Cancer Is NOT a Genetic Disease? Dr. Thomas Seyfried Explains the Metabolic Theory (Part 1)

Is everything we’ve been told about cancer wrong?

In this episode of UltraLife Today, Boston College biology professor Dr. Thomas Seyfried explains why he believes cancer is not primarily a genetic disease—but a mitochondrial metabolic disease fueled by disordered energy production.

Dr. Seyfried walks us through:
* Why the dominant “cancer is a genetic disease” model is breaking down
* The experiments showing that damaged mitochondria, not mutated DNA, drive tumor growth
* What Otto Warburg got right (and what he didn’t know) about cancer metabolism
* How cancer cells ferment glucose and glutamine even in the presence of oxygen
* Why this shift in understanding could change how we prevent and manage cancer
* The basics of the Glucose Ketone Index (GKI) and why metabolic health matters for all chronic disease

If you or someone you love is facing cancer, this conversation is essential viewing.👉 Share this with anyone who has an active diagnosis or is at high risk.

🔔 Part 2 coming next week – where we get practical about:
* Metabolic strategies and diet
* Exercise & mitochondria
* Supplements & common questions (including “repurposed” drugs)

🧬 About Dr. Thomas Seyfried
Dr. Seyfried is a professor of biology at Boston College and author of “Cancer as a Metabolic Disease: On the Origin, Management and Prevention of Cancer.” His work builds on and expands the Warburg hypothesis, arguing that mitochondrial dysfunction and fermentation are at the heart of cancer biology.

Listen to the full episode here our watch it on YouTube: https://youtu.be/l-_63d2Gkzc

⚠️ Important Disclaimer
This video is for educational purposes only. It is not medical advice, diagnosis, or treatment. Always consult your qualified healthcare provider before making any changes to your diet, medication, or treatment plan.

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Visit UltraBotanica.com to learn more about us and how you can get a free sample of our products.

Transcript

0:00:00 - (Dr. Thomas Seyfried): You can take the nucleus of a raging tumor cell and place it in the cytoplasm of a non tumor cell and you get regulated growth. That rules out any oncogene or tumor suppressor gene as being responsible for the dysregulated cell growth. And those experiments were done in vitro and in vivo. A broad range of these, that's what brought me to the idea that this cannot be a genetic disease by any stretch of the imagination.

0:00:35 - (Kyle Drew): Hi everybody and welcome to Ultra Life Today. My name is Kyle Drew, meat eating, tofu hating nutritionist. Glad that you're here joining us. Listen, we've got an incredible show for you today. Dr. Thomas Seyfried joins us from Boston College. What a guest. A lot of you have watched him, a lot of you have watched his podcast that he's been on and he has really moved the needle over in the ketogenic world now in the cancer space.

0:01:07 - (Kyle Drew): It is a tremendous interview. It's going to be a little dense, it's a bit technical at times, but it's well worth listening. If you know someone who has active cancer, please send them this link. This is crucially important. We've actually broken it up into two separate episodes. One long interview, but two separate episodes. We'll do another episode in the next week or so. I need you to know that Ultra Life Today is brought to you by Ultra Botanica, the makers of the super absorbable high intensity curcumin. You can feel.

0:01:45 - (Kyle Drew): It's called Ultra Cur, Ultra Kerr. That is powered by protosorb technology. Protosorb is just an absorption technology. A lot of people want to get the benefits of curcumin but they can't feel it. And it's because they're taking garden variety curcumin or an inferior absorption technology infused curcumin, something like black pepper or something like that. Liposomals are a lot better. Nothing touches protozorb.

0:02:15 - (Kyle Drew): When you take it, you can feel it. It's called ultracur. But more importantly, for the purposes of this episode, Ultra Botanica are the makers of the pathway system of products. Pathway system of products. Pathways 1, 2, 3 and 4. This is an adjunctive supplement. When people are going through cancer, it is not a treatment. We do not treat it, we do not prevent it. But it is nutritionally supporting the rebalancing of metabolic pathways that have been disrupted and corrupted by cancer.

