And we talk about where the levels of evidence exist for this and how we can kind of approach patients both with and without the evidence. I hope there's a lot of take home messages that you can take away from this interview to see how you can implement them in your lives, if you're suffering from any of these issues, but also sort of how to refrain this issue of insulin, its impact on our lives and our health and how we can implement fasting as a way to approach that.
Now, to be fair, fasting means a lot of different things to different people so we talk about the definitions and we talk about ways to make sure it's done safely, because that's very important. Just because something's good, doesn't mean more of it is better, and I think that's an important take home with fasting as well, doing it under supervision, doing it safely, can have a positive impact and that's part of what Jason has devoted a big portion of his career to.
Now, he's still a practicing nephrologist and that's sort of where all this started, but now with the IDM program he is reaching so many more people and spreading the word more about the benefits of intermittent fasting. So, enjoy this interview with Dr. Jason Fung, and if you want to learn more you can get the transcripts and you can see all our prior episodes on dietdoctor.com. Dr. Jason Fung, thank you so much for joining me on the Diet doctor podcast.
And then you hear so much, like it's going to burn muscle, it's going to wreck your metabolism and don't skip breakfast, and all these sort of things that make it sound really scary, until you realize that people have been doing it for thousands of years.
I mean I look at some of these studies they did and they're incredible, like one of them for example, they had like- I think they had nine people or something like that and they fasted them for like 30 or 60 days, then they gave them a big whack of insulin. It's like, I'm thinking why did they do that? And the answer was, "Just to see what would happen." So, they dropped the sugars to very low I think and it was like 1 point something in the Canadian unit so it's probably like 30 or something like that, it's ridiculously low.
And everyone was complaining they were asymptomatic, so you know these are the kinds of studies that no one would ever do, you don't do that kind of thing, it's you know you don't have to take those kinds of risks. So that's where people go more towards the shorter fast and there's no reason not to do them. And you've got to understand that fasting is a part of the normal life, like that's where the word breakfast comes in, you're supposed to feast then you're supposed to fast.
Well what's wrong with that? And you have a word that is actually part of your daily schedule, and now fasting for 12 hours is like insane, it's like everybody in the 70s did it like without even thinking about it. So it's sort of come all the way around that, you shouldn't even go like more than two hours without eating, it's like okay well, what about the normal nightly fast, right?
So, it's sort of ridiculous how quickly some people can get better and you know as I was saying this is something that really needs- people need to understand because it causes so much disease, type 2 diabetes, because I mean 20 years of diabetes, and we had just proved it was all completely unnecessary. Like do you know the amount of damage they did to their bodies with 20 years of type 2 diabetes to their hearts and to their kidneys, and to their eyes?
With type 1 diabetes, if you don't have insulin, you got to give it, that's how you're going to get better. So, it's not like the insulin is evil or anything like that, it's juts all context, like if it's too high you've got to bring it down, if it's too low you've got to bring it up, and that's how you're going to get better.
They are the ones that do measure resting metabolic rate, don't show any significant difference from chronic calorie restriction. In fact most of the studies and there is a number of them, so you have to kind of pick which one you choose, but most of them show that there's less of this drop in metabolic rate with alternate daily fasting and studies for example... one study where they did four straight days of fasting, their metabolic rate was actually 10% higher at the end of the four days compared to the day zero.
And again it all comes down to physiology because I don't know why, people get so bent out of shape. So if you don't eat, insulin drops, we know that, that for sure happens and when insulin drops, the counter regulatory hormones go up, we know that, that's why they are called counter regulatory hormones, they go counter of insulin, and one of the big ones is sympathetic tone, like that's not for debate, right.
That's medical school physiology, okay so if you think- and cortisol too, so cortisol is one of the counter regulatory hormones. So, if you think about it, okay so if sympathetic tone is going up, you know you're activating your body, that's what sympathetic is, parasympathetic, you're toning it down, but you're activating the body, what do you think that's going to do to your energy? It's going to raise your energy, it's going to increase your metabolic rate. It's like come on, this is medical school stuff, like why is this a debate.
And all the studies show that there's probably less effect on the basal metabolic rate from real world studies on alternate day fasting and stuff. Most of them allow calories and so on, so you have to interpret them a bit. It's like why do we worry about this? Where does this notion even come from? Because if you fast you're going to decrease you metabolic rate, that actually runs counter to what we all learned in medical school, of what happens when you don't eat.
