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Dr Rangan ChatterjeeDr Rangan Chatterjee

"This Is Feeding Cancer Cells!" - Fix This To Starve Disease & Heal The Body | Thomas Seyfried

To get 1 year's FREE VITAMIN D and 5 FREE TRAVEL PACKS visit When I started medical school in 1995, we were taught that one in four people were likely to develop cancer in their lifetime.

Dr. Rangan ChatterjeehostThomas Seyfriedguest
Sep 20, 20231h 52mWatch on YouTube

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  1. 0:00 – 6:14

    Why Cancer Rates Are Rising: Diet, Lifestyle and Metabolic Disease

    1. RC

      Almost 30 years ago, I started medical school in Edinburgh in Scotland, and I still remember sitting in the anatomy theater being told by one of our professors that one in four of us, at some point in our lives, were gonna get cancer. And I remember being shocked. This was back in 1995. I looked around thinking, "Wow, one in four." Now, I know as things stand today, that rate has gone up to one in two of us are going to get cancer at some point in our lives. So Professor Seyfried, you've been studying cancer for decades now. In your view, what's going on?

    2. TS

      Well, thanks. Um, well, you know, i- in any kind of a, a disastrous situation, um, there's never one thing that could be responsible, uh, for the rise in, in, in a particular disease. I, I think that, um, there are many factors that come together, uh, to account in part for this worldwide epidemic of cancer, uh, where most people, uh, that study epidemiology have now, uh, consider the view that it, it's just a matter of time before cancer overtakes heart disease a- as the number one killer of people in various countries. So what, what's going on? Uh, when you consider that our ancestral, uh, groups of people, um, cancer was extremely rare in, uh, in tribes and, and, and different populations that live by their standard ways, uh, ways that were common to those folks for, for centuries. All of a sudden now, we have this explosion within the last, say, 50 or 70 years, an explosion of, of cancer, and a lot of it has to do with our Western civilization diet and lifestyle. We, we have more contaminants in the atmosphere, we have less exercise, and we have far more foods that are poorly nutritious and provide, uh, high amounts of carbohydrates. I, I think you put all this together because there's a direct correlation between the obesity epidemic and cancer. Uh, a correlation between the obesity epi- epidemic, cancer, and Type 2 diabetes. You put all this together, Alzheimer's disease. All these chronic diseases are on a increased trajectory. So clearly, it's linked to a change in diet and lifestyle over the last, uh, 50 to 70 years, where we're really starting to see this, this increase. Even, even when we had the anti-smoking campaign here in the United States in the, in the, in the 1990s, you know, smoking was a major cause of lung cancer and other cancers. But now with the, uh, reduction of smoking, we're still seeing this relentless increase, and obesity now is replacing smoking as the num- as a number one or a major risk factor for the development of cancer. So I, I think it's a lot of factors coming together, uh, increasing our susceptibility to developing tumors in various, uh, organ systems.

    3. RC

      Yeah, it's really interesting. One of the ways in which we get trained as Western medical doctors, of course, is that these different diagnoses, these different illnesses are completely different diseases, right?

    4. TS

      Mm-hmm.

    5. RC

      We say things like, "Oh, you know, this increases your risk of Type 2 diabetes, and if you have Type 2 diabetes, it increases your risk of another condition called Alzheimer's disease."

    6. TS

      Mm-hmm.

    7. RC

      And what's really interesting hearing you talk about what's happened in the last... Well, my question was the last 20, 30 years, but you broadened it out to 50 to 70 years, is that it's not just cancer that's going up, as you say. We know that chronic disease is going up.

    8. TS

      Mm-hmm.

    9. RC

      Type 2 diabetes is going up. Alzheimer's is going up. Cancer is going up.

    10. TS

      Mm-hmm.

    11. RC

      And I know you have very much been trying to get the message across to people for many decades now that cancer is a metabolic disease. So clearly these things are not quite as separate as they might initially seem.

    12. TS

      That's absolutely right. And, and, um, metabolic homeostasis, uh, which is the, uh, um, absolute, uh, functioning of our cells in the appropriate way, uh, organ cells, it's called metabolic homeostasis. When you're basically a very healthy person, you're in metabolic homeostasis. So what's happening is our bodies are falling out of metabolic homeostasis as the result of a variety of insults from, uh, from largely from, from the environment, diet, and lifestyle, and these kinds of things. But when you look back and say, what is, what is, um, what is responsible for maintaining what... in metabolic homeostasis, and it comes back to our mitochondria within the cells, um, the organelle that, uh, ultimately is responsible for the metabolic homeostasis within individual cells and within the body as a whole. So this organelle, uh, when it becomes corrupted or dysfunctional, can manifest m- can manifest this problem in, in many different ways. Cardiovascular disease, Type 2 diabetes, cancer, um, uh, Alzheimer's disease, depending on the, on the tissue and the cells of the individual. In cancer, we, we, we know for sure that, um, every major cancer that I have studied has defects in the number, structure, and function of the, of the mitochondria.

    13. RC

      Yeah.

    14. TS

      And this then causes the cells to fall back on a, on a primitive form of energy, which is fermentation, and that leads to dysregulated cell growth. So we have... I, I have a very clear idea of the origin of cancer and how to manage it. Um, the ramifications of these to, say, other chronic diseases, um, we always find a mitochondrial connection. It may not be always the same as what we see in cancer.

    15. RC

      Yeah.

  2. 6:14 – 14:27

    Cancer in Traditional Populations and the Body's Resistance

    1. RC

      Well, let's just go- Initially to something you, you, you, you mentioned at the start of this conversation, which is when we look at these kind of indigenous populations, we don't see cancer.

    2. TS

      Mm.

    3. RC

      Now, some people may be thinking, "Okay, but how much are we, you know, examining these people? How much are we scanning these people?" So do we know for sure that actually they don't have rates of cancer, or is it just that we haven't found it? So I wonder if you could just address that right at the top.

    4. TS

      Yeah. Well, that's a good question. But, um, when w- when we read the, the work of, um, the humanitarian physician Albert Schweitzer, uh, he, he definitely knew what cancer was. He examined 40,000 Africans in-- living in their natural ways, looking for cancer, and he didn't find it, so, uh, so he absolutely knew. In other cases, with the In- Inuits of Alaska and the Arctic Circle, uh, some, um, British, uh, physicians reported that cancer was very, very rare. But I don't think it was done as comprehensively as what Albert Schweitzer did in the African populations. But others have looked as well, and they kinda conf- uh, concur what Schweitzer had seen. Ge-- In general, uh, human populations that lived according to traditional ways had a much lower incidence of cancer than those same populations that shifted to diet and we- uh, lifestyle. For example, the Inuits. I, I had the opportunity to visit, uh, the medical school at Thunder Bay, Canada, uh-

    5. RC

      Wow

    6. TS

      ... where they, uh, they, um, uh, service the, the medical problems of the Canadian Inuit population. And the Inuits now are, are, are raked with, uh, diabetes, cancer, dementia, uh, which their ancestral populations never had. So, uh, um, clearly it's the change in diet and lifestyle that's largely responsible for the onset of these chronic, uh, diseases, uh, including cancer.

    7. RC

      I've heard you say in a previous interview that our bodies are actually very resistant to cancer, and I've been thinking about that a lot over the past few days, that despite all the insults that-

    8. TS

      Mm

    9. RC

      ... are coming into our bodies, especially these days, although the rates are high, you could make the case that the rate should be even higher. So I guess-

    10. TS

      Mm

    11. RC

      ... whe- when you say our bodies are incredibly resistant to cancer, what do you kinda mean by that?

    12. TS

      Well, I, I, I think, um, uh, when we live traditional lives like the primitive folks and traditional ancestral groups, not getting cancer or having very low, uh, rates of cancer. Um, I think when we have the right diet and lifestyle, I, I think be-- it becomes much more difficult for cancer, uh, to develop. A, a, a kind of an example, uh, of this was the-- there was a study done some years ago, um, with, with, uh, uh, I think they were macaques, some sort of a monkey from South America or one of these places, and they rubbed carcinogen. They, uh, 20-methylcholanthrene is a known carcinogen. A- and they rubbed it on the arms of these monkeys, uh, for 10 years, injected them with it, and everything else, and they didn't get a ca- a single case of cancer, uh, from, from, from these. And they concluded that, uh, well, these monkeys are not good models for cancer. Um, but the monkeys were eating their, their diet. They were living in their natural environment, um, and they were quite resistant. The con-- the, the alternative experiment, which was never done, is why don't we give these monkeys, uh, high carbohydrate diets, uh, uh, uh, really change their diet and lifestyle, and then do these kinds of experiments? And, and I think that our members of our ancestral groups, uh, uh, having the correct exercise, diet, and lifestyle, even, even when exposed to carcinogens, would have a much lower risk.

    13. RC

      Yeah.

    14. TS

      So when you take folks that are now, uh, not exercising, getting obese, uh, you ha- you have them exposed to a variety of chemicals within the food systems, the type of poor nutrition, I think you-- even though we have a lot of resistance in our body to cancer, I mean, uh, we're really, we're really bashing down those walls of resistance by the diet and lifestyles that we're taking.

    15. RC

      Yeah. I really like that example, because I think it goes beyond cancer for me into all these chronic diseases. We can scare ourselves these days if we go online, if we read about the toxins-

    16. TS

      Yeah

    17. RC

      ... the pollutants, the air pollution-

    18. TS

      Right

    19. RC

      ... the diesel fumes that, that... You know, it can be really, really scary to think, "Well, what can I do? I'm going to be exposed to so much of this." But-

    20. TS

      Mm-hmm

    21. RC

      ... what you just explained there is really the approach I take with myself and with my patients, which is very much, "Okay, well, what can you do? Okay, what are the things you have control over? What can you do in your own house?" And the more good things you can do-

    22. TS

      Yeah

    23. RC

      ... the more of a buffer you create, the more strong these foundations become to then resist the attack and the onslaught from the modern worlds. Uh-

    24. TS

      Yeah

    25. RC

      ... as, as someone who's been studying cancer for decades now, do you think that's a, a kind of fair analogy?

    26. TS

      Oh, I think it's a really good analogy. I, I, I think-- I, I think... Uh, but it's hard, you know?

    27. RC

      It is hard.

    28. TS

      Uh, uh, we, we are confronted now, um, with food sources in abundance. Uh, our, our exercise levels are far, far lower than they, than they were, uh, when we evolved as a species. Um, it, you know, this, this whole way we live, sitting in traffic, in front of computers, um, with minimal exercise, uh, uh, chowing down on, on, on poorly nutritious, high carbohydrate [chuckles] foods. I mean, uh, uh, over years, you know, little kids, kids can do this, uh, because your body is strong and healthy. But man, you do that for 30 years, and it just, it just, [laughs] you know, it crushes you down.

