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SNI Digital, Innovations in Learning, Video Journal, Interactive with Discussion,
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now offering this program on podcasts on Apple, Amazon, and Spotify,
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in association with SNI Surgical Neurology International, an Internet Journal with Nancy Epstein as its editor-in-chief, is pleased to present another in the SNI Digital series of Dr. Blalock
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reports, and this report is on the molecular basis of cerebral aneurysm formation.
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This is an image of an aneurysm, as you can see the
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dilation
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in this blood vessel on the base of the brain into a big bulbous clot-filled area that can rupture and produces blood around the brain and can be lethal
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Dr. Blalock is the CEO of Theoretical Neuroscience Research, the associate editor-in-chief of the neuroinflammation section of Surgical Neurology International and SNI Digital. He is a
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board-certified clinical nutritionist. He is the creator and editor of the Blalock Wellness Report, author of multiple books, scientific papers on social health, political matters, he's a
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commentator for radio and TV, and also with the epic times. These are some of Dr. Blalock's publications and books. published on natural solutions for liver care, strategies for cancer patients,
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natural health, excitotoxins, which is going to be a topic of this discussion today, cellular and molecular mechanisms in the biology of autism. And together, we've written a book together on the
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China virus. What is the truth about COVID-19? And he publishes a monthly newsletter called The Blalock Wellness Report, which has been in publication for 20 years. You can subscribe at
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wellnessreportnewsmaxcom. This
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presentation is also co-authored by James Osmond, who is the creator and founder of CEO of SI and SI Digital, professor of a number of universities out of urinary surgery, and report health systems
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in Chicago, and the University of Illinois at Chicago. He's a futurist and entrepreneur in a health care consultant. This talk is about a molecular basis of cerebral aneurysms. There have been
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some historical treatments of this. The first one nobody knew what to do about it and was just waiting and observing and most of those patients or many of them died. Second treatment was to ligate
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the corotid artery in the neck for aneurysms distal to that and the next treatment was clipping an aneurysm with a clamp that separates it from the circulation or putting coils in the metallic coils
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in the aneurysm by interventional radiology treatments. These treatments have been helpful but they were not curative on about 20 of the patients and these treatments and the disease. is associated
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with a large morbidity and mortality. At this point, there is no way of preventing the disease, except knowing about its genetic basis, or ceasing smoking, or having blood pressure control. The
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fundamental cause that Dr. Blalock is going to address is what is the cause of aneurysm formation? OK Today, we have another in a series of presentations by Russell Blalock on the molecular basis
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of cerebral aneurysm formation. And this is a topic that's very important in neurosurgeons. And
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he's going to tell us how we've gone through a whole series of
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years in history here with various kinds of treatments. And it looks like we are getting to the point where there'd be a molecular specific drug treatment for it, and he'll lay this all out for us
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so we can understand that, and we'll talk a little bit about what that's gonna mean. So this is the talk you wanna start here, and then we can go into what it looks like in some of the introductory
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things, and you can go from there, and I'll pick out whatever slide you need to help you. Well, what we're basically doing and it's all of us as neurosurgeons, and very early in my career, we
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wanted to know what is causing aneurysm? Why do they form at all? And we knew there's a lot of hypertensities who never develop an aneurysm. There's hypertensities that are moderate. They develop
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not just one aneurysm, but several aneurysm, and we know that it's a highly fatal disease that anywhere from 30 to 50 of patients die before they ever gets to
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hospital,
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And another high percentage die once they're in the hospital and the survivors frequently have neurological deficits that they deal with. So we never could understand what is causing them to perform
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in the first place, if it's not hypertension, hypertension. And of course, this gets into modern biochemistry, modern pathophysiology, in which we see a lot of diseases, particularly affecting
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the nervous system, are inflammatory diseases, or at least the process begins with inflammation. And so we looked at aneurysms, and we discovered that it's not excluded. It's also an inflammatory
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disease. And there's a group in Japan that has done tremendous work demonstrate this connection to inflammation. Well, the first person to say an angioidodum was caused by inflammation was an 1847
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burn cow said it's inflammatory disease. It was ignored until recent. And so it's like most scientific discoveries are hundreds of years old. Somebody said it long ago, but it was ignored. And
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people looked at other things and they passed through, of course, the reditary. Well, only 10 of an aneurysms are the reditary. The rest are caused by something else.
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Russell is a picture you wanted which shows an aneurysm you want to describe that? Yeah, you see here the bass or artery and coming up at the base of the brain and a huge ballooning of an aneurysm,
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It's a fairly large aneurysm than it ruptured.
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and the blood is escaped into the subratinoid space in the cistern.
