How To Reverse Or Reduce Your Risk Of Alzheimer’s And Dementia

Coming up on this episode of the Doctor's Pharmacy.

There's the pre-symptomatic and then there's the symptomatic. I think that ketogenic diets make more sense in the symptomatic phase of the disease. It's been used to treat other brain.

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Episode of the Doctor's Pharmacy. Hi, this is Lauren Fein, one of the producers of the Doctor's Pharmacy podcast. Millions of Americans are affected by neurodegenerative diseases like Alzheimer's, dementia, ALS, and more. The good news is that there are many simple steps we can take every single day to protect our brains and reduce the risk for or even reverse symptoms of cognitive decline. In today's episode, we feature three conversations from the Doctor's Pharmacy about why it is so important to take care of our brains when we are young and what to do if we are experiencing a brain condition. Dr. Hyman speaks with Dr. Marwan Sabbah about the role of the APOE4 gene. With Dr. Richard Isaacson on lifestyle modifications that can prevent Alzheimer's and even reverse its decline. With Dr. Richard Isaacson on lifestyle modifications that can prevent and even reverse Alzheimer's. and with Dr. Jay Lombard about bacteria as the cause of neurodegenerative disease.

Let's jump in.

By the time somebody walks into my office with memory loss, they've had disease changes in their brains for two decades. And we understand that biologically now.

So you're seeing now a whole- and.

You can see that on imaging scans. We can see that on whole imaging scans. So we're now seeing now a big push to move the calculus beyond the time of symptoms to much earlier and try to find people and identify people at risk. Along the way, but most of that research has been focused on drug interventions to prevent or delay or forestall the onset of symptoms. But along the way, of course, if I'm going to, if I'm in my 70s and I know my disease started in my 50s or 40s, we can change beyond drugs. We can change to say lifestyle interventions have benefits. and there's now a whole new area of research. Exercise has really emerged as one of the areas that has grown with real biological evidence that it can prevent and improve brain function and brain health. And beyond that, we're seeing now people are looking at things like diet and supplements and other ways to manage the disease. And so I think this is an area that's just relatively new, but very exciting. Yeah, I mean, there was a recent.

Study called the Finger Study. The Finger Study is one of the.

Ones that we're going to talk about.

Which I talk about in the book. Yeah, I know. And this study was done in Europe and it was a very large study where they did an intervention with diet and exercise and stress and- and cog-stressing. Yeah, addressing cardiovascular risk factors. And tell us about the study. What did they find?

Yeah, so this study is done at the Karolinska Institute. The geriatrician, her name is Mia Kivipelto, a really, really sharp, very thoughtful physician scientist. and she said we're going to create a multimodal intervention including diet changes, managing health conditions, improving exercise, improving all their parameters. And one group was randomized to the intervention and one group was randomized to just kind of passive intervention. And in an objective way followed for over two years with aggressive intervention the treated group did much, much better over the two years. not only did they not get a decline, they actually got better.

Wow.

And these are people not young, they were starting in their late 60s into their 70s, so these aren't people in the middle of their life, they're kind of running into the senior age, and they actually got better. And this has been published in the journal Lancet, so it's a very respected peer-reviewed scientific journal.

Well, this is really remarkable. I just want to pause here because what you just said is pretty radical. Now, like I said, we spent billions of dollars on hundreds of studies, and none of them show this. We can't slow or reverse it. Now you're saying just by eating better, exercising, optimizing your health, we literally can slow and even start to reverse the disease.

That is correct. In fact, the US is taking the finger study, and in 2019-2020, there will be the US version of it called the Pointer Study. Pointer study, yeah. Which is being rolled out in about six sites in the United States. this year.

And the government has to pay for it because there's no drug involved. The government, well, this is to be.

Very clear, the point of study so far as I know is being funded by the Alzheimer's Association. I don't know if there will be federal dollars behind it. But the fundamental issue- But it's not a drug company. It is not a drug company. But the fundamental issue is we want to answer an important question. Do these things objectively work? The signal, the way the evidence suggests the answer is yes. And so having more evidence 'Cause I have to tell you, you and I are both physicians. Part of our day job is taking care of people with disease.

Right.

So here we are saying, let's step back from that. Let's say instead of treating disease, let's treat health.

Yeah. Did you take the course in medical school called Creating Health?

I did not.

I didn't either.

I did not take that course. We didn't learn that. We did not. But the advantage of that is that it's not prescriptive. health recommendations that come out from consensus panels and then it can have effect change at a larger level. This is actually easier to roll out if we can prove there's a signal than it is by just writing a prescription.

It's unbelievable, yeah. I think, you know, what you said is really remarkable that we need to focus on how do we create health rather than just treat disease or symptoms or pathways or some pathology. and that's essentially what functional medicine is. It's asking the question, how do you create a healthy human being? What are the factors that knock you off that path? And what are the things that actually help create health? And those studies, the finger study, the.

