On September 21, 2024, Professor Thomas Seyfried presented at a BSI Medical Society event in Boston. His talk focuses on cancer as a mitochondrial metabolic disease rather than a genetic one. Seyfried challenges the mainstream somatic mutation theory, which suggests that genetic mutations drive cancer. Instead, he argues that cancer arises from chronic mitochondrial damage and compensatory fermentation, highlighting the role of glucose and glutamine as key fuels for cancer cells.
Throughout his presentation, Seyfried discusses historical examples of scientific paradigms and how they were overturned, using these as a parallel to the current dogma surrounding cancer. He emphasizes the importance of addressing mitochondrial dysfunction and suggests that targeting the metabolic pathways cancer cells rely on, such as glucose and glutamine fermentation, is a more effective approach to treatment.
He also shares case studies, including successful outcomes in both humans and animals using metabolic therapies, such as the ketogenic diet and specific drugs targeting cancer’s metabolic vulnerabilities. Seyfried also discusses the need for a shift in cancer treatment strategies, away from traditional methods like radiation and chemotherapy, which he believes can exacerbate the disease.
Seyfried’s presentation is a call to rethink cancer research and treatment, advocating for therapies that target the metabolic origins of the disease rather than genetic mutations.
Transcript:
0:00Well, I want to thank Emily and Bob and Greg for the kind invitation to come here and present some of our recent, uh, historical information on cancer as a metabolic disease. Um,
0:12I don’t want this to be too loud, is it too loud? Am I blowing somebody’s eardrum out
0:17here or anything? No? Okay, um, yeah, so, uh, cancer is a mitochondrial metabolic disease,
0:26uh, is what I’ll be speaking about, uh, this afternoon. And, um, I have a couple of, uh,
0:33quotes that will introduce what we need to know about, I think Greg hit upon one of these in his
0:40presentation. Um, but when we talk about, and what Dr. Palmer was speaking about, uh, we have certain
0:49mindsets in people, uh, related to some of these quotes here from Carl Sagan, you know, “We live
0:55in a society driven by science and technology, and most people have no clue what’s going on.”
1:01Um, Tolstoy: “The most difficult subjects can be explained to the most slow-witted man if he
1:07has not formed any idea of them already, but the simplest thing cannot be made clear to the most intelligent man if he’s firmly persuaded in what he knows already without a shadow of a doubt.”
1:16We have these problems of assimilation bias or confirmation bias from Francis Bacon, uh,
1:23the originator of the scientific method. “Human understanding, uh, when it has once adopted an
1:28opinion, draws all things else to support and agree with it.” And of course, in our area, uh,
1:35follow the money. Upton Sinclair: “It’s difficult to get a man to understand something when his
1:41salary depends on him not understanding it.” This is, uh, really all of these together, uh,
1:48represent, uh, some of the challenges, uh, that we have that speak to your philosophy
1:54of science in one way or another. Um, but, but what we do is, um,
2:00we document every year, uh, the, the, uh, American Cancer Society. One of their major
2:05functions is to, uh, log the dead, uh, basically, uh, new cases, deaths per year, deaths per day,
2:13and you can see it’s always increasing, um, to some degree, uh, more new cases. Um, and, and,
2:21you know, we’re getting almost 1,700 people a day in the United States dying, dying from cancer. Uh,
2:27and if you divide that number by 24, it comes out to about 70 people per hour, okay? This is
2:34not an insignificant—this is an epidemic. We keep throwing massive amounts of money
2:40into these problems—billions and billions of dollars, both from the federal government and
2:46from private foundations, you know, the pink ribbon campaigns, you hear all about them. People just mindlessly run out and throw money at a problem, they have no clue where the money is
2:55going. There seems to be no accountability, either in the federal government or for the private foundations. It just seems to be a year-in, year-out ritual of throwing money at
3:04a problem with the expectation that something will be different, and generally, it doesn’t.
3:10What I do is I check the scientific advisory boards of the individual foundations that support it, and then you can know, uh, why we’re not making any progress.
3:19This is a lot of words—cancer statistics from 2024. What they want to say here is that we
3:25are making major progress in reducing the death from cancer. I spoke to someone the other day,
3:31who said, “This is the most exciting time for cancer,” and all this. And I said, “What about all the dead people?” They said, “Yeah, well, that’s an unfortunate problem.” Um, but,
3:41uh, but one of the things they tell us, uh, about all the progress we’re making—in the early 1990s,
3:48uh, there was this anti-smoking campaign, uh, where secondhand smoke was bothering people,
3:54right? You sit next to this guy, “Oh, you can’t.” So it was societal peer pressure on people that
3:59smoking was unacceptable. You know, years ago when I would go to scientific meetings, you’d have to wave the smoke away—you couldn’t even see the slides! Right? Scientists were all
4:07puffing away, everybody’s puffing away. Half the restaurant was smoking, half was non-smoking. Now if they catch you smoking, they have a team come out and beat you half to death!
4:17So as a result of that, we’ve prevented a lot of cancer deaths, okay? So the red
4:22line is all the people that would have died had we not stopped smoking. Alright, so if we didn’t stop smoking, we would have had all these dead people, but we’re still
4:31on a trajectory of increase. So the biggest reduction in cancer has been a prevention one,
4:38a behavior—personal behavior one—not from what we think of with all the advertisements we hear
4:44on television every night about how wonderful it is. They show you some smiling guy riding a bike,
4:49and then they give you 15 different ways the treatment could kill you. The problem is, it’s personal choice that does a lot to reduce this.
5:00So we’re going to talk about cancer. What is cancer? It’s just disregulated cell growth. People always say, “What is cancer?” It’s cell division out of control. Um,
5:10is this disorder caused by genetic mutations? And we’re going to talk about that. Uh, or is
5:15it caused by chronic insufficient respiration, coupled to compensatory fermentation, or what we
5:21refer to as substrate-level phosphorylation? Now, a little bit about theories in
5:28science: a scientific theory is simply an attempt to explain the facts. The data, the facts—reality is based on replicated facts, whereas interpretation of the facts is based on
5:36a credible theory. You collect a lot of data, and people have different ways to interpret it. And if everyone is interpreting it in a similar way, then we have a theory. We can test that.
5:44Credible theories move science forward, whereas flawed theories can stall scientific progress.
