So this is such an exciting time. I have to say we are all in the midst of a historical change. The changes since I was in medical school, I started medical school 42 years ago, I can't believe it. And I've seen so many things during that time, things like the first effective approach to HIV, which actually came from my college classmate, David Ho, and things like the first effective approaches to hepatitis C. And we're seeing now the first effective approaches to Alzheimer's disease. And I think I very much agree with Dr. Gundry. There should be no Alzheimer's disease. And I'll show you why I believe that.  And what they'll tell you is that there is no treatment, there is no reversal. And I very much disagree with that for reasons that I'll show you. But because of that, we have a really sad state of affairs. So as you know, patients tend not to go in until it's there. They do just the opposite of what they should do. They don't seek medical care because they know that the doctors are going to tell them there's nothing we can do for you. The doctors, as Julie says, say good luck with that. They really don't have something to offer. And so what happens is they wait longer, longer, longer. They finally go into the doctor and the doctor says, well, you know, I don't really need to send you to any place special because I can write a prescription for Aricept. And so I'll do that for you. They don't even have a firm diagnosis many times. So they're not sure what kind of dementia this is or if this is dementia, which is a huge problem. So finally, as it gets very late, what do they do? They finally now go to a specialist. They go to, for example, a memory and aging center at a university. And the university person says, well, you know what, I can't help you.  Second of all, I'm going to make sure that it says memory problems on your chart so you won't be able to get any long-term insurance. And would you mind coming in once every six months for a spinal tap because I'd like to renew my grant? So that's the sort of situation we currently live with. And this has to change. So this is from a real evaluation from actually a relatively well-known neurologist at one of the nation's most outstanding memory and aging centers, I won't say which one. And this is directly from his notes. I've got an MRI of the brain, blood for complete blood count, metabolic panel, thyroid B12. I asked the patient and his wife to keep an eye on his disabilities to manage money, medications, and transportation. I prescribed Denepazil five milligrams once per day. So here's what he didn't do. He didn't do anything about the genetics. So he didn't ask, what's the APOE status of this person? He didn't ask, what about TREM2, CD33? And these are things that are critical for immune activation. He didn't ask anything about the innate immune response. NALP1, so forth and so on. He didn't check HSCRP or IL-6 or anything regarding the ongoing status of inflammation. Didn't check homocysteine, despite the tremendous literature on homocysteine and its relationship and beautiful studies out of the UK, to look at atrophy in the brain and how you can stop the atrophy by normalizing and optimizing, actually, the homocysteine. No interest in the fasting insulin, even though that's obviously, and again, repeatedly published to be an important determinant for cognitive decline. Nothing on hormonal status. Nothing about the toxicity. Nothing about the innate immune system status. Nothing about gut health. Does this person have leaky gut, non-leaky gut? Is a person gluten-sensitive, not gluten-sensitive? Nothing. Nothing about the microbiome. We don't care about the microbiome in someone who's got cognitive decline. Why not? Nothing about what's the status of this person's blood-brain barrier. How do you know what's going on when you don't check anything? Nothing about MRI volume metrics. You don't want to know what the hippocampal volume in this person is. Is it less than 1%ile? Is it 75th percentile? Where is it, this thing? On and on and on. Prescribed in epizel without any diagnosis, as there was no what's actually, here's my diagnosis. Just give him denepizel. This person happened to have a BMI of 33, which wasn't even mentioned in the chart. Nothing, no plans to address it. It's as if this has nothing to do with the cognitive decline. And by the way, this person also had prediabetes as it turned out, which is again, a key risk factor repeatedly written about. So this is the best you get at our nation's most outstanding centers on dementia. This is what we need to change. It's as if dementia is divorced from genetics and metabolism and inflammation, all these things. So the question then we've been trying to address for the last 27 years since I opened my laboratory is how do we go about developing an effective treatment for an incurable disease? So what I wanna show you today is two fundamentally completely different approaches, but the exciting part is they end up at the exact same place. And when we start seeing that these things are coming together, we got very excited because it tells us, okay, if we're seeing it from multiple angles, we may be on the right track here. So the first angle I wanna take you through is the AHS angle. Let's talk about the canonical Alzheimer's disease. So about 65% of all people with Alzheimer's disease have at least one copy of ApoE4 and actually about 10% of Alzheimer's disease is homozygous for even though it's only 2% as Dr. Gundry mentioned in the population, it accounts for about 10% of the overall numbers. And so what we were asking a number of years ago and we started this about seven years ago now is how does this work? We know how we start. The people start with ApoE4. We know how they end up. They end up very commonly with phosphotau, with A beta. But nobody really understands what's in the middle.  But that doesn't really give you insight. Why is it, and as Dr. Gundry was mentioning, oh my gosh, this has to do with shortjevity as we say, very few centenarians who are ApoE4 positive. Why is that? It has to do with inflammation. It has to do with heart disease. It has to do with infection. Why is it, this is an amazing, amazing gene. This is the AHS gene. And why is that, how does this work? So we wanted to understand that in a fundamental, mechanistic way. And so we set up a series of experiments to understand this problem. And this has turned out to be a remarkable, remarkable story. If you go back here, I call this the chimp that killed the rhino, because if you look at what happened when we went from simians to hominids, there was actually a fairly small number of genes that were changed as we went from simians to hominids. And as Tuck Finch from USC pointed out, you know, a lot of these have to do with inflammation. Why would it be that if we were gonna go from tree dwellers to getting up and walking along the savanna, why would it be that we'd have to have all this pro-inflammatory state? This is a strange phenomenon. So his argument was a very interesting one. He said, well, what does it take? You are literally changing the way you live. You're changing your niche in the world. And so what happens?  