The Melanie Avalon Biohacking Podcast Episode #77 - Dr. Jason Fung
Dr. Jason Fung is a Canadian nephrologist. He’s a world-leading expert on intermittent fasting and low carb, especially for treating people with type 2 diabetes. He has written four best-selling health books, The Obesity Code, The Diabetes Code, The Complete Guide To Fasting and The Cancer Code. He co-founded the Intensive Dietary Management program on his own website thefastingmethod.com.
Dr. Fung graduated from the University of Toronto and completed his residency at the University of California, Los Angeles. He lives and works in Toronto, Canada.
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The Cancer Code: A Revolutionary New Understanding of a Medical Mystery (Dr. Jason Fung)
7:50 - what lead to writing cancer code
10:45 - paradigms of cancer
13:00 - Cancer Overgrowth Theory
13:50 - Gene Mutation Theory
15:45 - personalized targeted treatment
16:40 - human genome project
16:55 - cancer genome map
18:10 - the problem with millions of Gene mutations
20:20 - causation of Gene Mutation
21:45 - adaptive therapy
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24:10 - somatic mutation theory
25:20 - Henrietta Lacks
28:00 - the potential of cells to become cancer
31:25 - role of diet in cancer
32:35 - Proximate vs root cause of cancer
36:15 - diet and lifestyle
38:10 - unicellular vs multicellular life
40:05 - competition vs cooperation
41:55 - competitive strategy in a cooperative system
43:15 - cancers method of metabolism
46:15 - Efficiency of glucose
47:00 - lactic acid
48:45 - unicellular immortality
51:20 - LUMEN: The Lumen Breath Analyzer Tells Your Body If You're Burning Carbs Or Fat For Energy! You Can Learn More In Melanie's Episodes With The Founder (The Melanie Avalon Podcast Episode #43 - Daniel Tal, The Melanie Avalon Podcast Episode #63 - Daniel Tal (Lumen)) And Get $50 Off A Lumen Device At MelanieAvalon.com/Lumen With The Code melanieavalon50
52:50 - convergent evolution
53:50 - cancer and ketones
54:40 - growth signaling
56:55 - Fasting and Feasting Vs "Grazing"
58:40 - cancer and obesity
1:00:20 - HCLF Vs HFLC
1:02:20 - Glycemic index
1:04:40 - the factor of food variability
1:06:40 - refined carbohydrates
Melanie Avalon: Hi, friends, welcome back to the show. I am so honored and thrilled about the conversation that I am about to have. I feel like it is a long time coming. For listeners, as you guys know, I am also the host of The Intermittent Fasting Podcast, and one of the figures who comes up on that show all the time, in a good way, is a fantastic Mr. Jason Fung. He really needs no introduction. He is a figure in the whole world of obesity, metabolism, fasting, really one of the go-to figures for all of that. His previous books, I'm sure most of you have read. He has The Diabetes Code, The Obesity Code, The Complete Guide to Fasting. I've been a fan and a follower of his work for so long. So I had been dying to connect with him on this show, and I thought it would be about fasting, but the timing was absolutely perfect, and that he released a new book called The Cancer Code.
Friends, I admittedly, prior to this book hadn't really done a lot of research myself on cancer. Reading this book was-- Well, first of all, it read almost more like a suspense mystery novel than a science book, it was so fascinating, and the history of cancer and what is going on with that and the future and what paradigm is actually needed. But that will be the topic of today's show. Jason, thank you so much for being here.
Dr. Jason Fung: Thanks for having me.
Melanie Avalon: To start things off, I'm actually really, really curious. Like I said, my listeners are probably pretty familiar with you, but your prior work has been a lot with fasting, metabolism, obesity, things like that. What sparked your interest in writing a book on cancer? Was it just a natural progression of your work? Or what was the inciting incident that led to that?
Dr. Jason Fung: Well, it started out as a natural extension about obesity, because there's a link between obesity, type 2 diabetes, and cancer, which has not been very well appreciated by most researchers until relatively recently. If we go back a little bit, in the 80s, and 90s, and so on, nobody really talked about that. It wasn't until the obesity epidemic really got going in the 2000s, 2010s, that we really saw that there was a clear link between certain types of cancer, such as breast cancer and colorectal cancer, and obesity and type 2 diabetes. That's where my interest in the topic started. I started looking into the link, and then it became something different than what I thought it would be because I started learning about some of the new ways that we're thinking about cancer. The story to me was absolutely fascinating, in the way that views of change in terms of what this disease is, what it represents, and what causes cancer sort of thing.
The book got drawn into a slightly different direction from the one I had intended, but in a way that I thought was extremely interesting. I have to say something that I think is written about very much, like nobody talks about it. For such a massively important topic, there's virtually zero discussion about what this disease is, like, what is cancer? That takes up the first half or two-thirds of the book is a real discussion about what that question is. Nothing much to do with fasting or anything like that. Just a really interesting discussion of that topic. That's how it came about, it was just that the topic itself is so fascinating that I thought, “Well, if nobody else is going to write about it, then I need to write about it.” So, interesting to me.
Melanie Avalon: That is so true. Maybe that explains partly why, like I said, I myself hadn't done a lot of research on it, because people aren't really talking about it, I think, people's lives will get touched by it. Then they might look into particular treatments for whatever type of cancer they or their loved one experiences. In general, there's not a lot of just, I don't say every day, but every day conversation surrounding it. When I picked up the book, I really had no idea what to expect, but like you said, it's fascinating. Like you just said, friends, listeners, you have to just get the book because it's really long and there's a lot in there. But you go through the whole history of cancer and how it was viewed throughout history, starting back with the humors and bile and, and then even ideas of it being a virus and all these different manifestations and theories as to what it is.