5:51Now let’s look at some of these in historical perspective. The heliocentric theory could explain
5:58better the movements of celestial bodies than could the geocentric theory. Now, for 1,800 years,
6:05the ideas of Aristotle and Claudius Ptolemy, uh, focused on how to explain the movements
6:12of the planets when the Earth is immovable and stable. We see the moon, we see the sun,
6:18we see the planets, and then we see the stars, which are actually in a separate sphere. It was a series of mathematical epicycles, uh, deference, where the planet is moving in one
6:32way and then all of a sudden decides to turn and go in a different way. There was a lot of mess
6:43for 1,800 years. Then Nicholas Copernicus, up on the top, uh, struggled with all the epicycles and
6:52the mathematical problems with the celestial bodies. He said, “Maybe if we rearrange the
7:02organization of the celestial bodies—if we put the sun in the center and make the Earth simply
7:08another planet—maybe we can better account for the predictability of where these planets are
7:14supposed to be at the time they’re supposed to be there.” Again, we find predictability that was
7:21far more accurate than previously thought. Of course, the next guy, Johannes Kepler,
7:26understood that they were not just perfect circles but ellipses. He jumped all over that—he knew
7:32exactly what Copernicus was saying. Of course, Galileo developed the telescope to confirm
7:39the moons of Jupiter and also the angles of the planets’ movement. He was very excited. Of course,
7:45he was put under house arrest by the Catholic Church. You were threatening the power establishment at that time, which was the Catholic Church, the seat of all knowledge
7:54and predictability. Now the poor guy on the bottom—does anybody know who that guy is? The
8:01lowest guy here? Anybody know who that is? Nobody? Giordano Bruno—have you ever heard of Bruno?
8:10Bruno was a cleric in the Catholic Church, and he was a strong supporter of Copernicus.
8:19He ran around and told everybody that Copernicus was right—the Earth is not the center of the universe, the sun is. That didn’t go over well. They stripped him naked,
8:28held him upside down, and burned him alive in a plaza in Rome. He’s considered the martyr
8:33of science—Giordano Bruno, you should all know. Galileo got away with house arrest,
8:40but poor Bruno was burned to death. Why? He was challenging the power structure at the time.
8:47But there was one thing that Bruno said that really put the flame to the torch here: he said,
8:52″There might be life on another planet.” Oh, that was it—he was gone, forget about his ass, he was finished, and that was the end of Bruno. But the key is, it started what we call the
9:02Copernican Revolution, and the Renaissance of science in Europe is the result of this. Then we have the germ theory, which could explain better the origin of contagious diseases than the
9:10bad air (miasma) theory. The miasma theory came from Galen, a Greek-Roman physician,
9:19and his ideas about disease permeated all the way into the 1800s. It was Louis Pasteur who
9:26clearly showed with his experimentation that germs actually cause disease, not bad air, not miasma. He was vilified by the French medical aristocracy at the time because they said,
9:37“He doesn’t have an MD degree, therefore we can’t believe anything he says—he’s only a PhD!” But he turned out to be right—the MDs were not right. And then, of course, there’s the Darwin-Wallace
9:49theory of evolution by natural selection, which could explain better the origin of species than the theory of special creation. Those little numbers on the top there are the descendants of
10:02original ancestors. Each one of those horizontal lines could represent millions of years, hundreds
10:08of thousands of years. You can see all the extinctions that have occurred in the organization
10:14of biological plants and animals over time. I have a whole chapter in my book on
10:19cancer—nothing in cancer biology can make sense except in the light of evolution. So we incorporate evolutionary theory into our design of therapies that we use in the lab.
10:31And thank you to Chris Palmer for at least identifying what the mitochondria are. It’s actually a spaghetti network inside the cell. These diagrams you see in textbooks
10:41make them look like little beans, but they’re actually a spaghetti network—they fuse, they
10:47divide, and they have a very active participation in the energetics and vitality of the cell.
10:55So, can the mitochondrial metabolic theory explain better the origin and management of cancer than the somatic mutation theory? This is the next big transformation in medicine. Which of
11:08these theories is correct? We’re going to dive into this and let you, as rational thinkers,
11:14come to your own decision as to what you think might be what we’re dealing with here.
11:20Does cancer arise from nuclear somatic mutations, or from chronic mitochondrial
11:26damage with compensatory fermentation? There’s a two-step here: you have to have the chronic
11:32damage, and you have to have protracted compensatory fermentation, or what we refer
11:38to in our lab as substrate-level phosphorylation. Fortunately, I have my research crew back here—if
11:45I screw up with one thing, they will attack me! Not you good folks—those guys. Bob is there with
11:53the rest of them, so I have to be careful. So, we’re going to talk about these concepts.
11:59We’re looking at two organelles here—the mitochondrion and the nucleus. The somatic
12:06mutation theory of cancer says that disregulated cell growth is due to mutations in the nucleus that cause the cell to become disregulated or grow out of control. I
12:17will present evidence that challenges that. We put up this paper—this is by Hanahan and
12:24Weinberg. They’re down here—Robert Weinberg is at MIT. This is one of the most highly cited papers
12:32in all of biology—cited by 75,000 times—Hallmarks of Cancer: The Next Generation, a dogmatic view,
12:40an irrefutable truth, a silent assumption, if you will: cancer is a genetic disease. And cancer
12:47cells carry the oncogenic and tumor suppressor mutations that define cancer as a genetic disease.
12:52Page 661 in the paper—you can read it if you have the paper, if not, I can send it to you.
12:59Okay, so this concept has now permeated all of the textbooks of biology, biochemistry,
13:04and cell biology. All the medical students, when they get their first year of training, and they do
13:10biochemistry or whatever, they’re talking about cancer as a genetic disease driven by different
13:15kinds of mutations that we’re going to look at. Not only that, it’s also supported by the National
13:22Cancer Institute—our government’s cancer website, the National Cancer Institute. What it says right there: “Cancer is a genetic disease; that is, it is caused by changes to genes that control the
13:33way our cells function, especially how they grow and divide.” Down at the bottom there:
13:40″Cancer is caused by certain changes to genes.” This is confirmation bias.
13:50What this means is, in terms of Francis Bacon’s assimilation bias and confirmation bias, the whole
13:56field says cancer has to be a genetic disease because the NCI says it is, and everybody else
14:03thinks it is—not everybody, but a lot of people. So let’s look at this somatic mutation theory. If
14:09you’re going to understand what the current theory of cancer is, because ultimately,
14:14if you think you understand what the disease is, you should be able to strategize therapies that manage it. And you just saw all the dead people piling up—something’s not right.
14:24So, we have mutations in tumor suppressor genes and proto-oncogenes leading to cell division out
14:31of control. So we look further at this, and we see that a tumor suppressor gene is a normal product
14:37of some gene, a protein of a gene in our genome, and it keeps normal cells in a growth-regulated
14:42state. A mutation happens in that gene, and you get disregulated cell growth. This is called a
14:49tumor suppressor. These are tumor suppressors. But in addition to tumor suppressors, we also have these things called proto-oncogenes. A proto-oncogene is a normal gene in our body, but
14:58if it gets a mutation, some sort of mutation—there are several different kinds of genetic
15:04changes—you can have a mutation in the normal proto-oncogene, and that causes an oncogene,
15:10which makes the cells grow faster. You can have a mutation in there, or you can have extra copies,
15:16multiple copies of this proto-oncogene, leading to normal growth-stimulating proteins in excess,
15:22or you can have the gene move around the genome and find itself next to a different
15:27kind of promoter, forcing the product to be in excess, leading to disregulated cell growth.
