 Good evening. Welcome to the San Francisco Public Library and our program tonight featuring Dr. Robert Lustig. My name is Janet Tom, and I'm a librarian in the business science and technology section on the fourth floor. I'd like to thank Dr. Robert Lustig for coming to speak tonight. Also, thanks to the Reader's Book Store for doing the book sale, which will happen immediately following our question and answer session. Also, thanks to my colleagues, librarians Ruth Amernick and Melissa Riley for helping to make tonight's program happen. Dr. Lustig has requested that tonight with your questions you write them on note cards. You should have gotten one on your way in. If you need one, please raise your hand. Ruth and Cherise are in the back, and what they'll do is collect your questions. As you think of them, please jot them down and pass them toward the center aisles, and then Ruth and Cherise will collect them. And as we're wrapping up the lecture, we'll go ahead and collect them and bring them up. Also, we'd like you to fill out our half sheet evaluation. This is for us. If you want to see more programs like this, please fill it out. Let us know. Let us know how you found out about tonight so we know how to reach you next time. And also, let us know topics you'd like to see here. I mentioned all sorts of different topics that we cover in our department, and we'd love to do program ideas that you have in the future. We're taping tonight's session, so at this time, would you please turn off your cell phones and other electronic devices? Dr. Robert Lustig is Professor of Pediatrics in the Division of Endocrinology at the University of California, San Francisco, Benioff Children's Hospital. He is also Director of the UCSF Weight Assessment for Teen and Child Health Program, better known as WATCH. Dr. Lustig has been studying and treating obese children for the last 18 years, and has come to radically different conclusions about this epidemic in our society. If you tuned in on his talk, Sugar, the Bitter Truth on YouTube, you are one of over 3,400,000 people who saw it since it was recorded in 2009. His new book, Fat Chance, Beating the Odds Against Sugar, Processed Food, Obesity and Disease, was published on December 27th, and it's hit the New York Times best seller list. Dr. Lustig graduated from MIT and received his MD from Cornell University Medical College. He is currently on sabbatical from UCSF and is attending the UC Hastings College of the Law to pursue a degree of Masters of Studies in Law. The topic of his talk tonight is Darwin, Diet, Disease, and Dollars. While the sugar in processed foods has changed society. Ladies and gentlemen, please welcome Dr. Robert Lustig. Well thank you Janet, and thank all of you for coming tonight, for taking time out of your busy schedule on a Tuesday night when your kids should be fed. And I'm going to explain to you why they're not, because we all have busy lives, and this is part of what's happened. My job, my goal tonight is to try to explain in 50 minutes what's gone wrong with us for the last 30 years. So I've got to sort of speed it up, you know, everybody ever see that movie, History of the World Part One, you know, Mel Brooks got to move really fast. So I'll do my best to try to bring everybody along. I hope at the end I will have given you some tools or at least some ways to think about this issue for your own health and for that of your children. Okay, so first of all I have no disclosures, no food industries putting me up to this, and everything I tell you I believe is the God's honest truth, at least the truth that I understand, and I'm going to try to impart it to you in a way hopefully that you will understand how I got to this conclusion. Alright, so here's the past. 2001. Six million kids are seriously overweight. Well, with all of the NIH money, with all of the media attention, with all of the programs and all of the Jenny Craig's and, you know, neutrosystems and everything else that have popped up all over the country, with Michelle Obama's vegetable gardens we are now at 20 million. Here's the present. Currently there are 30% more obese people in the world than undernourished people. 20 years ago it was the exact opposite. So something has gone on, and it's not just going on here, it's going on all over the world. Every single country on the planet has seen an uptick in obesity prevalence. 366 million diabetics walking the earth, 5% of the world's population, and that is going up as we speak as well, and they are chewing through all the healthcare dollars. Soon there will be none. Here's the future. Experts predict 165 million Americans, that's half of all of America, will be obese by 2030. Okay, so WALL-E, everybody remember, see WALL-E? Okay, that's us. We're there now. 100 million Americans will be obese by 2050. That's one third of the adult population, and that means no healthcare for you because Medicare will be broke by 2024. And just two weeks ago we learned that Obamacare was going to cost 32% more than they said, so make that 2019. So we have six years to fix this, guys, okay? And I will tell you right now, we can't fix it doing what we've been doing. Obamacare is predicated on preventative services. There are no preventative services for this. None of them work, right? Because if any of them work, we wouldn't be obese. So we got a problem. We have to do something different. The question is, what? What should we do different? All right, so this is an 11-inch statue that lives in a museum in Vienna. It was unearthed in 22,000 B.C. And it carboned... Sorry, it was unearthed in 1908. It carboned days to 22,000 B.C., I apologize. And what it tells us is that the ancients knew about obesity before they knew about McDonald's. Obesity is part of the human condition. There are about 60 different medical diagnoses that have obesity as one of its cardinal features. There are a lot of reasons to be obese. And I'll tell you that there are a lot of different causes of obesity even today. But none of them explain what's happened over the last 30 years. How did we get so fat so fast? And how come we're so sick in the process? In order to answer this question, we have to turn to probably the biggest scientific thinker since a second to Albert Einstein, that's Charles Darwin. I'm going to try to explain to you what I think Charles Darwin would have told us about what's happened over these last 30 years. So let's talk about the explanation. Obesity continues to worsen in prevalence and severity, no argument. It's increasing in all developed and developing countries, no argument there. It's increasing in all age groups, including newborns. How do newborns get obese? They don't diet and exercise. But there are studies around the world, Russia, South Africa, Israel here, that show that babies born today weigh 200 grams more on average than babies born 25 years ago. And when you do dexa scanning to determine what the body composition of those 200 grams are, guess what they are? They're fat. So these babies are laying down more fat before they're even born. So what do you think fat cells like to do? They like to get filled. So that's why we have an epidemic of obese six month olds. So as far as I'm concerned, you want to talk diet and exercise. You might as well talk to the wall because it don't work. That's what I've, the radical conclusion I've come to is it don't work, ain't gonna work, and we have to do something different. But recidivism is high. Can't do anything about it once it occurs, right? Once you're obese, you know, I mean, how many people can actually lose weight? There is something called the national weight loss registry. Anybody who's lost 30 pounds or more and kept it off for a year or more can join this online registry, it's kept out of the University of Colorado. And there are 6,000 people who have entered their data into this national weight loss registry. And you know what our government says? Hey, if these 6,000 people can do it, so can you. Really. There are 60 million people who can't do it. 6,000 who can, 60 million who can't. And you're gonna tell me that they're the rule, they're the exception. So the question is what's going on. So the obvious explanation that the government would proffer to you and the food industry would proffer to you and everybody including the medical profession would proffer to you is gluttony and sloth. You eat too much, you exercise too little. But what would Darwin say? He would not say this. He would say that this is a mismatch. This is a mismatch between our environment and our biochemistry. That somehow the environment we've created for ourselves does not match our current biochemistry and this is the outcome of that. And the question is what about our environment and what about our biochemistry and what do we do about it? So the question to try to get to the answer to that is, all right, what's obesity for? Why do we even have it? Why did the Venus von Willendorf, why was she obese? Well, it's obvious. I mean energy storage for our rainy day. For how many zillions of years we had this thing called famine. We had droughts, we had dust storms, we had all sorts of things. Bottom line was those who could store energy better survived longer. So there's a genetic predisposition and there's an evolutionary pressure to want to store energy. So energy storage for a rainy day is a good thing to be able to do. So obesity kind of makes sense, sort of. So the question is how is this selective advantage achieved? And this is where the science comes in. So we're going to talk about two physiologic processes today. A little science. I'm going to make it as simple and as palatable as I possibly can. We're going to talk about leptin resistance and insulin resistance. And when you understand those two concepts, you will understand why we're in this boat that we're in today. So leptin, anybody heard of it? A few people. Discovered in 1994 and hasn't even made it into all the medical textbooks yet, but it's super important. So what is it? It's a hormone. It comes from your fat cell. Your fat cell is not a blob of jello sitting on your thighs looking bad. It actually has value and it makes this hormone called leptin. And leptin goes to your brain and tells your brain, hey, I've got enough energy on board so that I can burn it properly, feel good and not eat so much. When your brain can see the leptin signal, you're in energy balance. And I will show you that. And then there's this other one over here called insulin. And you've heard of that one, right? Diabetes. Is the diabetes hormone? Well, no, it's