Pointer study are looking at those factors. And there are more, right? There are more. And I think that's the exciting thing is that I think, you know, I have to tell you, I've been involved in all these clinical trials. Every time there's a failure, It breaks everybody's heart. There is no ego involved. It's not like haha, I told you so. Because I will say to you whether the drugs work or not, I'm going to clinic tomorrow or the next day, and I still gotta look at these people in the eye and say, you know, something good is coming, we just kinda hope that it's coming soon. And so I say this to you because if I can see a path forward, whether it's a drug, a device, a lifestyle intervention, any way forward to help my patients either prevent, postpone or delay.

Well, let's talk about the disease a little more in a medical way because the understanding was from my training was that the brain seemed to be disconnected from the rest of the body. We learned about this barrier called the blood-brain barrier where nothing except some nutrients got in.

That's correct.

It was like this thing that disconnected our head from the rest of us. Turns out that our body is one system and then our brains are connected to everything else that's happening in our gut microbiome, in infections, what we eat, everything is actually influencing our brain function. So can you share a little bit about how this understanding has changed the way we think about the brain and how some of these factors that are driving inflammation are actually causing this disease? Because it's a disease of brain inflammation. It is.

So the conventional wisdom that we're trying to look at is that Inflammation is a response to an injury, or is it the injury itself? At the end of the day, a lot of people think that there's an amyloid triggered event and then the inflammatory events occur because of the production of the amyloid.

And amyloid is this sticky gooey stuff that gums up your brain.

That is correct. And importantly, but we used to think, as you said, there was north of the neck and south of the neck, right? And that everything in the Alzheimer's was north of the neck and nothing, south of the neck was related to it. When in fact now we know that things like gut microbiome can alter your immune system and having a healthy microbiome can keep you healthy and by the innate and you can boost your innate immunity which might reduce inflammation across the body including the brain.

Yeah, and exercise helps reduce inflammation?

And BDNF. So the exercise, I have to tell you, I hated running.

Oh no.

But I've taken up running. because of BDNF. So what is that? That's brain-derived neurotrophic factor because of- It's.

Like miracle growth for the brain.

Miracle growth for the brain and the funny part about it is almost neuroscientists are runners. They don't do anything but run. They have to have something to it. It's the fastest way to raise your BDNF levels.

Which is basically this growth factor that connects your brain cells together. So it calls neuroplasticity which increases connections and helps neurogenesis which is the development of new brain cells. That is correct.

So we never thought that was possible. We never thought it was possible. was possible. They said once you're born with your neurons, you're gonna get it, but we.

Now know that the brain's making neurons throughout their life. Yeah, I mean, I read a study where they studied terminal cancer patients and they gave them this dye that only goes to dividing brain cells and they.

Found even at the point of death they're making new brain cells. That's correct. We did a, when I was in Sun City, Arizona at the Banner Sun Health Research Institute, we had a brain and body donation program and we had scientists that could take brains of patients who had just expired and culture out, bring out the stem cells that were still left alive in dead brain.

That's unbelievable, pretty cool stuff. So these things like diet and exercise and optimizing your gut microbiome and stress reduction, they all in a sense work by regulating this inflammatory process.

That's correct, that is correct. The inflammation of course is the unifying common pathway that we can manage. And, you know, at the end of the day, that's what we want to do as well.

The studies taking Advil never really worked.

They tried it. Well, COX inhibitors have not worked. So then the questions are scientifically, is it that pathway of inflammation? People are now looking at different pathways of inflammation, you know. Now looking at TNF-alpha, which is tumor necrosis alpha, they're looking at the fact that TNF-alpha might trigger enzymes related to Alzheimer's called base. So we think that there's a link that Inflammation is not just a broad category, but there are specific segments that seem to work and others that we've tried, like you said. We tried anti-inflammatories for years to treat or prevent Alzheimer's. It didn't work worth a darn. Right.

Well, that sort of goes back to the thinking in functional medicine, which is what's causing it in the first place. So if you're standing on a tack, it takes a lot of aspirin to make it feel better. Pull the tack out. So it's not necessarily the best logic, but it's something that we have to sort of begin to wonder about. I'm talking to one of your colleagues, Rudy Tanzi from Harvard, who said to me that they've done studies of patients who had brains full of this amyloid, but they had the gene somehow that didn't let them create inflammation and they weren't cognitively intact.

They didn't have dementia. Right, and that's amazing things that you can go to your grave with a brain full of amyloid and not develop dementia. And we want to study those people because there's something protecting them against the development of symptoms. And of course, they may have just.

Less inflammation as you commented.

Rudy Tanzi would be the guy to figure that out.

Yeah, and he talked about the microbiome of the brain. I don't think they're still trying to figure it out, but they're finding microbes in the brain. Right. We thought it was sterile up there, but turns out it may not be.

It may not be. And there's a new one that you probably have just hearing about. There's a company out of the Bay Area that found there's oral bacteria called P. gingivalis, which creates a protein called gingipain, which may be a neurotoxin and neuro trigger of neuroinflammation, and so they're.

Looking at a drugs to stop that.

