The Brain Doctor That Figured Out The Cause Of Dementia - Dr. David Perlmutter

In America, Alzheimer's is the third. leading cause of death. If you live to. be age 85, your risk of developing. dementia and generally Alzheimer's, it's. close to a high 40% or a flip of a coin. And women have twice the risk of. Alzheimer's in comparison to men. But. what people may not be aware of is it is. significantly preventable. And that's. the message that I've got to get out. I'm a boardcertified neurologist and. I've seen a lot of brains and thousands. of scans. Alzheimer's is primarily a. metabolic condition of the brain.

>> So, I've got some cards here and I want. you to write the top five things that. you think are contributing to. Alzheimer's and dementia. >> Number one, we have offloaded agency of. our brains to the pharmaceutical. industry. So, I'm putting forth to you. the most important things people can be. doing in keeping the brain healthy. And. number two, being sedentary. This is. huge. Exercise and movement is a. multi-tool for the brain. Then there's. food choices. You know, I've got a few. things here. This is a big problem. because if Wow, that's scary. That's.

worrisome. So, what we really understand. now is genetics loads the gun. Lifestyle. pulls the trigger. >> You know, we often hear from the family. what it was like to essentially lose the. person they loved. >> And I've been through this with my. father and when you see your parent like. that and you think back to who he was. and what he was, it's uh difficult and I. don't want people to go through that. Well, you're a dad yourself now and you. have this wonderful son called Austin. Austin wrote a letter for you. You know, uh, I'm thinking of my dad. right now and I'm doing my best so.

people don't have to experience what I'm. feeling right now. So, what does that. mean for us? >> My hope is that a lot of people get this. message that. Before this episode starts, I have a. small favor to ask you. 2 months ago, 61% of the people that watched this. channel weren't subscribed. We're now. down to 58%. My goal is 50%. So, if. you've ever liked any of the videos. we've made on this channel, if you like. this channel, can you do me a small. quick favor and hit the subscribe. button? It helps this channel more than. you know. And the bigger the channel. gets, the more we can invest in the.

guests and the production. Thank you and. enjoy this episode. Dr. David Pelato, what is the mission. you are on and why does that mission. personally matter to you? Well, the. mission I'm on is to let as many people. know that the the destiny of their. brains uh is really based upon how they. are choosing to live their lives today. So, we live in a world where we're sort. of message to really live your life uh. come what may, however you like, and.

there'll be some magic development in. the world of neuroscience that will save. you when your brain isn't working like. it should. We aren't there yet. I. welcome that day, but we aren't there. yet. What we really understand now, in. fact, the greatest development in. neuroscience is that our lifestyle. choices are really the architects of our. brain's destiny. >> And who are you, Dr. David? What is your. experience and what is the the education. that you've had? >> I went to medical school, got my MD, then became uh enrolled in a.

neurosurgery residency and became a. boardcertified neurologist. >> And why does this all matter so much to. you personally? Personally, I've been. through this well with. You just played that card, didn't you? I've been through this with my father. And uh. and it's rough. It's rough for in my. country, the 7.6 million Alzheimer's. patients. Not so rough for them as it is. for their families, the truth be known.

And it is significantly preventable. That's the message that I've got to get. out. We don't have a treatment. Would I. welcome a treatment? You bet. Would I. have used a medication and prescribed it. for my own father? Of course I would. have. We aren't there yet. What happened. to your father? Got a wonderful portrait. of him here as well. What a suave man. So uh he was a brilliant brain surgeon, compassionate, skilled, wonderfully. compassionate uh individual. And in his.

later years, he developed Alzheimer's. And you know, it's interesting because I. diagnosed him late in the game. I. remember the moment that I finally. realized, my gosh, he's demented and uh. I missed it. >> How did you know he had Alzheimer's? What is that? How do you diagnose it? >> It's what I do. I mean, I I diagnose. Parkinson's in the airport when I'm. coming to see you. I mean, that's what I. do. It's my skill set. You know, just.

the the type of memory issues that he. was experiencing, losing things, walking. into the room, forgetting where he was, it was very obvious. I mean, it it was. at least dementia and generally that. means Alzheimer's. >> And just my knowledge, what is the. difference? Because we I hear these. words dementia, Alzheimer's, >> Parkinson. >> Most of dementia is Alzheimer's. You can be cognitively impaired because. of poor blood supply to your brain. We. call that vascular dementia. There is.

dementia that goes along with the. accumulation of something called Louis. bodies in the brain. People can be. cognitively impaired with reversible. issues like as a consequence of uh. medications that they may be taking or. uh other types of medical problems. So. dementia is the sort of umbrella term. >> Exactly. Dementia means you know this. failure of cognitive function across. multiple domains. >> Okay. So Alzheimer's disease, vascular. dementia, Louisibody dementia and. >> fronttotemporal dementia. >> Okay. So everything underneath dementia,

it's a general term for a group of. symptoms. >> That's right. >> Okay. >> What has become so fascinating for me as. you look at those seemingly very. disperate diagnoses and they are but. they're all united by one common. mechanism and that is disruption of the. brain's immune system. That's the. fundamental. That is the the huge aha in. neuroscience right now. That disruption. of the brain's immune system is a. central feature across this incredible.

panorama of what makes a good brain go. bad. >> What is it the current medical. profession believes that you no longer. believe? I think that by and large at. least relating to Alzheimer's and I. think we can flesh this out across more. neurodeenerative conditions as we speak. but I think still the party line is one. that believes that the central player in. Alzheimer's disease is the accumulation. of a protein called beta amaloid in the.

brain. Get rid of the beta amalloid and. problem solved. That is not reality and. it's unfair. And how many people are. likely to get a form of dementia in. their life? Like how how many people are. going to be affected by these. neurodeenerative diseases that you have. studied and worked on and can diagnose? >> Lots. I mean, if you live to be age 85, your risk of developing dementia and. generally Alzheimer's is close to a flip. of a coin. It's close to, you know, high.

40%. And that is uh that's very. worrisome. In America, Alzheimer's is. the third leading cause of death. People. don't realize that. And it is largely. preventable. That gets back to our first. question. Why am I here? What do I do? And my mission is to message people that. what you're doing at your age, Stephen, is hugely influential in terms of. charting your brain's destiny. >> When does dementia start? Typically we.

discuss the idea that you know a patient. becomes not even a patient yet but. somebody is having issues forgetful of. names going into the room forgetting why. losing things that's when they go to the. doctor and that's when the process. begins of evaluation and ultimately. choosing some form of treatment. And the. reality is it it's like um a heart. attack. We don't wait for you to have a. heart attack to begin looking at your. blood lipids, looking at your blood. pressure, asking you, "Are you active?

How are you sleeping? What's your. physical activity like?" And we should. be doing the same thing as it relates to. dementia. We should be talking to people. in their 30s and in their 40s and asking. those very same questions. Alzheimer's. is primarily a metabolic condition of. the brain. Let me tell you something. that's really interesting that happened. in your country. Uh this past week there. is a new trial being started right here. in England called the ADS smart trial.

and the government has uh put up 33. million pounds 44 million to begin a. study of two medicines in the treatment. of Alzheimer's disease. One is called. metformin which is a diabetes pill and. the other is actually an ADHD drug. called strata. And this is a trial of. about a thousand people. It's going to. take 18 months to treat Alzheimer's. patients. Why I bring it up? As a matter. of fact, your prime minister is very. much in favor of it in that um his.

father died of dementia. Uh that said, the reason I bring it up is metformin is. a metabolic drug. It's a diabetes drug. Think about that. that they've moved. away from targeting beta amaloid to. finally recognizing that metabolism is a. central player here. Explain this to me. like I'm 16 years old. So beta amalloid. are these these brown sort of plaques. they found on the brain with people that. had Alzheimer's dementia. Um so they.

thought that it was part of the cause of. the dementia. >> Subsequently they found out that you can. have those plaques and still not have. the dementia symptoms. So we now know it. must be something else and you can have. the plaques a a a brain load of plaques. and not be demented. So now the working hypothesis is that. it's something else is causing it. And. you're positing that it's largely based. on metabolism. >> Yes. >> And metabolism as I understand it is. what we eat, what we do like our.

activity and our life, our lifestyle. decisions. It's a great question and I. think that you know the strict. definition is metabolism is the way that. our cells uh create energy and make. things. They make proteins, they make. things. So really uh upstream of what. makes a good brain go bad are changes in. metabolism. The metabolic markers, our. blood sugar, our blood pressure, our. body fat, our blood lipids. These are.

the metrics of metabolism that are so. important for the brain and the heart. and in fact your entire body. So when we. say that Alzheimer's is fundamentally a. metabolic condition, let's let's say. that in the context of where the. research is going. For example, 10 years ago about a third of. Alzheimer's research was really focused. on what we talked about this beta. amalloid protein. That number is down to. about 14% now in favor of looking at.

things like metabolism and looking at. the brain's immune system these micro. gal cells that are really the upstream. issue as it relates to not just. Alzheimer's but all manner of. neurodeenerative condition. So when we. understand metabolism and its effect on. the microgle cells, we're throwing a. very wide net indeed. Meaning that if we. can target our metabolism earlier in. life, keep our blood sugar under. control, exercise, get enough sleep,

have relationships with other people, who knew that was such a powerful tool. uh for brain health. we really are. creating an environment that helps us. reduce the risk across the spectrum of. brain degenerative issues, not just. Alzheimer's. I'm going to set you a. slightly tricky task. >> Okay. I I've got some cards here and I. want you to write in order of um. severity and consequence the top five.

things that you think from lifestyle. perspective. are contributing to Alzheimer's and. dementia. Okay. If you've got more that you want. to add, you can add more. Just tell me. how many you've got you've done. Okay. So, how many have you got there? >> I have five. And again, let's restate. what I'm doing here. I'm putting forth. to you what I think are the most. important things people can be doing as.

it relates to being in charge of their. brain. And that is in fact number one. And that is the biggest issue is not. embracing the fact that you are the. architect of your brand's destiny. Because if we don't do this, nothing. here will matter. nothing here will take. place. You've got to embrace that and. you've got to recognize that. we have offloaded agency of our brains. to the pharmaceutical industry, if you.

will, and other forms of technology. And. again, that's great if there were. something that were effective. There is. not anything meaningfully effective. right now. John Kennedy said that the. time to fix the roof is when the sun is. shining. And that's why I'm here today. So number two, sedentarity, meaning. being sedentary. This is huge. This exercise and movement is a. multi-tool for the brain. It targets the.

function of insulin. It targets. inflammation. It targets mitochondrial. function. It targets blood flow. These. are all hugely important mechanisms in. keeping the brain healthy. Are you. somewhat very focused on brain health in. part because of your father and does. that statistically give you a. predisposition to the same disease? >> It does. It does. >> I think you know when we talk about what. we inherit in terms of risk I think a. lot of people these days are focused on.

the Chris Hemsworth story that he. carries two of what are called the APOE4. genetic alals. Are you familiar with. that or can I walk through it? Okay. So. we have the the APOE alals. We can have. a two, a three or a four. >> Mhm. >> And you get two chances. >> What do you mean you get two chances? >> Well, you carry two of them. So you can. have a 22, you can have a 2 three, a 33, a 34, a 44, and a 24. I guess those are.

all the permutations that can can. happen. Carrying more of the APOE2s is. associated with a pretty dramatic risk. reduction. APOE3 is neutral, but. carrying the APOE4 alil like about 25%. of people is associated with an. increased risk of Alzheimer's. If you. carry one by about fivefold. 500%. >> 500% fivefold and if you carry two, in. other words, your APOE 44, the risk may.

be as high as 12fold. increase, >> 1,200%. And you're saying Chris. Hemsworth has he's been very uh public. about it. But here's what is so valuable. and on the list of things that you and I. have not covered yet and incredibly. valuable. Why? Because people are. getting their genome sequence now, you. know, left, right, and center. Everybody. knows and a quarter of people who get. their genome sequence are getting their. results back. and seeing that they might carry an.