You get cuts in your feet. You are infected. You are fighting with others for food. You go longer between meals. You're fighting also with various predators. Your food, and guess what? You're not cooking your food, of course. This is now millions of years ago. And so you're getting exposed to all these microbes.  So what happened is five to seven million years ago, of course, God came down and touched us. What did he touch us with? He touched us with DNA, right? So we had a finite number of changes between the simians and the hominids. So what happened here? You can see we developed great things happened with this. We were able to go forward in a way that we had never before. So it's a very exciting change. And yet, of course, as we heard, it also changes your response to many different things. How does this work? And specifically, why does it give you an increased risk for Alzheimer's disease? So if you look at this, from seven million years ago or so, until very recently, we were all ApoE4 homozygous. So here, in fact, just 220,000 years ago, so just the last 4% of hominid evolution. And interestingly, associating with things like the appearance of modern humans, the appearance of fire and cooking things, stuff like that, all came around this time. So for whatever reason, ApoE3 appeared, and of course now is the dominant allele. The allele frequency of ApoE4 is 0.15. So 0.15 squared is the possibility of being homozygous.  Okay, so ApoE2 is a new one just 80,000 years ago, as you can see. And what happened? If you look at this, the chimp ApoE is actually slightly different. So this arge 61 here appeared when we became hominids. This was previously a threonine. And actually there were a couple of different changes in the chimp ApoE to the human. But a critical one appears to be this arge 61. So what happened when the threonine of the simians became the argenine of the hominids? You had this interaction between the argenine and the glutamate, and that changes the shape. So what happens is you go from a nutcracker shape here to a column shape because pulls together you have positive and negative charges interacting.  And you can see here that ApoE4 has a fundamentally different shape than ApoE3 and also then the chimp. Then what happened as we went along just 220,000 years ago, another mutation occurred. And you can see here, this is cysteine 112. This is not in the E4 or the simian. So when that happened, these now paired up, allowing this now to move away. So there's a fundamentally different shape. And really this returned it to more of the shape that you saw with the simians than with the early hominids here. So they're fundamentally different molecules. And we wanted to ask, do they act differently? And if so, does that give us any sort of insight into what Alzheimer's disease is and how it is that ApoE4 predisposes us to getting Alzheimer's? And so this is work done in my lab by Ram Rao and Karen Pokesay and Vina Thinda Carr and others. And this has been published in the first couple of papers have already come out on this. And here's the interesting thing. If you look at this right here, what happens is rel A, which is a component of NF Kappa B. So this is part of your inflammatory response, right? When you get inflamed, the rel A and the NF Kappa B move into the nucleus and they affect the transcription of hundreds and hundreds of different genes. Well guess what happens here? Here you see what happens is that the rel A is sitting outside the nucleus, which is the inactive state. In the presence of ApoE4, it moves into the nucleus. So you're really changing the program. And how does that work? Why would you do that? So to summarize a lot of work, I'll show you here what happens to ApoE4, which was completely unexpected. So ApoE4, as we all know, binds to receptors and there are a number of different receptors that bind ApoE4. It then goes in and interacts with rel A and it drives it into the nucleus.  So and it turns out to bind to the promoters of 1700 different genes.  And that was such a shock. So we applied for an NIH grant on this recently. And what the study section said was we know you published a paper, we know it was peer reviewed, we will not give you the grant because we don't believe it. So they literally said we do not believe, despite all the stuff you've shown, despite the fact it actually binds DNA with low nanomolar affinity, we do not believe that ApoE gets into the nucleus. Now by the way, there's another group publishing that ApoE gets into the nucleus and affects cancer. So we're not the only ones saying this. And at some point, the NIH study sections, not surprisingly the people that did this were ApoE experts focused on that part of ApoE. So this is the way things happen. So in any case, what it turns out is it binds to 1700 different promoters. And by the way, it also binds to other interesting regions. But if you just look at promoters, and we do this by what's called chip seek, so it's a chromatin immunoprecipitation. What you do is you put in the ApoE, if it binds to DNA at all, now you isolate the DNA, you cut it up. So then you, now you take an antibody to ApoE. So if ApoE's not there with the DNA, you won't pull anything out. But if it is there, you'll pull out not only the ApoE, and you'll pull out the local hunk of DNA.  And interestingly, one of the promoters that came out of this turns out to be the CER-T1 promoter, just as Dr. Gundry was talking about. So in fact, ApoE4 binds to the promoter of CER-T1 in a specific region, and guess what, turns the transcription way down. So when you actually look in the brain of someone who has ApoE4, what you see is a low level of CER-T1.  