Dr. Jason Fung on the mystery behind cancer

Let's Say Hello

[00:02:51.670] – Allan
Ras, how are you doing?

[00:02:52.630] – Ras
Good. How are you today Allan?

[00:02:54.310] – Allan
I'm doing really well. I'm doing well. I'm excited about conversation that we're going to interview, we're going to have today with Dr. Fung and his books called Cancer Code. And, you know, it's it's a big, big problem. So I'm pretty excited about the conversation. You know, as we're getting into this as this goes live, I'm going to be in North Carolina visiting my mom, the last leg, sort of last leg of our trip through the states.

[00:03:18.790] – Allan
So kind of exciting, you know, a couple weeks ago. Then we got loaded all of our stuff in a truck. So it's now in a cargo container headed down to Panama. So when I get down there I'll have a lot of stuff to sort through and a rack to build and all that. And I saw the picture that you posted on the group of your rack. So now I'm Jonesing and get that thing going down there because it's a much better rack than the one I have.

[00:03:43.030] – Ras
Nice, that will be awesome.

[00:03:46.300] – Allan
So how are things going up there?

[00:03:48.310] – Ras
Good, good. Mike and I are doing our puppy training, so Puppy is learning good tricks from Stella and vice versa. Actually, Stella is learning how to be a good dog to a puppy. So they're becoming fast friends and they've been really entertaining for us lately, which is timely this time of year. So, yeah, everything's good here.

[00:04:10.570] – Allan
Yeah, a lot of times when you get a puppy, an older dog kind of livens up a little bit, a little bit more playful than they would have been otherwise.

[00:04:16.660] – Ras
Absolutely. I was actually really surprised at how well she's taken to having a little sibling. She's teasing her with toys and and they're just really entertaining each other, which has been a real treat to watch grow.

[00:04:29.290] – Allan
All right. So let's get into the episode with Dr. Fung.

Interview

[00:05:02.530] – Allan
Dr. Fung, welcome to 40+ Plus Fitness.

[00:05:05.210] – Dr. Fung
Thanks for having me here. Great to be back.

[00:05:07.330] – Allan
You're the kind of guest that I just love having on the show because you do your homework, and after you've done your homework and you have your your case, which you say in one of your books. I've had you, I've covered you for The Obesity Code (Episode 77), The Complete Guide to Fasting (Episode 175), and then had Megan on for The Diabetes Code (Episode 321). But you do your homework and then once you have your statement, it's like, man, you just you're just like a wolf.

[00:05:32.830] – Allan
You're on it, man. And I just love your approach to these things because people are always talking about this. And a lot of people don't know about this. The book we're going to talk about today is called The Cancer Code: A Revolutionary New Understanding of a Medical Mystery. And it's a part of your wellness code trail, I guess, at this point, and like I said, I was going through the book and I'm like, this is this is completely fascinating and scary because this is not what my paradigm of cancer was.

[00:06:04.730] – Allan
My paradigm was that it's growing and we've got to get it out of there any way we can. But we don't understand cancer nearly as much as I thought we did. But we're getting there.

[00:06:16.830] – Dr. Fung
Yeah, yeah, and I think that these things are very important to understand, because a lot of times specialists like doctors and oncologists and researchers, they get caught in the sort of weeds of the minutia, which is not to say that they're not important, like you should use this drug versus this drug. Those questions are clearly important, but the frame is often missing in terms of, how are we looking at this problem as a whole? And it gets into the same sorts of things as the Obesity Code and the Diabetes Code, which is that obesity medicine sort of you get you get locked into this frame of calories calories calories.

[00:07:03.210] – Dr. Fung
Then you start talking about, oh, this food versus food, but your frame is still defined by calories as opposed to sort of hormonal responses and so on. And that's the reason it's important. Same thing with Type two diabetes. You get locked into this frame where it's all about blood glucose and you forget that the disease is not about blood glucose. Right. That was the result of the disease. It's not the cause of the disease. It's not the disease.

[00:07:29.280] – Dr. Fung
So it's the same thing in cancer where people often get sort of really focused on these very small questions and sort of leave the big questions of what cancer actually is that sort of frame unanswered. And it's important because the way you frame a question has huge implications as to everything that sort of goes on afterwards. So not that these questions are not important, but they have to you have to understand both. And this is talking about the frames or the paradigms of cancer and how you approach the disease.

[00:08:07.560] – Dr. Fung
And it's one of these things that's been changing over time, because the real question we're trying to answer here and this is, the book is sort of an exploration of how far we've come, which is not to say that there's not going to be changes in the future. Right. It may change in 20 years. That's that's clearly a possibility. But where we are now and how much it's changed in the last sort of 10 years, this idea of cancer, because the question we're trying to ask is what is cancer?

[00:08:37.410] – Dr. Fung
What is the actual disease that we are trying to treat? Because if you don't know that, then you're sort of guessing a little bit at treatments. So for the last 50 years, the main paradigm of cancer is a disease that grows. And then you say, well, why is this growing, why is this tumor growing? And the answer to that, if you ask a lot of people like, oh, it's a disease where you have these random genetic mutations which cause excessive growth.

