Doctor's Advice On How To PREVENT ALZHEIMER'S & Cognitive Decline | Dale Bredesen

We want to get people as early as possible. The earlier you come in, the earlier you start on the treatment, the better the outcome typically. We spent 30 years in the laboratory looking at what are the molecular mechanisms of neurodegeneration? Why do you get Alzheimer's so frequently? And how does this actually work? What are the things that are driving this process? And what we found is that what we call Alzheimer's disease is actually a protective response. It's really a protective downsizing response to multiple different insults. And so the whole point of the protocol is that in previous studies of Alzheimer's and treatments, people would always try to treat without understanding what's actually causing it. So they would give you a drug that doesn't have anything to do with why you have Alzheimer's disease. So after the research, for the first time, we were able to say, here are the things actually drive this process. And you can see that what's at the heart of Alzheimer's disease is actually a molecular switch that is integrating and looking at all sorts of potential insults and on the other hand all sorts of potential positives. So we call this synaptoblastic, which are the things that are making synapses and synaptoclastic, the things that are pulling them apart. And there's a beautiful balance that you have during your lifetime. As you begin to get older, you can have an imbalance just as you would with osteoporosis. disease is very much of a synaptoporosis. You don't have the things. So if it's inflammation that can be from Borrelia, that can be from various organisms, that can be from leaky gut, if it is trophic loss, loss of nerve growth factor, brain derived neurotrophic factor, hormones, nutrients, if it's glyco-toxicity so you have insulin resistance, or if it's toxicity from metallo-toxins or organic toxins or biotoxins such as mycotoxins. These things are all contributors. So the whole purpose of the protocol is to identify all of the contributors and we typically find that people have between 10 and 25. It's usually not one. And then we want to trigger and want to look at each of those and target each of those contributors. So if you have a high homocysteine, we want to bring it down. If you have a leaky gut, we want to heal that and we want to bring down your HSCRP so that your inflammation declines. If you have ongoing exposure to mycotoxins, we need to flush those out and we need to remove the exposure to the molds and on and on and on. So there are dozens of things that we look at to determine what's actually causing this and as you can imagine, it's personalized so it's different for each person what is causing their decline. The other thing I should add is we want to get people as early as possible. The earlier you come in, the earlier you start on the treatment, the better the outcome typically. So oral health is absolutely critical for cognitive function. And here's the thing, when you actually look in the brains of patients with Alzheimer's, you find multiple different types of organisms from different people. For some people, it is P gingivalis or F nucletum from the oral cavity. For some, it's herpes simplex from the lip. For some, it's fungi from the sinuses. For some, it's actually the Borrelia, the the organism from Lyme. So on and on there are different organisms that gain access to your brain. Recently an interesting report of what happens when you get exposed to Candida and that that can actually enter your brain. So what we call Alzheimer's disease is actually a protective response and professors Robert Moyer and Rudy Tanzi at Harvard University showed a number of years ago that in fact the amyloid beta peptide has an antimicrobial effect. So it is part of of this downsizing response. A little bit like if people come across your borders and they're trying to attack you, you may put down napalm, which unfortunately now makes you have less arable soil. You are trying to kill the invaders, but in so doing you are downsizing. So absolutely oral hygiene is an important one, as are any of the other things, whether it's leaky gut, whether it's exposure, whether it's skin lesions, anything that creates systemic inflammation chronically. can be a contributor to cognitive decline. Bacopa monnieri is an herb that's actually been used for thousands of years by the Ayurvedic physicians and it supports cognition and it turns out to have a number of things called bacopasides and these things have multiple mechanisms of action. So one thing, for example, they inhibit the breakdown of acetylcholine. Acetylcholine is critical for making and storing memory. So you have a cholinesterase inhibitor that allows you to have more acetylcholine. Interestingly, they also increase the synthesis of the acetylcholine. So you've got a better cholinergic tone. They also have an antioxidant effect, and they also actually have an effect on some other what are called monoamine transmitters. So multiple actions of these bacopasides to support cognition. Bacopa is available generally. It's a good idea if you have cognitive decline for any reason, it's a good idea to have a practitioner and health coach to work with, but anybody can obtain Bacopa monnieri. Melatonin again has a number of positive effects. A lot of people like to take it because it has an anti-cancer effect, but of course it enhances sleep and it actually reduces the net production of the amyloid beta, which collects in the brains of patients with Alzheimer's. And so we tend to use it at least in part because we want people to get the best regenerative sleep. Sleep is such a critical time where you have autophagy going on, where you actually have cleansing of the brain going on, where you have a reduction in the production of amyloid. So you also have synthesis of human growth hormone, which occurs during sleep. So for many reasons, sleep is critical. And most people who have cognitive decline are actually getting too little sleep and low quality sleep. It's also important to know from oximetry, you can literally stick an oximeter on the finger, you can have your doctor loan one to you, it's very easy to do. You want to know if you're having desaturation events at night. Many people have cognitive decline effects and also effects on blood pressure and heart disease and things from having sleep apnea. So you want to know if you have that. That's a commonly undiagnosed. About 70% of people with sleep apnea go undiagnosed. So another thing that's helpful. So melatonin is one of the ways to enhance sleep and reduce the chances of cognitive decline. It's something that your body makes naturally. It starts to make less as you get older. Now, you don't necessarily want to take large amounts, so people typically find anything between a half of a milligram and three milligrams to be about right. If you take too much, you'll know it typically because you'll sleep hard for a few hours and then you'll wake up and have trouble getting to sleep again. So people But people have gone up to 20, 50, and even 100 milligrams. But the physiological range, you typically want to be in that 0.5 to 3 milligram range. PQQ is Pyrroloquinoline Quinone. And the reason people take that is because it actually increases your mitochondrial number. So that's been the outcome of PQQ and the goal. So as we age, again, we often have fairly poor function of our mitochondria. And in fact, it's helpful actually to have turnover of the mitochondria, so-called mitophagy. It's a little bit like throwing out the worn-out batteries. If you continue to try to work with the poor batteries without replacing them, in fact you're at risk for Parkinson's disease. So it's good to have new, fresh, and active mitochondria, and just as you support your gut microbiome to support your mitochondria, which of course come from ancient bacteria that are now inside your cells. So that's the idea. of using PQQ and other mitochondrial supports. So here's the interesting thing about hormesis. We have a range where we were meant to work, our bodies were designed to work. If you exceed that dramatically, you actually damage the system. And so in fact, chronic mismatch between the way the system was meant to work, brain, bones, etc. Is what leads to degenerative disease. You literally are downsizing what's there because you cannot handle the mismatch. However, right at the edge before you get to this dramatic mismatch between what your body was made to handle and what it is handling, what can handle, you're pushing the system and that's what you do every day with exercise. So exercise pushes your system a little bit and that's what hormesis is all about. You are literally producing a modest insult that allows your body to respond in a supportive, regenerative, and improving way. So that's the idea of Hormesis. And again, so you want to be very careful. You don't want to go off scale so that you actually damage the components. So it was noted years ago that the copper-zinc ratio tends to be too high in people who have cognitive decline, often typically over 1.3 in looking at serum copper and serum zinc. And those aren't actually the best ways to measure copper and zinc, but it's a common way to measure it. And if the ratio gets too high, that is associated with cognitive decline. how Professor George Brewer at University of Michigan spent his whole career looking at copper and zinc and cognitive decline. And his argument, and his takeaway from his years of research, was that most of us, in part because of copper piping, part because of exposure to various things that have copper in them, like vitamins that contain copper, tend to be too high on the copper side and too low on the zinc side. Now, there are other reasons. Zinc is also absorbed poorly, for example, if you are on proton pump inhibitors. so we see this very frequently for people who've been on PPIs for years, they have very low zinc. There are about 1 billion people on earth who are zinc deficient and zinc deficiency actually causes a number of the things that are associated with cognitive decline and Alzheimer's. So it changes your immune status, it changes your insulin sensitivity and your ability to produce and utilize insulin. So you actually want to bring your copper zinc ratio closer to one to one, which for many people means bringing the copper down a little bit and bringing the zinc up a little bit. You may have, for example, poor immune response. You may begin to get pre-diabetes. You may have some cognitive decline. And often the type of cognitive decline that we see with high copper zinc ratios is what we call type 3 Alzheimer's, which is a toxic associated Alzheimer's. That tends to occur