Written by Christopher Kelly
Nov. 27, 2015
Jason.Fung.on.2015-10-21.at.09.28
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Christopher: Hello and welcome to the Nourish Balance Thrive Podcast. My name is Christopher Kelly and today I'm joined by a nephrologist, Dr. Jason Fung. Hi, Jason.
Jason: Hi, how are you?
Christopher: I'm very well, thanks. How are you?
Jason: Very good, thank you.
Christopher: For those of you that don't know Jason, this might not be the best podcast or the best place for you to start. Jason has a fantastic website. It's called intensivedietarymanagement.com. I'll link to all these resources in the show notes for this episode. Jason has done a bunch of fantastic presentations on fasting and type II diabetes. He's also done a number of other great podcasts including one I listen to a couple of days ago on the Sigma Nutrition Radio show. I'll link to that as well.
The background is I asked for questions on the Optimizing Insulin Facebook group, which is a great place to be, by the way, if you haven't already found it. I got some fantastic questions for Jason. That's what this show is going to be. It's me asking Jason some of these questions that we've gotten from Facebook. But just to give people a little bit of context, Jason, why don't we start by you telling us about your background and how it would come to be that a nephrologist would care about type II diabetes?
Jason: As a nephrologist, I'm a kidney specialist, and by far and away the major cause of kidney disease is type II diabetes. That's really where I became interested in it because that's what I see all the time. And things started to change a few years ago, probably about eight, nine years ago because the thing is, the type II diabetes, it really wasn't getting any better. Because what we do is we treat people for their high blood sugars and with medications and insulin and so on and our entire treatment paradigm was based on lowering blood sugars.
So we believe that all the toxicity is caused by high blood sugars. And there's all these theoretical reasons why high blood sugars would be bad for you and people came up with all kinds of reasons, advanced glycation end products and oxidation products and stress and all kinds of reasons. But that was -- The thing is that nobody actually knew whether or not lowering blood sugars made a difference. So about in 2008 or so there are four very large well designed trials -- the ACCORD, the ADVANCE, the VADT and the ORIGIN trial.
Basically, all of which showed the same thing, that is that type II diabetes, the randomized two groups of people, one to very tight blood sugar control and one to kind of not as tight blood sugar control, with the idea that if you really control the blood sugars really well with insulin and other medications, that they would do a lot of better. It turns out though that there was basically no difference between the two groups. And it wasn't just an isolated finding. Every single trial showed the same thing.
These are multi, multi, multimillion dollars of trials. They last like four, five years. They're very well done and then all four showed the exact same thing which is that there was no benefits to lowering blood sugars. And that was a real shock to a lot of people. But what it really did is that it really pointed out that that paradigm of just control the blood sugar is entirely false. There are still a lot of people who cling to that sort of idea but really if you follow the evidence there's really no benefit to lowering blood sugars.
And the question really is why is that true? Well, I think the idea is that this blood sugar causing all the damage, that's where it really doesn't compute. Because we know that type II diabetes is a disease of too much insulin resistance. That's really what causes the high blood sugars. We don't treat the insulin resistance. That's the disease. The disease is too much insulin resistance. It causes the symptom of high blood sugar.
And yet we treat the high blood sugar, which is the symptom, as if it's the disease. But it's not. So take an analogy. Suppose, for instance, that you have an infection. You need to treat the cause of the infection, which is bacteria, with antibiotics. An infection will also cause a fever but that's just the symptom. If you treat the fever but not the underlying infection, you're not going to get better.
And that's exactly what we've done in type II diabetes. We've treated the symptom of the disease as if it's the disease and we haven't done a damn thing about the insulin resistance. So all along we give medications, insulin and so on to make the symptoms look better but the disease continues untreated.
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So what happens is that people get worse. So if you look at what happens to most people, they start with one medication then two then three then four then insulin then more insulin then more insulin. What happens is that over a period of ten, 15 years, their disease has not gotten better. It's only gotten worse. So that's exactly what we see. So that falls precisely in line with what we expect because we've been treating the symptoms. We haven't been treating the disease.
So yes, you have to go back and start thinking about how you're going to treat that insulin resistance in the first place. And it's not within insulin. It's not with some of these other drugs because those are medications for blood sugars alone.
Christopher: Okay. So briefly then, just before we go into the questions, what do you think the appropriate treatment is?
Jason: Well, you have to go back to what causes the insulin resistance. And you have to understand that in biological system, there is propensity for anybody to stay kind of in its comfort zone. It's called homeostasis. So if you kind of perturb that, it will kind of go back to that. So if you give any kind of hormone in a kind of persistent high level, your body will develop resistance to it. For example, if you give antibiotics all the time you'd develop antibiotic resistance. If you look at drugs, for example, for cocaine and marijuana or alcohol, if you give it all the time, people will start to develop resistance to it.
If you're in a dark room all the time you'll develop so called resistance. If you're in the light you'll develop resistance. If you're in a loud room, you'll develop resistance. It's just normal. If you expose the body to a constant high level stimulus, it will develop resistance because it needs to fight that, because it wants to get back to its comfort zone. So if you think about insulin resistance, the easiest place to look is for insulin itself. The most likely cause of insulin resistance is persistent high insulin levels.
