Transcript of #300 Louisa Nicola - Peptides, Cancer and the Deadly Habits That Lead to Alzheimer’s New

Louisa Nicola, welcome to the show.

Oh, it's so good to be here.

It's good to have you. So, uh, yeah, I saw you, I think it was on Diary of a CEO's podcast, and you were talking about Alzheimer's. And, uh, I've been looking for somebody to talk about Alzheimer's because that and cancer are pretty much my biggest fears in life. And, uh, my grandpa died from Alzheimer's, and, um, it seems— it just seems to be growing more rapidly. I just read something, I think it said 7 million Americans have Alzheimer's, and by 2060 it'll be almost 14 million more. More?

Yeah, it's going to triple by the year 2050.

Holy shit.

So currently the statistics are around 60 million people worldwide have that disease, so it's going to triple by the year 2050, man. Yeah.

Well, I want to dive into what's going on in the brain, how it, how it comes about, what we can do, all the, all these— there's some new, um, I think we sent you this new study they're doing in mice. Yeah, that, uh, 40 Hertz. Yeah, 40 Hertz. Do you— what is—

do you—

that sounds— do you know what a Rife machine is? No, it's like holistic type stuff. It shoots frequency through your body.

Oh yes. Yeah. And, and, and there's a lot of science. I love that you said it was a mouse study, right? It was done in mice because it's very hard to replicate these studies in humans. Although it's a, you know, I think it's really phenomenal. I think using these 40 Hz, you know, whether it's signals from light or sound, I think it's actually you know, really great for the brain.

It is good for the brain.

Yeah. And so do you know what brainwaves are?

No.

So brainwaves are— we've got different frequency bands in our brain. So when our neurons fire together, we've got around 87 billion neurons, which we're going to go through everything with the audience. But just as a helicopter overview, when they start to fire, when we're doing particular tasks, they shoot these oscillations of brain waves, and they're good things. And we can map those out using an EEG, and we can map out whether the brain is using alpha waves, beta, gamma, delta brain waves. Generally, the delta brain waves are these big, luscious, big brain waves that occur during deep sleep. Okay, so we know you're in deep sleep because what we see on an EEG are these big brainwaves. So we know they're delta brainwaves, but these gamma waves are around 30 Hz to 100 Hz, and these tend to happen when we're in deep focus or deep concentration or deep thinking. So, and it generally happens around the prefrontal cortex area and in the hippocampus as well. So it is said that these are the first oscillations to deteriorate during neurodegenerative diseases. So when we are—

those brain—

those particular brain waves, the gamma brain waves, yeah, because we lose our processing speed, we lose our thinking capabilities, right? So those neurons don't fire, therefore we don't get those oscillations. Now it's been said that we can mimic certain oscillations from the outside world. It's actually called entrainment, meaning that our brain can mirror the 40 Hz signals that are occurring outside of us. So if we can get into this place of— whether it's through lights, which I, I love, or whether it's through sound— if we can mimic our brainwaves, if our brainwaves can get on that 40 Hz bandwave, then it can start to heal the neural pathways that are degenerating. So that's where that comes from. And look, it's I think it's going to be the next big thing in terms of neurotech over the next 5 years.

Really?

Oh yeah. There's companies that are spending millions. I just saw a, a new company that has raised around $200 million to come up with a device that mimics this.

Interesting. I was at— I just saw you post something on your LinkedIn. It was like, uh, it was that.

Yeah, I saw that.

Yeah.

And I thought it was really fascinating. I think, look, this whole binaural beats error took place, uh, in the last 5 years where you could download an app and you could look at the binaural beats and, and kind of mimic this. But I think now we can start to, you know, move into more replication in human studies.

And so this is— this, I found this on Twitter, uh, right after, right after I saw you on Diary of a CEO and said MIT researchers cleared 50% of Alzheimer's plaques using 40 Hz sound waves. So this— so where does the— so if the 40 Hz is— where does the plaque go?

Yeah, it's, it's— so basically, oh, we're gonna have to do a whole, you know, we're gonna have to learn all about this. But that tweet wasn't entirely true because the study they're referencing actually used both light and sound, and they cleared it out in a mouse model. So when we accumulate these amyloid beta plaques, when they get cleared out, which we have the ability to do during deep sleep, by the way, they get cleared out through the perivascular space and into the lymphatic system.

Okay.

Yeah.

Okay.

So they're able to speed that up. I have a theory along with this, and the theory is that along with sound and light vibration, I believe, is going to take place as well. Being able to vibrate the, like, your, your lymph nodes in your face to clear the plaque out.

Why do you think that?

I think that because new research has just shown in mouse again, in mice again, that the amyloid beta actually accumulates in the nerves. So we've got two nerves that come into the face, the trigeminal nerve and the facial nerve, and they just sit— just imagine here, right? and they come from their cranial nerves. So they come from the brain and they go into the nerves here. And they found that when they vibrate these mouse models, they can clear out amyloid. And so this is now giving rise to, well, if I wake up every day and I start doing facial massages, can I clear the amyloid? Wow.

Wow. And what does the amyloid do?

Oh, the amyloid is It's one of the hallmarks of Alzheimer's disease. It's one of the things that's getting in the way of your brain functioning. And when it actually accumulates in what we call plaques, these hard plaques, that's what causes neurodegeneration. That's what we see if you look at a brain scan of an Alzheimer's disease patient. You can see their brain is shrinking or there's holes in their brain on neuroimaging because these plaques are getting in the way. They're stopping the brain, the signals from cell to cell which causes the collapse of your entire network.

Oh man, okay.

But we'll go through all of that.

Okay, okay. I got a couple of random questions too before we get really good going, but I just, I just read something this morning and I didn't even get to get the whole article because I was on my way down here, but I just ran across it. It was talking about that— I think it was saying there was a peer-reviewed study that said people that use AI are seeing a cognitive decline because they're not Do you know anything about this?

Oh yeah, it's this brain rot era. Have you heard of brain rot?

I'm pretty sure I have it.

It's— I'll tell you what, I'm actually afraid of kids right now because this brain rot era is basically what you're doing is you're looking and scrolling at dumb content, right? Content that is not allowing you to think. And your brain, which we'll learn, is basically uses the analogy use it or lose it. And if you don't provide it stimulus, right, just like your muscles, you know, you go to the gym, you need to lift weights for a muscle to grow. If you don't do anything, the muscle becomes dormant and it wastes away. Your brain is no different. So when you are not using your brain effectively, you're not providing it the stimulus, what happens? Well, you end up with cognitive decline in the end because you're not training it to think, to critically analyze anymore. And I see it for myself, actually. I was a mathematician, right? That's how I got into this entire space. And I tell you, Sean, like back in my early 20s, I was doing trigonometry. I was using sine, cosine without a calculator. I could do large mathematical equations. Now I put everything into ChatGPT because why not? You know, even when I'm working out the tip on a bill.

That's how like sometimes lazy and fatigued I am. And now I'm realizing that my mathematical skills are just diminishing because I'm not using it anymore.

Okay.

Yeah.

Okay. So could that— do you think that could lead to, to Alzheimer's disease or—

Yeah, I definitely think so. I think that if we don't use AI effectively and we're using it for this brain rot era and the more times that we're spending on social media scrolling this dumb content, we are leading ourselves towards mild cognitive impairment, which is the pre-dementia state. And once we're in there, we can't get out of it. And it's just a slippery road down to Alzheimer's disease.

So could that alter your genes? I'm just curious. No, it couldn't. No, it wouldn't. Like evolution or anything like that, it wouldn't, wouldn't be passed down.

I know what you think. I, I do, you know, I've actually like been thinking about this often, like what, what's our brain going to look like due to evolution in the next 1000 years, right? And you can map this out using AI, and it's quite interesting. It actually shows larger, larger brains, uh, but I don't think it can alter the genes. I think it can just, um, just change the functionality. Okay, of our brain.

Okay, it's going to be a fascinating conversation. Let me, uh, let me give you an introduction here real quick. Louisa Niccolo, an Australian-born neuropsych— neurophysiologist, neurophysiologist, human performance coach, and clinical brain scientist who has spent over 13 years studying the brain. Founder and CEO of Neuro Athletics, host of the Neuro Experience podcast, and have published peer-reviewed research in leading academic journals. You were on track for the Olympics as a professional triathlete representing Australia on the world stage until a car hit you, and that changed everything. Your mission now is to end the Alzheimer's disease. So I'd like to kind of start with, with, uh, with the Olympics and the accident, and, and I would like to know what happened and how, how that got you into this.

I, I think as an Australian— so my parents were born and raised in Cyprus, and then they migrated to Australia, and I think And I was born in Australia. As an Australian, we all learn how to swim, right? It's like part of our curriculum to actually move forward in a particular subject. PDHPE in year 8, you have to be able to swim a certain distance with your clothes on. So I was always a natural swimmer, gifted swimmer. And for fun, I decided to enter a triathlon and I ended up winning in my age group, right? As you do. I didn't have the best bike and running skills, but I won. And then that led to me led to my career in, in, in being a triathlete. So I, I had a team, I trained rigorously. Sean, I was training anywhere from 30 to 40 hours a week. We would do morning sessions, midday sessions, afternoon sessions. I lived and breathed triathlon. I only spoke to my teammates. I had my coach, obviously. He was an ITU, International Triathlon Union, uh, special trained coach, and he said, we're going to get you on track for the 2009 Beijing World Championship Series.

So in order to qualify for something like this, and they take 3 from every— in terms of like gender, age group, from every country. So you have to make top 3. And in order to do that in Australia, you have to race at least 10 races in that season and get a podium finish. So I did that and I qualified for the Australian World Championship category. So I was off to Beijing and it was probably the greatest time of my life. You know, you're in your— I think I was around 23, if I'm correct, and maybe 24. You're at your, your peak cognitive health. You are— you don't have too many demands. I was living at home. I didn't have any expenses really. So my entire brain was just set on triathlon. And 2 weeks prior to racing and going to Beijing, we set out to do a 200-kilometer bike ride. And I went out to do this with 2 teammates. And do you know anything about triathlon?

Not much.

So when you're on the road and you're traveling at a certain speed, I think we were going at around 30 to 40 kilometers an hour, and we were we were getting to the 100-kilometer mark and we had to do a U-turn, and this was on a road. And we, we do something where we, we tailgate each other, right? So we were doing 2 kilometers at a time and we'd switch. So it was my turn, I was on the back, and the back, the, the back cyclist is always the one that's directing because you have to look behind to see if there's any cars. And instead of, you know, going onto the road and merging, we stayed in the in the lane where it's the bike lane. So, there's two-lane road, bike lane, and then a guardrail. So, we were traveling up this bike lane and I looked behind and I saw a car and I said, hold up, there's a car. So, we stayed in the bike lane. We saw the car go past us. So, we merged into the lane. I saw another one coming really fast. So, the speed limit at that time was 80 kilometers and he was coming up really fast.

So, I signaled to my teammates, let's get back in the bike lane, he's going fast. As we were getting into the bike lane. The driver, who was 85 years old, traveling around 120 kilometers in an 80-kilometer zone, he caught out— he caught us, and he was looking at us, and he wasn't concentrating on where he was going. He actually followed us just by pure, like, I don't know. Oh man, pure signal. And because I was on the back, he slammed me into the guardrail, and then my bike obviously clipped the boys. The first one went flying like a couple hundred meters up. The second one, his bike snapped, and I was actually squashed between the guardrail and the car. So I had to forfeit my title, unfortunately, um, and I was devastated. I was in hospital, I had surgeries, my leg was in a cast, um, broke a few bones. And so I was out.

He had dementia, didn't he?

Well, To be honest, we don't know what he was doing. He was very shocked himself. I don't know what, uh, he had been driving for at least 2 and a half hours without a break, and I don't know if it was clear that he had dementia. But now that I look back, you know, I think to myself like, A, how lucky was I, um, B, it could have been worse, but what was he thinking? So I was in a cast and that's where I had a major intersection in my life. I felt like I was married to the sport and it was just taken away from me. So there's a bit of heartbreak. I wasn't going to training anymore. I lost my sense of identity and purpose, which I found, you know, I had to throw myself into my studies. So threw myself into medicine and science at that time. But funnily enough, I actually was so determined to re-qualify for the 2012, uh, Championship Series in Auckland. So I did that.

Right on.

I did that, um, and as soon as I crossed that finish line, I called it quits. I haven't been on a bike since.

Right on.

Yeah.

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After you sign up, they'll ask how you heard about them. Tell them we sent you. Welcome to Hollywood vs. Reality. They do it right. What does he do in the movies? Tell me if I'm doing this wrong because I don't watch any of this shit. A little flick like that, right? Seems pretty cool. It is pretty fucking cool. Gotta silence it. In another lifetime, I did gun reviews for a living. Proprietary fucking magazines, supposedly the best engineering in the fucking world. When that breaks, you're fucked. And now we're bringing them back. It does look pretty fucking cool. I got it. I got to admit that we've been making some serious waves in this, in this market now.

Yeah. Well, let me tell you, it's, you know, you can study human performance, you can study exercise physiology, but I've been there and I've done it. You know, you see a lot of people now on social media talking about brain performance and what it means to perform at an elite level. And it's good in theory to read a textbook or to read a science study, but unless you've actually been there and done that, you can't really grasp what that means. And at that time of training, I did everything to a T. Like I was doing VO2 max tests that, you know, the whole world has caught on now. I was doing those, you know, in 2007, 2008. We didn't have data back then to show what our heart rate was. We were using metronomes. Metronomes, you know, I would clip a metronome to my headband to figure out, you know, what's my pace. We didn't have watches and heart rates. Like every time I ran a lap, my coach would, you know, check my pulse and then we'd determine whether we know through a calculator, like what percentage I'm running at. So when you know that hardcore raw data and you can translate that into science today, it's, it's so much different than just reading.

Do you wear any of those wearables?

I do, uh, when I'm training, I wear a Garmin watch and I wear a heart rate monitor just because it's so natural to me, so I can check what my heart rate is. I've recently taken off my Oura Ring.

Why'd you do that?

Which I haven't done— like, I've got a dent in my, my finger for that. I did that because I'm so sick of it telling me that I'm sleep deprived because I'm in a stage of my life now where I'm traveling a lot. It was providing me— no, I tell you, it was— for somebody who's so deep on like biomarkers and numbers It was providing me more stress and I just said, that's it.

Really?

Yeah.

I don't have one. I've been thinking about using one, but I don't— I just don't know if I want all my data in the— in this. I get paranoid.

Well, guess what? They just— a lot of people don't know this. Another reason I took it off, Oura is now selling people's data.

Really?

Yeah. Not Whoop, but Oura Ring. It's another reason why I took it off. So all of your data in terms of You know, women are tracking when they ovulate. Women are tracking their menstrual cycles. You've got evidently your, your age, your date of birth. Everything is stored in here, your daily habits. And it tracks where you are because you set it to going for a run. It shows you where you've ran. So it's tracking everything and they're actually selling that data. And this is publicly available news.

Who would they sell it to? What would they—

large corporations, insurance companies, probably pharmaceutical companies.

Is it tied to you directly?

Yeah, it would be tied to— like, your data is now stored and being sold to companies. So I can only imagine what that can pose as a risk for you.

Can this stuff help too if you have, let's say, have years of data, you know, on your everything, that, that kind of stuff? I mean, if you gave that to a doctor, would that help them in any— that's the— that's actually why I wanted to determine.

Yeah, they've— so I I don't wear the Whoop band. I mean, I think I might go— I might go and do that actually, but they've got this new thing on there which shows if you have atrial fibrillation and it can detect whether you have AFib. And AFib is one of the biggest risk factors for a heart-related event or a stroke. So I think that's pretty cool.

Yeah, yeah, yeah. Right on.

Yeah.

Um, a couple things to knock out here. Of the Patreon account.

Okay, cool.