15:34So we have the tumor suppressor genes, proto-oncogene, and oncogene, and these
15:41kinds of things, and this is all part of the somatic mutation theory—the current dogmatic view of what we think cancer happens to be. So this is Dr. Vogelstein from Johns Hopkins.
15:54He says, “We now know precisely what causes cancer: a sequential series of alterations in
16:02well-defined”—and remember this term—”driver genes.” Not all the genes we found—oh my God,
16:07there are some that don’t do anything: passengers, valleys, hills, all this kind of stuff. Drivers are the key. So the key to managing cancer is going to
16:15be to target the driver genes that are causing the disregulated growth in a tumor in your body,
16:23okay, or causing a particular population of cells to become disregulated. All these things happen.
16:29Now, here we are today. Individuals’ cancer cells are genetically tested for personalized therapy.
16:35You hear about all this precision medicine, personalized therapy, all this kind of stuff.
16:40Breast cancer cells are being examined to see if they possess extra copies of a particular gene.
16:46There was a company down here in Kendall Square, Boston, that was bought out for $2.4 billion dollars. It’s a company that looks at tissue from cancer patients and looks at hundreds of
16:56different kinds of mutations. And you get this nice readout, “Oh gee, look at all the mutations I have.” They look at that and say, “We can give you a short list for $4,000,
17:04but if you really want the Cadillac list, you can pay another $7,500, and we’ll give you thousands of different mutations.” And you say, “Wow, what are we going to do with all this information?”
17:14But anyway, the information keeps a lot of people employed, looking at screens and things like this. But you also have the observer effect, which is the Heisenberg uncertainty
17:25principle applied in human tissue. By looking at it and disturbing it, you have changed it.
17:31So what you’re looking at may no longer be what’s happening inside your breast or colon or whatever, that tumor from which you’re taking the biopsy. Now, again, we already heard about Ioannidis
17:40and his papers before. This is a paper from his group showing that the new cancer drugs
17:47aren’t working. The bottom line is they looked at 92 drugs from 2000 to 2016,
17:54and what’s very interesting about these therapies is, if you look at the tumors of the patients
17:59that were treated with these various kinds of precision drugs or whatever you want to call them, it looked like the tumors were—wow, the tumors were really responding well. It’s unbelievable!
18:07But the people don’t live any longer. Very little—like two and a half months longer. What I understand is that the Food and Drug Administration determines whether
18:16a new drug should be given to human beings based on progression-free survival. That means what does
18:22the drug look like it’s doing to the tumor? And if there is some modicum of overall survival benefit,
18:27well that’s great, but we really should be looking at: does the drug keep you alive far longer than
18:33any of these other drugs? And they don’t look at that. That’s not part of what they’re looking at. Now, evidence challenges the somatic mutation theory, and whenever you challenge the dogma,
18:42you end up like Bruno, right? So you’ve got to be careful—people don’t want to look at it,
18:47they don’t want to talk about it, they don’t want to hear about it. We like to quote Einstein—we’re all big on whatever Einstein had to say:
18:55“No amount of experimentation can prove me right, but a single experiment can prove me wrong.” Well,
19:01let me show you stuff that should have proved the somatic mutation theory hopelessly wrong.
19:08Here we have Theodore Boveri, in 1914, who wrote this paper—a purely speculative paper—where he
19:20thought that cancer might have something to do with abnormal chromosomal behavior, movement of chromosomes. He came to that revelation looking at sea urchins, and he even said,
19:30″I have no clue how sea urchins are related to cancer.” Even his friends in cancer said, “You know, Theodore, I think you’re out to lunch.” He said, “I’m probably totally wrong, and I want to
19:39apologize to the entire cancer community because I’m wrong, I have no knowledge, I’m ignorant.”
19:45And now we’ve anointed him as the father of the somatic mutation theory. So go figure.
19:53Now, we’re looking at some cancers that have no somatic mutations. Greenman showed this, Baker,
20:01Parsons, and everyone—those are big papers. So you say, “Wow, look at that!” They found 30%
20:08of breast tumors using a very powerful genomic sequencing analysis had no mutations, yet some
20:14other breast cancers had thousands and thousands of mutations. I was looking for how you explain that in your somatic mutation theory. Nothing. The same with Parsons—they couldn’t find,
20:24in one of the glioblastoma papers, patients that had no mutations in any of the major signaling cascades. Well, interesting. Now, new data are showing us that these
20:37cancer driver genes are abundant in all of our cells that never become cancerous. It’s
20:43unbelievable! So if we took samples from all of us, we’re loaded with driver mutations. You go down to Dana-Farber, and they say, “Oh, we’re going to start radiating and poisoning you—you’ve
20:50got all these mutations.” And you say, “Well, what’s wrong with me? I’m perfectly healthy.” “Oh no, you’ve got the driver mutations.” This can also account, in part, for why when
21:01you give immunotherapies to some people, the immunotherapy sometimes kills you before the
21:07cancer does. The problem is, of course—and Martin Karis pointed this out—okay, we’re going to
21:13target precisely that mutation, precisely that epitope, but oh—my kidney also has that. Well, we’re going to take your kidney out along with the cancer. What’s going to kill you faster?
21:21We’ve got what’s called hyper-progressive disease, and it’s a well-known phenomenon in cancer. Some cancers don’t cause mutations, like asbestos, right? Asbestos—the rarity of
21:34cancer in Aboriginal tribes. People who live according to their traditional ways,
21:40like these Africans and Inuits from the Arctic—the British were shocked. Albert Schweitzer couldn’t
21:47figure it out. He looked at 10,000 Africans through his lens—nobody had cancer. It was strikingly different from the Europeans. The Inuits—I went to medical school at Thunder
22:02Bay, Canada, and they service the Inuits. They’re massively unhealthy—obesity, diabetes, dementia,
22:12all kinds of things. And yet, 100-150 years ago, they were some of the healthiest people on the planet. All they did was eat meat and fat—they weren’t eating vegetables or fruits or much else,
22:23except seasonally. It’s very interesting: when the western diet and lifestyle enters your population, brace yourselves—you’re
22:31going to have all kinds of chronic diseases. And of course, our closest biological relative,
22:37the chimpanzee, which is 98% similar to us in gene and protein sequence, has never had a documented
22:43case of breast cancer in a female chimpanzee. Breast cancer is a big problem in humans,
22:50but there’s a stark difference here. The chimp is living according to its diet and lifestyle,
22:57whether it’s in the forest, or at Franklin Zoo down here in Boston, or in the San Diego Zoo. I
23:04was at the San Diego Zoo, and I said to the vet, “Why don’t you get a big box of jelly donuts for
23:13these things? I’m sure they’d like it.” “Oh yeah, they’d like it, but it’s very unhealthy.” I said,
23:18“Well, I’m standing here eating a jelly donut!” You know, we’re not allowed to do
23:27these kinds of experiments on chimps—it’s called animal cruelty. Can you believe it?