You can show that experimentally. You can take normal healthy people and just continuously infuse them with insulin. They'll develop insulin resistance. You can do it within a few days. So normal healthy young men will develop 25% of insulin resistance within like a couple of days. If you look at insulinomas, which are these rare insulin producing tumors, what you'll find is that people develop high level resistance because the insulin levels are very high.
The body is very smart. That is if you give it tons of insulin all the time, if you don't develop resistance, your sugars will go to zero and then you'll die. So the body has to develop a resistance to it. So if you look at it that way then you can see that insulin is what caused this insulin resistance. But the knee jerk reaction for the body is to just give more insulin to kind of overcome this resistance. You can see that that's counterproductive because that's just going to cause more resistance.
Christopher: No, that makes perfect sense. That actually segues quite nicely into Marty Kendall's first question which is: Which one is worse insulin toxicity or glucose toxicity or both?
Jason: They're both different, right? I mean, if you have sugars which are extremely high for an extremely long period of time, that's probably pretty bad for you. The problem is that a lot of that data is confounded because it's a high insulin resistance which causes the high blood sugar just like the infection caused the high fever. Is it the fever that kills you? No, it's the infection that kills you. It's the same. Is it the high blood sugar that kills you? No, it's the fact that you have a ton of type II diabetes, a very high insulin resistance.
So all that data with the high blood sugars is all confounded by the fact that it indicates in the absence of medication. In the absence of medication, that high blood sugar indicates very bad type II diabetes. But giving medication to lower that blood sugar doesn't make you better just like giving Tylenol to lower the fever doesn't make the infection any better. You're treating the symptom. But all that data that comes out that says, "Wow, high blood sugars are really bad for you," well, a lot of times it simply means that type II diabetes is really bad for you.
But the studies have shown that except for very high levels, the high blood sugar probably doesn't make any difference. I mean, it's very interesting because that's what you should have seen in all those studies, the ACCORD, the ADVANCE, the VADT, that lowering blood sugar from a relatively -- levels were not super high. A1Cs were about 8.5. They lowered it down to about 7.5. So you went from slightly high sugar to, well, the kind of moderately high sugar to slightly high sugar. So the sugars came down but you didn't see any benefit. So it's hard to see except if your sugars are super, super high that there is any benefit.
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Now, if your sugars are running like 15 or 20 or 30, well, that's like off the charts high. You should probably do something about it. But the problem is that everybody forgets that that's really only the symptom. You got to treat the disease, which is high insulin.
Christopher: I'm almost slightly shocked by the numbers that you're talking about there. that's perhaps the kind of circles that I run in. What percentage -- we're talking about hemoglobin A1C here. So what percentage do you think means there is no diabetes?
Jason: What, A1C?
Christopher: Yeah.
Jason: The thing is that A1C is a continuous variable. There are definitions but like, for instance, people define in the absence of medication that A1C of 6.5 is labeled diabetes, 6.0 to 6.5 is labeled pre-diabetes and under 6.0 is labeled normal. That's just labels, right? That doesn't mean that 5.9, you're fine and 6.0 you're not fine. It's a continuous variable. Like height. What do you call tall? Is 6' tall and 5'11" is not tall? So you're short. It's like there's only an inch difference.
It's the same thing. When you look at people not on medications, then the A1Cs are very accurate reflection of how much insulin resistance you have. So the fasting blood glucose, the hemoglobin A1C, they're all very good to tell you how much insulin resistance you have. And the more you have the worse you are. So even in the normal range without medication a 5.9 is definitely worse than 5.4 but it doesn't mean that taking insulin to get from a 5.9 to a 5.4 does you any good.
Because now it does no longer reflect, that blood sugar no longer reflects the amount of insulin resistance that you have. And that's the whole point. You got to focus on the disease, which is the insulin resistance not the blood sugar. That's sometimes helpful if you don't take medication.
Christopher: Okay. And then so what markers do you track? So fasting blood sugar, hemoglobin A1C, triglycerides. Is there anything else that you track?
Jason: I mean, we track all of those things. I mean, everything tells you something different. But the point is which is the mistake that I think a lot of people make is that they look at the A1C, for instance, and they say, "My A1C is 6.9, that's good. Now I bring it down with insulin to 6.5, that's good." But it's like all you did was take insulin to bring it down. I can bring anybody's blood sugar down with insulin. It doesn't mean that I make them better. The whole point and to ask the most important thing is to get people off medication.
If you're getting off medication and your blood sugar is staying the same it means your diabetes is getting better. Not your blood sugars. I could care less about your blood sugar. That's only a symptom of the disease. I only care about if you're taking medication I want to get you off medication because that means your diabetes is getting better. And everybody confuses type II and type I. I mean, they're totally different diseases. You can't even talk about them in the same sentence, right?
