Читать книгу Summary of: Cancer as a Metabolic Disease by Dr. Thomas Seyfried. On the Origin, Management, and Prevention of Cancer. - Travis Christofferson - Страница 4

Well, thank you very much. I'd like to thank CrossFit and Greg for supporting us. I'd also like to thank Jeff Glassman for the good questions that he asked us in the past, to validate some of our theories. You know, we need people like that, it's good to have people that question the information that you present. It makes us better at explaining this.

For your information: I have no financial disclosures.

Alright, So what I'd like to do to start this off is, basically, to present a report card on our approach to managing cancer.

And as I said, I'm going to speak to you today about cancer in general and also focus on specific types of cancer, in particular glioblastoma. As an illustrative example of our approach to managing the disease.

Now, these are numbers that we can take from the American Cancer Society, and they publish every year data on the overall number of cases and deaths. The war on cancer and the success that we're having is not going well.

So I compiled the data, just over the last five years:

This is 2013 to 2017 and as you can see, these are pretty sobering numbers. We break them down into new cases, deaths per year and deaths per day, simply dividing by 365, to give an estimate. And you'll notice that the deaths per day and per year are exceeding that of the new cases. Not good.

Just to put things into perspective: The population increase in the United States over the same period of time was about 2.9 percent. So how is this war on cancer going? You look at the numbers, you can make your own decision. These are numbers you don't see on TV, right? You see Opdivo and Keytruda and that kind of stuff, but you don't see the constant increase in deaths per day.

So the question we have to ask ourselves is: What's going on here? We're not getting success here! This is a failure of monumental proportions, right? These are large numbers! In China it's over 8,000 a day dying from cancer. Cancer's already superseded heart disease in China!

We go out and we raise money for cancer, right? You all know, you run, jump... I don't know if you guys do 'CrossFit for cancer'. But everybody raises money for cancer, it makes them feel good. Nobody asks: How much of the money that we raise goes to cancer research? And what's more important: What kind of research are they doing with all that money?

The federal government's spending millions of dollars on cancer research. People are raising money, "Stand up to cancer!" Look, the more money we raise for cancer, the more cancer we get. So you have to say: What is going on here? How do you explain this?

And it has to do with a fundamental misunderstanding of what the nature of this disease is.

We've been led to believe, that this is a genetic disease and I'll present evidence to show that it's not.

Here's a simple cartoon of a cell with a nucleus and a mitochondrion, within a cell membrane:

So we know there are mutations in the nucleus, but we also know that there are defects in the mitochondria as well. And I'll be showing you data showing that the origin of this disease is a mitochondrial metabolic abnormality. It's not a nuclear genetic disease. The mutations that you see in the nucleus are actually coming from reactive oxygen species (ROS) produced by the mitochondria!

What the entire field has been doing over the last six or seven decades, is chasing red herrings! Consequently, you have 1,600 people a day dying from the disease.

So the current dogma says: Cancer is a genetic disease. And this is solidified in this major paper:

Hallmarks of Cancer by Hanahan and Weinberg, one of the more highly cited papers in the entire cancer field. What they say is: Cancer cells carry the oncogenic and tumor suppressor mutations that define cancer as a genetic disease.

And we say it's a dogma, because it's presented as if it is an irrefutable truth. A dogma is no longer questioned, it's a solidified viewpoint. If you go into any textbook of biology, biochemistry or cell biology and you go to the cancer section, it says "cancer is a genetic disease." You go on to the NCI website, the National Cancer Institute, "cancer is a genetic disease."

There's no discussion about anything other than the fact that cancer is a genetic disease. Many of you went to medical school, you probably learned that cancer is a genetic disease. All the college courses on cell biology: Cancer is a genetic disease.

What this concept has done now, is it has indoctrinated several generations of scientists and physicians into this viewpoint that cancer is a genetic disease.

The somatic mutation theory is the foundation upon which the viewpoint of "cancer is a genetic disease" is based. And, basically, what the somatic mutation theory says, is that "Well, we get random mutations":

Random mutations that accumulate. And eventually, you convert a normal appearing cell into this dysmorphic, mesenchymal kind of cell. But nobody really knows how many mutations it takes to cause... or how it is related to the formation of a tumor. Is it 1, 2, or 4 mutations?