0:02:54 - (Kyle Drew): Do not mistake it for a medication. It is not a medication. It's a series of dietary supplements. You can go to ultra today.com ultra today.com and see the full line of protozorb enabled products. We hope that you will and we know that you will love them. Now, without further ado, let's start part one to our conversation with Dr. Thomas Seyfried.

0:03:27 - (Kyle Drew): He is a professor of biology, biochemistry, genetics at Boston College. He is known everywhere and I first began to see him popping up years ago in the thick of the ketogenic craze. And he sort of became kind of like a patron saint. But where he really has made a mark is with his research into cancer. If you don't know his book, here's the title. Cancer is a Metabolic Disease. And if you don't know why that is such an earth shattering title and concept, you'll find out as we go along.

0:04:09 - (Kyle Drew): Professor Thomas Seyfried is with us today. Dr. Seyfried, thank you for joining us today.

0:04:16 - (Dr. Thomas Seyfried): Oh, thank you very much. It's nice to be here.

0:04:18 - (Kyle Drew): I was very, very interested in visiting with you again. We've spoken before on a radio show, but one of the things that I think about is that an awful lot of people probably don't know why even that title is so controversial for your book. And maybe before we really go into why, can we even go a little bit more granular? A lot of don't totally understand what we mean by metabolic and metabolism. Could we maybe start with that and then jump off from there?

0:04:58 - (Dr. Thomas Seyfried): Yeah, we can do that. The full title of my book was Cancer as a Metabolic Disease on the Origin, Management and Prevention of Cancer. And it was by John Wiley Press. Now I have to point out that there have been a couple of hijacked versions with my name that I didn't write. I've seen, you've seen these things, right? They take my stuff from podcasts and they use AI and synthesize it down and then they say I wrote it and I didn't.

0:05:26 - (Dr. Thomas Seyfried): So I only wrote one. It's John Wiley Press is the book from 2012, and it's actually a mitochondrial metabolic disorder. Cancer is a mitochondrial metabolic disorder. And I think it's important for people to start reading more and more about our mitochondria. It is the essence of our life and our existence on the planet. And when that organelle becomes corrupted or inefficient in certain ways, you can get a whole range of chronic diseases as, as well as cancer.

0:05:59 - (Dr. Thomas Seyfried): So it's important to know about that organelle, how it functions and how it can be disrupted in its function, leading to dysregulated cell growth, which ultimately is Cancer. So that's the essence of what we need to know. And that brought us into a very deep dive on mitochondria, metabolism, biochemistry and all of the different things you need to know about the origin of that organelle and how it participates in our overall general health.

0:06:33 - (Kyle Drew): One of the things that is a telltale sign that they have not gotten your book, even though the fake books still have your name on it, is the thickness of the books is dense, it is well researched and it is an easy read. But it is requires thought, particularly depending on if it's a rank lay person reading it or not. Would you explain why this is such a controversy and what the predominant theory of cancer has always been that you are challenging with this book?

0:07:12 - (Dr. Thomas Seyfried): Well, it's just, it's. The book was in 2012.

0:07:17 - (Dr. Thomas Seyfried): Which laid out a pretty solid argument against the prevailing view that cancer is a genetic disease. But since that time we have published many other peer reviewed papers and number of journals solidifying the view that cancer is predominantly a mitochondrial metabolic disease. The controversy.

0:07:40 - (Dr. Thomas Seyfried): Is, involves the continual belief that cancer is a genetic disease. And that's supported by the National Cancer Institute's website which says that cancer is a genetic disease. It says it right on there. It says cancer is a genetic disease, maybe made up of maybe hundreds of different diseases with many, many different kinds of mutations. All of that is nonsense. It's not data don't support that concept.

0:08:09 - (Dr. Thomas Seyfried): And I don't, I, I've written to the nih, they're, they're like bots. I don't think they think, they just do stuff and it's consistent with what everybody else thinks it should be. So the continual persistence of the view by the federal government and the academic industry and the pharmaceutical industry is that cancer is a genetic disease driven by all kinds of mutations and tumor suppressor genes and oncogenes. And you're constantly chasing these things around for diagnostic and therapeutic purposes and we're not getting anywhere.