Type I diabetes is a disease of too little insulin. So should you take insulin? Of course, you should. But if you have a disease of too much insulin, like type II diabetes, the last thing you want to do is give more insulin. All that does is lower your blood sugar. It doesn't make your underlying disease better because your disease is too much insulin. So it's really like treating an alcoholic with alcohol. Yeah, your shakes get better in the short term but your alcoholism doesn't. It can hide the problem. If you give an alcoholic alcohol, it will hide your problems for a short while until they need more and more and more and then you say, "Well, then we'll just give you more to hide the symptoms some more."
So if the disease is too much insulin, you got to get it down. If the disease is too little insulin, like type I, you got to give some. It's not that difficult to understand. But people confuse the two all the time because they're so focused on the blood sugars.
Christopher: Right. And you did a really good job of ripping through all these questions without ever having been asked them. There's just tons of people asking the same type of questions. What number should I strive for with a fasting insulin test? What blood sugar goal do you set for the elimination of all medicine? That type of thing.
Jason: Again, it doesn't matter what your blood sugar really is. I mean, you have to understand the disease. The disease is not a disease of high blood sugar. That tells you, in the absence of medication it tells you where you are. So you should strive for it to go as low as you possibly can. But going low with medication does you no good.
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So let's take the example of an infection. What should your fever target be? What should your temperature be? You'd like your temperature to be normal without any medication because that means your infections almost are better. But it doesn't mean that you keep taking Tylenol until your fever, until your temperature is 37. It makes no difference whether your temperature is 37 with Tylenol or 39 without Tylenol, it's the same thing.
The medication kind of distorts, it hides the problem. It makes you look better. That is if you keep taking Tylenol, Tylenol, Tylenol and no antibiotics, you can pretend that you're better. You say, "Oh, I have no fever. I'm a lot better." But you're not actually better. The infection continues to fester. And it's the same thing. There's no target really for A1C. What you're trying to do is get off of medication and then go as low as you can because the higher you go the more insulin resistance you have.
And the other thing that people never understand is that type II diabetes is a disease that develops over decades, 20 years, 30 years. If it develops over 20 years, it's not going to go away in like a month and a half. And everybody expects it to. But it doesn't happen that way. It takes time to develop, it takes time to go away. So you got to give it the time. And the number, the blood sugar number, if you're off of medication, it tells you, it indicates to you that, hey, you're doing a good job or not doing a good job. On medication, you really just can't tell.
Christopher: Okay, I understand. I've got another question that's going to make an assumption. Marty Kendall asked when is a low carb diet not enough and when do you need to try fasting? So the assumption here is that a low carb diet can help with type II diabetes. I'm assuming that you believe that that's true.
Jason: Yes. So again, if you look at what the underlying cause of type II diabetes is, the way I see it is it's basically a disease of too much insulin. Once you look at it that way, then you can say, well, then the treatment is pretty easy. What you need to do is lower insulin. How can you do that? Low carb diets do a fine job of that. But the other thing you have to understand is that sometimes there are non-dietary measures. If you have a lot of insulin resistance, the whole point is that insulin is too high. Carbohydrates are notorious for raising insulin so low carb diets are going to be helpful.
But the other thing is that insulin resistance itself can lead to high insulin levels. That is, think about the antibiotics and the antibiotic resistance. Suppose you have antibiotic resistance. Then you go out and use more antibiotics. That gives you more resistance. Then you use more antibiotics. It's a vicious cycle. Same thing happens in insulin. If you have insulin resistance, your body produces more insulin. Try and overcome that resistance. But that increased insulin causes more insulin. That increased insulin causes more resistance. And it goes on and on and on.
And that's why both obesity and type II diabetes, they get worse with time if you don't interrupt that cycle. Because you keep going back and forth, the high insulin needs the resistance, the high resistance needs the high insulin, the high insulin needs resistance. So it keeps getting worse. The problem is that after 20 years, if your major reason why your insulin levels are high is because of insulin resistance, then changing your diet is not necessarily going to help. Because it’s the insulin resistance that's really causing the high insulin levels.
So the thing is that if that's the case then you really need to target that insulin resistance and that may need something bit more than a low carb diet. Yeah, it will reverse the cycle. If you lower the insulin levels for your diet, you'll slowly reverse that cycle. But it could take you 20 years. Because it took 20 years to develop in the first place. So you need to do something a lot stronger if you want to see some decent results.
So the point is, I mean, the short answer to the question is if you're not seeing the results you want with a low carb diet, then you either have to go very low carb like ketogenic or you have to try something else to lower insulin levels because it's not necessarily just the carbohydrate that is leading to high insulin levels. And that is the whole point of the carbohydrate insulin hypothesis. What it says was that carbohydrates, this insulin leads to obesity and type II diabetes.
But the carbohydrate insulin hypothesis is not correct. There's lots of things that raise insulin and lots of things that lower insulin. So it's not just the carbohydrates. And if it's not just the carbohydrates then you really have to understand what is it that's causing the increased insulin and really target that so that you can get it. So if you're not getting good results on a low carb diet then you need to change it to something else. Ultimately, the most effective and the most efficient way to lower insulin levels is fasting which is why we use that quite a lot.