Michael Stratton from the UK says "We're going to have 100 million genes going to be found," and "look at the deep sequencing coming out of the Broad Institute," and these various places." Thousands and thousands of mutations have been identified.

And then they have to label them with different names, "drivers" and "passengers" and "go-alongs". A whole bunch of stuff is going on there.

And no one talks about those cancers that have no mutations! Kind of non-discussed.

So where does that all lead us to? Where have we come in this journey to manage cancer? We have now come to these terms "personalized therapy", "precision medicine"... all of this is based on the viewpoint that cancer is a genetic disease.

So you have these kinds of images, here:

You have this woman staring into a screen and she's looking at breast cancer information to see if this may possess extra copies of a particular gene. Which would be used, in theory, as a diagnostic tool with possibly some therapeutic application. Now, to get that information usually you do needle biopsy.

So you have to take a needle biopsy of a particular tissue, in this case it would be a breast cancer. So you stab the tissue and in the process of stabbing the tissue, to get the information that she's looking at on that screen. Biopsy changes the micro environment of the tissue. You have potentially taken a pre-malignant state and by stabbing it to get this information, you have now put that person at risk.

Now, very interesting: The information that you get for this kind of screening is about $7,200 to do one of these screenings. To get the information that you can look at and say "Oh, we have this kind of battery of genes." Now, this would be okay if it had any redeeming value, right? But it has no value.

But you put people at risk for cancer by the very process of taking tissue. The phenomena is called inflammatory oncotaxis: It's an observer effect. By looking at it, you've changed it.

Now, I want to talk to you about the evidence that does not support the somatic mutation theory of cancer. And whenever you challenge any kind of a solidified dogma you always get the same response. We saw one of these images yesterday. This comes from Nikko, Japan. These are the Nikko monkeys:

I went to japan, actually. They have carvings of them that are a little bit different than this, but it's basically similar: You don't want to look at the data, you don't want to talk about it, you don't want to hear about it. Anything that challenges your world view. I don't care if it's a religion, a political philosophy or a scientific concept. You generally get this kind of a response. I know it's hard, it's hard for people to look at things differently.

So what I did in chapter 11 of my book... This is a paper that I wrote a couple of years after the book, to update more and more of the issues associated with information that does not support the somatic mutation theory:

All I did was take articles from the literature that had been spattered about for years and brought them all together in one group of papers - and reevaluated the information from those papers in light of the two competing theories for the origin of the disease. So, bring them all together and then look at the data and then say "Do the data support more strongly one hypothesis, or theory, over the other?"

And you come to the conclusion that the somatic mutation theory makes no sense,- relative to the mitochondrial metabolic theory. You know, what's very interesting about this, when Gary gave his talk yesterday... about the difficulty in reproducing findings...

I find it remarkable that these different kinds of experiments were done by different individuals, with different tumor types, different protocols... but all coming to a similar conclusion that does not support the somatic mutation theory. But the data more strongly support Otto Warburg's theory of disturbed energy metabolism.

So let's just look at a couple of these experiments. And, you know, the important point about this paper is: Don't let anyone tell you what they think about it. You're smart people! I tell people "Read the original paper and you come to your own conclusion. You make your own decision." Don't ask "Hey, what do you think of that paper? Do you like it or not? Yeah, maybe it's no good".

You can't believe how many people take in information second, third hand, rather than going to the original source. Read it! You make your decision if you like it! Do what Dr. Glassman did, hit me with a thousand questions and I'll be happy to answer them!

So let's look at some of the data:

Now, this was done by McKinnell and his group, published in Science in 1969. I had the chance to speak with Dr. McKinnell before he passed away a couple years ago and we discussed these data at length.

So this frog has a massive renal tumor on the kidney. It's a kidney tumor, kills the frog, very aggressive. So what McKinnell and his group did is: They isolated cells from this kidney tumor and then they took the nucleus out of the kidney tumor cell and put it into a fertilized egg. The original nucleus of the egg was removed.