APOE4 AL. And then you read the little. print out from AI that says this puts. you at increased risk for Alzheimer's. That's scary. That's worrisome. Early in. the day, we as neurologists were told, well, when we know the APOE status of. our patients, if they carry APOE4, we. shouldn't tell them. Well, why should we. tell them? Because they're on the road. to Alzheimer's. Nothing is further from. the truth. If you carry an APOE4 alil or. two, you are not necessarily destined to.

get Alzheimer's. So incredibly. important. Your lifestyle issues can. offset this issue of a genetic. predisposition. It's a genetic. predisposition. I won't deny that. It is. not a genetic determinant. There's an. interesting study that came out in the. Journal of the American Medical. Association. in November of 2025. The author was. named Marino and what he did was looked. at people from the Frammingham Heart.

Study and he divided the group of. individuals uh there were about a. thousand in each group 4,000 total into. younger people 25 to 44 years, middle-aged people 45 to 64 and older 65. to 88. That's my age group. And he. followed these uh individuals uh for a. number of years and determined who got. dementia and who did not. And he. compared that to their level of physical. activity. And what he found was really.

quite remarkable that in in middle-aged. people, those who were the most active. compared to those who were the least. active had about a 45%. risk reduction for this disease, Alzheimer's, for which there is no. meaningful treatment. That's huge. Similar results in the. older age group. Those who are most. active and carried APOE4. They had about a 67%.

reduced risk of becoming an Alzheimer's. patient. >> if they exercised. >> If they were in the the group that. exercised the most in comparison to the. group that exercised the least. Again, exercise is the multi-tool here. It is a. a huge and readily available tool for. each and every one of us. That's what. doctors should be should be teaching. patients. Not well, it looks like you're. cognitively impaired. We're going to put. you on an IV uh therapy uh every 2 weeks. and hope for the best.

>> What is the exercise doing. physiologically? How is it helping the. brain? >> Well, it's doing a lot of things. Exercise means you're basically. activating muscle, right? That's how you. move. You need your muscle to to work. when you move. Uh, and as it turns out, you may not know this, but your muscles. are an endocrine gland. >> What does that mean? >> Well, great question and and I'm glad we. teed it up. We know our endocrine glands. are, you know, the adrenals, the. thyroid, the pituitary. And why are they. called endocrine glands? Because they. make chemicals that go elsewhere and do.

something. Your muscles create a suite. of chemicals called myioind. Myom muscle kind means they move around. and they do things at a distance and. they make their way to the brain. For. example, they help stimulate the brain. to produce something called BDNF. So, it'll grow new brain cells and nurture. your neurons and nurture the connections. between neurons, which are the synapses. When we activate our muscles, we uh. improve how insulin works so our blood. sugar can remain where it needs to be.

Elevated blood sugar is a powerful risk. for brain degeneration. A simple blood. test like the A1C, measuring your. average blood sugar, is a powerful. indicator, if it's elevated, of risk for. Alzheimer's. When we exercise, we reduce. inflammation. Inflammation is a key. mechanism that changes our brain's. immune cells from being supportive to. being destructive, and we're going to. certainly look at that in great detail. And exercise improves the blood going to. your brain. That's got to be a good.

thing. any particular type of exercise. or all exercises? >> I think all exercise is great. The big. discussion is well, what's best for my. brain? Is it aerobics or is it strength. training, resistance training? And it. turns out that a a recent meta analysis. asked that question and came to the. conclusion that it's both that we want. to strengthen our muscles and we want to. engage in uh aerobic activity such that. we can gain the metabolic benefits. But. you know, think about it. If these.

chemicals that your muscles are making. are good for your brain that the more. you have of these chemicals, the better. So, build muscle. When when you're my. age, uh it's harder. It's much more. challenging to keep your muscle mass and. to build muscle. So, it's something that. you really want to start at a younger. age. >> What's the next card? I think I mean, we've got a tool box here as well, which. has got some things in it. >> The goodie box. >> You're aware that some of these are. relevant to things you just said, right? >> They are. And I'm going to pull out a um.

something a very very high techch device. that I think people should get. >> Okay. >> That might be their most powerful tool. that they can um save up for and get so. that they can improve their brains. Ready? >> Yeah. >> And here's one. >> Mhm. >> And here is the other. Get moving. Movement moves all the needles. Movement. moves everything. So if I use these, you're not going to use those. are too. small for you.

>> This is better than any drugs or. medicine that I could possibly buy. >> It is. It's interesting because what. I've just described to you in terms of. the activity of muscle activation is. very similar to the drug that's now. being uh used in the Alzheimer's trial. right here in in uh in England. Think. about that. That metformin metformin. does many things that exercise does. Exercise does more. >> Sold. >> You're sold. >> I'm sold. >> Mission accomplished.

Lack of social connection. Who knew? >> Really? That's the third thing. >> From here on out, these are all equally. ranked. >> Okay, so this is the in the top five. >> In the top five. >> Lack of social connection. What evidence. is there that relationships and social. connection is correlates to dementia? >> It's a tough metric, isn't it? How does. one measure that? And we we first got an. inkling that social connectivity was. good for health, good for the body, and. good for the brain. uh from the blue. zones information that looked at uh.

people who lived long and had lower risk. of dementia. And these are individuals. who ate a certain diet, which we can. talk about and uh lived in in areas that. had a lot of verticality, meaning they. were going up and down steps. But I. think importantly what we learned from. the blue zone data is that these are. people who are connected to other. people. They've insinuated themselves. into community and that is good for the. brain. It's good for inflammation. It's.

good for metabolism. Now you would you. would ask as I have asked well what is. the mechanism here right? You want to. understand that as a scientist right? What's the mechanism because until I can. see a mechanism I'm not going to I'm not. buying in. And what we know when we. connect to people and when we develop a. relationship, our bodies, our brains uh. increase the its output of a chemical. called oxytocin. You've heard of oxytocin. It's called. the love hormone.

But it's more than that. This oxytocin. is uh secreted when we're uh feeling. trust for another individual, when we're. feeling connected to another. we're. feeling. I'm getting oxytocin from my. time spent with you today. >> and I'm grateful. Thank you for that. And hopefully I'm giving some back to. you. And this oxytocin um stimulates our. good brain immune cells, these microgle. cells, and helps keep them in their.

supportive, loving, nurturing role as. opposed to letting them drift to. becoming what I call uh the evil twin, increasing inflammation, increasing the. destruction of our synapses. Let me set. that up a little bit more because I. think we're going to rely on that uh. moving forward. Our brain's microgle. cells can exist in a supportive loving. We call this the M2 configuration. We have long arms that are able to reach. out and be effective and do good things.

>> What is a microgle cells? >> So microgle cell is an immune cell that. lives within your brain. Makes up about. 10% of your brain cells. You know people. say, well brain cells, those are. neurons. I used to say, well if you. drink a beer, you're losing 50,000 brain. cells. Well, there are other cells in. your brain aside from the neurons. There. are immune cells. There are cells, you. know, that are involved in in the. structure of the brain. So, these. wonderful, loving, nurturing micro gal. cells, M2, are going around. They're.

shoring up our synapses, the connection. of one neuron to the next. They are. making sure that our very valuable. bloodb brain barrier is working and. keeping the bad things out. Uh they are. making sure that our neurons are. functioning appropriately and are. healthy. They're basically doing good. things, but they can shift. They can. become what I call the evil twin. And this is the evil twin, the M1. microgal cell. The reason I call it an. evil twin is because they're genetically.

the same, like twins. But this is the. cell that is destructive. These are the. cells that destroy our synapses. And. when our synapses are destroyed, we lose. connection. We lose connection at a. microscopic level of course because our. synapses connections are lost and we. lose connection at a macroscopic level. whereby we no longer are able to uh. connect to other people to ourselves to. the world around us. That's what's going. on. This shift from M2 to M1 is the.

fundamental upstream event in. Alzheimer's disease. These cells are. sensitive to our metabolism. These cells are sensitive to. inflammation. When our blood sugar is. elevated, it shifts them to being. destructive. When there's inflammation. in the body making its way to the brain. from any source, it shifts the M2. supportive microglea to being. destructive. Any metabolic issue and most importantly.

most importantly the energetics of these. cells is playing a fundamental role. This is a cell that gets its energy from. active function of the mitochondria. It. contains a host of mitochondria that are. producing this currency of energy called. uh ATP. This cell uses a totally different. energy uh production facility called. glycolysis. So upstream of this shift.

are changes in the mitochondria. This is. what's upstream. This is the fundamental. here. Mitochondrial energy production is. what dictates the shift between M2 and. M1. Now, I fully recognize that there. are countless transitional states. between M2 and M1. It isn't a binary. issue. It's an analog issue going from M. M2 supportive to M1. But again, upstream. of all of this is the energetics. It's.

the mitochondrial function. And this is. what is so sensitive uh to our. metabolism, to insulin, to exercise on. the positive side, to metformin on the. medication side. We're damaging our. mitochondria and that's causing it to. malfunction and then change from the M1. to the evil twin. That's exactly right. There are two inputs. These M2 microgle. cells and M1 for that matter have. receptors that are receiving. information. inflammatory chemicals from.

anywhere in the body like a leaky gut. You've talked about that before on your. program creates increased inflammation. in the body. Those chemicals can make. their way to the brain and there are. receptors on the micro gal cell that. will shift it to becoming more. destructive. So is that the symptom like. is that the effect? The effect is the. shift from M2 to M1. >> From the normal twin to the evil twin, >> right? Okay. because something goes. wrong with my energy production system. i.e. my metabolism.

