Now, right now there's two schools of cancer that are kind of duking it out.  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.  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.  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 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.  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.  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.  That we need oxidation. The oxidation elicits what's called a mitochondrial damage response. That, you know, it's like exercising.   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 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.  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.  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.  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.


Today, we're going to show you a quick and easy way to clean your speed queen commercial dryer So the third first thing you always want to do with your speed queen dryer is Clean this little doohickey out here.   That's That's the easy part The hard part is cleaning or inspecting whether there's lint outside of your The dryer drum the thing that goes all the way around. So let's see what happens The next step is to take the bottom panel off Forgive me if the washing machine is making too much noise here. I hope not But so you need a seven six. I'm sorry five sixteenths inch. I'm using a Ratchet wrench, but you can use a screwdriver Whatever I like this because of the long handle. So take these bottom two screws out Now this is just inspect And you should really unplug the dryer before doing this and I'm going to do that right now I'll try to take this first screw out It comes out real easy Probably still charged up, but I'm still just gonna take these two pieces off comes off real easy So let's see what happens here Now you'll know right away as I still hit hinge there As I can see here There's definitely some lint in here not a lot Not a tremendous amount Should get my flashlight LED so It's gonna look a little As you can see, it's not so bad.   Anyway, as you can see, I'm just gonna just get whatever is in there out But that's that's all you really need to do if you Really need to take the whole thing off. There's a way to do it There's clips under here. You just you gotta yank Make the top off and then you could take there's a pie to screws you and this thing comes right right off, but The most important thing is to inspect whether there is a land problem. We don't have a land problem So that's how you do it. It's pretty simple. I'm gonna vacuum it out now and call it a day Easiest pot Putting the cover back on is really easy They make it easy because they have little Notches in this thing. You just Goes in like almost any There it goes with your screws in tight Love you that one of the things that I think Most homeowners should consider is Situating your dryer as close to the Output of the house the vent outside as possible we moved our dryer One side of the basement to the other So that we could have the shortest possible duct exhaust the less turns and Twisting you have for your For your vent the better so this this is just a good idea a very good idea And that's how we did it


First of all, of course, I want to thank the organizers to for giving me this opportunity. So this is. Well, this is my first foray into number theory seminar. All right, so let me start this. Oops, it's not. Okay, so I will start with some rather old questions, which motivate the investigation in the stock, and there are two questions so we start with a field of algebraic numbers, possibly an infinite extension of q, and we have a ring of integers of that field. And what we want to know is, is there first order definition of the other string of integers in the language of ranks, and is the first order theory of the ring of integers undecidable. If you may be unfamiliar with all this terminology and I will explain it shortly. First of all, what's the first order language of rings. The short version is that it is a language of polynomial equations. You could think of a sentence in this language as being a conjunction of polynomial equations and it's prefaced by some collections of quantifiers. So, if I'm thinking about a sentence as opposed to formula, so all variables will be in the range of some quantifier. So the coefficients of the polynomial, maybe in Z, or we can augment our language by adding countably many constant symbols to name elements of the ring. There are some silly sentences you can write. Okay, so the first sentence is clearly true for while I'm thinking about community friends with identity, nothing strange. And the first sentence is obviously true in every ring. The second sentence is true over some rings. And the third sentence is both in all rings. So, I mean, it's natural for us to want to know which sentences of the language are true over a given ring. So the collection of all sentences that are true over a particular ring is called the first order theory of the ring. And we say that the first order theory is decidable if we have an algorithm which can decide given a sentence whether it's true or not. Otherwise, we will call the theory of the ring undecidable. So let's use language of ranks to define subsets. And the basic idea is that you leave one variable outside the range of your quantifiers. And then the set you are defining is the set of values in the ring for which the sentence is going to be true. So there are some silly definitions and there are not so silly definitions. So, for example, this is the definition of the set of even integers over Z. And it's obviously very easy to tell what's going on. On the other hand, if you write something random like some random polynomial of random degree. If you want to know what kind of a set you have defined, it may be quite difficult. For example, I have no idea what's defined over Z by the formula by the sentence I've written. So easy to see that the difficulty of deciding what you have defined depends on the ring you're looking at. So if instead of Z I look at the ring of all algebraic integers, then I can tell what's going on in particular that have defined just the ring of all algebraic integers. So it could be that one of the sets you're interesting in defining is actually a subring of a given ring. Now, why would you want to do that? Well, there is some connection between definability and decidability. The connection is if you start say with the ring R1 contained in the ring R2 and the first order theory of R1 is undecidable and R1 happens to have a first order definition over the bigger ring R2. I conclude that the first order theory of R2 is also undecidable, because if it were decidable, then we could use the algorithm for deciding the truth of sentences over R2 and the first order definition of R1 over R2 to construct an algorithm for deciding the truth of sentences over R1. So the first ring undecidability result, though is due to Hilbert Bernays, that somewhere like they had several volumes on logic it's buried somewhere there, I understand, and it's also was in a paper by Rother. As you see, these results are quite old and of course the ringer question was Z. So it was shown that the first order theory of Z was undecidable. And that, of course, is the beginning of all the other results about undecidability. So if we apply the reasoning from the previous slide with the smaller ring B and Z, then we will conclude that if the answer to the first question is yes, then the answer to the second question is also yes. So the answer to the first question will give us actually more information than the answer to the second question. Sometimes we can give a definition of a set which is uniform of a collection of objects of rings. So what we mean by that, because the notion of uniformity can vary depending on the context. Okay, so let K be a field of algebraic numbers, L a collection of extensions of K in its algebraic closure, and a subset of the ring of integers of the algebraic closure. So we say that a has a uniform first order definition of a rings of integers of all fields and now if there's a single polynomial equation. It has two sorts of variables T, and then there are axis. And only T is of course is not in the range of any quantifier and the formula QT gives a definition of the intersection of our set a with a particular ring of integers save the field L for every field L in our collection. So, so one polynomial works for every field in the collection. There is one very easy set to define uniformly and that's the set of units. Right, so let you be the set of all units in the Q bar. In any field K containing Q bar, we have the units of the ring of integers of that field. I