And, um, they're the reason I get to sit with you here today. So they get the opportunity to ask every single guest a question. And this is from Corey Powers: From a neuropsychology standpoint, what do we know about the chronic exposure to operational stress and professions like the military and policing? Affects brain aging over decades? And are there specific evidence-based strategies like resistance training or metabolic interventions that can help maintain cognitive longevity for people who have spent their careers in those type of environments?

Yes, and thank you for that question. I think it's really, um, prominent. So there's many things at play here. First of all, the ongoing threat and stress to your brain over a substantial amount of time can cause some form of neurodegeneration or accelerated neurodegeneration. But if you talk about the military, then we have to bring up concussions, we have to bring up TBIs, and you've probably heard of CTE, chronic traumatic encephalopathy. And this here is actually— CTE and Alzheimer's disease, literally, if you look at them on autopsy studies, they look identical. Right. So there is some extreme risk right there with TBIs and concussions. Partly while I'm against the NFL in theory, I don't agree with what's happening there. However, if you have— if you are at that stage now where you've gone through all of that, you just have right now to intervene. You can't go back in time. There's no reversal of any cognitive decline. So you can intervene with metabolic interventions. One of the greatest ones that you can intervene with is Putting your brain in a state of ketosis. I'm so fascinated right now on the research of ketones and what they're doing to help with brain fuel.

So having exogenous ketones is one thing that I'll tell you, you're, um, the person who asked. Another thing, yes, evidently resistance training, exercise, nutritional interventions, staying away from sugar, and sleep. I think in this instance, sleep, when you're trying to recover, will probably outweigh exercise. And I never usually said— I always say that exercise outweighs everything, but when you're trying to really recover and regenerate a damaged brain, you need somebody to be sleeping.

I mean, that's a, that's a, that's a, that's a big challenge for veterans. I mean, I'm a veteran. I know I sleep like shit. I think pretty much anybody that's probably seen any type of combat sleeps like shit. PTSD, PTSD, traumatic brain injury. I mean, you just always switched on. Business stress. I'm sure you deal with a lot of business stress. I mean, it's just the brain's always running. It's just especially mine. It's just, it's going 1,000 miles an hour all the time. I wake up in the middle of the night thinking about whatever's bothering me. And, and so, so if that's— I mean, yeah, it almost like when you say, well, sleep better, it's, it's like, oh shit, that's probably not going to happen.

And, and this is the hard thing, right? Because then you also get new mothers. And so what's a new mother going to— you can't just tell her sleep more, right? You know that if you're a new mother, for the next 10 years of your life, whether you have one child, two, or more you're going to be sleep deprived, right? So I know the science, and then putting it practically is a completely different story, right? But there are certain things you can do for sleep interventions, and it really comes down to— instead of just sleep better, it comes down to let's locate what your problem is. And normally when it comes to sleep, people have two problems: I'm having trouble falling asleep, I'm having trouble staying asleep. And they then provide you know, the interventions that you need to start attacking. So if you can start with just looking at your sleep environment, I always say you have to train for sleep, and it comes down to like, what are you doing at 8:30 PM every night? What time do you go to sleep? How do you prepare your mind for sleep? For somebody like you who's got this racing mind, outside of supplementation, which would actually give you a lot of benefit, You could start, you know, warming up for sleep, like getting rid of your phone, not emailing anybody, not having any crazy conversations, sleeping in a dark room, setting the lights at like 8:30, 9, like dimming them, putting just red lights on to get your body ready for sleep.

Putting just red lights on?

I like to use red lights or dim the lights or just have floor lights at home because it signals to my brain, hey, we're getting ready for sleep. Melatonin starts to rev up from the pineal gland, starts to release it in small doses. If you've got the lights on at night, your brain thinks that you're awake. You can't go from awake to sleep. You want to have this transitional moment, right?

So you have red lights all over your house at nighttime?

Yeah, it kind of looks funny. I live in New York City as well, and some people walk past, they see this red light apartment, signals the wrong thing.

Yeah, I see. Yeah. Um, yeah, that's, uh, That's a challenge that I've been thinking about a lot, and I want to dig into a little bit more, especially when it comes to psychedelic therapy. Yeah, but before we get there, everybody gets a gift.

Wow. Are these—

Those are our Vigilance Elite gummy bears.

Oh, I love it.

Actually, don't triathletes love gummy bears?

Yeah, well, what depends on what's in them?

Well, nothing good. Okay.

I can't wait to have these. I travel a lot, so. This is going to help you. Thank you.

You're welcome. Well, let's dive in. I just want to read a couple of, uh, numbers when it comes to Alzheimer's so people understand how serious this is. An estimated 7.1 million Americans are currently living with Alzheimer's symptoms, projected to nearly double to 13.9 million by 2060, which you said actually will triple by 2050. Globally, over 50 million people have dementia, expected to hit 150 million by 2050. Someone in the U.S. develops Alzheimer's roughly every 65 seconds. It kills more people annually than breast cancer and prostate cancer combined. Nearly two-thirds of Alzheimer's patients are women. Why is that? Tied into estrogen, menopause, and hormonal shifts. So I think before we go any farther, can we just talk about What, what is Alzheimer's dementia and how does it happen?

Yeah, I love that we're talking about it because I just want everyone to know this is not a disease of old age. We used to think it was, and when I first started in a hospital, working in a hospital, I thought Alzheimer's and dementia was just a disease that you got in your 70s and 80s.

Is this even an organic disease?

What do you mean by organic?

Is this— so I've read several different articles that say cancer is not an organic disease, it's from all the pollution and shit.

Yeah, Parkinson's is a man-made disease. Alzheimer's disease is a preventable disease, and in my opinion, it is also a man-made disease. Alzheimer's disease. Let's talk about dementia. So dementia is the umbrella term. It's not a diagnosis. Dementia is not a diagnosis, right? It's a term that we use to describe symptoms. It actually comes from the word demented. So as you get older and you lose your processing speed, that's your ability to think fast, right? Speed of decisions. You get slow, slow thinking and your, your memory starts to decline. These are, you know, these are all cognitive functions. We use them every day. And when they start to decline, or become demented, that's what we call dementia. So that's what dementia is. Underneath dementia, right, think of it, it's the umbrella term. Underneath it sits various forms of dementia. We've got Parkinson's dementia, right? So if you have Parkinson's disease, you have some cognitive demented states. So you have Parkinson's dementia. Vascular dementia, that's the second greatest form of dementia. We've got Alzheimer's disease, which is called Alzheimer's dementia.

What is vascular dementia?

That's when you have the— so the vascular system of the brain, that's when that starts to deteriorate. It's when all the blood vessels—

so it's not getting blood flow?

Correct. Yeah, it severely attacks the blood vessels of the brain. Okay, so you've got dementia with Lewy bodies. Now, the part that we can't help, right, when it comes to genetics, there's around 30 to 40 different genes involved in all of the dementias. And there's only really 3, right, that if you genetically get these from mom or dad, you will get Alzheimer's, you will get a form of dementia, right? Now, you know Bruce Willis? He's got something called frontotemporal dementia, right? So this is generally when we have a mutation in specific genes, right? So the genes I'm talking about are— we've got presenilin-1, presenilin-2, and the amyloid precursor proteins. When it comes to our genetic code, we've got mutations and then we've got risk factors, risk genes. So let's take, if you've got a genetic mutation on chromosome 4, that's how you were born, you will get Huntington's disease. You will get it. We can't change that for you, and that's, that is it. But for Alzheimer's disease specifically, not frontotemporal dementia, not dementia with Lewy bodies, for Alzheimer's disease there's no genetic mutations in the genes. There's only risk genes, right? So meaning that you don't have to have these risk genes, and you can have these risk genes, but it doesn't mean you're going to get it.

Okay.

The problem is 95% of all Alzheimer's disease cases were driven through lifestyle.

Really?

Yeah. There's only around 3 to 5% of the total Alzheimer's disease patients or cases that possess the risk factor genes.

Could you say that again? Did you say only 3 to 5%?

3 to 5% of all Alzheimer's disease cases were driven through genetics, meaning that 95% of all Alzheimer's disease cases were driven through lifestyle interventions and factors.

I feel like that's good news.

It's good news. It is, because it means that you have agency over your brain. It means that you have agency over this disease. It means that you don't have to be scared. Like you mentioned earlier, I am not scared of Alzheimer's disease. I'm scared of cancer because this is something that I don't know anything about. A, it's also something that can just sporadically happen no matter how good you are with your diet and exercise. But when it comes to Alzheimer's disease in the brain— and we're going to have a look at the brain, I've brought Henry with me today— uh, we're going to discover that you have a choice whether you get this disease or not. And those choices start in your 30s, and they get accelerated in your 40s and 50s, and then in your 60s and 70s, that's what will determine how well you lived in your 30s and 40s. So these risk factor genes Okay, these are called the APOE genes, so apolipoprotein E. We all have them, right? And they come in pairs because you have one allele from mom and one from dad. Now we've got APOE2. They're just different variants of the apolipoprotein E gene, but we've got APOE2, APOE3, and APOE4.

So you have these, I have these, and if we have a copy of the APOE4 gene, it— right, just one copy, right? You could be E3, E4. If you have one copy, it raises your risk of getting the disease by 2 to 3 fold. So you have an increased risk, increased risk, right? If you have two copies, you could be an E4, E4 carrier. Now, 25% of the population has at least one copy. Right? 25%. If you have two, it raises your risk by tenfold. If you are a woman, it raises your risk by 14-fold. 14-fold if you have two copies of this gene.

What is the regular risk? One out of— do you know how many?

Oh, so around 2 to 3% of the population has two copies. Okay, so, um, The Australian actor, um, Chris Hemsworth has two copies of this gene.

I saw that they made a documentary series or something about that.

They did, because he doesn't want to lose his mind. Um, so he has two copies, but it doesn't mean that he's going to get this disease. In fact, there was a landmark study that was done, uh, in Africa which actually showed that they've got a high population of APOE4 carriers right, because it's genetics, a huge population. But then the lowest population of Alzheimer's disease cases in Africa. Yeah, why is that?

Probably because they're running around all the time, eating better, probably have, uh, access to a harder way of life. Yeah, so they have to be more active.

Yeah, they've got a better— they've got a— they've figured out something that the— that we haven't in the US.

What do you think that is?

I think it comes down to lifestyle. I think it comes down to primarily stress, uh, sleep, better sleep habits, uh, better food, access to food, crops, organic foods. They're not spraying their foods with all the pesticides. And then their daily living, you know, activities of daily living. That's what we call it in academic research. Like, what are you doing every day to increase your steps? What are you doing every day to exercise? What are you doing every day to keep your brain active? So I think that they're doing more of that. We are so technology-driven in this country, and I think that that's what's getting in the way, whether it's AI, whether it's sitting in our, you know, in front of a computer screen working every day, and that's preventing us from sleeping better, eating better food, exercising, etc.

Could it be— could it be an ethnicity issue? Is it higher in white people than it is in Black people?

No, I mean, it's, you know, it's said that it's higher in, um, ethnic, you know, in the European countries. And this is all just because of genetics. You pass down your genes. By the way, you can test for this. You can test if you've got— if you're an APOE4 carrier or not. Some people choose not to because they believe, well, I'm doing everything I can anyway. And while that's true, I believe that everyone should get tested because you want to know if the bus is coming right, if the bus is going to hit you, because then you can intervene even better and harder.

Okay.

Yeah.

Okay. So what, what? Damn.

Let's, let's, let me, let me introduce Henry. Okay. Um, so for everybody watching, so this is Henry and I'm going to just perform a craniotomy right now. We've just taken his skull and I just want to use the brain just to properly show you. So the brain is around 2 pounds, right? And it actually feels like hard Jello-like tofu, right? And it consumes 20% of all the energy that you consume every day. So it's a hungry organ, right? And it's comprised, you've got two hemispheres, you know, we can do this. So you get two of everything. In the hippocampus, we've got two 'cause you get two on each side. This green part here is called the cerebellum, which is Latin for mini brain. And here is the, brainstem. The brain has around 87 billion neurons. Neurons are brain cells. We've got different types of brain cells. We've got, uh, glial cells as well, which we'll go into. But here's the fascinating part. See these red vessels here? The brain is the most vascular-rich organ in the entire body. Actually, if you were to pull apart all of the blood vessels in your brain, which comprise of capillaries, veins, and arteries, right?

If you were to pull them all apart, it would span 400 miles.

Wow.

So it's, it's a vascular network tightly dense in this 2-pound blob, right? And these brain cells are responsible for everything you do, right? Everything you do, everything you are, everything you think, everything you feel comes down to how your brain is functioning. That's all. So there is, you know, the reason I got into this in the first place was when I was studying mathematics, there was a neurophysiologist that we had to study. And back then I was like, what's a neurophysiologist? And his name was Warren McCulloch, and he teamed up with a mathematician, his last name was Pitts, and they were able to come up with the algorithm for how neurons fire. It was phenomenal. It's such beautiful work. And in fact, that algorithm and that mathematical equation is what printed the neural network that we know today, which is AI.

Wow.

Yes. And it's so beautiful. And he's got a phenomenal book, which I've like, which I read all through doing my thesis. But when I figured this out, you know, I remember talking to my, my professor and he said to me, He said McCulloch knew that when that— like, neurons either fire or they don't, and that's dependent on a mathematical code. So your neurons either fire together. So neuroplasticity is when neurons fire together, they wire together. So we knew that, but neurons are either on or they're off, and when they're off, that's what ends up becoming neurodegeneration and deteriorating your brain. So we've got 87 billion neurons which are being fed from the vascular system, right? These little ones that you see here on the outside of the cortex are capillaries. In Australia, we call them capillaries. They're one cell thick. So they're not like arteries. So arteries are thick, right? They're like these tubes and they're supported by a muscular outer layer, right? So they can handle, they're like pipes, right? So they're big and we have branching off those from the aorta, and going up into the brain. But these little ones are the first things to die, right?

They die primarily when we have an insult, a neuronal insult like a TBI. If you get a TBI, you're most certainly going to be breaking these little capillaries because they're so tiny, they're so fine. These are the first things to go with hypertension. High blood pressure, right? So one of the best things you can do is buy yourself a $25 automatic blood pressure monitor on Amazon which can measure your blood pressure. And you want to maintain the 120 over 80 gold standard. Anything above that, you know that you are starting to break your brain, the small vessels of the brain. So then the next question is, well, Louisa, if we, you know, let's just say we kill off these little capillaries. What happens? Well, these capillaries are feeding the, the neurons in that area. If you cut off its blood supply, you cut off its oxygen and its nutrients, so the neuron itself can no longer survive. So what does it do?

Dies.

Correct. And then you think, well, there's 87 billion neurons, you know, am I going to feel it? Well, this is why it takes 20 to 30 years to feel your first symptom of Alzheimer's disease. One neuron, you're not going to feel it, but that one neuron stops communicating with the nearby neuron, and then that stops communicating with the nearby neuron. This takes, you know, and when you stop, when they stop accumulate, when they stop accumulating in a small cluster, that's when we start to feel symptoms of dysfunction. You know, if it happens on the left side, maybe you're getting in the way of your language processing. Does this make sense?

What would people notice?

Well, the first symptoms to go is memory, specifically short-term memory. Forgot my keys. What's that person's name? You walk into a room. Why did I come in here? What was I getting? You walk out of the room, faces start to become distorted, and you start to forget certain things. Short-term memory. Long-term memory doesn't really get affected. So that's the first thing to go. And that is because— let's just perform surgery here— that is because we have a deep structure in our brain, okay, called the hippocampus. The hippocampus is a seahorse-shaped structure. It actually means seahorse in Latin. And it lives, as you can see, it's so deep, it's part of what we call the limbic system. The, the temporal lobes are here behind your ears, and it lives deep in there. And it's the first thing to go during Alzheimer's disease. So that starts to deteriorate. The hippocampus holds all of our memory formation, our memory consolidation. This is where we learn new things as well. So that is it's very susceptible to oxidation, meaning that if it gets stressed, becomes oxidized, that's when we start to kill the neurons in that area. So if we start to kill the neurons in that area and they become dysfunctional, then, um, short-term memory starts to fade.