>> Yes. But again there there are two. inputs here. Uh and it goes both ways. When these microgleas shift to being. more destructive they downregulate or. reduce the function of their. mitochondria. >> Okay. So it goes back upstream. >> It goes back upstream creates a feed. forward process. And importantly, very. importantly, these cells are. pro-inflammatory, meaning that they are once they become. activated, they're secretting chemicals. of inflammation throughout their.

environment, their local environment in. the brain. And those chemicals come back. and target the healthy microbial cells. and further shift them over to the dark. side like zombies. How do we know that. these microbio cells are anything to do. with Alzheimer's and dementia? >> We can actually see that on a special. scan called a TSPO scan. And what we're. looking at right now, uh, this is the. healthy control right here. And when we. image on this PET scan for TSPO in the.

Alzheimer's brain, you can see it is. absolutely just lit up. And what is so. incredibly empowering. that takes this story uh to a very wide. net that it throws is that we see. positive tspo imaging meaning activation. of the brain's immune cells across a. wide variety of neurodeenerative issues. Here's the empowering part. These cells. can shift back and become supportive. again. And the influence that directs.

them back to being supportive is under. our control. I've seen this kind of. photo a few times. Um, is that really. what an Alzheimer's brain looks like? >> It is. >> And you've seen a lot of brains. >> I've seen a lot of brains. >> How many brains do you think you've. seen? >> Well, uh, real brains, um, hundred. >> And now that's real human brains in your. hands. >> Brains in my hands in my laboratory. That's right. >> And then scans. Thousands of scans. >> And have you seen an Alzheimer's brain?

>> Oh, countless times. Well, I think this. is an extreme example, but what we're. seeing here is we call it atrophy. The. valleys between the mountains are are. wider because the mountains have. shrunken and then the inside of the. brain here, these are called the. ventricles. They are filled with spinal. fluid are expanding to take up the empty. space. Now, we always have to be. careful. We only look at this image uh. and and don't look at the the whole. picture in in aggregate. This could be. an indication of something called.

hydrophilis where fluid is increasing in. the brain and makes these ventricles. larger. It's just expanding because the. brain is basically shrinking. >> Okay. So, and the brain could be. shrinking for any number of reasons. >> Yes. But uh you know, keep in mind that. your brain will shrink as you age, but. the extent that you're seeing in in in. these images is really extensive. So, this this is a characteristic. macroscopically of an Alzheimer's brain. You know, you there are microscopic. characterizations as well and there are. blood characterizations as well. My.

sister-in-law just had a baby. I vaguely. remembered some stat that some. neuroscientist on this show had told me. So, I Googled it and it said that we. have more brain connections at 2 years. old than we do when we're an adult. And. the brain basically up until two sort of. has all these incredible connections. which probably explains why kids are so. bloody good at learning stuff. And then. the brain kind of loses the connections. so it can reinforce the ones that. matter. And I in part I was trying to.

figure out if this explains why kids. have terrible twos. We are going to go. to a really cool place right now. Okay. >> And let me set it up first of all. So. what you're describing is something. called synaptic pruning. And it is where. the brain, you know, becomes much more. adept at what it's ultimately going to. need to do. the the rate of synapse or. connection formation at age one year is. about 1 million synapses being formed. every second. >> So what does that mean? >> That means that in this brain nerves are.

wiring up they're wiring up connecting. to each other uh at the rate of a. million connections per second in the. one-year-old. Now this idea of synaptic. pruning the refinement part is happening. at about 20% that rate means that while. these connections are being made about. 20% of them of those connections or. others are actually being destroyed. So. the brain is refining itself. We're. losing connections very rapidly. What is.

the mechanism whereby this synaptic. pruning this refinement takes place? The. microgal cells. The microgleal cells are. the ones that are appropriately. destroying or taking away these synapses. which is a normal activity. It's what we. want to happen. There are situations. when there's not enough synaptic pruning. and there are consequences. Autism spectrum disorder being one of. them. Fragile X syndrome is another.

These are situations where the brain. doesn't adequately synaptic prune and. they're called hyperconnection syndromes. where the brain is actually. overconnected. Think about it though. These same micro. gal cells that are involved in. appropriate synaptic pruning when we are. growing up in our when we're children. are the same microgal cells that. inappropriately digest away or destroy. our synapses uh when we are older. and.

that can manifest as Alzheimer's. disease. So the there's a thinking now. in neuroscience. that Alzheimer's is the reactivation. of a normal developmental event. How cool is that? That Alzheimer's, the. loss of our synapses, which is what's. characteristic of this disease, is a. reactivation of what would have been. normal when we were children. So the brain is printing itself. >> inappropriately.

>> Why might it be doing that? >> That is the million-dollar question. It's doing that for a number of reasons. Uh first because of the activation of. these microgle cells, which is not. appropriate. I mean, you know, to be. fair, the biggest input that relates to. the shift of the microgle cell from. supportive to destructive is our. chronological age. And I say that. because that's what the data says, but. it should I I believe it should be our. biological age. And the reason I say. it's our bi could be our biological age.

is because it opens the door then for us. to target our biological age like. exercise and diet. But that said, um it. is, you know, a consequence of aging and. helps us understand why the number one. risk factor for Alzheimer's is the. number of birthdays we've had. Can't. really change that, but we can change. these other input sets for sure. >> So, what is number? Is it four? >> Uh, let's see. Non-restorative sleep.

>> Nonrestorative sleep. >> Non-restorative sleep. So, sleep has. there are a lot of things we talk about. when we're talking about sleep, how we. metricize our sleep. But it's. non-restorative. We don't get enough and. it's not high quality. How would you. know? Wait. Hashtag ad. I don't know. Well, you'd wear a a. wearable device, right? I mean, you. could subject yourself to a formal uh. polyomnog, which means you're going into. a lab, and it's creepy. I've done it.

And you wear all kinds of things. measuring your heart rate, your brain. waves, your your blood oxygenation, and. somebody's watching you and recording. you all night long when you're sleeping. I found it very creepy. But you you have. access to an Aura ring, an Apple Watch, a Whoop, and you can measure your sleep. and with pretty good reliability get a. sense as to its quality and its. quantity. That's what restorative sleep is all. about. Restorative sleep is so. important. It allows us to consolidate. our memories, our experiences in REM.

sleep. It allows activation, as you. know, of the glimpmphatic system that. allows us to take out the garbage. basically, which new research indicates. happens when we move as well. Yet. another part of the uh motion. multi-tool. But sleep helps us reduce uh. inflammation as well. It improves. insulin functionality. These are key players that relate to. brain function and brain health function. preservation. So you know uh even one night's poor.

sleep dramatically changes the function. of insulin has a significant effect upon. our blood sugar control and really does. set the stage for degeneration. Not only. that but it significantly affects our. decision-m ability after just one night. of poor sleep. I've heard about this. glimpmphatic thing. And ever since I. heard about the glimpmphatic drainage. system, I have slept significantly. better, but I've also become a little. bit of an with my friends. because I I've told them about it many. times. And the way that I kind of.

describe it, which I'm sure is um being. scientifically butchered when I say it, is that at night time it's almost like. the street cleaners come out in our. brain. That is a perfect metaphor. And. they come out and sweep up the streets. >> But they're only coming out if you're in. deep sleep. >> Okay. And how long it does it take to. get into deep sleep? >> To get into it? What's something that. typically happens later on in your sleep. cycle? >> So for me it's around hour 5 and 1/2. >> Hour 5 and a half. Okay. So you have. more deep sleep further into the night. >> That's right. >> And you sleep in these cycles, right?

Like. >> you do sleep in cycles. >> Okay. And the cycles are like 90 minute. cycles or 60 to 90. >> Depends on pe on the person of course. But you know the fact is we cycle. through various aspects as you know as. the orchestra is is getting ready to. play its music. each each area gets to. practice a little bit and it all. converges on and ultimately cubrious uh. sleep cubrious means uh it's an. adjective it means health providing I. used to really think of sleep as. non-negotiable but now you know I really.

do prioritize it and um you know I used. to think in my earlier years that if I. slept I was being unproductive and now. I've kind of inverted that where I feel. like I'm being unproductive if I haven't. slept. >> you know the other thing I think that uh. fleshes out a little bit is the the idea. that sleep dramatically affects your. decision-m ability the next day. There. are two areas of the brain that are. fundamental for how we make our. decisions. The uh prefrontal cortex.

which is here is the frontal lobe. >> and the prefrontal cortex involves this. part of the cortex. It's uh takes up. about onethird of the entire cortex or. outside of the brain. And another area. for decision-m is deep within the. temporal loes. These are the temporal. loes and it's uh shaped like an almond. It's called the amygdala. Some people. call it the fear center. But these areas. are Oh, here we go. Okay. So, within the. temporal lobe, uh which is here, the.

temporal lobe, inside of it is this. almond shaped uh organ, or rather this. almond shaped area that's called the. amydala. And both of these areas play. important roles in decision- making. The. amygdala is an impulsive, self-centered. area that makes rapid decisions. >> Well, I'm tired. >> Well, we'll get there. I'm leading up to. that. We're. >> I just I just can relate to. >> I know you can. We all can. >> The prefrontal cortex, again, this area.

behind your forehead. is the adult in the room, basically. And. what happens as we reach our teenage. years is this prefrontal cortex sort of. takes control. The adult in the room. hopefully becomes more and more. influential and exerts what we call top-. down control over the amydala. So we're. less impulsive. We understand the. consequences of our actions. We can plan. for the future. We can do uh things that. we can think about how it's going to. affect not just me but how it's going to.

affect you, how it's going to affect the. planet. That's the prefrontal cortex. We. depend highly upon this top- down. control of the prefrontal cortex. reigning in the amydala. The problem is. things can threaten that connection and. one of the things is inflammation. Inflammation can dramatically reduce the. functionality the ability of the adult. in the room to be in charge. And if you. are chronically inflamed, then your. decision-m is suffering day in and day. out. Let me take this a little bit.

further because it's it's an interesting. uh concept here that food has a role in. inflammation. We used to call it the. standard American diet. I think kind of. blaming America for the crappy diet of. the world today. But it was the standard. American diet then became the western. diet and now it's pretty much the global. diet that so. aggressively features these. ultrarocessed foods that are. pro-inflammatory. Now think about what I just said. The. world is eating foods that are. increasing inflammation. And.

inflammation separates the connection. between the adult in the room and the. impulsive, we're the best. I want it for. me. That's it. It's going to be my way. globally. This allows us to relate the change in. global nutrition to some of the things. we're seeing happening in our uh in our. world today. And does this link to card number five. of your top five? Poor diet. I've got a. few uh few things here. Terms of food.

Let's see what I have. Some orange. juice. Can of beer. Big tray of food. We're close. We're doing great. We want. to do our best to avoid sugar. So, how. much Let's say this is 12 ounces. Why. don't you tell me, Stephen, how much. sugar? I'll put it in this glass here. Tell me when to stop. How much sugar is. in here? Do you know the answer? >> Do you know what?

I probably I'm closer to the answer now. I've done this podcast. I If you'd asked. me when I was younger, I would have said. one. >> Okay, one. Before I did this podcast, I. would have thought, yeah, there's one. sugar. >> No, there's a little bit more than that. You tell me when to stop. That's two. All right, here we go. All right, now. three. Can I stop? >> I mean, >> four. Okay, here we go. Five. Six. Look at this. Seven.