23:32So, I checked—go down there yourself and ask the vet. Now, the nail in the coffin came from what I simply did: I went out and looked at all these
23:41studies that transplanted the mitochondria or the nucleus from tumor cells into normal cells
23:47and moved both nucleus and mitochondria back and forth between different cells. I didn’t do these
23:52experiments—what I did, for the very first time, is reinterpret the data that’s already
23:58there in a different light. And I published this paper—I actually did it in my book in 2012,
24:04and then this was in 2015. It’s got over 100,000 views and downloads right now.
24:11This is the very simplistic summary of dozens and dozens of replicated experiments. Replicated.
24:20So green cells get other green cells, normal cells get normal cells—the nucleus is healthy,
24:27the mitochondria structure and function are healthy, and they produce cells that are regulated
24:32in their growth during normal turnover. Red cells are tumor cells. Tumor cells
24:38beget tumor cells, and tumor cells have genetic defects—that is true. Some don’t,
24:45but many do. They also have abnormalities in number, structure, and function of the mitochondria. So what is causing the disregulated growth? Is it the mutations in the nucleus, or is
24:56it something in the cytoplasm—abnormalities in the number, structure, and function of mitochondria?
25:01When the red nucleus from the red cell is placed in the green cytoplasm—this was done by Israel and Schafer, in vitro and in vivo—they got regulated growth, which left them scratching their heads.
25:13Then they took the nucleus from the normal cell and put it in the cytoplasm of the tumor cell,
25:18and they got disregulated growth. This is just the opposite of what you would have expected if driver
25:25genes were controlling disregulated cell growth. Newer experiments now—if you take the green
25:32mitochondria and purify them and put them into the red cytoplasm, you get regulated growth. If
25:38you take abnormal mitochondria and put them into indolent cells, they become explosive. Clearly, what nature is telling us is that this is a disorder driven by mitochondrial
25:50dysfunction, not by nuclear mutations. If somatic mutations are not the origin
25:56of cancer, then how do cancer cells arise? We need to know the answer to this, and this goes back to the work of Otto Warburg, the German scientist. There’s a fascinating book written
26:05by Sam Apple. Warburg was a Jewish scientist whom Hitler spared because Hitler feared cancer
26:14and hoped Warburg would cure cancer someday. What Warburg actually found is that cancer arises
26:21from chronic damage to cellular respiration. We’re all breathing, getting our oxygen through
26:30oxidative phosphorylation—this is what we’re working on. Substrate-level phosphorylation is a non-oxidative form of energy. You move a phosphate group from an organic molecule onto ADP to get
26:38ATP—it’s different from oxidative phosphorylation. It’s an ancient pathway. These are the ways cells got energy before oxygen came into the atmosphere two and a half billion years ago.
26:48Cancer cells upregulate these ancient substrate-level phosphorylation pathways. Cancer cells continue to ferment glucose in the presence of oxygen—aerobic fermentation shouldn’t
26:58happen. This is called the Warburg effect. There’s a lot of confusion about the Warburg effect. Our big contribution to the cancer field is that we now know that amino acid
27:10glutamine—the most abundant amino acid in our bloodstream—can also be fermented in cancer
27:16cells. This is different than what everybody thought—they thought it was respired. Derek Lee,
27:22sitting here, has some of the strongest evidence of that. We’re working with Christos
27:28Opoulos at Semmelweis University in Budapest, Hungary. He’s the world leader on substrate-level
27:34phosphorylation in the mitochondria, and we’re now doing research. Warburg didn’t know about this.
27:40They threw Warburg under the bus when Watson and Crick discovered the gene. Everyone said, “Oh,
27:46these tumor cells are full of mutations.” But Warburg was essentially right—he just
27:51didn’t have all the parts of the puzzle. We’ve now connected the dots and shown that he was essentially correct. Enhanced fermentation is the
28:01signature malady of all cancer cells. If you look at a tumor and you go down
28:06and get the woman to look at all the different mutations, every cell in that tumor has a different constellation of genetic mutations—they’re not all the same.
28:14This breast tumor, that breast tumor—they’re all different from each other. Nobody has the same mutations, even within the same tumor—all the cells are different from each other.
28:20But one thing is common to all of those cells: they are fermenting. They’re getting their energy from a non-oxidative source. So the key to managing cancer is to take away the fermentation
28:31fuels. I mean, it’s not complicated, and you’re going to come to realize that.
28:37So what’s the evidence? Are you sure about that? Well, let’s look under the electron microscope, because that’s where you can really see mitochondrial structure. You can isolate
28:46them and look at their function. So, the cells—those nice, beautiful stripes—they are the cristae. They contain the proteins and lipids that drive the
28:56electron transport chain. Chris showed a picture of the electron transport chain. That’s a healthy
29:02mitochondrion. The one on the right—that’s a glioblastoma mitochondrion, deadly brain cancer.
29:07You can see the cristae are missing—it’s called “cristalysis.” Structure determines function.
29:14It’s an evolutionary conserved concept—if the structure of the organelle is abnormal, the function of that organelle will be abnormal. Now, what about breast cancer? On the right,
29:24the healthy cells, there are normal breast cells—nice, beautiful stripes of the cristae.
29:31We brute-forced these mitochondria—we took out all the lipids, analyzed everything in incredible
29:36molecular detail. The cancer cells have a very abnormal lipidome, and you can see the vacuoles
29:43in the breast—the spots there are vacuoles. Colorectal cancer mitochondria—these are empty
29:48of cristae. Structure determines function. Now, what I did is I went back and looked
29:56at all human cancers that we have studied over the years, decades from the 60s, 70s,
30:0280s. In the early days of electron microscopy development, people were looking at everything
30:08and recording what they saw. So I just went back and said, “Look at this, guys—they’re seeing all these different cancers with abnormal structure and function in the mitochondria.”
30:18All of it represents over 90%—bladder, breast, colorectal, gliomas, blood cancers, liver,
30:25melanomas, osteosarcomas, pancreas, prostate—they’re all similar. They
30:30all have problems—abnormalities in the number, structure, and function of the mitochondria. In our most recent study with Dr. Tea, we put that together. When you can’t respire, lipids can be
30:43deadly because they’ll create reactive oxygen species (ROS) and potentially kill the cell.
30:49So what the cell does is evacuate them—they put the lipids in these lipid droplets (LD). That’s a
30:58sign that the mitochondria aren’t working, because if they were, they’d use those fatty acids. They’d explode from the ROS. So, to protect the cell from death, they store them in these droplets.
