Optimize Interview: The End of Alzheimers with Dr. Dale Bredesen

You're listening to Optimize with Bryan Johnson. More wisdom in less time. Hi, this is Brian. Welcome back to the Optimized podcast. Today I am thrilled to be chatting with Dr. Dale Bredesen, the author of the End of Alzheimer's subtitle the First Program to Prevent and Reverse Cognitive Decline. Dr. Bredesen is one of the world's leading authorities on neurodegenerative disease diseases. Caltech undergrad, duke Med School, UCSF postdoc. If I'm getting it right, Dr. Bredesen and then UCLA. Go Bruins. Now he's up north continuing his research. But just really appreciate you and the decades of work you've put into your peer reviewed research and just the message you have that as we discussed in the prelude here, that I'm gonna actually read the first sentence from my notes on your book. You said this. Let me say this as clearly as I can. Alzheimer's disease can be prevented and in many cases its associated decline can be reversed. And of course, in the book you give us your overview of how to go about doing that, backing it by the science you and your colleagues have performed. But once again, thank you for doing the work and thank you for taking the time to share your wisdom with us today.

Thanks for having me on, Brian. Appreciate it.

Right on. And I'll give the asterisks to our community. We had a little technical glitch in our studio, so I raced home from the studio. We've got the home office slash Spartan gym going on here, so we're going to get to work. Let's start at the top. The End of Alzheimer's. Tell us what you were thinking when you named the book the End of Alzheimer's.

Actually, I didn't name it that. I named the book the Wit's End. And the idea was Wit's End is about the way the research was going and Wit's End was also about what the disease is about. And in fact, my wife at first suggested that title. I thought that's a perfect title for what we've been looking for for all these years. Unfortunately, the publishing company hated that title. So they then came up with this alternative. But here's the point. I think the point they made was a good one, that in fact, with what we now know, we can make Alzheimer's a rare disease. And that's something that represents a major change from what has been the number one fear of people as we age, that we're going to have cognitive decline. So we really need now global programs, just as we had Programs to eradicate polio and smallpox. We need global programs to eradicate Alzheimer's or get as close as we can to doing so. And so what we're saying is pretty straightforward. When you're going to try to prevent or reverse a complex chronic illness like Alzheimer's or Parkinson's or. Or cancer or these sorts of things, you want to know what's actually driving straightforward? It turns out in Alzheimer's, as you know, it's more than one thing. So it can be various forms of inflammation, various pathogens, various toxins. And we typically find that most people have between 10 and 25 contributors. So we want to go after those contributors. And when we do that, we. We have unprecedented improvements and most importantly, sustained improvements. So we've got people now who have been on for over seven and a half years who are still doing extremely well. That was unheard of before. And we've published this in multiple publications, most recently one with 100 patients, all of whom had documented improvement. And this is not to say that every single person improves. Absolutely not. But that we have improvements that haven't been seen before.

Hmm. It's inspiring. And you mentioned the fact that we all know a cancer survivor, but where's the Alzheimer's survivor? And your research, again, that kind of holes in the roof metaphor that you use a number of times throughout the book. And one of the things, let's just go straight to it, because you talked about polio and you also talk about the strategy that worked for an acute infectious disease or, you know, acute illness vis a vis the chronic illnesses that we're facing today. And you say, look, we need a new strategy, checkers vis a vis chess. Can you. Can you talk to us about that?