Eight. And if this were a can of soda, just two more. There. Eight teaspoons of. sugar in your wonderful glass of. oranges. Oh, but what about the vitamin. C? What about the fiber? It doesn't. offset what this is doing to your body. >> Isn't it crazy that, you know, we wake. up in the morning and then we we drink 8. teaspoon of sugar? And there was a narrative at one point. that it was healthy for you. So, like. back in the Sunny D days, I I thought if.

I drank orange juice. >> Yeah. Sunny D days. That's not. necessarily juice. I mean, what is Sunny. D? >> I thought it was like one of my five a. day fruit and veg. >> Yeah. Yeah. >> You Yeah. It's crazy. >> How old are you? 34. >> 34. 34. Okay. You are the perfect. population that needs to get this. message because right now you know your. metabolism is is being formed. If we can get this message to your age. group, uh it will have a huge uh outcome.

and you know when you get to be my age. and you will get to be my age, you will. wish you had had known this. >> Why? >> Because you'll have set yourself up for. a good brain. I gave a talk the other. day in uh Vancouver, British Columbia. and I started off by asking everybody in. the audience to close their eyes. I. said, I want you to imagine when you. open your eyes, you're 85 years of age. I said, now open your eyes. Now look. around the room and I'm going to draw a.

line right down the middle of the room. Half of you have now been diagnosed with. dementia. Which half of the room are you going to. be in? And what we're talking about right now. allows you to be the arbiter, allows you. to be the architect uh and the decision. maker in terms of which half of that. room are you going to be in. Now, you. know, these issues can happen in your. 60s, they can happen in your 70s, which. is not to say that there are not some. very promising things in development.

right now that if we have time we can. talk about. The future looks bright from. that perspective. But again, you know, Benjamin Franklin said that an ounce of. prevention is worth a pound of cure and. it makes all the sense in the world. I. think this is probably one of the most. important things that I. >> Good for you. >> did in terms of figuring out. the truth about the foods that I loved. Why do you think this is um so useful? >> For the reason that you just described, and that is we're talking about a. continuous glucose monitor. So, uh, I.

don't know if there's really one in. here, but this is It. >> probably is. >> Yeah, it's personalized medicine. How do. your food choices affect your blood. sugar and your blood sugar affects your. brain's destiny and your heart and and. and your body for that matter? But this. is how you will know. For me, it was. cashews. I had no clue that cashews, nuts, would raise my blood sugar the way. they did. And I had the Lucas Monzer on, and it lit up when I ate cashews. I had a tendency to overeat cashews. I.

thought they were safe. I was also very. surprised at the degree of my blood. sugar elevation with exercise, though it. was transient while I was beginning to. exercise. That's a normal response and I. knew it. I kind of expected it, but um. when I finally saw it play out on my. smartphone while I was running, it was. it was impressive. But, you know, and. I'm not saying you need to wear a a CGM. at all times, but I think it's uh it's. extremely valuable and and now available.

without a prescription. There was a big. push back uh in America about making. CGM's continuous glucose monitors. available to people without a. prescription. You know, there were. editorials written in journals saying, "Oh my gosh, people are going to be. neurotic. They shouldn't know this. information. This is the purview of the. doctor." And my argument was, well, if. that's the case, if people shouldn't. have their data, then we shouldn't allow. people to buy a bathroom scale. Same. thing. I mean, that's a crazy crazy. thing to say, but. the continuous click. Yeah, there is one.

in here. >> These little devices, um, they don't. cost a lot of money. They're $ 20 $30. You can get them on Amazon and lots of. other places. Um, you stick it to your. arm. Um, or you, this one, you prick. your finger, but I think the best ones. are the continuous ones where you stick. to them. You can record your data and. you can upload it to uh. >> you know. >> puts on your phone directly to your. phone. >> but you can do a lot with that data and. you know the main thing is. >> how do you know what your changes are. doing unless you're able to measure. them. I mean if you want to lose weight.

you can you go on the bathroom scale uh. frequently and see if it if it's. working. You want to get your blood. sugar under control and you should. How. would you know? I mean, to go to the. doctor once a year and have a fasting. blood sugar measurement, uh, I'm not. going to say it's useless. I mean, it'll. give you a clue, but it's we can do so. much better. A few things that I've. discovered from looking at my own. continuous glucose monitor that. surprised me and things that I liked, but I am now, you know, I'm a little bit. more conscious of. One of them is.

barbecue sauce, which I loved. It's 40. to 50% sugar, which shocked me. Balsamic. glaze, 40 to 50% sugar. had this. commercial fat-ree French dressing which. was turned out to be 35% sugar. >> Why fat free? >> It said fat free on it. I thought it was. healthy. >> Yeah, they they do a lot of those sort. of tricks on labels. >> That's really worrisome that you. gravitated towards something that was. fat free. I mean, you know, fat-ree. cookies, fatree, and the other one's. gluten-ree. I mean, there's crap on the.

gluten-free aisle in the grocery store. >> Yeah. Uh this another thing I learned. from this podcast is um I learned that. roughly 1% of the world are truly like. gluten intolerant yet 20% of us. including me buy gluten-free stuff. I. actually used to go around saying I was. gluten-free but having learned a few. things on this podcast I think I might. actually be fru intolerant. Well I would. say respectfully that the number of. people who are gluten sensitive is. probably more than that. uh there is an. entity a defined entity now called.

non-seliac gluten sensitivity. So you. know the classic gluten issue is of. course celiac disease which is an. autoimmune condition. There are blood. markers for it. There are um diagnoses. made by looking at the small bowel with. an endoscope. And the reality is that uh a lot more. people have non-seliac gluten. sensitivity than have a full-on celiac. disease. So I think it's it's a big. number. I was very taken by the work. many years ago of a Dr. Marius.

Hajivasalu who's actually here in. England at Sheffield Hospital as well. who described uh issues related to the. brain that weren't related to celiac. disease but were related to gluten. consumption. That got me launched uh in. a big way to looking at gluten as it. relates to the neurological consequences. in some people of of consumption of. gluten. I remember one time as I was. beginning to learn this and uh reading. his work and he was describing how some.

people have headaches from consuming. gluten. Who knew? And I had a patient. with lifelong headaches was on narcotics. for her headaches. And I said, "Hey, what the heck? Let's give it a shot. Let's go gluten-free. See what happens. Come back in 6 weeks." She came back in. 6 weeks and remarkably, she was headache. free. She was just over-the-top happy. She was headache. She was off narcotics. So she went to she had a. gastroanerologist because she had gluten.

issues probably related to GI symptoms. as well. And uh she said, "I saw Dr. Prutater and he put me on a gluten-free. diet. Now my headaches are gone." And. the doctor said to her, "That's. preposterous. And to prove it to you, I'm going to do. an endoscopy. I'm going to look at your. small intestine and prove that you don't. have celiac disease. He does an endoscopy. She doesn't have. the hallmarks of celiac disease. And he. says to her, "Go back on gluten." And. she said, "But but but okay." She goes.

back on gluten. What happens? Headaches. returned with a vengeance. And so she returns to the office, you. know, bashfully and explain that story. to me. What I read was that roughly 0.5%. of the general population have. non-siliac gluten sensitivity. In terms. of ciliac disease, it affects roughly 1%. of people. And then 0.1% of people have. a wheat allergy. But when you ask. people, the general population, if you. survey them around being gluten-free, up.

to 20% of adults report feeling much. better on a gluten-free diet. However, double blind placeboc controlled food. challenge trials show that only a. fraction of self-dagnosed individuals. react specifically to gluten. And. generally, I think the um in this report. it says that the misunderstandings are a. lot of people are allergic to fructes. and fruins and gluten always appear at. the same time. And I think this also. explains why when you go to certain. countries and have really good. ingredients, I often citing um Italy for.

like the pasta and things like that. where they don't have fruans, you don't. have the same response. But also it. could just be the total net. carbohydrates that's causing you to feel. Could be the calorie reduction. that's causing you to feel Um or. many other things like you know so like. placebo is one of the things they think. it might be. I'll give you one other. thing not mentioned and that is that. in America um though we don't have GMO. wheat GMO genetically modified u crops.

are created such that glyphosate or. Roundup can be sprayed to kill the weeds. but the plant is resistant and will. survive. So they've not really done the. GMO wheat thing yet. So therefore you. would think there wouldn't be any. glyphosate on the wheat. That's a wrong. assumption. Glyphosate in America is. sprayed on the wheat to desiccate it, to. dry it out so they can get more wheat to. market more quickly. And that might be. another factor. Why? Because glyphosate. is residual in these foods that we eat.

And glyphosate has a significant effect. on the gut microbiome. >> Uh okay. So it could be the chemicals. they're spraying on the food as well. >> That's right. And you know, we were told. uh that the science was that the. glyphosate only affects plants and since. you're a human, you shouldn't worry. about it. Well, it affects plants and it. affects bacteria. But again, we humans, why should we care? Well, we've got. billions and billions of bacteria that. live within us we depend upon to be. healthy. So, here we are now consuming a.

chemical and it's in all of us that can. affect the bacteria that live within us. And here's another bit of a stretch, but. I think really fascinating. Mitochondria. were originally bacteria. And these uh. mitochondria are very much still like. bacteria. They have a circular DNA like. bacteria and they are sensitive to. glyphosate. Glyphosate is a. mitochondrial toxin. So that's what we. are consuming when we are consuming. foods that have been sprayed with this. herbicide.

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head to piperive.com/ceo. to get started if you're in sales and. you run a sales team. I don't think. you'll regret it. What I'm about to say. is an ad. the company paying for it. really, really, really have changed my. business. They reached out to me about. three weeks after I posted this. particular Slack message to my team. saying how obsessed I was with this. product. I almost feel like I'm letting. the cat out the bag by telling you guys. about it, but I'm going to because I. like them. Crockbot now sponsors this. show and I've already invested in. SpaceX, which is the company that owns.