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I have this.

You think you do? Oh, you have short-term memory loss.

I mean, I, I see. I don't know, I try to justify why things are happening to myself all the time, but yes, I mean, yes, I forget people's names. I don't forget people's names. My family, my team.

Do you know why?

Close friends.

When those memories are formed in the hippocampus, they get protruded out to the cortex, and that's where they live. This is why you can get somebody with Alzheimer's disease, right, in the end stage, and they'll remember their daughter, right? Or they'll become lucid and they'll remember their wedding day. But the short-term memory, it's also important to differentiate between short-term memory loss and just pure stress and lack of concentration in the moment of, you know, knowing that person's name. But you've, you know, you're a vet. You've been— I'm sure you've been involved. I mean, have you had a TBI? You've probably had multiple, right? And who knows what happened in that moment? You know, the most important stage right then is 72 hours of that insult. An insult is a hit to the head. What happens within that 72-hour time frame? Which is why the concussion protocols at the NFL really matter. Like, what are you doing to preserve this person's brain after they've taken a hit, right? You can stop the process immediately if you do certain things in that 72-hour period. But, you know, we don't know what happened back then for you. And then did that you know, did that evolve with you killing off blood supply to a certain area of the brain?

Like, what is, you know, going on in your brain? We— I haven't seen any of your images. I don't know if you've done any, like, MRIs or anything like that.

I don't want to.

Why?

Because I have a lot of friends with this, and I'm not seeing a lot of improvement unless it's psychedelic-assisted therapy.

And that's, you know, and I know that you've taken ibogaine. Yeah, I think that's going to be also something big, especially in the state of California where they're looking at this now on people with major depressive disorder, you know, people with clinical depression, they're going through this. And I think it's great as well. But I also think it's wonderful to see other interventions that we could use if you knew what was happening in your brain.

Mm-hmm.

Mm-hmm.

But I forget words sometimes when I'm talking. I mean, are these signs? They have to be, right?

Yes. I mean, they would be definite signs of mild forms of mild cognitive impairment. So when it comes to Alzheimer's disease, this is what happens, right? You have a— you get something called subjective cognitive impairment. It's when you first start to notice these signs. Brain fog, right? Brain fog where you can't remember things. And then after that, if it becomes more persistent and you see it in different areas of life as well, slurring of words could be a language processing issue. This, if you get diagnosed with mild cognitive impairment, there is a test that you can take. It's called the MoCA test, M-O-C-A. You get a score out of 30. It's a free test, Montreal Cognitive Assessment. You can do it. It doesn't take long. If you get 30, That's great, right? If you're getting like, you know, if you're getting around 25, you've got mild cognitive impairment, right? So, or even 26, mild cognitive impairment. This MCI state lasts around 20 years. And the problem is it accumulates and accumulates. It's like compound interest, right? It's not that you get it now and then you're just going to stop it.

Mm-hmm.

Now you're on the road. Okay, let's imagine, right, where we live our lives up until 25. The brain fully forms at around 25 years old. That's it. And that's why, that's why that age is so beautiful. You know, when I was training like triathlon, like my brain is still developing, it's firing 22, 23, beautiful. But then you are survived in those by, by your age. You can get hit in the head. Right? And yes, it's going to do some damage, but you are survived by your growing of your brain due to your age and the healing process that takes place. But at 25, evolutionarily— evolution stated, that's it, reproduction is over and we no longer need to survive anymore, so we're going to die. That's evolutionarily why we stopped growing at that age, our brain. But now we're living longer because of penicillin, antibiotics, and vaccines, right? So now we're living till 100. So our brain wasn't built for that. It wasn't built to survive up until 100, let alone 120 or 130, right? So we're at this critical point at 25, and that's when we really need to start to protect our brain.

Okay, so it cannot be reversed, but you can stop it. No, so you can stop the advent— the snowball effect.

No, you can slow it down.

You can slow it down.

Yeah. Um, to my date, there are— there is a prominent neurologist who believes that he has reversed Alzheimer's disease. He's written a book on it. I think that that is unethical. Um, I think it's extremely difficult. I've never seen it. It's never been seen in academic peer-reviewed literature. I don't believe it's true. I tell people that Alzheimer's disease is a diagnosis that is similar to end-stage cancer.

Okay, you know, how so?

If you've been diagnosed with an aggressive form of brain cancer, it's called the glioblastoma, right? I'm in neurosurgery, I work in neurosurgery, and we've got a tumor board, and we've got, you know, the neurosurgeons are constantly being thrown cases of glioblastoma. We know that that has a 1 to 5 year survival rate. You don't really survive that. That's end stage, right? And we don't know who's got it. It's not something that you can prevent. It just happens, right? So that's the same as Alzheimer's disease, meaning if you get it, you have a— after this, you've got maybe a 1 or 2 year survival rate. You start to lose everything, all of your cognitive functions. You don't even know who you are. I've had a patient looking in the mirror asking me, who's that? She's looking at her and she thinks it's another person. You lose your cognitive faculties, right? So to say that you've reversed that is a really serious thing, and I don't believe you can do that. Now, when it comes to mild cognitive impairment, as I mentioned, this is a 20-year process. You can slow the progression, right? So if you get MCI and we know that, okay, in 20 years this means you're going to get Alzheimer's disease, Let's make it 30 years.

Let's slow that progression. It doesn't mean you're getting off the treadmill, right? You get on the treadmill, that's MCI, you're going down this track. Doesn't mean you have to get the disease at 80, right? By the way, you don't die of Alzheimer's disease. I think it's really important for you as well. You mentioned a close family member died. I think it's important to know on the death certificate what it actually says. Sometimes it will say on a death certificate I think it was actually kidney dialysis. That's what it is. You don't die of Alzheimer's disease oftentimes, which is what makes it so devastating, is that you can die of asphyxiation, meaning sometimes people just forget to swallow.

Holy shit.

You forget to swallow. Or you may die of sepsis. You know, you get an infection, you don't know it. You know, a lot of these patients are walking around, they don't know if they've been hurt or you fall, you hit your head, and that's— it's really sad. The reason why it's so sad, Sean, is because out of all of the diseases, it's the one that you lose who you are. Why I love it so much is because I love my life and I love learning, and I've loved learning my entire life. You know, I didn't really grow up watching TV. I grew up with books and encyclopedias, and I read a lot, and Reading is one of my, my pleasures, and I love it so much that my brain gets to do that. And I love forming memories, albeit with myself or with, you know, my loved ones. And I would hate to lose those because you spend your whole life building those up for it to be robbed of a disease that was preventable. Right. So let's keep going down, down this, if, if I've got you right. So you've got this, this brain that is at the mercy of all these insults.

So every day when your neurons are wiring together, Right. And every, every time you produce a thought, your neurons are firing together. And at that time, they're producing a whole host of chemicals, dopamine, serotonin. If they're getting produced in the right way, you're releasing serotonin, which makes you feel happy, right? Dopamine, if you're releasing them in the right way, makes you feel vigilant and it gives you that drive and that motivation to pursue your goals in the pursuit of goal setting, right? Or it could be hormonal. So it's a beautiful— it's a beautiful structure. It's the most beautiful structure in the entire universe. There's so much I don't know about it. This here is called the Circle of Willis. It's just how the, um, the blood supply is shaped. And it's really interesting because you've got the aorta, which is this massive, massive blood vessel that comes out of the heart. From the aorta, you've got here— you've got the carotid arteries. We've got one on each side. And then you got the vertebral arteries, the vertebral arteries. The carotid arteries supply the frontal part of the brain with blood, and the vertebral arteries supply the back part of the brain.

I love the system because if one system breaks down, if you've had a stroke, right, in one of the arteries in the brain, the brain has a backup system. So if the stroke is happening in the posterior part of the brain that's supplying the posterior part, maybe the occipital lobe, here, which is responsible for our vision and our— everything that we see and how we process vision, then the front supply, the anterior part of the brain, the blood supply will use their backup system and immediately supply the brain with blood, which is why strokes— my father had a stroke in 2019, which is why a stroke is such a hard— like, for you to have a stroke, you have to think neurologically. All systems broke down in the brain, right? So that's your brain, that's Neuroanatomy 101. Okay, okay, let's talk about Alzheimer's disease. So we've got all of the dementias. Now, what separates— like, why is that the most prominent form of dementia, A, and what separates it from the rest of the dementias, right? There's two proteins at play here. We've got amyloid beta, okay? So if we have a— if we've got amyloid beta in the brain, that's one of the hallmarks of Alzheimer's disease.

That's how we can differentiate it from the rest of the, the dementias. And then there's another one called tau protein. Now amyloid beta lives outside of the neurons. Tau protein lives inside of the neurons. So we've got two attacks, one that's getting in the way. So these— the way the neurons are structured, the 87 billion of them, they've got a cell body just like the cells in your, in your body. But then there's an axon that comes off it. So think of a tree. You've got the roots and then you've got the tree trunk, right? So that's the axon.

Okay.

Okay. And then the branches are the dendrites and then the leaves are these little dendritic spines. The leaves, okay, the dendritic spines and the dendrites communicate with the other dendrites. So imagine two trees forming together and the leaves are touching. That's how you produce your actions. They're called synapses. Okay. And so, so when we get that pruning around of the synapses, that's what causes the degeneration and our network system starts to fail. Right. So outside of the tree trunks, in the air, which is also the cerebral spinal fluid, that's where amyloid beta lives. And in the tree trunks themselves, that's where tau protein lives. So you can imagine, first and foremost, if we get the buildup of amyloid, what happens? Well, the leaves can't communicate anymore. They get stuck like glue, right? They get stuck. And then if they can't communicate and they're stuck like this, they just die.

So where does that amyloid come from? Where does the buildup come from?

I'm going to take you in history now and I'm going to give you something that's really— it's going to make you maybe hate science or medicine or institutions, which I know that I already hate. You've got something to say about that. In 1901, the first ever— this is how Alzheimer's disease became a thing. A woman was experiencing a form of delirium and her husband thought she was crazy and she needed to be in a psych ward. So he took her to the hospital, and the neurologist at that time— he was around 34 years old, his name was Aloïs Alzheimer— and he took this patient, and over a 3-year period, he tracked all of her symptoms. And he's got a book. He tracked everything about her because he thought it was so mysterious, you know, what happens to her. She died 3 years later, but she came in with complaints of not remembering who people are, not remembering faces, and she actually quoted, 'I don't know who I am.' They couldn't understand why. They just thought that she had delirium, right? She ended up dying, um, of sepsis like 3 years later. What they did was they donated her brain, and Aloïs Alzheimer was able to look into her brain on an autopsy, you know, cut her brain look under a microscope, and he found these plaques, right?

And when he scanned it and investigated it, he found that it was amyloid, okay? It's a protein. It's an antimicrobial peptide, right? So stay with me. It's just a protein peptide. He found it. So since 1905, there was this whole theory that Alzheimer's disease— they called it after him if you get these forms, this form of delirium, it's not delirium anymore, it's called Alzheimer's disease after Aloïs Alzheimer. And they were able to stain these using silver staining to show that, okay, they've got these amyloid deposits in their brain. So then Alzheimer's disease became something called the amyloid cascade hypothesis, right? In 2003, this is what we thought was— if you get a head full of amyloid, you've got Alzheimer's disease. This is where it gets so interesting and really frustrating. In 2003, there was a scientist, his name was, he was a French neuroscientist, Sylvain Leszner, at the University of Minnesota, was working in a lab to try and figure out Alzheimer's disease. And he found that a specific type of amyloid in the brain, before it becomes these hard plaques, they're soft oligomers, right? So they become soft and then they accumulate and they become these dense plaques.

But before they do that, they're just these little oligomers that are floating around, and they're actually not neurotoxic, right? They become a monomer and then an oligomer, and then when they start to accumulate, that's when it becomes dangerous. He realized, or he found in 2003 in mouse models that these oligomers, which is actually called amyloid beta 56, that, that is the sole cause of Alzheimer's disease. So at— it was so monumental in 2003, right, this paper that he put out to show that we can solve the amyloid cascade pathos— hypothesis if we intervene and stop this oligomer from becoming the actual plaque, right?

Mm-hmm.

Foundational. Do you know what happened then? He got cited 2,300 times, which is huge, right? Immediately he got a $7 million grant for his own funding, and then the NIH put $300 million per year towards formulating or replicating these studies and formulating pharmaceutical interventions to attack this, right? And this was the biggest thing in academic research. And it wasn't until 2022 that they found that it was fraudulent.

Holy shit, are you serious?

So all of the papers he put out— he, he made— he did, yeah, around 40 of his own papers What he did was they've got these Western, uh, block— these Western plots that you have to put in academic research. They were all fake. So all of the images he put into— and by the way, guess where it was first printed in 2003? The journal Nature. Nature is the most prestigious academic journal in the world. It is a high-stringent journal. And yet a neuroscientist at the university— and he only, um, he only quit from his tenured position in 2024. He resigned or was fired. This is the biggest scandal in the amyloid cascade hypothesis, and I'll tell you why. A, $300 million went towards funding something that never existed. They were never able to replicate these studies. And like labs all over the world were getting funded to replicate this amyloid beta 56. They were going, okay, great, how can we replicate this? No one was able to replicate it over a 20-year period, right? Why didn't people intervene earlier? This is a high-stringent journal, the most stringent journal in the world. And yet you didn't realize that these images were manipulated.

How he manipulated them, I'm not sure. And when it came out, you have to think what this did over 20 years. A, they were putting all of these patients through these phase 3 trials to, to see if we could replicate these, you know, replicate drugs that could come in and clear it out. What was happening during that time? Well, nothing. A, like pharmaceutical companies, like spending billions of dollars for absolutely no reason. We lost so much. A, integrity in science. B, integrity in peer-reviewed processing and academic integrity. I mean, I just— it's the biggest, I would say, scandal that no one's really talking about. I'm not sure why. And it's fresh. It wasn't until I, you know, and it was a a scientist, it was printed in 2022. Like, you know, they went in, they investigated it, they found that this, these images were, were not real. And it's just like, what did we lose in that process? And now we are now being faced with people losing, you know, trust in Alzheimer's disease research. You know, the NIH has now cut the funding completely, which is so sad for people now. But imagine the patients who are going through You're giving these patients, millions of people over the world, false hope of going through these phase 2, phase 3 clinical trials.

Damn. 20 years of effort, all just right in the trash.

Yeah. From this one man, which I don't know what his motive was. Maybe it was money. Maybe it was prestige. Because let me tell you, for 20 years he was a king. It's now the retracted article. Is the most— it's the second most cited retracted article in the entire world when it comes to medical science. I think there's like— I looked on it yesterday, it was like 84,000, um, like, uh, I don't know, I saw 84,000, I was like, oh my God, that's climbed a lot. So people are now becoming more aware of it, but it doesn't stop there. So We have drugs now, IV drugs. One of them is called lecanumab. Okay, one of them is called— there was one called aducanumab, but that was pulled off the market, right? So now we've got something called lecanumab, right? And basically what this is, it's an intravenous drug. It's extremely expensive, it's around $26,000. And what it does is when it's administered, it goes through and it clears out the plaques from your brain. But what people don't realize is when the scientists were going through the Phase 3 clinical trial, deaths were occurring and something called ARIA, which is basically when you administer this drug, it's causing microhemorrhages in the brain, so brain bleeds.

And these brain bleeds are causing deaths. And during the Phase 3 clinical trial, it caused deaths. It caused 2 deaths, and this was never noted. And the pharmaceutical companies just— which formulated aducanumab— which formulated lecanumab went through and fast-tracked it to get it approved. So it's still on the market. I get asked every day. Just yesterday, I have a friend of a friend who messaged me. She said, look, I know you know what's going on. My dad just got Alzheimer's disease. And she's quite young. She said, my dad just got diagnosed. They want to put him on this IV drug. Can you tell me anything about it? It's the only thing we have right now in terms of pharmaceutical interventions, right? But when you actually have a look— and the New York Times actually posted this back in 2025, huge, huge article— when you look at what it's doing, A, it's a $26,000 administration. Not many people can afford that. You actually need 4 lots of it, right? You're taking—

we're looking at 100,000.

