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Diet Doctor Podcast
#23 - Dr. Jason Fung, MD
#23 - Dr. Jason Fung, MD

#23 - Dr. Jason Fung, MD

Diet Doctor PodcastGo to Podcast Page

Bret Scher, MD, Dr. Jason Fung
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25 Clips
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Jul 2, 2019
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Episode Summary
Episode Transcript
0:03
Welcome to the diet doctor podcast. Today. It's my pleasure to be joined by. Dr. Jason Fung from the IDM program. Now, Jason has been revolutionary in his use of intermittent fasting to treat obesity and to treat diabetes. And in this discussion, we cover a lot of that. But we take it a little bit further and you get to hear Jason's perspective about how other diseases such as cancer polycystic ovary syndrome and even little
0:30
Hints at longevity. How they can all be related to a similar process of too much insulin? And we talked about where the levels of evidence exists for this and how we can kind of approach patients both with and without the evidence. So I hope there's a lot of take-home messages that you can that you can take away from this interview to see how you can Implement them in your lives if your supper suffering from any of these issues, but also how to sort of reframe this issue of insulin its impact on our lives and our health.
1:00
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 talked about the definitions and we talked about ways to make sure it's done safely because that's very important. Just because something's good doesn't mean more of its 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 we still a practicing
1:29
Just and that sort of where all this started. But now, with 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 Fang. And if you want to learn more, you can get the transcripts and see all our prior episodes on diet dr.com.
1:52
Dr. Jason Funk. Thanks so much for joining me on the diet. Doctor
1:55
podcast. Oh great to be here. Finally.
1:58
That's great to have you. So we already had Megan Ramos who worked with you at IDM program and talked about the amazing work that you and she and your whole team are doing implementing fasting as a tool for metabolic health and reversing diabetes and weight loss, but it's not without its controversy. Is
2:17
it? No, I mean, I think it's because it's really
2:20
Not been standard for the last sort of 20 to 30 years, prior to that, people didn't care much. Right, but, you know, in the last 30 Years, everybody thought we had to eat, had to eat how to eat to lose weight and you know, all this other stuff. So it has been controversial and mostly because it goes against the grain. I mean, when I first thought about fasting, I thought it was a bad idea to write and then you hear so much like oh it's going to burn muscle is going to wreck your metabolism and don't skip breakfast.
2:50
And all these sort of things that make it sound really scary Until you realize that people have been doing it for like thousands of years,
2:58
your haste. And when you talk about fasting, I mean, I think the definition is really important because some people get in their minds, tend a 15-day, these prolong fast, but then really, it's mostly shorter fast that you're using in your program. Isn't that right? Yeah,
3:13
exactly. So in the 60s, for example, when people are doing all these studies, they would be doing like
3:20
30 to 60 days of fasting. And you got to remember these are not like obese people. It's our people that had, you know, very low body fat, because there were just wasn't that much obesity and they're going on 60 days of fast. And it's like, okay, that's not a very good idea. Right? And that's where people got into trouble, like, they should have been fasting, but they did it for some study. 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,
3:50
Nine people or something like that and they fasted them for like 30 or 60 days. Then they gave them a big whack of insula know Jesus. Like, and I'm thinking why did they do that? And when the answer was like just to see what would happen, sort of. So they dropped the sugars to like very low. I think in it was like one point something in the Canadian unit. So it's like probably like 30 or something like that. Something ridiculously low and everybody was completely asymptomatic. So, you know, these are the
4:20
Studies no one would ever do now, right? You don't do that kind of thing. And that's, you know, you don't have to take those sort of risk. So that's where people go more towards the shorter fast and there's no reason not to do them. And, you know, you gotta understand that fasting is sort of a part of the normal life. Like that's where the word breakfast comes in. You're supposed to feed, then you're supposed to fast. It's like, what's wrong with that? Right? You have a word that tells you that it's actually part of your daily schedule. And now, you know, fasting for 12 hours.
4:50
Is like insane. It's like, you know, that everybody in the 70s didn't write like without even thinking about it. So, it's sort of come all the way around that. Oh, you shouldn't even go like more than two hours without eating. It's like, okay. Well, what about, you know, the normal nightly fast, right?
5:10
Yes, and that's what makes interpreting the science of fasting, sort of difficult because depending on how you define it is going to depend on how you interpret the science.
5:21
You and the folks at your program recently, just published three case studies of some remarkable benefits with fasting with people getting off their insulin and reversing their diabetes within days with fasting. But it was it was an alternate day fasting. So never more than a 24-hour fast in, those three patients. All right,
5:40
so this is stunning. So all three people middle-aged, they had sort of between 20 and 25 years of type 2 diabetes.
5:50
Of them five plus years on insulin and big doses like 60 units sort of thing. And it took a maximum of 18 days to
6:00
get off of all their insulin, a maximum of 18 days. That's
6:04
incredible. It was ridiculous how quickly they got better in the schedule use because we had two protocol eyes. It somewhat is 24 hours fasting three times a week. So this is the thing is that within you know, less than a month. They had significantly.
6:20
Your type 2 diabetes, even a year later. I think two of them are off all meds and non-diabetic by the classifications, you know, by A1C. And one of them I think was on some metformin still but came off all the insulin and three out of the four medications or something. So doing ridiculously well for an intervention that is actually free available to anybody and has been used for thousands of years with this sort of ridiculous how quickly some people can get better.