Maybe brushing your teeth, flossing, and getting.

Them clean is a good idea. That's good for the heart. Not just good for the heart, it's good for the brain as well. That's right, I mean people don't probably know that, but one of the biggest triggers for heart disease is gum disease, right? That's correct. So let's talk about the genetics here for a minute. So, you know, most people think you get your genes, they're fixed, your fate is sealed, there's nothing you can do. It's not actually how genes work. you can modify these genes expression, which ones get turned on and off and how they work. And I remember having this patient years ago, who was a 90-year-old woman. She was a dentist. She had APOE double four, meaning she had two of the worst genes you could have that are triggers or maybe predisposing to Alzheimer's. And she was 90 years old, she was still working, and she was completely cognitively intact. And she was a health nut her whole life. She ate a perfect diet, she exercised, she never smoked, she never drank. took her vitamins. I mean, it was remarkable to see that.

That's impressive.

And this is what you talk about in this book with this woman, Jamie, she came to you because she had a family history of Alzheimer's. And you checked her genes and she had that dreaded APOE4 gene, which many people are afraid to test because they feel like it's just a, why bother? So you talk about why bother. Tell us why bother. So.

I'll answer the why bother in a second, but Jamie is like your dentist patient. She's a 4-4. She found, her story of course, she found out her genetic risk by accident. Now you and I know that if you are two copies of the APOA4 gene, your lifetime risk is 91% that you're gonna develop it. It's almost a matter of when, not if. And the problem is that fortunately there's only 2% of the population that are double copy, 20% of the population is a single copy of the APOE4. But people are now finding out because there's commercial genetic testing by accident.

23 and me.

23 and me, right? And then they go to Dr. Google. It's me and my friend Dr. Google. And they're like, well, what does this mean? And they go and they-- and so the Jamie's of the world are finding out day in and day out by accident, and they're trying to figure out what does this all mean? So the story is, on her half, is how she found out by accident and how it affected her. My half of the book is, is it a good idea to be tested? What are the consequences of being tested? What does it mean? And so that's what my half of the book is. It's a nice convergence of two storylines that help people to become informed because this is happening every day of the week.

It's happening anyway, but what your book, Fighting for My Life, suggests is that by knowing that it can motivate people to take control of their life and their lifestyle and address the modifiable risk factors.

That is exactly right. And I want everybody who reads the book to be like your dentist patient, right?

Yeah, she was amazing.

I have to say to you, I had one other.

Not sure I would go to her at 90 years old to clean my.

Teeth, but... Sure, but... She got to 90.

She was, right? And working, still working.

And I've seen only one other elderly person get to late 80s, 90s, a 44 who was unaffected. in my career, I've always said that if you have that genetic profile, it's almost a foregone conclusion you're going to get Alzheimer's dementia eventually, but there was one exception to that. So we want everybody to be the.

Exception, not the rule. Now, one of the things we haven't really talked about yet is the role of sugar in the brain. And many people may remember Ronald Reagan's favorite food was jelly beans. And he got Alzheimer's. Now, maybe there's a correlation, but it turns out that diabetics have four times the risk of getting dementia. That is correct. we sometimes talk about Alzheimer's as type 3 diabetes.

This is Susan Delamonte from University of Rhode Island.

Brown, yeah. Yeah, brown, yes. And the truth is that we all have control over whether or not we get diabetes. This is almost 100% preventable and reversible.

Disease by changing our diet.

Right.

And you know that insulin resistance, of course, is the hallmark of type 2 diabetes and that we can see insulin resistance in the brain and that's what the type 3 diabetes, even if you're not having insulin resistance in the rest of your body. And we think that, of course, and I strongly I strongly believe, like you, that that's a modifiable risk factor. We can alter that. We can alter it, of course, the epigenome, which we're going to talk about, I hope we're going to talk about epigenetics. But the diet and reducing the sugar intake and the diabetes risk is something we can alter and have a positive effect on. So we all learned, I mean, I.

Learned in medical school that your brain uses 25% of your glucose and it needs sugar to run.

Yes, it does. And the PET scans, show that you need sugar to make your brain light up. So the rule of thumb on a PET scan is you want your south of the neck, you want to be dark, north of the neck, you want.

To be bright on sugar PET.

Because if it's dark below, you got cancer. If it's bright below, you got cancer. If it's dark, that's why you put it in the brain, you want it to be nice and bright.

You want that brain to light up because it can so much of the sugar metabolism is in the brain. But you also say in your book, in patients who have Alzheimer's, that people are exploring the role of ketogenic diets, which means no sugar and lots of fat and the brain running on ketones instead of glucose.

And the issue that people are trying to decide is can you bypass insulin pathway mechanisms? So if you're relying on insulin and pathways related to insulin to nourish your brain and you have insulin resistance, either you can pharmacologically improve that or you can dietarily improve that.

