Is cancer really a genetic disease? I know I was taught that as a radiation oncologist, but today's episode is going to challenge that assumption because our guest, Dr. Thomas Seyfried from Boston University, is going to explain that cancer is a metabolic disease and other chronic illnesses that we are seeing take epidemic proportion in today's society are also metabolic diseases from diabetes to obesity. to neurodegenerative diseases. And he's going to share with us the simple steps that we can take to take back control of ourselves and our bodies and get healthy.
So stay tuned. I know you're going to get so much out of this episode. You're listening to the Born to Heal podcast, and I'm your host, Dr. Katie Deming. After two decades of practicing as an oncologist and caring for thousands of patients, I've seen firsthand how our healthcare system places obstacles in your path to true healing.
My guests and I will bridge the worlds of Western medicine and alternative healing to help you achieve optimal health. Expect to uncover new insights, share a few laughs, and maybe even shed some tears along the way. But most of all, we'll learn how to heal from within together.
So let's dive into today's episode. Welcome, Dr. Thomas Seyfried. It's a pleasure to have you on the show today. Thank you very much, Dr. Deming. It's a real pleasure to be here and have this opportunity to speak with you.
Thank you. Well, you know, I wanted to start just by asking you, how did you initially become interested in cancer as a metabolic disease? Well, you know, that's a 20 to 30 year story.
It doesn't, you know, a lot of people... Ask me this and you'll hear me giving this description of how we all got into this. Because as I said to people, we don't start our research scientific career thinking we're going to manage this cancer problem using metabolic approaches.
We were all predominantly indoctrinated into the idea that cancer was a genetic disease and we all studied oncogenes and tumor suppressor genes. targeted therapies. And we just heard a lot about all the mutations.
And you just talk about oncogenes and tumor suppressive genes as if you actually knew what was going on. And in reality, no one had any idea what was going on. All we knew, there was a lot of mutations.
And we just told my students, oh, yeah, cancer is a genetic disease. You have these different P53 mutations, does this, does that. And we didn't think about it because it was in the book.
And this is what you teach the students out of the book. But don't forget, we were deeply involved in research in ganglioside biochemistry, which is lipids that accumulate in the brain of patients with Tay-Sachs disease and these kinds of rare lipid storage diseases. But I was trained in fundamental neurobiology, biochemistry, and genetics at the University of Illinois State University.
Moved my program to Yale University, where I was in the neurology department. We were working on brain biochemistry and... at that time, Yale was one of the leading programs in epilepsy in the country.
So Dr. Gil Glasser was there and a variety of other distinguished physician scientists. So I knew as a PhD in a clinical department of neurology, I would need to do something that was related to the mainstream of that department if I wanted to stay in the department. And it was epilepsy. So we started looking at mapping epilepsy genes. And I actually wrote a paper or an internal grant.
at that time to the medical school at Yale University, indicating, you know, ketogenic diets for epilepsy are interesting. And we had all these animal models of epilepsy. And I wrote a nice little proposal up to see if we could treat mice with ketogenic diet. And they threw it back at me.
Nobody's interested in that. This is like passe. This was stuff from the 1920s. Today, we have all this new drugs and all these guys. As a young scientist, I didn't know what to say.
I said, okay, well, we just continued on mapping genes for epilepsy. But then I was involved and I came up to Boston College after I was an assistant professor at Yale. I came up here as an associate professor. And we were still working on epilepsy. And I got some really good epilepsy models and mapping the genes.
And we were looking at all these different kinds of things. At the same time, I was doing a lot of biochemistry and glycobiology. And one of my students, Dr. Mariana Tran, I went to one of the epilepsy meetings. I went to the epilepsy meetings to talk about the genetics of epilepsy.
She came back and said, oh, this guy Jim Abrams from California, the movie maker, he makes the airplane movies and these kinds of things. And she said, he's excited about ketogenic diets for epilepsy. So I told to Marianne, I said, forget it. Nobody's interested in that. That's what the guys at Yale told me.
They were the leaders in epilepsy. So she's, oh, no, this guy, Jim Abrams, because his son, Charlie, they started the Charlie Foundation. He got Meryl Streep to do the first do no harm.
So her influence, of course, being a superstar kind of brought the attention. And Jim, his son, Charlie, was on a near death being treated by conventional medications, standards of care. And he just his seizures were just unrelentless.
They were relentless and uncontrolled and couldn't be managed. Finally, he found. former colleagues at Johns Hopkins, John Freeman and Eric Sokoff and Kosoff and others.
And it turned out that Charlie was put on this diet and his seizures became managed. And that was the movie Do No Harm and all this kind of stuff. But then I became very excited about this.
I said, wow, let's look into this a little bit more deeply. So I was involved in setting up some of the early workshops on ketogenic diets for epilepsy. And then we brought in more and more people.
And at the first, it was only like a small group, maybe. five or eight, 10 physician scientists that were interested in this. And then by the time I stopped doing this, I mean, there were halls of people filled with wanting to know more about this.
So yeah, so we started. And then, you know, I was working on cancer at the same time, but it was brain cancer and it wasn't anything to do with management. It was all biochemistry, brute force biochemistry, just to look at differences between human brain tumor biochemistry and mouse brain tumor biochemistry with the hope of finding some sort of parallelism. But then, interestingly enough, as I tell others, we were working with these glycobiology synthesis, ganglioside synthesis inhibitors, with the hope that we could reduce the storage of material in the brains of kids with Tay-Sachs disease.
So, because if we could stop the accumulation of the ganglioside, the accumulating glycolipid, we might be able to help manage the disease called substrate reduction therapy. So they gave me a drug. And then, you know, one thing leads to another. We put the drug on some mice that had brain tumors.
So lo and behold, the drug that was going to work to stop ganglioside biosynthesis had a huge effect on shrinking brain tumor in these mice. So I called the company. I called the company that was making this drug. They got super excited.
They said, oh, my God, we may found this drug that can stop brain cancer. And it's a very, very simple drug. And so they gave me $200,000. This was 20 some odd years ago.
to figure out how this drug was blocking brain cancer. And because they were all excited that it was going to inhibit the ganglioside pathway, thereby gangliosides could be inhibited, play a big role in managing cancer. So we did all these studies and we noticed that the drug shrunk the tumors big time and stopped ganglioside biosynthesis. But at the same time, it was making the mice body weight was reduced.
So that was interesting. So we had this speculation. Do you think it... The reduction in the tumor side had anything to do with the body weight loss rather than the restriction of the ganglioside biosynthesis. So we repeated the experiments.
And this time, we put in mice that got no drug in their food, but we restricted the food so the body weight of the control group matched the body weight of the drug-treated group. And we found, strikingly, that the tumor shrunk to the same exact size as the guys getting the drug. And then we realized that the mice were always eating, but they lost weight.
And we couldn't figure this out because how is it possible the guys could eat the food and lose weight? The control guys were deprived of the food, so their body weight was matched, but these other guys are still eating. So it turned out, interestingly enough, that the drug blocked sucrases in the gut.