And that's one of the reasons for things like nicotinamide riboside and appropriate diets and things like that. So this is a novel mechanism, and it really gives us new insight into what ApoE4 does with respect to inflammation and longevity and Alzheimer's. So then the next question is, okay, if we group these 1700 different genes, do they show us anything that's new and interesting about Alzheimer's? Does it give us any insight into the reason we started this whole thing? Turns out it actually, you couldn't tell a better story for Alzheimer's, as I'll show you in a moment here. So what it says is, when you have ApoE4, you have a rel-A dominant system. Now what happens is, your cells literally go back and forth between different states. This is a little bit like the metabolic flexibility that we hear about with fat burning and carb burning. Same idea, but cells also will set themselves up in one of two fundamental ways. One is a rel-A dominant state. That says, I'm under attack. I wanna set up most of my resources for inflammation. My NF-Kappa B is gonna be activated. I'm not worried about longevity. I'm not worried about recycling, and I'm not worried about oxidative phosphorylation because I need rapid response to microbes. So ApoE4 gives you a rel-A dominant state. And interestingly, rel-A and ser-T1 are mutually antagonistic at about a dozen different sites. So they actually have micro-RNAs. They have multiple indirect interactions. When you go up on one, you go down on the other. When you go up on the other, you go down on the first one. So ApoE4 tends to create a rel-A dominant state. And it goes right back to what Tuck Finch said several years ago. This makes perfect sense.  But if you wanna keep yourself from having Alzheimer's, you wanna get rid of that rel-A dominant state. Now ApoE3 has a ser-T1 dominant state. That is more like South Korea. This is like the North Korea side, South Korea side. You're gonna put your resources into recycling, into longevity, into oxidative phosphorylation. It's a different cellular state. Well the good news is, through the sorts of nutrition that Dr. Gundry just talked about, you can drive this state. You can drive someone with ApoE4 to acting like ApoE3. You can drive them to the appropriate state. So here now, if you take those 1700 promoters and you say, okay, what are they doing here? It turns out you could not write a better story for Alzheimer's disease. So it has to do with glucose homeostasis. It has to do with inflammation. And specific genes now, I mean it's amazing to go through these genes one by one by one. Things, for example, that turn down the TNF response, that turn down the NFKAPB response. Those genes are silenced by ApoE4. So when you get an inflammatory response, you keep it longer. You have trouble turning it down. And here, things, neurotrophins, programmed cell death, CERT1, as I mentioned. So all of these things are involved. They are all specific genes that are bound by ApoE4. So it really gives us a new insight. And again, it tells us, if we're going to deal with this illness, we've gotta think about more than one thing here. We've got to think about the whole symphony, okay. So now let's take a completely different approach. Instead of starting with ApoE4 because of the genetics, let's start with the chemistry. Let's say, okay, we know that all these brains have amyloid in them. And it's about a thousand fold more amyloid than is there from a control brain. It's tremendous. So why do you make amyloid? Well, it turns out, surprise, surprise, this is not just something that's bad for you and all these companies out there trying to get rid of your amyloid. The key thing is to understand why the amyloid is there to begin with. So why do organisms make amyloid? The surprise is, it is a protective response to three fundamentally different metabolic and toxic changes. So you make the amyloid because you have inflammation. Whether it's infectious inflammation, you make it because you have mycotoxins or you have mold exposure or you have spirochete exposure, all these things. This is literally the neurosyphilis of the 21st century. The difference being that when you have neurosyphilis, it's always trepanema pallidum. But when you have this kind of neurosyphilis of the 21st century, it's many different organisms, CMV, Epstein-Barr virus. They all engender the inflammatory response that produces amyloid. So if you're gonna get rid of someone's amyloid, great. But first, get rid of the reason.   In fact, you'll get both the type one and the type two because you'll also cause insulin resistance. So then the second thing, if you wanna activate amyloid, what you do is you have a rapid withdrawal of trophic support. And it's actually part of a programmatic downsizing. Beautiful work from Calesano out of Italy. You take away the NGF from the neurons and what do they do? They make amyloid. So this is part of a downsizing response.  Trophic support that is rapidly removed from a system engenders amyloid. And that's why if you're a young woman and you have a hysterectomy and uferectomy, then you, from Mayo studies, twice as likely to get Alzheimer's disease in the future if you don't have optimal HRT. Then the third reason is if you expose an organism to toxins. Mercury's a good one. Divalent metals, copper, things like that. Or things like mycotoxins. Then what does the organism do? It sends out stuff that sticks to toxins. Amyloid. Amyloid is a great binder. It binds to copper with an affinity of about 10 to the minus 18 molars. So it's incredibly tight binder. So if you wanna get an organism to make amyloid, put in some toxins like this. So this really creates, these are the basis of what I call type one, type two, type three Alzheimer's. And of course most people have a combination of these things. And then of course you can get combinations, as I mentioned, and the best way for example is go out and you have too many simple carbs. You get both the type one because you have the inflammation of the AGEs.  Insulin is one of the most important trophic factors for your brain. So you wanna get rid of that trophic support.  And by the way, Ed Getzel from UCSF who looks at neurolexisomes. A good way to look at brain chemistry in the blood shows that basically everybody who has Alzheimer's disease has insulin resistance in the brain, whether or not they have it peripherally. So this is the way to give yourself Alzheimer's disease. And then of course if you wanna make sure you get it, have some sleep apnea, some trauma, some vascular insufficiency and things like that. So okay, what we found then is if you look at the central piece here, in fact the thing that is driving this is here's your amyloid, right? This stuff, amyloid is from right here. But where does amyloid come from? It comes from, when you make this response, it comes from this parent, which is called amyloid precursor, okay? Not a very inspired name, but that's the one we're stuck with. So amyloid precursor, now what's interesting, we found that this molecule, which is a receptor sitting in your cells, so here's the inside of your cells and here's the outside. And it's especially prominent at synapses, just as you might guess. So this stuff is a molecular switch. It is like the CFO of your company. So it's looking at all the different inputs.  