Could you talk briefly about the biggest dominating paradigms that there have been because you present a new paradigm in the book? Prior to this, there was the idea of excessive growth, and then somatic mutation theory. What has been the general dominating paradigms? And why are those not complete?
Dr. Jason Fung: Yeah. This is sort of interesting part is that the paradigms of cancer, that is, how we think about cancer as a disease really is important, even though nobody talks about it because it guides your entire treatment focus. We've come through three major paradigms of cancer, modern paradigms, anyway, humors was Greek sort of ancient Greece paradigm, but the first modern paradigm was this. cancer is a disease of cells that basically grow too much. If there are cells that grow too much, then let's find ways to kill those cells. That's basically the the the whole major pillar of modern oncology treatment. Let's find ways to kill cells.
There's surgery, for example, where you can cut out cancers, and you can use radiation, so you can burn those cancers, and you can use chemotherapy, which is a basically a type of poison. These are things that destroy cells and destroy cancer cells slightly more than they destroy regular cells. All of them are, in essence, sort of ways to kill, because you have things that grow too much. So that's a logical extension, and that's what took us to where we are, it's a big advance at the time, because of course, there was no easy treatment for cancer prior to that. Chemotherapy, what happened, of course, is that they developed chemotherapy, then they develop different ways to combine chemotherapy with the other agents, that's how we came. It didn’t answer the deeper question. That is, if it's a cell that grows too much, then why is it growing so much? That's the question that we need to answer in order to get a deeper understanding of what cancer actually is.
By the 60s and 70s, we came through the knowledge of genetics and so on, and we thought, “Okay, well, here's the answer then.” We have cells, and they have genes and genes control cell growth. Therefore, if you have a cell that is growing too much, is because the gene that controls that growth, has become mutated, and therefore changes the cell growth. The idea was that this is a random mutation. This is the so-called somatic mutation theory, which is that if you take something like smoking, for example, tobacco smoking. Well, it causes lung cancer, we know that, but it's not a targeted gene mutation way to mutate your DNA. It's basically a way that damages cells, so that because it damages cells, it damages DNA, it can introduce mutations. If you have a lot of mutations in genes, one of them randomly may hit a very important growth signaling gene, and therefore you get excessive growth.
The idea was that, just like if you buy more lottery tickets, you'll hit the lottery, you have a better chance of hitting the jackpot. If you have a lot of mutations, there's going to be more chances that one of them will hit this critical gene and turn it into a cancer. It seemed to make a lot of sense. This is the second-grade paradigm of cancer. Now, if you say, “Okay, well, this is a disease of gene mutations.” And this is the dominant paradigm that we've lived under for the last 40 years.
If you go to the American Cancer Society website, they will still tell you that cancer is a disease of gene mutations. Lo and behold, you looked at cancers, and there were these gene mutations. Again, the reason it's important is because if you have a paradigm of cancer that is saying, “This is a disease of gene mutations that causes excessive growth.” Now you design treatments to fix those genes. You don't design treatments to kill cells, you design treatments to fix genes. The first couple of treatments that we had were incredibly good. They basically cured certain types of cancer. So, yes, they were rare cancers, but it proved the paradigm. One of the mutations of breast cancer, for example, the HER2 to gene, it also did extremely well. Now we had this so-called targeted treatment, but it was more than that with what you could do is in fact look for these gene mutations and then only treat those people that had those gene mutations and not everybody. Now we are getting into the realm of personalized medicine and targeted therapy, so personalized is targeted treatment.
By the 2000s, we're thinking, “Okay, well, this is it. We're going to cure cancer because all we need to do is map out all the genes, look for all these growth signaling areas, find the mutations. The two or three or four mutations of each cancer, and then devise ways to block it.” You have a cancer paradigm of genetic mutation, you design treatments to fix those gene mutations, and you're going to cure cancer. This was the huge optimism that we had in the 2000s. We completed the Human Genome Project, which mapped the genes of the entire human being. What happened, of course, is that we didn't cure cancer. And so we did an even more ambitious research project called the Cancer Genome Atlas. Instead of surveying one human genome, we instead surveyed 33,000 cancer genomes. You take a couple 1000 breast cancers and compare them and say, “Okay, well, look, this is the gene that's important for breast cancer.” We thought, “Okay, well, we just need to identify these two, or three or four.” Unfortunately, it didn't turn out the way we thought it would. Instead of most common cancers having one or two gene mutations, a breast cancer, colorectal cancer, for example, had 100 gene mutations. That's a real problem.
So, if you had two people in a breast cancer clinic, for example, with breast cancers that looked identical, you'd have patient A with 100, gene mutations, and patient B in the chair next to her, with 100 completely different gene mutations. If you're trying to treat these people, it's a real problem, because you can't make-- and you can't give 100 different drugs, and develop 100 different drugs for the person sitting right next to her. It's basically an impossible task. By last count, when we got to 2018, when they said, “Well, how many gene mutations have we found in cancer?” You're talking about something on the order of 6 million gene mutations in cancer. This is a huge problem because it's simply not something that you can treat any longer because you can't make those many drugs, and it's always changing. There's differences in genes between patients, between a primary cancer and a metastatic cancer. It's just genetic variety everywhere. This is what led to the real slowdown and advance of cancer therapeutics. We simply couldn't develop these drugs. Therefore, there was no good treatment. The treatments were stuck in the 60s, chemotherapy, and so on. That's what happened by the 2010. We hit rock bottom.