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Because most foods, almost all foods raise insulin to some degree. So again, if you look at the disease as this is just the disease of too much insulin, how am I going to lower insulin? Well, if all foods raise insulin like -- sure, olive oil might not but who drinks olive oil for dinner? That's not realistic. So if all foods do raise insulin then the lowest you can go is to eat zero, which is fasting. So when you fast, your insulin levels may still be high because of all of that insulin resistance. But there's no way you can get it lower than that.
And the other point is that there's very few medications that lower insulin. There is one now but for many years there is no medication. In fact, we were doing the opposite. We're giving insulin which is exactly what the wrong thing to do. It's the knee-jerk reaction. You give insulin to shove that blood sugar down but you're making the insulin resistance worse. Again, it's the same thing. It's the alcohol to an alcoholic. You're giving insulin to a disease state that is characterized by too much insulin. Why would you ever think that would work?
Christopher: I don't know. I really don't know. That's an excellent question. So why don't you explain what do you mean by fasting then? So we're not talking about intermittent fasting, having dinner at 4 o'clock in the afternoon and then skipping breakfast. We're talking about something different.
Jason: Well, it's all the same. Intermittent fasting and fasting, they are the same thing. It's just a question of how long you do it for. And there's no set rules or anything that you have to do it. If you do a longer fasting you'll get your insulin levels lower and that's it. A lot of people do intermittent fasting where they do kind of 18 hours of fasting or so. You can do it longer, 24 hours of fasting. And those will be fine.
And if you do them long enough they'll certainly have some benefits. But for a lot of the people that I treat which are severely insulin resistant, it often isn't -- you'll still get results but it'll take you years to get the results that you want. So we will opt with fasting. So we'll do it but we do it in a very supervised setting. We check their blood work, we have to check their sugars. They come in all the time. And they'll do longer periods of fasting. Sometimes a week at a time, sometimes longer.
And we'll adjust their medications because we really can't do this without supervision. You can do shorter periods of fasting without supervision, probably okay, but longer periods, you really have to adjust the medications and so on. And by doing that, what we do is we basically force the body to burn off all that excess sugar. After it burns off all that excess sugar, the sugar comes down, you don't need to use as much medication. It's not really that hard to understand.
After it starts burning all that sugar, then it starts burning fat. And in the end you got to ask yourself, okay, if you don't eat, are your sugars going to come down? Sure. Well, what's wrong with that? If you don't eat, are you going to lose weight? Well, sure you will. What's wrong with that? Everybody tries to convince you that you can't do it, you can't do it. Well, people have been doing it for 10,000 years at a minimum. If we weren't able to last more than 24 hours without eating, we would never have survived the species.
Everybody worries about all kinds of things like, "Oh, you're going to eat your muscle. You're going to burn your muscles." It's like, right. So the body stores fat as energy and as soon as you need it you start burning muscle and you need your fat there. Well, that doesn't make a lot of sense. Why would we do that? Lions, for instance, might eat once a week. You think they're burning their muscle as soon as they stop eating? I doubt it. I suspect that people burn fat because that's the way it was designed.
It's like storing firewood. So you spend all winter storing firewood but as soon as the temperate goes down you chop off your sofa and throw it into the wood burning oven. Isn't that insane? That's the same thing. So we store energy as fat but then when it comes down to crunch time we burn our muscles? I don't think so. What you do is you burn sugar and you burn fat. That's the way it's stored and that's the way it goes.
So when we talk about fasting, intermittent fasting, they're just really the same thing. It's really just not eating anything but for various lengths of time. People put different labels on it. But I use it, a fair amount, for type II diabetes and even the most severe. I mean, we have people on 200, 300, 400 units of insulin a day. They go down to zero. We have them off everything. And that's the whole point. It's not that the blood sugar is the be all and end all which some people seem to think it is. The point is to get off these medications because that means your diabetes is getting better.
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Christopher: Let's just be clear about this. So some of the fasting protocols that you are talking about, they go as long as 20 days even.
Jason: We don't use a lot of protocols because there's so many things that are different. People's lives are different. So the most important thing is to find something that fits into their lifestyle, the medications, how well they tolerate. So some people love the long fast and some people think it's like the hardest thing in the world. So if you don't like it then don't do it. Do something else.
So there are all different, we use all different things but we individualize it. Some people, for instance, will love the long fast, the seven-day fast. And other people find it extremely disruptive to their lives. The way that they're used to living their life with their family and their job and all that doesn't really work. Then don't do it. So there's so much variability that we tend not to use so many protocols. We tend to talk to them and say, "Look, this is the best thing to do."
So everybody thinks that you can just make a protocol of it. Sure, you can. I can tell you do this and this. But if it doesn't fit into your life, it's not really going to work. It's kind of like if you tell somebody, "Oh, just eat tofu all the time." If they've never eaten tofu and they hate tofu, well, that's not a very good diet. It's the same thing with fasting. If the 36-hour fast three times a week works a lot better for somebody then do it. There's no reason why you have to force yourself into one specific thing.
