Surprising Weight Loss Tips | Dr. Jason Fung

Resistant starch is this really interesting thing.

Your brain can literally make your body make sugar. There's not hyperbole there, that is literally what's happening.

That one of the ideal sort of weight loss drinks.

What is better for blood sugar control, a hot baked potato or a cold potato salad with vinegar?

It's a great hack if you're trying to reduce the amount of glucose and insulin effect.

It'll taste the same. But the impact on your blood sugar and insulin will actually be lower because of this.

With weight gain, again, it's really all about the hormones.

Everyone back here with part 2 with Dr. Jason Fung, all about controlling hunger as a means to control weight and obesity. Part 1 was chapeau bloc with, um, great high-level overviews of different types of hunger. We went over homeostatic, hedonic, conditioned hunger. So you should listen to part 1 to get some tips and tricks from his new book, The Hunger Code. Which is a fun read. I actually want to get into some more tips and tricks drawn from the book that I found quite interesting. And the way I want to frame this is I'm going to ask a question and I want viewers to either pause the video or think to themselves what the answer is, or even guess in the comments what the answer is. And then Dr. Fung is going to reveal what the correct answer is. So I'm just going to kick it off with the first question. For weight loss, is it better to eat freshly cooked rice or rice that's been cooled and reheated? Dun dun, cue the Jeopardy music. Hopefully people have their guesses. Jason, what's the answer?

The answer is the cooled and cooked rice. And the thing about this is that it's all about resistant starch. Resistant starch is this really interesting thing. So starches are chains of glucose and they come in different forms, amylopectin and amylose, which also makes a difference. But when you cook the rice, then cool it, and then reheat it. What happens is that upon cooling the, so when you heat the rice, it becomes sort of fluffy, right? It's not hard like when you have cold cooked rice, and that's because it gelatinizes and that sort of semi-melts. And then when it cools, it recrystallizes in a structure. That's why it's hard and brittle and you really can't eat refrigerated rice straight. But what happens is that the nature of that glucose becomes a different, it, it's, it's formed differently into different crystals and they don't get absorbed. So that's called resistant starch because it's a starch, but it's resistant to absorption. So your body actually doesn't, doesn't absorb it at all. And then when you reheat that rice, some of that resistant starch remains even though it tastes perfectly normal. So it's, it's a great hack if you're trying to reduce the amount of glucose and insulin effect of that rice, because you can simply cook it, cool it, put it in the fridge or freezer, and then bring it back out and heat it, and you're gonna get less glucose effect and less insulin effect. And, you know, with, with weight gain, again, it's really all about the hormones, you know, but the insulin is one of the major ones, and that's gonna be reduced. So this resistant starch is a really interesting phenomenon. Works— doesn't work for potatoes. So if you cook, cool, and then reheat potatoes, All of that resistance starch just basically goes away. But if you cook the potato, cool it and eat it cold, like in potato salad, you actually also reduce that. Okay.

So to sum up, with rice, you want to cook it, cool it, and then reheat it. It'll taste the same, but the impact on your blood sugar and insulin will actually be lower because of this resistance.

Yeah.

How much is the glycemic, like, index reduced? Is there a number you can put to it?

The studies show that there's about a reduction of about 20% in the, you know, depends on what you're measuring. So either glucose or insulin effect, but it's around 20%. So it's substantial considering that it tastes actually exactly the same. I know because I, that's, I do that all the time now. So when I cook rice, what I do is I put, I cook a bigger pot and then I put little bits into the freezer and it stays good for months, right? And then that way I, one, I don't have to cook it again, but two, when I actually I want to eat, I'm actually getting the resistant starch along with it, which reduces that sort of insulin effect.

Wow. That's cool.

Tastes exactly the same.

