Dr Thomas Seyfried, Pierre Kory MD Unite for Metabolic Oncology - The Manhattan Project for Cancer
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Some of the leaders would say or said to him that if the nuclear transfer experiments are right, saying that the mutations, that something in the nucleus might be responsible for dysregulated cell growth. Well, if that's correct, then the whole field of cancer has to be turned upside down. And therefore, the stuff that Seyfried's saying cannot be correct. So...

I like the logic, Thomas. I love that logic. I got it in my feet. I got it in my walk. I got it in my head. I got it in my feet. I got it in my walk. I got it in my toe.

A neighbor's choice.

Well, we're going to have a really fascinating conversation for today's program. I'm David Gronowski, your host, and I'm joined today by two friends of mine. And I was excited to know that there's some overlap in the work they're doing. So first, to my left, I want to introduce again to the program, Professor Thomas Seyfried from Boston College. How are you doing, sir?

I'm doing well. Thank you, David. Nice to be here. Yes. And I also have Dr. Pierre Corey from the Leading Edge Clinic joining me. Thank you for joining me.

Thanks, David. Good to be here. Yeah. Now, I met Professor Seyfried. I used to have him on the radio all the time about his work and metabolic approaches to cancer, and it was fascinating work. He's since become quite the sensation on the podcast circuit now. Millions of people were talking about what his work is, and it's been exciting to see the world change.

take a reckoning. And Dr. Corey, you know, I met you during the COVID-19 situation when you were doing frontline work. And then I come to find out later on that you've also been working with Dr. Paul Merrick and some others about some fascinating insights with metabolic approaches to cancer that may have some overlap with Dr. Seyfried's work. So I just wanted to have this kind of different perspective angle approach to this topic of cancer. So

Yeah. Well, let me say, the first thing I want to say is not overlap between his work, directly derived from his work. So I find the story of the metabolic theory of cancer and how it came together over, you know, about 70 years, you know, best told in the book, Tripping Over the Truth, which I found a transformative book. I found it really gripping. Maybe you have to be a nerd like me a little bit, but I thought it was the most fascinating scientific story. And

all the individual scientific pieces and that culminated in Dr. Seyfried's, you know, finally finding the, you know, the final pieces and putting them together to show that really cancer is a metabolic disease, which he can talk much more eloquently about. But yeah, what I do is really, I, you know, it's derived from his work in a metabolic approach, understanding that cancer really starts with damage to the mitochondria. But I also, most of my practice and my approach is,

is also heavily relies on Paul Merrick's work where he did a scoping review of the world's literature looking for all sorts of therapies that have evidence of anti-cancer properties, right? So he looked at all repurposed drugs, you know, which are drugs used for approved for one indication but have many mechanisms which can also lend themselves to cancer.

And he grouped all of the things that he found in terms of criteria under strong, weak, and then equivocal levels of evidence. And I really draw and utilize the things that have a really strong clinical in vitro, in vivo, and epidemiologic evidence base. And so I find it really exciting. You know, I'm not an oncologist, but I'm

I'm very well versed in these medicines. And I think what I do is I bring a complementary approach to standard of care. I'm not in the business of telling people not to follow standards of care, although I have my reservations. I know Dr. Seyfried does as well. But anyway, that's sort of my intro on how I sort of got really interested and involved and developed a cancer practice.

Very good. Professor Seyfried, I wanted to have you give us your overall approach to getting into this topic and where it stands today. Yeah. Well, that's good. I appreciate the information that we get from different folks who are really on the right, eventually on the right path for keeping people healthy with approaches that actually have a

documented success. But, you know, Travis's book, Tripping Over the Truth, I know Travis very well. He supports us through his foundation for cancer metabolic therapies. He was going back to medical school, having worked in the moving and storage business for many years with his father and uncle. And he chose my book, Cancer as a Metabolic Disease, as his thesis project,

And couldn't he never heard of the stuff that I was writing. And he's a science writer. And he decided to do an investigation further. He visited my lab just to speak with me.

about what I had written and he said, I'm going to double check to see whether or not you're accurate or not. So I'm going to go around the country and I'm going to visit leaders in the field of cancer like Robert Weinberg at MIT and Bert Vogelstein at Johns Hopkins and a variety of other folks who are considered leaders

in the field of cancer and asked them about certain things that I that I had written or things that they had written about the origin of cancer as a genetic disease. And it turned out to Travis when he started to ask deeper questions, it became clear to him that some of the leaders in the field really didn't have the answers that he was hoping to have.

And when he raised the questions of the nuclear mitochondrial transfer experiments, which are some of the strongest evidence showing that cancer cannot be a nuclear-driven disease by somatic mutations, where some of the leaders would say or said to him that if the nuclear transfer experiments are right, saying that the mutations, that something in the nucleus might be responsible for dysregulated cell growth, well,

If that's correct, then the whole field of cancer has to be turned upside down. And therefore, the stuff that Seyfried's saying cannot be correct. I like the logic, Thomas. I love that logic. So Travis wrote the book, Triffing Over the Truth. And in that book, he interviews these guys.

And you can see their lack of understanding at the level that they should be. If they're writing all the textbooks and the whole NIH is saying cancer is a genetic disease, it says right on their website that cancer is a genetic disease caused by somatic mutations leading to dysregulated cell growth.

And the evidence to support that is on a bedrock of sand. It's no longer credible to even say something like that. It speaks to someone who lacks fundamental knowledge of the biology of the disease. So this is the great embarrassment that people do not want to talk about at the top medical schools, the hospitals, and the National Cancer Institute. So until they open their eyes and realize, like I said,

to David, we've got 1700 people a day in this country dying from cancer, which comes to 70 people per hour. And everybody is back slapping, feeling good about the so-called progress that we're making. The only real progress that we've made was the anti-smoking campaigns from the 1990s and

And they come on, even when President Biden was just recently diagnosed with prostate cancer, you had these wags from the NIH saying, oh, we've made such incredible progress over the last 30 years. We've dropped cancer death rates by 33 percent. That was all because they stopped smoking. It had nothing to do with new drugs. And the new drugs are based on the somatic mutation theory, which is now undermined, thereby deceiving people's

giving them false hope. Now, there are some immunotherapies that do show progress. I've seen the results from PD-L1, PD-1 inhibitors and CAR-T. But the problem is they're few and far between, and you can kill the patient just as much as you can help them. And they don't lie about that. Look at every night you see on the news, at least when you watch Starz,

national news where they know older folks watch that stuff. So the advertisers pitch their toxic therapies. They don't hide the fact that these drugs are going to kill you. They spend more time telling you all the adverse effects of the drug and how it could harm you and kill you than they do on telling you how you have a chance to live longer.

but you have a greater chance to die from the drug. Thomas, can I say something? I just want to, I don't want to go back because I want to say something about what you just said, but when, when, um,

These leading cancer researchers, I remember reading, I think it was either Vogelstein or Weinberg, they ended up leaving the field of cancer research. Wasn't that correct? At some point, like after writing some of the most influential papers describing cancer and its origins, and then they literally, they felt there was too much dark matter or something. They just didn't understand. They gave up. Well, I don't know if they gave up. They certainly are still involved with this.