[00:09:10.530] – Dr. Fung
So say you take a disease like lung cancer, you say, OK, well, we know that tobacco smoking is a cause of lung cancer and tobacco smoke is a mutagen. That is, it damages genes and causes mutations, and that in a chance mutation in a growth causing gene will accelerate growth. And that's been our sort of understanding of cancer for this entire time. But there's a huge problem with that paradigm of cancer, which is that the data simply didn't fit that sort of paradigm.

[00:09:50.680] – Dr. Fung
So where we were sort of 20 years ago, was that OK, so now we know that there's a mutation in a gene. So you take breast cancer, say, oh, let's look at the BRCA gene or colon cancer, let's look at this gene. So now that we identified this paradigm, we say there's a couple of mutations, two, three, four mutations. So the initial paradigm was, OK, we have one mutation, one cancer. Block that mutation, get rid of that cancer.

[00:10:19.180] – Dr. Fung
And it worked well for some stuff. Right. So CML was a great case where we did that and it worked extremely well. Then clearly, most cancers were not one gene. So then they said, well, it's two or three or four genes. So therefore, if your paradigm is that you have two or three or four genes which are mutated due to random genetic mutation, then let's find those two or three or four genes and we'll block them with drugs and then we'll do fine, we'll cure cancer.

[00:10:49.280] – Dr. Fung
And that's where we were sort of 20 to 30 years ago, where we had this huge optimism that we're going to develop great new genetic treatments of drugs, that we're going to cure cancer and wipe it off the map. And it's all predicated on this frame, this paradigm that this is what we're dealing with. So we started to look for these genes. So we had the Human Genome Project, which, you know, finished up around 2000.

[00:11:16.840] – Dr. Fung
So we sequenced the genes of an entire human genome. And that was a monumental accomplishment. And at the time, we thought, well, well, now we're going to find all these cancer causing genes and figure it out. But we didn't. So then they did something further, which is called the Cancer Genome Atlas, which was that the ability to sequence human genomes, had the technology improved so much by that time that you could you could sequence many, many, many genes. Like you could go sequence your gene for like 50 bucks sort of thing at 23 and Me or whatever it is. Right.

[00:11:53.890] – Dr. Fung
So the technology went from multiple labs in 2000 with multi-million dollar budgets to like you could go to a company, get your genome sequenced today. So by that time the human genome, by the time the Human Genome Project wound up, we did this further thing where we sequenced sort of thousands and thousands of genomes of cancer patients.

[00:12:16.870] – Dr. Fung
So we took the cancer and we sequenced the genome. So then it's like, OK, well, we take like a fifty or one hundred breast cancers, sequence and find that one or two or three genes that's causing it and boom, we're going to get some drugs to block them. So that was sort of the paradigm from 2000 to, say, 2010.

[00:12:36.760] – Dr. Fung
By the time the Human, the Cancer Genome Atlas finished, that paradigm was sort of shattered. It was like blown out of the water because we were not finding two or three or four mutations in a cancer genome, we were finding hundreds and millions of gene mutations. So that is if you take a cancer such as colorectal cancer example. One person with person A with colorectal cancer might have not two or three or four genes that are mutated, might have 80 that are mutated.

[00:13:17.580] – Dr. Fung
And so that's the number that is far out. Like you can't develop 80 drugs and give them all to that patient. It's just so far out of what we can do with cancer therapeutics. The problem was also that if you had the very next patient that you saw with the exact same identical appearing colorectal cancer, say it's in the same place at stage three, same metastasis, everything exactly the same clinically, they would have 80 mutations or a hundred mutations and they would be completely different than person A.

[00:13:53.690] – Dr. Fung
So you needed 80 or a 100 drugs for person A, and 80 to 100 drugs that were completely different for a person. Well, that's just not doable. So at last count that I saw in 2018, there was close to I think six million mutations identified in cancers. So it's just this genetic paradigm of cancer just sort of got blown out of the water. Because how can two gene genomes with, say, 80 to a 100 different mutations like different at many, many, many places, how can they appear exactly the same?

[00:14:37.220] – Dr. Fung
Like what is it that we're dealing with? We're obviously not dealing with anything random because remember, this is the whole premise of this so-called somatic mutation theory, which was that paradigm that we were using. Is that it's just this chance mutation in a growth causing gene. So you randomly mutate this growth gene that grows. And that's why growth. Right. That's, but that wasn't the case. You have all different mutations in all different genes, yet they were appearing identical.

[00:15:08.150] – Dr. Fung
So there's nothing random about this. That is, if you think about it, it makes sense, because if you take a colon cancer from a, you know, a 40 year old black woman today compared to a colon cancer from a Japanese man in the 1920s those two situations are very different. But those colorectal cancer is exactly the same. yet they evolve differently from that Japanese man and that black woman. Like they've evolved completely independently, yet they've appeared the same. Which is an interesting sort of conundrum, because if you think that cancer, is this sort of random genetic mutation, how does everything end up looking the same?

