 Welcome to the Dr. Gundry podcast. Ask almost anyone over the age of 50 what medical condition they most fear and probably all of them will respond with the same answer, Alzheimer's disease. And that's no surprise since it's now the third biggest cause of death in the United States. And depending on estimates over 75 to 90 million Americans are actually genetically predisposed to get it. In fact, I'd wager that almost everyone listening to this podcast knows someone and maybe has a family member who has suffered from Alzheimer's disease. Well, my guest today says there's no reason why Alzheimer's can't be a rare disease, one that we can nearly eradicate. Imagine that the same way we once got rid of scary diseases like polio and leprosy. So I'm joined by my friend and colleague Dr. Dale Bredesen. He's professor of molecular and medical pharmacology at UCLA, the author of the New York Times bestseller The End of Alzheimer's and like I mentioned he's become a good friend of mine through the years. Dr. Bredesen has a brand new book out launching tomorrow the end of Alzheimer's program, the first protocol to enhance cognition and reverse decline at any age. It's all about the lifestyle changes you can make to prevent and even reverse symptoms of Alzheimer's disease. And on today's episode, he and I are going to discuss the APOE-4 gene, what your blood sugar levels have to do with dementia and which diet plan is best for brain health. Dale, happy to have you back on the Dr. Gundry podcast. Hey, great to see you, Stephen. Great to talk with you as always. Alright, so what's new in The End of Alzheimer's program? How is this different from the last book? Yeah, great point. So the first book, The End of Alzheimer's, was really a conceptual book. So this looked at our 30 years of research in the lab, what happened with the transgenic mice, what happened with the bacteria, what happened with the cells. And moving forward, we started with the idea of these diseases, neurodegenerative diseases, as you know, Stephen, have been the area of greatest biomedical therapeutic failure. You know, you did all this great work with hard bypasses and all these wonderful things over the years. We just haven't had anything for neurodegeneration. So whether it's frontotemporal dementia, Alzheimer's, Lewy body, ALS, there just hasn't been anything. So we were looking at, could we understand the molecular basis well enough so that we could begin to fashion the first effective treatments. And as you know, we ended up coming circuitously over these many years of research and realizing, wait a minute, this is not a single drug disease. This is a many different component problem where you actually have to change network function and your network is related to your neuroplasticity in Alzheimer's. So when we published that, a lot of people said, hey, we want more details. What are the URLs? What are the workarounds? What brands do we buy? Where do we go to the store? All these detail issues. So that's, this book is about the details, whereas the first book was about the concept. And so I'm very excited because for the details, I worked with two wonderful ladies. My wife, Dr. Aida Lashine-Bretison, who is a clinician, and with Julie G. And Julie, you know, is a wonderful user and biohacker and someone who's now been on the protocol for over eight years. And perhaps the most important thing is, as you know well, when you get better, you stay better if you're getting at the root cause of the disease. Whereas if you're trying to circumvent physiology with a drug, you just go right back to declining again. And in fact, as you know, article published about a year ago showing that people who were on the drugs actually did worse overall than people who were not on the drugs. So this one is really about the details. How do you do it? It's the program. So, you know, we've talked about this. Why do you think mainstream medicine has failed in this? A lot of money has been thrown at this. Yeah, billions and billions of dollars, as you well know. And this has been the problem, I think. And you know, it's interesting, your career shows it. You had the first part of your career, where you did very standard medicine, as did I as a neurologist. And then you said, wait a minute, there's something else out here that actually works better. And you've devoted the rest of your career with it. You know, you made a fundamental change there. And you know, it's interesting to me, this is exactly what happened to us. We are following the test tube research. And we are following, okay, wait a minute, here we see that amyloid precursor protein is acting like a molecular switch. It can switch you towards synaptoclastic activity when things are bad, you're pulling back. But it can also switch you towards synaptoblastic activity, when things are good. Okay, let's look at what those things are. And in a mouse, we can make a genetic change, change everything. But in a human, as you well know, it turns out it has to do with your homocysteine and your ongoing inflammation, your NF Kappa B, your toxin exposure. So we realized to change that network of neuroplasticity in a human brain requires that you evaluate, which as you know, doctors haven't been doing, you evaluate the critical parameters, and then you address each