All right. Real quick, a teaser. After this interview, I was curious and provoked, so I did a deep dive on resistant starch. There's gonna be a letter on it, which I'll link below, but Dr. Fung is dead right. In fact, there are blinded human controlled trials showing that resistant starch supplementation can lead to fat loss and visceral fat loss in a calorie-independent manner. So just to give you a teaser of the data, what you're looking at here are MRIs before and after resistant starch supplementation. You can see visibly visceral fat reducing. So you can check the letter for more, but let's get back to our interview. All right. Next question then in the quiz, you kind of already alluded to it if people were listening. So, um, I'll let people have a hint, but there is another element. What is better for blood sugar control, a hot baked potato or a cold potato salad with vinegar? People should put their guesses in. Now, can you reveal to us the answer and the rationale?

Yeah, so it's the cold potato salad with the vinegar and the potato salad. The cold potatoes of course have the resistant starch, but the vinegar is actually another fascinating thing because the point about the, uh, weight gain is that our body responds to hormones. So when insulin goes up, then we respond in a certain way, right? Insulin is a, a hormone, which means it's a chemical messenger to tell our body to do certain things. In this case, store fat, generally. So the point is to have a low insulin response, and not necessarily— which is not necessarily the same as eating less carbohydrate. You can eat the same amount of carbohydrate and still have less insulin effect. And vinegar actually has a very fascinating role in this. If you eat carbohydrate, what happens is that your body breaks it down. So carbohydrates are starches, starches are chains of glucose, and the glucose gets broken down by a hormone, uh, called amylase. And the amylase there's salivary amylase and there's pancreatic amylase. So as soon as you eat, there's amylase in the saliva that starts chopping up your, the, the starch, which is a long chain of glucose into smaller glucose fragments because it needs to be in that smaller fragment for you to absorb it quickly. It used to be thought that salivary amylase didn't have a big effect because as soon as you got down into the stomach, then hey, it, it would get deactivated. So it's mostly pancreatic amylase. Turns out that was wrong and the, the thing is that it actually contributes probably about 50 or 60% of the total effect of the amylase, right? So it's a significant effect when you eat potato salad with vinegar. So any organic acid, the acid sort of inhibits the amylase. In other words, when you eat that potato salad with vinegar, or if you eat the bread with the vinegar, what happens is that your body can't start chopping up that, that glucose chain. So therefore the chains of glucose stay longer, which means that your blood glucose doesn't spike up, which means your insulin effect is substantially reduced and you don't absorb it as much, right? It's the speed of the absorption that makes the difference because when you absorb it quickly and your glucose spikes and your insulin spikes, that's sort of the worst thing. So any organic acid will do, but the main types of organic acid would be acetic acid, which is vinegar, lactic acid, which is found in fermented foods. So you see all these people talking about fermented foods and it's like, yeah, absolutely. They're really good for you, not just for microbiome and all these other things, but they're also going to help neutralize the insulin effect of your carbohydrates. So kimchi, sauerkraut, that kind of thing. And the third thing is something like lemon juice, which is citric acid.

Yeah.

So they've done experiments with, you know, bread and they've added some lemon juice and they found that the, the effect is much lower. The insulin effect is much lower. So the vinegar, super interesting. So again, you know, something that's easy to do. Like if you think about how people eat bread, like you could eat bread and dip it in the olive oil and vinegar, that's gonna help.

The only caveat I would add is certain vinegars have sh— so like a balsamic vinegar, which is, this is what I'm thinking, go to a restaurant, you get balsamic vinegar. Balsamic vinegar is actually pretty sugary. Would you agree that the choice of vinegar probably matters to optimize the effect? Yeah. Or do you think the sugar content of the balsamic's not that much?

Yeah, yeah. I mean, in Chinese cuisine, a lot of dumplings they serve with actually red wine vinegar with ginger. And it's again, same thing. You have a lot of carbohydrate there with the dumplings and so on, but you always dip it in vinegar. So yeah, the balsamic is sugary. Yeah, there is, there is definitely a lot more of that.

So if you wanted to optimize your potato, so rice, cool, reheat potato, eat cold. With vinegar. I'm imagining like a potato salad with like some apple cider vinegar or white wine vinegar, maybe as the, like the creamy bit, like a Greek yogurt for some like added protein and fat. So if you wanna optimize your potato eating intake, maybe that would work. But speaking of potatoes, next question, food order. So now I want people to imagine you have a plate of food with a roasted potato, sweet or regular, I don't care. Chicken thigh and grilled eggplant. What's the ideal order to eat these foods in? People should give their guesses if they're bold enough. Now, Dr. Fung, what's the answer?

