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The BIGGEST MISTAKES People Make When Trying To LOSE WEIGHT! | Dr. Jason Fung

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Dr. Jason Fung challenges the conventional wisdom of weight loss, asserting that counting calories and restricting energy intake simply does not work because it ignores the hormonal mechanisms governing metabolism. He explains that while thermodynamics suggests a calorie deficit leads to fat loss, this assumes a stable basal metabolic rate which is biologically incorrect; when caloric intake drops without addressing hormones, the body compensates by lowering its metabolic output rather than burning stored fat. The core issue lies in insulin, described as a nutrient sensor and storage hormone that signals the body to save energy for times of scarcity. When insulin levels are high due to eating processed carbohydrates or frequent meals, the body enters a "storage mode," effectively locking away fuel reserves and preventing access to existing body fat stores regardless of how few calories one consumes. Consequently, even significant caloric restriction fails if it is accompanied by chronic hyperinsulinemia, as seen in studies where diabetics on high insulin doses gained weight despite eating less than 700 calories a day. The discussion highlights that not all carbohydrates are equal and distinguishes between natural sources found in traditional diets versus highly processed refined sugars which lack satiety signals like ghrelin. While protein also stimulates insulin, it simultaneously triggers other hormones related to fullness and does not primarily serve as fuel for storage in the same way glucose or fat do; dietary fats bypass the liver's processing entirely and enter fat stores directly without requiring insulin. Fung emphasizes that weight gain is fundamentally a hormonal imbalance rather than a caloric one, noting that ice cream is far more fattening per calorie than salmon due to its impact on these regulatory systems. Furthermore, he points out that chronic damage drives obesity-related diseases like type 2 diabetes and kidney disease, making the reversal of insulin resistance critical for health longevity. Transitioning from metabolic health to oncology, Dr. Fung introduces "Cancer Paradigm 3.0," a shift away from viewing cancer solely as genetic mutations or uncontrolled cell growth (Paradigms 1.0 and 2.0). He argues that modern medicine has focused too much on correcting random genetic errors while ignoring the evolutionary nature of cancer cells, which revert to primitive, unicellular behaviors characterized by competition rather than cooperation. Using a vivid analogy of a wild bear wearing a tutu, he illustrates how these malignant cells are not necessarily new creations but ancient survivalist organisms that have stripped away their multicellular "civilization" layers due to chronic environmental stressors. This evolutionary perspective explains why cancer treatments often fail; they attempt to kill or genetically correct cells rather than addressing the underlying cause: an environment that selects for primitive, aggressive cell types. Fung elaborates on his "seed and soil" theory of carcinogenesis, explaining that while every human possesses the genetic seed for cancer in their unicellular ancestors, it requires a specific toxic environment—the wrong soil—to germinate. This chronic damage comes from persistent stressors like smoking, hepatitis B infection, or long-term exposure to low-dose radiation, rather than single acute events as seen with atomic bomb survivors who suffered minimal excess cancers because the damage was not continuous. The "soil" is created by a diet high in processed foods and sugars that induce chronic inflammation and hyperinsulinemia, both of which act as powerful growth factors for these primitive cells. By improving this environment through fasting, eliminating refined carbohydrates, reducing sugar intake, and managing weight to lower insulin levels, individuals can effectively starve the cancer seed before it grows, offering a proactive approach to prevention rather than relying solely on reactive chemotherapy or immunotherapy.
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Counting calories simply does not work at all. And people will say, "Oh, but it does, it does, it does." Well, if you look at the scientific studies, it doesn't. [music] Hey everybody, welcome to another episode of Health Theory. I am here with nephrologist and best-selling author Dr. Jason Fung. Jason, thank you so much for joining me. Oh, thanks for having me. Great to be here. Dude, I am really excited to um talk to you about two things that I think are really revolutionary um that I don't see anybody talking about as well as you or maybe even at all. And that is you've really um pushed for a paradigm shift in the way that we think about both insulin and its role in longevity, obesity, diabetes, and on and on the list goes. And then this whole idea of cancer paradigm 3.0, which I find really really interesting. Um I want to start with the role of insulin um in weight loss, in uh disease mitigation. What is it that was sort of that key insight for you that got you thinking about this in a different way? And how exactly is it that you think about it? Well, it's interesting because the question of weight loss is one that has really become more and more important as we've had more and more obesity. So, uh over the years we've seen more people with obesity, which has led to more people with type 2 diabetes, which has led them to get kidney disease, which is where I kind of come in cuz I'm a kidney [clears throat] specialist. So, it's become a bigger and bigger part of the practice. And it it uh sort of dawned on me that eventually got through my thick skull that uh really weight loss is sort of really critical to keeping people healthy because it's uh sort of obvious. Like it leads to type 2 diabetes, which is a huge risk factor not only for kidney disease, but for heart attacks and strokes and cancer and it's a leading cause of blindness and amputations and diabetic infections and all kinds of bad things. So, almost like you know, 50% of what I do is related to type 2 diabetes and the point was that if you can reverse your type 2 diabetes, then you're not going to get these diabetic complications and in order to do that you need to lose weight, which