So the animals were eating the food, but they couldn't digest it. So that accounted for why they shrunk. But then when we looked at the biochemistry, of the tumors in the brain. Yes, the drug guys had restricted ganglioside biosynthesis, but it wasn't that. It was the anti-angiogenic effect of the calorie restriction that was causing the shrinkage of the tumor.
And of course, the drug company was very unhappy by the fact that their super blockbuster drug would just deprive mice of eating and the fact that they weren't able to digest their food. shrunk the tumors down. So this was not the kind of blockbuster you want to really talk about. So of course, the funding was pulled, the plug on the funding was pulled immediately.
And we did publish it. So why are we going to publish it? It definitely reduces ganglia, shrinks the tumor.
But we don't want you to say that it was through body weight. I said, what do you mean? That's the reason. That's what it worked by. Don't give me any stuff.
So anyway, we published the British Journal of Cancer. That was the end of my affiliation with the government. But anyway, that's the way science works. It brought us to the idea, what was going on with this calorie restriction? Why are the tumors shrunk so much?
And we started to look, and I knew from the work of epilepsy, we knew, and this is another thing, we knew these ketogenic diets worked, but they worked by lowering blood sugar. And you can get the same effect of a ketogenic diet as you can with water-only fasting. So the epilepsy and the cancer were both going down as the result of managing lower blood sugars. And we showed that. We showed clearly that the level of sugar was responsible for both the maintenance of epilepsy, seizure inhibition, as well as shrinking tumors.
And then we also knew the ketone bodies were going up when you fast, water-only fasting and this kind of thing. Ketones go up. And that's the reason Wilder made the ketogenic diet in the first place.
back in 1921 at Mayo Clinic, mainly because he knew that water-only fasting blocked epileptic seizures, but it wasn't a long-term therapy. You had to have something. So he looked at water-only fasting, saw blood sugar go down, ketones go up. He said, let's build a diet that could do something like that so the patients don't have to start to death while we're managing their seizures. So that's how the ketogenic diet got started.
But for the brain cancer, we used a ketogenic diet unrestricted, did not shrink the tumors. It was only when you calorie restricted it. That's why you could either do it on a regular high-carb diet or a ketogenic diet, as long as the blood sugars went down and the ketones went up.
So it was that kind of a relationship. And then we said, had anyone ever noticed this before, other than anecdotal observations? And it all went back to the great scientist, Dr. Otto Warburg, who clearly said cancers are driven by sugar. They're driven by sugar because the mitochondria are dysfunctional.
So the cell... All tumors have dysfunctional oxidative phosphorylation or mitochondria, ability to get energy from oxygen. So he said they have, and in order for them to survive, they have to ferment, and they use glucose as a fermentable fuel, which is energy without oxygen. So he was saying that the cancer cells are all fermenters because their oxidative phosphorylation, their mitochondria are defective.
The reorgonell that's needed to get energy from oxygen is dysfunctional, and therefore the cells have to suck down a lot more glucose to survive. And it was a shift from oxfos to fermentation. So we confirmed that. I wrote a big book on this whole thing, doing a deep dive on what Warburg said and why they attacked him and what was all the fighting about and why people didn't understand that.
So over the years, we clearly showed that Otto Warburg was absolutely correct on defining the origin of cancer as a mitochondrial metabolic disease. He was correct that all cancers need to ferment. He was incorrect in using the quantitative readouts.
of oxygen consumption and lactic acid production to quantify how much energy was coming into these cancer cells. We have resolved all this now. And he did not know about the second form of fermentable fuel, which was glutamine. And that's our big thing.
I shouldn't say, when I say big thing, if you ask anybody in the cancer field, they're all going, oh yeah, we know glutamine. Glutamine is a powerful fuel for cancer. But they all think it's respired.
We're saying it's fermented. So there's a big difference here. It's how you use the fuel, okay?
How is the cell using the fuel? Our immune cells, normal immune cells, use glutamine and they respire it. It's an anaplerotic.
That means the carbons of glutamine are going into the TCA cycle, anaplerosis. But when cancer cells take in glutamine, they're not doing the anaplerosis, they're doing the fermentation and they're throwing out a waste product called succinic acid. So there's a big difference.
And this is the battle lines right now in the cancer metabolism field. Scientist to scientist, lab group to lab group. The battle is that cancer cells are fermenting an amino acid called glutamine. They're not respiring it. Normal cells can respire, but not the cancer cell.
They ferment. Normal cells can respire glucose. Cancer cells ferment it.
So Warburg was right. And then I went through the entire ancient. literature on electron microscopy, ultrastructure.
I had to go through and look at all these guys at the major hospitals looking at mitochondria under the electron microscope of all these cancer cells. And in every one, I saw damaged cristae, broken mitochondria, few mitochondria, all the things that Warburg actually said. But at his time, they didn't have the electron micro. He didn't actually see the structural abnormalities that we now can see very, very clearly.
So it explains the linkage for why. cancer cells are fermenters because the structure needed for them to generate energy through oxidative phosphorylation is defective. Now, that's still a major controversy in my area because they're using all these sophisticated new respiration instruments like a seahorse, and they say, oh, the cancer cells are sucking down oxygen real good, and they're making ATP through mitochondria.
And I'm going a little deep here on it, but some people always ask me, can you get to the guts of this problem? And the problem is that Cancer cells take in oxygen, but they're not using it efficiently for making energy. So they're using it for other things like making reactive oxygen species, ROS, which are carcinogenic and mutagenic.
So that's when we found out that all these mutations that the cancer field is studying are all downstream epiphenomenon of damage to the oxidative phosphorylation. So we have spent hundreds of billions of dollars on the genome projects and all these precision medicines and all this kind of stuff looking for things that are downstream effects. They're not the cause, they're the effects.
So this then brings everything back into perspective. So... when the National Cancer Institute says cancer is a genetic disease, they're wrong.
They're not correct. They don't look at the data. But it's become such a dogmatic view that all the grants, the NIH grants, the hospitals, the pharmaceutical industry, they're all in building immunotherapies and all these targeted therapies, precision medicine.
It's all based on a flawed theory. It's not a genetic disease. It's a metabolic disease.
And once you realize that, the entire paradigm of how you manage cancer will change. I could go on for, but you asked me to give you an overview and I'm sorry, I have to go a little bit deeper. And I found over these years, most of the folks in our country are scientifically illiterate and the people treating the disease, cancer, almost clueless as to the biology and biochemistry that underlies the dysregulated cell growth.
And the patients who come into these guys also have no clue. So you have the blind leading the blind. And as the result of this.
You have almost 1,700 people a day dying from cancer in the United States. And when I start my cancer class every Tuesday and Thursday, we have to recognize in the one hour of my class, we'll have 70 dead people from cancer in the United States. In one hour, you'll have 70 dead people. And this is going on every day, day in and day out, week after week, month after month, year after year.