If you look at those programs where they have skin surgery, they're taking, you know like 40 pounds of skin, that's not fat, that's protein. So, there is excess protein, when you're talking in that specific sort of obesity type 2 diabetes situation, and you have to think that the body is going to maybe use some of that because that's all protein that needs to go. And again if you look at studies that have compared intermittent energy restrictions or IER versus CR which is chronic restriction and there has been a few, most of them generally show that there is less loss of lean mass as a percentage.
So one study from 2016 that was published in obesity for example, showed that you know you get about 0.5 increase in percentage of lean mass, because people are losing weight with chronic caloric restriction but it goes up by 2.2% in intermittent energy restriction or fasting. So you're preserving lean mass much better if you're using the fasting strategy, but this is sort of short term, 24 hours or less strategies.
So, again if you think about it, it's like okay, if you think that the body is- when it has no food, it's going to bypass your excess protein skin connected tissue and go right for your heart muscles, it's like you must think that the body is really, really stupid. I mean, like honestly, you don't eat for 24 hours and oh you're going to start breaking down your diaphragm. Like why would the body do that?
What you do is you take the strain off the muscles, so you take the stress off and you immediately start losing muscle, so if you want to lose muscle, that is the way to lose muscle, sit in bed all day. Like why would the eating have anything to do with it? Eating doesn't make you gain muscle, otherwise we would all be a nation of like you know Arnold Schwarzenegger's, right?
It doesn't happen, they are two totally separate things. You build muscle because you are working it, then you lose muscle because you aren't working it. If you're working it and not eating, your body is going to come up with a way to build that muscle, just the way it is, otherwise, again if you look at these Native Americans and all these people that used to go through these feast and famine cycles, and it was not like they were little globs of fat running around the prairies when the pioneers came.
They were lean and muscular and, you know, strong because your body responds to that, and I think it's really silly to think that our body is just so maladapted to life.
So, it's about getting the proper education and that's what we provide with our IDM program and also providing a support of community and that's is what is really the secret behind a lot of things, not just for weight loss, like Weight Watchers for example... they started out not with a diet but with those meetings, those Weight Watchers meetings and that's the secret sauce right? Same for Alcoholics Anonymous.
It's not like they didn't know to- hey stop drinking. It was that you had a supportive group, a sponsor and that sort of thing. So doing it with a community is just way easier and that's the secret of how all these communities use to fast, they do Ramadan, hey everybody's fasting, hey it's lent, everybody's fasting, hey it's Yom Kippur, everybody's fasting, so it's not fun but it's as hard as it would otherwise be.
Because if you're trying to fast and everybody is telling you you're stupid and eating, like you know in front of you, that's not like the easiest thing to do, so don't you know you've got to set yourself up for success and that's what we hope to do for with the IDM program.
I don't think that exists, but there are certain practices that have sort of withstood the test of time, that is they were considered to be wellness practices 2000 years ago and I think that has merit because those practices have withstood the crucible of time, like if something is really bad for you and people do it, they'll like die out.
So, the fact that these practices or these foods or whatever have survived means that there probably is something and what's interesting is a thing that science is starting to catch up and fasting is one of these things and if you look at the science of longevity, the one thing that really stands out huge is calorie restrictions. That is probably the single most well studied mechanism for longevity in animal studies mostly.
But intermittent fasting is sort of a play on that and it is a way to restrict overall calories and maybe there's a better way to do it, but at least it's been used for a long time as opposed to sort of protein restrictions and or carbohydrate restrictions, those have not been used for as long. Intermittent fasting is a way to do that, and the physiology is... you know, a lot of these growth factors are also nutrient sensors and I think that this is a really interesting thing if you look at the theories of aging and why we age, or there's sort of, there's trade-off between growth and longevity.
Okay so if you look at a car for example, if you rev its engine, you can get high performance out of it, it's not going to last very long because it's just going to burn out. It's the same thing, if your body is growing, growing, growing like crazy, it probably does the same thing; it burns out quicker. So the growth program is probably at odds with the longevity program, because it's probably the same program.
So you can look at a population of Ecuadorian dwarves for example, called the Laron dwarves, and what was super fascinating is that this group of dwarves which- they were persecuted in Spain, the inquisition forced them into Ecuador and of course there's this founder effect where- because there's only a few of these dwarves and they all married each other, the small population, there's a lot of these- this dwarfism occurred, and a few years ago it was- when they were following these dwarves they realized hey these guys actually don't get cancer or diabetes either and then they're like, what's the difference between this dwarf and the other one. It's like they have no IGF1, it's like wow.
So, here's a you know- the thing is if you slow down the growth program, then you might be able to age better, it all depends also on what stage of life; so if you're a child, an adolescent, you want that growth program running.
