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I'm going to tell you tonight a story. And this story dates back about 30 years. This story has a little bit of something for everybody.
It has a little bit of biochemistry, a little bit of clinical research, a little bit of public health, a little bit of politics, a little bit of racial innuendo. The only thing it's missing is sex. But, well, we can see what we can do about that, too. Thank you.
By the end of the story, I hope I will have debunked the last 30 years of nutrition information in America. I would very much appreciate it if at the end of the talk, you would tell me whether or not I was successful or not. In order to get you in the mood, as it were, let's start with a little quiz.
What do the Atkins diet and the Japanese diet have in common? Anybody? Oh, you have the answers right, yeah.
Never mind. That's right. You have the answer right there. So the Atkins diet, of course, is all fat, no carb. The Japanese diet is all carb, no fat.
They both work. So what do they share in common? They both eliminate the sugar fructose.
So, with that, think about what it means to be on a diet and what macronutrients you're eating and which ones you're not. And then we'll go from there and I'll try to explain how this all works. You've all heard about the obesity epidemic.
Here are the numbers. These are the NHANES database body mass index. Everybody knows what that is now. Histograms. Marching ever rightward as time has gone on.
on. This was what was projected for 2008 in blue. We had so far exceeded and surpassed.
This is not even funny. This was from 2003. The reason I show this is not just to show that the obese are getting obese-er. Of course, that's true.
But in fact, the entire curve has shifted. We all weigh 25 pounds more today than we did 25 years ago, all of us. Now, it is often said that obesity is the ultimate interaction between genetics and environment. And Dr. Christian Weiss, who's sitting here, is a professor at the University of New York sitting in the back of the room will be talking to you next week about the genetic component, which I am also very interested in. But having said that, our genetic pool did not change in the last 30 years, but boy, oh boy, has our environment sure changed.
So tonight, we're going to talk about the environment rather than genes. Now, in order to talk about the environment, we need to talk about what is obesity. And of course, you're all familiar with the basic concept of the first law of thermodynamics, which states that the total energy inside a cloud closed system remains constant.
Now, in human terms, the standard interpretation of this law is the following. If you eat it, you better burn it or you're going to store it. Now, who here believes that?
Oh, come on, you all do. Okay. I used to believe that.
I don't anymore. I think that's a mistake. I think that is the biggest mistake.
And that is the phenomenon I'm going to try to debunk. over the course of the next hour. Because I think there's another way to state the law, which is much more relevant and much more to the point.
Before I get there, of course, if you believe that, these are the two problems, right? Calories in, calories out. Two behaviors, right? Gluttony and sloth. After all, you see anybody on the street, oh, he's a glutton and a sloth.
That's all there is to it. Tommy Thompson said it on the TV show. We just eat too damn much, right?
Well, you know, if that were the case, How did the Japanese do this? Why are they doing this? bariatric surgery on children at Tokyo Children's Hospital today.
Why are the Chinese? Why are the Koreans? Why are the Australians? I mean, you know, all these countries who've adopted our diet all suffer now from the same problem.
And we're going to get even further in a minute. There's another way to state this first law. And that is, if you're going to store it, that is biochemical forces that drive energy storage. And we'll talk about what they are in a few minutes.
And you expect to burn it. That is normal energy expenditure for normal quality of life. Because energy expenditure and quality of life are the same thing. Things that make your energy expenditure go up make you feel good. Like ephedrine, it's off the market.
Coffee, for two hours and you need another hit like me. Things that make your energy expenditure go down... like starvation, hypothyroidism, make you feel lousy.
And how many calories you burn and how good you feel are synonymous. So if you're going to store it, that is an obligate weight gain set up by a biochemical process, you expect to burn it, that is normal energy expenditure for normal quality of life, then you're going to have to eat it. And now all of a sudden, these two behaviors, the gluttony and the sloth, are actually secondary to a biochemical process, which is primary.
And that's a different way to think about the process. And it also alleviates the obese person from being the perpetrator, but rather the victim, which is how obese people really feel. Because no one chooses to be obese.
Certainly no child chooses to be obese. Oh, you say, oh yeah, sure, I know some adults who don't care. You know, Rossini, the famous composer, you know, La Gaza Larga, Marriage of Figaro and all that, he retired at age 37 to a lifetime of gastronomic debauchery.
Okay? Maybe he chose to be obese. But the kids I take care of in obesity clinic do not choose to be obese.
In fact, this is the exception that proves the rule. We have an epidemic of obese six-month-olds. Now, if you want to say that it's all about diet and exercise, then you have to explain this to me.
So any hypothesis that you want to proffer that explains the obesity epidemic, you have to explain it to me. you've got to explain this one too. And this is not just in America, these six-month-old obese kids, but these are around the world now. So open your minds, and let's go and figure out what the real story is.
Now, let's talk about calorie intake, because that's what today is about. We're going to talk about the energy intake side of the equation. Sure enough, we are all eating more now than we did 20 years ago.
Teen boys are eating 275 calories more. American adult males are eating 187 calories more per day. American adult females are eating 335 calories more per day.
No question. We're all eating more. Question is, why? How come?
Because it's all there. You know what? It was there before.
We're all eating more. There's a system in our body which you've heard about over the last couple of weeks called leptin. Everybody heard of leptin?
Okay, it's this hormone that comes from your fat cell, tells your brain, you know what, I've had enough. I don't need to eat anymore. I'm done.
And I can burn energy properly. Well, you know what? If you're eating 187 or 335 calories more today than you were 20 years ago, your leptin ain't working. Because if it were, you wouldn't be doing it, whether the food was there or not. So there's something wrong with our biochemical negative feedback system that normally controls energy balance.
and we have to figure out what caused it and how to reverse it. And that's what tonight is about. But nonetheless, there are 275 calories we have to account for.
So where are they? Are they in the fat? No, they're not in the fat. 5 grams, 45 calories out of the 275, nothing.
In fact, it's all in the carbohydrate. 57 grams, 228 calories. We're all eating more carbohydrate.
Now, you all know back in 19... In 1982, the American Heart Association, the American Medical Association, and the U.S. Department of Agriculture admonished us to reduce our total fat consumption from 40 to 30%. Everybody remember that? That's how Entenmann's fat-free cakes came into being.
Remember that? So what happened? We did it. We've done it. 40% down to 30%.
And look what's happened to the obesity, metabolic syndrome. non-alcoholic fatty liver disease, cardiovascular disease, stroke prevalence, all jacked way up. consumption as a percent has gone down. It ain't the fat, people.
It ain't the fat. So what is it? Well, it's the carbohydrate.
Specifically, which carbohydrate? Well, beverage intake, right? 41% increase in soft drinks, 35% increase in fruit drinks, fruit aids, whatever you want to call them. Okay.
Just remember, down here, one can of soda a day is 150 calories. Multiply that by 365 days a year, and then divide that by the magic number of 3,500 calories per pound. If you eat or drink 3,500 calories... more than you burn, you will gain one pound of fat. That's the first law of thermodynamics.
No argument there. That's worth 15 pounds of fat per year. One soda a day is 15 pounds per year.
Now, you've all heard that before. That's not news to you. The question is... how come we don't respond?
How come leptin doesn't work? How come we can't stay energy stable? That's what we're going to get to.
So I call this slide very specifically the Coca-Cola conspiracy. Anybody here work for Coke? Pepsi? Okay, good. All right.
So this over here, 1915, the first standardized bottle of Coca-Cola out of Atlanta. Anybody remember this bottle? Sure.
A lot of you do, right? I remember this bottle because my grandfather in Brooklyn took me on Saturday afternoon down to the local soda shop on Avenue M and Ocean Avenue, and every Saturday afternoon I had one of these. I remember it very well.
Now, if you drank one of those every day, assuming, of course, that the recipe hasn't changed, because, after all, only two people in the world know the recipe, and they're not allowed to fly in the plane at the same time, right? You know that, okay? Assuming the recipe hasn't changed, if you drank one of those every day for a year, six and a half ounces, that would be worth eight pounds of fat per year.
Now, in 1955, after World War II and sugar became plentiful again and wasn't being rationed, we have the appearance of the 10-ounce bottle, the first one that was found in vending machines, and you probably remember that one as well. Then in 1960, the ever-ubiquitous 12-ounce can, worth 16 pounds of fat per year, and of course today, this over here is the single unit of measure, 20 ounces. Anybody know how many? servings are in that bottle?