6:50
And you know, as I was saying it's like this is something that really need people need to understand because it causes so much disease. Type two diabetes. I mean 20 years of diabetes and we had just proved that that 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
7:18
and it was all completely
7:19
preventable.
7:20
Exactly, like in a month, they could have taken care of the whole
7:24
thing. Now, in this case series. They were following a low carb diet in addition to the intermittent fasting. So do you find the success varies with low carb and without low carb when you're instituting intermittent fasting?
7:36
Yeah, for sure. We recommend low-carbohydrate diets for all of the the the type 2 diabetics and its really along the same lines. I think. Type 2 diabetes, is largely a disease of hyperinsulinemia, so
7:50
Are for both low carbohydrate diets and intermittent fasting. The goal is to lower insulin as you lower insulin in a disease of too much insulin. You're going to get better just like PCOS if it's too much insulin, you gotta lower it right 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 like it's not the insulin as evil or anything like that. Right? It's just all context. Like if you're if it's too high, you gotta bring it down. If it's too low, you got to bring it up, right? And that's how you're going to get
8:19
better. A very simple procedure.
8:20
Active, but somehow it gets a lot confused, lot, more confusing for a lot of people. They just need to realize the perspective there, so that the concerns about fasting are the safety of it. So one being your resting metabolic rate. Is it going to go down with fasting? And again time frame matters, doesn't it?
8:38
Yeah, for sure. And if you're, you know, if you're looking at some of the studies now, so nobody does these 60-day fast sort of and studies it, but there's been a few studies of
8:51
Alternate day fasting. And it's a lot of these are not sort of true fast. So you have to extrapolate somewhat, but they're 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's 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. In some studies. For example, 1,
9:20
Study where they just 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 you know, I don't know why people get so bent out of shape. Like so if you don't eat insulin drops, okay, we know that that's for sure happens and when insulin drops the counter regulatory hormones, go up, we know that that's why they're called counter Reg.
9:50
Realtor hormones, they will counter of insulin. And one of the big ones is sympathetic tone. Like, that's not for debate. That's a
9:59
sympathetic tone. You mean adrenaline? Adrenaline?
10:01
Adrenaline? Adrenaline? Yeah. So it's the basically the fight or flight response. So if you see a lie in your sympathetic tone goes way up and you either prepare to fight or run, really, really fast. So, your body actually increases growth hormone sympathetic tone, our adrenaline to actually bring glucose into the blood, right? It floods, the
10:20
Body with glucose that you can use to run away. That's Medical School physiology. Okay. So if you think and cortisol to, so cortisol is one of the counter regulatory hormones, but if you think about, okay, if sympathetic tone is going up, you know, you're activating your body. That's what sympathetic is. Parasympathetic your 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 bags and metabolic rate. It's like, come on. This is medical school stuff.
10:50
Stuff. Like why is this a debate and all the studies show that there's probably less effect on the basal metabolic rate from sort of real-world studies on Alternate day fasting and stuff. Yeah, most of them allow calories and so on. So there there you have to interpret them a bit but, you know, come on. It's like, why do we worry about this? Where did this notion even come from? Because it actually, if you fast, you're going to decrease your metabolic rate that actually runs counter to
11:20
What we all learned in medical school of what happens when you don't eat
11:26
with one, two, three, day fast, at least we can say that with
11:29
certainty. If you're going 30 days and 60 days. Yeah, you're talking about something totally different and almost Nobody Does that like we generally don't recommend that either. I mean, for us, we're like why take the risk, so if you're doing 30 days, if you want to, it's great, but if you don't, if you look at it, it's more powerful, but there's our wrist. So why don't you just do?
11:50
Do more shorter fast and that's the sort of trend towards where we've gone. So, when the 60s, everybody was like, oh, fasting is like a month, right? And it's like, okay, fasting, nowadays like 16 hours is controversial,
12:03
right? Yeah. It's amazing how times change. Yeah, and so, the other big concern is lean body, mass loss, muscle loss nitrogen wasting, and depending on how you measure it. It seems like you can come up with different
12:15
conclusions. Yeah. So again, you can definitely measure, you know, nitrogen.
12:20
It's right. And then you have to say, well, is it muscle, or is it not muscle? Because, not all protein is
12:25
muscle, right? So actually should clarify nitrogen, waste, meaning measuring the nitrogen, sort of in the urine that you urinate out. And then the question is, where did that nitrogen come from in the bottom? Right? Right. And I
12:35
think it depends a little bit on what your perspective is. So if you're talking about a leadoff, but it's then, yeah, you're talking about something totally different than what I'm talking about. For the most part which is sort of middle-aged and elderly people who are mostly
12:50
Beast. So there's a lot of excess protein sitting there. So if you look at again, we're not talking, Elite Athletics, but if you're measuring it, there's been studies and they say that obese, people generally have both 20 to 50% more protein than a normal person. And that's all skin. That's all connective tissue, right? There's a lot of skin when you look at those programs where they have those skin surgeries are taking out like 40 pounds of skin, right? That's not fat. That's protein. So, there is a
13:20
As 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 it's all protein that needs to go. So and again, if you look at the studies that have compared intermittent energy restriction, so I ER versus CR which is chronic restriction. And there's been a few most of them generally show that there's less loss of lean mass and as a
13:50
Percentage, so one study from 2016 that was published in obesity. For example, shows that, you know, you get about 1.5 increase in percentage of lean mass because people are losing weight with chronic calorie restriction, but it goes up by 2.2 percent and intermittent energy, restriction or fasting. So in fact, you're preserving lean mass much better. If you're using the fasting strategy, but this is sort of short-term 24 hours.