Yeah, the dark matter doesn't make any sense at all. I mean, you got it. That's what we call groping. But but a lot a lot of the the the issues is they always say the search for the the key gene responsible for dysregulated cell growth is not yet complete, even though we have already defined hundreds of millions of mutations. But the search is not yet complete. What does that mean?

Why don't you throw the towel in? The search, as far as I'm concerned, is complete. And Dr. Weinberg, in an interview, was lamenting about his 40 years of research

and not having any significant impact on dropping the death rate. So clearly, but they will not give up their position that cancer is not a genetic disease. They continue to hold that belief, which is solidified in all the major textbooks of biology. Even the new books are coming out saying cancer is a genetic disease. And the NIH has not changed their website. You can still see that it's a genetic disease.

So despite all the evidence that cancer cannot be a genetic disease, the institutions have not yet moved to change their position. Yeah, that was another really, well, nothing shocks me in science anymore, but

You know, when I read about the massive efforts and funding into the Human Genome Project and then the Cancer Atlas, Genome Atlas Project, where they sequenced all these cancers, all these tumors, and nothing made sense, right? They found tumors without mutations. They had different mutations in each tumors. They had different mutations between the primary leaves and the other one. And it left such a mess for them to explain. And nothing, they couldn't put together a credible theory to support it. And they already have that data.

And yet they persist in calling it a genetic disease. Yeah, well, that's the power of...

Ideological dogma. It's very hard to shake dogmatic views. It's it's really it's really quite quite difficult and and then The the newer information now is even more is just as disturbing where they're finding in normal cells of our body if we did a Genomic screen now we have the massive advance in genomic screening technologies you find mutations in driver genes and

You see, that have no relevance to dysregulated cell growth. So what the field did was they realized that not all mutations are participatory in driving dysregulated cell growth. So they parsed the genes out to passenger genes, which kind of just hang around, they don't do much. And then the driver genes, which were considered the really important ones for driving dysregulated cell growth.

Well now with the advances in technology people started looking at normal tissues and normal people that had no cancer. And we're finding dozens and dozens of pathological mutations in driver genes in cells that have no dysregulated cell growth.

You find that some cancers have no mutations. Normal cells have the bad driver mutations with no dysregulated cell growth. And the nuclear transfer experiment, mitochondrial transfer experiments showed clearly that it was the mitochondria, not the nucleus that was driving the dysregulated cell growth.

That's too much of a bitter pill. Yeah. They can't they can't now. And what they do essentially is ignore it. So we don't want to give it any voice, because if we give it voice, more and more people will think about the contrary evidence and say, what the hell have you people been doing? Ignoring the data that says you're on the wrong path.

You know, when I talk to patients, you know, I tell them that I said the prevailing theory of cancer was overturned. I hope I get the date. I usually say 2010. I think that's when your paper came out. And I said that was definitively overturned in 2010. And here we are in 2025, 15 years later.

And most of oncology is still persisting. And you're right, they are ignoring that the real underlying cause of cancer has been found. And we know in medicine that when you have sort of paradigm shifts or novel therapies that are proven effective,

From that first report to being adopted into like a guideline and a standard of care, it's estimated on average about 17 years. But this one doesn't seem to be moving that fast in terms of changing the paradigm. It's like it inordinately slow. And cancer is a massive economic engine, right? And so I think that's why maybe it's a little bit more resistant. Oh, yeah. I think you're right on the spot on that. Well, first of all, you have a lot of oncologists saying,

who are unfamiliar with that. And they've been trained to administer the therapies that they think are working. So the radiation oncology guys, the chemotherapy oncology guys, the immunotherapy oncology guys, they're all working within their own sphere. And the patient gets passed around

The primary care physician identifies that there is a problem and then he's handed off to the oncologist who they do some biopsy. And then they have their standard surgical procedures followed by their chemo, followed by the radiation or whatever order they want to do it in. And the patient then gets discharged, the ring the bell, and he gets thrown out into the world. With the grace of God, he survives or he has to come back.

and doesn't understand why they told me I was cured, and all of a sudden, within five or six years, it's back again. And the treatments they're using are extremely provocative to damage healthy tissues, either facilitating the return of the original condition or producing a new type of cancer that you didn't have, but for the treatments that you received and attempting to cure the first type of cancer you have. And if you don't get any of those,

you get neuropsychiatric problems, digestive problems, hormonal problems, microbiome problems, all of these other problems that now are to be serviced by other groups of physicians who are trying to patch up the damage that the person who survived the toxic therapies. So it's almost like patients are just being passed off from one group to another when none of that stuff ever has to happen in the first place. You know, I have to tell you, that was the kind of most shocking, right? So I'm

By training, I'm a pulmonary and critical care physician. And I left the system and started getting interested in using kind of alternative approaches to treating vaccine injury and long COVID. And when I started treating cancer based on your work and my, you know, my study and work with Paul,

You know, what you just said was really kind of shocking to me, even though, yes, I understand. We all know that chemotherapy makes people sick. It's very hard to endure. Radiation has its problems. I knew that in general. But when I started seeing patients, I was shocked.

that in the vast majority of my patients their symptoms do not derive from cancer itself some of them have cancer-related pains but most of them are fine except for the treatments the treatments are making them inordinately sick and they're suffering every time i see them their litany of complaints are all treatment related in terms of standard of care therapies

You know, my repurposed approach using nutraceuticals and some, you know, repurposed medicines. I mean, occasionally I'll have a little issue where I'll have to stop a medicine, but in general, they're very well tolerated. And I don't make my patients sick, but as someone who's been treating patients from all my career, I had never seen a disease where the treatments were so toxic and so quality of life impacting. It really, it still shocks me today.