Here's the tumor cell, you take the nucleus that has the tumor suppressors and oncogenes and whatever - and you put it into this new cytoplasm that has normal mitochondria and you get a tadpole. And they looked very carefully, there was no evidence of the signature feature of cancer, dysregulated cell growth, anywhere. Everything looked perfectly normal.

The problem is, this tadpole could not fully develop into a mature frog. So whatever problem was in the tumor nucleus, it was not allowing the organism to fully mature. So the nuclear mutations didn't cause cancer, they blocked development.

These findings are inconsistent with the somatic mutation theory, which says, that the genes are causing the phenotype of dysregulated cell growth.

Another paper:

I'm only going to give you information from a few of these studies, I put a whole bunch of these in the paper. It could take, you know, two days going over those experiments, but I'm just going to show you a few of them.

Now, this study was by Rudy Jaenisch and his colleagues at MIT. Rudy is one of the best and most preeminent developmental biologists. And he took these melanoma, malignant melanoma cells, and he characterized many of the mutations in the nucleus of the melanoma cell. They then he took the nucleus and made embryonic stem cells and cloned mice from the nucleus of melanomas.

He says here "The presence of major genetic abnormalities in embryonic mice cloned from the tumor nuclei provides unequivocal genomic evidence, that the mice were cloned from the tumor nucleus" - but they did not show any dysregulated cell growth. These findings are inconsistent with the somatic mutation theory of cancer.

And there was another series of experiments that were done by Dr. Wong and her group at Baylor College of Medicine, where they swapped the mitochondria from one cell to the next. These are much more difficult experiments than the nuclear transfer experiments.

So they take aggressive, malignant metastatic breast cancer cells, remove the mitochondria from the cytoplasm and bring in normal mitochondria from normal cells that don't have cancer. And the oncogenes and the abnormal growth was suppressed.

On the other hand, they took the mitochondria from the aggressive breast cancer cells and put them into an indolent cell (a type of low growth cancer) they exploded into high growth. So you've got a very different result. The mitochondria are calling the shots, not the nucleus!

So what we did to convey and summarize all of these data from all of these kinds of nuclear/mitochondrial transfer experiments in this simple diagram, which is now making its way through the web:

What I show here is: The green cell, which is a normal cell, begets normal cells. They have a normal genome, they have normal respiration. The red cell is the tumor cell. Tumor cells beget tumor cells. One tumor cell begets more tumor cells. They have genetic defects in the nucleus and they also have defects in the mitochondria.

Now, what is the origin of the disease? Is it the defects in the nucleus or is it the defects in the mitochondria? The nuclear transfer and mitochondrial transfer experiments provide evidence for this: Take the red nucleus and move it into the green cytoplasm - and you get normal cells that behave normally, grow normally, form normal tissues, sometimes organs and sometimes whole mice or frogs.

On the other hand Israel and Schaefer took the green nucleus and put it into the red cytoplasm. And in that case, you got either dead cells or tumor cells. You did not get normal cells. These are the exact opposite findings you would expect if the disease were a genetic disease!

Nuclear/mitochondrial transfer experiments are the strongest evidence to date that undermines the gene theory of cancer. The strongest evidence. No one has yet been able to explain how we get all these findings based on the somatic mutation theory of cancer!

So if that's the case: Why is the oncology field continuing to persist with therapies that are based on a flawed underlying hypothesis?

If somatic mutations are not the origin of cancer,

how do we get cancer cells?

Well, Otto Warburg described this a long time ago, back in the early part of the 20th century:

 Cancer cells arise from damage to the respiration

 Energy through fermentation gradually compensates for the insufficient respiration

 Cancer cells continue to ferment lactic acid in the presence of oxygen

This is called the "Warburg Effect" and unfortunately the Warburg Effect has significantly confused this field, making it confusing to a lot of people. Because they said "Well, there's some tumor cells that don't show a Warburg Effect, therefore Otto Warburg must be wrong!"

