Everything You Knew About Obesity is Wrong!

Everything you thought you knew about obesity is wrong. There's no question we are eating more. The question is cause or effect.

Ladies and gentlemen, it's an honor to introduce Professor Lassig today. I'm Ronnie Jaffe, CEO of Emory Pharma. Rob's passionate dissemination of truth deeply resonates with us as a distinguished professor at ucsf, Professor Lustig's celebrity status in the scientific community precedes him. Without further ado, let's welcome Professor Lustig.

Thank you. Thank you, Rob. Thank all of you. Thank you for being here on a Wednesday instead of on a Friday. Appreciate that and happy holidays. As you know, this is my fifth time talking to Emory Pharma. And the first four talks were primarily about science tinged with a little bit of politics. Today's a little different. Today it's going to be politics tinged with a little bit of science. Okay? And you will see why. But very specifically to, you know, reiterate what Ron said, and that is that we are all seekers of the truth. I am a truth seeker. We are all truth seekers here. This talk is about the opposite. What is the opposite of the truth? So everyone has heard of the word epistemology. What is epistemology? It is the study of knowledge. It is the study of how we know what we know. I'm going to introduce you to a new word. The word is agnotology. Now, does anybody know what the word agnotology means? I didn't either until about a year ago. Agnotology is the science and the study of ignorance. It turns out this is an extremely important and breadth and depth field that is being investigated in a multitude of places. So in May of this year, I participated in a conference at Stanford University on agnotology. And there were 14 talks over the course of two days. And these were what the 14 talks were about. And it was very interesting. I have to tell you, it's probably the most interesting symposium I've been to in three to four decades. Really, really, really cool. So we had the tobacco people, we had the big meat people, the economics people, art. Can you believe art could be subject to ignorance? Firearms, climate change, reproductive choice. Kind of important issues for today. Yes, Deep fakes and generative AI, intellectual debt, data loss. Talk specifically about anti epistemology and how epistemology gets buried. Subhumanization atrocity. My charge was to talk about medicine and public health and agnotology within medicine and public health. You would say, well, doctors, we're supposed to be the ultimate truth seekers. You would be mistaken. That's exactly the point. And so we're going to talk about that today and how ultimately that impacts on both patient care and on society at large. Okay, so deliberate or culturally induced ignorance. This is not by accident. This is not just ignorance. Like, oh, you know, I didn't watch, you know, that TV show last night. This is a well formed plan or plot by specific dark forces within society to actually bury the truth on purpose. That's what we're talking about. Now, there are different definitions of agnotology or at least sub subsections of agnotology. Factual agnotology, you don't want to believe that something happened. Object agnotology is you don't want to believe that something exists. There's a lot of that technical agnotology. I don't want to learn, I don't want to have to learn how to do something. But we're going to talk today about emotional agnotology. That is, I don't want to understand what's happening within others. I don't want to empathize with others. And this actually has a name in medical parlance. It's called alexithymia. Okay, so dysthymia is when you feel lousy. Alexithymia is when you don't want to feel anything. So that's what we're going to talk about today, the phenomenon of alexithymia and how that works within medicine. Now here I have a list of, I think it's 15 different problems in society that all relate back to medicine and public health. Some of them are exposures, some of them are chemical addictions, some of them are behavioral addictions. Medicine touches each of these in a different way. But every single one of these was thought to be a personal responsibility issue. That is, it's your own damn fault if you get this or if you suffer from this, or if you exhibit this as opposed to a public health problem. But ultimately, every single one of them became a public health problem and had to be dealt with with a public health strategy. Leaving it to the devices of individuals did not work. It did not help, it did not save money. All it did was lead to misery and death. And ultimately society recognized that fact and led to the development of public health efforts to try to stem the tide of each of these. And you can recognize all of them? Yes. Okay. Each of these had its own agnotology, but ultimately we graduated from it. I'm going to talk to you today about the one I know the most about and the one that I've been most involved in. And that is Sugar, obesity, and type 2 diabetes and metabolic syndrome, which currently account for 75% of all healthcare costs. And we've talked about these in the past. So some of these slides may be redundant, but most of them, I think, will be new to you. Okay? Now, before we can discuss ignorance, we have to discuss the concept of choice. Right? Because you can't be ignorant if you have a choice. Or can you? You understand that free will is embedded in the concept of. Of choice, that you are able to exercise your choice. So we have to understand what free will is. Now, I'm not here to debate with you whether free will exists or not, by the way, my colleague, Dr. Robert Sapolsky just published a book three months ago called the Case Against Free Will, and he did a podcast recently, and I recommend it to all of you. It's actually quite, quite good. Okay. If you're interested in this philosophical question, okay, but the fact of the matter is, there are a lot of people who've lined up on the side of free will, but there are also a lot of people who've lined up on the side against free will that there is no free will. Okay? And I'm not here to debate that argument with you. I've got way too much to do in terms of the medicine of this. Okay? Just to point out to you that this is a debate that goes back hundreds and hundreds of years. Calvin believed in predestination, that basically, you