop feeding your fat cell
so, it’s got a dichotomist role, and it’s that dichotomist role that is the linchpin
in terms of understanding the physiology of obesity
and I’m gonna get… we’re gonna go there. So here’s how it works, let’s… we have to explain a paradox, here’s the paradox
Who has children?
Enough of you. What happens if you give a 5 year old kid a cookie?
Yeah, they eat it, yeah, I know they eat it, what happens after that…
they bounce of walls, is what they do, ask any kindergarten teacher what happens when the cupcakes roll out for the birthday party
ok? That’s the end of the lesson, ok? They are bouncing off walls, is known as the sugar high
so what’s going on, the fat cell gets filled, you know, because of the coookie,
the leptin goes up, tells the brain “hey, I’ve got extra energy on board”, it tells the sympathetic nerve system, the fighter/flight part of the nerve system
that innervates your muscles, and innervates your fat cells, “hey, I got too much energy”, so what happens? you burn it off, so the sympathetic nerve system tone to the muscles give you the fidgeting
and the sympathetic nerve system tone to the fat cells releases the extra fat
and that gets used for energy later, and so 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, so here’s the paradox? What happens if you give an obese 5 year old kid a cookie instead?
They are in the pantry looking for more cookies
Anybody ever see a sugar high in an obese kid? Doesn’t exist, doesn’t exist
and that’s why they are obese, it’s because they don’t get the sugar high, because they can’t see their leptin
’cause if they could see their leptin they’d have a sugar high. But they don’t, that’s the point
so something is blocking that leptin signal, that’s the paradox, the question is, what is it?
So we learned about leptin from this patient over here, ok?
This is the obi obi mouse, the leptin deficient mouse, who has a gene defect in the leptin gene, so this
animal’s leptin is zero
so his brain thinks he’s starving all the time, so 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
so, the only reason this animal ever gets off his hind is if 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. Ok, everybody got it? Now,
the reason? Because leptin tells the hypothalamus that you’ve got the energy to burn
so 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 any more, and I can burn energy effectively
and so it tells the sympathetic nerve 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 is a gene deletion or there is 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”
and so that means your sympathetic nerve system tone goes down, which means you sit on a 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, everybody with me?
and this is that same negative feedback pathway I showed you before, now schematized
and there are leptin deficient people, 14 at last count, 14
and they’re all of consanguineous marriages and they’re all of Pakistani or Turkish ancestry
and when they’re born the are 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
so here’s a patient, 220 pounds by age 9
but 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 are losing too
hormone replacement therapy, because now the brain can see leptin because we are 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, that’s my job
and here’s an example, here’s the patient at 3 and half years of age, looking pretty awful
and here’s after a shot of leptin every day for 4 years, indistinguishable from normal
because we fixed the problem, great right? 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
but if our brain could see that leptin we wouldn’t be obese
because we’d burn it off in the sugar high, right? Everybody got it?
So 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
’cause if you can’t… 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, and there’s your gluttony and there is your sloth
so this is all biochemical
so, 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 tells your brain stop. That’s the problem
So, this is the patient that got me started in obesity research, now 18 years ago, when I worked at the St. Jude Children’s Research Hospital in Memphis
this was a 15 year old boy, who weights 364 pounds in this photo
and at age 7 this kid was perfectly normal weight for height, and 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
and he started gaining weight at the rate of 30 pounds per year non stop
for 8 years until he was 364 pounds and I saw him, ok, 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
so you can have all the leptin in the world but if those neurons are dead, your brain thinks its starving
because it can’t transduce that signal
so this is called hypothalamic obesity and this is how I got started in obesity research many many years ago, ok?
So the question is how does this happen, well here are two different hypothesis
This hypothesis says well you damage the hypothalamus and you get obesity because it releases a satiety center
so now you become hyperphagic, except the data actually doesn’t support that, the date doesn’t support that there’s hyperphagia, that there is too much food intake
actually it supports that there’s too little burning, that’s what it shows
so now you become hyperphagic, except the data actually doesn’t support that, the date doesn’t support that there’s hyperphagia, that there is too much food intake
actually it supports that there’s too little burning, that’s what it shows
and that the obesity occurs and then, because of the obesity you have to secret more insulin to tend all that fat
and so that the insulin here is a result of the obesity
but there’s this other hypothesis over here that says, the damage to the hypothalamus yes, it leads to obesity,
but because it turns on that vagus nerve, because you can’t see your leptin
and 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, so which is true?