defined by very simple formula. So, now, in describing the language of the rings we stated that given a formula in that language we can add both universal and existential quantifiers. Now, we can restrict ourselves to using just existential quantifiers. So the result of this will be a so called existential language of rings. And the corresponding theory will be the existential theory of the ring. And then the question of decidability of that existential theory is essentially Hilbert step problem for the ring. And there is the same connection about existential definability and existential decidability as the connection between first order definability and first order decidability. Okay, so a bit more history. So, the story for us starts with results of Julia Robinson, 1949, when she produced a definition of the four rings of integers of every number killed, and thus showing that the first order theory of the strings is undecidable. Her definition was of a simple form it just had one universal quantifier followed by some existential quantifiers but it explicitly used the degree of the extension. Later on she produced a uniform definition of the across the rings of integers of all number fields, but the uniform formula was more complicated. Of course, by now we have existential definitions of Z of rings of integers of many number fields. So do you know for the first person to show that Z has an existential definition of our every about to break into just a number field, and he was looking at the dimensions of degree two. This is his result was followed by many more some results of his and ellipse and other people. And so here's a list of people, not in historical order but just an alphabetical order, who produced some definitions existential definitions of Z over number fields. In 2010, Maisa and Rubin showed that Shafarevich state conjecture implies that there exists an existential definition of the ovarian rings of integers of any number field. And later on in a paper of myrti and past and another paper of a stand it was shown that other conjectures will reach the same conclusion so what this means that assuming any one of those conjectures is that Hilbert step problem is undecidable over a ring of integers of any number field. Okay, so, um, due to results of Julia Robinson, we have a pretty good understanding of the first order theory of rings of integers of number fields. But it's quite different when we look at infinite outbreak extensions of here. For one thing there are infinite extensions where the first order theory of a ring of integers is decidable, and there are other ones where it's not decidable. For example, the results of wrongly and one address show that first order theory of a ring of wall algebraic integers is decidable. And it's also more annoying that sometimes the status of the first order theory of the ring of integers, and its fraction field can be different. For example, the first order theory of the field of all totally real algebraic numbers is decidable so that's a result of read Quran and folklore. And the first order theory of the ring of all totally real algebraic integers is undecidable and that's the result of Julia Robinson from 62. And Julia Robinson was the first person to produce example of infinite algebraic extension of q with the first order theory of the ring of integers is undecidable. So she developed a method for constructing first order definitions of Z for rings of totally real integers and a method for constructing a first order model of the and also thus proving undecidability for some rings of integers that are not totally real. Julia Robinson's methods were used and generalized for totally real rings of algebraic integers and rings of algebraic integers of degree to extensions of totally real fields by a number of mathematicians so. So here's the below is the partial list of people who have produced such results. So moving on to our contribution to the literature. And so, in our case, the decidability or so our undecidability results do not so much depend on whether the field is totally real. The extension of degree to a totally real field, but whether the field is not big. So what do we mean by a big field. Well, one way you could think about it. So the field is big. If it contains a sub extension with a degree over q divisible by N for any integer and so. There is one of our main theorems and so if a is a collection of all non big fields of algebraic numbers. There exists the first order formula of the form so to universal quantifiers followed by some existential quantifiers uniformly defining the other rings of integers of wall fields in a. And of course in particular that the first order theory of the ring of integers of all non big fields is undecidable. And we also have a consequence which pertains to fields. And the consequence of if K is the non big Galois extension of Q, then the first order theory of the field K is undecidable. And that follows from the fact that in the Galois Galois extension, which is not big and such an extension. You can give a first order definition of integers of the field. And then if you remember from earlier slides that tells you that the first order theory of the field is undecidable. Okay, so now I'll try to give you a flavor of Okay, so the proof starts with a very simple idea right. If you're in any ring. Well, let's say ring of characteristic zero though. It's still the sentence that's still true and positive characteristic but we are mostly we're discussing rings of characteristics zero only so might as well see in that. So, this is a simple formula from algebra x to the n minus one divided by x minus one is equivalent to n modular x minus one. All right, so you take this formula and take it to the next stream if you wish. So you start with some algebraic extension of Q and let you sub K be the group of units of the ring of integers of K. And then you look at the set define in the following fashion so X is on the set top set of the ring of integers. Even on the if for every unit different from one there is another unit such that X is equivalent to this ratio modular the original unit minus one. So, you know we are motivated by that simple formula just showed you before, because we know that the set are sub K will contain all positive integers, because we can always take delta to be epsilon to the power n.  And it is I mean so there's some not very difficult exercises that show that the site the status happened to be closed under addition and basically multiplication of deltas in the formula ends up being correspond to sums of access so and of course it's enough to prove it for two X one for two elements of our sub K. And it's just silly algebra exercise that you see that it works for two elements of our sub K. And it's also the set of K is also happens to be closed under multiplication. It's also not particularly difficult proof. So if you have X and Y in our sub K right and for every epsilon use of K you need to satisfy certain congrats. So you start with observing that since access in our sub K I have direct with the delta in use of K to satisfy the congrats. But then since why is also in our sub K then I can use the original delta as the epsilon and find another delta delta prime to satisfy the congrats with epsilon replaced by delta. So the end result shows you that the product is also in our sub K and the final exercise is to note that minus one is also an element of our sub K and that will complete the proof that that's in fact during again it's just an exercise with some congruences. But the end result is that minus one is equivalent to epsilon to the minus one divided by epsilon minus one modular epsilon minus one. Okay, so now now so we have a ring of integers and we can define a sub ring of that ring of integers using the units. So what do we get. Well, of course, it depends. Now, if we start with imaginary quadratic fields. Then the situation is not very difficult simply because the imaginary quadratic extensions of Q do not have that many units and you can directly see what all the possible outcomes. The first proposition is not difficult to see. Second proposition is a lot harder. So here you want to know other any circumstances where the ring you have defined is actually the original ring. And it is the case if every polynomial of the form x to the d a times x to the d minus one plus B has a root in your field. Now it's clear that if F is algebraic closure of Q that it will satisfy this condition for having roots to these polynomials. Of course, a much more interesting question is are there other fields with the same property and we do not know the answer to that. Okay, so in general what we have so if K is an algebraic extension of Q