 Now, right now there's two schools of cancer that are kind of duking it out. There's the traditional cancer is a genetic disease where you get a bunch of mutations and it turns a normal cell into a cancer cell that starts proliferating everywhere. And the other is the so-called metabolic theory of Otto Warburg that is now being picked up by other people like Tom Safebreed who say that cancer is a metabolic disease due to an addiction to glucose and that addiction to glucose is because of mitochondrial damage. If they can't use the mitochondria it's stuck using glycolysis. And what I'm going to be showing is that they're both wrong and they both not only are wrong but they both cannot be right. And for that I want to start out by un-teaching you. So here it says the most useful piece of learning for the uses of life is to unlearn what is untrue. Our ability to open the future will depend not on how well we learn but on how well we are able to unlearn. And that will also determine how many more people die unnecessarily from faulty cancer treatment and faulty cancer research. We spent half a century on the war on cancer and have made almost no progress as far as cancer being a genetic disease and trying to figure out which genes cause cancer that got us nowhere. And I'm afraid that the current theory on mitochondrial damage causing cancer will follow the same road. And I want to prevent that. So is cancer a genetic disease caused by the accumulation of several oncogenic mutations? And here we show that patients in leukemia could be divided into 11 classes and each of those classes had unique genetic profiles. In other words almost every case of cancer has a unique genetic array of mutations. There aren't specific mutations for each cancer. And that's really important. So if it were a genetic disease we'd be out of luck because every disease then would be a different genetic disease. Here's another study in Cedars-Sinai which is right here or close to it. Investigators dramatically illustrates the complexity of cancer by identifying more than 2,000 genetic mutations in tissue samples of esophageal tumors. The findings reveal that even different areas of individual tumors have various genetic patterns. And I should mention that in non-cancerous esophagus they find almost the same thing. Is cancer a metabolic disease? I'm going to spend a lot more time on this one. A disease, especially a chronic disease of aging, like cancer, cannot be genetic or metabolic. To me it's a silly argument. If you look at the origin of life, the genetics of life and the metabolism of life came together. In other words, the genes do nothing. They have to be read. And we know about genetic expression. So the genes make proteins, that's all they do. The proteins regulate metabolic pathways which turn around to then control genetic expression. You can't have one or the other. They're always intertwined, just like life. Atta Warburg and the Warburg effect. And he basically says that cancer relies on glucose and aerobic glycolysis due to mitochondrial failure to grow itself. It was noted initially I found by other than Warburg, in other words Warburg effect probably wasn't even discovered by Warburg. But Warburg was very well known. He came from a very prominent German family in the turn of the century or 1900. His father was a physicist and good friends with Albert Einstein. So he had a ready voice. And he noticed that cancer produces and tumors produce lots of lactate, meaning they're using glycolysis. Glycolysis is a fermentation process that produces lactate. And he went on from there to notice that even if there were a lot of oxygen, there was a lot of oxygen available, cancer would still prefer to use glycolysis. And he and his current proponents assumed that cancer had to use glycolysis to make the copious fuel necessary to make all sorts of baby cancer cells. So even when there was plenty of oxygen available, they did not use their mitochondria. Why would that be? Why would cells not utilize mitochondria if they were healthy? Since they can produce in a given amount of time supposedly at least 16 times more ATP than glycolysis. And our typical healthy cells, if oxygen is available, will always utilize their mitochondria. So he said that cancer had to be due to mitochondrial damage. In fact, not just mitochondrial damage, but irreversible mitochondrial damage. And he was adamant about that for many, many decades. He espoused that. And then in 1950s when they found their first so-called oncogene, his theory kind of fell into disrepute or at least was kind of covered up and is now being resurrected as they're finding that the genetic theory of cancer is probably not right either. So there's four elements to Warburg's theory of cancer. Cancer cells have irreversibly damaged mitochondria. That because of the irreversibly damaged mitochondria, cancer cells must ramp up glycolysis. That this effect is unique to cancer and differentiates cancer from normal cells and that this causes cancer. We're going to look at all four of