[00:15:57.410] – Dr. Fung
That's a real that's a real problem. So by 2010, this sort of random genetic mutation idea of cancer genetics was sort of blown out of the sky. And it had a lot of implications because what we saw, of course, was that from 2000, when there's this huge optimism with all these new drugs. But the amount of new drugs that have really seriously impacted cancer that is significantly improved the lives of cancer patients is sort of dwindling rapidly.

[00:16:34.880] – Dr. Fung
So, yes, there are new drugs. But if you look at the actual studies of these drugs and some of them are fantastically expensive, you're talking one hundred thousand dollars a year, two hundred thousand dollars a year for some of these drugs. The thing is that if you look at how effective they are, they're sort of like, well, they're either completely ineffective at adding months of life to somebody's expected prognosis to sort of barely improving life.

[00:17:08.030] – Dr. Fung
So. I think one study showed that on average, if you take all of these recent drugs, they improve the prognosis, like the life expectancy by an average of two point one month or something like that. It was it was really, really, really bad. And I think that that's something that we have to sort of look at, because if if these drugs are so poor, then there must be sort of this better way of looking at this disease so that we can identify new drugs because we're sort of twenty, twenty five years into this genetic paradigm. And if you go to the American Cancer Society website, for example, you'll still read what is cancer?

[00:17:48.300] – Dr. Fung
Cancer is a genetic disease of mutations. And it's like, well, that paradigm didn't actually help anybody. It's actually been a giant dead end. Not to say it's a waste of time because obviously this is a learning process. But now in the sort of last 8 or 10 years, there's been this new sort of idea of how cancer, what cancer is, how it came to be that is leading to sort of more improved treatments.

[00:18:17.490] – Dr. Fung
And that's the sort of story that I sort of sort of write about, is that what are, what is this new thinking about cancer so that we can improve people's lives, prevent cancer or identify more promising areas of research, that kind of thing. And that's the sort of evolutionary paradigm of cancer, that cancer is a disease that evolves, not a disease of random genetic mutations.

[00:18:46.110] – Allan
In one of the things that you got into in the book is in helping us understand what cancer is, you identified eight hallmarks of cancer and then you further refine that down to four main characteristics. Do you mind going through that real quick? Because that for me was a real good frame to kind of understand when we're talking about cancer.

[00:19:07.890] – Allan
And then as you took that forward, it's like, what else is like this? And you kind of took it, like you said, in that evolution, which I kind of read as a De-evolution back to basic or atavism. But it's one of those things where it's now it's a new organism. I mean, it's almost its own thing. Can you kind of talk through that?

[00:19:29.130] – Dr. Fung
Yeah, exactly. So this is what we're, so it's an interesting sort of way. We came to this because cancer, we know is, evolve, is sort of originates from our own cells. When you have lung cancer, it came from your own lung cells that when you have liver cancer, it came from your own liver cells. It's not some extrinsic thing that like an infection or a virus or something. It's something that came from your own body, but now somehow became perverted.

[00:19:58.350] – Dr. Fung
So there's lots of different types of cancers and there's, you know, lung cancer, and liver cancer, and breast cancer and so on. And they're all different in a lot of ways. So that's the way that we've always treated them. So you look at things like breast cancer and you have a different staging system compared to liver cancer, colorectal cancer, different things are important for different cancers. So one of the things that happened in about year 2000, which was a big change, was this sort of codification, not of how cancers are different, but how cancers are the same.

[00:20:35.820] – Dr. Fung
And it's an interesting story because the researchers, and it's actually one of the most highly cited research papers in oncology. So this is the sort of one paper that everybody reads and it's called The Hallmarks of Cancer. And it was published in 2001. And when you read about the story, it's like the researchers themselves didn't actually think much at the time about the paper. They said, well, they're very smart researchers. And what they did was they said, hey, like we all talk about the differences between cancers and then way talk about the similarities between cancer so we should write a paper.

[00:21:13.680] – Dr. Fung
So they wrote a paper about it and it became the most important piece of research in a long time, because when you look at the sort of lumpers litter problem. So in biology, you can either lump things together or you can split them apart. And this has important implications because you can lump things together like, OK, an apple and an orange or two pieces of fruit. So they're fruit. You can split them apart and say apples and oranges are different because they're different.

[00:21:46.110] – Dr. Fung
Like this, it's round, it's orange and so on. So you can lump them together, you can split apart. So cancer had always been a splitter. So you say breast cancer, stage one versus colorectal cancer stage four, they are different. And what you do when you split things apart is that you actually highlight their differences and you sort of investigate further how they're different. When you lump them together and say their fruit, then you can say, well, fruit share these two characteristics.

[00:22:15.360] – Dr. Fung
So it's the same thing in cancer. So what they're doing, instead of being splitters, they were sort of lumpers and said, let's look at all cancers and say how, what is it about cancer that is similar between breast and colorectal and leukemia and all these different types of cancer? So they came up with eight sort of characteristics, which is a great starting point, because in order to understand cancer, not just breast cancer, not just leukemia, but cancer, you have to know what it is.