I mean, you know, I remember this patient I had at the Ultra Wellness Center, my practice in Lenox, and she came in, she was about 78, and she started having what we call MCI or mild cognitive impairment, and she had a whole bunch of things wrong with her. Fibromyalgia was bad. She had gut issues. She had low vitamin B12. She had heavy metals and mercury. But she was able to fix a lot of these things and do a lot better for many years. And then she started to decline, and I'm like, well, let's try a ketogenic diet. and we got someone to work with her and cook for her. And it was like the lights went on again. It was pretty dramatic. And I think there's some preliminary studies that are showing that.

And, you know, people have been looking at, so the ketogenic diet all starts with the whole coconut oil conversation, which is coconut oil is controversial by itself. But the story behind ketogenic diets is that we do understand there's insulin resistance. The NIH actually funded a study looking at the ketogenic diets. So I think the science is there. It's just a matter of being able to prove it and more importantly to adhere to it. Ketogenic diets, not easy. Not easy. It's not new to neurology. We've been using ketogenic diet to treat childhood epilepsy for 30 plus years. So it's new to Alzheimer's but it's not new to brain disease. It's been used to treat other brain diseases for a long, long time. But fundamentally it's really hard diet to stick to.

Yeah, we're finding more and more people are doing it. It's one of the hottest diet trends out there. If you look at all the best-selling books, it's not mine, it's the keto books. And we're seeing much more interest and we're running keto programs at Cleveland Clinic. They're our most popular programs, which is pretty amazing.

So people seem to be willing to try it. I know you had Dan Pomerleau on a few weeks ago and Dan and I have- David Pomerleau. He and I have had an internet debate about this.

And.

I will say to you that I think it's more nuanced. I think that ketogenic diets that are insulin sparing make more sense in the symptomatic phase of the disease. And I have to tell you, I look at Alzheimer's disease in a dichotomous way. There's the pre-symptomatic and then there's the symptomatic. Symptomatic disease means mild cognitive impairment and dementia. And I think there is some logic to a ketogenic diet in the dementia phase.

I agree. I think an ounce of prevention is worth a pound of cure as Benjamin Franklin said.

Correct. I think the ketogenic diet is a pound of cure. It's a pound of cure. But I would not necessarily advocate for it in the mild, in the pre-symptomatic phase. I'm more advocating for the Mediterranean diet.

In the pre-symptomatic phase. And that's the beauty of your book, is you talk about how to create resilience. and health, so you don't need the pound of cure.

Correct.

Because the hope for life isn't to be restricted and restricted, it's to actually be more resilient, healthy, so you actually are resistant to these diseases.

That's correct.

So it's actually exactly the right idea.

There are so many things that we can do to put the ball back in our court, to write this script and tell our own story. Can you definitively 100% prevent Alzheimer's in every case? Well, no. I mean, there are certain, Pretty rare genetic causes where basically just about anything you're going to do, you're going to get Alzheimer's and it's going to probably start early and that's unfortunate. But that is an exceptionally rare number of cases. Most cases of Alzheimer's you can do something about. Based on the 2020 Lancet Commission.

An.

Amazing study based on 12 modifiable risk factors, we can, the person makes brain healthy choices, prevent four out of every 10 cases of Alzheimer's disease.

Wow.

We didn't learn that in med school. Medical students now aren't learning that in medical school. It takes 10, 15, 20 years for something to be learned in medical science to be translated into clinical practice. And I think it's important for this podcast and people like us to share this news because there are so many things a person can do. So you ask me what can a person do? I want them to know there's so many things. At least 12.

At least 12.

Well, so, you know, in our study, I think there's more, but there's at least 12. At least 12. You know, in our study, we recommended on average 21 different things that a person can do, and those were individualized per person. In our whole universe of our study, we recommended almost 50 things that a person can do.

50 things that influence the brain that you've identified.

Yep.

And it's, you know, this isn't radical. This isn't rocket science. This isn't like, you know, I'm a simple man. I did not graduate first in my med school. school class. I did, I did pretty good and I worked pretty hard. But, you know, I, I, I just, I try to just see things from the patient's perspective and there are so many things that are evidence-based and safe. The two categories I would start with just to kind of set the, set the stage are pharmacologic and non-pharmacologic and I want to get it, get granular because the word pharmacologic doesn't just mean drugs and prescription drugs.

It also means food is medicine.

Well, food is, food is, food is definitely medicine, although that got, that got sidetracked to non-pharmacological but I vitamins or medicine.

I would challenge you, Richard, because I think that food is actually real medicine. The phytochemicals compounds in food are biological response monophiles or single transduction changers and they have similar effects as drugs. In fact, many drugs come from the phytochemicals in plants. So I would just kind of make us think about that a little bit.

Well, actually, so I'm glad you brought that up. I would say that traditionally speaking, and let's talk through this. this is a great opportunity. So traditionally speaking, I've always framed it and I'm open-minded so this is great.

As pharmacology, I'm just teasing.