It's not changing. It's only getting worse. So it's never going to change big time until you recognize that this is a metabolic disorder and not a genetic disorder. The problem is it's too radical.
It's too disruptive to an entire system in an industry. So people, they just can't discuss it and they deny it. Well, there's no clinical trials. Oh, I haven't heard about that.
I would have had it in medical school. There's always some non-scientific excuse. It's happening.
And it works and it will work even better once the physicians understand what to do and how to do it. I couldn't agree with you more on so many of your points, but as being, you know, Western-trained medical doctor and then radiation oncologist, and actually, you know, in my specialty, we have to take two years of advanced cancer biology and radiation physics. Everything that we're taught is about the DNA, that the DNA is the cause. And that...
This is what's ingrained into us, even though, you know, my specialty was breast cancer and gynecologic cancers and in breast cancer specifically, I know that only five to 10% of it is genetically related. The rest is spontaneous and we say we have no idea. And so it's interesting that we're trained into this paradigm to think that it's the cause, but then in practice, it's clearly a minority where they have a genetic mutation. Well, even the genetic nation like BRCA1 or P53 for the leaf romani or some of the other mutations, I have tracked them all down.
And none of them are 100% penetrant, meaning that there's secondary risk factors. Because as women with BRCA1 mutations don't get breast cancer. But those who do get breast cancer, it damages oxidative phosphorylation.
So the mutation is a secondary risk factor. Some women could have breast cancer because of intermittent hypoxia, systemic inflammation. from radiation, from a viral infection.
There's a lot of ways that you can get the same thing that looks like the same under the microscope that have multiple different causes. But every one of those cells in that breast cancer are fermenters, regardless of what their genetic mutations look like. They're all fermenting.
Every cell in the tumor that's neoplastic and dysregulated in its cell growth is fermenting. There's only two fuels that drive fermentation, and that's glucose and glutamine. And they can't burn fatty acids or ketone bodies.
So now you have a clear plan to manage them. And I can't tell you how many women with stage four breast cancer, what these terminal, like you would use not these kinds of terminologies, but can be managed. And they have a high quality of life.
And I don't know how long they're going to survive, but they certainly feel better when they were at 35 with an advanced stage breast cancer and they die from old age. Then you know that person was obviously cured. But you wouldn't be able to say that until. until you know that they went that long, because you never can really know if you've cured.
It could come back 10, 20 years later. But the issue is that you have a level of control. You can control your destiny to a large extent if you know that the cells in your tumor, wherever it's a colon, ovarian, breast, brain, doesn't make a difference.
They're all very, they all ferment. But you have this extra control mechanism. We have Pablo Kelly.
I've been working with him now for... nine years, a glioblastoma. guy from England. He has a little website he can tell you all about. He just finished his third debulking surgery.
He never took radiation, chemo, or anything. He just used metabolic therapy. Is he cured?
No. Is he alive and doing well? Yes. He's had a family and all this since he's had his tumor. But he rejected all the standard of care because he knew it was going to damage him.
And we know in glioblastoma, I publish papers, a majority of people who die from glioblastoma are dying from the treatment. They're dying from the radiation that frees up massive amounts of glucose and glutamine in the microenvironment of the tumor, leading to recurrence and death. And we think that if we avoid radiation to the brain, we think we can keep these people.
I'm not saying we cure them, but they certainly can live a hell of a lot longer and a higher quality of life. And I don't think there's anything wrong with that. You know, if you're doubling their lifespan and they have a good quality of life, I think that's a major advance. And some of these guys, like Pablo, he's still alive. So how many more can we have like that?
So I am very hopeful for the future. I just don't know how long it's going to take for the system to understand this and change. Well, I mean, I think the incentives are against having a systemic change to adopt this because it's, you know, free to do a diet rather than doing some drug.
And so I think the incentives in terms of and also within the research and everything, like you said, you know, the grants were pulled when basically it showed it wasn't the diet. It wasn't the drug. It was. you know, the restriction of the calories.
One question that I have for you is basically you're saying that cancer is a dysfunction of the mitochondria and that this is what is leading to fermentation within the cells. The cells are using glucose and we can use the ketogenic diet as a therapeutic means to basically starve the cancer cells. But one of the questions that I have for you is like thinking, you know, I have a lot of listeners who...
don't have cancer yet. The statistics are not good in terms of where we're headed as a society with 50% of the population projected to develop cancer in a lifetime by 2030. What are the things that people are doing that they can help with their mitochondrial function even before they get cancer? And then also once someone has cancer, in addition to doing the ketogenic diet, what are other mitigating factors there that are affecting the mitochondria?
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Check the link in this episode's description to learn more and sign up today. Remember, you've got this. Yeah, well, that's an excellent, excellent question. I know a lot of people have that same question. As I wrote in my book, it's very difficult to get cancer if your mitochondria remain healthy.
And how do you then maintain healthy mitochondria? And that is you have to do exercise. And you have to make sure that your obesity is now replacing smoking as one of the most prominent risk factors for cancer. And I think, I mean, let's be honest, lack of exercise, obesity, systemic inflammation, all these kinds of stress, emotional stress is another provocative agent. All of these, in one way or another, will cause chronic damage to the mitochondria, leading to compensatory fermentation and the risk of dysregulated cell growth.
in some population of cells in some part of the body. So I said I did started working with ketogenic diets for epilepsy, which is kind of a more traditional thing now, rather than some alternative type of approach. But we learned the ratio of glucose to ketones in the blood. And we developed a meter.
The calculator is called the glucose ketone index. And you'll hear a lot of cancer patients or, oh, I don't want to do a keto. Oh, it's horrible. I get. diarrhea, constipation, or whatever they have.
But we found out that you can take any diet, as long as you can get your GKI down. to a ratio of 2.0 or below, you're going to make your mitochondria very, very healthy because they're going to be burning ketone bodies. And ketone bodies protect the metabolic efficiency of the mitochondria, prevent reactive oxygen species, maintains your mitochondria in a healthy state. So people say, well, how do I do that?
What can I eat? And the answer is water only fasting will do it. But, oh, I don't want it because there's anything else you can give me.
I You know, of course nobody wants this hard. You try to let people do it. I tried it. Brutal. The issue is we do low-carb for a week or 10 days because that allows the body to slowly transition away from the availability of dietary introduced carbohydrates.
And then we jump into water fasting. For cancer patients, the jump now becomes so much less stressful to the body because their body has already semi-acclimated to this new metabolic state, this new... homeostatic state. So ketones are naturally starting to elevate.
Your body is now going after your fat and the fat in your cells, your adipocytes are mobilized and put into the blood stream and it goes to the liver. And the liver, it's like those fats are like putting branches in a wood chipper. Out come the water-soluble ketone bodies, which then subserve the energy of almost all cells in our body. Okay. So the liver makes this.
a bouquet of energy for the heart, brain, and all these other cells that can use an alternative to glucose. So then when you jump into water-only fasting, it's not so traumatic. Yeah, it still is to some extent, but not as bad as if you go cold turkey. And the exercise is absolutely important for managing your health.