The answer is you should try to eat the carbs last. So eat your proteins and veggies first, and it actually has a massive effect. So the thing about, you know, again, when you're trying to think about digestion, 'cause it's not just about the foods, right? People always think it goes from food to weight gain, but there's actually a whole process of digestion absorption that's really important. If you eat the carbs first, whether it's potato or bread, you know how the restaurants always give you bread at the beginning of the meal, right? What happens is that when you eat, the food goes into your stomach and the stomach's actually a reservoir, right? So it holds the food, it churns it around, mixes it with stomach acid, and then it shoots it out into the small intestine in small boluses, right? And that's when you absorb it. It gets into the small intestine, the small intestine absorbs all the glucose. If you eat the carbs first, then what happens is that you've got this bolus of food in your stomach that's basically 100%, uh, glucose. You've got your salivary amylases chopping it up already. It gets down there. You've got easily absorbed glucose sitting in your stomach. The bolus of food comes out and it's just basically, you know, slurped up by the small intestine, goes right into your bloodstream. Your blood sugar goes like this and your insulin goes like this. If on the other hand you eating proteins and fats, so you eat the chicken and the vegetable, what happens is that it spends time churning around in there, right? Then when you, by the time you eat your carbohydrate, it all mixes in. So by the time you start shooting out the boluses of food into the small intestines, what happens is that it's not 100% glucose. You've got your proteins, your fats, and your carbs.

Right?

So instead of like 100%, like 30%, whatever percentage of carbohydrate you ate. But the other thing is that a lot of the proteins and the fats and stuff are going to slow down how quickly you go through. This is the stomach transit time. So instead of eating the bread and your, your, your stomach holds it but very quickly shoots it out, and as soon as it comes out, it gets absorbed, slurped up right away, what happens is that you're churning around it's coming out very slowly and what's coming out is absorbed very slowly. So instead of that big shooting up of glucose, you've got this sort of slow glucose rise and therefore your insulin effect is much, much lower. And it's actually dramatically lower. In some experiments, like 50% lower, it's a, it's a massive drop. So eating the naked carbs, which is sort of like carbs on their own, or eating carbs first before your other stuff is, is sort of this, you know, it's, it's not the ideal way to do things. And it's such an easy thing because 'cause you're talking about the exact same foods. You're simply changing up the order that you're eating it.

Yeah. Oh, for sure. Very practical. So let's complete the meal. We've gone through meal order, how to cook various carbohydrates, how to eat various carbohydrates. What about beverages specifically? I wanna talk about green tea and how it affects carbohydrate metabolism.

