Preventing Obesity: The Myth of Calorie Counting - with Dr. Fung | The Empowering Neurologist EP.156

So many of these academic doctors are like, yes, it's calories, calories, calories. So therefore artificial sweeteners is good because it's zero calories. It's like, okay, so let me ask you something. How many people have ever said, you know what, I switched to diet soda, lost 20 pounds? Like never, like nobody. Does not happen. The whole focus, this sort of obsession with calories has been highly detrimental

Well, hello everyone. I'm Dr. David Perlmutter. Welcome back to The Empowering Neurologist. Here's a question for you: what should we eat? And I ask that question in the context of the incredible increasing rates of obesity that we're now experiencing. It's expected that by the year 2030, 50% of Americans will be obese, not just overweight, but actually obese. There's been a lot of discussion in recent years about the value of a low carbohydrate diet and actually welcoming fat back to the table. And one of the pioneers in this whole idea of restricting simple carbs, highly processed foods, is Dr. Jason Fung, and he's our day— our guest today. This is an amazing book. That I'm going to tell everybody you need to read. This is a landmark book that really lays out what's going on in the human body and in the brain that relates to our continuing weight gain. What is the issue here? Is it really calories in versus calories out? Is fat the enemy? Sneak preview, no, it's not. And it's really all about hormones and most specifically about insulin. So, This is an important broadcast, and I'm very, very excited to welcome Dr. Fung to our program. Well, hello, Dr. Fung. Welcome to our program.

Hey, thanks for having me. This is great.

You know, I was saying before we hit the record button that we should have done this a long time ago. But on the other hand, I think it's good to visit this information now afresh in that I think it's really important for people to really get. What is the science here? You know, in terms of weight loss, because you know here we are, however many years later, and rates of obesity continue to increase in America. You know, we expect 50% of adults to be obese in the year 2030, and that's you know what is that eight seven years from now, and it's breathtaking. That's not just overweight. So let me ask you first of all: You're a renal specialist, a kidney doctor. Generally, we assume kidney doctors are going to focus on kidney disease, obviously, and perhaps hypertension, but you got into pursuing weight loss and diabetes. How did that happen?

Yeah, and it really came out of the kidney disease. So I trained at UCLA, and there was a lot of kidney disease, and the 2 biggest diseases, of course, were high blood pressure and type 2 diabetes. And it was Sort of, you know, as I started practicing, I sort of realized that it was not really doing very well. My specialty wasn't doing very well because the number of people on dialysis from kidney disease from type 2 diabetes predominantly was just going up and up and up. And the numbers were almost like never-ending. It was just a flood of people. And it occurred to me gradually that we were sort of chasing the wrong thing. That is, we had thought that type 2 diabetes Diabetes was a chronic and progressive disease, and and and it was on every every diabetes association had it. The American Diabetes Association said so; everybody said so. But even as they said so, I realized that it was really just a complete lie because everybody knew that if you lost weight, your type two diabetes would either get much better or go away completely. Everybody knew that, and we had studies on say bariatric surgery, and we knew people who had You know, developed type 2 diabetes and then they got serious, they lost weight, diabetes went away. So, I saw it every day. And so, this idea that it was chronic and progressive was basically a lie, even though everybody's saying it. And then it occurred to me that even if you think about the term diabetic kidney disease, it really tells you what you need to know. If you don't have the type 2 diabetes, then you won't get the diabetic kidney disease. So therefore, the best way to treat people was not to treat them after they got their diabetes, then they got their kidney disease, and then put them on dialysis. The best thing was to get them to lose weight, which was the sort of the root cause, then they won't get type 2 diabetes, then they won't get diabetic kidney disease, then I won't have to put them on dialysis. And so that's where I really started to get very, very interested.

Yeah, yeah, you've said a lot already. I really want to drive home a point here, and that is, that you as a kidney doctor began seeing more and more patients having to go on life— possibly lifelong dialysis because their kidneys had basically shut down as a consequence of this ever so common type 2 diabetes for which people are being told on television ads that take this pill and you'll get your A1C below 7 and everything's going to be great and you can continue to eat whatever you want and maintain a lifestyle that you choose as long as you're taking whatever that magic pill seems to be.

