 Welcome everyone, this is Dr. Steven Gundry and I'm talking today with a colleague of mine who I've gotten to know over the past year. We've actually known each other's work for many years and I'm a huge fan of this man and what you're going to hear today about his new book, The End of Alzheimer's, I think it's going to be really revolutionary. And I'm just delighted to have you, Dr. Dale Branson, today talking with me. Thanks very much, Steven. I'm a huge fan of your work and you as well. In fact, I'm actually starting phase one of your protocol right now myself, which I think is fantastic. It actually fits very much with what we've found in the test tube over the last 28 years on Alzheimer's disease. Yeah, I think that's very true and so what I want to do today, Dale, is get a feeling of what, first of all, what compelled you to write this book, The End of Alzheimer's? We have been looking for the last 28 years in the laboratory, basic neuroscience at what are the actual driving factors? Why do people get Alzheimer's? Why is it so common? As you know, it's now the third leading cause of death in the United States and by the way, number one in the UK. So this is a major and growing problem and as you know, complete failure on the therapeutic side. So we wanted to understand the basic mechanisms of this disease in enough detail that we could ultimately do something about it. And over the years, what we found is that this is very different than something where there's just one cause and it's one disease and it's the same thing each time. It's not like pneumococcal pneumonia. You don't take penicillin and it goes away. This is, if you could imagine looking at a car to say, why is the car not moving? Imagine that you found a hundred things. You found that the gas is a little low, the transmission fluid is a little bit low, the bolts are rusty, on and on and on. So what we found is that there are many different mechanisms and they all interestingly come together on a balance. So just as you get osteoporosis when your osteoblastic activity is chronically exceeded by your osteoclastic activity, so it turns out you get Alzheimer's disease when your synaptoblastic signaling and there are dozens of these signals are exceeded chronically by your synaptoclastic signals. And you can actually see this at the molecular level and you can actually see it at the human level. You change that balance, people start to get better. And many of the things that you've talked about in your book, especially some of the immune related things, leaky gut, chronic inflammation, all of these fit in. So we realize we now have actually over a thousand people who are following this protocol started back in 2012 after the research guided us here. We said, well, wait a minute, this should actually help human beings. Of course, I actually thought I would die still studying mice and cells, but we started to see humans getting better. And we've now seen this in hundreds of people. So very excited. So I wrote the book actually so that people would understand that this disease is different than what we've actually been told. It's a very different disease. And in fact, there's a lot you can do about it. The reality is Alzheimer's should be a rare disease. Yeah, I think that's an amazing point. This disease didn't exist really when when you and I were growing up, there was the odd case that everybody knew about. But it's a brand new thing. And there are societies that you and I know about where even if you carry the quote Alzheimer's gene, the apo E4 gene that you don't develop the symptoms of Alzheimer's disease. So can you give me maybe you can share a little of the background of your studies with maybe some of your patients that have had, you know, reversal of their Alzheimer's or cognitive decline? Yeah, thanks, Stephen. So let me start by saying that the concept of this disease that has could literally come out of the test tube research is very different than what we've been told about this disease. So what we discovered is that Alzheimer's disease, the thing we call Alzheimer's is actually a protective response to three fundamentally different insults. One, we've already talked about chronic inflammation, anything you do to give yourself chronic inflammation, whether it's Lyme disease, whether it's HSV one, whether it's leaky gut, whether it's problems with your rhinocinal microbiome. What have you? Chronic inflammation causes your brain to make a protective response. Why? Because amyloid is a wonderful antimicrobial, as Rudy Tanzi and Robert Warren, their colleagues at Harvard, showed beautifully. Second thing, if you withdraw trophic support, so things like estradiol, nerve growth factor, BDNF, vitamin D, testosterone, progesterone, pregnenolone, free T3, we can go right down the list. Your brain actually cannot support any longer. At this massive network, you have close to a quadrillion connections in your brain. If you can't support them, your brain does the same thing your company does. It says, okay, we can't hire any new people, can't add any new memories. And so that is the canary in the mind. And that is part of a programmatic downsizing. It is, and it is mediated by amyloid. The third thing, if you have specific toxin exposures, be they biotoxins like mold-related mycotoxins, things from stachybotrys or penicillium or aspergillus, or their chemical toxins. Mercury is a big one. Copper, too much iron, all of these things. What do you do to protect yourself? You make amyloid because it binds these toxins. In fact, it's one of the best binders known of copper. 