So it's like it doesn't matter but now if you're trying to get out to like 80 or 90 years old, you have to be a bit smart, so just like that engine, you can't run at full speed, you've got to cut back at some point though if you look at what stimulates growth the most, it's things like insulin, like growth factor mTOR and AMPK, which are all nutrient sensors and this is what's really interesting is that the nutrient sensing pathways are actually the same growth pathways because the body has to know when the nutrients are available.
So, now if you want to say, okay well this growth pathway after, you know age 30- I don't really want to go full boar on growth because I want to live until 80. If you want now longevity, you actually have to cut down your growth pathway, which means reducing those nutrient sensing pathways, which is insulin, which is mTOR and AMPK, which is something that fasting does.
Because we can't necessarily measure mTOR and AMP kinase. It's harder to measure so we have to use surrogate markers, so what do you use as your guidelines to say here is where you're getting the biggest bang for your buck to do this level of fasting to help promote your longevity?
It's going to give you heart attacks, it's going to give you all kinds of stuff, cancer and so on. And that's dependent on not body weight but waist circumference, type 2 diabetes and hypertriglyceridemia and all that sort of thing, so we know that those are all very important and those are obviously highly linked in to hyperinsulinemia and so on. So you're looking for a surrogate marker that's been clearly correlated to disease and that's going to affect longevity and all those things.
So if you are fasting and your weight is just way, way down, then yeah, you probably don't need to be doing that. But on the other hand, doing it so often might be something that is very beneficial and again if you look at it, it's like there's that sort of ancient wellness practice that people have done for thousands of years. Once a year, do a longer fast, just to sort of clean everything out, reset everything and then go from there, do you need to do it for longer? Maybe not.
But if you're 300 pounds and have type 2 diabetes, you probably need to be doing more, because you know that those insulin growth pathways are way, way too high. It's harder for mTOR right and that's really the tough part and we spend a lot of time talking about sort of optimal protein and stuff but that's really, really hard to measure because it's not as easy to see.
So this is another field you've been fairly vocal about, about fasting and insulin as it relates to cancer and that can be controversial as well because cancer, there's the one theory that it's sort of all of a genetic mutation and you know the drugs we're developing is high powered weapons so to speak to target specific genetic variations of cancer, and then there's the sort of the opposite side of a metabolic disease or maybe it's a combination of them both.
So, how do you incorporate that into your thinking and fasting in terms of cancer prevention or treatment?
So, we got the human genome project because it was going to cure cancer and then you had the cancer genome atlas which was an even more ambitious attempt to find out the mutations of cancer because we thought there was one or two mutations. It turns out there were like hundreds of mutations and not only mutations like between people, so one breast cancer cell to the next person's breast cancer might have like a hundred mutations and 100 complete different mutations on the other guy, even within the same tumor there are different mutations.
So there's mutations everywhere and clearly you're not going to develop 100 medications to block every single- 100 different medications to block every single mutation, so that was sort of a dead end theory. And the other thing is, it's not about genetics, it's about the interaction of genetics and the environment, that we sort of forgot that it depends on the environment. So looking at obesity for example, the World Health Organization lists 13 cancers as obesity related, and including breast cancer and colon rectal cancer, sort of the number two and number three cancers after lung.
So what's the difference? The difference is clearly the diet and the environment in which that breast cancer cell is living, so again what is going to stimulate breast cancer cells to grow- And in the lab the answer is very clear, insulin is what breast cancer cells need. You can't barely grow breast cancer cells in a dish without insulin. If you take away the insulin, they all like die. And if you give them lots of insulin, they grow, because the nutrient sensing pathways are the same as the growth pathway.
So you take this breast cancer cell, and remember the obesity didn't cause the cancer, but after that cancer cell is there, you're going to stimulate it to grow if you have a lot of insulin, so type 2 diabetes, a disease of hyperinsulinemia, higher risk of cancer, obesity, disease of hyperinsulinemia, higher risk of cancer, and then you say what about the other ones? What about AMPK for example... what blocks the AMPK or what affects the AMPK? Metformin.
It's like, oh well you know that metformin in a lot of studies has been associated with a significantly decreased rate of breast cancer and is it like the effect on AMPK, it's a very interesting hypothesis, what about mTOR? It's like because they are the three nutrient sensing pathways. Well, mTOR, you can block mTOR with rapamycin, which is an anti-cancer medication, right.