Well, exactly. And the key realization was that this, in fact, was a disease that was reversible, that you could put this into remission. And remember, at the time, it was a hugely controversial sort of thing to be saying as a physician, even though everybody I knew, like doctors knew it, patients knew it, everybody knew it, it was reversible. Nobody would ever say that. And it wasn't until 2021 until the American Diabetes Association put out criteria for remission, basically admitting what I had been saying for 10 years, which is that it is a reversible disease. Because the point is that if it is reversible and it's largely a dietary disease, then you need to fix that diet. Right. You cannot simply give drugs for a dietary disease and expect it to get better. So that's why I focused so heavily on trying to understand what causes weight gain, how are you going to get people to lose weight, and so on. And that's where I got very interested. And again, the other striking thing coming into the field was the incredible sort of lack of success that we had as physicians. Yeah. in getting people to lose weight. And that the predominant paradigm, which I was taught and pretty much all my classmates were taught in medical school about focusing on calories, calories, calories, a calorie is a calorie, count your calories, that paradigm had stunning, stunning rates of failure. Yet we continued to accept it as true. And scientific, and anybody else, anybody who said otherwise was sort of considered outside the orthodoxy. And I kept thinking, how strange that we accept— like, if a drug had a sort of 99% failure rate, like the counting calories strategy, we'd throw it out within 2 seconds, right? We'd say, this drug is garbage. Get it out of here. And yet, this sort of paradigm sort of lived on for 50 years, you know, not looking at the sort of quality of the diet and, you know, the macronutrients. It's all calories, calories, calories, right? So that was very, very strange coming in when I was actually looking at the evidence for myself.

I recall giving a lecture in New Jersey several years ago to a very mainstream group of physicians, and I asked the question, what's your go-to treatment for type 2 diabetes? And people raise their hand, you know, sulfonylureas, metformin, insulin, which we'll certainly talk about, and other various drugs. And I said, put your hands down because please understand you're not treating diabetes, you're treating the blood sugar, a manifestation of the underlying problem. You know, the high blood— the drugs we use to treat hypertension aren't treating the underlying problem. They are treating the symptom, the manifestation, which is the hypertension. You know, and what you talk about in this and your other book, The Diabetes Code, is basically about finally approaching the underlying problem, which is insulin resistance. It's very popular today to treat type 2 diabetes with insulin. And what Dr. Noakes said in the— in your introduction or your forward to your book, he said it's like treating the alcoholic by giving them alcohol. And, you know, he— that hit the ball out of the park for me. Um, you know, I have a lot of love and respect for his work. And when he did that, I just— because he does, you know, he does not hold back. But so what's wrong? Why are people getting all this wrong? What's, what's changing their minds in favor of thinking that all they need to do is take their pills and their insulin and everything's going to be fine?

Yeah, I think that it was the sort of— again, it was what I was taught and everybody was taught, that you just give insulin And you're absolutely right. What we did was we confused the symptom, which was the high blood sugar, for the disease, which is sort of type 2 diabetes, right? So, you have type 2 diabetes as a disease which causes high blood sugars. And we treated the symptom with the high blood sugar with insulin and it got better. But the problem was, and patients knew this, right? This was the stunning part. Patients knew that if I gave them insulin, Their sugars got better, but they gained weight. So, as they gained weight, they came back to me and said, hey, doc, you gave me this insulin, I gained like 30 pounds. How is this better?

Yeah.

So, they knew that this was actually a vicious cycle, right? So, you gain weight, you get type 2 diabetes, you get insulin to lower the blood sugar, right? Not treat the type 2 diabetes, but lower the blood sugar, which is the symptom. Then you gain weight, which makes your type 2 diabetes worse, which makes me give them more insulin, which makes them gain more weight. And you see how it's going, right? They're spiraling into the drain. And for years, I had no answer to why this was wrong because I believed that it was the right treatment, as did everybody else, of course, until I realized it's actually the wrong treatment completely. Because a couple of things struck me. One is that Type 2 diabetes is a disease of hyperinsulinemia, right? Insulin resistance, hyperinsulinemia, they're very much the same thing. And why would you treat a condition of too much insulin with more insulin, right? It makes no sense at all. It's completely wrong. If somebody has an overactive thyroid, you don't give them thyroid replacement because that's the wrong treatment. So, So if your insulin levels are high, you should actually lower insulin, not make it higher. And after a while, it just seemed like that seems such a wrong thing. I mean, and mistaking the symptom for the treatment is very easy to do, but it's completely wrong. So it's sort of like if you have an abscess or an infection and you get a fever, the fever is caused by the infection, right? The fever is symptom. So you can treat the fever with acetaminophen, but everybody knows that ain't going to make you better. That's just symptomatic treatment, right? You can lower the fever, but you need antibiotics, right? Same thing. You've got to—

but in actuality here, this is making it worse. It's not even just avoiding the treatment. You're actually making the situation worse by giving them insulin, causing more weight gain, ultimately increasing their leptin resistance, will We'll get to that later, but it's a terrible pun, but it's clearly a feed-forward cycle that's making people worse. And who benefits from this? The pharmaceutical companies.

It's ultimately the pharmaceuticals, yeah. And the cost of insulin had been going up a lot, right?