This is exactly why we're doing this. This is exactly a meeting of the minds. Gloves are off. Let's go. So, drugs, vitamins, supplements, and medical foods are the classic things that I personally have categorized in the pharmacology session. And then, in the non-farm section, included diet, exercise, sleep, stress, a whole bunch of things, learning new things. But what you bring up is important. And, you know, I have a colleague named Dr. Robert Krikorian, and he's an amazing guy. He's a neuropsychologist, and he's fought the good fight, you know, kind of like us. He's, I don't want to say he's had, yeah, in some ways, that contrarian views because he's tried to do randomized studies using nutrition. He's done studies on the ketogenic diet and Alzheimer's and Parkinson's, and he's done, you know, studies on blueberries and omega-3s. And what he's done is he's taken the food and he said, okay, it's not just about the blueberries. we did a study in wild blueberries are better. Well, why? Because of this thing, it's called anthocyanin and then he gets down deep into it. So, I completely agree that food is medicine, 100% agree. I completely agree that the specific chemical nutrient compounds can be isolated, but I think it's too reductionist to just say, let's just put a pill of anthocyanins and prescribe them.

100%.

Because it's the milieu. It's right. It's like with caffeinated coffee is good for brain health. well, is it the caffeine? Is it the coffee? Well, no, they think it's like some substance X during the brewing process. Right.

So.

So, you know, depending on which way you look at the science, I would prefer that food is medicine. It's just sometimes I agree with you.

I understand the bucket. So I'm just kind of playing with you.

But I love it.

But I think, I mean, when I, when I put a patient, for example, on a ketogenic diet with Alzheimer's, and they wake up and their brain becomes alert and they remember their son and their daughter. And I'm like, well, how is that less a drug than some other drug that doesn't even work that we're using like Aricept, right?

Yeah.

It's impressive.

Yeah. No, I mean, I just feel like all of the different paths, some people call nutrition, I don't know, not mainstream medicine. To me as a Western doctor, that doesn't make any sense to me. Nutrition is like I got very little nutrition education in medical school and I think that's a terrible thing. I learned a ton and I had to, my better half has a master's degree in nutrition from Columbia and she's taught me a lot, I think through osmosis. Ah, there we go. It's always the better half and she informs the less enlightened one. So, you know, I guess what I'm trying to say is nutrition is the cornerstone of how we practice. Physical exercise and precision exercise, precision nutrition, these are all the things that are developing and really become the cornerstone of our care.

So, you're talking about the 12, then the 21, and then the 50, and maybe there's going to be 100. Tell us more about the granularity on that.

Sure.

You were using these, you know, and I just want to sort of frame it for people. You did a study that you published, I think in 2019, which surprised even you. We're using this approach, looking at a personalized assessment of these biological factors that could be modified and then individualizing the treatment that you not only slowed the decline, you not only stopped the decline, but you reversed the decline, which is something that has never really been seen except in a couple of trials like the finger trial and I think there's a new one coming out, the pointer trial. So those are also lifestyle trials. And so you really have sort of cracked the egg and published something that should have been on the front page of every major newspaper, the lead story in every evening news. And yet, It was like crickets. Yeah, well, I mean, we got the.

Wall Street Journal and CNN and the Smother. So I'm okay.

But for me, it was like, it.

Should have been like the NIH should have gone, oh, Richard, here's $10 billion to get going on this. Like, that's what it should have.