2.5 8 ounce servings, that's right. Anybody know, anybody who gets 2.5 8 ounce servings out of that bottle? That's a single serving, right?
Okay, so that would be worth 26 pounds of fat per year if you did that every day. And then of course over here we have the 7-11 Big K Thirst Buster, Big Gulp, whatever you want to call it. 44 ounces worth 57 pounds of fat per year. And if that wasn't bad enough, my colleague Dr. Dan Hale at the University of Texas San Antonio tells me that down there there, they got a Texas-sized Big Gulp.
Sixty ounces of Coca-Cola, a Snickers bar, and a bag of Doritos, all for 99 cents. Okay, so if you did that every day for a year, that would be worth 112 pounds of fat per year. Okay, so why do I call it the Coca-Cola conspiracy?
Well, what's in Coke? Caffeine, good, good. So what's caffeine?
It's a mild stimulant, right? It's also a diuretic, right? Makes you pee-free water. What else is in Coke? We'll get to the sugar in a minute.
What else? Salt. Salt.
55 milligrams of sodium per can. It's like drinking a pizza. So what happens if you take on sodium and lose free water? You get thirstier, right? So why is there so much sugar in Coke?
to hide the salt. When was the last time you went to a Chinese restaurant and had sweet and sour pork? That's half soy sauce.
You wouldn't eat that. Except the sugar plays a trick on your tongue. You can't even tell it's there.
Everybody remember New Coke? 1985? More salt, more caffeine. They knew what they were doing. Okay?
That's the smoking gun. Okay? They know. They know.
All right. So, that's why it's the Coca-Cola conspiracy. So, are soft drinks the cause of obesity?
Well, it depends on who you ask. If you ask the scientists for the National Soft Drink Association, they'll tell you there's absolutely no association between sugar consumption and obesity. Okay?
If you ask my colleague, Dr. David Ludwig, remember, I'm lustic. He's Ludwig. Okay?
He's... does what I do at Boston Children's Hospital. Someday we're going to open a law firm.
Each additional sugared sweetened drink increase over a 19-month follow-up period in kids increased their BMI by this much and their odds-risk ratio for obesity by 60%. Okay? That's a prospective study on soft drinks and obesity.
The real deal. If you look at meta-analyses, everybody know what a meta-analysis is? Okay, it's a conglomeration of numerous studies subjected to rigorous statistical analysis.
Okay? Eighty-eight cross-sectional and longitudinal studies. Regressing soft drink consumption against energy intake, body weight, milk and calcium intake, adequate nutrition, all showing significant associations, and some of these being longitudinal.
This came from Kelly Brownell's group at Yale. I should comment, disclaimer, those studies that were funded by the beverage industry showed consistently smaller effects than those that were independent. Wonder why.
Now, how about the converse? What if you take the soft drinks away? So this was the fizzy drink study from Christ Church England, James et al., British Medical Journal, where they went into schools and they took the soda machines out, just like we did here.
in California. We haven't seen the data yet, but they went and did it for a year. So the prevalence of obesity in the intervention school stayed absolutely constant, no change, whereas the prevalence of obesity in the control schools, where nothing changed, continued to rise. over the year.
Okay, so that's pretty good. So how about type 2 diabetes? Are soft drinks the cause of type 2 diabetes? Well, this study from JAMA in 2004 looked at the relative risk ratio of all soft drinks, cola, fruit punch, and found a very statistically significant trend of sugared soft drinks, fruit aids, et cetera, causing type 2 diabetes.
And you know, we've got just as big a problem with type 2 diabetes as we do with obesity for the same reasons. And this was a sugared sweetened beverage against risk for type 2 diabetes in African-American women. Looking here at sugared sweetened soft drinks, just the downward arrow shows that there was a significant rise as the number of drinks went up. You can see that here, whereas orange and grapefruit juice, interestingly, did not.
So two different studies, two different increases in type 2 diabetes relative to soft drink consumption. So what's in soft drinks? Well, in America, it's this stuff. right?
High fructose corn syrup. Everybody's heard of it, right? It's been demonized, something awful.
So much so that the corn refiners industry has launched a mega campaign to try to absolve high fructose corn syrup of any problems, which we'll talk about in a moment, okay? But the bottom line is, this is something we were never exposed to before, 1975. And currently, we are consuming 63 pounds per person per year, every one of us, 63 pounds of... of high fructose corn syrup?
That's American. Yes. Now, what is high fructose corn syrup?
Well, you'll see in a minute. It's one glucose, one fructose. We'll talk about those at great length.
One of the reasons we use high fructose corn syrup is because it's sweeter. So here's sucrose. This is cane or beet sugar, standard table sugar, you know, the white stuff. Okay.
And we give that an index in sweetness of 100. So here's high fructose corn syrup. It's actually sweeter. It's about 120. So you should be able to use less, right?
Right. Wrong. We use just as much.
In fact, we use more. So here's lab fructose over here, if you had crystalline fructose, and they're starting to put crystalline fructose into some of the soft drinks. They're actually advertising it as a good thing.
And that's got a sweetness of 173, so you should be able to cut that way back, right? They're not. Lactose down here, milk sugar, it's not sweet at all.
Okay? And glucose, I should point out over here, is 74. It's not particularly sweet. sweet, and we're going to get to that at the end, and what goes on with glucose. But anyway, there's why we use it.
It's sweeter. It's also cheaper, as I'll show you. So here's high fructose corn syrup. One glucose, one fructose. Notice the glucose is a six-membered ring.
The fructose is a five-membered ring. They are not the same. Believe me, they're not the same. That's what this whole talk is about, is how they're not the same.
And here's sucrose, and they're just bound together by this. this ether linkage. We have this enzyme in our gut called sucrase. It kills that bond in two seconds flat, okay, and you absorb it.
And basically, high fructose corn syrup, sucrose, it's a non-issue. It's a wash. They're the same, okay? And they know that they're the same, the softening companies and the corn refiners, because here are their missives, okay? This comes from the Corn Refiners Association.
Obesity research shows high fructose corn syrup metabolizes impact satiety similar to sugar. Indeed it does. I agree.
Okay? You know, decent, you know, meetings, you know, academic meetings around the country. Okay? Hunger and satiety profiles energy intakes following ingestion of soft drinks. Bottom line, research supported by the American Beverage Institute and the Corn Refiners Association.
They are correct. There is absolutely no difference between high fructose corn syrup and sucrose. So much so that the Corn Refiners Association and an attempt to capture market share, came out with this entire ad campaign.
You probably saw it on the back page of the New York Times. It was on TV. My hairdresser says that sugar is healthier than high fructose corn syrup. Wow, you get your hair done by a doctor?
I didn't know I could cut hair. Okay? If you want to see all of them, there are a whole bunch of them, you can go to www.sweetsurprise.com and see how you're being...
hoodwinked. But indeed, this is true. High fructose corn syrup and sucrose are exactly the same.
They're both equally bad. They're both dangerous. They're both poison.
I said it. Poison. My charge before the end of tonight is to demonstrate that fructose is a poison.
And I will do it. And you will tell me if I was successful. Nonetheless, here's Center for the Science and the Public Interest and the Corn Refiners Association.
Everybody remember last year when Gavin Newsom floated a soda tax? Okay, last February. Okay, Governor Patterson of New York has since floated one. people are starting to talk about it. So why are they saying this?
Well, they're saying obesity is a problem. Kids are drinking soda. Let's tax it.
So they're talking about soda like it's empty calories. I'm here to tell you that it goes way beyond empty calories. calories.
The reason why this is a problem is because fructose is a poison. It's not about the calories. It has nothing to do with the calories.
It's a poison by itself. And I'm going to show you that. Nonetheless, I just want to read you this paragraph here in yellow. We respectfully urge that the proposal be revised as soon as possible to reflect the scientific evidence that demonstrates no material differences in the health effects of high fructose corn syrup and sugar. I agree.
Here's the important sentence. The real issue is that excessive consumption of any sugars may lead to health problems. I agree. That's exactly right. Not may.
Does. Does. So here's the secular trend in fructose consumption over the past hundred years.
Before we had food processing, we used to get our fructose from fruits and vegetables. And if we did that, today we would consume about 15 grams per day of fructose. Not sugar, fructose. So sugar would be 30 grams, it would be double.