14:20
Les strategies. So again again if you think about it, it's like okay.
14:28
If you think that the body is when it has no food, it's going to bypass your, you know, excess protein like skin, connective tissue and go right for your heart muscle. It's like, you must think that the body's really, really stupid. Like, honestly, like, you don't eat for 24 hours. Oh, you're gonna start breaking down your diaphragm. Like why would the body do that? Like
14:56
a muscle is a muscle base.
14:58
So it how does it know to Target certain muscles and not
15:01
others? It wouldn't lay, it wouldn't it's gonna go for the stuff that's not needed. And how would we have survived? If our body was so incredibly stupid, that every time you don't eat, it starts breaking down your muscle. Like, let's think about this for a second, like I do is fairly regular fasting. So if I'm losing like a quarter of a pound of muscle every time I
15:28
You know, fast for 24 hours. It's like yeah, I should have like zero muscle right now, right? I should be this giant blob of fat. Instead. I'm pretty much the same, you know, composition as I was a couple years ago when I didn't fast, right, it just didn't make any
15:46
difference. Do you recommend resistance training to try and stimulate muscle growth or maintain muscle during the faster. Do you think even that's not necessary?
15:55
I think it's always good to do it.
15:57
No doubt, but the thing about it is that the body is like, honestly the body is incredibly smart. So if you put a strain on the system, it will respond by getting stronger muscles. Work like that. Right? So you put a little bit of damage on your muscles, it rebuilds it to get stronger. You put weight on the bones and they respond by getting stronger. So if you, you know, look at astronauts, you take away gravity and all of a sudden. Hey there bones tr8 like
16:27
Crazy their muscles deteriorate like crazy. You put a man hospitalize them and put them in bed. Rest only which was remember the whole to change what you do is you take the strain off the muscle. 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 to sit in bed all day. Like, why would the eating have anything to do with it? Eating doesn't make you gain muscle, right?
16:57
Otherwise, we'd all be a nation of like, you know, Arnold Schwarzenegger's right? It doesn't happen. The two, totally separate things, right, you build muscle because you are working it. Then you lose muscle because you aren't working it. Yeah, if you're working it and not eating, your body is going to come up with a way to build that muscle. That's just the way it is, right? Otherwise again, if you look at these these Native Americans and all these people who used to go through these
17:27
He's feast and famine Cycles. Right. And it's like they were not little Globs of fat running around the Prairies, right? When the Pioneers came, they were lean and muscular and you know, strong because your body responds to that. And I think it's it's really silly to think that our body is just so maladapted to life
17:50
interesting perspective, right? That the body knows and we just have to listen. Yeah, help it on its way. Yeah.
17:57
And then they're obviously number of other issues about making sure you're well hydrated, and have adequate sodium intake. And, you know, reduce medications, if necessary. And I think that's a big issue of doing this on your own versus doing it, with professional guidance. So yeah. Yeah. Tell us some of your perspective on that and some other things you're doing to help with that.
18:16
So yeah, that's that's our IDM program and it's basically to provide the education people need because it's not easy. I mean, it's it worked, but it's not easy. It's not fun, right? I'd rather be eating.
18:27
Donuts myself, but it's healthy. And that's the thing is that, it is something that will improve your health. So you need to get educated as to what to expect. So, if you know that, for example, headaches are very common, but they'll go away, then you can deal with it. If you know that you're going to get hungry on their tips that might help you deal with that hunger, then that's going to help you in terms of the fasting. So it's about getting the proper education. And that's what we provide with our eidm program and also,
18:57
A supportive community and that is really sort of 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, right? The Weight Watchers meetings and that's the secret sauce. Right? Same for Alcoholics Anonymous. It's not like, you know, they didn't know to, hey, stop drinking. It was that you had a supportive group, you had a sponsor and you had a thing. So, so doing it with the
19:27
Community is just way easier, and that's a secret of how all these communities used to fast. You do Ramadan. Hey, everybody's fasting. Hey, it's landed, everybody's fast ahead, jump, where everybody's fasting. So, it's not fun, but it's not as hard as it would otherwise be because if you're trying to fast and everybody's telling you you're stupid and eating like, you know, in front of you, it's like, that's not the easiest thing to do. So don't, you know, you go out of set yourself up for success, and that's what
19:57
Up to do with with the IDM program. That's a great point. And
20:01
there are a lot of communities built around fasting that are sort of popping up. So people can support themselves and I think that's valuable. Now with fasting, you can look at it from two perspectives in terms of, what do you treating? And one is treating diabetes and obesity and insulin resistance. And another is just promoting longevity. That's a whole another field of research, which now with your book, the longevity solution, your it seems like you've sort of delve more into longevity. So tell us a little bit how the
20:27
And set changes when you're, when you're focusing on longevity, rather than just treating a reversing a medical
20:33
condition. Yeah, that's a great question. I think it's really a matter of how to sort of maintain Health throughout life. And so we look then this book on a lot of sort of ancient Wellness practices because I'm not about selling the latest supplement that's going to make you live forever, right? I don't think that exists but
20:57
Are certain practices that have sort of withstood the test of time that is, they were considered to be Wellness practices, two thousand years ago. And I think that has Merit because those practices have kind of sort of withstood The Crucible of time. Like, if something's really bad for you and people do it. They'll like die out. Right? So the fact that these practices are these Foods or whatever, have survived means that they're probably
21:27
E is something. And what's interesting is that the science is starting to catch up in fasting is one of these things. So, if you look at the signs of longevity, the the one thing that really stands out huge as calorie restriction, so that is probably the single most well-studied mechanism for longevity and animal studies mostly. But intermittent fasting is sort of a play on that and that it is a way to restrict overall calories, and maybe there's a better way to
21:57
It but at least it's been used for a long time as opposed to sort of protein restriction or carbohydrate restriction. Those have not been used for as long. So intermittent fasting is a way to do that. And the physiology is that you know, a lot of these growth factors are also nutrients sensors and I think this is actually a really interesting things. If you look at the theories of Aging of why we age or there's sort of this.