And it's doing exactly the same thing that your CFO is doing. It's saying, do we have enough support? Are we in good enough shape to continue to build? If so, it gets cleaved here and it makes two peptides, SAPP alpha and CTF alpha. And these things both support, guess what? Neurite outgrowth and synaptic maintenance. These are literally memory peptides. On the other hand, if you're in the red, it makes three cleavage events here, so different proteases are activated. And a simple example, NFKB activates at the transcriptional lever, both this protease, which is beta secretase, and this protease, which is gamma secretase. So it activates this side. On the other hand, estradiol activates when it goes into the nucleus. SAP, this one here, which is the alpha secretase. So this is a beautiful molecular switch.  It does not have homeostatic feedback. It has what we call prionic loop feedback.  And no surprise, you see a lot of amyloid, yes. But that's a small part of a much, much bigger picture. And this is just like your CTO sending out, or your CFO, sending out four memoranda here. So four memos that are saying two for internal consumption, two for the public. And they say, you know what? Our company's in the red. We're going to downsize. And that's exactly what happened. So when your company's struggling, what's the first thing you do? You say, we can't hire anybody new.  You can't hire anybody new. So we have people, they can drive, they can play tennis, they can do everything, but the husband or wife will say, you know what, they just can't remember anything anymore. That's the canary in the mind. And it's just like not hiring new people. That's the way it starts. If you address it at that point, then you can shift this. So, all right, so let's talk about that. All right, so everything else is downstream from this, and we want to look at what happens. So what we wanted to ask is, okay, in the mice, we do this with a genetic mutation. But what about in humans? It's much more complicated. The vast majority of people with Alzheimer's don't have APP mutations. What they have is all the things that feed in to the APP. And that's everything that you've read about the epidemiology of Alzheimer's disease, which is why we got so excited when we saw this. So we published this connectomics paper about a year ago. And it shows you all the different hormones that feed in this NFKAPB, the inflammation, all this stuff feeds into that. So what we want to do with Alzheimer's, we want to alter that balance. We want to send you toward the two good guys instead of the four bad guys. That's the idea. So, coming back for a moment to ApoE4, we asked, okay, do these two things link? Does ApoE4 affect that ratio? And you can see here, there is a huge effect of ApoE4 on that ratio. So what I tell the patients then is, it's like you have a roof with 36 holes. The idea of filling one hole with a drug really doesn't make biological sense. That's not to say that drugs aren't important. They will be very important with the overall program. But you've got to fill as many as you could. So if you wanted to get a perfect Alzheimer's drug, what would it do? This is what it would do. So this is why it's hard to screen for one drug that is a cure for Alzheimer's. And so what we want to do is we want to address all these things, and we can address all these things with a functional medicine approach. This is why programatics are the future of medicine instead of what we call philosophy. So we don't want to do that. So what we want to create then are physicians. And now we're working with Lee Hood at the Institute for Systems Biology and Mike Mersennek from POSIT to create a much better way to understand the disease and how we treat these chronic illnesses. Now the 21st century physician, great. They understand DNA and RNA, but they're really not very good at the whole person.  That's not really what you want to do. You want to ask why does the person have hypertension? These guys, the traditional Chinese doctors were great at looking at the whole body, right? But they didn't know anything about metabolomics or RNA. So we want to create a new group of physicians that will understand both of these things, right? So they'll understand DNA, RNA, that have much larger data sets, but they also understand that the body works as a beautiful symphony. You've got to put the whole thing together. So I want to just quickly show you a couple of people here. This is a woman who is 67. She's now 71, doing absolutely great. She works for the U.S. government. She was having trouble with her reports. She couldn't recall even four digit numbers. She had a positive retinal scan for amyloid, so she had Alzheimer's disease. We treated her with what we described at that time as metabolic enhancement for neurodegeneration. She talks a little bit about this here. So tell me a little bit about how things were a year ago. Well, a year ago, I was having a lot of difficulty. I was very frustrated because my memory was poor. I had issues of being spatially disoriented, particularly when I was driving. I would get off the freeway at the wrong exit or not know where I was getting back on, on familiar routes. I would reach in my house for a light switch. I'd reach on the wrong wall, even though the light switch has always been on the right side. I'd start reaching to the left. I'd call my animals a different name, my pets. I was really worried about it. I was very stressed about it. So it was a very stressful time. And how are things at work? I have a job that requires a lot of mental analysis, a lot of thinking. I do a lot of research. I have to collect data and design a study and then do the analysis and write a report, usually under pressure. And I was finding that I just couldn't complete an assignment. I couldn't think about the analysis. It was just a jumble to me and I would start procrastinating and putting it off and the longer I put it off, the more stress I felt. So I was worried that I was not going to be able to continue with my career. Tell me a little bit about how things are now. Things are much improved now. My memory is much better. In fact, I would even go so far as to say I don't think that I have a problem with memory now, which is a great surprise to me from where I was a year ago. My thinking, cognitive ability and ability to do work, ability to do reports, I am back into the stream of things, being productive and being able to do my analysis and writing, which is fantastic. And how's the driving? Driving, no problem. I drive at night, I drive in the daytime. I know where to get off, where to get on. I'm on the highway, so I feel like that's the problem. I'm not reaching for the wrong side of the room for the light switch. I'm