31:08We went through all the major cancers—colorectal, breast, blood
31:14cancers—they’re all storing lipid droplets. It’s a marker for deficient oxidative phosphorylation,
31:20meaning that those cells need to ferment. What do they ferment? Glucose and glutamine. Right?
31:28How come nobody’s targeting the glucose and glutamine? Too simple. Very simple. Can’t do simple things. So when we look at energy metabolism in
31:38normal cells, here’s a very simple overview. Glycolysis—called the Embden-Meyerhof-Parnas pathway—is documented well. Glucose is metabolized through a 10-step process to
31:48pyruvate. Pyruvate goes into the Krebs cycle, fully oxidized, producing reducing equivalents
31:55like NADH and FADH2, which deliver their electrons to the electron transport chain, and we get tremendous amounts of energy with waste products of CO2 and water. CO2
32:08and water come right out. We also get a little energy from substrate-level phosphorylation.
32:13These are the ancient pathways that existed for energy metabolism before oxygen came into the atmosphere. The cancer cell, though, you see
32:25the shift. You get a lot of energy now from these ancient fermentation pathways—called
32:30substrate-level phosphorylation—and you can see that. We’re not really sure of
32:35the percentage—that’s one of the debating points where we’re not sure. But energy through oxidative phosphorylation is neither necessary nor sufficient for driving disregulated cell growth.
32:46Glucose and glutamine fermentation in the cytosol and mitochondrial substrate-level
32:51phosphorylation are necessary and sufficient for driving disregulated cell growth.
32:56I don’t want to bore you with these. We love these things, you know—we could spend hours looking at this stuff. But you can see glycolysis and glutaminolysis—those are
33:04the two driving pathways that provide the energy for disregulated cell growth and the
33:10metabolites needed for new growing cells. You see these starbursts here—glutamine,
33:16glutaminolysis, glycolysis, and energy. These cancer cells are, in fact, taking in oxygen, okay,
33:23but they’re blowing out reactive oxygen species (ROS) that are carcinogenic and mutagenic. So, we’re not getting very much energy from oxidative phosphorylation. We’re getting more energy from
33:30substrate-level phosphorylation, with succinic acid and lactic acid as waste products—not CO2
33:36and water, but succinic acid and lactic acid. And we’ve measured that—Derek’s measured that.
33:41Now, this is Derek’s gift to mankind. He put a lot of energy into this. Derek,
33:47stand up there! Let people see who you are! There he is, right there. So he put a lot of energy into this, and we thought about how we’re driving disregulated cell growth
33:59through using glucose and glutamine as fermentable fuels. Derek came up with the idea that this is a high-throughput system. These cancer cells are sucking down these two
34:08fuels in enormous amounts relative to normal cells, and they’re blowing out lactic acid and
34:13succinic acid into the microenvironment. You know, one of the biggest things in oncology is: “My immunotherapies don’t work. My chemo doesn’t work. My radiation doesn’t
34:22work.” There’s so much acidification in the microenvironment, it’s blocking all these things from working. Where’s the crisis? Where’s it coming from? Glucose and glutamine.
34:31If I take away glucose and glutamine, these things now become vulnerable. But nobody’s doing that,
34:36right? Nobody’s doing that. But anyway, Derek showed all the linkages—these two powerful pathways are feeding off of each other in a synergistic way,
34:45driving the disregulated cell growth and the metabolites needed to make new cancer cells.
34:52And then we put this together. Okay, we’ve got the beautiful normal mitochondria on the left, and over time, chronic disruption of oxidative phosphorylation leads to ghost mitochondria.
35:01The Delta G prime of ATP—this is the key that you have to know—that is underlying the energy efficiency. So, we’re keeping the energy efficiency, but we’re shifting.
35:10The green line goes down—that’s oxidative phosphorylation. Then there’s a protracted increase in substrate-level phosphorylation. To bring Einstein back again, substrate-level
35:19phosphorylation is linked to malignancy as strongly as gravity is linked to the red shift.
35:27Anybody know what Einstein’s red shift is? The pull of gravity on photons? It’s an unbelievable
35:33thing. That’s how strong the linkages are. So we can now put all the parts of the
35:38puzzle together again. The common pathophysiological mechanism for cancer is damage to the mitochondria. That damage can come from radiation, chemical carcinogens,
35:47intermittent hypoxia, systemic inflammation, rare inherited mutations, oncogenic viruses,
35:54older age. Every one of these things impacts negatively on the structure and function of the
35:59mitochondria, producing reactive oxygen species (ROS), which are carcinogenic and mutagenic. So,
36:05most of the mutations that we see in the nucleus of the tumor cell are downstream effects of mitochondrial damage and dysfunction. Yet we’re chasing tails—we’re not chasing the origin.
36:14So ROS go on, now the oncogenes turn on, and their floodgates—those are the high-throughput pathways of glycolysis and glutaminolysis—are driven because the mitochondria are suffering.
36:24So how is the cell going to survive? It has to get an alternative energy. The alternative energy is substrate-level phosphorylation, driven by glucose and glutamine.
36:32Now, we can take all of the hallmarks of cancer produced by Robert Weinberg and
36:40Hanahan and link every one of those back to dysfunctional failing mitochondria.
36:47Now, there’s a book—Sid Mukherjee wrote The Emperor of All Maladies. Mukherjee struggles
36:59in the book: “I don’t understand what’s the common pathophysiological mechanism. I don’t understand.” And the end of the book is very bleak. Read it—it’s very depressing. I said,
37:10“For Christ’s sake, didn’t you read some of our papers? You wouldn’t have been so depressed. You should be on a ketogenic diet or something!” Now, if most cancer cells obtain energy through
37:27fermentation, what therapies might be effective for managing cancer? Well, one approach is to target those fermentable fuels. Now, I’m going to show you the evidence. I’m going
37:36to show you the power of predictability. As Greg would say, “If you’re on the right path, you should be able to predict something,” right? So, here’s the strategy: metabolic management
37:48of cancer, following changes in plasma glucose and ketones. Let’s lower the glucose—water-only
37:54fasting. I’m going to talk about that in a minute. Calorie restriction, restricted ketogenic diets,
38:00and then raise ketone levels, because it’s the glucose that’s driving the disregulated growth. Now we’re going to give them fatty acids and ketones to choke on, right? And not only that,
38:10it’ll make the rest of your cells healthy. We’re going to increase the Delta G prime of ATP hydrolysis. This is the key to why ketones are effective—they increase your Delta G prime.
38:24Now, look at this: the ad libitum mouse is given all he likes—let him eat as much as he wants. The
38:30other group is the calorie-restricted group, restricted by 40%—calorie restriction three days post-inoculum. And you can see we got a huge reduction in the size of that tumor. It’s
38:40obvious. People say, “Wow, all I have to do is cut my calories back by 40%?” No, wrong. Forty
38:47percent in a mouse is water-only fasting. Do you have another option? There’s something else you
38:52can do? You know, they don’t want to water-only fast. You can’t get people lining up for that, but anyway, the mouse had no choice. We put him in a cage, and we just give him what we want.