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So the question is, what made this basilar artery balloon? What weakened the wall of that artery to produce that ballooning? And why did some area of that aneurysm eventually ruptured and allowed
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the blood to enter that subratinoid space in that cistern?
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Next slide
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This is the one of that you were going into, you started in. Yeah, the historical treatment is basically Vircal, who was a famous pathologist, neuropathologist. And he was of the opinion that
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aneurysm were caused by inflammation. He didn't know why, he didn't understand the mechanism, but he said every case we look at, there seems to be inflammatory cells in the wall of the artery
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that's involved And so we're mistaken. over a hundred years to finally see well he was right and the people that found the proof that he was right was a group of Japanese researchers who looked at
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this and next slide and they did a study on aneurysms and what they found was that in every case there was an infiltration of immune cells in the wall of the artery from the very beginning and that at
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the very beginning of this process there was inflammation and so you asked well what caused inflammation well if you look at the bifurcation of the artery there's a stress at this artery and we see
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that most aneurysms are formed at the bifurcation of vessels and the
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stress produces an area of inflammation in the wall of the vessel And you know, the histology of arteries, there's several layers, an outside layer, the adaptation. And then there's a schmoo
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muscle layer, which is the media and internal elastic layer. And then outside of that is the endothelial cells. Well, the endothelial cells of the artery, I call the brains of the artery, 'cause
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this was responsible for the dilation, the constriction control of the blood flow of the vessel. It contains a lot of ability to control that vessel. And so they looked at this area
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of inflammation and they saw, well, it's like most inflammation in the body, it's through the NF-cap of B, being activated, and NF-cap of B moves to the nucleus of the cell, activates the
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inflammatory genes, And this starts to produce localize inflammation at that
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bifurcation. What makes the anger to progress is that the endothelial cell secretes
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MCP1, which is a chemocan. Chemocan is a tract immune cells. That's their function. And MPC1 attracts primarily macrophages, leukocytes, neutrophils, and
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basophils as
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a minor cell, and in case of natural killer cell. Very few. But the number one cell attractive seems to be the macrophage. Well, that enters the wall where that vessel is inflamed before an
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aneurysmium formed. And it begins to destroy the wall of that vessel and weaken it so that the media is damage begins to thin, the internal elastic and the external elastic membranes are weakened,
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and you get this bulge, and that's what causes it to bulge, is the pressure from the artery at that vivrication, stress, we'll make that aneurysm start to get larger. Well, they knew that these
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immune cells, particularly
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the macrophage, release a number of destructive chemical, particularly the proteolytic enzymes, there's 14 different proteolytic enzymes called MMP, which is a metalloprotonase and, MMP2 and
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MMP9 are released by the macrophage into the wall of the vessel and begin to destroy the media, the internal and elastic layers, and so the vessel is weakened at that point of the inflammation and
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it begins to form the aneurysm, which you see down below, the aneurysm is now formed in that rectangle. And so then the process began. More and more macrophages are attracted to that area. And we
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see, if you look at the timeline of an aneurysm, more and more inflammatory cells begin to arrive and filtrate even a wall of that vessel, the aneurysm
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becomes thinner because it's destroying the media, the internal elastic, extra-enelastic layer, and then the adventition. And eventually, what we call the fondness of the aneurysm in about 84 of
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cases, the erupts are there. And because it just dissolves the outer portion of the fondness of the aneurysm and the pressure can break loose and then it forms this overachnoid hemorrhage.
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Next law. Okay, this is uh, so what they did is they they said well gee if that's going to happen Maybe I can give them a chemical which will stop Macrophages from Coming in and destroying the wall
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and they did an experiment and here they gave them a An agent that's the agent that's the name of pfo for four. That's an experimental drug This is an animal that had an aneurysms ever induced and
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you can see what happened is that The aneurysm size was was diminished and here
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is the aneurysm here And actually it went back to a more normal appearance here And the control animals which only got which is a vehicle got that so What they did is proved what you said is right if
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I stomp the macrophages from getting in here and slow down this inflammatory process, I can reverse this. Is that what you got out of this? Yeah, what they're showing is that if you allow the
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macrophage to enter the wall of that aneurysm, that fund us. It's gonna secrete digestive enzymes, and later what I'll say is exciter toxicity and destroy the wall of that aneurysm, that fund us,
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and it's gonna rock, which is your top diagram there. If you do nothing, if you give a drug to block the macrophage from ever in here, the wall of the aneurysm, then the aneurysm can restructure
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itself. It's always remodeling itself. And it remodels, strengthens, and then you can prevent an aneurysm and prevent any other ones from forming. Do you wanna talk about immunocidotoxicity now,
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or because this is the concept that you've really pioneered. And this is an inflammatory cell, which is going into this little pathway through the aneurysm wall.
