Change Your Brain Every Day - The End of Alzheimer’s: Part 1 with Dr. Dale Bredesen

Episode Date: November 7, 2017

Everyone knows someone who has survived cancer, but until now no one knows anyone who has survived Alzheimer’s Disease. In the first episode of a three-part series with Dr. Dale Bredesen, author of the new best-selling book, “The End of Alzheimer’s”, Dr. Daniel Amen and Bredesen discuss the fully integrative approach to treating Alzheimer’s disease outlined in the book.

Welcome to the Brain Warriors Way podcast. I'm Dr. Daniel Amen. And I'm Tana Amen. Here we teach you how to win the fight for your brain to defeat anxiety, depression, memory loss, ADHD, and addictions. The Brain Warriors Way podcast is brought to you by Amen Clinics, where we've transformed lives for three decades using brain spec imaging to better target treatment and natural ways to heal the brain. For more information, visit amenclinics.com.

The Brain Warriors Way podcast is also brought to you by BrainMD, where we produce the highest quality nutraceutical products to support the health of your brain and body. For more information, visit brainmdhealth.com. Welcome to the Brain Warriors Way podcast. Welcome to the Brain Warriors Way podcast. I am here with a friend of mine who I just have great respect for, Dr. Dale Bredesen, who is an internationally recognized expert in Alzheimer's disease, the mechanisms that underlie it. He graduated from Caltech and earned his medical degree at Duke, served as chief resident in neurology at UC San Francisco.

And he and I have collaborated on a number of patients who have Alzheimer's disease or mild cognitive impairment. And Dale really got international acclaim publishing a study showing he could reverse Alzheimer's disease. Welcome, Dale. Just such a joy to have you and, uh, help, uh, and tell our audience about the end of Alzheimer's. Fantastic. Thank you so much, Daniel. I really appreciate your having me on. Thank you. So, so both, both you and I are considered mavericks, uh, that we think outside of the box. And when did this become purposeful for you? When did this mission really start? Yeah, thanks, Daniel. So let me start just by saying I really appreciate your work in psychiatry because you are asking how these diseases actually occur. Instead of just saying we're going to follow some arbitrary rules, you're saying, you know, what is the biochemistry?

What is the neurophysiology of psychiatric diseases? And I think that's huge and that's exactly what should happen in the 21st century. I came from a probably fairly similar background to you, being trained very classically, and I've spent my whole career in academia. And we wanted to ask a fundamental question, which is, why do neurons degenerate? We've spent 30 years in the lab asking the basic molecular biology and genetics of neurodegeneration. And what happened over all those years is that we saw that this problem is a multifaceted problem. It's not a simple thing like pneumococcal pneumonia. As you know, we were pretty much all dying 100 years ago of these infectious illnesses. You get the

pneumococcus, you're okay. You get the TB, you kill it with a drug, you're fine. These complex chronic illnesses, Alzheimer's, Parkinson's, cancer, cardiovascular disease, psychiatric diseases, they have more than one component. And as we looked at the basic biology of these neurodegenerative diseases, we could see there were many, many different inputs. We've published over 220 papers on various aspects of Alzheimer's. But we realized at some point, hey, wait a minute, there's a bigger picture here. And we tell the patients, imagine you have a roof with 36 holes in it, and because we initially identified 36 different contributors, maybe you have to cover all those holes to make a big difference. And that's exactly what happens

with the human patients. So many years ago, when I started looking at the brain, we use a couple of studies here, but the most important one to us is SPACT that looks at blood flow and activity. Almost right away, I went, oh, ADD is not one thing. Depression is not one thing. Bipolar disorder is not one thing. Schizophrenia is not one thing. And what you're saying is Alzheimer's is clearly not one thing. And it's got many different roads to devastation. And if you're going to prevent it, reverse it, slow it, you actually have to attack all of the risk factors. Yeah, that's a really good point. And in fact, as you pointed out, you look at things that we call one disease, but there are different roads and different contributors. And in fact,

when we started looking at larger data sets, instead of simply looking at sodium and potassium and the kind of usual stuff. We said, well, let's look at a larger data set for people with cognitive decline or risk from cognitive decline. And what we found is that they fell into groups. And we published this a few years ago. So you can see people who have dementia associated with chronic inflammation, which we call type 1 or inflammatory Alzheimer's, and people who have problems with trophic loss so that you've got a situation where you're withdrawing trophic support, be it from estradiol, vitamin D, B12, testosterone, what have you,

that is associated with cognitive decline. That that we call type 2, or people who have essentially sugar toxicity, which we call type 1.5, because it has both some inflammation, as you know, and also trophic loss, insulin resistance. And then we also found a subgroup of people whose main problem is toxic exposure, be it from biotoxins like mycotoxins or things like mercury. You can see that these people have the decline, and until you treat that and remove it, you will not see improvement. So the big surprise was what we call Alzheimer's disease is actually a protective response, surprisingly, to these different insults.