not. It's the energy storage hormone. Insulin's job is to take what you eat and put it into fat cells for storage. That's the energy storage for the rainy day. And if you don't have any insulin, not only do you lose weight but you get super sick and you die, that's called type 1 diabetes. But what we're talking about today is type 2 diabetes or comes along with obesity but is not due to it. We'll talk about that in a minute. And then there's some other hormones that have to do with satiety versus hunger which we're not going to talk about today. Anyway, the hypothalamus transduces all of these signals and basically says I'm hungry and I'm going to eat and I'm not going to burn energy or I'm not hungry, I'm not going to eat and I'm going to burn energy and you'll see that on the next several slides. And what it does is it tells the nervous system, the autonomic nervous system, the fight-or-flight part of your nervous system to either burn energy called the sympathetic nervous system here to tell the fat cells to give up its energy or it tells the vagus nerve here which innervates all the organs inside your intestine. Hey, I'm hungry, I want to eat and I'm going to metabolize it and store it. So it's the yin-yang between this sympathetic nervous system which causes energy to be burned and the vagus nerve which causes energy to be stored as to exactly what's going on. Everybody got that? Okay. So the hypothalamus is ground zero for energy balance. It decides what's going to happen and it all depends on whether or not it sees these hormones or not. So let's go through that and I'll try to explain how it works. So here's the paradox that basically tells us what's going on. Anybody here got children? A few people? Yeah, okay. So if you give a five-year-old kid a cookie, what happens? They bounce off walls. Ask any teacher about what happens when it's cupcake time. This is called the sugar high. And what's going on during the sugar high is so the adipocyte, the fat cell, gets energy. It therefore makes leptin to tell the brain what's going on. The brain interprets that leptin signal and says, hey, I can burn it off. And so it increases the sympathetic nervous system tone which goes to the muscles and that causes the muscles to twitch and we call that fidgeting. So when a kid's going like this in class, good, you're preventing obesity, that's good. And then that energy expenditure then causes the adipocyte to shrink. And so what you've got here is a nice negative feedback pathway between the fat cell, the brain and your nervous system to keep you in relative energy balance. So far so good? Okay, so here's the paradox. What if you give an obese five-year-old kid a cookie? They're in the pantry looking for more cookies. Anybody ever see a sugar high in an obese kid doesn't exist. Does not exist. And the reason is because the kid's not seeing his leptin because if he was seeing his leptin he wouldn't be obese. So when he eats the cookie, there's no sympathetic tone being increased so there's no burning off. And the kid's just looking for more cookies. Now, here's the animal that explains all this. These two are brothers. But this animal over here makes no leptin. No leptin. Fat is all get out but makes no leptin because he has a gene defect so he can't produce the protein. So his brain sees starvation all the time even though he's as fat as all get out. Now, even more to the point is this animal is the biggest couch potato in the world. Rats or mice like to nest in their cages. They like to build up with a sawdust and they go into the corner and they have a little ritual they do. This animal does nothing. You put him down in the center of the cage, he just sits there. And the only reason this animal ever gets off his heiny is if you put the food on the other side of the cage then they'll waddle over there, eat the food, and stay there instead. And the reason is because this animal's brain thinks he is starving all the time because he can't read his leptin signal because there ain't no leptin signal. Everybody understand? So here's what's going on. So here's your fat cell making leptin and your leptin then tells your hypothalamus what to do. When your leptin reaches your hypothalamus and your hypothalamus sees it, it tells you you're not hungry and to burn energy. We call that anorexigenesis. Not eating. And it tells the sympathetic nervous system turn on, burn it off, and it tells the vagus nerve turn off, don't store. So far so good. If your leptin is low, below a leptin threshold for that animal, then you get this one instead. You get orexigenesis. I am hungry. I want to eat. I want to store. And I certainly don't want to burn because I'm trying to store up for a rainy day. So what happens? You do the opposite. The vagus nerve goes into overdrive so you eat and that tells the pancreas to make insulin and it tells the sympathetic nervous system tone down. That's why after Thanksgiving you feel like crap. You can't get out of your seat because your insulin basically went super high because you're in storage mode. Now, believe it or not, there are 14 leptin deficient people in the world. 14. A total of 14. And they are all of Pakistani or Turkish extraction and they all have two genes bad. So the parents were usually related to each other to get two bad genes. And here's an example of a patient who has leptin deficiency. Normal weight at birth but gained weight right out of the box by six months already obese. And by age 10 the kid weighs 220 pounds. But look what happens. You start giving the kids daily shots of leptin to make up for the fact that he's not making it himself because he's got a gene defect and look what happens. He loses weight on a dime. And it's all fat mass that he's losing. Hormone replacement therapy. Kid can't make the hormone. We give the hormone back. Kid becomes normal. But the rest of people are, we're not leptin deficient. We're leptin resistant. We got plenty of leptin, see? And it correlates with how much body fat we have. So the fatter you get the more leptin you got. But if the more leptin you got and it were working you'd burn it off and you wouldn't eat so much and you'd stay stable. So what this is telling us is that obesity is not leptin deficiency. That's for the 14. Obesity is leptin resistance. We make it but we don't see it. Everybody understand? What's blocking the leptin signal? So here's that leptin telling the hypothalamus what to do. Uh-uh. Because something's getting in the way. The question is what's that question mark that's blocking that? Because when your brain can't see your leptin then you go into aerexigenesis you eat and you don't burn. That's called gluttony and sloth. So gluttony and sloth is actually secondary to this biochemical process. And when you can actually fix it the gluttony goes away. And guess what? The sloth goes away too. And I'll show you that. Okay, so what does insulin do? Remember I told you there were two hormones doing this? Insulin. Insulin's funky. Because insulin tells your fat cell store but it tells your brain something else. Normally it tells your brain, hey I'm in the middle of metabolizing a meal. I don't need to eat so much. And so it's actually part of the satiety system. So when you eat something and your insulin goes up that is one of the things that tells your brain hey calm down, don't need to eat so much. And you can stop for that meal. So it does one thing to your fat cell and it does the exact opposite thing to your brain. So that's kind of cool. It has this dual mechanism that seems to be in opposite directions. And it's that that we're going to talk about because that's where the holy grail of this is. Now this is the patient that got me started in obesity way back when I was at St. Jude Children's Research Hospital in Memphis, Tennessee. And I am a neuroendocrinologist. I take care of kids with brain tumors. That's how I got started in this. And this is a kid. This kid is 15 years old in this picture and he weighs 364 pounds. Now when he was seven he was completely normal weight for height. Normal kid. And then he developed this. This brain tumor sitting in the middle of his hypothalamus in that middle of his energy balance pathway. And this required surgery and radiation and he started gaining weight at the rate of 30 pounds a year nonstop to the point where he's in this picture. Now does anybody want to tell me that this is gluttony and sloth? This is because his brain was damaged. He now cannot see his leptin because those neurons in his brain are dead. Everybody got it? He is now leptin resistant on an anatomic basis. On an anatomic basis. His brain can't see his leptin therefore he's always hungry and he doesn't want to move because he's a glutton and he's a sloth but it ain't his fault. It's the brain tumor's fault. Everybody got that? So how does this work? Two different hypotheses. The first that you damage the hypothalamus and that causes you to overeat and that causes the obesity. And we know that these kids make a lot of insulin and that this hypothesis says that the insulin is because of the obesity. It comes after. On the other hand, this is another hypothesis that's been out there for a long time that damage to the hypothalamus does cause obesity but because it increases the vagus nerve because you can't see your leptin. And if that's the case, if the vagus nerve is firing that makes your pancreas release more insulin and that extra insulin then drives energy into fat and that's the reason for the obesity. Now if this is the case nothing I can do because I can't fix a brain. But if this were the case I could potentially intervene right here between the vagus nerve and the pancreas and there's a drug that does just that called octriotide. Now I know how to use that drug because that's an endocrine drug, that's a hormone drug. It normally blocks growth hormone but it also blocks insulin. So I said many, many years ago, 18 years ago now, what if we gave octriotide to these kids who have obesity due to brain tumors? What would happen? Well, here's what happened. Here's a patient. 