I have to be careful, but, you know, the NIH doesn't really fund what we do. And that's been, you know, it's very hard. And listen, the NIH, I've engaged with the NIH over the last year or two, and there's definitely been more interest. But, you know, I, I, you know, talk about crickets years ago, a decade ago, when I started this whole thing, more at 15 years ago, there was nothing. There is no, there was no funding for any of this. So, you know, what I would say is what our work shows is that when you individualize care and you give people a plan, and I know you've asked me at least three times now, what should people do? What I'm trying, why I'm, why I'm delaying things is because it really, truly needs to be individualized. And what we, what we use is a term called the C's of Alzheimer's prevention management. Based on the data, we get data on A's, the B's, and the C's. A stands for anthropometrics. Anthropometrics is basically a fancy A word for body composition. What is your body fat? What is your waist circumference? What is your muscle mass? Depending on these factors, we're gonna change the recommendations we give. The B stands for blood-based biomarkers. We're gonna look at markers of lipids, cholesterol markers, also advanced markers that preventative cardiologists use, for example, that you know, most neurologists honestly don't really pay attention to. We look at metabolic markers, insulin resistance, we look at inflammatory markers, we look at nutrition markers, you know, instead of, you know, saying, okay, well, go eat fish, it's good for you. We're going to look at the markers in the blood. We're then going to tell you based on your blood and based on your genetics how much fish you should be eating, what types of fish. So so the the take home point is we're going to get granular with every patient. The other thing we do is in the blood based biomarkers, we look at genetics, we look at the APOE4 variant. It's the most common risk Gene doesn't mean you're going to get Alzheimer's if you have the variant, but it increases your risk. Well, if I know that you have the APOE4 variant, they checked for this in 23andMe and millions of people have gotten this checked. I'm going to personalize your care differently. If you have the variant, I'm going to give you plan A, B, and C. If you don't have the variant, I'm going to give you a little bit modified plan X, Y, and Z. If you have two copies of the variant, you have a different plan altogether. That's only 1% of the population. So, you know, the take home is we take all these markers and then the C is cognitive function. And we understand a person's cognitive baseline. We look at memory function, language abilities, learning abilities, speed of processing, attention and executive function, which is higher order processing. We take all of this and the patient's medical history. We learn about the patient. We learn everything we can about them, about their family, and then we personalize a plan. So those 21 different things are based on that person individually. And, you know, there's a lot of overlap. If you want me to say, okay, well, what are the core things? exercise on a regular basis. Okay, well, exercise on a regular basis is good, but every person gets a different plan. If we're putting someone on a plan for body fat loss, we're going to give them a different plan. Steady state cardio, for example, some people would call that zone two training. Steady state cardio at 60 to 65% of your heart rate. There's different ways to do this through lactate testing, through a variety of things that we do, you know, more precisely in our clinic. But we put people on these, steady state cardio plans fasted in the morning as long as they can tolerate it because that way it jumpstarts body fat loss. If we have people that don't do any muscle strength training because they don't like it, we educate them to say, I don't like it either. I'm not, you know, Mr. Big Muscles over here, but I have to do strength training once or twice a week minimum because if you don't have muscles, you can't boost metabolism. So we put people on these very specific plans. high intensity interval training. I really believe that high intensity interval training is almost necessary for people with at least one copy of the APOE4 variant. And this is what has been studied down in a couple of studies. And, yes, we need more research and the studies out of Norway were good, but we need to personalize an exercise plan. We need to personalize a nutrition plan. We need to personalize a vitamin and supplement plan. In some people, we do use drugs. Drugs are actually not commonly used at all in our research. although we do use them on occasion. We'll use a variety of drugs, usually at much lower doses than maybe the regular community uses. But when it comes to management, equal opportunity, if there's data and it's relatively safe, I'll entertain it. So we recommend cognitive activities that will have a spillover effect, learning something new, learning how to play a musical instrument, learning a new language. These are things that may have a protective effect, build backup pathways, Believe it or not, even learning how to play a musical instrument in midlife has protective effects on cognitive outcomes in late life. And that's- There's hope for me yet. There's hope for you yet. I got my bass guitar over there. I got blisters on my fingers.

I'm gonna learn to play the guitar. I'm gonna learn to play the guitar. But my big problem is I don't know how to tune it and I don't, I am so musically inept that I probably there are good apps and.

Things to do it. There's a website, it's called, you got a pen, it's called YouTube. YouTube. YouTube.

You may have heard of it.

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

That's my December.

Excellent.

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

So, let me ask you this because, I mean, you know, first I want.

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

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

Yeah.

Full stop. That's it. There's this thing called the skull, and it's a hard thing that protects you when you fall. But it's just like it.

It.

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

So essentially what you're saying to paraphrase is that Alzheimer's is not a brain disease.

Correct.

It's a systemic disease that affects the.

Yeah, I really believe that. I have to be careful saying that. Is this being recorded? Oh, no.

And it's gonna be broadcast to billions of people around the world.

Great, great. My field, I was just trying to, I was just gaining some fans in my field and now it's all last decade of work.

Oh, no, no.

You are at the forefront of a paradigm shift that's happening throughout medicine, which is the breakdown of the old concepts of disease from simply this reductionist organ-based, symptom-based model to systems thinking and network medicine. And, that's really all you're talking about.

There's very strong compelling evidence at this point that bacteria are the cause of neurodegenerative diseases.

Not my- yeah, we talked about Rudy Tanzi, who's a Harvard scientist, one of the discovers of some of the presenilin genes, which are the genes that show that people at risk for early Alzheimer's. He actually said they were discovering all these microbes in the brain, which we thought was sterile. And that we had this blood-brain barrier that protects us. And you're saying, and he's saying, that that barrier is not always 100% and that stuff can leak through. Not only can you have a leaky gut, but you can have a leaky brain.

Look, bacteria, not to scare people, bacteria love the brain. Why? 25% of the body's glucose is used by the brain. They know where to eat. They're going to, you know, Le Pen or that fancy restaurant is downtown. Everyone else is eating downtown. They're getting, you know, our brains.

Bacteria live on ketones?

100%. But not, wait, that's very important. They prefer simple sugars. Why? Because they're lazy, right? They want, you know, they want instant gratification. So they like sugar better than ketones.

But ketones, and ketogenic diets work for some of these neurodegenerative diseases like Alzheimer's and even LS and brain cancer.

That's right. That's right. And I think one of the mechanisms, to be honest with you, is that ketones actually improve, first of all, they improve mitochondrial function, but they're not a good substrate for bacteria. They're a great substrate for us. Bacteria don't like them because they like eating fast food, basically.

So feed them sugar, we eat fat.

That's right.