39:02Now, here’s something I want to share with you for Greg’s amusement. He doesn’t know about this. When
39:12he first saw my book, what does he do? He turns it over to his father to ask if I’m right! Funny,
39:20right? He suffered having to measure nail lengths as a punishment when he was a kid. So what he did
39:27to me, he punished me by giving his father my book and having him eviscerate my data.
39:34All these red lines are Jeff Glassman’s critique. I had to sit down and spend days
39:40paging out exactly what we did, how many mice, I gave him the raw data from the experiments,
39:46and I let him look at it. I explained every one of his little red lines there and what he was concerned about. I did paraphrase—Perna said to me, my other staff member, “Boy,
39:57this is a smart guy, but we’re not that dumb!” So, we had to spend our time going back to address
40:04every one of Jeff’s criticisms. Finally, he writes me a letter, “Maybe you did more satisfactory work
40:12than I thought.” He actually accepted what I said. I got it. I got it better than you! He actually
40:20thought you understated your case mathematically. Well, he might be right about that, but I wasn’t
40:26understating. I had to present it the way we looked at it. But it was a great experience and exercise for us to look at how someone else’s brain would view the information,
40:38and if we were able to communicate the information back and forth to satisfy both groups.
40:43Yeah, you know, regardless of what he said, I was kind of done with it at the nuclear and mitochondrial transfer experiments. That was enough. But for a lot of people,
40:54it wasn’t. But you tell me—you’re the guy with all the answers, right?
41:01No, I don’t know either. It’s called confirmation bias—dogma. Dogma. You can’t change religion in people. Yeah, well, I put everything out there,
41:16and people still say cancer is genetic. What are you gonna do? Anyway, we got a lot of work from Jeff’s criticisms. When you have people that are
41:25not directly in your field, and they see the data, you have to examine how they are viewing this information. Therefore, our explanations need to be more clear and accurate
41:36to make others recognize what we’re doing. I thought you’d enjoy that because we had to spend a lot of time addressing those issues. But anyway, predictability, which is very
41:47important. Each square is a mouse under a different dietary condition. We did linear
41:56regression analysis, which is actually choosing one as the cause and the other as the effect. So, glucose was the independent variable—beta-hydroxybutyrate is the ketone body
42:06in the blood—and the tumor weight is the size. What we see here on the left is that as blood sugar goes down in these animals, ketones go up. This is an evolutionary conservation of
42:17energy—when you stop eating, if the brain doesn’t get energy, you’re going to go unconscious. So the body mobilizes fat, turns it into ketone bodies—water-soluble fat breakdown products.
42:26And that’s clearly related to low insulin, higher glucagon, more ketones. But on the right, you’ll see that as the glucose goes down, the size of the tumor goes down. The tumors got
42:35smaller as the blood sugar went down. The higher the blood sugar, the faster the tumor would grow.
42:42This is the first evidence in the scientific literature that I’m aware of, predicting that the rate of tumor growth is linked directly to blood sugar. Since this has been pointed out,
42:52we’ve seen it in glioblastoma, colon cancer, breast cancer, bladder cancer—all the different cancers that have been looked at. The higher the blood sugar, the more likely
43:02the patient will die sooner. There is definitely a predictability in cancer for blood glucose levels.
43:10Now, what we did—based on a lot of interaction with cancer patients—is
43:15build the glucose-ketone index (GKI) calculator, which is a quantitative assessment of the ratio of
43:23glucose to ketones. Glucose is usually measured in deciliters—we convert that to millimolar,
43:29and then we measure ketones, so you have this GKI. What we’ve determined is that levels
43:34of 2.0 or below put one in nutritional ketosis. And what is nutritional ketosis? It’s essentially
43:41the way we existed during the Paleolithic period. We didn’t have highly processed carbohydrates in our diet—we had a lot of exercise, and almost no highly processed carbohydrates. We had to move a
43:54lot. We ate predominantly low-carbohydrate plants and animals—mostly animals.
44:03What we’re doing is simply taking people back to that. People ask, “What do I have to eat to get a GKI?” You can do it with a ketogenic diet, a Mediterranean diet, a pescatarian diet—you can
44:11do it with any kind of diet. Each person will have to adjust for themselves, whether it’s cultural,
44:16religious, or whatever, to get their GKI. I built this for the glioblastoma patients,
44:23and then we switched it to all cancer patients. But now, as a prevention of cancer,
44:29healthy people like these CrossFit folks and others want to see how low they can get their GKI. My good friend Dominic D’Agostino lives in this environment constantly. It’s a very good way
44:43to prevent cancer as well as manage it. Now, what we did here was we took the concept of “press-pulse” from paleobiologists. They use it to describe the destruction of
44:58plants and animals on the planet, but we actually adopted the concepts. We have press therapies and
45:03pulse therapies. Press therapy—you put patients on restricted ketogenic diets, water-only fasting,
45:09that kind of thing. Even ketone supplements. Stress management, like Chris was saying, is very important because when you’re under stress, glucocorticoids go up. So, you’ve got
45:18to keep your glucocorticoids down, reduce stress. A lot of people with cancer are freaked out—they
45:24all think they’re going to die. So stress management is very important—it lowers glucose, makes the metabolic therapy work better. Then you come in with dosed timing and
45:34scheduling of glucose targeting, glutamine targeting, and hyperbaric oxygen,
45:39which can eventually replace radiation for killing tumor cells. Hyperbaric oxygen kills tumor cells by producing ROS, but it enhances the health and vitality of the normal cells
45:49while selectively destroying the tumor cells. So we move the patient from a diseased state to
45:54a managed state, and then, with improvements in dosed timing and scheduling, we can move from management to a state of resolution. Dr. D’Agostino is also working in my lab. We have
46:06a major paper under review right now in a major medical journal, with more than 20 MDs and PhDs,
46:15for the metabolic management of glioblastoma. This is the framework, but the nuts and bolts of how
46:21to treat cancer patients on a day-to-day basis, and all the things you might encounter in trying to treat individuals—personalized nutrition, all of these kinds of things—are in that paper. So,
46:32when that paper comes out, there’s no excuse for anybody not to treat cancer patients, because here’s the “how-to” manual to do it. Let me talk just a little bit about
46:42glioblastoma—terrible brain cancer. This is what killed John McCain, Ted Kennedy, and Bo Biden,
46:50the president’s son. It’s a terrible disease. You can see how bad the brain looks—the patients die
46:57from intracranial pressure. Those purple cells on the right—those are the tumor cells. They go
47:03across the surface of the blood vessels, called Virchow-Robin spaces, and they seed the entire
47:08brain, even though you can’t see the tumor cells. You see only this discoloration in cystic areas, but the tumor cells are out there. That’s why they always say, “We can never get all the cancer, it’s
47:18always there to some extent,” because the tumor cells have already seeded out into the parenchyma. Now, here’s another very interesting thing—let me just talk about predictability. Emily,
47:35didn’t you say that Greg talks about failure to replicate? Well, nothing is more replicable
47:41than how fast you’re going to die with a GBM (glioblastoma). Look at these survival
47:47curves—this is five surgical institutions. You can’t design more replicable survival data than
47:53this. All these—and we can go all over the world to every major brain cancer center—you’re going
47:59to get a survival curve that looks like that. Highly replicable. We just heard about how
48:06hard it is in the oncology field to replicate data—look how replicable this is. And there hasn’t been any improvement in 100 years. In 1926, the median survival was 8 to 14
48:16months. In 2024, the median survival is 8 to 16 months. What’s going on? We’ve
48:23got the Webb telescope for crying out loud, and we can’t move the needle on glioblastoma? Why? What is going on? Why are we not moving the needle in survivability for this cancer?