[00:22:44.280] – Dr. Fung
And nobody had sort of defined that. So the best sort of scientific definition of what cancer is could be defined by these eight hallmarks. Which is very is a little bit technical. But I break it down into something a little bit more sort of simple to understand, which is that one, these cancers, so cancer as opposed to normal cells, and this is sort of irrespective of what type of cancer they grow. So cells don't normally grow, tissues do not normally grow.

[00:23:10.990] – Dr. Fung
Your liver doesn't continue to grow and grow and grow until it's sort of the size of a small boulder. Because it's going to impact everything else. And that's what sort of partially was so deadly about cancer. So they grow. Second thing is that they move around. So, again, this is not something that happens in normal cells. So when you consider a sort of lung cell versus a lung cancer cell, lung cell never moves around. It's always anchored to the lung, whereas the lung cancer cell moves around the body.

[00:23:45.930] – Dr. Fung
It can go anywhere. And that's why it's so that's why it kills you, because it metastasize to the liver, to wherever. So it grows and moves around. Third is that it's immortal. So the mortality, again, is not something we see in normal cells. So this is called the hay flick limit. And this has been talked about a lot in the longevity sphere. But the hay flick limit is basically if you take a human cell, so you take your lung cell and you try to grow it, it will split into two daughter cells.

[00:24:20.160] – Dr. Fung
That's that's how cells divide. But you can't do that sort of indefinitely. So when you get to a certain number of replications, that cell will no longer replicate. And we know how this works. So when cells divide, the genetic material sort of splits in two and and that's what you get. But at the end of each chromosome, which is where all this genetic material is as telomeres and the telomere is this sort of cap on the end of the the chromosome.

[00:24:52.680] – Dr. Fung
And every time you replicate it sort of shaves off one. So in other words, every time, you do the cell divides, the telomere cap gets a little smaller and smaller, smaller and smaller. When it goes away, you can no longer divide. And so that was sort of Nobel Prize winning material 20 or 30 years ago. So but it's another way that cancer cells are different than normal cells. And the fourth way that they differ is that they use a different way of generating energy, which is very anomalous.

[00:25:25.620] – Dr. Fung
And it's very interesting because it's anomalous and that's the war of effect. That is, the cancer cells and normal cells generate energy, cellular energy differently. So when we, normal cells generate energy, we use glucose in a process called oxidative phosphorylation. Which means that we take oxygen, we take glucose, we burn them together and we get energy. So we measure cellular energy as ATP and get 36 ATP per glucose in this oxidative phosphorylation, so you get lots of energy.

[00:26:00.820] – Dr. Fung
When you, but cancer cells don't do that. And it's very anomalous because cancer cells which are growing and moving and stuff, you think that they need a lot of energy. So you think that they use oxidative phosphorylation but they don't. They actually use glycolysis. Where you take the glucose and you metabolize it through a different pathway called glycolysis and you get two ATP and lactic acid. So this is, all cells can do this. So when you sprint, for example, and you run and you can't get enough oxygen to your muscles, they generate anaerobic energy, which is glycolysis, which is gets you all the lactic acid, which gives you the muscle burn and all this sort of stuff.

[00:26:43.360] – Dr. Fung
But the point is that you get a lot less energy than you generate more quickly, so that's the trade off. In cancer cells almost always use this sort of less efficient way of generating energy. At the same time that we know cancer cells need a lot of energy, so it's like that is very, very anomalous. And those are the ways that cancers all stay the same in any theory of cancer as to what is cancer.

[00:27:08.950] – Dr. Fung
So we take a paradigm like, cancer is this random collection of genetic mutations that happens to kill you? Well, it doesn't explain anything of why cancers grow like it does and that you have the growth gene, but why they're immortal, like how does it affect the telomeres? Why do they move around? Because to move around, you have adhesion molecules for example. You have blood cells which are trying to kill you, like the body has defences against the lung cell moving around the body.

[00:27:41.050] – Dr. Fung
If it's lung cell detaches and tries to move around the body, it'll get slaughtered. So these sort of genetic mutation, random genetic mutations doesn't explain why. Why is it going to grow? Why is it immortal? Why is it moving around? Why is it using warping effect? Because each of these each of these hallmarks and those aren't, those are just sort of characteristics. Those are not the actual hallmarks. But each of these characteristics requires many, many, many genetic mutations to make it happen.

[00:28:10.210] – Dr. Fung
So why is every cancer independently, so every cancer in history for the last five thousand years of humanity where cancer has existed, each cancer has independently sort of reinvented the wheel. Because like the cancer of the person Queen Atosa in the year 20 AD or whatever, has reinvented the wheel to develop all these characteristics just as the person in 2020 has. How is that? Right?

[00:28:44.440] – Dr. Fung
That's that's a very interesting question that needs to be answered. And the answer is that this is sort of an evolutionary process. And as you say, it's not a forward evolutionary process. It's actually a backwards evolutionary process. And that's how we get to there by understanding what it is that cancer is doing.