Yeah, green tea's very fascinating because it actually affects it in by with several mechanisms and it actually blocks an enzyme called COMT. COMT affects the sympathetic, you know, that's adrenaline or adrenaline, and it raises it slightly. So it's supposed to break down sort of adrenaline, noradrenaline. When you block it, you leave the adrenaline or adrenaline, so your sympathetic tone actually goes up a little bit. And the thing is that people don't realize often is that when you increase sympathetic tone— so sympathetic tone, so remember there's the, this autonomic nervous system which is the parasympathetic and the sympathetic system. One is the parasympathetic is sort of the resting relaxation and the sympathetic is the sort of fight or flight response. But the other thing that happens when you go into the sympathetic stimulation is that your appetite, your hunger goes down significantly, right? So if you're increasing sympathetic tone, you're decreasing hunger. So if you think about drugs that increase sympathetic tone, there's lots of them, but the classic one that causes weight loss is nicotine. So nicotine increases sympathetic tone, but the way it creates the weight loss is that it kills your appetite. So just like Ozempic, it's not about the calories, it's about the hunger because you're suppressing your appetite because you're increasing the sympathetic tone. You're getting that effect. You see beta blockers, when you block the sympathetic tone, people respond with weight gain, right? And the other thing is, um, there's this old drug called Fen-Phen. Which was, uh, fenfluramine, phenteramine. And it was basically taken off the market 'cause it caused heart problems, but it's actually very effective. It caused 17% loss of body weight, which is on par with Ozempic, right? The lower doses. And people often forget that fenfluramine was a sympathetic agonist, that is increased sympathetic tone, and therefore killed your appetite just like heroin or speed or, uh, crack. They're actually— if you look at the class of drugs that these belong to, they're called anorexians, which means that they're drugs that cause loss of hunger or anorexia, right? So it's like increased sympathetic tone equals decreased hunger. That's why when you increase the sympathetic tone, you get less hunger in any drug. But it happens with the green tea as well because you're blocking COMT. You get an increase in sympathetic tone and therefore a decrease in hunger. And it's, it's not huge, right? It's like 4% or something like that. Interestingly, it may be more effective for Asians because their genetic variation means that the COMT is actually a bit more powerful. So they, they actually estimate, I, I think that it's, it's about a double effect for Asians compared to Caucasian. So very interesting from that standpoint. So I think green tea is a, a fantastic drink from several standpoints. One is that it's got the, the blocking of the COMT. Two, it's got no sugars. So you're basically able to displace the need to drink other sugary beverages, which is always sort of a temptation at times. 3, it also has a bit of caffeine, which is going to stimulate again the sympathetic tone, but also stimulate metabolic rate because, you know, that's what caffeine does. It's a stimulant. For a number of reasons, green tea is actually one of the sort of ideal sort of weight loss drinks. And of course, you look at places where they drink a lot of green tea like Japan and They love it there, but they also, you know, they also, they've done actually most of the studies on green tea, but you know, you see there's very little obesity. That's not the only reason, but maybe it's a, it's part of the reason.

Yeah. Well, we've now gone through rice, potatoes, food order, beverages. If you want more tips, there are in Jason's new book, The Hunger Code. Again, it's no pay for play or anything here. I just enjoyed reading the book and wanted to talk to Jason about it. With that, I want to pivot in our conversation and just talk about some new data beyond the book, things that I found interesting that kind of dovetail with what we've been talking about, practical things for people to be aware of. So I thought one of the most stunning and underappreciated papers from last year was a basic science study in Nature. And one of the things it showed— and I showed you these data, but I wanted to get you to react to them, uh, on this, on video— is that your brain— we're talking about mindset in the the part 1 of this conversation, but your brain can literally make your body make sugar. And there's not hyperbole there. That is literally what's happening, that there's a direct neural line goes from your amygdala to your, um, hypothalamus and then a neural line to your liver and it says, hey liver, make blood sugar. So it not only dumps blood sugar, but it actually creates new sugar through gluconeogenesis. Basically what it's, this mechanism shows is that your brain can tell neurally your liver, hey, we're stressed. Pump quick burning energy into your bloodstream. What do you think about these data and their implications?

Yeah, I think again, I think is fascinating data to be sure. And again, shows you how much of our body depends on these neurohormonal stimuli, right? Your whole body basically runs on either the neural signals or the hormonal signals, right? Your body only does what it's being told to do. And what I thought also thought was interesting, 'cause they, you showed me the paper, it was new, I hadn't seen it before. But I was saying that if you look at the amygdala link, it actually links to the ventromedial hypothalamus, the VMH, which was fascinating to me because it's actually one of the very earliest, you know, syndromes of obesity experimentally. You could, in rats, destroy the ventromedial hypothalamus and these rats would become obese, right? So, the interesting thing is that did they become obese because they ate more calories than they burned. Yes, but that's not the reason. The reason is because you induce this lesion in the ventromedial hypothalamus, and it basically, um, you know, this is sort of additional evidence of, hey, here's the link like between your hypothalamus. And then this is sort of, you know, to me is interesting because this is, uh, it causes hyperphagia, right? It causes rats to eat a lot, and that's why they gain weight. But there's an intermediate part too that, hey, maybe it has to do with the liver gluconeogenesis adipogenesis and insulin, right? It's, it's, it's a fascinating sort of thing to be fleshed out a little bit more for sure.