Why? Because you're blocking the pathways. So rapamycin is super super interesting because it blocks mTOR right. So, it's developed as an immune suppressing drug and the thing about immune suppressants, is that they generally increase the rate of cancer and the immune system sort of destroys cancer on site. So, if you give a drug that suppresses the immune system, like you give these transplant patients tons of drugs to suppress the immune system, cancer goes crazy and that's why-
So it all seems to fit, but yet we don't quite have those human trials, to say yes it works which can make it a little bit uncomfortable for you to recommend fasting for that.
Those trials don't exist so now we're talking about going into treatment and that's a totally different thing. One I don't think there's much data whatsoever but there is some super interesting data about sort of combination therapy, right. So, you say okay well diet is not going to cut it for a treatment, like you can't have breast cancer and think you're just going to fast and yes there's a few case reports and so forth but for the most part that is not going to work for most people.
But can you combine it with say chemotherapy to make it better? And that's something that's really, really fascinating because for example fasting reduces the side effects of chemotherapy. We know that because chemotherapy, and there's been a couple of papers on that, the chemotherapy affects the most rapidly dividing cells so in the human body the normal body, the cancer cells are growing faster, that's why you are targeting rapidly growing cells, the hair follicles grow quickly, the epithelial cells in the intestinal system for example are very rapidly growing so therefore you get nausea and vomiting and hair loss.
So, if you put these, if you now fast for 48 hours for example, and you get these cells to ramp down their growth, they will enter a sort of a more quiescent state, now you whack them with big doses of chemotherapy, you're going to get less side effects, so if you get less side effects, one you're going to be able to get a lot of treatments have to be ramped back, because there's too many side effects, so you would get the full treatment.
Or maybe you can get a higher dose treatment because you're looking for this maximal tolerated dose, and then there's some interesting data to suggest that maybe that- So the worry there of course is that the cancer cells will also go into this protective state, but apparently some preliminary data suggests that this doesn't happen because they are stuck in this sort of on mode, that's the whole point of cancer that they are in this sort of growth mode.
And they say what if you down regulate insulin by eating a ketogenic diet and then by giving the drug, like can you do better than doing either one alone. Those studies are very interesting, there's not a lot of data, so cancer is more of an evolving story that I think you know would be. You know, it's super interesting but ...
So it was sort of part of that whole metabolic syndrome spectrum that I had been talking about, but I hadn't really looked closely into it and you know as I got interested I said okay let's look at what happens with it, let's look at the path of physiology, why are people getting PCOS. And it's been well worked out and I showed a New England Journal of Medicine review article that sort of spells it all out so under the influence of too much insulin, your ovaries start to actually produce a lot of testosterone.
And when you have a lot of insulin, the liver decreases sex hormone binding globulin, so the effect of the testosterone is increased because there's not a lot of globulin to bind it so the free testosterone is more active. So, therefore you get all the symptoms and the hair growth and the acne, clitoral enlargement, things that are sort of typical.
So, if you have too much insulin, then you get follicular arrest and that means that the follicle stops developing at a certain point, so it never ovulates, it never reaches the size that it's going to ovulate and if it doesn't ovulate then there's no egg and you can't get pregnant. so that's another- that's the infertility. And the thing is if it doesn't ovulate, it doesn't become the luteal body which then involutes, which means that it just sort of gets reabsorbed into the body.
So, you've stopped the follicular development at a stage where it doesn't ever go away, so you've got these cysts that develop over time. So, okay so those are the three sort of criteria of PCOS. You've got too much insulin which causes the follicular arrests which causes the cysts, you've got too much insulin which causes the follicular arrests which causes the unovulatory cycles and then you've got too much insulin which causes the hyperandrogynism.
So the whole disease is a disease of too much insulin and it's been well worked out and it's been in this review article... So it was like are okay... well like if it's too much insulin, then bring down the insulin, that's how you're going to make the disease better. That's the root cause treated. Instead, that's not how we treat it, we give drugs.
And intermittent fasting hasn't been used. When I started talking about it like six years ago, like I was really just a lonely voice in the wilderness. Nobody, but nobody was studying this. So, are the studies going to come? I hope so. I don't know that there's a lot of people interested in it, but here's the thing and this is sort of the art of medicine as opposed to the science of medicine. Everything in medicine comes down to risk versus reward, so if you give a drug like a beta block or you do a stent or something, what's the risk of doing a stent? Because there's risk, because everything has risk, and what's the reward?
If the risk is more than the reward, then you don't do it. If the reward is more than the risk, you go ahead and plop in a stent, or you give aspirin or you give beta blockers or whatever it is. So, what's the risk if you don't eat, you know for 16 hours of the day. What's the cost like... zero? What's the risk? If you are overweight, there's practically no risk, so then you say well okay there's no risk so any reward you can get is a plus and here's the thing, you don't have to prove.