Yeah, you're taking with you the plaques, the amyloid beta plaques, right? But what they're not reporting is that a lot of these patients who went through the— who went through the trials, who survived and didn't have microhemorrhages and didn't obviously cause any death, it wasn't preserving their cognitive functions. So they were clearing out the amyloid, but they're still not themselves— they're still not remembering things. So what was the point?

But so there's no improvement.

There's no improvement. Which brings me to my next thing. You can have a person with a head full of amyloid and have Alzheimer's disease. They've got no cognitive functions. Subsequently, I can have the same— another person, same age, same gender, same genetic profile, if you will, with a head full of amyloid, but they've got their cognitive functions. What does this mean? It means that amyloid is not the demon. But we have been led to believe that this protein, which is a naturally occurring protein, a naturally occurring peptide, that it's not the problem. We can't— we need to stop focusing. But pharmaceutical companies don't want to stop because they've formulated a drug that can eliminate that. But that's not the problem. That's like, that's like putting a Band-Aid on it. By the way, you get rid of amyloid, it's, it's going to come back.

Wow. Is that what the 40 Hz is getting rid of?

Supposedly, yes.

So it doesn't do anything.

So, I mean, it gets rid of it. So what we're doing now is, what we're trying to say is, I don't know, it's like, let's, let's give a financial analogy, right? It's like going and spending spent so much money on a credit card, you know, not thinking about anything, over a 20-year period, and then it creeps up to you. It's okay, you have billions of dollars in debt. What now? And you're like, oh, I don't know. But you were warned about this 20 years ago. You've— that compound interest has been accumulating. So the problem isn't amyloid. The problem is, why is the amyloid accumulating in the first place? So what is amyloid beta? Well, as I mentioned, it's an antimicrobial peptide. Your brain is so strong. Remember, prior to antibiotics and penicillin, it had to survive. So how does it survive evolutionarily? Well, amyloid actually lives in your neurons, and it actually gets ejected out of the neurons in the event of an attack, a microbial attack. So think of a virus, right, or pathogens that get into your brain. How does the brain protect itself? Because if the pathogen gets in the brain, it starts to attack the neuron.

The neuron's smart. It's like, I need to protect myself. So what does it do? It releases amyloid and the amyloid goes, it traps the microbe or the virus, it engulfs it and it kills it. This is like what white blood cells do with cancer cells. It detects cancer, goes through, it engulfs it, kills it, right? So you eject the amyloid, it goes in, it kills the virus and then there, but it's outside now. So now we have to get you into deep sleep at night, which is why we sleep. In fact, before antibiotics and penicillin, we were sleeping 11 hours a night, so we'd be able to clear it all out, right? That's how you do it. So then you've got tau protein. Now tau protein lives in the, um, in the axon, as I mentioned, and if that builds up, it actually causes the collapse of that tree trunk.

Shit.

So then the question is, well, how do we stop it from being ejected? Why would— like, how do we— like, it makes sense, right, mathematically? Well, let's just stop the, the brain from ejecting the amyloid in the first place. That, that'll solve it. But why does it get ejected? Well, because it's— because it's an antimicrobial peptide. It actually gets released every time you activate your innate immune system. Every time you get stressed. Remember, the brain doesn't know the difference between you getting hit by a car or you just receiving a text from an ex. It depends on your emotional security at that time. If you get stressed and you release all of this cortisol, it signals to your brain that you are under attack. You're running away from a lion. Massive amount of cortisol, the stress hormone, gets released. So your brain is like, I'm under attack, let's release, uh, amyloid to protect our brain cells. We get an influx of inflammatory cytokines, these, these neurotoxic protein— these neurotoxic cytokines that go into the brain, just like inflammation in your body, but inflammation in your brain, neural inflammation. If your brain senses it's got inflammation, it starts to release amyloid to protect you.

And when it's first released, when amyloid is first released, it's, it's not harmful. It's soft, it's a monomer. It turns in, it turns into this, a lot, these different fibrils, and then it actually comes together. That's when it becomes toxic. So amyloid's not the demon, and yet Pharmaceutical companies know this, and yet they're still spending money giving you a medication to clear the amyloid when they should be spending their money figuring out how do we get people to, you know, stress less, sleep interventions, natural things to help people in their daily lives to prevent this from happening.

Why aren't they doing it? Just because of the business?

Well, there's no money in it. You can't make money on an exercise intervention because it's free. You can't make money really on a sleep intervention because it's free. You can make money on a monoclonal antibody, which is the IV drug, Lecanemab and Donanemab. That's what they are. If you ever hear the word MAB on the end of a pharmaceutical, it's a monoclonal antibody. So these are used to go in and clear the amyloid, but that's not the problem. So there's another phenomenon that I want to bring, you know, shed light on, which I think it's really, really fascinating. We have something in our brain called cognitive reserve. I mentioned to you 87 billion neurons. By the way, every neuron has around 15,000 connections. Do the math on that. 15,000 times 87 billion, that is your neural network, and it's firing, right? So the, the leaves, again, when they communicate with one another, that's a connection. You have 15,000 per neuron. Those connections are your cognitive reserve, right? So we want to keep it in reserve. And the reason why you can have a head full of amyloid at the end of your life but preserve your cognitive functions comes down to your cognitive reserve.

Your cognitive reserve is built through everything that you do, right? When you go for a run, you build new connections in your brain. When you see something new for the very first time, you build new connections. This is why a baby's brain is formulating so rapidly because everything is new to them. Sound, color, anything, light, buildings, everything. Imagine seeing something for the very first time. Your brain has to build a connection. So this happens throughout our life and you can keep building cognitive reserve. It's really beautiful. But what happens is we stop doing it because we get older and we stop exercising. Actually, a huge risk factor for Alzheimer's disease and all-cause dementia is retirement. Because you stop interacting socially, you stop using your brain, you stop providing it stimulus, therefore it's not creating new connections. And also those connections that were preserved, the ones for mathematical reasoning or social connection, if you stop using those, those connections die off.

I mean, that's interesting because you would think it would be less stress after retirement, but that's not what your brain is.

Your brain is it needs stimulus. Just, I mean, you would think that as well, like, oh, why would our muscles deteriorate if we just have less stress? Well, you have to use them and you have to provide a stimulus for them to grow and adapt. That's actually evolution, right? Adaptability. So you provide a strong stimulus and it grows and it adapts. So if you want to preserve your cognitive functions, you need to be deliberately doing things in your day-to-day that's going to be effortful, right? Yes, exercise. But how about reading? I don't know if you agree with me on this. I'm, you know, in, in your amazing studio, you've got so many books and I'm an avid reader. I think we have a literacy problem in the US right now. I don't like, I'm like, a lot of people are finding it difficult to articulate words, uh, to articulate their thoughts and to even read because they don't have to because we've got AI now. Or we've got videos on YouTube, you know, growing up we— I didn't have the internet. I know it kind of makes me feel old, but every time I needed to study something, my father would say, get the encyclopedia.

So you'd have to build those connections. We're losing those. So seeing culture, you know, new cultural things, you know, if you want to age somebody fast, get them talking to the same people every day, get them doing the same things. Not challenging their brain, living in a secluded form, talking to the same person every day and not seeing new things. If you wanna grow your brain and have an enriched environment, travel, travel somewhere cuz you see something new that your brain's never seen before. And every time you see something new, your brain creates a new connection and you add to that cognitive reserve bank. Let me tell you, you want that bank, you want it there cuz you never know what's coming your way. You don't know if you know, you have a tragic accident where you'd be concussed in the head. You don't know if you're going to get a virus that will engulf your brain. You want to be able to have so much reserve there to overcome any insult that it takes.

What is the— what is a person with Alzheimer's experiencing? I think, I think pretty much everybody knows what it is from the outside, but what is, what is the person actually experiencing? Is it stressful for them? Do they— yeah, how do— how does it—

how is it at the core? Loss of sense of self. What is yourself? It's your— it is your cognition. So they're losing sense of— look, you've got in some aspects loss of spatial awareness, right, where they can come closer towards you. I've noticed this, you know, with my father. You know, he had his stroke, and a stroke obviously causes deterioration in a certain part of the brain, and you lose the cognitive faculties around there. I've noticed he's lost spatial awareness, and you see him sitting close to you, and it's so interesting. Um, you know, he sits so close to my mother now on the couch. He doesn't realize where he is in space and time. He can forget Obviously you can forget certain things like walking into a room, yes, but to a larger extent you can be driving, which happened to my father as well, which he— I don't think he should have been driving. He was cleared from the doctor because his eyesight was fine, cognitive faculties were fine. He was driving, he forgot to hit the brake, right? He went straight through a traffic light, car tumbled down, he was left upside down, and he had no idea what happened.

In that moment. And he was— he's miraculously, because of, of God, I believe he was fine. He came out without a scratch, but the car was torn apart. I asked him like, what, what happened? His brain didn't relay in that moment, in that split second, red light, stop, which he knows, but just didn't happen in that moment. So people are feeling, you know, they don't want to be surrounded. You know, you can get auditory dysfunction. Actually, the American Academy of Neurology actually put down mild hearing loss as a symptom of cognitive impairment. So you get mild hearing loss and it is now a risk factor for Alzheimer's disease and dementia. Why do you think that is? That's because I told you every brain cell in the brain needs to be utilized. It needs to be, or it starts to think that, hey, she's not using me, I'm gonna die, I'm gonna— I'm just gonna die because she doesn't need me anymore, to preserve my energy. Your ears are here, right? And your ears are connected to the cells in your brain, which is in the, uh, in the temporal lobes of the brain. Remember, that's where, deep in the temporal lobes, that's where the hippocampus lives.

If you're not using the cells around here, because when you hear sounds, you need to process those sounds. In your brain. So you need to use this part of the brain to process sounds. And if that's becoming dysfunctional because you can't hear anymore, then those cells in the temporal lobe start to die. Which is why with the military— I spoke at the inaugural military convention on TBIs and sounds. People think the TBIs, it's just the hits to the head. It's no, it's the sounds, the massive explosions that can cause mild hearing loss. And actually a lot of the vets there had hearing aids, which I love. Hearing aids are phenomenal because they can help you preserve your cognitive functions. If you start to, you know, lose a sense of sound, then that can deteriorate your brain. The back part of our brain, the occipital cortex, we don't see with our eyes, we see with our brain. You've got your eyeball there, the retina, then you've got the optic nerve that comes out of the, literally from your eyeball goes into the brain. And the signals travel down here to the back of the brain where you make sense of— you've got a black hat on.

The only reason I know that is because this part of my brain is functioning. It tells me what the image is and then it relays it back to the frontal cortex. That's the executive processing part of the brain that gives you the idea that, hey, that is a black hat that you are wearing. That becomes slower over time. Right? If you've got Alzheimer's disease or if you've got mild cognitive impairment, that rate and that speed becomes slower. So you'll see something happening, but it takes you a long time to process it.

Oh God.

This is why some people who have got a lot of cognitive overload when they're driving and they're trying to figure out where they're going, you just need your eyes, but they're like, turn the music down. I need to see where I'm going.

Hmm. Are they aware? I mean, how a lot of them get angry.

Of course they're angry. They're frustr— they're frustrated because they don't know what's happening to them. They're experiencing a loss of their faculties that, you know, think I know for myself, and I'm in my 30s, right? When things become— I'm not as sharp as I was in my 20s. When I was 25, oh my God, you should have seen me. Like, I was, I was able to do so much with little sleep, right? Now I, I need my 7 hours, 7 and a half hours a night, or I'm not, I'm not myself. Things are becoming slower. For my father especially, he gets very frustrated and his frustration turns to anger when he has to do something that is a bit mathematically challenging. So he took care of everything in our house, and now my mother does when it comes to bills and, you know, their properties and investments. And my mother has to take care of all that because my dad simply just— he looks at it and it's— he just cannot make out what to do, and it frustrates him. And he's spoken to me about it, and he very much frustrates him to the point that, um, it— that's when you start to lose— you start to question, who am I in this world?

Damn.

And depending on where— look, Alzheimer's disease, as I mentioned, it starts in the hippocampus and it starts to go out into the temporal lobes and then the, the frontal part of the brain. Remember, your frontal lobe It's the biggest part of the brain. It has the most amount of neurons.

It—

that's where our executive functions live in the prefrontal cortex. I kind of think of the prefrontal cortex as the federal government, right? It's making all the decisions and that starts to deteriorate. And that because it's so got the most populated amount of neurons, those start to become dysfunctional. And that's when we start to, you know, our thinking and our intellectual capabilities start to decline. Let's keep going if you're okay.

Mm-hmm.

I said to you that it takes around— it's a highly metabolic organ. So how is it powered? So how are neurons surviving? It uses glucose as its primary fuel source, right? So glucose is its primary fuel source. Have you heard that, you know, in some aspects that Alzheimer's disease is type 3 diabetes? That's what they say, right? Why is that? Well, as we get older— and it actually occurs more in women, so this is where we're going to be a bit gender-specific— why are 70% of all Alzheimer's disease cases female? Right, why is that? Well, A, because the first— the, you know, the biggest risk factor of Alzheimer's disease is age, right? As you get older, you've got an increased risk of getting the disease. The second biggest risk factor is being a woman.

Really?

Yes, the second biggest risk factor is being female, and that is because of two reasons. A, on average, women live around 4 0.5 to 5 years longer than men. So it increases their age, so they've just got a greater susceptibility of getting the disease. The second one is because women go through the hormonal transition, which is causing the increased risk factors of getting this disease. We start to lose estrogen and progesterone, and you know what this is called? This is called menopause. Okay, when you get the complete cessation of our primary hormone, which is estrogen. Right, so just with the amyloid cascade hypothesis, we used to think that estrogen was just a reproductive hormone. That's all we thought it was. Women, you know, start, you know, stop to, you know, they stop producing estrogen, that means they can't produce children anymore. That was it. But it's only been in the last 10, 15 years that we now know that estrogen is a neuroendocrine hormone. Meaning that it is a hormone that we need for our brain cells to survive. Now, you are a male, you have estrogen too, and your brain is more protected because you go through your own type of menopause.

It's called andropause. But for women, it's this steep, steep collapse. Okay, so at age 45, right, this is what happens. The decline of our hormones start to go down like this. For men, it goes down really, really slowly. So you can maintain your estrogen and your testosterone. You have estrogen too, believe it or not. And what happens with testosterone in the brain is testosterone aromatizes into estrogen. So you have that protective barrier in your brain of estrogen throughout your life, whereas women downfall. So we've lost our estrogen, right? We can help that with hormone replacement therapy. But why is estrogen so important? Well, on our cells we have receptors, right, for estrogen. Imagine a receptor like a key in a lock. That's the receptor sitting on the, the cell body. This is estrogen. Estrogen's floating along, it gets in, and then it can get into the brain cell. And what estrogen does is it helps with neural inflammation. So it detects, okay, she's got inflammation in her brain, brings it down. It also helps shuttle glucose into the cell. So if I don't have estrogen in my brain anymore, where's the glucose going? It can't get into the cell.

So therefore I've got two problems. I've got a buildup of glucose in the brain because it's not getting into the cell, it's not getting utilized, right? Just like the glucose in your bloodstream, in your body, you become insulin resistant, so higher risk for diabetes, insulin resistance in the brain. So it starts to deteriorate the blood vessels of the brain because it's just floating around in there, it shouldn't be there. And B, that means the cell doesn't have energy, it doesn't have its fuel source because it's not being able to get shuttled in So what does it do? Well, the brain cell in that state, that's what's causing the brain fog in the menopausal women. We've heard, you know, brain fog, um, is deteriorating the thalamus, which is where our temperature control mechanism is. So this is why 60 to 70% of all women experience hot flashes during the menopausal transition, because their hypothalamus doesn't have the estrogen anymore, so it's not supporting the hypothalamus anymore. So the the thermoregulatory system in your brain doesn't know what it's doing, so it's making you go really, really hot, and then it's making you go really, really cold.