Well, myself and some of my colleagues, we proposed that cancer cells can not only ferment sugar (glucose), but they can also ferment amino acids. And that amino acid is primarily glutamine, through the succinyl-CoA-ligase step and this is not well known to a lot of people. Basically, this is the missing link in Warburg’s central theory.

So the cells are fermenting, but not only lactic acid, they can ferment amino acids and particularly glutamine. I'll present evidence for that.

 Enhanced fermentation is the signature metabolic malady of all cancer cells

Now, if we take a tumor and we look at this tumor and we separate the cells of the tumor: Every single cell in that tumor has a different genetic profile. No two cells in that tumor have the same kinds of mutations! This has been demonstrated over and over again.

However, every cell in that tumor is fermenting. Now, the question I ask to you: Is it more logical to focus on the common problem that exists in all of the cells of the tumor - or do you think it makes more sense to focus on the individual, unique differences of every cell in that tumor? Right? I mean, the answer should be clear.

But we do it wrong! We focus on the unique, individual differences at the expense of the common pathophysiology - and that's what we call the somatic mutation theory of cancer. Consequently, we get 1,600 people dying a day.

Now, let's look at this, energy:

Alright. So, in a normal situation (this is a cartoon of just the mitochondria) most of the energy that we get in our body comes from breathing. About 89 to 90 percent through oxidative phosphorylation, respiration. We get smaller amounts of energy through these ancient pathways of substrate-level phosphorylation. In the cytoplasm, in the form of glycolysis and in the mitochondrial Krebs cycle through the succinyl-CoA-ligase step.

And we all know this, this is biochemistry, right? We're all breathing! We all are... well, I think. Any zombies out here? They don't breathe. But the issue is: Most of us breathe and when you exercise you breathe more and this is where we get our energy from, right?

Okay, now look at the cancer cell:

This is the same picture, but you'll notice that there's a major shift in where the energy is coming from. Much less energy is coming out of oxidative phosphorylation and a lot more is coming from these ancient, primitive pathways: substrate level phosphorylation.

And you see that... we now know, and we're learning more, that the majority of the energy is coming out of the mitochondria, but not through OxPhos [oxidative phosphorylation], but through the Krebs cycle. This is the new understanding that we're talking about, this is the missing link in Warburg's theory.

So tumors get a lot of energy from fermentation metabolism. Tumors can get energy without oxygen and this is where the cancer cells are getting their energy from! So people say "How do we get cancer then?" Well, all we have to do is take all of the data that was published in the cancer field over the last, you know, 100 years and just reconfigure it, along with Hanahan and Weinberg's Hallmarks paper.

Then we take the information and just rearrange the picture. And now we can put together, in a more logical way, the origin of "How we get cancer" - and once we know that, then we'll know how to manage the disease. It becomes much more clear to do that:

So what we have here on the on the left is the mitochondrion and people say "How do you get cancer?" Well, you can get cancer from any number of different things, right? Carcinogens cause cancer. You can get cancer if you're exposed to carcinogens. Radiation will cause cancer. Hypoxia (absence of oxygen) can cause cancer. Systemic inflammation, we heard that from Axel, he was telling us about the systemic inflammation and others.

Rare inherited mutations: People say "It must be genetic, because you got BRCA1 and P53... Angelina Jolie had her breasts and ovaries removed because of the BRCA1, she's trying to reduce her risk...

That's all secondary. It's secondary, because those BRCA1-mutations do not cause cancer, unless it damages the respiration. And there are people around that have BRCA1s who'll never get cancer, because the gene is not damaging the respiration.

Ras oncogene damages respiration.

Hepatitis C, and papilloma viruses enter mitochondria and damage the respiration. Age increases risk for cancer... so all these disparate risks factors was referred to as the oncogenic paradox, right?

Hepatitis C, papilloma viruses enter and damage the respiration. The older you get... so this was referred to as the oncogenic paradox, right?

This was first pointed out by Albert Szent-Györgyi, who said "Hey, there's so many different ways to get cancer - but the common pathophysiological mechanism is not clear!" Well, once you understand that it's a mitochondrial metabolic disease, the mechanism becomes very clear!