22:27
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, but it's not going to last very long because it's going to burn out and it's the same thing. If your body is always growing 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
22:55
program and as part of that when you're
22:57
Green growth or stimulating growth. You're going to grow the healthy cells, but you're also not going to be able to just limit it to the healthy cells. So potential cancer cell growth or abnormal cell growth to leave to chronic disease. So exactly, we can't necessarily differentiate it.
23:12
Exactly. Because their part and parcel of the same thing. When you look at the growth Pathways, for example, you have something like igf-1 which is insulin-like growth factor 1 and so insulin. And both both insulin and Insulin like growth factor, 1 are very similar.
23:27
And their growth hormones. So you can look at a population of Ecuadorian doors. For example, a called the lehren dwarves and what was super fascinating, is that this group of dwarves, which they're persecuted from 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 or the small population. They all a lot of these.
23:57
This dwarfism occurred and a few years ago. It was when they're following these dwarves. They realized hey, these guys actually don't get cancer and they don't get diabetes either and then they send their like what's the difference between this dwarf? And the other one is like they have no IDF one. They just and it's like, wow. So here's a, you know, here's the thing is that if you slow down the growth program, then you
24:27
You might be able to age better. So it all depends also on what stage of life. So if your child, if you're an adolescent, you do you want that growth program
24:35
running right? Growth isn't by its definition bad. We need to grow. We need to build muscle that's part of Health as well. So it's exactly finding the balance which can be tricky.
24:44
Yeah, but if you're going now for longevity, so, if your average age of like a, you know, if you're like, in the Middle Ages or am, your average age is 30, then, yeah, it doesn't matter. You run that as hard as you want.
24:57
It don't matter because you're gonna die of like the black death or something. Right? And so it's like it doesn't matter. But now if you're trying to get out to like 80 90 years old, you have to be a bit smart. So just like that engine. You can't run it full speed, you got to cut back at some point. So if you look at the what stimulates growth the most, it's things like insulin insulin like growth factor M. Tour and ampk which are all
25:27
And 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 whether nutrients are available.
25:42
If so nutrients, sensors, meaning they're turned on or inhibited just by having nutrients in your body.
25:48
Exactly. So, if you have like, you know, an ovary for example, its way on the inside. How is this supposed to know if
25:57
Food coming in while it knows it because when you eat insulin goes up and when you have protein mtor goes up for example, and if you eat fat ampk as also goes down. So those are nutrient sensors because it's the body's way of sensing if nutrients are available and they are actually the exact same ones as growth. So now if you want to say, okay, well this growth pathway after, you know,
26:27
Age, 30 or whatever. I don't really want to go full bore on growth because I want to live to 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, which is ampk. And, of course, that's something that fasting
26:48
does. And so, the question always is, where is the threshold for this, right? Because again, chronic calorie restriction, can sort of lower the stimulation of it, but you know, the old
26:57
In may not make you live longer, but it sure makes life feel long. That's not as enjoyable to do. Yeah. So with the intermittent calorie, restriction, or intermittent fasting, where's that threshold? And how do we know? Because we can't necessarily measure mtor, an EMP kinase and 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.
27:23
Yeah, that's a really good question and it really comes down to
27:27
Maintaining a sort of stable body weight and get making sure you don't have the visceral. Obesity says because the one thing we know of course is that the metabolic syndrome is going to shorten your life, right? It's going to give you heart, attacks is going to give you all kinds of stuff cancer and so on and that's dependent on not body weight, but waist circumference, you know, type 2, diabetes, and hypertriglyceridemia and all that sort of thing. So we know that those are all very important and
27:57
Those are obviously highly linked into hyperinsulinemia and so on. So if you're looking for a surrogate marker, that's been clearly correlated to disease and that's going to affect longevity. It's all those things. So if you are fasting and your weight is just way, way way, you know down and yeah, you probably don't need to be doing that. But on the other hand, doing it every so often might be something that's very beneficial. And again, if you look at it, it's like there's that sort of
28:27
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 longer? Maybe not. But if you are 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
28:57
Protein and
28:58
stuff. But that's really really hard to measure because it's not as easy to see. Ya
29:03
for something. That's so hard to measure mtor. Sure gets a lot of air time and a lot of discussion and it is pretty controversial because we needed to grow. We need it for immune function. But yet we can't have. We shouldn't have it turned on all the time. And part of that concern is cancer. So, this is another field that you've been fairly vocal about about fasting insulin, as it relates to cancer. And that can
29:27
Be controversial as well because cancer, there's the one theory that it's all sort of a genetic mutation. And you know, the drugs were developing our these high-powered weapons. So to speak to, to Target specific genetic variations of cancer, and then there's the sort of the opposite side saying, no, it's more of a metabolic disease, or maybe it's a combination of the both. So how do you incorporate that into your thinking and fasting in terms of cancer, prevention or treatment?