Yeah, yeah. Well, that's— gosh, it's entered even the— at least here in the States, you're in Canada— it's entered the politic about, uh, Allowing people to get their insulin. Gosh, they shouldn't. God forbid they wouldn't get it for for a lower price. Let me let me wind the tape back a little bit because in many years ago, probably about fifteen years ago, the data started coming out about the relationship between type two diabetes and Alzheimer's. So that obviously piqued my interest, with data indicating that with type two diabetes there was up to a fourfold increase of an a condition for which we have no pharmaceutical treatment, Alzheimer's disease. And I began looking at those statistics and looking at the statistics that related to risk of developing Alzheimer's based upon your average blood sugar or the A1C. And I really came to a very similar place as a neurologist that you came to as a nephrologist that, you know, yet another complication of type 2 diabetes related to the foods that we are eating. And I sure know what it's like to be looked upon as being the outlier and outside of the box. And I've always said, well, maybe the work we're doing is outside the box. The mission though is to make the box bigger. I mean, that's what you're doing in your book is to be more inclusive. And the other thing I'll say before we really dive into everything is that people might be critical of these Perspectives that we offer up, but your book is there. There's not a statement that's not referenced in peer-reviewed science. There's a there's a study for everything. There's a study, you know, indicating how or several studies how when we cut calories, we have we are confronted by an equal reduction in our metabolism. So there's no change. And you know that that's I think a very valuable lesson for people wondering why gee whiz I've cut my calories so substantially and I still don't see. Seem to be losing weight. But, um, the last thing I want to bring up, I don't want to forget, is we turn to our doctors because they're educated and they have the answers. They're going to tell us which drug to take, etc. You ask the question in your book, then why are there fat doctors? I, you know, I— you asked it, I'm going to put it out here on the podcast. I thought it was great because, you know, it's not a question, do as I say, not as I do. I mean, if you're— if you want to teach and and lead by example, then this is what you've got to present to people. Look, it works. I'm doing it for myself. So let's now look at some of the dynamics, the mechanisms of insulin. We've described now how type 2 diabetes is a situation in which there's excess insulin because the cells are less receptive. We've become resistant to what insulin is trying to do Let's go a little bit deeper into that mechanism and how that ultimately translates into weight gain.

Yeah, so insulin resistance is a very interesting thing because this is basically the sort of cause— like, that's the underlying problem in type 2 diabetes, insulin resistance. But I think it's actually sort of not a great name because I think a better name is hyperinsulinemia. Insulinemia, because there's 2 ways of looking at it. And so what we know is that if you have type 1 diabetes, for example, you have insulin and its job, one of its jobs, is to move glucose from the blood into the cell and the cell can therefore use the glucose for energy. If you don't have any, and, you know, and people talk about it like a lock and key, right? So insulin is a hormone, it's like a key, it goes to the cell surface like the liver cell, for example, interacts with the cell receptor, cell surface receptor, sort of, which is like a lock. It opens the lock, the gate opens. Now glucose can go into the liver cell and the liver can use that for energy. So that's great. So in type 1 diabetes, of course, there's no insulin because the pancreas has been destroyed. So therefore, the gate is closed, the glucose in the blood stays high, but inside the cell There's nothing. There's no energy. So people, kids, right, untreated, would just keep losing weight until they died. And it didn't matter how much they ate because that glucose, that energy, those calories couldn't get into where it needed to go, which is the cell. So that's fine. And type 2 diabetes, of course, is a completely different situation. What you have is plenty of insulin, and the insulin that's circulating is normal insulin. It's not defective in any way. So the key is sort of normal. Then you can look at the cell surface receptor and you can look at the lock and you can look at it and say it's completely normal as well. So then why is this glucose, why is this gate, you know, not allowing this glucose to go in? And the idea was that, hey, maybe there's like a piece of gum in the lock, right? There's something that's gumming up the lock. So even though the key and the lock are there, you can't open it up and so on. But there's a problem. And that was the sort of predominant paradigm, this sort of underfill. So there's a piece of gum, the lock is therefore still closed, the gate is closed, the blood glucose is high, but inside the cell there's no energy. This is an underfill or a sort of situation of internal starvation. The problem is that it didn't fit any of the proper sort of clinical phenotypes. That is, People weren't skinny; they were really, really fat, and they had big fatty livers. So you know that's strange because if your glucose is not getting into your liver cell, why is your liver full of fat? Right? It didn't make any sense. It's the complete opposite of type one diabetes. So what we knew is that there was insulin, but there was also a lot of glucose. So the alternative explanation, because there's always another way that it can happen, is that it's not. Underfilled, it's overflowing. That is, this liver cell, it's not that there's too little insulin, too little glucose, there's too much. So over time, you have too much glucose, too much insulin, you've shoved all this glucose into the insulin— into the liver cell, and now it's sort of bursting, it's full, and therefore you can't push any more in. Sort of like if you have a bar, it's Super Bowl Sunday, the bar is full, you can't push any more people in. But not because the door is closed, but because there's simply too many people there already. So the problem is that you've already put too much glucose into that cell, and therefore you can't push any more in. And therefore, the body produces more insulin to try and shove more in, which works temporarily, but then it can't do that. And, you know, you have to produce more and more insulin to keep shoving more in. So that's the sort of overflow hypothesis. Okay. Of insulin resistance, which is really looking at it as a disease of too much glucose, too much insulin, or the disease is hyperinsulinemia, which makes a lot more sense. And it in fact explains everything about type 2 diabetes because that's why you have obesity associated. That's why you have fatty liver. That's why when you lose weight, you are going to reverse the type 2 diabetes because you can't explain it with the sort of underfill hypothesis. Right? So if it's overflowing, then it's a different situation. Now, if you look at these diseases— obesity, type 2 diabetes, Alzheimer's— as diseases of hyperinsulinemia, that sets you up immediately to ask the right question. If my insulin is too high, how am I going to lower insulin? Because that is the root cause, and that is how I am going to be successful. And one of the ways would be to reduce Carbohydrates because carbohydrates are glucose, and carbohydrates stimulate insulin where proteins and fats do not. For example, and in fact, now you have the studies these days looking at you know low carbohydrate diets. There's more and more studies in the treatment of type two diabetes. Some have been extremely successful. I mean, even the American Diabetes Association says low carbohydrate diets have the most scientific evidence behind them for. Reversal of type 2 diabetes. And then the other way to lower insulin, if the disease is too much insulin, how do you lower insulin? So one is to change the foods that you eat, to eat lower carbohydrate containing foods. And the other is intermittent fasting, which is sort of a natural solution. If you don't eat, your body will simply burn off the excess glucose and therefore, You're going to be able to reverse your type two diabetes. So, in fact, again, just just this month, actually, two randomized control trials looking at intermittent fasting and type two diabetes were both extremely positive. Almost fifty percent remission rate of type two diabetes. If you think about the millions of Americans who have type two diabetes, a fifty percent remission rate is absolutely stunning. Like this is a treatment which is free, which is available to anybody, which has been used for thousands and thousands of years. There's nothing to stop them, 50% of them, from actually reversing the disease completely. And that's stunning.

