 Hello, a little volume, a little bit, how are we doing? Hi, I'm Jay Stanton of Knowles.org. Now, it's important to remember that people aren't obese because they enjoy being obese. And diets don't fail because people dislike being slim and healthy. Diets fail because hunger overrides our other motivations. Now, there's an inflection point somewhere around 1980. What happened? The standard explanation is that fat people are just gluttonous and lazy. So, well, yeah, maybe not. So, it's also popular to blame junk food. But, you know, so much for that idea. And lately it's become, of course, popular to blame fast food. But as we see when we plot that together, the data doesn't seem to really support that either. And by the way, the top blue line is food away from home, and the top red line is fast food. So, you can see it's flattening out just about the time obesity starts getting very steep. Now, before I explain the science of hunger, there is a very simple and seductive model which is wrong. And if we fall into it, we've made a logical error from which we can never, ever recover. And that error is food has a special property called palatability or reward, which causes us to eat it. So, if food has too much palatability, it's hyper palatable, so we can never eat it and we get fat. Well, first, as we've just discussed, that doesn't fit the data. The second problem is palatability is a lot like pornography. We all know it when we see it, but it's surprisingly slippery to actually define. Now, for instance, why do different people like different foods? Hundreds of millions of people around the world find these foods delicious. Why can I get 12 different sauces for my chicken wings and 31 flavors of ice cream? Because just like pornography, palatability is subjective. It is a property we assign to food. Now, the second problem is why do we ever stop eating? All Oreos taste the same, but at some point we don't want any more. The Oreo didn't change. We did. Now, the third problem is that the foods we overeat aren't the foods often that taste the best. The classic conundrum is, well, I like prime rib more than I like ringles, but I can't stop eating the Pringles. Why not? And low carbers get this all the time. Your food isn't really rewarding. It just tastes like it. So what happens now is that the naive model has to do a little shuffle step. It redefines palatability as that which we can't stop eating, or you'll sometimes substitute the generic term rewarding. And in other words, we overeat that which we overeat because it's overeatable. And of course, if we're writing grant proposal, we use the word obesogenic. And with that little shuffle step, we've just bypassed the entire science of hunger. Now, I'm beating this dead horse for a very, very good reason, which is that like phlegiston, spontaneous generation, and the luminiferous ether, this very simple and very seductive error absolutely prevents us from understanding hunger. So once again, palatability and reward are subjective properties that we assign to food based on our past experience and our current nutritional and metabolic state. So what is hunger? It turns out there's a very large body of established science. And I could easily teach a semester-long class in this. I asked for 40 minutes, and well, they gave me 20, so I'll do my best to try to keep up. Let's go. Hunger is not a singular motivation. It is the interaction of four different clinically measurable, provably distinct biochemical processes. Satiety, our body's nutritional and metabolic state, and includes both our biochemical response to the absorption of nutrients and our access to stored nutrients. Satiation, an estimate of future satiety based on the sensory and cognitive experience of eating. Hedonic impact are likes. The pleasure we experience from an action. Palatability is the hedonic impact of food. And incentive salience, or our wants. Our actual motivation to obtain something we like. And it is largely but not exclusively a product of the other three motivations. Now, two more factors interact with hunger to modulate our food intake. Availability, how easy it is to get something we want. And willpower, the conscious overriding action of our forebrain known as executive function. So, let's talk about availability for a moment. No, I'm good. So, let's talk about availability. Even though we might want prime rib much more than we want leftovers, well, we eat the leftovers because they're all that's available to us. Now, if I want prime rib, that's three hours on a trip to the store or 40 bucks on a trip to the restaurant. In contrast, we don't have to want processed snack foods very much at all. Because all we have to do is open the bag. They're not hyper-palatable, they're hyper-available. So, now, unfortunately, time does not permit me to explore the biochemistry and neuroscience of the reward system. So, for the details, I will point you to the pioneering work of Dr. Kent Barrage, whose work I was proud to introduce to the community last July. And just a couple quick notes about that. First, it is important to note that likes and wants are not limited to food. Any experience we like that has hedonic impact is capable of producing a want for more incentive salience. And it is also very important to note that is what is colloquially called reward, is a mashing together of hedonic impact and incentive salience. And both vary independently and both are subjective properties. So, the term food reward, which implies a singular property of the food itself, is intrinsically misleading. Because it drops us right back into the cognitive trap of the naive model. So, if liking and wanting are subjective, though, what determines them? Yeah, taste