Okay, so this is just a breakthrough idea and this isn't just an idea. You've actually treated patients using this approach and seen some really extraordinary things.

Yes.

So can you share with us a little bit about this case you were sharing with me earlier about ALS, which is a horrible condition. Stephen Hawking had it. It was called Lou Gehrig's disease. the baseball player, essentially is where your nervous system is affected by the killing of the neurons in your spinal cord, which makes you basically paralyzed. You got fasciculation, which is twitching. You eventually can move your arms and legs. You're in a wheelchair. You breathe. You need a respirator.

You wouldn't wash it off on your worst enemy.

It would not work. It's like slowly getting paralyzed, right? Yep. That's right. never has there been a treatment that has stopped or reversed it.

Right.

And you're saying that you've seen patients where this has actually happened?

So, well, we are in the process of validating that sort of that data. Yes.

So, yes, we need more studies. Yes, we need to do research on multiple patients. But even if there's one patient, Right. Where you've seen a change. It raises the question of-- oh, by.

The way, it's made me go crazy, by the way, because, you know, I am so-- I'm finally glad to be a neurologist. You know, being a neurologist is like being a nihilist or a masochist. Diagnosing adios, right? Well, it's worse than that. It's like diagnose and let me not tell the patient that they have ALS. Let me treat them for, you know, like a CIDP picture, because they don't want to actually make that diagnosis for people. It's the hardest diagnosis you can make for a patient, because everyone knows ALS is incurable disease, right? I mean, it's 100%, even pancreatic cancer is better. Well, you have a five percent chance of living a pancreatic cancer. You have zero chance of living through this disease.

Zero. So, based on your hypothesis that it's infectious, that plays a big role, if not is the main role. Right. You know, I personally shared on this podcast that I went to a place in Mexico called San Aviv where I and my wife both went through this treatment called hyperthermia, which essentially is where they heat you up to 107 degrees, which sounds crazy and is scary. But actually, we did both fine and it killed a lot of infections that we had. Lyme, my wife, her viral loads of very tough to treat infection called CMV came plummeting down. She felt much better. I felt much better. and so this is a therapy that is not much used in the United States, but is used widely in Europe, is used in Mexico and other countries as the therapy for some of these types of infectious diseases and even cancer. Right. So how does the theory work behind this with something like ALS?

Well, the idea is that fever, is the way of actually denaturing spores.

Okay, that's a big sentence. Can you unpack that?

Sure. So human cells have their proteins that either fold properly or not fold properly at a certain temperature. Bacteria have their own temperature zone, like their ideal climate. And spores have another ideal climate, meaning that to kill a spore- A spore.

Is like a baby bacteria.

A spore is a baby bacteria. And that's what I believe personally is the reason that patients have amyloid accumulation, that the spores are creating this protective cover against antibiotics that actually is in fact the amyloid being produced.

The amyloid is like the armor for the bacteria.

Yes, they're like the bomb shelter. The biofilm is the bomb shelter for these little baby bacteria.

Yep.

And so how does hyperthermia work to disrupt that? And what is that procedure?

Because.

Well, so it works, hyperthermia works by, it's a very narrow window of temperature. Meaning if you give too much temperature, you can actually hurt normal cells as much as, you know, bacterial cells. If you don't give enough temperature, you've done nothing.

So it's like Goldilocks.

It's like Goldilocks.

You gotta get it just right.

Exactly right, okay? And that's part of the way that the hyperthermia technology has been developed is by really understanding that the brain itself can provide feedback on the tolerability for human cells because brain cells are going to tell the brain, hey, this is pretty hot in here.

You don't want to fry your brain.

Can you turn the thermostat off now? So the part of the part of the device actually is to get the brain temperature back into the feedback system where it's self-regulating so that you never reach a point where the temperature is harmful to your own cells.

And so, often in places where they do this, they'll give at the peak of the temperature, they'll give antibiotics or antivirals.

Right.

Does that make sense?

To give antivirals.

Or, yeah, to give antimicrobial treatment to patients when they're at the peak of the fever because the idea is that it sort of flows through something.

Oh, I see. Yes, for acute infection, yes. I would argue that. Lyme or? Well, if the Lyme is acute, certainly. I mean, I don't think that, I mean, I think you gotta be weary of the issue that by, you know, robbing Peter to pay Paul, for instance. Let's say that C. diff is, let's say, for argument's sake, say this is a polymicrobial disease. as opposed to a... Like lots of different bugs. Lots of different bugs, as opposed to just one ringleader everyone else is following. So Lombard believes that C. Diff is the ringleader, and all these other guys, Lyme, HSV, they're just tagging a ride because it's such a great killer that it's like, okay, great, we'll take the leftovers, no problem here. We'll take the leftovers. So my concern is clinically that if we start treating patients with bacterial drugs like Roseffin, whatever it is for chronic Lyme, yes, you're dressing chronic Lyme.

I mean, the C. Diff gets worse.

Yes, exactly. Exactly.

So the heat alone is enough to disrupt the C. Diff?