10 to the minus 18 molar. It's incredible. So you are protecting yourself. So the last thing we want to do is get rid of the amyloid. What we want to do is get rid of the reason for the amyloid. Then get rid of the amyloid. That's fine then. So what we realize is, okay, we need to now address all these different things that we need to determine for each person. Why is this happening? So we started to do that first person back in 2012. We actually tried to do initially a clinical trial. We were turned down because the clinical trial was, quote, too complicated because we were manipulating more than one variable. We said, yeah, but this is more than a one variable disease. This is a complex chronic illness. So we've had now, as I said, hundreds and hundreds of people. I'm going to give you a couple of examples. One person who is now 73 had had problems. ApoE4 positive, PET scan proven, Alzheimer's, showed with quantitative neuropsych testing over the years to decline down to where his CVLT was at the third percentile. Started the program in December of 2013. Came back for retest. Did very much better subjectively, but came back for neuropsych retest after 22 months. Did absolutely beautifully CVLT at 84th percentile. Auditory memory went from 19th to 78th percentile. So this guy is going from doing very poorly, not remembering much of anything to actually having a better memory than most of us. So did very, very well. And he's now three and a half years into this and a little more than three and a half years and has actually done exceedingly well. He was actually shutting down all of his offices. He's opened new offices doing great. Another person who has done very well and had a low mocha score of 24, which means pre Alzheimer's, now has a mocha score of 30, which is perfect. Had amyloid PET scan proven Alzheimer's and actually got worse on a drug trial and has actually done exceedingly well. Again, with addressing all of the different things. And just as you talk about in your book, you have to address the root cause of the problem. To try to trick nature with a drug that is basically trying to trick your physiology really makes no sense. That's 20th century medicine. 21st century medicine is no longer about the what, it's about the why. Why did you get it? What are all the contributors? How are they acting? Is leaky gut among your problems? And then in microbiome changes, whatever they are, they need to be identified and addressed. And we see, again, repeatedly improvement after improvement. Yeah, I mean, it's fantastic. I'll throw in a very interesting story that you taught me last August. You suggested that I start measuring pregnenolone in my patients. And quite frankly, unless it came from you, I would be skeptical. Pregnenolone is not usually measured in a standard endocrine test because you need a mass spec machine to run it. But I started measuring right after we talked a year ago, pregnenolone. And you told me that 95% of adults I would find deficient in pregnenolone. And I can tell you that you are absolutely spot on. About 95% of my adult patients are basically completely deficient in pregnenolone. And as you taught me, pregnenolone is an incredible neuro-stimulating hormone. And your observation is so spot on. And unless you had done this fundamental research, practicing physicians like myself wouldn't be knowledgeable of that. And I personally thank you and my patients, thank you for that. It's an amazing observation. And you're right. There are so many factors that we, because we're a drug-oriented society that there's a magic bullet like you mentioned, we can knock off pneumonia with an antibiotic. And we've been very naive to think that we could knock off amyloid plaque and solve the problem. And really thanks to your research, we're beginning to figure that out. So you brought up all these different factors. There are these different types of Alzheimer's or cognitive decline. And can you kind of talk about those three that you've defined and then maybe tell us how a functional medicine approach or what I call restorative medicine approach makes this possible? Yeah, a very good point. So when we started the research, of course, I knew nothing about functional medicine. My wife had told me 25 years ago, and she's an integrated physician. She had told me 25 years ago, you know, whatever you find in the test tube over the years, all these years of research, we're going to have something to do with things like nutrition and exercise and stress and sleep and all these basic things. And I laughed at the time and said, no, no, no, we're going to find, you know, one molecule, one domain. We're going to get a drug that's going to interact with one domain of one tiny molecule and everything's going to go away. And of course, the research showed just the opposite. That it showed that there's this beautiful network. You know, we were taught in medical school to think about Occam's razor and to think about silver bullets. And what we realized, we now, in the 21st century, must think about Occam's network. What is the network that is contributing to your disease and about silver buckshot, not a silver bullet? Yes, you want to target all these critical things, that's great. But it's not just one thing. That was pneumococcal pneumonia. That's not the way