Grockbot. Grockbot is an app on my. phone, but it's also on my computer. And. basically I have all of these different. agents. You can think of them like team. members that are working with me to do. work right now. Like this graph here is. a graph showing my usage and my team's. usage. In 4 weeks, daily use rose from. 100 requests by one person. to about 63,000 requests. It has taken. hold. It's freed me up again to do the. things that only I should be doing as a. creative, as an entrepreneur, as an.

investor, which is the sort of higher. level things around taste, creativity, judgment. You will get more done with. Grockbot today. And you can get 50% off. your first month by heading to x.ai/ac. x.ai/doac. What about these other things? What's. your take on some of these other foods. here? What I'm seeing here are wonderful. foods. This looks like chocolate, on uh. onions, uh blackberries, uh I think this. is supposed to be Himalayan tartar, buckwheat. So, these are foods that are.

rich in We'll leave the alcohol here off. the plate for just a moment. These are. rich that are foods that are rich in. what are called polyphenols. That's what. gives them their colors. Uh that's why. the blackberry is black. It's why the. onions are colored. We have blueberries. and I guess raspberries as well. You. know, do they contain sugar? Yes, they. do. But they contain sugar in a way that. is released more slowly into the body. and again coupled with the polyphenols. These are are chemicals that are read by.

our gut bacteria. In other words, these. are signaling our gut bacteria to do. good things to increase their. antioxidant production to create. chemicals that are good for the entire. body. So, uh we're in a sense nurturing. ourselves but we're also nurturing our. gut bacteria. This Himalayan tartery. buckwheat is probably one of the richest. sources of these polyphenols on the. planet. What's a polyphenol and how does. that help my brain? >> So again, a polyphenol is a a targeting.

molecule that uh activates pathways to. create antioxidants in the body. They. activate a a pathway called the NRF2. pathway and that increases our. detoxification. It increases our. production of antioxidants and it. reduces inflammation. So all the good. things. What I'm not seeing here is the. number one source of polyphenols on the. planet at least in terms of consumption. That is coffee. So there's a vote. Oh, well close enough.

>> So there's a vote for coffee. But. there's very little polyphenols in these. uh highly processed or what we call. ultrarocessed foods. In America, 60% of. the calories that adults consume are. derived from ultrarocessed foods. They're processed such that these. polyphenols are processed out of the. foods and what we're getting are foods. that by and large have added sweetener. and have all kinds of issues uh related.

to their even just the processing of. them. I'll put up all the foods with. strong levels of polyphenols on the. screen now so everyone can see. Um and. I'll rank them by how much polyphenols. they contain per 100 g in order so you. can see if you eat some of those. Um, extravirgin olive oil is one of them. that I love and I eat a lot of because I. had it contains lots of polyphenols. >> It does. And you know, it's really one. of the keys we've now come to understand. of the so-called Mediterranean diet. Uh, you know, unfortunately now, if you.

travel the Mediterranean, you'll see. that they're eating not the. Mediterranean diet anymore. And I'm I. like that you have chocolate on the. plate, by the way. Chocolate's good. >> Chocolate's good. Polyphenols. >> Dark chocolate, though. I'm guessing. >> dark chocolate. So the number that you. look for is you want to go north of 80. >> 80%. >> 80%. Yes. Because the higher that is, the lower generally is going to be the. sugar content. >> I had the opportunity to make some. chocolate in uh Peru, and it I'll never. forget the day. >> Well, tell me about it. I've said this.

story before, but they gave me this like. massive tub that was like this big. And. he and he was like, "We're going to make. white chocolate first." And there was a. big bowl of sugar like this. And he. goes, "Pour in 60% or it might have been. 70% of the white sugar into the into the. bowl." And I was like, "What?" He was. like, "Pour 70% of the sugar." And I. filled it up to here with sugar. And. then he was like, "And then there was. this liquid we poured in.". >> And I was like, "Wow, the white. chocolate I eat is 70% sugar. Milk. chocolate.".

>> I love white chocolate. >> Really? >> Abs. Why wouldn't why wouldn't you? >> I know. Your brain is programmed to find. sweet. That's your survival mechanism. It tells you that the food in nature is. not poisonous and it helps your body. store fat for for the winter. I mean, it's that's what our genetics do for us. That's through activation of uric acid. >> And then milk chocolate was like half. the size. It was about 50% and then. obviously dark chocolate is. >> right. And and you know, you could go. overboard on any of this and certainly. go overboard on the chocolate. But you.

know the traditional diet that humans. and protohumans consumed was one that. was rich in fiber uh which these foods. are rich in polyphenols as demonstrated. by the different colors that you see. here and and had very good levels of fat. the the castigated fat the lowfat this. the lowfat that that we were so. programmed to gravitate towards and and. you know it gets I think to the broader. theme we'll do we'll do some alcohol in.

a moment. broader theme of of really the central. issue here in terms of what's making us. sick is this mismatch between what our. genetics expect and what our genetics. are seeing. In other words, our genome. that we are gifted from all generations. who've come before us, it's been refined. generation after generation. in our. genome. Right now, we are experiencing. this incredible mismatch between our. evolution, meaning our genes, and our.

environment. I mean, I think that's a. central issue related to modern. ailments, that we are living a life that. just doesn't send the appropriate. signals to our genome. And I've been. interested in this for since I was 15. I've heard you say that people with type. 2 diabetes have a 300 to 400% higher. risk of Alzheimer's. Some studies have. shown that. I think a number that we can. uh absolutely support by more recent. data is at least 75 to 85% increased.

risk. Wow, that's a big number. But what. people may not be aware of is that even. Parkinson's disease is increased in the. type 2 diabetic by about 85%. Why would. that be? Because when you look at the. the Parkinson's brain, and this data. became evident in the late 1980s, you. see activation of the microgal cells. destroying that part of the brain called.

the substantion, the black substance. that makes dopamine. It's an activation. of the microgle cells. The original work. was was fascinating. It was uh it was. seen at Stanford University when. suddenly people started showing up in. the emergency room who developed. Parkinson's in one day from shooting an. IV designer drug. that was contaminated with something. called MPTP. and that was a mitochondrial toxin and. it it basically fried those cells in.

their brains that made dopamine and. became a powerful research tool. I was. at a conference last week where MPTP was. used in laboratory mice to create uh to. damage that part of the brain, create. Parkinson's. And now they've developed a. an offset for that. They're giving the. mice MBT, but giving them something else. called RNS60. that was able to keep these mice from. having that damage occur by activation. of their microgal cells. So, what is. this?

Well, it looks like a brain of a very. long animal like an alligator, but I. think it's body fat or I think it's fat. >> Not that pleasant. That's a pound of. fat. And you don't want it here. You do not. want it here. >> You don't want it on your belly. >> No, you don't want on your belly. You. don't want it around your organs. That's. called visceral fat. So, um, you know, when you're 30 lb overweight, over ideal. body weight, that's 30 of these. Think. about that. And that's common. I mean, it's so incredibly common. So, this is.

an organ. It looks like just stuff. We. used to consider fat as being pretty. inert, but as a resource for calories, we could tap into body fat if we needed. calories if we were starving. That's. what it's intent is. But it is creating. chemicals that have function throughout. the body. And by and large, these are. chemicals that are damaging. They're. pro-inflammatory chemicals called. cytoines. We think of flat fat as just. being the byproduct of its storage for. the food we ate, >> right? And it we don't think of it as an.

organ or that it's secretreting or doing. anything. But you're telling me there's. chemicals coming off this? >> You bet there are. There are. pro-inflammatory chemicals that are. secreted by uh by body fat. And they're. not necessarily always bad. I mean, even. the notion of inflammation always being. bad, we challenge. We need inflammation. If we suddenly were able to reduce uh. all the inflammation in your body. immediately, you would perish. You need. to have the inflammatory response. It's. a life-saving activity. It's the.

excessive inflammation that gets us into. trouble or lower levels of inflammation. over a longer period of time. You know, people talked about. the cytoine storm in COVID. the cytoine. storm in COVID with this sudden. explosion of cytoines, inflammation. throughout the body damaging uh. everything. And I I think that we should. consider things like Alzheimer's as not. a cytoine storm, but as a cytoine. drizzle, that this is still an uptick of. inflammation, though slight, but it.

happens over a long period of time. And. we've got alcohol there as well on the. table. What is your point of view of. alcohol? I mean, they used to say that a. little bit of alcohol is contributing. Well, there was a lot of data that. showed that there was what we call a. U-shaped curve in terms of dementia. risk. What is a U-shaped curve? The very. lowest level, i.e. no consumption of. alcohol, there was a certain risk for. dementia. With consumption, then the. risk went down a bit. One glass of wine. per day for women, two glass wine per.

day for men, but then the U comes back. up. So, we thought there was a sweet. spot. uh and it turns out that. reassessing that indicates that really. any alcohol consumption is probably not. good for the brain even and I think. context is important. The argument was. well red wine has polyphenols visav our. previous discussion you know have a. glass of red wine we know that uh many. people in the blue zones for example. will drink some wine as do I from time.

to time but uh I find it threatening. alcohol itself is a neurotoxin and I. think it's let's get our polyphenols. from what you just described what you. just showed from coffee and extravirgin. olive oil I think I'll tread lightly. here at risk of becoming an internet. meme but Um, how does alcohol harm the. brain? >> It is directly toxic to neurons. and uh from my perspective, I think you. probably guessed through the lens. through which I see brain science these.

days, it helps polarize our microgal. cells away from being supportive. >> These things. Yep. >> The bad twin, the good twin. >> That's the good. That's the bad. >> The good twin and the bad twin. So, it. turns these into these. >> That's right. Are these all over the. brain? They're all over the brain and. they move around. They move around. >> Yeah. Uh that was what was so exciting, that discovery that, you know, originally when when they were first. discovered, you would see these little. cells interspersed between the neurons.

on a slide, you know, that of a dead. slide. And it was thought that they are. small, they're called micro, and they're. ga meaning glue. It was thought that. they glued the brain together. Glu glued. the brain cells together. Then. technology evolved that allowed the. observation in living tissue and noted. that they're moving all around. They're. swimming around looking for something to. do, looking for something to repair or. conversely looking for something to. destroy. And let's be clear, that is.

something over which we have control. So this good micro gleo cell is the M2. >> That's right. And then the bad one, the. evil twin is the M1. >> That's right. And alcohol flips the M2. into the M1. Alcohol, high blood sugar, inflammation, stress, sedentarity, um lack of restorative sleep, all the. things, even social isolation. And then.

when we have the M1, the evil twin, how does this then. directly increase our probability of. getting dementia? What's the mechanism? Those microgle cells create uh havoc in. the brain. They destabilize our neurons. They destabilize the bloodb brain. barrier. So now we're letting things in. that can make the problem even worse. Most fundamentally, they destroy. synapses. So neuroscience is now looking at. Alzheimer's as what is a new term, a.

synaptopathy, a disease of the synapses, a loss of the synapses. And you know, interestingly, I'll connect this segue. for you. What is our answer for the. question, why do women have twice the. risk of Alzheimer's in comparison to. men? Is it because they live longer? Not. really. What's going on in the female. brain? And what has recently been. identified is this sudden drop of. estrogen, particularly one estrogen. called estradiol at menopause. causes the synapses to be labeled with.

signaling molecules called compliment. That is basically uh what what is called. an eat me signal. There's a Dr. Beth. Stevens at Harvard who's done some. amazing work. >> What you mean eat me signals? >> Destroy me. The syninnapse binds a. chemical called compliment. And. compliment triggers these microglea and. it says for you M1 micro ga come and. destroy this syninnapse. I mean she's. she's demonstrated this. You can.

actually see it happening. It's pretty. breathtaking. So the evil twin is. receives a signal to come and destroy. parts of the brain. >> It's directed right to the syninnapse to. destroy that syninnapse. >> Why would the brain be doing that? >> Well, good question. These cells are. activated for the reasons we've talked. about. These metabolic changes, the. inflammation, the exposure to polluted. air, breathing these PM2.5 particles. from wildfire, all of the things that. are known to activate this microgle and.