So talk more about that. I mean, that's revolutionary that, you know, I'm involved in imaging. And so I've talked a lot to my friends at GE. They make the medicine we use, Ciritec, for doing spec scans. But they also make the amyloid imaging agent. And I think they spent $100 million developing it. And I'm like, expect will actually give you more

information that sort of says Alzheimer's or not but what what you're saying you're saying that actually differently that if you have a high amyloid load yes you could be on your way to Alzheimer's disease, but amyloid is not the cause. It's the reaction. It is the reaction. So what happens is, as you know, amyloid has turned out, and very nice studies out of Harvard on this, to be an antimicrobial. So you are producing this because it damages microbes. You are producing it because it responds to inflammation. It's produced in response to NF-kappa B activation. You're producing it because it actually is part of a downsizing program for trophic withdrawal. Or you're producing it because it actually binds

divalent metals like copper. So my point is, it's all well and good to think about removing the amyloid. But more important, let's think about removing the causes. And there are often many contributors, we typically find 10 to 25 contributors for each person. So don't take the amyloid away until you take the inducers of the amyloid away. And we've had a number of people come through who had their amyloid removed by antibodies who did much worse when they had that removed. So you want to remove the cause, the inducers first. Are there any studies showing that removing amyloid in humans improves cognitive function? No, not to date. And there have been many attempts, as you know. There is one suggestion,

as you know, adenokinumab, which, again, very, very early. So people keep saying, oh, we must not have removed it early enough. Let's go earlier. So that has been the paradigm. Let's just keep doing that. But what's really coming out of all this is, no, it's not an issue of removing it early. It is an issue of recognizing that this is a response to insults and therefore let's remove the insult and then remove the amyloid george perry who's uh editor-in-chief of the journal of alzheimer's we published five papers there and so i follow his work and he's talking about the death of the amyloid hypothesis, which I thought was really interesting. And there's sort of a food fight going on in the Alzheimer's research community. You know, is it Alzheimer's? Is it not?

How do you think the issue is going to get settled? You know, it's a great point. And you remember the famous old quote, you know, the reports of my death have been greatly exaggerated. And I think this is a great example where you've got a whole bunch of people that are spending, as you pointed out, hundreds of millions of dollars on the amyloid theory. And then you have other people, and certainly I know George, who say, wait a minute, you know, this really doesn't fit. When you press hard and you say, prove this theory, there's no proof for the theory. The best, you know, I think the best suggestion for the theory, of course, would be the people who have mutations, the rare people who

have mutations in the APP gene that lead to an increase in amyloid and do develop familial Alzheimer's. However, I think the problem has been people want to make this simple. So they say, is amyloid the cause? Yes or no. Instead of saying, isn't it more likely that amyloid is part of the overall story, but it's not the entire story. I think that's what we're seeing here. And in fact, again, it is a protective response that is associated with a downsizing of your overall neuronal network. And so when we look at the parent of amyloid, the amyloid precursor protein, we can see directly in a molecular way what feeds into whether it's going to be on the amyloid side or whether it's going to be on the anti-amyloid side.

And the really interesting thing is that the amyloid precursor protein can be cleaved in two opposing ways. So literally it can support neurite growth and synapse formation, or neurite retraction and synapse loss. So it literally can make amyloid and be part of the downsizing of Alzheimer's, or it can go the other direction

and support synapse formation. It is literally a molecular switch. Oh, how interesting. In 2005, when I wrote Preventing Alzheimer's with Rod Schenkel, the amyloid hypothesis was in full swing. And one of the interesting things I learned was that kids with Down syndrome, and we've seen a fair number of them here at Amen Clinics, have an extra chromosome that actually increases the production of amyloid precursor protein, and they have a higher incidence of Alzheimer's disease at much younger ages. So I wonder if that's in that genetic group where amyloid is much more of a problem than in the typical Alzheimer's patients you have. So this is a really good point. When you make it genetically, as you said, when you overproduce this, you do see this downsizing effect. And I think that's one of

the things that has misled people in general. So no question, you overproduce this stuff, then you're going to see the downsizing. But for most of us, and this is about 95% of people who get Alzheimer's, they're not getting it because of a genetic predisposition in terms of APP itself. Instead, what they are doing, they are responding appropriately to insults, just as you would put, you know, lay down plaque in your coronary arteries. You're laying down this stuff. And in this case, you're actually protecting yourself against these various insults. And therefore, you're not genetically predestined to have this. In other words, we really can control our future with respect to dementia for the vast majority of us. Do you think it makes sense for the average person who has the genetic risk, who has one of the E4 genes, to do simple strategies to try to clean up

the excessive beta amyloid, such vitamin D curcumin sleeping better blueberries those are the things you know as I was writing memory rescue that there were published studies showing those things can decrease beta amyloid load this is a really good point I agree and this is actually why I wrote The End of Alzheimer's. The whole point here was after we published the paper that you've mentioned earlier, we had over 5,000 emails and calls saying we want more information and what do we actually do here? So what I recommend is for everybody over the age of 45, And again, especially if this is running in your family, just as we know that when we hit 50, we're supposed to have a colonoscopy. We recommend

that anyone over 45 have a cognoscopy. And by that, I mean getting your biochemistry checked, right? You want to get a cognoscopy, get your basics checked to understand you know do you have a high hscrp do you have a low vitamin d just as you mentioned now do you know so many of us are deficient in vitamin d so many i usually tell people look um if you if you wear clothes or you live indoors you're probably deficient in vitamin d so you know the reality is most of us are deficient in vitamin D, you know, we should get it checked, get it checked, you know, we can actually look at the various contributors. So I would say just the opposite of what we've all been told, there's nothing you can do about this disease. I would say there's a tremendous amount and obviously you're doing it.

There's a tremendous amount you can do about this disease, both in the prevention and in the reversal. So get these things checked out so that you will know where you stand. Just as everybody knows their cholesterol, get these things checked and find out where you stand because we can reduce the global burden of dementia today. When we wrote Preventing Alzheimer's, we actually argued if you could put it off five years, that you could dramatically decrease the incidence in the country. And it's just such an exciting message. And it's not giving people false hope i know that's the the

criticism but um you know my experience working with you know thousands of patients with dementia over the years it's you have to understand what's causing it in you and go after all of the risk factors. Thanks, everybody. You're listening to The Brain Warrior's Way. Dale Bredesen. I'm Dr. Daniel Lehman. Thank you for listening to The Brain Warrior's Way podcast. Go to iTunes and leave a review and you'll automatically be entered into a drawing to get a free signed copy

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