Fat Chance Fructose 20

This program is presented by University of California Television. Like what you learn? Visit our website or follow us on Facebook and Twitter to keep up with the latest UCTV programs. Good evening, everyone. Welcome again to our penultimate class in this semester's course on nutrition. Reminder that next week, we'll be talking about vitamins and minerals and vitamin mineral supplements, so please join us for that last class. Dr. Jeffrey Tice will be the professor joining us that evening. Tonight, we have, what I guess for some of you has been the lecture you've been waiting for since the beginning. Dr. Lustig gave a similar lecture in 2009. Little did we know at the time that it would have 3.5 million downloads since then. But it was in this room, and a course very similar to this that I also chaired, and it's really, I think, changed his life more than anything else. I think the hope is that it's also changed the field and the topic, and the policies and the politics of what we're going to talk about tonight. Many of you know, Dr. Lustig is an internationally known neuroendocrinologist in pediatrics. He trained for part of his time at UCSF, then went back East to do clinical neuroendocrinology and came back to UCSF in 2001, where he's continued to do his clinical science on factors that control appetite, particularly the interaction between the hormones of insulin, leptin and ghrelin and appetite control and the metabolic syndrome and obesity. More recently, in part, around the time of the video and certainly in the four years since, Rob has become an international leader in the efforts to improve our nutrition, not only in the United States but around the world. He's focused a larger part by putting a real microscope on the issues of fructose and sugar in general and refined foods in general. The relationship to dietary fiber and many of the other topics that we've been talking about over the course of the course. Rob just returned from Europe this morning. In fact, arrived here at five o'clock this evening. We think he had dinner. We know he hasn't had sleep. It's four o'clock Europe time for him. So this was really a heroic effort. Our fingers were crossed that all the flights would be on time, and I'm very pleased, more than you can imagine, that is here tonight because I didn't want to give this lecture as well. But in addition to his work, Rob recently took a sabbatical in order to further this work and spend a large part of that time at Hastings School of Law, getting a master of studies in law. Part of his aspiration I think is really to add his legal training now to his science and medical training to continue to advocate for good nutrition around the world. We're very anxious to hear about his newest thoughts on this topic. We've entitled the talk the same title as his best-selling book, Fat Chance, and added the subtitle, Fructose 2.0. Rob? Thank you, Bobby. Thank all of you for coming. To some extent, this is like deja vu all over again. Having done this four years ago and it really did change my life, and hopefully it changed a few people's lives in the audience and certainly around the world. I still get emails from that video today. People who have seen it for the first time. That video, we're going to refer back to it to some extent tonight because I am not going to redo the biochemistry. There's no point in doing it twice. What we're going to talk tonight about is primarily the physiology. In a sense, the two videos will end up being complementary on YouTube, and hopefully people who watch it will end up watching both. So keep that in mind. Well, a lot's happened in four years, and the data just keeps rolling in. Unfortunately, for us, all the data is pretty awful. You'll see why as we go and I will try to delineate that as we go. First of all, I have no disclosures. No food industry is putting me up to this, you can be sure of that. Here's the past. This is 2001. Six million kids are seriously overweight. Well, with all of the media attention, with all of the NIH money, with all of the clinical programs, and with Michelle Obama's vegetable gardens, we are now up to 20 million. Here's the present. Currently, there are 30 percent more obese people on the planet than undernourished people. This has happened only within 15 years because 15 years ago, it was exactly the opposite, and it's occurring in countries that still have under-nutrition. How do you explain that other than to say, that can't be behavior, that's got to be an exposure? This looks like any standard pandemic; influenza, typhoid, etc. This looks like a microbial phenomenon rather than a behavior phenomenon. We're going to go there. Three hundred and sixty six million diabetics walking the Earth, that's five percent of the world's population. They are chewing through all the health care resources. This was just three months ago, diabetes costs the US $245 billion. Now, if we could recoup even a fraction of that, we wouldn't even need health care reform. In fact, it's been suggested that we wouldn't even need financial reform. Forty one percent rise in five years. This is going up so fast, it makes your head spin. Here's the future if we do nothing. Experts predict 165 million Americans, 42 percent will be obese by the year 2030, 100 million Americans that'll be 33 percent will have diabetes by 2050. But fear not, because it won't really matter because Medicare will be broke by 2026. As the Soup Nazi once said, "No health care for you." Well, the fact of the matter is, I'm going to be 69 in 2026, and I want my frigging Medicare. So should you all. The point is, we have to do something different than. You know the old adage, or the definition of insanity is doing the same thing over and over again and expecting a different result. Well, I'm here to tell you for the last 30 years, we have done the same thing over and over again, and there has been no change in the result. So we have to rethink this, we have to re-frame the argument, and that's what we're going to try to do tonight. I'm going to do it right now. Here's the way people view this issue. This is a Venn diagram of all the adults in America. Thirty percent obese over here and 70 percent normal weight over here. Everybody assumes that the problem is this group over here, because 80 percent of the obese population is sick in some fashion with type 2 diabetes, lipid problems, hypertension, cardiovascular disease, cancer, dementia, non-alcoholic fatty liver disease, polycystic ovarian disease, etc. If you do the math on this, that's 80 percent of 30 percent of 240 million, that's 57 million sick, and it's those 57 million that are bankrupting the country. So it's the obese person's fault only, and that's the way everyone views this. This is wrong. This is a mistake. This is a disaster actually, because it's not correct. Here's the real story. In fact, 20 percent of the obese population is completely metabolically normal. They have normal insulin dynamics, they don't get sick, they will live a completely normal life, die at a completely normal age, cost the taxpayer nothing. They're just fat. Conversely, up to 40 percent of the normal weight population have the exact same metabolic dysfunction that the obese do. They're just normal weight. They don't even know they're sick until it's too late, because normal weight people get type-2 diabetes, they get hypertension, they get dyslipidemia, they get cardiovascular disease, they get cancer, they get dementia, etc. When you do the math on that, that's another 67 million, so that's actually out classing the obese. The total is 124 million. That's more than half of all of America. Now, you may remember HIV. Remember HIV? When did HIV become a public health crisis? In the '80s. No, not in the '80s. In 1991. 1979, patient zero. We first learned about the diagnosis. Throughout the entire '80s, it was all about the gays and the addicts. It was always, well, it's their problem, their personal responsibility, their behavior, their fault. Then something happened in 1991. Anybody know what it was? Magic Johnson. Magic Johnson got HIV. All of a sudden everybody went, "Holy, Mother." You know what. Everybody realized, you know what? Everyone's at risk and all of a sudden, it became a public health crisis. When does a personal responsibility issue become a public health crisis? That's what we're going to talk about tonight because this is a public health crisis. Here's the slide that demonstrates the phenomenon. Here are two equally weighted adult men, which one's healthy and which one's sick? Anybody know? The one on the bottom is sick. Right, he's sick. Why? All that visceral fat, all that fat surrounding the organs. See, this guy over here, he's got big love handles. So what? In fact, this is perfectly healthy, there's no problem because subcutaneous fat is actually good for you. There are actually studies that show more subcutaneous fat, more longevity. Whereas this stuff, this is the bad stuff, this is the poison stuff over here. The fact is standing on a scale doesn't tell you where your fat is. What does? Well, your waist circumference is a good start, and then there's some lab tests you can do as well. The bottom line is, there are a lot of normal way people who have this phenomenon called TOFI, thin on the outside, fat on the inside, probably some right here in the audience and they get type 2 diabetes, they get dyslipidemia, they get hypertension, etc. You get the picture? Everyone's at