220 pounds one year later down to 172. And there's an apocryphal story that goes with this patient. She said, the mother called me up after a week on the medicine. It's given by injection. Mother calls me up after a week. Kid hadn't lost any weight yet. She says, Dr. Lustig, something is going on because normally we would go to Taco Bell and she would eat five tacos and an inch of Rideau and still be hungry. And we just went to Taco Bell and she ate two tacos and she was full. And she just vacuumed the house. Vacuumed the house. What does she charge? Anyway, this was very interesting. So we did a few more of those. And here's another patient. Here she is, BMI of 28. And here she is. Six months later on the medicine down to BMI of 24. And this kid became a competitive swimmer. This is a kid who sat around the house, ate Doritos and slept. And now she's a competitive swimmer and she lost all this weight. Fantastic. But then the study was over and the medicine went away and the insurance company wouldn't pay for it. And we couldn't get it for her. And here she is two and a quarter years later trying her best. Here she is in her swim talks and her BMI has swollen all the way back up to 35. Not cool. Well, we finally got the insurance company to pay for the drug and I will tell you that her BMI went back down to 27. So that was good. Now does anybody want to tell me this is gluttony and slough? This is the problem with the brain, right? And here's that pro band patient I told you about before. 364 pounds over here. And here he is 326. First time he took a picture with his shirt off. And then finally the best. This isn't even my patient. This is a beautiful 13 year old girl living in Hawaii who was in a car accident. And she stroked in the car accident. She stroked out her hypothalamus and this is her a year later. Very sad. Well, I was giving a talk at her hospital, Kaiser Honolulu and they invited her and her mother because they were thinking about putting the kid on a tritide. And they wanted me to, they wanted to hear the talk and everything. So there she is with me. And here she is a year and a half later at her high school graduation. And that's pretty good, huh? Now does anybody want to tell me that this is gluttony and slough? So what's going on here? So I would pose to you that this is the way you should think about obesity in general. Each of us is two compartments. You, your heart, your liver, your kidney, your lungs, your brain, your muscles, your lean body mass which burns energy and then there's your fat which stores it. Now the substrate for both compartments is glucose, right, in your diet. But glucose is never at saturation for both compartments at the same time. No one can eat that much. Which means there's a competition going on between the two compartments for the glucose. Which compartment gets the glucose? Well, what decides it is your insulin because when your insulin goes up more goes to your fat because that's insulin's job is to store energy and fat. That's why it's the energy storage hormone. Now normally your insulin's tied to your food. So the more insulin you make, the more fat you store. Everybody got that? But normally your fat would then single the brain with leptin and would tell the brain hey, I don't need to eat so much. Because that's leptin's job. And so that would then reduce your food. So you reduce your glucose and so your insulin would go down and then more would go to you. And this is your negative feedback pathway that I was talking about before. Right over here. It's like so. Except that these patients because of the central nervous system insult they can't see their leptin. So their vagus nerve goes into overdrive because they think they need to store like crazy so their pancreas makes more insulin all the time and so it's always going to them, them, them, them to the fat. Right? Everybody got it? So they gain weight no matter why and they feel lousy doing it because they don't have any energy for themselves, for their lean body mass. So gluttony and sloth but it's completely insulin driven. What we did was we got rid of that by giving them octriotide to block the insulin release. Now the glucose goes to them. They feel better. They start exercising spontaneously and they start losing weight. Cool. So the question is, you say to me, okay Dr. Lustig, that's a really good parlor trick but what the hell does that have to do with garden variety obesity out on the street? They don't have brain tumors and I would say to you it has everything to do with it. Let me show you why. So we asked the question exactly thereafter, could there be adults without brain tumors who do the same thing and if we gave them the same medicine would they lose weight too? And here's an example. Now not everybody does. Okay? It's 20% of the total but here's a lady, 1998, holding up food I believe, Christmas 1998 and here she is 35 pounds later after six months. In her jogging clothes she wanted to show me she actually liked to exercise. We changed her behavior because we changed her biochemistry because the biochemistry comes first. Everybody thinks the behavior comes first. Everybody thinks if you're fat it's because you're a glutton and a sloth and that's behavior and it's your fault and it's your choice. Obesity is not a choice. Nobody chooses obesity. The quality of life of an obese child is the same as a child on cancer chemotherapy. You think kids choose that? You think that newborn chose to have 200 grams extra fat? Give me a break. Okay? So I don't want to hear any of you ever saying to somebody you're a glutton and a sloth or it's your fault because it ain't their fault. The question is what has their environment done to their biochemistry to cause it? That's the question to ask. So the cause of leptin resistance is insulin. Insulin is the thing that blocks that leptin signal. And as the insulin goes up it gets in the way of the leptin signal and now there are biochemical studies which show exactly how that occurs in the brain. Now I'm not going to show those to you because you guys are not scientists. You're not neurologists, neuroscientists, et cetera. It's not worth spending the time on it. Trust me on this, okay? There's real science that shows how this works. So what we have learned from these original studies is that insulin is an endogenous, meaning you make it yourself, leptin antagonist. It gets in the way of leptin signaling. Okay? That's what the data say. Why? Why would God do that to us? What's the selective advantage? Why does this happen? What would Darwin say? Here's what Darwin would say. Well, you know what? There are two times in your life when you actually have to gain weight and they are puberty and pregnancy. And if you don't gain the weight, guess what? Species dies out. If you're leptin worked right every day all the time, you could never gain the weight because you'd start eating, you'd make the leptin, and you'd get your sugar high, and you'd burn it off, and you couldn't eat more, and you'd stay in energy balance like the 97-pound weakling on the beach who couldn't bulk up. So during puberty you got to make more fat or more muscle. During pregnancy, you know, the baby's got to grow, you need more energy, right? And then when the pregnancy's over and you cut the cord and all the sex hormones go down, then the insulin goes down too, so you can lose the weight and start all over again. So it actually makes perfect sense that insulin should block leptin twice in your life. Here's the problem. So doesn't it make sense that the same hormone that causes the weight gain peripherally should also inhibit the leptin centrally so that energy storage can actually take place? It actually makes perfect Darwinian sense. Here's the problem. We're not hyperinsulinemic twice in our lives. We're hyperinsulinemic 24-7-365. If you look at studies of insulin release to say a glucose challenge from 35 years ago versus today, we are making three times as much. We used to go up to a peak of 50, now we go up to a peak of 150 on average. So the question is, how come we're releasing double to triple the insulin that we used to? What made that change? Because when we understand that, then we understand how come we're eating more and how come we're gaining so much weight and how come we're getting so sick. So where did the hyperinsulinemia come from? Anybody know? I'm not going to tell you. But I'll tell you it's diet, but what in our diet? I'm not going to tell you. I'm going to let Will Smith tell you. Okay? Sorry, let's do that again. I'm trying, I was here. Can you hear it? There we go. Sorry, I can't talk right now. I've got some secret cases of my own I'm working on. I need to tell you away from the video again. All right, I'm hanging up. The most destructive force in the universe? Sugar. If Hollywood knows it, why don't you? I don't get it. I mean, how come? How come you don't know this? Okay? They know, they know. Okay, well we know too. So here's this paper that was written about our research back in 2011 called Is Sugar Toxic? That was in the New York Times Magazine. Maybe some of you saw it. And this is a comment that we had in Nature Magazine last year called The Toxic Truth About Sugar. And exactly what it does to insulin and what it does to your body in general to cause all of this disease. Okay? So what is this stuff? Okay? Well, it's two things in America. It's high fructose corn syrup, right? Most demon-ived food additive known to man. Okay? What is it? Okay, here's a glucose molecule. Here is a fructose molecule. High fructose corn syrup is 42 or 55% of this five-membered ring here, fructose. That's the sweet stuff. That's the stuff we like. Glucose. Eh, we can take it or leave it. Okay? You don't see people going around chugging K-rose syrup, do you? Eh, you know, I mean it's sweet, but very interesting, you know? Maybe it's good in a pecan pie, but that's about it, you know? But this stuff over here, we will go to the ends of the earth to find. Okay? This stuff does something special to our brain in terms of reward. And that's what this is all about, too. Okay? But here's this other stuff called sucrose. Cane sugar, beet sugar, table sugar. The stuff you put in your coffee, the white stuff, right? One glucose. One fructose. O-glycosidic linkage linking the two. So what? The enzymes in your intestine, cleave this in about a nanosecond. You absorb both. Bottom line, they're the same. And that's what all the studies show, is that they're the same. When you compare high fructose, corn syrup to sucrose, head-to-head, in terms of its metabolic effects, they're exactly the same. I agree. They are equal. They are equally bad. They're equally poisonous. They're equally toxic. And I use that word very specifically, that it is toxic in high dose. Now, can anybody think of another substance that is okay in low dose and toxic in high dose? Alcohol. Alcohol, right, alcohol. Perfect. Any others? Caffeine. Caffeine, you bet. What else? Salt. Salt. Yes, keep going. Water. Perfect! Ding, ding, ding! Everything is toxic in high enough dose. Paracelsus said in 1537, the dose determines the poison. Indeed. That's right. Everything is poisonous. Hey, oxygen is poisonous at high dose. Ask any preemie with retinopathy or prematurity. Everything is poisonous in high dose. The point is, we are over our limit. That's the point. Low dose? I don't care. Do what you want. Okay? High dose? Another story. Here's what's happened. Our ancestors, consuming sugar coming out of the ground in fruits and vegetables with the occasional honey, consumed about 15 grams of fructose per day. Double that for sugar because glucose is the same weight, so that's basically one ounce of sugar a day. That's what we got pretty much our entire history until the 20th century. Prior to World War II, we got up to about 20 grams with the nascent candy and soft drink industries. 