that is not big. Then either R sub K is B or R sub K is an order in some imaginary quadratic field F contained in K. Now it follows from this theorem that if K say contains two different quadratic imaginary extensions of Q. Only one of this extensions can potentially contain R sub K. Now, this asymmetry seems entirely unnatural. I mean how does R K select which quadratic imaginary extension to lend in. So that leads us to suspect that actually what happens is that if we start with something which is not an imaginary quadratic field then R K is going to be Z always whether K contains an imaginary quadratic field or not. It's just too strange that the process of constructing R sub K would discriminate between quadratic imaginary extensions of Q contained in K. Okay, now our initial goal was after all to define Z and so there could be an impediment right we cannot show that R sub K is always going to be Z even for non big fields the ring of integers of non big fields. So we have to do some work to compensate for the fact that we can land in a quadratic imaginary subfield of our original field instead of Q. Unfortunately it's not that big of a deal because you can modify the original results of the nerve to show that there is a uniform existential formula defining the ring of integers of any imaginary quadratic field. And basically what you need to do you append this uniform differential definition to the definition of R sub K and then you will get Z. So so far it looks like to define Z of the ring of integers of a non big field, we need just one universal quantifier. So an element X and OK is actually in Z if and only if the function of the following statements is true so the first you recognize that's a construction of R sub K. And then we append some existential statements in case we do land in a quadratic imaginary extension of Q instead of Q. But in this case appearances are deceiving if you look more closely. So the problem is we're not allowed to quantify over the set of units. So the best we can do is a statement of the following sorts. So you start with two elements of OK. And either you're looking at units and more specifically units not equal to one. And then essentially you do what we did in the previous slide. Or you don't have a unit. So that's the other term in the disjunction. So in order to get rid of the second universal quantifier for the case that's always not a unit, we would need a uniform existential definition of non units. But we don't know how to construct such a definition or even if it exists. At the moment we are stuck with two universal quantifiers. All right, so there is another interesting field where we can say something using this methodology and the field is called QUP is the largest Abelian extension of Q. So the question of decidability or undecidability of the ring of integers of QUP is also a rather old one. Still unanswered. So what do we know? We know that we know that the real number of integers of Q. There is a sub extension of degree two of QUP, the field we call QUP plus. It's the field of all totally real number of numbers contained in an Abelian extension. And that ring of integers has an undecidable first order theory by a result of Julia Robinson. So if you look at the first order definition of the ring of integers of Q. Then the ring of integers of that totally real extension has a first order definition over the ring of integers of QUP. Of course, the existence of such a definition would now imply that the theory of QUP is undecidable. So before we get to QUP, we need to revisit some properties of the rings we construct. Now, the idea here is that instead of using the full group of units to define O sub K, we can actually use a subgroup of units. It will also generate a ring, but essentially by the same argument as for the full group of units. But of course it can very well be a different ring depending on the field and the subgroup. So under some circumstances, the real extension of the subgroup of units can lend you in a subfield. So if it happens, okay, so if F is a subfield of K and VK contains elements of infinite order, and the subgroup itself happens to live in the subfield, then the ring we will produce is a subgroup of units. If it is in the subfield, then the ring we will produce will be a subring of the rings of integers of F. So we will lend in a subfield. And the other modification one can make, well, maybe I should say one can choose a particular subgroup VK. And the subgroup will first of all consist of nth powers of units, and all those units will be required to be equivalent to one module of sum ideal. So what happens in this case is you get some other ring, but the original ring times n will be sitting inside the new ring. Now it takes some work to show that the first part of this lemma is true, but the second part of this lemma is not hard to show. And we will use some properties of our rings. So what we want to show is if we start with an element of the original ring R sub K, then n times this element will land in the new ring. So let's choose an epsilon in the subgroup. Now since element X was an R sub K, there must be a delta in use of K such that the required equivalence is satisfied with that delta. Of course, we're not done yet because delta is only in the group of units. It's not necessarily in the subgroup. If you remember, delta has to be an nth power of some other unit. Now the requirement that delta is equivalent to one modular selected ideal, that will be satisfied automatically if we select epsilon in the subgroup because then epsilon itself will be equivalent to one modular that ideal and it will force the same thing on delta. All right, so what we can do is use our addition lemma, which basically tells you that multiplication of delta leads to our addition of Xs. Here's a reminder of that lemma. And we will apply this lemma so with all Xs being equal to X and all deltas being equal to delta. So the end result will be so we add all Xs and we'll have n of them and we multiply all deltas so we'll have delta to the power n and we get this new equivalence. So delta to the n is now in the required subgroup. So what we see is that n times X is going to be in this new ring. Okay, so how are we going to use in our situation? So if k is an extension of degree two, a totally real field and k itself is not an imaginary quadratic field, and f the maximal real subfield of k, then what will happen is that our ring R sub k is going to be sitting inside this totally real subfield. Well, why so? First of all, let's choose a subgroup and the subgroup will contain only squares of units of the original field and every unit will have to be equivalent to one modular some integer bigger than one. Then, okay, that's an exercise to show that units like that are actually totally real. I mean, basically the argument depends on the fact that if you go from totally real number field to a totally complex extension of degree two, the rank of unit groups do not change. So that's so. So now we will use our lemma on subgroups on some fields. I just want to remind you what it was. This lemma, this part, the second part of this lemma. In our case, n is going to be two. So what we conclude is that two times original ring R sub k is a ring generated by the subgroup V sub k, but the subgroup sits inside the totally real field. So we conclude that two times R sub k is in the real subfield. Well, then, of course, R sub k itself has to be in the real subfield. So if we are looking at an extension of degree two, totally complex extension of degree two of a totally real field, then R sub k is going to be contained in this totally real field. So if we apply this argument to OQAB, what we will see that OQAB contains a first order definable totally real subring. Now this totally real subring is not necessarily a ring of integers of any field. It may be smaller, but it takes very little effort to actually convert it to a ring of integers of some totally real field contained in OQAB. Now Julia Robinson conjectures in 1962 that the first order theory of any totally real ring of integers are nondecidable. Of course, this conjecture would immediately imply given our result that first order theory of OQAB is undecidable. But in fact, we don't need to conjecture that much. It's enough to conjecture that the first order theory of the ring of integers of every totally real abelian extension of Q is undecidable to deduce the undecidability of first order theory of OQAB. And or alternatively, we can try to figure out exactly what we have defined. What is this ring R sub VQAB that is defined using units and try to see whether the first order theory of that is undecidable. And as usual, I finish ahead of time. Thank you.


