← Moonshots with Peter Diamandis
Moonshots with Peter Diamandis
David Sinclair (Harvard Professor) Reveals Age-Reversing Science to Look & Feel Younger
02:23:37
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- [00:01]
A
Have we reached some state of age reversal technology that truly works?
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We can cure diseases and injuries that have never been cured before. And so imagine in 10 years, you just take a pill for four weeks and you get younger.
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Why do we age?
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The epigenome is the issue, because going through sperm and an egg and fertilization resets the epigenome. But the good news is we've figured out a way to safely reset that without having to clone yourself. We've gone from the idea that, oh, we just take a supplement or we do some exercise to slow down aging. Now we're talking about the ability to truly reset the body, reset all of the cells in the body to be young again. Teenager today will live into the 22nd century.
- [00:48]
A
Now that's a moonshot, ladies and gentlemen. Welcome to moonshots, everybody. Today's episode is delivering on a state of the union on age reversal, focusing on one of my favorite moonshots, longevity. We'll be discussing epigenetic reprogramming, when we might reach longevity, escape velocity, and the role of AI in our longevity quest. My guest here is a dear friend, a brilliant scientist, Dr. David Sinclair, professor at Harvard Medical School, author of Lifespan, one of my favorite books. We'll talk about what comes next from David's authorship and one of the leading thinkers in the realm of age reversal, epigenetics, and longevity science. We'll discuss what's here on the near term, how you can support it, how you can be involved in it, how you can benefit from it. We'll also discuss why, at age 55, David looks like he's 35. I believe we're living during the most extraordinary times in human history. And if you want to see more of this future, if you want additional decades in your life, this is the episode for you. All right, let's jump in with Dr. David Sinclair and. And a whole download on the state of Adri Bristol. David. Welcome, buddy.
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B
Hey, Peter. It's good to be back.
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A
It's good to have you back.
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B
How are you doing?
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A
I'm doing well, you know, I'm having a blast. I am more focused on my health than I ever have been.
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B
You're looking really good. I was commenting on your biceps. That's why I'm wearing a jacket here, because I don't have them.
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A
I think we can talk about this. That in fact, muscle mass and exercise still remains one of the primary pro longevity drugs out there.
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B
Absolutely, yeah.
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A
And, you know, we'll get into the details of what the best state of the art is and what's coming, because, you know, eating right, sleep, diet, all of these things can only get you so far. And then the question is, can we turn back the clock of time? So here's my opener for you. It's 10 years from now. It's 2035. Have we reached some state of age reversal technology that truly works? How well does it work? How often are you taking this treatment and what does it cost? Give me a vision of the future here. Right? I'm not asking for promises. I'm asking for your best guess.
- [03:13]
B
Yeah, sure. I'm not shy to talk about what I think is coming. And as I wrote in my book Lifespan, I predicted a future where we would have wearables and we would have video conferences with our doctors and you could order medicines online. And I thought that was going to take 15 years, and it happened in three. And so sometimes I'm actually. I underestimate what we're actually looking at. So here's what I see. So I sit on the front row of the future, right, for this long
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term, the bleeding edge, I would say.
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B
Yeah. And so I want to share my thoughts with the listeners. What I'm seeing in my lab and labs that are competing with us or collaborating with us is something quite remarkable. And the pace of change is making my head spin off. And I'm an optimist, but I just can't comprehend right now how fast things are going. So let's just go back a few years, and then we'll project into the future going back a few years. So 2017, it was just a theory that we could reverse aging. Even the word reverse and still to some extent is abhorrent to my colleagues. But we've actually, we proved that and published in 2020 that you can reverse most aspects of aging by reprogramming cells, which we'll talk about. And that changes everything. If my information theory of aging is correct, which is we'll talk about the idea that you don't just lose information as you get older, like software corruption, you can actually reset that. If that's true, and it looks like it is, then it changes everything. Because we've gone from the idea that, oh, we just take a supplement or we do some exercise to slow down aging. That's basic. That should be on everyone's protocol. But now we're talking about the ability to truly reset the body, reset all of the cells in the body to be young again, and not just slightly, but by 50, 75, 80, 90%. And this isn't science fiction. We do this in my lab. My graduate students are doing this all the time. We talk like this in my lab. Whereas outside is like, we. What are you talking about? How do you reverse aging? But what we do is we use a set of genes that are normally only on in embryos. We turn them on in adult tissues, mice and monkeys, and we can cure diseases and injuries that have never been cured before, even blindness. And so we published that in 2020. And since then, what are we now? We're at the five years later, middle of 2025 currently. What I see is that with the advances of AI and we're doing a lot of AI in my lab, which I'm happy to share, things are going so fast. Now. We're doing experiments in a matter of a month that would take hundreds of thousands of years to do. As you can probably imagine, trillions of molecules coming through, screening virtually. And so we're coming up with alternatives to this gene therapy that we published in 2020. So you ask me, first of all, how much might it cost? Well, right now, the technology which is going into humans next year in January,
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A
hopefully, this is with Life Biosciences.