these chronic complex illnesses work today. So we need to measure all these things. We need to look at them. We need to look at why they have changed. What is actually going on? When we started to do that, we now look at 150 different things. And by the way, this is, of course, what the cancer research centers are doing. They're looking at the whole genome of the tumor, the whole genome of the host. Of course, we want to go beyond the genome. We want to look at the metabolome and the lipidome and all this sort of thing. But we look at all the things that are actually driving the cognitive change or risk of cognitive change. And the first thing we found was that there are these multiple subtypes, as you mentioned. So these go very much with the idea of what amyloid is actually doing to help you. So number one, we find people who have cognitive decline. And this is, when I say cognitive decline, these are Alzheimer's patients. So they have amyloid, and they're making it because of chronic inflammation. And as you know, many causes. These are people with gut leak. These are people with Lyme disease. These are people with eating trans fats. These are people with high hemoglobin A1Cs, with all sorts of advanced glycation end products. Autoimmunity, all the things that you've talked about. This does contribute to what we call Alzheimer's disease. And in those cases, we need to identify why that is, and then we need to reduce it. So we use, for example, the specialized pro-resolving mediators. We use the appropriate omega-3s. When we need them, we use everything possible. And the critical thing, again, is to identify the source. Then we see people with metabolic syndrome, what we call type 1.5, which is glycotoxic. These are people who have this combination of the inflammation from the sugar, but also the trophic loss from the insulin resistance. So their neurons are no longer sensitive. And in fact, a beautiful work by Professor Ed Getzel out of UCSF, who showed that virtually 100% of people with Alzheimer's disease, if you look at their neural exosomes, so you're actually looking at fragments of brain cells that are in the blood, he could show that they all had insulin resistance. They've literally changed their IRS-1 signaling molecule through phosphorylation events to reduce its sensitivity to insulin. So you are insulin resistant at that point in your brain, whether or not you are peripherally. Very scary. Then second one, of course, we see many people where that's not the problem. They don't have a lot of inflammation. They don't have a lot of sugar-related problems. But what they have is no longer the support. Their estradiol is low. Pregnenolone, as you said earlier, they may have Pregnenolone steel, as you know, where you're basically taking that Pregnenolone and you're moving it into cortisol instead of to estradiol or testosterone or progesterone or things like that. So they do not have the support. Their brain-derived neurotrophic factor may be too low. Their NGF nerve growth factor may be too low. Their vitamin D may be too low and we see these people and they tend to present differently. So the typical person with the atrophic, this type 2, is in their 70s. The typical person who has a type 1 is in their 60s and the typical person with type 3 is in their 50s. And again, you mentioned diseases we didn't see as medical students and I've actually talked to a few of my neurology colleagues recently saying, have you ever seen this disease before, this type 3 Alzheimer's? Nobody has seen it. It is a hidden epidemic hidden underneath the umbrella of Alzheimer's disease. But when you and I were training, when did we see a 52-year-old woman with severe Alzheimer's disease? It just didn't happen unless they had familial mutations, which these people do not. So this is a toxin-related Alzheimer's. And by the way, if you have any doubt about toxin-related Alzheimer's, take a look at the World Trade Center first responders. 12.8% of them now have cognitive decline in their 50s. This is very concerning and some beautiful work done out of New York looking at the follow-up. So there is this toxin, which is the type 3 related. It looks different. It's typically non-amnestic. These are people who have trouble organizing, trouble planning, trouble calculating, trouble word finding, trouble with visual perception. This is very different than type 1 and type 2 Alzheimer's. Yeah, you know, Michael Greger, the author of How Not to Die, who is a vegan physician who I respect a great deal, likes to point out that executives in the Miami, Florida area, where they consume a lot of fish, actually have marked cognitive decline because of the mercury levels in the grouper that's very popular in southern Florida to eat. And he makes a case of not eating fish because of that, but the more important case, which you would make, is, well, it's the mercury toxicity of, in those particular fish, that was actually part of their cognitive decline. And as you well know, you want to have smashed fish. So, you know, salmon and mackerel, anchovies, sardines and herring. You know, you don't want to have the large mouth and long live fish. Absolutely. Yeah, I was, last month I was down in a small village in southern Italy called Aciaroli, which I talk about in my book. These are actually now the greatest percentage of over 100-year-old people of any town in the world. About a third of the town is over 100 and functional. And they