one. The assumption is kind of stuck in 20th century medicine is what classic medicine has been, including all the pharmaceuticals, assuming making a huge assumption that a single drug will cure all of the ills of a complex chronic illness. And it actually makes no sense. No, you're right. In fact, I know we've mentioned this before. A few years ago, I was asked to come to major Alzheimer's University Center and give a lecture. And the head of the program after I was about 20 minutes in, he says, Well, this has nothing to do with drugs. And, you know, everyone knows that drugs are the only hope in treatment of Alzheimer's. And thank you very much, Dr. Gundry, but I don't want to hear any more about this. This is this literally happened. Oh, my gosh. Yeah, it's, you know, it is amazing to me, people will literally stand there, knowing the truth, and just say, you know, this is not what it is. We've got in fact, some of the crazy comments we've gotten are the drug companies will never go for it. You know, the FDA doesn't like a multivariable approach. You can't do a clinical trial with more than one variable. I mean, it's just amazing. In the face of people getting better and being published, we published 100 so in 2018, we published 100 patients with documented improvement, improvement in electrophysiology, improvement in MRI volume metrics, improvement on their quantitative cognitive assessments. But in the face of that, people simply deny it. We're going to go after the drug. And as you know, one large group has said, you know, someday out there, we want to find the first survivor. Well, there are hundreds of them. You're seeing them. I'm seeing them. So many people are seeing them. And they're literally denying the existence of these people. Yeah. All right, so there's a lot of people want to know about the apoE4 gene. Yes. Why do why do so many people carry it? And how is it connected to a higher risk of Alzheimer's? Yeah, Steven, great question. And you know, I think that the apoE story is one of the most interesting stories in medicine. As you know, it impacts your field of cardiovascular disease. It impacts your longevity. It impacts, you can own, you know, people have called it the God gene because it impacts so many things. Of course, it is the most common risk factor for all genetic risk factor for Alzheimer's disease. So to make a many year story very quick, apoE4, as you know, the apoE comes in two, three and four, and you get one copy from your mother or one copy from your father. So for example, I checked myself, I'm a three three, which is kind of the vanilla. It's the most common thing. My wife is an apoE2 three, which actually gives her some decreased risk. So she's very fortunate for that. And so I told her, you know, you're going to be taking care of me, sweetie. And hopefully, if I do the right thing, that won't that won't come to pass. But as you know, the story is fascinating because in our in our forerunners, the simians, the simians had apoE simian basically, which was different. And it underwent a few mutations to become our primordial. The original hominid apoE is apoE4. So for 96% of our evolution as hominids, we have all been apoE4 for the one that is the highest risk. And today, if you have zero copies of four, your chance during your lifetime of getting Alzheimer's about 9%. If you have a single copy, about 30%. If you have two copies, well over 50%. More likely you will develop it then that we will avoid it. Of course, we'd like to make all of those zero by doing the right things. So there is a fundamental difference in these molecules, they look different, they act different. And of course, one of the things about apoE4 is that it increases your your inflammatory response to virtually anything. So just as we've been hearing so much in COVID-19 about the whole issue of cytokine storm and the whole issue of inflammation as being a real determinant, of course, Alzheimer's same story. Inflammation is huge. But what takes decades in Alzheimer's COVID-19 has compressed down to two weeks, as you know. So what happened was, it's only 220,000 years ago that apoE3 appeared. And then 80,000 years ago, apoE2 appeared. Now some believe that apoE3 then thrived because it was after we had fire and things like that. The bottom line is we don't know. But for whatever reason, we have a less pro inflammatory gene. And as Tuck Finch, the professor from USC has pointed out, that inflammation was probably helpful five to seven million years ago when apoE4 appeared, because we were stepping on things, stepping on dung, we came down out of the trees onto the savanna. You know, we're eating meat that's full of microbes. So you need a pro inflammatory gene just for survival. We don't need that in the first world today. And by the way, as you know, in the third world, you still need that if you go down to the Chimane Indians in Bolivia, what do you see they in fact do better with apoE4 because they're all they have many, many parasites and things. Exactly. So what what we found, which was really striking, and we published this a number of years ago in the lab, everybody was wondering, how does apoE4 the thing that carries your lipid around? It's it's like your butcher, it carries fats. How does that give you Alzheimer's disease? And what we