The most important part of fasting is to fit it into your life and your lifestyle. If an 18-hour fast everyday is what works for you then do it. If you don't get the results you are looking for then change it, intensify it, do something. But you have to really look at the person and kind of fit it in. But any of them will work. If it's a shorter fast, you probably have to do it more frequently. If it's a longer fast, you don't have to do it as frequently. But that's about it.
Christopher: Okay. And do you worry about -- So I've got someone here asking about their fasting putting too much stress on the adrenals. I'm not sure how much I'd really agree with this idea but there's some people out there saying that you need to eat more often if you have so called adrenal fatigue or low cortisol. So I have seen -- We've done in our practice hundreds of these saliva cortisol panel. And I nearly always see low cortisol. So I know it's common at least amongst the people that I work with. So is that something you worry about whether it's going to, somebody with already fried adrenal is going to get worse if they're going to a fasting protocol?
Jason: I have never really seen it. I think a lot of people worry about it more than it being real. Cortisol levels, they can change. It's a sign of stress. So it depends. A lot of people do fasting. If they're totally stressed out by it then it's fine. But other people don't find it very difficult so their cortisol may not change. It's variable. I mean, you can look at what does grow up, things like noradrenaline levels go up.
So if you look at resting energy expenditure, it tends to stay stable, growth hormone levels go up. So blood glucose can actually go up because a lot of the counter regulatory hormones are actually stimulated, right? So that's a normal thing. So if you're fasting, if you're not eating, then your body is supposed to produce glucose because you're not putting it in your mouth.
And in type II diabetic situation, you can have high blood sugar. It doesn't matter. That's not the point. Everybody focuses on the blood sugar but think about what insulin does, for example. So insulin takes the sugar from your blood and it doesn't get rid of it. It just shoves it into your body. So if you thought that glucose was toxic in your blood, why isn't it toxic in your body? Basically, what we do is we take that sugar that's in the blood and we shove it into the body with insulin.
And it sends it elsewhere. It turns it into fat, it sends it into the eyes, into the kidneys, everywhere. So the sugar goes in everywhere. Yeah, exactly. So that's what the insulin does. It takes the sugar from the blood but it doesn't get rid of it. It just keeps forcing it into the body. So if you thought that the sugar is toxic in the blood, why wouldn't it be toxic in your body?
So think about what we do to type II diabetics. We haven't take lots of insulin to get their blood sugar down but we keep forcing all that sugar into the body. And eventually everything just starts to rot -- your eyes, your kidneys, your nerves, everything and that's why type II diabetes affects every single organ system in the body because you're not getting rid of it. You're just hiding away the problem. And that's all the outcome of focusing so purely on the blood sugars. It doesn't matter.
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But in terms of adrenal fatigue, so the cortisol level can sometimes go up. And I've seen it go up with fasting and people are very unnerved or they're having a lot of tough time with it. And sometimes the blood sugar goes up with that cortisol because cortisol, growth hormone, noradrenaline, those are all counter regulatory hormones. So they actually tend to raise the blood sugars. In the adrenal fatigue, I can't say I've ever seen it.
Christopher: Okay. And then you don't worry about the differences between men and women. So I've got Denise asking that fasting for women might be a bad idea. And I think you've addressed it in other, on your blog in particular. Maybe I should link to that. But if you wouldn't mind briefly.
Jason: Yeah. It's a funny thing because there's this idea that women shouldn't fast. And I'm not really sure where it came from but there's some posts that are very well read that say it doesn't work and they shouldn't do it. It's not really true. First of all, you have to understand there are people that really shouldn't fast. People who are severely underweight, people who are pregnant, children, people who are breastfeeding, people who are malnourished, you shouldn't be fasting. That's not the hardest thing to understand.
But if you're [0:31:28] [Audio Glitch] or you're overweight, then what's wrong with fasting? Nothing really. Some people worry that you're going to [0:31:44] [Audio Glitch] or situation. Or people used to fast or they used to be -- If you're 300, I think that's probably 60% of our clients in the program are women then there's really no difference that I noticed. And funny because I read these posts where they talk about women shouldn't fast.
I'm thinking, okay, I put probably 500 women on fast on various durations. I've never seen a problem. In fact, women, if anything, do better than the men because that's just what happens. A lot of them are more dedicated to it and so on. And these people are right about how women shouldn't fast, I'm thinking have you actually ever -- the bottom line though is that clinically we put many, many, many on fast. We see no difference between men and women. They do just fine. But you don't put pregnant women, you don't put breastfeeding women, you don't put malnourished women on fasting. That's just kind of common sense.
Christopher: Right. Right. And then what do you think the difference, say, you have an athlete -- Some of the people listening to this podcast will be athletes and maybe some of them are concerned with body composition as it affects their performance. What do you think would happen if somebody who was just maybe had a few pounds to lose but not much really were to go on to a fast? Do you think you would see a change in some of the physiology that you've already talked about? Do you think you would start to see a lean person catabolizing lean muscle mass in order to produce glucose?