is why I go became very interested about 8 years ago in the question of how to lose weight. And I didn't know much about it at the time, but people were always, you know, what I had learned in medical school was all about sort of calories in, calories out sort of thing. But the more I looked into it, one it's a very, very unsuccessful way to lose weight. Counting calories simply does not work at all and people will say, "Oh, but it does, it does, it does." Well, if you look at the scientific studies, it doesn't. Every single study that's looked at sort of say, you know, trying to restrict calories leads to at best a couple of pounds of weight loss over like 8 years. So, you acknowledge that if you if you take calories out of somebody's diet long enough, they are going to get lean regardless of anything else. So, where is where does that paradigm break down in reality and is it just willpower that people aren't sticking to it or is it something else? Well, it's something else and the whole point is that it's not the number of calories, it's what your body does with those calories. Because if you take 100 calories, if you eat a cookie for example, you take 100 calories, [snorts] your body has a decision to make. Do I store that as body fat or do I burn it for energy and say increase body heat generation for example. And that's the basal metabolic rate. That's the number of calories that your body uses in a day. So, which your body does with that same 100 calories, you can either become fatter or you can have a bit more energy during the day. And which one your body does really depends on the hormones that are associated with the foods that you're eating. And that's the real key because if you simply cut calories, and this is the way that, you know, I was taught and everybody was taught, you simply cut the fat, you eat less fat because fat is very dense in calories. You get less calories and therefore your body is going to lose body fat. But that's not necessarily true. If you eat 500 calories less, your body could simply decide to burn 500 calories less and you won't lose any body fat. And it's not a matter of thermodynamics because that's that whole idea that it's just about thermodynamics assumes that your basal metabolic rate remains absolutely rock stable. That is if you're using 2,000 calories a day today, you go on a diet, you'll still use 2,000 calories a day. But you won't. We know we've known that for at least 100 years of basic research that your body will actually use less, fewer calories. So, cutting 500 calories a day, which has been the standard advice, is very unsuccessful because if you don't change the hormonal system in your body, the the the and different foods contain different hormonal instructions. Your body could simply decide to burn 500 less and you will not lose body fat. So, it's it's it's simply false to say if you cut 500 calories a day down, you'll lose a pound of body fat a week. It's actually not true in any way, [laughter] shape, or form. Um just like if you say, well, if you make an extra $100, uh you know, this week, that you'll be $100 richer. You may or may not be. If you make $100 more and you spend $100 by going out, you're not richer. Same thing with your body. You You You You take 500 calories or less that day, but you burn 500 less because your metabolic rate goes down, you're not losing body fat. And that's the whole point. So, it's It's not the total number of calories that's important. It's what your body does with those calories, and that depends on hormones. And in fact, everything in our body runs on hormones. Those are the instructions that we give to our body as to what to do. So, everything your body does or doesn't do depends on hormones. Those are the sort of mediators. Do you have any sense of why different foods have different hormonal cues? Like, why is it that carbohydrates signal the body to secrete insulin, I think, the most out of all the macronutrients? Given that that is the signal to the body to store, like, why doesn't protein, for instance, signal the body to store? Why is it specifically carbohydrates? Yeah, actually protein does stimulate insulin as well. And Equal amounts? Um some of some proteins can actually stimulate quite a bit of insulin. It doesn't So, if you eat carbohydrates, your glucose goes up, and then your insulin goes up. In protein, your glucose doesn't go up, your insulin does go up. And And it's really to do with the way the body metabolizes. So, insulin in a more general sense is a nutrient sensor. So, that tells your body that, "Hey, food is on the way in. Therefore, let's switch over to storing calories as opposed to burning calories." The reason dietary fat doesn't do that is that it doesn't get metabolized through the liver. Dietary fat actually gets absorbed through the intestines, goes into the lymphatic system, and sort of goes directly into your fat stores. So, because it doesn't go through that whole processing through the liver, it actually never metabolizes and therefore doesn't really need insulin for that. But, one of the things is that insulin you know, different hormones, our body needs to know what's coming in and what proportion. So, insulin is a nutrient sensor, but so is something called mTOR, which really is very specific for proteins. It goes up quite a lot, tells your body that there's a lot of protein coming in. And there's a lot of associated things, but one of the things that's important these nutrient sensors are also linked to growth pathways. So, therefore, your body really only wants to grow when nutrients are available. And therefore, when you do get take a lot of carbohydrates or even protein, your body senses that there is food coming in and therefore will turn on growth pathways to grow muscles, to grow, you know, stores of body fat, that kind of thing. Is the key in this then, cuz the thing that I found most interesting about what you talk about is a focus on insulin, at least that's been sort of my read on what you talk about. Moving away from, you know, for a long time you hear people talk about glucose, blood glucose, the body tightly regulates that. But, this idea, the analogy that you use of the suitcase, right? And sort of where this starts to become a problem is what we call insulin resistance. It's probably not the right way to think about it. We'll get to that in a second, but first I want to talk about low-carb