And if you look at what happened in cancer, of course, is that if you look at the number of deaths in cancer, compared to overall, it's always been the number two killer of Americans. Heart disease has always been number one. In the 70s, you're twice as likely to die of heart disease compared to cancer. Now they're basically neck and neck. Where people have made huge progress in treating heart disease, there's been virtually, comparatively very little progress in treating cancer. The reason is that that paradigm that we focused on, simply couldn't deliver any treatments. That's where I was, that's as much as I knew about cancer. But it turns out that the story was far more interesting. We've gone in a brand new direction, and we've gone into the third great paradigm of cancer treatment, which is, again, doesn't invalidate any of the paradigms that came before it. But basically went another step further to say, “Well, if genes are mutating in cancer, then what is causing the genes to mutate?”
It turns out that this is an evolutionary process, not a forwards evolution, but this backwards evolution into a more primitive survivalist cell, if you will, a backwards evolution to a more primitive state, and that's likely what's happening in cancer. Again, the reason that's important is because it informs different treatments. Instead of saying, “Let's fix genes.” What we can say is that, “Hey, this cancer is actually a cell that's mutating into a foreign invasive species. The body actually has a way to deal with foreign invasive species.” We have an immune system, and therefore we can bolster the immune system, and this has opened up a whole new area of treatment called immunotherapy, which now gives hope that we might be able to do something in the future. We can also apply the lessons of evolutionary biology because it's an evolutionary process, to the cancer problem. We can do things like adaptive therapy, which is instead of just giving the maximum dose, maybe we have to time it a little bit better. All these new treatments, which are coming out of this sort of new paradigm of understanding that it's an evolutionary process.
I spend a lot of time going over the evidence for this, and it really answers a lot of sort of key questions that the genetic paradigm left wide open, which was there's a lot of holes in that theory, it didn't explain anything. Whereas the evolutionary process takes that into account, but takes it a step further, takes our understanding, step further in trying to define what this disease is.
Melanie Avalon: Yeah, this is so fascinating. Some questions about the somatic theory, which was such a dominating theory. Those mutations in cancer, were they all related to growth? Or were they mutations for different characteristics that that they were looking for as the traits?
Dr. Jason Fung: Yeah, there was actually a whole lot of different mutations. There was a number of ways that cancer cells differed from regular cells. They grew, but they also exhibited other traits, that is, the cells became immortal cells, that is, if you take a human cell, and just grow it in a lab somewhere, it will only divide a certain number of times before it will stop. The cell line cannot propagate itself indefinitely. Cancer cells, as well as single-celled organisms, well, so you take a bacteria, and you grow it and grow it and grow it and just keep going, it will go on forever, cancer cells do the same thing. One very famous example of that is the story Henrietta Lacks, which is a lady in the 30s, I think, who had cervical cancer. They took ourselves without her permission, I might add, because they didn't do it very ethically. They took her cancer cells, and they've kept growing them for the last 80 years, or whatever. The cell keeps growing. As long as you give it nutrients, you can take some cells out, keep growing it, keep growing it, keep growing it. S, they're mortal cells.
The other thing is the cells tend to move around, and so on. There's a lot of different things about cancer cells, which are different than normal cells, which is strange, if you think about it, because remember that these cancer cells are derived from our own normal cells in everybody. Person A has a cancer and Person B has a cancer, these cells have turned into cancerous cells independently from each other and from every other person in history. The question is, how can that be? That's a very interesting question because if you say, these genes are mutated, you can mutate genes in 100,000 different ways? Why would all the cancers look alike at the end of that, and that's one of the questions that the somatic mutation theory because it says, it's a random mutation. ‘Well, it should lead to infinite variety, cancer should look completely different from one person to the other.
Just like if I gave you a pencil and a paper and said, draw something, you're not going to draw the exact same thing as me, because we're different. If we don't talk to each other or see each other, we're going to come up with something completely different. Cancer’s the same. If cancer is moving, say a breast cell is moving towards a breast cancer cell, since they're evolving independently, why do they look exactly the same at the end of it. Which is a fascinating question, and one that the somatic mutation theory could never answer, but one that the evolutionary theory does, and it says that, “Well, because you're moving towards a more primitive form as we evolved,” we all had that same original sort of cell blueprint and therefore that's why. It's a super interesting theory, with a lot of really important implications as to how we should treat it and how we should further research it, and so on. The other thing, I think, fascinating, of course, is that it gets almost zero attention.
Melanie Avalon: Let's say that cancer is a robber, for example, is it like in the somatic mutation theory, it would be like trying to find a robber by looking at the different characteristics that a robber might have. A pistol or literal things that the robber might have, or they might more likely be a male, or I mean, I don't make generalizations, but characteristics about them, and then trying to just address those things in the general population to get rid of robbers. Compared to the idea that anybody can actually become a robber, they just need to have the reason to do it, like attacking that reason.