risk because everyone's exposed. The question is, what is it you're exposed to? Because obesity is not the problem, it never was. They want you to think it's the problem, but it ain't the problem. What is the problem? Metabolic syndrome is the problem. The cluster of diseases that I've just described to you because that's where all the money goes. Obesity costs almost nothing. Metabolic syndrome is 75 percent of all healthcare costs today, and there's the list right there. Everybody with me now? Do I have your attention? How does this work? This actually is a redundancy from the previous YouTube video, so I apologize for that. It has to do with how you view the question of obesity and what does it mean. Of course, obesity obeys the first law of thermodynamics and I don't argue that. The total energy inside a closed system remains constant. It's a law. If I didn't believe in the first law of thermodynamics, you'd have me written out on a rail. I would be the ultimate heretic and zealot and I would be discredited. Of course, I believe in the first law of thermodynamics. It's a law. The question is, as I've learned from my legal training, whose truth? Which interpretation? The Supreme Court always comes down five, four on everything. True. Because there are two interpretations. I mean, basically, that's what the Supreme Court's for, is interpreting the law. The law is the law, but the interpretation is something else. Here are the two interpretations. If you eat it, you better burn it or you're going to store it. If that's true, then this is a matter of energy balance. That's what everyone will tell you, and it's the result of two aberrant behaviors, calories in, gluttony, calories out, sloth, and that's what everybody assumes is, if you're obese, well, you must eat too much or exercise too little or both, and therefore, it's your fault. That's what we believe and to this day, we still don't have insurance for obesity, although just today, you know that the AMA finally said obesity is a disease. This is funny because actually in 2004, HHS said obesity was a disease. It took the AMA nine years to catch up with HHS. Figure that out. It's based on this dogma. The dogma is that if you eat more than you burn, you'll gain weight. If you eat less than you burn, you'll lose weight because all calories are the same. A calorie is a calorie. This is the biggest pile of, you know what? There is. This is absolutely not true. But if you believe it, then the corollaries of a calorie are, that this is free will, you get to choose what you put in your mouth. It's personal responsibility because if you're obese, you chose to be. Gluttony and sloth, that's your problem and diet and exercise will fix it. That's what everyone believes from a calorie is a calorie. Who says that a calorie is a calorie? Well, the food industry says a calorie is a calorie and that's because it serves them well. This is the fiction, this is Coca-Cola's coming together video on YouTube released just before the Super Bowl that says, "Beating obesity will take action by all of us based on one simple common sense fact. All calories count, no matter where they come from, including Coca-Cola and everything else with calories." A calorie is a calorie. Why pick on Coca-Cola? Why pick on Burger King? Why pick on any individual because it serves them well, because it diffuses the issue? Is that what we've got? We've just got a caloric bacchanalia. Sorry, wait, this is wrong. That's better. Indeed, we are all eating more, I don't argue that; 187 calories per day more for men, 335 calories per day more for women, 275 calories more per day for teen boys than 25 years ago. We are all eating more, I don't argue that, of course, we are. The question is why? So you'd say, well, this is why. This is the evolution of fast food over here. 1957, we have the original White Castle hamburger, 210 calories right there, one ounce. Over here, we have today's Bob's Big Boy over here at 618 calories, and of course, in the midst of the obesity epidemic, Hardee's had the temerity to offer us the thickburger at 1,420 calories. Of course, you can go to Carl's Jr. and get the six dollar burger, which is 2,000 calories. That's the entire caloric allotment for the day, and people are proud to go do it. Anybody here had a Trenta? Yes, no? So that's this guy over here, so it's not hot coffee, it's a cold coffee drink flavored with, you know what? It is 916 cc's. Well, your stomach is 900 cc's, it's bigger than your stomach. You'd say, well, there's your answer, QED, it's all over. How about this? I love this. This came in the mail, free chicken sandwich from KFC with the purchase of a 30 ounce drink. The food's gotten so cheap, we're giving it away, that's where we are. Or is it the opposite side of the equation? Is it an activity famine? This is a study that was done looking at physical activity here on the y-axis against age, nine-years-old to 19-years-old for white girls and black girls, and you can see that by the time they hit age 15, the black girls are just lying prostrate on the floor because there is no physical activity whatsoever. So you say, well, there's your answer, that's why everyone's obese because they're eating too much and they're exercising too little; gluttony and sloth, diet and exercise, just like common sense tells you. Well, you know what? I don't believe in common sense. I believe in data, and that's why we do research, because education consists mainly of what we have unlearned. In fact, if everything that we knew were true, there would be no reason for research, would there? I would never have to do any research because everything we knew was already right. In fact, everything we learned 10 years ago is already wrong, and everything we know today will be wrong 10 years from now, and that's why you do research, and the fact is the research tells us something very different. Is this behavior? Is it personal responsibility? What do you think? There are six reasons to doubt this. Number one, no child chooses to be obese. The quality of life of an obese child is the same as a patient on cancer chemotherapy. Why would anyone choose this? In fact, children are ostracized. Second, does diet work? Now, everybody knows somebody who lost weight on a diet and then of course, they gained it all back, and that's what all the data shows. The number of people who can actually maintain their weight loss for any length of time is vanishingly small. If that weren't true, you wouldn't be sitting here listening to me because you'd say, "Well, why do I have to listen to him?" Does exercise work? Here are studies of exercise, and this is the identity line here, and you can see when compared with no treatment, exercise resulted in very small weight loss across the board, one BMI point, vigorous exercise, 1.5 BMI points. Considering we are all 78 BMI points more than we should be, that ain't going to cut it because exercise does not cause weight loss. What does exercise do? It causes muscle gain, and that's good because muscle have mitochondria. Mitochondria burn energy, so you stay insulin sensitive because you have a place to put your energy instead of in your liver where it causes problems. Exercise is the single best thing you can do for yourself but if you think it's going to show on the scale, think again. When you stand on the scale, what do you measure? You're measuring four compartments at once; bone, more is better, muscle, more is better, subcutaneous fat, more is better, I just showed you, and finally, visceral fat, more is worse. Now, the visceral fat usually encompasses about 46 percent of your total body weight. When you stand on the scale, what are you measuring? You don't know. You can't possibly know. We have all these doctors telling their patients, well, if you'd only exercise, you'd lose weight, and then of course, they don't because they've built muscle, which is good, but it doesn't show up on the scale, and then they get depressed because, "Oh, I was doing this to lose weight and it didn't work, and so I might as well stop because obviously, it doesn't work for me." This is the single most egregious thing doctors do to their patients today, and as far as I'm concerned, that's almost malpractice because the data say otherwise. Number three, this isn't just about America, and it's not just about the UK, it's not just about Australia. Yes, we are the three fattest countries and we spend the least amount of our GDP on food, that's true, but it's going on everywhere, every country. Every single country on the planet has shown an uptick in obesity. Some have shown an uptick in diabetes and some have shown a downtick, but for obesity, everybody's gone up. It doesn't matter where you look. Every country has shown an increase. Number four, the poor are disproportionately affected. They don't have access to choices. They can't even leave their house for fear of crime. How are they going to exercise? How are they going to leave the kids out to go play in the yard when they might face a stray bullet? They don't have supermarkets. They live in food deserts. If you don't have a choice, how can you call it personal responsibility? This is one of the most egregious pejorative statements that there is. Number 5, the prevalence of obesity is going up in the group that you can least ascribe personal responsibility to. The toddler, the 2-5 year-old group is going up the fastest. You want to say that that's personal responsibility, or you say it's the personal