cause it to do that. But I think more. importantly, you know, this explains why. uh when we age, we're at higher risk. It's really, I think, the most exciting. and fundamental uh area of neuroscience. research right now. So, how does it. work? What's the research doing now? Well, all kinds of cool things are. happening. There's a Dr. Leeway Sai at. MIT, and what has she done? She's. demonstrated that the nonAlzheimer's. brain has a beautiful background rhythm.

called gamma oscillation, a beautiful. syosoidal rhythm underlying the brain. The Alzheimer's brain has a disrupted. rhythm. It doesn't have that beautiful. syosoidal rhythm. and she stumbled upon. the idea that brain rhythms change based. upon frequencies of light that are put. in front of a laboratory animal. And she. found in the laboratory uh rodent that. is geared to get Alzheimer's that is one.

of the experimental tools that we use. that a light flashing at 40 times per. second 40 hertz. How how do we discover this stuff? who. knows, restores the background gamma. And she said, "Well, that's interesting. I wonder what effect that's going to. have in humans." And what she found was. 40 Hz light and 40 Hz sound. She has a. device that does this. Restores this. gamma oscillation in the brain and. reverts microgle cells back to being.

supportive. >> The evil twin cells, >> the evil twin back to being supportive. So she's actually done this technique in. humans with Alzheimer's. >> So what does that mean for us? Like for. the average person, >> I have a 40 Hz light generator on my. desk, you know. >> Oh, really? So you can go and buy. >> that I do. I mean, >> what what does that do for you according. to the science? >> Oh, according to the science, it is. keeping my micro GA uh doing what they. need to do. She's actually done. interventional trials in patients with. existing Alzheimer's disease, and her.

results are better than any drug that. targets beta amaloid. The beta amaloid. drugs are the FDA approved treatment for. beta amalloid. And I make it very clear. uh in my recent book that these drugs. are for the most part ineffective and. significantly dangerous. And my vote is. that they are not to be used. 40 Hz sensory stimulation most famously. pioneered through strobe lighting, flickering LEDs or audiary clicks, has. emerged as one of the most intriguing.

non-invasive approaches to recruiting. micro glear to clean up the brain. >> Wow. Can you imagine? I mean, that is a. why that's fantastic #WTF. a moment. It's breathtaking. You flash a. light and you hear a sound and your. micro gle cells revert back to being on. your side. So I I keep a device right by. my by my computer screen and it's. passively shining that light into my. eyes. Can I prove that it's doing. anything wonderful for me? No. But am I.

a believer in the science? You bet I am. In animal models, just 1 hour of daily. 40 Hz light stimulation drove. significant drops in plaque and tangle. burden. H I mean it goes on and on and. on. I'll put some of that data on the. screen. Um just closing off on this. subject of of alcohol, you said in your. book on page 102 about this study uh. where they found that microia exposed to. binge level alcohol for 24 hours showed. a 15% decrease in their ability to clean.

out beta amalloid. Exactly. So someone binge drinks for 24 hours and. the microia. drop in their ability by 15%. um as it relates to their ability to. clean out that beta amaloid which is the. plaque associated with Alzheimer's. >> Yeah, it's the plaque associated. It's. not the pivotal player, but it's. important. I mean, uh we need to unpack. a little bit more about this kind of. misdirection of targeting beta amaloid.

It's a player. There's no question. But. I can't afford uh a 15% reduction. I. mean, they're already downregulated. uh towards M1 because of my age. So, you. know, uh that's the vote against. alcohol. And you know, even one uh night. of non-restorative sleep does the same. thing. Even more so. >> Interesting. >> One night of not getting a good night's. sleep dramatically reduces your ability. to clear beta amaloid. >> Can you recover from that? Cuz there's. going to be a lot of people thinking,

"Fuck, I had, you know, seven bad nights. last week.". >> Or or does. >> I'll tell you one thing. I mean, I know. you travel a lot between LA, New York, and Monday, and I don't know how you do. it. >> Yeah, it's a lot. Yeah. And then fly. back to Europe. But I I do this is why I. think about all this stuff so much. because I'm like what I do now at the. age of 34 really is going to compound. >> Yep. It really really is. >> And I'm gonna figure it out the mistakes. I made. >> Yeah. I mean, you know, in neurology. school they again they teach you, well, how do you what do you do for the. Alzheimer's patient once the problem has. begun? And great. I'm glad people are.

looking at the doing research, but it's. setting, you know, sewing the seeds at. your age is when it really begins. Let me take this. There's one. interesting study that was just. published and it just blows my mind. It. was done uh looking at women who. conceived in the year 1953. right where you and I are sitting right. now here in England and whether they had. sugar rationing or they didn't have. sugar rationing at that time. The sugar.

rationing from World War II was still in. place in 1953. And it it looked at a large cohort of uh. women and followed them. for a number of years uh to when people. became I guess so followed at least 50. 60 70 years and what it found was the. women who had sugar rationing who. weren't able to get sugar while they. were pregnant and for one uh thousand. days so through pregnancy and then the. first couple years of life the risk of.

that child now that that child is 60 70. 80 years old developing Alzheimer's was. reduced by 40%. because mother didn't have access to. sugar when she was pregnant. Wow. I mean, you know, people are always. saying, "Well, Dr. Promoter, when should. the Alzheimer's prevention program. begin?" You know, my standard response. is, "Well, you know, we got to be paying. attention in our 30s and 40s." Uh, but.

this really winds the clock back, doesn't it? What is the mechanism though? I think. there are multiple mechanism. I think. you know sugar in and of itself raising. blood sugar uh compromises brain. function and even the genesis of the. brain. But I think sugar also changes. the millu the makeup of the gut bacteria. and the study actually didn't really. comment on that but I'm kind of. sensitive to that. Higher levels of. dietary sugar change the array, the. function, the diversity of the bacteria.

and other organisms that live within the. gut like yeasts for example. >> And the baby has the mom's gut. microbiome. >> Uh actually no, the baby does not really. have much of a microbiome until such. time as it's born. The method of birth. is really fundamentally important for. the development of that newborn's. microbiome. In other words, cesareian. section versus a vaginal delivery has a. huge impact. When a baby passes through. the birth canal, it's being anointed. with a special concoction, a special.

array of organisms in the birth canal. >> Bacteria, >> bacteria and viruses and yeast, all. kinds of organisms that get in the. baby's eyes and its nose and its mouth. And it I call it an anointment. It's. it's a blessing, right? that this. newborn gets his or her microbiome. started seated at that moment based on. how it's birth uh birthed being born by. cesareian section that newborn will.

develop a microbiome based upon what was. on the surgeon's glove at the time that. baby was delivery delivered in fact. there is research uh being done I think. at NYU. many women are probably familiar with. this where if they're going to have a. C-section they take a swab of the birth. of the vagina. Baby is born by. C-section. Then that swab which still. contains those secretions is placed in. the baby's nose and its mouth to help. restore that um specific type of of.

microbiome. >> What is the link between the microbiome. and Alzheimer's and dementia? >> Well, I think the link is is uh is quite. profound. And I think that we've got to. understand that these organisms are. making things that are good for the. brain. uh they're making very types of. short- chain fatty acids for example. that are important for brain. functionality. The microbiome these. organisms are secretreting chemicals. that are changing gene expression. throughout our bodies and of course in.

the brain. I think the biggest issue. when we have uh changes in these. microbes that can be brought on for. example by taking certain medications. Oh we we happen to have them here for. example proton pump inhibiting drugs. These are acid blocking drugs that. people take because they think they need. to lower their stomach acid based upon. what they're seeing on television or. elsewhere. And when you change the pH of. the gut, you're changing the organisms. that live there and their function. And.

when you do that, it can lead to. increased leakiness or permeability of. the gut lining. That sets the stage for. inflammation in the body. Those. inflammatory chemicals can then make. their way throughout the body and make. their way into the brain. What do they. do there? They polarize our supportive. loving M2 microg GA to being. destructive. Remember those TSPO images. that show. >> TSP? >> TSPO images that show. >> what's that? These are the images the.

the type of receptor the TSPO receptor. that is found on the M1 dangerous micro. glea that we can actually attach. something to and then scan it. Uh PET. scan remember that that shows activation. these micro ga explain it's like on 14. So again, the TSPO is simply a way in. living humans to demonstrate activation. of their microgal cells, >> which are these. >> immune cells, >> these evil twin things. >> Yeah. Let me let me be a little kinder.

to our M1 microglea. There's a time and. a place. when we have an acute injury, acute. infection, we want to have that type of. microbial cell to do its job to destroy. or to neutralize. When we have a head. injury, for example, we activate our our. M1 microglea, >> but we have to be able to revert back to. being the supportive microgle cell, >> the the healthy one. >> When we keep our micro glea in their. destructive um phenotype or.

configuration after the event has. occurred, it leads to delays in. improvement or even lack of improvement. >> Improvement in what? >> Good question. We know that these uh. football players for example get this. encphylopathy that when they bang their. heads playing football too many times. they experience this progressive. neurodeenerative condition that. ultimately may kill them but they're not. banging their heads anymore. Why so?

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cometier.com/stephven. today. That's cometier.com/stephven. >> Oh, so it's kind of like boxers who. finish boxing, but then gradually you. watch them deteriorate. You watch their. speech slur. >> memories. >> We're both right now thinking about. Muhammad Ali. >> How tragic was that? Right. That's. called pugilistic Parkinsonism. Impugilist means a boxer. But any bump. to the head uh you know whether it's uh. playing soccer uh there was a study that.

came uh out last week that looked at F1. drivers as being at risk. The first F1. driver I think that developed the CTE. chronic traumatic encphylopathy made the. news uh just a week ago. I mean you know. I guess you're banging your head around. when you're in in that car going that. fast. But you got to protect your head. You really got to protect it against. trauma. interesting study that shows that if you. have head trauma, it's going to happen, you know, to all of us maybe that your.

risk of poor outcome is increased if you. happen to have been a type 2 diabetic. prior to the head trauma. Outcome of. head trauma in type 2 diabetics is much. worse. Why? Because that type 2 diabetes. is shifting their micro GA, preventing them from coming back and. being uh being helpful, being. supportive. Shifting it to the evil. twin. >> The evil twin. Exactly. Right. Okay. So, one of the big takeaways from this. conversation is the decisions I make in.

my everyday life, what I put in my. mouth, the exercise I do or don't do, the alcohol I do or don't drink, um is. all going to impact this ultimately. That's that's the event. And upstream of. that. are the changes in the mitochondria, the. energetics of what is going on here. That is playing a really important role. such that you know we are now looking at. what can we do to enhance mitochondrial. function because when mito mitochondrial.