have a diet of anchovies, rosemary, olive oil and wine. And they have anchovies for breakfast, lunch and dinner. And they actually have fried anchovies, but they fry them in olive oil. And I got to sample quite a bit of it. And you're right, they're eating tiny fish. And I think if we could get Dr. Greger to realize that a fish is not necessarily a fish, that there may be beneficial fish for us that we'd all agree it's the toxins that these fish acquire that are the problem. And as you've pointed out, you want to stay away from the farmed fish. Oh, yeah. You know, we have to understand that when we feed animals and fishes and animal things that they're not designed to eat and we lace them with antibiotics, we totally change their microbiome and our personal microbiome and we actually change really the cellular constituencies of those animals at a basic level. In fact, I was just talking with the medical director of our hospital yesterday who was actually trained as a veterinary scientist. And he was telling me about their poultry courses. And he said, I can tell you to this day, because I'm still involved with the research, that 100% of our free-range chickens in this country are fed antibiotics. And he said, do not believe anyone who claims that they're antibiotic-free because you have 100,000 chickens in a warehouse crammed in together. And if one chicken gets an illness, you are not going to single out that one chicken. You are going to pan-treat them with antibiotics. And he said it is one of the great lies that's been told to us that these chickens are antibiotic-free, because the FDA, even though condemning antibiotics in chickens, allows the veterinarian on site to make a decision to give antibiotics to save the flock. And guess what? They always make that decision. And the thing is that we have found that there were a lot of assumptions made in the last 100 years with increased industrialization in food, for example. And of course, in the pharmaceutical industry, lots of assumptions made that have simply turned out to be incorrect. You can feed these animals anything, all sorts of things. You can put them together as closely as you want. These are just incorrect assumptions, and we're now paying the price with our health. Yeah, absolutely. You and I both think that a great deal of this at the cellular level has to do with mitochondrial function. And can you kind of tell our listeners today where mitochondria, the little energy organelles in the neurons fit into this grand scheme? You know, this is a great question. So for one thing, amyloid actually interacts with the mitochondria. So it actually has a direct impact on mitochondria. And again, it is part of a downsizing phenomenon. As I mentioned, it literally changes your metabolism. However, we published a paper actually a few years ago with an expert, Dr. Martin Brandt is one of the world's experts on mitochondrial physiology. And interestingly, we used the mouse model and said, okay, can we detect mitochondrial abnormalities in their synaptosomes early on? So in just the area where they're actually having neural transmission. And the surprise was we did not see any changes early on. And one of the things we realized is that mouse Alzheimer's, what we call mouse Alzheimer's, is quite different than human Alzheimer's. When we give it to the mice, what do we do? We give them a mutation that is very, very rare in humans. So it's a horrible model. In humans, you have many, many different things feeding into this. But as you know, it is very difficult in a human patient to measure and with an easy lab test, you know, you can measure things like organic acids, but these tend to be abnormal very late in the process. In fact, we need better tests of early mitochondrial changes that can be applied to people early in the course and people who are at risk. I believe that the neural exosome work where we're now starting to look at these exosomes, you're literally looking at brain chemistry in a blood sample, which is very exciting. And that's the coming thing. I think that will be very helpful for pointing us in the direction of what are the actual changes, as you probably know. In fact, the data are much better for absolutely clear complex one abnormalities in the mitochondria in Parkinson's disease. What data we do have suggests that it is more complex four in Alzheimer's disease. So I have no doubt that you're right. I have no doubt that these will play an important role. But it's actually been quite difficult to tease out where it's coming from and whether, in fact, people early at risk actually have such changes. You know, you and I are both big advocates of fasting speaking of mitochondria. Absolutely. And you know, why is fasting good for brain health? And what do you think about the optimal timing for fasting? You and I both agree on this, but I want to hear it from you. You know, this is a great point. It's so funny that, you know, when I was training, I was much younger. I would see, you know, what's, I would see what's going on with these various, sorry. I forget to do that all the time. I apologize for that. So in any case, you know, when we were younger, we would hear about these old civilizations and things that, you know, Ramadan, things like this. You've got to do this. This has started hundreds of years ago. And I would say, what's the point here? And in fact, obviously someone knew what they were doing. And in fact, there