And if you read Sid Mukherjee's book on the Emperor of all maladies, the one that was on the New York Times bestseller list, and it was the Pulitzer Prize-winning book on cancer... he struggles with this! If you read pages 285 and 303 in his book, he says "You know, it's just like, we don't... we just can't figure out how you get cancer from all these different things!"

You get cancer from all these different things, because they damage respiration and they form reactive oxygen species [ROS]. And reactive oxygen species are carcinogenic and mutagenic!

So the mutations that you see in the nucleus, that everybody is following - these red herrings - are all coming as a secondary cause to the damage to the respiration.

They are not the cause, they are the effects!

Alright? And then when the ROS are generated, they damage further the respiration, the cells are suffocating! Where are they going to get their energy? They have to upregulate substrate level phosphorylation.

So you see here at the bottom, the green line going down and the red line going up, substrate level phosphorylation. Which means a fermentation metabolism. So what are they fermenting? They're fermenting glucose and glutamine! Those are the two fuels that are driving up the energy. Because without energy nothing lives! Period!

Energy is everything. Without energy, you don't survive!

So what's happening with these cells is: They're shifting their energy away from respiration to a fermentation metabolism, using available fermentable fuels. So now we can put together all of the hallmarks of cancer in a more logical way, all linked back to damage to the respiration.

The first three hallmarks of Hanahan and Weinberg are all the result of the cell falling back on its default state, the state that the cells had before oxygen came into the atmosphere, some 2.5 billion years ago! Where everything on the planet was fermenting. They were fermenting amino acids and whatever else they can get!

And during that period of time the cells were in a state of unbridled proliferation and they would proliferate like crazy, until the fermentable fuels in the micro environment disappeared and they croaked. And they'd throw out all this waste material into the micro environment. In cancer this leads to vascularization or angiogenesis - another multi-billion dollar industry that's all based on, you know, indirect findings.

Okay. Then you say "Well, if this cancer cell is starting to suffocate, it should die, right?" Yeah, it should undergo programmed cell death and drop dead, that's called apoptosis. Why are they not undergoing apoptosis? Because the mitochondria control the apoptotic signaling system in the cell. Mitochondria are the cell’s 'kill switch'! And your kill switch is broken and these cells are now bypassing apoptosis. They're not dying, they're proliferating.

So the big dog in this whole thing is metastasis. Okay, you know, I can agree with this. Where do you get metastasis from? Which is ultimately the biggest challenge in managing cancers, trying to control when it spreads through your body.

Now, you have to understand the biology of the disease. Once you understand the biology of the disease, you can start putting the pieces of the puzzle together:

Here's some blue cells, they're columnar epithelial cells. They could be in the breast, the colon or whatever. They get damaged by anyone of the provocative agents in the micro environment. They start entering the default state, they start proliferating.

Our body has a sensory system to know what's going on, this looks like an unhealed wound. So we have cells in our immune system that come into these places to heal wounds. And these are mostly macrophages. So they sense this, chemically, in the blood. They come in, out of the bloodstream, and they go right to these incipient cancer cells, growths of cells, to put out the fire, to heal the wound and then heal the tissue.

The problem is they throw out growth factors and cytokines, which are actually stimulatory towards these cells, which lost their growth control because of their fermentation behavior.

Now, they're making the situation worse, because it's the wrong context. What these red cells, our immune cells, do is to facilitate wound healing. They fuse together – they are very fusogenic cells, which is well documented in the scientific literature. So what's happening then with this continual fusion in this inflamed micro environment, is: You're diluting the cytoplasm of the red cell with the cytoplasm of the tumor cell, thereby shifting the immune cells from a respiratory system to a fermentation system, locked in.

These immune cells are already genetically programmed to enter and exit the bloodstream. You don't have to have this epithelial–mesenchymal transition, it makes absolutely no sense. (This is the gene theory explanation for metastasis.) This is the real thing! And we have evidence to support that in a number of different ways.