responsibility of the parent for letting them have the sugar pops and the sodas and the fruit juices and everything else, it's the parent's fault. Except for one thing, we've been having epidemic of obese six-month-olds and they don't diet and exercise. Any hypothesis you want to proffer, you have to explain this as well. It's even worse than that because we have obesity in newborns. Birth weight's gone up by 200 grams all over the world over the last 25 years. When you do DEXA scans to figure out what the body composition is, it's all fat. These babies are laying down more fat before they're ever born and fat cells want to get filled. That's why we have obese six-month-olds because everybody's laying down more fat. The question is, how? Why? Why they're laying down more fat today? Most clearly mother's diet. But you want to blame the newborn for that problem? Is that their problem? Is that their fault? You want to blame the pregnant mother. Well, then, it just goes backwards like that. You basically blame everybody or blame nobody. I blame nobody. Actually, I do blame somebody. We're going to get there at the end. We're talking about behavior. This is the definition of behavior, this is all from the original video, a stereotyped motor response to a physiological stimulus. Let's take that apart. Stereotyped, same every time, so yes, eating is a behavior. Motor, muscles have to move. A thought is not a behavior. Finally, physiological, and that's where I come in. What's the physiology behind the obesity epidemic? Why do you eat too much and exercise too little? All behaviors have a biochemical basis. Now sometimes we're smart enough to know what it is and sometimes we're not smart enough to know what it is. Give me an example. Schizophrenia. For a 100 years, schizophrenia was behavioral disorder. Now, we know it's a defect in dopamine neurotransmission and probably actually a defect in glucose transport across the brain. These are biochemical problems that ultimately manifest themselves as a behavioral disorder. This is no different. What are the biochemical underpinnings behind gluttony and sloth? That's the question. That's what we're going to try to answer now. In order to answer that, you actually have to know some science. I'm gong to make this very brief and very quick. We're going to talk about these two hormones right over here called leptin and insulin. Leptin is a hormone that comes from your fat cell, goes to your brain, and tells your brain, "You have enough energy on board to engage in normal, expensive metabolic processes. You can burn energy at a normal rate and feel good doing it." It tells your brain, "You've got enough energy on board." If your leptin goes down or if your brain doesn't see your leptin, then your brain sees that as starvation. Everybody got that? Insulin is equally interesting because insulin tells your fat cell one thing it says, "Store energy" and it tells your brain something else. It tells your brain, "Stop. I'm in the middle of metabolizing a meal I don't need anymore. Let me deal with what I got." It's part of the satiety signal. It tells your fat cell, "Get bigger" and it tells your brain, "Stop feeding your fat cell." It's got a dichotomous role and it's that dichotomous role, that is the linchpin in terms of understanding the physiology of obesity. I'm going to go there. Here's how it works. We have to explain a paradox. Here's the paradox. Who has children? Enough of you? What happens if you give a five-year-old kid a cookie? They eat it. Yeah, they eat it. Yeah, I know they eat it, yeah. What happens after that? They bounce off walls is what they do. Ask any kindergarten teacher what happens when the cupcakes roll out for the birthday party. That's the end of the lesson. They're bouncing off walls. It's known as the sugar high. What's going on? The fat cell gets filled because of the cookie. The leptin goes up, tells the brain, "Hey, I've got extra energy on board." It tells the sympathetic nervous system, the fight or flight part of the nervous system that innervates your muscles and innervates your fat cells, "Hey, I got too much energy." What happens? You burn it off. The sympathetic nervous system tone to the muscles give you the fidgeting, and the sympathetic nervous system tone to the fat cells releases the extra fat and that gets used for energy later. This is a nice negative feedback pathway that keeps you in energy balance as long as your brain can see its leptin. So far so good. Here's the paradox. What happens if you give an obese, five-year-old kid a cookie instead? They're in the pantry looking for more cookies. Anybody ever see a sugar high in an obese kid? It doesn't exist. That's why they're obese is because they don't get the sugar high, because they can't see their leptin. If they could see their leptin, they'd have a sugar high, but they don't. That's the point. Something's blocking that leptin signal. That's the paradox. The question is, what is it? We learned about leptin from this patient over here. This is the OB/OB mouse, the leptin-deficient mouse who has a gene defect in the leptin gene. This animal's leptin is zero. His brain thinks he's starving all the time. He'll eat anything in sight. Not only will he eat anything in sight, but this animal is the ultimate couch potato because his brain can't see his leptin, so he thinks he's starving, so he doesn't want to burn energy, he wants to store it. The only reason this animal ever gets off his high knee is you put the food on the other side of the cage and they'll waddle over to that, sit down, eat it there, and stay there instead. Everybody got it? Now the reason? Because leptin tells the hypothalamus that, "You've got the energy to burn." If the hypothalamus sees the leptin signal, then this diamond over here gets activated. Anorexigenesis, that is, "I'm not hungry, I don't need anymore and I can burn energy effectively." It tells the sympathetic nervous system, "Turn on to fidget" and to release fat from the fat cell, and it tells the vagus nerve, the energy storage nerve, "Hey, I'm not hungry. Appetite down and stop releasing insulin." Everybody with me? Conversely, if the leptin doesn't reach the hypothalamus because there's a gene deletion or because there's something blocking it, then you get this diamond instead, which is orexigenesis. "I'm hungry. I need more food because I'm starving, and because I'm starving, I'm going to try to conserve." That means your sympathetic nervous system tone goes down, which means you sit on the log and your vagus nerve goes up to increase your appetite so that you'll generate more calories in order to put more into the fat cells to try to get more of a leptin signal. Everybody with me? This is that same negative feedback pathway I showed you before, now schematized. There are leptin-deficient people. Fourteen at last count, and they're all of consanguineous marriages and they're all of Pakistani or Turkish ancestry. When they're born, they're perfectly normal weight, and by age six months, they are already massively obese because their brain is constantly starving. It doesn't matter how much weight they gain, their brain can't see it because it ain't there, because they have a leptin gene defect. Here's a patient, 220 pounds by age nine. You start giving them shots of leptin every day and look what happens. They lose weight on a dime and it's all fat mass that they're losing too. Hormone replacement therapy because now their brain can see leptin because we're giving it to them from a bottle instead of from their own fat cell. Hormone replacement therapy, that's what I do as an endocrinologist. That's my job. Here's an example. Here's the patient at three-and-a-half years of age looking pretty awful, and here's after shot of leptin every day for four years. Indistinguishable from normal because we fixed the problem. Great for those 14 people. The problem is the rest of us are not leptin-deficient. The rest of us are leptin resistant. We got boatloads of leptin and the leptin correlates with how much body fat we have. If our brain could see that leptin, we wouldn't be obese. We'd burn it off in the sugar high. Everybody got it? There's something blocking that signaling right there, that X. That's the holy grail of obesity right there. What is blocking leptin from working? If your hypothalamus can't see it, then you are in this box over here and you can see things just go in the wrong direction. There's your gluttony and there's your sloth. This is all biochemical. What role does insulin play in this leptin debacle? That's the question. Remember I told you, insulin tells your fat cell one thing and your brain the exact opposite. It tells your fat cell store and it tells your brain, stop. That's the problem. This is the patient that got me started in obesity research, now 18 years ago, when I worked at St. Jude Children's Research Hospital in Memphis. This was a 15-year-old boy who weighs 364 pounds in this photo. At age of seven, this kid was perfectly normal weight for height. Then he developed this brain tumor sitting in the middle of his energy balance pathway, and he required surgery and he required radiation to kill this astrocytoma, tumor of the brain. He started gaining weight at the rate of 30 pounds per year, nonstop for eight years until he was 364 pounds when I saw him. Everybody with me? Now, this form of intractable obesity due to a brain lesion, now, that area of the brain that controls this energy balance is dead. You can