We are sitting in traffic, on cell phones in traffic, listening to books on tape in traffic. But sitting in traffic is stressful and doesn't do... anything for your cardiovascular system. Our Western diet and lifestyle puts us at risk for all the chronic diseases that are presently crippling the health of our nation.
So I sometimes look at it as a national security risk. We're putting so many people at risk. And don't forget, we evolved during the Paleolithic period.
There weren't Dunkin'Donuts and delicatessens on every corner. during a Paleolithic period, we were always in a level of semi-ketosis because it was hard to get food. We had to use a lot of energy to kill and eat something or catch something. That was before the agricultural revolution in the Neolithic period.
So most of it, we evolved as hunter-gatherers. Only did we, in the near 10,000 some odd years ago, did we start planting corn and rice and wheat and this kind of thing, where we can build civilizations around the food. So we didn't have to spend all our time chasing down buffaloes and whatever else we ate. But that was our historical history.
We have an incredible capability of storing energy because we evolved in an energy-depleted environment. Now the obesity epidemic is evolution in action. People want to know what evolutionary biology is?
It's the obesity epidemic because now we have all this energy that we never had access to and we store it. We store it because we're going to be starving to death if we don't. So the obesity epidemic is evolution in action, but now it's putting us at risk for cancer, type 2 diabetes, dementia, macular degeneration, cardiovascular disease, you name it, go right down the list. It's all diet and lifestyle.
And that's kind of a cliche, diet and lifestyle, diet and lifestyle. Okay, if you're walking three to four miles a day, every single day, and you're not eating a lot of carbohydrates, you're putting yourself at a better place to be resistant to some of these things, including cancer. We are in charge of our own destiny, but we are tempted.
We have temptations all over the place. Just walk out to any downtown section, oh, the aroma of the baked goods, the aroma of the barbecue grills. I mean, it's just like, wow, this is unbelievable.
So I'm not saying we should not do any of this, but to do it every day and highly processed carbohydrate foods, this is like semi-poison to us. And it stores wasted energy, poorly nutritious food, but yet the calories... the glucose is stored in fat.
So the glucose from what we eat is stored as fat. And people always say, how is it possible you would a fat diet, like a ketogenic lose weight? Because you can't store fat well. You either burn it or excrete it. You don't store it very well.
But glucose is stored. Glucose is gold. You don't pee out glucose unless you're a diabetic.
Glucose is stored in fat. And that's how we get. So it's the sugar that's making the fat, not the fat. And the food industry puts on all low fat diet.
What low fat means high carb. So you eat low fat, you're going to get fat. So, you know, it's just the marketing of how the industry works.
And don't tell me I this stuff is delicious. I mean, you eat a jelly filled for me. I had jelly filled.
Are you kidding me? Especially with these special shops. It's delicious, you know, but I know if I eat too many of them, I'm going to be in the ward. Yeah.
I'll be demented, type 2 diabetes, cancer, some damn thing. Well, and I think the point that you're making is that the rise in all of these diseases are related to the same cause. It's not like we think of them all as different, like cancer is different from diabetes, from neurodegenerative disease, but it's all related to lifestyle and metabolic disease. This is basically we're in an epidemic of metabolic disease. But I want to come back.
So you said, you know, low carb for 10 days. I'm wondering if you can just explain what to you is low carb. Like what is the grams that you would say is considered low carbs?
Well, again, we try to do it based on the glucose ketone index. So as long as their GKI is less than two, that's basically okay. Yes. And everybody is, not everybody, but many people are different from each other. So what might be easy for one person may not be as easy for another person.
So if someone were a vegetarian. They may have to choose foods that would be a little different from the carnivore, from the pescatarian, from the Mediterranean. So everybody would have to look at what they like.
And they always ask me, can I eat this? Can I have no idea? Eat it and see what it does to your GKI. If it makes it go up, don't eat that. No, absolutely.
And I think actually this is an important factor because, you know, recently I've done some work using continuous glucose monitoring and seen that gosh, with different clients, they really respond so differently. And our bodies are all different. And I actually just got a meter from Keto Mojo to test this to see because I hadn't used GKI before. But, okay, so if you do 10 days of low-carb, keeping the GKI less than 2. Well, don't forget now, this is what we have for the cancer patient.
Okay. And sometimes we have to work with them a little different. than the healthy young or the healthy person.
Okay, a healthy person might do three or four days of low carb and realize that. So you start off by measuring your glucose ketone index, and you'll see how it changes during the course of a day. So in the morning, it could be high.
We call it the dawn effect. And then during the course of the day, you can see it changing. And most of the time, ketones are very low in the bloodstream.
I mean, they're there at a 0.1 millimolar or 0.2 millimolar. But as you stop eating and exercise, you begin to see the GKI go down. And what that means is the blood sugar is going down while the ketones are going up, and you divide the glucose by the ketones in millimolar, and then you can get a singular number. And it's the ratio of one fuel, the glucose, to another fuel, the ketone body, in the bloodstream of the person at that moment in time.
They can match how it goes. all of a sudden you'll say, man, this is tough, man. I can't get my GKI down to 2.0. What do I have to do?
I said, stop eating or stay on the low carb. So anybody that would be a vegetarian or a vegan, they would have to choose those foods that would have low glycemic index, which means how fast sugar would be produced into the blood from eating that. Okay.
So they asked me, what about fruits? Oh yeah, fruits. Well, I said, eat the fruit and see what it does to your GKI.
If it makes it go up, don't eat that. But when we worked with epilepsy kids, my colleagues, my physician knew that grapefruit was a good way to get a vitamin C and it was a low glycemic fruit. So it provided the great vitamin C and minerals, but it didn't have a high glycemic index as opposed to a banana, you know, or something like this. But everybody will have to... experiment in their own lifestyle going through.
And it's kind of a game. As you go through, you can start to see your GKI going down over the days. Oh, and you get all excited. Jeez, it went down by 10 points. Oh, look, it's going down by another 10 points.
Let me eat this thing. Boom, back up there. Now I know I can't eat that. And you're right about the free Libra. I understand from my colleagues that there might be a similar kind of measurement for ketones as well.
So you might be able to get your GKI directly real time. But I think that technology is on its way. The Keto-Mojo right now, you have to prick your finger and get a drop of blood and measure with the glucose strip, the glucose. And then with the ketone strip, the ketones, the meter does the conversion, and then you get the results.
But if they can do it with a free Libra, then you don't have to be pricking your finger. And in the epilepsy field, this was always a problem for us because the little kids didn't want their fingers pricked to determine what their glucose and ketone levels were. So I think that's coming down. It would be a great technology.
And it allows the patient then, the individual, to take charge of their own destiny with respect to their diets, what they can eat. what they can eat. They'll come to know. Now, we built glucose ketone index calculator for cancer patients, in particular, glioblastoma patients.