more with the toxic form of Alzheimer's and may contribute to it. So what the type 3 often presents with a non-amnestic Alzheimer's. So people instead of the first thing going is learning new things and new memory, the first thing that goes tends to be things like organization. They just can't do their jobs anymore. They're the ones that actually get fired from their positions the first. Because if you've got a bad memory but you can still do everything else, you can get along really well for years with what you've already learned. On the other hand, if you can't organize things, you can't calculate, you just can't set things up, then you tend to do very poorly at your job very early on. so lion's mane is a mushroom. It's Hericium erinaceus, and it's been shown to increase the production of nerve growth factor, which again supports the very synaptoblastic to synaptoclastic ratio that is critical for Alzheimer's disease. And so there are actually ongoing trials of Hericium in Alzheimer's disease. But again, we prefer it as part of an overall program so that you're addressing the various things and you're going to be increasing the trophic support of the synapses and so we include lion's mane with that. So we do encourage people, especially if they're at high risk for Alzheimer's or if they already have some cognitive decline, then as part of an overall program that may include many pieces, yes, lion's mane is one of the ones that we would suggest because of its effect to increase nerve growth factor. We also suggest whole coffee fruit extract, which increases brain-derived neurotrophic factor. We also suggest to get your hormones optimized because again, that provides support for synaptic maintenance. Looking at what actually increases brain-derived neurotrophic factor, a number of things that have come up from research, and one of them is this whole coffee fruit extract, which increases the production. Now, you can exercise and also increase your production. Also, whole coffee fruit extract, both good ways to increase production of brain-derived neurotrophic factor. And then there's another thing that's actually been, it was discovered by Dr. Yee at Emory University. which is called 7,8-dihydroxyflavone and that actually binds to the to the BDNF receptor. So it's essentially one step downstream from producing the BDNF. So these are all ways to enhance the trophic support of your synapses. So you can literally trace the molecular pathways that that goes to APP, which is the amyloid precursor protein, which is the critical switch. When times are good, when you have appropriate support, you cleave this at a single site, you produce two peptides, SAPP alpha and alpha CTF, that actually signal growth and maintenance in your synapses. So that's when things are good. When things are bad, in fact we've got inflammation, you've got insulin resistance, you've got nutrient and trophic loss, you've got toxicity. This thing now senses literally and gets cleaved at three sites, which are the beta, gamma, and caspase sites, to produce four peptides that literally signal your nervous system, things are bad, we need to pull back, we need to downsize. So literally trying to live within the means of what is available at the time. Now, you can trace direct paths from specific hormones, such as estradiol, and you can trace beautifully the path from inflammation. so whether it's related to gut leak, whether it's related to specific microorganisms, poor diet, what have you, you activate a mediator called NF kappa B, which literally enters your nucleus and turns on hundreds of different genes. And two of the genes that it affects are the ones that make the cleavage of the APP to produce the the four pulling back peptides. So you can trace directly from inflammation to change in gene expression to cleavage and now signaling downsizing. And so the inflammation from whatever cause is critical. Now, I should add, people always say, well, you don't want inflammation, so just take an anti-inflammatory. Well, remember, the inflammation is there for a reason. So before you take the anti-inflammatory, you want to remove the causes of the inflammation. For all these things, you want to go to the root cause. That's critical. Once you've removed that, you want to resolve the inflammation and there are things called resolvins that do that and then you want to prevent the inflammation in the future. But the most important is to determine what's causing it and remove that. The cytokines are simply signaling molecules. They're messengers that come typically with they can be pro-inflammatory or they can be anti-inflammatory. So these are modifiable they're modulating molecules that are sent from cell to cell with respect to inflammation inducing spreading the word essentially and then spreading the word that hey now we're going to decrease the inflammation when it is appropriate. So for example, people with Alzheimer's typically have an increase in their pro-inflammatory cytokines such as interleukin-6 and interleukin-8 and things like that. So in the past it was always said that people should not find out if they have ApoE4. This is the most common genetic risk factor. Now about 75 million Americans have a single copy. If you have zero copies and that's about 240 million Americans, that's the common one, your chance through your lifetime of getting Alzheimer's is right around 9%. It's not zero, but it's not too high. If you have a single copy, it's about 30%. If you have two copies, it's over 50%, so most likely you will get it. One of the things that we recommend is to, first of all, is to check it out. Find out what you have, because in the past it was said you don't want to know because there's nothing you can do about it. Nothing could be further from the truth. There's now a treatment tremendous amount you can do about it. What it really says is that you have a mismatch in that having ApoE4 makes it so that you have a quick trigger for inflammation. Great if you are walking on the savannah five million years ago and you're stepping on dung and puncturing your feet and you're eating micro-bladen raw meat. All these things, it's great to have ApoE4. And that was the dominant one for 96% six percent of hominid evolution. But in the last 220,000 years, Apoe3 appeared, and then the last 80,000 years, Apoe2 appeared. So most of us now are Apoe, about three-quarters of us are Apoe4 negative. So first of all, there's a wonderful website, apoe4.info, started by a woman, Julie G. And very helpful, and people share information and share their sorts of protocols and the sorts of things they're doing. Second thing is to recognize that you are at risk for inflammation. So you are more sensitive to things like poor dentition, leaky gut and things like that. Third thing is to recognize you also are better at absorbing fat and so you have an increased risk for cardiovascular disease. But the good news is you can adopt an appropriate lifestyle and appropriate supplements where they are necessary. And you can change your risk with this approach. So in fact, you have no more risk than if you were APOE4 negative. And it is one simple example. The magnitude of the effect of one copy of APOE4 is approximately equal to the magnitude of effect of routine exercise. So that alone is very helpful. But there's a series of things you can do to make it so that your risk is minimal. So we coined this term cognoscopy simply because it's easy to remember. It's a silly term but it's easy to remember that when you turn 50, you know, everyone should have a colonoscopy. Good to know because it can reduce your risk of future of getting colorectal cancer and you can catch them early and make it so that you don't die from colorectal cancer. Great thing to do. so whether you're 45 or older, you want to get a Cognoscopy. Now if you're younger than that, probably just wait, but if there's a strong family history, you may want to check as well. It's a relatively straightforward thing to do and so with a Cognoscopy you want to know what are all of my risk factors? Do I have ongoing inflammation? Because most people aren't aware of it until it gives them problems down the road like cognitive decline. Do I have insulin resistance? Again, you're headed for a problem potentially cognitive decline or type 2 diabetes, vascular disease, things like that. Do I have reduction in critical nutrients or critical hormones? Do I have exposure to toxins that I'm unaware of? Do I have a poor vasculature? All of these things are good to know about and you can do it with a simple set of blood tests, then to add to that you want to have a simple online cognitive assessment. Now if you're completely asymptomatic that's all you need blood testing and a cognitive screen. If you already have symptoms you want to add a volumetric MRI. So you want to have an MRI and you know you want to know what is the status of my Hippocampi, what's the volume? And so that's a fairly straightforward way to determine where you stand. And the hope is going forward we want to reduce the global burden of dementia by having people look at these things before they actually have Alzheimer's disease. So you can go on the End of Alzheimer's, the book, and look at all the different tests and get all the specific ranges for those. In general, we recommend that people go by the target. In other words, we personalize this based on what you need. However, yes, there are some supplements that for many people is partly because so many of us are deficient in some of these things. So one thing to think about, we talked about Bacopa earlier. Bacopa monnieri is benign and actually can support cognition. Ashwagandha is another one that is benign and that supports cognition. And then omega-3s and cytidine. So omega-3s support synapse formation. As you know, they're anti-inflammatory. Cytidine, work done from Professor Wortman at MIT for years, also supports synapse formation and maintenance. Magnesium threonate, this came from Dr. Guosong Liu in his work also at MIT and that also supports and in fact they've published trials showing improved cognition with that. So in as a general rule we say look at your look at your status to see what is going to be best for you. But there are definitely some basics for everyone. You want to support gut health, you want to support your microbiome and therefore you want to know if you have leaky gut and you want to have probiotics and prebiotics and if you can get those in your food, that's even better with your fermented foods and of course your prebiotics, things like jicama. So these are all helpful optimizing gut function, optimizing synaptic function and optimizing your nutrients. For most people taking some vitamin D is helpful. You don't