found really surprising, apoE binds to receptors that had been known. But the surprise was it actually enters the nucleus, not all of it, but a significant fraction of the apoE enters your nucleus. And apoE4 interacts with 1700 different promoters. So it actually changes the programming of your cells to among other things, a more pro inflammatory state. So it affects, for example, things like tumor necrosis factor. So you acting now again, that's great when you need that inflammation. But in the long run, what you want to do is keep that down so that you'll live a longer life without Alzheimer's without cardiovascular disease. So that's why apoE4 gives you that risk. So how do people find out if they carry it? Very simple. You can go on you can either go to 23 and me and check very easily. You can go on mycognoscopy where we do a whole looking at all the different critical pieces that give you risk for Alzheimer's disease. And then one of the many things, in fact, is apoE4. So you get that and you also get your, you know, HHS, CRP, vitamin D, all the things that we know are putting you at risk and are contributing to that beautiful balance that your amyloid precursor protein makes. So I, you know, I check apoE status on all my patients when they walk through the door. And, and some of my patients say, I don't want to know if I have it. What, what say you about this? Yeah, this comes up all the time. I think it's very important for people to know their status. So I'm glad you're checking it. And, you know, the reality is, everything has been upside down in the Alzheimer's field, because it's based on we can't do anything, don't know, don't help put your head in the sand, and it'll happen to you one day, and you won't be able to do anything about it. And it's just the opposite of that now, the truth. So in fact, people tell you, the armamentarium is nothing. There's nothing you can offer that does anything. In fact, the armamentarium is huge. And it has to do with your inflammatory status and your detox abilities and your vascular status and your nocturnal oxygenation and on and on and on. So everybody should know their status. Now, again, we're told, Oh, don't check your status because there's nothing you can do about it. Yeah, check the 3,500 people on ApoE4.info who are all doing a tremendous amount about it. Yeah. And I think that's the point of this book. And you've done a great job of really saying, Okay, I'm glad you have ApoE4. And because here's the steps that we now know that you can mitigate this. So what Okay, so let's suppose and again, 30% of Americans carry at least one copy. And so this is not a freak little thing. Right. So what give me kind of step us through what can people do who particularly are carrying this gene do you know today with your program where where are the steps? Yes. Great question. And of course, Julie G is herself an ApoE4 force. She's almost like it. And she has taken her own cognition from 35th percentile to the 98th percentile where she remains after eight years and doing just absolutely beautifully. So you know, she's living proof as well as many other people that there is a tremendous amount you can do about this. And so start by saying, Okay, this is not a disadvantage. It's an advantage in certain areas. As you know, you're better at fat absorbing, you're better at dealing with various infections. You know, just this is probably why we did so well with it five million years ago as early hominids. But if you are going to eat things that are pro inflammatory, if you're going to have a high carbohydrate diet, if you're going to have a leaky gut, in that case, it's going to potentially hurt you. And so therefore, all you have to do is adjust things to take into account the fact that you have a slightly different programming of your cells. We see people, you know, people all the time just doing exceedingly well with this gene. And again, you know, if they took someone with and without and took the food away, the person without the floor is going to die first before the one who who is with the gene, if you expose them to certain pathogens, the one with the gene is going to do better. So you have advantages and disadvantages. But overall, there's, you know, it's not that one is better in any way than the other. So what you can do is the program that we developed and I know very similar to what you are using, you want to make sure that you have a fasting period. And typically, you know, 14 to 16 hours, maybe you consider time restricted eating, if you are ApoE four positive, very helpful, make sure to heal your gut. You want to minimize your exposure to any sort of inflammogens. If your home is filled with molds, you know, get an army score or a hurts me to score. See where things stand. You want to then change, you know, your eating habits to having a we call it keto flex 12 three. And I think again, similar to what you suggest, it is a low carbohydrate, mildly ketotic, ketogenic, plant rich diet. And of course, we're well aware. And I congratulate you for the tremendous work on plant paradox. And, you know, and also on your subsequent work on longevity, you know, you're really the first one to come out and say, you know, plants are not all good. Let you know, this is let's be fair. Again, duh, this is life, right? But