Dr. Jason Fung: I think that's the from saying, we go and say, okay, well, if you have a robber, then what we've always said, is that, well what was wrong with them sort of thing? How are they different from other people, as opposed to saying that, well, anybody can become a robber, given the right circumstance, if your family is starving, and you have to steal to feed them. Well, I think most people in that situation, may well become a robber because you take that sort of step in that you have to take care of a starving child, or whatever it is. The idea is that cancer is exactly the same. It's not that it's an unusual thing. It's not that it's so different. It came from us. It has evolved from a normal cell, but what is the circumstance that made it into a cancer cell? This gets into the sort of idea that this is not just the seed, but the seed and the soil. That potential to become a robber exists in everybody. What is it about that circumstance that is going to make him into it? The same with the cancer.
Any cell in the body has that potential to become a cancer, because it is a sort of evolutionarily earlier remnant, so that kernel of cancer exists in all of ourselves and all animals basically. What is it about the soil that allows this cancer seed to bloom as opposed to stay dormant. That's the important thing, because when we focus on the genetics, we focus just on the seed. You can't do anything about your genetics, like, you can't change them, I can't change them. There was this fatalistic, “Well, if he had cancer, that's just a bad roll of the dice.” But it's not. There's so much that we can do to influence our risk of cancer because it's the soil that provides the necessary growing conditions for the evolution of your normal cell into a cancer cell. And so that's where the diet and lifestyle and all these sort of things comes in.
It's interesting when you look at the determinants of cancer, that most people think it's just genetics, but genetics plays actually an incredibly small part of what cause of cancer, like age is a big thing, of course, but can't do anything about that. So, you might as well forget about it. Other things like the diet plays a huge role. If you look at diet, for example, its role in cancer causation is very close to that of tobacco at this point. Actually far outstrips any other risk factor by a longshot, all the stuff we worry about, like radiation and chemicals and pesticides and herbicides, and all these sorts of things. They actually are maybe 1% or 2% of cancer causation compared to diet, which is somewhere around 30%, and tobacco smoke, which is about 35%. It's at the same time that it's interesting, it's also hopeful because it's like, “Look, if we can understand what causes cancer, then we can try and prevent it. I mean, it's not a one-time thing. It's not like, “You do this and you'll prevent cancer,” but it's over your lifetime, you're going to be able to make the slower sort of soil, hostile to cancerous growth. That's what's really important being able to control it in the end.
Melanie Avalon: You talk about the difference between proximate and root causes. By all of that logic, is the actual root cause of cancer, carcinogens or carcinogenic lifestyles diet, is that the actual cause? Or is it something else, like we talked about, the actual characteristics that come about from those causes?
Dr. Jason Fung: Yeah. I think that's where diet plays a big role, as does other things, like tobacco smoke, for example, and asbestos and viruses or certain types of cancer, so cervical cancer, for example, is largely caused by human papillomavirus. What's important, of course, is that when you talk about proximate causes and root causes, it's really, really important to treat the root cause, not proximate cause. To differentiate, you have to say, “Well, the proximate cause is what goes right before,” but it's not sort of what's most important. For example, if you have an airplane, you say airplanes, they fly because lift is greater than weight.” The proximate cause, you might say, well, if a plane crashes is because the force of gravity is more than the force of lift. That's true. But it's not really useful, because if you were to say, treat the proximate cause, you'd say, well, in order to prevent plane crashes, all you need is bigger wings, because you have more lift. That's it. That's all you need to do.
Well, small wings is not the cause of most plane crashes. It's weather or it's pilot error, or it's whatever it is. Then you say, okay, well, if the ultimate cause is actually pilot error, then you need better pilot training. That's going to prevent your plane crash, not bigger wings. The treating the proximate cause is such a reactionary thing. It seems it's useful, but ultimately, it's not useful. That is to say, if you're to say, let's take the example of lung cancer, and we've identified a whole bunch of different gene mutations in lung cancer. If you're to say, what causes lung cancer? What is more correct? If I say it's a mutation in ALK1 gene, or tobacco smoke causes cancer. You got to get to the tobacco smoke, because then you say, well, then to prevent lung cancer, stop smoking, that's treating the ultimate cause. Whereas saying, I'm going to make a drug to treat the ALK1 gene mutation. Well, that's a proximate cause, and you're not going to get very far, like you might get somewhere but not very far, by doing that. The problem, of course, is that we spent so much time and money trying to figure out the proximate cause, which is the gene mutation instead of the ultimate cause, which is, “Hey, stop smoking.”
We figured out for smoking, of course, and asbestos, but there's a lot of other cancers, like breast cancer, where there's a huge, huge risk. We talk about these gene mutations and so on. The thing is that if you take a Japanese woman in Japan, and move her to San Francisco, within a couple of generations, her risk of breast cancer like doubles or triples. Even though she marries Japanese people. There's no change in the genetics. What's changed is the diet and the lifestyle. It plays such a huge overwhelming factor, same with colorectal cancer.
In the 1950s, Denis Burkitt in Africa, observe that the Africans who are eating a traditional African diet and following the traditional path and lifestyle did not get colorectal cancer. When those same Africans adopted a Western lifestyle, mostly with refined grains and sugar, they got cancer. Again, not the genes, it's the lifestyle. Now you're getting to the root cause, which is the lifestyle, and then to focus so much and say, “Oh, well these Africans got colon cancer because they have the mutation in gene X, Y, Z. No, that's the proximate cause. They got cancer because their diet and lifestyle change to a more westernized diet and lifestyle. We know that that's the cause. Getting to that ultimate cause is so important.