want to have a low vitamin D because that's also important for cognitive function. So the diet that we recommend is called Ketoflex 12-3. And the idea is we're trying to drive a specific biochemistry that supports synapse formation and maintenance. So the first part, keto, it induces mild ketosis. And we'd like to see people, and you can get a simple ketone meter, we'd like to see people between 1.5 and 4 millimolar beta-hydroxybutyrate. so it's helpful and in fact your brain tends to function better when you're running on ketones than when you're running on glucose. We'd like to get rid of insulin resistance and so that's part of this. So the second part is flex, so keto flex, that means it's flexitarian. If you want to be a vegetarian, no problem. If you want to have some meat and fish, that's fine as well, but you want to have the right kinds. You want to have wild caught fish of course. You want to have grass-fed beef if you're going to have that and you want to have pastured chicken if you're going to have that. You don't want this stuff filled with toxins and hormones and things like that. And so, in general, as a general rule, we'd like to recommend that people use meat as a condiment. So you don't want to use massive amounts. The main thing you should be eating is vegetables and typically non-starchy vegetables. You want to have a plant rich, high fat, medium protein, low carbohydrate diet. That seems to work best. And then the 12:3, 12 is the minimum in terms of hours between finishing dinner and starting your breakfast, brunch or lunch. If you're APOE4 positive, you actually need to go a little longer, 14 to 16 hours. If you're APOE4 negative, 12 to 14 hours is enough. that will help you to get into ketosis, help you to induce autophagy and improve brain support. And then the 3 means three hours minimum between finishing dinner and going to bed. So KetoFlex 12:3 is the overall approach. It's a plant-rich ketogenic diet. Autophagy is what happens inside the cell where when you have not enough support, so you're giving a rest literally to the system. You literally undergo a cleaning effect inside the cell. And this is triggered and there are three different types: macroautophagy, microautophagy, and chaperone-mediated autophagy. And these function a little bit like vacuuming and cleaning your house. If you had people coming into your house 24/7, you never had time to clean it. It would be a disaster, right? So this way, people go home, you have a few minutes alone here, now you can actually do the vacuuming, you can actually put back things where they're supposed to be. That's what happens. By the way, one of the things you do is recycle proteins, lipids, and you break down mitochondria. These things all enter an endosome and ultimately interact with a lysosome so that you break them down inside the lysosome and recycle the components. Chronic Inflammatory Response Syndrome is a name coined by Dr. Shoemaker that is for people who have a response which can be from several different causes. It can be from mycotoxins from molds. It can be from various building materials. inflammagens, volatile organic compounds, it can be from Lyme disease, anything that is triggering your innate immune system, that's the evolutionarily older part of the immune system, to be active chronically. And what he found is that this induces a number of different responses that affect your health. For example, you can develop asthma, You can develop rashes, you can develop nosebleeds, you can develop changes with your visual contrast sensitivity, you can develop changes in your cognition, you can develop arthritis, you can develop Parkinson's and cognitive decline is one of the things that we found occurs with this. Now, what was surprising is that when we started to see people who have what we call type 3 Alzheimer's, these are the people who have toxic Alzheimer's. They have the sort of lab tests that Dr. Shoemaker described. However, they typically don't have the peripheral components. They typically don't have the asthma. They typically don't have the rashes. So these are closely related phenomena, the SIRS and this type 3 Alzheimer's. So we had to come up with some term for something that is like SIRS but doesn't seem to have the peripheral markers. So we call this iSIS, which is innate system immune stimulation. The bottom line is the amyloid that we associate with Alzheimer's disease that collects in the brain is actually part of the innate immune system's response. So as long as you are responding to something with an inflammatory response, you are producing this and putting yourself at increased risk for cognitive decline. So the things that affect immunity, and there's a two part here, one part is what actually induces the inflammation and then the response to it, but the other is the ability of your immune system to have an appropriate response. Too brisk of a response, you get an autoimmune condition like multiple sclerosis. too weak of a response, you don't respond and you now have more spread of the inflammatory process itself. So you have, if you've got, for example, if you've got Lyme disease, if you've got mold exposure, these things now can go farther. So in fact, there is this cold war that is ongoing. So we want to do both. We want to support the immune system and there are a number of ways to do that. And certainly the Ayurvedic physicians like to do it with a triad of tinidazole, amalaki, and ashwagandha, which some people like to use. Others want to find what the specific microbes they're dealing with, target those directly with specific antifungals or antimicrobials. Then, what are the things that are actually causing this? For most people, there are several things. So, if you have a leaky gut, and this comes up again and again and again. It's a common problem. You are spilling things like lipopolysaccharide from the cell walls of the bacteria. You are spilling bacteria, foods that you're interacting with, as opposed to well digested food. So now you are at increased risk for things like rheumatoid arthritis and things like that. And so you've got ongoing inflammation. the other thing, of course, poor dentition, another way. Air pollution has turned out to be a relatively common way to have an inflammatory response. And so organisms, poor diet, leaky gut, sinusitis. Many of us have a chronic mild sinusitis that we kind of ignore for years. And this again, this has access, and so you you have to be concerned about the exposure to your brain. So all these different things can give you neuroinflammation. Not only can alcohol cross the blood-brain barrier, but alcohol actually affects vitamin B1, thiamine, which has a dramatic role in memory. So we recommend if you've got cognitive decline, if you're going to have a glass of wine, a few times a week, that's probably fine. But you don't ever want to take enough alcohol that you're actually damaging your cognition because you are having a direct effect. It is a neurotoxin and it is a neurotoxin that also has this effect on thiamine which is critical for memory formation. And so people get ultimately what's called Wernicke syndrome, Wernicke-Korsakoff syndrome, and can lose their ability to form new memories. Now most people don't go that far, but we'd like to have people keep their thiamine appropriate. In fact, it only takes a few weeks to get low on your thiamine. It's not one of these vitamins that's stored for years. So alcohol has multiple mechanisms by which it can create problems with cognition. So Marcon's is again something that was pointed out by Dr. Richie Shoemaker. this stands for multiple antibiotic resistance coag negative staph. So these are organisms that tend to form biofilms. And when you have bacteria that are together, it's a little bit like having a community of bacteria that's all embedded in a fort. It's much harder to get rid of them. Interestingly, if you look at what amyloid beta does, it looks like not only an endogenous antimicrobial, but an endogenous antibiofilm because one of the things that you need to do when you want to get rid of biofilms is to chelate the metals that are in the biofilm. That helps the biofilm to dissolve and now you can get at the bacteria with antimicrobial. Well, that's what amyloid beta does. It has both a metal chelating and an antimicrobial effect. So it literally looks like an endogenous antibiofilm. Now, marcon can contribute to SIRS and can contribute to cognitive decline. You're basically giving a protective region for microbes to live. They can produce, for example, proteases and peptidases that decrease your, for example, MSH that affect your cognitive function and that lower your trophic support as a whole. And of course, keep keep the ongoing inflammation going. So you can literally do swabs that test for marcons. And it's been pointed out by Dr. Shoemaker that what you're really testing for, it's a surrogate marker for biofilm. So you want to know, is there marcons and is it part of biofilm? So there are multiple ways to go after marcons. Some people use biocidin, some people use a colloidal silver. Some people use a combination antibiotic regimen called BegSpray. So we just recently published a paper with 100 patients with documented improvement. And the idea is that it has been claimed in the past that you couldn't see improvement for people who have Alzheimer's or pre-Alzheimer's. And these people, we had some with Alzheimer's, even some with advanced and some with pre-Alzheimer's. And this came from from 15 different sites. So this isn't just one group claiming that they're seeing it. These are 15 different sites that showed demonstrated and documented improvement in cognition in a hundred different patients. In addition, some people showed also improvements in quantitative EEG. Some people showed improvements in evoked responses, so-called P300. Some people showed improvement in Hippocampal volume. So all these objective measures showed improvement in these particular patients. Now, this doesn't mean that every single patient improves, but this is a collection of 100 that showed documented improvement. In the past we've dealt with scourges. We had the scourge of black plague, the scourge of leprosy, the scourge of polio. We don't worry about these scourges today. We should not have to worry about the scourge of Alzheimer's. So our goal is that within a few decades, the scourge of Alzheimer's would be seen just as the scourge of the black plague or the scourge of polio and taking an approach with prevention and early reversal and targeting the things that actually can do this. We can reduce the global burden of dementia and in fact we can view Alzheimer's as a very rare disease and as a past scourge. So that's the goal.