those. So number one, do cancer cells really have significantly and irreversibly damaged mitochondria? Well, it's well known that glutamine is a well-known fuel for cancer. Cancer gobbles up glutamine. And glutamine is metabolized in mitochondria. So that makes the scratcher head a little bit. If mitochondria damage, how can it use so much glutamine? Not just glutamine, but lactate. We mentioned that glycolysis is the fermentation process that produces lots of lactate. But then the cancer then eats the lactate. And here they say the researchers see that lactate is like candy for cancer cells and cancer cells are addicted to the supply of candy and indeed they are. And also I might mention that cancer uses lactate for other things too. It uses lactate to penetrate tissues and implantant tissues. So lactate is actually a really good thing for cancer. So it wants lactate. Taken together, our results demonstrate a link between lactate metabolism and the mitochondria of fermenting mammalian cells. In other words, lactate is utilized in mitochondria. They can't be too damaged. Ketone body utilization drives tumor growth and metastases. Nutrition deprived hepatocellular carcinoma cells employ ketone bodies for energy supply and cancer progression under nutrient deprivation stress just like us. You don't have a lot of nutrients. It just burns ketones. But the thing is ketones are also burned in mitochondria. In other words, mitochondria are apparently used for lots of things here. And not just ketones and not just lactate and not just glutamine, but fatty acids. Many cancers use fatty acids, especially those cancers that have a ready supply of fatty acids such as the omentum, the fat in the belly surrounding the pancreas, for instance, pancreatic cancer we know also utilizes fatty acid oxidation. Breast cancer uses fatty acid oxidation. And of course, fatty acid oxidation is done in exclusively mitochondria. In particular, the proliferative clonal expansion of cancer stem cells appear to require mitochondrial metabolism related to the reuse of ketones and lactate. In other words, cancer stem cells. We know now that cancer isn't just a single type of cell. It's a society. It's a colony of cells. And just like we have stem cells, cancer has stem cells too. And it's the stem cells really that perpetuate the cancer. And in particular, they're the ones that are instrumental in metastases and proliferation. And so our effort to research cancer in Petri dishes almost exclusively misses the cancer stem cells. Cancer stem cells are a tiny, tiny fraction, you know, fraction of a percent of all the cells. So when they take a biopsy and put it in a Petri dish, the chances of them even getting a single cancer stem cell is somewhat remote. And yet it's the cancer stem cells that are really instrumental in determining where that patient is going to die or live. And it's really the cancer stem cells that we have to focus on. And cancer stem cells have different metabolism than other cells. In particular, they use a lot of mitochondria. Mitochondroloxfos. And here they say they like to use ketones and lactate and fatty acids and anything that they can get. And ketones and lactate increase cancer cells' stemness, driving recurrence, metastases and poor clinical outcome in breast cancer. Lactating ketone promotes the cancer stem cell phenotype, resulting in significant decreases in patient survival. Consistent with the idea that cancer cells use their mitochondria to generate energy, the metastatic phenotype is directly associated with an increase in mitochondrial metabolism in cancer cells. An increase in oxidative mitochondrial metabolism in cancer cells is associated with tumor recurrence, metastases and poor clinical outcome. Here, oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. A lot to burn fatty acids. The oncogene ablation-resistant pancreatic cancer cells, by the way, is the most virulent kind that kills almost everybody. The entire premise of Warburg and its current proponents, such as Tom Seyfried, was, is based on the assumption that an uptick in glycolysis means reduced mitochondrial activity. They figure why would cells not use mitochondria if they were healthy? So the entire theory is based on the assumption that cancer is having to use glycolysis, but it can't use mitochondria. We'll see why it uses mitochondria anyway. But does an uptick in glycolysis even mean reduced mitochondrial activity? And here it shows no. The assumption is wrong. There's another alternative. And that is that this is what is typically thought that you turn up glycolysis and mitochondrial oxfoss is turned down. There's like a switch, one or the other. But here they're finding there isn't a switch, one or the other. It's both. Cancer is proliferative. It wants all the energy it can get, not just the energy, but the components that glycolysis makes during the pentosephosphate pathway is a component manufacturing pathway from glycolysis. It doesn't even use glycolysis for most of the ATP. It doesn't use it for fuel. It uses it