diets, right? So, low-carb was wildly effective for me in terms of reducing the body fat that I had. That's certainly something I've heard you and other people say that reducing your carbohydrate intake is, you know, going to have a disproportionate response in terms of body fat than something like, you know, dietary fat or protein. Help me understand then the relationship, if protein is spiking my insulin and insulin is the thing that's storing things into my fat cells, why are carbohydrates more, quote unquote, problematic when it comes to storing fat. I think it comes down to several things. So, proteins is actually quite complex because it's not primarily fuel. So, carbohydrates and fat are primarily fuel. We we burn it and we store it. So, our body stores glucose, our body stores fat, but our body doesn't really store protein. So, it's primarily a structural thing. So, your body isn't So, even though insulin is stimulated, there's it's actually quite complex because glucagon is stimulated which keeps the glucose normal. Um but then protein also has very strong effects on satiety. That is there are certain other hormones that when you eat, for example, protein are going to tell you, "Hey, you're full. You you need to stop eating." So, if you think about eating steak, for example, uh you can eat a certain amount of steak. And then at some point, you can't really just keep eating. Uh you will actually just get nauseous. As we've all done at the buffet when we've eaten too much. You can't just say, "Oh, that looks good. I'm just going to have another pork chop." It's really hard to do that because those satiety hormones are very powerful. Uh the reason carbohydrates are very problematic is that they tend to be processed. So, processing removes a lot of these satiety signals. So, even if you've eaten a huge buffet and somebody says, "Hey, do you want a few sips of uh my soda?" You'd say, "Sure. No problem." Because they don't activate your satiety mechanisms. And same for like a cookie. You could easily eat a cookie after after you're full from dinner where you would not eat another, you know, pound of steak. So, it's it's a bit more complex because there's multiple interacting hormonal systems that regulate how we respond. Protein doesn't seem to be nearly as bad. Even though it has a lot of insulin effect, it has probably a lot of these other hormonal effects that are just as important and really stop us from eating. Just like if you were to eat steak and eggs in the morning, a lot of fat, a lot of protein, it tends to keep you more full than if you were to eat white bread and jam. You eat that and then at 10:30 you're looking for a low-fat muffin, for example. And And this is one of the things which I always say is like when you're thinking about weight gain, weight loss, really have to think about hormones because it's really a hormonal imbalance, not a caloric imbalance because the the calories in all these foods can actually be exactly the same. Um and that's why I'm not and I you know, not all carbohydrates are bad for you. Like clearly there have been many, many um societies that have lived primarily on carbohydrates. Yet if you measure the insulin um response, they're actually quite good. So, something like they they did a study in Kitava, for example, which is a South Pacific island and um they measured their diet and it's about 70% carbohydrates, but natural carbohydrates and they didn't weren't eating all the time. Then when they measured their insulin, their insulin level was below the fifth percentile of a reference sort of Swedish population. So, that means that even though they're eating a lot of carbohydrates, their insulin levels are still very low. So, there's lots of things, not only the foods that you eat, but also the frequency which with you eat them plays a really important role and the amount of processing that goes into it. And you can see that effect in something like the glycemic index where when you eat white bread, things just spike way up, but if you were to eat beans, which is all carbohydrate, the glycemic index is much, much, much lower. And most natural foods are like that. You don't see that huge spike that you get. So, the the processing of the carbohydrates makes it especially problematic because it is a fuel source for our body that our body is able to use very easily. And it's highly refined so that you don't have any satiety and then you're getting it sort of absorbed very quickly because you've removed all the fiber, you've removed all the fat. And that's, you know, that's that's sort of what goes into it. But focusing on the hormones is really important because it leads you away from focusing on something like calories. The only implication of focusing on the hormones as opposed to calories is that some foods are more fattening than other foods. That's really the only implication. It's like, boy, if you were to ask your grandmother or great-grandmother, she'd say, "Well, duh. I hope you didn't have to go to university to learn that. [laughter] Of course some foods are more fattening than other foods. Like cookies are fattening. Like anybody could have told you that. Anybody with an ounce of common sense would have told you you don't get fat eating broccoli. Like these are just like things that we take for granted that we should know. But you get so people get so so focused on, "Oh, it's all calories. It's all calories." that they say ice cream is as fattening as salmon. It's like, no. Obviously not. If you've ever lived, you know, in on this earth, you would know that [laughter] ice cream and salmon are not equally fattening for the same amount of calories. That's just common sense. So, um this distinction between chronic caloric restriction and fasting, um that I find really interesting. And let us, for the sake of this discussion, assume that we have a person who is willing to endure an unlimited amount of suffering. Um and you even you've talked a lot about the book Unbroken that you read about World War II um people in Japanese concentration camps, and they were literally being starved. And obviously all of them got lean. So, what I want to understand is, okay, fasting seems to have all these tremendous benefits, chronic caloric restriction has some, but also has like this really damaging psychological component. If there was no damaging psychological component, would they be equal, or is there