function is restored it helps keep our. microglea in their supportive role. There are transplant uh techniques now. for transplanting healthy mitochondria. into human hearts and very soon into. human brains. There are ways that we. increase our our mitochondria in terms. of their numbers, in terms of their. function, and in terms of our ability to. get rid of defective mitochondria. Exercise does it and metformin does it. as well. This drug that is being used. right here in England now as part of a.

treatment pro protocol for Alzheimer's. Metformin is that metformin supplement. >> It's a diabetes drug. It's not targeting. beta amaloid, >> but the average person shouldn't be. taking that, should they? >> That's a great question. I was at a um. at a conference uh dealing with uh a. health span uh aging and it was very. small uh conference about 20 people. The. question was asked, how many of you are. taking metformin? This about eight years. ago and I think 80% of the scientists.

raised their hands. What you're not hearing from me right. now is that we should all jump on board. and take metformin. I prefer to. exercise. But there is a a big study. called the TAME trial. Neil Barzai at. Albert Einstein is trying to get this. started but looking for funding. It's uh. I think about a $70 million project. He. can't get funding because metformin has. gone off patent so nobody's going to get. the the brass ring at the end of the. day. But it's looking at the.

intervention of taking this drug. metformin uh to see what effect it has. on longevity and and dementia for that. matter. For generally healthy. non-diabetic people, the current. scientific consensus is not to take. metformin because there are some. potential consequences. Why routine use. in healthy adults is problematic. Number. one, it blunts the benefits of exercise. Apparently, exercise is the single most. validated reproducible longevity. intervention available. Multiple. randomized control trials have.

demonstrated that metformin actively. interferes with exercises adaptations. Number two is risk of masking lifestyle. fundamentals in long form clinical data. Intensive lifestyle modification. consistently outperforms metformin in. reducing cardiovascular risk. relying on. a pill to simulate metabolic health. cannot replicate the systemic vascular. and psychological benefits of movement, sleep, and whole foods and there's a. bunch of other known side effects. Okay.

So, interesting. It's almost like. replicating some of the effects of. exercise. Yes. But as you wonderfully. point out, look at the potential. downsides. And I I don't think mentioned. in this uh article was the uh. possibility of B12 deficiency that we. see uh in people taking metformin. you. know, um, Dr. David Sinclair, you've had. him on the program on the podcast. He. recently put out a paper several months. ago that looked at all these kind of. cool interventions as it relates to. these aging clocks that he he talked.

about and uh, it ranked them and Mitt. Foreman was described and rap was. described. what led the list and you. know and he's a big NAD guy as you know. uh what led the list was exercise in. terms of these age aging clocks so again. it gets back to this what did our. ancestors do they were active they. didn't suffer from you know this. sedentarity this idea that we're just. sitting on our butts all day flying here. and there in front of the computers and.

you know I to me this has been the the. central focus of my understanding as to. Why we are sick? I wrote a paper about. this when I was 15. And. >> 15. >> 15 I think you may even have a you have. a picture here of it uh in in one of. your photographs. Uh yeah, I wrote a. paper uh about it and it was published. in the Miami News. I think that is no. longer uh a newspaper in Miami. But I I. I I simply concluded that the world in.

which we live, we are not able to adapt. uh quickly enough, genetically enough to. be able to survive in the world that has. suddenly, you know, turned the tables on. us that we are not able to uh there it. is to the editor. >> So what is what is this? This is when. you were 15 years old. It is. Perhaps. the human will change rapidly in the. next centuries to adapt himself to beer. cans, concrete, and shattering noise. Our generations are each contributing to.

the evolution of pollution resistant. lungs. But what about the people of. today who are stuck with the outdated. machinery? And that was written by this. young man. You're about 17 years old. there, but nearly. >> No. Yeah, I guess. Uh I No, by 17 I had. grown long hair. >> Okay. >> So, yeah. Uh, I was a pudgy little one, wasn't I? That was my bar mitzvah tie, too, as a matter of fact. Yeah. >> Got a picture here of your son as well, >> Austin. >> Austin,

you look very similar. >> You look more similar now than. >> Well, I'm going to take that as a very. big compliment compliment. And uh more. than that, I would say uh. uh he's taught me a lot. >> He really has. uh in many ways he's a. mentor and it it's so wonderful watching. him become a father. >> Uh it has it's changed him in ways he. you know he cannot uh begin to to. appreciate. I think not yet but he will. and our daughter um watching her blossom.

as a an artist on the world stage. It's. just breathtaking to watch the two of. them. And again when when you have your. children I'm I'm going to come back or I. don't know what we'll do. I want to stay. in touch cuz that's it's going to be a. real gamecher for you. >> Did it change a lot of how you think. about the brain and the body and. longevity and all the subjects we've. talked about today? Preserving oneself. now that you've got a grandson um a. granddaughter. I would say that I've. doubled down uh I I have absolutely.

doubled down on everything that I do uh. to to be a grandfather. I mean I became. a grandfather kind of late in life. You. know, here I am 71 become my grandpa. Most of, you know, my friends who have. grandchildren, you know, their. grandchildren are, you know, in her late. teens already. So, I got to do the best. I can. And I think, you know, I don't. want to be do as I say, not as I do. I. don't want to be that person. I want to. be as transparent as possible with my. foibless and, you know, with the things. that I I I think are important. You.

know, I think fundamentally that. what we're talking about today. changes the ownership and the. responsibility. And perhaps there's a criticism there, but my my goal is to give agency. You. know, we offload our agency to the hope. of the development of cures, right? And. and James Cameron, the movie director, famously said that hope is not a. strategy. I want to provide a strategy.

to improve your odds of not experiencing. this cognitive decline that is not just. you know the a devastating issue for you. but by that time who knows your wife. your children and uh it's an awful. situation and the cost is profound. So. when I say that the drugs are. ineffective in the context of hope that. there will be effective drugs, I just. saw a powerful study come out of Havanic.

Huba of all places giving an intraasal. treatment of something called ariththrop. poetin which is something made by the. kidneys that had effects in existing. Alzheimer's patients that were. mind-blowing. I mean patients who would. have declined who did decline in the. placebo group by four points on a. standard scale that we use improved four. points. So what didn't just stabilize. they they got better. For those people. that do have Alzheimer's or have a.

relative that has Alzheimer's now I. imagine there's a lot of them listening. I I know that because when I have. conversations on this subject matter the. comments typically fill with stories. People who have been diagnosed, loved. ones have been diagnosed. A lot of the. reasons why they click on these videos. is because they've just received a. diagnosis or they're living with it and. they're in search of answers. What what. is there that we can offer to people who. unfortunately are now dealing with. dementia in their family or within their. own brain? Well, what what do we offer? And why. should you believe me, right? Why should.

you believe some guy that's on your show. that is, you know, I'm swimming upstream. here. I am indicating that what at least. in America the FDA has approved is not. the way to go. I'm indicating that when. we look at a relatively small study from. Harvard University obviously well. respected by Tany and Rudolph Tany Dean. Ornish where they took a group of 51. individuals who have Alzheimer's disease. or mild cognitive impairment going to.

have Alzheimer's and they changed their. lifestyle. They increased their. exercise. They changed their diets. They. reduced their stress and they had to. meditate for an hour a day. So these. people didn't just slow their decline in. the relatively short intervention of 20. weeks, but 70% of them either stabilized. or improved. What did they do to their. diet? >> They put them on a plantforward more. Mediterranean type diet. A diet rich in. the things that we just looked at. Rich.

in polyphenols, rich in color. welcome. back to the table fat but the good fats. and encourage social interaction is. people improved. So that's what I say to. this hypothetical. That's what I say to. anyone who's listening that pay close. attention to your blood sugar. Get your. weight down. And most importantly, this. powerful tool that we looked at, a pair. of running shoes. That is the salvation.

in my opinion. What did the Cochran. analysis that was just published say. about these Alzheimer's drugs? We've got. to talk about it because I wrote in my. last book the idea that I am not in. favor of the use of these amalloid. targeting drugs. And why would I say. such a thing? I mean after all they are. FDA approved. I said it because they are. for the most part ineffective and they. have a significant risk profile. So this. cockrine analysis looked at 20,342.

individuals in 17 different studies 18. months each study and asked two simple. questions. Do the drugs work in the. Alzheimer's patient that target beta. amalloid and are they safe? Right? Those. are risk and benefit. Right? They found. that the drugs basically have no. meaningful effect in slowing the. progression, much less leading to. improvement. >> What about the ketogenic diet as a way.

to deal with the symptoms of dementia? >> Well, I think more than the symptoms, I. think when you're talking about. ketogenic diet, you're targeting, as you. well know, the mitochondria. Ketogenic. diet along with exercise, we're. targeting mitochondrial function. And. remember that that is a the pivot point. for determining supportive versus. destructive microglea. >> And by keto diet, for anyone that. doesn't know, we basically mean a very. low carb diet, less than maybe 50 grams. of carbs per day. >> significantly with the addition of more.

fat to the diet, good fat, the extra. virgin olive oil with nuts and seeds. In. clinical trials on mild cognitive. impairment and early Alzheimer's, a keto. diet or ketone supplementation, which. you can get through various ketone. shots, rescues roughly 10 to 18% of the. brain's total energy supply, directly. closing up to 80% of the fuel gap left. by impaired glucose metabolism. This. energetic boost translates up to 15%. improvement in standard memory and test.

scores alongside a 20 up to 20% gain in. daily functioning, helping patients. manage basic self-care and everyday. tasks with greater independent. independence. Sorry, who knew? When you. target mitochondria, it's a good thing for the brain. I mean, it's a metabolic issue. The brain. requires glucose and when we become. insulin resistant, certain parts of the. brain suffer. Not all of the brain cells. require insulin, but some parts do. The.

hippocampus, the memory center, the. hypothalamus that controls our. metabolism, the prefrontal cortex, which. allows us to make good decisions and. helps direct our behavior, and finally. an area called the olfactory bulb, which. is involved in smell. When you think. about it, everything I just mentioned. are are issues in Alzheimer's. We become. forgetful. our metabolism goes. catawwampus, we lose executive function. and we lose our sense of smell. So you are so right to point that out.

that this is an upstream energy. deficiency, the inability of the brain. to use energy. You can bypass that with. the keto ketogenic diet and also in. Parkinson's. There is a researcher in. New Zealand named Matthew Phillips who. has published papers on each of those. and I wrote a book chapter with him on. the use of the ketogenic diet in in. Parkinson's. >> It's hard to adhere to the ketogenic. diet though, isn't it? >> And I'm not saying one needs to do that. at all times. I think what you want to.

try to establish is flexibility. such that when you do decide you're. going to fast for a day or two or one. meal and and stick to the very low carb. and higher fat regimen that you're able. to jump into ketosis relatively quickly. as opposed to having to adapt to uh. ketogenic state which may take you know. a couple of weeks. Dr. David, what is. the the most important thing we haven't. talked about that we should have talked. about as it relates to Alzheimer's, dementia, and generally just having a.