know, the world was already, you know, constructed. And you. You are just a cog in the wheel, and you don't even know what's going to happen to you, but God does, all right? And. And you're predestined to whatever your fate is. Laplace believed in something called causal determinism. That is, you ultimately don't get to decide what happens. It's already determined. Hobbes believed in compatibilism, which basically said the concept of free choice and fate are eminently compatible because you think you're choosing, but in fact it's chosen for you. Schopenhauer believed that free will was an illusion. That is, you are free to do what you want, but you are not free to want what you want. That was Schopenhauer's great insight. Darwin and Einstein and Crick and Jerry Edelman were all about consciousness. Was it a cause or was it effect? Are we all living in somebody else's dream, or is this our dream and everyone else is living in ours? Most recently, Anthony Cashmore and Robert Sapolsky sort of developed this notion that free Will is actually a concept that was developed by the criminal justice industry to be able to punish perpetrators. That free will is actually a combination of our DNA and our environment and some random stochastic processes, which are random. Well, our DNA hasn't changed in 50 years, and those random stochastic processes are random, which only leaves the environment as something that is actually manipulable. So that's the big question is what has happened to our environment that can have led to all of this obesity, diabetes, metabolic syndrome, and ultimately societal devolution? That's the question here. Okay, so this is where I come into the story. This concept of obesity being sort of a great way to take this concept of free will, personal responsibility apart. Everyone with half a brain believes in the first law of thermodynamics. The first law is a law. And what is the first law? State? It states the total energy inside a closed system remains constant. It's been tested 50 ways from Sunday and always comes out the same. The first law is a law. And I subscribe to the first law. But like every law, the law is subject to interpretation. There are two interpretations of the first law. The first interpretation goes like this. If you eat it, you better burn it or you're going to store it. Now, in this interpretation, where the eating and the burning come first, that is the result of behavior, eating behavior, burning, exercise, activity, behavior, and therefore the weight gain, which is the object of this is actually secondary to two behaviors in the case of obesity, to aberrant behaviors, gluttony and sloth. And therefore, if you believe that, then it's calories in, calories out. Therefore, it's about energy balance, it's about gluttony and sloth, it's about diet and exercise. It's about any calorie can be part of a balanced diet. And it's about if you're fat, it's your fault, right? And the food industry loves that because that assuages their culpability for anything they might have done to either the eating or the burning to get you to this obesity. That's the politics of, of this current belief system, which is this interpretation of the first law. Everybody with me so far? But that's not the only interpretation. But that's the standard interpretation which you can see on this Dilbert cartoon, which I think I've shown here before. But it's my favorite Dilbert, so you got to read it. Even though you know Scott Adams is in the toilet right now. Health problems and absenteeism are a huge cost to this business. So. So give me a raise or I'll eat unhealthy food and avoid all forms of exercise. You already do those things. How could you possibly know that? That's. That's what we have today. Now, this is unfortunately, you know, resonating throughout the entire zeitgeist of America. And I'm going to give you just two quotes that you know from politicians that you're probably all familiar with. What happened to willpower? I love fat people. Every fat person says it's not their fault they have gland trouble. You know, which gland? The saliva gland that can't push away from the table. That's, you know, that's what's out there. And everyone believed it. Right? Here's another one, okay? This bill says, don't run off and file a lawsuit if you're fat. It says, look in the mirror because you're the one to blame. The cheeseburger. Bill Sensenbrenner. Okay, so you get the idea. This is all based on an interpretation of the first law, which unfortunately has become dogma. And the dogma is that it's about calories, and that calories are fungible and it doesn't matter where the calories come from. Okay. That a calorie from a, you know, kumquat is the same as a calorie from a cheesecake, and a calorie burned is a calorie burned no matter what. Okay? So the corollaries to that are that this is personal responsibility because it's about two behaviors which ostensibly you are in control of. And the question, of course, is, is that true? Therefore, you have to be able to exercise free will to be able to invoke that personal responsibility, because it's about gluttony and sloth and diet and exercise. And that's what pretty much the world still believes. This is a belief system. Okay. Now, how hard is it to change a belief system? Pretty hard. Okay. How many of you are Christian? Wow. Two. All right. Did you ever think about being Jewish? Yeah. My last name is Shapiro. Shapiro? Yeah. Okay. The question is, like, why wouldn't you change? It's what you're exposed to when you're a kid. It makes sense to you. It works for you. When I was a kid, only 2% of the population changed religions. Today, 24% of the population changes religions. So clearly, this belief system is not working for a lot of people. Okay? It has nothing to do with Christianity. It has nothing to do with Judaism, has nothing to do with Islam. It has nothing to do with Anything, whatever it is, is not working for a lot of people. Therefore, you have reason to challenge your belief system. So I'm going to give you reason to challenge this belief system. So is it just a caloric bacchanalia? Actually, I take it back. This is. This is much more to the point. Right. Okay. In fact, if you look at calories in, there is very clearly a difference. I. No argument. Okay. 187 calories per day in men, per day. 335 calories per day in women, up from 25 years ago. 275 calories