If you're a patient with PCOS, if you're somebody with PCOS, you don't have to prove that it works in everybody, you only have to prove that it works in yourself. So, if you have type 2 diabetes, if you have PCOS or any of these diseases, you can simply say, I'm going to try it. I'm going to try it for two months because it's not going to cost me anything, I'm going to do low carbohydrate diets, I'm going to do intermittent fasting and see what happens.
If nothing happens and your disease is just as bad as before then you haven't lost anything, you can go ahead and just do it, but what if your disease completely goes away? Right, now you've done something that all the drugs haven't been able to do for you and the thing is that it's big money here. So IVF is big money, it's like four plus billion dollars a year, so these people who are doing fertility treatments and all the sort of stuff- like if you ever go into one of those clinics they are really nice, they look like a spa.
If the risk is very low then the need for evidence is also a little bit lower if there's a potential upside, it seems like one of those circumstances. Yeah it was sort of a whirlwind tour through the fasting, through longevity, through cancer, through fertility and it all tends to have a common theme, doesn't it.
I mean you're talking about the biggest killers in America, so heart disease, stroke, diabetes, cancer are sort of like at least four of the top five and all of them are impacted by hyperinsulinemia. I think that's a better term than insulin resistance as it immediately tells you what you need to do. So, insulin resistance doesn't tell you what you need to do.
Cut the carbs and don't eat, so it's much more powerful. So just changing that word, makes it so much more powerfully clear to people, what you're supposed to do because there's been a shift in medicine, right. If you look at the causes of death, there's a complete shift from sort of 100 years ago and you're talking-
So, and those are diseases which are going to be impacted by metabolic syndrome and also we know cancer, like for so many years was thought about as a genetic disease, it's like what about the genetics when you put it in a high growth environment, which is a high nutrient environment, and it's like okay, well you know that cancer, you go back to sort of those traditional African societies and stuff.
They had cancer right, a lot of them were viral cancers, lymphoma and so on, but those cancers like breast cancer, they practically didn't exist. The Eskimo, or the Inuit that we call them now, in the far north of Canada, they actually studied them, very intensively to see why they were immune to cancer.
So, we pretend that cancer is this disease of all genetics, genetics, genetics but it's not because two of the sort of- okay if you talk about the big three cancers, lung cancer, obviously it's just smoking, right? Let's forget that. So the next two are breast cancer and colon rectal cancer, prostate cancer is number four and is actually very common, but doesn't kill as many people because it's slow growing and it doesn't sort of effect the younger groups as much.
So, breast cancer and colon rectal cancer, which we've already declared are obesity related cancer, so it's like let's face the fact that these are actually diseases that may have something to do with insulin and reducing a state of hyperinsulinemia might be highly beneficial for them, and again what's the downside?
Just talking about sort of, it's not like a how to cure cancer, because that's not going to happen, but it's sort of this, you know I'm really, really fascinated because the whole story of cancer has changed so completely from what we thought it was. We thought it was just a bunch of randomly accumulated genetic mutations and sort of from 1990-ish, you know when I went into medical school in 92 sort of to 2010 probably, it was all considered genetic mutations.
But now the whole theory of what cancer is has completely changed and now we're talking about evolution, using evolutionary biology and trying to understand how cancers develop and we're trying, talking about, you know- One of the really fascinating things about cancer is why it occurs in every single cell in the body, like almost every single cell in the body can become cancerous, and that's really weird, and it's not just that.
Almost every multi cellular animal in existence can develop cancer, even a hydra which is one of the most primitive multi cellular organisms can develop cancer. So cancer is not a disease of just humans, it actually predates humanity by a lot. It's a much, much more ancient than we knew, and it actually probably dates back to the transition between uni-cellularity and multi-cellularity, which is, you know what is, and that's really what the fascinating story of cancer really is, and that's ...
So we go from a time where we consider the Inuit to be completely immune to cancer, these people don't get cancer ever, to hey they get a lot of cancer over here, and it's because of the environment, not because of the genetics. So, that is the sort of story of cancer, so it's not really just about fasting and so on, actually you know, I'm more interested in the deeper story which is changing and I don't think it's the end of-
I don't think it's the final answer, there's just so much more to be learned about it. But it's just very interesting as we move from that transition, from a paradigm of pure genetics to a paradigm of evolutionary biology, which to me is a much more fascinating.
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