Yeah, well, that's the problem. And, you know, it's hard to make someone healthy when you're treating them with poisons, nuking them and and surgically mutilating them.

Not to say that surgery is not important, and not to say that any of that stuff does not have a place in the overall treatment strategies. It just has to be done in the right way at the right time and the right place. When you use metabolic therapy to shrink a tumor down, removing the angiogenesis, the inflammatory microenvironment,

the way we can do, then the tumor becomes extremely vulnerable to perhaps a very low dose of chemo, perhaps a small dose of radiation, or if surgical procedure to remove the residual mass.

the outcomes will be far, far more favorable to the health of the patient. So you will not see the devastation from high dose radiation, chemo and removing organs and doing all the other things that you do to these poor folks. So we don't throw out any part of the standards of care at this point, but only to use them in a different way, in a different context where they might be problematic.

If you can shrink a tumor down to some residual mass but it's still seen in non-invasive technology, cat, pet, or whatever you want to use, there's still something there and you'd really like to remove that something there. Now, a strategic surgical procedure could remove it or a beam of radiation could remove it with minimal collateral damage to surrounding tissues or to the general physiology of the individual.

You know, I appreciate that so much what you just said, because that's really the paradigm shift. You articulated very well. I hadn't thought of it that way, is that if you have a primary metabolic approach and then have standard of care as secondary at lower doses,

the outcomes and quality of life and survival and really just quality of living, right, would improve. And I think, but, you know, I guess we've talked about it already, but to get that paradigm to shift is going to take a while. Well, the paradigm shift is happening as we speak. More and more folks are realizing, even the oncologists are beginning to realize, the medical professions are starting to realize that

as we and others have shown, these tumor cells cannot survive without fermentable fuels.

and we've interrogated tumor cells to know what the fermentable fuels are that drive their dysregulated cell growth. And it's the sugar glucose and the amino acid glutamine. And because of their mitochondrial dysfunction, they cannot shift to a fatty acids or ketone bodies. So the, the, the simplistic, uh, strategy is bring patients into a therapeutic ketosis, uh,

and simultaneously target the two fuels, glucose and glutamine. And there are drugs that are available to target those pathways using strategic low dose levels to do that.

And then but that's all there. And we just completed a huge treatment protocol. We've published it in BMC Medicine, which already has like 40,000 views a short period of time. And it was a very comprehensive protocol treatment with the recommendation, all the like the nutraceutical, all that kind of stuff, where it should be used, how it should be used as the patient moves through the process of being healed.

And we did it in excruciating detail with my colleague, MD, PhD, Thomas Duret from Spain and the Czech Republic. We put all this together with 30 authors of scientists, nutritionists, dieticians, surgeons, all kinds of folks on there. And we've just started a new society, International Society of Metabolic Oncology,

which is now a group of people all over the world that are beginning to think more carefully about how to manage cancer. So we're using, it's happening. The paradigm change is happening because physicians go into this profession to help heal people. And we have a strategy that will work and do better than the current strategies that are there. And we are perfecting and improving those with the knowledge base of the clinicians

They bring in new knowledge for us and our preclinical work here at Boston College. We get feedbacks from clinicians around the world, what they're seeing. We use all natural models of cancer, not these genetically engineered monstrosities.

or these absurdities that the NIH likes to fund. We use all natural models, and then we have feedforward feedback, feedforward feedback. So we're getting information from the clinicals. We're giving information to the clinicians about how this, we think, might help their practice,

They tell us they saw something that might help us. And then we go back and that's the way we're working from preclinical to clinical to preclinical, back and forth, perfecting these systems.

allowing people to live far longer than they would have been predicted to live based on their original, their prediction from the original diagnostic treatment. And that's what I'm doing. I mean, obviously my practice is exactly what you just described. It's, you know, ketogenic diets, really trying to limit as much glucose, other combinations of metabolically active medications, right?

And, you know, we're doing an observational study right now. So we don't have a control group because I'm in private practice. But that is what our essentially our design is, is we're going to be following these patients over time and then comparing them to historical predicted prognostic timelines. And we've begun data collection. I haven't had a look at it yet. But my my kind of spidey sense already, just from my clinical experience, is

Those that are more adherent to the diet, because for some I'm finding on the clinical level, it can be difficult to get patients to adhere. But the better they do, I think the better they do in terms of adherence. Yeah, no, you're absolutely right. In fact, the new paper we just had come out from our Greek colleagues on glioblastoma, their diet was a calorie restricted Mediterranean diet.

And if you look at the composition, it wasn't that bad. I mean, it was salmon, olive oil, a little broccoli, different kinds of oils and avocado. And the ones who adhered to the diet survived three years or longer.

And the ones who didn't, only one of the 12 people that didn't survive three years. And it's a knowledge of both the patient and the physician working. And the reasons for not adhering to the diet were not the palatability issues, like, oh, I don't like eating this stuff every day, or the variations that they gave you. We put that into the paper. I'm one of the co-authors. It was...

Pressure from the family. It was it was weird. If you look at each patient that didn't adhere to the diet, I think there was only one or two that didn't like the fish every day. But most of the other folks were for one guy. Every one of these glioblastoma patients received standard of care. So they had radiation and chemo.

And a couple of guys. So I had that. I don't want to do any more. I don't want to eat any special stuff. So it just didn't even want to do it. He did. He's dead. You know, all the guys who didn't stay on the we had a couple die that were on the diet. But I've written a paper showing that the standard of care is actually very provocative to reducing the lifespan of the patient.

When you irradiate somebody's brain, you free up massive amounts of the two fuels, glucose and glutamine, that are driving the dysregulated growth in the surviving tumor cells. So the last thing you ever want to do to a glioblastoma patient is irradiate their brain. The fact that we got such an incredible response and the people who did have their brains irradiated using metabolic therapy speaks to how effective it is. Wow.