not calling my pets the wrong name, which I think they're probably grateful for. And how overall are you feeling? I feel great. I feel really, really good. I feel energetic. I feel more peaceful. Okay, so I'm being told to stop, which is the same thing that the NIH, the Alzheimer's Association and pharma are telling me. But I'm gonna tell me, I apologize, I'm gonna run a couple of minutes into the questions. I apologize, I wanna just show you a little bit more here. So this is a guy who, 70 year old, now actually 71, ApoE4 positive, PET scan positive, I mean, very clear case of Alzheimer's. Neuropsych testing showed that, especially in the last 18 months, he had really gone downhill, which is why his wife brought him to see me. Went from 84th percentile to third. Unable to remember, lock combinations, all sorts of problems. Interestingly, he's much, much better. He's back at work. I'll show you his numbers here in a moment. But his wife called me and said, what you missed the most important thing. And I said, well, what do you mean? And she said, well, what happened when he started the program, he had been declining with a more and more rapid pace and he just completely stopped. And then after about six months, he started to improve. So he talks a little bit here about his own story. And went to open the locker at my gym and I could not remember the combination. Which is, as I know myself, that'd be very unusual. Clearly, I mean, math has come back. That's a real measurable thing. I mean, I'm fast with math again. People I had met, maybe even taken to lunch. I did not know who they were. I mean, it's like a new encounter. And then afterwards they'd say, you actually know this person. So that's gone away. So here is his number. So I tried to get this guy to go back and get one more follow up after he'd gotten a number of these. And so he didn't wanna do it at first because he said, look, I know I'm doing great. My wife knows I'm doing great. If the neuropsychologist tells me I'm not doing as great as I think I'm doing, I'm gonna feel lousy. And so you can see the neuropsychologist actually called Aida and me when we were driving north in California and said, I come and see these numbers. I've never seen anything like this. So this guy's been in practice for 30 years. So you can see here just dramatic, dramatic improvements in this guy's neuropsychability. Here's another person also ApoE4 positive. Also went back to work improvements here, not to perfect but better with his metabolic status. And you can see your hippocampal volume from 17th to 75th. And of course the neuropsychologist called me up and said, well, we must have made a mistake because you would just don't see that. 75,000 scans were done at this particular hospital.  We were hearing before about 50 millimeter cubed volume, this is over 1200 millimeters of volume. So dramatic increases in his hippocampal volume. Here's another person you can see here, ApoE4 homozygote who improved with hers as well. So the last slide here just to show, so people always ask, so what is practical? What do I do differently tonight? And these are all just metabolic things but I'll show you very quickly here and it's difficult to show everything in two minutes but let me quickly show you where are we here, okay. So here's, so what we do is we gather, here we go. We gather information, so this just shows we gather over 100 different pieces of historical genetic metabolic information. So we wanna know all the things that function in that balance. We wanna know the direct molecular interactions to that balance. Okay, then when we have that, we actually put this through an algorithm that we developed with a group in Silicon Valley. And so let's go here. So then we create a report. So this is a real person here and so we can see this particular person here. Overall, not doing terribly well but what about the subtypes of Alzheimer's that we described? So this person you could see as biggest problem is glyco toxicity. Then secondly also has some contribution from trophic loss that's type two and then toxicity. So this person also has some type three. Not so much on the type one inflammation or the type four, the vasculature. And then you can look at the key contributors, you can look at the nutrition. And again, thanks to Julia and Aida for their work on the optimal nutrition. We call this keto flex 12-3 and there are obviously a lot of tremendous experts on nutrition and I certainly can't claim to be an expert on nutrition. The goal that we have is to take everything to make it so that we change that balance so that we are literally telling the brain, you do not have Alzheimer's disease. You can now signal again, you can now grow forth, maintain your rights, all that sort of stuff. And then we'll look at what sorts of things that you're gonna do with exercise, hormonal optimization, so forth and so on. So various supplements or all these things are critical. And then all the various tests that they have in the results. So I will stop there to leave time for some questions. Thanks very much again for the invitation to this wonderful symposium. Hi there, thank you so much for an awesome talk. I was a philosophy degree here at University, I mean philosophy degree, for reals. I guess my question, it goes back to Abram Hoffer and using the high-dose niacin and I'm just curious if you could speak to that, if you use that or you don't recommend it anymore or and how that was working for work. You mean for cholesterol? No, no. Were you talking about nicotinamide riboside sort of approaches for increasing NAD or for what? He used it to treat dementia in massive doses like six gram doses. So everybody who's proceeded what was currently going on has used monotherapies because we're all taught in medicine that we should use a monotherapy because that way you can be scientific. The problem is the disease didn't listen. The disease is not a monotherapy disease. So it is true, everybody who's gone before has used vitamin E, by the way vitamin E, statistically significant result, minimal exercise, minimal niacin, minimal testosterone, minimal estradiol, minimal, these things are all fine but using them by themselves is ignoring the beauty of the program. So the future is not philosophy. The future is programatics with appropriate targeted pills at the right time for the right targets but all these things that have gone before where they used one thing and said I saw and the interesting thing it tells you why they saw what they saw. The people that they're seeing have 36 holes in the roof and some of them have the big hole where the niacin is and small holes everywhere else. Those are the ones that respond but as you could see in all those studies