What our work shows is that when you individualize care and you give people a plan, and I know you've asked me at least three times now, what should people do? What I'm trying, why I'm delaying things is because it really truly needs to be individualized. And what we use is a term called the ABCs of Alzheimer's prevention management. based on the data, we get data on A's, the B's and the C's. A stands for anthropometrics. Anthropometrics is basically a fancy A word for body composition. What is your body fat? What is your waist circumference? What is your muscle mass? Depending on these factors, we're going to change the recommendations we give. The B stands for blood-based biomarkers. We're going to look at markers of lipids, cholesterol markers, also advanced markers that preventative cardiologists use, for example, that most neurologists honestly don't really pay attention to. We look at metabolic markers, insulin resistance, we look at inflammatory markers, we look at nutrition markers. Instead of saying, okay, well go eat fish, it's good for you, we're gonna look at the markers in the blood. We're then gonna tell you based on your blood and based on your genetics how much fish you should be eating, what types of fish. So the take-home point is we're gonna get granular with every patient. The other thing we do is in the blood-based biomarkers, we look at genetics, we look The APOE4 variant, it's the most common risk gene. Doesn't mean you're gonna get Alzheimer's if you have the variant, but it increases your risk. Well, if I know that you have the APOE4 variant, they checked for this in 23andMe and millions of people have gotten this checked, I'm gonna personalize your care differently. If you have the variant, I'm gonna give you plan A, B, and C. If you don't have the variant, I'm gonna give you a little bit modified plan, X, Y, and Z. If you have two copies of the variant, you have a different plan altogether. That's only 1% of the population. So, you know, the take-home is we take all these markers and then the C is cognitive function. And we understand a person's cognitive baseline. We look at memory function, language abilities, learning abilities, speed of processing, attention and executive function, which is higher order processing. We take all of this and the patient's medical history. We learn about the patient. We learn everything we can about them, about their family, and then we personalize a plan. So there's 21 different things. are based on that person individually. And, you know, there's a lot of overlap. If you want me to say, okay, well, what are the core things? Well, exercise on a regular basis. Okay, well, exercise on a regular basis is good, but every person gets a different plan. If we're putting someone on a plan for body fat loss, we're going to give them a different plan. Steady state cardio, for example, some people would call that zone two training. Steady state cardio at 60 to 65% of your heart rate. There's different ways to do this through lactate testing, through a variety of things that we do, you know, more precisely in our clinic. But we put people on these steady state cardio plans fasted in the morning as long as they can tolerate it because that way it jump starts body fat loss. If we have people that don't do any muscle strength training because they don't like it, we educate them to say, I don't like it either. I'm not, I'm not, you know, Mr. Big muscles over here, but I have to do strength training once or twice a week minimum. because if you don't have muscles, you can't boost metabolism. So we put people on these very specific plans. High-intensity interval training. I really believe that high-intensity interval training is almost necessary for people with at least one copy of the APOE4 variant. And this is what has been studied down in a couple of studies. And yes, we need more research and studies out of Norway were good, but we need to personalize an exercise plan. we need to personalize a nutrition plan. We need to personalize a vitamin and supplement plan. In some people, we do use drugs. Drugs are actually not commonly used at all in our research, although we do use them on occasion. We'll use a variety of drugs, usually at much lower doses than maybe the regular community uses. But when it comes to management, I'm equal opportunity. If there's data and it's relatively safe, you know, I'll entertain it. So we recommend, you know, cognitive activities that will have a spillover effect, learning something new, learning how to play a musical instrument, learning a new language. These are things that may have a protective effect, build backup pathways. Believe it or not, even learning how to play a musical instrument in midlife has protective effects on cognitive outcomes in late life.