We're just talking about fructose today. Prior to World War II, before it got rationed again, we were up to about 16 to 24. about 20 grams, so a small increase from the beginning of the century to World War II. Then, in 1977, just as high-fructose corn syrup was hitting the market, we had increased that. We had basically doubled up to 37 grams per day, or 8% of total caloric intake. By 1994, we were up to 55 grams of the stuff per day.
Remember, if you want to do sugar, then double the number. So that's 10.2. So you can see that more and more of our... caloric intake, higher percentage is being accounted for by sugar every single year.
So it's not just that we're eating more, we're eating more sugar. And for adolescents today, we're up to almost 75 grams, 12% of total caloric intake. 25% of the adolescents today consume at least 15% of their calories from fructose alone.
This is a disaster. An absolute disaster. unmitigated disaster. The fat's going down, the sugar is going up, and we're all getting sick. Now let me show you why.
Okay. How'd this happen? Why did it happen? So this is where the politics comes in.
This is the perfect storm, and it was created from three political winds that swirled around all at the same time to create this perfect storm. So, the first political wind? Everything bad that ever happened in this country started with one man. Okay, and it's still being felt today. Okay, so Richard Nixon in his paranoia back in 1972, okay, food prices were going up and down and up and down.
I'm going to show you that on the next slide. Okay, and he was worried that this was actually going to cause a lot of trouble. So he admonished his secretary of agriculture, Earl Rusty Butts, I love that name, to basically take food off the political table.
To make food a non-existent food. issue in presidential elections. Well, the only way to do that was to make food cheap. So he was out to find all methods to be able to decrease the price of food. Remember Nixon's war on poverty?
This, we're suffering from it today. Okay, that's what this is. Okay, second political win, the advent of high fructose corn syrup. Okay, so this was invented in 1967. at Saga Medical School in Japan by a guy named Takasaki, who's still alive.
As far as I'm concerned, this stuff is Japan's revenge for World War II. Except, of course, that they're suffering from it now themselves. Like everything, you know, it always comes back to haunt you.
And it was introduced to the American market in 1975. So what do you think happened to the price of sugar when this thing hit the market? Here's what happened. So here's the U.S. producer price index of sugar going up.
and down and up and down. This is not good. Stability is at 100%. If it stays nice and stable at 100%, that's what you want if you're a politician.
Up and down. Here's where corn sweeteners entered the market in 1975, 1980, and you can see that since then the price of sugar has remained remarkably constant. And it did so not just in the U.S., but also on the international stage.
Here's the London price doing the same thing. when you look at the difference in price between sugar and high fructose corn syrup, you can see that high fructose corn syrup is about half the price. So in other words, it's cheap.
So high fructose corn syrup is evil, but it's not evil because it's metabolically evil. It's evil because it's economically evil. Because it's so cheap that it's found its way into everything.
It's found its way into hamburger buns. pretzels, barbecue sauce, and ketchup. Almost everything. Somebody emailed me the other day and told me they went into their local grocery store and went through every single loaf of bread on the shelf, and out of 32 types of bread on the shelf, only one of them did not have high-fructose corn syrup in it.
So we are being poisoned by this stuff, and it's been added surreptitiously to all of our food. Every process. food. And the question is, why? Well, you'll see why in a minute.
So the corn refiners like to point out, well, you know, it's just been a substitution. As the high fructose corn syrup's gone up, the sugar's gone down. You know, we're just replacing, you know, like gram for gram.
Well, not exactly, because here's 73 pounds of sugar per year. This is from the Economic Research Service of the U.S. Department of Agriculture, okay?
So disappearance data, okay? 73 pounds. up to 95 pounds by 2000. And there's something missing from this slide.
Anybody want to tell me what it is? What's missing? Juice.
Juice is missing because juice is sucrose, right? Sugar. And juice causes obesity. Okay. So this is a study done by Miles Faith, a prospective study in inner city Harlem toddlers.
And the number of juice servings per day predicts the change in. BMI score per month in these inner-city Harlem toddlers. Now, where do these inner-city Harlem toddlers get their juice?
From what? From where? From whom?
From WIC. Anybody heard of WIC? You know what WIC is?
Women, Infants, Children, right? A government entitlement program set up under who? Nixon, okay? To prevent failure to thrive. They did.
This is the equal and opposite reaction. So, let's add juice in. Here it is.
And so, most fructose items, when you put it together, now we're up to 113 pounds on this graph, and I just heard from Brian Williams of NBC News after the most recent study came out that was in the Journal of Clinical Investigation. that we are actually up to 141 pounds of sugar per year, each of us. That's what we're up to, 141 pounds of sugar per year.
Now, do you think that this might have some detrimental effects on you? Hasn't stopped you, has it? That's the point.
It hasn't stopped you. That's why we need to talk about this. So, juice consumption increases the risk for type 2 diabetes. So this is the relative risk ratio as juice intake goes up.
the nurses study, showing again, juice consumption, sucrose, obesity, diabetes. The third political storm that's swirling around to create this disaster, this mega typhoon. That thing that happened in 1982. The USDA, the American Heart Association, the American Medical Association, all telling us we had to reduce our consumption of fat.
Now, why did they tell us that? To stop what? To stop heart disease.
Did we? No, we didn't, did we? In fact, it's worked the exact opposite. We've only created more.
So now how did this come to be? Why did they tell us to stop eating fat? Well, in the early 1970s we discovered something in our blood called LDL, low density lipoproteins. You've heard of that, right? Is it good or bad?
Not so bad. We'll talk about it. In the mid-1970s, we learned that dietary fat raised your LDL. So if dietary fat is A and LDL is B, we learned that A led to B. Dietary fat definitely increases your LDL, no argument.
It's true. And then, finally, in the late 1970s, we learned that LDL correlated with cardiovascular disease. So let's call cardiovascular disease C.
So we learned that B led to C. So the thought process by some very smart nutritionists, et cetera, the USDA, et cetera, said, well, if A leads to B and B leads to C, then A must lead to C. Therefore, no. No A, no C.
This was the logic. Now, any logicians in the room? Anybody see any problems with that logic?
Go ahead. That's right, the premise is incorrect. And I'll tell you why the premise is incorrect.
Because this suggests that this is all transitive. But in fact, only the contrapositive is transitive. So it's not no A, no C. It's no C, no A.
Okay? So the logic isn't even right. There's faulty logic here. So this doesn't work on any level. So I'm going to show you why this doesn't work.
But before I show you why it doesn't work, I'm going to show you that this was a battle royale. back in the 1970s. This was not a simple thing.
There were people lined up on both sides of this story. So this over here is a book, 1972 it came out, and it was called Pure, White, and Deadly. It's all about sugar. Written by a British physiologist, nutritionist, endocrinologist by the name of John Yudkin. Now I never knew John Yudkin.
He's passed away. But I read this book about a year ago and without even knowing it. it.
I was a Yudkin acolyte. I was a Yudkin disciple. Every single thing that this man said in 1972 is the God's honest truth. And if you want to read a true prophecy, you find this book.
It's not easy to find, but you go find this book, and I'm telling you, every single thing this guy said has come to pass. It's astounding. I am in awe of this guy. But on the other side, we had this guy over here. here.
His name was Ancel Keys. Anybody heard of him? So Ancel Keys was a Minnesota epidemiologist, very interested in the cause of cardiovascular disease, and he performed the first multivariate regression analysis without computers. Now, anybody know what that means?
Multivariate regression analysis? So this is where you take a whole lot of data, and normally you would just run a few computer programs, but basically the object is to try to figure out what causes what. and to try to factor out other things and determine what the contribution of various things all at once are to an outcome that you're looking for.
So he was interested in cardiovascular disease. And so what he did was he did this study, along with other people around the world, called the Seven Countries Study. Very famous, front page of Time magazine in 1980. So here's the data on the Seven Countries Study. So we have the U.S., we have Canada, Australia, England, and Wales. Wales, Italy, Japan.
And here's percent calories from fat on the x-axis, and here we have coronary disease death rate on the y-axis. And so you'd say, well, look at that. I mean, it's very obvious, isn't it?