Well if this is true, nothing I can do about it, ’cause I can’t fix a brain
If this is true it gives me a place I can potentially intervene, right between the vagus nerve and the pancreas
and we have a drug that does that, and it’s called Octeotride, and it’s an endocrine drug that I know how to use
and so 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
So here’s that same patient I showed you, 364 pounds, and here is a year later 326 first time he took a picture with his shirt off
so he did pretty well, ok, I’m gonna show you the ??? over here, this isn’t even my patient
this is a beautiful 13 year old girl from Hawaii, notice the flower, ok?
who, like a month after this picture was taken, was in a very severe car accident
on a Honolulu road, and she was in the intensive care unit for a month
and she survived but she struck her hypothalamus, and so this is her a year later
now, does anybody wanna tell me that this is gluttony and sloth?
This kid now can’t see her leptin because those neurons are dead
now just so happens I happened to be giving ground rounds at Kaiser Honolulu in 2008
and so they invited the patient and her mother to come to the talk
because they were thinking about putting this kid on octreotide even though she’d never’ 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
Now, who here wants to tell me that this is gluttony and sloth?
Do I have your attention? Ok, it’s never gluttony and sloth
It’s always biochemical, the question is are you smart enough to figure out what the biochemistry is
So we said, maybe this could be true in adult obesity without brain tumors or without hypothalamic damage?
So we did a study, actually 2 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 togs, 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
and when her insulin when 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
so, the cause of leptin resistance, that X up here? It’s insulin
and 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, now why?
What’s in it for us, why would God do this to us?
And the answer is because there are two times in your life you actually have to gain weight, what are they?
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 weight
you’d be the 97 pound weakling on the beach who couldn’t bulk up
and the species would die out
so 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 lose the weight and you can start all over again
So 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
‘Cause our insulins are high, 24/7/365
so the question is, how come? Where did the increased insulin come from?
That’s the question, the 64 zillion dollar question
why are we all hyperinsulinemic today
If you look at glucose tolerance tests done today vs 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 gonna tell you
I’m gonna let Will Smith tell you
“Guess I owe you some answers, hoss”
“What, you’re feeling chatty all of a sudden?”
“Sorry, I can’t talk right now. 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?”
You know, if Hollywood knows this why don’t you?
Indeed, he’s got it right, ok?
So, 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, so there are the two papers… you know, popular press items
this was from the New York Times magazine in 2011, is sugar toxic, from Gary Taubes based our work here at UCSF
and this is a, Comment, that we had 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
So, hazardous to your health, and the reason is because
that common sense notion, a calorie is a calorie
it ain’t true, ’cause a calorie is not a calorie
So, what are we talking about? Here we’re talking about this stuff called High Fructose Corn Syrup
55% fructose, so they say
there are actually some studies that suggest that dispenser sugar, like from McDonald’s, or Burger King, or 7eleven
might actually have 65% fructose sometimes, and that would be a problem
but most of the time it’s 55%
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… the stuff you put in your coffee
one glucose, one fructose
O-glycosidic linkage linking the two
The enzyme in your intestine, sucrase, cleaves this in about a nanosecond
so when you absorb the two moieties they are exactly the same and that’s what all the data say
is that they are exactly the same, high fructose corn syrup and sucrose are metabolically equal
Metabolically bad, metabolically equally bad, ok?
This is what our consumption of fructose, so double it for sugar, has done over the last 100 years
so our ancestors, getting foods and vegetables out of the ground with the occasional honey, got about 15 grams of fructose a day
prior to WW2 with the nascent candy and soft drink industries in the country we got 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 8% of total caloric intake, by 1994 we are up to 55 grams a day, that was 10% of total caloric intake
and adolescents currently consume 75 grams per day, that’s 12% of caloric intake
and 25% of adolescents consume 100 grams of fructose per day
double that for sugar, that’s 200 grams of sugar, multiple by 4.1 calories per gram, that’s 840 calories in sugar
so for 2000 calorie allotment, that’s 40% of calories are 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?