    29. RC

      Yeah.

    30. TS

      Um, a- and so it's a, it's a combination of all these exposures and the lifestyle that we have. And it's-- it cuts across, um, uh- ... racial and, uh, and, uh, different groups. I mean, clearly it's, it's a common... I- once that Western diet and lifestyle enters into a population, all of a sudden you see the onset of these chronic diseases. It's very clear. So, so, uh, that never existed-

  3. 14:27 – 25:26

    How Cancer Develops: Mitochondrial Damage and Fermentation

    1. RC

      Can we say cancer adopts a, a similar kind of model? That, you know, you, you get the diagnosis at some point, but things have been building up for a period of time. I wonder if you could just expand on that and help us understand how one actually develops it in the first place.

    2. TS

      Yeah. Well, you're right about that. I mean, it doesn't happen o- You don't, you don't wake... You don't go to sleep, uh, looking healthy a- at night, wake up with a big tumor on y- on your lung or your kidney or something like this. I mean, th- these, these things, wh- when you have something that can be obvious now and detected, uh, um, by, um, you know, uh, pathology, pathological report or non-invasive imaging, I mean, there's gotta be a large number of dysregulated cells in, in that mass, uh, before you actually, uh, see it, uh, with, with some diagnostic tool. Um, but you know, when I, when I wrote, uh, my book on cancer, Albert Szent-Györgyi, uh, who was a Nobel Prize recipient, did work on vitamin C, he called, he called this cancer thing the, uh, an on- an oncogenic paradox. How is it possible that so many different provocative agents, uh, could, could elicit a dys- a dysregulated group of cells in a particular organ or, um, part of the body in a c- in a common way? What is the common pathophysiological connection, uh, a- among all the provocative agents? Like we know carcinogens. They call chemicals that cause cancer as carcinogen. This is a, a chemical that has been, been determined to, uh, cause cancer, so we refer to these chemicals as carcinogens. We also know that we have certain viral infections like hepatitis, uh, C, uh, papillomaviruses, and some of these other kinds of carc- uh, uh, carcinogenic viruses. They produce cancer. Uh, we also know radiation can produce cancer. We also know that chronic inflammation can produce cancer. We know that intermittent hypoxia can produce cancer in certain cells. What is the common pathophysiological mechanism by which all this happens? We know that there are certain, uh, uh, inherited genes in our body. These are called secondary risk. They're not primary risk factors, but they, in the right environment, they, they will elicit cancer, like the, uh, Li-Fraumeni syndrome. You have the BRCA1 mutations for breast cancer. Um, so a woman might get breast cancer for her, uh, having a BRCA1 mutation. They might get breast cancer from a, a, in a clogged milk duct. Uh, they may get cancer from systemic inflammation. But when you look at it under the microscope, uh, the pathological report, they say, "Oh, you have breast cancer." So what was the origin? Why one woman? Why all these women that would have various kinds? They all might all have different provocative agents that elicited, uh, the p- the common path... Now, what the common pathophysiological mechanism, mechanism is to all cancers is a chronic disruption of energy metabolism in the mitochondria of the cell, followed by a compensatory fermen- fermentation. Now let me break that down because this is what Otto Warburg initially said. He just didn't connect all the dots like we have. He, he said cancer elicits from chronic damage to the ability of a cell to generate energy from oxygen. So we know that all of the cells in our body use oxygen to generate ATP, which is the currency of energy in our body. Adenosine triphosphate, okay?

    3. RC

      Mm-hmm.

    4. TS

      So w- you and I are breathing, we're talking, uh, because the air that we breathe in has oxygen in it. Oxygen serves as a, uh, the acceptor of electrons, w- uh, which allows the mitochondria to produce a vast amounts of, of energy, and the waste products are CO2 and water of oxidative phosphorylation. All of our cells in our body, the majority of cells except red blood cells, are using this process so that we can remain alive. What happens in the cancer cell? Over time, that organelle, that process becomes corrupted or deficient in some way. But the, but a- as Warburg said- If you disrupt oxidative phosphorylation or energy through oxygen too acutely, the cell will die, and you'll never get a cancer from a dead cell. So whatever causes the cancer, whatever the provocative agent does, it doesn't do it acutely, it does it chronically.

    5. RC

      Mm.

    6. TS

      And by chronic disruption of oxidative phosphorylation, it allows the cell to, to replace oxidative phosphorylation with the ancient pathways of fermentation. The fermentation pathways is energy without oxygen, and all the cells on our planet existed, uh, in using fermentation before oxygen came into the atmosphere, and that was about 2.5 billion years ago. So the cancer cell adapts to a fermentation metabolism as a way to compensate for the chronic disruption of oxidative phosphorylation. Interestingly enough, that same organelle, the mitochondria, controls the cell cycle. It allows the cell to remain in a quiescent, differentiated state, and as that organelle becomes corrupted over time, the s- transition to fermentation causes the cell to lapse into the default state, which is proliferation. So in this, in this, all of the cells on our planet, uh, were highly proliferative, dysregulated cell growth before oxygen came into the atmosphere to form metazoans and-

    7. RC

      Yeah

    8. TS

      ... more complicated, complex, uh, organisms. So the cancer cell is doing nothing more than falling back on ancient pathway, living in the a- living as if it were in the absence of oxygen. That's what cancer cells do. They can absolutely survive without oxygen. They don't use oxygen anymore. So they're living without oxygen, anerobiosis, as Warburg called it. They're life without oxygen. Even when oxygen is present, the cancer still is, the cancer cell is still fermenting. So now you know what this cell is.

    9. RC

      Yeah, it's so interesting. So let's just unpack a little bit, uh, of what you just said. First of all, you said that, I guess, or my interpretation is that there are infinite numbers of insults that we can have on the human body, and with respect to cancer, it can be from pollution, from radiation, from, you know, whatever it might be, we can have these insults, but whatever those insults are, for us to get a diagnosis of cancer, there is a specific abnormality in mitochondrial function which occurs.

    10. TS

      Mm.

    11. RC

      And at that point, the cancer cell is no longer utilizing oxygen to make energy. It's doing it using fermentation products. And you're saying that-- So, so if we go down that logic, is it fair to say then that cancer is not really the diagnosis, cancer is a symptom? It's a symptom of problems in the mitochondria.

    12. TS

      Yes, exactly. You're actually right. And then, uh, Warburg had said this, and at that time, he only knew about glucose fermentation, lactic acid fermentation. Because ATP, uh, synthesis through oxidative phosphorylation is highly, highly efficient, so you can generate 30, 32 to 36 ATP molecules for one mole of oxygen consumed. But fermentation is a very inefficient system. So what is the raw material to generate fermentation? Yes, glucose, but, uh, but the glucose can only generate a couple of ATP relative to the vast number from oxidative phosphorylation. So in order to make up the difference in energy, you have to take in massive amounts of glucose, uh, to know- in order to replace the energy that you would've gotten from ox- that the cell would've re-received from oxidative phosphorylation. So consequently, the transporters for the, the, the sugar glucose are massively upregulated on the surface of cancer cells, and this is one of the reasons why you can detect tumors using position, uh, uh, p- uh, PET scanning, uh, uh, positron emission tomography. You c- you can, you can see cancer because it's sucking down so much, so much, uh, glucose. Um, but what we have found, and Warburg did not know, um, we have also discovered that these same tumor cells also ferment the amino acid glutamine. So they can, they can use glutamine in the absence of oxygen in a fermentation mechanism. So the two fuels, the glucose and the glutamine, are the two predominantly, the predominant fuels for fermentation. So, um, uh, once you know this, once you know that these tumor cells are dependent on, uh, non-oxidative energy, uh, which is called fermentation, energy without oxygen, what, what generates-- Well, listen, without energy, nothing can grow, period. Energy is absolutely essential for life. So if the cancer cell is using a different type of energy metabolism, what is it? It's fermentation. Wow. Okay, great. What are the fuels that are driving the fermentation? Well, one of them is glucose, as Warburg said, and the other one is glutamine, as we have now found as the second major fermentable fuel in these tumor cells. And these two fuels work together, driving all of the necessary processes for rapid development, rapid proliferation, and for, um, its, uh, the constant dysregulated, dysregulated growth. DNA, RNA, protein synthesis. The glutamine has the nitrogen and carbons to make new DNA and RNA. The glucose has the carbons for fatty acids and proteins, and these two fuels are driving the beast. And once you underst- And then the other thing you need to know is that they can only use fermentable fuels. Fatty acids and ketone bodies are non-fermentable fuels. They're not, they cannot be used by tumor cells, but they are, they can be used by normal cells that have normal mitochondria. So the solution to the cancer problem is simultaneously targeting the ferment- fermentation metabolism of the cells, which is the glucose and glutamine, but by transitioning the body over, over to ketone bodies, which allows the normal cells in the brain and all other organs to, to function. And fatty acids for the liver. Tumor cells can't use fatty acids and ketone bodies. So the solution to the cancer problem is very simple. You have to simultaneously target the fermentation while transitioning the body over to fuels that cannot be fermented. And this now puts massive pressure and kills the tumor cells without toxicity.

  4. 25:26 – 28:04

    Glucose, Glutamine and the Press-Pulse Strategy

    1. RC

      Wow. I mean, [laughs] it's so clear when you, when you say it like that because, look, if you were not medical, right? If you knew nothing about cancer and the pathophysiology, but you knew that, hey, listen, a cancer cell cannot use oxygen. Even if oxygen is around, it doesn't use oxygen to generate energy. It can only use glucose and glutamine, right? I- if that's all you knew, you told a child that, I reckon a child would say, "Okay, well, let's not give the body any more glucose or glutamine. If that's what a cancer cell feeds on, let's stop it," right? Now, that may be overly simplistic, but it kinda sounds like that's the conclusion from what you're saying.