Jason: No. Again, that doesn't really happen. There's a short, very short period of time where you are burning protein but not necessarily muscle. In fact, if you look at the physiologic changes during the fasting, they actually should be highly beneficial to many athletes. So if you look at what happens then noradrenaline goes up so you're basically going to get more energy so their workouts are going to be more intense, you're going to have higher levels of growth hormone which means that building up muscle is going to be easier and post workout kind of where we did the recovery period is going to be shorter.
And you're going to burn fat instead of sugar which is also highly beneficial. So in fact, there's a ton of these people, ton of these elite athletes like Olympic level athletes and higher who all talk about just training in the fasted state. It's funny that people think that they have no energy, they can't exercise or burn their muscle. In fact, even if you go back to the ancient Greeks and stuff, a lot of their Olympic athletes, the original Olympic athletes, they had tons of fasting all over the place.
Because what you want to do is you want all these changes. So, for instance, there is a movie called Serial Killers 2 which talks about the guy who did -- he rode from San Francisco to Hawaii. It was an amazing feat. And when he talked about his training and stuff, he talks all the time about training in the fasted state.
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What he means is that he'll fast for 24 hours and then he'll do his workout. So the benefits he's going to see is that he's going to have a higher level of adrenaline. He's going to have a more intense workout. He'll have higher growth hormones. He'll recover faster. And lay down muscle faster. That's great.
If you're looking for every edge that you can get, that's a huge advantage. And there's a lot of research about that, about pseudo adaptations and so on. It does take a bit of time for your body to get adapted to it but once it gets adapted to it, you wind up being able to do these ultra marathons and so on much longer. Professor Tim Noakes talks all about this sort of exercise physiology and so on. It's a very fascinating area. Fasting is really just kind of outgrowth of that sort of thing. They both do similar things. But yeah, if people want to look for an edge, there's an edge.
Christopher: I wanted to ask you about gluconeogenesis in lean individuals. We know that certain tissues in the brain and anything without a mitochondria, so red blood cells, have an absolute requirement for glucose. So where is the substrate for that glucose coming from? That's my question. I guess you've already alluded to the fact that primarily we're burning fat but still where do you think the substrate from the glucose is coming from?
Jason: So in terms of the fat, the triglyceride, what happens is that what you do is that you take the fatty acid chains, make that broken off, and most of the body is going to be powered on fatty acids. So the muscles and the liver and so on, most of it is going to be powered off of the fatty acids. Now, you also produce ketone bodies so the brain, which is the biggest user of kind of glucose is actually going to be powered off of ketones. But not entirely.
So about 75% of your brain's power is going to come from ketones and the rest will require glucose. And then you have the renal medulla and the red blood cells which require glucose. So the glycerol backbone actually gets turned into glucose. And that's really how you power yourself. In the initial phase when you're moving between kind of burning sugar, using glycogen and lipolysis, that's where you're breaking down the triglycerides, there's a short interval there where you may breakdown some amino acids.
But it's fairly short lived. During prolonged fast, you really don't have a lot of muscle breakdown. And that's what almost all the studies show. There's a normal turnover of proteins. You do need a certain amount of protein for a day but it doesn't have to be taken kind of day after day. You can take it when you break your fast. So a lot of the gluconeogenesis substrate is going to come from glycerol. That's where it comes from.
Christopher: Okay. Yes. I was just wondering. I did spend some time looking at this and I wonder whether you had any good studies that you could reference that maybe we could look at. So what we're talking about is triglyceride consisting of a glycerol backbone with three fatty acids attached and then you can take two of these glycerol molecules to make single glucose. I was kind of struggling to find any good studies that show that glycerol can make a meaningful contribution to gluconeogenesis. Did you have any in mind?
Jason: Yeah, I mean, I have a link on my blog. So if you look at all the Cahill studies, it shows much the same thing. You're going to have a daily, so there's a daily turnover of protein. Every day you break down a bit of protein and you replace it. So there's a daily turnover of protein. And that continues. So you do need a certain amount of amino acid daily. But what you don't see is that spike up. You don't spike up your protein burning to turn into glucose.
So if you look at the -- So Kevin Hall who recently did that six-day kind of metabolic ward study from the NIH, he's done some studies of fasting. He shows where the energy is coming from. Cahill has done the same thing. That was back in the '80s. And there's basically studies all through showing where the energy is coming from. Most of it is not coming from protein. Again, there is a baseline protein turnover. That doesn't change.
So at some point you do need to take the protein again. But it's a small amount. And a lot of it, don't forget that when you break down protein -- So if you turn protein into, if you turn amino acid into glucose then it's lost. But if you simply break down amino acids because of turnover of protein then you can recycle those amino acids into new proteins. If you look at the amount lost in urine, if you look at the amount lost in feces, for instance, it's much less.
[0:40:05]
You don't have to replace all those daily amounts of amino acids. But that baseline level continues, that baseline turnover of protein does continue. So you can't go indefinitely. For sure you can't go indefinitely fasting. You do need protein every day. But you don't turn all this protein into sugar which is what everybody says.