have all the leptin in the world, but if those neurons are dead, your brain thinks you're starving because it can't transduce that signal. This is called hypothalamic obesity, and this is how I got started in obesity research many, many years ago. The question is, how does this happen? Well, here are two different hypotheses. This hypothesis says, when you damage the hypothalamus, you get obesity because it releases a satiety center, so now you become hyperphagia, except the data actually doesn't support that. Data does not support that there's hyperphagia, that there's too much food intake. Actually, it supports that there's too little burning is what it shows, and that the obesity occurs, and then, because of the obesity, you have to secrete more insulin to attend all that fat, and so that the insulin here is a result of the obesity. But there's this other hypothesis over here that says the damage to the hypothalamus, yes, it leads to obesity, because it turns on that vagus nerve, because you can't see your leptin. When you turn on the vagus nerve, that tells your pancreas to release more insulin, and that extra insulin drives energy into fat, energy deposition, not energy balance because of the high insulin and the insulin is driving the obesity, which is true. If this is true, nothing I can do about it because I can't fix a brain. If this is true, it gives me a place I could potentially intervene, right between the vagus nerve and the pancreas. We have a drug that does that, and it's called octreotide. It's an endocrine drug that I know how to use. We asked the question, if we take these kids who have this intractable obesity due to brain tumors and we give them this drug to suppress their insulin, might it help? That was the question. Here's that same patient I showed you, 364 pounds, and here he is a year later at 326, first time he took a picture with his shirt off. It did pretty well. I'm going to show you the piece de resistance over here, this isn't even my patient. This is a beautiful 13-year-old girl from Hawaii, notice the flower, who, a month after this picture was taken, was in a very severe car accident on a Honolulu Road. She was in the intensive care unit for about a month. She survived, but she stroked her hypothalamus, and so this is her a year later. Now, does anybody want to tell me that this is gluttony and sloth? This kid now can't see her leptin because those neurons are dead. Now, it just so happens I happened to be giving grand rounds at Kaiser Honolulu in 2008. They invited the patient than her mother to come to the talk because they were thinking about putting this kid on octreotide even though she didn't have a brain tumor because she might have the same disorder, and so there I am with her, and here she is a year and a half later on the drug at her high school graduation. Now, who here wants to tell me that this is gluttony and sloth? Do I have your attention? It's never gluttony and sloth. It's always biochemical. The question is, are you smart enough to figure out what the biochemistry is? We said, maybe this could be true in adult obesity without brain tumors or without hypothalamic damage. We did two studies, double-blind, placebo-controlled. This is a patient, adult, Christmas 1998 holding up food, and here she is 35 pounds later in her jogging tags showing me that she wanted to exercise. She actually wanted to exercise and the reason was because she wasn't storing it. Because her insulin went down because the drug suppressed her insulin. When her insulin went down, she had the energy to burn and she wanted to, and she did, and she's showing you right here that the change in the biochemistry changed her behavior. The biochemistry drives the behavior. The cause of leptin resistance, that X up here, it's insulin. There's actually numerous studies now, biochemical, molecular, genetic, that show that insulin blocks leptin-signaling by acting on the same neurons in the brain as leptin does, and that's the point: insulin blocks leptin-signaling. Now, why? What's in it for us? Why would God do this to us? The answer is because there are two times in your life you actually have to gain weight. What are they? Pregnancies. Pregnancy is one, and the other is? Puberty. Puberty and pregnancy, both necessary for survival of the species. If your leptin worked right all the time, you could never gain the weight because you'd be in the sugar high, you'd be burning it off before you ever had a chance to actually gain the weight. You'd be the 97-pound weakling on the beach who couldn't bulk up and the species would die out. There are two times in your life you actually have to gain weight, and both puberty and pregnancy are insulin-resistant states where your insulin goes high very specifically to cause the weight gain, then you cut the cord, baby's out, sex hormones go back down, the insulin resistance goes away, you'll lose the weight and you can start all over again. It actually makes perfect Darwinian sense that insulin should block leptin, twice in your life. Twice in your life, insulin should block leptin. Problem is, now it blocks leptin all the time because our insulins are high 24/7, 365. The question is, how come? Where did the increased insulin come from? That's the question, that 64 zillion dollar question, why are we all hyperinsulinemic today? If you look at glucose tolerance test done today versus ones that were done 35 years ago, we're releasing double to triple the amount of insulin today that we were 35 years, and the question is why? I'm not going to tell you. I'm going to let Will Smith tell you. What? Guess I owe you some answers, hoss. What, you're feeling chatty all of a sudden? Sorry, I can't talk right now. I got some secret cases of my own I'm working on. I hate to tear you away from your video game. All right, I'm hanging up. You know the most destructive force in the universe? Sugar? If Hollywood knows this, why don't you? Indeed, he's got it right. We know that there are substances out there that are addictive and hazardous to our health. Here's a perfect example, and we regulate it. Well, guess what? It's not the only one. This is too, and I'll show you why. These are the two papers, popular press items. This was from the New York Times magazine in 2011. Is Sugar Toxic? from Gary Taubes based on our work here at UCSF. This is a comment that we had in nature, last year that got quite a bit of heat more than light, unfortunately, called the Toxic Truth About Sugar that I wrote with my colleagues here, Laura Schmidt and Claire Brindis at the Institute for Health Policy Studies. Hazardous to your health. The reason is because that common sense notion, a calorie is a calorie, it ain't true, because, a calorie is not a calorie. What are we talking about? Here we're talking about this stuff called high fructose corn syrup. Fifty percent fructose, so they say, there are actually some studies that suggest that dispenser sugar, like from McDonald's or Burger King or 7-Eleven might actually have 65 percent fructose sometimes. That would be a problem. But most of the time, it's 55 percent, one glucose, one fructose, six-membered ring, five-membered ring. Now, this stuff is essential for life. Every cell on the planet utilizes glucose for energy. It's so important that if you don't eat it, your body makes it. That's how important it is. This guy over here is completely vestigial. There's not one biochemical reaction in the body that requires it, but it's very sweet and we like it a lot. The question is, what do we do with it if we don't need it for any biochemical reaction? That's one of the key questions. But over here is sucrose, this is table sugar, cane sugar, bee sugar, the stuff you put in coffee, one glucose, one fructose, or glycocidic linkage, linking the two, the enzyme in your intestine sucrose that cleaves this in about a nanosecond. When you absorb the two moieties, they are exactly the same and that's what all the data say, is that they're exactly the same. High fructose corn syrup and sucrose are metabolically equal. Metabolically bad. Metabolically equally bad. This is what our consumption of fructose, so double it for sugar, has done over the last 100 years. Our ancestors getting fruits and vegetables out of the ground with the occasional honey got about 15 grams of fructose per day prior to World War II, with the nascent candy and soft drink in the streets in the country, we got up to about 20 grams per day. By 1977, we got up to 37 grams per day. This is just before high fructose corn syrup invaded our shores at eight percent of total caloric intake. By 1994, we were up to 55 grams a day. That was 10 percent of total caloric intake. Adolescents currently consume 75 grams per day. That's 12 percent of caloric intake. Twenty-five percent of adolescents consume 100 grams of fructose per day. Double that for sugar. That's 200 grams of sugar, multiplied by 4.1 calories per gram, that's 840 calories in sugar. For a 2,000 calorie allotment, that's 40 percent of calories of sugar. The question is, can you handle it? Can your liver handle it? Can you metabolize all that sugar before something bad happens? Remember what Paracelsus told us. The dose determines the poison. Could this be an overdose? Could that be hazardous to your health? Indeed. As far as I'm concerned, our entire food supply has been adulterated, fructose related. Because of the addition of fructose for palatability, especially with decrease fat, and also sensibly as a browning