And could that be hazardous to your health? Indeed
So as far as I’m concerned, our entire food supply has been adulterated, fructoselated
because the addition of fructose for palatability, especially with decrease fat
and also sensibly as a browning agent
because, food browns better, right? You paint it on your barbecue ribs
to brown it better, right? And the caramelization, actually you know, we like that
and the removal of fiber for shelf life and freezing
we also have substituted trans fats, but those are coming down ’cause we know those are poison
although they are still legal and they are still on the generally recognized as safe list of the FDA
figure that out, ’cause we know they are poison
Now, does sugar cause obesity? Yes, no
Food industry will tell you “Everything causes obesity”, and you know what? They are right, it’s true
because if you look at this study from Mozzaffarian at New… 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
And 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
so there is a significant increase in weight, but when you actually look at the… do the math
it’s only 0.8 BMI points
remember I told you, we got 7 or 8 BMI points to deal with
so, does sugar cause weight gain?
Does sugar cause obesity?
A factor. Is sugar THE cause of obesity?
Not even remotely close
Ok? And 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, ’cause I’m a doctor, ok?
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 that of glucose
and this is what the first Youtube video went into, in exhausting detail and I will not repeat it
but I’m gonna show you very quickly that chronic fructose exposure alone promotes the metabolic syndrome
so, this again is from that first video
when you consume glucose, say rice, white bread, you know starch
80% of the glucose goes to all the organs of the body, only 20% hits the liver
and where does it go? It goes to this guy over here, glycogen
Glycogen is liver starch, and 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
ok, that’s what, why marathoners carb load before a marathon race
is to try to build up their glycogen stores, because glycogen is non toxic
so if you can up your glycogen stores, your liver has more energy in reserve, and that’s a good thing
now 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 carbohydrates 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
so your liver is protected
everybody see that? Your liver is protected
so this for a lack of better word is normal, now let’s talk about something that’s not normal
this guy, alcohol, that’s not normal, CH3-CH2-OH
but alcohol is at toxin, right? It’s to toxins in one
you wrap your Lamborghini around the tree, right, 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, so you doesn’t get any of those CNS symptoms because it doesn’t get there
so let’s consume the same number of calories as alcohol,
now most of ’em go to the liver, instead of going to the periphery
and what happens to it? You see glycogen anywhere?
No glycogen, it bypasses 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 got that lipid droplet, that’s alcoholic steatohepatisis
and you’re gonna make lot’s of triglycerides, and so you are gonna have hypertriglyceridemia
and that’s gonna end up in the muscle, now you’ve got muscle insulin resistance
and it serves as a substrate for weight gain as well
and we also know that alcohol has this dis inhibiting effect on your brain
which causes you to drink more, “oh, I’m just gonna have one drink” and you end up with 5
and of course if you do that too often, maybe you’ll live and become and alcoholic
and that’s addiction right there, positive feedback effect
so here’s a problem, because this is toxic
and abused, and so we regulate it
now let’s do fructose, so we are gonna consume sugar now, we are gonna consume orange juice
same number of calories, but glucose does the same 20/80 split it did before, 12 and 48
but all the calories from fructose are gonna go to the liver, because only the liver has the transporter for fructose, called glut-5
and, you see glycogen anywhere? No glycogen
Go straight down to the mitochondria, just like alcohol did
and because there’s so much of it, your mitochondria got no choice but to turn the excess into liver fat
there’s your lipid droplet, so now you have non alcoholic steatohepatisis
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
so now you’ve got liver insulin resistance, which makes your pancreas have to make more insulin
in order to make the liver do it’s job, now the high insulin goes to the brain, blocks leptin
and now you can’t see your leptin, so what does it do? It makes you think you are starving
So what does it make you do? Consume more fructose
so now you’ve got a positive feedback effect between a compound that is 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’d never think about giving your kid a beer, but you don’t think twice about giving your kid a coke and they do the same thing
that’s one problem, now there’s a second problem
here are 5 photographs, what do they all have in common?
There’s one thing they have all…, they’re all
Brown! Good, thank you, they are all brown. This is the browning reaction
The Maillard reaction, anybody you know what HbA1c is?