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And then I won't, I'm going to not see any more here, but if you wanted to start to talk a little bit about what's happening here, and this leads to some more things that are going to cause
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destruction. Well, what you see with aneurysms is that in that local area, the TNF alpha, which is inflammatory cytokine, goes sky hot. And another inflammatory cytokine called in leukin-1 beta
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begins to elevate. And both of those are triggering not only these destructive enzymes that are described to MMP-1 and MMP-9, but they're also triggering the exciting toxicity within the wall of
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that vessel.
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And so if you look at that slide there, it says acute microglial activation. But what we know is a microglia and a macrophage look almost identical. They have a identical function. A macrophage
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can enter the brain and it's very difficult to tell the difference between them. So they do the same thing. And so if you just change that from a microglia to a macrophage, it's releasing high
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levels of glutamate and inflammatory chemicals, quinoleic acid, rachidonic acid,
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and other inflammatory cytokines. And high level, just like a microglia was. And that would trigger free radical generation. The free radicals will further destroy the wall of that blood vessel.
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And then you get down to the stage where it starts interfering with the mitochondrial function.
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hard reach have mitochondria as well. So it's not able to produce the energy it's supposed to produce. And that will cause a further increase in the pre-radical generation and a further death of the
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cells and the elastic fibers within the wall of the aneurysm. And this is just showing what happened to the microfay, but this is what we call immunoexciter toxicity. We also know that TNF-alpha
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can interfere with the
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release of
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glutamate and dramatically increase the exciter toxicity by that mechanism. And so this also explains why the TNF-alpha is producing all this damage. It's just like, Huh? we look in the brain when
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cells are destroyed and when the TNF-alpha is high, the same thing's happening in the wall of the vessel. But I just threw that in. I think that more research needs to be done in this area 'cause
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nobody measures the glutamate in the wall of aneurysms. Nobody looks at the macrophage and seems to realize that all immune cells when activated release very high levels of glutamate and that you can
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produce excitotoxicity in every tissue. So if we go back to the macrophage in the earlier floods,
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and so what we see is the inflammation that I said was caused with the bifurcation by arterial stress is triggering inflammation. The inflammation is triggering the release of MCP1, which is a chemo
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gun and a tractor.
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macrophages and it draws the macrophage into the area of inflammation at that
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bifurcation. Then as the vessel becomes weaker at that area, it balloons more macrophages that will arrive and secrete more protolytic enzymes like MMP2 and MMP9. The TNF alpha continues to arrive,
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so there's more destruction of the wall of the vessel, more destruction of the fundus of aneurysm, eventually it becomes so weak that it'll burst and then you have a rupture of aneurysm. If you
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stop that, like if you take an experimental animal, we can experimentally produce aneurysm, but if you block macrophages in that animal, it's very difficult to produce an aneurysm and then it's
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very difficult to get the aneurysm to rupture and we find, well, if you also stop the
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At the very beginning, it's also very difficult to produce aneurysm. And it's very difficult for them to grow and to rupture. And so now we have through these various experiments that were done
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demonstrated that indeed, if you block the inflammation, if you block these enzymes, if you block the TNF alpha, aneurysm is a form. The aneurysm does it rupture And in the experimental animal,
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it's very, very difficult to form an aneurysm. And if you even have these cells arrive, but you block
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all these
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toxic factors, an aneurysm won't form. So it's the toxic factors being released from the macrophage. And these other cells are producing the destruction and the eventual rupture of the aneurysm.
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with this drug that they use, which I think is too toxic to use, that's often. But we know there's some natural substances that can do many of these same things. And so what they did is they
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looked at, well, we know that vitamin D plays a big part in the increase of all these destructive factors, that if the vitamin D is low, there's an increase in TNF alpha, an increase in leukin-1
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beta, an increase in Mm2, Mm9. So all of the factors that are responsible and have been demonstrated to cause the aneurysm and to cause the rupture are linked back to this process and can be
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blocked by natural substances like vitamin D And so they found that if an animal has a high vitamin D level
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It's very difficult to form an aneurysm just like if you block the macrophage.
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And so then they try to other light, like riboflavin. We know riboflavin has a similar flip. It lowers TNF alpha. It interferes with MMP2 and MMP9. It lowers and luke in one beta. All of the
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toxic factors that are producing the aneurysm and causing the introduction of block And so if you do that, we find that aneurysm, whether in the head or the aortic aneurysm, will not form and will
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not rupture. And
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so then they started looking at other, like a piscetin. Piscetin is one of the most powerful natural substances or any substance found to prevent senescence of cells. And they found out as you get
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older, your arteries, the sales line in your orders becomes senesis.