Well, we haven't demonstrated that yet, to be quite frank. But what's been demonstrated is that by applying hypothermia, that we're able to actually see improvement in clinical symptoms of patients with ALS.

People's muscle strength, this is a progressive disease, so it gets worse and worse and worse. Every visit they're worse. You're seeing patients that it stops or.

Gets better, which never happened.

Correct. So this is a major breakthrough? I think so. Major breakthrough. And this is not something new. This has been around for a long time. So where in the world is most of the research being done on hyperthermia? For ALS?

Period.

I mean, it's- oh, most of the.

Research on hypothermia actually is cancer research. So they call it chemothermia, chemohypothermia. So people can look up a lot of data on how hypothermia affects cancer, but as far as I know, there's zero data until now applying hypothermia for ALS. We will be the first people to actually talk about applying hypothermia for treatment of ALS.

What about things like Alzheimer's or Parkinson's or MS?

The difference in those diseases are that in Alzheimer's, it's very difficult to induce hypothermia in a patient with Alzheimer's disease. Why? Because you need to be compliant. The treatment itself is, it's fairly rigorous as you know from your experience. They put me to sleep.

They put you to sleep, right?

We don't want to put them to sleep though, right? Because we're concerned about protecting their brain. So, you have a patient who's got end-stage Alzheimer's disease, for instance, I don't see how this is going to be healthy for them. But early, 100%.

Early.

Early. In fact, I will talk later, not about the case now, because we're really just in the beginnings of this case. But yeah, I think it will be applicable for Alzheimer's disease as well.

Have you seen any patients reported or in the literature? No, not really. No. But you serve as a theory.

Yes, still a theory.

And MS, what about MS?

MS, there's data on actually the opposite, right? Which is how do you induce hypothermia, right? Because in MS, it's an inflammatory disease obviously, right? Which by the way, I also believe is caused by Clostridium, but not C. Diff, where it's especially important to actually identify at that stage that this is bacterial. So, I don't know what they're- yeah.

So what, what, what, is the idea with MS that you wouldn't want to use hyperthermia, that you wouldn't want to.

Use heat because it makes it worse? Well, because remember, when you heat up a patient with MS, what happens? They usually get worse.

So the trick is- But maybe not enough, right? Maybe it's not enough.

That's right. Maybe you haven't reached the threshold to actually, you know, use the body's fever.

Mechanisms against- Because there's links to MS and Epsom virus and other infections. There's links to Alzheimer's and herpes virus infections. Right.

So yes, the whole principle is applicable for all those diseases, but we don't know yet if it is applicable yet until we clinically demonstrate that. But yeah, I think that this is going to be a treatment that's going to be very important for a lot of different diseases, Mark.

So there's this whole theory that the body has a mechanism for dealing with this and it has its own proteins that are produced in response to heat. And there are things we learned about in medical school. They're called heat shock proteins.

I learned something very important about heat shock proteins from Dr. Lesler because we remember that, you know, people looking at how to induce hypothermia, right? So there's all sorts of research, there's actually even a drug in clinic for ALS that is the mechanism of action is based upon increasing heat shock protein through a pharmaceutical agent. So I was at this lecture and I thought I knew everything, basically, and I learned that actually you can induce-.

Because you thought MD stood for medical deity, is that it?

Medical deity, yes, exactly.

We all got that draining. The truth is we know close to nothing.

That's why I said at the beginning of this talk, thanks for inviting me, but I really know nothing. Just disclaimer. But anyway, so yes, actually in MS, The goal is to induce heat shock protein through hypothermia. Hypothermia.

So you get people cold?

Not people. The brain.

The brain.

Right. How do we do that?

Chill the brain.

Chill the brain.

How do you do that? Ice blocks around the head?

No.

No. Well, I'll invite you up and you could see for yourself what that looks like.

All right. Dunk your head in ice water. Nope.

Nope. Nope. None of the above.

Okay, so we have to be in mystery here.

A mystery about what the device looks like, you mean?

Yeah.

It's basically the same concept as building a hyperthermia device, except remember now that technology itself was developed basically for anesthesiologists. This was developed at Yale by Dr. Abreu, who's the person who actually discovered a way of measuring brain temperature objectively externally. Okay, so that's kind of where this whole thing started from, to be honest with you.

You don't have to stick an electrode in your brain, you can literally map it out from the outside.

You can map it out from the outside. So the ability to do that now allows a clinician to not only, you know, heat the body to create hyperthermic states, but through other types of modalities to actually cool the brain safely externally with the same, in the same way, meaning that you can actually apply a small device to a region of the skin, its periorbital location, and you can actually change the temperature of the brain through this, what's called the brain thermal tunnel. And that also creates heat shock protein 70. Heat shock protein 70. I didn't know that until I was in Australia.

That's amazing. so you're hopeful about the future of neurology, it sounds like.

It's the first time I've been hopeful.

About anything in my life, to be honest with you. I hope you enjoyed today's episode. One of the best ways you can support this podcast is by leaving us a rating and review below.

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