For many years, we got stuck on trying to identify all these intervening steps without making much progress, and that's why, hopefully, as we develop new tools and so on, and that's where understanding the bigger level, higher-level view of cancer like, what is this disease? What is the paradigm that we have to follow because that's how you're going to develop new and effective treatments, rather than focusing on the same thing.
Everywhere you look, every everything you read about these days, in terms of cancer, is still stuck in that old paradigm. This is a disease of gene mutations. It's nobody's fault. We can't control our genes. It's just bad luck that causes cancers. There's luck, for sure, there is, but there's so much more to it than that. To say that it's just luck is, it's not correct and it doesn't help people.
Melanie Avalon: It's echoes being stuck in the calories in and calories out model, or a lot of the other paradigms that we've had in health that we can't seem to crawl out of. There was a part of the book where literally, my mouth dropped open. I was so on the edge of my seat, and it was when you lay out the different characteristics of unicellular versus multicellular life. The differences and the comparisons, they're basically how-- their differences and comparisons and growth and their movement and their immortality and how they generate energy, and how it perfectly aligns with cancer cells. I was wondering if you could talk a little bit about that, because I just found that completely mind-blowing.
Dr. Jason Fung: Yeah, honestly, I was totally blown away by that myself because I didn't know any of that. It was just as I was reading it, I was learning about this new paradigm that some oncologists were going into, but really only like the researchers and stuff and nobody had ever talked about it. The idea was that if you look at the way that single-celled organisms are different than multi-celled organisms. Remember, all our body is composed of trillions of cells, but the most primitive organisms are only one cell. If you live in New York City, for example, which is a city with millions of people compared to a lone survivalist in the woods, there's a big difference. The survivalist in the woods, he has to do everything himself, he can't specialize. You're always going to be small. The difference is between single-celled organisms, and cells within a sort of a community or a city, if you will, of cells is completely different, because their overriding paradigm has changed from single cell where you compete with everybody else, to a model where you have to cooperate with everybody else.
The survivalist and the city, he has to compete with everything for resources. In the city, you actually try and help each other. That allows you to become specialized, and same thing in our body. Our liver becomes specialized to do a certain thing. But it can't do other things, we rely on other cells to do that. That's the difference between a single-celled organism and a multi-celled organism. That's the difference between cancer cells and normal cells is that cancer cells act almost exactly like a single-celled organism. When you're looking at cancer cells, they do everything for themselves, just like a single-celled organism.
Remember, in our bodies, our cells are part of a team. Everything has a certain goal to make a winning team. Your liver doesn't compete with your heart, for example, for resources there, it's divided, you got a common goal, just like if you have a soccer team, everybody's trying to win the game. Certain players will be in goal, and certain players will try and score and certain players will try to defend. You each have your role, and you do your role in a very specialized and efficient manner, as opposed to say tennis, which is a single person game where you must do everything yourself, you have to hit backhand, forehand, whatever serving. Everything is on you.
The point is that cancer cells are this movement from a cell within a community back towards a cell that now is trying to survive on its own sort of thing. The problem is that when this cancerous transformation happens, and it turns into from this cooperative strategy, into this original competitive strategy, that's when it becomes a problem because that liver cancer cell, now is trying to survive for itself only. Its goal is to-- it tries to grow, it tries to move around and tries to get as much resources, but it also try and kill other cells around it because it's trying to compete. That's the huge sort of evolutionary jump is from the unicellular to multicellular. When you look at cancer, what's so fascinating is that when you look at the genes that are mutated in cancer, they're not random. They're actually concentrated at that point in evolutionary history between the unicelled and multi-celled organism, so that is the critical differentiating stage between cancerous cells and non-cancerous cells.
When I was reading it, honestly, I was just like, wow, this all makes sense, and it's so interesting that people have come up with these sort of ideas and this huge advances in knowledge of cancer that I had no idea about, and nobody's talking about.
Melanie Avalon: Yes, it's absolutely fascinating. I was also really fascinated by one of those characteristics you just talked about, as far as the energy generation of the cells and cancer cells and how they use the Warburg effect. Basically they choose to use glycolysis, even though they're in the presence of oxygen, and they could be generating more energy in a different manner. Why do cancer cells choose that as their preferred method of metabolism?
Dr. Jason Fung: Yeah, this has been the object of a lot of speculation over the years. The thing about normal cells is that they can generate energy in two different ways. Glycolysis is where you take the glucose, and you burn it without oxygen into 2 ATP, which is the unit of energy, loss to lactic acid. That's what happens when there's not enough oxygen. If you're running a very fast sprint, you're our sprinter, the blood flow is not enough to deliver oxygen, so you actually generate a lot of energy through glycolysis. When there's plenty of oxygen, you can take the same glucose molecule and burn it with oxygen to generate not just 2 ATP, but 36 ATP. You're generating a lot more energy per unit glucose in oxidative phosphorylation. If you think that in a very energy-- in a situation where you need a lot of energy, such as growth, like cancer cells growth, you need a lot of energy. You think that you choose oxidative phosphorylation, but they don't. Almost all cancers choose glycolysis. That's been a very big paradox. So, you'd say why should cancer do that? It's like making a nice race car and making it nice and sleek, and then taking out the big 600-horsepower engine and putting in a nine horsepower lawnmower engine. It's like, why are you doing that? It doesn't make sense. So that's been the speculation for a lot of years as to why cancer does it.