And the idea that if we didn't irradiate those guys and did the metabolic therapy the correct way, we may have been able to keep guys even further in health and survival, like Pablo Kelly, who lived 10 years with a glioblastoma and died. He was never cured. That's an interesting thing. His brain tumor was never cured, but it grew very, very slowly in an indolent way where every two, three years he had a surgical debulking.

and lived a good life. He had got married, had two children. He died from the fourth debulking surgery from a complication of a cerebral hemorrhage.

He never died from the tumor. Glioblastoma, he died from a broken blood. He came out of the operation with his thumbs up, talking and everything else. And 12 hours later, he was dead from a cerebral hemorrhage from a complication of surgery. Thomas, you said something just before, which I kind of had interesting, which I think I need to think more about is that

You seem to say that some of the lack of adherence to the dietary protocols was because, I guess, friends and family somehow gave them their opinions that it was not necessary and they should eat different things. Because I see the converse. The patients that do the best, and this is going to be very kind of a generalization, but...

When the wife or the spouse is invested and like really, you know, totally into making sure their loved one with cancer is on that diet, those do the best. So when they have that close kind of family support in adhering to the diet, they seem to do wonderfully.

Yeah, well, that's why the guys that did the best on where they had those same support groups. Yeah, that's exactly what you're saying. I mean, this is when we see the knowledge of the physician and the compliance and motivation of the patient. Those those are the ones that do spectacular. So when when when we when we try, we can't do big clinical trials yet.

because we don't have all of the variables identified, but we have enough of it to do, and we're getting bigger. That trial in Greece involved 18 glioblastoma patients, which is a small type of clinical trial, and they did standard of care. The group that we're hoping for, and we have another group at Cedars-Sinai Hospital,

hospital in California, Los Angeles with Dr. Jethro Hugh. He's doing a clinical trial right now on glioblastoma with metabolic therapy. But the group that we never seem to be able to get, at least for glioblastoma, are the people who do metabolic therapy without brain irradiation.

And the IRBs will not allow that. So this we've gone through this over and over again. The IRB says. And yet, when you look back in the historical literature about starting the radiation procedures for brain cancer, it was very ambiguous. And there was a lot of resistance to that on the part of oncologists. Yet it was a push forward.

that eventually became standard of care. But at the very beginning, there was a lot of resistance and a lot of concern about irradiating somebody's brain. But yet that was all pushed aside. And now it seems to be you can't get rid of it. It's very hard to convince IRBs that we should never irradiate the human brain. They don't want to hear that. That's an interesting point. I think you're when you think about trial design, right?

In order to get a trial that receives ethical permission, the challenge is what you're proposing, right, is do metabolic therapy first and then rely on standard of care interventions secondary when needed.

they're going to want you to do standard of care first, right? And like the metric study, which was that really remarkable study from 2019 on glioblastoma, where they added four drugs to standard of care, even though they got, you know, Timolazole and radiation and surgery, those patients' lives changed.

were extended by significant amounts. And what I thought was also interesting about that paper is on average, those patients showed up six months after diagnosis. So they weren't treated from the time of diagnosis, yet still they had a very remarkable result. The other point you made, and going back to that point about paradigm shifting, is a couple of months ago, I was very encouraged to learn, and I'm sure you know about this, but there are three large

double-blind randomized control trials of repurposed drugs added to standard of care. Beyond that metric study, there's this CUSP-9. They're adding nine drugs to standard of care. I didn't really understand some of those drug choices, but I hadn't researched them. They certainly, Paul didn't find them to have a sufficient evidence basis, but then there's also two other trials. And so at least there seems to be some developing research interest into studying the additions of these repurposed drugs and metabolic approaches.

Yeah, well, that's that's absolutely correct. And they're realizing because what they're doing, they're still groping to help people, you know.

The standards of care, as I said, when you have 1,700 people a day dying, the system is not working. It's clearly broken. And people will start to say, we better think of different ways and metronomic approaches where you use various drug combinations and things like this. The resistance to that is because you can't really figure out which of the combos of drugs might be between.

participatory in in helping people. But, you know, when you understand the the the the fuels, everything comes down to energy because without energy, nothing can live. And a lot of people seem to discard that or not understand that our bodies are we we combust fuels.

This is how we live. We breathe in air and the air serves, the oxygen serves as an acceptor of electrons in the electron transport chain. And we break carbon hydrogen bonds of the foods that we have eaten. And those carbon hydrogen bonds were originally created by the energy of the sun and

And we simply break down those bonds, recapturing the energy of the sun to combust the fuels that we are using to stay alive. And cancers no longer do that. They rely on ancient pathways of fermentation. They don't use oxygen because they can live in the absence of oxygen. Cancer cells can live without oxygen. Cancer cells can survive life.

You know, if you and I drink cyanide, we're dead real quick. But cancer, we tested cancer cells. They don't die in cyanide. So they're living on fermentation metabolism. And we interrogated what they can survive on. And it's the sugar, glucose and the amino acid glutamine.

And we found out that the glutamine is fermented, not respired. And this is a big breakthrough in the field because they all said cancer has normal oxidative phosphorylation because it can use glutamine. Glutamine is fermented. It's not respired. And that's a big breakthrough. So we now know how these tumor cells are getting their energy back.

to grow and the mitochondria is the organelle that controls the differentiated state and the cell cycle through calcium signaling. So when that organelle becomes dysfunctional, the cells fall back on their ancient proliferative pathways driven by fermentation.

And then once you know that, then you say, well, if I take away these fermentation fuels and allow the body to adapt to fatty acids and ketones, these tumor cells should up and die. And that's exactly what we see. So we now know how to manage cancer without toxicity and repurposed drugs come in to

to facilitate the targeting of the glycolysis and glutaminolysis pathways. So that's why we're using m-bendazole and fenbendazole. Our research here at Boston College

we found that those drugs target the glycolysis and glutaminolysis pathways. So when I looked at the literature, I saw it. Why do people had reported fenbendazole and embendazole, these parasite drugs as being therapeutic for cancer? So I said, well, why the hell would that be? So we discovered that the cancer cells are using mitochondrial substrate level phosphorylation, a fermentation mechanism within the mitochondria itself that

And then when I went back and looked at how parasites use the same damn pathway to survive. So...

So I said, well, these parasite medications are killing cancer cells because the cancer cells and the parasites are both dependent on the same energy pathway to survive. Makes perfect sense now. Now you know that there are repurposed drugs that will target these things and make a, whoa, voila, what's going on? You got to bring everything back to the mechanism by which it's targeting energy metabolisms.