And that's a hot flash, and that's keeping women up at night, not allowing them to get into deep sleep, not allowing them to clear out the plaques. So we've got so many problems. And that was another flawed study back in two— in the early 2000s, the Women's Health Initiative by far the most fraudulent study in all of medicine. And it, it starved and wronged millions upon millions of women out of taking hormone replacement therapy. Millions. And so now we're, we're suffering, right? We've got all these baby boomers. My mother is one of them. She's 72 years old and she's got her cognitive faculties intact. She's fine there. But she was scared out— like, she, her, her doctor never told her to take you know, 20 years ago to take hormone replacement therapy because this study went out there and said that hormone replacement therapy increases your risk of breast cancer.

Does it?

No, no, that has been retracted. We now know that hormone replacement therapy is safe. They used a different type of, um, of estrogen back then when they were testing it on women. There was many things wrong with the study. A, they were putting conjugated estrogen, which is they took the estrogen from the urine of female mare, so horses, horse urine estrogen. And so it's a synthetic form of estrogen. They were putting it into these women. These women on average were around 63 years old, so they had already surpassed menopause. And so it wasn't working, um, and it actually increased their risk of dementia. So what we have now is we have a safer option for women It's bioidentical hormones. So you can take a hormone patch, an estrogen patch, you put it on your body and you replace that. I believe, I'm not on HRT yet, but I will in my 40s. Basically, we have a window of opportunity. So women must get on their hormone replacement therapy between the ages of around 42, 45, and 52, when you still have circulating estrogen in the, in your body, for it to go in and mimic that hormone, and it becomes bioidentical.

So you have that, you have now a safeguard. It's called the window of opportunity.

So women need to start hormone replacement in their 40s?

Correct. So generally you want to get on it when you're in the perimenopause stage, which again, just like mild cognitive impairment, perimenopause happens 10 years prior to the onset of menopause. Menopause is just one day, right? It's when you have been 12 months without your menstrual cycle.

Okay.

So if you reach that 365-day and you haven't had a period, that is the first day of menopause. It generally happens at around 52, right? So women can get into perimenopause in, in their, you know, at 42, at 40. It varies, and that's when you need to go to the doctor and discuss your symptoms. And it can help you. It can help you stave off dementia and Alzheimer's disease, and it can help you with your symptoms, which is the biggest thing affecting these women.

Is there any data that shows how— what percentage, uh, it, it deters dementia? Alzheimer's?

So we haven't got the research yet, okay? The research is underway, and actually this is a huge controversial debate amongst, um, academics right now because we can't solely say hormone replacement therapy prevents dementia. We can't say that. But what we can say is we know for sure that it helps with the symptoms involved in the risk factors of dementia, meaning If a woman's going through perimenopause and she's experiencing hot flashes, that means she's getting up at night, she's frustrated, she's hot, she's sweating, right? That's keeping her up at night. That's a— so sleep deprivation is a risk factor for Alzheimer's disease. If I can correct that in a woman, then that's going to help her stave off Alzheimer's disease, right? What is another risk factor? Well, Diabetes, osteoporosis— huge risk factor as we get older. A lot of women who are in menopause have osteoporosis because we have estrogen receptors on our bones. When we lose those, then we stop the formation of our bones growing and they start to deteriorate. What happens if we get osteoporosis? Well, our bone actually communicates with our brain first and foremost, but A woman, if she experiences a fall in her 60s or 70s, it's a steady decline to death after that.

Shit.

Yeah. So there are so many things. So I, I like to think of hormone replacement therapy— it's not your be-all and end-all, but it's going to help you go to the gym, it's going to help you lift weights. Estrogen is anabolic to muscle, so it's going to help you build more muscle. It's going to help you with your mood swings. It's going to help you with your hot flashes. So that's, that's what it— that's what it's there to do. It's to help your symptoms so you can then do the things that you're meant to do, like go to the gym, sleep, eat well, so then you can have a better healthy brain.

Oh good. Oh good. Mind if we take a quick break?

Yes.

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See you later.

World's tallest building. What do you think, Sean? We're high. All right, Luisa, we're back from the break. We just kind of wrapped up women's hormone replacement therapy. I wanted to go back just a little bit about what the what a person with Alzheimer's is actually experiencing. And we, I can't— we kind of talked about the beginning of it.

Yeah.

But I have— I don't— my wife actually, one of her really good friends, her, her father has it, and they sectioned off the house into two different basically apartments. And her dad's just completely gone. And, uh, you know, my wife has asked her, like, you know, how do you, how do you deal with this? And she's, she says, I don't even visit him anymore. He's, he's legitimate. Like, she considers him dead. It's just not him.

Exactly. But remember, at that stage, you're— that's it. You don't know. You don't even— you don't, you don't have control over anything. It's— you are not in control anymore when you're— it's your brain has now taken control because your brain has decided that it's time now to like decompose, really, because it's, it's thinking, well, I'm no longer— like, it's that the signals are all cut off, so you are not in charge. Your cognitive faculties that are responsible for you going to the toilet, or you don't have control over those anymore. It's another force, and that force is the accumulation of those amyloid plaques. And so what you'll notice though is a lot of patients who have got Alzheimer's disease— we're not talking about mild cognitive impairment anymore— they kind of feel like they want to do this from the world. A lot of them, you'll see, they start— they stop to— they stop going out and communicating with people and socializing and They become so secluded, it's like they just want to stare at the wall. I've had, um, the daughter of somebody tell me that their mother, she noticed that she started sleeping facing the wall only, and she didn't want to see anybody.

She just wanted to face the wall, and that's it. Um, that's what makes it so devastating. So they're feeling lost, they're feeling confused, but they're waking up every day not themselves. So it's, it's not who they are, and it's so devastating. You know, we think two-thirds of all Alzheimer's disease cases are female, and then also a third are carers.

A third are what?

Are carers. So it's usually the females who then end up taking care of a person with Alzheimer's disease, albeit mother, father, husband, whatever it is. So you've got enormous pressure placed— and Emma Willis speaks about this, the wife of Bruce Willis— like caregivers, enormous, uh, financial burden, and seeing a loved one forget who you are. So it's actually hard on both parties. It's hard on the person itself. You have to think, this person who has Alzheimer's disease, they don't know if they've eaten. Sometimes a lot of These people starve as well. They don't know if they've eaten. They sometimes— they forget to swallow. They don't know if they've hit their head. They don't know if they're feeling pain or not. They don't know if they've been to the bathroom. More often than not, it's, you know, just the wedding themselves or something like that. So they don't realize any of this because your brain is not functioning. And your brain does not function, your life doesn't function.

Do they go in and out of it?

They can become lucid at times, yeah. And that's very unpredictable.

Why does that happen?

That just happens. Well, we don't know. You know, you can become a— it's just a small moment in time where you can be laying there on your bed and you can recognize your wife or your child. You can recognize them for a very short period of time. There's a movie that was made and it was so beautiful. I forget the actress's name, but it's called Still Alice. And, and basically it chronicles the woman who gets diagnosed with dementia in her 40s, and that's called early onset Alzheimer's disease. That's the one that's predominantly genetic. As I mentioned earlier, when you do get those genes, if it's presenilin-1, presenilin-2, amyloid precursor protein, if you've got it, you will get the early onset Alzheimer's disease in your 40s, right? But most of diseases occur due to late onset Alzheimer's disease, which is the genetic— which is the lifestyle ones. So if you see her in this movie, you can see the fast deterioration of who she is to death, really. And you should watch it because she starts to lose everything. Like, first of all, she, she's driving, and then out of nowhere she's looking around, she's like, where am I?

Where am I driving to? What am I doing? And that's the mild cognitive impairment stage. But I was asked on Tarja Vasillo, which is quite a funny question to me, when he's— after I explained, you know, over a 3-hour period what Alzheimer's disease was, he said, Stephen said, well, what would you do if you got Alzheimer's disease? And it's like sort of a question. I don't— I couldn't do anything in that moment. I could not do anything. Nothing. No, no therapy would help me. Um, no amount of exercise would help me. No amount of sleep would help me. My sleep would be completely disrupted. I wouldn't know who I was. I wouldn't know if I'm walking on the road. I wouldn't know if I'm eating out of a garbage trash can. I wouldn't know what I'm doing.

The reason I was just— I'm wondering, you know, is this— is it harder on the family or the caretaker, or is it harder on the person? Does the person even realize what's happening?

I mean, exactly. And that's what's so devastating.

Or are they just staring off into space all the time?

And they don't know.

They don't know.

No. Just like this beautiful patient that I say came to me, literally. And I have seen— and this is how I really started in this, um, going on this journey of wanting to end this disease and focusing on women as well, because I did have this one woman I was tasked with them. I mean, neurophysiologist, so, um, usually somebody who you'll see when you've had, um, when maybe you've suspected of having MS or you've had a seizure, and we assess the functionality of your brain. And I was tasked with heading up an entire Mild Cognitive Impairment or Alzheimer's disease unit. And I had to do that by scanning brains, and I scanned thousands of brains. And every time I would go to a meeting, these, you know, biweekly meetings, I'd say, you know, I'm giving a diagnosis of MCI to 90% of these patients, but like a third of them are women. Why? And every time I asked why, they would, you know, the attending would always say to me, it's just what happens. We can't do anything about it. It's just, they've got it. You know, genetics. They could never give me an answer.

It was frustrating because one woman came in, I tracked her over a 5-year period, husband, 2 kids, came in addressing me by my name. And over that period, like at the end of those 5 years, she'd come to me and she'd say, are you my daughter? And I, And at that time I was troubled because I had built a relationship with her and her family. You give the diagnosis of there's nothing we can do. And this was, you know, somewhat 10 years ago when we didn't know as much, but then you're the, the, the spouse, you've lost somebody. It is like a death. They are no longer there.

Yeah. When it comes to habits or anything that increases risk, is there, is there increased risk with alcohol, marijuana?

Yeah.

Drugs, certain medications? What, what, what are some, what are some common things that people are doing that increase risk?

So there is the famous Lancet study. Lancet is another academic journal that came out with 14 modifiable risk factors, meaning that these are risk factors of getting the disease, but if you modify them, you lower your risk. And turns out that there's 14, right? So they include things such as, first of all, smoking, right? We all know this. If you smoke, you increase your risk of all-cause mortality. We all know that. Hypertension, so your blood pressure, if that's high, I told you We want to maintain blood pressure. We want to maintain 100 over, uh, 120 over 80 as the gold standard. I don't know, do you measure your blood pressure?

Every once in a while.

Every once in a while. There's now actually, um, continuous blood pressure cuffs, so I'm going to buy one for my father because that increase— this is what caused his stroke, right? So this is a really great and easy way, uh, non-invasive and inexpensive. Obesity. One of the biggest risk factors of getting Alzheimer's disease is obesity, which I think now we've got a grip on because of GLP-1s, which is what makes GLP-1s, you know, Wegovy, like Ozempic and Triseptide, which what makes them so phenomenal.

So these are good drugs?

Oh yeah. Oh my God, I am— they are remarkable. GLP-1s are absolutely remarkable. And I think, you know, when, when, when we first founded as humans penicillin, it was like this breakthrough moment. Then there was insulin, which is also a peptide, breakthrough moment. Now we have, you know, we can help people with type 1 and type 2 diabetes. Now GLP-1s, and I think it's definitely on par, and I think it's going to be something that is going to eradicate diseases.

Wow.

GLP-1s will eradicate diseases that in 100 years— I don't think you and I won't see them, uh, but I do believe in 100 years people will be saying people were obese. You'll look— we will be— our nation will be in— our society will be in medical textbooks and people won't recognize it. I don't think people will know what Alzheimer's disease is either.

You think it will solve that eventually?

I think it's going to solve a big portion of it because we're now— there was a huge EVOKE trial which tested, do GLP-1s prevent dementia? And it failed. But it failed because of many reasons. A, we can't directly say that just take the GLP-1 and you're going to lower your risk. Just like hormone replacement therapy, it's doing other things. A, it's helping with insulin resistance, and B, it's helping with obesity. C, we're seeing a lot of patients who are, um, they don't feel like they want to drink anymore, so it's stopping alcoholism. In fact, I think, was it this year, in 2024, um, alcohol sales have completely gone down. Have you seen that? Now there's—

I have, I've heard that.

Yeah. Which is phenomenal, right? Because alcohol increases your risk of Alzheimer's disease. So trisepatide, um, these— we're now getting retatrutide, which is, um, has got 3 hormones in it now. Trisepatide has 2. I think this is going to be even more remarkable. So yes, so obesity is a risk factor. Uh, type 2 diabetes is another modifiable risk factor. So you mentioned like, what am I doing to increase my risk? Well, drinking alcohol— no amount of alcohol, no amount, I don't care what anybody says— is good for the brain. Alcohol is actually diminishing the white matter of the brain. So you know that, that, you know how I told you about the axon, the tree trunk? So that's part— that's coated in this myelin sheath, right? And if you have a look on imaging, it's called the white matter of the brain. The white matter of the brain is the myelinated neurons. It's the tree trunks of the brain. So when you drink alcohol, and this was actually done in a UK Biobank study, when you drink alcohol, even as moderate drinkers, which is around 7 drinks a week, on neuroimaging, when they took photos of their brain with an MRI, they showed what we call white matter hyperintensities.

So in the white matter of the brain, They've got these, these deteriorated portions. You're also affecting the gray matter of the brain, which is the cerebral cortex where the neuron cell bodies live. So alcohol is detrimental for the brain. Okay, so don't do that. Evidently, like I said to you, smoking, um, social isolation is now becoming a huge, huge one as well. Um, we're becoming—

why is that? Why is that?

Well, we're becoming more isolated because we're obviously on our computers more. But why is that? Well, there was an 80-year-long study done at Harvard which showed— they wanted to track over an 80-year period, at the end of this 80 years, who has the best health and who has the best brain, like who's aged their brain well. It turned out that it comes down to the quality of your close relationships. Out of everything, out of— they accounted for every variable. They accounted for sleep, nutrition, exercise, and it turns out that those who maintained good quality relationships showed better signs of brain aging than those who don't. Why? Well, basically, if you have somebody that you can lean on, throughout your years. This doesn't mean romantic partner, doesn't mean you have to go and get married to preserve your brain, right? Um, it means that if you can feel safety in another person that you trust, that knows who you are, it regulates you more, regulates your nervous system better. Secondly, if you have somebody that you can talk to who knows your life and that you can have deep conversations with, also challenging conversations, that's another human that you're interacting with.

Remember, every cell in your brain is getting utilized. The way I'm looking at you right now, your facial features, my— me being able to pick up on everything. You're different too, obviously. You look different to somebody else, so my neurons have to accommodate for that. So having somebody by your side that you can talk to— and this is why, you know, close friendships that take, you know, that take long, long years to accumulate really matter.

Is there any— is there any information on how many relationships you should be maintaining?

No, but I mean, it's very hard to maintain close relationships. I've got a close group of friends, and you know, you're not just like acquaintances, you, you know. And this is, you know, I've built my close friendships, and I spend a lot— you invest a lot of time in them because you have to. And I've maintained my, my close, and some of them have fallen off. And yeah, build new ones.

Any other risk factors? Um, well, not exercising.

Probably the biggest one is lack of physical activity. In fact, um, inactivity is now a disease state. Inactivity and sedentary lifestyles is an actual disease.

Are you serious?

Yeah.

What is that disease called?

Inactivity. Sedentary. Well, it's called sedentary. Yeah, sedentary lifestyle. It's now classified as a disease.

When did that happen?

Uh, back in 2024.

How many people are suffering from that disease? Uh, that's a choice. It feels like a choice, not a disease.