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And so, they're stiffer, they're weaker, they're more likely to perform an aneurysm, but with the five-seatin, it reduces the stiffness and it reduces the incidence of an aneurysm. And we see
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the same thing with Kirkman. Kirkman goes even further. Kirkman blocks all the factors we know that calls inflammation. It blocks NF-CAPA-B, it blocks
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the release of a rachidonic acid, it lowers the prostaglandin, plantaroid prostaglandin, which you see on the left there, the PGE2. And so it's virtually it's COPs too, lots. All of the things
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we know that produce inflammation are blocked by Kirkman. And so if you feed Kirkman, you also prevent aneurysm formation And it's a comprehensive one. It's not just attacking the traction.
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of macrophages, it's inhibiting the inflammation that started the process off. So
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we have in our armamentarium this being ignored, some natural substances that indeed can alter this mechanism.
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Okay. So I think much of what you're really saying and
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we're trying to help neurosurgeons understand and neurologists where the biochemistry of this is. So it gets into the areas that we don't talk about very much. But basically what he's saying is, is
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this starts out as a molecular disease with a very minor injury, which leads to an inflammatory process and the inflammatory process then degrades the aneurysm wall or degrades the vessel wall
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producing an aneurysm and makes it weaker. and there are all kinds of other inflammatory substances, pro - and anti-inflammatory substances which come in there. And if you are able to treat this as
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we showed you in some of the images that they did in our laboratory, they were able to reverse or reduce the aneurysm-sized formation. And so that's the fundamental observation, which is really a
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major step forward because for what we've been doing this for 50 years, either treating them with clipping them or putting coils in there or something, and there's a failure rate in there and
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there's a high mortality rate with rupture initially. If you get that, you're gonna imagine if something's out, like that's in your brain in a rupture and not gonna do very well. And so this is a
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major advance in mineral science and medicine and it gets to some basic body mechanisms. that are pro-inflammatory and anti-inflammatory. Is that right? That's right. I mean, it breaks down to
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what we see in other neuro-water group condition that the beginning of that condition and throughout the condition is inflammation and all the biochemical effects of inflammation. In the artery, the
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special thing that's happening is also the excitotoxicity is occurring and we know that once an aneurysm ruptures and there's a brain, the prognosis of that
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subratinoid hemorrhage depends on the glute mate level in the CSF in the brain. That people with higher glute mate levels have a poor prognosis. Those with the lower level have a better prognosis.
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Now you talked about this in previous videos, you talked about this as a, a fundamental mechanism as long as we got this slide in front of us for the formation of atherosclerosis. And if you look
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at the
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process, if you look at the process of atherosclerosis, it's virtually identical. As you have inflammation along the endothelium, the endothelium secretes
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MCP1, it attracts the macrophage to the vessel wall and filtrates the fatty streaks, which are the earliest change of atherosclerosis in the vessel and begins to produce destruction of the wall of
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the vessel and the calcification and the other effects that we see with atherosclerosis. And that if you take animals and you block the MCP1, it's very difficult to produce atherosclerosis, even an
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animal that is genetically prone to produce rampant atherosclerosis. it's difficult to produce it in them if you block the macrophage. So
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this is an underlying mechanism of a whole bunch of diseases that we see, and this is the fundamental principle mechanism by which all this is happening. That's right, I mean, if you look at an
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aneurysm, all aneurysms have atherosclerosis in them. So here you have this process occurring in an aneurysm, it's producing both events It's producing an aneurysm and producing atherosclerosis,
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which you would suspect if it's the same mechanism. And when we look at the atherosclerotic lesion, we see
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the same process going on. Well, when we talk about bacterial infiltration of vessels leading to atherosclerosis and even bacterial aneurysm, we see the same process, it's triggering inflammation
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that weakens the vessel, it produces acid sclerosis and it can produce angurism. And then we can have bacterial angurism.