you've done a great job with showing. So what is it about plants that's not always perfect? And so, you know, life is complicated. And when you've got to look at these neural networks, and you've got to look at the physiology. And as you indicated in your book, some people don't do well with specific plants like nightshades. Other people not so bad. And of course, that's similar to the gluten story. And it's similar to the dairy story. And it's similar to other things that people are sensitized to. So we're all a little different. And I notice again and again, I suspect you do as well. Certain, you know, people that do the best are the ones that are able to kind of go with the flow and say, okay, this is working better for me. This is working a little less for me. I'm going to keep evolving my own personal program. This is personalized precision medicine based on what's driving it. So there are a lot of things you can do to answer your question about ApoE4 starting with an appropriate fasting period, an appropriate food, exercise, critical, beautiful study a few years ago, showing that the magnitude of the effect of regular exercise on your risk for dementia was approximately equal to the magnitude of effect of one ApoE4 gene. So in fact, again, tremendous amount you can do. And then one of the things, Stephen, that we're finding that I was actually surprised by is that the very commonly people who are slipping into dementia have or a high risk for dementia have poor oxygenation at night when they're sleeping. They don't realize it. Their doctors don't check. They say, oh, I don't think I have sleep apnea. I don't snore a lot. Please, everybody check. It's turning out that you have got to support those 500 trillion plus synapses and critical to have the oxygenation. Of course, we're hearing about this with COVID-19. Everyone's checking their oxygenation. Great idea. Please get an oximeter or ask Dr. Gundry or your doctor to loan you one or get a sleep study. And if you're dropping into the low 90s or the high ages, we've had people as low as 71% while they're sleeping. Just unbelievable. And there was a beautiful study that came out about two years ago showing that if you just look at the average oxygen concentration while sleeping, that directly correlates with the volume metrics of multiple nuclei within your brain, including ones that are critical for Alzheimer's disease. So there's this beautiful correlation. If your oxygen is dropping at night, you are increasing your risk and your doctor's not checking it and you're not aware of it. And so it really allows this to sneak up on you. Critical thing to do. So, you know, that brings up a point. We used to have this wonderful test that was available from only one company looking at cardiac tropon in eye in pica grams per milliliter. Most of them are nanograms per milliliter. It was incredibly sensitive. A hundred times more sensitive. And we were using it to look for the subtlest signs of cardiac ischemia. But one of the interesting things we found was it was extremely sensitive for predicting sleep apnea. And yeah, so you're right. The heart was getting ischemic at night. And you couldn't see it on a regular blood test, but we could see it on the super sensitive test. And we'd get sleep studies on these folks. And sure enough, you're right. They may not have had a big history of snoring. They denied it. And some of these guys were the worst ones. And so when we got them on CPAP, or we got them to lose weight on my program, their cardiac tropon in eye normalized. And it was very fascinating. So you're right. Yeah. And you know, this is interesting to me because what you're seeing in the heart, we're seeing in the brain, you are getting these areas. You're just not functioning as well as you should. And I'd say, again, with this idea of you've got to support that brain, you know, it's running like a Maserati. You have really got to support it well. And the other thing that's come up is continuous glucose monitoring. As you know, this has been huge. Not only will people see spikes, which of course are very damaging and helping to give them insulin resistance. But also so many people who are waking up at 2 30 a.m. 3 a.m. 3 30 a.m. So I why am I waking up at night? Well, guess what? Your glucose is dropping to 40 or 45 or 50. You are getting hypoglycemic, also bad for your brain and heart and not realizing it until you got the CGM that showed you. Yes, you're getting this burst of adrenaline in the middle of the night, and it's harming you because you don't have a nice, smooth, high fat diet. You've actually got a too high carb diet and you're getting this reactive hypoglycemia. So these things, again, people don't look for them and they're so critical in our cognitive function. All right now, Dale, as the devil's advocate, somebody's listening to this saying, now, wait a minute, I know that the brain runs on glucose. And so the proper way to avoid Alzheimer's is a high carbohydrate diet. And there are a number of our colleagues, we will call them that, who clearly advocate for a low fat high carbohydrate diet for this very purpose. So what do you think? Yeah, well, I understand that they're trying to say, OK, this is about your vessels. Let's see if we can remove the lipids from your vessels. And