That’s the lab test they do for diabetics to see how they 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
so the common link is this browning, or Maillard reaction, or non enzymatic glycation
so 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, ok? 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, and we know it, 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 gonna do damage, and that’s what non alcoholic steatohepatisis is
so here’s that reaction, here’s the aldehyde of glucose
and it binds to the amino group of lysine of the hemoglobin molecule
forms what is known as a shift base, which then… decomposes and develops this mid linkage here
and bottom line is, it’s non enzymatic and happens all the time, the question is how much?
and this shows that it’s very very specific to fructose in terms of a mapped ?
so this is a animal model of non alcoholic fatty liver disease, called the 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 non alcoholic fatty liver disease clinic
at Duke University, this is Dr. Manal Abdelmalek’s work
showing that the grade of steatosis or fatty liver is dependent on
the… how much fructose consumption, whether it’s daily or not
and the stage of fibrosis same thing
Ok, so two problems:
fatty liver and cell aging
so far, so good? All right, so now we are gonna get into the weeds
so 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, you know what I’m talking about, right, …it’s those ribs, yeah, I know [laughter]
10 most obese 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 is soda per capita soda consumption, now what you see?
Pretty significant overlap, wouldn’t you say? Ya?
Well now this is correlation, not causation
and I’m very clear on the difference, we are gonna talk about the difference, ok?
So 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
’cause it’s one snapshot in time, you can’t tell which way the data went
Here’s what happening world wide
So 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 to 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
So 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 are a BRIC country, right? They sell
? jets, and biodiesel, and you know like… world cup… you know, 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
doesn’t have the highest prevalence, that’s reserved for Saudi Arabia, Kuwait, United Arab Emirates, Qatar and Malasia
Why them? Why do they have the highest diabetes rates in the world?
No alcohol, no alcohol
But they got soft drinks like they are going out of style, why? ‘Cause it’s hot,
and the watter 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, right? 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, just came out 3 months ago, very proud of it
Sanjay Basu, one of my colleagues at Standford Prevention Institute,
took 4 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 to 2010
which has food supply as total calories
foods excluding wine, oils, roots, tubers, pulses, nuts and vegetables, meat, cereals, and sugar, sugar crops and sweeteners
as separate items
we then linked 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? Ok
So 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
we did a lot of statistics, this is called an econometric analysis
now a standard, percent vs percent, would be called an ecological analysis
this is not an ecological analysis, this is an econometrical analysis
this actually won 2 economists Nobel Prizes for being able to predict stock market crashes
ok, based on what’s happening before, to predict what happens after
ok? Cause there is causation 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
’cause you can’t infer causation if something didn’t come first, right?
Proximate cause, you need proximate cause
and period effects to control for secular trends, so we did all of this really really neat statistical analysis and Sanjay Basu is an absolute genius
and 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
So, during the decade diabetes prevalence rose from 5.5 to 7 percent world wide, not good
and 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%
and here’s the adjusted associated 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
only changes in sugar availability predicted those changes in diabetes prevalence worldwide, only
if you consumed a 150 calories extra per day,
in total calories, diabetes prevalence only went up by 0.1%, pffft, nothing
but if those 150 calories happen to be a can of soda
diabetes prevalence went up eleven fold
1.1%, and we are not consuming one can of soda per day, we are consuming two and a half
so that’s 2.4%
given that American diabetes rates are 8.3%
that means that 26% 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 wanna do something? You want something actionable? You want something that’s gonna change how much money we spend
so we can salvage Medicare? Here it is,
and of course our government is doing absolutely nothing, ok?
Our data show that 25% of diabetes worldwide is explained by sugar
and more importantly, this is causation
because these data meet what’s known as the Bradford Hill, 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, 3 year time differential
so every country when their sugar went up
3 years later you saw the change in diabetes, in either direction
that’s causal medical inference, now
it’s not scientific proof, so there are different kinds of proofs
there is 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, ’cause it’s a snapshot and you can’t tell,
then there’s this thing called causal medical inference, we’re gonna talk about that right now
and then there’s this thing called scientific proof that everybody keeps harping on
so, in medicine today, what percentage of what we know
is scientifically based, evidence based, scientific proof, randomized control trials?
That’s the standard. How much of what we know, what percent of what we know today, is due to scientific proof, what do you think?
Wanna give me a percentage? 10, 10? 10% of what we know is due to randomized controlled trials
that means 90% of what we know is causal medical inference
so here’s the question, what level of proof do you need?
You tell me. Who here believes in global warming?
Why? Got any proof?