are a lot of advantages to fasting, as you know. And we should all be doing it. So what we recommend to the patients as part of the overall protocol that we call RECODE for reversing cognitive decline. And I go into this in the book in detail. What do you need to check? What do you need to do? And when you do this, so we recommend between 12 and 16 hours. Between finishing your dinner and starting your breakfast or brunch or lunch, whatever your next meal is going to be. So you need to have that fasting period. And then three hours before bed. And here's the reason that there are many reasons as you know. For one thing, as your brain now is shutting down and as in terms of new food exposed to it, it literally changes. Number one, it will start to remove amyloid. It will start to clean out. It will induce a process called autophagy so that you're actually going to start cleaning out your brain. You're going to reduce your amyloid. And interestingly, while you're sleeping with this fast, you actually change fundamentally the micro anatomy of the brain. So you were literally flushing out the brain during that time. So you're actually doing your brain a disservice if you eat late in the evening before bed. And if you don't have that fast. You pointed out if you are ApoE4 positive, and that includes about two-thirds of people with Alzheimer's disease. And it increases your chance of Alzheimer's if you are ApoE4 positive. Then in fact, you should probably make that 14 to 16 hours. If you're ApoE4 negative, then you can make it 12 to 14 hours. But you want to have a significant fast to allow your brain to cleanse itself and actually to help reduce the inflammation, to help reduce the accumulation of abnormal proteins. Yeah, I think that's a really critical point. With my patients, what I grew up and like you did after you ate lunch, your mother would say you have to stay out of the pool for an hour after you eat because you'll die of muscle cramps. And there was actually a little bit of truth in this wives tale because we know that the gut is actually a huge digestion, is a huge demand of energy. And we actually shunt a huge amount of blood flow to our gut in digestion. And what your work and others have shown is that during sleep we have to have increased blood flow to our brain to do this deep cleaning that you and others have discovered. And I think what people have to take away is we don't tell you, well, fast three hours before you go to bed. It's actually because you don't want blood flow going down to your gut and stealing what would naturally be happening in your brain. And so if we put this in practical terms that people can understand, oh, okay, I don't want to get a cramp in my brain. I need big time blood flow at night when my brain is cleaning itself. And we're beginning to discover, you're right, that so much of the brain can be cleaned as long as we have the opportunity for the brain to clean itself. So your message is well taken here. It's amazing how important the combination of optimal nutrition, exercise, sleep, and stress reduction, and then of course that relates to microbiome as well. It's remarkable how powerful these are and how often they are forgotten by many physicians. So what are the other practical things that you talk about in your book, The End of Alzheimer's, that people can do in their everyday lives? Well, again, the thing we recommend first and foremost is to get a cognoscopy. Everyone knows when you turn 50, you get a colonoscopy. So anyone over 45 should have a cognoscopy. And that means they should have blood tests. They should know their genetics, their evo-E status. They should know they're pregnant alone, their vitamin D, their estradiol, their progesterone, their free T3, reverse T3, RBC magnesium, their B12, their homocysteine. You can go right down the list and we go through all of this. So you should know these things because they are important to you. These aren't strange things that you don't need to know. This is determining your future. Your risk for Alzheimer's. And then when you know what your risk factors are, you want to optimize each thing. So we tell the patients, imagine you've got a roof with 36 holes in it. You can look at those holes with your cognoscopy and then you can plug the appropriate ones. But you don't want to just plug one, which is what the drug does. You want to plug all of them. In fact, I believe the drugs work much better if you actually would plug the rest of the 35 holes. So to get back to what you said, yes, you want to include optimizing your microbiome. You want probiotics. You want to heal your gut if it is leaky. And as you point out, many people have leaky gut and are not aware of it. You want to help bring down your HSCRP. And that may take some pro-resolving medias, but it may just take some good fish oil and some good antioxidants. You want to make sure that your vitamin D is optimal. There's so many people who are deficient in vitamin D, as you know, deficient in magnesium, deficient in iodine, deficient in zinc. These are so common in our society. You want to make sure to get off the proton pump inhibitors. You want to make sure to get on the appropriate vegetables. These are all powerful things. You want to optimize your hormones. So as we tell the patients, we're now going to treat you like a competitive athlete. It's no longer good enough to have a B12 of 350, even though that is, quote, within normal limits. It's