healthy brain for those that maybe. aren't thinking so much about a. disorder, but just want to be able to. show up in their lives on a daily basis. and be their best. I mean, I'm one of. those people because obviously, you. know, I have conversations with doctors. sometimes and. >> Yeah. But who isn't one of those people? >> I mean, true. Who could you speak to uh. who would say you know I really am not. so invested in having my brain perform? Everything that we have talked about. today in terms of brain degeneration is.

equally valuable in terms of brain. performance. So that was a wonderful. segue. So if you want your brain to. perform at its optimal level, these are. the exact same keys to the kingdom. >> We've got a few. >> you've got some goodies in here. There's. other things in your toolbox here. We've touched on some of them. Um, are. you a fan of supplements? >> I am. >> You are? >> I absolutely am. >> What particular supplements do you take? >> Well, I have a bit of a first the.

personalized medicine part of that. answer is I have a little bit of a. genetic quirk. >> Uh, goes by the name of MTHFR. And what. that means is I don't handle B vitamins. as well as I should. And as such it's a. complicated story but my homocyine level. was elevated. Homocyine level homocyine. itself is an amino acid that is a. significant risk factor for heart. disease and Alzheimer's. >> Okay. >> So because of my unique genetics I have. to take a different type of B vitamin.

called methylated B vitamin. So that's. first and foremost for me. >> vitamin B methylated. Yeah, >> methylated for me and for probably about. 25% of the global population. >> What else do you take? >> I take DHEA from fish oil. >> So, is that omega-3? >> Omega3. But we want to look at the DHA. content. So, my fish oil that I take uh. contains uh I'm getting about 1,000. milligs a day of uh DHA. When.

we talk about people that are living. with someone with Alzheimer's, you know, we often hear from the family what it. was like to essentially lose the person. they loved. >> Yeah. >> What is it like for the person that has. Alzheimer's? It's a great question. I. think early on it's incredibly. distressing. And you ask people what. disease do you fear most? Overwhelmingly. the answer is Alzheimer's. It's not. cancer. It's not heart disease. It's not. anything else. It's losing the ability. I think uh to make your own decisions.

and selfcare. >> Do they know that they're losing it? >> Early on, yes. >> Early on they do and it gets to a point. where they don't realize and that's a. blessing. I watched that happen to my. dad. >> Really, >> he was, you know, ultimately became. unaware. You know, when you lose these subtle. cognitive functions early on, you know. damn well something's going on. >> How long did that take in his case? >> Yeah. between diagnosis to his death I. should say from when you know when his.

behavior changed to his passing took. about 5 years. >> 5 years. and is it the disease that. ends up killing the person or is it. something else it's the disease it's the. disease yeah everything ultimately just. shuts down he did not I don't believe. carry AP E4 I don't know what his. genetic profile looked like I do not and. I don't know my mother so I can't figure. out what whether my dad did carry the. APOE E4 or and to be sure there are 80.

other genetic issues that relate to. Alzheimer's risk. But again, genetics uh. loads the gun. Lifestyle lifestyle pulls. the trigger. >> What were those five years like in terms. of how he changed? >> Well, you have to start at his baseline. He was a towering human. uh just in. terms of you know his contribution and. his compassion and to be fair to others.

more so than to family call it out like. it was which is something I've I've. worked through which I think helps. explain why I've been as driven as I. have been throughout my life to um get. recognition that perhaps I could have. gotten earlier in life. I'm not sure I. had planned on going to this part of uh. this topic in our conversation, but what. what the heck. But that said, um when he. was aware of it, uh his uh he was one to. deny uh and off offload blame. I never.

said that or you must have misplaced. this or and became a bit accusatory of. things that were happening. When he. couldn't find things, he would accuse. people of of moving things around. And. then as um as it progressed, you know, his uh issues became less and less of an. issue for him and more and more of an. issue for all the rest of us. >> Was there a moment where he realized he. had his brain was changing?

>> Yes. And so did he shift out of that. accusatory state and start understanding. that this was. >> No, I don't think he had the tools at. that point. and and um by circumstance. the nursing home in which he lived, his. apartment in the nursing home was across. the uh parking lot from my clinical. neurology Alzheimer's practice such that. I could see his room from my examining. room and I'd be meeting in the examining.

room with families of patients and um I. could see his room while the. conversation ations are going on. And. they'd say, "Doc, you have no idea what. we're going through with mom or dad.". And I would stop and I would say, "Let. me hold you right there just so we can. relate as humans. That room that you see. across the parking lot, that's where my. father lives now and he's dying from. this disease. So, I get it. So, now you. know who your team player is.".

And gradually the decline meant that he. didn't know. who he was. Oh, beyond that, he didn't, you know, he was totally unable to. function. That's the end endgame in in. Alzheimer's. It's a a total lack of. ability to engage any meaningful. interaction with others or any. meaningful activity. You're just in bed. with a blank stare on your face. It's it's uh and when you see your.

parent like that and think. and you think back to uh to who he was. and what he was, it's uh it's difficult. and I don't want people to go through. that. I really don't. And if I'm a pain. in the ass by saying the things that I. say about don't put your faith in the. drugs and make these changes today cuz. they're hard and I wish medicine would. do these things. I'm not going to.

apologize cuz that's what answers your. very first question. What am I doing? I'm doing my best so people don't go. through to have to experience what I'm. feeling right now. And you know I'm this. was a long time ago and I'm a 71y old. man and I'm not over it. And I realize. I'm not ever going to be over it. And. that's not a bad thing because it's um. it motivates me. It gives me the courage. to go before your audience. I know that.

it is vast and to make these statements. because if one person gets this message, then I've done my job. And my hope is. that a lot of people get this message. that. we need to regain agency and not be. persuaded to. hope that there's a wonder drug out. there. That's just inappropriate. It's. wrong and it's absolutely cruel and I. object to it. Well, you're a dad. yourself now and you have this wonderful.

son called Austin. I actually spoke to. Austin and Austin wrote uh wrote a. little letter for you. Here you go. This. is from uh your son Austin. Okay. And the winner is. you can read it. I will.

that. for the entirety of my life, you've been an example of passion. personified. Whether it was for your patients, your. family, or the millions of people you. reach on podcasts like this one, you've always cared so much about. helping others and empowering us with. tools to make our lives better. I'm so proud to watch as you help people.

understand and improve their brain. health. It matters. I see it in the messages I get from. people telling me just how much you did. for them and their families. I hear it. at conferences when people tell me about. the things you did for them decades ago. I'm honored to have you as my father. And most lately, I'm filled with the joy to see become an. exceptional grandfather.

You are an incredible continuation of. the work of your father. I can't wait to see you soon. Love from all of us across the pond. Austin. Well, uh, Stephen, you you you really did it. here, didn't you? Um, you know, uh,

I'm thinking of my dad right now and we. go through our lives trying to, um, do the right thing and he set a very. high bar. He really did. You know the. Daly Lama said that if you want others. to be happy, be compassionate. And if you want to be. happy, be compassionate. In many ways, these are tears of joy. I. am so.

happy with how it's playing out because. I'm in my lane. It feels really good to. be in my lane and doing having. identified what my skill set is and. exploiting it to the ends of the earth. That's what it's all about. Probably a. better answer to your uh opening. question. I think that's enlightenment. I think enlightenment is identifying. your skill set and using it to. contribute. And uh and there you go. And I guess uh.

I will continue as I'll continue as long. as my brain holds up and I'm doing all. the right things. So hoping that it it. does. As Austin said, you are a wonderful. continuation. of your father's work. Um, at his. eulogy, um, I sang, I think it's a Dan Fogleberg. song. Um, just a line from a Dan Fogberg. song. I think I got that right. Attribution. And it was, uh, my life has been a poor.

attempt to imitate the man. I'm just a. living legacy to the leader of the band. And. why not, you know, why not uh continue. on the legacy and. teach by example? Doctor means teacher. It doesn't mean healer. So that's what. we do. That's what you do. You know, all. the things that go on on this podcast, it's all about teaching. whether it's.

about you know um should we take. creatine or or should we not take. creatine and what's our dosage and. what's the research or what is the cause. of aging. You've asked that question so. many times. How do you define aging? It's teaching and it's it's um. it marries curiosity with compassion and. that's a great marriage because. curiosity gives you the tools to really. be compassionate and at least in. medicine it sure does.

Amen. Everything we've uh talked about today. comes back to this old fella, the brain. What are your closing words for people. about their brain? What can we say to them to to make sure. that they walk away from this. conversation and they do everything they. can to protect this? And I'm going to. amplify that a bit uh from a personal. perspective, what matters and from a global.

perspective. In a word, reconnect. If we reconnect with others and. reconnect with relationships, it will go a long way to improving our. lives, improving our brain health, and. improving the planet. Austin, as you know, and I wrote a book. uh called Brainwash. It's right there on. top. And we define in this book. something called disconnection syndrome. at a microscopic level. And we talked.

about that how the brain gets. disconnected from its prefrontal cortex. Our gift as humans and on a macroscopic. level how disconnected we're becoming. from each other. There's personal. benefit. We talked about that through. oxytocin. But we've got to reconnect. with each other. We got to reconnect. with the planet. And we're all in this. together. That would be I think my most. important message. Well, you certainly. are one for a message. I mean, you've. written so many incredible books here. Your most recent book called Brain.

Defenders. um is came out I think the day after my. birthday, August 27th. I'll link it. below. Brain Defenders: Harness the. power of your immune cells to protect. your brain for life. And I know there's. lots of my audience that are especially. keen to avoid dementia and Alzheimer's. because it runs in their family. Um and. they've seen the horrific consequences. of of of the disease. And this is a. wonderful book to feel to sort of take. back a bit of agency as you describe and. feel like there is some control over. something that feels so helpless.

>> You bet. And um. you're a good man. You're a sweetheart. And um I'm sure grateful to to meet you. and spend time with you today. I am too. It's wonderful what you've. done. you know, the consequence of, I. guess, your father is is you and the. millions and millions of people that. you've reached and helped, given them. some information, turned the lights on. in their life, which gives them that. agency that we describe. And I think. agency's most valued at times when we.

feel hopeless and that's certainly what. you've done for so many is give them. both actions that they can take, but a. sense of hope and that's really truly a. wonderful thing. So, thank you for doing. that work, Dr. David. >> Thank you, Steven. >> It's incredible. We we do have a closing. tradition where the last guest leaves a. question for the next. Oh, wow. Not. knowing who they're leaving it for. And. the question left for you is. Oh, no. I usually don't let guests see this, but.

I'm going to break the tradition in this. case. This is the question left for you. Oh my gosh. So, it's from Mark Hubin. and we've answered the question. The question is, Mark, to answer your. question, what makes you emotional? It's. an excellent question, but uh I think. we've answered your question, >> Dr. David. Thank you. >> Thank you. YouTube have this new crazy. algorithm where they know exactly what.

video you would like to watch next based. on AI and all of your viewing behavior. And the algorithm says that this video. is the perfect video for you. It's. different for everybody looking right. now. Check this video out and I bet you. you might love it.