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[00:30:19.930] – Allan
One of the things that came out of this is when I was thinking about the treatment, so, you know, you hear a friend is going in for chemo or you hear they're going in for surgery. And, you know, the principle is how do we reduce the tumor size? How do we get rid of the tumor? How do we make sure we got it all? And that's because we know that cancer has the opportunity to metastasize and spread, which is how it tends to kill most of us because we'll get a cancer that's not necessarily deadly.

[00:30:45.400] – Allan
And then it's going to spread to the bone or to the heart, I mean to the brain or to the liver. And then then it is something that could absolutely kill us. Why is there still a big focus on tumor size when that's not really what's going to preserve us? That's not really going to get rid of cancer? Just seems that that's still the paradigm of most of what I hear in treatments as we need to get the tumor size down. If we get the tumor size down, we're winning.

[00:31:11.980] – Dr. Fung
And I think it comes back to the sort of old paradigms, which is to people who are thinking, well, this is a disease of random genetic mutations, which causes it to grow. So the less growth you have, the better you're doing sort of thing as opposed to saying where are we in this sort of evolutionary process of cancer development? That is to say that cancer is, so we focus on this sort of growth and it's easy to measure. So therefore it's easy to put a number on it.

[00:31:43.930] – Dr. Fung
And a regulatory agency such as the FDA can sort of say, OK, well, that's where we go. It's sort of what led us to this sort of inpass of how we got so many marginally useful drugs at this point? Like fantastically expensive, but marginally useful because of this sort of focus on size. Like the focus on size is extremely misguided because we know that it's not the size of the tumor that kills you. So about 90 percent of the deadliness of cancer is the fact that it moves around.

[00:32:24.940] – Dr. Fung
So that's metastasis. When when cancer metastasizes, your prognosis becomes very, very poor. So you have benign cancers like comas, for example. They grow very large or cysts, grow very large. It doesn't matter so much because as long as it doesn't move around, you can always just cut it out if you have to. Most of times you don't even have to. So the whole point is that, you know, you get to this stage because years ago so we know that the size of the tumor is probably a very, very, very minor part of what causes cancer to kill you.

[00:33:08.530] – Dr. Fung
At the same time, the larger the cancer is, the more likely it is to be a more advanced tumor, which means it's more likely to spread. So you get this sort of confusion between the size, which is sort of a marker for how advanced it is compared to the size, which is important in and of itself. Right. I mean, it's a very important thing, just like saying that gray hair, for example, is a marker of mortality.

[00:33:35.500] – Dr. Fung
Right? If you have more gray hair, you're more likely to die. That's true because it's a marker for age. If you're older, you're more likely to die. If you're older, you're more likely to have gray hair. But there's this confusion between sort of gray hair is going to kill you because the gray is a bad color sort of thing versus gray is just a marker for age. It's the same thing as size is. It's the size that's going to kill you.

[00:33:59.980] – Dr. Fung
Or is it because the larger it is, the more likely it is to be advanced? Right. And it's really the light. It's really that if it's bigger, it's more likely to be more advanced. And therefore you've probably had longer and therefore it's more likely to spread. So it's a very important, because if you say that gray hair is a marker for mortality, we know that the gray hair actually causes mortality. You make that sort of leap, that horrible leap of association and causation which we do all the time.

[00:34:31.660] – Dr. Fung
So when you make that horrible leap into causation and say gray hair will kill you, then you say, well, I just need to dye my hair and I will reduce my mortality by 50 percent. Well, obviously that's not true, but we've done the same thing. So a big cancer means that it's more likely advance, which would more likely kill you. So we say, well, let's make it a smaller cancer, and that is the equivalent of dying your hair.

[00:34:54.340] – Dr. Fung
It doesn't do anything, though, and we know that it doesn't do anything because, for example, in surgery. When we have a cancer that has metastasized, there's no point cutting it out or cutting it, you know half of it, because it doesn't do anything yet. Yet when we measure this sort of partial response in cancer trials or drug trials, they say, well, we reduce the size from sort of by 50 percent. That's considered positive. And you can get your drug approved on the basis of these sort of measures, which is like reducing the size or something called progression free survival, for example.

[00:35:39.200] – Dr. Fung
And there's all these sort of logical fallacies as to why these sort of markers don't work. But what happened in the sort of in the 2000s is that the Federal Drug Administration, which approves these drugs, created this sort of expedited way of accelerating drug development. So the reason we never use these sort of markers of approving drugs is because they weren't effective. But in the sort of 2000s the FDA said, well, we need more drugs, so we're going to make it easier for you to get your drug approved so you can use these half measures like gray hair and so on, so you can use these half measures like tumor size to get your drug approved as long as you go back and study to see if it actually improves things overall, that is overall survival.

[00:36:38.300] – Dr. Fung
That's the only thing that matters, overall survival. So the problem was that a lot of drugs got approved based on these surrogate measures. And they when they look back at first, a lot of drugs never went back in to see if they're actually effective. A lot of them, when they look back, found that they weren't effective. So then they actually got pulled down from the market. And other drug companies say, well, we just won't look then, because once we are approved we're just selling stuff.