Thomas, I got to just, you know, second what you just said, because one thing that I find a little, how should I say, just troubling or even disturbing is, you know, when a cancer patient, you know, develops cancer, they go on the internet and they start reading, they, you know, they all have these, they rightly so obsessed and

When you'll hear people conflate what you just said and say that parasites cause cancer, and that's why these drugs work. And so there are clinicians who think that they're actually treating parasites without understanding it's the metabolic similarities between the two rather than the fact that there's a parasite causing the cancer. Oh, absolutely. Absolutely. They think, you know, but the outcome is the same, right? Yeah.

I guess you're right. So I guess, you know, the... Again, if you're being scientific, the discriminating scientist, he wants to know the mechanism. Yeah. And we have shown that. And in fact, we have a paper on pediatric brain cancer, which is a great tragedy, irradiating and poisoning these little kids, surgically mutilating them. And you can see their swollen faces from the massive doses of steroids they're giving the kids.

And we know we have a model that replicates what you see in high grade children brain cancer. Their cancers often invade the spinal column in these little kids. So you get spinal involvement from cerebral initiation. The tumor cells move down the spinal column. In our glioblastoma, natural glioblastoma models that we work with in the adults, we never we don't see that. We don't see that in adults with GBM as well.

But in little kids with GBM, they call them pineal blastomas. They're very similar. They get spinal involvement. So when we took our adult glioblastoma cells and put them into very young mice, we got spinal involvement, just like what you would see. So it has to do with the age of the brain and the ways the cells can move through their neural parenchyma to achieve these different phenotypic characteristics. But

But when we put them on the parasite medications with targeting glutamine and put these young mice in keto therapeutics, oh my God, we knock the crap out of these tumor cells. Now, we can do that in the clinic, in pediatric oncology clinics.

Yet nobody's doing that. And that's what I consider one of the great tragedies. We have a way to keep these little kids alive so much more healthy and so much more. Their survival and overall quality of life will be so significantly improved because we have the science. We have the preclinical evidence. Why are they not doing that in these pediatric oncology? I have a question about the therapeutic ketosis. Yeah.

There's that means, you know, keto means a lot to a lot of people. Most people are not eating. And when they do a keto diet, they're not probably anywhere near what you're probably requiring, I would imagine. Right. Because, for example, if you eat too much protein, your body can turn on gluconeogenesis and then you got sugar glucose coming out of the protein you ate.

So you have to kind of watch your protein, right? For example, there's some that would say a therapeutic ketosis would be four to one fat to protein. So you're basically living off of fat primarily with a little bit of protein. Do you get into that? Is there a threshold you like in terms of the ratio where the sweet spot where you're... Is it about producing a lot of ketones in that therapeutic state or do the fatty acids, it's okay, we just...

How much is it about restricting the protein to make sure that doesn't have a pathway for sugar in this feeding mechanism to the cancer? And then how much of it is just kind of whatever the patient wants? How do you guys work through that? Well, we've addressed that already with the glucose ketone index calculator, with the GKI calculator.

which takes away all the ambiguity that you just mentioned. Any diet that can lower blood sugar and elevate ketones will be therapeutic against cancer. And the way we do that, we use Keto-Mojo or other meters that can measure simultaneously the ratio of glucose to ketones in the blood.

Now, we have continuous glucose monitors that are already available, the free Libra. But that only gives you one part of the ratio, the glucose ratio. The glucose value in millimolar doesn't give you the ketones. But now, they're already available. They're just not available for purchase. It's continuous glucose ketone monitors with a patch on your arm. Oh, wow.

So you can you can now manage. And not only that, it works on your cell phone. So there's we're working on an app that can do all this. And therefore, eat whatever you want to eat and see what it does to your GKI. And yeah, protein. I did that. We had we do all we test all this stuff on ourselves. You got to realize this. We're not just blah.

blowing crap out of her ass and telling people to do this. My wife is yelling at me, oh, you tell these people to do this and you don't do anything. So anyway, we have... So I ate a carnivore diet. I ate prime ribs and Philly mignons and all this kind of stuff, right? With sauce beurrenaise on it. I got my GKI down to 10. Now, to kill cancer cells, in five days, I went from a 50 to a 10. In...

in cancer, to kill cancer, it's 2.0 or below. So I would have... And if you do exercise, you can bring it down a little bit further. And some guys like to eat different foods and different things. And I said, well, what does it do into your GKI? And you'd be surprised. You can kick in periodic fasting and eating... The amount of energy that you get from gluconeogenesis is minimal. It's...

And don't forget the organ that takes in most will be the brain and the muscles. But the brain has the capacity to shift over to ketones and what little glucose would be picked up by the brain. And higher ketones suppress utilization of glucose.

And the muscles will take it. So when you exercise, you're sucking glucose out of the bloodstream by doing the exercise. So these tumors get hammered. You get into a low GKI and do exercise, man, you're going to hammer the tumors. I'm sorry. I just wanted to, how, how, how soon do you think those glucose ketone monitors, continuous monitors would be commercially available?

Well, we can't get them in the United States, but if you're in Europe, you can get them because Dr. Durai, who's working with me, got one through Czech Republic and he wears it and he cheated. OK, he got the lowest GKI. He said he was doing carnivore diets like the rest of us. But but what he did was he took a couple of spoonfuls of medium chain triglyceride oil, which the liver immediately threw into beautiful ketosis. Yeah.

lowering his GKI lower than everybody else's in the lab. So, so, but we realize how come, you know, we can't say he's, he got the lower GKI because he's from the Czech Republic, but he was, he was taking some medium chain triglyceride oil. And this is what's beautiful about repurposed drugs and the nutraceuticals that you guys are working with. You now have, once you have this quantitative measurement, which is we're taking the meat,

history out of all what you should eat, what you can't eat, what ratios of fats to proteins and all this kind of stuff. When you bring it down to the quantitative measure of blood sugar to ketones in the blood, and every person is different. So one guy might want to do a pescatarian diet. Another guy want to do a Mediterranean, a carnivore, whatever. Vegans are a little tougher because it's harder to get your blood sugar down

on that, but they have to come to know that. They might have to do warm water only fasting. But it can be adjusted for every type of a person, cultural differences, religious differences, age differences, because you're looking at it now, a blood quantitative marker. You have taken the mystery and the ambiguity out of the system. And people mix and match. As long as you can keep a low steady glucose ketone index

And then you can and you don't have to stay there all the time. You can flop out of that zone, but get back into it because you want to make your life interesting and enjoyable. So but at least you have a quantitative biomarker to know where you are at any given time. Can you say a little bit more precisely about what you just said in terms of you don't have to stay there all the time, like in a general sense, like how often, how much portions of the day do you think you need your GK under two, you said?