not optimal, as you know. This is a fairy tale that the two standard deviations is the way we should be optimizing things. So we want to have your B12 level over 500. We want to make sure that if you're a male, your testosterone is not too low. That's absolutely critical for your cognition. If you are a female, of course, same idea with your estradiol and progesterone and, of course, pregnenolone and DHEA. These are all critical parameters. Many people, as you know, are mildly hypothyroid. We want to understand why that is. We want to make sure that your thyroid is hitting on all cylinders, that your reverse T3 is not too high. We look at the free T3 to reverse T3 level, which many people do. We want to make sure that your TSH is not too high. Many people are walking around with TSHs of 3 1⁄2 and being told those are normal, but they're not optimal once again. So these are all critical. The type of exercise you do, you want to get some cardiovascular, but you also want to get some strength training. One of the most critical things is you want to achieve insulin sensitivity. So if you're walking around with a fasting insulin of 10, although your doctor may tell you that's normal, it is not optimal. We want to see it below 5. We want to see your hemoglobin A1c, you know, 5.5 or below, preferably. We want to make sure that your fasting glucose is below 92. So we want to optimize your insulin sensitivity. And now, of course, with the neural exosomes, we'll be able to look directly and say, do you have phosphorylation of your IRS1 that is preventing signaling in your brain? So that will be a very powerful addition to this. So we want to optimize your insulin sensitivity. And of course, that's fasting as part of that, as is exercise. And so all of these things are critical. And then one of the things that's ignored by most people, and it's just shocking how many people are ending up with type 3, toxic related Alzheimer's disease. We want to know what toxins you are carrying in your body. And you know, Dr. Joe Pizzorno made a really good point recently that as people get to 50, get to the menopausal time or andropausal, they start losing some bone. And as they release the bone, of course, mercury is coming out, which they've stored for years. And what we now believe is that many of these toxins, not just mercury, are all sitting there. You've stored them away. You've kept them from harming you. And this, we believe, is now why so many people are turning up with type 3 cognitive decline right around the age of 50. And in fact, when we include in the treatment an optimization of their BHRT, of their hormone replacement therapy, they do much better. So this is likely to be preventing continued release of this because you need to find the source of the toxins and you need to remove it. So this is another absolutely critical thing to optimal performance. And then, of course, as we talked about earlier, what's your magnesium status? We want to know your RBC magnesium. What is your copper to zinc ratio? If you're walking around with a high copper to zinc ratio, that was shown 30 years ago to be associated with dementia. So all of these things are critical to evaluate and optimize. You know, speaking of TSH, I do a complete thyroid panel on all my patients. And one of the interesting things, one of the probably only smart things the government ever did in the early 1900s was to mandate iodine in salt. And we're seeing, at least in my practice, and I talked to other restorative medicine docs, that this switch to sea salt or Himalayan salt, I'm seeing a kind of all of a sudden an iodine deficiency in so many people. And they're running a slightly high TSH and their docs tell them everything's fine. And in fact, their docs, if they measure a thyroid function at all, it's TSH. And if they're lucky, they get a T4 and a T3, but never the free form. And I've been fascinated. All I do is either ask them to go get iodized salt again or iodized sea salt, it exists. Or I just ask them to take some spirulina tablets so that they can get it Trader Joe's. And kelp, seaweed, any of them. And, lo and behold, their TSHs fall down to the normal range. So I'm seeing just this easy to fix fundamental problem that the government recognized 100 years ago and we've forgotten it. And so let me say, so the average person is sitting here listening to you and me going, holy cow, that's a lot to look at. And my doctor, he doesn't even, what's a fasting insulin? And in fact, I will tell you that I've yet to see a fasting insulin on any blood test that's brought to me from any practicing physician from around this country. And personally, I'd much rather see a fasting insulin level than a fasting glucose or even a hemoglobin A1C. But how does the average person who picks up your book put this into effect? How do they get these tests? Is there a system? Can you make your doctor do this? Where do you go? This is such a great point because we are all in the early days of a true revolution. And my argument is this is the bloodiest revolution ever because so many people are going downhill without realizing that there's a lot that can be done. So this is a revolution. We are changing from 20th century medicine that asked what is the diagnosis but didn't look for the root cause of 21st century medicine that asks why and looks at the root causes and identifies and treats the root causes. So the first thing to do, very simple, grab a few of