0:08:42 - (Kyle Drew): No.

0:08:44 - (Dr. Thomas Seyfried): We got 1700 people a day dying, 70 an hour. And we've been doing the same stuff for the last 50 years and nothing's changed. And it's getting worse.

0:08:52 - (Kyle Drew): Nothing's changed.

0:08:54 - (Dr. Thomas Seyfried): You know, that's the sad thing.

0:08:57 - (Kyle Drew): Well.

0:08:59 - (Kyle Drew): I asked you before we started recording the show if this has been your prevailing view. I said that you were a professor, among other things, genetics. And if you think of yourself as an expatriate of the genetic model and you have always, it sounds like questioned that model for cancer.

0:09:20 - (Dr. Thomas Seyfried): Yeah, no, I didn't. I just bought onto it like, like everybody, all the other non thinkers. So, so because that's what it said in the textbooks. And when you're teaching genetics out of the textbooks, you know, and you say, well, okay, it's a genetic disease, tumor suppressor genes, and then in biochemistry you got the same thing and cell biology you got the same thing. But, but I wasn't focusing on that in those days. I was working in the field of epilepsy. So it really wasn't genetics of epilepsy and glycolipid biochemistry. So it really wasn't central to what I was doing anyway. And I just went along with the crowd. If everybody says it, it must be right.

0:09:55 - (Kyle Drew): Hard to push against it.

0:09:57 - (Dr. Thomas Seyfried): Yeah. You know, and then when you start pushing against it, you get, you get weird looks by people.

0:10:04 - (Kyle Drew): Uh huh.

0:10:04 - (Dr. Thomas Seyfried): You may have lost your bearings. Yeah.

0:10:07 - (Kyle Drew): Well, what began your shift into a metabolic model?

0:10:15 - (Dr. Thomas Seyfried): Well, that started, it sprang from our work with ketogenic metabolic therapy for managing epilepsy, which is a standard practice for managing seizures in children. The question is, what is the mechanism by which shifting from a regular high carb diet to, to a low carb high diet that elevates ketones. What does that, how does that stop epileptic seizures? I mean this, this is still a very active research focus, but we also were studying angiogenesis in brain cancer, which is abnormal blood vessels. And we started to see similarities.

0:10:51 - (Dr. Thomas Seyfried): When you calorie restrict animals with epilepsy, the seizures go down. And when we calorie restricted mice with brain tumors, the angiogenesis went way down and the tumor shrunk. So I said, wow, this seems to be something here. And then we, we ran into the, look big into the work of Otto Warburg. And he said that cancer was a, a metabolic disease and that all cancers have this dependency on glucose because respiration was inefficient.

0:11:22 - (Dr. Thomas Seyfried): So I looked at, and we started looking at blood sugar and ketones in the animals that were restricted. And sure enough, blood sugar went down and ketones went up and the tumor shrunk. And then Warburg said this a long time ago. That initiated probably around the year 2000, 2001.

0:11:41 - (Dr. Thomas Seyfried): Brought my attention to that. And then when we started doing research in the lab, we were corroborating what Otto Werburg had said. Then I started to do a real deep dive on Otto Werburg. Who is this guy? Of course, he turns out to be one of the giants in the field of biochemistry. Giants and you know, a very arrogant German who actually had, he thought he had all the answers to the cancer problem. And in the end, they threw his under the bus.

0:12:08 - (Kyle Drew): Uh huh. Yeah, well. And part of the work that you've done that I think is every bit as profound as laying out the metabolic model. There's work that I. The way I think of it, Professor Seyfried, is you've stood on the work of Otto Warburg. You've seen what he got right, but you also saw something that he got wrong. I believe you and a colleague from Budapest have published on this. Talk about the additional thing that you guys have found.