agent. Because food browns better, right? You painted on your barbecue ribs to brown it better. The caramelization actually, we like that. The removal of fiber for shelf-life and freezing. We also have substituted trans-fats but those coming down because we know those are poison, although they're still legal and they're still on the generally recognized as safe list at the FDA. Figure that out. Because we know they're poison. Now, does sugar cause obesity? Yes, no? Food industry will tell you everything causes obesity and you know what they're right. It's true. Because if you look at this study from Mozaffarian and at Harvard School Public Health, looking at what foods cause the most weight gain, potato chips and french fries. Indeed, I agree with that. Those are the bad guys in terms of weight gain. Sugar, distant third. When a meta-analysis was done earlier this year from the University of Otago, you'll notice the diamond doesn't cross the identity line. That means that it's significant. There is a significant increase in weight. But when you actually do the math, it's only 0.8 BMI points. Remember I told you, we got seven or eight BMI points to deal with. Does sugar cause weight gain? Yes. Does sugar cause obesity? A factor. Is sugar the cause of obesity? Not even remotely close. The problem is, it's not about obesity. Remember it's about metabolic syndrome, and that's where the money goes. I don't even care about obesity. What I care about is people getting sick because I'm a doctor. Here's the problem. Common wisdom says that sugar is just empty calories and you can get your discretionary calories from anywhere. The problem is that hepatic fructose metabolism is completely different from that of glucose. This is what the first YouTube video went into in exhausting detail and I will not repeat it. But I'm going to show you very quickly that chronic fructose exposure alone promotes the metabolic syndrome. This again is from that first video. When you consume glucose, say rice, white bread, starch, 80 percent of the glucose goes to all the organs of the body. Only 20 percent hits the liver. Where does it go? It goes to this guy over here, glycogen. Glycogen is liver starch. Liver starch, for lack of a better word, is good. Because that's your energy store for a rainy day. That's the first energy that's used when you fast. That's why marathoners carb-load before a marathon race, is to try to build up their glycogen stores because glycogen is non-toxic. If you can up your glycogen stores, your liver has more energy in reserve, and that's a good thing. Now, a little of it will sneak down here and get metabolized by the mitochondria and throw off a little of this stuff called citrate, and that will then get turned into liver fat. This process here in orange is called De novo lipogenesis, new fat-making. This is how your liver turns carbohydrate into fat, is through this process here. But you're not dealing with very much carbohydrate here because it all went to glycogen and most of it actually got metabolized elsewhere anyway. Your liver is protected. Everybody see that? Your liver is protected. This is for lack of a better word, is normal. Let's talk about something that's not normal. This guy, alcohol, that's not normal. Carbon, hydrogen, oxygen. But alcohol is a toxin, right? It's two toxins in one. You wrap your Lamborghini around the tree, acute alcohol toxicity, and you fry your liver. Chronic alcohol toxicity. We keep it out of the hands of children. Here's acute alcohol exposure. Here's acute sugar exposure, none. Why? Because the brain doesn't use fructose for energy. It does use alcohol, but it doesn't use fructose for energy. You don't get any of those CNS symptoms because it doesn't get there. Let's consume the same number of calories of alcohol. Now, most of them go to the liver instead of going to the periphery. What happens to it? You see glycogen anywhere? No glycogen. It by-passes glycogen and goes down to the mitochondria, and since there's so much of it, you get big-time fat-making and some of it won't make it out. Now, you get that lipid droplet, that's alcoholic steatohepatitis. You're going to make lots of triglycerides, and so you're going to have hypertriglyceridemia and that's going to end up in the muscle. Now, I've got muscle insulin resistance and it serves as a substrate for weight gain as well. We also know that alcohol has this inhibiting effect on your brain, which causes you to drink more. Oh, I'm just going to have one drink and you end up with five. Of course, if you do that too often, maybe you'll even become an alcoholic. That's addiction right there. Positive feedback effect. Here's a problem because this is toxic and abused. We regulate it. Now let's do fructose. We're going to consume sugar now, we going to consume orange juice. Same number of calories. The glucose does the same 20-80 split it did before 12 and 48, but all the calories from fructose are going to go to the liver because only the liver has the transporter for fructose called GLUT5. You see glycogen anywhere? No glycogen. Go straight down to the mitochondria, just like alcohol did. Because there's so much of it, your mitochondria have no choice but to turn the excess into liver fat. There's your lipid droplets. Now you've got nonalcoholic steatohepatitis. You've got high triglycerides, just like you did with alcohol. You get the muscle insulin resistance, substrate for obesity, and it tells your insulin receptor not to work. Now you've got liver insulin resistance, which makes your pancreas have to make more insulin in order to make delivered to its job. Now the high insulin goes to the brain, blocks leptin, and now you can't see your leptin. What does it do? It makes you think you're starving. What does it make you do? Consume more fructose. Now, you've got a positive feedback effect between a compound that's toxic and abused, causing damage to the liver, damage to the pancreas eventually, and damage to the brain. But we don't do anything about that. You would never think about giving your kid a beer, but you don't think twice about giving your kid at Coke and they do the same thing. That's one problem. Now, there's a second problem. Here are five photographs. What do they all have in common? There's one thing they have all hung come, they're all brown. Good, thank you. They're all brown. This is the browning reaction, for the maillard reaction. Anybody you know what hemoglobin A1c is? That's the lab test they do for diabetics to see how the blood sugar control is. That's glucose binding to proteins in the blood. Well, that's what this is. This is the maillard reaction: glucose binding to proteins in the actual food. The common link is this browning or maillard reaction or non-enzymatic glycation. Here's the deal. You can think of it this way. You can roast your meat at 375 degrees for an hour, or you can roast your meat at 98.6 degrees for 75 years, the answer is the same. We all brown. It's part of aging, it's normal aging, and everyone does it. The question is, how fast do you do it, and if you don't believe me, here's just an example. Here's newborn rib cartilage nice and white and here's 88 year old rib cartilage nice and brown, and if you had orange juice this morning, you are browning faster. That's the deal. That's what we know and we know it, and we know it's true, because every time this reaction occurs, you release a hydrogen peroxide, and that hydrogen peroxide does damage inside the cell unless it's quenched by an antioxidant, and if you don't take enough antioxidants, you're going to do damage and that's what nonalcoholic steatohepatitis is. Here's that reaction. Here's the aldehyde of glucose and it binds to the amino group of lysine off the hemoglobin molecule. It forms what's known as a shift base which then decomposes and develops this amid linkage here and bottom line is, it's non-enzymatic and it happens all the time. The question is how much, and this shows that it's very, very specific to fructose in terms of amount. This is an animal model of non-alcoholic fatty liver disease called methionine-choline deficient rat, the MCD rat. Not the McDonald's rat but it might as well be because what happens is when you give the animal sugar or starch with normal amounts of methionine-choline, no problem, the liver can handle it, but if you're deficient which happens when you have a bad diet, then only sugar causes the problem, starch doesn't, and you can see here in a nonalcoholic fatty liver disease clinic at Duke University. This is Doctor Manal Abdelmalek's work showing that the greatest steatosis or fatty liver is dependent on how much fructose consumption, whether it's daily or not and the stage of fibrosis, same thing. So two problems; fatty liver and cell aging. So far, so good? All right, so now we're going to get into the weeds. Here are the 10 most obese states in the nation. Anybody surprised? Anybody from any of them? I used to live in Memphis, you know what I'm talking about, right? North Carolina. North Carolina, you know what I'm talking about, right? I'm turning to those ribs. Yeah, I know. Ten most of these states. Here are the 10 laziest states in the nation. What's going on over there in Nevada? I guess you can only burn so much energy going like this. Here are the 10 most unhappy states in the nation. Here's the adult diabetes rate, here's the adult heart disease rate, and finally, here's soda per capita consumption. Now, what do you see? Coke. Pretty