Well, you could say the same about type 2 diabetes. It is a choice. You could say the same on some part— I know this is controversial because of, um, you know, GLP-1s— but obesity to some extent, apart from, you know, different genetic risk factors, could be somewhat a choice. You do get a choice in everything you do, uh, which is the choice to get up and move. So that actually is a really good segue to what I focus most of my, my academic research on, and that's exercise. So if you want, we can delve into that.

Yeah, let's dive in.

How many days do you have?

We've got as long as we need.

Um, I do want to point out, because I, I just— I mentioned women. Men have something else that's not often spoken about. It's called EMLOI, where 17% of men actually lose their Y chromosome. Yeah, and they lose it in the immune cells. So you're obviously, you know, we have different genes, X and Y, XX. 17% of men lose their Y chromosome in their immune cells, which actually is increasing their risk of getting dementia and different neurodegenerative diseases as a whole family. And it hasn't been specified yet, but my hypothesis, you know, I think about, well, why, why are men at an increased risk of a) Parkinson's disease and b) amyotrophic lateral sclerosis? I don't know if you saw, um, McSteamy from Grey's Anatomy. I forget his name in, in real life. He, oh, one of the leads in Grey's Anatomy. Um, just passed away of ALS. I think it was 2 weeks ago.

Oh man.

Uh, which is very— it's probably the most— it is so scary, Sean, to see in real life because it's so fast-acting and deteriorating. So I— you can test for this. You can test whether you're losing your X chromosome through a genetic test, um, generally over the age of 50. So that's one thing that we didn't pick up. It's called MLOI. Okay. So now let's segue to exercise. I think, I think it's so prominent to talk about because A, exercise is free. B, the only reason we call it exercise, it wasn't called exercise 200 years ago because people were running and doing things. We have to now because of technology and the way we're living, we've now formulated the word exercise, right? Which doesn't mean, which I tell my mother every day, doesn't mean you walking around the house and getting the clothes off the line. That's not exercise, right? Exercise is structured programs where you are increasing your heart rate or moving your muscles or contracting your muscles. So first of all, we'll separate into 3. You've got the aerobic exercise and the fast-paced VO2 max exercise. You've got resistance training. Or strength training, and then you've got what I call neuroathletics or neurocognitive training.

The relationship between aerobic exercise and brain health was the first one to ever be discovered. Marian Diamond back in 1960 or 1961, basically she got two sets of rats, right, two sets of mice, and one were put on a protocol of wheel running. So she got these mice running on wheels, and she got them in what she called an enriched environment. She was the first female neuroscientist, by the way. Enriched environment, so really nice cage, lots for them to do, and with other people as well, or other mice. Over 6 months of wheel running every single day, what she found was that their brains grew. She's like, why were their brains growing? And not just— so they were, they were growing new new brain cells in their brain. And she figured out that the mechanism was every time they were running and their blood was flowing through their body, they were releasing a hormone called BDNF, brain-derived neurotrophic factor. And it turns out that this is a growth factor for the brain. So when it goes into the brain of these mice, it grows the brain, right? What she found was with the other mice who didn't do anything— obviously they weren't in an enriched environment, they were in a depressive environment— actually their brains shrunk, especially the hippocampus.

So that was the start. That's where we first knew that exercise is good for the brain. When replicated on humans, it works the same. So when we exercise, we get this massive bolus, okay, massive release of BDNF. It goes into the brain and it helps our brain function better, but it doesn't help us grow new brain cells. In fact, We can't as humans grow new brain cells. That's called adult neurogenesis. It doesn't exist, which is sad because if you've taken a huge hit to the head, a TBI, and you kill off brain cells, you can't revive those. Like my dad, when he had a stroke, killed off certain neurons in the brain. They can't grow back. But what we can do is we can grow new neurons in the hippocampus. Isn't that beautiful? Because remember, the hippocampus is the first structure to go during Alzheimer's disease. Disease. So if we exercise— now, this beautiful study, which is one of my first, uh, most favorite studies, uh, in 2011, um, Ericsson et al., basically what they found was if you exercise for 30 minutes a day, aerobic exercise, you can grow the hippocampus by 2%. The volume of the hippocampus, you can grow it just by 30 minutes of exercise.

A day. Not just that, 30 minutes of exercise a day. You know what else it does? It downregulates 13 types of cancer.

No kidding.

Yeah, there's now— it's so prominent that there is now a new field in research or in medicine called exercise oncology. I've done a whole episode on it. It's one of my best performing episodes, which showed that through exercise interventions you can mitigate your risk of tumor cell growth.

No shit.

Yeah. Most prominently breast cancer, colorectal cancer.

Wow.

Yeah, that's prostate cancer.

Those are the three. Yeah.

Mm-hmm. Just from 30 minutes of exercise. So exercising for these long periods of time using the aerobic system gets the massive release of BDNF, and that's what's helping the brain. Now we didn't stop there. That was the first ever studies. Then they moved on to what does the high-intensity exercise do? You know that one that, um, I don't know what your exercise regime looks like, but the VO2 max exercise where you're going so hard you feel like you're going to vomit. And when I was a triathlete, we would call them spew sessions. I don't know if you ever do these.

Not anymore.

You should, okay? Spew sessions, right? So it's when you're going hard out, you're in that zone 5 cardiac zone, right? Where your heart rate is reaching around 90% of your maximum heart rate. What is this doing? Well, A, to go to that effort, you're using the anaerobic system, right? So when we're in the aerobic system doing the long exercise bouts where you can last for 30 to 60 minutes of running, you're producing energy in something called the mitochondria. Okay, the mitochondria is the energy powerhouse of the cell. So we're, we're in there, it produces energy for us, and that's how we get our energy to run. But when we're going so hard out at 90% of our maximum heart rate, it's, it's the mitochondria can't produce that energy in that fast time. So when it does, when we produce the energy, it happens outside of the mitochondria. A byproduct of that Okay, during the, the byproduct of producing glycolysis is lactate. And lactate produced in that moment is a fuel source for your brain. So the lactate, it's a, it's a myokine. So basically it comes out of the cell and it goes into the brain, and that's what can produce better brain energy.

It can help neurons that are dying survive better. It can help with brain energy metabolism. So it helps your brain produce more energy and utilize energy better. It's just such a phenomenal, phenomenal fuel source for your brain. Right? And this is where most of the studies are done on cancer. In fact, what we find in the cancer research and exercise research is exercising at that intensity, right? What happens is you get this shunting of blood, right? Imagine the tubes, like the highway system, like your blood is pumping, boom, boom, boom, boom, boom. And in that moment, when it's pumping, it's taking with it and clearing out something called circulating tumor cells, right? So when you have stage 1 cancer, it's local, okay? It's a, it's a, it's a growth, it's a tumor that's formed somewhere in your body, right? Let's just say prostate. Stage 1, meaning it hasn't metastasized. But the way tumors work is the tumor cells off that one tumor break off and they, they go through the bloodstream and they think, where can I lodge myself again? And if it does, if enough tumor cells break off and then they form another little family, that's metastasized.

Now you're moving into stage 2 and stage 3. Exercise at that zone 5 is clearing out those circulating tumor cells.

Wow.

And that's how it's downregulating tumor cell growth.

Wow.

Yes. And a study was done on this in the journal Cell, which showed the effects of this, of inhibiting prostate cancer in men. So that was pretty interesting to me.

That's good to know.

So it's doing a whole host of things. Where my area of research is, is really taking place— I, I first authored a paper that was printed in The Journal of Aging was I wanted to look at what are the effects of resistance training on the brain. It turns out that there is far more effects of resistance training on the brain than these two categories. First of all, when we, when we, you know, lift a, lift a, a dumbbell, right? And we're, we're shortening our muscles, we're contracting our muscles. What happens is we produce and shoot out something called myokines. These myokines live in the skeletal muscles, right? They live in the cells of your skeletal muscles. They just live there. And when you squeeze them hard enough, like literally under tension, they get released. And when they get released, they go into the bloodstream and they travel. And we've got receptors just like the hormone receptors of estrogen. We've got receptors all over our organs, our heart, our liver, our pancreas, and our brain. And when these myokines get released, they do so many different things. They go in like instructions. I call them care packages.

They go into different cells and they help the cell perform better. So cells are— they're really phenomenal, right? Whether at the DNA level or whether just in the cell itself, the cytoplasm, they've got instructions on how to do things. How to keep you from dying pretty much, or how to, you know, survive, like how to— how your cell survives. When those instructions, like when the mitochondria becomes dysfunctional, that's really at the root cause of all diseases. But we can fix this mitochondria, right, by sending in instructions to fix itself. Right. It's called autophagy. We can grow new mitochondria or we can just correct the bad ones. Right. And we can do that from these myokines. So when the myokines go into the brain, They're helping the brain do better things. They're helping the synapses of the brain, the ones, the synapses that are like, you know, where do we— they form the synapses again. It's called synaptogenesis. Um, they grow new neurons in the hippocampus. They help your, your different areas of your brain grow and proliferate. They work together as a camp. There's like 100 different myokines. They work together as a camp to help each other express themselves.

They help with immunity. They help with the clearing out of amyloid beta. They're doing so many different things for your brain and your organs that I've got to tell you, pharmaceutical companies are trying to replicate these myokines. They're trying to replicate them in pharmaceutical forms to make them injectable drugs, and they can't do it.

Really? How long have they been working on that?

Years. Ever since we first found out about myokines, like back in, like, you know, the early 2000s.

You think they'll figure it out?

I hope not, because that means we're just going— we're just going to sit there for the rest of our lives and inject ourselves, right? I mean, look, this whole— I don't even want to get into peptides, but look, I think in 5 years everyone's going to be using peptides.

Really? Why?

Because we're— people are becoming more, you know, the gray market, the black market is infiltrated. Like, people are buying these black market, which I— it's so dangerous, by the way, peptides, right? A peptide is an amino acid. Amyloid beta is a peptide, right? And I think in theory they can do well. We've seen them, you know, in mice studies, but not one human randomized controlled trial has ever been done on peptides, which is why it makes it so dangerous. We don't know what the safety and efficacy is of peptides yet, but I do say that they will start funding it because of who's currently in charge. And yeah, I think that people, you know, will start to see human studies in 5 to 10 years and that's what's going to happen.

So you're not— you are not a fan of peptides?

I'm not a fan. I went out really public with this because one of the things that BPC-157 does, that's the most prominent peptide right now, Body Protection Compound 157. What it does is it's, it's meant to help with cartilage health and, and recovery. That's— a lot of people are taking it. What we don't know yet is it's doing this by inducing vascularization, meaning that it's helping you around the cells of injury, it's helping you form new blood vessels. When you form new blood vessels, what happens? You get oxygen and nutrients. It's great, right? Better healing. But it can't detect whether it's causing vascularization on a cancer cell. And what a cancer— how does cancer survive and grow and proliferate? It forms blood vessels to feed itself. Cancer cells are so hungry when they form a tumor site, they say, okay, great, now we need blood vessels to survive. So they form its own little blood vessel supply, and that's what grows, and that's what metastasizes, because they're like, yes, they become so greedy and so hungry, these tumor cells, they go out and metastasize all over your body. You have no control over that, right?

Whether it goes to your brain, your spinal cord, you don't know. So why would I accelerate that? Because we can't test yet whether you've got stage 1 cancer. We could all be walking around right now with it. It's just too small to detect on neuroimaging.

These imaging things, they don't even detect it.

They can't detect it yet. No. I mean, look, on some cancers, yes. Look, prostate cancer, yes, we can detect it. This is, you know, colorectal cancer. Yes. This is why, you know, everyone should be getting screened and doing colonoscopies because around 95, 99% of all colorectal cancers exist from the polyps that are built up. But you can get rid of those. This is why everyone should be getting screened and doing their colonoscopies and endoscopies. But, you know, breast cancer, I believe so. But I'm talking like, you know, pancreatic cancer, you don't know whether you've got it until stage 4, and then it's— you're done. That's what took my grandmother, um, that's what took my aunt. Ovarian cancer, you don't know. Glioblastoma, forget about it. So, you know, this— how— why would you—

I mean, a lot of people are taking peptides.

And yeah, and not knowing the harmful risks.

I took them.

BPC-157, I believe that's what it was. Everyone's on something called the Wolverine stack, which is TB-500 and BPC-157. There's melanotan, and then there's these secretagogues, which, um, somoralone, ipamoralone, and everyone's taking them. But my question is First of all, I don't know if you know this, but it failed. It failed its trial. You do phase 1, phase 2, phase 3. It failed when they found out how dangerous it was. So the FDA cut it completely. They said this is too dangerous to move forward in human studies.

Okay.

That's why there's not one randomized controlled trial done. This is why you can't go to and get a prescription for BPC-157. So I don't know where you got it from. I'm scared because when you get it on a gray market, or scarily on a black market. Let's just say you get on the gray market. The gray market means that it's not FDA approved, but it comes with a form that basically says, you know, this is what's in it. You don't know what's in it. It could— you don't know what you're injecting. You're injecting it systemically. GLP-1s are peptides, but they've passed Phase 3 clinical trials, they're FDA approved, you get a script, they're not compounded, meaning that, you know, if you go and get it from Wegovy or Zepbound, like they are, you know, they're safe. The safety and efficacy, they have passed with flying colors. How do you know that when you're using BPC-157 that you are not inducing vascularization of a tumor cell?

I guess you don't.

You don't, and you won't know.

Shit.

And so that's my problem. Now, I got a lot, you know, I put this out on social media and I got, you know, even Andrew Huberman messaged me. I'm sorry, like, I, I would, you know, there's another one that's great for the skin, copper GCU. I'm not even sure what it is. I'm into anything that's going to slow me the aging process, right? You know, I spend thousands on my skincare products, for God's sake. If I thought that these were safe for me and my mother and my future children, I'd— everyone get— I'd be telling my mom every day, get, you know, do it. Of course I would, right? But I can't take that risk. Now, if you could go to the doctor and get cleared, and the doctor can say, hey, listen, we've scanned you, we now have technology to pick up you have not one cancer cell inside you that is going to grow and proliferate, then yeah. And they— these have passed clinical trials and they're safe, then yeah, take your BPC-157. If not, to put an ice pack on, like, why are you taking it?

Why are you asking me?

I'm asking you. Yeah.

Shoulders.

And what happened?

They may have gotten a little bit better, but yeah.

And look, it could be placebo, or it could well and truly have downregulated inflammation and helped the healing process. This is why you inject it at the site. You've probably injected it into your—

then that's not what I was on, or I took it wrong.

Yeah, but okay, I'm not sure then what you were on. I'm usually— what happens if you've, if you've got an injury, usually injected at the site. You don't have to, but a lot of people do. They're like, okay, I've got a shoulder injury, inject it here because it goes in systemically and it does a number of different things. But one of them is the formation of the vasculature. So it helps with the healing process around that site.

What did Huberman text you about?

He believed that I got something wrong, which was in one study, and I've put this out on social media. It's funny when you do, you know, a 1-hour-long episode and the thing that gets clipped needs more nuance, right? And what got clipped was I mentioned that in a phase 2 clinical trial— I don't— correct me if I'm wrong, but maybe it was melanotan, it was one of the peptides— it caused death in one person. And I stated that, but I think when it got clipped, it said that, you know, I was referring to every, you know, BPC-157, which I wasn't. You look at the full clip on YouTube. But, you know, he wanted to correct me, and I re-corrected him and said, well, I didn't say that. Um, and because I think he's a proponent of, of peptides. I'm not sure if he—

well, that's where I got my, uh, doctor from, was a recommendation from Andrew. Yeah, which I love that doctor. I love that doctor.

No, look, he, he's phenomenal. We've known each other for so long. Um, and I think he, he sits on the same bandwagon as me. I think he believes that it's going to be a big thing in the next 5 to 10 years. I know he knows that there are no human randomized controlled trials that have been done outside of GLP-1s and insulin, which is another caveat. People were telling me GLP-1s are peptides. I know that. I'm not talking about those. I'm talking about the ones that you buy on the gray market. And secondly, I wouldn't even— you know, I, I don't even buy my supplements on the gray market. I make sure that my supplements, which are nowhere— doesn't pose the risk that a systemic injection does. I don't even buy my supplements on the gray market. That's how like, like adamant I am on safety and efficacy.