All right. Good morning. Well, I hope all my jokes land today. And if they don't, Chris is OK with pretending not to know me anymore. And you guys just play along. It'll be great. With that in mind, here we go. There are hundreds of citations to this talk today. I do not have time to cover even part of them. The slides would go on endlessly. So if you have any questions about particular papers or anything afterwards, feel free to ask. And I will send them to you. So what I do is I am a writer of both fact and fiction. Today is facts only. I am a researcher. Last year, I had a paper published on canine genetics. I hope to have a paper published next year if I have the time on murlocular dysgenesis. And neither of those have anything to do with iron. But I'm kind of busy. I am also a health nutrition and genetics consultant. A lot of what I do is I look at my client's iron profiles, and I see if they're in optimal ranges. And if they aren't, I get them back where they should be. And also, some of what I do is reverse related conditions like heart disease and type 2 diabetes. And we'll talk a little bit later about how those are related to iron. And yeah, Chris's introduction was fantastic. And thank you so much. He's amazing. OK, so iron. I'll be talking about iron regulation and dysregulation this morning and its role in the disease process, which is widely underappreciated. But first, we should talk a little bit about iron itself. It's a mineral. It's all over the place. And it's necessary not only for survival, but for thrival. It's a very, very important mineral. So iron is found in every cell of the body. It is the most common mineral in the body. And from there, it is the most common metallic cofactor, meaning its presence is required for all sorts of biochemical functions in the body, including all of these really necessary and exciting tasks. Couldn't get by without it, not anywhere. And it has both direct and indirect effects on essentially every cell in every function of the body. So we want to plough through of it in our systems, right? Not so much. Iron is toxic or pro-oxidative in its free state, meaning that it will cause free radical formation. And it'll damage cellular membranes, proteins, and DNA. So having too much of it floating around the body is bad. However, having said that, you would want a tiny amount of iron floating around the body. And that's not great either because a lack of a requisite amount of iron is pseudo-inflammatory on its own. And it can cause things like arthritis and fibromyalgia and rheumatoid arthritis even. And in the cases of toxic, it can cause Alzheimer's and Parkinson's. So an iron surplus or an iron shortage is a problem. It's to that whole survival and thrival thing, meaning we need to find a way to maintain iron homeostasis in our bodies. In order to do that, the body has come up with various iron binding proteins that allow the iron to be used and moved about and stored safely. Very useful. So next question is, how do we get our iron? And what do we do with excess iron? We get our iron from food. We ingest it. It goes into our small intestine. The first chunk of the small intestine is the duodenum, and most of it is absorbed through there. And this is really the only natural iron accumulation method. Modern accumulation methods, which I am very thankful for, include supplementation, transfusion, and injection. So iron removal, how do we get that out of our bodies besides a giant leech? Intestinal sloughing, the enterocytes of the small intestine slough off every few days. And any iron that isn't absorbed from there goes out that way. Perspiration, athletes, heavy exercise, you are going to sweat out plenty of iron. So you can easily, as I have done in the past, become severely iron deficient just from exercise. Minstrel tissue sloughing, I'm pretty irritated about this one. It's rather common in about half the population. And for related reasons, this is why many post-menopausal women and men are higher in iron sometimes than pre-menopausal women, children, and the elderly. But not always, and we'll get into that. Blood donation, prophylactic blood loading, those are pretty obvious. Kind of intentional parasitism, pregnancy, versus unintentional parasitism like helicobacter infections and intestinal worms.  It's important to have your iron right in case you become pregnant, and we'll get to that. And then other potential injuries, because humans are a bit of a mess, we can lose iron in all sorts of ways. And the first world kidney dialysis is now also a common cause of iron loss. So the natural ways of losing iron aren't exactly specific, and you can't really rely on them. So instead, the body relies primarily on regulating its absorption of iron from the outset. So if we have iron regulated highly on every single level, you would think, oh, tiny particle, bound up, harmless iron. What could go wrong? Well, it turns out that iron regulation is extremely common. Billions and billions, at least a Sagan's worth of people on this planet are iron deficient. Or not iron deficient, I'm sorry. Iron have iron dysregulation. They could be iron deficient. They could have iron overload. And there are, I would say, three primary causes of this. The first cause being genetics. Your body can genetically be predisposed to absorbing too much iron, which is iron overload. Or it could be genetically predisposed to not absorbing very much iron at all, like me. Second potential cause is injury or illness. And that can be anything from trauma to bacterial, viral, other parasitic infections. And then a couple causes of malnutrition, so excess or inadequacy in your diet. All three primary causes occur nowadays, but they also occurred in our ancestral populations, with one exception, that being a particular dietary excess. So no matter what the cause of iron dysregulation, it can run havoc on the body, can really do a number. So you start off life carefree and optimistic and literally somewhat lily-levered. But if you live in a Western country, like the United States, you have an 88% chance of things going metabolically wrong. So you start to get to middle age, and things start to go noticeably wrong. And you're not sure why, but you find you can only party ironically. So this downhill slide is regularly linked to iron dysregulation. Too little iron in body will cause the body to stop going burr for a number of reasons. And too much iron in the body will keep the body from going burr for a different number of reasons. It's all a problem. And paradoxically, it might not seem obvious on the surface, but you can also have functional iron deficiency at the same time you have iron overload. Takes decades of work on this to achieve and unlock that level. But it's common, very common now. And all the organs are affected by iron dysregulation. All the tissues, all the organs, poor Bevis, not knowing where his liver is, it's terrible. So these are just some symptoms of iron dysregulation. If I had time and there would be two or three different slides with just symptoms of iron dysregulation, either too much iron, too little iron combination, all those problems. Now, everybody is an individual. We all have different genetic inputs. We all have different environmental inputs. We all express ourselves differently when it comes to those inputs. And so some people might be