[00:37:10.650] – Dr. Fung
But you're selling stuff that has never really been shown to be useful. And that's how you get into this situation. We have so many very expensive drugs that have very marginal benefits, if any benefits at all. And it's the use of these sort of surrogate outcomes. And it's the equivalent of saying we measured gray hairs and you colored all your gray hairs black and therefore you did really good for reducing mortality is the same thing. So that's the reason in surgery you never cut half the tumor because it's not useful.

[00:37:43.970] – Dr. Fung
You might as well not cut any of it in. If you could give a drug that reduces it by 50 percent, it probably doesn't do anything. And that's that's the sort of thing that we get into in the book, because there's all these fallacies. People say, well, if you're reducing cancer deaths as opposed to overall deaths, well, how can it not be good? So let's take an example, you have one hundred patients, for example, and they get cancer at age 60, they all die at age sixty five, for example.

[00:38:16.380] – Dr. Fung
So a group of one hundred patients, they get at sixty, sixty five. Now you have one hundred percent of them die of cancer. If you treat them with this drug they, like twenty five percent of them will die of chemotherapy related causes, heart attacks and infections and so on. Now everybody still dies at sixty five. So same overall effect, but now twenty five percent have died, of heart attacks and infections and whatever. Seventy five percent have died of cancer.

[00:38:52.160] – Dr. Fung
So now you have seventy five percent cancer deaths versus one hundred percent cancer death. And so you say now my drug is useful because I've reduced my cancer deaths by twenty five percent. You haven't reduced your overall mortality. In fact, you did harm by causing all these other deaths when the data will actually make it look like you could actually argue that you're actually improving things. So that's that's a big problem. Same thing with lead time bias, for example.

[00:39:21.590] – Dr. Fung
So if you and this gets into the question of screening, for example, where if people talk about screening and they say, well, how is screening bad? Because there's actually a move backing away from a lot of screening and the same thing, you have this lead time bias, which is that if you take a group of people that have cancer at 60, they died at age 70. So with screening, you discover them immediately. They survive 10 years with their cancer.

[00:39:48.530] – Dr. Fung
Say you didn't screen them and they got to that age 60. You didn't find it till age sixty nine. They only survived a year with cancer. Sixty nine to 70. So you say, OK, well, I improve my survival with cancer. From 1 year to 10 years, but it's completely artifactual. Because, in fact, the both groups got to that 60 died at 70. So you see there's all these sort of statistical things when you start to make measures that are like cancer deaths and, you know, survival with cancer and progression free survival and all these sort of terms that get used in the development of disease that actually don't make any difference.

[00:40:29.970] – Dr. Fung
So that's sort of where we got all these where we got into trouble with a lot of these things, such as the screening, which we thought more screening is better. Turns out more is not always better. There's been a lot of screening that's been a complete dud and has been sort of walked back a little bit. And that's how we got to this situation with with cancer therapeutics, where we've got a lot of marginally improved marginal improvement drugs by looking at these measures like size that just were not important in and in and of themselves.

[00:41:06.470] – Allan
Now, insulin is a is a growth hormone, it's a it's a hormone we need for a lot of different purposes in our body. It pulls in sugar into our muscles and our liver when we need it. Stores body fat when we need it. But insulin is also a very big problem for us, and it's intricately tied into cancer growth. And that has when you take that one step further, it's like, what control do I have actually over my insulin? And that's what I put in my mouth. So can you kind of talk us through that?

[00:41:35.900] – Dr. Fung
Yeah, this is the fascinating part. So again, when as we're moving from a paradigm of genetic mutations to something a little bit more nuance like the evolutionary thing. So as cancer is an evolutionary process, almost the development of this sort of new species, then you have to say, well, if it's going to be a new species, and I say that because the human body actually recognizes cancer cells as foreign cells. So it's not our cells. Right.

[00:42:07.040] – Dr. Fung
So the human body has this unique immune system. And if you are not part of the human body, it will attack and destroy you. So bacteria that come in, the immune system will recognize it and kill the bacteria because it recognizes it as non-human. Same thing as a cancer. It will actually, if you put a cancer cell, a cancer cell develops, the human immune system will just innately, without any training, just destroy that. So it is a foreign invader almost, but it came from our cells.

[00:42:38.150] – Dr. Fung
So if you see that as a genetic mutation problem, then you say things like, well, what you eat doesn't make any difference because, or your lifestyle doesn't make any difference because what you eat is not mutagenic. That is, if you like to eat sugar, it doesn't cause a lot of cellular damage. If you eat a lot of refined carbohydrates, it doesn't make your genes mutate. So therefore it shouldn't make any difference. But it turns out it makes a huge difference.