Exactly. So the point is that the great success of 20th century medicine was that we used public health approaches and infectious disease approaches, things like penicillin, amoxicillin, cephalosporins, et cetera. These together had a big impact on these simple illnesses like pneumonia. So, Brian, if you get pneumonia, it may be there are all sorts of risk factors, everything from your glucose control, your immune system, toxins you may have on board. But much more important than any of those is the pneumococcus itself. So we as physicians got away with treating just that one thing. Now, fundamentally different diseases are the diseases we are all now dying from in the 21st century, like Alzheimer's and cancer and heart disease. These are complex chronic illnesses. So as you indicated, we're using our checkers strategy for a chess match. Now, when you look at all the things. Take Alzheimer's as an example. So you're going to be looking at someone's methylation status, the toxin status, various pathogens that you have to look at. What is the status of their insulin resistance? Do they have glycotoxicity, do they have vascular compromise? On and on and on. And no. One of these is head and shoulders above the rest. Therefore, when you try to target a treatment, you either need to look at all those or you need to find just one. And so far, we're not finding that it's one for most people. Therefore, what you want to do is not a drug, although the drugs are going to be very important as part of the overall program. But what you want to have is a precision, personalized program or protocol. And that's what we've used.

That's great. I want to hear you describe that. And again, one of the metaphors that I remember. Was it 36 holes in the roof that you talk about in the book?

Yeah, that's exactly right. So the idea was, we went back and said, okay, what we studied for 30 years in the lab was what are the molecular drivers of the degenerative process? Could we kind of wrap our heads around what is actually going on here? When you look at that, what you find is at the center of Alzheimer's is really a sensor, which is called app, amyloid precursor protein. And it senses things like hormonal status and inflammation status and trophic factor status and interaction with other contacts, the extracellular matrix, things like this. So that when things are good, this central switch is cut at a single site, and it gives you two peptides, one for essentially outside and one for inside the cel, essentially, say, things are good. Go ahead, grow. Make contacts. Good. Just no different than what you would do as the president of a company or president of your country. Now, when things are bad, you've got pathogens, you've got inflammation, you've got toxins, on and on. It's actually a different way to cut it. So you now have three different cleavage sites. That gives you four pieces, four fragments or peptides. And these things now say, oh, things are bad. Protect yourself and downsize. So it is literally a downsizing program. And so therefore, what we want to do is look for, why are you actually doing this? And then address all of the things. And they're, of course, different from person to person. So that's the approach. And the 36 holes came from the fact that if you look at all the mechanisms, the molecular mechanisms involved, so you want to increase the good cleavage, you want to decrease the bad cleavage, you want to prevent the amyloid from increasing, you want to prevent the interaction with specific receptors. You just go on and on. There were 36 different mechanisms that we counted up at the beginning. Now we know of a couple more now. But the bottom line is this is not a single mechanism disease. And that's the most important part to realize. So it is as if you had 36 holes in your roof. Now, drugs are important, as I said earlier, and hopefully they're going to be better and better for Alzheimer's, but they only patch one hole at a time. So you're going to want to use other pieces here. This is not rocket science. We want to hit those holes. We want to address each one. If you have insulin resistance, that's been shown repeatedly to be an important contributor. If you have specific pathogens, as you know, herpes simplex has come up again and again in the brains of patients with Alzheimer's. You look in Alzheimer's brain, it's amazing. There are often herpes family viruses. HHV6A is another one. Besides herpes simplex, there are often dental organisms like Porphyromonas, gingivalis, P. Gingivalis, or T. Denticola, or F. Nucleatum. All of those things can be found in the brains. There are various fungi that you find in the brain, such as, for example, such as Candida. People often have A. Sinusitis, a chronic fungal sinusitis. You also find exposure to mycotoxins. These are toxins made by mold species such as Stachybotrys and things like that. So all of these things we want to identify, and then we want to go upstream, of course, and we want to use the most appropriate upstream method to stop this. So you're literally stopping the signaling that's telling your brain, hey, you've got to protect yourself.

Yeah, that's awesome. Let's step back and talk about your actual protocol. So it's called Recode. Can you give us kind of the overview of that?