obese. Some people might be real thin. Other people might have anxiety. You could have GI problems. You could have what we've taken to calling a dad bod. Little pudgy down here, but no matter what it is, it's usually a sign that something is very wrong underneath the surface and you need to get it looked at and addressed before things really go out of control. The cool thing about this, however, is that if you solve your iron dysregulation, it doesn't, sometimes it can take months or even years if you do it in certain ways to resolve these issues. Other times, you can resolve them overnight. And that's really exceptional to see that happen. So these are diseases, the presence or severity of which track with ferritin levels. Again, ferritin is an iron protein. And so these are not necessarily caused by iron dysregulation, but their presence or severity tracks with the dysregulation. And to use one example from the previous list of sleep, poor sleep. Lots of people have poor sleep. Sometimes it's due to all sorts of things. Sometimes it's due to iron. So this is one person and two sets, essentially a sleep data. The first set, the first three, is from when that person had severe iron dysregulation. You can see that the red is awake time, the light blue is REM sleep and the dark blue is deep sleep. Now, the next three are from the very same person. The one and only change in their entire life was their iron. They got their iron in their Goldilocks zone for them and you can see what a difference it made in their sleep. So it's not just a matter of the length of sleep. It's the quality of sleep you get. Another example is thyroid function. So thyroid dysfunction and iron dysregulation, they're indistinguishable symptomatically. Oddly enough, they are very closely related and one can in fact cause the other. So you get to a situation where without the right amount of iron you cannot make thyroid hormone. You cannot convert T4. You cannot utilize T3. It's sort of like in depression where without the right amount of iron, you don't make serotonin, you don't make dopamine. So no amount of pills or therapy, although those are fantastic for their own reasons and for their own uses, are never going to solve an underlying iron problem. So, you may or may not get either joke there, it's fine. I'm laughing inside. So we've gotten to a point in modern medicine that doctors really haven't been trained to understand what's going on other than a lot of pharmaconetics lately. So it's important, it's vital for physicians to test essential blood markers, find the underlying cause of the problem and treat that cause rather than putting band-aids on the symptoms they're seeing. And this is the perfect time to mention reference ranges. So in the middle there is where you're living the dream. You want your iron wherever it is for you right there. You can, you have some fudge room for when things happen to you and then you don't want it going out of bounds there. Whoops. The problem is reference ranges. Now reference ranges tell you what is common in a typically sick population that that lab has tested. It does not tell you what you want to have. It does not tell you what you should have. You don't look at them when you get your results back. You toss them out, it has nothing to do with you. But again, those are the reference ranges and it'll tell you from 12 to 300 is just fine for say Faradayn or, you know, 50 to 150 or something would be fine for ceramide. Whatever it is, it's not. You have to find what's right for you and it's not gonna be that huge number. So it's not fine. So iron deficiency. All of this, this dude here, that's iron deficiency. This little chonker down here, there we go, is iron deficiency anemia. Now, I didn't list it before but iron deficiency anemia is but one potential symptom you can have from iron deficiency. Two thirds of people with severe iron deficiency are never going to have anemia. This is a problem because doctors are trying to think, oh, if the hemoglobin's low, it's anemia, we treat that. They never look at the iron and you cannot judge iron levels by hemoglobin. So iron deficiency does not get treated and only the anemia gets treated which doesn't necessarily help all that much. The other problem is people with severe iron deficiency will have more severe symptoms and they will have more varied symptoms which seems, again, paradoxical. But iron deficiency anemia is but a symptom of the bigger problem you have to look at. So we have a lot of stuff going on. Our symptoms are right up at the big levels. It's not fine. How did we get here and how can we fix our problem? One of the causes of iron dysregulation is genetics. On the left there is iron deficiency. That's me. And on the right, there we go. And on the right is my friend Ryan who is just seen in a festive hat and skirt. So, simple iron deficiency. There are mutations. A lot of them have not been looked at yet but some of it is genetic adjacent just by being female menstruating, that sort of thing. Oddly enough, you can have severe iron deficiency and not be menstruating and that's fun. So, iron overload. Genetic, there are half a dozen different kinds. Overagulation is what causes that. The body keeping the iron load low had the evolutionary advantage of acting as protection against certain bacterial diseases, particularly malaria, and we'll get to that in a minute. So, at least I won't die of malaria, I guess, great. Here in Kansas City, Missouri or here in LA. Malaria is not common but for a lot of people it is. So, health risks from iron deficiency. It's a problem for mothers, it's a problem for pregnant women, it's a problem for children. And so, when you are iron deficient and you have a child, you essentially pass on the iron deficiency because they're not getting it from the new fangled food we have, right, that we talked about yesterday. So, it causes all sorts of problems that can be avoided. So, people just need to get out more and enjoy more nutritious food. And by nutritious food, I mean meat and organ meat. And by more people, I mean pretty much everyone. Need more iron, right? Except for the people who don't need more iron. So, under regulation of iron absorption causes this problem. It's common in Northwestern, people of Northwestern European descent, more common in men than women. And it's proposed that it might have helped with some other diseases. So, hemochromatosis is what the genetic version is called. And citerosis, or citerosis if you prefer, is what happens when iron accumulates in different organs and tissues of the body, such as the heart, liver, or pancreas, brain. Causes all sorts of serious defunction, degeneration, and high morbidity and mortality. So, on to the next one, injury and illness. The obvious things, of course. But surgery, a lot of people come out of surgery and they feel miserable for quite some time and nobody knows why, oh, it's just surgery. Just recovery time, well, not necessarily. Malabsorption, a lot of gut dysfunction, especially with modern foods. And especially as you get older, that system breaks down so it's harder to absorb iron. And then you get psychological stresses, which are not talked about very often, but they can absolutely mess with your iron regulation and cause citerosis. So, immune dysfunction and infection, let's get into that. Lots of people know that low vitamin D predisposes to infectious disease. Some people know that low cholesterol predisposes to infectious disease. Not a lot of people appreciate that low iron also predisposes to infectious disease. They're steaky and a neutrophil. And there's a close relationship between iron status and immune function. So, the presence or absence of iron effects pretty much everything that's going on. Functionality and diversity of the body's microbial landscape, your susceptibility to disease, your ability to recover from the disease, and then everything that can go into hospitalization or immunization.  