Where do you buy your supplements?

Well, I make sure that I'm buying it from a reputable company that has got their manufacturing standards on their website that have been third-party tested, that don't contain contaminants. Like, I go through, I look at their safety scores to make sure that they're not full of lead and full of gunk. And filled with things that I don't want to be putting in my body. In saying that, I'm sounding so much un-pharmacocentric, meaning like I'm not against pharmaceuticals, meaning, you know, I don't live my life like, you know, in an organic, you know, way like that. No, I think that there are certain things in life that you need to realize, like what's safe and what's not.

You're not anti-vaccine, that's what you're saying?

I'm not anti-vaccine, no. And I can tell you why.

Sure.

Are you?

No.

Why?

Why am I not anti-vaccine? Um, because they— I mean, I don't know, my dad's a pharmacist. Oh, good.

So because they save lives and they have eradicated diseases. I want to put that out there so loud because we are here because polio doesn't exist anymore. Smallpox doesn't exist anymore because of vaccines. A reason why I'm, I'm really upset with the decision of the current administration when they decided to eradicate certain vaccines from the vaccine schedule, right? Flu vaccine, basically for children, they took around, you know, which is, which is really scary, by the way. Some of the vaccines, you know, that they've taken off the schedule, um, could be very scary and detrimental.

I mean, vaccines scare me, they do, especially, you know, I've, I've, uh, two young ones, and, and the amount of vaccines that they want to give them when they have an appointment is like, uh, I I don't think we need to do 6 in the next 5 minutes here, but I don't think people understand.

I get that, I get that completely. And I'm not also pro-vaccines if you don't need them. I supported the initial rollout of the COVID vaccine schedule, the initial role, because we saw that it lowered hospitalizations and death. What I didn't support is the second and the third and the fourth vaccines. I didn't support that. So that's me not being pro-vax or anti— I just didn't support that because we didn't see that it made any meaningful difference, especially, um, you know, keeping 10-year-old kids inside. I, I didn't see this, you know, I didn't see that to be effective. My problem is in, in education. Now I'll tell you something, the largest studies ever done I'm talking in Wales. I've got a huge study. I'm talking millions of people. A huge study out of Wales, Australia, and the US for the shingles vaccine has showed that if you receive the shingles vaccine after the age of 50, you lower your risk of all-cause dementia and Alzheimer's disease by 50%.

No kidding.

The shingles vaccine can reduce your risk of getting Alzheimer's disease by 50%, and that is even more pronounced in women. So why are we telling you to stop getting vaccines? Do you want— do you know what shingles is?

No.

You get chickenpox as a, as a young kid, right? You end up in Russia, you get chickenpox. That never leaves your body. It goes and it lies dormant in the spinal cord, in the dorsal root ganglia we call it, which is in the spinal cord. Under times of high stress and low immunity, usually in your 50s and above, when you get stressed, it reactivates. So basically, the chickenpox virus that lives in the spinal cord gets woken up. It was dormant, now it's woken up. And what happens is it travels and depending on where it's asleep in terms of a nerve root, it travels up your spinal cord. And we've got things called dermatomes, right? So if it traveled up this nerve root here, you would see that the rash, the skin rash comes in the form of the dermatome. So it won't just be a skin rash all over your arm. It causes these painful sores in that spinal cord nerve root. So now you've got this virus in the spinal cord, and what happens then? It goes up into the brain. And what happens to viruses in the brain? What did I teach you about amyloid beta?

Brain cells are like, oh my God, we're under attack! It releases all this amyloid beta to try and engulf it, but in the process, you're increasing the amyloid beta plaques in your brain, you know, and you're causing a massive influx of neural inflammation, increasing your risk of Alzheimer's disease. So getting the shingles vaccine can prevent this from occurring, not just Alzheimer's disease, but can prevent you from— like, this is a really painful rash. Why are we— why do not more people know about this, right? Why are we saying no to the shingles vaccine? People are so scared of vaccines. So that's my thing. I think that education needs to come to the forefront right now. mRNA cancer vaccines. I think that there's so much research that can be done in there. These mRNA-like vaccines, like, I don't think people understand that it's just— you're actually injecting the virus, a very small amount of it, into the cell. Doesn't go into the DNA or anything, the mRNA vaccines, and it helps your body fight off the virus if it's, if it's going to come and attack you. That's all it's doing. It's not— people are under the impression that you get a vaccine and it's causing lead buildup or something, or you don't know what's in the vaccine, I don't trust them.

The same people that are scared of vaccines are the ones buying peptides on the gray market. It's like, make it make sense. So As I mentioned earlier, we have a huge literacy problem here because all you have to do is go and research and you will realize what the mechanism of action is of the vaccines. And by the way, the US and Australia have very strict vaccine protocols in terms of what they put into the vaccine. There's no lead in them. I don't know what this thing is with lead. I don't know who started that. So that's my take on it. I made my mum— my mom and dad went and got the shingles vaccine a few months ago.

What age should people be taking the shingles vaccine?

In their 50s.

In their 50s.

In fact, they— in the studies, this one out of Wales, they actually accounted for age and birth date. So yeah, you don't need to be getting it before then.

So probably at 50.

Yeah, 50, 55, go and see your doctor. And ask for the shingles vaccine. I asked my mother, I said, did I ever have chickenpox? Because I don't remember it as a kid. She doesn't remember it either.

So, so if you didn't have chickenpox, do you need it?

I could still get it though.

Yeah.

So, you know, I know I've got a friend, a girlfriend, who's got a 2-year-old, and she got chickenpox because he got chickenpox. Yeah. So So that's my, that's my take on vaccines. Um, and I, I, I just urge everybody to read a little bit more and become a bit more educated.

And I think people just get, you know, the COVID COVID just really fucked everything up. Oh yeah, you know, and people don't know where to look. I don't know where to look.

No one knows.

I've interviewed a bunch of you guys. I always ask about vaccines, but You open your—

every time I say the word vaccine, did you know that Australia was the first country to eradicate, um, HPV? So because of the vaccine, cervical cancer.

I didn't know that.

Yes, as of last year, 2025, we are now the first nation to have eliminated cervical cancer. Why? Wow. Because of the vaccine. I mean, that's phenomenal. When you go against the HPV vaccine, you go against women. Like, why are we— what are we— what are we scared of? I, I would love to know. I'd love to hold a press conference. What are we scared of? Is it because the very person that is, you know, HHS Secretary, the very person who we are supposed to trust and look to, is actually— he's confused himself. I don't know if you know this, but he went on back in the early 2000s to say that I believe in vaccines. All my kids are vaccinated.

Are we talking about RFK?

Yeah.

Well, I mean, RFK also just came out and supported an immunity— what do they call it— immunity for pesticide companies.

Why?

How the fuck is that making America healthy again?

And do you know the number one cause of Parkinson's disease?

I'm gonna guess it's pesticides.

Paraquat. Found in dry— it's part of what is found on our crops and on our fruit.

Great.

Yeah. And another trimethyl something, it's another chemical ingredient that is found in dry cleaning products. These—

this is why they call dry cleaning products.

Yeah. So all dry cleaners should be shut down if they use— if they use this. It's trimethyl— if you just type that into Google, I forget what it's called. Um, but, um, this is what is causing, uh, Parkinson's disease. But we're getting off track here. But yeah, so this is good stuff.

Um, I use a lot of dry cleaning, so yeah, shut it down. All right.

Um, Secretary Kennedy said in the early 2000s that he got his kids vaccinated. He believes in vaccines. Then fast forward like 10 years He went on to say vaccines, uh, I don't trust them, they're full of lead and you shouldn't be taking them. And he seems so confused. In fact, in a press conference, he actually went on air to say to the American people, do not trust your doctor, take your health into your own hands. I work in a hospital. If we let patients take their health into their own hands— I'm talking the very patients that don't even know where their neck is or where their knees are— would be in a lot more trouble than what we are now. You're— it's like saying, right, it's like getting on a flight and asking the passengers, saying to the passengers, don't trust your pilot, you must take this flight into your own hands. No wonder everybody's scared of vaccines. No wonder we are confused when the very person we should be turning to for our health advice is confused himself.

I mean, even the— with back to that immunity thing, I mean, we just did a big episode on glyphosate, which is, you know, the main chemical that they are giving immunity to.

Yeah, yeah.

And Iowa has the highest concentration of glyphosate in the country, and Iowa also has the highest rate of cancer in the country. So I don't know why they would give immunity to all these pesticide companies. I mean, that right there is pretty good fucking indication that the shit's not good for us. But then they called it a— what do they say— it was a national security concern. Yeah, but then I looked it up. 600 and something thousand— 600— I think it was 618,000 people die of cancer Uh, was it 22? It might have been 2024, 2024, 2025. Yeah, we're calling the fentanyl crisis a national security concern, and the cancer rate is 6 times— over 6 times that of the fentanyl crisis. So how is cancer not a national security concern?

You know what it reminds me of? The saga, the Tylenol saga with pregnant women, or even the vaccines and autism. There is not one, one corollary, not one reported case of the vaccine causing autism. Not one. Where did it come from? Fabricated numbers? But they can't because there's no numbers to prove it. So I feel like the administration are waking up and they're like, oh, what should we pick on today? Let's just, let's just put our blindfolds on and eenie meenie miney moe, autism. Okay, what we're going to just pick on autism today because that's how we feel. And let's just say that vaccine's called autism and, you know, people don't want autism. That's how I really feel like we are running, um, science here. And it's just, it's scary. Even when it comes down to Thailand, how many poor pregnant women were scared out of taking Tylenol during their pregnancy. The first line of action in the event of—

what was that? My— I remember my wife was—

she didn't want to take anything, of course, because they said that if you take Tylenol, you increase, uh, your kid's risk of getting autism.

And that's not true.

No. The first line of defense for— there is like— and that, I think they retracted that as well. even at the secretary level, even RFK came on and said, sorry, I'm— I made a mistake. After like scaring the nation for, I think, like 2 months, scared, like, like, don't take Thailand, like all these— imagine, imagine, right? I can't imagine how it must feel not knowing anything about health because you're not in that field. There's many areas of life I know absolutely nothing about. I feel so blinded.

I can tell you how it feels.

Yeah, I'm so susceptible to confusion. Yeah, when it comes to like makeup, I don't really know too— I'm so susceptible to that, I'll just buy anything because I don't know too much about it. But I can't imagine how it must feel to know nothing about health, to be a— to be first-time mothering a child, or even being pregnant for the first time, to say, don't take Tylenol, it's going to increase the risk of autism. Imagine how you must feel, so scared, so lost. So he retracted that, so that's fine now. Take the Tylenol, it's just for God's sake. In the, in the event of a fever in pregnancy, the first line of action is Tylenol. It's safe. Uh, we got offline. Now the only other thing I would argue there is there seems to be this very big confusion around statins, right? Statins, uh, decrease your risk. We've got two huge randomized control trials that show that statins, which is a cholesterol-lowering medication, reduce your risk of getting dementia and Alzheimer's disease by upwards of 32%.

Really?

Yes. Let's go back to Henry's brain here. Um, just like cardiac— do you know what atherosclerosis is?

No.

You know, when you build up, so you get cardiovascular disease, which is the number one cause of death.

Okay.

In the United States. Alone. Alzheimer's disease and dementia is the number one cause of death in Australia and the number one cause of death among women in the UK. In the US, it's cardiovascular disease and then cancer. So cardiovascular disease is just when the arteries are getting clogged up with plaque, right? And that's built up because your cholesterol— this is a very layman's term— but your cholesterol builds up in your bloodstream and it goes into the arteries and and over time it gets lodged there, and that's what can cause a heart attack. The same thing's happening to your brain. You get a buildup of cholesterol in the brain and it causes a stroke or a hemorrhage, right? So why would we want a high cholesterol, mainly LDL and ApoB? We don't. So we can lower that risk by taking a cholesterol-lowering medication like a statin. For example. Um, the, the people who have got APOE4, the risk factor gene, they are at an increased risk because what APOE4 does is it helps transport cholesterol through the brain. So if that becomes faulty, which it does in APOE4 carriers, that means the cholesterols can't get transported to the brain cells where we need them.

So they're going through the brain, they're going into the arteries of the brain, and that's where they're causing havoc. So if you have ApoE4, you've got an even better chance of lowering the risk if you take a statin. And yet every time I— that's such an— along with vaccines, that's what I've seen as the most controversial pharmaceutical. As soon as I put it up, like, I'll put up like a massive study that has just been published, like amazing, right? And people are just traumatizing me. For it, saying that I'm getting paid by pharma.

What is the— what is the scare about statins? I, I had this conversation with Peter Attia, uh, probably a year or two ago.

Yeah, and he's very pro. He's on, I think, a PCSK9 inhibitor. I think this— I don't even know, people saying, um, you're increasing your risk of getting dementia, which is crazy. Oh, um, another scare is that it's causing muscle weakness. I'm like, great, uh, it doesn't. I mean, in a very small percentage of people it might. Um, I don't know what the scare is, but I know it's very controversial amongst that family of, of people.

Do you know the, uh, medication that helps with acid reflux, heartburn? It's like omeprazole, or— yeah, is it? So that has supposedly has an increased risk for dementia. I have to take that shit. Yeah, the doctor said also take a B12 shot.

Are you doing B12 shots as well?

Well, she said that the reason that the— for the increased risk in dementia with whatever that medication is called, is that it creates a B12 deficiency.

Yeah, you should actually check as well on your blood panel if you've got, um, if one of the biomarkers, homocysteine, is raised as well. But if you're taking a B shot, it should be able to bring that down. Um, yeah, look, it's, it's funny, like that. And you know, you get— you go in for an app, you know, you say you've got acid reflux, the first immediate course of action is just take this medication, right? Have you heard that Listerine, um, you know, the one that you drink, is, um, causing the same thing? It's actually, um, increasing blood pressure. Yeah, it's the same mechanism basically. And actually, I would caution people against taking Listerine. That I do believe.

Okay.

Yeah, so mouthwash especially, um, don't take that. But for acid reflux, I do believe it in some part. Yeah, because I've also read about— I'm not obviously— because I'm not able to go deep into— I don't know too much about it, but I did interview, um, somebody who said the same thing.

That— what do they say?

Um, that it's increasing blood pressure, decreasing nitric oxide.

Hmm.

All right, well, um, we spoke about exercise and then we went down this field of our pharmaceuticals and went into why— I don't know, you know more about politics than me. I don't know why, um, we're doing certain things in the way that we're doing it.

I don't think anybody knows anymore. No, it's a lot of confusion out there and a lot of different sectors of politics. Um, I want to talk to you about psychedelics— ibogaine, psilocybin. I mean, it seems like there are a lot of— I mean, if you read the studies at Stanford for the veterans that have gone down with TBI and, oh yeah, in the black spots in the scans are full color. I did it.

Yes, you, you— I, I read about your experience too. You credit ibogaine to you feeling better, and mentally, no booze.

Yeah, no Adderall, no sleeping pills, no, none of that.

How did you administer it? How long did it take you? What was your protocol?

For ibogaine, or I went down to Mexico and took a couple of pills, woke up and didn't want any of that shit ever again. And I still haven't.

The confusion comes in, and this is why I think it's, you know, because then you would ask us then, why is this not getting approved everywhere? Why are we still, you know, SSRIs are going through the roof, like prescription SSRIs, antidepressants are going through the roof. A lot of midlife women who are experiencing these symptoms I mentioned of perimenopause will go to their doctor who doesn't know anything about menopause and diagnose them with a mental health disorder and give them an SSRI. So then you think to yourself, okay, why, why can't we replace SSRIs with psychedelics? Is that where you're sitting now? If it's done so well with you, is that the question you have really?