Right. So the idea of recode, and it was named that just because it's for reversal of cognitive decline. So that's Recode. And the idea was, okay, instead of going after one specific thing, let's go after the drivers. Let's first identify. So the beginning of Recode is you have a series of blood tests, essentially what we call a cognoscopy. It's telling you just we all know when we turn 50, we should get a colonoscopy so if you're 45 or older, you should think seriously about getting a cognoscopy. Now, it's easy to do. You can literally do it directly online. So you go in and you're going to get some blood tests and those are going to now tell you, where do you stand, how is, is your methylation doing? What toxins have you been exposed to? Do you have good gut health? All these things are critical. And so then what we do is we have an algorithm now where the computer will now tell you what subtypes you have exposure to. Where are you at risk? So some people, the cognitive decline is mostly inflammatory. Some it's mostly from glycotoxicity. That's what we call type 1.5. Some of it, it's atrophic. You don't have enough hormones or enough trophic factors or enough nutrients. That's type 2. And then the type 3 is toxic. And this can be metallotoxins like mercury. It can be organic toxins like benzene or toluene or glyphosate, or it can be biotoxins like trichothecenes or aflatoxin A or gliotoxin, all those things. And then of course, vascular is another and traumatic is another. So it'll give you subtyping and then it will spit out for you an initial program. And you can do this, you can work with your physician on this, you can work with your health coach on this. And the health coaches are turning out to be the most important part of the whole equation because they are the ones that have the most interaction with the patients and can help keep them on the right path. Because you have to remember, this is a protocol. It's not just a pill. It does include some pills, but it's a protocol. So you need to get people, you need to make them insulin sensitive, you need to get them into mild ketosis, you need to start detoxing them, you need to heal their gut. One of the things that we find is people will improve and then they kind of go along and they plateau. And then, okay, now they address something more. Now they go to a higher plateau. Now they address something more, they go to a higher plateau. So it's really about addressing the things that are driving the process and then.

Creating the behavioral changes that allow for those plateaus to be reached and then continue to spiral up. So much we can talk about there. You mentioned, okay, so we code checkers versus chest. We've got inflammation vis a vis nutrients and toxins. The three different rough ways we can expose ourselves. And then you have a playful section in the book where you say, hey, how to give yourself Alzheimer's. You basically walk us through the typical modern life, but give us a fun overview of that, of, hey, if you want to give yourself Alzheimer's, this is what you should do.

I wrote that because I wanted people to realize so many of us are doing just that. You want to give yourself Alzheimer's. It's actually pretty easy. You don't get much sleep. You start with, don't worry about your sleep. Get four or five hours of sleep a night. Don't worry about more than that. If you have sleep apnea, don't address that. Go ahead and live in a place that's full of mold. Go ahead and eat the standard American diet. Run your insulin up high, get type 2 diabetes, get overweight, stress yourself out, expose yourself to toxins, eat all processed food. Don't worry about organic foods. Go ahead and develop a very high LDL particle number. So you've got vascular disease. Get your HSCRP through the roof. Get metabolic disease. Go ahead. Don't wear helmets. Smash your head around a little bit. These are the things that are all contributing to that change. And what I wanted people to realize is that so many of us, when you read the chapter, people say, oh, I'm doing about half these things already. And that just shows many of us are putting ourselves at risk for Alzheimer's disease and we don't have to do that.

Yeah, that's great. And then you can pull the levers behaviorally of starting with that good night of sleep and then kind of moving from there. So let's talk about that for a moment. Sleep. Why is sleep so important in general and specifically with ending Alzheimer's?