With innate immunity, iron regulates the macrophage, polarization, neutrophil, recruitment, and case cell activity, and an adaptive immunity. It does things like activates and differentiates certain T-cells, and mounts an antibody response with B-cells. So, we need iron, but also pathogens need iron in order to survive and multiply. So, it can nourish infections. See, steaking is a little bit there. Yeah. OK. In order to start pathogens and avoid oxidative stress, the body's reactive process usually entails any of the following tasks. And we can go through these really quickly. But the important thing to note is that serum iron tends to drop with an infection, and stored iron tends to increase in order to get it out of the system and away from pathogens. So, when getting it out away from pathogens into tissues, again, ceterosis, it can cause all of these problems. So, we get too much iron. It's a problem for immunity. Too little iron. It's a problem for immunity. We have to figure out how to work with that. So, immune function incredibly complicated. And when iron's involved, it's also pathogen-specific. So, how everybody starts reacting to a pathogen, any particular pathogen is how your body is likely to continue reacting to that pathogen, which is good to know for the course of disease progression. Malaria, like I said, this is a very important pathogen because it affects many people and kills many, many people. Modest iron deficiency is protective for the reasons I just explained. And this is, in fact, why people think humans developed sickle cell trait because one copy of it will keep you from having severe malaria symptoms and possibly death. Having two copies is, of course, a bad time, but differently. So, sometimes the iron deficiency can get severe in these populations and it can lead to iron deficiency and anemia of inflammation. So, tuberculosis is another one. Infection results in the typical low iron and high ferritin because you don't want to feed the pathogen. If you supplement the patient with iron thinking they're too low, which I mean they are, but you want to get rid of the infection first, you can trigger all sorts of problems. So, by both iron deficiency and iron overload are independently likely to result in negative outcomes in disease progression, treatment failure, disease recurrence, and or mortality. HIV, same thing. Iron disruption in HIV stays low, even in chronically-traded cases. It's deposited, cirrhosis, and the activity is lowered. Iron status is predictive of how things are going to go. Lower reactivity, better outcomes. Lower storage, better outcomes. Hepatitis. Again, this one alters with disease progression, so it changes a little bit over time between acute and chronic. And again, similar situations, the rona. So, a lot has been said about coronavirus. And there's also a lot that hasn't been said about coronavirus. So, again, predictive of disease severity. Low serum iron, they found in many studies, can cause respiratory failure in clinical settings. And high serum ferritin can lead to what they call that. And they have different designations for children and adults for that. And that can occur at the same time. It can occur after infection when you aren't quite expecting it. So, this long rona may or may not resolve for a while on its own. And going into it with the right iron seems to work well. So, loads of news articles pop up on your screen all the time. I'm sure you've seen. That could be ceterosis. Yeah, one in eight adults. Pretty common. Reinfections, long COVID. Huge impact on economic and personal situations. And, gee, we still don't know what's causing this. It's a mystery, right? Well, here's some of the most common symptoms of a long rona. Oddly enough, there are some of the most common symptoms of iron dysregulation from any cause. I'm sure they have nothing to do with one another. Yeah. Besides having that in common, apart from everything else, iron dysregulation alters mitochondrial morphology and functionality and causes mitochondrial damage, which they think is going on with the long rona. So iron should not be discounted. It can help you, and it can hurt you. So getting into the chronic side of things. Over half of all Americans live with one chronic disease. Many live with multiple diseases. Again, this is not normal. It never used to happen. We're coming from a place a century and a quarter ago where nobody had heart disease. Nobody died of that. And now, one out of every three people, as Dr. Kenobi will be talking about later. So chronic inflammation. It causes all sorts of dysfunction and all different tissues. And of course, the cirrhosis can develop which can begin a feedback loop and make things worse, such as metabolic disease, which we'll talk about. So any condition that causes inflammation and therefore alters immune function has the potential of causing chronic iron dysregulation of inflammation. And that's one of the other things, is they've termed this anemia of chronic disease or anemia of inflammation. But once again, it's not the anemia that's the problem. It's the iron deficiency that's the problem. So that's what I tend to call it. And that way, I can look at the big picture and see what's really going on and treat appropriately. So malnutrition. So this show contrasted two different populations to contrast two different types of malnutrition. But the truth is, most populations in the world now have both types of malnutrition. And it can be either a dietary deficiency or an excess, and they're not exclusive. So first world, we have both going on. This is not uncommon at all. Most people never test some of these things, and they won't know ribophyte is a big deal. Any deficiencies in any one of these can lead to poor iron status. And it can be due to obvious starvation, but it can also be due to dietary choices we make. What we don't eat when we eat it, because iron has a circadian rhythm, oddly enough. Iron absorption, I should say. And if there are any absorption inhibitors ingested at the time. So lots of inhibitors, I'll just quickly go through these. Overcooking can also convert heme iron to non-heme iron, and the thing about heme iron is it's found only in meat. Oh my God. Okay. And yeah, so it's the most bioavailable version. You need that. And so plant material less available, not as good. So that's a problem because lots of Americans wake up first thing in the morning, or all day long, and are chugging coffee, and they're tired. Symptomioid disregulation is being tired. And so the cycle continues, and you keep making yourself more tired. Lots of plant problems, and cow boobs squeezes are kind of a favorite of mine. However, the calcium will compete for entry into the enterocytes with iron. So that can