Yeah, 2.0 or below. Yeah, it's hard. Listen, you've got to be really compliant.

But what would happen if you're in this zone, you're taking drugs that target help. Once you're in that state of metabolic therapeutic ketosis, the tumor cells are already suffering. You're reducing the inflammation in the microenvironment by shutting off the fuels that produce the acidification, which is glucose and glutamine. We've identified the waste products that cause the acidification. Well, the inflammation starts to go down.

Now, when I worked in the epilepsy field for years, I ran the ketogenic diet workshops and all that stuff because I was part of that whole thing at Yale University. We would know the kids that would be low and steady on their glucose levels would have very few breakthrough seizures. But in difference to cancer, you could see that immediately when a kid took a piece of a cake or a fruit juice. Within a few minutes, you would have a breakthrough seizure.

because his blood sugar shot up. But his ketones remained somewhat stable. So epileptic seizures became so sensitive to the level of glucose. But the cancer patient...

If you were keeping low steady glucose, it takes a while for the tumor to start re acidifying the micro environment. So if you spike, so I want to have a slightly different, I want to eat some pizza for Christ's sake. Okay, eat the pizza, you're going to notice your GKI is going to go high, and then see how fast you can get it back down into the zone again.

So because the cancer cells may grow a little bit, but you slaughtered a lot of them already. So it's a it's a slow degradation of the tumor already.

and a reconstruction of the micro environment without a disturbance of your the micro microbiome. And also your immune system, which picks up the dead corpses, is dependent on the same fuel that drive in the cancer. So you have to then you have to know how to the physician and the compliant patient work together as a team, because you you don't want these people to be stuck in a rut.

of having to eat a four to one ratio of fat to carbohydrate diets, making their life miserable. And then they lose interest and they become noncompliant.

So, again, everything has to be worked into who we are as a species, what makes our lives enjoyable. But at the same time, what we need to do to control the dysregulation of this of this growth, we can do all this and we can make it a lot of fun. And the issue, of course, people say, well, what are your adverse? What are the adverse effects of doing something like this? You know what it is?

It's increase in cognitive engagement and overall life survival on the planet. Yeah. You got to love it. Yeah.

You're not going to come back to the poor doctor and say, oh, my bone density is bad. My liver problems. I got all these problems. You know, you're going to find out you get rid of a lot of chronic diseases at the same time you're managing your cancer. But this is a transformative thing. This is completely paradigm shifting. And we have the evidence and we're working on all this right now. So you're going to see within the next couple of years an explosion of

of interest using technology and physiological transformations where everybody can know what they're doing and why they're doing it. And they have free choice to do this. Nobody's going to tell them if they want to maintain a high. We've had people that say, I don't I don't want to do this. We'll keep your blood sugar high. If you want to see how fast your tumor can grow, get your damn blood sugar up as high as you possibly can get it.

But bar none, take as much carbs into your body as you possibly can. Keep that GKI up in the 500 to 1,000 range like some diabetics and see how fast you can get your tumor to grow. And if you don't want it to grow fast, keep your damn blood sugar low. I like it. I like it. You know, Thomas, the other kind of, and I guess I would call this a paradigm shift in cancer, which

You know, Paul Merrick got really interested. And you and I were on a Zoom conference recently. But the cancer stem cell discovery was interesting to me because that was first identified in 1996 in a leukemia study.

and then in a solid tumor like 2006. And the interesting aspect of it is that they're relatively resistant to chemo, quite resistant actually to chemo radiation. It's one of the explanations for why there are recurrences and it's hard to keep someone cancer-free. And there are only 1% of these tumors

But what's interesting is they most of them, I think, do have the same metabolic defect, but not all. I think some stem cells actually still have oxidative phosphorylation. And so what's what's interesting about that aspect is.

We have to pay attention to cancer stem cells, and these repurposed drugs, when they've studied cancer stem cells over the last 20 years, many of their in vitro models, they were using repurposed drugs to see which ones inhibited the proliferation of the stem cells. And so we have this host of repurposed drugs that we know we can address stem cells with, whereas...

In oncology, I was looking at this the other day, there is research into trying to address cancer stem cells, but they're all leading to what I think are going to be very expensive and invasive therapies like monoclonal antibodies that look for antigens on those. And so, you know, I like that in my practice, I already have a way to kind of pay attention and address, theoretically, the cancer stem cell proliferation.

Yeah, well, we in our preclinical systems, we have cancer models of cancer stem cells and we have models. We have the we've identified the difference between stem cells and metastatic cells because the metastatic cell ultimately is what most people deal with, which is which represents you can't cure metastatic cancer with surgery or radiation. The stem cells are interesting. They can't metastasize.

We've we've interrogated their behaviors. They have they grow faster than the metastatic cells. They create a great deal of angiogenesis, blood, a lot of blood vessels, blood

They disturb the micro environment, but they're blowing out lactic acid and succinic acid. They do not have oxidative phosphorylation capacity. So they don't. Okay. I think there was a couple of cancers where they thought, I saw a paper where they identified that, but most of them, I think you're right. I think you're right. So what we found is there is a difference in their utilization of glucose and glutamine.

That seems to be one of the differences. Metastatic cells have a rapacious consumption of glutamine because the metastatic cell, as we and others have identified, is in fact one of our immune cells, the macrophage.

So the macrophage is a part of our immune system that protects us from bacterial infections and plays an important role in the inflammatory parts of wound healing and this kind of thing. They circulate in our bloodstream as monocytes.

Every tissue in our body has resident macrophages that take care of local disturbances like Kupfer cells in the liver, that we have alveolar macrophages. We have various kinds of cells with different names like

microglia in the brain. These are all derived from the immune cells which have macrophage characteristics. When those guys become corrupted, they are already genetically capable of spreading from one location to another.