per day, up in teens from 25 years ago. So there's no question we are eating more. The question is cause or effect. Is that the reason for this? Is that. Is it? Well, you know, there's a lot of, shall we say, circumstantial evidence to support that. I mean, here we have the original White castle hamburger at 210 calories, okay? Here we have Bob's Big Boy, you know, at 618 calories. And in the midst of the obesity epidemic back in 2003, parties had the temerity to offer us the sick burger at 14, 20 calories. And of course, there's the Carl's Jr. $6 burger, which is 2,000 calories. So you could say, well, QED, Dr. Lustig. I mean, you know, we're all eating more. And it's true, we are. But the question is, is that the cause or is that the effect? Okay, correlation is not causation, and we all know that. Or is it the other side of the equation? Is it just an activity famine? So here we have what's known as mets, okay? So it's a measure of physical activity based on accelerometry. Okay? And here we have American girls, white here, black here. And you can see that as they get older, from 9 to 19, their physical activity goes down so significantly that by the time they reach age, what, 15, okay, the black girls are basically prostrate on the floor according to this. So is that the reason? And again, you would say, well, that's clearly why there's obesity. Or is it, is it cause or effect? You don't know. Correlation is not causation. But we do have these data and we have to explain them. So I'm here to tell you that everything you thought you knew about obesity is wrong. Okay? And I've given this talk as this room before, and we're going to go through a little bit of the data and we actually have some new data to Talk about. Okay, but ultimately, changing a belief system is what this is all about, because we had to change our belief system for those 15 personal responsibility issues and recognize that they were really all public health crises. Well, education consists mainly of what we have unlearned. We all thought we knew something. We find out we actually didn't know anything at all and had to relearn it. Doctors do this, have to do this all the time, and they don't do a very good job of it. All right, so there are four reasons to doubt this formulation of personal responsibility. Let me show you those four reasons. First, if it's just about gluttony and sloth, how do you explain the fact that body temperature is going down in the American population over the last 150 years? So this is from Civil War records, and this is from most recent gathering of data from EPIC off electronic medical record. And you can see for whites, for blacks, doesn't matter the age. Okay. There has been a decline, a steady decline in body temperature in everyone. Everyone says, you know, we're supposed to be 98.6. Well, guess what? We're not 98.6 anymore. We're more like 97.3. How come we're all burning less energy to give off less heat? Is it because we're starving and don't have the energy to produce? Clearly not. If anything, we have more energy, but something's not working to generate that heat because the heat is a byproduct of energy metabolism. So we're not burning energy in order to maintain our body temperature. Second problem, related. Every one of these crosses is a different species in captivity. And what you can see is that over the last 25 years, every species in captivity has increased their body weight, living in the same captive environment and eating the same captive food as they always did. They're not humans. They're not gluttons and sloths. They only eat what you give them, and they're all gaining weight anyway. How do you explain that something else is going on? Is it the same thing that's causing our defective energy metabolism? Maybe so. Second problem. No child chooses to be obese because the quality of life of an obese child is the same as the quality of life of a child on cancer chemotherapy. No one chooses to be obese. No one. Okay. It happens to people, but no one chooses it. Okay, number three, this isn't just about America. You know, you can say, hey, we're gluttons and sloths, or the UK they're gluttons. And sloths or Australia, they're gluttons and sloths. It's happening everywhere. The whole world is having this problem. There is not one country on the planet that has a stable rate of obesity. It's climbing everywhere. In places that don't even have our diet. Okay? 175 out of 185 countries, even in countries that don't exercise this notion of personal responsibility. And number four, which I think is the kicker, we have an epidemic of obese 6 month olds and we have an epidemic of obese newborns. Newborns don't diet and exercise. How come the mean birth weight of babies born in the US, South Africa, Israel and Russia are all up by 200 grams? When you actually do the DEXA scanning on Those babies, those 200 grams are not muscle, they are fat. How come babies are laying a half a pound of extra fat down even before they're born? You really want to say that that's about gluttony and sloth? Well, any theory you want to advance about the cause, the pathophysiology of obesity has to be able to explain that too. And you can't, because it ain't true. It's not about calories. It never was. The industry wants you to think it's about calories because that way they get to hide behind it. The government wants you to think it's about calories because that way they can basically not pay. But ultimately it doesn't work. I happen to have edited a book back in 2010 called Obesity Before Birth, Maternal and Prenatal Influences on the Offspring, which talked about genetics, epigenetics, developmental programming. Okay, so I've shown this slide before. I know I have. Okay, this is a Venn diagram of the United states adult population. 260 million adults, okay? 42.4% obese, 57.6 normal weight, BMI over 30, BMI under 30. Okay? And the standard mantra is that 80% of those obese people are metabolically ill. That is true. 90% of 42.4%. So that's 110 million adults metabolically ill. No argument. However, that's not what's going on, because what's really going on is because 70% of the normal weight population have the exact same diseases as the obese. Normal weight people get type 2 diabetes, hypertension, dyslipidemia, cardiovascular disease, cancer, dementia, fatty liver disease, polycystic ovarian disease too. And they get it at a normal bmi. So it can't be about obesity because normal weight people get it, too. When you do the math on the entire sick population, that turns out to be 204 million out of 260 million. In fact, 93% of all Americans manifest some form of metabolic dysfunction when it's 93%. You really want to call that personal responsibility? You really want to say that's an individual's fault when 93% of a population suffers from the same thing? Really? And I've shown you this slide before, too, okay? I can prove it. So here are two CTs from two equally weighted patients. Notice trunk fat, 12.8. 