29:52
Yeah, and I think that the cancer is like a fascinating story because for
29:57
You know, since I was in medical school, we all talked about genetics. It was all a genetic disease, right? Is just genetics, genetics, genetics. It's a mutation. It's genetic mutations. If we can find the mutation and block it, we're going to cure cancer. Of course, that didn't happen. Right? So we got the Human Genome Project was going to cure cancer, and then he had the cancer genome Atlas, which was an even more ambitious, attempt to find out, you know, the mutations of cancer because we thought there is one or
30:27
R2 mutations turns out there's like hundreds of mutations and not only mutations like between people. So one breast cancer, cell to the next person's breast. Cancers might have like 100 mutations and 100 completely different mutations on the other kind, but even within the same tumor there, different mutations, so, there are mutations everywhere and clearly you're not going to develop a hundred medications to block every single, a hundred different drugs, to block every single mutation. So that was sort of a
30:57
Dead End Theory. And the other thing is that it's not about genetics, but it's about the interaction of genetics and the environment, and we sort of forgot that it depends on the environment. So looking at obesity. For example, the World Health Organization list, 13, cancers as obesity-related, right? And including breast cancer and colorectal cancer, sort of the number two. And number three, cancers after
31:25
long, which doesn't mean that
31:27
Obesity causes these cancers, but plays a role plays a role in, makes it more likely so sort of. Yeah, if you have a genetic mutation and you're obese. Now, the deck is really stacked against you,
31:39
exactly. But now there's something you can do about it. Because if you have a genetic mutation, there's nothing you can do about it. You have it, like, I'm not going to change it. If you have it, you have it. I can't do anything about it, but I can change the environment in which that cancer cell lies, because we know it's
31:57
Vitally important. So you take a Japanese woman in Japan, and you move her to Hawaii and then San Francisco the rate of breast cancer. Like, triples, even though the genetics are exactly the same. 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
32:27
AB, 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, right? And if you give them, lots of in some, 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, and it didn't cause the cancer, right? That, but after
32:57
Cancer cell. Is there you're going to stimulate it to grow if you have a lot of insulin. So that so type 2 diabetes, a disease of hyperinsulinemia, higher risk of cancer. Obesity disease of hyperinsulinemia, high risk cancer. And then you say, okay. What about the other ones? What about ampk, for example, what blocks ampk, or what effects ampk metformin? It's like, oh, well, you know, that meant Foreman, a lot of studies has been
33:27
Associated with a significantly decreased rate of breast cancer. It's like, is it the effect on ampk? The very interesting hypothesis? What about mtor? It's like, because those are the three main nutrient sensing Pathways. Well, mtor, you can block them tour with rapamycin and guess what it is.
33:50
And anti-cancer medication, right? Why because you're blocking the pathway. So rapamycin super super interesting because I blocked them to. All right, so as developed as an immune suppressing drug, and the thing about immune suppressants is they generally increase the rate of cancer because the immune system sort of destroys cancer on site. So if you give a drug that suppresses, the immune system like these transplant patients, you give tons of drugs to suppress the immune system cancer goes.
34:19
Crazy and that's why actions infections absolutely, but sort of unique amongst these immunosuppressants cancers went down. It's like wow that is
34:31
specific one with rapamycin
34:33
rapamycin. Yeah, it's like fascinating because you're blocking MTAR. So because you're blocking growth Pathways, you don't have the you know, that's why it blocks the immune system, but it also blocks cancer because it very specifically Targets this nutrients.
34:49
Seeing growth pathway. We turn the same thing which is now amenable by the diet.
34:56
It's like so it's a fascinating field and one of the things that's important though is to talk about the level of evidence of support. So what you've been talking about is a mechanistic level of evidence of support and with the Japanese women, moving to the United States, sort of the epidemiological or observational. So we don't know. It was the diet. We know it was environmental change and the diet, too.
35:19
Part of that and the mechanisms you're describing. Certainly makes sense. So it all seems to fit, but yet we don't quite have those human trials, to say. Yes, it works, which can that make it a little uncomfortable for you to recommend fasting for, for that, right? Oh, yeah, for sure, for
35:34
sure. Because you don't know what the effect is. But you know that, for example, if you use fasting to reduce obesity, you're likely going to have a beneficial effect. They can't say that for sure. Like, and the other thing is that, where this is.
35:49
Mention, right? So this is you're talking you don't know if you're you don't know if you're going to prevent it because you know now if somebody's going to get it or not and you're not doing those big trials that are going to say, well we fasted sort of a million women and a million didn't and you know, this is what happened, those trials. Don't exist. So now you're talking about going into treatment and that's a, you know, a totally different thing. One. I don't think that there's much data whatsoever, but there is some super interesting data about sort of
36:19
Of combination therapy, right? So you say okay. Well, diet is not going to cut it for treatment. Like you can't have breast cancer and just think you're going too fast. And, you know, yes, there's a few case reports and so on forth, but for the most part that is not going to to work for most people but can you combine it with say chemotherapy to to make it better? And that's something that's, you know, really really fascinating.