Once you apply the veil of evolutionary biology, you start to see some of the advantages of using glycolysis for the cancer cell, that is the cancer cell needs to not only generate glucose for growth and generate ATP, I should say, for growth, but it also needs to generate organic molecules to grow. That is if you're building a new cell, new cancer cell, if it divides, and it grows, you need not just energy, but also mass. It's like if you're building a house, you need the builders, but you also need bricks, like you can't go anywhere without bricks. The idea is that if you generate the energy through glycolysis, you take your glucose you take. you get 2 ATP, which is energy, but you get two lactic acid, which you can then use to grow. Maybe that's a big enough advantage, because you're providing both the sort of energy and the building materials. It's actually a much more efficient way to grow.
The second thing is that in a situation where you have lots of glucose, that higher efficiency is just not that big an advantage. That is you get 36 ATP per glucose, but what if you have hundreds of thousands of access molecules of glucose just sitting around in a dumpster? Well, being more efficient user of glucose isn't any big advantage. In these days, when people are generally overweight, and perhaps have excessive amounts of glucose, such as type 2 diabetes, that energy efficiency is not a big advantage, so what looks like a huge advantage, isn’t.
Then the third thing is that that lactic acid may actually play a role in making it easier. Remember, these cells are growing and competing with other cells, so dumping lactic acid and making your surroundings more acidic, is a way to prevent other cells from invading your territory. There are several advantages to glycolysis which may explain why cancer’s preferentially choose glycolysis over oxidative phosphorylation. It's an interesting theoretical point, but one that's only made clear once you start looking at it from this different paradigm and understanding it. Well, I think of it from the cancer standpoint, it's way better to use glycolysis. So that's why it does what it does.
Melanie Avalon: Do normal cells use the byproducts of glycolysis in beneficial ways, or just cancer cells?
Dr. Jason Fung: No, just cancer cells, because there's no reason. The only reason we use glycolysis is when there's not enough oxygen. If there's plenty of oxygen, our cells almost always choose glycolysis, because remember, our cells are not trying to grow, that is your liver is not trying to get bigger and bigger and bigger, until it's the size of the whole body. Your liver only wants to stay the same size. Whereas cancer cells are trying to get bigger and bigger and bigger. That one centimeter cancer wants to get to two centimeter and three, four or five, that cancerous cell is trying to keep growing as much as possible. Whereas normal cells are not trying to grow, they're trying to just stay the same.
Melanie Avalon: This is a super theoretical question. Does studying cancer possibly hold the secrets to immortality for us, like the mechanisms of action that cancer is using?
Dr. Jason Fung: It has some applications, but it's mostly interesting as a disease of itself. Cancer is an immortal cell, but that immortality is part and package of a whole different suite of differences. That is, it's a competitive, it's less-- even though the cell itself is immortal. It's like a unicellular organism. It's a much more primitive existence. It's hard at this point to really take those lessons and say, “Can we apply this and then say, make our own cells immortal? It does have some implication in terms of, if you're trying to make mortality, you may wind up getting a lot of cancer, too, because all these things go with each other, but it's an interesting theoretical construct to say, “Well, can we get certain parts of this cancerous cell than not others? Right now, it'd be very difficult to do so.
Melanie Avalon: I guess, the direct correlation would be a multicellular cell turning into a single unicellular cell, it'd be like a human reverting to a yeast to become immortal.
Dr. Jason Fung: Yeah, exactly, because not only, yes, you would be immortal, but you'd also lose specialized functions, like a yeast has to do all of-- a single cell has to do everything. Grow and feed and reproduce. It's so less, so much less specialized than what a human can do. You actually can't get any of those additional functions. As we move from unicellular sort of immortal organisms, we actually had to build in, so these new genes on top to control those urges, where cells were immortal, we actually had to make a whole way to make them not, that's during our evolution, that that's what happened, because otherwise, we couldn't control that those unicellular urges in another way. It's an interesting theoretical point. Yeah, it's a fascinating way to look at cancer as this evolutionary movement forwards or backwards in time.
Melanie Avalon: I did want to touch sinceyou just brought it up backwards in time, that was one part of the book I really loved, was your discussion of convergent evolution, compared to atavism. Basically, the idea that-- but you already mentioned it before, but that we are evolving backwards and rediscovering traits in a way that the cell already has.
Dr. Jason Fung: Yeah. The whole idea is that if you have that original programming, that original kernel of cancer, that was never destroyed as we evolve. We just built on top of it. Therefore, when we remove all the stuff on top, we expose the core, which is what cancer actually is. Which makes a lot more sense than evolving forwards, and then everybody looking exactly the same, which was always a strange-- it was what the somatic mutation theory postulated, but it was truly preposterous to say that.
Melanie Avalon: One big question also involving what we just talked about, and tying everything in together with the larger bulk of your work, but as far as energy generation goes. We just talked about how cancer preferentially often uses glycolysis and glucose, but you do talk in the book about how it can really fuel on a lot of different things. Fasting, does cancer can it run off of ketones ever? Can it run off of fatty acids fasting and cancer, what goes on with all of that?
Dr. Jason Fung: It can actually. People used to say, “Well, cancer needs glucose.” But that's not strictly true. There are other cancers that live on certain proteins, for example, glutamine. They've also shown that certain cancers can live off fatty acid. Remember, if you look at the cancer as a single-celled organism, it's advantageous to be able to use different fuel sources. It can use carbohydrates, which is easy for it to do, but it can also use proteins and fats, if it needs to as well. That is something that, again, is a relatively new information. The point is that, if you have cancer cell, the way that you control it through fasting is that you're decreasing growth signaling. When you eat foods, you actually have nutrient sensors in your body, that will tell your body, for example, that food is available. When you eat insulin, for example, goes off and tells you're eating. Another nutrient sensor called mTOR tells you you're eating protein.