unfortunately, as you know, this simply hasn't worked. And so there are multiple publications, you know, everything from Mediterranean diet, mind diet, the stuff that we've published. There's no question, getting into ketosis is critical for support. So you mentioned, you know, fueling your brain. OK, you can look at that directly by getting an FDG PET scan. When you get a PET scan, as you know, with someone even 10 years before their diagnosis of Alzheimer's, you see a loss of the ability to metabolize glucose in the temporal and parietal regions. It's a classic signature of Alzheimer's and pre Alzheimer's. So you really got your engine that's now sputtering. You cannot utilize this. So you really have an energy failure, an energy gap. And as you know, Steven Kinane has done very nice work on this and others. The way the best way to bridge that energy gap is with those ketones. And so what we recommend, yes, in the long run, you know, you want to burn your fat. You want to make your own ketones. But for the short period, the first couple of months, just go on exogenous ketones. It's fine. Just just, you know, get rid of that gap. Give your brain, your brain is sputtering. Give your brain enough fuel. And of course, that includes making the blood pump in there, doing the exercise, and includes getting the oxygenation and includes making sure that you don't go into significant hypoglycemia. All of these things are playing together just like an orchestra to give you the optimal ability, the optimal function. And by the way, as we mentioned in the book, this is also true for younger people who just want better function. People who are in there, you know, 20-somethings and 30-somethings and early 40-somethings, we used to think of Alzheimer's as a disease of the 60s, 70s and 80s. But guess what? The pathophysiology starts 20 years earlier. So Alzheimer's is really a disease of your 40s, 50s and 60s that gets diagnosed in your 60s, 70s, 80s. So that's a good segue. I've said to whoever would listen, if I had one blood test, the only one, to tell me my fate or my patient's fate, it would be a fasting insulin level. So what does insulin sensitivity have to do with all this? And you speak very eloquently in the book about this. Yeah, this is such a good point. And you know, Professor Ed Getzel from UCSF has published some beautiful studies using neural exosomes, literally taking these little lipid dots that you have, billions in your blood, taking these out and evaluating them because they actually come from the neurons in your brain, little pieces that are coming off of there. And showing that if you look at the insulin signaling, so as you know, the insulin binds to its receptor, the receptor signals largely through a molecule called IRS1. And that IRS1, when you have high insulin, because you've had a high-carb diet for years, your insulin is high. And then what happens is your IRS1 actually gets phosphorylated on specific serines and specific threonines that are basically like putting earmuffs on. So if you've got a son who's playing the drums 24 seven, you've got those earmuffs, okay. And then what happens, your wife comes home and puts on a Brahms lullaby, you can't hear a word. And when we used to, you know, we used to grow neurons in the lab, you had to include insulin, transparent and selenium to get them to live. The insulin is a critical growth factor for neurons. Well now what you've done by eating all the carbs by ramping up your insulin, you have turned off your ability to respond to insulin. So that's the worst thing you can do. You've now got insulin resistance and now it doesn't give you that same sort of kick, either metabolically or trophically, that is so critical. And that's why this is such an important risk factor for Alzheimer's disease. Now you mentioned your program is called the KetoFlex 12-3. Right. What the heck is a 12-3? Yeah, so it's 12. 12 hours is the minimum fasting period. And again, if you're ApoE4 positive, you want to make that 14 to 16 hours. If you're ApoE4 negative 12 to 14 hours, good enough. Between finishing your dinner, starting your breakfast, brunch or lunch, it turns out to make a big difference. Of course, it helps with your autophagy. It helps with your ketosis. It helps with cleaning up your brain with the various things that you're developing, the damaged proteins and damaged lipids and carbohydrates, advanced glycation end products, all of these things. So that 12 hour fast is helpful. And then, of course, the three hours, you want to finish your dinner at least three hours before you go to bed. And again, same reason. Because if you're not spiking your insulin while you're sleeping because you've just eaten, you're going to have a tendency to get a hypoglycemic episode in the middle of the night, wake you up and mess up your sleep, mess up your sleep stages, all of the above. So this is why we call it KetoFlex123. It's ketotic. It's flexitarian. You can have some fish and meat and things like that. If you want to, you don't have to. You can be, you know, vegetarian if you want. But you want to drive your bio chemistry toward the biochemistry that supports synaptic production and synaptic maintenance. And you want the 12 hours and the three hours to give you the best shot at improving. OK, so all right. And