Yeah, it's a great point. As you know, there's a wonderful book by Professor Matthew Walker on sleep as well, why we sleep. And so sleep is a critical part. And we think of the basics. You know, diet, exercise, sleep, stress, brain training, things like that. When we first started our research 30 years ago, it was funny. My wife, who's an integrated physician, said, you know, whatever you guys find, it's going to have something to do with the basics of diet, exercise, sleep, stress. And I said to her at the time, no, no, no, no. We're going to find one molecule, one fold of one molecule, and we're going to be able to target a drug to that and boom, all over. Well, of course I should have listened to my wife 30 years ago. She was Right. There are. This is not a simple illness. There are many things that feed into this. Now, sleep is one of the most important for multiple reasons. And it's not just about the length of sleep. And of course we'd like people possible to get eight hours. A lot of what Alzheimer's is about is the fact that we are as a species living in a way that we were not evolutionarily designed to live. We got lights on all night, we got WI fi going here and there. We're not taking rest, we've got a chronic stress, we're eating too much sugar, more than we can handle. We're getting leaky guts, we're getting ongoing inflammation, on and on and on. So in sleep, number one is the amount that you have, but the quality is critical. And here's one of the biggest things that we're finding again and again and again, people drop their oxygenation when they sleep. Now we think of this with sleep apnea, but that's the tip of the iceberg. There are many people who don't have full on sleep apnea, who nevertheless for other reasons. It can be something called upper airway resistance syndrome, or it could be for other reasons they will drop their oxygenation. So again, your brain is an amazing organ, right? You've got about 500 trillion synapses or so. It requires sensitivity to insulin. It requires that you don't have too much a beta in there. It requires all these things. And one of the important ones is that you have enough oxygen while you're sleeping. And we have people. You should be between 96 and 98% saturation. And it's easy to check. You can check it with an oximeter, your doctor can loan you one, or you can go and get one on your own and check it.

I just put my oximeter on.

You're doing well. Perfect. Imagine that you're dropping to 85 every night while you sleep. What do you think your brain does? It's not happy. You may wake up feeling a little groggy, you may feel sleepy during the day. So that's turning out to be an important one. So absolutely for those reasons, of course, Consolidation of memory. Critical. Having appropriate REM sleep. If you're drinking alcohol late in the day, you're going to affect your sleep, as they call it a REM robber. So there are all these things that are critical about sleep.

What's the number one practical tip you'd recommend if we want to optimize our sleep?

Number one practical tip actually is to get a sleep study Check and see and make sure that if yours is dropping low that you bring it up. But beyond that, good sleep hygiene. Try not to have a lot of food or drink late in the day. Try to slowly. I know this is one of my problems. I tend to work late at night and then just go, boom, straight to bed after that. And it's not the right thing to do. You really want to wind down. You'll have a better sleep if you do that.

Yeah, I think it was Dr. Gundry. He may have been referencing some of your work too, on the glymphatic system. Who? You know, I've heard enough times to eat X hours before you go to bed, but frankly, it was one of the few things I didn't really pay that much attention to. And I got my. I have my aura ring and all of that and started, you know, testing the eating. Four hours before I go to bed, right. Which for me, I go to bed early, you know, an hour and a half, two hours after the sun goes down. Right. And so it was a very early window at which I needed to have my last meal. But it was astonishing to watch my resting heart rate go down and my heart rate variability go up by something like 10% and 30% respectively. Just astonishing. Overnight maintained. And if I violate that, I'll watch it go back to the prior baseline. So I found that amazing. And just to reflect on your eating and drinking a little earlier, these little marginal gains add up as we aggregate them and compound them. And we'll talk in a moment about our genetic vulnerability. And if we have the genetic vulnerability, it's that much more important that we pay attention to these more marginal potential gains. And it's funny too. Matthew Walker, in our coaching certification program, I say, look, if there's one book that we need to read, it's that it's why we sleep, the foundation of our well being. Melissa, you've mentioned insulin resistance a number of times. You talk a lot about sugar and flour. Why is that so important?