when they then tried to look at large cohorts of people they never saw an effect where just about everybody got better. So that's for the future, it's programatics. I think that's the, and we're seeing this, this is what's happening with every, this is what's happening with cardiovascular disease. This is what's happening with type two diabetes. This is what functional medicine is all about. So I think that all these things have been very helpful in telling us what's important but I don't think that any monothe, at least I haven't seen a monotherapy yet that really is the optimal way to go. Thank you. Thanks. Good afternoon. Dr. Gundry was saying that he doesn't think of the, didn't want us to think of the April 4 gene as the Alzheimer's gene. You wanted to think of it as the fragility gene and I'm wondering if there's a correlation between people who have it in other neurological conditions besides Alzheimer's like Parkinson's or multiple sclerosis and if they, and if, you know, treating someone who has APOE4 and those diseases that would be beneficial to them. It's a very good point. So I see it very differently. I don't see it as a fragility gene. I see it as an optimizing gene for early hominids. So what happens, it's a different situation. So in fact, if you are living in a squalid environment and you're not getting fed enough and you're in infection, then you tend to do better if you have APOE4 than if you have APOE3. But we're living in a different world now. We're living in a different environment and that's why AHS is so critical for people who are APOE4 positive. To learn to see we want a match, not a mismatch. So of course the Gladstone group, Bob Maley and the whole group, Yadong Wang and all these people have been studying for years what other diseases are. And so Lewy body disease, for example, Parkinson's disease, these all have increased risk with APOE4. Okay, great, thank you. Hi, first I wanna say I have followed your work for years and I'm fascinated and I just wanna thank you because I think I'm a veteran and in the military we call what you're doing tip of the spear. You are at the leading edge of this and I think that when reversal and prevention of Alzheimer's is the norm, we will have people like you and Dr. Gundry and Dr. Veach and Sam Henderson to thank. So first of all, thank you. Second, two quick questions. The first is when you talk about optimizing the hormone levels, specifically some like testosterone estrogen, do we know that somebody over 50 or over 65 is supposed to have the same level as someone who's 25? I don't know what optimal means in an aging population. And then second question, in the non APOE4s, I've read and I see so much literature to the effect that the chronic hyperinsulinemia is really the leading cause in the non APOE4. So if you could comment on those things. Yeah, great questions. And first of all, let me just say, I think that the DOD and the armed forces are gonna be leaders, especially with the TBI related work, because with all the people coming back, this is a huge issue. And of course, Posit is working with this group and we're now gonna be interacting with Posit to try to optimize their cognition. This is a huge issue. And I got a note. Do you know the work that Ken Ford is doing? No, I don't. Who's Ken Ford? He's doing like the same kind of fat field, ketogenic leaning, you know. Makes perfect sense. Yeah, and we didn't talk about ketosis, but mild ketosis is probably the best way to go. This is why we call a keto flex 12-3. So I got a note from a guy who said, I'm writing you, I'm in the special forces. I can't tell you what I'm doing. I can't tell you who I am on and on, but I'm gonna come to your course. So I figured he probably came. I probably never saw him. He probably came to our last course, but very interested in trying to optimize people with post-traumatic stress and with TBI. So with respect to hormones, this is the most controversial area. No question, it is the most controversial area. And my wife and I argue about this on a weekly basis because my argument is, when you get early cognitive changes, this is an emergency. This is a branch point in your life.  So I worry less about should you take your estradiol to 80? Okay, get your mammography. Evaluate your uterine lining thickness. These are all important, but you've gotta address optimization. Once you get your brain optimized, you can start changing other issues, right? So that's the first thing. And so yes, I don't know if someone's testosterone should be above 500. I only know that if I get cognitive changes, I'm gonna optimize everything before I start throwing things away. What I often say though is do the other things first. Then you can jump on that. Okay, hyperinsulinemia in the non-E4s, absolutely huge issue. But also in the ApoE3's toxicity is a huge player we're finding it again and again and again, which is why I tell everybody get your C4A, your TGF beta one, your MSH, and your HLA DRDQ. All these things should be checked. And we should have a world with very, very little Alzheimer's if we do prevention and early reversal. We gotta M it, 45. So when you're 50, you'll get a colonoscopy. When you're 45, you should get a cognoscopy. Okay, all right. Thank you.


All right, Cyber Traders welcome on back to close out the week this Friday, February 18th, shortly after 2.30 PM Eastern time and welcome on back here for our afternoon meeting. Great to see Chuck C. Loud and clear. Chuck Z with a call out just before him. Draft King's pushing up a bit. You know, Mark, it's trying to make a small bounce heading into this afternoon. Great to see the mics in tandem. Chris, Lewis, Loud and clear from all and all of us. I'm sure joining us just coming up in the next couple of seconds, but great to see all of us as well on social media, Facebook Live or YouTube folks. We got to go right into it here because we have a pretty exciting afternoon, but we also have class finishing up phase one lesson number four for all of us live inside the trading room at least or rather I should say any of our bronze, silver or gold students and of course platinum diamond, you know, all of our students nonetheless, you have access to the phase one course this afternoon. We're going to be talking all about journaling. Not the most exciting topic to talk about, right? Well, we're going to break down really why we need to journal. You know, listen, if you're a long time student here of CTU like Kathleen or Lewis or Michael D, you know, it's to say, Hey, you folks know why we need to journal, but how could be progressed? How could we become better traders like going through our journals, you know, on downtime? So that's what we're here to talk about this