12.8. Okay, one's healthy, one sick. Which one's sick? A or B? No radiologists here, obviously. B, B, B is sick. That's right. A has subcutaneous fat. Love handles, if you will. Okay, but the organs inside, not so much. B, on the other hand, has all this fat in and around the organs. Intra abdominal fat. So subcutaneous fat, intra abdominal fat, they are not the same. Turns out subcutaneous fat is cosmetically undesirable, but functionally or metabolically inert, it's not the cause. This is where your body wants to put excess adipose tissue is in your subcutaneous space where it's not going to hurt anything. Intra abdominal fat, on the other hand, that's the metabolically active fat. When you exercise, that's where your body lifts energy from, is the visceral fat. And that's why when you exercise significantly and chronically, okay, your waist circumference goes down before you lose any weight, your belt size gets better before your weight gets better, because you're losing visceral fat. You might actually be. If you're exercising, you might be gaining muscle, and so it won't even show on the scale. But in fact, you are clearly doing yourself a metabolic favor. And As I said, 93% of Americans manifest some form of metabolic dysfunction. So let's talk about this notion of gluttony and sloth. This is the definition of behavior. A stereotyped motor response to a physiological stimulus that comes straight from the dictionary. That is the definition of behavior. In other words, behavior always has a biochemical basis. Sometimes we're smart enough to know what that biochemistry chemical basis is, sometimes we're not. Example, a mother loving her child. Is that behavior or is that biochemistry? That's biochemistry. That's the hormone oxytocin. Okay? No. Oxytocin. Mother doesn't love her child, period. Okay? That is biochemically driven. We see it outwardly as behavior, but it has Nothing to do with a conscious choice. It has everything to do with a biochemical drive. What we want to know is what are the biochemical underpinnings of gluttony and sloth? That's what we want to know. Everybody with me so far. Now, remember, Cashmore said that free will was about our DNA and our environment and our random stochastic processes. But DNA hasn't changed, and the random stochastic processes are random. The only thing that is actually manipulable is the environment. So what has happened to our food environment? Kelly Brownell, in this book Food Fight, labeled this the toxic environment. And here are all the things that have happened to our food and our activity. And this is old news to all of you. And this is what you hear about all the time on tv from all the obesity pundits, whether they're on the Today show or anywhere else. Garbage. These are all the results of the problem, not the causes of the problem. In fact, the toxic environment is just a euphemism for the altered behaviors. The question is, is there really something insidious and poisonous going on in the environment that is not just causing the obesity epidemic, but actually lowering our body temperature by 1.5 degrees and causing animals to increase in weight? And at the same time, because we have to factor that in, too. So is there an environmental trigger to this obesity epidemic that we have mistakenly placed on the individual? Because if that's the case, then this is not about personal responsibility at all, is it? Well, there are a whole bunch. There's a whole bunch of obesogens, chemicals in the environment that promote weight gain, and they do it through several different mechanisms which I'll outline really quick. This is a paper that we published. As you can see, I'm right there. Establishing causal links between chemical exposures and obesity. Okay. Bisphenol A is an estrogen. Estrogen binds to the estrogen receptor and causes fat cell differentiation. Okay. Resins and can lines and thermal paper. Okay. It's everywhere. Okay. Every time you get your receipt at Target, you've just gained weight before you ate what you ate at what you bought at Target. Okay. Just from handling the paper, the thermal paper. How's that? Vinyl flooring. Every time we have carpet here. Every time you walk on a vinyl floor, okay. You've gained weight. Okay. Personal. Every time a baby sucks on a pacifier, that baby's gained weight. Because all of these things drive interactions between ligands and receptors that promote weight gain, that promote adiposity, personal care products, food preservatives. Things that are in the food rather than the food itself. Pharmaceutical drugs of various sorts, like atypical antipsychotics, clothing. Flame retardants. So every baby is clothed in clothing that has embedded in it. Flame retardants. Guess what they gaining weight from the clothes they wear? Electronics. Polychlorinated biphenyls. Every time you drink water that went through a plastic pipe, you're getting it, okay? You get the picture, okay? Oh, organo tins, like tributal tin. That's what they paint on the bottom of boats so that barnacles won't attach to the hull. It's in our environment. Okay? All of these things are going on as we speak. And of course, they happen to be in our diet as well. Okay? So this. You see this? You see where it says impress? It is impress. As of this morning, we just got this paper accepted, okay? A new theory of obesity. Because there are two overriding, you know, two popular models of obesity today. One is the energy balance model, the calorie model, and one is the carbohydrate insulin model. That refined carbohydrate and sugar drive insulin, which causes adipose tissue deposition. Okay? And of course, these two models have been fighting it out now for the past ten years or so. I subscribed to the carbohydrate insulin model myself for a long time, and I still do to some extent. But