1977, before high fructose corn syrup hit our shores, we were up to about 37 grams a day. That was 8% of our total intake. By 1994, we were up to 55 grams. That's 10% of our total caloric intake. And finally, adolescents currently today, 75 grams per day on average. That's 12%. 25% of adolescents consume 100 grams of fructose per day or more. Double that for sugar. That's 200 grams. Multiply by 4.1 calories per gram. That's 840 calories in sugar. So for a caloric allotment of, say, 2,000 calories a day, which is normal, that's 40% of calories of sugar. And the question is, is that okay? Can your body handle that? Can your liver handle that? Might it have some problems because of the dose? Everybody got it? So, a little's okay. A lot is not. And I'm going to show you what happens when you eat a lot. And we're eating a lot. And where did we get it from? Well, guess what? Of the 600,000 items in the American grocery store, 80% of them have added sugar. Added by the food industry for its own purposes, not for yours. Like salad dressing, barbecue sauce, tomato sauce, hamburger buns, hamburger meat, et cetera, et cetera. You cannot pick up a processed food package and not find sugar in it somewhere. And do you know why it's there? Because when they add it, you buy more. That's why they add it. So if a some unscrupulous cereal manufacturer laced your lucky charms with morphine instead of sugar, what would you think of that? Would that be okay? Well, guess what? They did. It's just not called morphine. It's another white powder instead. In fact, all white powders have this effect. It's okay when it's in the sugar cane. It's not okay when you purify it. It's okay in the cocoa leaves. It's not okay when you purify it. Everybody get the idea? It's okay in the poppy. It's not okay when you purify it. And that's what raises the dose. And here's what's happened worldwide. American Heart Association says 150 to 200 calories per day in added sugar. That's the max. That's the limit before you start seeing pathology. So what do you see? Everybody's over it. Everybody's over it. Why? Because Western diet has basically taken over everywhere. That's right. And now every country has obesity. And every country has chronic metabolic disease like diabetes. Sorry, China too. China too. Well, here's what's happened in world sugar consumption tripling over the past 50 years. This is per capita consumption. Look at Brazil. Brazil used to be a sugar exporter, but they were so poor they couldn't afford their own sugar. They were not sugar consumers. Well, guess what? Now they are because they're a brick country, right? They got an expanding economy. And so now they can afford their own sugar. And now guess what? They have the highest increase in rate of type 2 diabetes prevalence, the highest increasing acceleration of type 2 diabetes in the world. Now they don't have the highest type 2 diabetes prevalence. Who is that reserved for? That's reserved for Saudi Arabia, the United Arab Emirates, Kuwait, Qatar, and Malaysia. Why do they get that? No alcohol. But they got soft drinks like they're going out of style. And why is that? Because it's hot. And the water supply is a question mark. And no alcohol. This is their reward. Right? This is their reward. And so they have diabetes coming out of their wazoo's. I'm telling you. It's just crazy. So, here's the point. Everybody thinks that sugar is empty calories. Right? It's just, you know, and you get discretionary calories. You don't, you know, and you can spend them on sugar if you want to. But the problem is that a calorie is not a calorie. And that's what the whole book is about, is a calorie is not a calorie. If you believe a calorie is a calorie, then it's, you eat too much, you exercise too little, diet and exercise, and guess what? We will never get out of this. Because we haven't gotten out of it in 30 years with diet and exercise and calorie is a calorie. It's because a calorie is not a calorie. I'll give you four things right now that say a calorie is not a calorie. Almonds. You eat 160 calories in almonds. How many do you absorb? 130. What happened to the other 30? The fiber in the almonds prevented those 30 from being absorbed early in the intestine. They go further down the intestine, the bacteria got them. Because you got 100 trillion bacteria sitting in your intestine. You only have 10 trillion cells in your body. They outnumber you 10 to 1. You are really just a bacterial delivery vehicle. Okay? Because they actually outnumber you. They got to eat something. What do they eat? They eat what you eat. The only question is how much did you get versus how much did they get? And the more fiber that was in the food, the more they get. Now sometimes that's not so good. Because when they get it, sometimes they make some hydrogen sulfide. So sometimes it's fat or fart. But the bottom line is foods that contain fiber, a calorie is not a calorie. How about protein? It turns out to burn protein for energy, you have to expend energy to get the protein in a form that you can actually burn it. It's called thermic effect of food. You have to put in energy to get out energy. It's called catalysis. It costs twice as much energy to burn protein as it does to burn carbohydrate. So that's why they tell you to eat protein, because it actually helps with weight. Because you have to put more in to get some out. Because a calorie is not a calorie. How about fats? So over here we have omega-3s, which are heart-healthy and really good for you and save your life. And over here we have trans fats, which will kill you. They are the devil incarnate, true poison. And there's reasons for why that is. They both burn energy at 9 calories per gram. But one will save your life, and the other one will kill you, because a calorie is not a calorie. And finally, fructose is not glucose. Fructose is seven times more likely than glucose to bind to proteins, cause them to become less flexible, and therefore cause cell damage. Anybody here have diabetes? Yes, no? What does your doctor measure in your bloodstream? Every once in a while he does a lab test. It's called the hemoglobin A1C. You've heard of that? Okay. That's to see how high your blood sugar has been, because glucose binds to proteins. Well, fructose does it seven times faster. You think that's good? That's bad. Fructose does not suppress the hunger hormone, ghrelin. Ghrelin is the hormone that comes from your stomach, tells your brain you're hungry. Then you eat, and ghrelin goes down, except fructose doesn't suppress it, so you keep eating more. So, you take a kid, you prepped them with a, you preload them with 150 calories and a soda, and then you let them lose at the fast food restaurant. Does he eat less, or does he eat more? He eats more. He took on 150 calories. Why doesn't he eat less? Because a calorie is not a calorie. And finally, liver fructose metabolism is completely different from that of glucose. They bear no relation to each other. In fact, liver fructose metabolism looks more like liver alcohol metabolism. And in fact, fructose and alcohol bear very striking similarities. And fructose alone causes the metabolic syndrome, which I'll show you. That's the constellation of diseases that we're talking about here. So, here's the basic story, and I'm not going to bore you with all the arrows. You can watch it on the YouTube video, Sugar of the Bitter Truth. It's 90 minutes of carbohydrate biochemistry, but 3.4 million hits so far. That's pretty good. Here's what happens. Glucose comes into the liver, and it gets turned into this stuff over here called glycogen. Glycogen is liver starch. That's what happens to glucose when you consume glucose. It becomes glycogen. And we know that because we have marathoners who like to carb load before a race. And that's to try to build up the glycogen. Now, is glycogen toxic? No. Glycogen is completely non-toxic. So, your liver can store whatever glycogen it wants and whatever it needs. No problem. Now, let's talk about alcohol. Alcohol is a carbohydrate. It's a structure right there. But you know that alcohol is a toxin, right? It's two toxins in one. You wrap your Lamborghini around the tree. That's acute alcohol toxicity. And you fry your liver. Chronic alcohol toxicity. Two toxins in one. We keep it out of the hands of children. Here's acute alcohol consumption. Just take a read through it. Okay, you all went to college. Over here, fructose exposure. Nothing. Why? Because the brain does not metabolize fructose. So, you don't get the acute toxic effects of alcohol when you consume sugar. But let's consume those alcohol calories. Here's what happens to the liver. You see glycogen anywhere? It doesn't make glycogen. It comes straight down to the mitochondria down here and makes fat. This is the fat making pathway called de novo lipogenesis. New fat making. De novo lipogenesis. And so, basically, you get liver fat and there's the lipid droplet. And that's why you get fatty liver disease with alcohol. And when you get fatty liver disease, that means that your insulin doesn't work right. And your pancreas has to make extra insulin to make the liver do its job. So now let's see what happens with sugar. So, the sugar, here the fructose, comes in. Only the liver can metabolize fructose. No other organ in the body. And what happens? You see glycogen anywhere? No glycogen. But you see an awful lot of arrows. And it all comes down here to the liver, to the mitochondria. And here's that liver pathway, that de novo lipogenesis pathway. And here's the lipid droplet. And here are all the things that happen. And here's the blockage of insulin action right here called insulin resistance. And what happens? The pancreas has to make extra insulin. It gets in the way of the leptin, you know, it gets in the way of the leptin, signaling. And now what happens? Now you have disease and extra consumption, gluttony and sloth. So what's the difference? Over here we got a can of coke. Over here we got a can of beer. They're both 150 calories. But obviously they're not the same, are they? Oh yes they are. Here's why. Because the coke has 75 glucose, 75 fructose. The alcohol has 90 alcohol, 60 moltose, that's glucose. 