is one part of it. But the interesting question is not why we eat. It's why we can't stop eating. So, we move on to satiation and satiety. Two quick examples. You have just left the all-you-can-eat-Brazilian steakhouse. What tastes good right now? Yeah, pretty much nothing. Now, you have just hiked 17 miles over three mountain passes with a 40-pound pack and that dehydrated lasagna is the best thing you've ever tasted. And the food didn't change. But somehow, its hedonic impact, how much we like it, and therefore its incentive salience, how much we wanted, did change. Now, satiation and satiety are synonyms in common usage, so why do we distinguish them? And the answer lies in gastrointestinal transit time. It takes hours for the nutrients and food to be digested and absorbed, which means that the satiety response is not a useful signal to stop eating. So, furthermore, because satiation is the sensory experience of eating, it can be fooled. It is well known that, for instance, people eat more in groups than when eating alone, people eat more when they're able to eat more quickly, and hidden calorie preloads are never completely compensated for. However, the failure of dietary fiber to affect body weight or fat mass and controlled interventions suggests that faking satiation with indigestible bulk is not a useful long-term strategy for weight loss, because you can fool satiation, but you cannot fool satiety. And satiety is the key to understanding hunger because, as we've seen, satiation is just an estimate of future satiety, and both our likes and our wants are very strongly modulated by satiation and satiety. Now, if we do an experiment where we sit teenagers down at the mall food court and let them have all the food they want for an hour, which is like a challenge for your teenager, right? Now, what we find is that the lean kids eat a huge amount of food, just as much as the obese kids do. The difference is that the lean kids compensate for that over the rest of the day, whereas the obese kids do not. And this strongly suggests that obesity is primarily a failure of satiety. So, we're clearly converging on a primarily nutritional model of hunger here, because, well, that's the definition of satiety, nutrients absorbed. So, let's explore some of the evidence. We can begin by asking the obvious question, well, what else could hunger possibly be for? Any animal whose faulty perceptions and motivations caused it to become obese, emaciated, malnourished, or poisoned by excess would very quickly have been strongly selected against. But, let's talk about the science. So, taste receptors are not located. Taste receptors are located throughout our bodies, not just on our tongues. In our intestines, they modulate the release of satiety hormones. All those great acronyms like CCK and NPY and VIP and GLP-1. In the pancreas, they modulate the release of insulin, among other systems. And those effects are so powerful that, quote, the post-absorptive effects of glucose are sufficient for the post-ingestive behavioral and dopaminergic reward-related responses that result from sugar consumption. Yes, satiety is rewarding in itself. So, by eating food that doesn't produce satiety, you're chasing a reward that never comes. All right. Our taste buds both produce and respond to satiety hormones, which directly alters the perception of taste, so it might not be your imagination that food doesn't taste as good when you're satated. There are opioid receptors in the walls of their portal vein, and they're not there because your liver wants to get high. They're a protein sensor. They're bound to freshly digested protein fragments. So, now that I've convinced you that a nutrient-driven model of satiety and hunger has both biological and evolutionary basis, let's review some of the experimental evidence. So, the obese tend to be deficient in many different macronutrients. Iron, calcium, zinc, vitamin A, vitamin C, vitamin D, E, K, B1, B2, B12, and folate. But that's associative data, so let's talk about some interventions. Protein leverage. We don't have time to go into all the details, but animals from rats to people very much tend to eat until they've ingested a sufficient amount of complete protein to eat their daily needs. And if you feed them a protein-poor diet, they will continue to eat surplus, quote-unquote, surplus calories until they've met that protein need. So, women given multivitamins lose weight and fat mass, whereas women given placebo do not. If calories are held constant, weight and fat remain the same, as we would expect, but the placebo group experiences greater hunger than the multivitamin group. And calcium and vitamin D supplementation alone can decrease body weight and fat mass, but only if you're calcium deficient to start. And here's the blockbuster courtesy of nutrition pioneers Dr. Donald Davis and Dr. Roger Williams, which I dug for way back in the wayback machine. So, take rats and feed them a completely plausible human diet, not a cafeteria diet, not a high-fat diet, not a research diet, a whole food diet of meat, flour, eggs, vegetables and fruit all ground up together so it's uniform. Split the rats into two groups and supplement one group with a very comprehensive list of vitamins, minerals and other micronutrients to help them feed freely. Then, after several weeks, do some experiments. The interesting one is you give both groups free access to granulated sugar in addition to their chow for an entire day. And guess what happens? The non-supplemented rats, again, eating a plausible whole foods diet of meat, flour, eggs, vegetables and fruit consumed 67% more sugar than the supplemented rats. How about that? And this is something we absolutely