in fact, there's actually some problems with that model. Like, for instance, the epigenetics, like what happens prenatally to cause that. 200 grams. Where's that coming from? Why is it that babies are gaining weight even faster? And why is it that everybody's metabolism is going down because of the body temperature going down? Those are not explained by the carbohydrate insulin model. There's something else going on. Well, we have postulated in this new paper that just got accepted this morning at International Journal of Obesity, a pretty good journal, that it's this guy here. Reactive oxygen species. Now, you're all familiar with reactive oxygen species, right? Hydrogen peroxide, oxygen radicals. Okay. Rusting. Well, it turns out every cell has its own redox potential. Based on what? Reactive oxygen species are either oxidized or reduced at any given moment, correct? Every cell has its own redox potential intracellularly. The idea is that that redox potential is going to affect the regulation of multiple enzymes in that cell at any given moment. Because virtually every cell that's a regulatory pathway is a kinase. And that kinase, the phosphorylation of that Kinase is completely dependent on that redox potential. So the cell decides whether to burn energy or store it or where to move it around inside the cell based on the redox potential within that cell at any given moment. So anything that changes that reactive oxygen species concentration within that cell is going to change the metabolic fate of that cell. That's the idea. Everybody got it all right. Now that ultimately can influence what happens to calories, and it can also influence what happens to the pancreas in terms of whether it releases insulin or not. So both, this is basically a method for being able to combine these two models into one. So obesogens, many of them, most of them, generate reactive oxygen species just by their very nature. And so obesogens and diet can ultimately impact on Ross, which then alter cell signal transduction, which lead to weight gain. That's the idea. Okay, now this is a complicated slide, and I don't want to belabor it, but you know that there's this thing called nad, and you know that there's this thing called nadp. They are not the same. They run different enzymes. Well, you know that you have to reduce it in order to be able to oxidize it later, right? So NAD becomes nadh, NADP becomes nadph. Well, if you're basically, if you have an altered reactive oxygen species, you might be basically fixing one at the expense of the other, because there's only so much hydrogen ion that you can get onto reducing that NAD or that nadp. Everybody get the idea? So these reactive oxygen species that are coming from the electron transport chain are going to ultimately influence the degree of mitochondrial function. So reactive oxygen species can reduce, for instance, cause oscillations in glutathione that convert those Ross to water in order to be able to restore the glutathione. And then the NADP will basically not necessarily go to nadp. The membrane potential will change. And that means that the mitochondria will not necessarily work the same way as before because the proton gradient in the mitochondria has been affected. So you can change what's happening in terms of energy metabolism based on what's happening to the by based on the redox potential of the cell. That's the idea. So diet and obesogens change the redox potential. Redox potential in the liver can cause glucose release or uptake in the fat cell, can cause lipolysis or lipid synthesis in the brain, can cause hunger or satiety in the pancreas, can cause insulin secretion or not. Those tend to actually work in concert. And there's data for each of these that these things work in concert when the redox potential in any given organ changes the redox potential and the other organs change the same way. So they're all working in concert to either store or burn, Having nothing to do with the calories themselves, but rather with the degree of oxidative stress. Everybody got the picture. Now, the thing that causes the most oxidative stress is this. My favorite. You've heard this one before, right? Fructose. Because fructose is not glucose, it exerts metabolic effects having nothing to do with its calories. In fact, fructose is like alcohol. And alcohol is the ultimate metabolic stress. Oxidative stress. Right? Alcohol is not dangerous because it's calories. Alcohol is not dangerous because it causes obesity. Alcohol is dangerous because it's alcohol. Right? Because it leads to acetaldehyde. And acetaldehyde causes the most reactive oxygen species because it's an aldehyde. That's how you get reactive oxygen species is with aldehydes. Well, guess what? Fructose has reactive keto group, which is the same as the aldehyde. And fructose explains the metabolic syndrome as I've talked about in this room before. Okay? And fructose also has has effects on the brain to limit the ability of leptin to signal, because leptin is the hormone that tells your brain you've had enough. Well, if you're inhibiting leptin signaling, your brain thinks you're starving, okay? Fructose exhibit exerts effects akin to alcohol, especially with respect to reactive oxygen species. And fructose inhibits mitochondrial function in three ways. Three separate enzymes. AMP kinase. AMP kinase is the fuel gauge on the liver cell. ACAD L ACYL CoA dehydrogenase long chain, which is necessary to break the fat into two carbon fragments so that it can be oxidized in the mitochondria. And finally, CPT1, a carnitine pulmidol transferase 1, which is the enzyme that regenerates carnitine to allow for the shuttling of fatty acids into the mitochondria for burning in the first place. So everything that fructose does is based on Ross inhibiting enzymes that would normally lead to burning, except now they lead to storing instead. There's a perfect example within the liver. The point is, this can happen in the pancreas to release insulin. It can happen in the brain just to induce hunger instead of satiety, et cetera. And it's coordinated and we know that fructose is a metabolic toxin that targets the gut liver axis. I'm not even the one who said that. Somebody else did. And of course, we also know that fructose is addictive because it induces reactive oxygen species in the reward center, making you crave more. In fact, this is a