still some difference? It all depends on how you do the caloric restriction. So, because it's not just about the calories, it's about the hormones, right? So, you have to sort of take it not to sort of this two-compartment problem. You have to take it to like a three-compartment problem, right? There's what's coming in, there's what's stored, and there's what's being used, okay? So, most people only think of sort of the two compartments, and then the storage is sort of left over. But, that's not the way the body works. If insulin is high, your body is going to store calories. Remember, insulin is a nutrient sensor. It tells your body that, "Hey, energy is coming in. You're eating. You need to store some of this." Right? It's so it's so you eat breakfast, lunch, dinner. get somebody on a low-calorie diet, like if you were on 700 calories a day, but I gave you insulin, could I make you fat? Yeah, absolutely. Whoa. Because think about it this way. If you have insulin, your body And so, if you think about it physiologically, if you have insulin, your body goes into a storage mode, because it's a hormone, insulin is a hormone. It tells your body food is coming in, and even if you don't give food, if you just give insulin, you're going to switch your body into this mode where it thinks that food is coming in. So, it's going to store energy. So, imagine that, for example, you are a coal, you know, a coal plant, right? A power plant. You get 2,000 tons of coal coming in, and you burn 2,000 tons of coal. That's fine. You have a storage compartment, too. So, if you're, you know, if you do a thought experiment, say say you have 2,000 tons of coal coming in, but you divert the whole thing over to uh or 1,000 tons of coal into storage, well you only have a thousand left. So, you're going to feel tired and cold and hungry. And you're going to get fat at the same time, right? That's what's going to happen. But it's because of the way that you've diverted off the energy. So, think about it from a human body standpoint. [snorts] Suppose you have 2,000 calories coming in, 2,000 calories going out. Now you artificially inject insulin. Well, you shuttle a thousand calories immediately into body fat and you have a thousand calories left to burn. Well, what's going to happen? Your your your body heat generation is going to go down, your heart rate is going to slow, you're going to feel tired, you're going to feel hungry because you want to get more energy, right? That's the signal for you to get more energy so that you can get more you can burn more. Guess what? That's exactly what happens when you go on a chronic calorie restricted diet. And the the point is that if you do it correctly and you you correct that insulin part of things so that none of it's going into storage and you can do that with chronic calorie restriction, you certainly can. You have to know that you have to do it properly like cutting out processed foods, cutting out refined carbohydrates, that kind of thing. But it all depends on that sort of that sort of toggle in the middle that says how much goes here, how much goes here. Insulin it what it does is it tells your body to store fat, but it also turns off fat burning. Remember, fat is purely a store of energy. It's a store of calories. So, you're immediately shuttling all your energy into storage and you have nothing left. So, say you take 700 calories of it, you're pumping people full of insulin. So, that energy is going to go into into storage. And 700 is probably the lower limit of what you could really do, but your body would then try to subsist on say 5 600 calories of energy. You'd get really hungry because you you you've got no energy coming in. You probably wouldn't be able to last very long, but you could still gain weight. There's a great experiment a few years ago where they actually took the type 2 diabetics and they gave them a lot of insulin. So, they went from zero uh units a day to 100 units a day over a span of 6 months, which is a lot. And they dropped the number of calories that they ate by 300. Okay, so they're taking insulin, but they're eating less. 700 300 calories a day less. So, over the span of 6 months, on average, that group gained 20 lb. 20 lb by eating 300 [laughter] calories a day less. Why? Because so, let's take an example. You're eating 2,000 calories, you go down to 1,700, but the insulin is shuttling 700 of that immediately off to storage. So, you're gaining body fat. Now, your body can only burn 1,000 calories a day. So, you feel like crap, you feel tired, you feel hungry, and you're still gaining weight. And guess what? If you do it wrong, which is constantly snacking and eating cutting out all the dietary fat and eating all refined carbohydrates, which remember is almost precisely what we told people to do in the '80s and '90s. Oh, I remember it well. Yeah, actually [laughter] I had a tub of licorice because it was fat-free, and I would just eat it and eat it. I'm like, it's fat-free. What What's happening? Why am I getting fat? Yeah. [laughter] That was a very confusing time. It makes perfect sense from like because but you have to think of that additional step, that is what is the body actually doing? It's this sort of flip this switch. So, when you eat, you're storing body fat. When you don't eat, when insulin is going down, you're going to burn body fat. You're going to actually going to You can't burn body fat if insulin is high. Let's ask then the reverse question. So, I fully accept that all food is a signaling molecule that's triggering a some cascade of hormones. I know what to do if I want to store a lot of fat. I'm going to eat a lot of processed carbohydrates that are going to remove all my society mechanisms and it's going to spike my blood glucose like crazy. My body's going to pump a bunch of insulin to make sure that that gets pulled out of the bloodstream. I'm going to get fat. Okay. Is there a diet that's optimized on the exact opposite side where I'm taking in very satiating amount of calories but it's dropping my insulin or failing to trigger my insulin is maybe the right way to think of it and therefore I'm eating maybe more than your average bear but I'm actually getting leaner. Yeah, there's there's certainly lots of them. There and and the the principles are much the same. One is you want to avoid sugar cuz sugar, the way that we process fructose is sort of particularly bad and