Well, it's not like we haven't heard parts of this story for many, many years. I mean, we can all think back of Dr. Atkins' books, of Pure, White, and Deadly by Dr. Yudkin in 1975, for example. Our grandparents told us that, you know, sugar and starch is what's making you fat. We've— humans have always eaten fat for an awful long time, and by our nature as hunter-gatherers in Paleolithic times, we underwent— it's not like we tried to fast intermittently, but that was just part of the, you know, part of our lifestyle. It certainly has taken off as of late, though, the notion of intermittent fasting, and And certainly ketogenic diet as well. We've had on the program Dr. Sarah Hallberg, who reported just remarkable success in terms of getting people off of their insulin and their sulfonylureas, drugs used to treat diabetes, by putting them on a very strict ketogenic diet. So what is it about— first, why was fat so demonized, and why were we told that fat was the enemy? And then we'll get in a moment to why we should reconsider.

Yeah, I think it's it's an interesting story. I think, and I think that it's it's sort of this started with the dietary guidelines for Americans in 1977. I think where Yudkin and others were sort of like, hey, it's the sugar, whereas Ancel Keys and so on were hey, it's. Fat. And the whole story of the fat was simply that Americans in the '40s and '50s were getting a lot of heart attacks for no specific reason. It's like the rate of heart attacks was going up and nobody knew why. When they looked back, it became sort of obvious. They were smoking a lot more, right? And smoking caused a lot of heart attacks. So, they were getting heart attacks. So, no big mystery, right? Through the world wars and everything. So, The problem was that at the time, of course, the tobacco companies strenuously denied that it caused any kind of heart disease. So, they needed something to blame it on. And I think Ancel Keys believed very strongly, and he was very influential, that it was dietary fat. Although the rate— the amount of dietary fat in the American diet didn't change from 1900 to 1950. So it's hard to imagine why eating the same amount of dietary fat all of a sudden spiked your heart attack rates if it was causative, right? But nevertheless, he was very persuasive and his view sort of held out. And then, you know, in science, there's always a back and forth. But, you know, when you have official pronouncements like the dietary guidelines in 1977, they basically just said, nope, Fat is the enemy, and everything had to change to conform to that view. Right? And everything else, if it was if you're sort of like Atkins and saying, "Oh, it's probably the starches and the sugars," you know that didn't fit the narrative. So you got sort of marginalized, which is unfortunate because that really stifles scientific debate where legitimate points of view could be brought to mind. So that's the idea that hey, dietary fat can cause. Heart disease, which prevailed through the '80s and '90s. So as I did my medical training in the '90s, we used these American Heart Association— you may remember this— the Step 1 and the Step 2 diets, right? So if you had a heart attack, you got a Step 1 diet, which was like, I think, 10% fat, total fat, which is quite low actually.

And 2 grams of sodium.