You know, it's really amazing. This is one of these things where we are so evolutionarily designed that's really incorrect for the way we are currently living. You mentioned behavior earlier. I think that's one of the most critical concepts because people will often say, okay, the research is now showing us what people need to do, but they won't do it. And so therefore, an example of a guy who actually ended up with kidney disease, and he said, I would rather die of kidney disease than stop eating meat. Okay, for this particular guy, it was actually kind of important to lower the nitrogen load. So the same sort of thing happens with insulin. So the fact of the matter is, human beings, as organisms, were not designed evolutionarily to eat large amounts of sugar. And unfortunately, we're now consuming massive amounts of it in all sorts of different foods, of course. And so what happens is we have. It's essentially like an emergency. It's like a shock to your system. So what do you do? You pour out the insulin. Your insulin binds to the insulin receptor, and it signals through the insulin receptor. And of course, multiple changes in metabolism, including entry and fat storage and all these sorts of things to bring that glucose, which is actually a toxic molecule, it gloms on like remoras to a shark, to all these many, many proteins. We measure it as hemoglobin A1c, of course, but it's glomming on to all sorts of proteins and it is affecting their function. So we bring it back down. Well, what happens now? We've got to get rid of that insulin. The insulin signaling is essentially hyperactive. And so what do we do? We actually now tamp that down. It's a little bit like, imagine you spend years and you've got a son or daughter who's playing, or maybe you're playing incredibly loud drums. And so now what you do is you're going to put on some earmuffs so that you can tamp that down. Now someone comes in, your spouse comes on and puts on a Brahms lullaby. You can't hear it. And so what happens with the insulin resistance? Our insulin goes up for years. And now, as we start to have more normalism, you literally don't respond. You can actually follow this in a molecular pattern of phosphorylation of a signaling molecule called IRS1. And as Professor Ed Goetzel from UCSF showed, everyone with Alzheimer's disease has this altered signaling pattern from your neural exosomes. So what's going on in your brain is that you are now resistant to the signaling effects of insulin. Now, the problem, of course, is that also insulin is an important growth factor for your neurons in your brain. So now you are not responding to this appropriately. You're going to increase your vascular disease, which is another contributor to Alzheimer's. You're going to decrease the trophic nature of insulin. So for multiple reasons, you're in bad shape. And by the way, the stuff that breaks down the insulin also breaks down, interestingly, the amyloid. So it's called insulin degrading enzyme, or ide. And it's one of the things that breaks down the amyloid. So here you can see there are multiple mechanisms by which simply eating too high of a simple carbohydrate diet, which so many of us do, contributes to cognitive decline. And reversing that, on the other hand, is a critical part of the toolbox that's so powerful.

So we've got sleep, we've got eating, reducing sugar, the ultra processed, fast acting carbs to get the insulin under control. Hemoglobin A1C is going to be our primary measure there. I want to come back to the cognoscopy and where to get that in a moment, but let's go to the third kind of the triad here. Eating, moving, sleeping, to look at the basic fundamentals. Moving. What happens with movement as it relates to the brain and why is it so important?

Yeah, huge. And again, as someone who did the lab work for all these years, we're really interested in the biochemistry of this, what's actually happening. So when you exercise, a number of things happen that are critical. One of the things of course is that you do increase your ketones and it turns out ketones are a great fuel both for your muscles and your brain, as you know. And so you're increasing ketones that actually interact with, with specific histones and alter the way they interact with DNA so that you now increase your brain derived neurotrophic factor which has a wonderful anti Alzheimer's effect. Of course you also improve your oxygenation also by the way, as you start to build some muscle, you make yourself more insulin sensitive. So again, there are multiple biochemical mechanisms that are all involved, coming from movement, coming from strength training, coming from aerobic training, whether you like to do HIIT or whether you like to do it another way. These things are all critical.

Burpees, Dr. Bredesen. Burpees, doctor.

There you go.

A good trailer. Let's step back. So eating, moving, sleeping, core fundamentals that you talk about a lot. And I love the way that you playfully say, look, I would have been a skeptic. I was a skeptic 30 years ago. My wife, the integrative physician told me, look, these things are solved through basic evolutionarily adaptive fundamentals. And it took you, whatever it was, however many decades to get to the point of, oh wait, the science is demonstrating this. I love that part. Cognoscopy, where do we go to get one? What's the recommended protocol there?