good model for all of addiction and reactive oxygen species in the reward center. Okay, now, we also know that the sugar industry doesn't want you to believe that. And they've done a lot of work to try to bury this information over the years in order to keep people, you know, to keep the food industry intact and keep people consuming. And so that in and of itself is its own problem. And I think I've shown you this slide also. The Sugar Research foundation paid off to Harvard School of Public Health scientists back in 1965 to publish two papers in the New England Journal which signal out fat and cholesterol as the dietary course of heart disease and downplayed the evidence that sucrose consumption was its own risk factor. So, you know, this has been going on a long time. So this is where the politics come in. So remember our first law. Remember our interpretation of the first law. If you eat it, you better burn it or you're going to store it. That's the common wisdom, that the weight gain is secondary to two behaviors. There's another interpretation, and the data I've just shown you about Ross says that it goes like this. Instead, if you're going to store it, that is an obligate weight gain set up by biochemical forces out of your control, like, for instance, Ross, in the liver or in the brain or in the pancreas. And you expect to burn it because normal energy expenditure equals normal quality of life. Because energy expenditure and quality of life are synonymous. Think about it. Things that increase your energy expenditure make you feel good, like exercise, caffeine, right? Thyroid hormone. Things that reduce your energy expenditure make you feel lousy, like starvation, hypothyroidism. So if you're going to store it and you expect to burn it, then you're going to have to eat it. Same first law, but turned on its head. Because after all, who said the first law ran one direction? Maybe it runs the other direction. In this interpretation of the law, obesity is the result of the biochemistry, not personal responsibility, that the behaviors are actually secondary to a biochemical process. And we've already shown you that every behavior is secondary to a biochemical process. In fact, it's embedded in the definition of behavior. Everybody get the picture? Everybody see the. You know, where the belief system came from. Because you have to be able to see where it came from in order to undo it. Okay, now we get to some fun stuff. Okay, everybody with me so far on the science and the politics. Now we get to fun, fun stuff. The history. Where'd this come from? The history of personal responsibility. So a lot of people think the history is that personal responsibility is in the Constitution. It's not. A lot of people think the personal responsibility is in the Declaration of Independence. It's not. A lot of people think that personal responsibility is in the Magna Carta. It's not. In fact, it's nowhere. It's not anywhere. Okay, we're going to talk about how did we get to this notion of personal responsibility. The very first time anybody even brought up the concept of personal responsibility was Homer in the Odyssey. Because this is the line right here. It's line 32. Zeus asked the people to stop blaming their bad choices on the gods. And it says, look you now how ready mortals are to blame the gods. It is from us they say, that evils come, but they even of themselves through their own blind folly have. Have sorrows beyond that which is ordained. It's your own damn fault. Right? Homer said so. Okay. The next time anything having to do with responsibility of any sort is in any form of print anywhere is the Constitutional Convention of the United States, 1787. And it wasn't personal responsibility at first. Edward Rutledge of South Carolina. If you ever saw the movie or play 1776, he's the one who sings molasses to rum. Big deal. He said a single man would feel the greatest responsibility and administer the public affairs best. He was talking about the presidency at the time. Hmm. To which Jonathan Pinckney of South Carolina warned that investing power in a president could mean a monarchy of the worst kind. To wit, an elective one. Strains of Today to which James Madison responded. The responsibility of all to the will of the community seemed to be generally admitted as the true basis of a well constructed government. The will of the community, not the will of the individual. To which Randolph in Virginia said that they should keep a public record of senators votes in order to impose personal responsibility. That was the very first time anyone ever mentioned the concept of personal responsibility. And it was basically to hold people's feet to the fire. Politicians feet to the fire. Interesting. I think Hamilton also then picked it up in Federalist 69, which was published in 1789. The American executive would not be sacred and inviolable, but Impeachable and removable ruling in a delicate and important circumstance of personal responsibility. In other words, the President has to be able to account for his choices. Personal responsibility. And then we never hear about personal responsibility again. Never had nothing else in the history of America. Nothing else until the 1960s. This is the Dahl paper. Richard Dahl and Austin Bradford Hill. They were the first people to equate smoking with lung cancer in 1950. What you're seeing here are the number of newspaper articles on the dangers of tobacco in the Washington Post and the New York Times. You can see there's this big blip here after the Dahl paper when this concept first came out, then the Bradford Hill paper over here in 1960, which basically told us how we can determine causation. It's dose, duration, direction, and precedence that got everybody up in arms about that. But notice nothing about personal responsibility. Yet here we are now in 1966, and we're still looking at the same New York Times, Washington Post. Okay? This is when the Federal Cigarette Labeling Advertising act was enacted after the Surgeon General's report in 1964. Okay? And all they were doing of all the food the tobacco industry was doing at the time was denying it and saying, no, it's the other way around. It's not that smoking causes lung cancer, that people with lung cancer decide to smoke because it makes them feel better. Swear to God, that's what they said. Then we had people start suing. We had individual plaintiffs start suing here. And that's when they started with the concept of assumption of risk. Well, they assumed the risk because they knew, so it can't be our fault, because they knew what they were doing and they assumed the risk, which was the precursor, the prequel to personal responsibility. And that's when this happened. And the thing that triggered that was Cipollone versus Liggett, which was like the first major broadside. 