to make components. It's like ribose to make genes and NADPH to make fatty acids and glutathione to prevent oxidative damage. There's two kinds of metabolism. It's not just how you're burning fuel. Thank you. Thank you. But also even more important for cancer or any proliferating cell is how rapidly you can accumulate the parts you need to make new babies. Here, limiting glycolytic ATP production fails to prevent tumor genesis, suggesting that the major role of glycolysis is not even to supply fuel, ATP. Many studies have demonstrated that the great majority of tumor cells have the capacity to produce energy through glucose oxidation in mitochondria. Moreover, mitochondrial metabolism is necessary for cancer subproliferation in tumor genesis, like we've seen. Thus, despite their high rate of glycolysis, most cancer cells generate the majority of their ATP through mitochondrial function. The observations that cancer cells simultaneously oxidize and ferment glucose has engendered confusion over the role of respiration, mitochondrial respiration in the Warburg effect, particularly as Warburg misinterpreted his own early observations and promoted the erroneous idea that damaged respiration is the synquanon that causes increased glucose fermentation and cancer. How many people have heard of Herbert Crabtree? Nobody. Herbert Crabtree was kind of an obscure English gentleman. People that know him are wine manufacturers. All wine manufacturers know about the Crabtree effect. And he lived virtually identical time as Ida Warburg. But Ida Warburg was, as I say, much better known because of his family. And he was German. And this was the heyday of German science. Everybody listened to the German scientists. And rightfully so. They were really smart. They did a lot of really great things. And here's little Herbert Crabtree noticing some things. And in 1929, so Herbert Ida Warburg started publishing his papers on mitochondrial damage causing cancer in 1926. 1929, Herbert Grace Crabtree states that Warburg postulates a disturbance of respiration, meaning mitochondria, as beating the fundamental cause of the development of aerobic glycolysis. Aerobic glycolysis again is when glycolysis is used even when oxygen is present. When typically cells would kind of switch over to more mitochondrial oxfos. In many of the tumors, the respiration is very high, exceeding that of any tissue, normal or malignant, so far examined. This respiration is ineffective in checking the aerobic glycolysis. In other words, they're both being used. He was right on. And nobody was listening. His cancer, the second part of Warburg's theory is that cancer is forced to use glycolysis. Well, we've already cast doubt on that, but we'll continue. Glycolysis has great advantages. Not just to make ATP, but first of all, it's anaerobic. And you can burn glucose without needing oxygen. So for those cancers that don't have enough oxygen, of course it uses glycolysis. But the pentose phosphate pathway is needed to make components that we've talked about. So it's a little detour. It's an anabolic pathway off of the catabolic pathway that manufactures ATP from glucose. You can also make ribose and other components that are really necessary for making any cell really. But here's a real kicker that even for fuel, you can make ATP far faster using glycolysis than mitochondrial oxfoss. And cancer is dividing rapidly. And if there's enough glucose available, it'll far prefer to continue to use glycolysis, whether oxygen is present or not, because it can make sometimes up to 30 times faster ATP than mitochondria. So in a given amount of time, given the resources, you can actually make more ATP using glycolysis than you can mitochondrial oxfoss. That's a little known. Also, I mentioned that cancer actually wants to use the galactic acid that it makes in fermenting glucose. Also, it's been shown now pretty interestingly that cancer purposely tries to steal glucose from white blood cells. It's competing with white blood cells. White blood cells are rapidly proliferating too. And we will show that they prefer glycolysis also. In other words, glycolysis, you'll see, is not just unique or aerobic glycolysis is not unique to cancer cells. It's found ubiquitously in all rapidly dividing cells. They all prefer aerobic glycolysis. And so we have white blood cells that are trying to kill the cancer and the cancer doesn't want to get killed. And one way that cancer can outpace the white blood cells and avoid being killed by them is to steal the glucose from them. So the more rapidly it can take glucose, the better off it will be. I mentioned this much faster. At least half the carbon atoms required for nucleotide synthesis are derived from the pentose phosphate pathway intermediate ribose phosphate ribose is made in the pentose phosphate pathway, the detour off of glycolysis. You can't make new genes, which means you can't make new cells without ribose, which means you have to use glycolysis. What this is telling us is that cancer doesn't have to use glycolysis because