48:36We published this paper, and you ask me why people don’t listen to what we’re saying. When you debulk
48:42the tumor—cut it out en masse—you create a wound. Then, as soon as the patient wakes up, you start irradiating them. That breaks apart the glutamine-glutamate cycle in the brain, freeing
48:51up massive amounts of glutamine—the fuel. That’s one of the two fuels! And when you irradiate the
48:57brain, they give you high-dose steroids to reduce the inflammation, which gives you hyperglycemia. I just showed you—the higher the glucose, the faster the tumor is going to grow. It’s
49:07obvious. The two fuels driving the disregulated growth are created by the standard of care.
49:14What we’re doing to these poor people is denying them, for the most part. You saw how replicable it
49:21is because everybody on the planet is getting the same treatment—there are no differences. Standard
49:27of care happens in India, Germany, Japan—all over the world, they’re doing the same thing.
49:32This is explainable—it’s explainable because you’re not allowing the person’s brain to
49:38recover from the surgery and targeting the glucose and the glutamine simultaneously. So we developed the therapy using the VM3 glioblastoma mouse model, which has all the growth
49:49characteristics that we see in human GBM. And we use this drug DON—6-diazo-5-oxo-L-norleucine,
49:58which is a glutamine analog. The glutamine analog looks like glutamine and blocks glutamine
50:04utilization. So we put the mice on a ketogenic diet, lowering blood sugar and elevating ketones.
50:12I can spend hours with you, but the overall success is survival. Survival is success.
50:20What you get is—the blue line is the untreated mice, dying fast. The green line is the diet by itself. The red line is the drug by itself. And the purple line is when you combine the diet
50:30with the drug. You can see how powerful it is. We tried this on an Egyptian guy—he did really
50:37well at the beginning, but they insisted on irradiating him. I said to Elsaka,
50:45the attending physician, “The guy’s doing great! He’s back in the field, he’s a corn farmer, he’s a young guy!” “Oh no, we’ve got to irradiate him!” I said, “Jesus!”
50:54Anyway, I’m here in Boston, he’s there in Alexandria, Egypt. I ask, “How’s the patient?” “He seems to be doing okay.” We published the paper. Then, at 30 months of age,
51:03he starts getting headaches. He dies at 30 months of age. When they did the autopsy,
51:08he had died from liquefaction of the brain due to radiation poisoning, not from the tumor.
51:18It was very disheartening to me. Then I also wrote this paper, “Provocative Question,” for Harold Varmus, who runs the NCI. He had provocative questions—“change the standard
51:30of care for GBM.” Oh, can’t do that, right? Anyway, we’re not going to move the needle
51:36until we stop irradiating the brains of these poor GBM patients. I say that in the big treatment paper as well—radiation brings huge amounts of revenue. Follow the money.
51:48Once we have this protocol, the one we’re writing is going to have a major impact if we can stop radiating these poor folks. I always show this one—poor Brittany Maynard,
51:57remembering Brittany. She was a young woman, January 2014. Here she is with her husband,
52:03right after they got married. She gets a glioblastoma, actually from a lower-grade tumor that exploded into a GBM. She puts her story in People magazine, “I’m going to kill myself rather
52:13than take the standard of care.” But you can see her face is swollen—that’s moon face from the
52:19high-dose steroids. When you give people high-dose steroids, they get this thing called moon face. So she dies with dignity with her family on November 1, 2014.
52:29Now, this is our man Pablo. We wrote a case report on him. He came to us the same year as
52:35Brittany—glioblastoma, no radiation, no chemo, no steroids. He didn’t want any of that. The
52:41attending physicians told him, “You’re going to be dead, Pablo, in nine months—start getting your affairs in order.” He said, “The hell with it!” He wanted to have kids. He said, “If I
52:49take radiation and all that stuff, I’m not going to have kids. I won’t even live to have kids.” So, he rejected that, and I’m going to talk about him in a minute. He survived
52:58with good quality of life until just this month. But anyway, we look at his brain tumor. You can
53:04see it when it was this big thing with the arrow, then in 2016, you can see it’s bigger. He had his
53:10first debulking surgery in early 2017. It grows for another three years, and it’s cut out again.
53:35In the meantime, he gets married, he has one child, he has two children.
53:42We found out that, in addition, he had the IDH1 mutation, which actually inhibits the
53:47glycolysis and glutaminolysis pathways, giving him a survival advantage—slight. I don’t have
53:54time to talk about that, but if anybody’s interested, I have the crew here that can go into a deep dive on that. But the idea is, Pablo did have an advantage—he used a special
54:02diet and lifestyle together with God’s gift of a therapeutic mutation. Not all mutations are bad.
54:09Now, here’s Pablo. Thomas and I had a discussion with him in August,
54:14and we were laughing about Pablo surviving 10 years, which was… He had survived four
54:24operations on a previously inoperable tumor. So we had a big laugh about this—“Pablo,
54:30how many more? Are you going to outlive me? Are you going to have 20 operations on your head?” We were laughing—he was perfectly healthy, there was nothing wrong with Pablo. Then two days later,
54:39after that conversation, to our surprise, they say, “Oh, we want to go in again. There’s some
54:44residual—we think we can get it out.” So he comes out of the operating room—thumbs up,
54:50talking and everything. Then 12 hours later—cerebral hemorrhage, dead from the operation, not from the tumor. He was our poster child for how long you can
54:59live with glioblastoma. Everybody was looking at him for hope, and everything… Poor guy.
55:06And then I know poor Danny Sheehan, from Marshfield, Massachusetts, right down here on the coast. He was diagnosed in 2017 with pineoblastoma. It goes through the
55:16spinal cord and everything. You can see his fat face from all the steroids, radiation, everything they gave this poor little kid. Then he died in 2021 from standard of care.