that's why sugar is particularly fattening really and that's that's true if you're a bear. You're eating a lot of ripe berries and stuff because you're trying to gain fat. And it's also true as anybody knows if you're eating a lot of cookies and brownies, you're probably going to gain weight. The The other thing is you can't eat all the time because again, it's a cycle between feeding and fasting. That's what we're supposed to do. If you don't give your body time to burn off all those calories that it's taken in which means the fasting period, you're going to overall gain weight. It's like a one-way valve. If you go in but don't come out, eventually everything just gets bigger. Same thing. [snorts] That energy cannot come out if your insulin levels are high. That's just the way it's designed and it's it's sort of like, you know, if you if you see a tanker, you know, those tanker trucks on the side of the the road. Sometimes they you think, "Oh, they'll never run out of fuel because they have all this fuel." But they do run out of fuel, of course, because you can't access that fuel that's in that big container. Same thing with your body fat, right? It's locked away. If you do not lower your insulin levels, you will never have access to those stores of energy. Once you lower it, hey, all that energy just comes flowing in. And and for people who are who are on long who have done longer fast, and this is what's so interesting about the whole process when you actually do it is that the hunger starts to go down significantly. The psychological hunger goes up because people are like, "Oh, I really want to eat that." But, the physical hunger actually tends to go down. Meaning measured by things like ghrelin or whatever. Ghrelin. So, hunger hormones and so on. And and people you talk to people and you know, I've done it live. I know lots of people have done it. And they they all say the same thing. By day three, day four, the hunger's almost completely disappeared. And why is that? Well, because you're fueling yourself from your body fat stores. And therefore, you actually have no no need to eat. It's It's It's It's an interesting process which people never think about, but it's completely physiologic. Yeah, so I've done my longest fast was 5 days. Um I've done many fast that are 24 hours to 72 hours. I find 72, while not pleasant, I find it relatively easy. I don't decline in performance. But, day four and five, I do. And I'm super curious to know um if I am doing something wrong. Like, am I supposed to be supplementing? And and I'm talking a true water only fast. Um should I be eating salt? Should I be taking magnesium? Like, what what is it? Yeah, everybody's different. Certainly, some people salt is probably the main thing people get into trouble with because we're on a relatively high salt diet. And then to go to a sort of zero which is water only zero salt is a bit of a transition sometimes. So some people find that their pressure blood pressure goes low and that that makes them not feel so good. So a lot of people have found better from taking salt either salt and water or just a salt like a under the tongue even. Magnesium is another one that that tend to know and some people find it helpful to supplement there as well. The other things that people find useful is to take some broth for example which is going to give you it's not a true fast none of these are. I was going to say that sounds like cheating to me. Yeah they're they're they're sort of like I call them variants because they're not water only fast is really a true fast. But you can get a lot of the benefits by taking some of these other things and it makes it easier. So it's a sort of a trade-off it's sort of like bulletproof coffee which is of course not fasting but it's a very very pure sort of fat and therefore it's going to provide a lot of satiety and then let you go through the day maybe allows you to go long and overall you might wind up positive in terms of weight loss and so on. So lots of people certainly have found that useful not everybody. But certainly it's it's that but water only fast can be more difficult because of the associated electrolyte problems. Your body is supposed to handle it but it doesn't always. Sure. So if we're looking at longevity and we want to prolong life as much as possible and anti-cancer in fact this might be the perfect transition into your brilliant synthesis of what's going on from cancer paradigm 1.0 to 2.0 to 3.0 I found that absolutely fascinating in your new book cancer code. It was subtle and yet changes everything. And if you can just like give a a sort of thesis on that 1 2 3 thing I think that would really help people. Yeah. Yeah, and and you know, I'm I'm not the one who made it up. I just was the one to sort of explain it sort of in an accessible way. And honestly, it's it's the most fascinating story in medicine today, I think, is cancer [clears throat] because it's undergone this tremendous change in the last sort of 10-20 years, and nobody even talked about it. And what I talk about is sort of the the these modern paradigms of cancers, the way that we look at cancer. And the reason they're important is because they determine what sort of treatments we use. So, the first sort of modern paradigm of cancer is sort of this cancer is a cell that grows too much. So, you have breast cancer, for example, you have a breast cell. Now, something happens to that normal breast cell, okay, so it starts off as a normal cell, but somehow mutates into this breast cancer cell or this lung cancer cell. And this lung cancer cell then grows and grows and grows, and then it moves around, it spreads, or this is called metastasis, then you die. So, the first paradigm is, "Hey, this is a cell that grows too much." So, therefore, our treatments are actually ways to kill cells. And that's the sort of core of modern oncology is to cut it out, which is surgery, you can burn it with radiation, or you can poison it with chemotherapy. Chemotherapy is really nothing more than a selective toxin. It kills some cells faster than it kills another cell, so that's why you have these horrific side effects. Their hair falls out, they're nauseated, all this stuff you think about with chemotherapy is because the idea of chemotherapy is to kill the cancer slightly faster than you kill the patient. That's really it. It's a selective toxin. But that's the paradigm, and it