Christopher: Okay. So you don't get your patients to be really careful with protein or having them restrict protein for fear of it contributing to gluconeogenesis.
Jason: No. We don't. We don't really worry about that. Most diets in North America are way, way, way over the actual minimum amount that we need. Probably like three, four, five times the minimal daily requirements of protein. So most people get more than enough protein. We were talking people here eating 20%, 30% of calories as protein. I mean, you could go as low as 5% and do fine, so really about five, six times the amount of protein that we need in a regular diet.
Yeah, at some point you have to resume a regular diet. You can't go on forever, of course not. But those amino acids are going to be replenished without very much difficulty. And that's exactly what we see clinically. The thing is that you have to understand the physiology but then you have to look clinically at what happens. And we don't see any problems with protein deficiencies. We measure all of that. We measure urea, we measure albumin, we measure electrolytes.
We don't see any of those problems. And it's funny to me because we put maybe 700, 800, a thousand people on fast. We measure their electrolytes and everything kind of weekly and then monthly and then somebody always comes up to me without ever having done a fast, without ever putting anybody on fast, "Oh, you're going to get a problem with this."
I'm like, okay, you're telling me. Having never supervised a fast and I've like a thousand and measured all their blood work and followed them clinically and talked to them, you're telling me there's a problem. Right. Strange. The internet is a strange place, right? You get people that just give their opinion and sometimes they're taken seriously. I'm thinking, but you've never actually done it so how would you know?
It's like maybe I should give Michael Jordan some basketball tips. You should do this when you should pass. It's like, come on, that's ridiculous. Michael Jordan is the greatest basketball player who ever lived. What do I know about it, right? It's crazy. There are people who have ever done it think that they should give advice on how to do it and why you shouldn't do it and stuff. It's like, wow, it's a topsy-turvy world here.
Christopher: Well, this has been fantastic. Thank you very much. Where do you point people? Where should people come to find you if they're just kind of new to this idea of using fasting as a therapeutic measure. Where should they go?
Jason: You can go to my website. That's www.intensivedietarymanagement.com. And we talk about all kinds of things. We talk about obesity. There's a lot of misconceptions there. We talk about not so much type II diabetes although we're getting into that. We talk about fasting quite a bit as a therapeutic measure. I have a number of videos. They're linked on the website but they're available on YouTube for instance. They talk about, again, diabetes and so on.
That's probably the easiest place. I have a book that's coming out in March of next year called The Obesity Code which again talks about a lot of these ideas not so much with relation to type II diabetes although it's a very similar thing but more to do with obesity. But it also coves a lot of the ideas of fasting and so on. Obesity is also very interesting in that we get bugged down in this entire concept of calories. It's like, okay, well we've been doing calories for 50 years and it just hasn't worked.
But then you get these people who insist that it's all about the calories. If it's all about the calories, don't just think we would have a little bit of success treating this, right? But we haven't. I mean, the proof is in the pudding. There's this huge obesity epidemic even as we've eaten low fat, low calorie and at least our advice has been to eat low fat, low calorie. There are those who argue that, oh, people just don't follow the advices. It's like, well.
I think it's more likely that the advice is just not good. So it talks about that a bit. That's what we spend a lot of time on our blog. But it's a similar, the obesity and type II diabetes, they're really, I think, both diseases of too much insulin. I think both are caused by the same thing and both can be treated by the same thing. And that's why they're so tightly linked together.
Christopher: Interesting. It's a fantastic blog. I will definitely link to that in the show notes so people can find that easily and the presentation too which is fantastic.
Jason: Thank you.
Christopher: Well, this has been great. Thank you very much, Jason. I really appreciate your time.
Jason: Thank you. This was great.
Christopher: Cheers then.
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Christopher: Okay. So Jason Fung said a couple of things in my podcast which I thought were curious. I want to learn from him but he said something which I thought was very strange which was that someone with a hemoglobin A1c of 6.5 is cured of diabetes and could be off of medicine and that he couldn't care less about blood sugar. I'm kind of quoting him out of context here a little bit. What do you think, Tommy? Would you be happy with a hemoglobin A1c of 6.5?
Tommy: No, absolutely not. But if it had come down significantly -- Because what it basically tells you is it gives you an idea of your blood glucose, your average blood glucose over a period of time, so two to three months, the average life of your red blood cells. And 6.5 is pretty high. That would still put you just in the bottom of the diabetic category, which I think starts at 6.5 or they say 6.5%. So I think it's just within or just around the cutoff range. So that might be kind of what he's talking about. You're sort of out of the full blown diabetic range and into the pre-diabetic range. And then at that point you can say you no longer have diabetes, you have pre-diabetes.
Christopher: Okay. Yeah, the context maybe important here. Maybe this person that he's been working with has come down from an A1c of eight, say.
Tommy: Yeah, absolutely.
Christopher: And so that would be relevant. But he said something else which was that anyone can lower blood glucose. I can give you medication. I can give you supplements. But where do you think those sugars are going to go? They're going to end up in the delicate tissues of the kidney, in your eyes, somewhere else where they're going to cause damage. I mean, again, he's the nephrologist but I didn't think that was right. I thought that the sugar would be stored either as glycogen or as fat.