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B
Correct. So Life Biosciences has proven that it works, this reversal of aging in the optic nerve to cure a variety of ailments in the eye. And we chose the eye because. For business reasons, mainly. So we're going to treat glaucoma and stroke in the eye called Nyon. And this is a gene therapy. So gene therapies typically cost 3, $400,000
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A
per hour, or it could be as much as $2 million for gene therapy, right? Yeah. For a rare disease, it's a lot.
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B
And the reason is there's a lot of hurdles to get through to get to the market. And just producing this stuff is expensive, costing us more than $10 million just to make the first batch to go into humans. But my lab is in existence to make this for everybody. We're not here to charge as much as we can. We're here to make it, hopefully, eventually pennies on the dollar every time someone takes a pill. So what we've been doing since the last, well, five years is to try to bring that cost down. And using AI, we're now at a point where we've got molecules that really would only cost $100 to make or less for a month's course.
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A
For a month's course, like three bucks a day.
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B
You. Yeah, yeah. And we're seeing that those work really well in mouse studies to reset an old animal's physiology within just a matter of four weeks. So this holiday season we did a Hail Mary experiment. We gave them just orally this cocktail and we weren't expecting anything, but we thought why don't we just measure how fit and healthy they are? And all the mice that were on the treatment and not the controls end ended up behaving and being physiologically younger. And then when we tested their biological age, which you can do with real quantitative tests, they were younger as well. And that's just giving them this stuff Monday, Wednesday, Friday for four weeks.
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A
Wow.
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B
So now we want to do a lifespan study. If we can raise the funds to do that and see if we can blow away the lifespan record for mice.
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C
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A
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A
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A
So 2035 you're saying we will have a age reversal therapeutic working well.
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B
That's where it's headed. So if you extrapolate where we are next year, if all goes well, we'll have shown that you can reverse aging in a human in a tissue safely. So curing blindness.
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A
You've done this in primates already?
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Yeah, it works in green monkeys every really amazingly well. And some of the data is just stunning. You know you can map whether you reverse the age of the optic nerve in these animals and it's looking like 95% of the age goes backwards.
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A
Wow. Yeah, I mean this is to a youthful state of the optic nerve and
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B
semi permanently this isn't that you have to keep the genes on, you can switch them off again and which we do. We have an on off system that we've patented and works really well. If you do it for about six to eight weeks, then turn it off, and the eyes stay young, they're gonna age out again, but then you just turn it back on for a few weeks. That's the plan.
- [10:20]
A
That's the plan. I like that plan. And what type of age reversal do you see? I mean, putting this into human terms, someone's 50 years old, they turn this on. Is it taking them back to teenage years? Can you control how far back they would get?
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B
Yeah, we can control it. The longer you leave it on, the younger the tissue gets.
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A
Beautiful.
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And it seems very safe. There's no untoward effects of this treatment so far in the monkeys either. But here's what I see. I see that within the next 10 years, we'll have the ability to not only use gene therapy throughout the body, but, and we're already working at life biosciences on getting away from viral delivery, which is the current one.
- [11:06]
A
And just for folks to know, gene therapy has been something developed since the 80s. It ran into some troubles early on, but it's where you basically are using a virus to deliver, typically what's called an aav, adeno associated virus, to deliver a set of genes into targeted cells. But that's expensive and, and sometimes maybe goes off target, you don't get all the cells you want.
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B
Well, that's the big problem with AAV is that tissue distribution is tough. And so we need better ways to either get those viruses evenly throughout the body or use other things like what are called lipid nanoparticles. Those are also like MRNA vaccines. Exactly. Though you know, for those that questioning. What. What about the vaccines? Maybe we won't get into that.
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A
I know vaccines got a bad name in the last course.
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B
This is obviously not a vaccine. This is. You deliver genetic material inside these little particles and those. There's really good technologies. Actually, there's a company that I'm advising called Legandal, and they use AI to find proteins that you could put on the outside of these little particles and direct them to anywhere you want them to go. So getting back to what you asked me about, what does the future look like? I think we can either go into the doctor and have an injection of that genetic material and we become transgenic humans that we can turn on. These three youthful Yamanaka genes, they're called, and every time we want to get rejuvenated, or we have an injury we need to heal quickly, we turn them on. How do you do that? Well, we've engineered it so you can just take an antibiotic for a few weeks. It's doxycycline. So you take a course. It's pretty safe, actually. Very, very safe. And you turn it on. Now that's what I can see happening with already technology that's going into humans. But if we are successful in what we're doing in my lab, these AI generated molecules are mimicking that. So the reason for having a molecule rather than a gene therapy is not only are they cheap, you can just swallow it and they evenly go throughout the body, typically. And so imagine in 10 years, you just take a pill for four weeks and you get younger. That's what we're headed towards. And I can see that being realistically possible in the next 10 years. In fact, I can see how this is going to happen. That's what we're working towards in my lab.