of mitochondrial damage or anything. Cancer, like all rapidly dividing cells, wants to use it. It's purposely going out of its way to use glycolysis. It doesn't care if oxygen is present or not. When it's rapidly dividing, initially, it's going to use glycolysis. And so the whole premise that cancer is using glycolysis because of mitochondrial damage, just gets thrown out the window when you find out that cancer is not forced to use glycolysis, but is actually desirous of it. Is the Warburg effect unique to cancer? Does it differentiate cancer from normal cells, which is the third part of Warburg's theory? The answer to that is absolutely not. It's in all rapidly dividing cells. It's in rapidly dividing white blood cells when they're called upon the T killer cells, the NK cells, all the cells that rapidly divide to try and fight an infection or cancer has an almost identical metabolism to cancer. Also, when we're a fetus, you start out sperm hits the egg and they start rapidly dividing. Same metabolism. And they use aerobic glycolysis. The Warburg effect is no Achilles heel. It's common to all rapidly dividing cells, including immune cells. Now mitochondrial damage, what Warburg noted, was correlated with cancer. I cannot tell you how many times correlation is confused with cause and medicine. You see that with cholesterol. You see it with calcium. It's all over the place. And in other sciences, you just don't make that mistake. But in medicine, it's made all the time. And this is just another example of it. Yes, mitochondrial damage may be correlated with cancer. But does that mean that mitochondrial damage caused the cancer? Or possibly did the cancer actually cause the mitochondrial damage? And we'll find it's actually the second. We have found that mitochondrial dysfunction in cancer cells correlates with abnormally increased mitochondrial replication. Okay, you have rapidly dividing cancer cells. That means you have to have rapidly dividing mitochondria. Rapidly dividing mitochondria has less quality control. You're going to have more damage to mitochondria. And indeed, also, that mitochondria are destroyed by lysosomal degradation leading to the production of highly energetic nutrients to support cancer cell growth. It's finally promotes the onset of robotic glycolysis in cancer associated fibroblasts because of the mitochondrial dysfunction. Translation. Cancer eats mitochondria from their neighbors. They're nice and nutritious. So when they're multiplying rapidly and they want to use glycolysis, there's no need for the mitochondria. They'll eat them. Obviously, producing fewer in number and some damage to the mitochondria because they're being used as fuel. The cancer is actually causing whatever associated mitochondrial damage there might be. Also, they're talking about the cancer associated fibroblasts, by the way, are non-cancerous cells. We find the cancer is a society and it's made up of cancer cells and non-cancer cells. And the non-cancer cells are basically captured and coerced into doing metabolic functions that the cancer wants. And cancer will eat the mitochondria of the fibroblasts, forcing them into glycolysis so that then cancer can use the components of that glycolysis like ribos for themselves. Slavery, basically. Now, Tom Seyfried is probably the leading proponent of this so-called metabolic theory of cancer and mitochondrial damage. And he's written papers currently. And he uses the results of hybrid experiments that Warburg didn't have the use of at that time. So I wanted to look at some of the hybrid experiments. So this is a paper in 2015 from Tom Seyfried and he states that in contrast to the somatic mutation theory, emerging evidence suggests that cancer is a mitochondrial metabolic disease, according to the original theory of Otto Warburg. The findings are reviewed from a nuclear cytoplasm transfer experiment that relates to the origin of cancer. The evidence from these experiments is difficult to reconcile with the somatic mutation theory, but is consistent with the notion that cancer is primarily a mitochondrial metabolic disease. We're going to see that that's also a correlation. Tumors reappeared in some clones after extended cultivation of the cells in vitro. The effects of the unnatural cell culture environment on mitochondrial respiration could account in part for the reversion to tumorigenicity. So what these hybrid experiments do, they take a cancerous nuclei and fuse it with a non-cancerous cell and they find that the cell does not become cancerous. Well, they're thinking, well, if cancer is due to genetic mutations, if you take a cancerous nuclei with all the genes and stick it in a non-cancerous cell, it should become cancerous. But he's saying it doesn't for a while. They carried out these experiments for like three, four months or three, four weeks, but he did notice that after a while the cells did become cancerous. And he's blaming that on the unnatural cell culture environment on mitochondrial respiration, which could account in part to the