So monocytes come in out of the bloodstream to a wound and they differentiate into mature macrophages that facilitate wound healing. And when the wound is healed naturally from a contusion or a lesion of some sort like that, some of these cells, they actually become pus, the dead white blood cells. They throw themselves at these bacterial infections.

And after they heal the wounds, the ones that haven't died, they go back into your lymph nodes and they hang out in the lymph nodes for a while to determine whether or not they're going to be needed again if the wound was not completely healed. The cancer cells are these cells. They're corrupted macrophages. And what happens is they fuse with the stem cells.

So in this lesion of cells that are continuing to dump out end products of fermentation, which are lactic acid and succinic acid, you create an unhealed wound, a wound that seems to not be healed. And our immune cells keep throwing themselves at this unhealed wound, and they're extremely fusogenic.

So the stem cell, which is the origin of some of these cancers, becomes fused with the macrophage, which is in there to help heal the wound. And now you have the combined genome and cytoplasm of a stem cell with one of our macrophages.

And that macrophage leaves this environment, spreads around your body with a dysregulated cell growth, excessively driven by glucose and glutamine, but more glutamine than glucose, where the stem cell seems to have more glucose than glutamine. But they're both corrupted in their ability to generate energy through oxidative phosphorylation.

So you have to be cognizant of the biology of what's going on in the local environment of the tumor. And the resistance to the resistant to chemo and radiation is because they're throwing out so much acidification into the micro environment. They're living in a hypoxic environment.

So so that reduces the efficacy of immunotherapies, chemotherapies and radiation therapies, all being protected by the waste products of the fermentable fuels that they're being produced. So you stop the fermentation fuels. Now these damn cells become super vulnerable to these other treatment modalities.

So, but the cell that gets into our bloodstream and seeds, like say if you have lung cancer, it goes to the liver, it goes to the brain, breast cancer goes to the liver, to the brain. All of these disseminations are the result of these fusion hybrid events. And you have to then, again, target glucose and glutamine simultaneously.

Then your repurposed drugs come in to help facilitate the clearance of these metastatic cells. So, Thomas, what is why are stem cells considered to be more resistant to those therapies than tumor cells?

Well, they're all tumor cells. You have tumor stem cells and you have the metastatic cells. And their resistance comes from the fact that the fermentation rate differs from these different cells.

So not that they have effective oxidative phosphorylation. We just published a big paper showing that you have three sources of energy in any given cell. One is in the cytoplasm, cytosolic glycolytic activity. This happens in the Emden-Meierhoff-Parnes pathway because we have, as we're breathing right now, we produce a little bit of

bit of energy in the cytoplasm through glycolysis. Most of the product pyruvate is fully oxidized in the mitochondria. And then, of course, we have that one step in the TCA cycle, the succinyl-CoA ligase reaction, and you get a little ATP coming out of that pathway. And this is normal respiration. The problem in cancer is that those peripheral minor pathways become major pathways, but you still have oxidative phosphorylation.

A little bit. You get you get three sources. You get cytosolic ATP, mitochondrial ATP through oxidative phosphorylation, which is a major one in normal cells. And you have substrate level phosphorylation in the glutaminolysis pathway within the mitochondria itself.

So what happens with cancer is you do a reshifting of those, the energy coming out of those pathways. Yes, you get a little oxidative phosphorylation. You get more from cytosolic substrate level phosphorylation and mitochondrial substrate level phosphorylation. They are the two big ones. So we have found that oxfos is neither necessary nor sufficient for driving dysregulated growth.

whereas glucose and glutamine are both necessary and sufficient for driving dysregulated growth,

So so we now know how to pare down. And the idea is, is that when you say, well, I did metabolic therapy and the tumor didn't didn't go away completely. Yeah, but it's a hell of a lot smaller and indolent than it was at the beginning. Now we can come in with these repurposed drugs and with different ways of using the standards of care to finish off these these surviving tumor cells.

But you've got to pare down and you've got to make this angry, malignant growth much less angry and much less malignant by doing these strategic targetings.

So all we have all of the necessary procedures and processes for managing cancer effectively as a chronic disease. We're just not using all of this in the right way, using it in the best ways. So when the clinician comes and says, you know, OK, I got my tumor down. You got how you feel? Pretty good. I still got this lesion here. OK, now we can say, OK, we have better chance now. We have more time. We're not so rushed anymore.

We want to take the fear away from the patient to know that this is a process of healing. Let's take each step as it comes. What used to be really angry and malignant is less angry and less malignant. Now we can go through. It's up to you to do what we need to do with these conditions to bring that thing into a complete recovery.

residual mass or get rid of it completely. And that was our press pulse therapeutic strategy. So everybody wants a cure right away. I want my cancer gone so I can go back and do what I was doing. You know, this is a life changing event. You get cancer, you better make damn well sure you know this is a process. But you don't want to become sickened by the very therapies that you're using to heal you. You really want to be healed

the correct way to know that you have this under control. You need to know what to do and how to do it, working closely with your knowledgeable physician. If the physician says, "Eat jelly donuts and get your sugar as high as possible," you might want to consider someone else. You don't want to work with that guy.

Dr. Corey, you're not recommending jelly donuts, are you? Not at all. No, I follow his advice. No, but you can't believe I go down here to Dana-Farber and they give me that. I saw the other day I was down there. They got a guy sitting there being infused with chemo in their cafeteria and he's eating a big hamburger with a half gallon of Coca-Cola. Unbelievable. This is Dana-Farber, right? Dana-Farber.

Thomas, I got to tell you something. So the patients that come see me, they're all, they've been informed by your work. They have a knowledge of the metabolic approach. And sometimes they don't. They just know that, you know, repurposed drugs have a role. And when I explain to them a little bit of the science and they understand the importance of like a ketogenic diet, I think they do this for fun. But when they see their system oncologist, they'll ask the oncologist, so what should I be eating, doc? Yeah.

generally tells them whatever you want. And so like, and so then, you know, it's, it's my patients tell me this all the time. They're like, it's my oncologist. No, I have, I get like 50 emails a day from all these cancer all over the world. And they get all excited about what I'm saying. They hear me say all this stuff. And then they go in and the oncologist slaps them down. Oh, there's no evidence to support that glucose drives. What are you kidding me? Don't you read this? What do I have to do? Write it in crayon. Yeah.