10% first pass GI metabolism on the alcohol. Bottom line, the number of calories hitting the liver? Equal. So in America we have this thing called beer belly. Well guess what? We also have soda belly. That's what our kids are suffering from is soda belly. They have non-alcoholic fatty liver disease. Just like alcoholic fatty liver disease looks exactly the same. The only difference is it's sugar, not alcohol. But they do the same thing and they cause the same diseases. So fructose induces insulin resistance. Then the high insulin from the insulin resistance induces the leptin resistance. Everybody get this now? So the higher the insulin goes, the more weight you gain. And the higher the sugar consumption, the more the insulin goes up. Everybody see that? Okay. Now why would God do that to us? What would Darwin say? What he would say is, you know what? We used to only have sugar one month a year. It was called harvest time, right? And what happened after harvest time? Winter. And what happened during winter? No food, right? So doesn't it make sense that when the fruit would fall off the tree and the animals would, or the humans would gobble it all up because after all it tasted so good. And they would put on some weight because they became insulin resistant during this one season called harvest time. That that was actually adaptive because it let them make it through a period of four months of famine. And then they could start all over again in the springtime. The problem is now fructose is available 24-7-365 and consumed in unlimited amounts called soda. And it's unopposed by the fiber which was in the fruit like orange juice. So guess what? We got a problem because we are not adapted to this sugar glut that we currently find ourselves in which was made by the food industry because they know when they add it, you buy more. So far so good? So you say to me, okay, Dr. Leslie, how do you know this is true? Well, I don't know that it's true, but here's an example. This is what they call a fruit orgy that they see in orangutans in Papua New Guinea. And in January, there's lots of availability of fruit right over here. See it? And when that happens, they go hog wild. They eat nothing but fruit because after all it's so good. So tasty. And when that happens here, as you can see, it's all fruit at this point. And the calories go up during this period of time because they're trying to put on weight because you know what? When the fruit disappears, when harvest is over, they're going to be in trouble again. And here the ketones disappear. The ketones disappear because insulin blocks ketones. So this shows you that they have high insulin during this period of time. So guess what? This is actually adaptive. This was adaptive for zillions of years until modern food processing. And now we got a problem because now it's everywhere. And we got high fructose corn syrup because now it's super cheap, right? And they put it in all the food because they can and because they know when they do, you buy more. Absolutely. We're going there. Thank you. Jump the gun, but that's all right. And guess what? Sugar is addictive, too. Now it's not strongly addictive. It's not heroin or cocaine or morphine, you know. But it's weakly addictive, like alcohol. Now is everybody addicted to alcohol? No, about 20%. And can some people consume a little bit and be okay? And other people, they consume that little bit and then it's a lot, right? Because they're addicted. Sugar's about the same thing. And probably because sugar and alcohol are so similar. So is sugar addictive? Well, you know, lay public seems to know this, but the scientists are not so convinced. Here's what I want to tell you. You know, there are five tastes on your tongue. There's sweet. And then there's salty, sour, bitter, and this other one called umami, which is savory, like roast beef. Sugar hides the other four. It hides salty, like chex mix or honey roasted peanuts. It hides sour, like lemonade or what they call the sister's herb in German wines, because German wines are very acidic, because they don't get enough sun, because they're in Germany. It hides umami, like sweet and sour pork, that's half soy sauce, you wouldn't eat that except that the sugar hides it. And it hides bitter, like milk chocolate, because caffeine is bitter. Bottom line is you can make dog poop taste good with enough sugar. Because sugar basically negates all of the negative aspects of foods and the food industry knows that. So does this make Darwinian sense? And the answer is yes, this does too. Why? Because there are no food stuffs anywhere on the planet that are sweet and also acutely poisonous. This was the message to our ancestors that any given food stuff was safe to eat, because they didn't know what was safe and what wasn't, so sweet they knew they could eat it. This is ingrained into our DNA that if it's sweet it's acutely at least safe. Chronically is another story, but acutely safe. And how do we know this? Well, how about this? Anybody know what this stuff is called sweeties? This is a super concentrated sugar solution that you dip the pacifier in, that you stick in the newborn boy's mouth and then you do the circumcision. And what does it do? It releases opioids in the brain in the reward center, which deadens the pain. This is the baby narcotic. So anybody want to tell me that sugar is not addictive? All right, now let's move to disease. We've gone through Darwin and diet, now we're going to go to disease. I want all of you to forget everything that the federal government has told you. Because what they have told you is that obesity is the cause of all of those bad diseases, diabetes, hypertension, lipid problems, cardiovascular disease, cancer, and dementia. They will tell you obesity is the cause of those problems. So here's the way to think about this instead. Here's a Venn diagram of all the adults in America. 30% obese, 70% normal weight. And everybody thinks it's just the obese's person's fault, that's all, just them. So 80% of the obese population has chronic metabolic disease of some fashion. So 80% of 30%. And those 57 million people are costing you money. And so you say, you suck. You miserable fat slob. And you are costing me money. After all, the obese are still, they're the last group you can be pejorative against. Everybody can still make fun of fat people. And everyone still makes fun of fat kids. And that's why kids are so miserable. Obese kids have a quality of life like cancer chemotherapy. Because everybody thinks it's their fault. This is wrong. This is a mistake. Because it ain't true. Ain't true. And I'm going to show you right now. Let's go back. Here we are. And here's what's really going on. Yes, 80% of the obese population has chronic metabolic disease. That's true. But so does 40% of the normal weight population. They get type 2 diabetes. They get problems. They get hypertension. They get heart disease. They get cancer. They get dementia too. But because they're normal weight, no one thinks they have chronic metabolic disease. They think they just get it. No. They have the same disease as they're just thin or normal weight. Because obesity is not the cause of these diseases. Obesity just travels with them because it's a marker for the process that causes these diseases. So if you think you're normal weight and you're out of the woods, think again. This is for everybody. And it also means that whatever is causing the disease in the normal weight people, it's causing the disease in the obese people too. It means everyone's at risk. Everyone's exposed. Which means that whatever we're going to have to do, we're going to have to do it for everyone. Not just for the fat people. Everybody got that? So that turns this whole friggin' thing on its head. And it says to the federal government, you're screwed because Obamacare ain't going to fix this. And here's an example of why that's true. These people right here are equally fat. And this one over here is perfectly healthy. He's in that 20% who is not going to have a problem. He's just fat. He's going to live a normal life, die at a normal age. He's just fat. He's got big love handles out here. That's what he's got. But this guy over here, same amount of trunk fat. See? 12.8, 12.8, right? But this guy over here, he's got organ fat. He's got liver fat. He's got much smaller love handles, but he is sick as a dog. Okay? Everybody see? Equally fat. But one's sick and one isn't. Because it's not fat versus thin. It's sick versus healthy. And thin people can be sick. And I would rather be fat and fit than thin and sick. And so would you. Believe it. Because the key to the kingdom is it's not about obesity. It never was. But the food industry wants it to be about obesity because then they can actually deflect and say it wasn't their fault because there's so many different things that contribute to obesity. And there's this thing called exercise that they can always pin it on. Right? Because it's not about obesity. It's about metabolic dysfunction and anyone can get it. And obesity is a result of that. Not a cause. All right? I'm going to show that to you now. So here are the 10 most obese states in the nation. Anybody from any of these? One over there. Okay. You know what I'm talking about, right? I used to live in Memphis, Tennessee. I know what's going on. Well, join the club. 