reversion to turning into a tumor. In other words, the effect only lasted for a while and he's blaming the rest on some weird thing on culture. The other part is if you take a non-cancerous nuclei and put it in a to a cancerous cell, or fuse it with a cancerous cell, the cell will stay cancerous. What he's saying is then cancerous resides in the cytoplasm and not the nuclei. And he's saying this is really good evidence, or he calls it almost proof, of the mitochondrial cause of cancer. Well there's another thing wrong with that, number one, there's a lot of other things in the cytoplasm other than mitochondria, such as ribosomes that make all the enzymes that carry on chemical reactions. So you set up the genes, make ribosomes that are in the cytoplasm that make proteins and their factories they keep churning out the proteins, the cytoplasm continues to do its job and you have all the chemical reactions are continuing to take place because the ribosomes are still there, the factories that make all the enzymes that dictate all the chemical reactions that are taking place. They didn't know about this paper apparently. Preservation of normal behavior by enucleated cells in culture. In other words, if you take the nucleus out of a cell, it just goes about its merry way as if nothing has happened for at least three to four weeks. It takes that long before the genes can actually manufacture new ribosomes that can manufacture new enzymes that can then dictate different chemical reactions and make the cell do something different. In the meantime the cell is just going on its merry way with the stuff that's already been made previously. This is why it took four weeks that you know Tom Safrey noticed that, oh yeah, tumors reappeared in some clones after extended cultivation, like four weeks, the effects of the unnatural cell culture environment. No, it's not the effects of the unnatural cell culture. It's the fact that cells are not able to make new proteins. So the cyber experiments you can throw away, they mean zero. Suppressing mitochondrial function conversely inhibits cancer rather than encouraging it. Oh, I've only been going for 25 minutes. I got 15. So, 12 minutes. Do I hear 13? 14. Okay, because I don't need it all. We know now that one of the really good ways to suppress cancer and to treat cancer is actually to inhibit mitochondrial function. Metformin, we know inhibits mitochondrial function. Now it's being used quite extensively to treat cancer and really extend life. It's being used as a life extension drug. One of the major reasons it extends life is by suppressing mitochondrial function and inhibiting cancer. Antibiotics. I mean, mitochondria used to be like bacteria that got gobbled up. And antibiotics will kill, not kill, but inhibit the function of mitochondria. All of these things they find inhibit cancer stem cells and that inhibits cancer and metastasis. Metastasis is what kills everyone. And so it kind of flies in the face of this mitochondrial theory. In other words, injuring mitochondria, inhibiting mitochondria hurts cancer, not causes it. The mitochondria damage theory is just another genetic mutation theory. So here they're saying, well, you know, we don't believe in genetic mutation, but that's what they're talking about when they talk about the mitochondrial theory. They're saying it becomes mutated and irrelevant, doesn't work. It's an offshoot of the mitochondrial free radical theory of aging. My background is in the biology of aging, and I can tell you right now that the mitochondrial free radical theory of aging is passe. It's like archaic. Nobody really believes in it anymore. Here we find things that suggest that the age-dependent mitochondrial dysfunction is not sufficient to limit lifespan. Mitochondroreactive oxygen species are not always deleterious, in fact, can stimulate pro longevity pathways. They find that, like, we take too many antioxidants, you actually can increase your risk of cancer, and you actually shorten your lifespan. That we need oxidation. The oxidation elicits what's called a mitochondrial damage response. That, you know, it's like exercising. You damage your muscle, you get stronger. You know, you damage the mitochondria, they actually get stronger. You get healthier. And here what they did is they in mice, the proofreading function of the DNA polymerase, was mutated. And these mutated mice are born with a mitochondrial mutation burden 30 times higher than that of wild-type mice, yet they lack overt phenotypes and have a normal lifespan. In other words, causing mutations 30 times more rapidly doesn't hurt anything. That's not where the problem lies. It calls in the question whether naturally occurring slow mutation of age-related mitochondrial DNA mutations has a leading role in causing aging, rather than representing only one of the types of damage accumulation that accompany aging. That's true. So Warburg interpreted tumor lactate secretion as an indication that mitochondrial oxfoss was damaged. However, numerous studies, including Warburg's original