I thank you for mentioning in the book that certain lectins may be problematic. And I, of course, agree with you. But how do pathogens and toxins fit into this Alzheimer's equation? I mean, aren't the ApoE4s protected against these guys? Well, they have a more brisk inflammatory response to them. But this is a good point that you bring up. So again, we're, again, we're agnostic, whatever helps. And of course, as you pointed out in your work, for some people, they're very sensitive to lectins and they're not going to get rid of their arthritis or their other problems until they get rid of those. And so there are specific toxins and pathogens that are associated with cognitive decline. And in general, the pathogens tend to be chronic pathogens. So when you look in the brains of patients with Alzheimer's, what do you see? You see P. gingivalis, which comes from your oral, your dentition, right? And you can actually measure these things now very easily with an oral DNA test. This is the stuff that's giving you periodontitis. We'd like to see low levels of P. gingivalis, low levels of T. denticola, low levels of pre-vitella intermediate, low levels of fuzobacterium nucleotom. All of these things are pathogens. You want to have the good bacteria. So the oral microbiome is absolutely critical, just as the gut microbiome is for neuro degenerative diseases such as Alzheimer's and Parkinson's. You find those very bacteria in the brains of patients with Alzheimer's. You also find herpes simplex from your lip. And there's a beautiful study out of Taiwan showing that people who actually treated their outbreaks had a much lower, less than 50% of the likelihood of developing dementia as those who did treat them. So if you're treating them much better than not treating them as it turns out, and as you know, treating them is pretty simple. And then HHV6A, which appears to be coming in actually through the sinuses, and then various mold species that again come in typically through the sinuses. And then even Candida is found in Alzheimer's disease brains. So part of if you think about the amyloid, the amyloid that is produced in Alzheimer's is a response to insults. And it is actually a part of your innate immune system. So again, just like with COVID-19, cytokine storm bad, adaptive is what you need to get rid of this. Same thing in Alzheimer's. There is a gap between what's coming in in your innate response, which is chronically activated, which is what's giving you that amyloid, and the adaptive response, which should be clearing. And in fact, people with Alzheimer's have a increase in their innate response and a decrease in their adaptive. And that's one of the things to give you better phagocytosis, better antigen presentation. Omega 3s, vitamin D, some of the very things that help reduce your risk for Alzheimer's. No surprise. So this all fits together beautifully. And as you say, toxins and pathogens, the toxins come in three forms. It's metals and other inorganics. As you know, air pollution has turned out to be one of the important risk factors for Alzheimer's disease. So be careful when you're on the 405, right? And then secondly, organics, things like toluene and benzene and formaldehyde and glyphosate. So again, if you're out there burning paraffin candles all the time, please beware you're getting exposed to some toxins, switch over to some beeswax or something like that. And then third group is the biotoxins. So things like trichothesenes and ocarotoxin A and gliotoxin. Of course, these molds are just trying to survive. So they're producing toxins to kill bacteria. Of course, that's where we get penicillin. They're trying to kill the bacteria and survive. And unfortunately, they make toxins that are very damaging to human brains, to human immune systems and to human kidneys and livers and can even increase your risk for cancer. So those are the big toxins. So you want to know if you've got exposure to pathogens or toxins and you want to direct your treatment toward those as part of the overall plan. Well, so how does someone go about finding out all of this about themselves? Yeah, great point. And unfortunately, as you know, at the Alzheimer's centers, they're not checking these things. And they're basically saying, you know, you've got Alzheimer's, there's nothing we can do. We're going to give you a drug. It doesn't work very well. You're going to continue to decline, which really makes no scientific sense. And so the idea is you need to know these various pathogens, toxins, et cetera. And so we set up something we called a cognoscopy. It's a silly word, a kind of corny, but it's it's easier for everyone to understand. We all know when we turn 50, what do we get? We get a colonoscopy. So hey, let's not forget about the brain. So if you're 45 or older, please everyone get a cognoscopy. And it just consists of three things, a series of blood and urine tests, looking at the very things you were talking about, things like fasting insulin, HSCRP, you want to know am I systemically inflamed and looking at things like vitamin D and omega three status and all of these things that are the players that determine whether you are going to get Alzheimer's or if you already have it, why you got it. So that's one second one, simple online cognitive assessment. You're