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A
I love it. I love it. I can't wait. And I volunteer to come first, the concept of longevity escape velocity. So Ray Kurzweil, who's been a dear friend and a mentor, his prediction is that we'll reach longevity escape velocity by the end of the year 2030. And longevity escape velocity, for those who haven't heard the term, hopefully if they're listening to this podcast, they've heard it. It's the idea that at some point in the future, for every year that you're alive, science is extending your life for more than a year. And at that point it basically departs and you're going as long as you want. I've had the conversation with multitude of different people and everybody's got a different guess. I just had a conversation with Demis Hassabis not long ago, and when he was on 60 Minutes, he said he foresaw the end of all disease by the end of the decade. So all disease by 2035. And then Dario Amadei, the CEO of Anthropic at Davos, said he expects that we could see a doubling of the human lifespan in 10 years time. Those are good people to have in the same camp you are. So what do you think about longevity escape velocity is a concept worth thinking about. When do you think we might hit that?
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B
I don't have a number. I'm actually just on the ground working as hard and fast as I can with my team. But I do think now it's feasible. There was a time in my career five years ago, maybe 10, I thought this was so far into the future it wasn't worth talking about. It's all speculation. But now that we the information theory of aging and the reset seems true and that we're entering the clinic with these age reversal technologies that can be used multiple times, not just once, but you can keep doing it maybe twenty times, hundred times. I think it's possible that within our lifetime we'll see such the ability to reset yourself. Now, I don't think we're going to live forever because there's always noise and information is hard to preserve, even indefinitely. But I do believe that we could double the human lifespan now. And I'm on record, and I've taken some flack over the years from colleagues who didn't like me saying that the first person to live to 150 has already been born. But I still stand by that because teenager today will live into the 22nd century. We have to remember that it's not about today's technology.
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Two 14 year old boys that I keep on telling that.
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Yeah. And just think about what's happened in the last 10 years. We just can't imagine what's going to be in their lifespan. And so that's why I think that it's quite possible that they will be able to live 150 or more. But for us, the question is, were we born one generation too early? Us in our 50s, actually, since I was 18, I decided, damn it, I, I don't wanna be part of the last generation to live a normal human lifespan. That's not right. And I know it's coming. Just a question of can we do it in time for all of us? And I think the best way to ensure that we reach that point if there is an escape velocity, is to stay healthy. And that's why we should talk today about what we can do in our lives to stay healthy into our 90s and 100. Because certainly by the time you and I are 90 or 100, the technology is gonna be there to reset our reach.
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A
I mean at this exponential age and what's going on with AI And I was with Eric Schmidt recently in our last podcast and he's like, we will reach digital superintelligence within the decade. Right. And this is not just AGI, whatever AGI means. This is, you know, billions of fold more intelligent than human. And of course the work going on right now of being able to model a cell in silico will get there and then we'll have a cell with David Sinclair's genome or my genome and you know exactly which molecules activate that or don't.
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Yeah.
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I want to go to a basic question which I think is important for everybody to understand. The answer to, and I'd like to understand how you express it, why do we age in the first place? Right, so we have. We have the Greenland. We have the, you know, bowhead whale lives to 200 years old. We live. And the Greenland shark lives to 500 years old, has pups at 200 years old, and we make it to 100 on a routinely regular basis. But why do we age? And why were there no factors selecting for us to live longer than that?
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B
Yeah, well, the first answer to the second question is there was no need. And evolution doesn't build things that there's no need for. And on the savanna, we're likely to die from war or infection or starvation within 50 years. So living to 100 was really not helpful. The reason why we age is debated among academics, but what I strongly believe, based on the evidence that my lab's been garnering, gee, 25 years now, is that it's not just wear and tear. We're not just breaking down. There aren't just things going wrong, but it's all about information and entropy. And that what keeps us young is that we have great information. We've got our pristine genome and our pristine epigenome, which are the structures that read the genome. And those two elements of information, they get lost over time due to noise. And we've identified some of the causes of that noise. DNA breaks of chromosomes as part of that noise. Stress on a cell. If you crush a nerve cell, it will accelerate its aging, we showed in a 2020 Nature paper. And so I think of the body, not like a lump of meat now. I think of it like a computer, and the software gets corrupted over time. And then the great news is we found that there's a backup copy of that software that can be reset.