work, failed to demonstrate effective respiration as a general feature of malignant cells. Instead, mitochondrial respiration and other mitochondrial activities are required for tumor growth. In fact, help tumor growth, especially cancer stem cells. Furthermore, in non-cancer cells, the Warburg effect is a reversible phenomenon tethered to proliferation, indicating that it reflects proliferation-associated changes in metabolism rather than a unique feature of malignancy. Okay, that's kind of a summary of this. So, if cancer is not a disease of glucose and mitochondria, just like... Cancer is not a disease of glucose and mitochondria. Just like diabetes is not a disease of glucose, coronary disease is not a disease of cholesterol, osteoporosis is not a disease of calcium. Why not? Because life isn't in the parts. That's not where life is. Life is in the interaction of the parts. It's in the communication of the parts. All disease, like life, is due to communication or miscommunication. That's where you have to look. You have to look. What's being miscommunicated between the parts? It's not a defective part. If it's defective mitochondria, then why are they accumulating? Why aren't we getting rid of them? Where's the communication that allows mitophagy, so-called the the gobbling up of defective mitochondria? Everything's going to be in in some sort of defective communication that otherwise would preserve life and health. Here's what's missing. Okay. This is metabolism. This is communication. Somewhere in here, there will always be a problem. It's not going to be in the mitochondria. It's not going to be glucose. It's not going to be calcium. It's not going to be fat in arteries. It's not where you look for disease if you want to really get to the root of it. So if cancer is not a disease of fuel or mitochondria dysfunction, then what? Well, it looks like I don't have any time they're saying. Okay. About five minutes? Ten minutes. Seven minutes. Okay. Seven minutes. Okay. Cells don't mutate into cancer. They start out that way. That's one clue. Okay. We come from an ancestral history of unicellular organisms whose main directive was to out-replicate their neighbors. All of that predilection is in all of ourselves. It has to constantly be suppressed. You don't have to mutate cells into cancer. All you have to do is prevent them from not being cancer. And that's what happens. Cancer is obviously a disease of growth. So it would make sense to look at what controls growth. And sure enough, Hans Krebs, you've all heard of the Krebs cycle? Very famous German who was actually a protege of Ada Warburg. And he wrote a biography of Ada Warburg. But he stated, and rightfully so, and he also won the Nobel Prize for his citric acid cycle, you know, the Krebs cycle. Also another German. Warburg neglected the fundamental biochemical aspect of the cancer problem that the mechanisms which are responsible for the controlled growth of normal cells and which are lost or disturbed in the cancer cell. No doubt the difference in energy metabolism discovered by Warburg are important, but however important they are at the level of the biochemical organization of the cell, not deep enough to touch at the heart of the cancer problem, the uncontrolled growth. Warburg's primary cause of cancer may be a symptom of the primary cause, but is not the primary cause itself. Exactly right. This was actually taken out of another book, Tripping Over the Truth, by Travis Christopherson, who used it as an example of how people wouldn't look at the truth when they saw it on Ada Warburg. It was actually, he was advocating for Ada Warburg and using this as an example of why people were ignoring the truth. But in fact, this is the truth. And I was talking about this, you know, back, what is this now, 20 years ago. I was talking about what insulin does. Insulin is a growth factor and it causes, it affects cancer right there. Insulin increases cellular proliferation. What does that do to cancer? It increases it. And then in teleclinic with Joe Merkola in 2005, two of the major factors that will determine whether a person has cancer are the amount of sugar and insulin. Sugar is just listening to orders. It's listening to orders from insulin and leptin. You get insulin and leptin right, your sugar is going to be right. However, the converse is not necessarily true. You can bring down sugar with drugs, but you're not really improving that person's health if it's causing insulin and leptin to increase, which is what almost all the drugs do. All you're going to do is increase your risk of cancer. And then I see stuff like this that drives me crazy. This was just published August 3, 2019. In a new study, researchers have demonstrated for the first time a causal link between high insulin levels and pancreatic cancer. They still are not linking growth factors to cancer. And insulin, by the way, you've heard of IGF, insulin-like growth factor, produced from growth hormone. We'll talk about growth factors. Growth hormone and IGF. Obviously, that ought