36:49
Because, for example, fasting, it 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're targeting rapidly growing cells, but the hair follicles grow quickly, the the epithelial cells of the intestinal system. For example, are very rapidly growing.
37:19
I'm so therefore you get nausea vomiting and hair loss though. So if you put these if you now fast 48 hours, for example, and you get these cells to ramp down their growth, they will enter sort of a more quiet and 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, you know, a lot of a lot of treatments have to be ramped back because to my side effects so you can get the
37:49
Treatment or maybe get higher dose treatment because you're looking for this maximum tolerated dose, right? And then there's some interesting data to suggest that maybe that, you know, so the worry of course, is that the cancer cells will also go into this sort of protective state, but apparently, there's some preliminary data that suggests that doesn't happen because they're stuck in this sort of on mode, right? That's the whole point of cancer that they're in this sort of growth
38:18
mode. I don't have.
38:19
The normal feedback loops. So yeah, exactly. Is that? So for
38:23
prevention, you might be able to do something about it, but for treatment maybe you can combine it and then of course they talk about combining a ketogenic diet with drugs. For example, does that going to be beneficial? So they do these things? So the pi3k pathway is actually the growth pathway. They have drugs that can block it, and they say well, what if you down regulate insulin by eating a ketogenic diet and then give the drug like can you do?
38:49
Better than doing either one alone. And those studies are very interesting but there's not a lot of data. So cancer is more of an evolving story that I think we really, you know, would be, you know, it's super interesting. But
39:03
yeah, safe to say it's in its infancy but shows promise and so maybe the next five to ten years. We're going to have a completely different discussion and say yes, here's what the evidence shows. Yeah. One way or the other.
39:13
But the the one thing you know, for sure is that in the prevention, if you can prevent the
39:19
Lisa T and you can prevent the type 2 diabetes. There is a good chance that you're going to prevent some of these diseases. So remember, colorectal and breast cancer are the big ones in terms of obesity related cancers because they've already been declared obesity related cancers, right? So, with the idea that hey, reducing obesity is going to reduce the breast cancer. For
39:42
example, yeah, certainly makes sense. So now transitioning from longevity and cancer to procreation.
39:49
So you gave a talk today about PCOS polycystic, ovarian syndrome and, you know, you're a nephrologist, right? So you Dimension. What is a kidney doctor doing? Talking about the ovaries? So, draw draw the line, connect the dots for us.
40:03
Yeah, and I say that I'm not, I wasn't very interested in the whole disease until a few years ago when we started really treating people and Nadia who works with us at the IDM program. She's one of the educator she was like, well, you know, all these women are getting
40:19
Pregnant. There's like 15, 20 women who have gotten pregnant. I'm like, whoa, that is really interesting. And we've always known that PCOS polycystic. Ovary syndrome is related to obesity and the insulin resistance and type 2 diabetes. So it was sort of part of that whole metabolic syndrome, sort of spectrum that I had been talking but I hadn't really looked at closely into it. Then I you know, as I got interested I said, okay, let's look at
40:49
What happens with with it? Let's look at the pathophysiology. 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 you get under the influence of too much insulin, your ovaries actually start to produce a lot of testosterone and when you have a lot of insulin, the liver, decreases sex hormone-binding,
41:19
Globulin, so, the effect of the testosterone is increased because there's not a lot of this globulin to bind it. So, the free testosterone is more active. So therefore you get all the symptoms and the hair growth. The acne, clitoral enlargement, other things, that that is sort of very typical
41:39
and infertility.
41:40
Yeah, the infertility comes from the an ovulatory cycle. So, you know, if you look at the insulin, what it does is it causes something called follicular?
41:49
Rassa, during the normal menstrual cycle, you have a developing follicle and then the sort of, you know, the big pops out and then it becomes the corpus luteum that, that in volutes. That's a normal menstrual cycle. If it doesn't get pregnant, then you get the the bleeding and the period. So if you have too much insulin, then you get follicular arrest. And that means the follicle stops developing at a certain point. So it never ovulates. So, never reaches the
42:19
The size that it's going to ovulate and if it doesn't ovulate, there's no egg and you can't get pregnant. So that's another, that's the infertility. And the thing is that, if it doesn't ovulate, it doesn't become the luteal body. Which then in volutes, which means that it's sort of just 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
42:49
Those are the three sort of criteria of PCOS. You've got too much insulin, which causes the follicular arrest, which causes the sis. You've got too much insulin, which causes the follicular arrest, which causes the anovulatory cycles, and then you've got too much insulin, which causes the hyperandrogenism. So the whole disease is a disease of too much insulin and it's been, well, worked out and it was in this review article. So it's like, okay, well, like that.
43:19
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 treat it. Right instead. That's
43:31
not how we treat it. We give drugs, we get stuck.
43:36
This is a total replay of like, 9 2 diabetes. So here, you know the cause and you know, the answer, the answer is, if to insolence too high, you gotta drop it. How are you going to do?