be a problem if you drink too much milk, or to eat too much cheese. You might have to compensate for that. So dietary excesses, Dr. Knobey, will be talking at length about the potential one that we believe might be causing most of the problems. So I won't get into much of that. So metabolic syndrome, however, is the effect. That's what happens. And it doesn't matter what size you are. Like I said, most Americans are metabolically unhealthy. And so these are typical symptoms which you may be familiar with. So this is what happens in iron deficiency of inflammation or metabolic syndrome because the body treats it like an ongoing infection. So you got iron deficiency with anemia, without anemia, inflammation, and iron overload. So the body alters the iron and systemic metabolic dysfunction causes inflammation and re-regulation of iron and mimicry of transient pathogen infection. So never, ever, ever, ever treat iron deficiency if you see it in a metabolic syndrome patient unless there are severe symptoms and the ferritin isn't crazy. Basically, treat the metabolic syndrome. Sometimes the hyperferritinemial will resolve on its own and then you can treat the hypoferemia. Otherwise, you could have a bad time. So what about ancestral dieting? Yes, it's absolutely possible to have iron deficiency if you're eating only meat and severe iron deficiency at that. Things you wanna make sure to do. Nose to tail if you can. Just get some organ meat in there. Eat the right things at the right times. That's important. Don't overcook your food. Don't ingest too many inhibitors unless you're like me and I'm kinda living my best life here and I just pop iron at the right time. It's important. So, good news. Keeping track of all these things will keep you healthy and will keep the healthcare system from being overburdened. You can avoid a lot of problems. Maintaining ideal iron status. Keep a healthful diet. Keep track of your labs. Find somebody who actually knows what they're doing and not just an internet forum where there are 49 different interpretations of what's going on and all of them are wrong except for one that might be right for the wrong reason. Just find somebody who knows what they're doing who can guide you and how to alter your iron if you need it. Some people are just fine. So, you have to compensate for other issues that you might have and avoid injury and illness as one is wont to do.  Live longer. That's great, right? We want both health span and lifespan. We want those to coordinate very well. So, this is my talk and like I said, I could have gone on for about 10 hours but I really had to compress it. So, I hope you learned something from this and can pass it on to other people that it might help. Thank you very much. Great talk. Thank you. Quick question. Yes. I do a lot of spleet dentistry and so we're always looking at iron. Particularly in our circles, we talk about restless leg syndrome. So, maybe you could talk a little bit about that. I'd appreciate it. And is there anything else going on with the circadian rhythms and sleep particularly? Yeah, I can spend a lot of time on that. Okay, so, restless leg syndrome. They've recently come out with a bunch of pills for that, right? So, the problem is with, it's very, very common in iron deficiency, especially if you get under like 70 ferritin and you have to check out CRP while you're doing that. Otherwise, you won't know what you're looking at. So, some people, again, get it at different levels. You can get severe hair loss at 100. It depends on the individual. That's why I'm never gonna tell you exact numbers for anything. You have to know the individual and their history and their genetics sometimes. But so, yes, restless leg syndrome. You can often cure that overnight with siren supplementation. And it's a lot better than spending multi-million dollars on pills and stuff. But I mean, I'm sure there are reasons why you would need it that don't have to do with iron. So, they are important. So, don't get me wrong. And as far as circadian rhythms, yeah, so, hepsidon is the peptide hormone produced by the liver that is highest and about 3 p.m., lowest, roughly the opposite time. And so, you can absorb the least amount of iron at that time. So, you might wanna move your eating schedule around depending on your particular iron status. And that's the main thing. So, I take my pills right before I go to sleep, maybe 3 a.m. Yeah, thanks. Thanks for your talk. Three years ago, I got diagnosed with SIBO and I found a functional medicine doctor and we went through the process of working on that and healing my gut. At the time, I had crazy high ferritin. I have one of the genetic snippets, I guess, we're holding on to iron. And my thyroid levels were crazy. They thought I had cancer and all this stuff, which I didn't. But anyways, long story short, one of the things we did over the few years was I donated blood every two months and that helped get my levels normal. Like last month, I did my blood work and it was the first time ever that my iron was too low then.  Anyways, I'm just curious if you're, in examples like myself, if you've seen people get to sort of a homeostasis just by healing the gut and maybe how often should I be measuring it? Cause I'm kind of concerned that it's like here and then here and then here. Right, so yeah, with the gut issue, SIBO, you know, Crohn's CLA, all those things, kind of modern diet situation. Some of it is also for medications and so anacids can cause the microbial situation to get all out of whack down there. And yeah, so things can go wrong, but so yes, it can heal. It absolutely can. Iron's the right amount is gonna help and sometimes symptoms and iron, it's hard to tell what's causing a lot sometimes. So you really have to go through that. But also you have, so yeah, with people with hemochromatosis or, yeah, I don't really recommend donating blood if you have metabolic syndrome in that sense because you're causing a different issue, but you don't want low serum iron. But so you probably got to a point where your ferritin was what, maybe 30, 40 or something. I don't know when you're donating. And so yeah, that can actually be fine. It might get rid of more symptoms if you get down that far because if you've been iron overload for decades or if you've been iron deficient for decades, sometimes you have to massively overcompensate for a while. So it's not necessarily detrimental, but you have to go by your own symptoms. Symptomology is the most important thing. Thank you. Yeah, you're welcome. Thank you, Kevin. In a book called Survival of the Sickest, it's mentioned that hemochromatosis, speaking to what you said about pathogens need iron too, not just us, that hemochromatosis was protective against bubonic plague. Have you heard that? And it's somehow the iron isn't in the cell, it's extracellular and it starves the bacteria. Have you heard this? I haven't heard of that in particular. I haven't done a deep dive because it's not my specialty, so to speak, but it could be that they're talking about macrophage load of iron and that happens with tuberculosis and typhoid fever too, I think. So it could be that. Yeah, I mean, there's probably a reason Northwest Europeans had all these mutations and that might be one of those reasons. But I assume it's macrophage. Okay, thank you so much. Thank you. Thank you.