Those happen not only to be nutrient sensors, but they also happen to be very powerful growth factors. When your body senses that food is available, it tells your cells grow, grow, grow. When you have cancer cells, it will follow the exact same thing and trying to grow, grow, grow. Therefore, if you have a situation where you have too much insulin, not only are you going to be overweight, because you're eating more than you should, but you're also signaling your body to grow more than it should, and therefore, it's going to tip the scales towards cancer because you're got more growth signaling compared to signals to stop growth. That's important because if you know that insulin is a very important growth factor for cancer, you can change your diet, to the way that you're going to minimize this insulin signaling, you can do intermittent fasting, which is again, going to lower your insulin levels and tell your cells to not grow. That's, hopefully, one effective strategy to lower the risk of cancer. We don't have that data, of course, but if you fast, then you're going to try, you're going to hopefully be able to maintain a normal weight. We know that being overweight increases your risk of cancer a significant amount.
Melanie Avalon: What are your thoughts on the potential cost benefit of, let's say, fasting coupled with periods of overeating? Higher mTOR stimulation, higher insulin stimulation, but then fasted periods, compared to like, low to moderate, constant baseline. So more like snacking throughout the day, but maybe never intensely punctuating insulin or mTOR because of your dietary choices, because Gen and I, on The Intermittent Fasting Podcast talk about this a lot. If somebody had to choose between a “healthy diet” eating throughout the day compared to fasting, but maybe less helpful choices in your eating window. Do you have any thoughts on the comparison between there, or is it even a comparison worth making? What are your thoughts on that?
Dr. Jason Fung: Yeah, I mean, I think that there's certainly something there. There's clearly a huge, and not all of this is very well defined at this current point. We've got a very little research into diet and nutrition at this point. It'd be great to be able to pinpoint these, you shouldn't do this, you shouldn't do this, you should cycle this way. We're not at that stage, I don't think where we can say that what we've done, of course, in terms of nutrition, and cancer, we've studied all kinds of risk factors. We haven't zeroed in on insulin and that sort of thing. We've looked at fiber, we've looked at dietary fat, we've looked at the various vitamin deficiencies. We've looked at all different reasons that people thought that diet might influence cancer risk, none of them turned out to have any influence.
At this point, the best you can say, it's not very satisfying, I suppose, but the most you could say is, well, if you're overweight, then you should try to lose weight because we know being overweight increases your risk. I mean, the World Health Organization lists 13 different types of cancer as obesity-related cancers. Therefore, if you have an obesity-related cancer, we know that going to likely reduce your risk by being normal weight. The second thing you can say is that type 2 diabetes significantly increases your risk of cancer as well. If you have type 2 diabetes, you should try to reverse your type 2 diabetes. Again, both conditions of obesity and type 2 diabetes are diseases of too much insulin. Therefore, fasting is going to help you reduce that insulin, and by reducing the insulin, you're going to lower your risk of cancer. It's not a very satisfying thing to say, but that's really as far as you can take it right now.
You can't say, “Oh, you should fast for 16 hours twice a week and you won't get cancer.” We're not that granular yet. We're really at that very basic level. There's lots of different ways, of course, lower your insulin levels if you have too much insulin, it's not necessary that you have to fast all the time, you could change the foods that you eat, for example, and you could even lower carbohydrate diets. Even within the carbohydrates, you could change the type of carbohydrates you eat, because certain ones are going to be more stimulating than others to insulin. There's lots of different ways to do it. It's not all sort of one size fits all.
Melanie Avalon: I just have one really last quick question. I'm just dying to know your thoughts. I brought on a lot of people on this show who are advocates of low carb diets and fasting and things like that for managing insulin. Then I've also brought on people like Cyrus and Robbie, who wrote Mastering Diabetes, and people in the high carb, low fat world. Do you have any thoughts on those approaches for managing insulin. I just feel like I'm constantly seeing both sides of that the low carb versus high carb, or--
Dr. Jason Fung: It's not the carbohydrates per se. It's really a fact that you have excessive insulin. You can eat a high carb diet and still not stimulate insulin. If you look at the Kitavans, the South Pacific Islanders, they ate a diet that was somewhere around 70% carbohydrate, in the 70s, I think. They were being studied. One of the researchers there from Sweden compared these Kitavans to a reference Swedish population. Remember, the Swedes are very fit. What he found was that the insulin levels of these high carb diet, the Kitavans was at around five percentile. That is 95% of the Swedish population. The healthy Swedish population had an insulin level that was higher than the average Kitavam, he's eating this very high carb diet. It's not necessarily the carbohydrates that is driving your insulin. The disease is the disease of too much insulin, and lowering the insulin can take one of many ways to go down. If you eat a high carbohydrate diet, you certainly can and still have very low insulin levels, but you can't be eating all the time, and you can't be eating a lot of refined foods. If you're eating things like white bread, it's much more stimulating to insulin than say, even a boiled potato or something like that. You can see it on these glycemic indexes, where you look at beans, for example, which is carbohydrate, compared to say a cookie. There's a huge gap. It's not just about the carbohydrate, it's a useful construct that is if you're eating less carbohydrate, you certainly can do well.