847 patients suing the tobacco industry. Now, this did not work, by the way. Cipollone v. Liggett was not, you know, was not found for the plaintiffs. It was found for the defendants. But it was after that that the Mississippi Attorney general sued Big Tobacco for recoupment of Medicaid costs related to lung cancer. So you can see that this became the order of the day. Personal responsibility. So it was the tobacco industry that invented personal responsibility out of this notion of assumption of risk in order to basically act as a bulwark against these lawsuits. That's where personal responsibility came from. It didn't come from anything inherent in American life. It's new. The tobacco industry used personal responsibility in a very, shall we say, surreptitious way because they disguised freedom to blame as freedom to choose. Yes, you can choose whether to smoke or not because you're the one to blame. And that's where the Cheeseburger bill came from. Freedom to blame. Everybody with me. So can the toxic environment be changed without governmental or societal intervention? When this is a public health problem, not a personal responsibility problem? When everything you touch could be driving weight gain, when your Target receipt might be driving your weight gain? Is that personal responsibility? Should you stop getting receipts at Target? Maybe. Maybe. Anyway, but you get the idea when there are toxic and addictive substances involved. So fructose is toxic. It's also addictive. But there are other things in this story as well, right? So in summary, this concept of alexithymia is emotional ignorance and the way it expresses itself as. It's your own damn fault. Personal responsibility. That's the, shall we say, the colloquialization of not needing or wanting to empathize with others over your problem, over their problem. Okay? One manifestation, personal responsibility in its freedom to blame rather than freedom to choose. It's really the health care version of schadenfreude. Everybody familiar with schadenfreude, right? There's a great song in Avenue Q called Schadenfreude. If anybody's not ever seen the musical Avenue Q, just play, pull it up on Spotify and just listen to the one song, okay? It's very dirty, but it's very good. And it explains everything you need to know about this concept. It's your own damn fault, okay? Taking delight at the misfortune of others. And that's what's going on in America today. And the reason is because of this phenomenon called alexithymia, which has a biochemical basis and actually has a. A prefrontal cortical dysfunction basis. And we can talk about that. I have the slides, but I very specifically cut them out of this talk because it's just too long. If I show you the neuroscience of this. So obesity and type 2 diabetes demonstrate that biochemistry drives behavior as opposed to the other way around. And personal responsibility does not explain how to prevent chemical and behavioral addictions or exposures, for that matter. An education alone has not solved any substance of abuse. And fructose, for lack of a better word, is addictive. Personal responsibility does not have a long history in the United States, despite what people will tell you. In fact, it's actually very recent, okay? It's a new idea, especially in medicine. We never believed in personal responsibility for all those years until tobacco, Big tobacco adopted only as a defense against lawsuits. That's where this all came from, was tobacco. The tobacco industry invented it. It wasn't around before that while individual intervention for medical care is essential, societal intervention is also warranted. That we're not going to be able to solve this by doing this one patient at a time. You have to do this one population at a time. And that is what public health is. That's why the talk is called personal responsibility or public health. So what I hope I've done is give you a reason for rethinking your belief system, not just about obesity, but about all medical problems and possibly even all societal ills like climate change, like gun violence, like vaccination, that these are public health issues that need to be addressed in a public health context and not expect that individuals are going to be able to solve this for themselves, especially when they are biochemically driven. It's not possible. In the same way it would be impossible for a mother not to love her child. Happy to take questions. Mention that newborns obese. Yeah. Is there any like, correlation there with the mothers, like being obese or what the mothers assume during pregnancy? Without question. The obese mothers give birth to more obese kids. Absolutely. And the question is through what mechanism? Reactive oxygen species. Gotcha. Okay, that's, that's, that's the driver. Okay. And it has to do with their diet, of course, because it all crosses the placenta. Right. Okay. Fructose crosses the placenta and is going to induce alterations in redox potential within the fetus. And that's one of the reasons why you get the adiposity. It's. Yes. What mother ate or what mother breathed. Because air pollution does this too. That's not anyone's fault either. Except for the, you know, transportation industry and the, you know, the oil industry and the rubber industry and what other. You know, you get the idea. Okay. We live in an obesogenic environment and it works through all of these receptors. And there's a whole bunch of different receptors that are involved, involved in this. Okay. You know, the thyroid hormone receptor, the estrogen receptor, the androgen receptor, the hydrocarbon receptor, and, and the list goes on. Lxr, fxr, the ones in the, in the liver. Okay. Individual biochemicals will affect these in different ways and basically activate them, but they're all kinases. So the redox potential of any given cell is going to basically determine which, which direction that kinase is going to work at any given moment. Gotcha.