55:26Now, because of that, we got a grant from a British UK Childhood Center to study childhood
55:32cancer, thankfully. We developed the pediatric high-grade glioma model in our lab—Per, Muki,
55:38and myself—where we can put tumors into the brains of young mice, at the same age as Danny Sheehan
55:43and other little kids, and we could see the tumors going down the spinal cord. We replicated key aspects of pediatric oncology in these mice. Now, I don’t know if I can—yeah, maybe I can get
55:55it. So, you can see the difference. The guys on the left are the ones that were not treated with
56:02metabolic therapy, and they’re all going to die—one has already died. But you can see the ones on the right—we gave them ketogenic diet, Bendamustine, and DON, targeting glucose and
56:12glutamine simultaneously while raising ketone levels, and we’re keeping these guys alive.
56:17This is going to be a blockbuster in the pediatric clinic, but they don’t use it
56:23because cancer is a genetic disease, haven’t you heard? It’s unbelievable.
56:29This woman here was treated by Ikiki, of this clinic in Istanbul, Turkey, and you can see she
56:38was from Ohio. She had breast cancer that spread to the brain and many other organs. All those dark
56:44spots are the spread of the breast cancer. They gave her metabolically supported chemo
56:50for managing it. They said she had one month to live—”Get your affairs in order, radiation, chemo,
56:57did all these horrible things to her.” Nothing was working, so she jumped on an airplane, went to Istanbul, and almost died in the ICU for two and a half weeks, according to Abdel Slok told me.
57:08Then they put her on this metabolically supported low-dose chemo—very low doses, we’re not throwing out anything. Like Chris said, we’re not throwing everything out—there are some
57:15things that can work if you do it the right way. Anyway, here she is celebrating her life with her
57:20husband in Hawaii in 2021. Last week, I had to call because I know people are going to ask me,
57:26“What’s going on with the woman?” So I called up Slok. I said, “Abdel,
57:31how’s this woman doing? I don’t want to say…” “Oh no, she’s fine. She sent me a nice letter thanking me for all the wonderful life she’s had.” She was a goner, but she’s doing fine.
57:40We got this guy from Greece—he had lung cancer that spread to the brain. Restricted ketogenic diet, primary lung cancer. Amazing guy—he’s doing fine, he’s out 10 years.
57:50I wrote a puff piece for Nature on how we can manage prostate cancer—I did all these things. And then, of course, the dogs. Jimmy’s dog, with the big blueberry tumor on his face.
58:02This woman came to me and said, “Can you publish this, right?” So I had to drum up a veterinarian to make it look like… Lauren Nations is a friend of mine. I said, “Lauren,
58:11come on, join us,” because I’m not a vet. In fact, the woman treated her own dog. This was a mast cell tumor on the dog’s nose. The first thing she did was say, “Okay,
58:22no more carbohydrates for you, poor dog.” It’s a pit bull. So, what happens is that it shrinks
58:28down. She gave it raw eggs, raw chicken, fish oil, and 40% calorie restriction, just like the mice.
58:35And lo and behold, the tumor disappears. Here’s the dog in 2013 and in
58:422016—completely healed. They said, “Oh, you’ve got to have radiation and chemo, it’s going to cost a lot of money, the dog will be very sick, diarrhea, all kinds of stuff.” She said, “No,
58:49I don’t want that.” So no surgery, no radiation, no chemo. Look at this—the dog died at 15 and
58:55a half years of age from heart failure. It didn’t die from the therapy—in fact, the therapy kept the dog alive even longer. And don’t forget, I published this on autolytic
59:05cannibal autophagy, like Chris was saying, where you rearrange mitochondria and organelles within the cell. But there’s also autolytic cannibalism. When you put the body under nutritional stress,
59:15every cell in your body has to justify its existence to function as a whole. You’ve got a tumor, those cells aren’t functioning well—eat them. So the body will turn on them
59:26and attack and eat the tumor for the good of the survival of the whole. We have stage 4 cancers—we don’t consider terminal cancer anymore. This is not right.
59:37If you do metabolic therapy, we don’t know whether you’re going to die or not.
59:42There’s this book, Cancer Revolution, by Maggie and Brad Jones. Maggie is a long-term survivor of lung cancer that spread to the brain, and she is collecting all these folks. She’s got a
59:52registry of all these people who are alive, who should have been dead, and she’s got
59:57dozens—“I’m alive! I’m alive!”—she’s got all these people that are doing various therapies. We haven’t even standardized this yet, folks. Once we standardize this,
1:00:06we’re going to drop the death rate on cancer by 50% in 10 to 15 years. The problem is,
1:00:12how do you get through the wall of obstacles that say you can’t do this? Everything is “You can’t, you can’t, you can’t.” Remember that guy telling us, “You can’t do that.” The hell we can’t! These
1:00:21people need to live, for Christ’s sake! Yes, the mitochondrial metabolic theory
1:00:30can explain better the origin and management of cancer than the somatic mutation theory. When are we going to get rid of this noose on our neck with the somatic
1:00:37mutation crap? We can keep people alive. And yes, our conclusions—it’s not a genetic
1:00:46disease, it’s a mitochondrial metabolic disease, driven by substrate-level phosphorylation.
1:00:51And not only that—press-pulse ketogenic therapy for chronic diseases.
1:00:56We’re right about this. Chronic disease—it’s all related to the lack of exercise, too much
1:01:02carbohydrate. Get your GKI to 2.0! Everybody should have a 2.0 GKI. The hospitals would be
1:01:08running down the streets looking for somebody to treat! Everybody would be like a CrossFitter for
1:01:13crying out loud—they’d all be healthy. But no! You know, we have a picture in the lab. It says,
1:01:19″Pills and surgery,” and you have a hundred obese people all lined up trying to get the pills. Diet and lifestyle change? One guy in the line! So, you know, we’re up against a tough sell.
1:01:30We’re having a global society for cancer metabolic therapies. We’re collecting collaborators from all
1:01:35over the world. We want to set up clinics. We have people talking to us, saying, “Okay,
1:01:40once the paper comes out, how are we going to set up clinics? What are we going to do? What are the nuts and bolts of this whole thing?” And, of course, we have to thank so much of our
1:01:48support—Greg, Broken Science, and yes, CrossFit when Greg ran it. That was definitely helpful to
1:01:55us. Broken Science, the Corkin family for sure, philanthropy from Maroon and Edward Miller,
1:02:02Kenneth Rainin, Children with Cancer United Kingdom. Our university has been helping us tremendously. Delaware County—the deputies have been helping us. This
1:02:09fund is really a blessing for us. And in the past, the National Cancer Institute and the NIH supported us. So, I thank you for your attention,
1:02:16and I’ll be happy to answer any questions if there are any. Thank you.