[00:43:12.470] – Dr. Fung
And we started to recognize this sort of with with in the 2000s. So this is why I say a lot of what we think about cancer has changed in the last 20 years without people quite recognizing it. We found out that there's this huge link to obesity. So a lot of cancers are actually obesity related. The WHO recognizes that leads 13 types of cancer is obesity related. So this was not something that we actually knew about in the past. So we actually, I went to medical school in the 1990s and we never talked about obesity as a cause of cancer.

[00:43:52.670] – Dr. Fung
Turns out when you look at the population attributable risk, that is, you know, in a whole population of people, what percentage of risk can be attributed to, say, smoking? It's about 35 percent. Then you say what can be attributed to diet, it's about 30 percent. So it's actually just below tobacco smoke as an attributable risk for cancer. So it's like, wow. And it far, far, far outweighs everything else you think causes cancer, which is things like radiation and pollutants and chemicals, manmade chemicals and plastics and all that.

[00:44:32.840] – Dr. Fung
Those all can cause cancer. But your population attributable risk, in a big population. It's going to be one percent, two percent, whereas diet is like 30 percent. Tobacco smoke is like 35 percent so far outweighs everything else. And then you have to go back and say, well, what is it about this diet that is making people get cancer? And that's where you start to get into these hormones that change with your diet. Things like insulin and other things.

[00:45:03.830] – Dr. Fung
So mTOR, for example, goes up when you eat a lot of protein and that turns out to be very involved in the cancer making process. And 20 years ago, people would laughed at you if you said stuff like that. But now we know that it's true. And the link is that all of these sort of diseases, sort of these hormones that are implicated in nutrition, that is you eat certain hormones, go up like insulin. Well, these sort of nutrient sensors.

[00:45:36.890] – Dr. Fung
So these are specific ways that our body knows that nutrition is coming in. So towards one, AMPK insulin, the others. So insulin goes up when you eat. So we know nutrition is coming in. Turns out that they're also growth factors, that is. And the reason their growth factors is because your body wants to grow when nutrition is available, when nutrition is not available. So if you're in the middle of famine and you're not eating anything, insulin is going to go down very low and your body doesn't want to make more cells.

[00:46:10.910] – Dr. Fung
They don't want the cells that are there to grow. They want the cells that are there to shrink or die. So that's the whole point that that these hormonal mediators of nutrition are actually the growth factors. So it's important because if you have a disease where you have excessive insulin, so Hyperinsulinemia, which we talked about in the Obesity Code, the Diabetes Code, if you have foods that are causing you to have way too much insulin. You're going to have very high signaling for growth, that is, you're telling your body not only to store fat, but you're telling all the cells of your body, hey, you should grow because lots of food is available.

[00:46:55.340] – Dr. Fung
Please grow. Please grow. And the things that are going to grow better than anything else are those cancers. So things such as breast cancer cells are very insulin sensitive. So they're very responsive to insulin. Same with colorectal. So we see this also in obesity, which is also a disease of hyperinsulinemia, where you have a huge risk increase with obesity as well as Type two diabetes. So both diseases of Hyperinsulinemia and both diseases are associated with sort of increased risk of cancer.

[00:47:28.910] – Dr. Fung
So that's the sort of link because these are independent organisms almost. These cancer cells, but they do respond still to growth signals and nutrition, so you increase nutrition such as you eat a lot of sugary food, you eat a lot of high, highly refined carbohydrates, which really spikes your insulin up. You get into the state of obesity where you have insulin high all the time, or type two diabetes, well, you're signaling increased growth, which is going to translate into an ideal sort of growing environment for cancer cells because cancer is like a seed.

[00:48:14.170] – Dr. Fung
Just because you have the seed doesn't mean that it will grow. That is, you take a seed of a plant of whatever plant or flower or something. It's not going to grow if you just put it in a little bag, but you put it in soil and give it water and it grows. Same thing with cancer. So the seed is there because it's actually in all of us, but it doesn't grow until you have the fertile soil which is provided by these nutrient sensors that is giving it the nutrition, you're making nutrition available at the same time, you're signaling it to grow as much as it can and you're in a disease of too much insulin is a disease of too much growth, which is bad for cancer.

[00:49:00.950] – Allan
OK, so knowing what we know now, we want to reduce our risk or minimize our risk. What are some recommendations that you would make now?

[00:49:10.300] – Dr. Fung
Yeah, and that's a great question because I don't think there's a lot of good recommendations that we can make right now. However, the only thing you can say is that if you are overweight or obese, then you should try to lose weight because there seems to be a clear reduction in cancer because you have all these cancers that are related. If you're not obese, then you're going to reduce your risk. Whether or not low carbohydrate diets, for example, versus a plant based versus paleo versus whatever diet, there's not the amount of data that you can say, well, you should follow this diet.

[00:49:51.730] – Dr. Fung
I'd love to be able to say that, but the science just doesn't allow us to. All you can say is that maintaining normal weight is going to be very likely to reduce your risk of cancer. So that seems fairly uncontroversial. But how you lose that weight is you can't sort of at this point say this diet is better than this diet. So whatever diet works for you to lose weight, that's probably the most important thing. A few other things, such as fasting, will it work?