significant overlap, wouldn't you say? Yeah. Well, now this is correlation, not causation and I'm very clear on the difference. We're going to talk about the difference. The question is, which direction does it go? Is it that soda causes heart disease and diabetes or is it that people with heart disease and diabetes like to drink soda? You can't tell, because it's one snapshot in time, you can't tell which way the data went. True. Here's what's happening worldwide. This is global consumption of sugar and sugar crops. Here we are at 629 calories availability here in blue and here's the rest of the world. Now, the American Heart Association says 150-200 calories in added sugar per day right here, this color blue. How many countries are above that? How about all of them? In fact, that's why diabetes is skyrocketing everywhere. Here's world sugar consumption tripling over the past 50 years. Per capita consumption, notice Brazil. Brazil used to be a poor country. They were always a sugar exporter, but they couldn't afford their own sugar, but now they can because they're a BRIC country. They sell Embraer jets and biodiesel and World Cup, and all that stuff, and the fact is that Brazil now has the highest increase in rate of prevalence of type 2 diabetes in the world. It doesn't have the highest prevalence. That's reserved for Saudi Arabia, Kuwait, United Arab Emirates, Qatar, and Malaysia. Why them? Why do they have the highest diabetes rates in the world? No alcohol, but they got soft drinks like they're going out of style. Why? Because it's hot and the water supply is a question mark and no alcohol. This is their reward. Now the difference is alcohol, for lack of a better word, is self-limiting, because you end up under the table, but soft drinks, you can drink them all day, and they do, and that's why they have diabetes. Now, how do I know that the sugar cause the diabetes? Because correlation is not causation, but we have causation too and this is our work. It just came out three months ago. I'm very proud of it. Sanjay Basu, one of my colleagues at Stanford Prevention students and I took four databases and melded them together. We took the Food and Agriculture Organization or FAO statistics database from the World Health Organization which for the whole decade, 2000-2010 which has food supply as total calories, fruits excluding wine, oils, roots, tubers, pulses, nuts and vegetables, meat, cereals and sugar, sugar crops and sweeteners as separate items. We then link that to the International Diabetes Federation statistics database for diabetes prevalence worldwide for the decade, and then we linked that to the World Bank gross national income database to control for GDP, urbanization and aging, and then we linked that to a physical activity database to control for physical inactivity, and we asked the question, what about the world's diet? Predicts diabetes prevalence change over time worldwide. That was our question. Everybody with me? Here's what we did: 204 countries, we had complete data for 154, the 50 that we did not use were no different from the 154 by a very fancy set of statistics, and we did a lot of statistics. This is called an econometric analysis. Now a standard percent versus percent would be called an ecological analysis. This is not an ecological analysis, this is an econometric analysis. This actually won two economists Nobel Prizes for being able to predict stock market crashes based on what's happening before to predict what happens after, because there's causational inference in this. Generalized estimating equations with a conservative fixed-effects approach called the Hausman test, a hazard model to control for selection bias called the Heckman test. This is the important one. Since we had the whole decade, we didn't have a snapshot. We had the movie and you can learn a whole lot more from a movie than you can from a snapshot, can't you? That's called the Granger causality test because we can determine what came first. Because you can't infer causation if something didn't come first. Proximate cause. You need proximate cause, and period effects to control for secular trends. We did all this really, really neat statistical analysis and Sanjay Basu was an absolute genius. What we did was a control for GDP obesity, urbanization, aging and physical activity, so the question was, is it the obesity or is it something specific in the food supply? That was the question. During the decade, diabetes prevalence rose from 5.5-7 percent worldwide. Not good. Here's the effects model. Sugar, sugar plus controls plus period, bottom line. Remember that diamond that can't cross the identity line? Well, it doesn't. It's very significant. In fact, for every 100 calories, you increase your diabetes prevalence worldwide by 0.8 percent and here's the adjusted association when you took all the factors into account between sugar availability and diabetes prevalence. Here's what you need to take home. This is the take-home slide. Only changes in sugar availability predicted those changes in diabetes prevalence worldwide only. If you consumed 150 calories extra per day in total calories, diabetes prevalence only went up by 0.1 percent. Nothing. But if those 150 calories happen to be a can of soda, diabetes prevalence went up 11-fold, 1.1 percent, and we're not consuming one can of soda per day, we're consuming two-and-half. So that's 2.4 percent. Given that American diabetes rates are 8.3 percent, that means that 26 percent of all diabetes in America today is due to sugar and sugar alone. Not due to obesity, not due to total calories, sugar, and sugar alone. You want to do something, you want something actionable, you want something that's going to change how much money we spend so we can salvage Medicare, here it is. Of course, our government is doing absolutely nothing. Our data show that 25 percent of diabetes worldwide is explained by sugar. More importantly, this is causation because these data meet what's known as the Austin Bradford Hill criteria for what we call causal medical inference. Now, what does that mean? It means that you can show dose effect, you can show duration effect of sugar on diabetes and you can show most importantly directionality. That is, those countries where sugar went up showed an increase in diabetes rates, those countries, the few of them where sugar went down, showed decreased diabetes rates and precedence. Three-year time differential. So every country when their sugar went up, three years later you saw the change in diabetes in either direction. That's causal medical inference. Now, it's not scientific proof. There are different kinds of proof. There's anecdotal data which of course is absolute garbage, and you can't do anything with that because an N of 1 means nothing. Then there's correlation but correlation suffers from this directionality question, which came first because it's a snapshot and you can't tell. Then there's this thing called causal medical inference. We're going to talk about that right now. Then there's this thing called scientific proof that everybody keeps harping on. In medicine today, what percentage of what we know is scientifically based, evidence-based, scientific proof, randomized controlled trials? That's the standard. How much of what we know, what percent of what we know today is due to scientific proof? What do you think? You want to give me a percentage? Five. Ten. Ten, good. Ten percent of what we know is due to randomized control trials. That means 90 percent of what we know is causal medical inference. So here's a question. What level of proof do you need? You tell me. Who here believes in global warming? Why? Got any proof? [inaudible] Causal inference? Can you a randomized controlled trial and show me that that's what's going on? No. Who here believes that football trauma causes Alzheimer's? How come? You got proof? No, [inaudible] Causal inference. Who here believes that tobacco causes lung cancer? How come? You got proof? Who's done the randomized control trial where you take naive people and expose them to cigarette smoke for the next 50 years and see what their lung cancer rates are. Number one, it would be too expensive. Number two, it would be damn unethical, wouldn't it? In fact, most of these studies would be damn unethical. You ever think we're going to get the actual scientific studies, the scientific proof for sugar causing diabetes. Number one, nobody's got a zero baseline, nobody's naive. Number two, this is something that happens over 40, 50, 60 years. How are you going to keep people on the same diet for that long? How are you going to figure out what they actually ate when we can't even figure it out after one day? Don't you think it'd be a little unethical to do that to people? You'll never get this data. But of course, the food industry says, well, we don't have the data, we need more research. We always need more research. Of course, we need more research. The question is, do we have enough proof to act? Them saying we need more proof, is them moving the goalposts because we'll never get enough proof for them. The question is, what do you think? Do you think we have enough? We have causal medical inference for sugar and diabetes. Do we have enough? Yes. Is for you to decide. Addictive, the last piece of this. Binging on high-calorie foods may be as addictive as cocaine or nicotine and could cause compulsive eating and obesity according to a study. Here are all these books that came out on obesity