Sure, percent calories from fat correlates very nicely with coronary disease, except for one little problem. Anybody see it? Japan and Italy, so how much sugar did they eat? Didn't I tell you the Japanese diet eliminates fructose? They never even had it until we brought it to them after World War II.
Italy, you know, aside from gelato, I mean, what else they got? They get a lot of pasta, there's a lot of glucose, but no fructose. There's no sugar in the Italian diet other than the occasional sweet, which they moderate.
They're very careful about moderating, and they cost a lot. But here we got a little bit of a difference. got England, Wales, Canada, Australia, US, you know, we are sugarholics, aren't we? We're also fataholics. So, in fact, the fat migrated with the sugar.
So, here's, this is from Keyes'own work, okay, page 262, if you want to pick up the 500-page volume, okay, and I'm just going to read you the one paragraph, okay, that talks about this. The fact that the incidence rate of coronary heart disease was significantly lower than the incidence rate of heart disease correlated with the average percentage of calories from sucrose in the diet is explained by the inter correlation of sucrose with saturated fat in other words donuts ok wherever there was the fat there was sucrose too because these guys here eat donuts partial correlation analysis show that with saturated fat constant there was no significant correlation between dietary sucrose in the incidence of coronary heart disease. Okay.
When you do a multilinear regression analysis, you have to do it both ways. You have to do holding sucrose... a fat constant showing that sucrose doesn't work, and then you have to hold...
sucrose constant and show that fat still works. You see that anywhere? He didn't do it.
He didn't do it. He didn't do the thing that you need to do to do a multivariate linear regression analysis. Now, this was done before computers. We can't check the work. He's dead.
He died in 2004. So we're left with a conundrum. Do we believe this? Do we believe this study?
Because we based 30 years of nutrition education and information and policy in this country on this study and as far as I'm concerned it has a hole as big as the one in the u.s. coal USS Cole all right you got it everybody am i debunking yes no all right let's keep going Remember I told you LDL may be not so bad? Well, here's why. Because there really isn't one LDL.
There are two. There are two LDLs. Here's one over here.
It's called pattern A or large, buoyant LDL. So everybody knows that LDL correlates with cardiovascular disease, and that's true, and I'm not going to argue that. That is true. But it's not this one, pattern A LDL.
These guys are so light. They are buoyant. They float. So they get carried through the bloodstream, and they don't even have a chance because they're so big and they're so buoyant, they don't even get underneath the edge of the endothelial cells in the vasculature to start the plaque formation process.
But over here we have this other guy over here called pattern B, or small dense LDL. You see the difference? These guys are dense.
These guys don't float. These guys are small. They get underneath the edge of the surface of the endothelial cells, and they start the plaque formation. And it's been shown by numerous investigators now that small, dense LDL is the bad guy. Okay, now, when we measure LDL in the bloodstream, when you do a lipid profile, you measure both of them together because it's too hard to distinguish the two.
So when you get an LDL, you're getting both LDLs, the neutral one and the bad one. Now, how can you tell whether your LDL is the neutral one or the bad one? What you do is you look at your triglyceride level.
in association with it because your triglycerides tell you which one it is. So here, here's pattern A over here, okay? Big, large, buoyant LDLs, okay? And you'll notice that the triglycerides are low and your HDL is high.
That's what you want. You want a low triglyceride, high HDL because that's the good cholesterol. You want high, good cholesterol.
Over here, you have pattern B, and here you have high triglyceride, low HDL. That's the bad guy. That's the guy you don't want to be because you're going to die of a heart attack. No question about it. Triglyceride to HDL ratio actually predicts cardiovascular disease way better than LDL ever did.
Point is, when you measure LDL, you measure both. So, dietary fat raises your large buoyant. What do you think raises your small dense?
Carbohydrate. Okay, so here's percent carbohydrate and here's your pattern B going up. Everybody got it? So what did we do? What did we do in 1982?
What did we do? We went on a high-carb diet, which was supposed to be a low-fat diet, right? Right.
So, here's the low-fat craze, okay? Took America and the world by storm. Because the content of low-fat, home-cooked food that you cook by yourself in your house, you can control the content of fat.
But when you process it, low-fat processed food, it tastes like cardboard. It tastes like crap. Okay, so the food companies knew that.
So what did they do? They had to make it palatable. So how do you make it something palatable that has no fat in it? You add the sugar, right?
So everybody remember Snackwell's? Okay, so two grams of fat down, 13 grams of... Carbohydrate up, four of them being sugars, so that it was palatable.
Well, we've just shown you that that's the worst thing you could do, and that's what we've done, and we're still doing it today. So when you find a mistake, what do you do? You admit the mistake, and you right the ship. We haven't admitted the mistake, and we haven't righted the ship.
So we've had our food supply adulterated, contaminated, poisoned, tainted, on purpose. And we've... allowed it and we've led it through the addition of fructose for palatability, especially because of the decreased fat, and also as a, ostensibly, browning agent, which actually has its own issues because why it browns so well with the sugar in it actually is what's going on in your arteries because that's causing what we call protein glycation and cross-linking, which is actually contributing to atherosclerosis. So it works on your steak on the grill.
It works in your arteries the same way. Okay? And removal of fiber also.
Now, why did we remove fiber from our diet? We as human beings, walking the earth 50,000 years ago, used to consume 100 to 300 grams of fiber per day. We now consume 12. Why? What did we do? We took the fiber out.
So why did we take the fiber out? It takes too long to cook, takes too long to eat, and shelf life. So people ask me, what's the definition of fast food?
Fiberless food. I dare you, other than a salad, I dare you to go to any fast food restaurant and find anything on their menu that's actually... have to cook that has more than one gram of fiber in it because there isn't any and that's on purpose because they take the fiber out because that way they can freeze it ship it around the world and cook it up fast and not only is it fast cooking but it's fast eaten which also causes its own So, on satiety issues, bottom line, we have a typhoon on our hands. And then finally, the last issue was the substitution of trans fats, which are clearly a disaster.
But those have been going down because we know that those are a problem. So we've actually gotten rid of most trans fats. fats, not completely, but most. So this is it.
This is what we've done over the last 30 years. Okay, now to the biochemistry. Now, how many of you here have taken biochemistry? About 25%. I am going to show you a lot of reactions in excruciating detail.
If you've studied biochemistry, you will have an anaphylactic reaction. If you haven't studied biochemistry, you will fall asleep. So what I'm going to suggest that you all do is just let me do my thing to show you that at least it works, and just count the arrows.
Okay? Okay? You can do that, right?
Can you count the arrows? It's not like counting sheep. You can count the arrows and just stick with me. Just let me do my thing and let me show you why fructose is not glucose. Because what the liver does to fructose is really unique and you've got to understand it to understand everything I've just told you.
So number one, fructose is seven times more likely than glucose to do that browning reaction, the advanced glycosylation end products. The thing that happens on your grill happens in your arteries for the same. same reason.
You can actually see the color change too. Fructose does not suppress the hunger hormone. There's a hormone that comes from your stomach called ghrelin you've heard about already.
So if you preload a kid with a can of soda and then you let them loose at the fast food restaurant, do they eat more or do they eat less? They eat more. They just took on 150 calories yet they eat more. Reason? Because fructose doesn't suppress the hunger hormone.
mongrelin. So they eat more. Acute fructose ingestion does not stimulate insulin because there's no receptor for fructose, no transporter for fructose on the beta cell that makes insulin. So the insulin doesn't go up.
Well, if the insulin doesn't go up, then leptin doesn't go up. And if leptin doesn't go up, your brain doesn't see that you ate something. Therefore, you eat more. And finally, I'm going to show you liver, hepatic fructose metabolism is completely different between fructose. fructose and glucose.
Completely different. And I'm going to show you before the day is out, the evening is out, that chronic fructose exposure alone, nothing else, causes this thing we call the metabolic syndrome. Everybody knows what the metabolic syndrome is? Okay, so this is the conglomerate of the following different phenomena. Obesity, type 2 diabetes, lipid problems, hypertension, and cardiovascular disease.
Okay, those all cluster. together. called metabolic syndrome. I'm going to show you how fructose does every one of those.
I want to show you the difference between glucose and fructose in a way that will be glaringly apparent. So let's consume 120 calories. in glucose.
Two slices of white bread. What happens to that 120 calories? Now, you eat the 120 calories, 96 or 80% of the total will be used by all the organs in the body.