Same thing in China in the 1980s. People are eating white rice all-- a lot of white rice, like 300 grams of carbohydrate a day. Yet very, very little obesity, very little type 2 diabetes. It's the other things that were important. How often did they eat? What else did they eat? Did they eat a lot of sugar? There are other things that are important in the diet that will control your insulin, it's not just the carbohydrates. Getting into this sort of, “Oh, it's the carbs,” or, “It's not the carbs.” It's not the whole answer. If your car breaks down, it's because you ran out of gas. Yeah, might be or might be because your fan belt broke. Or it might be because your spark plugs didn't work, or whatever it is. There's lots of different things that can go wrong. There's lots of different ways to get there. People confuse the insulin part with the carbs. Just because you eat a lot of carbs, doesn't always mean that your insulin levels are going to be high. If you eat refined carbs, and you're eating 10 times a day, then yes, you are going to have a high insulin level. Unfortunately, that's been the standard American diet.
There's lots of other things that control it. If you eat a certain food all the time, you're not going to lose weight, because the problem with foods-- lots of people like pizza, but if you ate pizza, four or five, six times a day, every single day, for three years, you would probably lose weight, you know why? Because you probably wouldn't be able to stand another slice of pizza. You would eat as little pizza as you possibly could, so that you're not hungry, and then that would be it. When you take away food variability, for example, so in China, you've got white rice and vegetables, every single day, that's all you eat, you really just don't really want to eat because you don't want another meal of white rice and vegetables. It'd be the same if it was pizza, it’d be the same for almost any other thing, that's a highly restrictive diet.
Now you've taken away all variety, and after eating it for so long, you really just don't want to eat and therefore you don't. Well, you're going to lower your insulin level. So you can do that with a vegetarian diet, you can do it with a high carb diet, you can do it with a low carb diet. Any of those will work just fine. In the end, what happens, of course, is that you're eating in a way that your insulin levels are going to be lower, your nutrient sensors are going to be lower. There's lots of different ways, and that's why I'm never really one to say, “Oh, you have to eat this way,” or, “You have to eat that way.” Fasting is really just a tool that you use to bring your insulin levels down. It allows you some flexibility, because if you want to eat a variety of foods, then you can, as long as you're not eating all the time, it's just a different strategy. Instead of restricting certain foods all the time, you restrict all foods some of the time. It's a different strategy, and it works very well for a lot of people. This is why I try not to get in the middle of these sort of high carb versus low carb debates because you certainly can do very well with a high carb diet, it's been done for years, like the Irish ate a lot of potatoes, the Chinese ate a lot of rice, the Mexicans ate a lot of beans. These traditional diets have had that. Indians ate a lot of rice. Most of Southeast Asia ate a lot of rice. People ate a lot of bread in the past. It can be done. That's my take on it.
We're confusing the diet, like the things that we eat, and we're trying to become these great, say that, “All carbs are the same.” It's not. All carbs are different. The how refined carbohydrate is, plays a big role in the insulin effect. It's not just your grams of carbohydrate. It's also how refined they are, and how often you eat them.
Melanie Avalon: Bringing everything full circle, it's the confusions and misconceptions with cancer and the mutations and not for taking in the bigger picture in the context and the environment and everything. Well, thank you so much. This has been absolutely amazing. My listeners, like I said, are probably very familiar with your work, but is there anything else that you'd like to touch on put out there? How can people best follow your work?
Dr. Jason Fung: Follow me on Twitter and Instagram. For example, my handle is @drjasonfung. That's D-R Jason Fung. Also doing a lot more YouTube videos these days, covering the basics of all that. So that's also good, so you can check me out on YouTube. Then my website is called thefastingmethod.com. And there's a lot of sort of blogs and other resources that might be of interest to people. So, yeah, you can check me out there.
Melanie Avalon: Perfect. I will put links to all of that in the show notes. Very last question, I promise. It's easy. It's the last question that I ask every single guest on this show. It's just because I realized more and more each day, how important mindset is surrounding everything. What is something that you're grateful for?
Dr. Jason Fung: I'm always grateful that I have the opportunity to get the message out there. It's an opportunity that's, for example, didn't exist before social media and blogs and all this sort of stuff. Where you can just give information to people for free. Hopefully, they can take that information and make their lives better, or lose weight, or reverse type 2 diabetes, or lower their risk of cancer. It's a real privilege to be able to do that because it always makes me feel very good. When somebody says, “Oh, I listened to this guy, and I started doing it, and I lost all this weight and I got off all my medications, and even my doctor is astounded.” That's great because we have such an opportunity here to help other people. It's not by selling them stuff or putting them in a program or whatever it is. It's just by sharing knowledge and stuff that's logical. I'm always grateful that I live in a time I suppose that this is something that can happen and hopefully brings a lot of good to a lot of people. Fasting, of course, is not new, it's been around for thousands of years, but it's been forgotten about, and hopefully we can bring it back to a point where people actually will be able to make themselves healthier. It would be amazing to be able to do that, that's what I want to do is just make everybody healthier and give them the tools they need to control their diseases. Not put them on medications and do surgery and all that. That's not healing. That's just the business.
Melanie Avalon: Well, I love hearing that so much, and you are definitely 100% truly doing that. I am truly forever grateful for your work, and so is-- I'm sure the entirety of my audience. Thank you so much for this and hopefully, we can connect again in the future. This has been incredible.
Dr. Jason Fung: Thank you so much. Thanks for having me.
Melanie Avalon: Thank you. Bye.
Dr. Jason Fung: Bye.