makes sense from that you know, because if it's if it's growing too much, then kill it. That's basically it. Now, that reached its limits probably by the '60s. And by then we were talking about genetics, so everybody started to look at genetics, and then that's the sort of next huge paradigm shift. Is that we were trying to understand at a deeper level not we weren't saying that cancer cells didn't grow. The question we're trying to ask is why are they growing? And so we said, "Well, the answer now is that they have genetic mutations that lets them grow too much." And sure enough when we looked we found these oncogenes and tumor suppressor genes, so genes that control growth. And when the cell gets a mutation in one of these critical genes, then it would grow too much. And that made perfect sense. So, the point of something like lung cancer and smoking, cuz we know smoking for you know, clearly causes lung cancer. Smoking is not a targeted mutation device. It's very non-specific. You're just creating damage all over the place. So, what they said was that this is a random genetic mutation. So, you're just creating damage in the genome. And if you're damaging a lot, you're getting a lot of chances to hit this critical growth gene area, and it's going to let cells grow. So, this was the the genetic paradigm, which really has dominated cancer medicine for the last 50 years. And so, instead of trying to kill cells, this led to new treatments. And instead of trying to kill cells, we're trying to correct the genes that controlled it. And the first few drugs of the sort of genetic paradigm were just amazing. So, by the 2000s, we were like, "We are going to cure cancer." So, we did this whole human genome project. We said, "All we need to do is map out all the genes, look at the cancers, map out those genes, and see what's different. We're going to find one or two genetic mutations. We're going to find a drug to cure that one or two genetic mutations, boom, we're going to cure cancer. And that was really what we thought at the time. It was a time of incredible promise. But it didn't work. That was like if you look at the number of genetic treatments of cancer that really made a difference, you're talking maybe five. Right? In the last 40 years, five really good drugs. That's not a lot. And that's a long way from curing cancer. And the problem is when we went back, so they did the Human Genome Project, then they did this Cancer Genome Atlas, where they mapped out all these genes. They took 30,000 cancers, mapped out the genes, and said, "What are the one or two critical genetic mutations?" They didn't find one or two. Each cancer had like 50 or 100 genetic mutations. And And it was crazy because if you had a cancer clinic where one patient had lung cancer, so patient A had lung cancer, patient B had lung cancer, patient A's lung cancer had 50 mutations, patient B had 50 mutations, completely different mutations. So, how are you going to treat this? You can't get 50 drugs for patient A and 50 completely new drugs for patient B. It's just impossible. And that's why cancer treatment just sort of slowed to an absolute crawl. It was just uh you know, a huge amount of disappointment. Um and that sort of spelled the end. It wasn't a random genetic mutation. So, it wasn't that genes weren't mutated. It was what is driving these mutations? And that sort of spawned this whole next paradigm shift to cancer paradigm three, which so few people people talk about. And I don't understand why, cuz I I I find it endlessly fascinating. And what we were trying to do, we weren't trying to uh invalidate that the these genetic mutations, cuz clearly these genes had mutations. What we're trying to understand was, once again, try and get to that one level deeper of why. Why are these genes mutating? And the totally fascinating answer that they came up with is that it was an evolutionary process, not a forward-moving evolutionary process. It was a backwards evolutionary process towards a more primitive form of our cell, which was there from evolution. And what's fascinating is that if you look at pathologists, like the way that people who look under the the microscope at cells, that is exactly how they describe cancer cells, primitive, uh undifferentiated. You've got to use You use a an analogy or a metaphor in the book about a bear in a tutu that I thought, "Oh my god." Like it lets you conceptualize what this is so perfectly. Will you walk people through that? Yeah, and the point is that the cancer is actually a reversion to a more primitive form of a cell, and it's a sort of like if you have a wild bear, you can raise it and teach it to dance and wear a tutu, but it's still a wild animal. So, if you provoke it, it'll still kill you. Like it'll still wear a tutu, but it'll still kill you. So, it reverts to being that wild animal, and our cells are very much like that. So, we came from unicellular organisms. So, all of us sort of evolved from small bacterias and so on, fungi, and so on. And under the right conditions, these cells actually undergo an evolutionary process back towards this more survivalist sort of primitive cell, a single-celled organism. Its primary mandate is to compete with other cells, as opposed to a multicellular organism which its mandate is cooperation. And they are fundamentally against each other. As we move from cellular competition to cellular cooperation, we had to put on all these instructions on top, these genetic instructions to suppress all these competitive urges. When you cause genetic damage and strip away you damage all these sort of controlling layers, what shines through is that competitive nature. And then the cells, the cancer cells actually behave exactly like unicellular organisms. And that's fascinating again because our own immune system has actually identified these cells as foreign cells. Like there are, you know, immune cells in our body that identify sort of self, our own cells versus other cells, so you avoid friendly fire. And cancer cells are actually identified intrinsically, without being having seen them ever before, your own body will identify these as foreign cells and destroy them. And that's really the reason why we don't have cancer sort of with 99% of the population cuz when you suppress the immune system, of course, you increase your risk significantly of developing these cancers because it's our immune system which