But since we built that, now we've learned the web, all these young athletic men and women, they all want to be buff and they want to be looking tough. And they all go on, what's your GKI? I'm looking like, look at the muscle.
Look at this. I have no fat and all this. I didn't make it for that. I didn't make it for those people.
I made it for the cancer folks. But then we know the cancer folks have a much more difficult time getting into these low GKIs, sometimes because of emotional stress. What we found is that, and I think you know very much about this, the fear of the diagnosis creates a hormonal glucocorticoids, which is a fear response, raising blood sugar.
Consequently, the fear of the diagnosis makes it a little harder to get into a low GKI. So one of the big parts of our... Press Pulse therapeutic strategy for managing cancer is stress management. You have to bring the individual stress down so that the metabolic homeosis begins to take hold.
So again, stress management is an extremely component for effective cancer management because once you get that glucose down, then we take drugs. And when you get into the low GKI levels, cancer-killing drugs become super powerful to kill at low doses. So it's really amazing. You don't have to have hair loss.
You don't have to have all of these horrific adverse effects to kill cancer cells once you've taken away their fermentable fuels or significantly reduced them. And then we can slowly degrade the tumor over time. And like some of the folks that I know, if they had hypertension, high blood pressure, diabetes, all that other stuff goes away while you're degrading your tumor.
So you emerge as a kind of a new evolved guy. You don't have cancer. You don't have diabetes. Now this is... This is not good news for the pharmaceutical industries.
In other words, I can target all these things simultaneously by using a glucose-ketone index. Well, and can you speak a little bit to water fasting? Because you started to talk about that. But so with someone with cancer, and I know you're also doing the press pulse therapy with the glutamine, but I'm just wondering, and I actually did have Lauren Lockman on the show who does prolonged water fasting in Costa Rica.
you know, talk about that. But I'm wondering if, but the interesting thing is he denied, it was interesting because he was telling me that the fasting was detoxifying the cells and then also in improving immunity. And that was the mechanism.
And I said, but you're missing, it's also basically putting them into ketosis. And it was interesting because he kind of downplayed that part of it. But I'm wondering if you can speak a little bit to water fasting and what type of fasting, like how long are you?
Well, I'll. when we did calorie restriction in the mouse, published a big paper on this, Nutrition and Metabolism, where we were characterizing the blood changes in a mouse with a 40% restriction of its food versus a human water-only fasting. And because the difference is in basal metabolic rate between a mouse and a human, you can't use value in the mouse like what would be equal to a human. So 40% restriction in a mouse is comparable with lowering blood sugar and elevating ketones.
and reducing blood triglycerides as well. So we matched human and water-only fasting in human is like a 40% calorie restriction in a mouse. But don't forget the mouse has a seven-fold higher basal metabolic rate than human. Don't forget their heartbeat.
You know, we're talking about about 70, 60 to 70 beats per minute. Mouse has 600 beats a minute. Wow.
So you have to do these conversions. Like imagine if a head would blow off the guy if he had a 600. So the So we're trying to match the basal metabolic rates to figure out what's going on. So yes, water-only fasting is comparable to a 40% restriction in calories to a mouse to produce the same physiological changes in the blood. When I and my students and associates first started to realize how you kill cancer cells by lowering blood sugar and elevating ketones and targeting glutamine, we didn't want to appear like nuts, like some whack jobs. Oh, yeah, you want to get rid of your cancer, don't eat for 21 days.
You know, what a jackass. Who's going to do that? You know, so I said, well, why don't we try these, like, ketogenic diets restricted and make it a little bit less. traumatic to tell this poor, poor cancer guy, oh, come in today. Oh, how?
Okay, doctor. Instead of, we used to say, you know, take one of these pills a day with water and that's all you take each day for three weeks. Well, without food, you know, we say take the pill without, with food, right?
They always say, take this pill with a meal. Oh, yeah. Take this pill once a day with no meal for 21 days.
Well, they think you're nuts. Can I get a second opinion on this? So we said, let's, let's move the field.
slowly into this realization that a change in metabolic homeostasis can be done with restricted diets and maybe some modifications. But now I'm seeing more and more folks are telling me, oh no, you got a 21-way water-only fasting. And I've met so many people, cancer patients, who have eliminated their tumor, like Guy Tannenbaum, doing this. And I didn't tell them to do that. First of all, I'm not a physician.
I can't tell anybody what to do or what not to do. I just have educational material that they can look at, make their own decisions. But Guy got rid of all of his diabetes, cancer, and everything. And I've seen more and more people.
Here's what happens. You ask the question. Okay, I wrote this paper called Autolytic Cannibalism.
All right, I have it in my book. The body is a unique machine. All the organs are working together. The brain, the colons, I mean, the gut, the liver, kidneys.
We all have this machinery in our body, all working together for the good of the whole. And when there's enough energy consumed, the cells of the body are all sufficient in their energy. So there's no lookout for anything that's not efficient. There's no surveillance because everybody, all the cells seem to be, the brain, everything is satiated.
But then when you start lowering the blood sugar by water-only fasting, The body starts to look around, okay, you start mobilizing fats out of your post-tissue. And then as you continue to do that, the normal cells of the body, the brain cells and the liver cells and the kidney cells, all start looking for the valuable fuel, which is glucose. And there's a threshold.
So now these cancer cells that are absolutely dependent, that were not recognized by the normal body because everybody was fat and happy. But when you start lowering this level of energy, the body then will turn on any group of cells. It's called autophagy.
And the mitochondria in the cells are then recognized as being not efficient. Parts of the mitochondria go to the lysosome and are digested. Only what remains is the singular most efficient metabolic system. And if you have cells that are consuming excessive amounts of a valuable fuel for everybody else, the body will turn and eat those cells.
and redistribute the energy to the rest of the body called autolytic, self-cannibalizing cells in your body that are not energy efficient. And those are cancer cells. So then if you can stay in these zones of low sugar, elevated ketones, the body will eventually attack.
And this is the shot, the thing that we're seeing. Some of these guys that come out cancer, what happened to my tumor? Where did it go?
The body ate it. And this you have to know is evolutionary biology. So once you understand... evolutionary biology, all this cancer stuff makes sense.
The problem is almost nobody knows anything about evolutionary biology. So you're doing all these crazy things that are not consistent with how we all evolved on the planet. And that's what we go back to the cancer cells.
They're using ancient fermentation pathways that existed before oxygen came into the atmosphere 2.5 billion years ago. So they're just falling back on heirloom pathways. All of our cells have those same heirloom pathways, but they're only very minor in producing energy.
But when the cancer cell can't get good energy from oxidative phosphorylation, they fall back and those pathways become the dominant form of energy. So they're fermentation. There's just nothing more than what we evolved at this before.
This was, we had a lot of organisms on the planet before oxygen came into the atmosphere. Don't forget, our Earth evolved in a hypoxic environment billions of years ago. There was, yet we have fossils of these cells that lived and they were all fermenters. And they would...
dysregulated growth until the fermentable fuel was used up and they would die. And we do the same strategy to kill cancer. We just take away their fermentable fuels while enhancing the health and vitality of the normal cells with ketone bodies.