So you now have a rogue cell, part of our immune system, that's already programmed to spread through your body. Very difficult, they're already programmed to live in hypoxic environments, therefore anti-angiogenic drugs probably won't work - and they haven't worked.

So we now know the biology of the metastatic cell: It's a rogue macrophage! What do they eat? They eat glucose and glutamine! Okay. We know that.

Now, if most cancer cells obtain energy through fermentation, what therapies might be effective in managing tumors?

Well, one of the things, logically, is simply take away fermentable fuels and replace them in the body with non-fermentable fuels. And one of the ways to do that is: Stop eating! Calorie restriction [CR], ketogenic diets [KD], these kinds of things!

What calorie restriction and ketogenic diets do is:

 they differ from starvation

 they maintain normal levels of minerals

 they enhance mitochondrial biogenesis, and also, they replace fermentable fuels

You can't ferment ketone bodies! You need good respiration to obtain energy from ketone bodies. So you're going to remove or lower the glucose levels, and raise the ketone bodies which the normal cells are going to shift over to and the tumor cells are going to be marginalized because they can't use the ketone bodies!

And don't forget: We just heard from Michael about the basal metabolic rate. I do this in the mice. The mice, we give them 40% calorie restriction [CR] - but that's like water only fasting in humans, okay? People have to have to realize that because of the 7-fold difference in basal metabolic rate between mouse and human.

So ketogenic diets:

A lot of misinformation, a lot of misunderstanding. Basically, these are low-carb diets, high-fat diets. But it's the types of fats and proteins that play an important role.

Basically, you eat these diets in a restricted amount. The ketogenic diet, unfortunately it was labeled with the word 'diet', right? Whenever you put 'diet' on something, everything becomes like mysterious. It's a medicine! The ketogenic diet is a medicine, it's called ketogenic metabolic therapy and it should be respected as a medicine! If it's not used properly, it won't work, just like any medicine.

Not to say that it will harm you, but if you do eat too much ketogenic diet, you can in fact get insulin insensitivity. We worked in the epilepsy field for years and we understand how some of these diets can be not as effective as they should be.

But the whole strategy is not complicated, right? If the tumor cell needs fermentable fuel, then you take the fermentable fuel away from the tumor cell and you transition the body to a non-fermentable status:

So you lower the blood sugar that the tumor cells need and you elevate ketone bodies, which the tumor cells can't use - but the normal cells can. You just simply marginalize the tumor.

Now, the tumor needs fuel, it can't live without energy. Where is it getting its fuel? It's fermenting. You're taking away a prime fuel - what's going to happen to those tumor cells? They're either going to die or they're going to slow down. And that's what happens!

Now, the first person that did this work was Linda Nebling, in a human situation, I should say:

She took two little children, hopeless cases. Brutalized. Brutalized by the system. If you read her PhD dissertation, you'd be crushed about what they did to these little kids. They surgically mutilated them, gave them massive doses of chemo, radiation, all kinds of stuff. And they gave them up for hopeless, they said these kids aren't going to live more than two or three months.

She says "Can I try a ketogenic diet?" She was in nursing, getting her PhD in nursing. "Yeah, it's not going to do anything, they don't have long to live". So anyway, she rescued both of these kids! Their quality of life improved dramatically, they lived far longer than what was predicted. And it was based on the whole shift of the body's metabolism and I said "Wow, this is unbelievable!"

This was back in 1995 and I said to my students "You know, we should try some of that with our brain cancer and the mice!" And we were building these animal models, beautiful animal models of human brain cancers and we had the CT-2A, a neural stem cell tumor. Everybody's excited about neural stem cell cancers.

Anyway, we just gave them a standard diet [SD] - which is a high carb diet - but calorie restricted by 40%. Which is like a water-only therapeutic fast in humans:

And these tumors started to shrink big time! You know, go down 60 to 85 percent reduction in size.

And we said "Geez, what? Wow!" You know, I never saw anything like this before, so powerful, "What's going on?"