    2. TS

      Yeah. Well, I think the ... Uh, you can't stop the glutamine because, uh, it- it's a non-essential amino acid, and it's the most abundant amino acid-

    3. RC

      Yeah

    4. TS

      ... in our body. It plays an, uh, mo- a, a massively important role in our gut, our immune system, the urea cycle. So glutamine is, is ... They call it a non-essential amino acid, but for cancer, it's an absolutely essential amino acid. You can use diet and lifestyle to lower blood sugar, for sure, but you need drugs, uh, that will interrupt the glutamine pathway, the glutaminolysis pathway, essentially. So we use a combi- a combination of, of diet and, uh, repurposed drugs, uh, in the, what we developed called the Press-Pulse therapeutic strategy for managing cancer, where we can tr- we, we bring the body into a state of very low glucose, high ketones, and then we hit the surviving tumor cells with, uh, drugs that target, that can target and disrupt the, the glutamine pathway. But we do it over very p- ... We pulse it. We don't do it too aggressively. Knowing, knowing the value of glutamine for the normal physiological function of our body, you can't go after glutamine, uh, aggressively because you're gonna harm the body. So you have to know the biology. You have to really understand biology, evolutionary biology, to manage cancer. And, uh, once you understand that, like you said, it's quite ... It's not that complicated-

    5. RC

      Mm

    6. TS

      ... uh, once you break down, uh, the issues. So, uh, um, once you understand the issues and dissect them, y- it ... I mean, sure, there's ... You, you have to know about energy metabolism, and you have to know about a, a variety of these things, for sure. But once you know that, then the, the path to resolution, the path to long-term management without toxicity becomes obvious.

  5. 28:04 – 33:06

    Aerobic vs Anaerobic Energy, Muscle, Liver and Metabolic Flexibility

    1. RC

      You mentioned oxygen, making energy in the presence of oxygen or making energy, well, in the presence of oxygen, but without utilizing oxygen, and I think a lot of the public have heard about aerobic exercise and anaerobic exercise. So they understand, I think, a lot of people will, will remember from biology class at school that when your body's utilizing oxygen, you can do certain forms of exercise. But if you push up the intensity, and let's say you're playing football or doing lots of high-intensity sprints, that at some-

    2. TS

      Mm

    3. RC

      ... point you go to anaerobic, where actually you're generating energy no longer using oxygen, or not exclusively using oxygen. For people who are thinking about that, can you help us understand, like, is, is there a similarity there between what you're saying about cancer and the difference between aerobic and anaerobic exercise?

    4. TS

      Yeah. Well, I think that's, uh, that's really an, a, a, an important point. With the sprinting, you build up lactic acid because the, uh, the muscles are working at such an incredible speed, uh, that the amount of oxygen delivered to the tissue in the blood, uh, is not, is not, uh, uh, enough to keep the muscles, uh, working through an aerobic mechanism. But the muscle can generate tremendous energy using anaerobic, uh, short periods of time. For short periods of time, your muscles can burn energy, uh, through anaerobic mechanisms, which is, which is taking in a massive amounts of glucose and getting energy. Now, as soon as the muscle stops contracting, you're breathing oxygen so that the, the muscle can recover, uh, ATP synthesis through oxidative, uh, uh, phosphorylation. But when they were in that sprinting condition, uh, they were dumping out lactic acid, which ... And this was the, how they found the Cori cycle. Uh, Saul and Gerty Cori, that received the Nobel Prize, when the muscles were dumping out massive lactic acid into the bloodstream, uh, from this, uh, very active, uh, activity, the lactic acid would go to the liver, and the liver would conjugate the lactic acid back into a glucose. Two lactic acids were reconfigured-

    5. RC

      Mm

    6. TS

      ... into glucose molecule to replenish the, the blood sugars. Now, muscle is very interesting because it's, it ... Muscle conserves ... Muscle does not share glucose with other organs. This is a very interesting thing.

    7. RC

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    8. TS

      And it's an evolutionarily conserved adaptation. So muscle stores energy in the form of glycogen. You have glycogen in your muscles, and that energy, that can be broken down very quickly for rapid, for rapid, uh, r- uh, rapid energy. But muscle does not share, uh, uh, glucose with any other organ for, for mo- of, uh, mo- mostly, and that's because when a lion would chase us, we better damn well have enough energy in our muscles to run away. [laughs] Because if you're sharing, if you're sharing your energy with some other organ, you're not gonna be able to run as fast when the lion chases you. So, um, uh, so clearly, the con- conservation of energy within muscles in, is an evolutionary adaptation for survival. Uh, liver, on the other hand, will store glycogen, and that glycogen in the liver can be shared. In fact, it's shared ma- majority, mostly with the brain. And, uh, a- as we stop eating, blood sugar goes down, glycogen is mobilized largely from, from liver, uh, which can then subserve the function of the brain. Brain burns a lot of, uh, uh, a lot of glucose. On the other hand, if the glycogen stores, that's why it takes about 36 hours after you stop eating for the glycogen stores in the liver to be depleted, and then all of a sudden we then mobilize energy out of the adipocytes in our body, and the adipocytes release the fatty acids back into the bloodstream. Those fatty acids go to the liver, and the liver makes ketone bodies, water-soluble breakdown products of the fat, which can then provide the brain, the energy for the brain. So we are s- an unbelievably, uh, sophisticated machine, that we have these different organs and different populations of cells that can be flexible in how they generate and use energy. The cancer cell, on the other hand, is trapped. It's linked only into a fermentation energy. So knowing that this cell is massively limited in its capability of survival, we now have strategies. We can take advantage of knowing how the body works to eliminate and kill cancer cells, uh, without toxicity. Once you understand evolutionary biology and systems physiology, you now know the strategies for managing cancer.

  6. 33:06 – 36:55

    Cancer Cells as a Return to Ancient Energy Metabolism

    1. RC

      Through the lens of evolution, you mentioned before oxygen came into the atmosphere and before we evolved into being multicellular, those single cells would generate energy through the process of fermentation, which is what cancer cells do.

    2. TS

      Yeah.

    3. RC

      So is the cancer cell then moving towards a more primitive form of energy production?

    4. TS

      Yeah. You're actually right. I mean, we can't, we can't say the cells before oxygen came into the atmosphere as cancer cells, because cancer cells develop from cells that were differentiated. They were, they were-

    5. RC

      Mm

    6. TS

      ... a part of the society of cells.

    7. RC

      Okay.

    8. TS

      However, they share a common, uh, energy me- mechanism. They ferment. Um, and, uh, fermentation before, uh, oxygen came into the atmosphere was the way, the way all cells, uh, uh, got energy, was a fermentation mechanism, and they would ferment, um, whatever carbohydrate or whatever a- amino acid would be in the environment. And interestingly enough, it was called the alpha period of, of life on Earth, as Szent-Györgyi called it. Uh, all of the cells at that time had dysregulated cell growth. They were, uh, unbridled proliferation, and they would proliferate like crazy until the fermentation fuels in the environment dissipated, and then they would die. Uh, cancer cells are the same. They, they, they will survive as long as there are fermentable fuels in their microenvironment. And when you remove the fermentable fuels in their microenvironment, they die very quickly, just like cells did in the old days. The, the old days, uh, [laughs] let's put it this way, i-i-in, in, in, in the time before oxygen. So, but their behavior is very, very similar. And, and when you say cancer cells look very primitive, like when you, uh, uh, when you look at cancer under a microscope, I mean, it's just a massive pile of cells in all different dysmorphic stages. Um, they look very primitive. They look, they look, uh, uh, very, uh, uh, undifferentiated compared to the normal cells of the organ from which they arose. But the commonality is that the cancer cell is surviving on fermentation, um, because its oxidative phosphorylation is defective. The cells before oxygen came into the atmosphere had no mitochondria. Mitochondria were a, a fusion between two different organelles-

    9. RC

      Mm-hmm

    10. TS

      ... two different organisms. Uh, uh, an organism that could capture the oxygen and use it for energy. So we had this symbiotic, and that led to the formation of metazoans, which are, are multicellular organisms, of which we are all metazoans, multicellular. You couldn't have multicellularity until you were able to capture the energy from oxygen in the, in the fusion hybridization between these organ- between these different organisms.

    11. RC

      Yeah.

    12. TS

      So the cancer cell is simply using the heirlooms of energy metabolism from the past to grow in a dysregulated way. And th- and that dysregulated growth will continue as long as the cancer cell has access to fermentable fuels in the microenvironment.

    13. RC

      Mm.

    14. TS

      So our way of managing cancer is simply to restrict the availability of the fermentable fuels in the microenvironment using both diet and specific drugs, uh, and then using the normal cells of our body to outcompete and digest and destroy the cancer cells. It's unbelievable. When you really understand the mechanisms-

    15. RC

      Yeah

    16. TS

      ... and the strategies involved, you can get very excited about this.

    17. RC

      Well, it's absolutely fascinating to hear it, how we've evolved, how we get energy, and then what happens to that cancer cell and how it reverts back to actually maybe the oldest form, the oldest way that we have of generating energy. The cancer cell is utilizing that. So that's, that's really, really interesting.

  7. 36:55 – 45:41

    Genes, BRCA1 and Somatic Mutations as Downstream Effects

    1. RC

      I wanna talk a little bit about genes and genetics because we hear a lot of things, like in the media, let's say over the last 10 years, there's been a growing awareness of BRCA1 and BRCA2 and how that potentially can increase the risk of things like breast cancer or ovarian cancer by 50 to 80%, depending on which study you read. Now, I'd love to know your thoughts on that, but I'd also love to know just more broadly about ... this relationship between genes and cancer. I have heard prominent oncologists in the UK, professors, say things like, "We are born with the genetic codes for cancer within ourselves, but they're kept locked in place by suppressor genes. And then something happens, whether it be from, you know, carcinogens in the diet or the environment or whatever we're exposed to, and then what happens is that genetic material becomes rearranged. And once it becomes rearranged, those cells no longer stop growing, and they become cancerous, and they spread." So that's a viewpoint I've heard. What is your view on that? And I guess more broadly, where do genes fit into this whole conversation around cancer?