[00:50:26.530] – Dr. Fung
Again, theoretically, fasting is going to be very, very effective for prevention of cancer. But that's all you can say. Theoretically, we don't know that that's true. So fasting, of course, reduces all of your nutrient sensors. So insulin is going to go down and talks are going to go down AMPK is going to go up. So it's going to affect all of them because it's not just insulin, right? There's other nutrient sensors in the body.

[00:50:54.070] – Dr. Fung
So you're going to affect all of them simultaneously versus a low carb diet or a ketogenic diet where you're really only lowering insulin. So the point is that if you're able to lose weight, that's probably a good thing. Fasting is probably a very important part. And that's the argument I make, is that fasting is an important part of weight loss. So therefore, fasting is likely going to reduce your risk, future risk of cancer by allowing you to maintain a normal weight.

[00:51:21.820] – Dr. Fung
The second thing, of course, is type two diabetes. Type two diabetes also happens in people who are normal weight. So it's not just the weight of the Hyperinsulinemia. So, again, fasting is going to help reduce your insulin because when you don't need insulin goes down. So therefore you're reducing the sort of nutrient censor's which is going to likely translate into a reduced risk of cancer. But that's all you can really say. You can say that theoretically this should work, but whether it actually works, you couldn't say with any confidence, there's a few other things in terms of chemo-prevention.

[00:51:55.690] – Dr. Fung
So this was a term coined by the NH to talk about substances which will reduce cancer. And this is always interesting to people to say, well, if I eat this, I'm going to protect myself against cancer. And there's very little that actually is proven there. There's some data on metformin. Some metformin is used again in the longevity circles. It increases AMPK, which is actually one of the nutrient sensors. So it actually signals low food availability. So if you are on metformin for type two diabetes, it seems that there's a lower risk of cancer than other types of diabetes treatments. So if you're on if you're a Type two diabetic, maybe you should consider metformin. There's a little bit of data on that in terms of chemo-prevention. The other one that is interesting to me, but there's not a lot of data is also is green tea, because, again, a lot of these compounds have been studied mostly by the Japanese.

[00:52:58.370] – Dr. Fung
You drink a lot of green tea that it might reduce the risk of cancer. So some of the some of the data coming out of Japan are very interesting. But of course, it's not a randomized control trial. You can't say for sure that this is or isn't going to reduce cancer. But on the other hand, when you look at a chemo-prevention, you have to say, well, what are the risks of drinking green tea? And you have to say, well, almost nothing.

[00:53:25.780] – Dr. Fung
I mean, people drink five, six, seven cups of green tea a day. They don't seem to have any harmful effects and it's pretty cheap. It's just go to the grocery store, buy a big box of green tea. And so it's pretty, seems pretty safe. Seems like there's a fairly inexpensive and potentially you could lower your risk. So, again, as a chemotherapeutic, as a chemo preventative agent, it's probably one of the more interesting things.

[00:53:56.250] – Dr. Fung
But again, mostly I would. I would. That's all the science can say about that. So maintaining normal weight and getting back to the Obesity Code and the Diabetes Code, you know, I think that a rational strategy involves sort of reducing carbohydrates, intermittent fasting, sort of reducing snacks and reducing processed foods.

[00:54:16.510] – Allan
Dr. Fung, I define wellness as being the healthiest, fittest and happiest you can be. What are three strategies or tactics to get and stay well?

[00:54:25.730] – Dr. Fung
Yeah, I think I think that those are the main things which I cover in these sort of these books, which is it all kind of comes back to the same sort of things, which is, you know, cutting out processed foods largely like it's not just the process carbohydrates, but they are the biggest culprit. But most processed foods are not going to be very good for you. So reducing processed foods, reducing the frequency of eating, because and this was different of course, in the 1900s versus the 2020s, we're all sort of more towards the obesity side than in the past. So therefore we should try and bring it back in order to be healthy.

[00:55:13.010] – Dr. Fung
And then more specifically with regards to cancer. I mean, I think that the main thing is really just sort of maintaining this balance of understanding of what it is so that we can, and it's not just diet. Of course, there's lots of other determinants, but also things such as avoiding unhealthy habits like smoking. And there's always these things. In terms of stress you should you know, it's probably not good, the chronic stress, because it's this chronic sort of damage that happens when your cortisol is always high. So sort of maintaining this balance of diet and also the lifestyle, which is going to keep you free of cancer.

[00:56:07.000] – Allan
Great. So, Dr. Fung, if someone wanted to learn more about you, learn more about your book, The Cancer Code or your other books, where would you like for me to send them?

[00:56:16.310] – Dr. Fung
Yeah, so you can go to my website, which is thefastingmethod.com. You can follow me on Twitter or Instagram. That's at Dr. Jason Fung. That's Dr Jason Fung. Those are great ways to get in touch. And of course you can get my books, The Cancer Code, The Obesity Code, and The Diabetes Code.

[00:56:34.880] – Allan
Well, Dr. Fung, thank you for being a part of 40+ Fitness.

[00:56:38.100] – Dr. Fung
Thank you so much.

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