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A
Amazing. You've not done, really any podcasts in the last few years. So I'm super happy to have you here. So I really want to go into what you've learned. So the information theory of aging, you published that as part of your book Lifespan Time did an amazing piece on you and the information theory of aging. So I was so happy that Marc Benioff ownstyme did that. It's like, yes, it's good to get the exposure for this. So let's take it a step further in explaining what that information of what that aging theory means. And have you had any new proof points supporting that in the lab?
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B
Yeah, we've come a long way since 2020.
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A
So just to settle things, you get 3.2 billion letters from your mom, 3.2 billion letters from your dad. That's your genome. It doesn't change over the course of your life. So I like to ask people, like, why do you look different at 20 and 100? Why don't you look the same? And that genome codes for. What's the current estimate? 22,000 genes? Yeah, thereabouts. So epigenetics is effectively which genes are on and which genes are off. Right. As you age, If I just have this right, as you're aging, the wrong genes turn on and the wrong genes might turn off, and that's causing some of this aging effect.
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B
I can't add a lot to that. You summed up the theory well and I did put it in Lifespan, the book. So if anyone hasn't read Lifespan, it's all in there. And book two, hopefully next year will come out. But it was a risk putting it in that theory and all of our results into the book because we hadn't published it yet. But since then, since 2020 when the book came out, we have published a couple of big papers, one in Nature and one in Cell. And it's really strong evidence now that the theory is real. Stands up. Yeah. What have we learned since? Well, we're trying to figure out how is it possible to reset a cell and get back the original structures of the epigenome. And if we were to dive into the cell, okay, let's say we're going to pierce the membrane, go inside a cell, then you swim down and then you see the nucleus, there's another membrane. There are little pores in the membrane. We can swim through those. Now we can see the chromosomes, and that's really the epigenome. And if we unwrap those chromosomes, what we would see is the 6ft of DNA that's in the cell of every cell. And then. But the DNA is wrapped up in proteins. And that wrapping is important for two reasons. One is that's how you fit six feet into a microscopic cell. But also, whether it's wrapped tightly or not determines whether a gene is on or off. And if it's tightly bundled, we call that silent chromatin or heterochromatin. And a lot of the genes you want to be switched off because you don't want a liver specific gene on in the brain and vice versa. So there are these bundles of DNA and loops of DNA, and when it's
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bundled tightly, it can't be read, it can't be transcribed.
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Because it's hidden.
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Exactly.
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It's tightly bundled. And actually one of the big clues that this was relevant to aging was when I was in the lab of Lenny guarenti as a 25 year old postdoc and as a team, we uncovered that there were these silent information regulator genes called the sirtuins, and their job is to bundle up DNA. And at the time we're thinking, what the heck has bundling DNA got to do with aging? We were expecting to see antioxidant genes and telomere extending genes, but we found these silent information regulators, and that's why information has been key to my research ever since. Getting back to what happens during aging is that these bundles and these loops, they change over time. In part because the cell loses the ability to bundle them and you get these loops open up, but also because the epigenome is changing all the time. Our genome is stable, we don't change our genome much. And in fact, mutations are not as abundant as we thought. And you can actually, I could take one of your cells and clone you. And even though your cells are old, we can start new life with those cells.
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A
I love that. Right? And so I know one experiment, set of experiments were done, actually took cells from 23 sequential mice, clones that showed, you know, you could take a cell, clone the mouse, grow it out, take a cell, clone the mouse, grow it out. And they just, I think they got bored and stopped at the end of
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B
the day and they're still healthy. Right. These mice aren't getting old. But if the old theory is correct that mutations cause aging, then you just end up getting older and older babies. That doesn't happen. So therefore, I'm very convinced so far that the epigenome is the issue, because going through sperm and an egg and fertilization resets the epigenome, you can start life again. But the good news is we've figured out a way to safely reset that without having to clone yourself. But think of it like that, as resetting the system, like going through conception without having to be reborn.
- [24:26]
A
Amazing. So the control of the epigenome. I know, for example, skin has a multitude of different proteins, collagen molecules. And as you grow older, one of the reasons your skin ages is those collagen molecule, the genes, those collagen molecules get silenced. And so one could imagine unsilencing them.
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B
So we do that in the lab all the time. We have a skin project. So yeah, you don't have to imagine it.
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A
Okay, great.
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B
I will show you.
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A
I can't wait for the product to come out.
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B
Yeah, we think skin is a good model. It Also may help some people with wound healing and how they look. But we actually grow bundles of human skin and hair in the lab. And for those of you who are queasy, you may not want to hear this, but we, we open up that organoid of human tissue that we grow, and these are engineered to be able to drive aging forwards and backwards. So we can study that, but we put them in the backs of mice. And now it's pretty funny. You can see the.
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A
And the mice give the blood supply and keep it alive.
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B
Yeah, but you get human black hair growing out of the back of a mouse. Now we can age that hair, make it gray, make it old. And now we test if we can reverse it. And so far it looks good.