cannot explain by the palatability model. The sugar didn't change. The diet didn't even change. The only difference is micronutrient content. So, satiety modulates reward and junk food is self-reinforcing. The more empty calories you eat, the more you'll crave empty calories. So, why it's critically important to understand hunger, the problem with popularizing for mass consumption is that it's very easy to simplify a concept until it's no longer true. In the process of oversimplification, concepts can also become politicized. And the naive model in which palatability is a property of food that causes obesity is being used to resurrect the diet-heart hypothesis and here's how the story goes. You have not become fat-sick and diabetic because we've been telling you to eat the wrong things for 35 years. These massive surpluses of corn, soy and wheat we've created via agricultural policy that subsidizes the destructive, chemically-based monocropping of genetically modified birdseed by giant multinational corporations are completely a coincidence. Our dietary edicts from the original dietary guidelines for Americans to the food pyramid, to the food plate are not just excuses to turn you into passively compliant grain disposal units which consequently require heroic doses of highly profitable patent pharmaceuticals to keep you alive. No, no, no. That is not the problem. Pay no attention to the $500 billion profit stream behind the curtain. You are the problem because you did it wrong. You didn't eat those hard, bitter, dense, whole-grain breads we told you to. You've been putting salt and butter on your vegetables. You've been eating food that tastes good, not that dry, tasteless, low-fat whole grains we told you to, but that's okay. It's not really your fault. We know you're weak and stupid and can't be trusted to make your own decisions and the fault lies with those evil corporations who have been making food that tastes too darn good and you just can't resist it. So we're going to save you. We're going to tax sugar because just like liquor taxes have stopped us from drinking, sugar taxes will most definitely stop us from drinking soda and eating candy and also we're broke. So that is the new narrative. And there are people here playing footsie with it and that is why we need to understand the true science of hunger. First, because we quite literally cannot afford not to. 35 more years of the OBCD epidemic will bankrupt Medicare, our government, our healthcare system, and us. But far more important is that the cost in human lives and human suffering will be incalculable. Millions will suffer terribly and die needlessly. Been to a cheap nursing home lately? It's ugly. It's an ugly reality. However, there is good news which is that the real science of hunger is not complicated and if I have done my job here, you now have enough of a handle on the concepts to figure out for yourself how the science of hunger applies to your own research as well as your own issues around food. And I challenge each one of you individually and collectively to follow the path of science, not the path of politics. So, we'll close with some takeaways. First, hunger does not exist to make us fat. It exists to keep us alive. Second, hunger is the interaction of four biochemically and neurologically distinct motivations likes, wants, satiation, and satiety. Our resulting desire to consume is modulated by availability and willpower. Cells and organs throughout our bodies are full of taste and nutrient receptors that sense their external and internal environment. In response, they issue hormonal and neural signals in order to maintain an environment which keeps them alive and functional. These homeostasis define our current nutritional and metabolic state, our satiety. Palliability and reward are not properties of food. Our likes and wants are subjective properties we assign to food based on our past experiences and our current state of satiation and satiety. Remember the rats. Our food consumption is primarily determined by its ability to produce satiation and satiety, not its hedonic impact. Conclusions. Obesity is primarily a failure of satiety. And your mother was right. The problem is in hyperpallidability. It's empty calories. Thank you. And apparently we have time for some questions, so come on up. Seth Roberts. Awesome. I really like that. I really like your talk. And I would like to know, so what did change in 1980? I don't think one thing changed in 1980. As when I talked about homeostasis back there, you can make the diagram of human biochemistry. It's that giant seven by nine poster in fly spec three type. And to be able to point to one part of that poster and say the one over there, he did it, I think is a little bit optimistic. We all want to explain everything in terms of the part we understand. I know I don't understand enough to make that judgment. However, I do think there are several things that most certainly contribute to that. When you look at the, how diet actually changed during that time, one thing you have is the removal of a lot of nutrient dense foods from the diet because they have cholesterol, saturated fat in them. Another thing you have is a gigantic increase in trans fat because all the beef tallow got pulled out of all the fast food restaurants and all the French fries we loved eating so much, suddenly were fried in 30% trans fat. And there are a lot of other consequences and really you look at, and again, I don't want to say those are a sole cause of anything. I think there are a lot of things that contribute. Those are a couple things that come first to my mind. Well, can I say something? Please. I think the fact, I mean, I think it's great the way you