is playing that anti-cancer role. So what you're trying to do is weed out so our body has these very efficient anti-cancer mechanisms where we go around and we're hunting down these sort of, you know, anarchists and stuff trying to these people who are not going to follow the rules, who are who are competitors, not cooperators. We try and hunt those down and we kill them so that we stay cancer-free. It's only at the end of, you know, only with time uh when stuff falls through or with chronic damage such as with lung uh lung cancer, for example, with smoking that that you're you're damaging the genome and those controlling organisms and allowing to shine through, which is called an activism, which explains a huge amount. Like that this theory just explains so much about cancer because if if you think about say let's take lung cancer again. So you have a 50 mutations uh in patient A, 50 different mutations in cancer in in patient B, but their lung cancers look exactly the same under the microscope. How does that happen? Like if you have a 100 mutations, your cell should look completely different than this other guy's cell, yet they look precisely the same under the microscope. It's because it was the original sort of cell. You're simply stripping stuff away. You're not adding mutations on. You're actually stripping those away. And what's fascinating is that the genetic So all this genetic stuff that we've done, when you look at the mutations of cancer, they're all concentrated in this area, it which is the the the the difference between unicellular and multicellular organisms. So they did these studies where they take all the genes and they say, "Let's rank them by evolutionary age." So these are the ancient genes, these are the recent genes, and they put them on and then they say, "Where are the cancer mutations?" And they're all clustered right around the point between unicellular and multicellular organisms. And like that is so interesting. So then of course the reason it's important is because now you have if this is an evolutionary problem, if these are actually unicellular organisms, well now we actually have ways to fight these unicellular organisms, and that's our immune system, and that's led to this sort of explosion in interest in immunotherapy because we're not trying to kill cells with immunotherapy. We're not trying to We're not trying to fix genetic mutations. What we're trying to do is treat these cancers like a foreign species, like an invasive foreign species, and be able to identify them and also bolster our own immune system to attack them. But now you're getting a totally different paradigm because you're the concept of what this disease is, it's an evolutionary disease, which requires immune system to fight it cuz that's our own defenses. That's fascinating. Like that's a totally different paradigm and such an interesting way to look at it and it's going to lead to all these new treatments. So in the book I talk about immunotherapy, we talk about the abscopal effect, which is how radiation plus immunotherapy may actually help unearth these things. We talk about adaptive therapy where perhaps you don't have to give maximally tolerated doses of chemotherapy because you may not need it. It may be more effective to use smaller doses. All stems from the understanding of the evolutionary paradigm of cancer as opposed to the genetic paradigm of cancer where you would never be able to understand why these treatments that are coming up now are going to be effective. Man, this this is really feels and you talk about sort of the hope this brings in the book and it really does feel hopeful, you know, cuz if you've pursued something to a dead end, it's like until you have another path to go down, it's a pretty ugly place to be. One of the things that you outline in the book that I thought was really enlightening is what it is exactly. The you you talk about the seed in the soil. So what is it about our modern life that creates this soil, that stresses the cell just enough that it is like sort of in scramble mode of whoa, I have to I'm constantly looking for this new mutation or stack of mutations that's going to allow me some path through this cigarette smoke, this dietary problem, this whatever. Um if you can walk people through what we've sort of done to the soil. And please, if you can, mention the when you talked about the bomb in in Hiroshima and Nagasaki, how they were expecting a certain cancer rate, but they didn't get it. And why that is. I thought I thought that so interesting. Yeah, I thought I thought so, too. [laughter] Thanks. Um this concept is that you need both genetics as well as the environment. Like both are important. I'm not saying one is more important, but you have to have a seed, which is obviously all the genetic material that you need to become a plant, for example. [sighs and gasps] But you have to plant it in the right soil. So, you take a seed, you put it in the desert, it doesn't grow. You put a seed, put it in proper soil, and give it water, it grows. So, cancer the seed is there in every single one of our cells. And not just us, but every animal practically that we know has that seed of cancer, because cancer, of course, is our sort of genetic ancestor. That was the unicellular organism from way, way, way back. So, that's Be selfish. Yeah, exactly. The selfish sort of the unicellular organism. But that seed of cancer is there. Luckily, if we prevent it from growing by using proper soil, we can actually prevent it. And you you look at these things that cause you know, cause cancer called carcinogens. Turns out our diet is one of the biggest ones. So, other than tobacco smoke diet is sort of way up there. And when you look at carcinogens, there's a specific sort of thing that have to be chronic, and they have to be sort of sub-lethally damaging, which is the point about Hiroshima. That is radiation we know causes cancer, for sure. So, when they dropped the atomic bomb, they thought, "Man, we're going to get a lot of cancers coming down the pipes, but it was a single large dose of radiation, not a chronic low dose of radiation, which does cause a lot of cancer. So, they did these atomic they did they did these studies where they followed people for for years and years and there was a little bit of extra cancer, but like on on average, way less. So, when they estimate how many months of you know, months or