Okay? 80% off the table. Why? Because every cell in the body can use glucose. Every bacteria can use glucose.
Every living thing on the face of the earth can use glucose because glucose is the energy of life. Okay? That's what we were supposed to eat. Okay? 24 of those calories, or 20%, will hit the liver.
Okay? So let's watch what happens to those 24 calories. Here they go. So the glucose comes in through this transporter called GLUT2. the glucose is going to stimulate the pancreas to make insulin.
The insulin is going to bind to its receptor, and it's going to take this substrate over here called IRS1, insulin receptor substrate 1. That's not important right now. Don't worry. And it's going to tyrosine phosphorylate it. And it's going to be tyrosine IRS1, which is now active.
That's active. And it's going to stimulate the second messenger here called AKT. Now, what AKT does is it stimulates this guy down here, SREBP1, sterol receptor binding protein number one. Don't worry about it.
about it. But this is the thing that ultimately gets fat mechanics going. So you'll see in a minute.
So one of the things that SREBP1 does is it activates this enzyme here called glucokinase, which takes glucose to glucose 6-phosphate. Now glucose 6-phosphate can't get out of the liver. The only way to get glucose 6-phosphate out of the liver is with hormones, glucagon or epinephrine.
That's the way you can get it out. So now the glucose is fixed in the cell, but it's only 24 calories worth. So it's not a big bolus of it. Now, the glucose 6-phosphate, almost all of it is going to end up going over here to something called glycogen. Now, glycogen is the storage form of glucose in the liver, okay, because glycogen is easy to fish the glucose out with glucagon and epinephrine.
So my question to you, and granted this is a physiology question, is how much glycogen can your liver store before it gets sick? The answer is any amount. It's unlimited.
We have carb loaders who run marathons, right? Does it hurt them at all? We have kids with a disease where they can't get the glucose. of the glycogen called glycogen storage disease type 1a or von geerkes disease they got livers down to their knees they're so big they're hypoglycemic like well get out because they can't lift the glucose out of their liver okay but they don't go into liver failure because glycogen is a non un-toxic storage form of glucose in the liver. So the whole goal of glucose is to replete your glycogen.
So this is good. This is not bad. This is good.
Now a little of that glucose is gonna fall down here. It's gonna get metabolized down to this stuff here called pyruvate. And the pyruvate is going to enter your mitochondria over here.
Remember your mitochondria are the parts of your cell that actually burn the energy. They're your little factories. They make the stuff that lets you live, okay, called ATP.
ATP, adenosine triphosphate. That's the energy of life right there. So the pyruvate comes in, gets converted to something called acetyl-CoA, gets metabolized by this thing called the Krebs cycle, TCA cycle, and you throw off ATP and carbon dioxide, which you breathe off. So far so good?
Have I snowed anybody yet? You're with me? I snowed one guy back there.
I'm doing my best. I swear to God, I'm doing my best. Anyway, so this stuff over here, this acetyl-CoA, gets burned off in the TCA cycle.
Now, maybe you won't burn all of it off. And so some of it may exit as citrate. And the citrate then leaves the mitochondria through a process known as the citrate shuttle.
And then that citrate can then be broken down by these three enzymes, which are all subservient to this SRABP1. This is ATP citrate lyase, acetyl-CoA carboxylase, fatty acid synthase. They're not important. The only thing to know is these three enzymes together turn sugar into fat. This is called de novo, meaning new, lipogenesis.
fat making. This is de novo lipogenesis. So you take the citrate, which came from the glucose, and you end up with something called acyl-CoA, which then gets packaged with this protein here, and you end up with something called VLDL, very low density lipoprotein.
Now, anybody heard of that before? Is it good or bad? It's bad. That's bad. VLDL is bad because that's one of the things that causes heart disease.
It's also a substrate for obesity. obesity. So you don't want to make much of this. But the point is... You started with 24 calories, maybe a half a calorie will end up as VLDL.
So that little Japanese guy with the little hat, you know, working out in the field, eating rice for the next, you know, 90 years, you know, can he die of a heart attack at age 90? Sure. Okay?
But that's not so bad. Okay? If you make it...
to 90, you're doing all right, okay? Because of that VLDL coming from glucose, okay? Glucose made a little bitty VLDL, okay?
And that serves as a substrate for adipose deposition into your fat cell here, triglyceride. In addition, because the insulin went up... in response to the glucose, your brain sees that signal, and it knows that that is supposed to shut off further eating.
Okay? In other words, hey, I'm busy metabolizing my breakfast. I don't need lunch. Okay? And so you have a nice negative feedback loop between glucose consumption, the liver, the pancreas, and the brain to keep you in normal negative yin-yang energy balance.
This is good. This is not dangerous. This is what's supposed to happen.
All right, so now let's talk about a different carbohydrate. Let's talk about my favorite carbohydrate, maybe yours too. Okay, ethanol. Ethanol is a carbohydrate, isn't it? Here's the structure, carbon, hydrogen, oxygen.
It's a carbohydrate. But we all know that ethanol is a toxin, right, a poison, right? You can wrap your Lamborghini. around the tree or you can fry your liver your choice depends on how much you drink and how often right okay so we know that ethanol is not good for you except of course a little bit is good for you you right so we can talk about that too later if you want okay let's talk about how it's bad for you so here's acute ethanol exposure okay cns depression vasodilatation hypothermia tachycardia myocardial depression pupillary responses respiratory depression diuresis hypoglycemia loss of fine motor control you all went to college here's fructose nothing doesn't do any of those because the brain doesn't metabolize fructose okay Alcohol gets metabolized in the brain to cause all of those things, but fructose doesn't.
So fructose is not an acute toxin. Ethanol is. We control ethanol, don't we?
We have something called the Bureau of Alcohol, Tobacco, and Firearms. We have all sorts of things. We tax ethanol.
We do all sorts of things to limit consumption of ethanol. The Nordic countries, all the liquor stores are state-run in an attempt to try to set the price of ethanol high enough to... so as to discourage consumption for public health reasons. We have 1,500 years of alcohol control policy in this world to draw on in terms of how to limit consumption.
Got it? Because ethanol is a toxin, and we know it. So let's consume 120 calories in ethanol.
Shot a maker's mark. Anybody taste it? Yeah, good.
Okay. So, 24 calories right off the top. Okay, the stomach and the intestine have something called the first pass effect. So 10% off the top.
And kidney, muscle, and brain will consume the other 10%. So there goes 20% or 24 calories right off the top. 96 calories of the 120 are going to hit the liver. Now, how many was it for glucose?
It was 24. So four times the substrate is going to hit the liver. and there's the rub. Okay?
This is a volume issue. Okay? We're going to show you how.
So the ethanol comes in, passive diffusion, there's no receptor for it, no transporter. First thing that happens is ethanol gets converted to this guy over here called acid aldehyde. Okay?
Anybody know anything about aldehydes? Like formaldehyde? Right?
Are aldehydes good for you or bad for you? They're bad, right? Because what do they do? They can cause cancer.
They cross Cross-link proteins is what they do. So if you cross-link enough proteins in your liver, what do you think happens to it? You get something called cirrhosis.
Right, exactly. So this guy over here is bad. And it generates something called reactive oxygen species.
And reactive oxygen species damage proteins in the liver. And the more alcohol you drink, the more of this stuff you get. So far, so good?
Okay, so this is one of the reasons why alcohol is bad. Now the acetaldehyde will come down here. to something called acetate.
The acetate will enter the mitochondria just like the pyruvate did before. We'll get converted to acetyl-CoA and participate in the TCA cycle just like before to generate energy so that alcoholics don't die from lack of energy. They got energy.
It's everything else they don't have. They're going to have a whole lot of citrate, right? Because they have 96 calories that have to get metabolized.
How many calories made it to the mitochondria with glucose? About a half, right? Because most of it went to glycogen.
So we've got a big citrate. So it's in big font to show you that we're talking about big citrate now. And so the big citrate is going to get metabolized all the way to VLDL by this SRIBP1.
And so... So you're going to get a lot of VLDL, and this is the dyslipidemia of alcoholism right here. Okay, everybody see that? So the liver's going to try to export this VLDL out so that it doesn't get sick because when fat builds up in the liver, that's not good. good for it.