And that's hope for me yet.

There's hope for you yet. I got my bass guitar over there.

I got blisters on my fingers. I'm going to play the guitar. I'm not, but I just, so, but my big problem is I don't know how to tune it and I don't, I am so musically inept that I, probably there are good apps and things to do it.

There's a website, it's called, you got a pen? It's called YouTube.

YouTube, you may have heard of it.

Almost as many people watch YouTube as listen to your podcast. So you can learn how to play guitar on YouTube. I think you can do it. Okay, I'm gonna try.

For sure.

That's my December.

Excellent. And January and February and March. So the take home point is engage your brain. Treat your brain with respect. Love your brain. Make a plan for your brain. What does that mean? Make a plan for sleep. If you exercise and exercise and exercise, some people say colloquially that that loosens the amyloid, the bad protein that gets build up in the brain of a person with Alzheimer's. But if you're burning the candle at both ends and you're not sleeping during sleep, especially deep sleep, that's when a person has the trash come. The trash man comes, they pick up the garbage and they take it out and they take it to the trash heap. That is the restorative part of sleep. And if someone isn't sleeping at least seven, seven and a half, eight hours of sleep is usually the goal as we get older. It's harder to sleep that much. But making a plan for sleep, prioritizing sleep. We have people that track their sleep, that track their exercise. I'm wearing a wrist device here. I have nothing to disclose, but we've done several research using this device. I track people on my phone. I have my phone right here, and I can check how much exercise they've been doing, how their sleep, how much deep sleep. I can see their blood sugar control. I can see all these different things on my phone because my patients share their data with me. and when I talk about data sharing, it's not just about tracking sleep, it's not just about doing exercise, it's about tracking it, determining the response, talking to your physician about it. Granted, it's hard to find physicians that will take the time to talk to you about this kind of stuff. Tracking your blood sugar, there's, you know, at home devices called continuous glucose monitors. In our program, we take a very, very deep dive and we learn about all of these different metrics and we refine or fine tune the plans that we give them based on their real-time measurements. So, you know, I can keep going. There's stress modification. You know, transcendental meditation. Bob Roth's taught me a ton about this. What about mindfulness-based stress reduction? You can take a course online. Mindfulness-based stress reduction has amazing outcomes when it comes to brain health. The list goes on and on. There's no one magic pill or one magic cure, but there are a variety of I was going to say pharmacological and non-pharmacological, but you're reevaluating how I say this now. There are a variety of interventions that are evidence-based and safe that I think all of us need to learn about. Whether we talk about fasting, and I like the term time-restricted eating better, meaning not eating for 12, 14, 16 hours overnight, at least four or five days a week. I use the term fasting for a more prolonged fast, 24 hours or more, and that's a different discussion. There's the ketogenic diet, there's the Mediterranean-style diet, there's the mind diet, There's components of each diet, green leafy vegetables, wild salmon, grass-fed beef better than non-grass fed beef because of the omega-3s. There's so many devil is in the details. Half a couple blueberries and strawberries two to three times a week, you know, leads to better brain health outcomes and cognitive outcomes in the nurse's health study, you know, many years later on. There's dark cocoa powder. There's so many things that I can drop in as key things. But, the take home point is all of these things need to be individualized. So, let me ask you this because.

I mean, you know, first I want to just kind of feedback because what I'm listening to you thinking, you're a neurologist, but you're also an immunologist, a cardiologist, an endocrinologist, a gastroenterologist, a nutritionist.

I mean, right?

You're breaking down the paradigm of medicine, which is we should stay in our lane, focus on our organ, and leave the rest to everybody else.

Yeah.

And your Insight here is that the body is a system, that everything's connected to everything.

Yeah.

But you can't just pick out one thing and work on that, like amyloid or TAO or whatever, and get to the problem.

Yeah.