Let me address your last point first here. Yes, I was a skeptic, absolutely. And the thing is, I Didn't train as a functional medicine doctor. We were doing neuroscience in the lab. But the interesting thing to me, and the reason that I am such a fan of that approach now, is that following the pathways led us straight to say, oh, wait a minute, this is about all these different factors playing a role. So that the lab data really supported the functional medicine approach. So to get to the cognoscopy. Very good point. And this is, it's very simple. You can go on mycognoscopy.com and you can get the cognoscopy. But the cognoscopy is simple. It's three things. And if you're completely asymptomatic, you only need to do two. So step one, there are some simple blood tests, and you can actually get them at your home, or you can go in to get them. There are mobile phlebotomists that will do them. You can do it however you want. But what they do is they look at the various things that typically your doctor doesn't look at that are critical. And we've had a number of people say, well, I went to my doctor. My doctor said, I don't do those tests, or they're not reimbursed, this sort of thing. But we want to know these things because we want to know where you stand. Is your HSCRP high? Do you have activation of your innate immune system that's associated with Alzheimer's? What's your triglyceride to HDL ratio? What's your homa ir? All these things are critical pieces, and they're relatively easy to do. So we want to do that. And that'll tell us, are you most at risk because of vascular changes, because of inflammatory changes, because of pathogens, et cetera. And then the second step is you simple online cognitive assessment. You can do it in about 30 minutes. So it's a pretty easy thing to do. And it'll tell you, are you doing really well? Are you doing so many of us? And this has been one of the problems. It is a disease that sneaks up on you. And I just had a call from a guy yesterday. This guy has a very high risk. He's got APOE4.4. So it's the most common genetic risk. Seven million Americans have two copies. The majority of them will develop Alzheimer's during their lifetime if they don't get on active prevention. 75 million Americans have a single copy. This guy happened to have two copies, already had symptoms, had been to a major university center that told him there's nothing to do with just when you get it, come back. I mean, that makes me sad because there is a tremendous amount. And this guy is in the earliest stages. Now's the time to jump on this. So that's the second piece is to get the online cognitive acceptance. And by the way, his show that he was already in there and so many people, it sneaks up on you. You don't know. We had a woman who said, you know, I want to make sure it's in my family. Want to make sure I'm okay. We did a simple thing called the MOCA test. You should score 28 to 30 out of 30. She scored a 23. And so she was already well into the early stages, and yet she didn't know it because it had happened so slowly. And so it can fool you sometimes. So that's. The second piece is simple online cognitive assessment. Now, if you're completely asymptomatic, completely, no symptoms at all, you're really sure about that, and you score well, fine, you're done. Those are the only two things you need to do. You want to get on an active prevention program. If you have any symptoms, then you want to do the third thing as well, which is simply to have an MRI with volumetrics. We want to know what percentile you are with your hippocampal volume, for example. That's a critical thing to know, and that's been very helpful. If you've begun to have shrinkage atrophy of your hippocampus, that's something that you want to address. You want to make sure that you are on appropriate treatment. So those are the three things. That's the cognoscopy. It's a relatively simple thing to do.

Fantastic. Mycognoscopy.com we can find it there and get on that. I'm excited to 45. I'm due. So then let's talk about genetic risk. We've got the three different, from my understanding, the three different broad categories we can fall into. Can you walk us through that and what all this means?