these books, the one that you wrote very helpful, I've enjoyed it very much, looking at all the different pieces that contribute to these problems of chronic illness. And thank you very much. And grab the end of Alzheimer's. We go through every single one of the tests that you need to get. But you're absolutely right. Many doctors will not order it. So then what you can do is, we've trained now 450 practitioners from seven different countries and all over the United States to do our protocol, to order the right tests, to get the right computer based algorithm that we use, and then to generate the correct and optimal program. This is no longer about monotherapeutics, this is about programatics. And so we'll have more, we'll have 1,000 trained by the end of this year. The Institute for Functional Medicine is working with us. We have our next training in Dallas, actually, in September. And then another one in Miami in December. We had an earlier one in Los Angeles back in April. So we will continue to have these different times where we train people. And my hope is people will begin to slowly see that in fact these are the critical things for your health. All timers should be a rare disease. If we all get these parameters evaluated when we're relatively young, or if we start to have symptoms as early as possible. Now, fortunately, lately, we've seen people even late in the course with some response. But the earlier, the better, no surprise. And so I think when this becomes standard of care and people realize, yes, you need to look at these. And you're, of course, the insurance companies to help and say, you know what, we can save. There is a, as you know, over $220 billion price tag per year on Alzheimer's disease in the United States. It is shocking. It is going to bankrupt Medicare if we don't do something about it. And in fact, we can all do something to reduce that bill by getting a cognoscopy and by getting on the appropriate prevention or early reversal. You know, and I bet that a cognoscopy is a lot easier than a colonoscopy. Much easier. And probably far more pleasant. Much more pleasant. Nobody sticks anything in your head. It's a little, you know, a few blood tests and an online cognitive assessment. Easy to do and really, it really can save you time in a nursing home. And your book will show people, well I know it does, but your book shows people how to do this. Exactly. It goes through, and it goes to the West and says, you know, why would you want to know your fasting insulin? Why would you want to know your copper zinc ratio? And so hopefully, you know, it was written actually both for doctors and for patients so that anyone, caretakers, et cetera, health coaches, et cetera, anyone can pick this up, look through this and look at, you know, why do you get this test? Why is this so critical? Well, you know, you're someone who does this and all of this, what you're recommending is certainly not your first rodeo, as I like to say. So what are you working on now? Now that you've figured out how to end Alzheimer's, where to next? So what we're doing, first, we're doing two things. Number one is that we are looking at how can we make this effective later and later and later. So even if someone is at end stage, can we really bring them back? And then, can we now add things to bring them all the way back? So that's the question. We know that we basically, anyone who's early stage has done very well. But the people later stages, it's more difficult and we want to know, what do we need to add? Do we need to add specific neural stem cells? Do we need to add specific intranasal, trophic support? What are the things that do we need to add antibodies to remove the amyloid once we've gotten rid of the cause of the amyloid? There's lots of questions about that. And then, of course, as you can imagine, we're also looking at what if we do the same sort of thing, but directed again at the biochemistry of ALS, Lou Gehrig's disease, or Parkinson's, or Lewy body. So we're just beginning to see if this sort of approach can be applied, of course, with the appropriate modification or again for Occam's network of those diseases. Can we now improve ALS? Because as you know, neurodegenerative disease in the area of greatest biomedical failure, we have not previously had anything to do about these problems. So that's where we're going and in fact we're writing up a paper right now on the next 50 people who've responded objectively and very well to the protocol, and another one on the type 3's what's the best, because there's virtually nothing in the literature about how do you manage type 3 optimally and how do you prevent it? This is the toxic form. So you know, in that light, let's suppose you or a loved one, or a family member has been given a prescription for aerosept or an exhalon patch and say this is the best treatment there is you've got it good luck what do you do? Yeah, and again there's nothing wrong with the drug, it patches one hole, beautifully. There's of course the one concern that has been pointed out over the years for aerosept where you have to be careful, aerosept inhibits your colonesterase so therefore you have more acetylcholine at your synapses, but the problem is your body responds by making more colonesterase, so if you suddenly cold turkey the aerosept you can actually decline quite significantly so you simply don't want to cold turkey it and we recommend for people who come in on it, stay