Yeah. And then if you had another heart attack, which they usually did, Then you went to the step two diet, which was seven percent total fats, which was really like eating cardboard. And it and and this was thought to prevent heart disease. Turns out when they actually did these sort of studies head to head, they did terribly. These low fat diets did horribly. Remember, there's the Lyon Dietary Trials, and and and and there's the whole French paradox where hey, how come the French people are eating all this butter? And cheese and they're getting half the rate of heart attack. That was a huge paradox, right? It turns out dietary fat wasn't really the culprit. And then through the 2000s, we started to discover, hey, Mediterranean diet's pretty good and nuts are very good and olive oil is very good, all these fats, right? So then we had to bring the whole thing about fat back. So that was where fats got demonized. It was through this sort of just this one pronouncement in 1977 that fat is the enemy. All science must now conform to this. And what happened, I think this also ties into the story of intermittent fasting, is that as people ate all their sort of white bread and jam for breakfast, what happened is that they didn't replace their fat with sort of broccoli. They replaced it with refined carbohydrates. So we know now that if you're eating a whole bunch of, you know, sugary cereal or white bread and jam, what happens is your glucose spikes up, your insulin spikes up. By 10:30, it spikes down, you're ravenously hungry. So now you're looking for your low-fat muffin, which did the same thing. It spiked up your glucose, spiked up your insulin. By 12 o'clock, you're ravenously hungry. So now instead of eating 3 times a day, which people were doing in 1977, they were eating like You know, 6 times a day, 8 times a day. But they're saying, hey, I'm eating the right food. So therefore, eating frequently must be good. So then, this sort of got entrenched that, hey, you should eat 8, 10 times a day, which was the situation I was going into in 2012, 2013 when I was saying that, hey, you should really be eating less often. And people thought I was completely off my rocker. They're like, no, you got to eat 6, 8, 10 times a day.

I hope you are because I know I am.

They sort of went hand in hand. People thought the idea of not eating for more than a couple of hours before stuffing a muffin in your mouth was really unhealthy for you. There's this whole idea that, hey, if you didn't eat breakfast, you're going to kill yourself. It's better to go stuff a donut in your mouth instead of not eating anything. I said, this makes no sense, right? How are you going to lose weight while you're eating all the time? When you're eating, your body wants to store those calories. It's only when you don't eat that your body uses those calories. And it's basic sort of first-year medical school stuff, right? When you eat, insulin goes up, your body stores energy, right? You turn off breaking down of— you turn off lipolysis, you turn off glycogenolysis, right? So you can't burn fat, you can't burn glycogen. You turn on de novo lipogenesis, so you're actually creating new fat. You're laying down more glycogen. That's normal. That's what you're supposed to do. It's only when you don't eat, insulin goes down, and your counter-regulatory hormones go up—growth hormone, noradrenaline, sympathetic nervous system—that's when you break down fat. That's when you break down glycogen into glucose. So, you know, the human body knew what to do with. energy. Otherwise, we wouldn't be sitting here in 2022. We would have died like long ago in the, you know, in the caveman days.

I'm puzzled why we are sitting here in 2022 having this discussion, and it still seems a little bit outlandish. I mean, I think many people, maybe not as many people watching this podcast, but in general, this type of information is so counter to what continues to be parroted in the mainstream, that if you just simply cut back on your calories, you're going to lose weight, uh, based upon the laws of thermodynamics. And to this day, we have low-fat, uh, cookies and the low-fat aisle in the grocery store, and you still see products labeled in hopes that they will sell as being low-fat, despite the fact that they're high in sugar. And I recall back in 1995, you actually characterized it in your book, that the American Heart Association was recommending soft drinks and fruit punch because they had no fat. That's what we should be drinking. And then we saw the rise of understanding the threat that sugar posed, and, and in response to that, the, the rise of the artificial sweeteners, the artificially sweetened, uh, soft drinks, for example. And you unpack that in your book as well, that that's not an answer for us.