    2. TS

      Yeah. Uh, well, of course, [clears throat] that's the basis for the somatic mutation theory here in the United States. National Cancer Institute, on their website, they say cancer is a genetic disease caused by mutations in specific genes, uh, tumor suppressor genes and proto-oncogenes, and these kinds of things, and this leads to a dysregulated, uh, cell growth. And this is the dominant co- uh, consistent view we have right now, the somatic mutation theory, uh, where, uh, the, uh, mutations arise randomly in a population of cells, which then leads to a disorder of the cell cycle and the, and the proliferation. [clears throat] But you have two different kinds of genes. You have those inherited in the germline, and you have those that are acquired through, um, various insults in, in the environment. When you mention about BRCA1, the hi- the ... That's a inherited mutation, uh, that contributes to, uh, a greater risk for breast cancer. And when you look at what does the BRCA1 mutation do, it disrupts oxidative phosphorylation in the mitochondria. The most, the most, uh, prominent inherited mutation is the P53 mutation-

    3. RC

      Mm-hmm

    4. TS

      ... in, uh, the Li-Fraumeni, uh, disorder, syndrome. The Li-Fraumeni sy- the ... Where about 80% ... You have about 80 to 85% penetrance of that gene, leading to ovarian cancer, breast cancer, brain cancer. There's a vari- variety of cancers that are linked to the Li- Li-Fraumeni. The Li-Fraumeni encodes a protein in the electron transport chain of the mitochondria, cytochrome C oxidase II. So what you're do- what these inherited mutations are doing, we went through all of the inherited mutations, and all of the inherited mutations, risk factors, uh, damage mitochondria in a, in a particular way, um, putting them on the path to destabilized energy metabolism and a consequent fermentation metabolism. So, so the inherited mutations are what we call secondary risk factors, not primary risk factors. Because in order for a, an inherited mutation to ha- be a primary cause of a disease, like, like, uh, the presenilin mutation in Alzheimer's disease, that's 100% associated with the development-

    5. RC

      Mm

    6. TS

      ... of Alzheimer's disease. There is no cancer gene-linked, uh, uh, a germline-linked mutation that is in, w- is 100% associated with the onset of a particular cancer. So we call those secondary risk factors, just like being exposed to a carcinogen. If you inherit a mutation in BRCA1 or one of these, your, your risk for the development of cancer is certainly higher, but it's not 100, 100%. Now, the ... In somatic mutations, this is where the cancer ... Th- this is where a cell in the body will randomly accumulate mutations, uh, some of which will then lead to destabilized growth, okay? So where do the somatic mutations come from? And they come from destabilized energy metabolism in the mitochondria. How does that happen? So ROS, reactive oxygen species, are a byproduct of dysfunctional, uh, oxidative phosphorylation. So the oxygen that the tumor cell is taking in is not being used efficiently for ATP synthesis, but rather is throwing out these radicals, these reactive oxygen species. What do they do? They cause mutations in the DNA. They lead to the mutations in the DNA. So the mutations that we see in cancer are largely downstream epiphenomenon of the damage to oxidative phosphorylation, forcing the cell into a fermentation metabolism, leading to acidification of the microenvironment, which further damages the nuclear genome. So that most of what we see in cancer, the genetic mutations, are largely downstream epiphenomena of the damage to oxidative phosphorylation. So they're not effects. They're not causes. They're effects of this whole process.

    7. RC

      Okay. So let's just get this really clear. So 'cause a lot of people will have absorbed the idea that cancer is genetic, and of course, you know, that there's been a, there's been a conversation online for, uh, I would say at least 10 years, about what a woman might want to do if they have one of these BRCA mutations. And I think there's some very prominent examples of women having prophylactic operations-

    8. TS

      Mm

    9. RC

      ... removing both breasts to try and ensure that they don't get breast cancer in the future. And I definitely wanna, uh, get your perspective on that and your view o- on, o- on these kind of procedures. But the big picture I'm getting from what you're saying is that, look, these genes may increase the likelihood that you are going to develop cancer, but they're not 100%. They're not deterministic genes fully. So-

    10. TS

      Yeah, yeah. They're risk ... We call them risk factors.

    11. RC

      It's a risk factor, right?

    12. TS

      Yeah.

    13. RC

      It's a risk factor. But if you make, uh, significant modifications to your diet, your lifestyle, your environment, the amount of stress you're under, all, all kinds of things, that you try your best to, to significantly change your environment- You can then also significantly decrease your risk of developing that cancer even if you have the gene

    14. TS

      Yes, you are absolutely correct. So you have cho- you have, I guess, at least two choices. If you are detected to have, uh, the BRCA1, let's just use that, but there are, there are several other genes that this would also apply to. But the BRCA1 you res- uh, because you, some women, uh, have done prophylactic removal of breasts and ovaries and things like this to reduce their risk for getting cancers in those organ systems, or, uh, recognizing that they would have this ris- risk factor. How would they reduce the probability of that inherited mutation causing cancer? And you're absolutely right. Y- y- that cancer cannot occur if the mitochondria in the cell remain healthy. And how do you keep mitochondria in your cell healthy? By exercise and enhancing ketogenesis. How do you do that? Well, you can do water-only fasting. You can do a variety of, of, of, of, of diets, uh, that will reduce glucose and elevate ketones. Ketones are a super fuel for mitochondria. They reduce reactive oxygen species, the damaging, the damaging byproducts of respiration. So ketones can significantly reduce damage to mitochondria, allowing that organelle to function in a highly precise manner for long periods of time. So yes, diet and exercise in the right foods, in the right context could take the risk of a inherited mutation that we would say 50% chance of getting a, a, a cancer with that mutation. You could reduce that down massively. I don't know to what extent, because the studies haven't been done in the correct population. But, but we do know that we can significantly, just as you said, you can significantly reduce your risk knowing that, and you can't get cancer without w- uh, uh, w- for you get cancer from damaged respiration, prot- protect the mitochondria, and the risk will go down.

  8. 45:41 – 54:57

    Informed Consent and the Epilepsy Ketogenic Diet Story

    1. RC

      Look, I'm all for informed consent, like real informed consent. So you tell a patient, you know, what all the options are, and of course, a patient is entitled to do what they want, right? And they're entitled to do what they want with their own body. But what I'm passionate about, why I work so hard on this show each week, is to help give people information, so actually they're empowered to know, well, actually, there are some options here. There are some options. Now, someone may say, "I don't wanna take that option." Fine. Informed consent to me means, or one part of it, is giving people all the options. So if you have been diagnosed with epilepsy, as well as the anti-epileptic drugs, if there's good evidence, as there clearly is, that ketogenic diets can be of use, and in some people can be transformative, surely you should also be told that at the same time. Now, you may go, "Well, I don't wanna do a ketogenic diet. It's too difficult. It doesn't fit my life." Fine. You're entitled to make that decision. But you kinda need to be given that choice if we're gonna be evidence-based, if we're truly practicing informed consent, right?

    2. TS

      Yeah, absolutely. I, I was on, on those, um, decision committees when I was a member of the Epilepsy Society of America. I was the society's representative to the corporations [chuckles] on this whole thing. And, you know, um, uh, uh, the, uh, ketogenic diet developed from, um, Wilder in 1921, only when he realized that many of these intractable seizures could be modified significantly with water-only fasting. But water-only fasting is only good for a certain period of time, and you have to eat something. So, uh, what he found was that when you water-only fast, blood sugar goes down, ketones go up. Is there a diet that can do what water-only fasting could do? And that was the, the ketogenic diet. It was managing a lot of different se- in children. Uh, it works in adults, but it's the, the children. The problem is with kids is that when they have a f- a, a blown seizure or they have, uh, absent seizures or whatever, it disturbs the parents tremendously. And the parents have control over the child's diet, uh, uh, at what they're doing. So in order to avoid seeing your child writhing on the floor and foaming, they would say, "Okay, you're gonna stay strict on this diet, uh, because I don't wanna see you seize." Uh, in the 1930s, certain drugs, uh, c- became available that would also stop seizures, and obviously, it was much easier to take the drug than to adhere to a, kind of a rigid diet. The problem with these drugs is long-term, they have very adverse consequences. And then in the 1990s, uh, mid-1990s, Jim Abrams, uh, of, of, a movie producer from Hollywood, his son Charlie, uh, uh, had this t- uh, terminal kind of epilepsy where he was actually dying. And then he contacted folks at the Johns Hopkins Medical School in Baltimore, the late John Freeman, uh, who was one of the few guys left that, that liked to study, uh, ketogenic diets, and they rescued Charlie, uh, from his condition. They made a movie out of it. First Do No Harm was the movie by Meryl, with Meryl Streep. Uh, a friend of Jim Abrams, uh, made this movie, which then brought tremendous attention back to this ketogenic diet, uh, uh, because, uh, it had been f- it had fallen by the wayside. When I was at Yale University in, in New Haven, Connecticut, I wanted to do a project on ketogenic diet internal support, and the people in the neurology department and the medical school in general said, "Ah, ketogenic diets, nobody's interested in that stuff anymore." So my grant was just like, "Oh, no, no more." So when one of my students came to me in the late '90s when I was here at Boston College and said, "Hey, there's a, there's a meeting in Wash- in Seattle, Washington on ketogenic diets" st- um- Uh, spearheaded by Jim Abrams because his son Charlie, uh, did so well on this ketogenic diet. He wanted to bring the concept to the world that this ketogenic diet should be resurrected as a non-toxic management, uh, for epileptic seizures. So I told my seizure, "Ah, nobody's interested in ketogenic diets." She said, "Oh, please send me anyway." So I, I sent her out there to the meeting. She came back, "Oh my God, you can't believe how powerful the diet is. Everybody's so excited about this diet for epilepsy." So we started working on ketogenic diets because we had the best animal models of epilepsy, just like humans with absence seizures and all this kind of stuff. And we started to see, wow, this, uh, this diet does work on the animal models as well. And I said, we published all these papers and everything, and, um, I said, "Wow, what's the mechanism of action? I know you gotta lower glucose and elevate ketones." Well, we were doing research on cancer at the same time looking at angiogenesis, which is the, the vascularization of the tumor cells. So we put the, the... When we put the epileptic mice on, on calorie-restricted diets that lowered blood sugar and e-elevated ketones, we knew from, from Warburg. I said, "What the hell, Warburg?" He said, "You lower bloo- you lower blood sugar, and you can manage cancer." So we started to put, uh, move the, uh, the diets that we were using to manage epilepsy in the mice onto our cancer models, which were the best models that we... Spontaneous models of cancer in the mice. And lo and behold, we said, "Holy crap, this, these, uh, calorie-restricted diets knock the hell out of angiogene- Everybody's getting excited about angiogenesis. You can, you can completely manage angiogenesis with these diets. And, you know, uh, holy-- Napoleon Ferrara and all these other guys that were making all these an- a-anti-angiogenic immunotherapies and, and stuff, and a lot of them don't work, and they cause the cancers to be worse. But when you, when you start using metabolic therapy, you... So after we saw that, and not only that, we started killing these cancer cells through a variety of different mechanisms, okay? Uh, and then we said, "Oh, we should be shifting, shifting our power away from the... We, we use-- We actually had two, uh, parallel programs, uh, metabolic management of epilepsy and metabolic management of cancer. But of course, uh, folks from England and the United States got together, and they wrote up a clinical trial. They said, "Well, we can't believe, uh, epilepsy, uh, managing epileptic seizures with ketogenic diets. There's no clinical trials." Um, uh, well, Dr. Cross from England and, uh, our group here at Johns Hopkins got together, and they wrote up a, a really nice publication showing in a clinical trial that ketogenic diet absolutely can manage a variety of epileptic seizures in children. So you'd say to yourself, "Well, they, uh, uh, like you said, well, then we should use, uh, this." Uh, but no, they'll only measure-- Or they'll only do ketogenic diet for managing seizures only after your expensive drugs don't work. Then you'll do that. That... But we've all argued that you should be doing metabolic therapy for epilepsy first. If the, if that doesn't work, maybe you can consider low-dose drugs.