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A
Well, if you can do that, I think you got another huge winner. I'll never forget at the Abundance summit, which I've had you speak at a couple of times, and you're gonna be in 2026. Thank you for that.
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B
Sure.
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A
Eric Schmidt will be our opener. You'll be our closer that year. That'll be fun. I remember had a biotech longevity scientist on stage and he was talking about his technology, how it could cure cancer, it could increase the health of particular organs. And he's giving this entire list of what it could do. And then he says, and it can grow hair. And the crowd erupts in applause.
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B
You know, it's like, yeah, I remember that. Yeah. So people do care about skin and hair, but we're also, we're learning fundamentals about what makes cells old and how do we reverse that. And skin is just one.
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A
So the original data set that, you know that is there, that that helps the cell remember its original state. Have you found out where that lives?
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B
Oh, well, the answer is probably, though I'm going to wait to reveal that in detail. But I have some very good students working on that right now. I wrote a review in one of the Nature journals about this, so if anyone's interested, you can go see my ideas. But basically what we need for, for this to be real is there's a memory of youth in every old cell. So what is that memory? It's gotta be probably something physical. Could be a chemical modification of the DNA, chemical modifications of the proteins, like
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A
a methylation or an essential.
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B
Could be methylation, could be something else. Could be some other type of novel genetic material. Or it could just be proteins that permanently stick to the chromosome and stay there until we need them to reset.
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A
I figure you would have. People would have seen this by now.
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B
Oh, well, What I can say is people have bumped into this and ignored it because they didn't think it was important.
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A
I read through all of your tweets as we got ready for this, and I love one of these says, your cells remember how to be young. We just need to remind them.
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B
Exactly. And my students are great in that they are.
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A
And I came to your lab, was it, a month ago, and I met many of them, and they are brilliant.
- [28:05]
B
Yeah, they're like my children. Actually, on some days, I love them more than my own children. But, yeah, they're a very special group. And they are working so hard to change the world and make these medicines a reality.
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A
Yeah. And we'll talk about the insanity of funding cuts in a little bit and the importance of the work that you're doing. So anything else you want to add on the information theory? Do you have experiments planned that will just nail this down? How does a theory become just accepted gospel?
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B
In fact, I think it happens at one funeral at a time. I've been very pleasantly surprised that the theory, which is called ITOA for short, itoa, is being well accepted by the community. And there's more and more evidence every few weeks about this. I think what'll really convince people is when we disrupt the observer, we call it. So this backup copy based on Claude Shannon. I'm a big fan of his, and you know that. And so for those of you who don't know about Claude Shannon, just briefly. Claude was a scientist at MIT and Bell Labs who figured the information theory of communication. So the reason we have an Internet is because of him. And the same mathematics and concepts, I poached and used them for aging. And so the information theory of aging is all about the preservation of information and having a backup copy, which at the time he called it the Observer. So we still talk in my lab about finding the Observer. And the observer keeps a backup copy of the original signal. And if you lose it by the time it gets to the sender, you can go back and retrieve what's missing from the observer. And so what we think is that the observer has a physical, as I mentioned, a state. It's got information there. We think we've found that information. It's novel biology. And when we show. If we show that breaking that system prevents age reversal from happening, then I think that the community will believe us.
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A
Love it. Love it. So we just launched about 18 months ago, something called the $101 million Healthspan X Prize.
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B
Thank you.
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A
Yeah, absolutely. I think you're in the process of registering for that competition.
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B
We are registered.
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A
Oh, you're registered.
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B
Fantastic.
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A
So we've had like 625 teams from around the world. And for those who haven't heard me speak about it before, this is an Xprize, one of our largest. We raised $157 million. GSK is a big sponsor of it as well. But our primary two sponsors are gentleman Chip Wilson, the founder of Lululemon, who has a muscular dystrophy called FSHD, and he put in 36 million. And then a group out of Saudi Arabia called Hevolution, Think health and Evolution, they put in 40 million. I'm a multimillion dollar donor. We have a lot of incredible people who are supporting this. And the goal is, can we get the smartest people in the world, including you, working on reversing the loss of cognition, immune and muscle? And I'm amazed the variety of different approaches. And I'm excited that your lab will be participating. But we're seeing a huge range. I mean, from cellular medicines to gene therapies to. So I want to ask you, beyond your own work, the state of the union for age reversal for longevity, is it still an uphill battle in the scientific world, in the funding world? Because it used to be a stigma. If you said you're doing age reversal work, it was like, oh, this person's insane. Yes. Has that gotten better?
- [32:06]
B
Not much, especially age reversal. There's still the old school in my field that doesn't like the word reversal, but it's somewhat better that at least saying that you work on longevity isn't a stigma. And there's a lot more funding outside of academia for this, of course, but in academia there's less money than ever to study this topic, which is surprising given how much potential it has to change Medicare.