Tommy: Yeah. He's right that those are the tissues where you see damage. You get diabetic nephropathy or you get diabetic retinopathy, so you get problems with various things that could go on in your eyes and that's why diabetics get their eyes checked and their kidneys checked very frequently. But if you're disposing of glucose, if you're lowering somebody's blood glucose, that is going into the main tissues. It's going into muscle or it's going into the liver or it's going into the fat. Because those are the real sinks. The eyes aren't a sink for glucose. They're not that so metabolically active that they can take up that glucose.
And if the blood glucose is being actively lowered then you're actually exposing those tissues to less glucose. I think we talked about this. There's been some nice animal data that basically shows that the effects of hyperinsulinemia and hyperglycemia have sort of an additive effect. So all the people focus just on lowering blood glucose. Other people focus on just lowering insulin. But I think actually the best approach would come from trying to manage both at the same time. So you can't completely discount one or the other.
Christopher: Right. Yeah, I know. It's funny because he makes a similar analogy and I'll touch on this in just a second. If you had all this sugar floating around in your bloodstream and your body wanted to get rid of it real quick, you wouldn't just shove it into your eye, right? I mean, how does that make sense? And then he said something else about glycerol. Triglyceride has a glycerol backbone. So if you could think of this chemical structure there's a glycerol molecule and you can take of these glycerol molecules and glue them together and make glucose.
So you can effectively make sugar from this glycerol backbone in a process called gluconeogenesis. And he said that that's where the glucose comes from when you're in a fasted state. Imagine you're doing an extended fast and you still need some glucose to power your brain and your red blood cell and maybe some other tissues. Then that's where the gluconeogenesis substrate is coming from and that you're not catabolising lean tissue. And we looked into this before I did the interview and I don't think it's true, is it?
Tommy: No. So just to correct you quickly, there's one glycerol per triglyceride. But you would combine two glycerols into a glucose molecule when you're sort of--
Christopher: Right. Sorry. I thought that's what I said.
Tommy: Yeah. Or you may have said that and then I misheard you. So two glycerols make a glucose. I think there's two main studies where you can look at data and one is worked by George Cahill. There's a huge amount of work on fasting. And then there was also a study looking at the men in the Minnesota starvation experiment, which a lot of people talk about. It's probably one of the robust studies we have in terms of long term fasting, effects of long term fasting or long term caloric restriction. And in both of those, they show that in lean people, you can sort of start to prevent--
[0:05:11]
So basically, you need to generate some glucose because some tissues in the body need glucose, say, the red blood cells and certain parts of the brain. And if you're not taking any of that in, then it has to come from somewhere else. And a lot of where it's going to come from initially is from muscle tissue. It's going to come from protein breakdown and you'll get some gluconeogenesis from protein and certain amino acids.
As you fast for longer, it sort of stays about the same, the amount of muscle that they end up using. But people will have more fats on offer. So in obese people, the amount of protein that they end up turning into sugar drops over a few days and stabilizes within a couple of weeks probably. But that's very variable actually how much people access their fat stores in that way. But even in the people who had been fasting for a long period of time, say a month or more, and maximally using glycerol for gluconeogenesis, they can probably still only use about, get about 60% of their glucose from glycerol. So from the breakdown of fats. And the rest has to come from muscle tissue.
So even in those people who are really good at using glycerol to make glucose, they're still losing about 20 grams of protein a day. And you can look at that by looking at the nitrogen that ends up in the urine, sort of a turnover of protein. And 20 grams of protein doesn't sound very much. But if you think that 20 grams of protein is 100 grams of muscle, so in a week, you're still losing upwards of a pound of muscle potentially and that muscle is going to be really metabolically important.
So I think there's a real risk particularly -- So I think one of the ways that you can mitigate this is with exercise. So we see the same thing in patients with cancer cachexia. So basically, you have a metabolically active cancer and you have a lot of information going on, very similar thing happens as if your sort of long term starving yourself. And those people, if they do exercise, resistance exercise and walking particularly, so you're actually getting a stimulus into the muscles, then you preserve muscle mass.
So I think if somebody is fasting for a long period of time and they can do a reasonable amount of movement, particularly resistance exercise, then they could mitigate a lot of those effects. But in a sedentary person who's just plain fasting. I think that's a real risk to lose a reasonable amount of muscle mass.
Christopher: I hope this has been helpful. So my fear is that people will hear the interview and then start asking me questions, "Hey, this guy Jason Fung said that blood sugar doesn't matter, so why are you getting me to check it?" That's the situation I'm trying to avoid. I think it is important to check your blood sugar. And the other thing I'm trying to avoid is having you believe that fasting, especially if you're kind of lean to begin with, is not going to lead to a decrease in lean muscle mass because I'm pretty sure it will.
Tommy: Yeah, absolutely.
Christopher: Okay. Well, thanks a lot, Tommy. I appreciate it.
Tommy: No problem.
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