    3. RC

      Mm.

    4. TS

      No, but they still, they still have it reversed. In the cancer field, the, the stuff right now, what I'm saying, is p-predominantly unknown. Uh, people have no clue that you can manage cancer in a very similar kind of way, obviously with certain, certain, uh, differences. But now that's the, the situation. So, so the argument is, well, we can't use metabolic therapy for cancer because there's no clinical trials to prove it, despite the fact that the science is rock solid to support why you should do that. So that's the conundrum that we have right now, is that no one on the planet has yet-- And, and we can't do a clinical trial yet because the people needed to do that aren't trained. And you need to know what to do and how to do it, and we're working on that right now. So as soon as we have the, our treatment protocol, we'll be able to move into the cancer field with the same, with the, with the same, uh, uh, uh, um, uh, uh, intensity as we did in the epilepsy field to manage, to manage the epileptic seizure. So it's a, it-it's an evolving situation-

    5. RC

      Yeah

    6. TS

      ... with parallel studies, uh, knowing how the brain works under different-- the ketosis issue and all of these different kinds of things coming together to know how to enhance the health and vitality of your normal cells without harming the body. I know I said an awful lot in a very short period of time.

    7. RC

      No, it's-- I, I mean, you're clearly very passionate about this and, and with good reason. How long have you been studying cancer for now?

    8. TS

      Oh, I, well, I studied cancer for probably forty years, but it was not, not in the way to manage the disease. Uh, I studied cancer like ninety percent of the people studying cancer. We do research on some aspect of cancer.

    9. RC

      Mm-hmm.

    10. TS

      Like, I was doing glycolipids. We were looking at, uh, you know, all the different abnormalities in glycolipids in cancer cells. So it had nothing to do, uh, with actual, uh, design to manage the disease. Uh, but of course, everybody in their papers, everybody, many, many people put it, "Oh, this information could potentially be important at some future point or whatever." Um, but it wasn't a direct, it wasn't a direct assault, uh, on the management of the disease, uh, where you could actually cons-- where, where you, you can actually see an observable outcome in someone that would be riddled with a stage four cancer. Uh, h-uh, okay, how would understanding the glycolipid dys-dysregulation in that s- in that person with a stage four cancer in a very short period of time lead to a management strategy?

    11. RC

      Mm.

    12. TS

      And the answer was none. So, and that's the m-majority of people, signaling cascades and looking at this and looking at that. I mean, you can do that for the next hundred and fifty, two hundred years, and you're not gonna have any impact in the clinic. So the idea is how are you gonna im- how are you gonna make your research impactful to the person dealing with a stage four cancer today?

  9. 54:57 – 1:04:51

    Is Every Cancer the Same? A Common Metabolic Target

    1. RC

      We've used the word cancer a lot during this conversation so far, and of course, there are lots of different types of cancer. You know, you can differentiate them depending on location in the body, brain, pancreas, prostate. Uh, of course, the different pathological types of cancers as well. So when we say cancer, do we need to be a bit more specific about what we're talking about, or would you state based upon your research that actually- All of them are fundamentally the same. There is a problem with respiration. There's a problem with generating energy in the mitochondria. Like, y- just help us understand that if you, if you will.

    2. TS

      Yeah, well, that's really so important because we were all led to believe, and we still are pounded by information saying, "Your, your... We have a therapy for your specific kind of cancer." You hear this all the time. Like, breast cancer is different from colon cancer, different from brain cancer, different from bladder cancer, different from the leukemias. You hear, you hear this all the time. And, and that's based, again, on the somatic mutation theory of cancer. When you start to look at the mutations in all these different cancers, they're all quite different from each other. They're even different from each other within the same, within the same type of cancer. Within the same tumor, you'll find all kinds of different mutations. But all of the cells... Now, what I, what I did, I, I went back and I said, "Well, if, uh, um, if all, all the cancers that we know are fermenting, uh, to get energy, that says there's some commonality between them." So in order to, in order to justify that, I had to go back and go through historical records on ultra, um, um, uh, histology, mi- the, the, the, um, you know, uh, the way electron microscopy, ultra structure of the cells in a cancer. So I would look at lung cancer, breast cancer, colon cancer, pancreatic cancer, bladder cancer, blood cancers, and I was looking for a commonality. And that commonality, uh, was abnormalities in the number, structure, and function of mitochondria in all of the major cancers. And, and that's what I found. And in the, in the concepts of evolutionary biology, structure determines function. This is a, uh, a, a, a well-established concept. Structure determines function. If the structure of the organelle that generates energy through oxygen is abnormal, the function of that organelle will be diminished in some significant way, leading to an alternative energy, which would be fermentation. So when I went back and looked at all of the major cancers, I found abnormalities in all of these different cancers. Uh, and then that would lead to the explanation that they would all need to have fermentation in one way or another. Uh, and that leads to the, the concept that if they do ferment, there's only two fuels that they can ferment, which is glucose and glutamine, and that we know every major cancer is dependent on glucose and glutamine fermentation. So it comes right back to the, yes, they look different under the microscope, they look different in their genomic profiles, but metabolically they're all very, very similar and will respond quite effectively to a singular strategy of metabolic therapy.

    3. RC

      The ketogenic diets, or certainly the presence of ketones in the body, is now... You know, the research is accelerating so fast. We're seeing benefits, potential benefits of ketones in neurodegenerative disease, in Alzheimer's, in mental illness, in cancer, of course, in weight loss, and it's really interesting, isn't it? That how can this one fuel source or potentially this one diet, ketosis, and of course, there's many ways to get into nutritional ketosis, but it's, it's, it's very interesting to me how this could potentially have a wide variety of different benefits for a wide variety of seemingly different conditions. Now [laughs] let's look at this methodically.

    4. TS

      No.

    5. RC

      Sorry.

    6. TS

      Yeah, you're right. You're, you're absolutely right. I mean, okay, let- let's go back to our, um, Paleolithic ancestors. All right? So, uh, our, uh, uh, for, uh, uh, thousands and thousands of years, um, uh, we were in a state of ketosis, uh, mainly because food was not available.

    7. RC

      Mm-hmm.

    8. TS

      Carbohydrates were certainly very limited to seasonal, uh, situations. So our ancestors, we were always in a state of therapeutic ketosis. We, we know that in the Aboriginal populations, not only was cancer rare, diabetes was rare, uh, cardiovascular disease was rare, uh, Alzheimer's was never heard of, uh, or rarely discussed or rarely identified, um, uh, as some... Uh, all of these things, uh, that we see, that you've just, uh, mentioned are all linked to mitochondrial, uh, function.

    9. RC

      Mm-hmm.

    10. TS

      So, uh, ketones, as I said, as, as my late good friend, um, uh, Richard Veech from the national, uh, uh, uh, NIH, ketones are a super fuel. Uh, they allow the health and vitality of our mito- mitochondria. They, they allow our mitochondria to, to remain very, very healthy. So when you, when you talk about, um, you know, all of these different linkages for all these different diseases, it all comes back to energy metabolism. And we didn't have, uh, uh, all of these chronic diseases when we were existing in the Paleolithic period. We had other things that would kill us like, uh, infections, bacterial infection. We didn't have antibiotics.

    11. RC

      Mm-hmm.

    12. TS

      Uh, falls, uh, arthritis. You would have a variety of things that would limit your capability of sur- of longer term survival. But cancer, dementia, cardiovascular disease, all of these kinds of things, uh, were not there.

    13. RC

      Yeah.

    14. TS

      So... Or very, very rare. So you're-- when you say ketogenic diet, it's actually, you gotta be very careful because it's not necessarily a ketogenic diet. It's the state of being in therapeutic ketosis is, is... And a ketogenic diet can put you in therapeutic ketosis, but many of these so-called ketogenic diets, uh, are not done correctly. People go out, eat too much of it. Uh, they don't do it the right way. It's nutritionally imbalanced.

    15. RC

      Yeah.

    16. TS

      I mean, but, uh, but the bottom line, the, the underlying theme here is nutritional ketosis prevents chronic diseases.

    17. RC

      That's a really interesting point there, right? So if we're gonna talk about, as I hope we get to during this conversation, nutrition and cancer and the link between it, and you've covered bits of it throughout this conversation so far, a lot of people will talk about... So and this, there's, there's lots of N equals one studies, there's lots of anecdotes of people, uh, saying that, "I got a cancer diagnosis, and it caused me to stop and look at everything in my life, and I changed dramatically my lifestyle. I started to meditate. I lowered stress. I stopped traveling all the time for work. I went on a keto diet, for example, and, you know, my cancer never came back," right? Or whatever it might be. You, you hear that a lot with, uh, a ketogenic diet, and of course, that can be practiced in many different ways. But you also hear people saying that if they radically change their diet to plant-based diets, right? There's many case studies out there that I've heard or certainly people reporting. Now, it's really interesting to me, so I'm trying to put it all together and go, well, okay, what Thomas just said was that it's not necessarily a ketogenic diet, it's the state of ketosis.

    18. TS

      Yes.

    19. RC

      So I guess what I'm trying to get to, a plant-rich diet, uh, will have lots of polyphenols, right, within it, and I know there's been quite a few studies showing the benefits of polyphenols in terms of their role as signaling molecules and what they can do for cancer risk. Given what you know about cancer, how do you put these two things together, where some people say they revolutionized their health with a keto diet, other people will say that they've done it with a plant-based diet? H- how does that sit with you when you think about cancer? Just taking a quick break to give a shout-out to VIVOBAREFOOT shoes. Now, I've been a huge fan of VIVOBAREFOOT for over 10 years now, well before they started supporting my podcast. They are the only shoes that I wear, and they really have had a huge impact on my own life and the lives of many of my patients. You see, when people start wearing minimalist shoes like Vivos, you can see improvements in things like back pain, hip pain, knee pain, foot pain. Even things like plantar fasciitis can often get better. And scientific research shows us that just wearing Vivos for about four months or so improves the strength in your feet by over 60%, which is absolutely incredible. One thing people don't realize about these shoes is just how flexible they are, which allows your feet to do what your feet naturally want to do rather than the shoe dictating your foot's movements. VIVOBAREFOOT are giving my audience a 15% off one-time code when you make your first order, and they make it really easy for you to give them a try. They give a 100-day trial for new customers, so if you don't like them, you just send them back for a full refund. I'm a huge fan. I really hope you take advantage of this offer. To get your 15% off code, all you need to do is go to vivobarefoot.com/livemore or click on the link in the description box below.