So, yeah, there are several dozen genes that give you risk for Alzheimer's. And so it is a multigenic disease. But the way it parses out is there's one most critical one by far, which is your APOE status. And I should say over 95% of Alzheimer's is considered sporadic. So in other words, the gene isn't going to determine whether you get it or not. It just determines your risk. There are very few people who have a gene that says you're going to get it 100% or the penetrance is 100%. The vast majority of us, it's about these other things. What do we get exposed to, what pathogens do we have, what's our lifestyle, all these things. But the critical gene to know that everybody should know, just as most people know what their cholesterol is and should know what their homocysteine is, and should know what their HSCRP is and should know what their gut status is, whether they have a leaky gut. The critical one to know for genetics is APOE. And so there are basically three possibilities. Either you have zero copies of APOE 4, you have one copy, or you have two copies, and you get, of course, you get one copy of APOE from your mother, one from your father. So, for example, I check myself, I'm a three, three. That's kind of vanilla. That's the most common one. My risk for Alzheimer's during my lifetime is about, in a population level is about 9%. It's not zero, but it's not terribly high. If you have a single copy of Apoe 4, and that's about 75 million Americans, your risk is about 30% during your lifetime. And if you have two copies, that is about 7 million Americans, it's well over 50% more likely than not you will develop it. So we'd like to see it so that nobody develops it. And the reality is, if everybody went on appropriate prevention or early reversal, we could make this a rare disease. And the time is here for us to do exactly that.

And the easiest and best way to find that, to get that data.

Yeah, you can get it a number of ways. 23andMe is an easy way, by the way, the cognoscopy has it so that it's included in there. You can get it from any of these genetic tests that you do.

Okay, fantastic. And then just to emphasize, although your risk may be over 50% if you have both these APOE 4, what is it? Just genes? Is that what you'd call it?

Yeah.

So alleles.

Oh, yeah. They are alleles of the genes. So you can be a 2, a 3 or a 4. So you could be like a 2, 3 or a 33 or a 43 or a 4, 4. Any of those combinations.

But the genes are not going to be 100% determinative. So 95% of it is going to be determined essentially by our lifestyle choices, exposure to toxins, and all the other things you're talking about. If you have the vulnerability to repeat myself, that just means we need to play the margins even closer. We need to be that much more engaged in the protocol and take it, and then we can use it as actually a catalyst to be stronger, turn that weakness into a strength, and avoid not just the Alzheimer's, but the other systemic chronic illnesses of cancer and diabetes, et cetera, et cetera.

We're working with a lot of people who are APOE 4. 4 who are doing great. And for example, a woman named Julie g. Who is a4.4 who founded and is the current president of Apoe4.info good website for anyone to go to who has Apo Boe4, because there's a lot of social networking and most of the people from that site are on some version of the protocol that we developed and doing very, very well. And so, yeah, you want to get on active prevention or at the very latest early reversal. The longer you wait, and we do see people who are very late who still do well, but in general, the longer you wait, the harder it is to turn things around.

I appreciate you bringing up. Can you repeat that website just to make sure everyone hears that?

Apoe4.info apoe4.info Perfect.

Apoe4.info A great community with community support, wisdom, etc. I think that's fantastic. And the other thing I reflected on in the note that we created was you and kind of living the hero's journey and having kind of pushed up against the tide and just the cultural bias toward that checkers like, hey, let's solve it like we've solved the other diseases and just how hard you've worked to bring, you know, more awareness to this and to kind of lead the charge of, look, we can prevent and we can reverse this. So I was deeply moved by your stories of Hero's journey and how you've lived it and, you know, just the battles you've needed to fight, you know, internally and privately that a lot of people may not know about, but just want to shine a light on that and just thank you.

I appreciate your. I appreciate your kind words. I'm definitely playing the heel more than the hero sometimes. And we've had a lot, as you know, we've had a lot of pushback people. Some people will say we just don't believe it. So I always say, look, talk to these people, talk to the people who've improved. And there's actually a documentary that's just been finished in Japan from nhk, which is, of course, the, you know, the BBC of Japan that's about this protocol and about people who've been on it. They've interviewed a number of people in the United States who've done well. So I always suggest, you know, talk to these people and see, look at their scores. We're just publishing a few more papers now on people where we have documented improvement. But we are now in the midst of the first clinical trial in which you actually ask what's causing this. You know, all previous clinical trials on Alzheimer's have predetermined a treatment. Just say, okay, this is what people are going to do. Blank. It might be a drug, it might be exercise. Whatever it is, it's a treatment. But in this case, what we're doing is different. We're asking for each person, what are all the things driving your cognitive decline? And then we address each one of those things that should be finished next year. So it'll be very interesting to see how people do.