- [32:33]
A
Yeah. The interesting thing is it's coming. A lot of the funding from this is coming from the crypto community. There's a great alignment between people who believe in crypto, bitcoin, long term vision for capital as well, and longevity. We've seen Jeff Bezos and Yuri Milner back altos. We've seen Brian Armstrong back New Limit. We've seen Sam Altman back retro. So it's good to see some of these multibillionaires backing these things. I mean, I for one, if I had that level of capital, I'd be backing like all of them.
- [33:07]
B
Yeah, well, one or more of these companies could dominate pharmaceuticals in the 21st century.
- [33:13]
A
I mean, it is a multi trillion dollar marketplace. I mean, I'M on stages and perhaps you are too. And I ask, okay, you're 70 or 80 years old. You know, this is a room of family offices, wealthy individuals. And you know, you're slowly degrading as people do in the last decades. And someone comes up to you and says, listen, here is a therapeutic. It will give you an extra 20 healthy years. Not 20 healthy years right now, like where you were in your 50s. How much of your wealth would you give for that? What do they say? If they're honest, it would be the vast majority, 80 plus percent. And when I think about that, that is tens of trillions of dollars. So I think it's a giant market. I'm hopeful that we'll see a lot more funding coming in from people both philanthropically and investment wise.
- [34:10]
B
Me too. Me too. Actually, the story I like is if you ask someone in their 30s, what would you do to trade with Warren Buffett? No one says they'd trade with him, no matter how much money he has because he's older. So the years you have are worth everything to you.
- [34:28]
A
Yeah.
- [34:28]
B
More than money.
- [34:29]
A
Agreed. Agreed.
- [34:32]
C
Everyone, as you know, earlier this year I was on stage at the Abundance Summit with some incredible individuals. Cathie Wood, Mo Gadot, Vinod Khosla, Brett Adcock and many other amazing tech CEOs. I'm always asked, hey Peter, where can I see the summit? Well, I'm finally releasing all the talks. You can access my conversation with Cathie Wood and Mogadot for free@diamandis.com summit. That's the talk with Cathie Wood and Mo Gadot for free@diamandis.com summit. Enjoy. I'll ask my team to put the
- [35:04]
A
links in the show notes below. What else are you seeing out there that could be a viable age reversal therapeutic? Are you seeing any particular, without naming necessarily labs or anything but approaches?
- [35:20]
B
Well, there's a few. I work on epigenetic reprogramming at Life Biosciences and these companies you just mentioned, they're also chasing us. So we started a little earlier than they did, but they're trying to catch up. So that's a big area and why I'm hopeful that one or more of us is going to succeed. So that's a whole, I think that's for me, the most promising. That's why I'm putting my own money into it as well. What else is important? Well, I think that there's factors from the blood. So we know that plasmapheresis exchanging your plasma has some benefits and Looking better all the time.
- [35:56]
A
Like therapeutic plasma exchange.
- [35:57]
B
That's right.
- [35:57]
A
Yeah. I've done that five times now, right?
- [36:00]
B
Yeah, I think I've done it maybe a few times, but I really believe in it because there's a lot of animal data and some human data coming that looks good. But what is it about that that's beneficial? We're actually trying to turn that into a pill. But stay tuned for that because it'll be easier than sitting for an hour. But that sounds promising, right? That there's something in our blood that's keeping us old or fresh, that comes in that makes us young. There's some factors already companies are working on. I think there might be a few really good ones that you could take as a drip and rejuvenate.
- [36:31]
A
There was a promise of GDF 11 years ago. I mean, the problem is a lot of these companies get funded with seed capital. But being a biology medical company is expensive and they run out of capital.
- [36:47]
B
Yeah, it is. And I think there's something that we haven't found yet that's going to be more rejuvenative. So we're screening these proteins in the blood and genes that do epigenetic reprogramming. And so you could imagine that there's a peptide perhaps or a protein that is circulating in the blood, and when it circulates, it triggers these genes that give rejuvenation. So we're looking for that. Stem cells. It's been a bit slow, but we're starting to see a resurgence of stem cell interest and approval. So the FDA now approves certain types of stem cell therapy.
- [37:24]
A
Yeah. And we've just seen states begin to become much more lenient. So Florida is in the process of passing regulation to allow you to do stem cell treatments in state. I think it was Utah. Is there already other places? Which is great because, you know, before this you'd go to Panama or Costa Rica or Antigua to do it, which is fine, except you don't have your medical team around you and you're operating ex us. Right.
- [37:51]
B
So presumably Fountain Life is going to get into that.
- [37:53]
A
Yeah, Fountain Life. We have two centers right now in Naples and Orlando, and we're opening up Miami. And those will all have hopefully the most advanced stem cell therapeutics available, as well as other cellular meds like NK cell supplementation.