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Okay, so we're explaining a number of diseases with this. There's a few more things here that they talked about. Do you wanna get into this anyway, this signaling pathway which stimulates the
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macrophages from coming in and then doing its job? Or do you think we've covered that enough? Yeah, the CCL2,
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that is the same thing as
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MPC1. The CCR2 is its receptor. And we know that the front that we discussed before is the one that makes the MPC react with that CCR2 receptor. And so what you're doing is you're blocking it with
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that cell phone to prevent. it from interacting with its receptor, triggering this whole chain of events. And so you're interfering with the cell signaling that we know is the basis of the
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formation of both atherosclerosis as well as aneurysms. So what they did here in this experiment when they gave them
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this disulforam or this chemical that essentially was inhibiting the macrophages, basically what they were doing is they were stopping this signaling mechanism that was attracting more macrophages to
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this area, right? And that stops the disease. Yeah, it stopped that cascade that was triggered initially by the inflammation, the localized inflammation. So what you're seeing here on this slide
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is what's happening is this is, and you see the yellow arrows and the red arrows where this is all being self stimulated and basically you're shutting that down So you don't run, it's disease.
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you're stopping all the factors we know that cause inflammation, and you're stopping
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the chemocyanne that's attracting the immune cells, particularly the macrophage, that's gonna make it even worse. So there's a whole bunch of chemical reactions and molecular reactions that are
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going on at all this time, and the body is adapting the various signals it senses from the environment and so forth And this is going on in all 36
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trillion cells in the body, the body was all attacked, but it's going on in areas where there are organs and injuries and so forth. So this is a, almost a massive orchestra of all kinds of things
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going on. And to get this to be productive and helpful, you have to have, this has to be almost like a symphony conducted. together, so it all makes sense. Well, you also have to realize that,
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because of the complexity of process, we have natural substances that can interfere with key areas of this process. These natural substances are not being used. We're using drugs that attack only
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one aspect of it. So if you use a Cox-2 inhibitor, well, that's helping So that didn't have any effect on Cox-1 lots. Are the other factors like PG-E2, arachnoid acid, release, the phospholipid
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process? And
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so we are using drugs that are barely putting a chip in an armor where we have drugs that are natural we have substances that are natural, they can affect numerous.
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process. That's a good point. And you're trying to stop this while all these chemical reactions are going on. And you're making free radicals, which are highly reactive molecules. You're trying
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to really shut that down and modify that. So all this series of events doesn't continue. Correct? That's right. And you see, what people don't know, we know that a lot of people know that
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there's good mate receptors in the brain. And this is a number of types of receptors. A great number of physicians don't know, there's good mate receptors virtually everywhere in the body.
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It's in your pancreatic islets, it's in your vessels, it's in the endothelium, it's in your heart, it's in your liver. So we have it everywhere. If you stimulate that, those receptors and those
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tissues. It were critter. a series of destructive reactions which will destroy that tradition. Well, you talked about that in diabetes that we, you had a Dr. Blalik reports on, talked about it
34:17
in atherosclerosis, and
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it talked about it in a number of other processes, and they can go back and look at some of those videos. Let me ask you a question here, now we're at a point in science where during our lifetime,
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we've now seen the entire history of aneurysms, basically, in which it was treated initially by simple methods, or by either clipping it or putting a clamp on it or putting a coil in it, and those
34:53
were not 100 successful. It's not working now, we're at a point where there's a biochemical treatment for this, and it's also a treatment for the underlying inflammatory diseases that you're saying
35:06
are associated with this, how long is this going to take? And you mentioned some natural substances which will add into the talk so that they know about it. They've tried disulfur and they tried
35:19
some other substances which are too toxic,
35:22
but you say there are some natural substances that aren't toxic that are very helpful and can be used We'll list those for the readers. Well now, what's the progression here? How is somebody going
35:36
to get this into the clinic and use it on patients? And I'd like to hear your view on Epa. My view is you've got a very complicated patient and for some reason other is either he failed all the
35:49
other treatments and he's still got these or he's got other aneurysms as they may have multiple aneurysms. That might be a patient that you would get special permission and they tried to do that.
36:01
The government gives you a special permission to use drugs for certain things they did in COVID, but it was corrupted because they suppressed all the other drugs that were helpful. But here you
36:11
don't have any other choice and you do something and you track it and you'd say, gee whas, it worked in five patients, I did it and then the studies would expand and eventually it becomes part of
36:22
the treatment. You agree with that? Yeah, I mean physicians should know that this is the mechanism, it's been shown like an aortic aneurysm, one of the principles of treatment of aortic aneurysm
36:36
is you watch it, but you don't know which ones are gonna rupture. So you surgically treat them all. Now we know that if you scan that patient and you see very little inflammation in the wall of the
36:51
aortic aneurysm, it's not likely to progress. But if it is highly inflammatory, You better operate on it. because it's gonna rupture soon. And when you look at intracranial aneurysms, we saw the
37:04
same thing, is that the ones that ruptured had the highest immune cell infiltration, the ones that were least likely to rupture had very little immune cell in them.