Some of it's going to exit as free fatty acids and those free fatty acids will take up residence in the muscle and you get something called muscle insulin resistance. So insulin resistance, that's a bad thing. That makes your lip muscles and your liver not work so well. And can cause all sorts of other problems like diabetes. Some of the acyl-CoA won't even make it out and will precipitate as a lipid droplet.
So there's your alcoholic steatohepatitis. This acyl-CoA and this ethanol and these reactive oxygen species can start this enzyme activated. It's called C-Jun N-terminal Kinase 1 or Junk 1, and it really is Junk 1 because it is the bridge between... metabolism and inflammation. So when you generate junk one, you do bad things to your liver, which I will show you when we talk about fructose.
So let's talk about fructose. Fructose is sweet. We like it a lot. We like it in everything.
We like it in our bread. We like it in our pretzels. We like it everywhere we look.
So let's consume 120 calories in sucrose, a glass of orange juice. Everybody got it? So two slices of white bread, a shot of Maker's Mark, a glass of orange juice. All the same 120 calories, but three different substrates.
Let's see what happens to the fructose. So, number one, the glucose, remember, because sucrose is half- glucose, half fructose. So 60 of the calories of the 120 are glucose. 12 are going to make it into the liver.
48 out here for the rest of the body. Okay? The same 20-80 split we had before with glucose. So far so good. But all 60 calories of fructose are going to be metabolized by the liver.
Why? Because only the liver can metabolize fructose. So what do we call it where when you take in a compound that's far into your body and only the liver can metabolize it and in the process generates various problems. What do we call that? We call that a poison.
So let me show you how it's a poison. So let's watch the fructose. So the fructose comes in through this transporter now. Before it was GLUT2, now it's GLUT5.
No insulin, remember, because fructose does not stimulate insulin. The fructose then gets metabolized by this guy over here called fructokinase to form something called fructose 1-phosphate. In the process, ATP has to give up one phosphate to ADP because the phosphate has to come from somewhere.
So it comes from here. Now, before we had 24 calories that had to be phosphorylated. Now we have 72 calories that have to be phosphorylated.
So we have three times the substrate, and there's the rub. It's a volume issue for right now. So we're going to lose a lot of phosphate, aren't we?
So there's a scavenger enzyme in your liver called AMP-Diaminase-1 to rescue. the phosphates off the rest of the ATP molecule. And it takes ADP down to AMP, adenosine monophosphate, down to IMP, inositol monophosphate, and finally to the waste product, uric acid. Anybody ever heard of uric acid?
What is it? It's a waste product. It goes out in your urine. It causes what disease?
Gout, right. It also causes another disease. called hypertension.
Okay, let me show you how. Because uric acid, turns out, blocks the enzyme in your blood vessels called endothelial nitric oxide synthase. And that's the enzyme that makes this stuff called nitric oxide, NO. And that is your endogenous blood pressure.
lower. That keeps your blood pressure low. So when you can't make it, your blood pressure goes up.
So this just shows that fructose consumption increases gout in adults. Okay, so this is a study that came out last year. showing that fructose consumption increases the risk for gout, showing that uric acid is going up. And this is a study done by our pediatric renal fellow, Stephanie Wynn, just published in Journal of Pediatrics.
Okay, it's not submitted anymore. It's long in press. Okay, showing that this is in the NHANES database in the adolescent. showing that sugar sweetened beverages as it goes up your uric acid goes up and not only does your uric acid go up but here's your sugar sweetened beverages and here's your systolic blood pressure going up.
Here's a study done by Dan Feig at the University of Texas San Antonio where he took obese adolescents with hypertension and he gave them the drug allopurinol and allopurinol is the drug that you treat gout with to lower the uric acid and look Look what happened to the blood pressure, systolic, diastolic, went down, showing that in fact uric acid is an important part of hypertension. We have a hypertension epidemic in this country. Here it is.
It's the sugar. Okay, so, so far we have high blood pressure. Let's keep going. The fructose will get metabolized down to pyruvate.
The pyruvate will enter the mitochondria just like before, throwing off a lot of citrate. Now here's a little trick that fructose does. does that glucose doesn't.
Because these two can reform this stuff over here called fructose 1,6-bisphosphate, which can then reform with glyceraldehyde to form this guy over here called xylose 5-phosphate. And I'll get to xylose 5-phosphate in a moment. But I want to point out this asterisk that's there to remind me to tell you something. That's there to remind me to tell you that this is why the sports drink companies put high fructose corn syrup in the sports drinks. Because if you are glycogen depleted, in other words, if you just ran a marathon and you have no glycogen left in your liver because you burned it all, and you take in a sports drink with high fructose corn syrup, you can replete your glycogen faster than with glucose alone.
That's true. So for elite athletes, a high fructose corn syrup containing sports drink actually makes sense. And so indeed, sports drinks have high fructose corn syrup. The question is, who's drinking the sports drinks?
Any elite athletes you know? Who's drinking the sports drinks? The kids, right? Why are they drinking it?
Because it's cool, right? Because it's cool and it tastes good. Okay, so before we go on, I just want to now digress for a moment. Okay? 1967. University of Chicago.
of Florida patents Gatorade. Everybody remember Gatorade? Okay.
1970, the Florida Gators win the NCAA championship in football. Gatorade makes a big splash. Okay?
Big deal. Anybody ever taste the original Gatorade? Yeah? What it tastes like? Tasted horrible.
It tasted like something that you might find coming out of you instead of going into you. It tasted awful. 1992, Pepsi buys Gatorade. And they say, how are we going to market this swill?
So what did they do? They added the high fructose corn syrup. Okay? So now who drinks it? Right, fat kids.
Right? Not even skinny kids. Fat kids drink it. Okay?
So there's a problem here. Okay? And we're going to show you how that works.
Okay. So xylose 5-phosphate, just to show you. So here's, if you take a rat and you glycogen deplete him by making him run on an exercise wheel. And then you refeed them with starch or with sucrose.
The xylose 5-phosphate goes way up with the sucrose. So you get more xylose 5-phosphate through this pathway here, going over here. So why do we care about xylose 5-phosphate? Well, here's why.
Because it... It stimulates this guy over here called PP2A, which then activates this transcription factor here, carbohydrate response element binding protein, which then activates what three enzymes? New fat making, right?
The novo lipogenesis. So here's the citrate, right? We got lots of that. And here we've got acyl-CoA, which is the way into fat, okay, which then gets packaged, all right, oops, with the VL, to the VLDL.
Now you've got the dyslipidemia. of obesity, of fructose consumption, which has been known for many years. So here's normal medical students, if you can call them normal. Taking in a glucose load, notice almost none of it ends up as fat. Taking in a fructose load, same number of calories, 30% of it ends up as fat.
So when you consume fructose, you're not consuming a carbohydrate, you're consuming. fat. So everybody talks about a High fat diet?
Well, a high sugar diet is a high fat diet. That's the point. That's exactly the point. Okay?
This is a study where they gave acute administration of fructose, and you can see the triglycerides going up compared to the control. Okay, serum triglyceride right there. Here's normal medical students again, six days of high fructose feeding.
Triglycerides doubled. De novo lipogenesis went up five times higher. And here's free fatty acids, which then cause insulin resistance, doubled.
Okay, six days. So here's the dyslipidemia. of fructose consumption. We're not done.
Some of the fat won't make it out of the liver, just like with ethanol, and now you've got a lipid droplet, so now you've got this non-alcoholic steatohepatitis. So this is work that we did in our clinic, looking at sugar sweetened beverage consumption against the liver enzyme marker ALT, alanine aminotransferase, which tells you about fatty liver. And sure enough, here's sugar sweetened beverages against ALT, and you can see a nice... linear relationship in Caucasians. African-Americans, it's a different relationship, and that's a whole other story all by itself.
So there's the lipid droplet of non-alcoholic steatohepatitis. Some of it will come out of free fatty acids and populate the muscle. It will also tell the insulin to go up higher. Remember that junk one? So here's what junk one does.
So the acyl-CoA and the fructose can all activate junk one. And what junk one does is, remember, when we use glucose, this This IRS became tyrosine IRS1, and that was good. Remember that? Well, junk 1, what it does is it's serine phosphorylates IRS1, and serine IRS1 is inactive.