- [38:10]
B
Yeah. Which kill cancer cells.
- [38:11]
A
Yeah. And natural killer cells, your innate immune system, you know, kill cancers. We're always developing cancers. And we depend on our immune system to find them and kill them. And the same NK cells also Hunt down, you know, infected, virally infected cells.
- [38:25]
B
Yeah. Well, we're working on a new type of stem cell, a very rare type. Okay, we should talk because there's something that. There's a stem cell that actually turns into the tissue that it lands in, and that's different than current stem cells.
- [38:38]
A
Interesting. Okay.
- [38:39]
B
I think that area has promise too. Senescent cell killing chemicals. Somewhat promising. I saw Altos bought a company or is merging with a company that works on that. It's been a little slow, a little bit disappointing with Unity.
- [38:56]
A
Yeah. So surprised. So Unity Biosciences goes public, and then their data comes back and they crash and they're slowly eking their way back.
- [39:04]
B
It wasn't a complete failure, just they didn't reach the end point. So there's a lot of variability, so that's part of the issue. But I think they'll keep pushing on and they'll find something. These senescent cells are important. We know from a lot of studies that if you delete these cells, you can improve metabolism and a bunch of other things.
- [39:23]
A
Can you use epigenetic reprogramming to move senescent cells back to normal, healthy cells?
- [39:28]
B
We have a. A project in my lab on that, and so far it looks like yes, we can do both. Rejuvenation of stem cell of senescent cells so that they don't cause havoc. They normally cause a lot of inflammation and even cancer. So we can stop that with reprogramming, but in some cases we can even rejuvenate them so they grow again. Normally they're sitting and they don't grow just for folks.
- [39:52]
A
There's something called the Hayflick limit. Right. Which is. Was it 50 cell replications? Thereabouts. That a cell should replicate 50 times and then have the decency to die. And if it doesn't, it can become a cancer cell or a senescent cell, which is pumping out these inflammatory factors.
- [40:09]
B
Yeah. And so you can either kill them or you can cure them. And so it looks like we can cure them, but we're not sure if that's a good thing. We have to figure out if curing a senescent cell will just give us more problems. But at least in tissue culture, it looks like reprogramming does work in that regard. And also, somebody might be asking, you, might be asking, if you reprogram a cancer cell, what happens?
- [40:30]
A
Oh, yeah. Fascinating.
- [40:32]
B
I have good news on that front.
- [40:33]
A
Okay.
- [40:34]
B
Nalan, one of my graduate students has been working on this for a few years, and we have a lot of evidence that many types of cancers are killed by reprogramming, which is interesting if you think about it.
- [40:44]
C
Oh, so you have a cancer cell, it's growing.
- [40:47]
A
You've discovered it at stage three or stage four, and it's through different parts of the body. You hit it with an epigenetic reprogramming cocktail and it has a decency to die.
- [41:00]
B
Well, I think it freaks out and realizes it wakes up from its zombie like state and says, oh, my goodness, my chromosomes are messed up. I better kill myself. Because one of the ways to become a cancer, how honorable of it, is to ignore its DNA damage. They're filled with DNA damage, and when we wake them up, they can. So if you wake up a normal cell, it goes back and it gets younger. But if you wake up a cancer cell, it looks like it realizes it should kill itself. And it does.
- [41:27]
A
Amazing. That's crazy. Amazing. All right, so I want to dive into a couple of your companies that I'm tracking. I've had them on my stages at the Abundance Platinum event, which I do every fall. For those of you interested, David and I will be together in Boston. Our Abundance Platinum trip this year is the last five days of September. If you want more information, you can go to abundance360.com Longevity, Life Biosciences and Metro Biotech, two very cool companies. Let's talk about each of those.
- [42:06]
B
Should we start with Life Biosciences?
- [42:07]
A
Let's do it.
- [42:08]
B
This is the more recent one. This was founded in 2017 18, and they're the ones that have shown in monkeys that you can basically cure blindness and get vision back. And so the first studies will be in January if all goes well.
- [42:20]
A
So you've gone originally from mice to monkeys, so non human primates. And it worked as expected in both cases.
- [42:32]
B
It worked better than expected, actually. And so far, there's no signs of any reason why we shouldn't go into humans next year. It's going to depend on the fda, but we're planning to submit what's called an IND shortly, and hopefully by this time next year, we'll know if it's working because the studies are straight into patients.
- [42:50]
A
And so is it a single injection? What is it?
- [42:54]
B
Oh, good question. It's a single injection. So with macular degeneration, it's very common to get one injection or more. You don't feel it's nothing bad. And what this virus does. So the AAV you mentioned goes into the nerves at the back of the eye, and we Just turn it on by giving the patient some antibiotic doxycycline.