37:17
So my point here, and what you're saying is very, very key, if people are looking to learn how our surgery is gonna go in the future, it's gonna take some time for this to get into the clinic and
37:30
be approved and so forth and so on. And I'm sure some of the natural substances that you've talked about are gonna be very easy to approve because these are basically have zero to no toxicity.
37:45
And we just have to show that that works and it looks like it's gonna work from all the other knowledge you've had in other systems.
37:53
This can become part of an armamentarium And if I'm going to have a department - the thing to do is you start getting into these areas. And you look at them, what is the basic biochemistry or
38:05
understanding of diseases? Because as Russell has just shown us, this is fundamental atherosclerosis and a whole bunch of other diseases. And you ought to be the one who knows about it rather than
38:17
some other specialist who's going to take the patient from you. That's fine. But the problem we have, and you know it, we all know it, is there's too much money involved. And so if it's a cheap
38:31
treatment, a natural product that will cure the problem, prevent the problem, they don't want it because they're making a lot of money off of this pathophysiology. So they don't want something
38:44
that's simple. You
38:48
could just take orally and prevent atherosclerosis or an aneurysm or a neurodegenerative disease. They want it complicated. they want you to take a drug forever. And they want that drug to be very
39:02
expensive, or they want the surgical procedure to be very expensive. So we're fighting an uphill battle against money. Yeah. Profit. Okay, anything that we've left out, I think you did a
39:17
terrific job of explaining what is an extremely complicated and involved problem that we know we didn't understand for years And now we have an understanding and the Japanese did a wonderful job on
39:31
this. I think some other people around the world got into this, but nobody's pursued this to this level as this fella has. And obviously people are doing it for aneurysms in the aorta. We didn't
39:42
show that information slide, but that's happening. So anything else we didn't cover on this particular subject? Well, one of the things that was kind of a sad item
39:56
The observation was that riboflavin prevents abdominal aneurysms and intracranial aneurysms. And it
40:03
does it again by inhibiting all these factors that produce destruction of the walls of the bustle. Well, riboflavin is very cheap. It's very well absorbed. It's extremely safe. So there's no
40:19
reason not to do that It was also shown that the risk of rupture of an aneurysm was directly related to the vitamin D, vitamin D3. That was shown in humans. And so that's very easy to correct
40:35
orally or by exposure to sun. And you can get the vitamin D level up, reduce your risk tremendously And you can take the riboflavin, reduce all of the factors that are known to be responsible for
40:50
the destruction of the bustle and the formation of aneurysm. There's no reason not to do it. It's safe, it's inexpensive, it's readily available. And we've told people, and you've told them
41:03
through many of these videos, that because of our dietary change, because of our change in farming methods, people are deficient in various vitamins and minerals that they need in their diet,
41:18
right? That's wrong. And also, if you wanna look at some of these, you've talked about patients who are profoundly deficient in vitamin D, vitamin B12, which also helps you on an nervous system,
41:32
and a whole bunch of other factors that you think you're getting in your diet. And then we have 50 of the people obese in the country and around the world, actually. And they're eating all this
41:42
junk food, which has glutamate in it, which is an extremely toxic substance in the diet, but they put it in there, so it makes it taste good. And so it makes you addicted more to that. And so
41:56
you're taking the wrong things and only promoting these diseases, which is why we're seeing more of these diseases than people as they get younger. Is that all true? Yeah, almost all of it can be
42:07
related to diet. For instance, vasospasm with ruptured aneur. That was always our big enemy when I was in training. What do we do about vasospasm? Well, I did a lot of study back then and I
42:20
found out, well, magnesium prevents most of this vasospasm
42:26
and all these drugs that's preventing vasospasm, they're no better than magnesium. And most people are magnesium deficient. And in the heart, the coronary arteries, if they're magnesium deficient,
42:40
are highly likely to go into spasm. And that if your magnesium level is higher, the blood flows through the coronary arteries and the cerebral vascular system, before graded Well, this has been
42:54
known for a long time. we've done enormous experiments throughout that time. So there's no reason for not knowing that, except it cuts into profits. We can sell this drug that's a vasodile layer.
43:07
And
43:08
you can take that to prevent supposedly the vasospasm after aneurysm rupture, which can be delayed, which you can also take magnesium. Raise your magnesium level in these vessels, or walled about
43:23
and block it all.