years of life lost, it was like two months, something like that. So, people these people were living like 82 years and they estimate that that that atomic radiation maybe cost them like two months of of life. Way less, cuz we are thinking that these people were going to get you know, cancers at age 20 sort of thing and that didn't happen because it wasn't this chronic thing. And that the reason it has to be chronic is that cancer is an evolutionary process. If you do not have chronic selection pressure, you don't get this change. If you just have one and then another the mutations and you need they're going to be random and they need to occur over time. They have to occur continuously because that's the way that selection pressure works in an evolution in a in a population of cells. That is, if you if you select for certain cells and do it once, that's not going to be that effective. If you keep selecting for those cells, like you only take the the the the the cells that are sort of survivalist, which are the the sort of more primitive cells, then you over time you're going to select the population that's going to have more of those sort of survivalist cells. If you have a single event, there's no further selection pressure. That is, if you look at you know, if you look at evolution of species, it's the same thing. You can't simply have one event. It has to be a continuous selection pressure that produces that change. And that's why it has to be a chronic thing. So, tobacco smoking for example, You look at viruses. So, if you have a single terrible virus, like hepatitis A, which is causes fulminant hepatic failure, it kills you, but it doesn't give you cancer, as opposed to hepatitis B, which is a chronic virus. It doesn't kill you, but it certainly does give you cancer. H. pylori in the stomach, for example, a very low-grade chronic infection is what gives you cancer, not a single sort of fulminant episode of of inflammation. That doesn't give you cancer. So, um you know, all of these these sort of things, UV light and so on, they're all chronic damage, and that's part of that soil, and diet plays a huge role. And the promise, of course, is that if you look at traditional populations, like when they looked at uh populations that lived very simply, so very low sugar, very natural foods, they weren't eating all the time, very little obesity, so people in Africa that they had studied, Dennis Burkitt in the '50s and '60s, and then in the Inuit people, which uh and live in the far north, for example, uh they used to send these expeditions up to the Arctic Circle to find why these these native peoples, these Inuit, were immune to cancer. Then, of course, they became civilized, we we gave them uh you know, sugar, we gave them white flour, because they didn't go bad, then they got all the same cancers. Turns out they weren't immune at all. It was their environment, it was the soil that was so important. But, the promise is that if you can fix that soil, that means you could actually overcome the genetics. Not in all cases, but in many cases, especially of these obesity-associated cancers, the breast cancer, colorectal, and so on. And that's the sort of really important thing, and the sort of take-home message for a lot of people is that the diet actually plays a massive role and by understanding it, perhaps you can reduce your risk of cancer and that's where fasting as a way to control your weight, as a way to control type 2 diabetes, which is a risk factor, as a those are going to lower the risk factor for obesity, which is a big risk factor for those obesity associated cancers, but it's your lifestyle that's going to play a big role, not necessarily some drug that's or anything like that. So, it's all in your own hands. It's amazing. That That is truly amazing. Now, as one sort of final point on this, is is the chronic stressor, is that simply being tipped into growth mode or is it inflammation coupled with the fact that we're tipped into growth mode? Like, what is it specifically about our diet that's causing this perfect soil for mutations over time um that leads to cancer? I think they're I think both are are correct. So, if you have uh chronic hyperinsulinemia, insulin is a very powerful growth factor. Uh inflammation as a cause of chronic damage in itself will cause cancer. So, you look at the disease such as ulcerative colitis or Crohn's colitis, these are called the the so-called inflammatory bowel diseases. There's this chronic inflammation in the bowel and what you get is a super high risk of cancer down the down the line. So, uh both inflammation and uh hyperinsulinemia and obesity, all of them are risk factors and and this is the important thing is that there's a lot of different things that can contribute to the risk of cancer. It's not just that if one is right, then the other is wrong. I mean, both are correct. So, if you eat foods that are highly inflammatory and a lot of people feel that, for example, omega-6 seed oils perhaps are in in these big doses that we take, perhaps those are highly inflammatory. That, even if it doesn't cause obesity, could be a factor because we know inflammation, chronic inflammation, can certainly do that. So, both can be very important. Whoo, man, I really hope people read your book, The Cancer Code. It it was very insightful. If people want to stay connected with you, learn more, follow your extraordinary clinical-based thinking, where do they go? Uh you can follow me on Twitter. Uh my handle's @drjasonfung. That's drjasonfung. Um also, uh my website is thefastingmethod.com. And you can also find me on YouTube. Uh my channel is Jason Fung and uh I have a number of videos on fasting um and and other things. Uh so, check me out there and you know, I hope uh you know, and then my books, of course, The The Obesity Code, The Diabetes Code, The Cancer Code. Love it. Awesome. Jason, thank you so much for joining me today. I really, really enjoyed our time together and I really enjoyed researching you as well. Um so super grateful. And speaking of things you'll be grateful for, if you haven't already, be sure to subscribe. And until next time, my friends, be legendary. Take care. Thank you guys so much for watching and being a part of this community. If you haven't already, be sure to subscribe. You're going to get weekly videos on building a growth mindset, cultivating grit, and unlocking your full potential.