0:12:43 - (Dr. Thomas Seyfried): Yeah, well, he got something wrong, but he also did not know about something else. So there's. There's two issues here. The first issue is that he assumed that every mole of oxygen consumed by either a normal cell or a tumor cell was comparable to seven moles of ATP produced, which is the currency of energy in our cells. And he. And he got that calculation from Hans Krebs of the Krebs cycle. So. And Krebs was one of Warburg's students.

0:13:17 - (Dr. Thomas Seyfried): So because Warburg trained Krebs, Krebs cannot be wrong.

0:13:24 - (Dr. Thomas Seyfried): So we started to look deeply into. And of course, everybody was saying that Warburg cannot be right because there are some tumor cells that consume oxygen just as avidly as normal cells. And normal cells consume like tumor cells. So he says they were using oxygen consumption as an accurate surrogate for ATP production through oxidative phosphorylation. We and others have done some really comprehensive experiments to show that in cancer cells, oxygen consumed is not quantitatively linked to ATP produced.

0:14:01 - (Dr. Thomas Seyfried): It is in normal cells for sure, but not in tumor cells. Not in tumor cells, yeah. So tumor cells consume oxygen, but they use the oxygen for the production of reactive oxygen species, which are carcinogenic and mutagenic. So you cannot quantify and make an assumption that the oxygen consumed in a tumor cell is equivalent in energy production to oxygen consumed in a normal cell. And Warburg made that mistake. And everybody make that mistake. And they still make that mistake. They're still using all of these devices. Like the Seahorse is spending $75,000 on the seahorse instrument, which is all calculations and not direct measurements anyway.

0:14:46 - (Kyle Drew): So I didn't realize that. Really?

0:14:49 - (Dr. Thomas Seyfried): Yeah. You're not. You're not doing direct. It's all based on adding these different chemicals. And it's over a short term, like 30, 30 minutes of experimentation, maybe an hour at the most. You got to look at these tumor cells over hours. We use a reservoir resvere oxygen consumption device that we have here in the lab. And we can monitor all over, over days oxygen consumption on these tumor cells.

0:15:15 - (Dr. Thomas Seyfried): So we were finding that in normal cells, if you add cyanide, which blocks cytochrome C, oxygen consumption goes. Goes way down. So we were given. We were giving cyanide, potassium cyanide to the cancer cells, and oxygen was going way down. But ATP wasn't interesting.

0:15:34 - (Kyle Drew): Right. So there's no respiration going on.

0:15:39 - (Dr. Thomas Seyfried): Cancer cells can live in cyanide. They can live without oxygen. So then, then what we did is we put them in glutamine alone with no glucose and no oxygen. And then we were measuring ATP production. And where was this ATP production coming from? Is coming from mitochondrial substrate level phosphorylation, which is a very interesting mechanism inside the mitochondria itself that produces ATP independent of oxygen. It's unbelievable. So interesting. Yeah. So this is where they're.

0:16:10 - (Dr. Thomas Seyfried): So they're using a fermentation mechanism in the very organelle that's supposed to get energy from respiratory.

0:16:17 - (Kyle Drew): Wow.

0:16:18 - (Dr. Thomas Seyfried): This is an ancient. We have a big paper coming out on this and this. Let me give you an example. When people have heart attacks and they stop breathing, the bloodstream fills up with lactic acid and succinic acid. This is because you're not breathing. And it's been known for a long time that lactic acid is coming from the fermentation. It's called lactic acid fermentation using glucose as the fuel. And Warburg knew this, and that was one of the interesting things about cancer. They continue to ferment even in the presence of 100% oxygen.

0:16:49 - (Kyle Drew): Hmm.

0:16:50 - (Dr. Thomas Seyfried): But he never knew anything about the succinic acid. So we started looking into succinc. The guys in the heart attack field knew it all. They knew it and they were saying that this succinic acid is coming from a amino acid fermentation. And that amino acid seems to be glutamine. So, so we, we added labeled glutamine in cells that were no oxygen and no glucose. And we were finding labeled succinic acid.