Yeah, because it's not really the calories. And this is the sort of where everybody sort of gets bogged down. It's like, if it has no calories, it must be fine. It's like, no, it's not necessarily fine. Because if you're still stimulating sort of the sweetness, you're still stimulating insulin, you're still stimulating your appetite, for example, then No, taking these artificially sweetened beverages is not going to be the answer. I mean, and really this is where sort of getting out of the ivory tower is very useful because so many of these academic doctors are like, yes, it's calories, calories, calories. So therefore artificial sweeteners is good because it's zero calories. It's like, okay, so let me ask you something. How many people Yeah. Have ever said, you know what, I switched to diet soda, lost 20 pounds. Like, never. Like, nobody. Does not happen. It's far more frequent that I say to somebody, get off all that diet soda, because they're drinking 10 a day, and they're like, oh, all of a sudden I lost like 50 pounds because I'm not stimulating my appetite anymore, so therefore I'm not eating all the time, and therefore, you know, I'm losing weight. So it's like this is, you know, the whole focus, this sort of obsession with calories has been highly detrimental. And it's a very strange sort of situation. And I think it's, you know, it's an easy, as I mentioned in The Obesity Code, it's sort of an easy target, right? Because all of a sudden you're changing the complexity of sort of obesity, which is really a hormonal disease of hyperinsulinemia, as well as other things, into something extremely sort of, it's just calories, therefore it's just willpower. And it gets back to the question that I came back at, which was originally like, well, why are there fat doctors? And everybody thinks that's an insult, but it's not. Most of my friends are doctors, right? These are like very smart people. Very like they don't lack for willpower. When they set their mind to something, they do it. So if you have the knowledge and the willpower to do it, why can't these people lose weight? The only the only way that happens is that the information that we all believed, myself included, right? I mean, you know, was not correct. This idea that calories are the sort of be-all and end-all, and it still pervades through academic circles, right? That's that's all you hear about is calories. Even now, even now, and interestingly, the public has sort of moved past that because they've seen the sort of folly of these calorie-reduced diets. So even as those academics are claiming, oh, it's all about calories, all about calories. Everybody else in the world knows that you can't just count your calories. You can't. And this is where I remember there were doctors that were saying things like, you can eat ice cream for dinner because if you eat ice cream and it's 1,000 calories and it's the same amount as your steak and salad, it's the same. And I always thought, if you told your grandmother that, she'd say, you're completely off your rocker. If you think eating ice cream for dinner is the same as eating real food like steak and, you know, a salad or something like that, right? And I'm like, crazy.

Well, in terms of calories though, there is this idea that, oh, if I eat the ice cream, I'll just exercise more, and therefore it'll be a net neutral and I'll— I won't gain weight, maybe even lose weight if I can Just keep exercising. And this comes to mind when I— at my gym, when I, I see people who are clearly significantly overweight just pounding the treadmill day in and day out. And they're the same people that have been there for the past couple of years. And, you know, I'm just, as an observer, not seeing any significant changes in their morphology. And there is this notion that if I can burn more calories, I'll lose weight.

Yeah, this focus on calories is, is very strange. And that's why I said it's really a hormonal imbalance. Not a caloric imbalance. Because think about it this way. So there's— you have 2 foods. So one food is, say, salmon, for example, or eggs, uh, and another food is cookies. Okay? So you have the same amount of calories. So say 200 calories of eggs versus 200 calories of cookies. The minute you put those foods in your mouth, the hormonal response to those 2 foods are completely and utterly different. We can measure them. Easy, right? One of them glucose spikes way up, the other one it doesn't spike up at all. One of them insulin spikes way up, the other one it doesn't spike up at all. So we know that insulin is going to spike with the cookies. If you, you know, if insulin is going to then take those calories, that energy, and put it into storage because that's its job, right? That's what it's supposed to do. We know that it stops burning of fat and puts, you know, lays down more fat. So you're going to take those 200 calories, you're going to put it immediately into Well, what's your body going to use for energy? It has nothing. So, what's going to happen? Well, your body's going to say, hey, I still need some energy here. Go out and eat some more, right? Whereas with the eggs, your insulin's not going to spike up. You have all that energy to use for storage. So therefore, you're not going to be hungry. And everybody knew this, of course. If you ate eggs for breakfast, you're full until lunchtime. If you ate white bread and jam for breakfast, you're hungry at 10:30. Every person knew this already. The physiology was fully worked out, but it's not about the calories because the calories are the same. It's about the hormones that are precipitated by eating those foods are different. And you have to pretend that the hormonal difference is completely irrelevant to say that we shouldn't be looking at the types of food that we are eating in addition to the calories. I'm not saying calories is not important, but it's not nearly as important as we think it is. In fact, you know, of course, most ancestral peoples never counted calories.

Well, it's been said that nobody binges on avocados, and I think that gets back to what you're talking about. Let's, let's look at that in a little bit more depth. The hormones of satiety. How do we know when we've eaten enough? How does that compare eating a high-carb meal versus versus a higher-fat, lower-carb meal.

Yeah. And that's very—

That's from the hormonal perspective.

Yeah. That's very interesting as well because this is the same notion. If you eat highly refined carbohydrates like white bread, we know that there are very powerful hormones in our body to tell us to stop eating. So, if you go to a buffet, you can only eat so much. You can't keep eating indefinitely because you're going to be nauseated or whatever. Right? If you've eaten until you're well overfilled and then somebody says, hey, why don't you eat this pork chop? You'd be like, I don't think so. Right? But that's the same pork chop you ate at the beginning of the meal. So, it's not the food, it's the hormones that are telling you that, hey, you shouldn't be eating anymore. So, those satiety hormones include things like peptide YY, which is in response to protein, cholecystokinin, which is in response to dietary fat, And if you have a lot of bulk in your stomach, you activate stretch receptors in your stomach, which again tell you not to eat. So therefore, those are very powerful stimuli. You can't just override them. It's like those restaurants that say, eat a 60-ounce steak and we'll give you a free steak. They're not giving away a lot of free steak. So the point is that if you eat highly refined carbohydrates like the white bread and jam, there's no protein. There's no fat and there's no bulk because you've taken all that bulk out. You've taken all the fiber out. You have no satiety signaling. If you eat steak, you've got protein and you've got fat. So you've got a lot to keep you full. Therefore, simply eating the white bread and jam, you can just keep eating and eating. And that's why when you— after you've eaten your all-you-can-eat buffet, Somebody says, hey, do you want to have some cookies or ice cream or other highly refined carbohydrates?