Can you randomize a controlled trial and show me that that’s what’s going on? No
Who here believes that football trauma causes Alzheimers?
How come? You got proof?
Causal inference. Who here believes that tobacco causes lung cancer?
How come? You got proof?
Who’s done the randomized controlled 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?
Number 1, it would be too expensive, number 2, it would be damn unethical, wouldn’t it?
In fact most of these studies would be damn unethical
You ever think we are gonna get the actual scientific studies, the scientific proof
for sugar causing diabetes? Number 1, nobody’s got a zero baseline,
nobody’s naive, number 2, this is something that happens over 40, 50, 60 years
how are you going to keep people on the same diet for that long
and how are you gonna figure out what they actually ate when we can’t even figure it out after one day
Ok? And don’t you think that would be a little unethical? To do that to people?
You’ll never get these 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?
It’s for you to decide, ok?
Ok, addictive, the last piece of this
Bingeing on high-calorie foods may be as addictive as cocaine or nicotine, and could cause compulsive eating and obesity according to a study, ok
So here are all these books that came out on obesity, and addiction, and reward,
you know, they are all popular books, ok?
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
so here’s a control brain with nice hot dopamine receptors, which is good
and here’s a cocaine brain where they’ve been damped down
This is the neuroanatomic equivalent of the phenomenon of tolerance
Ok? Because dopamine down regulates its own receptor, so
once this happens you need more substrate to get the same effect, that’s called tolerance
Ok? And then of course when you withdraw it, 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 here’s 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
and so how fast this gets transduced
has everything to do with what level of reward you achieve
with any given stimulus, whether be power or gambling, or shopping or
cocaine or alcohol, or for that matter, sugar
and this just shows what happens, so here’s that dopamine neuron
and you see it’s going blip, blip, blip, right?
So you add nicotine, blip blip blip blip blip blip, you get more reward, that’s basically what we are talking about, that’s why people start smoking
and then of course the dopamine receptors go down and they can’t stop smoking, that’s addiction
If an food readout… a food intake is a readout of reward
’cause 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
and 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
so when we see a patient in our clinic
that’s the question we ask ourselves, is this patient obese because they are hungry?
and I know what to do about that
or is this patient obese because of the reward system, it’s defective?
and they are addicted? That’s a lot harder to deal with, but we know how to do that too
Or is this person eating because of stress?
Which is enormous problem, especially in America
And that one is really a hard one, because it’s not the stress, it’s the response to stress
So if you think you are stressed, you are stressed, whether you are or not
and most kids today are stressed like never before
and you know what stresses them the most?
And this is going on in every animal, see us humans right there, big dopamines there
receptors here, when obese, dopamine receptors go down
here are Bonnet macaques, same thing, and here are rats, same thing
bottom line, obesity means downregulation 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
ok, that’s what it’s all about
So these people are eating because their brain says they have to
So, the question is, is fast food addictive? What do you think?
Yes? No? Ok, so we actually looked at that question
So everybody familiar with this book?
Michael Moss put this out, “Salt, sugar, fat, how the giants hooked us”, right?
This is wrong, this is a mistake
‘Cause there is one thing not on the list
‘Cause there is one thing not on the list
Now we’ve got fast food! Ok, salt, sugar, fat and caffeine, right?
So 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, lot’s of people do
specially when they have to go low salt for some reason
and we know because we take care of a disease in endocrinology called “salt-losing congenital adrenal hyperplasia”
were 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
and if they were addicted that wouldn’t happen
so when we fix their physiology their
preference gets a lot better. So salt? Not addictive.
Now let’s take fat. Is fat addictive? What do you think?
Nope, rodents binge but show no signs of dependence, and humans
they always bing on high fat high carb or high sugar
items, like pizza and icecream, you don’t binge on high fat per se, otherwise the Atkins diet would have everybody addicted and they’ll tell you
you know they are losing weight, how could they lose weight if they are all addicted?
Energy density actually has a stronger association with obesity and metabolic syndrome than fat does
so, fat? Not addictive
So we are left with these two
Caffeine? Oh man, caffeine is addictive
and if you take my Starbucks away from me I’ll kill you
model drug of dependence, gateway drug in fact
dependence show in children, adolescence, adults, 30% who consume it meet the DSM criteria for dependence
and physiological addiction is well established with the headache, and the test performance, and everything else
Mega addictive, ok?