And it, you know, it's sort of like trying to, you know, bail the boat while there's holes in it. You gotta fix the holes. Yeah. And essentially, the holes that you're talking about are all these. ways in which our brain gets injured by our lifestyle and by our environment. And you didn't mention toxins, but that also plays a large role. And so all of a sudden, we have to sort of rethink our whole approach, which has really been a reductionist approach. Single disease, single drug, with a single outcome. There was an article in Jam a number of years ago called Shifting Thinking in Dementia. You probably saw it. And they said in that article that we combine categorical misclassification, with etiologic imprecision. And in English, for those listening, that means we categorize dementia according to symptoms, not the causes. And we are not very focused on the etiology or the causes. We're focused on the symptoms. And we say, well, you can't remember this and you fit this profile on your neurocognitive testing. You have Alzheimer's, you have this kind of dementia or Lewy body or blah, blah, blah. And the reality is that you could have 10 people with Alzheimer's who need 10 different treatments. And that's exactly what you're talking about. That's heresy, Richard. That's heresy in medicine, honestly, because we really have a very, very restricted reductionist view of disease that doesn't let us actually even study these things. And I've literally had arguments with top leading researchers, like heads of research at major institutions, saying, these are all the factors that affect the brain. We want to study them together. So, oh, no, you have to study one thing at a time and then see how that works. Then one thing. So study exercise and then study nutrition, then study vitamin D, then study fish oil. I'm like, no, that's not how things actually work. It's like, it's like you have to use all the whole picture. The other thing I sort of wanted to sort of touch on was that you're sort of introducing a concept of the personalization, which again is very different in medicine. It's not one size fits all. And, you're talking about very sophisticated personalization based on a whole set of biomarkers and tests and things that are easily accessible, but that aren't normally looked at and that aren't normally tested. You know, you get your typical panel, you get your thyroid, your B12, you get your spinal fluid done, you get your MRI, and you go, okay, you got Alzheimer's. It's sort of a little bit more complicated than that, but it's really a fairly narrow window of biomarkers and metrics, and there's bazillions of them. And I think we're just sort of touching the sort of tip of the iceberg on this. And I've seen in my patients when you start to apply these concepts of personalized care around around food, around exercise, around sleep, around stress, around supplements, around everything that you really begin to see dramatic changes in brain function.

Yeah, I often joke that I'm a one-third neurologist but a preventative neurologist at that. I'm a one-third make believe. I will full disclosure, I'm not a preventative cardiologist but I may make believe preventative cardiologist. I one-third primary care doctor and make-believe preventative endocrinologist. I don't even know any preventative endocrinologists. If you find one, introduce them to me. I was trained in an environment. I went to a six-year medical program where I was in med school from day one, University of Missouri, Kansas City. I knew I wanted to be a doctor when I was five, 17 years old wearing my white coat, and I did so much internal medicine during med school. I had like an extra year of medicine because that's the way our training was. and I don't know if it was that or I'm not sure exactly what it was, but Alzheimer's disease is a medical disease.

Yeah.

Full stop. That's it. There's this thing called the skull and it's a hard thing that protects you when you fall, but it's just like it it it's like when you have medical conditions, you can affect your kidneys. When you have medical conditions, it can affect your eyes, it can affect your heart. The same thing, it can affect your brain. And I couldn't agree with you more. People can take different roads to Alzheimer's. and you have to figure out what world they're on and get the, get them the heck off that road. Women, for example, are unfortunately many times in the fast lane to Alzheimer's. Women, two out of every three brains affected by Alzheimer's are women's brains. And five, 10 years ago, I would say I didn't know why. And now I think I can answer that question. And it's related to the perimenopause transition. It's related to specific life factors. It's related to women being maybe a little bit more at risk. if they have the APOE4 variant. So the take-home point here is if you understand a person's individual risk factors, whether it's biological sex, whether it's medical conditions, whether it's what's floating around in their blood, whether it's what is their cognitive function at baseline, you have to figure these things out and then you have to target that plan and personalize that plan. And I mean Alzheimer's disease and brain health needs to be treated in a medical way. Because if it's not, if you're just targeting amyloid, you're missing the boat. You know, amyloid's a marker and I think hopefully one day we're gonna have just like we treat diabetes with lifestyle interventions and exercise and as well as certain targeted drugs that honestly some of them actually do tend to work pretty well. I'm not the biggest fan of insulin like that doesn't—Dr. Justin that's—Justin: that's maybe band-aiding to me. Dr. Justin: that's probably too late. Justin: I mean, I'm not the best—Justin: whatever. but some of these new, you know, new things that are pretty interesting. I won't get into specifics, but I hope that one day we treat Alzheimer's disease and cognitive decline like any other chronic disease of aging where we hit things with a multimodal evidence-based and safe approach that requires a medical intervention. So essentially what you're saying to paraphrase.

Is that Alzheimer's is not a brain disease.

Correct.

It's a systemic disease that affects the.

Yeah, I really believe that. I have to be careful saying that. Is this being recorded?

Oh, yes. And it's going to be broadcast to billions of people around the world. Great. Great.

My field, I was just trying to, I was just gaining some fans in my field and now it's all last decade of work. Oh, no, no. What are you gonna do?

You are at the forefront of a paradigm shift that's happening throughout medicine, which is the breakdown of the old concepts of disease from from simply this reductionist, organ-based, symptom-based model to systems thinking and network medicine. And, that's really all you're talking about. And, you've touched upon some of the most easily accessible and modifiable factors, which is what we eat, how we exercise, how we handle and manage stress, how we sleep. Those four pillars are huge. And then, there's the fine-tuning with managing metabolic risk factors or getting their nutrient levels up to a certain level. but there's a whole treasure trove of stuff that we, I think, still haven't even dug into. It's like, it's like I visited Ephesus in Turkey, and it's the largest Roman city during the Roman Empire. It was incredible. It was all buried under dirt and, you know, rubble, and they excavated it, but they're still figuring, they're still, you know, excavating it 100 years later, and it's just fascinating to see that there's so much we don't know. And I would in my experience as a functional medicine doctor, I've seen things that have impact on the brain that aren't really included, like heavy metals. Do we even have a way of testing that is in conventional medicine? Not really. We just do a blood test and then we don't worry about it if it's okay. But there may be total body burden of toxins we don't look at. The microbiome is another huge factor that affects the brain and Alzheimer's. And mitochondrial function is something we talk about, but it's often ignored. and we have latent infections that may be affecting the brain that cause inflammation, whether it's, you know, herpes two may be linked, but there may be other things. I mean, Chris Christofferson had Lyme disease and got diagnosed with dementia. There may be environmental factors like mold that have impact on inflammation. So we know that the brain with patients with dementia is inflamed, and then the causes of that inflammation can be multiple. And so part of the diagnostic dive that you're doing. And I would just sort of encourage you to think about this is that you're getting to all the stuff that we do know that's so clearly evidence-based. But then there's a whole treasure trove of things to look at that we're kind of ignoring. And I'm just gonna take like two seconds. I know it's your podcast, but you're talking. But I'm just gonna just talk about this one patient because it was the first patient I had where I'm like, came in the guy with Alzheimer's, I'm like, can you do anything? I'm like, I have no clue. I don't know. But I'm just gonna apply the model of systems of biology and functional medicine. Let's see what we we do. We found he was severely insulin resistant. He had, which is, you know, we talked about Alzheimer's type 3 diabetes in the brain. He had very high homocysteine levels and methylation problems. So his, his genetics were off around metabolizing B vitamins in the right way, which we know is a risk factor for Alzheimer's. He had the APOE4 double4 gene. So he's the one percent. he was seven years old, cognitively impaired, diagnosed with Alzheimer's, basically at home, not able to do anything, depressed, not functioning. It was the former CEO of his company. He also had other nutritional deficiencies like vitamin D and he had been living in Pittsburgh and in Pittsburgh, it's the capital of steel. And for a century, they've been burning coal for the steel plants. and they use cold air for the streets, on the winter for ice. They put it on the fields for fertilizer, what they do. It's, it's everywhere. And all my patients in Pittsburgh have high mercury levels. And he had very, very, very high mercury levels. When we did a challenge test, he also had a mouthful of fillings. And we know that if you look at, you know, amalgam scores, surface area, and you look at animal studies, the more amalgams you put in their mouth, the more Mercury ends up in their brain. And, and so I said, well, I don't know, I don't know if anything I'm going to do is going to work, but let's fixure in some resistance. Let's fixure. also, he had terrible gut issues. He had irritable bowel for 30 years and was on stellazine for his stomach, which is a psychotic, anti-psychotic drug to kind of calm his stomach down. And I fixed his stomach. I cleaned up his diet, fixed the insulin resistance, I fixed the B vitamin thing. I got rid of the metals, and the guy came back to life. And it was really, really remarkable. And he was able to go back to work and function again and be part of his family and be part of his Society in a I was just shocked. And so, I think that there's a level of stuff that we're looking at and then there's a whole bunch of stuff we're not looking at. So, I'd love you to comment on that and what your thoughts are about all that other stuff that's going on.