  10. 1:04:51 – 1:10:10

    Radical Remissions, Diet Differences and the Glucose Ketone Index

    1. TS

      Yeah, well, I think those are important points and, you know, we don't have answers, uh, to all of that yet. I, I, I know Kelly Turner wrote a book on ... called Rad- Radical Remission, and, um, uh, in her book on these cancers that you've just mentioned, like some people just do something different and cancer goes away. She, she kind of cataloged all of the different kinds of things that were linked to rad- so-called radical remissions. And, and a large amount of it had to do with a dramatic change in diet and lifestyle, uh, whether y- whether you were a carnivore going to a vegan or a vegan going to a carnivore. It, it seemed, it seemed as though there were radical changes in diet and lifestyle that were, um, uh, linked to these, uh, these remissions. Uh, you have to, you have to realize, um, the cancer, the cancer cell is a cell, uh, uh, hovering near death all the time because it can't get energy efficiently, so it has to depend upon the fermentation fuels i- in the microenvironment. And ever- whenever you change the whole physiology of your body, you are creating ... All the ... We evolved as a species to survive under incredible, uh, stresses in our environment, whether it's cold, hot, food, uh, uh, absence, food abundance, or whatever it was. Uh, Rick Potts of the Smithsonian Institution described it, uh, as our flexibility in, uh, survival. Cancer cells can't do that. They, they're very limited. So when you have these radical changes in your body going from one state to another, sometimes it's just the tumor cells just simply cannot handle the change in some people making these radical changes. So you don't have a, a very, uh, clin- a good clinical trial or a sophisticated approach to say, you know, what is responsible for the elimination of your cancer by, by this radical change? All we know is the tumor cell's up and died, and they disappeared, and you're now healthy. Um, in the movie that's coming out, the documentary film called, um, Cancer Revolution, um, by Brad and Maggie Jones. Brad is a professional documentary filmmaker, and his wife, Maggie, who contacted me lo- she had, um, um, stage four breast cancer that metastasized to her brain. Uh, she went on one of these radical keto, uh, changes, and she, her cancer disappeared, and she's still doing very, very well. But they've collected a lot of these N of 1s, uh-

    2. RC

      Mm

    3. TS

      ... a lot of these people that you just mentioned, and put them in the movie. Um, and they're all, the faces are there, and I'm a survivor, I'm a survivor, one after another, after another, and she's collecting more and more of these individuals that had stage four cancers of a broad range, lung cancer, brain cancer, colon cancer, breast cancer, and they're all alive. Now, what is it, what is it about this? And there's no, there's no comprehensive clinical trials on this, because how would you design such a clinical trial to look at some sort of a radical change in your diet and lifestyle? Um, there's a lot of variables that have not yet been pinned down that we should need to focus on. And this is the whole thing with using ketogenic diets for ma- managing cancer. Uh, what kind of ketogenic diet? That's why we developed the glucose ketone index calculator. We published this, and what it does is it allows the, any patient, healthy or sick, uh, to know whether they're going to be in a state of maximal metabolic homeostasis. And, uh, it's a meter, you can buy it on Amazon, the, the Keto-Mojo meter, and it's a, you take a dr- uh, a, a blood, uh, a drop of blood, and you can measure with one stick your blood sugar, and with another stick your blood ketones. And if you can get the ratio down to 2.0 or below, you are going to be in a state of metabolic homeostasis. And that, that really puts tremendous pressure on cancer cells, uh, diabetes, uh, all of these variety... In other words, you're bringing yourself back to a state of metabolic homeosta-

    4. RC

      Yeah

    5. TS

      ... with a quantitative measure to let you know when you're there.

    6. RC

      Okay. I wa- I wanna talk about that. I just wanna finish off, um, from the previous question about keto diets, plant-based diets. Another way I was thinking about it as you were talking is that if we, if we develop cancer, based on everything we've said so far, I think it's fair to say that there's something going on. You have been receiving a variety of inputs, whether out of choice or not out of choice, whether you're aware of or whether you're not aware of, but whatever's happened, your current environment has resulted in you developing cancer, right? We don't know maybe what exactly it was, but it was multiple signals from your environment and lifestyle. So if you then undergo radical environmental and lifestyle change, I'm not saying no matter what, but, you know, if you're significantly making changes so the environment in which the human body is now existing is fundamentally different, well, it kinda stands to reason that in some cases, depending on how advanced that cancer is, depending on the type, it stands to reason that, yeah, in some people, the environment has shifted and you're no longer getting the inputs, so cancer cells are no longer sort of growing and proliferating, right? Does it, does that sound like a reas-

  11. 1:10:10 – 1:15:38

    Combining Metabolic Therapy with Conventional Treatment

    1. TS

      No, it's absolutely corre- you're absolutely correct.

    2. RC

      Yeah, so-

    3. TS

      Uh, es- especially if you catch it, like, early.

    4. RC

      Yeah.

    5. TS

      Well, when you're... Many people, not all people, many people are first diagnosed with cancer, they never knew, "Oh, gee, I'm just diagnosed with cancer." "How do you feel?" "I feel great." Uh, it's at that stage, uh, where the body is pretty healthy other than you have a growing tumor somewhere, where you can do this radical change and blast out these, uh, uh, marginalize and blast out these cancer cells. The problem, the problem is many cancer, many folks devel- uh, who are diagnosed with cancer, immediately, without any alternative thinking or recognize, they go in for toxic poisons and radiation and, and, and what happens is that undermines the health vitality of the rest of the cells in the body, making them less capable of challenging the vitality of these, of the, the, the existence of these tumor cells. So then all... I get so many people contacting me who have failed every kind of a cancer treatment, and the cancer is still growing, and now they wanna do one of these metabolic therapies. And their bodies are rigged. Uh, you know, they're, they're emaciated. They, they, they have all kinds of adverse effects and all kinds of stuff. And now you're gonna ask your body to go through this, uh, tough, uh, radical change, uh, to try to eliminate. Y- They should've been doing that at the very beginning. Not to say it can't happen, uh, because when you have, sometimes you get a stage four diagnosis, you're still in pretty good health. "Oh, I got stage four diagnosis." Okay. Well, great. Now you do metabolic therapy to pound out those cancer cells. Not to say that we can't use radiation and chemo, uh, but they would be used in a very strategic way, in very low doses at the right time, at the, at the right setting, but not, uh, massive poisoning at the beginning of this disease.

    6. RC

      Yeah, that, that-

    7. TS

      It doesn't make any sense

    8. RC

      ... that, that is such a key point, because I, I really think that, that, that message has to come through loud and clear, which you're not necessarily saying, that we shouldn't be using some of these modern advances, like chemotherapy or radiotherapy. What I think you're saying, a- as you've just pointed out there, is essentially that, look, let's get involved with the metabolic side of things right at the start, you know? And I'm guessing you're gonna say that in some people that may be sufficient. In others, it's gonna reduce the size. It's gonna allow some cancer cells to die off, so you can be a bit more targeted and use lower doses of chemotherapy or radiotherapy, right?

    9. TS

      Absolutely. Absolutely. We have seen that ourselves. You know, uh, you shrink the tumor down and make it extremely vulnerable. Now you can come in with, say, uh, one of these, uh, therapies, um, modern, more modern therapies at a lower dose in a more strategic way to finish off the cancer survivors that the metabolic therapy wasn't able to kill. Because one thing is gonna be in common. When you pare down, the cancer cells are all kinds of... As you said, they're all genetically different from each other. They're all fermenting, uh, but they're all genetically different from each other. But when you pare them down, the survivors of metabolic therapy will have something in common, and that, that common, commonality, uh, makes them extremely vulnerable now to some sort of targeted therapy, because all your [laughs] all, all the cells are gonna have the same target on.

    10. RC

      Yeah.

    11. TS

      Uh, so that's the strat- So in other words, we need, we have a lot of tools for managing cancer. It's just that we haven't been using them in the correct way or understanding the concepts of evolutionary biology to enhance the success of the, of the treatments that we already have.

    12. RC

      Yeah. We kinda need to embrace this approach more, not going either/or. It's like, well, why can't you do both? Why can't-

    13. TS

      Yeah

    14. RC

      ... why can't we do both?

    15. TS

      No, no.

    16. RC

      But, but we're not. But going back to what I said at the start, that I was in, I started medical school in 1995, right? We were taught how to diagnose, and we were taught to treat with pharmaceuticals.

    17. TS

      Yeah

    18. RC

      ... end off. Right? That is literally what we were taught. And again, that can be very useful for certain conditions, but there's a big piece missing there, right? So the training needs to evolve, and I, I honestly don't feel it has evolved [laughs] even now-

    19. TS

      No

    20. RC

      ... you know, almost 30 years on.

    21. TS

      Well, ex- well, you're, you're 100% correct. And, and, uh, what we know, we base it on, on the science. I mean, I, I do the experiments h- here in the lab. I, I, I have the best animal models for cancer, so we know what... It's dosage, timing, and scheduling. This is not what we call sexy science. This is just knowing how to, how to manipulate the tools that you have to the maximum, uh, efficiency. And then we can translate that directly to patients in the clinic. When I have all, uh, these, my physician colleagues say, they're coming to me and they're saying, "Wow, you can't believe how powerful this stuff is," uh, when you do it the right way. Uh, our group in Istanbul, uh, Turkey are using, uh, metabolic therapy with conventional, uh, uh, treatments, and they're using far lower dosage and the, and the outcomes are, are, are so much better. So this is an evolving, uh, process right now. But I agree 100%, we have to do, we have to know, uh, the tools that we have, what will work the best, and how to, how to blend the system. Um, but the, we're not doing that.

    22. RC

      Yeah.

    23. TS

      Uh, w- we're not doing that at all. I have all this information. I publish all these papers. We do all this kind of stuff, and then when the cancer patient goes to their oncologist, "No, there's no evidence to support that. If it were really true, I would've learned it in medical school."

    24. RC

      Yeah. Well, we'll get into that-

    25. TS

      But we-

    26. RC

      ... 'cause I've got a few things to share about that.