0:17:22 - (Dr. Thomas Seyfried): So that's the waste product of mitochondrial substrate level phosphorylation. All major cancers are crapping out lactic acid and succinic acid, the two fuels driving the fermentation metabolism. And they've been knowing, and they do it in 100% oxygen. So in other words, they're not respiring, they're fermenting, even in the presence of oxygen. So Warburg knew the lactic acid story. He did not know about the succinic acid story, nor did he know about amino acid fermentation.

0:17:53 - (Kyle Drew): There's. And that's the key. And this is something that's really important because there are a lot of laypeople, a lot of cancer patients who once they begin reading, they will see the glucose link. But many of them have not heard about the glutamine link. And this is what is so important. And I think that there's implications with regard to therapy, even diet. But the glutamine link is fascinating, and I think that it has not filtered its way into the general public yet the way glucose has.

0:18:29 - (Dr. Thomas Seyfried): Yeah, well, in the scientific literature, you'll see many, many papers from top journals calling it cancers are glutamine addicted.

0:18:36 - (Kyle Drew): Addicted.

0:18:37 - (Dr. Thomas Seyfried): Yeah, glutamine. They'll call it glutamine addicted. They know that tumor cells need a lot of glutamine. But here's the situation. There's what we call anaplerosis. This is a term that means the replenishment of carbons to the, to the TCA cycle, the Krebs cycle. And many investigators were under the assumption that the glutamine entering the cancer cell was respired, not fermented, because the cancer cell is taking in oxygen, is producing ATP in the mitochondria, and glutamine is being used.

0:19:10 - (Dr. Thomas Seyfried): And they said, oh, it's coming into the mitochondria, it's being fully oxidized. But if that's the case, they should not be ever producing succinic acid as a waste product. So the glutamine is metabolized to glutamate, and then through a transamination reaction, it, it, it's. It's metabolized to the metabolite called alpha ketoglutarate, which is part of the Krebs cycle. Alpha ketoglutarate is then metabolized to succinyl coa, and that succinyl coa to succinate produces ATP through a substrate level phosphorylation reaction. It's unbelievable.

0:19:48 - (Dr. Thomas Seyfried): Now, in normal cells, it's doing that, but it's a tiny amount of ATP produced in the cycle. In the cancer cell, it's a buttload of ATP.

0:19:57 - (Kyle Drew): No kidding.

0:19:58 - (Dr. Thomas Seyfried): Yeah. So the succinic acid should. Succinate, should stay in the cycle if it's going to be fully oxidized. But because it has an incapacity of oxidative phosphorylation, it blows the succinic acid out as a waste product of amino acid fermentation, just like it blows lactic acid out as a waste product of Cytosolic substrate level phosphorylation. So the cancer cell is Getting energy from 2 substrate level phosphorylation reactions.

0:20:27 - (Dr. Thomas Seyfried): It's independent of oxidative phosphorylation, which is inefficient.

0:20:31 - (Kyle Drew): Right, inefficient. And to me, what that does is change the game that you've already, you and others have already helped to change even further. It moves it further downstream into the metabolic model. It just, it becomes irrefutable. And yet the conventional docs, the conventional researchers that are relying on the textbooks, it's just so hard for them to turn around. It seems like.

0:20:59 - (Dr. Thomas Seyfried): Yeah, well, they're locked into molecular biology and gene chasing. And when you're chasing genes, you're not thinking of the biochemical reactions responsible for energy, because without energy, nothing can survive. ATP is the gold standard. So all of the stuff that most people are studying are downstream effects of all kinds of things. All of the hallmarks of cancer are all downstream effects of the shift from oxidative phosphorylation to substrate level phosphorylation.

0:21:26 - (Dr. Thomas Seyfried): And, you know, the HIF1 Alpha, which is a transcription factor that becomes stabilized and drives the glycolytic pathway producing lactic acid. That Greg Semenza received the Nobel Prize for his work on HIF1alpha. And how in hypoxia it becomes stabilized to increase cytosolic substrate level phosphorylation as a means to get energy. Well, here's a very interesting phenomenon. When you have hypoxia, you also produce succinic acid through the ferment. Like I said, the heart attack patients are dumping out succinic acid. Succinic Acid also stabilizes HIF1 alpha, thereby driving the fermentation in the cytosol. So it's our view now that the key to cancer is mitochondrial substrate level phosphorylation, producing succinic acid, which then stabilizes hif.