going to do either mocha score, CNS vital signs, that sort of thing. You want to know where do we stand with respect to ongoing cognition takes about 30 minutes, very easy to do. And then if you're completely asymptomatic, you're done. You just need those two things. If you're symptomatic, you're going to also want an MRI with volumetrics. You want to know is my hippocampus beginning to atrophy. And as you know, you want to atrophy your hippocampus, increase your cortisol, eat some sugar, things like that are associated with hippocampal atrophy, which in turn is associated with poorer outcome with cognitive decline. So that's the third piece only necessary if you're symptomatic. When you have those three, we generate, we have an algorithm that's computer based and then we can generate something we call a recode report. It simply says, here are the things. Do you have mostly an inflammatory cause for cognitive changes or risk? Is this mostly a trophic? Is this mostly glycotoxic, vascular toxic? What have you? It'll tell you because as you know, it's different for each person. You want to know what are the things that I have to be concerned about so that I can avoid decline. So if our listener goes into their doctor and says, I want a cognoscopy, is there somebody going to stick a tube up their nose and look inside their brain? I mean, how do you find out about this? Great point. And the easiest thing is just to go on MyCognoscopy.com and you can actually get these directly. You can get the blood test and then you can take the report to your doctor and say, here I got my report. Here's where I stand. Can you help me with this? And we've got, we've trained as you know, over 1500 physicians from 10 different countries now and all over the US. So there are many people who are now doing this sort of thing. If you go into your doctor and the doctor hasn't been trained in this, the doctor will probably say to you, what the heck is a cognoscopy? Yeah. And, you know, in congratulations on doing that, I know that's been a labor of love for you to train thousands of healthcare providers now in your methods. So and it is, it's starting to appear. And I, you know, sent some patients who live in various parts of the United States. And sure enough, they have found physicians that you have trained. And so, you know, thank you for doing that. Thank you, Stephen. And we've got new training that's actually coming out next month in August. So recode 2.0 training. And we've got some fantastic things. Dr. Neil Nathan, who's really the world expert on biotoxins talks about his approach and Dr. Chris Shade, who's an expert in chemotoxins talks about his approach. So I'm really excited about that. All right. So we've talked kind of on this in preventing Alzheimer's and cognitive decline. What if you're, you know, you suspect you have it or someone has told you you have mild cognitive impairment or early Alzheimer's, same steps here? Or do we have to go even further? Very good point. And so, as you know, the earlier the easier and the earlier, the more complete, which is why we suggest to everybody, either come in for prevention or come in as early as possible. This idea of Leo, you hear it all the time from doctors, you're not that bad yet and there's nothing we can do anyway. So just come back next year. Terrible idea. You want to get going as early as possible. And yes, you're right. The farther along the more you've got to tweak this, the more you've got to look at all the different contributors and address them. However, the idea is the same. You are changing the underlying neurochemistry to allow your brain once again to make and keep synapses. You are restoring neuro plasticity. The later you wait, of course, the more you've lost and so the more you've got to restore that. But again, there is a lot to do. There are stem cell trials ongoing and I think stem cells are going to be an important part of the overall restoration. So you start by removing the problems that are actually causing this, seconds that you want to create resilience, optimize these various factors. And there's so many good things to do now along those things like, you know, whole coffee fruit extract, which helps to increase your BDNF. It helps you with, you know, your exercise, which is also increasing your BDNF and optimizing specific hormones for its specific times depending on whether your hormones are contributory. You can do all these things. And then ultimately, the third piece is regeneration. So you want to now bring back the synapses that have been lost. And this is where stem cells can potentially be so helpful. Some of the ongoing trials of stem cells are just as a monotherapy. This is very much like trying to rebuild a house as it's burning down. So yeah, great. You're throwing that next brick and every time you put anything in, it's now being, it's burning down again, you know, so you've got to get rid of the fire first, get rid of all the contributors. Now rebuilding makes a lot more sense. Now, that's a really good point. I have a number of patients who've had stem cells for arthritis in their knees. And a number of them have had some early benefits. And then six months a year later, they're back to square one because you're right, the underlying process was not treated. Absolutely. Yeah. So