Yeah, I can't wait to see it and help spread the word. Share with us. You have a great R. Buckminster Fuller line on affecting change. Can you share that with us?

Right. So his point was simply that you don't try to compete with what's there. You design a system that makes the current system obsolete. And that's, you know, that's obviously, that's paradigm shifting. So that's the way to go when you want to change the world. And I would add another favorite quote is from Margaret Mead and she said, never doubt the ability of a small group of committed individuals to change the world. Indeed, it is the only thing that ever has. I think it's a great quote because it really takes people getting enthusiastic and saying, we are going to change this.

It's so inspiring. One of our coaches who just went through the program had no intention. She has Ms. For decades and has her annual neurological scan and whatnot. And at the end of it, this year, it was year to year and she had done all the things that we're talking about, the eating and the moving and the sleeping, but. But really prioritizing them. And at the end of it, apparently some of the black spots had actually been cleaned up a bit. And the neurologist look at her and said, what are you doing that I don't know about? Our message is, look, be that change. And as we do that, it's not about, hey, the lecture and hey, this is it. Obviously the scientific data behind it is so important and why I have so much gratitude toward you. But at the end of the day, it's what's demonstrated, what's proved that this data works and in mass effect change. That I think is only going to happen as more and more of us embrace these ideas and demonstrate the efficacy of these models by our own brain scans and by our own prevention. Reversal of these diseases.

Right, yeah, well, so we're all pushing the envelope. Be part of pushing that envelope because we're all trying to push it open. Otherwise you just sit there in the middle of it and get crushed. So there's so much that can be done. And for the people where it's not perfect yet, don't give up, you know, keep on optimizing. We've had a number of people where they try a few things, it's not really helping much. Then they find the next thing, hey, now they really get a bump up. And as you know, Dr. Terry Wahls, who has Ms. Herself, has done a tremendous job over the years with healing herself by doing things very relevant. Again, she's targeting the way Ms. Works just as we are targeting the way Alzheimer's works.

So it's funny and so many parallels. When you get to the end of the day, end of the discussion, all these metabolic drivers, whether it's the hemoglobin A1C and the HSCRP, all these things, we're finding them to be at the root of all these chronic diseases. Obviously different expressions. And I'm really excited about the cognoscopy and identifying our own personal vulnerabilities, et cetera. The end of Alzheimer's, the first program to prevent or reverse cognitive decline. Highly recommend the book. Where else can people learn more about you and your work?

Yeah, so you can just go on the website drbredison.com, easy way to do it, or look at Apollo Health.

So.

And we've got another book coming out next summer, so there's going to be more and more information. Hopefully we'll have, as I said, by the end of next year we will have the clinical trial finished, so we'll know much more about this. But yeah, thanks for all the stuff you're doing. And, and I do think that for people to understand that behavioral change is critical and get in there. The people we see who do the best are the ones that just go in with all their feet, like jump in. Okay, we're going to do this, get on the right things, keep tweaking and we see these wonderful stories. That's been the best thing of all of this. Getting either emails or phone calls, et cetera, hearing from people who have done so much better and sustained their improvement and said, wow, I'm really glad I got into this. There's nothing better.

I agree with that completely. Dr. Bredesen, thank you so much. Appreciate you.

Thanks very much, Brian. Thanks for having me. I appreciate it. We hope you enjoyed this episode of Optymyze with Brian Johnson. To find out more, go to Optimize Me.

Hey guys, this is Brian with a quick little psych. I'm really excited to let you know about an event we're working on. Plan is to make it the premier self optimizing event of 2020. We're calling it Optimize 2020. You the modern hero. Basic idea, five days, 101 world class luminaries, 1 million people. You can learn more and get your tickets to the online and offline event at optimize me 2020. Again, that's optimize me 2020. Hope to see you there.