43:26
So Russell is really telling us, and he's has a whole series of videos on SNI digital going into these various disease processes, and these natural substances that have been found to be very, very
43:40
helpful, not toxic, and are very protective. I think you can go into SNI digital look up in the index for Dr. Blalak reports, or put Dr. Blalak in the search, and I'll come a whole series of
43:54
these. studies where he talks about it. These are things that are gonna be very important for you
44:01
to know, even though you're a neurosurgeon, you wanna just get in there, take care of the disease and leave. Your patient's not gonna do as well. He's even got some studies in there showing that
44:10
the patient immediately after surgery, surgery represents an extremely traumatic experience for the body. It's almost like he was taking care of burn patients earlier in his history The patient
44:24
patient's coming in with third-degree burns. That's what the metabolic disturbances are. And if you treat those instead of just giving them water and glucose, that's not gonna do anything. So
44:30
there's a lot to learn. And
44:32
this is just another example of
44:40
another disease
44:43
that has a similar mechanism that's causing it. You agree with all that? Sure, that's what it's exactly right what we found recently wrote about. the danger of excess glutamate in the diet over 20
44:57
years ago. Now, there's a whole new set of articles demonstrating significant organ damage from glutamate that can last very, very long periods of time. Well, the argument was always well, the
45:11
brain's detected to get glutamate by the blood-brain barrier. Well, I showed that nonsense, but there's no barrier for your other organs, your heart, your liver, your pancreas, your intestine.
45:25
They all have glutamate receptors. There's no barrier. And so whatever you eat and raise your blood level of glutamate, it's triggering those receptors and triggering the excitotoxic reaction.
45:41
Well, okay. I think you've done a terrific job of explaining a very complicated issue and back to some fundamental basic principles that people should know about.
45:52
Yeah, they should. And all neurosurgeons should understand this. I mean, Birkow hit the nail on the head in 1847 and we're just now understanding the biochemistry of this process. And it's been
46:06
very well demonstrated, both in humans and in experimental islands. The references I provided you make no question that all this is true. This is not a hypothesis It's not a theory anymore. It's
46:24
demonstrated that every way you could demonstrate.
46:28
Okay terrific, we'll have all the references in for some of these papers in here. And I really appreciate it. I think it was a very good explanation for something that's very important to
46:41
neurosurgeons. Okay? Thank you, Jim. Thank you very much, Russell.
46:50
These are the key references, slides, and charts from this presentation. We suggest you take screenshots with your camera for records or on your computer, and you can use them for future reference.
47:08
These are some key topics that were key papers that were discussed and that form the basis of this talk They're all developed by Tomohiro Aoki, who's in the Department of Molecular Pharmacology in
47:26
the National Cerebral Cardiovascular Center in Osaka in Japan.
47:33
This paper is on intracranial aneurysm as a macrophage mediated inflammatory disease. Dr. Boylak discussed this in his introduction. This is the figure you've seen. mostly which deals with many
47:47
biochemical reactions involved with the
47:51
macrophage, which is a screened cell here, which goes through the endothelium, and then multiplies by a chemo-attractant mechanism to draw more macrophages to the lesion and destroy the cell wall
48:07
and the muscle wall so that an aneurysm forms.
48:11
This is from the experiments that Dr. Aoki and his colleagues did in which animals, in which they were able to produce animals or aneurysms, were fed a certain compound that they had, its compound
48:24
PFO441894A8, and that compound basically would stop the accumulation of macrophages in the aneurysm wall. And you can see here in A there was an aneurysm that was formed when they were given this
48:42
drug, this drug listed here.
48:46
You can see that the aneurysm formation was suppressed. You see that in the red line and the chart here. In other words, there are very small bubbles in the blood vessel, but without it, the
48:57
blood vessel continues to large and to develop.
49:02
Dr. Yoyuki and his colleagues went on, had another paper in 2019 on macrophage imaging of aneurysms. Because in Japan, they wanted to predict when these aneurysms would rupture and they thought if
49:15
they could identify the macrophages in the aneurysm wall, they would know which ones would rupture. And in this study, you can see with a little aneurysm bulge on the blood vessel here, they were
49:27
able to give the animal these iron-loaded
49:33
particles, which were taken up by the macrophages.
49:38
Now, if
49:43
the macrophages were not active, the macrophages would not take up this iron loaded. material, and you could see here it's in the macrophages here, but there are no macrophages in this aneurysm.
49:49
So the imaging didn't turn out to be positive here, but was positive in
49:58
those which had macrophages in it, and they thought that this would be a way of identifying the aneurysms. The problem was that the substance that used to identify it was
50:08
too toxic for patients and it couldn't be used, so they did some more studies.
50:15
And this is the last study that was the most recently published study in 2025 February, which is a study showing that there is a signaling agent and its receptor, which then attracts macrophages to
50:33
the wall of the aneurysm, and that leads to destruction of the cell wall and aneurysm formation. He talked about this in his presentation. This is an excellent paper you should screenshot this with
50:46
the others and use this for references.