Yeah. And thanks for sharing the story because every story is instructive because this is...

I'll send you the article that I described as an editorial I wrote for a medical journal.

I'll just... because you'll go, wow, this is interesting. So, you know, the thing that resonates me with the story is, you know, when you have people with APOE4-4s, those are just different eggs. And, you know, E4-4s may be, you know, for example, E4-4s may be preferentially responsive to vitamin D, for example. So, you know, some studies show that vitamin D, eh, maybe it's not really that preventative. Oh, some studies show, oh, maybe it is more preventative. Well, people with two copies of the E4 variant, which is, again, not super common, those people really need to have their vitamin Ds up. And that's, and, you know, that's just an example there. But, you know, people with the APOE4 variant, pesticides, DDT and DDE, the interaction between E4 and pesticides increases Alzheimer's risk several fold. If people don't have the APOE4 variant, maybe they're not as exposed or maybe they're not as increased risk to Alzheimer's. So, when you look at a whole population, you don't tease out for E4 positive versus negative, the studies may not show any correlation but in practice we see the correlation and in other studies you do see the correlation. So, I think I think, you know, something I learned, I was at a conference in Canada. You have a lot of fans in Canada, by the way, just definitely.

Your name came up there. True, it's everywhere I get. I'm in Istanbul at the airport and some guy from the security comes running up to me, I thought I was gonna get arrested for smuggling something. Smuggling my Turkish delights back to America. And you're like, Dr. Hyman, can I take a picture with you?

And I'm like, oh, fine, okay.

International.

So I was at this thing in Canada and amazing people, just smart people and we were giving presentations and of course I'm like the science guy and I'm a clinician. I'm like a regular doctor, I don't say Joe Schmo like you and me, but I was thrown into this clinical research thing and again I had resources, infrastructure, did work hard to learn, hired the right people. So yes, I've done research and when you do research you need to have objective measures to follow that you can track. I was at this group in Canada, this guy named Gary and Elizabeth, Elizabeth's a naturopathic doctor and Gary is just really, really, really smart. And they were working together to present on a topic and it's kind of like a bulb light bulb came off of my head and I said, you know, I'm so focused in the objective because I need to be because I'm a researcher. If I'm going to say something and think it, I need to then prove it because if I'm in an academic environment, you know, I was at Weill Cornell Medicine for a New York Presbyterian for almost eight, nine years and now I'm at Florida Atlantic University. doing a really, a really exciting program in brain health and Alzheimer's prevention, Parkinson's prevention, dementia with Lewy body prevention. You get to do some really cool things. It, maybe I'm missing the boat a little bit because if I'm just focusing on the objective that I need to track and prove, there's a lot of stuff under the surface that I can't really track and prove because I don't have a biomarker to do that. So I guess what I'm trying to say is as, as I've I know what I know and I don't know what I don't know. I'm consciously incompetent about things. And the story that you say is, yeah, I know. There are people that are unconsciously incompetent and those people drive me a little bit batty.

But I am on your team. I know what I don't know.

Yeah, I know what I don't know and I'm willing to have my eyes opened. And the stories that you say, it's like, as a physician, you have to treat someone in a certain way to try to make them better, but we don't always have all the objective evidence and the types of work that we do on patients, it's really hard to study. I have empathy for people in our boat who are trying to study the rigorous, rigorously study because what's moving the needle? To me, I don't care what's moving the needle. People were criticizing one of my research paper, oh, you recommended 21 things. Whatever. if 18 of them are helping and three of them are harming, you'll never know. And I said, okay, but look at the results. 18 months later, people with amyloid in their brain with mild cognitive impairment due to Alzheimer's disease that followed this plan, 18 months later, as long as they followed 60% or more of what I recommended, had better cognitive outcomes. 18 months later, we were able to improve symptom. There's no drug that can improve symptoms. at 80, slowing decline is one thing, improving symptoms. So, I'm Zen with not being able to precisely understand which of my 21 things are working. But I think, you know, as clinicians, I think we just have to do the best we can. And we want to, you know, promise not to over promise. I think that's important too. You said at the beginning when you were seeing that patient, I'm not 100% sure yada, yada, but I'm going to try all the usual things and something worked. So I think as long as we have honest conversations with our patients and do the best, people like us that have academic appointments and are in that realm, I think it's my duty in some ways at this time in my life, in my career, to try to prove as much as I can. But I think the field and I think people need to realize that some things are really hard to study and prove. proof.

Yeah.