So now the insulin can't even do its job in the liver. So now you have liver insulin resistance as well. That's going to make the pancreas work that much harder, generating higher insulin levels, which raise your blood pressure even further, cause further fat-making, cause more energy to go into the liver.
into your fat cell, there's your obesity. And finally, our research has shown that the higher the insulin goes, the less well your brain can see its leptin. And so there you've got continued consumption because your brain thinks it's starving.
And it's been shown in many different ways that fructose consumption changes the way your brain recognizes energy, all in a negative fashion, so that you basically think you're starving. Your brain gets the signal. that you're starving even though your fat cells are generating a signal that says, hey, I'm full like all get out.
So this just shows you how it goes. So the high insulin generates the obesity because this is that, remember the first law of thermodynamics, the biochemical force generating the energy storage as the primary phenomenon. Remember, if you're going to store it and you expect to burn it, then you're going to have to eat it. So here's the store it. Normally, that would make leptin, and the leptin should feed back and turn everything off.
But it doesn't because the insulin gets in the way and the high-fat diet gets in the way. Also, the hyperinsulinemia stops the leptin from acting on that nucleus accumbens, and so you get an increased reward signal. So that continues your appetite, continues more fructose, more carbohydrate, generating more insulin resistance, and you can see you generate a vicious cycle of consumption and disease. And no stopping.
So here we are. Hypertension, inflammation, hepatic insulin resistance, hyperinsulinemia, dyslipidemia, muscle insulin resistance, obesity, and continued consumption. Looks like metabolic syndrome to me. So here are the phenomena associated with chronic ethanol exposure. Hematologic disorders, electrolyte abnormalities, hypertension, cardiac dilatation, cardiomyopathy, dyslipidemia, pancreatitis, malnutrition, obesity, hepatic dysfunction, that's alcohol, Alcoholic steatohepatitis, fetal alcohol syndrome, and addiction.
Here's fructose. Eight out of 12. Why? Because they do the same thing. Because they're metabolized the same way. Because they are the same.
They come from the same place, right? How do you make ethanol? Naturally. Right.
You ferment sugar. Hasn't changed. Because it has all the same properties. Because it's basically taken care of by the liver in exactly the same way and for the same reason.
Because sugar and ethanol are the same. Every which way you turn. So here's our clinic intervention.
This is what we do in our clinic. It's as simple as you can imagine. We write this on the back of a matchbook.
It's just as simple as you can make. We have four things we teach the kids to do, and the parents. Get rid of every sugared liquid in the house, bar none.
Only water and milk. There is no such thing as a good sugar beverage, period. Eat your carbohydrate with fiber. Why?
Because fiber is good. Fiber is supposed to be an essential nutrient. And we can talk later, if you want, after the cameras turn off, as to why fiber is not an essential nutrient. Because the government doesn't want it to be. Okay, because then they couldn't sell food.
abroad. Wait 20 minutes for second portions to get that satiety signal. And finally, buy your screen time minute for minute with physical activity.
That's the hardest one to do. If you play for half an hour, you can watch TV for half an hour. You want to watch TV for an hour, play for an hour. That one's a hard one. But anyway, we follow our patients every three months.
So here's my question. Does it work? What do you think?
Yeah, it works. So this is BMI Z-score time from initial visit. It works. But we were interested in what made it work and what made it didn't work, so we did a multivariate linear regression analysis, right?
The thing that made it not work, sugared beverage consumption. The more sugared beverages the patients drank at baseline, the less well the lifestyle intervention worked for all the reasons I just showed you. Okay? So why is exercise important in obesity?
because it burns calories? Come on. 20 minutes of jogging is one chocolate chip cookie. You can't do it.
Are you joking me? So why is exercise important? I'll tell you why.
Here's why. Number one, it improves that skeletal muscle insulin sensitivity because your insulin actually works better at your muscle, which then brings your insulin levels down, which is good for you. Number two, it's your endogenous stress reducer.
It's the single thing that actually stress reduces. And if you stress reduce, what do you think your appetite does? Goes down. Because stress and obesity go hand in hand, right? For all sorts of reasons which are beyond the scope of this lecture.
today, but we can talk about it in the question period if you want. And then finally, remember that de novo lipogenesis? Remember those three nasty enzymes?
Okay. What if you burned the stuff off before you made the fat? That's what exercise does, because it makes that TCA cycle run faster, so you don't get the citrate leaving the mitochondria, so it doesn't get turned into fat, so it doesn't precipitate and cause all the problems you just saw. That's what they mean by a higher metabolism, yes. Okay?
But it has nothing to do with burning of calories. That is the stupidest reason that I've ever heard of for exercise. You've got to be joking me. Okay?
You can't do it. I mean, one... Big Mac, you know, and you've got to, you know, mountain bike for 10 hours. Are you joking? Okay, so why is fiber important in obesity?
So this is my motto in clinic. When God made the poison, he packaged it with the antidepressants. antidote.
Because fructose is a poison. I think I've hopefully shown you that. But wherever there's fructose in nature, there's way more fiber. You ever see a piece of sugar cane?
It's a stick. You can't even chew the damn thing. You got to suck the stuff out like that.
I mean, how many calories do you think you're going to get out of a piece of sugar cane? Okay. They actually did studies on the sugar plantations back in the early 1900s. Okay? All of the workers were healthy and lived longer than the sugar executives who got the processed product.
How about that? Wonder why. Okay?
So eat your carbohydrate with fiber. That's why we say that. That includes sugar. That's why fruit's okay. Because number one, it limits how much fructose you're going to take in.
And number two, it gives you an essential nutrient, which you needed in the first place. And you get some micronutrients along with it so that you actually can... your liver works healthier.
So here's what fiber does. Number one, it reduces the rate of intestinal carbohydrate absorption. Now, sometimes that's bad.
I'll tell you when that's bad. You know when that's bad? That's bad when you're at a formal function. Because what happens if you reduce the rate of carbohydrate absorption in your gut? The bacteria get to it.
So as far as I'm concerned, in life you've got two choices. It's either fat or fart. It increases the speed of transit of the intestinal contents to the ileum. And that raises this hormone over here called PYY, which goes to your brain and tells you the meal's over. That's your satiety signal.
So when you add fiber to your diet, you actually get your satiety signal sooner because the food moves through faster. And then finally, it also inhibits the absorption of some free fatty acids all the way to the colon, and then those get chopped up into little... itty-bitty fragments called short-chain fatty acids, and those actually suppress insulin as opposed to long-chain fatty acids, which stimulate insulin.
So there are a whole bunch of reasons why fiber is good. Anybody ever heard of the Paleolithic diet? Okay, go home and read it.
read up on it on the internet. The Paleolithic diet. Basically, if you eat everything as it came out of the ground raw, with no cooking, you would cure diabetes on a dime.
It takes about a week because you're getting that 100 to 300 grams of fiber I mentioned before. That's why. Because fiber is good for you. And the more, the better. Type 2. Type 2, right.
Type 2, not type 1. I stand corrected. Type 2. Okay, now for some fun. Okay, that's the end of the biochemistry. How'd I do?
I told you I'd get you through it. Okay, so now comes the fun part, okay? The racial innuendos and all the political stuff, okay?
The fructosification of America and, of course, the world. Ready? Another quiz. Can you name the seven foodstuffs at McDonald's that don't have high fructose corn syrup or sucrose? No, mustard has it.
Oh, come on, come on, the big one. French fries. But they have salt, starch, and fat, so they're not so good either. Okay, what else?
We'll get to coffee. Hash browns, for the same reason, right? Salt, starch, and fat. Okay, what else?
Chicken McNuggets. I was shocked. I was shocked.
No sucrose or high fructose corn syrup in chicken McNuggets. But as the circuit court judge in New York called them, they are still a McFrankenstein creation. Okay, but nonetheless, no sucrose.
I was really shocked. Sausage. Oh, they're terrible.
They're just disastrous. But, I mean, there's nothing good in them at all, but there's no fructose. Sausage.
Diet Coke. I eat coffee, if you don't add the sugar, and iced tea, if you don't add the sugar. By the way, the Chicken McNuggets have, you know, we have a disclaimer, because no one eats the Chicken McNuggets without the dipping sauce. And there's a whole bunch of high-fructose corn syrup in the dipping sauce, right? Okay, good.
All right. So who's really drinking this? We talked about this before. Gatorade AM.