Give me 2.

Yeah, it's fine. And as kids, we used to say, hey, I have a second stomach for desserts. The truth is that those foods, or if you drink some soda or something, you can certainly drink soda. You could drink 500 calories of soda after you've eaten all that because there's no satiety signaling at all. So therefore, you can just keep pounding it in, which of course is a problem if you're trying to lose weight.

So we're leading into the leptin discussion, and I'd like to lead into it by a quote that you put in your book from our friend Gary Taubes, who said something along the lines of, we don't get fat because we overeat, we overeat because we're getting fat. And the more fat we have, the more leptin it seems that we have, and the less sensitive we become To leptin, a hormone that's telling us to back away from the table. So how does that integrate into what we're talking about?

Yeah, so leptin is an interesting hormone because it sort of went through its heyday in the sort of late '90s. And the way it works is that if you gain body weight, so body fatness is actually tightly controlled, it turns out. If you are in the wild, for example, if you are too fat, you're not going to survive because you're not going to be able to catch food or somebody will eat you, right? So, body fatness is actually very tightly controlled. If you get too fat, your fat cells release leptin. The leptin goes to your hypothalamus, which tells you stop eating. And therefore, it's going to, as you stop eating, your weight is going to go back down, your body fatness is going to go back. So, it's a homeostatic sort of relationship. And so people thought that giving leptin was going to be the cure for obesity. Turns out obesity is not a leptin deficiency state, so therefore you simply cannot just give more leptin. It's a leptin resistance state. That is, your body has leptin, it just isn't signaling it properly. And probably one of the things that is a problem is that if leptin Or any hormone, right? Any hormonal system, any body system. If something stays high and stays high for a long time, your body develops resistance to it, right? And it happens in all biological systems. If you're listening to loud music, you get a little deaf. That's your way, your body's way of protecting yourself against the loud noise. If you go in a dark room and you go into light, all of a sudden it's very, very too bright, right? Because your body's trying to protect yourself from the darkness. And the same thing, you know, all the way through. So if you have continuously stimulating leptin, then at some point your body just stops resisting. So if you keep eating, so it's almost like a seesaw between insulin and leptin because if the insulin keeps making you, you know, if you have hyperinsulinemia that's keeping your weight up, now all of a sudden your leptin is always high, you're going to develop the So therefore, you can't simply just give leptin to reverse the situation. The only thing you can do is try to sort of lower the leptin by getting the body fat down. And that's a lot of hard work, right?

It's a lot of hard work, but insulin is working against you in that— in terms of achieving that goal.

Yeah, exactly. So, the insulin is sort of trying to make you fatter versus the leptin, which is trying to make you leaner. So, it's sort of the seesaw balance. So, it's very hard to affect it on the leptin side of the seesaw, whereas it's a lot easier to affect it on the insulin side of the seesaw because the foods you eat and how often you eat are going to play a large role in how much insulin you secrete, whereas you can't do the same thing and say, well, I'm going to eat this and leptin is going to go up or down or So in that seesaw between insulin and leptin, you almost have to go on the side of— you have to change it based on your side, which is the insulin side. You can't change the sort of leptin side because that's sort of automatic.

So, Dr. Fung, in your book, of course, you talked about sugar extensively and refined carbohydrates, but in the sugar department, you specifically called out fructose or fruit And why don't we explore that a little bit? What is so threatening about fructose as a sugar?