I think I have a lot of questions. I mean, I've read that it could help with Alzheimer's dementia. I've read that it actually— I just, um, I just connected somebody to the guy that I go to because his, his mother, father just got diagnosed with Parkinson's, and they were asking if that can help with that. So I was like, I said, I have no idea, let me just connect you. And they sent me a whole article on, yeah, how it could potentially help with that. I mean, it's helping with, with, with, with overcome addictions, opiate addictions, alcohol, stimulants.

Do you believe in microdosing? I've done microdosing, but to a smaller extent. Obviously you can't microdose that one, but people are microdosing psilocybin. Yeah. How do you feel?

Uh, sometimes if I do it, uh, I'll feel jittery at the very beginning of the day, and then and then it'll kind of level out. But I feel sharper.

Yeah.

And I felt sharper after I took ibogaine. So at the beginning of this, I told you sometimes I'll forget my words or I'll get— I won't be able to describe what I'm, what I'm trying to do. I'll read better. And I noticed all these things that like right after, right after I did it, I was like, I'm not forgetting. I'm not forgetting my keys. I'm not forgetting words. I'm not forgetting— I'm not really forgetting anything. I'm reading faster and better than I normally do.

My, my, my concern with this, and by the way, I'm so happy that you were able to get out of the state that you were in because that's so scary to be in. And the fact that you, through this therapy, which all you did was take some pills, you said you didn't go through an actual like experience.

Oh no, I would— I didn't. That's what I mean.

It was the whole Yes, that exists because what I believe is happening at a mechanistic level, one thing is, you know, it's, it's actually helping produce more BDNF.

What is that?

So, you know, BDNF, the one that I said in the mice studies from exercise.

Okay.

Massive bowls. Every time you exercising, you're running, you're producing all this BDNF, right? Brain-derived neurotrophic factor. So it's a neurotropin. So it basically helps the brain in many ways. BDNF is like fertilizer, they call it in neuroscience, fertilizer for the brain. My problem is, and I'm, I'm not deep into psychedelic research, but what I've heard and read, and I was talking to a surgeon about this a few days ago who did the experience, he said it enhances whatever state you're in when you're doing it. So my, my, what I'm scared about when people do this is could they induce psychosis in that moment? Could they induce schizophrenia? Could they induce paranoia? I'm not sure. I don't know if you've heard about anything like that, if they could induce a mental state that they don't want to be in. And could that mental state last a long time? Hmm.

You mean well after the experience?

Yeah.

I've not heard that from anybody.

So the thing is, what you're doing is you're enhancing the neural patterns. Right? And this is why the experience matters. You're not going to just go into, into Central Park and pop these pills, right? I don't know what your experience is that you went through, right? But I do know that you do need to go through an actual guided psychedelic experience rather than just doing it by yourself, which is actually what poses the risk with, um, the psilocybin usage. Like, I think people are doing that as unguided. I don't think it's as unsafe, you know. I don't think it's unsafe, but I think like, you know, do it in a— don't do it recreationally, do it in a proper manner.

How do you explain the black spots on the brain?

Well, what sort of spots were they? Were they white matter hyperintensities?

I don't know, I don't speak that language.

If they had an MRI scan, then it would have been the increased production of BDNF creating the— and recovering the neural patterns that were lost during whatever trauma that you went through. Remember that the mathematical equation from Warren McCulloch says a neuron fires or it doesn't. In order for a neuron to fire, it needs a lot of energy and it leads— needs a lot of help from nearby neurons. So when it fires, and it creates another neural pattern with another one. You can do that synchronously with the help of BDNF. So if you're going to— if we produce, let's just say, 200% BDNF when we try 100% on top of your resting state when we're running, I would dare say that the psychedelic experience is doing it by tenfold.

So are you, are you excited about something?

I'm very excited.

You are?

Yeah, I'm excited about it for the treatment. I know that Dr. Dave Rabin. He's a psychiatrist, uh, he's doing it out of California, doing a lot of the studies on psychedelics, um, to help with major depression. I think anybody in that stage, if we can do anything outside of pharmaceuticals— we're seeing that pharmaceutical interventions are— yes, SSRIs are necessary if somebody is suicidal, of course, but if we can get a better non-pharmacological way, then I'm so excited about it. I mean, look, we've even seen, um, Charles Raison, uh, believe he's a neurologist. I interviewed him. He's working on people with mild depression— with, uh, major depression, and he's seeing if he can replace an SSRI with sauna therapy. And he did.

With sauna therapy?

Yeah. He got these patients, right? And he basically split the two— split them up into two groups, okay? And he put one group— he gave them all, you know, he put one group into the sauna therapy and gave them a sugar tablet. So not an SSRI, they didn't know that because it was an RCT, randomized controlled trial. They thought they were still taking the, um, SSRI. He subjected them to really, really hot saunas, and I think around 200 degrees or something like that, uh, 7 days a week. And he did this for a period of time, and he found that over a— over the, the course of a few months, he was able to replace— they felt, they felt good. There was no suicidal ideation. All of the depressive-like symptoms eliminated just because of the heat. So they found out that the heat shock proteins are actually having a natural therapeutic effect that can mimic SSRIs. So when I found that out, I thought that that was so interesting. So he could actually eliminate the SSRIs from these patients. But obviously you're not going to be doing sauna therapies, you know, 7 days a week at this extreme heat.

And I think it was like 8 hours a day as well. It was a long period of time, but there is a mechanism there. So that's what got me excited about the potential mechanism of psychedelics.

Do you think that there are any possibilities that it could be some type, some type of a cure for, or deterrent for Alzheimer's dementia?

Yes, I think not a cure. I think it could be a therapeutic agent. I don't think— there is no elixir, there is no cure. There is no cure for Alzheimer's disease. What you're basically saying is if we have a head full of amyloid and we've lost our cognitive functions, we don't know who we are. Could we take a pill?

I guess I meant more of a preventative.

Preventative is a different story. I think eventually we'll have a cocktail of, um, of therapies that can be your prevention bucket for saving you from Alzheimer's disease. It may even be, can we Can we inject lactate into our brains or into our, you know, peripherally, which can go up to the blood-brain barrier? Could we do that? Could it be this? I do think psychedelics will fall under that, that bucket, mainly because if we can solve for the depression problem, that's another risk factor. If we can solve for that, then we've eliminated a risk factor, just like GLP-1s. If we eliminate obesity then instead of having 14 modifiable risk factors, we go down to 13.

Well, for people with— do people that have psychedelic experiences or therapy, do they have less, um, shit, what are we, less, uh, especially for people with PTSD, the cortisol dump, does that take care of that?

Oh, I'm not sure. I mean, I don't even know the complete mechanism of action of what it would do, you know, if it would increase— I don't think it increases, maybe it does, uh, parasympathetic activation, which is the rest and digest, which is what will probably slow down cortisol. But I could probably, like, posture that if it is getting into the brain and it's helping neural networks and eliminate these depressive-like symptoms, then yeah, it must also have something to do with the neuronal energy. Because we're seeing now that you can alleviate depressive-like symptoms with creatine, and that's because of the energy crisis that's happening in the brain.

So people should be taking creatine?

Yes.

How much creatine should they be taking?

We can segue into creatine if you like. Uh, well, over the last, what, 50 years from the Arnold Schwarzenegger days, people have been taking 5 grams of creatine a day. And what 5 grams does is it saturates the muscles because the muscles are so hungry, they get first dibs. As soon as you have creatine, they get first dibs of it, right? Saturates the muscles. But after that 5 grams, if you have more, then that gives it room to go elsewhere. So we now have studies to show that taking 10 grams to 12 grams a day can effectively raise your brain creatine levels. So remember, creatine, what it does, it's a naturally occurring molecule and we release it every day, but we release it in really small amounts, or maybe around 1 to 2 grams a day, right? So when it gets released, when we, when we take that 12 grams, it goes into the brain, it helps the brain cells produce energy better, namely the mitochondria. So it helps the mitochondria produce more energy in the form of ATP. And it's been said that in diseases like neurodegenerative diseases, like Alzheimer's disease, we have an energy crisis, right?

The brain's trying to repair itself, so it needs a lot of energy to do that. It doesn't have energy, right? The mitochondria is all dysfunctional. We've got plaque to deal with. There's so many things that the brain has to deal It needs more energy. So if we can give it more energy, then it has more energy to fight, right? And this is the same thing with depression. People don't realize it takes energy to be happy. Our brain didn't want us happy. That's not what evolution put, you know, put the brain there for. It was here for two things: survival and reproduction. It wasn't there to make you happy, didn't care about that. So every day we have to fight to be happy. It takes energy to do that. And imagine a person who has got clinical depression. They're fighting with every— everything that they have in their brain to not feel that again, to not have those suicidal ideations. Like, it's a— it's a brain chemistry problem here. And the psychiatrists that are actually working on these studies and who have clearly showed the effectiveness of creatine on major depression, the effectiveness of creatine on sleep deprivation.

You can almost eliminate a bad night's sleep with a bolus of, you know, 15 grams of creatine. The first ever pilot study done on Alzheimer's disease patients, very small group, 20 groups of Alzheimer's patients, not mild cognitive, Alzheimer's disease, meaning that they've gone to the doctor, they've gotten a spinal tap, meaning they've gotten fluid from their spinal cord, and they've seen that they've got amyloid beta, which means they've got the clinical diagnosis of Alzheimer's disease, took 20 grams of creatine per day for 8 weeks. And then after the 8 weeks, they increased their global cognition scores, right? They did tests, they increased their global cognition scores, they felt happier, their mood increased. And on top of that, they were able to go to the gym.

Wow.

Yes. Um, people are fighting against this because they're saying, but it was only a group of 20 patients. I said, great, that's— we have to start somewhere. And if you're going to get at that end stage, you're going to get somebody to increase their cognitive scores and go to the gym and feel better, why wouldn't you do it? But the reason why it needs 20 grams is because the barrier on your brain is called the blood-brain barrier. It becomes dysfunctional. That's what allows drugs to get into your brain and other drugs to not pass the right brain. And this can get into the brain, okay? Creatine can cross the blood-brain barrier, but it takes a lot for it to get past the bouncer. That's why it takes a lot of, of grams of it per day.

Okay, okay. Interesting. Creatine. What— I'm rabbit hole here. What do you think of Neuralink?

I mean, it sounds exciting. They've done the first one, haven't they?

Oh, they did. I forgot about that.

Yeah, they did the first one. I mean, whoever's deciding to get elective brain surgery just for, um, Elon Musk— I mean, interesting character, um, I think that it, it's, it's scary. But look, do you know what deep brain stimulation is?

No.

That's when we can go into the brain. We literally drop electrodes into the brain, just like if you were to have a pacemaker, and we can stimulate different parts of the brain to do certain things. And a lot of neurosurgeons are doing it right now, and it's phenomenal. I've been in surgery where they've done that. And it's helping in patients with Parkinson's disease. So where you have tremors, so where patients that you can stop the tremor by doing deep brain stimulation. So this shows it's just so hard to do. Like, it's so hard to do to stimulate, like the brain is like, it's so intricate. Like when you see it like the way it is to stimulate a certain part of the brain to stop doing a certain thing or stop producing its actions. Um, it's very hard to get to, but I think it's phenomenal. Um, Neuralink, I mean, look, if it can help in disease states, like if you can help you walk again, maybe. I just don't know what he's doing it for.

Is it— would it be possible to, to, to project an entire false reality into somebody's head with that?

Probably.

That's scary.

Of course, it's very scary. I mean, if we can do that with drugs, right? I've seen somebody very close to me started, you know, going down a bad path and started with cocaine and ecstasy and then moved on to— in Australia we call it ice— and methamphetamine. One with the pipe, and induced psychosis and schizophrenia. So if you can do that, that's a lifelong thing.

Wow.

Yeah. So if you can do that with a drug, and I, I saw it come alive, right, over a 7-year period. So if you can do that with a drug, then you could most likely do that with a chip.

What about marijuana?

Terrible.

There's— it's terrible.

Yeah.

Why is that?

Apart from its ability to induce, um, you know, psychosis and hallucinations, which happens with heavy marijuana usage over a given period of time, most, most people are taking it to help them sleep better. But what they don't realize is it's not helping you sleep, it's pretty much sedating you. Right? And so you're not getting into the deep sleep and the REM sleep that we need. You're pretty much just sedating yourself, and it's highly addictive, and it's not doing anybody any good. There is a part of the THC plant which is the, um, the other one. Let's see, now I need my creatine. Um, I did have 10 grams today. Um, anyway, it's a part of the plant that is actually not psychoactive, and it's helping with patients with epilepsy. See, now, do I have Alzheimer's disease, mild cognitive impairment, or I know just malnourished?

How many people do you guys— how many people do you get that think they have it that are just paranoid?

Oh, depends on, uh, your gender, your age. Look, I don't think I have, uh, mild cognitive— I feel so on point right now. I can't get that. CBD. CBD.

CBD.

Yes. So CBD oil, which is part of the plant as well. This is fine. It's, it's not psychoactive and it's been shown to help patients with epilepsy.

Okay.

Yeah.

All right. Is there anything, anything I should be asking you that I'm not?

I think when it comes to nutrition, like one thing that a lot of people can be doing is they can be taking omega-3 fatty acids. I think it's up there as well. If you get it from a reputable brand, a lot of the omega-3 fatty acids on the market are highly rancid and they exceed the normal oxidation level. So you have to make sure you go to a good brand. But oh God, I gotta tell you, like, 70, you know, 70% of your brain is made of fat, right? It's fat and water. And most of the fat that it's made from is DHA. And omega-3s comprise of 3 molecules. You've got EPA, DHA, and ALA. So when you feed the brain EPA and DHA from omega-3 fatty acids, you're literally feeding the brain what it's made of. and there's abundance amount of research on Alzheimer's disease patients and omega-3 fatty acids. In fact, there is a transporter on the outside of your brain, MFS2DA transporter, that actually helps shuttle in DHA into the brain. That becomes dysfunctional in Alzheimer's disease patients. So if you can be helping your brain with omega-3 fatty acids every day, that's another thing.

That is really good. So 2 grams of each, 2 grams of DHA and 2 grams of EPA per day. It's also been shown to eliminate and clear out some of those plaques.

Wow.

Yeah, so that's a huge one. But look, if you are exercising every day, at least 2 days a week of resistance training, if you are doing your, your aerobic training and your high-intensity training, if you're sleeping 7.5 hours a night I say that because PNAS, okay, it's a very big journal, they showed in humans that just one night of sleep deprivation, which was classified as 6 hours or less, increases your amyloid beta just after one night by 5%. That was a well-established landmark study, so you don't want that. So you want to be sleeping more.

So I need to get a sleep study.

Yeah, or you need to stress less.

Yeah, that would be great.

But other than that, uh, my message is just read more, do more, do what you can to be happy, invest in yourself, you know, exercise, get outside, increase your daily steps per day, because we don't, we don't realize this in our 20s and 30s, but you'll regret it.

And get your shingles vaccine after 50.

Get your shingles vaccine. Yes.

Well, Doc, I appreciate you coming.

Thank you so much.

That was so informative. Thank you. Thank you. Thank you. What's next for you? So many things, actually. I want to— tell me about your consulting business.

Yeah. So I take on private clients and I run them through— I'm basically your private health consultant. So you can come to me. We do everything from extensive blood biomarkers, imaging, everything.

All of it.

We do. Yeah. Head to toe. Absolutely. Every single, every single cell in your body and whatever goal you're optimizing for, whether it's health, whether it's its longevity, um, we help you there. So yes, I'm taking on people. All right, got an entire team around me as well.

I'll be putting my name in that hat.

Definitely.

Thank you. Thanks, Sean. All right, cheers. No matter where you're watching The Sean Ryan Show from, if you get anything out of this at all, anything, please like, comment, and subscribe. And most importantly, share this everywhere you possibly can. And if you're feeling extra generous, head to Apple Podcasts and Spotify and leave us a review.