So this is an attempt by Pepsi to capture market share on the juice. market, right? Do you think there are any elite athletes who actually drink this stuff?
You got to be kidding me. Okay, this is for kids, right? So this really blew my socks off. This was my daughter when she was in second grade two years ago, Miriam Lustig, okay, brought these two cartons of milk home for me and said, Dad, you're not going to believe this, okay, second grade, okay?
So here's the calorie. in Berkeley Farms 1% low-fat milk, 130 calories, 15 of them are sugars because it's lactose, right, which is okay. And here's Berkeley Farms 1% chocolate milk, 190 calories, 29 grams of sugar, all high-fructose corn syrup. it's like a glass of milk plus a half a glass of orange juice and that's what we're giving to our kids and you know what the nutrition department at the SFUSD says well we have to get our kids to drink milk somehow Now, is that brilliant or what?
I don't know. Now, what about WIC? So we talked about the 112 pounds of orange juice that the kid down in Salinas was drinking.
What about WIC? So remember what we started with? We have an epidemic of obese six-month-olds.
Remember? So could this be the reason? So here's a can of formula.
43.2% corn syrup solids, 10.3% sugar. It's a baby milkshake. Soda, Coca-Cola, is 10.5% sucrose. formula is 10.3% sucrose any difference and There's a huge literature. That's now coming of age that shows that the earlier you expose kids to sweet the more They're going to crave it later Plus there's a new literature that shows the more sugar the pregnant woman drinks or eats dirt During the pregnancy, the more that gets across the placenta and actually causes what we call developmental programming, changing the kid's adiposity even before the kid is born and driving this whole epidemic even further.
So, we'll close in a few minutes, okay? But I just want to point out what's the difference, okay? Here we've got a can of Coke.
Here we've got a can of beer. And I'm not picking on Schlitz or anything. I mean, it's any beer you want, okay?
So 150 calories each, no difference in terms of total calories. Percent carbohydrate, so 10.5% from sucrose here, except there's high fructose corn syrup, but who cares? 3.6% alcohol. Here's the breakdown, 75 fructose, 75 glucose for the Coke. 90 alcohol, 60 maltose for the beer.
Remember, the first pass GI metabolism takes 10% of the alcohol off the table. So when you actually compute the number of calories hit in the liver, which remember was the big... Big difference between glucose and fructose, remember? 72 versus 24 and started the whole thing into motion as terms of what happens that's bad.
Okay? Bottom line, no difference. So, we have something called beer belly. Well, welcome to soda belly because that's what America is suffering from. No ifs, ands, or buts.
That's what it is. Okay? Now, you wouldn't think twice about... not giving your kid a Budweiser. But you don't think twice about giving your kid a can of Coke.
But they're the same, in the same dosing, for the same reason, through the same mechanism. Fructose is ethanol without the buzz. So, fructose is a carbohydrate.
Yes, it is. But fructose is metabolized like a fat. And I've just shown you that 30% of any ingested fructose load ends up as fat. Okay, so when people talk about high-fat diets doing bad things, no, what they're really talking about is high-fructose diets.
And that's what Ansel Keys was looking at. So the corollary to that is, in America at least, and around the world too, a low-fat diet isn't really a low-fat diet, because the fructose or sucrose doubles as fat. It's really a high-fat diet.
That's why our diets don't work. And fructose, just like ethanol, for the same reason, through the same mechanism, and in the same dosing, is also a toxin. Now. Last, what can we do about it?
Can we do anything about it? How about the FDA? You think they can do something about it?
After all, aren't they supposed to regulate our food? Aren't they supposed to regulate what they can put in food? Right?
Weren't they supposed to regulate tobacco? Now they are, actually. So, you know.
weird things. So I want to just show you what the tobacco company thinks of all this. So here's, this is actually from the UCSF Legacy Tobacco Documents Library that Stan Glantz runs right across the street.
Okay, Stan's a good guy. Okay, likes Stan a lot. Okay, and he showed me this. He said, under the regulations governing food additives, so this came from an Altria or Philip Morris executive, it is required that additives be safe, defined as a reasonable certainty by competent scientists that no harm harm will result from the intended use of the additive. Now, does fructose meet that standard?
Well, the FDA says that fructose, high fructose corn syrup has what's known as GRAS, G-R-A-S status, generally regarded as safe. Now, where'd that come from? Nowhere.
It came from nowhere. It came from the notion that, well, fructose is natural. It's in fruit.
It must be okay. Right? Yeah, well, tobacco's natural too.
But it's not. Ethanol's natural, but it's not. A whole bunch of Jamaican aki fruit's natural, but it's not either.
It kills you. Okay? Keeping on going. A food shall be deemed to be adulterated if it bears or contains any poisonous or deleterious substance which may render it injurious to health.
Fructose fits that description, right? Uh-uh. But not with the... prevention of chronic diseases, even though its own regulations explicitly postulate the connection between such products and such diseases.
In other words, the FDA will only regulate acute toxins, not a chronic toxin. Fructose is a chronic toxin, right? Acute fructose exposure did nothing, remember, because the brain doesn't metabolize fructose. The liver does. And the liver doesn't get sick after one fructose meal.
It gets sick after one meal. after a thousand fructose meals, but that's how many we eat. So the FDA isn't touching this.
The USDA isn't touching this. Because if the USDA touched this, what would that mean? That would mean an admission to the world that our food is a problem.
So what do you think that would do? There are three things in this country that we can still sell overseas. Weapons, entertainment, and food.
Cars? Computers? I don't think so. I mean, can anybody think of anything else that another country wants of ours?
What? Tobacco, right, tobacco. All right, you get the picture, all right?
So the USDA doesn't want to know about this, okay, because this is bad news. And so who runs the food pyramid? The USDA. It's the fox in charge of the hen house, okay, because their job is to sell food.
And who's eating it? We are. So, in summary. Fructose, and I don't care what the vehicle is, it's irrelevant.
Sucrose or high fructose corn syrup, I don't care. Fructose consumption has increased in the past 30 years, coinciding with the obesity epidemic. A calorie is not a calorie.
And the dieticians in this country are actually... perpetrating this on us because the more you think a calorie is a calorie the more you think well then if you ate less and exercise more it would work it doesn't all of the studies show it doesn't work here's why it doesn't work work because a calorie is not a calorie. Fructose is not glucose.
We know a calorie is not a calorie because there are good fats and bad fats. There's good protein and bad protein. Okay, there's good carbohydrate and bad carbohydrate. And glucose is good carbohydrate. Glucose is the energy of life.
Fructose, okay, is poison. You are not what you eat. You are what you do with what you eat.
And what you do with fructose is particularly egregious and dangerous. Hepatic fructose metabolism leads to all the manifestations of the metabolic syndrome. Hypertension through that uric acid pathway, de novo lipogenesis, dyslipidemia, hepatic steatosis through that DNL pathway, those three enzymes, the new fat-making pathway, inflammation through junk one, hepatic insulin resistance because of the serine phosphorylation of IRS1, obesity because of the VLDL transport to the adipocyte, and leptin resistance promoting continuous consumption, basically starving your brain, making you think you need more. Fructose ingestion interferes with obesity intervention, as we showed in our clinic. The more soft drinks, the less well diet and exercise actually worked.
Fructose is a chronic hepatotoxin for the same reason that alcohol is. The only difference is alcohol is metabolized by the brain, so you get alcohol effects. Fructose is not metabolized by the brain, so you don't get those effects.
But everything else it does is the same. But the FDA can't and won't regulate it. It's up to us. I'm sorry. standing here today to recruit you.
Okay, that's a famous saying here in San Francisco, right? I'm Harvey Milk and I'm here to recruit you. Okay, I'm Robert Lustig and I'm here to recruit you in the war against bad food.
Okay, and this is what's bad. With that, I want to thank my colleagues at the UCSF Department of Pediatrics in our Weight Assessment for Teen and Child Health Clinic, the UCSF Department of Epidemiology and Biostatistics, and also the Department of of Nutritional Sciences at UC Berkeley, in particular Dr. Jean-Marc Schwartz, who is a card-carrying fructose biochemist, PhD biochemist, who vetted all of these pathways that I've shown you today and looked at this and said, oh my God, it is a toxin. He worked in this stuff for 15 years and he didn't even realize it was a toxin until he saw this.
So with that, I'll close. Thank you.