0:22:19 - (Dr. Thomas Seyfried): So hif again is another downstream effect of mitochondrial substrate level phosphate.

0:22:24 - (Kyle Drew): Another downstream effect. You've mentioned mitochondria. Let's talk about that for a minute. You know, the evidence that you've compiled and published and written about is really talking about what happens when mitochondria fail or break down and it shifts from efficient energy production to a backup primitive function vis a vis fermentation. One question that's very basic is what is causing those mitochondria to fail in the first place?

0:22:55 - (Dr. Thomas Seyfried): Well, that was Albert St. Giorgi's oncogenic paradox, which we solved. We solved the paradox because people were Always asking, what is the comp? In fact, if you look at Sid Mukherjee's book, the Emperor of All Maladies, which was a New York Times bestseller, he asks in there many, many times, what is the common pathophysiological mechanism that could link all of these disparate cancer causing agents to a dysregulated cell growth?

0:23:21 - (Dr. Thomas Seyfried): And Albert Sink Jorgi asked the same thing and he called it an oncogenic paradox. So what we did is I went through all of the things that we know have been linked to cancer, like carcinogens. When you say, what is a carcin? A carcinogen is any chemical that has a potential to cause dysregulated cell growth, which is cancer. But how does a carcinogen cause cancer? Well, according to the somatic mutation theory, it causes DNA mutations and that's how they think you get dysregulated cell growth. But you also find that many of these carcinogens enter the mitochondria and they biofluoresce and they damage oxidative phosphorylation.

0:24:05 - (Dr. Thomas Seyfried): So you have this conundrum then, well, which is the chicken and the egg. Does carcinogens cause cancer because they cause mutations in the DNA or does it cause cancer by disrupting oxidative phosphorylation leading to a compensatory substrate level phosphorylation? Before I get into the actual nitty gritty of the mechanism that happens, you have to then look at radiation, intermittent hypoxia, inflammation, rare inherited mutations.

0:24:36 - (Dr. Thomas Seyfried): You have to look at microplastics, forever chemicals. We went through every kind of a risk factor. We found out that all germline cancer risk factors, all damage oxidative phosphorylation. So the genes are all BRCA1LI, Fraumani lynch syndrome. We went through, we have a big paper coming out on this showing that all these so called genetic risk factors all damage oxidative phosphorylation leading to a compensatory substrate level phosphorylation.

0:25:03 - (Dr. Thomas Seyfried): But, but the question is, okay, carcinogens do cause mutations in DNA. How do you know whether those mutations are responsible for dysregulated cell growth? And the answer is in general, only, only if they damage, only if mitochondria are damaged do you get dysregulated cell growth. The nuclear mitochondrial transfer experiments excluded genetic mutations as the origin of dysregulated cell growth. Because you can take the nucleus of a raging tumor cell and place it in the cytoplasm of a non tumor cell and you get regulated growth.

0:25:39 - (Dr. Thomas Seyfried): That rules out any oncogene or tumor suppressor gene as being responsible for the dysregulated cell growth. And those experiments were done in, in vitro and in vivo. A broad range of these. That's what brought me to the idea that this cannot be a genetic disease by any stretch of the imagination. But here's the key, and this is the golden all of these downstream effects, like the hallmarks of cancer, which is, you know, angiogenesis, dysregulated, regulated growth, and all this.

0:26:08 - (Dr. Thomas Seyfried): When mitochondria become corrupted and they can't generate energy efficiency through oxidative phosphorylation, as we said, you get a compensatory substrate level. Phosphorylation, which is replacing the availability of energy from fermentation. Fermentation is replacing oxidative phosphorylation. But that still doesn't tell us. It just tells us where the energy is coming from to drive the dysregulated growth. But where do you get the dysregulated growth from in the first place?