Alright guys, so it's been a long time since I made a video and I apologize for that But today is gonna be a different video Now I don't normally do this, but this is a very cool conference Guys if you live near the Bay Area, or you would just want to visit this and see this online, please Register for Samsung developer conference 2023 now. Why should you come here? Basically Samsung developer conference. There's a lot of things to do here This is a free event. You don't have to pay for anything. It is completely free You just show up and you get to meet new developers new things. You get to meet Engineers developers and there's good to be a ton of cool things that you're gonna be at this event So here just register There's gonna be a lot of things One thing they're gonna do is they're going to explore a lot of the latest tech news in Samsung so one of the cool things is that Tizen and also the latest SDK, they're gonna go over the latest SDK They're gonna go over many different things in Samsung and they're gonna go over Just the coolest tech news and this is a great way opportunity for you to network with people and for you to just Learn the latest tech news more than other people. Also, you get to try out new things in Samsung developer conference. So Basically, they're gonna go over the latest tech news in Samsung and they're going to go over many different things and you get to try out many cool things and There's a lot of events and a lot of things is gonna happen at this developer conference As a developer, it's very easy for us to just sit down at home And then just code all day and then not actually meet new people But in the Samsung developer conference, you will meet a lot of people you will go to Have a lot of things activities. You'll see the latest trends many different things And you'll just have a great time at Samsung developer conference So I encourage all of you guys to register for this event Personally just go there register for the event and meet different as many people for Samsung and as many different things So yeah, just go online Samsung developer conference calm register register for the event and then just you don't go to any of these things So they have the recent tech square, which also where they're just going over the latest things in Samsung They have the hackers playground, which we're gonna it's like a hacking competition We're you're just gonna try to write secure programs and hack things and just a cool thing to hack And then there's gonna be an after-party.  It'll be pretty cool There's gonna be arcade games and you're just gonna have fun There'll be a live performance and it is pretty cool. All right, this whole thing is pretty cool So when is this event? This event is in October 5th So if we just go here and just go to the event tag main events October 5th remember October 5th and just register for this event Samsung developer conference Register for it. It's completely free. Just go to this link Samsung developer conference October 5th Thursday 2023. It's near sands from Francisco and Moscone And it's also available online. So to watch it register for it. I hope you guys enjoy this video We're gonna come back to more a leak code videos tomorrow. I'm gonna start uploading daily now I apologize for a lot of things. But yeah, register for Samsung developer conference I hope you guys see you there and yeah, just enjoy the time and just come and have a good time That's what you should do. All right. All right, peace


We can all agree, 2020 was up, and now it's finally over.  That's right, the sun is back in action, like the Terminator. I'll be back. But the second movie, where he's a good guy, good robot, good robot guy, and it just announced its first piece of legislation will be the Four of the People Act. If passed, it would be the most comprehensive anti-corruption reform since Watergate. You know Watergate. The scandal's so bad it's the whole reason we say gate after scandals. The grandpa to banana gate, cargo gate, pickle gate, pizza gate, Sharpie gate, Russia gate, Trooper gate, and all the other gates. The Four of the People Act is a motherload of a package that'll make government work fairly like governments are supposed to, unless you're into these governments, and it would take dark money out of politics, which everyone likes, unless you're one of these people. And the Four of the People Act introduces all kinds of reforms to fight corruption, like ending gerrymandering, securing our elections, increasing ethics, and cracking down on the abuse of presidential powers. It's about getting Congress to listen to the people and start solving our major problems like this, this, this, and this. Otherwise known as doing their jobs. And we have a real opportunity to pass this bill right now. All these organizations dig it, and 67% of Americans across party lines say they support it. Yeah! Almost everyone likes it. It's the Tom Hanks of bills. Thank you. Because it will strengthen democracy for all Americans. Donkeys, elephants, dog events, elkies, independence, and whatever animal represents libertarians. Lizard terriens. So we all need to flood our members of Congress with calls and email messages. You've got mail. Nice messages. Not this. Tell them you want the Four of the People Act passed and on the president's desk ASAP. Because the only thing that's going to stop America from going back to this is all of us.


Toxocera can cause a variety of symptoms depending on which organ or system it affects. It is important for doctors from different specialties to be aware of these symptoms so they can make an accurate diagnosis. In the most serious cases, cerebral toxicoriasis can lead to brain damage and death if not treated promptly. Imaging tests such as MRI and blood tests can help identify the condition and determine the best course of treatment. Albendazol is an effective medication that can reduce the severity of symptoms and prevent further complications. Early detection and proper treatment can ensure a positive outcome. This article was authored by E.R. Rachmanov, N.M. Goliimova, and A.A. Boymiradov.