yeah, I think they're going to be a marvelous edge on what you got to stop all the other trouble first. And the same goes with drugs. As you know, people are now trying to say, well, take away you, let's take away the amyloid because things will be better if you just take away the amyloid. Well, no, you want to take away what caused the amyloid to be there. I know the thing that's been interesting to me, it's the same thing we're seeing with the reopening in COVID-19. You've got a problem in this case, the virus, and you're saying, okay, the protection from this is a downsizing. It's unfortunate. We've entered a recession because we are protecting ourselves from this virus. This is exactly what we see with amyloid. You are downsizing the brain to protect itself very much like we see it with COVID-19. So then you say, okay, now what we want to do is reopen everything. Everybody start going back. Just just ignore that there's a virus there. This is what happens when you remove the amyloid. You're removing both the downsizing, which is the good part, but you're also removing the protection. And we've seen a number of people now that when they had the drugs to remove the amyloid, they clearly tanked each time they had these administered. So please, remove the insult first, and then I think removing the amyloid is a great idea after you've removed the insult. That's a very important point and probably not recognized by a lot of our fellow practitioners out there, unfortunately. Yeah, important. All right, I've got to let you go. This is a great book not only for the end of Alzheimer's, but it is a one of the best disease preventing books that I've ever read and I was pleased to be able to read it beforehand and give you that blurb. And I mean that sincerely. So I don't care if you're worried about Alzheimer's or not. If you want a lifestyle book to protect yourself from chronic disease, I couldn't recommend this more thoroughly. So Dale, where do people find you? You've mentioned Cognoscopy and what else we got? Yeah, you can go on DrBredesen.com, mycognoscopy.com, on Facebook, DrDale Bredesen, any of those easy to find me and get more information. And please, everybody, stay safe from COVID-19 and let's make sure that we reduce the global burden of dementia. We absolutely can do that now. And Stephen, I know you're doing it every day. Thanks so much for the great work you're doing. Thanks so much for speaking up on lectins. I think this is really important. I think you've got as many arrows in your back as I've got in mind. And thanks so much for the discussion today. Always enjoy talking to you. Always pleasure to see you and write another book and we'll get you back again. All right, thanks, Stephen. All right, take care. All right, stay safe. All right, it's time for our audience question. And this is a perfect Paul S. on YouTube asked, if you have Alzheimer's symptoms and then determine that you have the apo-E4 gene can reducing saturated fats reverse symptoms? Or is it too late at this point? Well, that's a great question. And I think both Dr. Bredesen and I have talked a lot about this. What is happening at this point if in fact you have symptoms is exactly what he talks about. You've got to remove the underlying causes that have brought you to this point. And you've got to get in a position to start having insulin sensitivity. That is, having your brain be able to use ketones as an alternative energy source. And quite frankly, the only way to do that is to practice excuse me, time-restricted eating, which I spend a huge amount of time in the upcoming energy paradox, teaching you how to do that easily and safely. There is a point where saturated fats, particularly medium-chain triglycerides, have a good effect in getting you insulin sensitive. And I've talked about that in all my books, so I'll refer you there. But no, there's far more important things to do than removing saturated fats from your diet. We've got to retrain your cells to be responsive to insulin and retrain your mitochondria, how to use both sugar and free fatty acids, fats, as fuel, like switching from one to another. And about 80% of us have lost the ability, what's called metabolic flexibility, to burn fat as a fuel versus sugar as a fuel and do it instantaneously. And that's actually what the energy paradox is about. And the end of Alzheimer's program is a good starter for that as well. OK, now it's time for our review of the week. This week's review comes from Sabine Schultz, who wrote me an email after our recent episode with Dr. Lisa Mosconi. Dear Dr. Gundry, thank you so much for this podcast. I've been thinking about that topic so much, as my mother suffered from Alzheimer's disease and Parkinson's. And I'm understandably quite concerned about my own health. This podcast is really helpful for me. I always love hearing from you. So remember, you can rate and review us on Apple Podcasts or drop us a comment on YouTube. You can even sign up for our weekly podcast newsletter at drgundry.com. So I can't wait to hear from you soon. That's all and we'll see you next week. Before you go, I just wanted to remind you that you can find the show on iTunes, Google Play, Stitcher or wherever you get your podcasts. Because I'm Dr. Gundry and I'm always looking out for you.