on it, fine you'll add all the other things which should actually help it to work even better so what I would recommend is no problem if you want to work with your doctor and be on a medication but it's good also to seek the counsel of someone who knows about a protocol that is a functional medicine associated protocol that will then look at the actual drivers, when you're giving a drug you're saying I'm not bothering to look at what's actually driving the process, I'm just because I only have a few minutes I'm just going to cover it quickly with this and then sorry you're not going to do very well well if you bother to look further you're going to find for each person what is driving the process on that same line I've heard you talk what do you think about statin drugs in the brain, any opinion you know this is the statin drugs again probably the areas of greatest controversy right now are no identical hormone replacement and statins people tried for years to look to see whether statins could actually be a treatment for Alzheimer's it never showed to be a treatment my belief from all the data we have so far is that the problem is you're seeing both a positive and a negative effect so for some people the net will be slightly positive and for some people the net will be slightly negative no question some people go on statins and they really lose their memory that's well described it's in the brochure etc it's a well known side effect but for many people they don't have that problem and so on the one hand you will get an improvement for example because of less inflammation however my argument is there are lots of better ways to decrease your inflammation so you don't need to use that because there are the negative effects and in fact years ago when we started looking at this balance this synaptoplastic balance we thought look let's screen all the drugs in the pharmacopeia because of course Bruce Aims years ago developed the Aims test and told us about carcinogens how we could screen for carcinogens but nobody had ever tell you about dementogens and we realized yes there are lots of dementogens out there when we screened through all the drugs guess what came up first as putting you on the wrong side and that was specific statins and interestingly the one that was the worst was the one that had already been taken off the market which is the Seriva statin which has some bad side effects so in fact statins do have this potentially negative effect but they also and there are publications showing they have potentially positive effects so my argument is if you can control your lipids with other ways go there first if you can't control it any other way and it's not going to damage your cognition acutely then you might play with fire and use these but if you can do it another way if you can do it with diet with exercise with all the other things that we now know are available then in fact that's probably for your brain the better way to go yeah, statins I think actually prevent lessen heart disease by actually reducing inflammation they actually hit the mute switch on toll-like receptors but I use them as a band-aid or a cast on someone until I get those factors that are causing their inflammation affected and gone and then I try quite frankly to get people off of statin drugs we usually find they don't need them once we fix the underlying cause yeah, again they're trying to subvert physiology yeah, absolutely so any last words of advice, obviously first last word is get the book my quote's on the back this is quite frankly a life-changing book this is something that really all of us need to be aware of no matter what our age no matter what our health because as you said and I said this is an epidemic that unless we do something it's going to break care it's going to break all the insurance companies and you and I both believe that all of us have the power with the information that you're providing in this book to take control of this and to actually reverse this and you know once again folks Dr. Bredesen has devoted his life's work to understanding all this and he has taught me a huge amount of at the cellular level at the molecular level how this is happening and in the book he actually makes it accessible for Joe Blow to understand what they need to do and you know it's brilliant writing Dale and congratulations so any final words just that this is a trillion dollar global problem and of course the number of dollars doesn't begin to describe the suffering all the pain that people and families go through it affects the workforce all the caretakers another thing to notice this is a female centric disease 65% of patients and 60% of caregivers are females this is a huge global problem that is growing and in fact we absolutely do something about it literally no one should get Alzheimer's if you do the right prevention and the right early reversal we can all take a huge bite out of this there are 45 million Americans who are currently living who will develop Alzheimer's it's a huge problem and in fact we can reduce that dramatically if we all get the appropriate tests and get on the appropriate prevention or early reversal all right well I'm gonna show the book the end of Alzheimer's by Dr. Dale Bredesen my colleague and friend and Dale it's always good to see you and I'm sure we'll see each other again very shortly I look forward to it all right thank you Stephen all right thanks a lot take care bye bye