and addiction and reward. They're all popular books, based on no data. But what do you think? You think that science could catch up to this? So here's neuroimaging studies, PET scanning of dopamine receptors. Dopamine is the feel-good neurotransmitter, the pleasure neurotransmitter in the reward center here. Here's a control brain with nice hot dopamine receptors, which is good. Here's a cocaine brain where there had been damped down. This is the neuroanatomic equivalent of the phenomenon of tolerance. Because dopamine down-regulates its own receptor. So once this happens, you need more substrate to get the same effect. That's called tolerance. Then of course, when you withdraw, now you get withdrawal and you get symptoms. Everybody with me? Well, here's a control brain, and here's an obese brain. What do you see? Same thing. Not quite as bad, but same concept. So this is the reward system. Here's the ventral tegmental area here where the dopamine neurons live and here's the nucleus accumbens where the dopamine information gets received. How fast this gets transduced has everything to do with what level of reward you achieve with any given stimulus. Whether it'll be power or gambling or shopping or cocaine or alcohol or for that matter, sugar. This just shows what happens. So here's that dopamine neuron and you see it's going bleep, bleep, bleep. So you add nicotine and you get more reward. That's basically what we're talking about that's why people start smoking and then, of course, the dopamine receptors go down then they can't stop smoking. That's addiction. Food intake is a readout of reward because here's injecting morphine into the reward center and you can see that as the morphine goes up, the food intake goes up because food intake is a readout of reward. You can see that all the reward centers are all linked together into the nucleus accumbens including the hypothalamus, which is the starvation area, the amygdala, which is the fear area, and of course the reward area. So hunger, reward, and stress, all reasons to eat and they all conspire against us all at the same time. When we see a patient in our clinic, that's the question we ask ourselves. Is this patient obese because they are hungry? I know what to do about that. Or is this patient obese because of the reward system is defective and they're addicted? That's a lot harder to deal with, but we know how to do that too. Or is this person eating because of stress? Which is enormous problem, especially in America. That one's a really hard one because it's not the stress, it's the response to stress. If you think you're stressed, you're stressed whether you are or your not. Most kids today are stressed like never before. You know what stresses them the most? Facebook. This is going on in every animal. See here's humans right there, big dopamines. There are receptors here. When obese, dopamine receptors go down. Here are bonnet macaques, same thing. Here are rats, same thing. Bottom line, obesity means down regulation of dopamine receptors, which means you need more food to get the same level of reward, or you might as well crawl in a hole and die. That's what it's all about. These people are eating because their brain says they have to. The question is, is fast food addictive? What do you think? Yes. Yes, no, what do you think? Yes. We actually looked at that question. Everybody would be familiar with this book? Michael Moss put this out. Salt Sugar Fat: How The Food Giants Hooked Us. This is wrong. This is a mistake because there's one thing not on the list. What's missing? Caffeine. Now, we've got fast food; salt, sugar, fat, and caffeine. The question is, of these four, which are addictive? Let's talk about salt. Is salt addictive? No, it's not addictive. In humans, the threshold is physiologically fixed. Higher levels are attributable to preference, but you can alter that preference. Lots of people do, especially when they have to go low salt for some reason. We know because we take care of a disease in endocrinology called salt-losing congenital adrenal hyperplasia, where their kidneys are losing salt non-stop. But when we give them the salt retaining hormone that works in the kidney called aldosterone, their salt intake goes way down. If they were addicted, that wouldn't happen. When we fix their physiology, their preference gets a lot better. Salt, not addictive. Now let's take fat. Is fat addictive? What do you think? No. No. Rodents binge but show no signs of dependence. Humans, they always binge on high fat, high carb or high sugar items like pizza and ice cream. You don't binge on high fat per se, otherwise, the Atkins diet would have everybody addicted and they'll tell you they're losing weight. How could they lose weight if they were all addicted? Energy density actually has a stronger association with obesity metabolic syndrome than fat does. Fat, not addictive. We're left with these two. Caffeine? Caffeine's addictive. If you take my Starbucks away from me, I will kill you. Model drug of dependence, gateway drug, in fact. Dependence shown in children, adolescents, adults. Thirty percent who consume it meet the DSM criteria for dependence, and the physiologic addiction is well-established with the headache and the test performance and everything else. Mega addictive. But do you see anybody going out and regulating Starbucks or pizza or anything like that? Why? Because it's not toxic. It's addictive but not toxic. Unless you mix it with alcohol and then you got something called Four Loko and that we're banning. Everybody got it? When it's toxic and addictive, we ban it or we regulate it. Caffeine, alcohol together, that's a bad deal. But caffeine alone, keep your hands off my Starbucks. Caffeine; yes, addictive. That leaves this one. Sugar; is sugar addictive? What do you think? You know, we've known this for a long time. Anybody know what this is? It's called Sweet-Ease. This is a super concentrated sucrose, sugar, solution that you dip the pacifier in and you put in the newborn baby boy's mouth before you do the circumcision because it releases opioids and It deadens the pain. This has been known forever. Then you mix it with a little wine and then you got a real good cocktail. Is there really such a thing as sugar addiction or we have to look for similarities to other drugs of dependence like nicotine, morphine, amphetamine, cocaine? The one I think is most appropriate is alcohol, because after all, alcohol and sugar basically metabolize the same way. Because after all, where do you get alcohol from? Fermentation of sugar. It's called wine. We do it every day up in Napa Sonoma. The big difference between alcohol and sugar is that for alcohol, the yeast does the first step of metabolism called glycolysis, for sugar, we do our own first step. But after that, when the mitochondria see it, it doesn't matter where it came from. That's the point. That's why they both cause the same diseases and they do the same thing to the brain. The criteria for addiction in animals are binging, withdrawal, craving, and then this one down here called cross sensitization with other drugs of abuse. That means that if you expose an animal to one drug of abuse like cocaine for three weeks and addict them and then you expose them to a second drug they've never seen before, like say amphetamine, they're addicted to the amphetamine even though they'd never seen it before. Because the dopamine receptors are already downregulated because they're the same dopamine receptors. Everybody got it? Does sugar do this? Absolutely, QED, slam dunk, sugar's addictive in animals. What about humans? Who saw this movie? Did you like it? Yep. More or less? I have big problem with this movie because if you watch the movie, his doctor, Morgan's doctor keeps saying,"You got to get off this high-fat diet." Not the high fat diet, it's the high sugar diet. That's what caused all the problems. Can sugar be addictive? Watch. I was feeling bad in the car. I was feeling really sick and unhappy. Started eating, I feel great, feel really good now. I feel so good, it's crazy. Isn't that right baby? Yeah, you're crazy all right. This was on Day 18 of his 30-day sojourn through McDonalds. He just described withdrawal. That's withdrawal. He needed another heap in order to feel good again. He just described withdrawal. He was a vegan, because his girlfriend was a vegan chef. In 18 days, he's a sugar addict. You tell me. This is what we're dealing with. We are dealing with an industry that wants us to consume its product. Every industry wants us to consume their product in some fashion or another. The question is, what if it hurts you? Here, this is an example, this is the Federal Trade Commission versus Sugar Information back in 1972. This was an arm of the Sugar Research Association. The fat time of day; you're really hungry and ready to eat two of everything, Here's how sugar can help. Any data? They can advertise any way they want, they're allowed. How about this one? The birth of the Uncola, why we have the youngest customers in the business, from 7 Up. You're okay with that? This was going on. How about this one? This was in Publix, the supermarket chain in Florida just a year ago. Drinks are on us; Publix is rewarding top grades with free apple juice and sodas. Students, we salute your thirst for knowledge. The American Heart Association gets it. I'm a proud member of the American Heart Association because they get it. The fat hypothesis has been debunked and they've