43:49
That low carbohydrate diets ketogenic diets intermittent fasting. Instead. We give birth control pills. We use Clomid which is a, you know, causes the ovary to start hyper secreting and let's like, okay, that is not the answer, right? It's like
44:06
so again, mechanistically makes complete sense. And now the level of evidence to my understanding is low carb. Diets can reverse a lot of the hirsutism, the hair growth, but I don't know that we have any
44:19
Any evidence saying it, improves fertility, but yet, there's lots of anecdotal evidence of that happening. Right? Do you think that we're going to bridge that Gap? So that this will become a more common
44:29
trip ends if anybody's interested in actually looking at it now drug
44:33
companies are interested. That's for sure.
44:35
That's right. And, you know, and this is one of the reasons that they use metformin because they use it as a sort of, you know, insulin sensitizer, which makes a little bit of sense. So at least that makes a little bit of sense, but
44:49
You know, it's the question is, who's who's looking at it? Like these low-carbohydrate diets haven't been, you know, used for a long time because of the worry about the dietary fat and intermittent fasting hasn't been used. I mean, when I started talking about it, like, 6 years ago, like, I was like, really just a lonely voice in the wilderness, so nobody, but nobody was studying this. So, yeah, it's are the studies going to come. I I hope so. I don't know.
45:19
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 science and medicine. It's like everything in medicine comes down to risk versus reward. Okay. So if you give a drug like a beta blocker, you do a stand or something. It's like what's the risk of doing a stent? That's because there's Risk, Everything has risk. And what's the reward? If the risk is more than the reward, you don't do it. If the reward is better than the wrist. Then you go ahead and just plop in a stent, right? Or you give a
45:49
And I give beta blockers, 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 and what's the risk? If you're overweight, there's practically no risk. So then you say okay. Well, there's no risk. So any reward you get is a plus. And here's the thing that you don't have to prove if you're a patient with PCOS, if you're somebody who has P. Cos you don't
46:19
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 peace, you as 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
46:49
Your disease completely goes away. Right? Right. Now you've done something which all the drugs haven't been able to do for you. And the thing is that it's big money here. Right? So IVF is big money, right? So it's like four plus billion dollars a year. So these people who are doing fertility treatments and all this sort of stuff. Like if you ever go into one of those clinics, they're really nice. They look like a
47:13
spa right? But and it's also miserable for the women. I mean it is so uncomfortable and difficult to
47:19
To do and it can all be changed. Potentially potentially potentially nutrition know
47:24
and and it's not just the discomfort of the IVF. But like if you want to baby, it's like you want a baby. It's like very like it. Totally, like you have some emotional cost. It's a huge emotional cost and the time is ticking because people are getting married later. We know that people are having their babies later, right? So it's funny because, you know, my
47:49
Sister got married at like 20 to and had her kids. I like 24 and she was like, the latest of her, you know, friends, right? It's like nowadays. If you are getting married at like 35 and having their baby, I like 38 or something like that. Right? So if you're having your babies, I like 35 Plus, I mean that used to be considered sort of low fertility
48:11
time, right? That's Advanced maternal age
48:13
exactly. Because fertility sort of Peaks around 20, right? It's like you can't stop.
48:19
Getting pregnant at 18 and 20, right? But at 35 it's not as easy as it was. And so if you're if you're wasting time because you're like saying, oh, you know, I got to wait for the evidence and, you know, I'm going to do cycles of IVF. It's like, well, why not? Like you can do that, but why can't you add it to, or just use it instead of like it just, it just makes no sense. And that's, that's what I mean. It's like, sort of the art of the, the art of medicine because it's not like, do I have evidence that it works?
48:49
No, but
48:50
it's a good perspective. We talk a lot about evidence-based medicine and that is important to understand the quality of the evidence. Especially when there's a risk to the treatment like you're saying, so I think that was a good perspective for you to talk about, weighing the risks and benefits, which is what we do for everything. And if the risks is very, if the risk is very low, then the need for evidence is also a little bit lower. If there's a potential upside and that seems like one of those circumstances. And yeah, it was a sort of a whirlwind tour.
49:19
Or through the, through the fasting, through longevity through cancer, through fertility, and it also tends to have a common theme, doesn't it? Yeah, and this is
49:28
the thing is that we look at the and I went over this and the diabetes code is that if you look at the five sort of things that deal with metabolic syndrome, so the waist circumference and the type 2 diabetes, the hype triglycerides, low HDL and hypertension. They're actually all linked to hyperinsulinemia, but there's actually
49:49
So much more to it because it's like after the metabolic Center, you got obesity linked I think mechanistically really to hyperinsulinemia type 2, diabetes linked hyperinsulinemia piece you as like link to hyperinsulinemia, but also things like cancer where it may play a not a sort of causative role but a sort of facilitative role. I mean you're talking about the biggest killers in America from heart disease. Stroke diabetes. Cancer are sort of like
50:19
At least four of the top five. All right, and all of them are impacted by hyperinsulinemia, and I think that's a better term than insulin resistance, because it immediately tells you what you need to do. So, insulin resistance, doesn't tell you what you need to do good point. So if you say I have insulin resistance, then people will say, well what caused it? And then there's all this debate. Oh, maybe it's a high fat diet cause insulin resistance, right? I don't think so. But if you say now that the problem is hyperinsulinemia, then you say, okay. Well I have too much in.
50:49
Bring it down and then it's like, well, it seems pretty obvious how you're going to bring it down. Right? And I cut the carbs and don't eat right? It's so it's so it's a 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 a hundred years ago and you're talking tropical infections exactly infection.