I mean, I think the thing I wanna highlight for people is whenever we talk about any of these cascades, they're not a single linear causal pathway that is the be-all and end-all of something as complex as obesity. They're like threads on a web that we're just fleshing out. And that's what I think is so beautiful with that. There was another paper also on the stress domain we were talking about, you know, conditioned hunger and other forms of like hunger related to environment, one of which could be stress eating. So there's another paper that came out showing that people with metabolic diseases, particularly diabetes, are characterized by gut microbiomes that make molecules. One was called imidazolepropionate, IMP, that at least in preclinical models can go to the brain and basically lower the stress eating threshold. So the idea here is that poor metabolic health can, via the microbiome, perpetuate a vulnerability to stress eating. Thoughts on that?

Yeah, again, a fascinating thing because microbiome is really, I mean, there's, it's, it's sort of relatively new from an experimental standpoint, right? Within the last 10, 15 years sort of thing. So I think that there's a lot more to do with it, but it, what it shows is that the, you know, it, it sort of validates this hypothesis that the bacteria that you have in the gut, they're important because when you eat certain foods, it metabolizes it and then creates these other molecules that can then go into the brain. So it's not that the bacteria and, and, you know, are good or bad, it's that their byproducts can go into the brain and then become active, right? Just like fiber. What I think is interesting is if you eat a lot of fiber, it goes to the colon, it actually gets broken down into short-chain fatty acids, it gets fermented into short-chain fatty acids, which then stimulate GLP-1. So it's like, hey, that's really interesting because if you're thinking about fiber, not only is it, you know, not digestible, it's gonna, you know, create bulk in this, in the foods that you eat and all this sort of stuff, but it's also gonna stimulate GLP-1, which we all know is very important from studies on GLP-1 agonists, for example. Just, just to note it with GLP-1, I always think it's really funny because glucagon, so GLP-1 stands for glucagon-like peptide. So glucagon's basically, or can be thought of as sort of the opposite of insulin, right? It's, it's sort of, they, they, they sort of seesaw a little bit. That's a little oversimplification. I always think that it's funny because, you know, so many people say insulin's, that's not the important, that's not important, that's not important at all. Okay, okay. But what happens when you stimulate the opposite of insulin? Like, glucagon or glucagon-like peptide? Well, you get a hell of a lot of weight loss and everybody says, wow, what an important breakthrough. It's like, yeah, I'm friends with intention in medicine.

I won't get into a rabbit hole on this. I was reading the paper, it was Cell Metabolism 2024, and it was a human-controlled trial using the single most profitable drug in history. So statins as a class, but specifically atorvastatin, Lipitor, literally the single most profitable drug in history, human-controlled trial. And there was a graph showing in a 16-week study how atorvastatin crushed GLP-1 levels. Like an 8-year-old could read this graph, plummeted them into the floor. And I'm not even going to go into the clinical implications. That's not the point of the discussion. The reason I bring it up is because, as you just mentioned, there's a lot of selective attention in medicine and in the media. And I just don't think— this is now going to be me getting on my soapbox a little bit, but without any conspiracy theories, without pointing fingers at all, the compass of healthcare and scientific education is not driven by what's best for people. It's driven by business models, incentive structures, economics. Again, that's not anybody's fault, it's just the reality we live in. And I think that's a point where a point I wanna highlight and, and what I kind of wanna wrap up on because I framed the discussion starting in part 1 with the idea that as I went through medical school, I was very frustrated by the fact that everything seemed to be set up against people succeeding on their weight loss journey. And I just wanted people to be like aware of, you know, what's really guiding what you see so that they can educate themselves, pick up a book, look, read, learn, and hopefully get in a better place.