afternoon, right at 305 Eastern. I know that Rich just posted the link for the class right there in the chat board. All right. So for Henry, Lewis, Chris, Chuck, all of us otherwise just make sure that you click that link before we begin. But let's hop right into it though. We have Goko. It's on the screen. It's not necessarily the fastest. It's at the highs. It's up 17 plus percent. So, hey, you know, we only hope to see a stock like this make not only a bigger push, but perhaps a bit faster of a push heading into the market close. The issue on this trade is that although it's at the highs, it's just not really trading a lot of volume per minute. You know, at least looking at the order book right now, the stock's trading about 70,000 shares a minute. And if we stop seeing or if we see less and less volume being traded over the next couple, that number is only going to drop off. So I'm not fully committed to this Goko trade yet. You know, it's more of like a level one stock. Don't get me wrong. It doesn't hurt us to put this on our list, but I'd rather follow at least, you know, some of the ones that are making better moves right now.  We'll come we'll go to that one just on the loser side. That's number 10. So nice catch from Mark and you know, hey, that one could very well be on our list here coming up. Alright, so we'll start off the top percent gainer here. This one we're not going to put on our list for obvious reasons. This thing looks like a trade wreck. This sky age trade. I mean, this obviously ended up making a big move today early in the morning, but it reminds us of the CPTN trade.  I mean, it's easy to say that it was right there. But you know, for a stock like sky age, I mean, it's a very similar type of pattern in the sense that when it ended up reopening off of a halt, it instantly ended up getting halted again. And then after that again, and then after that, it was just very choppy and messy. And you know, for right now, this stock isn't worth it here. But a stock that may be worth it. Hook. We have another push on hook here. I ended up making a nice pop at least heading into Wednesday afternoon this week. It took a breather yesterday and then obviously here this morning made a nice push upon the market opening up. And then for right now, it's still near the highs, right? It's trading about 81, 82,000 shares a minute. So looking, looking at the order book that you see there, you know, that's actually a decent amount of volume right now. So hopefully this hook trade can give us one more push. I would be more inclined to put this on our watch list here. And then we have Brian inside Cyber Group, a couple of us picking up some good trades here at this time. Brian picking up 42 cents on stock QSI. You got in from 418. It's a steady, easy trade. Well, that one's on the gainers list, I think, right? Yeah, number probably 13 here, probably. We'll jump to that in a bit. So nice trade from Brian and let's see what else we got. Definitely a nice push on the spy right now for what it's worth. NRGV not doing a whole lot here and we'll kind of just skim through. I definitely want to jump to that QSI that Brian just got out of. MTech still holding near the highs. You could say the same with this as I said on hook. This one's trading about 12, 13,000 shares a minute. That number will probably drop off in a bit. But you know, that means it's actually trading good volume comparative to what you see on the order book right now that put hook on our list. I feel like I definitely should put this MTech for right now on the watch list. All right, what else we got here? KPTI. I don't know why I was having trouble saying that. Ended up making a nice push earlier today. It's actually a familiar name. We've done really well on KPTI more often on, but over the years, like, you know, I've been seven to eight years now.  We would see these big 100% moves at points. So at least it's a stock that we know fairly well and it's trading good volume here. Also, shortable. So if it fails to break higher than perhaps the opportunity could be seen on the way down. So it just is a tradeable stock for the meantime. I'll come back to this at the very ends. Put this on the side list. Odds are all actually put this on the main watch list. But I definitely want to jump to QSI. I want to jump to some of the stocks that may move with the market like the AMC trade, perhaps. That one was a great short from this morning. Obviously, draft came as we did really well on today just a short. So yeah, we'll come back to this at the end if we need to AMPL. Here we go. This one's a no brainer AMPL right back on our list here looking really strong for the afternoon ended up making a big drop yesterday. It's making what we call the dead cat bounce abbreviated DCB, you know, pushing up to 20 right now. So yeah, definitely that's what's expensive. I, you know, it's funny. My trader's dyslexia folks gets the best of me. Sometimes I thought this was this was APR and Louis for not APP and little expensive at least, but a nice push for the afternoon. I reckon, but it's a Friday. I want to just kind of keep within price range. This takes me right to QSI. All right. So QSI is making a steady move as Brian commented. It's yeah, it looks good. I mean, it's trading about five, six thousand right now per minute. Order book looks, you know, not too thick. So that's a good sign. So yeah, for right now QSI I'll put on the list here. See what else we got here. I'm in one trade right now folks. And I mean, for people inside the live trading room like Mike or Chuck or Henry, Kathleen, Lewis, I mean, I've been commenting only on a couple of stocks throughout the afternoon. You'd probably take a quick guess. We'll jump to it in a bit. If I could stop that on second, I have my position held on for a little while, but did a pretty good through the day. We took care of our chores or errands early in the morning, able to play around a bit right now. So I got out of part of my position on the stock that I'm currently in, but I still have half left. SLQT, nice little push right now. This one's actually doing all right. And what's peaking my interest more for this type of stock is pretty much the same reason that we were following. What was it? The AMPL, the dead cat bounce ended up dropping off probably from the end of last week. It seems like, you know, just dropped from like seven all the way down a three sub and right now pushing up for the meantime here. So I don't know if it's ready to, you know, fill the gap, but perhaps this could be a decent trade. I don't mind putting this on our list here. Also is shortable, so if it fails, then I guess that could be an opportunity as well. All right. I think that just about does it on the