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. Okay? But now they just go like this. Here are the 10 most unhappy states in the nation. No surprise. Okay. Here's the adult diabetes rate. Here's the adult heart disease rate. And finally, here's soda per capita consumption. What do you see? Right. Correlation. Correlation. Clear correlation. Now, I have been accused of pandering to the audience because scientists will say, Dr. Lustig, come on. Get with the program. You know as well as we do that correlation is not causation. Who says that the soda caused the diabetes? Maybe the diabetics all drink soda. Really? Okay. Well, you know, it's true. You don't know. Directionality. Epidemiology is not directionality. Epidemiology is not causation. Agreed. I agree with that. So we did something to try to get to it. This is called an econometric analysis. We just published it a month ago in a very reputable journal. Got a lot of press. I'm going to show it to you now. What we did was, and this was Sanjay Basu, who's my colleague, who's now at Stanford. What we did was we took four databases and we melded them together. And anyone can do this if you, you know, have access to the internet. What we did was we took the food and agriculture organization statistics database, which had food availability of different kinds of foods. So we had total calories. We had fruits, excluding wine. We had oils. We had roots, tubers, pulses, nests, and vegetables and all the fiber containing foods. Meat, cereals, and we had sugar, sugar crops, and sweeteners as a separate category. We then melded that with the International Diabetes Federation statistics database for diabetes prevalence country by country over the decade. And we then melded that with the World Bank gross national income database to control for purchasing power for poverty, for urbanization, for aging. And then we also melded that with a database from NHANES, which had obesity and physical inactivity. And we asked the question, what about the world's food supply predicted the diabetes prevalence over the decade around the world? 175 countries. We had complete data for 154. The ones we didn't evaluate were no different. We did a lot of fancy statistics. Okay. I mean, Sanjay Basu is a statistics genius. He, Ph.D. in statistics from MIT. And he is a superstar. Okay. And he's going to be chairman someday. And we control for these various things. Okay. To make sure that it wasn't something else causing the problem. And here's what we found. During the decade diabetes prevalence rose from 5.5 to 7% worldwide. That's bad. That's a bad thing because that means more money going out the window. Okay. More disease, more disability, more decreased productivity, more death. And here's what we saw. This is sugar prevalence for every 100 calories against everything else in the diet. And you can see very clearly a 1% increase in diabetes prevalence for every 100 calories. So here's the adjusted association of sugar with diabetes prevalence. Here's what you need to know. This is your take home. Only sugar predicted diabetes worldwide. Nothing else. Not even total calories. Everybody thinks it's about the calories. It ain't. Because a calorie is not a calorie. Because if a calorie were calorie, then total calories would have predicted it. And it didn't. For every extra 150 calories and total calories that the world consumed, the diabetes prevalence went up by 0.1%. Nothing. But if those 150 calories happen to be a can of soda, diabetes prevalence went up by 1.1% 11 fold. And here in America, we are not consuming one can of soda. We are consuming 2.5%. So when you do the math on that, that's 2.75%. Considering we have a diabetes prevalence of 8.3%, that means that 29% of diabetes in this country is due to sugar and sugar alone. And around the world, 25% of diabetes is due to sugar and sugar alone. You want to do something about this problem? Here's where you start. That's what we showed. And those countries where sugar consumption declined showed a decreased diabetes prevalence. That's called the Granger Causality Test. And this is why we know we have causation, not just correlation. Sugar causes diabetes, period. And if that ain't true, God strike me down. And it has nothing to do with obesity. Sugar is toxic. Sugar is poison. Now, a little, as I said, is okay. A lot is not. A little is what we used to do. A little was the occasional birthday cake. The problem is that yogurt your kid ate this morning had as many grams of sugar as that birthday cake. And he doesn't get it for dessert. He gets it as a diet staple. That's the problem. Now, there are lots of limitations to this kind of analysis, but I'm just going to make it very clear none of them get in the way of the data. None of them, okay? And if you want, we can talk about those limitations later. Bottom line, this is a slam dunk. This is a complicated slide, but I'm just going to try to take you through it and show you how this all works. So here's the sugar coming in, the fructose coming in. Blinds to proteins throws off hydrogen peroxide, reactive oxygen species which damage the cell. They get metabolized in the mitochondria. Also generates reactive oxygen species damage the cell. In addition, some of it's going to get laid down in visceral fat, like I showed you that picture, and that's going to generate reactive oxygen species damage the cell. Now, those ROSs can do damage, but we have an organelle in our liver and virtually every organ in our body called the peroxasome, and the peroxasome is where those hydrogen peroxides go to die. Anybody ever heard of Actos? It's a diabetes drug. What it does is it makes more of these peroxasomes, and so what happens is you detoxify these ROSs so you don't get so much damage, and that's why it helps with diabetes. But if you don't do that, then the ROSs go over here where you fold proteins and what that causes is less insulin. That's diabetes. Now you've got metabolic dysfunction. Everybody understand? So getting rid of this is really important, and the more you make, the harder it is to get rid of them, and sugar makes boat loads. That's what it comes down to, seven times more. And some of that fructose will get converted to fat through that de novo lipogenesis, and that will cause that insulin receptor not to work, and you've got insulin resistance, which drives the insulin up, which does all the other bad things I showed you too. This is not cool, and it's all sugar-driven. And worse yet, there is no drug target, because there's no way to take those things away. Mitochondrial overload means more of those hydrogen peroxides. That means cell dysfunction, aging and death, and mitochondrial overload promotes all that fat, which promotes all that insulin resistance and metabolic syndrome. The only options are reduce the availability. That's called diet. Reduce the rate at which the sugar gets absorbed from the gut into the bloodstream to get to the liver. That's called fiber. That's what fiber does. And finally, burn it off before it ever becomes fat, and that's called exercise. Diet and exercise again. But it's not just any old diet and exercise, okay? Because you can't eat less, because your leptin won't let you. Because as soon as you eat less, your leptin goes down, your brain says, I'm starving, and so you eat more. But could you eat less sugar? That you could do. And guess what? When you eat less sugar, you eat less, because now your insulin works, and your leptin works. And when your leptin works, you don't need to eat so much. So when you correct the metabolic dysfunction, your health improves, and your weight goes down, and your appetite goes down, and you feel better because you have it to burn instead of store, and you reverse the entire metabolic process. Just by making one simple change in your diet. The problem is you can't, because the food industry won't let you, because they have poisoned your food supply. And that leads us to dollars. So here's what has happened to your dollars. 1982 to 2012. This is your food dollars. Meats, 31% down to 21%, because of the low-fat directive. Fruits and vegetables, about the same. Grains and baked goods, up slightly, 13 to 14. Dairy products, down, because now everyone's lactose intolerant. True. Processed foods and sweets, 11.6 up to 22.9%. We have doubled the processed foods and sweets in our diet in that 30-year period. The average is about the same. Everybody got it? So who's making out like bandits? The stockholders are. And that's why the food industry can't change, because the stockholders are making money hand over fist. Here's the S&P 500 over the last five years. And here's the economic downturn of 2008, right over here. Now, notice, McDonald's, Coke, and Pepsi, all doing better than the S&P, no surprise. And here's Hormel, Archer Daniels Midland, General Mills, Kraft, Con Agra, Procter & Gamble, all doing better than the S&P too. Want to make money? Invest in a food company. Now, what does this mean? It means we have to do something. Can you do it alone? What do we need? This is what government is for. We need some sort of regulation, because we can't do this ourselves. It can't be done. You can help yourself in your house, but that ain't going to help your neighbor, or your neighbor's neighbor, or anybody else. Right? So I'm telling you what you need to do, but I'm also telling you what we need to do, because you want your Medicare. I want my Medicare, and there won't be any Medicare unless we do something. So the question is, do we have enough to actually make the case that we need to do something? Societal intervention requires externalities, meaning when you smoke or drink or take drugs, it's bad for me. That's how we justify regulating those things, because when you smoke, you create secondhand smoke. That makes me sick. When you drink, you get in a car accident, and you kill me, that's not okay. If you take drugs, you turn your house into a crack den, and that reduces housing prices all over the neighborhood. And of course, I have to do your job for you, because of your absenteeism. So all of those things are reasons why we regulate. They're toxic and abused, and they affect society in a negative fashion, and we regulate them. We regulate tobacco. We regulate alcohol. We regulate drugs. So how does your obesity affect me? $274 million extra for jet fuel. Discomfort on the subway. Sinking of boats due to the weight. 