But d’you see anybody going out and regulating Starbucks or Pits 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 loco
and that we are banning, everybody got it?
So when it’s toxic and addictive we ban it or we regulate it
And so, caffeine and alcohol together that’s a bad deal
but caffeine alone? Keep your hands of my Starbucks, ok
So caffeine? Yes, addictive
Ok, that leaves this one. Sugar, is sugar addictive? What do you think?
You know, we’ve known this for a long time, because, anybody know what this is?
It’s called “sweeties”, “sweeties”
This is a super concentrated sucrose, sugar solution, that you dip the pacifier in
and you put in the newborn baby boy’s mount before you do the the circumcision
because it releases opioids and deadens the pain
and this has been known forever
Ok? Then you mix it with a little wine and then you got a really good cocktail, eh?
So is there really such a thing as sugar addiction, 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 are basically metabolized the same way, because after all where do you get alcohol from?
Fermentation of sugar, it’s called wine
right? We do it every day, up in 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
and that’s the point, and that’s why they both cause the same diseases
and they do the same thing to the brain
so for the criteria for addiction in animals are bingeing,
and then there is 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 3 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 ’cause they are the same dopamine receptors, everybody got it?
Ok? And so, does sugar do this? Absolutely
Q.E.D. slammed on, sugar is addictive in animals
What about humans? Who saw this movie?
Right? Did you like it?
More or less?
I’ve a big problem with this movie, because if you watch the movie
his doctor, Morgan’s doctor keeps saying:
“You gotta get off this high fat diet, high fat diet, high fat diet, high fat diet, high fat diet”
Not the high fat diet, it’s the high sugar diet,
high sugar diet, that’s what caused all the problems
So, can sugar be addictive?
Watch. “I was feeling bad”
“In the car, feeling like…”, sorry, “…really”
“I was feeling really, really”
“sick and unhappy”
“started eating, feel great”
“feel really good now”
“I feel so good as crazy”
“Ain’t that right baby? Yeah you’re right darling”
This was on day 18, ok?
of his 30 day ? through McDonald’s
He just described withdrawal, that’s withdrawal
and he needed another hit in order to feel good again
he just described withdrawal, he was a vegan, right? ’cause his girlfriend was a vegan chef
and in 18 days he’s a sugar addict
so, you tell me. So this is what we are dealing with
We are dealing with an industry that
wants us to consume its product, well gee, every industry wants us to consume their product in some fashion or another, the question is
what if it hurts you? What if it hurts you?
So… this is an example, this is the Federal Trade Commision vs Sugar Information
back in 1972, this was an arm of the Sugar Research Association
“The fat time of day you are really hungry and ready to eat two of everything, here’s how sugar can help”
They are allowed to do… they can advertise any way they want, they are allowed
How about this one, the birth of the un-cola
“Why we have the youngest customers in the business” from 7up
You ok with that? And this is, you know this is going on
How about this one, this was in Publix supermarket chain in Florida just a year ago
“Drinks are on us! Publix is rewarding top grades with free apple juice and soda. Students”
“we salute your thirst for knowledge”
Well, the American Heart Association gets it
and I’m a proud member of the American Heart Association
because they get it, the high fat hypothesis has been debunked
and they have taken it back, 2010 American Journal of Clinical Nutrition, Krauss et al, ok?
But this is dietary sugar intake in cardiovascular health
I was a coauthor of this, and very proud to have been so
and we recommend a reduction in sugar consumption from 22 teaspoons of added sugar per day
down to either 9 for males or 6 for females
that’s a reduction by two thirds to three quarters
How we gonna do that? How we gonna ever accomplish that?
Especially since we don’t even know we are consuming it
Because only 1/3 of our total added sugar intake comes from sugar sweetened beverages, like soda, juice, sport drinks
1/6 comes from things we that call desserts, you know, candy, icecream, 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 yogurt is healthy?
I got a bridge to sell you
Plain yogurt? Sure! You wanna take some whole fruit and mix it with plain yogurt like they do in Europe?
No problem! Off you go, ok? But
processed yogurt? You know, the stuff they are selling on the shelves of the supermarket?
Take a look, just take a look at the amount of sugar
Now it’s total sugar, so some of it is lactose, which is milk sugar
the question is, how much of it is lactose and how much of it is added sugar
You can’t know. You are not allowed to know.