gainer side here. Just checking out all these others at the bottom right now. You know, hey, folks, if there's anything else that's making a decent move up that's actually on the gainer side, type it in the chat board, let me know. But otherwise, let's hop on over to the losers list here. ISPO, we're not going to follow CPTN, Dunzo, ANGH, same thing. I'm just going to skip over those. Roku just want to check in with it. Obviously a pretty expensive stock, but for as much as it dropped off from after hours yesterday, you know, this would be the exception when we would look to follow a more expensive trade. You know, we've done that, of course, here in the afternoons before on stocks like Square or PayPal more recently. And, you know, Roku isn't exactly near the lows of the highs. So that's more the main reason why I'm not going to put this on our list. If this was, you know, closer to the lows or trying to make a dead cap bounce on the way up then, I would see more reason with us putting a more reason for us to put this on our list, but keep it moving. Same here on Blaze, the stock I'm in right now is just making a great move for me back down again. So I'm going to jump to that next. Redfin, so Mark picked up 17 cents on Redfin at least. This is not the stock I'm in, but I, you know, hey, it's making a decent move up. It's just very tradable like the KPTI, right? So I would group this with the KPTI kind of just on the top of the side list, if you know what I mean there. And hey, in particular, if you're Mark or if you're someone else that's done pretty well on this trade through the day, I'm sure you would be more, you know, gravitated to it personally for the afternoon, right? And there would be no harm doing that, right? It's very tradable stock still, this RDFN. All right, let's get to it. DraftKings currently short right now from 1831. In short, very similar play, almost carbon copy play as Palantir yesterday, except for the fact that Palantir was even steadier as a short heading into the afternoon than this. But right now this just ended up re-breaking under a major support level at 18. So this could be a really good sign right now for continuation. We have to make sure 18 holds as resistance. And if not 18 itself, then perhaps just the VWAP, the volume weighted average price in 1809. But man, this was a really good short earlier today folks. Literally for the same exact reason. I shorted PLTR yesterday, I shorted this today. And it's not just because of the earnings and it was down from the after hour or down from pre-market this morning. You know, that's part of it, but in terms of volume, right? And I'll tell you what, I'm going to go over this trade in particular in the journaling class at three o'clock. So that's any more of a hook to get you into the phase one course later on this afternoon. Now we'll go over this stock. I'll explain my actual reasoning for why I took this trade and we'll journal it, all right? With that said, Jeff King's will put on our list. I wouldn't have put, I wouldn't have been as inclined to put this on our list to be very transparent if it didn't just drop right back down. That's why I'm like really emphatic about this. This just rebroke a big support level at 18.  I think this could be a great trade for you folks since the close now it just needs to hold this 18 though. If it breaks back over 18, then there's a good chance I get out on the second half of my short position.  But follow the SMP, follow the spy here, namely heading into the afternoon laser, LASR, familiar name at least, not doing a whole lot right now. Dropped off big early this morning. That's just about it folks. I see CleanSpark down big. I'll at least check that one out. Familiar name from I think last week ended up making a nice drop off this morning as a short. So, you know, this is tradeable. I'm not going to be as committed to this though. I even like KPTI or Red Fit Board this one. But folks, what else you got for me here? I think this just wraps it up for me. I think that's all I have for you. Got someone on YouTube today, Ashen. Welcome aboard, Ashen. Saying DTSS is up 20% but even Fit and Vis doesn't show up on the gainers. Okay, so maybe, you know, maybe DTSS not popping up for us here. Wow, good call. Yeah, well it's number five right now. I may be, maybe I personally skipped over it. Maybe I just quickly glanced at that gainers list and kept going. You know, maybe at the time, I didn't think there was no volume but it's at the highs. Ashen, this is a really good call from YouTube right now. You know, in the sense of just at the highs. And right now, I wish it was trading a little bit more volume per minute but the order book is not really that filled it. It's like kind of more in the thin side. So, you know what? This DTSS, I'm sold. I like it so far. From Mitch, welcome back, Mitch. There we go, man. Sound or sound, however, however you may nickname it. S-O-N-D just popped up and got halted up over 15% right now. It seems like just like one of these others, you know, runners that we've had from the last 36 hours, right?  So, be really careful on this type of stock but, you know, given what we've seen so far from the latter half of this week, you know, it's hard to not put this on our watch list. No problem at all, Ashen, you as well. Enjoy your weekend. Remember, folks, keep in mind, markets are closed for Monday, President's Day, so we're not gonna be live on Monday. All right, that's just about it for me, folks.  So, you know, obviously, markets took a hit the last, you know, day and a half and with that, Bitcoin's pulled back. It's dropped off quite a bit and it's exactly at the 40,000 level that we were talking about for the last two to three weeks, right? You know, with these videos that I've been pumping out on YouTube, so if you haven't seen it yet, just go right to the YouTube link. I just posted inside the YouTube stream and for all of us inside Cyber Group, same deal. Give us a thumbs up. Give us a subscribe on YouTube if you haven't already. We're gonna be putting out these types of videos pretty much every week going forward, all right? But that's all you got for me here this afternoon, folks. So, for all of us on Facebook Live, for all of us on YouTube, enjoy the weekend. Again, markets are closed on Monday. Any questions that you have, please let me know. Send it right on over to Josh at ctutrading.com for Chuck, Brian, Leda, Mark, Jeffery, all of a sudden just otherwise here inside the trading room. I look forward to speaking to most of us live in class just in about 20 minutes. Take care. Come a Cyber Group member today. Just click the link below and receive all these amazing products and a world of knowledge for just $9. Do it today.