So then we analyzed, using linear regression analysis, using glucose as the independent variable, and either ketones or tumor weight as the dependent variables and glucose as the independent:

Each square is an animal on a different diet. And you can see on the left here: As blood sugar goes down, ketones go up. And this is an evolutionarily conserved adaptation to food restriction. When our bodies are not getting the carbs, we're going to start mobilizing fats, bring them to the liver, chop them up, make water-soluble ketone bodies and these are going to go to the the tissues.

And on the right side: The blood sugar goes down, the size of the tumor goes down. The higher the sugar, the faster the tumor grows - the lower the glucose, the slower the tumor grows! Right?

So the higher the sugar, the faster your tumor grows.

The lower the sugar, the slower your tumor grows.

So if you want your tumor to grow fast, get your blood sugar up as high as it can get! Right? You go to oncology clinics and you see everybody eating ice cream and cake and candies! Don't they read the literature? This has been supported now in human gliomas, breast cancer, colon cancer... if you want your tumor to grow fast, get the sugar as high as it can go!

Now people say "Well, this looks wonderful and great, but we don't understand the mechanism." Bullshit! You understand the mechanism! We published so many papers and so many other people published papers on the mechanisms by which this works!

It's anti-angiogenic, anti-inflammatory, pro-apoptotic. No cancer drug is known that can do this without toxicity! And therapeutic fasting can do it! So we and others have shown in many papers the molecular mechanisms by which this process works.

When you hear people say "Well, it's not proven!" – Well, they don't read the literature, nor do they contribute to it!

So this woman had this dog with a big mast tumor on his nose, right? Minka. You know, she listens to our YouTube videos and reads our regular papers. She's a lay person, doesn't have any training in medicine or anything.

This dog has this big tumor, she goes to the vet, who said "Well, yeah we're going to have to cut it out and then we're going to give radiation and chemo. 'about ten thousand dollars, maybe the dog will live seven more months. But it's going to be sick..." and blah blah, you know. The same stuff.

She said no. So she went to the butcher and she got the fresh chicken meat with the bones in it. Cut the calories by 40 percent, threw in some medium chain triglyceride [MCT] oil and some raw eggs in the mix. The dog lost about five percent of its body weight.

And you can see: The tumor started to shrink and disappear!

And, you know, Minka is still alive today, doing fine! This was back in 2013. Impressive, how fast the dog responded, and there's many dogs now. They're putting them through these metabolic therapies that are doing really well.

Of course, the veterinarians were all over me about this. They don't think they should feed the raw meat to the dogs because of salmonella poisoning! Give me a break! I mean... have you ever seen what dogs eat? It's like, give me a break, you know! Salmonella poisoning!

So you're looking at this stuff and you're saying "Jesus!"... and then we did a YouTube video on this, about the dog cancer thing, got 5.3 million hits! Can you believe this? So there were all kinds of trolls out there, writing all these negative reports, giving me all kinds of grief. The hell with them, you know.

Okay. Now I want to talk about a really serious issue here, glioblastoma multiforme. And this is a really bad tumor with poor prognosis:

And unfortunately Senator John McCain is now struggling with this kind of a tumor. It's a nasty cancer, many multiple different kinds of cells, no effective therapy. So you get a whole bunch of different kinds of cells. Consequently the name "multiforme": Highly invasive.

So when you look at a brain tumor... here's a poor soul that sacrificed their brain for the study. And you can see: This nasty necrotic area, a cyst, large cyst:

But, if you look at the midline of the brain, you can see it shifted to the left. This is called "midline shift", okay?

So these tumors grow and they cause intercranial pressure. And people die from intracranial pressure, most of the people who have these kinds of tumors. The problem is: You can't surgically resect them, because the tumor cells have already spread out into the normal appearing brain areas. And the tumor cells use blood vessels as one of the mechanisms to disseminate: They go across the surface of blood vessels in the Virchow-Robin space.

So they use these blood vessels as kind of a railroad system to get through the brain. So it's very, very hard to do any kind of surgical resection. And you can see them, the dark blue cells around the blood vessels are the way... you can see on histology. Histology will tell you. This is how they spread through the brain and make it very difficult to get resolution.

And we all know that mitochondria are abnormal in brain cancer.