to be linked to cancer, and it absolutely is. Dwarfism. This is a group of people in Ecuador that have a syndrome called Leron syndrome. It's a defect in the growth hormone receptor. So they have low growth hormone, and cancer is almost unknown. And this doctor, Guevara Guire, noticed this. And they're talking about why. Leron syndrome is almost completely avoided cancer and diabetes. It could be because cells must invest energy in either trying to grow and reproduce or in repair and preserving themselves. Ponies are longer than horses. Small dogs are longer than large dogs. It's a fascinating field in aging. We notice a lot. And a good friend of mine who won the Methuselah Prize in aging research, the biggest prize in aging research, did so by mutating a mouse so that growth hormone was suppressed. And these mice lived over four years, normally two years. That's the longest living mouse. And maybe you actually got them to live longer than that. So there's a huge theory in aging that growth plays a huge role in the aging process itself and cancer. Ungrowth hormone increases longevity. If you restrict growth hormone, you increase. You limit and inhibit cancer, including prostate, breast, brain, and lung cancer. IGF is associated with cancer, very much so. In fact, almost all cancers have some sort of IGF signaling increase. Leptin, not a lot of time to talk about leptin, but leptin is at least as important as insulin, and it is a growth hormone also. And it works through proteins. Dietary protein increases IGF, increases leptin, and most of all increases the target of rapamycin. Target of rapamycin is not a hormone. It's a kind of a switchboard where all the other growth pathways and nutrients kind of feed into it. And it then makes the decision in all cells whether that cell should replicate or whether it should up-regulate maintenance and repair. We want repair. We don't want cells to replicate out of control. They're finding now that the vast majority of cancer cells have up-regulated target of rapamycin. And so they're using drugs to lower the target of rapamycin, like rapamycin. That's why it's called the target of rapamycin. Rapamycin is a natural product actually found in the 70s, only recently found what it does, and it lowers the target of rapamycin, and it greatly decreases cancer. It's kind of a new drug for cancer. I mentioned that. It is one of the most common molecular alterations in human cancer is an up-regulation in the TOR pathway. The emerging studies indicate that the TOR modulates mitochondrial function. So any of the mitochondrial damage that you see, a lot of it is due to TOR being too high. So that when TOR is too high, you don't gobble up defective mitochondria. Lower TOR, you increase autophagy and mitophagy, you basically eat all your junk. TOR is responsible for ketosis. A lot of stuff is going on ketosis. You have to lower TOR to produce ketones. Here is a study that showed that longevity and health were optimized when protein was replaced with carbohydrate. I mean, excuse me, when protein was replaced with carbohydrate, in other words, when you, between protein and carbohydrate, you will increase longevity by lowering protein as opposed to carbohydrate. That doesn't mean carbohydrate is good for you. It's not. But protein is what actually controls almost all of these growth factors, including IGF and MTOR. One minute. We see that a long lived diet is a low protein diet. And we have found there's a mechanism how that may be working. TOR, a recent study appeared in Nature showing that feeding rapamycin to mycin inhibited TOR and extended their lifespan. And here they're using it now for breast cancer. You can read more about TOR in a talk I gave in 2006, protein, the good, the bad, and ugly, it's all over the internet. The best drug to reduce TOR signaling to slow aging and the chronic diseases of aging associated with it is already available, avoid high protein. Avoiding high protein is probably the most important thing you can do to both treat and prevent cancer. Lower TOR, increase autophagy, mitophagy, eat and recycle your own damaged proteins. The protein content of breast milk, how much protein should you eat? Well, the protein content of breast milk is about one gram per kilo per day. Nobody will ever have more rapidly dividing cells than when you are an infant. Nobody should need more than one gram of per kilo per day. And in fact, most of us certainly as adults shouldn't need more than 0.75 kilograms, or if you're 75, 0.75 grams per kilo per day. And if you have cancer, I'd go down to even six grams per kilo per day. Your health and lifespan will mostly be determined by the proportion of fat versus sugar you burn over a lifetime, and that will be determined by the communication of insulin, IGF, leptin, and especially TOR. Cancer is not glucose driven. It is not driven by mitochondrial dysfunction. It is driven by growth signals, particularly TOR, and that is most controlled by the protein that you eat. You've got to be careful of your protein. Done. Thanks.