  12. 1:15:38 – 1:30:41

    Measuring GKI and Seyfried's Cancer Protocol

    1. RC

      Let's go to that glucose ketone meter that you mentioned. That sounded really interesting, right? So you're measuring the ratio between glucose in your blood and ketones. Is that right?

    2. TS

      Yes.

    3. RC

      Now, if you were to take, you live in, I think, Boston. If you were to go out into the center of Boston and pick the first 10 people who passed you on an average street downtown on a Saturday afternoon-

    4. TS

      Right

    5. RC

      ... what do you think the glucose, uh, ketone ratios would be in that population typically?

    6. TS

      I, I know exactly what they would be because we, we've done these kinds of things [laughs] .

    7. RC

      Okay. Okay [laughs] .

    8. TS

      Not to guys walking through the streets, but to the students in my [laughs] there, there at the university here. So we can, uh, all of us, we test. Uh, it's about 50 to 60, sometimes 70.

    9. RC

      Hold on, hold on.

    10. TS

      So-

    11. RC

      So 50 to... Is that to one? So it's basically-

    12. TS

      Yeah, yeah. So, so it's, um, you would have glucose levels, um... Well, you can do, uh, uh, normally, uh, your glucose levels would be, uh, let's say 100 milligrams per deciliter. What does that come out to be? You have to divide that by 18, and that gives you the millimolar, uh, ratio. What is that, 4.5 or something like this? Um, you know, four point... And the ketone value in millimolar would be 0.1. So you divide the, uh, 4.5 by 0.1 or one of these kinds of things.

    13. RC

      Okay.

    14. TS

      It, it, uh... You, you, you come up with a value about 50. I, I, I have all the, the numbers here somewhere.

    15. RC

      It's about 40 to 50 times higher based upon that.

    16. TS

      Yeah, yeah, yeah. Okay. So then you stop eating, like, for how... Like, when we did the water-only fasting here with the students, um, it takes about four days, and then you start to see the ketones rise and the glucose drops. So, uh, um, because you stop eating, once you stop eating, you're not bringing glucose back into your system. Um, the only way you're gonna get glucose now is through the process of gluconeogenesis, where your body will make glucose-

    17. RC

      Mm

    18. TS

      ... from breaking down, uh, proteins. And also, you mobilize the fats, and most of these are called triglycerides. So the two glycerol backbones could be conjugated to make one glucose molecule. But the majority of the fats are gonna be used to make ketone bodies. So the ketones are gonna gradually increase in your bloodstream, and then glucose gradually goes down, and you come to a, a ratio where the ketones and the glucose are about the sa- similar millimolar or in your blood, or the ketones are higher in millimolar than the glucose, therefore you get numbers below one, and that becomes super healthy.

    19. RC

      So were you... Did you say before you wanna get to two or below ideally?

    20. TS

      Well, for killing ca- for killing cancer cells, for sure. Um, but for just general health, yeah. You can get down to five or even, um... Like my, my good friend, Dom D'Agostino from University of South Florida-

    21. RC

      Yeah

    22. TS

      ... he's always in ketosis, right? He's always in this kind of a state. Uh, he's like one of these Paleolithic guys, you know? He likes to eat, uh, alligators and squirrels. I mean, it was one of these kinds of guys [laughs] . He's always like living the, he's like living the Paleolithic life.

    23. RC

      I, I, I really like Dom's work, and I, I'm hopefully gonna-

    24. TS

      [laughs]

    25. RC

      ... try and get him on the show later in the year. And h- and he shared... Well, we'll get to this maybe later, but he did share one of his colleagues, I think, in a, was it a mouse model where they had GBM glioblastoma? Um-

    26. TS

      Yeah. It was our model. It was our model. Yeah.

    27. RC

      It was your model. Yeah.

    28. TS

      Yeah, yeah, yeah.

    29. RC

      And actually, um, by using ketosis-

    30. TS

      Yeah

  13. 1:30:41 – 1:39:02

    Oncology Resistance, Glioblastoma and Pablo Kelly

    1. RC

      Yeah, I mean, there's so much to unpack there. I'm loving my conversation with you. I think this is so important we get this message out. But one of the frustrations will be, I'm sure, for some of the listeners or viewers on the back of this, is they'll hear this information, and maybe they have cancer or a family member has, and they may go to their oncologist and have this conversation, and chances are this will be shut down, and it will be like, "Look, I don't know about that stuff." I mean, four years ago, a really close friend of mine, his son, I think at the age of maybe six or seven, was diagnosed with an optical pathway glioma.

    2. TS

      Mm.

    3. RC

      And of course, very scary to, you know, for your child to have this tumor inside your brain. And, you know, initially they started, I think, down the conventional route. I think initially, um, he had a course of chemotherapy. But as my friend started to read up and, you know, he went all in, spent hours a day researching the papers, experts like yourself listening, and he thought, "Wait a minute, I'm not sure about this. I'm not sure I like what's being offered versus what I think we can do." He has basically for four years, there has been no increase in size at all, and he's done it all, and he, to be fair, I feel for... He's done it all through a huge amount of stress. He's taken on to, you know, seven days a week, obsessively research the literature-

    4. TS

      Yeah

    5. RC

      ... trying to get help. He's not getting help from his oncologist. You know, he told me recently, he said one of the first things his oncologist said to him was, "Oh, are you gonna do the ... the, the no sugar thing. Don't worry, in four weeks you'll be back eating McDonald's. They all are. That's the first thing, which is a pretty, um, I just don't know why or how a doctor would say that. What, what... Even if that's what the doctor believes, I'm not convinced that that has any benefit at all, uh, to, to saying that, uh, to a parent of a child with a tumor. I mean, what would you say to that?

    6. TS

      Well, that, uh, well, I, it speaks to a profound lack of knowledge-

    7. RC

      Yeah

    8. TS

      ... on the part of the oncology community. And it's not just where you are. I see it all the time here in the States as well. Um, at the Mayo Clinic, uh, which is supposed to be, you know, a top-notch medical center, and for certain, uh, aspects of medicine, they s- they are, but when it comes to cancer, um, they, they're clueless. Uh, one, a pa- uh, one of the people who emailed me said they went to the Mayo Clinic with, with glioblastoma, and one of the on- the neuro-oncologists there said sugar has nothing to do with glioblastoma. And I said that we, we were the first to publish a direct, uh, association between glioblastoma in the mouse and how fast the tumor, uh, how, uh, the, the sugar and the, how fast sugar could make a tumor grow, and then that was replicated in humans, uh, with glioblastoma. Hyperglycemia is an accelerant to rapid tumor growth, and it's been repeated dozens of times, and now it's been shown for almost every major cancer that the higher the blood sugar, the faster the tumor grows. The lower the blood sugar, the slower. This has been now repeated. Uh, and yet for a person treating patients to say that sugar has nothing to do with glioblastoma speaks to a profound lack of knowledge on the part of not only that person, but the entire establishment. Another person you might wanna talk to is Pablo Kelly from Devon, England. Um, Pablo, uh, chose no radiation, chemo, or steroids to manage his glioblastoma. He's still alive eight, eight, uh, almost nine years. August will be nine years.

    9. RC

      And, and just, and just, and, and just explain to people how bad the prognosis is when you have a diagnosis or when you have, uh, glioblastoma.

    10. TS

      It's a brain tumor. It, it killed John McCain of our country, Ted Kennedy. It killed the President Biden's son, Beau Biden. I did, uh, uh, studies for, for many, many, uh, decades on glioblastoma. The issue is why is survival for glioblastoma so poor? There's been not a single major advance in 100 years, and I keep pointing this out. In 1925, survival was 8 to 14 months. In 2023, survival is 8 to 17 months. So I mean, you're talking about no progress in 100 years. Uh, and what we have found, what I have found in my research is not only is the tumor very bad, it grows, it grows rapidly. Um, radiation, uh, treatment frees up massive amounts of glucose and glutamine in the microenvironment. When you irradiate somebody's brain tumor, uh, the head swells. Uh, the, the radiation fo- forces blood sugar into the, i-i-into the stratosphere. A-and not only that, they give you high-dose steroids to reduce the inflammation from the radiation, which raises blood sugar even higher. So you're, you're actually contributing a microenvironment rich in the two fermentable fuels that drive the rapid growth of the cancer. I have published this over and over again, and I said, "As long as you continue to, continue to irradiate the person's brain, you're never going to achieve a, a, a level of success that you would expect." Now, Pablo Kelly rejected radiation. He rejected temozolomide. He rejected it all and went for metabolic therapy alone. People say, "Oh, he's only an N of 1." Yeah, an N of 1. He could be the, he could be the, the rule rather than the exception, but to stop the radiation of the brain by, by onco- by radiation oncologists is an absolute essential, uh, part for incri-

    11. RC

      Wow

    12. TS

      ... to, to... If you wanna keep people alive longer, you have to stop irradiating their tumors. And we, we have a treatment protocol that will, that will hopefully do this. But I tell you, when you're, when you are indoctrinated and, and wrapped into a, in-into this constant system, it's very hard to break, uh, the habits of what you're doing.

    13. RC

      Yeah. I think that's the problem. You know, I, I genuinely believe that all doctors, nurses, healthcare professionals are doing the best for their patients based upon what they've been taught, based upon what they know, based upon the current paradigm. It... And I know you've been shouting [laughs] from the rooftops trying to shake up this paradigm and go... You know, the, the other, the other thing to really think about here is that, and I always say this when we're talking about nutrition changes, is that, look, like, there's, there's very little downside here, right? [laughs] Improving your diet, whatever that means, depending on what you're doing, whether it's cancer or anything else, there's no downside here, right? Rarely, you know?

    14. TS

      Well, you know, that's a, that's an interesting point. You'll hear some of the people in the oncology center said, "Oh, that ketogenic diet is very dangerous. You're gonna get cardiovascular disease," or something like this. And, and I, I said, "What? You got a brain tumor. You got a glioblastoma. You're worried..." And, and, and the i- the issue is relative- you're exactly right. Downside. Do you think a, a, a metabolic therapy has more downside than toxic radiation and poisonous chemicals?

    15. RC

      Yeah.

    16. TS

      I mean, give me a break.

    17. RC

      And also, what you were saying, Thomas, before, is that you could do them both. You could use-

    18. TS

      Right

    19. RC

      ... the metabolic therapy to reduce the cancer size, improve the health of other cells, and then use small targeted doses which have less side effects. So it's not either/or. So Pablo Kelly, you're saying, what, has, has been alive for what, eight, nine years? Is that right?