Cancers can't use the ketones. It becomes a restricted fuel only for normal cells, not the tumor cell. It's beautiful.
It's unbelievable when you start to see the power of what your body can do when given the opportunity to heal itself. It's amazing. And I love talking to you because you know the science so deeply, which is fascinating to listen. I have a question for you.
Is the idea of cancer cells growing more rapidly? And if the DNA changes are really just effects of this malfunctioning mitochondria? Why does it appear that they're growing faster? And actually, so Dr. Tom Cowan, I read his book, Cancer and the New Biology of Water, and he talks in there about that maybe the cancer cells aren't growing faster. And also he says that the DNA damage is in effect.
And I'm just wondering if you can speak to that idea of why would the cancer cells be growing faster if they're dysfunctional and using fermentation for their metabolism? No, they use fermentation for their metabolism. Yeah, they do.
Why do they grow faster? Okay, brace yourself. Brace yourself.
Do you want the answer to this question? I want the answer, yes. Okay, okay.
The organelle that maintains the differentiated state is the mitochondria. Okay, the mitochondria controls the differentiated quiescent state of the cell. The cell is alive, whether it's a liver cell, a lung cell, colon, whatever it is.
And it's doing its programmed activities. They call them housekeeping, whatever it is. All that energy is efficiently distributed from the mitochondria through oxidative phosphorylation.
When that organelle also, if the cell has to repair or in the gut you have these constant crypt cells that come in there, there's a regulated replacement of cells. There's growth. But it's a regulated growth, not a dysregulated growth.
It's the mitochondrion that maintains the quiescent state and the growth of the cell. When that organelle becomes corrupted, losing its ability to produce energy through oxidative phosphorylation, the cell begins to grow out of control because the regulatory system itself loses the control. And all this is very, very intriguing because we know about the thing called the cell cycle.
the mitosis, the DNA synthesis, the resting and all this, this is all controlled by cyclins, checkpoints and all this kind of stuff. That's all regulated by the calcium gradients from the mitochondria. So if the mitochondria calcium gradients start to fall because they're no longer getting energy from respiration, the controlling mechanism of cell division and control of growth goes out the window. So the cell gradually loses the controller.
of the destiny of the cell is now taken off. You know, people always say, oh, cancer cells are, they have a growth advantage. Such an incredibly stupid statement. It's not that they have a growth advantage.
They're dysregulated because the regulator is broken. You want to see what regulation growth looks like? Liver regeneration.
You know that a lobe taken off of someone's liver, the liver will regenerate that lobe, and those regenerating liver cells grow faster than any tumor. than any hepatoma, liver tumor. So why? They know exactly when to stop.
They don't continue to grow out of control. It's under control growth, and that's because the mitochondria are directing that. That is amazing. Because that has always not made sense to me.
Like if they're dysfunctional, then why do we talk about them being, you know, growing more aggressively and faster? It's like having a car that works better when it's broken. Then, you know.
when it's fully functional. So that makes sense to me. Oh, everything.
People have been nuclear-centric in biology for centuries because they could see the nucleus under the microscope. It was very hard to see the mitochondria. It was kind of amorphous stuff. But now we're realizing that it's the mitochondria that are the controllers, not only of the cell cycle, not only of the functionality of the cell, but also aging.
When we die by natural causes. Our bodies just simply shut down energetically. That's because the mitochondria have reached their end point. And none of us are going to live to be 200 years old, but we can certainly allow us to live a little bit longer if we keep our mitochondria healthy.
And this is the mitochondrial theory of aging, that reactive oxygen species, by just breathing air for decades, causes wear and tear on your mitochondria and eventually sustain. You cannot avoid equilibrium. And I always said equilibrium is death.
When the mitochondria can no longer produce energy, the ionic currents across the membrane reach equilibrium and you're dead. That's it. We have no longer any energy. And energy is life.
Without energy, we don't live. Cancer cells are immortal as long as they have fermentable fuels in the microenvironment. And this was exactly what happened before oxygen came in 2.5 billion years ago.
They were dysregulated in their growth. They have no regulation because the mitochondria had not yet merged to be the symbiosis. Between cyanobacteria and these other bacteria that came together to form this hybrid thing, which was the beginning of metazoans, where we get a multicellular division of labor within everything. Before that, it was just...
Growth out of control. No mitochondria. So a cancer is just falling back on this ancient pathway.
They do not have a growth advantage. They have no growth control. And it looks like they're growing out of control.
There's no control here. And once you know that it's driven by fermentation, glucose and glutamine, and they can't burn fatty acids or ketones, this is the path. It's very clear how to manage cancer.
Well, and I love, too, that you brought in the whole role of stress, because that's one of the things with GMs is monitoring patients'glucose, they'll say, I ate the same thing as I ate yesterday. Why is my glucose higher? And it's really, you know, what happened?
What just happened that day before you had that measurement? And I love this, that you're bringing attention to it, that stress, you know, I put it together for like weight loss when we're trying to help patients lose weight, understanding that stress plays a role in that. But I love how you connected the diagnosis and the fear related to that. not only is releasing stress hormones, which ultimately affects our ability to heal, but it's also raising the sugar, which is further complicating the problem. And the other thing, too, seen from many published papers, people who get radiation, regardless of where it is, if it's any part of the body, it creates a stress and blood sugar goes through the roof after you irradiate somebody.
And chemo and a lot of the things that we do to people raises all this blood sugar. All these things can make the cancer, it's hard to kill a tumor cell when it has a load of its fermentable fuels in the microenvironment. So we, in our Press Pulse concept, we use spirituality, prayer, massage therapy, aquaponics, anything that lowers the stress that a person feels comfortable doing, while knowing that if you have a low GKI, you take small doses of the drugs that target glutamine and glucose.
You can degrade slowly your tumor while maintaining a very high level of overall health. It doesn't have to be all this toxic treatment. It doesn't have to be all this. That speaks to a fundamental lack of knowledge and understanding the biology and biochemistry of the disorder you're trying to treat.
So we put all that together over years. And I have to be honest, without an understanding of evolutionary biology, none of this stuff would be known. I have to know that because I read this stuff. I look at this stuff. I...
tested in my lab. And then, of course, metastatic cancer is interesting because we have shown that the metastatic cancer cell, regardless of whether it's a breast, a colon, a lung, they're macrophage. They characterize macrophage.
Macrophage is an immune cell in our body. It's like the Marine Corps. It's either your best friend or your worst enemy.
It's designed to attack and kill bacteria in our body, okay? If you get a stab wound or a broken bone or anything like that, you're dead. and the skin is breached, bacteria get in.
And then we have monocytes pouring out of the bloodstream, maturing into macrophages to kill the invading bacteria, because if we don't beat that down real quick, we're going to be dead from an infection, sepsis or something like this. So those cells are macrophages, and they're heavily glutamine dependent. Now, when you have an incipient cancer, like a wound that doesn't heal, and it's there for long periods of time, could be decades, the macrophages are always in there trying to facilitate wound healing.