50:52
This is just an example of what he did. In the animals who had the aneurysm formation, these are aneurysms
51:06
who were treated in a certain way so they would form aneurysms. And the second set of animals were treated with disulfuram, which was
51:15
the ancient esol, which is an ancient use in alcoholism to prevent alcoholism, to reduce the number of macrophages in the cell wall. And you can see here that there's a significant reduction. And
51:28
here the top diagram with a little bit of reddish standing in there shows the thinness of the wall here where the aneurysm is going to develop. And when they gave them the disulfuram, The wall
51:40
became thicker and the aneurysm disappeared. And again, the incidence of aneurysm was much less than the animals that had disulfuram. Here is another experiment done, which specifically tags
51:54
macrophages, and you can see they're reduced in number.
51:59
And this is a staining he did, which showed the staining in a superficial temporal artery, which has no reason to have inflammation in it. And it doesn't show in a green, very much inflammation
52:12
And this is a nuclear stain here of the nuclei of the cells. And here in this next slide, in animals that have the aneurysm, you can see the red shows a marker for macrophages, as does the green,
52:25
which attaches to macrophages. And this shows the macrophages in the lesion in the aneurysm.
52:34
Basically, what is involved here is a signaling pathway, which known as a monocyte chemo attractant protein. And that binds to its receptor CCR2, which is part of the signaling mechanism. And
52:48
that initiates a cascade of downstream signaling events, eventually playing a significant role in the recruitment and activation of immune cells, particularly monocytes and macrophages, which are
53:02
crucial in the development of the aneurysm and its disease progression.
53:08
Now, these are the references Dr. Blalak has assembled for this talk, there are 39 references. So I make a screenshot of these references. It goes on for five pages. And I'll just pause for you
53:23
to have make a screenshot on each page. These are the first seven references. Here's the next seven references.
53:34
Here are the next seven references
53:38
And here's seven more references.
53:42
and the final last up to 39 references.
53:49
This is the key reference that was a significant piece of work that Dr. Aoki and his colleagues did. You can screenshot that. And
54:02
Dr. Blalock also mentioned that besides using disulfuram, there are other natural agents which are available which can stop the attraction of macrophages to areas of damage or injury and stop this
54:22
inflammatory process of immuno-excitotoxicity. He said he would give us a list of them. Here is the list. Those in yellow he mentioned multiple times. What happens is these are substances and I've
54:36
read the literature on this There are many, many articles which support all of these. these claims that he's made. And what needs to be done are further clinical studies to define the toxicity in
54:49
humans. And these are very low toxic lesions and their uses and
54:57
the dosage. So those important compounds that he's mentioned have been listed in yellow.
55:06
Here is one list, take a screenshot of this, is a list of two very important macrophage chemo attractant protein
55:16
inhibiting agents. One is nano curcumin, which reduces inflammation. And the second is luteolin, also, which affects this macrophage chemo attractant protein he talks about. Take a screenshot of
55:33
this page. Other agents that reduce microglial activation, which is important in this process of immuno-excitotoxicity, are nanocircummon, resveratrol, which is really terrogastilobene. It
55:49
comes out, it's cheaper under that name, and it's the same. Luteoline, which we've just mentioned, switches microglia to the resting state, riboflavin, which is a vitamin, lowers the level of
56:03
the conoid in the vessel so they cannot be disrupted, and fycetin. This is another one to take a screenshot of vitamin D, among these others listed here, increases in, well, it increases in your
56:20
rupture when levels are low, and it turns out that most people in this country are vitamin D deficient. low levels increase all factors associated with growth of the aneurysm and ruptures and there
56:33
are other factors involved here that he mentions. Again, he mentions riboflavin
56:39
and thiamine, but these other agents have found to be also active. Another one which suppresses macrophage activation and
56:48
here are some more that increase endothelial function, again, nanocaracetin.
56:56
Others lower TNF-alpha, riboflavin, again, as mentioned, luteolin, again, inhibits monocyte macrophages
57:04
and other riboflavin lowers TNF-alpha, and there's nanocaracetin.
57:13
Others that are lowing TNF-alpha are asperidin and rospheritro, we mentioned those before, or there are other agents that are anti-exocytochicity.
57:26
the exocytoxic phase of immuno-exciter toxicity. Nanocircomin, nanocursitin, magnesium, which he's talked about in the presentation as being valuable against phasmus spasmin as to xanthin, one of
57:40
the most powerful antioxidants in dome.
57:46
These again have been written about in his books, on many books on this subject. You can get these books on Amazon.
57:55
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