But yeah, and I think that's the thing, like people get into these, and I don't think it's people, I think it gets, it gets rammed down their throats, these sort of ultra simplistic models that wind up being completely untrue. The low-fat model being like the sort of the prime one, right? So in the 1980s, which I lived through in the '90s when I went to medical school, it was basically, we all know that fat causes heart disease, right? It was unquestioned, right? Everybody said it. We all took it to be true because everybody said it, right? Turns out there actually wasn't a shred of evidence behind that whole model. It was crap, right? And then in the late '90s, people started noticing, hey, when you eat lots of nuts, people are healthier. When you eat avocados and olive oil and fatty fish, you're healthier, right? So they then, they had to sort of backtrack into this healthy fat, right? And then there's the whole discussion about butter and stuff, right? And coconut oil, right? It's like, you know that people have been eating coconut oil for like millennia, right? Like everybody who lives on an island is like eating tons of coconut and coconut oil. And it's like, okay, It's the same thing with the calories. You get fed this sort of really simplistic, simplistic to the point of imbecility, sort of fat causes heart disease, calories in, you know, calories a calorie, all calories are equally fattening, you know, calories in, calories out. When it's actually not true, there's so much more nuance to it. And it, people try to bring it down to that sort of one very—

I mean, they just do.

Yeah. And, and, and it's, it's, and it's detrimental because the more you know, the better you can, you know, design your solutions, right? Because you're, you've got more nuanced understanding. So instead of trying to, you know, and this is the thing that I'm always like, you know, it's a complex disease. There's not just these hormones. Like, so when I go into, I'm like, Okay, look, you don't go from calories to weight gain. You go from foods which contain nutrients, carbohydrates, proteins, fats. Then there's a whole process of digestion, right? And I list 10 factors that affect digestion. Then you have absorption and there's like 10 factors that affect absorption, which affect your hormones. And there's like 10 hormones, right? So the number of ways you can change from food to weight gain is virtually like unlimited, but it depends on those things. Food order, like, you know, what you eat the foods with, like, you know, vinegar and all this other stuff, resistant starch, all these other factors. By simplifying it down, it's, it's, it's like you can't ever appreciate the sort of importance of all these other factors. But we do because, and then what happens is that to the person with the hammer, every problem is a nail, right? So every time it's weight, You need to lose weight, eat less calories, right? Oh, your problem is ultra-processed foods, eat less calories. Your problem is food addiction, eat less calories. Your problem is conditioned hunger, eat less calories. Your problem is, you know, too much sugar, eat less calories. Like, what? What are you talking about? If your problem is— or your problem is stress, eat less calories. Like, how is that solving the problem? If your problem is you're not getting enough sleep, eat less calories. Is how you lose weight. What? No, your, your solution should be get more sleep, right? Isn't that logical? But you know, it gets sort of so, you know, you just get dumbed down to this point and, you know, you just reminded me, I mean, like, like statins, there's other effects that, that happen, but GLP-1 is one of these really important hormones that we have to pay attention to.

I have this little thing I call with me and my friends, Snarky Nick. It's like a little shoulder angel and everybody sits, everybody, every time someone says eat less calories, I think Snarky Nick says, tell them their neurons are in a caloric deficit.

'Cause it's just such a stupid thing.

That aside, I wanna be respectful of your time. Thank you for joining me for this two-part discussion. Dr. Fung, tell people where they can get your new book and where to go to find out more.

Yeah, so you can go to my website, which is drjasonfung.com. That's D-O-C-T-O-R or you can follow me on x.com or, you know, or Twitter or YouTube, and you can order the book wherever you want. But again, I think it's, you know, I— it is— it's sort of a follow-up to The Obesity Code, but actually goes much, much more deeper into the sort of understanding of sort of the systems, the eating behaviors, the sort of, you know, hedonic hunger, homeostatic hunger, conditioned hunger, a lot of the social environmental determinants that I think are really underappreciated and nobody really talks enough about. So I think it's actually really important, but simply because I actually don't see a lot of people talking about this stuff. I think people, the more you understand, the more you know, the better you can, you know, figure out a good plan for you, right? Because if there's different problems, you need to know what that problem is, then you can solve it. But yeah. Yeah, for sure. For sure.

I thought it was a fun read. I was actually laughing throughout and there was a lot of practical tips. We gave you a taste at the beginning of this video, but thanks for your time and have a great evening. Thanks so much.