51:19
Is and diarrhea. And you know, that sort of thing to what are now, you know, well the top to sort of if you like it, the cause of death, there's two and then there's everything else heart disease and cancer are just off the scale in terms of the amount of people they kill. And then everything else is actually quite a bit lower than that. So, if and those are diseases, which are going to be impacted by metabolic syndrome, and also we know cancer,
51:49
So, for so many years we just thought about as a genetic disease. It's like but what about the genetics when you put it in a high growth environment, which is a high nutrient
51:59
environment. Right? And it's
52:01
like, okay. Well, you know that cancer you go back to sort of, you know, those traditional African societies and stuff. They had cancer, right? But they had a lot of them are viral. Cancers, burkitt's lymphoma and so on but those cancers like breast cancer and stuff.
52:19
They practically didn't exist. So the Eskimo or the Inuit that we call now, so in the far north of Canada, they actually studied them very intensively to see why they were immune to
52:30
cancer and mean
52:32
they're immune to cancer, except for EBV. They got nasopharyngeal carcinoma and stuff, but they didn't get breast cancer, didn't get colorectal cancer soon. And then, of course, we took them away from their traditional lifestyle of hunting and Gathering and gave them.
52:49
Brad and, you know, seed oils and sugar and all of a sudden cancer just goes way way, way up. So, we pretend that cancer is this disease of all genetics, genetics, nice, 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 it's smoking, right? That's, let's forget that. So, the next to our breast cancer and colorectal cancer prostate, cancers number four. It's actually very common but actually doesn't
53:19
Kill as many people because it's mostly slow-growing and it doesn't affect the sort of younger age groups as much. But so breast cancer colorectal cancer, which we've already declared our obesity related cancers. 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,
53:49
That's the downside. What's the risk? Yeah, exactly. So when done safely, and that's the key. When done safely, when fasting with low carb nutrition, when done safely, can make a big impact with very little downside. Yeah. Absolutely. I was a great, a great summary and a great discussion of all that. So thank you very much for taking the time and give us a little hint, what's next for you and where can people learn more about you to hear more.
54:11
Yeah, so they can go to our website, which is IDM, program.com, which stands for intensive dietary management.
54:19
And there's lots of resources, a lot of free resources and paid resources. If you want more you can go on Twitter, usually fairly active there. I've got the books, you know, next up. We've got some, you know, I'm writing a book about PCOS which is sort of a you know, about what we talked about and also and I'm doing that with Nadia and then also a cancer book as well just talking about
54:50
Sort of, it's not like a how to cure cancer because that's not gonna 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. So we thought it was just a bunch of randomly accumulated, genetic mutations and from sort of 1990.
55:19
Ish, you know, when I went into Medical School 1992 to sort of 2010, probably it was all considered genetic mutations, but now the whole the whole theory of what cancer is has completely changed. And now we're talking about Evolution that using evolutionary biology in trying to understand how cancers develop. And we're trying talking about, you know,
55:49
The really fascinating things about cancer is why it occurs in every single cell in the body. Like almost every cell in the body can become cancerous and that's really weird and it's not just that but almost every single multicellular animal in, existence can develop cancer. So even hydro, which is one of the most primitive multicellular organisms can develop cancer. So cancer is not a disease of just human.
56:19
It's it actually predates Humanity by a lot. It's a much much more ancient than these than we knew and it actually probably dates back to the transition between unicellular and multicellular T, which is you know, what is and that's really what the fascinating story of cancer really is and
56:39
that's that's what that almost speaks against insulin resistance as being a contributor. So I think it's it's more complicated than the definitely more complicated.
56:49
But the insulin resistance or hyperinsulinemia is going to play a sort of facilitative role that it's going to make, it's not going to cause
56:58
cancer but I think it's important differences.
57:00
Yeah, exactly. If the cancer is there, it's going to make it grow faster. And that's the difference. A, you take a Japanese woman Japan. She may get breast cancer, but you put them in a high nutrient environment, which is a high growth environment. That is give her. Lots of, you know, Brad and Insulin goes way up and mtor goes way up.
57:19
Well, you know, all of a sudden that breast cancer which wasn't a problem back then or you take a look at the enemy, for example, like they clearly have the potential to develop cancer, but they're keeping insulin solo. For example that those cells never get the growth environment. There's what exactly it's the environment that matters, but then you put them in, you give them, you know, fry bread which has basically like white bread fried in oil. That's what they eat. Great.
57:49
Now, you get him a high growth environment. Now, those cells, that would not have grown do grow and that's when you start to see cancer. So we go from a time where we consider the enemy completely immune to cancer. These people don't get cancer, ever to. Hey, they got a lot of cancer over here, right? And and it's because of the environment. It's not because the genetics so that that is the story sort of story of cancer. So it's not purely just about, you know, fasting and so on. It's actually.
58:19
Lee, you know, I'm more interested in that sort of deeper story which is changing and I don't think it's the end of the, you know, I don't think that's the final answer. I think actually there's just so much more to be learned about it, but it's just a very interesting as we move from that transition, from a paradigm of pure genetics to a paradigm of evolutionary biology, which is to me a much more
58:44
fascinating and interesting structure change for sure. Well, thank you. Thank you for all.
58:49
Your information and all you're doing online and all you're doing to help people and promote the idea that insulin matters environment matter, so, it's wonderful. Thank you very much. Thank you.
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