Yeah, fructose is really an interesting molecule because for years people thought fructose was actually good for you. So the thing is that there's 2 types of sugar. So there's more than that, but there's 2 main ones: glucose, which is what you find in most carbohydrates. So, if you have bread or rice, they're chains of glucose and they're in chains called amylose or amylopectin and they get broken down into glucose. And that's why if you eat bread, your blood glucose or blood sugar goes up because it's glucose. If you eat 100% fructose, for example, then your blood glucose does not go up at all. So, people thought, hey, this is really good. But eventually, it turned out that people realized that, hey, it was really bad. Okay. People who use, say, high fructose corn syrup, which was this artificially fructose-enriched substance. Table sugar is sort of 50% glucose and 50% fructose. It turns out that it's in the way that the fructose is metabolized that it's so bad for you. So even you can't see it in the blood glucose, but the fructose cannot be metabolized by any cell in the body other than the liver. So, when you eat bread, you get glucose. Every cell in your body can use that glucose. So, if you take too much glucose, your brain is going to burn it, your heart is going to burn it, your kidneys are going to burn glucose. If you get a fructose load, none of the other organs can actually burn that fructose. So, instead of having like 150, 180 pounds of body burning glucose, All of that fructose goes purely straight into the liver, right? Which is like a you know a ten-pound organ or less. So therefore, the the liver then has to decide what to do with it, and it gets metabolized either into glucose, but then your body has glucose, so it doesn't turn it into glucose; it turns it into fat. It stimulates de novo lipogenesis, which gives you fatty liver, which then You know, worsens this whole cycle of insulin resistance. So the key organ in metabolism and a lot of metabolism is the liver. And it's going sort of straight to the liver. It's like a guided missile that goes straight to the liver and causes a lot of havoc right at the liver. And that's why it's so bad for you. And I don't think any nutritionist these days much disagrees that sugar is actually one of the things that we should be cutting out. There's other problems too with it. The added sugars, for example, we know that when you eat them, it lights up a lot of the dopamine reward systems in the brain, for example. So you get rewarded. Of course, that's why people eat sweets. But then it can set up things like food addictions and that kind of thing. But yeah, fructose, because it goes straight to the liver and sort of wreaks havoc on the liver specifically, It's just much, much more likely to give you problems with type 2 diabetes than just glucose.

Well, you know, fructose doesn't stimulate insulin production and does not require insulin for its metabolism. I think that's why early on that was the sugar of choice as it related to diabetes, because it didn't interfere with this whole insulin cascade. That you're talking about. So should we not be eating fruit?

I think that fruit is like, you know, it's sort of one of these things that is here and there. Like, fruit has fructose, which is chemically no different than the high fructose corn syrup or table sugar that you get. It really comes down to sort of how much fruit it is, how much fructose it is. So a lot of the Fruits these days are sort of engineered to be much sweeter than they used to be, so then therefore we're getting a higher load of fructose than before. If if you're if you're also taking a lot of glucose with it, for example, then there's not that runoff pathway where you can take turn the fructose into glucose. So fruit is probably not the best thing to be eating if you're trying to lose weight or. Reverse your type 2 diabetes. For other people, you know, there are fruits that are probably lower in fructose, which may not be as bad for you. A lot of the berries and stuff, for example, may not be bad. But yeah, I would probably limit the fruit. I don't think it's nearly as good for you as people had imagined it to be, just because it is there. On the other hand, it has vitamins, it has minerals, It also has fiber, so that prevents you from overeating it as opposed to drinking fruit juice, for example, is going to be much worse because there's nothing to stop you. There's no satiety signaling there, so there's nothing to stop you. It's easy to drink a glass of apple juice, not so easy to eat 5 apples, for example, because there's other things that are going to stop you from eating it. Fruit is sort of a mixed bag. I would be careful on fruit.

I was at breakfast the other day at a restaurant in New York, and, you know, you can't help but look at what's going on around you. And a man and his wife were at the table next to us, and he got a cup of coffee and asked for artificial sweetener. I don't know whether it was pink or blue, but he put it in his coffee and then had several glasses of orange juice. I mean, orange juice fruit juice in general has about 36 grams of sugar in a 12-ounce glass, and he went through a couple of those. So that's about 14 teaspoons of sugar. And yet he didn't put a teaspoon of sugar in his coffee, so I guess that's a good thing. But it's really, um, I think valuable for people to recognize that there's a big difference between drinking a glass of concentrated sugar in the orange juice versus having an orange or an apple. And I think your points are very well taken. Let me say thank you for spending time with us today. Your information is so valuable, and I think the main thing that you've done is, you know, validated what's really going on here with an incredible work of science. So I want to say just thank you for being here today.

Thank you so much, and thank you to you too for also for also sort of bringing, shedding light on this entire, you know, debate because I think you're, you know, the books you've written, the stuff that you've done have really, I think, helped a lot of people sort of understand that, hey, it's a lot more than just the calories here. And that translates into sort of directly actionable advice that people can take to improve their health. So thank you also for, for all you've done.

Great. Well, we'll talk soon. Bye for now. Thanks again.

Okay. Thank you.

Bye. Wow. That really told it like it is, didn't it? We recognize that this whole notion of calories in versus calories out— in other words, if you can burn more calories than you take in, you're going to lose weight. Is really interesting, but it's not founded on any science whatsoever. The fat phobia that made its way into our lives over the past 3 decades is based on really no science whatsoever, and that it turns out that insulin signaling is primarily the issue as a life-saving issue in terms of why we gain weight. You're telling your body, make and store fat for the upcoming time of food scarcity. scarcity that obviously doesn't seem to be coming. It is central to why we are continuing to gain weight and the ever-increasing rates of obesity. So if you want to rein in your weight gain and in fact lose weight and regain control over your blood sugar, this is a great book for you. The Obesity Code, as well as The Diabetes Code, also by Dr. Jason Fung. I'm Dr. David Perlmutter, and I thank you for joining us today. On The Empowering Neurologist.