taken it back. 2010, American Journal of Clinical Nutrition carries it all. But this is dietary sugar intake and cardiovascular health. I was a coauthor of this and very proud to have been so. We recommend a reduction in sugar consumption from 22 teaspoons of added sugar per day down to either nine for males or six for females. That's a reduction by two-thirds to three-quarters. How are we going to do that? How are we going to ever accomplish that? Especially since we don't even know we're consuming it. Because only one-third of our total added sugar intake comes from sugar sweetened beverages like soda juice, sports drinks. One-sixth comes from things that we call desserts; candy, ice cream, things like that. That means one-half of our sugar consumption is hidden in foods that we didn't even know had sugar, like salad dressing, yogurt is a big one. Anybody here think yogurt is healthy? I got a bridge to sell you. Plain yogurt, sure. You want to take some whole fruit and mix it with plain yogurt like they do in Europe? No problem. Off you go. But processed yogurt, the stuff they're selling on the shelves in the supermarket, take a look, just take a look at the amount of sugar. Now, that's total sugar. Some of it's lactose, which is milk sugar. The question is, how much of it is lactose and how much of it is added sugar. You can't know. You're not allowed to know because the food industry won't let you know. Because in 1989, the food industry lobbied the Food and Drug Administration when they were coming out with the Nutrition Labeling and Education Act of 1990. They said, if we told our consumers, our customers, how much added sugar we put in each of our processed foods, our competitors could duplicate our recipes. This is proprietary information and you're not allowed to know it. You know what the FDA said, okay, sure. Let's just show. Here's what you need to know. Of the 600,000 items in the American grocery store today, 80 percent of them are spiked with added sugar. That's not for our purposes, that's for the industries because they know when they add it, you buy more for all the reasons that we've just discussed. Worse yet, there are 56 names for sugar and you don't know them and you're not allowed to know them. Does anybody know what Florida Crystals are? Sugar. Anybody know what evaporated cane juice is? If you evaporate cane juice, what do you get? You get sugar. That's what they use in yogurt because cane juice must be healthy. Juice from cane. Here's how your food dollars have been bastardized and reallocated for you. Meats, this is 1982, 30 years ago, here's 2012. Meats down 10 percent because of the low fat directive. Fruits and vegetables, the same. Survey says eat your fruits and vegetables. You know what? We're eating just as much as we were before. Grains and baked goods, 13-14 percent, so all the carbohydrate. That's only up a little bit. Dairy products 13 down to 10 percent because now everyone is lactose intolerant. Processed foods and sweets, 11.6, 22.9; a doubling in 30 years. That's what's happened. That's the change, and that's what we're talking about tonight. Because processed food is high sugar, low fiber, and real food is low sugar, high fiber. Every diet that works is low sugar, high fiber because every diet that works is real food. That's what this is about. This is a process food disaster. But the food industry is making money off it. In fact, lots of it. Because here's the S&P 500 over the last five years. Here's the economic downturn of 2008 right here, and here's the stock price of McDonald's, Coke, and Pepsi. They're doing very well. Thank you. Here's General Mills, Hormel Conagra, Kraft, Procter & Gamble, Archer Daniels Midland. I said Hormel, I think already. Bottom line, they're all doing better than the S&P. Want to make money, invest in a food company because they have a winning formula for getting you to eat more. Back to that first law. Remember, it's not about common sense, it's about the science. Let's restate it. Let's re-frame the argument. If you're going to store it, that is an obligate weight gain due to energy deposition. The most obvious of which is high insulin, and you know where that came from, and you expect to burn it. That is normal energy expenditure for normal quality of life because energy expenditure and quality of life are synonymous. Things that make your energy expenditure go up make you feel good like ephedrine off the market, caffeine for two hours, exercise. Things that make your energy expenditure go down make you feel lousy. Hypothyroidism, starvation. If you're going to store it, energy deposition, and you expect to burn it, then you have to eat it. Same first law, but now reinterpreted based on the science, not the common sense. Because the aberrant behaviors are a result of our biochemistry, and our biochemistry is a result of our changed environment. The only way we're going to fix it is to change the environment back. Here's a list of diseases. Every one of these was a personal responsibility disease until the sheer weight, magnitude and gravity, and the money that went into it, made it very clear that it was a public health crisis instead. Here are some more newer ones and these are very clearly personal responsibility diseases. Except they're not, they're public health crises. How about this one down here? What do you think about guns? It's San Francisco, so I know what you think about guns. John Howard, the Australian Prime Minister, perhaps the most conservative politician in the last 100 years in any country, banned assault weapons in Australia back in the late '90s. He was on CNN about two months ago and they asked him, "How could you do that? You're a conservative politician, libertarian, how could you ban guns?" He said, "Look, this is not a Democratic issue, this is not a Republican issue. This is not a liberal issue, this is not a conservative issue. This is a public safety issue." That's exactly right. Even he got it. But we don't get it. Well, this is a public safety issue because we will have no Medicare. The questions I'm going to leave you with, I have two homework assignments for you. Can our toxic food environment be changed without government or societal intervention? Especially when there are potentially addictive substances involved? Has education worked for any substance of abuse? Not one. Did Nancy Reagan's Just Say No work? Does the Surgeon General's warning on a pack of cigarettes stop people from smoking? No. The thing that stop people from smoking was secondhand smoke. When your smoking affected me, that's when we started getting legislation. Then the tobacco documents came out and we realized there was corporate malfeasance involved. That's when things changed. But not one lick of education made any difference in the amount of tobacco consumed and Stan Glantz right here at UCSF showed that very nicely. Second question; can we afford to wait? The food industry will say, we need more research. Of course, they're going to say we need more research, it's moving the goalpost. Can we afford to wait to enact these public health measures when healthcare will be bankrupt due to chronic metabolic disease in just 13 short years? That's your homework assignment. This is my second to last slide. This is a paper that just came out in Lancet in March. Profits and pandemics: prevention of harmful effects of tobacco, alcohol, and ultra-processed food and drink industries. What it says is that what we used to practice was called the old medicine, and we focused on infections as the problem, and microbes as the vectors. Now, the new medicine is all about chronic disease and the vector has changed. It is now multinational corporations instead. That's who we're battling. For further reading, I refer you to a whole bunch of academic articles, and more academic articles, and more academic articles, and more academic articles, and more academic articles, and finally, non-academic. If you should choose to pick it up, Fat Chance, which is written for the public, but really to be honest with you, I wrote it for doctors. My publisher says, "You cannot write a book for doctors, we won't publish it." I said, "Okay, fine. I'll write it for the public." But I really wrote it for doctors because the whole medical profession has to change. The problem is, they bought the bill of goods that the food industry was selling and we got to fix it because a calorie is not a calorie. It never was and never will be. Lastly, we have started a non-profit very specifically to provide medical, nutritional, and legal analysis and consultation to promote personal and public health against Big Food, called the Institute for Responsible Nutrition. There is our website and contact me if you would like any more information. I want to thank my collaborators here at UCSF, the Weight Assessment for Teen and Child Health clinic, where we do the actual boots on the ground, changes in people's lives to actually make kids better. Stanford Prevention Institute, my colleague Sanjay Basu, who is an absolute genius. Touro University, my colleague Jean-Marc Schwarz, who's a card carrying fructose biochemist and vetted all the biochemistry on this. Kathleen Mulligan at UCSF Clinical Translational Sciences Institute, who is my right-hand. Berkeley Department of Nutritional Sciences, and also my colleagues Claire Brindis and Laura Schmidt at the Institute for Health Policy Studies here at UCSF as well.

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