looked at that graph of the 1980 change. But the fact that it's so sharp really does suggest it was one thing. You know, as weird as that is. But it's really weird to see a sharp change like that. It is. And you do have to keep in mind that it looks possibly a little sharper than it is because it's about eight or ten years between the N. Haynes. So what we know is the curve started turning up sometime after 1978. And before 1988, we don't know exactly when. But the thing is it can't get less sharp because you can only get more sharp. The more you delay it, the sharper it has to be. So yes, we know it is sharp. And yeah, I have some speculations, but I don't have the answer. I admit that. Thank you so much. Hello. Hi. So I just wanted to say that I think that, you know, one of the ways that you discussed palatability was by saying that palatability or more palatable foods are those that we eat more of. But eating more of a food is not part of the definition of palatability. Palatability, as you said, it's a subjective concept. But we study many subjective things that are important, such as depression and cognitive characteristics that are very important to understand. But the other thing I wanted to mention is that the quality of palatability actually does have a substantial impact on food intake. And in fact, as far as I understand, every single controlled trial that's ever been conducted on the question, and there have been quite a number, have determined that more highly palatable foods are rated as more highly palatable. So the way these studies are done, essentially, they give subjects a small taste of different foods. They have them rate the palatability. And then after that, they give them unlimited access. And what they find is that there's a tight correlation between palatability and subsequent food intake. And in fact, those excess calories are not compensated by eating less and further meals typically. So we're talking about excess food intake occurring over long periods of time. So anyway, I just wanted to point that out. Well, and let me say first that, no, I absolutely agree. As far as I understand, the actual definition of palatability is, yeah, the hedonic impact of food. It's not really a circular definition. It's just easy to slide into that by mistake. So, yeah, and I'm not suggesting anybody in particular does that. It's an easy cognitive trap. And yeah, and again, there are a lot of different studies. Does palatability affect food intake? Absolutely it does. The question is, to what degree is that compensated for later? And that depends on a host of different, obviously different data, and which study you're looking at and everything else. So yeah, I'm certainly not making the claim that, oh, everything's satiety, palatability doesn't matter. I'm making the claim that, I think, according to how I see things, that's a primary motivator, because why we start eating is less interesting than why we stop eating, so. And why we stop eating is determined both by palatability and satiety. And that's the question. How much does palatability enter that versus satiation and satiety? And I'm not personally aware of experiments that directly measure that, because I'm not sure you can measure it or disentangle it, but it's a very, very interesting question. All right, cheers. Thank you. J.S., you're brilliant. I love this stuff so much. I think we see people coming to a paleo-style diet in part to avoid this trap, to get back to micronutrient-rich satiety-inducing foods. But can you talk about how you can fall right back into this trap while still eating technically approved 100% paleo foods, the micronutrient-poor stuff, with the lack of satiety? Yeah, well, I mean, the whole concept of paleo approved is kind of strange, because... APPLAUSE Number one, you know, who's the regulatory board for this and who's on that and who makes the decisions? And really, what I think we find is you've got sort of the intersection of two things. You've got the intersection of nutrient density and you've got the intersection of that with toxicity. And toxicity is possibly too strong a word for something like lactose intolerance. But, you know, the fact remains that however nutrient-dense raw milk might be, some people are just simply not going to be able to consume it because they don't have lactase persistence and that's that. So really, yeah, I don't like to think of things in terms of directly paleo-approved or not paleo-approved. I like to think of things in terms of, yeah, nutrient density and anti-nutrient density, as it were. And there's a lot of things we don't know about that. There are a lot of foods, yeah. There are a lot of things we don't know that are bad for us. You know, is that particular lectin a biological problem? We're not really sure. So depending on the degree of the issues you personally have, it can be prudent to be more or less conservative about your judgment in that area. For instance, if you've got autoimmune issues or other things, it may be prudent to eliminate a lot of things that other people might not be so concerned about because even if you don't know which one or if any of them are responsible or if any of the chemicals are bad it's still probably a good idea because you know you're more sensitive to that than others. So yeah, I don't have a simple solution. But yeah, to me it's the sort of two concepts of nutrient density and anti-nutrient density. You want as much of the nutrient dense stuff and you really want to avoid the anti-nutrient dense stuff. And if you want to call that paleo or whatever you want to call that, you want to call that Whole30, which is a pretty strong intersection with that particular template. Great. Okay.