2003, Lake George, a ferry taking people across Lake George in Plattsburgh, New York, coded for 17 people at 140 pounds. They were carrying 25 people at 240 pounds. Boats sank. That ain't gonna do it. Huh? No, it wasn't a carnival cruise. But it might as well have been. You ever been on a carnival cruise? Oh, man. Here's the reason. $65 billion reduction in work productivity, 50% increase in absenteeism, 50% increase in health insurance premiums. That's a big one. Okay? Your employer pays $2,750 extra for you, whether you're obese or not, because of obesity. And guess what? That cost gets passed on to you. It's affecting you, whether you're obese or not. Too bad. $150 billion wasted in health care resources. Obesity is a threat to national security because 27% of the recruits can't qualify their foreeft for being overweight. And this is the most important one. The government pays twice. They pay for the corn subsidy and then they pay for the ER visits. And it can't get better if they pay for the corn subsidy. So if they stop paying for the corn subsidy, then they stop paying for the ER visits. The question is, how are they going to stop paying for the corn subsidy? Why can't they stop paying for the corn subsidy? Because I'm going to... I'm going to... That... Thank you. That's exactly right. The most... The dirtiest four-letter word in the English language, Iowa. That's why. Iowa. Iowa is the first presidential caucus because you can't win the presidency without Iowa. And so nobody wants to piss off Iowa. So you think the government's going to do anything about the food subsidy? The corn subsidy? Not a chance. They are on the other side. Government's on the other side because 6% of our exports are food. And do you think the government wants the rest of the world to know that all of the food that we're shipping around the world is poisoned? What happened when that one downer cow came from Canada to Washington state? That was the end of meat sales to Britain and South Korea for two years. Job of the U.S. Department of Agriculture is to protect the food supply. And that includes protecting it from people like me. So you think anything's going to happen? Not a chance in hell. So let me sum it up for you. The dirty truth. Obesity means leptin resistance or brain starvation. When your leptin works, you're not obese. When your leptin doesn't work, you are. It's that simple. The starvation response is what causes recidivism. So you try to diet. Your leptin goes down. Now you have leptin deficiency on top of leptin resistance. You think you can solve that yourself? Forget it. You're back to eating just what you were before and there goes your diet. That's not your fault. You're not weak. You're biochemical. Energy expenditure and quality of life are the same thing. How fast you burn energy is how good you feel. And when you don't burn energy because you're storing it, you feel lousy. So people whose insulins are high feel lousy like my brain tumor kids. Defects in insulin signaling promote leptin resistance. So the higher the insulin goes, the less well your brain sees its leptin. When your brain can't see its leptin, what do you do? You eat more and you exercise less. So you see the behaviors, but it was biochemically driven. Just because you see the behaviors doesn't mean that's the first thing. It's the second thing. It's secondary. Insulin is an endogenous leptin antagonist. Insulin blocks leptin because there are two times in your life you actually have to gain the weight. But now we gain weight all the time because we're insulin resistant all the time. Fructose, the sweet part of sugar, because of how it gets metabolized in the liver, causes this insulin resistance, driving the metabolic syndrome and all those bad diseases, and that is what's wasting all these healthcare dollars. And fructose is addictive to boot. Causes you to eat more, and that's why the food industry put it in there in the first place. It drives excess food consumption. Our entire food supply is fructose-fied. We have to get the insulin down if we're going to get this turned around, and we can't get it down as long as the sugar is in the food. And the food industry has no impetus to change its practices because they're making money hand over fist. You are fracked. Sorry? Yeah. There are a lot of these. Yeah, yeah. Guess what? Guess what? This is not just guns. This is not just food. This is global warming. This is basically all societal ills because of something like this. Because somebody is making money on your misfortune. That's what this is. And the question is, you plan on taking it? I need you. I need all of you. I need you guys to get with the program. I need you guys to figure out what the real story is. And when you do, then you're going to get mad. And then you're going to call your congressman. And then, when there are more votes than dollars, then something will happen and not one minute before. So you guys have to get mad. Okay? So for further reading, lots of stuff, academic stuff. And for further reading, more academic stuff. And for further reading, more academic stuff. And for further reading, more academic stuff. And then finally, not so academic stuff. Okay? So fat chance. It's here somewhere. If you want, you can buy it here. You can buy it on Amazon. You can buy it at the bookstore, bottom line. Buy it. Buy it. Because it will explain what happens and how this works, and you need to give it to your family to protect them. Okay? And lastly, we have started a nonprofit, a 501c3 nonprofit to provide medical, nutritional, and legal analysis and expertise. I am putting my law degree to work because we're going to try to take down big food. Called the Institute for Nespansal Nutrition. Okay? For education, research, advocacy, and action, you can go to responsiblefoods.org. And let me know if you want any other information. The bottom line is, we can't solve this without you. We need your help. You need my help. Okay? Because I get it. The bottom line is, government doesn't want to get it. They have to get it. You can't expect government to do the right thing. You have to coerce it into doing the right thing. That's why it's called democracy. And with that, I will be happy to close and answer any questions that will come on the little pieces of paper. And I thank you for your attention. We have some questions. Please push them to the center of the aisle and Shreese and Ruth will collect them. We have to work. Feel free to, you know, get up and leave and it's no problem. We're running a little bit over because, you know, I took my time, but, you know, I'll stay as long as you guys want me to. Sorry? I'm not a JD. No, I'm getting an MSL, Masters of Studies in Law. So it's not, I can't sue, but I can talk to lawyers who can. That's basically what it is. My goal, basically what we're going to do is we're going to look at the tobacco playbook. Okay? How did tobacco get defeated? Through regulation, through litigation, because the states sued tobacco for recruitment of Medicaid costs. And we're going to follow the tobacco playbook and we're going to do the same for metabolic syndrome. You know what? The gun playbook should be the same and people are talking about it. You know, actually, let's talk about guns for a minute. Okay? Everybody want to talk about guns? Sure. Anybody know who John Howard is? John Howard was the Prime Minister of Australia. Okay? The most conservative politician Australia ever produced. Okay? He made Ronald Reagan look like a liberal. Okay? Now, I was not a John Howard fan, but John Howard got rid of assault weapons in Australia. Okay? And he was just interviewed on CNN about three weeks ago or so. And they asked him, I mean, you know, I mean, look, you're ultra conservative. Like, why would you ban guns in Australia? And he said, because it's not a conservative issue. It's not a liberal issue. It's not a Republican issue. It's not a Democrat issue. It's a safety issue. That's right. It's a safety issue. All right? This is a safety issue. Has nothing to do with libertarianism. All the libertarians say, keep your hands off my food. Get your hands out of my kitchen, Dr. Lustig. Guess what? Your food's already been altered. Your food has been changed under your nose over the last 30 years. That's all that processing that went on. Okay? And the libertarians don't get it. They think I'm the one that came after their food. That's coming after their food. They've already been co-opted. They just didn't know it and they were happy to do it because they applied them with sugar. You know, religion is the opiate of the people. Wrong. Sugar is. And I showed you why. Everybody got it? They did this with our tacit approval. And now we've got to fix it because now we're sick from it. This is a safety issue. This has nothing to do with libertarian or communitarian or liberal or Democrat, you know, or liberal or conservative or Democrat or Republican. This is a safety issue because there will be no Medicare. Yep. So that, I mean, I should get to these, but no, very good point. Okay. So Michael Bloomberg's big gulp ban failed. At least for the moment. Okay. It's going to be appealed and I'll tell you about that because I know about it now because I'm in law school. Who here was for the big gulp ban? Who here was against the big gulp ban? Come on. Be honest. Come on. Usually it's about 50-50. Really? More for it than against it? That's surprising. Anyway, the judge in New York cited a case called Boreali V. Axelrod. Now Boreali V. Axelrod was about smoking in public places and it was struck down in 19, Boreali V. Axelrod said, you know, stop ban smoking in public places and the judge struck it down in 1986 saying there was no compelling state interest to prevent people from smoking. Well, that was four years when we learned about secondhand smoke. Guess what? There's a compelling state interest now. It just hasn't been tested because they passed statutes. So for that judge, Tingling, to invoke Boreali V. Axelrod as the reason to knock the big gulp ban out, he's a friggin' idiot and it's going to get overturned on appeal because that was an inappropriate case to use to cite because that's why they needed the legislation was because of that decision four years earlier before we knew about secondhand smoke. We know about diabetes. We know that sugar causes diabetes. Now, is the big gulp ban going to fix obesity? Of course not. Is the big gulp ban going to fix diabetes? Probably not. But it's a step in the right direction. It's a baby step and it's within the police power of the New York City Board of Health to be able to do that. It is their responsibility and their job. They did it for smoking. They did it for trans fats and they can do it for sugar and they're entitled to and they will. It's just going to take a little longer because Tingling's an idiot. Okay. All right. Does that answer your question? Okay. All right. Is the damage done by sugar reversible? We don't know. We don't know. We think some of it is. Probably not all. If you get fatty liver and you scar your liver, so the same thing that happens to alcohol, that's not fixable for sure. That we know absolutely. Once you scar your liver, you're done for. You're going to die and you're going to die of cirrhosis of the liver. Okay. So right now, 33% of Caucasians, 25% of African-Americans and 45% of Latinos have fatty liver and of those, 5% of those categories have scarring and they are going to die of their chronic liver disease. We have already done two liver transplants on 400-pound, 15-year-old soda drinkers at UCSF. 400 pounds. Okay. So some of it is definitely not reversible. The