That's a good line. I like that one. So, you know, you mentioned the repurposed drugs, and that reminds me of my friend, Dr. Lasante, who has published a lot on doxycycline and azithromycin. He did a limited trial with breast cancer patients and had great success with metastatic, the cancer stem cells.

and breast cancer, and he's also shown it repeatedly in his other papers. What is the proposed mechanism? If you guys have looked at those or thought about those, why would an antibiotic help take out these stem cells?

What's it doing there? Any, I thought, I'd have to look at the data. I was going to say, Thomas, I was hoping that you'd jump in and answer that. My answer would be just like Thomas's. When I look at the different mechanisms of action of all the medicines, it's dizzying because they do interrupt several different pathways. I do know that there's good data for doxycycline inhibiting the proliferation of cancer stem cells, particularly it's one of the more effective ones. Um,

But I can't keep in my head all the individual mechanisms and pathways. So I generally, you know, would look it up or I send my patients like brief summaries. Yeah. Sometimes some of these, you know, one of the one of the indirect effects of some of the treatments is nausea. When you're not eating any food, your blood sugar goes down. Yeah.

You know, this was one of the things with temozolomide that they gave to the cancer patient, the brain cancer patient, fatigue, diarrhea, nausea and vomiting. You know, all of these are indirect forms of calorie restriction. And I asked some oncologists one time and they say, yeah, we don't we never had a controlled experiment to determine that.

How effective is nausea, vomiting, diarrhea, and all this other stuff? But you can do water-only fasting and get the same thing, and that really works well. So again, we always have to be cognizant of the types of interactions that might happen. But the bottom line is the tumor cell cannot grow at all without the fuels glucose and glutamine. So if antibiotics are working in some way, it might be through that mechanism, but I don't know evidence to support that.

And of course, if you, you know, you can kill cancer cells with radiation and chemo by, you know, if you kill enough, they can't divide and you block the DNA replicating mechanism or your cytoskeleton like these vincristine and some of these, god damn, these toxic cytoskeleton things. You know, you can kill cancer cells, but at the same time, you risk damage to normal physiological function.

Excess use of antibiotics can damage your microbiome. You can do a lot of different kinds of collateral damages that you have to be careful about. And our goal to manage cancer is how selectively can we kill the tumor cells without causing any harm or even enhancing the health and vitality of the other organ systems in the body. Cancer should be looked at as a systemic disorder, not just a localized area in a particular organ.

Because your whole body is responding to this growth in many different ways, not only in response to putting out the wound, healing the wound, but also the cytokines that are released by the tumor into the bloodstream, causing a whole change in your physiology. So you have to put all that together in a global way of healing this condition. And that's what our goal is. And we know we can do this.

I want to land the plane here, let you guys have your final thoughts or anything you want to share with each other. And also just kind of keeping in mind, you know, Dr. Jay Bhattacharya has been on my show before. Now he's the NIH director. And, you know, I know several of the folks that are going to be in decision-making capacity at HHS under Bobby Kennedy. What needs to happen in the regulatory scene? Dr. Seyfried, you're as a biologist and Dr. Corey as a medical doctor.

both operating in this paradigm, what can we do with this potential change of guard in the regulatory world to make your lives easier?

Let's leave it there. Well, you know, I can tell you that they have to and National Cancer Institute has to recognize that cancer is a mitochondrial metabolic disorder. They have to come to that recognition. Once they recognize and make that a statement, then the kinds of research that will be shifted in that direction will have a very short, a very close interpretation.

impact on reducing cancer deaths and suffering. Without that statement, you're going to continue with absurdities that are actually harming people and not helping the majority of people. So they have to come. If he's the head of the NIH, then he has to, and they're interested in dropping chronic diseases. Cancer is the most feared of the chronic diseases, the most lethal and feared of the chronic diseases.

If cancer and these other chronic diseases are all ramifications in one way or another for mitochondrial dysfunction, they have to make that the statement. Mitochondrial dysfunction underlies cancer and these chronic diseases. If they don't do that, you're not going to get major changes in dropping death rates.

Yeah, I'll just play off of that. If they do that, I would expect a sea change in terms of the focus of research, even clinical research. And I'm going to finish by just saying, like, I just, like I started by saying, you know, discovering the metabolic theory of cancer and reading Tripple of the Truth and now having a cancer practice, I'm just really excited to be involved. I think...

you know, the approaches that we're bringing are the scientifically and biologically correct ones. And so I think I'm delivering, you know, the best care that affords them the best outcomes. And I'm looking forward to research aiding us and clinical experience aiding us in refining and really improving these kind of approaches, although there's difficulty because when you use combinations of medicines,

It really is hard to see or really identify which one is contributing the most and in what combination. But I think we'll get there. I mean, we're on the right track. We just got to go further.

Well, I think, you know, you might email me and I'll put you in contact with Janak Nathan from Mumbai. He's our secretary for the new organization, the International Society of Metabolic Oncology. And the discussion of repurposed drugs is a key aspect of this.

So we have a lot of folks just like yourself wanting to talk to others to see how their practices are responding to what they're doing in relationship to this overall re-evaluation of the cancer system. Yeah, please do. And I think I'm going to join, become a member. I'd be really interested to contribute and learn from them. Yeah, so email me and I'll put you in contact with Dr. Janik. Thanks.

Thanks, Nathan. And then and then he'll he'll we have a lot of committees that we're setting up for folks in all different aspects of managing cancer. And you might want to look through the different committees and see which one you'd like to participate in. Right now, it doesn't cause there's no there's no fees required.

We're still in a very early stage of developing this society, but it's international. We have all major continents, physicians and scientists and nutritionists throughout the whole world that are all just like you said, you're very excited. There's a lot of folks that are very excited about this because they see they're starting to see responses in patients that they've never seen before.

And they want to know what the hell is going on and how to improve this. So this is the society to do all that. And so, yeah, people get excited. So anyway, yeah, please email me. And I'll give you the the the the link to the Janik and he'll he'll explain. He'll give you the we're writing a new mission statement on this whole thing. So it's exciting. Yes, it's this is the new future.

Well, thank you both for what you're doing. You guys are pioneers, and we're cheering you on, and I know the public is going to respond very favorably to this interview, so thanks for your time, guys. Thanks, David. Okay, thanks, Thomas. Take care.

I took the boat.