And what happens, sometimes they release growth factors and cytokines that are supposed to facilitate wound healing. But in that context, it actually stimulates these dysregulated cells to grow a little faster. And then they're getting bigger, causing a bigger disturbance in the microenvironment.
And macrophages have this unique biological capability. They're fusogenic. They will fuse with each other. and sometimes fuse with these cancer cells.
The cancer cell at that point, the dysregulated cell, has no capacity to spread anywhere other than in that focal area. So what happens is it fuses with the very cell trying to heal the wound, and then the cytoplasm of this macrophage becomes diluted with the abnormal mitochondria from the cancer cell, and now you have this dysfunctional macrophage, a rogue, what already is programmed. to enter and exit tissues and spread around your body. So when I found out that all these metastatic tissues are essentially fusion hybrid between one of our immune cells, I went back to the Newskoms in Oxford, England, and they studied these macrophages for years.
And I said, what do they eat? And they eat glutamine. When a person is burned and you open the skin up to all kinds of bacteria, they give high dose glutamine to these burn patients in order to keep our immune system healthy to kill the invading bacteria. So I know the cancer cells are sucking down the glutamine because they need it to ferment.
So now they're fermenting this glutamine. So we know exactly how to kill metastatic cancer cells. We know how to kill all these cancer cells if you understand the biology and biochemistry of the system in the context of evolutionary biology.
And so is that only important in the setting of metastatic disease, the glutamine inhibitors or depriving of glutamine? Yeah, because I think most people fear when anybody says they have a stage four, that's metastasis. Okay, so that...
was considered terminal. We don't consider that terminal anymore. We consider that susceptible to metabolic therapy.
So glucose-glutamine targeting. I don't want to make it sound like we have a panacea here. All I want to say is that we are on the cutting edge of dosage, timing, and scheduling for using the body's healing capabilities together with strategically placed drugs. Because if we become too aggressive on the glutamine, we paralyze the normal macrophages and immune cells in our body. to prevent them from doing their job.
So that's why we developed the pulse concept. So you press the glucose hard because the body can switch to ketones. And then we hit them with small doses of glutamine inhibitor because that'll kill the tumor cells, but it'll not kill our immune cells.
Because if you kill a lot of tumor cells or any tumor cells, you have to have immune cells picking up the dead bodies, getting rid of the corpses. And if you do this in the wrong context, you end up with a potentially infectious area and the tumor cells are not... being effectively killed.
So again, it's how you do what we know to do. And this is where, if we had trained physicians that understood all this, they would be on the front lines experimenting with dosage timing and scheduling, writing the papers and telling us what their strategy is for various types of young people, middle-aged people, older people, and what the best strategy is for managing these folks. But right now, we're not doing any of that because they all think cancer is a genetic disease. It's not a genetic disease. It's a mitochondrial metabolic disease.
Wait until you see what happens when the field comes to recognize this. Cancer death rates are going to drop. It's going to drop like the AIDS epidemic that it was years ago. But how do we get that? I don't know what to say.
When I tell people this, and when I go to medical meetings with the physicians, it's like a deer in the headlight. I don't know. They just stare at you. It's like they never heard any of this before. Well, we haven't, though.
I mean, this is the thing is they... nutrition is not taught in medical school. We're not the teaching kitchen.
I was at the teaching kitchen conference back in 2022, I think. And they had like an attorney on their team lobbying to get something passed. I forget whether it was the Congress or Senate to actually ask medical schools to include nutrition in the curriculum.
And the only thing that they could get passed was that it would be optional. for them to include nutrition, which is just mind-boggling. So the reason why they don't understand is because we are literally not taught anything about this. Well, that's what I'm saying. You guys all take this oath for do no harm, and then you're trained to push pills and use treatments that are not as effective as they could be if they were combined with a good nutritional strategy.
So we do diet drug therapy. We're not against drugs. You have to realize that.
But we want to use the power of the body to work with the drugs. And the drugs don't have to be these super expensive things. There are a lot of them are repurposed drugs. And I know I've spoke to many. I put so many of my kids in medical schools and they never they only hear is that cancer is a genetic disease and they never hear the power of nutrition on how to use specific drugs to make not only kill the tumor cells, but make the patient healthy.
So so it's a failure on the part of the medical training. And that's what I call the system. OK, the system is the.
National Cancer Institute, the National Institute of Health, the pharmaceutical industry, the hospital industry, all of these are in the same bubble. And a lot of people are making fortunes on these drugs that don't really work well. And the idea is because they're not based on an underlying theory that it's a metabolic problem.
And if you understand metabolism, and it's just not nutrition, it's evolutionary biology. And very few people really understand that either. So even if you say, oh, I'm going to eat this and eat that, to know how it all works mechanistically in the body, you have to understand these other concepts. And that's how you connect the dots.
And that's how you'll really be able to move the field forward for managing health care in this society. Yeah. And I have a question for you. Where would you recommend someone start to learn about evolutionary biology? I think that's a very good question.
It's not easy. And even here at BC. very few people read Darwin. When I read Darwin, it made no sense to me in a medical sense. He wasn't talking about cancer.
He wasn't talking about type 2 diabetes, but he was talking about how things happen and change over time. Where does all these integrated systems come from? Because we can see, I mean, you guys, we studied the section of a frog.
We just studied the section of a rat or a cadaver. And we see all the linkages between where did all this stuff come from? You know, it evolved over millions of years to subserve functions.
And then you're looking at the molecular and biochemical level, and you can see... You can see the unbelievable connections between all these units. And then you have to know how different systems use different fuels. The liver doesn't use ketone bodies.
It makes ketone bodies, but it burns fatty acids, okay? But the liver is garnishing everybody else with fuel. So you really have to know how all this is working, why the brain can burn ketones so effectively.
If we were dependent on glucose and our blood sugar, everybody would go unconscious. But the brain doesn't do that. The brain can...
function under ketogenesis, it evolved to do that in order for us to remain alive as a species. So again, it takes time to read these things and understand them. But I think most students, they just read it, oh, this is painful.
Look at a Krebs cycle. Oh, this is painful. I got to memorize all these pathways. Oh, everything is painful because they don't see it connected to who they are as an entity on the planet. Well, I think that there's a disconnect between, because when I learned the Krebs cycle, it was like, you just have to learn this.
But if I understood that disease was, you know, related to metabolism and respiration, oxidative phosphorylation of the mitochondria, it would have given me a whole different context to learn those systems. Yeah. Well, I had the same problem, you know, when I looked at that when I was a student, oh God, it was painful.
Well, you know, all these steps and the reducing equivalence and all this, you know, stuff. But I'll tell you, after you start to learn, well, Otto Warburg, you know, brought me and I started doing it. You have to reach a certain point in your development of an intellect to be able to see these connections because you couldn't, I couldn't see them when I was younger.