question is, how about the rest? And the answer is, we don't know for sure. I think some of it is. I don't know if all of it is, but the bottom line is never too early to start. There are lots of studies now documenting increased risk of diabetes and heavy metal exposure. Yes. Why aren't physicians screening for these risks? That's a very good question. The bottom line is, it's not across the board and we don't know that it's causative, it's causative and it costs a lot of money to do that and so we do not yet know that that's the cause. I do know about this and it's not just heavy metals. Actually, one of the things that is associated with diabetes is processed red meat like bacon according to the Harvard Department of Health. So there are a lot of things that are associated, but they're associated. We don't know causative. I just showed you data that showed causation. So when you see causation rather than correlation, then you have to do something and that's why I showed it to you. Okay. So the answer is, maybe it's important too, but we don't know that yet. The statistical analysis showed sugar responsible for 25% of diabetes worldwide. What are the causes of the other 75%? Well, obesity is one. I'm not going to tell you what obesity does and cause diabetes. It almost assuredly does. The insulin resistance that goes with diabetes can cause diabetes. There are probably many other reasons, including what we just talked about like heavy metals and processed red meat and other things as well. Genetics, clearly there's genetic susceptibilities that are very different. In addition, different racial groups have different propensities at different weights. So for instance, African-Americans get five BMI points higher before they get sick. And Asians get five BMI points lower before they get sick. So we say that obesity is a BMI of 30. That's for Caucasians. For African-Americans, it should be 35. And for Asians, it should be 25. And we have a population that's running between 25 and 30. Well, that might be causing diabetes in the Asians and the diabetes rate in the Asians are going up astronomically. Astronomically. So that's a huge problem. Dentistry and medicine are just now discovering the effects of untreated dental disease. Yes, periodontal disease and dental carries on various organ systems. Well, you know, that's a little complicated. There's no question that sugar causes periodontal disease. Can you hypothesize about the possible role of various bad metabolites on bone health related to teeth? Okay. Complicated question. When was the toothbrush invented? Anybody know? About 1500. Okay. If you look at skulls of prehistoric man that have been unearthed, they got really bad teeth, right? But no cavities. They're all over the place, but no cavities. No cavities. How come no cavities? They had no toothbrush. No sugar. Right. Exactly. No sugar. They had no sugar. So, they ate carbohydrate. They ate glucose. They, you know, they learned to farm irrigation, you know, I mean, agriculture, you know, way before 1500. Glucose forms a biofilm on the teeth. It causes really bad breath, but actually protects the tooth from getting carries, from getting cavities. What causes the cavities? The fructose, the sucrose, the sugar, because sucrose is metabolized by the bacteria, not, it doesn't get part of the biofilm, it basically forms lactic acid and burns a hole in the tooth. So, the bottom line is that it's the sugar that caused the teeth problems, not the carbohydrate. And what it does to bone is complicated. Certainly sugar's not good for bone, but it might be that the phosphoric acid in the soda is actually worse for bone than the sugar is. So that's a complicated question, but, you know, there's no question that we are seeing more osteoporosis today than ever before. That is true. And it may be because of the phosphoric acid, we're not sure yet. Also sodium, the sodium, because sodium causes calcium loss in the urine. So you lose more calcium in your urine when you consume more sodium because of the way the kidney works. That might be part of it too. What's the connection between depression and sugar consumption? Oh, super question. Really good question. And there is data that actually supports that. One of the reasons is because of leptin. Because when your leptin is not working, you feel lousy. So that's one reason. But there may be other specific reasons why sugar consumption causes not just depression, but causes irritability, causes violent behavior. So this is San Francisco. Everybody knows what the Twinkie defense is, right? Right? Right? Does anybody need explanation as to what the Twinkie defense is? So 1979, Harvey Milk and George Mosconi, right over here at City Hall, next door, were assassinated by Dan White, a supervisor who was a little crazy and ultimately committed suicide after he was released from jail many years later. His lawyers invoked the Twinkie defense. They said, because he went on a junk food binge, he went insane and was not responsible for his actions. The court didn't buy it. And he went to jail for 25 years, got released and killed himself two days later. There was a paper that came out last year from a group in Boston, Skolnick, Skolnick and I forget the other author, called the Twinkie defense, correlation of sugar-sweetened beverages and violent behavior in Boston high schools. And I have a friend in England, Alex Richardson, who runs a group called Food and Behavior Research, where they have looked at the issue of sugar and also omega-3 fatty acids in terms of neuronal function. And it's very easy to understand why sugar causes so much emotional liability. One of the things that can actually fix that is omega-3s. Omega-3s seem to actually block that effect. Problem is, we went low-fat. No omega-3s. That's a problem. We have time for two more questions. We talk about the link between sugar and tumor growth. All right, so another complicated... These are all good questions, by the way, super questions, but complicated. There are two issues with regard to sugar and tumor growth. The first is that because sugar causes insulin resistance, insulin goes up, insulin is a growth factor, causes cell proliferation, and causes tumors to grow. That one is a slam dunk, no ifs, ands, or buts. Take it home to the bank. Lou Kent Lee, who used to be at Beth Israel, now is the head of oncology at Mount Sinai. He's demonstrated this. If anybody saw the 60-minutes piece last year, his work was shown. And that, we know for sure. In addition, more recently, a group at UCLA led by Michael Heaney showed that certain tumors, not all, but certain tumors, especially pancreatic tumors, have an enzyme called transketolase, which can actually metabolize fructose for energy so that when you consume extra sugar, you're basically feeding the tumor and causes increased tumor growth. Now, that's not true for every tumor, but it's true for at least the tumors he looked at. And so that might be another reason why sugar can cause cancer growth. Bottom line, it's bad stuff, in case I didn't tell you. Is stevia a healthy sugar substitute? Okay, all right. Best question, no answer. Let me try to make this very clear. Everybody wants to know about diet sweeteners, everybody wants to substitute with something because they still need their food to be sweet. I get it. Here's the problem. We don't have the data. It's not that I don't know. We don't have the data. Why don't we have the data? We have no data on any of the artificial sweeteners with respect to this. Here's why. There's something called pharmacokinetics, and there's something called pharmacodynamics. They are not the same. Pharmacokinetics is what your body does to a drug. Pharmacodynamics is what a drug does to your body. They're not the same. We have all the pharmacokinetics for all the diet sweeteners because the FDA demands it, because that tells you whether something's acutely poisonous or not. Pharmacokinetics, okay? What that drug gets metabolized into by your liver. That we have. And you need that in order to get any compound on the market, including foods. We have none of the pharmacodynamics. So we don't know what Asa sulfame K does to your leptin or what aspartame does to your ghrelin or what sucralose does to your long-term energy intake or what stevia does to your hypothalamus or anything like that. We have none of that information. And the reason we don't have it is because the FDA isn't demanded. That's not part of the FDA's decision-making process. And the food industry says, well, why should we do that if we don't have to do it for the FDA because it can't help our sales, why would we do it? So they don't do it. And the NIH says, that's the food industry's job. No, we're not going to pay for that. So the bottom line is we have an impasse. So there's no pharmacodynamic data on any of the diet sweeteners. Second problem. You put something sweet on the tongue. What happens? Impulse goes from the tongue via the cortotempani nerve to the hypothalamus. The hypothalamus says, sugar bolus is coming. Get ready to metabolize it. And that vagus nerve that I showed you before sends an impulse down to the pancreas and says, get ready to release the insulin because the sugar is coming. But then the sugar never comes because it was a diet sweetener. What does the pancreas do? Does it say, oh, I was waiting for all that sugar. I guess I'll just wait until tomorrow. Or does it say, you know, the insulin vesicle is ready to go, primed, packaged, ready to be released. I'm going to go work on something now. And you end up overeating because of it. We don't know that. So how can I tell you that a diet sweetener is the answer to taking sugar out of the diet? Bottom line is we need to de-sweeten our lives. Okay? Sugar is pleasure. Agreed. We are over-pleasured people. Okay? The Declaration of Independence said the pursuit of happiness, not the pursuit of pleasure. And we have abdicated happiness for pleasure in the last 30 years because happiness is hard and pleasure is easy. Happiness is problematic. Sugar is cheap. Okay? And guess what? Dopamine, which is the feel-good neurotransmitter, down-regulates its own receptor, which means that every time you get exposed to sugar, you need more the next time to get the same level of effect. That's called tolerance. And then you pull it away and you get symptoms. Now you've got withdrawal and now you've got addiction. And the whole country is addicted. So what we need to do is we need to de-sweeten our lives. By the way, FYI, turn off the camera. Just turn off the camera for a second. That's my next book.