0:26:35 - (Dr. Thomas Seyfried): Okay, so here's the situation. In the inner membrane of the mitochondria, there's a. There's a. An enriched lipid called cardiolipin. Cardiolipin is enriched in the inner membrane of the mitochondria.

0:26:48 - (Dr. Thomas Seyfried): It intimately interacts with the proteins of the electron transport chain. It interacts with what we call.

0:26:58 - (Dr. Thomas Seyfried): Calcium transporters in the inner membrane of the mitochondria. Okay. Mitochondrial calcium transporters are controlled by cardiolipin. Electron transport chain proteins are controlled by cardiolipin. So what we have never found. There's no tumor ever found to have normal content or composition of cardiolipin. So cardiolipin controls calcium signaling. Mitochondria control calcium signaling throughout the cell. The cell cycle. Cell cycle itself has checkpoints to control cell division, and those checkpoints are under the control of mitochondria generated calcium signaling.

0:27:36 - (Dr. Thomas Seyfried): So when the cardio. When the cardiolipin lipid is abnormal, calcium signaling gets haywire. The cells no longer respect contact inhibition, and they. It's like the cell cycle no longer has any checkpoints. It falls back on the ancient pathways of fermentation, which were unbridled proliferation. Exactly. Well, you put all this stuff together. Goodness.

0:27:58 - (Kyle Drew): It becomes a unifying theory.

0:28:01 - (Dr. Thomas Seyfried): Absolutely. We now know exactly how to. We know exactly what's causing dysregulated cell growth, why there's no contact inhibition, why they're blowing out fermentation, metabolism. And better yet, we know how to Manage the disease very simply.

0:28:15 - (Kyle Drew): And that is ultimately what it comes down to, is what the implications are both for prevention and for treatment. Again, a lot of people who have been just casually ketogenic for whatever reason have keyed in on a lot of what you're saying. I am wondering first if you have any sense of. Of what the implications are for preventing cancer in the first place. Lifestyle changes, dietary changes, et cetera.

0:28:50 - (Dr. Thomas Seyfried): Yeah, well, that's why we developed the glucose ketone index calculator. It was first produced to manage brain cancer. But now we know that all chronic diseases in cancer stem from damage to mitochondrial dysfunction. So if you can keep your mitochondria healthy, the probability of getting cancer is very low. The risk.

0:29:10 - (Kyle Drew): Incredible.

0:29:11 - (Dr. Thomas Seyfried): Very low.

0:29:12 - (Kyle Drew): Incredible.

0:29:13 - (Dr. Thomas Seyfried): And also other chronic diseases as well. Type 2 diabetes, cardiovascular disease, dementia, you name you go the issue about some of these other conditions which. Which you have mitochondrial dysfunction without corresponding dysregulated cell growth. Usually that happens. The cells die because there are certain cells that can't switch to fermentation because of the types of cells, they are like neurons in the brain and cardiac.

0:29:39 - (Dr. Thomas Seyfried): They never become cancer, rarely, if ever, because they can't transition to fermentation. So they up and down. Interesting. So you know why certain cells can become cancer and why other cells cannot become cancer. So in using a gki, you always keep low glucose and elevated ketones, putting our cells metabolically back in the paleolithic state of our existence.

0:30:01 - (Kyle Drew): There we go. There we go. All right. I hope that you enjoyed the part one to our conversation with Dr. Thomas Se. And I'll tell you what, part two becomes very, very practical. Dr. Seyfried gets really, really practical. We talk about diet, we talk about exercise, we talk about supplements, we talk about fenbendazole, mebendazole, and these antiparasitic drugs that so many people are taking and why they seem to be having an effect.

0:30:32 - (Kyle Drew): This is worth sending to your friends who have an active diagnosis. Again, we are not doctors. We are not giving medical advice. This is just the sharing of information. We're so glad that you watched it. Make sure and send it to your friends. And thank you so much for watching Ultra Life today.

0:31:03 - (Dr. Thomas Seyfried): Sam.