    20. TS

      Yes. Yeah. And he, he was given nine month, uh, uh, nine months to live.

    21. RC

      Wow.

    22. TS

      And, uh, like, uh, and he said... No, it's all over the English newspapers. There was many-

    23. RC

      Where did you say he lives? Devon?

    24. TS

      Devin

    25. RC

      Devin

    26. TS

      Yeah

    27. RC

      I might try, I might try and get ahold of him

    28. TS

      Oh, get ahold. He's a, he's a character. He, he, he can tell you what he did and then-

    29. RC

      Oh

    30. TS

      ... he, now he since got married, he has two children. Uh, he would have-

  14. 1:39:02 – 1:48:00

    Sugar, Obesity and Cancer Prevention

    1. RC

      Thomas, one thing I, I really wanna make sure we make clear, right? You'd have mentioned how hyperglycemia, so elevated blood sugar levels, is an accelerant for tumor growth, right?

    2. TS

      Yes.

    3. RC

      And that fits with everything we've been talking about so far. Metabolic dysfunction, a problem in the mitochondria. You know, what happens when a cancer cell is there, it no longer, uh, is using oxygen appropriately. It's getting its fuel from fermentable sources, which is glucose and glutamine.

    4. TS

      Yeah.

    5. RC

      So it makes sense when you have a diagnosis of cancer, you may want to reduce sugar, reduce glucose, maybe go into ketosis. But if we shift our lens to prevention, right, of course, there are many things that can cause cancer. You ... We've already mentioned that. Diet, lack of exercise, um, environmental pollutants, carcinogens, whatever it might be. Can we say that sugar is causing cancer? Because I think that's ... This is where we really need to be very careful with our messaging, right? What, what's ... There's something to do with our diet as a therapeutic intervention if we have been diagnosed. But what if you are, I don't know, in your 30s and 40s and, and pretty well, and you listen to my podcast, you try and stay healthy, try and make small changes. You know, w- what's the relationship there between sugar-

    6. TS

      Yeah

    7. RC

      ... and cancer?

    8. TS

      Well, I, I think we can never call sugar, uh, a carcinogen.

    9. RC

      We cannot. We cannot. Yeah.

    10. TS

      No. Sugar is not a carcinogen, okay? But sugar, uh, creates a systemic inflammation in the body over time. Uh, C-reactive protein goes up. Now, how do we know this? Obesity. The obesity epidemic, which is now becoming worldwide in, in industrialized societies, the obesity epidemic, is the result of, of the storage. You get fat by storing carbohydrates. You don't get fat by eating carb. That's why you lose weight with a ketogenic diet. You, you, you, you can't, you can't store fat. Uh, uh, you store carbs as, as fat. You don't store fat as fat. People, this is a t- another tremendous mis- mis- uh, conception, misunderstanding. So we have an obesity epidemic. Obesity has now replaced smoking as a major risk factor for cancer. How do you get obese? By consuming too much carbohydrate in the diet, especially poorly nutritious carbohydrates. Not complex carbohydrates that you see in certain plants and in certain grains, but you get it from consuming those foods that have minimal nutritional value with high levels of processed carbohydrates. High fructose corn syrup and all these kinds of things. Um, they are provocative to s- becoming obese, elevating blood sugar. Elevated blood sugar is an accelerant to growing tumor.

    11. RC

      Mm.

    12. TS

      So, so clearly all of these things come together, and it's basically diet and lifestyle. Yeah, we all th- would like to prevent cancer, but when we have fast food stores on every corner, we have Coca-Cola, we have everything that's in our environment that makes us feel good. We evolved as a species to love sweets. Our brains are geared to-

    13. RC

      Yeah

    14. TS

      ... love sweets, and we have sweets everywhere. So it, it's, again, it's mo- moderation. We try to do what we can do to moderate our consumption of highly processed-

    15. RC

      Yeah

    16. TS

      ... carbohydrates, and that will reduce the risk for ca- not only cancer, but a lot of these diseases as well.

    17. RC

      I think, you know, the, the, the truth as I see it, at least, is that many people are really struggling, right? They, they do have ... They either live in a food desert where they can't get-

    18. TS

      Yeah

    19. RC

      ... access to decent foods.

    20. TS

      Yeah.

    21. RC

      They're in poverty. They're-

    22. TS

      Yeah

    23. RC

      ... they've had a problematic relationship with food. So I, I think on an individual level, I think that it's complex as to why so many people are overweight. Certainly that's my experience as a clinician.

    24. TS

      Yeah. Yeah. Yeah.

    25. RC

      Um, but I think we can say as a society, we're not really putting this front and center. If, if government, for example, really wanted to address, frankly, beyond reducing our risk of cancer, reducing our risk of obesity and type 2 diabetes, you know, they could, uh, [laughs] put in place a lot more policies. For example, I don't know, make sure that there's, uh, affordable, healthy food for-

    26. TS

      Yeah. Yeah

    27. RC

      ... all of the population. Make sure the food in hospitals and schools is healthy and health-promoting rather than health-decimating. We'll be back to the conversation in just a moment. Now, many of us struggle to find time to eat all of these incredible whole foods. That's why I'm a big fan of good quality whole food supplements like this one that's been in my own life for over three years now. It contains over 75 whole food source ingredients, vitamins, minerals, pre and probiotics, and can help us support our energy, focus, digestion, and our immune system. AG1 are giving my audience a fantastic offer, one year supply of vitamin D and five free travel packs with your first order. You can see all details at drinkag1.com/livemore, or just click on the link below. And now, back to the conversation. Right, so-

    28. TS

      Yeah

    29. RC

      ... I just wanted to clarify that, 'cause I'm sure you would agree-

    30. TS

      Oh, you're 100% it. But you know, it's an industrial thing. Uh, the food industries are extremely powerful. Uh, they control politics as well as the pharmaceutical industries.

  15. 1:48:00 – 1:52:44

    Practical Prevention Tips, Intermittent Hypoxia and Hope for the Future

    1. RC

      Professor, it's been a real joy, uh, talking to you. I know you've been in this field for, for many decades now, and you're, you're still banging the drum. You're trying to get people to see that there's a metabolic cause to cancer, and that maybe we need to, you know, relook at how we view cancer and how we treat cancer. There's plenty more we haven't got to. Maybe I can tempt you to a, for a part two at some point in the future. I, I'm pretty sure my audience are gonna love this conversation. But just to finish off then, for people who've heard that and are inspired and go, "Okay, I'm with you. I can see how poor metabolism, metabolic dysfunction, mitochondrial dysfunction is gonna increase my risk of getting cancer. What can I do right now? I don't have cancer, but I wanna reduce my risk of getting it in the future," I wonder if you could share some of your top tips for people as to what they can actually practically do.

    2. TS

      Well, I think exercise is absolutely essential. Um, keeping your ... Because, uh, bringing oxygen into your blood, having, uh, good blood flow increases, uh, physiological function. If you can reduce the amounts of high carbohydrate foods that you eat with exercise, and o- occasionally look at your GKI, your glucose ketone index, uh, you're going to ward off not only cancer, but probably type 2 diabetes, cardiovascular disease, and even dementia. So, uh, all of these things are linked to a common problem in, in disturbed metabolic homeostasis. So, um, so I think there are definitely things people can do. And it's hard when you're sitting in traffic, uh, traffic jams, and then you have to rush up and sit in front of your computer in s- or in an office somewhere.

    3. RC

      Mm-hmm.

    4. TS

      So all, all of these things are not consistent with our, uh, evolutionary origins. But I think if people become aware of these things, at least they can, in their own lives, try to adjust the, adjust their, uh, their, their situation to, to recognize this.

    5. RC

      And sleep, chronic stress, these sort of things?

    6. TS

      Well, that's another thing too. Sleeping, you know, uh, good sleep. Yeah. Right. Who would, who wouldn't like to have that?

    7. RC

      [laughs]

    8. TS

      Uh, yeah. [laughs] And stress, what do you do for stress? You know, I mean, we're all stressed out. People would used to smoke like crazy to reduce stress. Now they stopped smoking, and now they got fat, and now they g- [laughs] they got this, they're back in the same spot for a different reason.

    9. RC

      Yeah.

    10. TS

      So, uh, you know, it's just, it's just, um-

    11. RC

      But, but the po- but the point is, is that all of these things really do make a real difference at reducing your risk of cancer in the future

    12. TS

      Yeah, absolutely.

    13. RC

      Yeah.

    14. TS

      Absolutely. You know?

    15. RC

      And maybe this is just a little teaser for the next time we talk. You mentioned earlier on that intermittent hypoxia is one of the things that can drive the mitochondrial dysfunction. I wanted to really expand what you meant by that. Did you mean obstructive sleep apnea, things like that? Because you also, th- 'cause you then mentioned exercise as being a way of delivering more oxygen.

    16. TS

      Right. Yeah, no. That's what Warburg even showed, that it was intermittent hypoxia that he thought was responsible for the majority of cancers. We, we've expanded upon that, and we've shown the mechanisms by which that can happen. So yeah, that's another story. I mean, we've done, we've done a lot of, uh, re- uh, research and, and r- we recognize these things. And, and intermittent hypoxia can be prevented by a- by, uh, oxygenation and exercise, and eating the right foods. So again, you're coming back to a similar kind of thing.

    17. RC

      Well, we'll get to that in our next conversation, hopefully. But just to finish off then, are you hopeful? Are you hopeful that we can do something different to make an impact in our rates of cancer?

    18. TS

      Oh, absolutely. I mean, uh, uh, absolutely. A- and Warburg even said that we could reduce 80% of our cancers, and I believe that. If w- but now we, we have a plan. We know what's going on. We have an understanding of the mechanism by which cancer occurs, and we really understand how we can manage it. The problem is getting that to be adapted in the, uh, in the clinics and, and the education that requires, uh, i- in the medical schools, uh, to train the physician that diet, lifestyle issues are really important for managing, uh, chronic diseases, and here is the strategy and, and, and protocols for doing that. And that, I think, will be the future.

    19. RC

      Well, Professor, thank you for your tireless work. Thank you for giving up some time. Thank you for coming on the show.

    20. TS

      Yeah. Very nice. Thank you very much for having me.

    21. RC

      [upbeat music] If you enjoyed that conversation, I think you are really going to enjoy this one about the four common causes of decreased longevity and what we can do about it.

    22. RC

      Today, we're at a point where not only has life expectancy flattened, but in many parts of the developed world, it's actually declining a little bit. And more importantly, quality at the end of life is going down. The question is, why?

Episode duration: 1:52:44

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