‘Cause 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, and 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 are not allowed to know it”
and you know what the FDA said?
“Eh… ok, sure”. That just shows
Here’s what you need to know, of the 600000 items in the American grocery store today
80% of them are spiked with added sugar
and that’s not for our purposes, that’s for the industry’s, ’cause they know when they add it
you buy more
for all the reasons that we’ve just discussed
and worse yet, there are 56 names for sugar
and you don’t know them, and you are not allowed to know them
so, does anybody what florida crystals are?
Sugar, anybody know what evaporated cane juices
If you evaporate cane juices what do you get? You get sugar, ok?
And so that’s what they use in yogurt, because
“Oh, cane juice must be healthy, right? Oh, came… juice from cane, right?”
So 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%, because of that little fat directive
Fruits and vegetables? The same
so everybody says eat your fruits and vegetables, you know what? We are eating just as much as we were before
Grains and baked goods, 13 to 14%, everybody says it’s all the carbohydrate, it’s all up a little bit
Dairy products, 13 down to 10%, 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 are talking about tonight
because processed foods is high sugar, low fiber
and real food is low sugar, high fiber
and 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 processed foods disaster
but the food industry is making money of it
in fact, lots of it
because here is the S&P 500 over the last 5 years
Ok? Here’s the economic downturn of 2008 right here
and here’s the stock price of Mc Donald’s, Coke and Pepsi, they are doing very well, thank you
and here’s General Mills, Hormel, ConAgra, Kraft, Proctor & Gamble, Archer Daniels Midland, and
I said Hormel I think already, bottom line, they are all doing better than the S&P
Wanna make money? Invest in a food company, ’cause they have a winning formula
for getting you to eat more
so, back to that first law, remember?
It’s not about common sense, it’s about the science
so let’s restate it, let’s reframe the argument
If you are gonna 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 a ? off the market
caffeine, for two hours, exercise,
things that make your energy expenditure go down make you feel lousy
so, if you gonna 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 the result our biochemistry
and our biochemistry is a result of our changed environment
and the only way we are gonna fix it, is to change the environment back
so, here’s a list of diseases
everyone 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
and here are some more newer ones
and these are very clearly personal responsibility diseases, right?
except they are not, they are public health crises, how about this one down here?
What do you think about guns? San Francisco so I know what you think about guns, but
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
and he was on CNN about two months ago, and they asked him: “I mean, how could you do that?”
“A conservative… you know, politician, how could… libertarian, how could you ban guns”, and he said:
“Look, this is not a democratic issue, this is not an 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,
even he got it, but we don’t get it,
well this is a public safety issue, because we will have no Medicare
So the questions I’m gonna leave you with, I’ve two homework assignments for you
Can our toxic food environment be changed without governmental or societal intervention?
Especially when there are potentially addictive substances involved
Has education worked for any substance of abuse?
Not one, did Nancy Reagan just said “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 second hand smoke
when your smoking affected me
that’s when we started getting legislation
and 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 Glance ? right here at UCSF showed that very nicely
Second question: can we afford to wait?
The food industry will say “we need more research”
“We need more research”, of course they’re gonna say we need more research, it’s moving the goalposts
Can we afford to wait, to enact these public health measures, when health-care will be bankrupt due to chronic metabolic disease in just 13 short years?
That’s your homework assignment
So, 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 food industries”
And 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
and 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
so for further reading I refer you to a whole bunch of academical articles
and more academical articles,
and finally, non academic, if you choose to pick it up
“Fat chance” which was 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 “Ok, fine”
“I’ll write it for the public”
but I really wrote it for doctors because the whole medical profession has to change
and the problem is they bought the bill of goods that the industry was selling
and we gotta fix it, because a calorie is not a calorie, it never was and never will be
so, lastly we have started a non profit
and we gotta fix it, because a calorie is not a calorie, it never was and never will be
so, lastly we have started a non profit
very specifically to provide medical nutrition 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’d like any more information
So I wanna thank my collaborators, here at UCSF, the Weight Assessment for Teen and Child Health Clinic
were we do the actual on the ground, you know 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
Touro University, my colleague Jean-Marc Schwarz who is a card carrying fructose biochemist and vetted all the biochemistry on this
Kathleen Mulligan at the 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.