I didn't see anything. I couldn't put these connections. You're focusing on brute force biochemistry, isolate lipids from a brain.
It didn't have anything to do with energy. But then you begin to say, you know, what's going on? Why are we killing these tumor cells?
Why are they up and dying? Why can't they survive under these conditions? And you start to put the dots of the puzzle together and you say, oh my God, it's unbelievable.
So the most important thing that we should focus now on is changing the paradigm for how we're treating cancer patients. Because the current paradigm is a failure. It's one of the greatest tragedies in the history of medicine that we would have 1,700 people a day dying from cancer. And the only advance that we've had is the anti-smoking campaign and the cancer statistics that comes out every year from Dr. Dr. Siegel from the American Cancer Society, always gives a picture. We've dropped cancer rates by 33%.
Well, yeah, because people stopped smoking. If you didn't stop smoking, we would have 33% more cancer than we have today. So it's all just prevention, not any treatment. Because the treatments, immunotherapies, you hear them advertised on television at night.
CAR-T. Oh, look at this guy, Optivo, Contruda. We got this and we got that.
You always show some smiling face, not sitting on a toilet. with diarrhea or anything like this. So, and that's all based on the somatic mirror. It's wrong.
It's not going to work. It does work for 20% of the people. I have to be honest with you.
20% of the people die faster from those drugs. All right. So it's kind of a crapshoot.
And then, you know, 60% of people doesn't do anything better than what standard care would have done. And they charge you like $100,000 or more for this. And then they cause financial toxicity.
That's another thing. One of my students write a big paper. Okay.
A lot of folks in our country. They're living on paycheck to paycheck. They can't afford $20,000 for cancer treatment.
So the marriages fall apart, suicides. I mean, it's unbelievable. This is called financial toxicism. This is immoral.
So we're dealing with an immoral system here right off the bat. Yeah, I hear you and I agree with you. You know, I wanted to ask a question and this is like putting two things together that I don't know if you'll know the answer to this, but One of the things that Dr. Cowan has talked about, I've been studying Dr. Gerald Pollack's work with the fourth phase of water, which I'm not sure how familiar you are with that, with easy or exclusion zone water. And one of the things that Dr. Cowan has talked about is that actually, the role of ATP is creating a conformational change within the cells to structure the water, and that actually... ATP is less related to energy and more related to structuring the intracellular water.
And I'm just wondering if you know anything about this or you have any understanding or insight. Well, when we grow ourselves in water, buffered water, phosphate buffered water, and measure their ATP through bioluminescence technology, which is what we do. The cells die. Okay.
Without energy, nothing lives. So water is there. No energy is there. The cell is dead.
And then I can't speak specifically to that role. I speak specifically to energy. And as Otto Warburg said, without energy, nothing can survive. Okay.
So energy in biochemistry is ATP. So ATP is the currency of energy. It creates the conformational changes in proteins, enzymes, synthesis, degradation. It's the energy of life is ATP. Ultimately, it comes from the sun.
The energy comes from the sun in carbon-hydrogen bonds that the plants produce. All right? So we break that.
We eat food. We break the carbon-hydrogen bonds. That was embodied. The energy of the sun is in the food that we eat. Okay, you can burn wood and you release the carbon-hydrogen bonds in the form of entropy.
Disordered heat is what you feel. But when we eat food, we break those same bonds, capture that energy in the form of a proton-motive gradient. So when I say water, we grow cells in water without any food. Just put the cells in there, and in 24 hours, they're dead.
So what will keep them alive if we just add in the buffered water, salt water, buffered water? We add back fuels. We see what, boom, all of a sudden, man, you add a little glucose, they start perking up. And then you add all these different amino acids, you add the gluten, boom, you get the big explosion right there. So we know, and the light comes on, so they're burning, they're making energy.
So that's how we were interrogating these cancer cells to figure out what do they need to survive? And you go through the litany of things that they, and we only found glucose and glutamine as the two fuels that keep these guys alive. And vitamins are important for the cancer cell as it is for the normal cell.
Sometimes the cancer cells need even more vitamins. So you always have to be careful. You don't want to be pumping all this crazy stuff.
The thing of it is, is you just got to deprive them of the only two fuels that they need to survive, which is these two fuels. And then it becomes a very manageable problem. You don't have to be chasing things, all these things that are not as pertinent to the survival of the cell. Because what do they need to survive and grow?
They need energy. Where does the energy come from? It comes from fermentation.
What are the only things they can ferment? Glucose and gluten. How do you know?
Because I tested it. Well, this has been really helpful for me. I feel like since I've stepped out of my traditional Western practice, I really feel like a student again and also open to hearing different ways of thinking about things. And I have learned so much from just spending the past hour with you.
And I know that my listeners will as well. So. I want to thank you for your time and generosity of information. Thank you.
If people would like to find you or your work or learn about the studies that you're doing, where is the best place for them to find you? Yeah, well, that's another important point because people hear me on these podcasts. Oh, he didn't talk about this. He didn't talk about that.
But we publish all of these in open access. So all you have to do is go to Google, put my name into Google and say publications, and then they'll come right up. You'll see a whole bunch of them.
on the press pulse therapy, Pablo Kelly, dog, we have a beautiful response in a dog put on metabolic therapy. Unbelievable, the tumor just went right off his face. I can say, works of all the animals that we've looked at, that therapy works best on us.
And our research is supported predominantly through philanthropy and private foundations. So Travis Christopherson's Foundation for Cancer Metabolic Therapies supports us. And there are people who hear this And they say, I want to be part of the change.
I want, there are people who donate money and they're not expecting something in return other than the fact that we keep people alive a lot longer than they should have been. And this is a work in progress. And I think it's going to be the eventual standard of care. Right now, we're writing a big treatment protocol for cancer, a how-to manual, a physician's desk reference, if you will. And we're going to try to get that published.
And we have a lot of number of physicians and scientists on this. And once we would have that, then primary care physicians can play a huge role in helping these patients. They don't have to be handing off patients to so-called more special specialists.
So I think the system is going to definitely change for the betterment of the population. Yeah, this benefit everyone. Yeah, yeah, right.
And I think this is going to happen. And as long as we can test everything preclinically. here.
And then I write up sometimes case reports with my physician colleagues. The movie Cancer Revolution is coming out, documentary on this. They put in all their so-called terminal patients that are all happy and waving to everybody. Well, I love that. I mean, this is the thing.
People take very toxic chemotherapy drugs to live like an extra two months. The fact that you have the GBM fellow who's here, what did you say, 11 years. That's 10 times what the average survival is for someone with a GPM.
So it's just, you know, you know, not toxic drugs. Yes. So I love it. Well, thank you so much again for your time.
That's a wrap for today's episode. Thank you for joining me on Born to Heal. It's been a privilege to share this time with you.
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You can find additional resources in the episode show notes linked below. And remember to join us next week as we continue to explore more holistic approaches to healing. Until then, this is Dr. Katie Deming reminding you that just like me, you were born to heal.