Next, Rob, Reactive oxygen species. There are many kinds of reactive oxygen species. Do all obesogens create the same or different or. And then do you, have you been able to show this in some kind of an in vitro model? Such.

Really? So both very good questions, Rob. So the, the answer to the first question is we don't know. We have no idea at this point whether or not these things are different based on what ros it is because it could be, you know, the O2 radical or it could be a sulfite radical. Okay. Either way. And we don't know whether or not one would be different from the other. I my guess is that they would not be because I think it's electrical. I think it has to do with ph, you know, in the cell affecting that phosphorylation status, I think, but I don't know that. Now in terms of models, we have loads of data in animals. We have boatloads of data in animals. That paper that I pointed to, the One that started Obesity 2 that I'm a co author on, is 150 pages long. That is not a little paper. That is a big effing paper is what that is. It's a book. It was going to be a book and we said, no, it can't be a book because we have to actually get it into the literature so everybody can see it. So we put it in an open access format. Okay, that's exactly right. And 43 authors, you know, it's a huge magnum opus. And it's got all the data. It's got all the data. We have mechanistic causational data in animals. Slam, bam, thank you, ma'. Am. You know, no ifs, ands or buts. It's hard and fast. Nail in the coffin f you. I mean, it's just real for humans. It's much harder for obvious reasons. What we have for humans is perspective. Correlational data that goes in the same direction. Okay. That's not quite the same as human causational data. And we understand that. We know the difference. The point is we have to be able to do those experiments and they're very hard to do in humans for obvious reasons because of IRBs. Not going to let you do unethical. That's unethical. So the only way to do that then is natural history experiments like the one I just described for sugar and diabetes, where you do it in a timed approach. We don't have that yet. That needs to be the next Step on the clinical side is to do an econometric analysis of these going forward to demonstrate that not only did these predict the change in weight over time, but that they are actually the cause of the change in weight over time. And in humans, we don't have that yet. It's one of the reasons this is a hypothesis, not a proof.

You know, for example, we talked about PFAS in receipts you get from store. Let's not talk. Let's not focus on Target. Let's not Target. Target Everywhere, everywhere.

It's not just Target. I was just picking on Target. My wife likes Target too much.

So you have these PFAS on this paper. You receive and you get it.

No, it's bpa. It's not PFAS on the receipts. PFAS is basically everywhere now because it was Teflon, you know, perfluoro octanoic acid, pfoa. So. And, you know, so it's perfluorate, perfluoro alkylating substances. And there are a whole bunch of them, and they're in the water and you can't get rid of them. They're for forever chemicals. They're with us forever. Just like DDE is the metabolite of DDT. We haven't used DDT since 1972. But I can still measure DDE in all of your urine. And the concentration of DDE in pregnant mother's urine predicts obesity in the offspring at age 5.

The point I was trying to make is even if you see it in animal, it means it's in the environment, of course, affecting our environment. So why isn't anybody doing anything about it to stop?

Well, that's why. That's why we've done all this work and that's why we've published this paper, is to get people on the Prevention kick. Because there's no other way to deal with this other than prevention. There's no treatment for this. There's no way to block those receptors. You'll basically, you know, lead to Italy to. Yeah, three heads or missing feet or worse, missing brains. Yeah. No. The only way to deal with this is prevention. Ken asked, is there anybody at the CDC or USDA or FDA listening? And the answer is not really at nih. Yes, at nih, they know. And Jerry Heindel, who ran the Endocrine Disruptors Unit of the niehs, the National Institute of Environmental Health Sciences, he's the first author on this paper, and he was the first author on the Obesity 2 paper. I was the author on first author on the Obesity 1 paper which basically talked about mechanisms of obesity. We know and NIH knows. Now the question is, how do you get cdc, usda, FDA to agree in order to be able to ultimately influence Congress? And how do you do that? I don't know. You tell me. How do you do that? It's, it's a, it's a long road.

It's missionary work and he's on that road.

It's tough. The question is, does it relate to mental health issues in humans as well as metabolic health issues in humans? And I will tell you, metabolic health and mental health are basically the same thing. So I'm very prepared to believe that. Okay. I have every reason to want to believe that. I don't know of any data that actually has looked at in environmental obesogens and mental health yet, but that would be really interesting to do. And then my philosophical question is, if you take the focus off personal responsibility, where do you leave the agency? Is it on the government? Is it on the local communities? Where is the agency to try to remove these obesity? Well, ultimately the only way to affect this is to have regulation. So it has to be at the governmental level, at the federal level. If you're going to ban a substance or restrict a substance, and has to be at the federal level, you can't do that at the state or the city level. So it has to rise to the level of, of at least the executive branch and preferably the legislative branch, because if the executive branch knows it, you know, the legislative branch doesn't really care. And we've seen that enough times as well. So this is, you know, it's a big problem. It's a huge problem.

So thank you so much once again.