And they are. But, you know, what's happening now is, is with the acceleration of our understanding of how to map biology and things we couldn't even measure before, we're able to start to, you know, look at different Diagnostics than we ever did before and find things we never found before. And, and within the diaspora of medicine, which is where I've been most of my life, there, there has, there's a lot of people doing really interesting Diagnostics that are ignored, like heavy metal. for me, that's like a, that's like a blood pressure. When someone comes in and they have any kind of, you know, toxic or immune or cognitive or any chronic symptoms, I look at it because it's often an underlying factor. It was actually how I figured this all out was through my own mercury poisoning from living in China. And I had severe cognitive impairment and also immune dysregulation and gut issues. And I, I think the, you know, the gut stuff is such a big deal, and that's something we can start to understand with the microbiome and its effect and there's data coming out. But the question is, as clinicians, we never learn, well, how do we repair a microbiome that's off? Right? How do we do that? Like, that's. Okay, well, we may know. Okay, if you're low in vitamin D, take vitamin D. But, like, if we test the microbiome and there's all this inflammation and dysbiosis and, like, the average doc has no clue where to start. So I think that's part of the problem, is we just don't have one, some of the Diagnostics we need, or. Or if we do, the average practitioner has no clue what to do with it. And I think we're. We're all. all that's going to change. I think what you're talking about is managing something that until now, I don't think has been able to be managed by the average doctor, which is, God, there's a hundred things we could find that could affect the brain. I think there's probably a thousand, or maybe there's 10,000, but the average person and the average doctor cannot process all that and make the connections. But with the advent of quantified self metrics, which you talked about, with the advent of advanced diagnostic metrics and metabolomics and the, you know, to understand even the microbiome metabolomics, for example, nobody talks about that, but it's the metabolome of the microbiome in your blood. There's probably 20 to 50% of the metabolites in your blood come from the bugs in your gut.

Right.

And, and how does all that work? Well, that's going to require big data and machine learning and artificial intelligence and start to see the data and the patterns and connections. So I think that's where this all headed. And, and, you know, it, you know, we have to stop this Paradigm. of being reductionist and saying, just take this one drug for Alzheimer's. And I get so frustrated when I hear these studies come out and they had big news articles and, oh, this helps or that helps. I'm like, what about all the rest of the stuff that Richard's talking about? It's got to be frustrating for you too because you see it, you see your patients get better and you go, hey guys, why don't you try this? And what do your friends say who are also neurologists or memory specialists? Do they think you're a quack or.

Do they like listening? you know, I'm a pretty resilient guy. I gave my first talk in 2007 about, you know, how MCI, mild cognitive impairment due to Alzheimer's and, you know, in this pre-symptom, I didn't like that term. I just felt it should be, you know, prodromal at risk, you know, I felt like we should be treating people before they had dementia. And when I kind of set that stage, and I wrote about this in one of my books, names, not naming names, but, and I didn't name the name there, too. But one of the Giants in the field was sitting there and, like, just, I don't say rolled their eyes, but just, just, but there's no evidence. There's just, there's no evidence. There's nothing you can do. There's no evidence for die. There's no evidence for this. There's no evidence for that. But there was no impetus to even aim to study it. You know, I started seeing Alzheimer's prevention patients in 20, 2009. Dr. Arthur Agatson was one of my mentors. Oh, yeah. Arthur. Yeah. Amazing guy. You know, he my attending at Mount Sinai Medical Center when I was an intern. Yeah, before the South Beach Diet, before, you know, he's the South Beach Diet guy. But to me, he's the Agatston Calcium Score guy. To me, he's the visionary that was one of the first preventative cardiologists. And preventing disease and starting before there are symptoms, it was so, the tomatoes that were thrown at me were, you know, the big vine-ripe tomatoes. Now, I don't know if my reflexes are better. I have cat-like reflexes now, I have a cat behind me, but I can dodge the tomatoes better. My armor is thicker. The tomatoes are not being thrown as quickly. But it's also because we've now published, we've published results. And I would talk to a journal editor five, six years ago and I said, well, this, this, and this, and this, and this is what I see. And it's clear. And he said, well, it may be clear to you, but you need to prove it. And then you need your peers to review the article and accept that your thoughts and your observations are substantiated by evidence. And I feel like in the last five years, just eight years actually, we've been able to do about as good of a job as possible with the limited resources that we have.

Now.

If 1% of the billions of dollars, or heck, 10% of the billions of dollars, would have come in the prevention bucket, I can tell you if someone drops a very large sum of money in our research program to prove this, we can do it, but it's hard. Prevention studies are expensive because they take longer. Prevention studies, you need to follow people for years rather than, you know, six months or nine months or a year. Yeah. So, so, so I think, you know, the reason that my colleagues are coming around is because of the Publications and building the, you know, the body of evidence. I think the other reason that my colleagues are coming around several of them have come visit. I've had over 45 other physicians and other healthcare providers come visit me and sit next to me. And if someone isn't willing to sit next to me and if someone is willing to criticize the work we do but not willing to come sit next to me and spend a couple hours and just watch, just look, it's oh, this is only one patient. It doesn't mean anything. When you see this once and you see it again and you see it Nine o'clock, 10 o'clock, 11, and then one o'clock, two o'clock and 3:30. You just, you know, like, okay, fine, prove it. I get that. But there are still skeptics out there. There are still skeptics and I still get criticism every day. And I don't want to say I'm jaded, but, you know, haters gonna hate. I'm gonna keep doing my thing.

And, well, you know, you know what Max Plank said, right?

No.

He'S cool.

He said, he said that.

No, he said, he said science. But you could say medicine doesn't evolve by convincing your opponents and helping them see the light. But because they eventually die and a new generation grows up that's familiar with it. In other words, medicine progresses one funeral at a time. That's kind of mean, but that's what he said. And, and I think, you know, the other point is that the absence of evidence isn't the evidence of absence. If we haven't spent billions of dollars studying nutrition and Alzheimer's, how the heck do we know anything? We spent billions of dollars studying drugs that don't work, but not the right things. And the other thing, Richard, I'm gonna push back pretty hard on this for you because you keep talking about preventive neurology and preventing Alzheimer's. And yes, yes, we should do all that. But your study, your own study showed that you cannot only prevent it, but reverse the symptoms. Now, how far can we go to reverse it? How much can we reverse it? How far can these treatments work? What if we added 10 other things that maybe we haven't even thought of that might be as or more impactful than the 25 things you're already doing? You know, I would push back and start to encourage you to think about treatment studies, not reversal studies, because those you'll see outcomes much quicker. And if you can take a group of 10, 20, 50 people, and be really aggressive. And it's not easy because changing, and I, and I have these patients, I'm treating many of them right now, it's the roughest thing because if you have an engaged patient, you know, someone had a heart attack and you tell them to change their diet and their vitamins and exercise, they'll go, I get it. But you've got someone with dementia or who's cognitively impaired, they can't remember stuff. You need a full-time like bodyguard, literally with them, telling them what to do and helping them do it. But if you did those kinds of studies, I, I think you would the dramatic changes. If you loved that last video, you should check out the next one for sure on getting the root cause of all disease. Pathogenic microbes, bacteria, yeast, viruses may be doing the seeding of the plaques where the plaques are actually forming to protect.