- [43:12]
A
Doxycycline, right, yeah. Which is, by the way, is just the trigger that turns on that segment of DNA.
- [43:21]
B
Yeah. So we put in those three genes inside the virus. So we normally have these genes. We're not changing the genome. But by putting these three genes in the virus, we can control them better. And now they're what's called Dox inducible. And we could have used any chemical. Doesn't have to be docs, but dox is such a safe drug and it's been in research for decades, so we chose that. But yeah. So by this time next year, we should know if it can improve vision in people that have gone blind, either from a stroke in their eye or from glaucoma.
- [43:53]
A
Amazing. How big will your phase one be?
- [43:55]
B
You think it's a small study, right? You start with 1, then 2, then 10.
- [43:59]
A
Yeah.
- [44:01]
B
And we're just raising money to go into our phase two study already.
- [44:05]
A
Awesome. Any other elements of life biosciences besides that specific?
- [44:11]
B
Well, some of it's, you know, I'm bound by confidentiality, but I can say in general that the company has. That's phase one for the company. Let's call it stage one. Not to confuse it with clinical trials. Stage one is proof of concept in the eye. Does it work? Two shots on goal. Two diseases. Stage two for the company, which is already underway, is using AI to convert to chemicals. So you have a pill instead, or an lnp, which is the lipid nanoparticles. You don't use viruses. Whole body rejuvenation, they're already doing that. And then, so stage three would be going into multiple diseases and eventually whole body rejuvenation.
- [44:49]
A
All right, so let's pause right there and focus in on this. So I think one of the realizations is for those who develop a disease when you were younger, you didn't have the disease. And so if you're able to actually induce some type of age reversal, you know, does that cure the disease in mice?
- [45:08]
B
It's working great. So for instance, glaucoma is an age related disease. You make the eye young again in the animal, the disease goes away, the body can heal itself. And that's been really not the approach of medicine as we know it. Medicine as you know, you're a trained doctor, is, oh, we treat the symptoms of this disease and slow it or cure it, but we don't use the body's own healing properties. Now we've uncovered the ultimate healing property. We believe that we've uncovered the ability that salamanders have to regrow limbs and fish grow new tails. It's similar process. And we just turn on these embryonic genes, and now we get youth, and now the body can heal itself. So besides vision, what else have we tried? Well, in my lab, we've done Alzheimer's disease. Cured.
- [45:53]
A
Wow.
- [45:54]
B
Some muscle diseases. Cured. Als, Pretty cured. And that's important because in my partner's family, we have als, so we're rushing to fix that one. We published it with a collaborator that we could alleviate multiple sclerosis with this as well. So so far, we have not seen a disease or an injury that could not be effectively treated with this therapy. Now, doesn't mean everything can be cured. But what it's telling me is that diseases that we've been treating really, we've just been addressing the symptoms, not the underlying cause. And finally, now we're treating what's really underlying most diseases, which is the aging, universal aging process itself.
- [46:38]
A
And the challenge is today's medical system is built all around, you know, just treating the symptoms. It's built around keeping you alive and treating what's possible, but not curing you. I mean, it's really quite insane. Whole body rejuvenation again by taking a set of pills. Do you. So we don't see, like, one arm get younger than the other arm. We don't see any of that going on. So the notion is that if you're going to be able to reverse the aging of a particular system, skin or muscle or hepatic, that it's going to hit all tissues, all organs.
- [47:30]
B
Well, that's the ultimate goal. And we're already testing in mice how that works. There was another lab, our collaborators out of George Church's lab, where we. Collaborating with George. You know George?
- [47:41]
A
Yeah, I love George.
- [47:41]
B
He's in my department at Harvard. We collaborated initially on building these viruses. And they did the experiment that I thought was really interesting, which was just to inject the virus not just into the eye, but inject it into the vein of a mouse. And if we're right, the mice should live longer. And even though this was a Hail Mary experiment, not optimized, those old mice that they treated lived another 109% longer.
- [48:06]
A
Huh. Okay, so I have to ask you this question. At this point, we talk about mice. Mice are the lab. Mice are experimented on, everything. And a typical lab mouse lives how long? 24 months, 36 months?
- [48:22]
B
Yeah. Yeah, 28 months.
- [48:25]
A
28 months. Okay. Why aren't we seeing mice that are living not two years, but 10 years at this point. What's going on there?
- [48:35]
B
Because I think we were taking the wrong approach. What happened to the field, unfortunately, in the.
- [48:39]
A
And by the way, I just noted this real quick for reference. In June of 1982, Richard Weindrud and Roy Walford at UCLA showed that life extension of 30 to 40% was possible through calorie restriction to get a mouse to what is currently the record of 53 months. So you just have to starve the mouse and you can almost double its lifespan, which I don't think anybody here wants to do.
- [49:07]
B
No, it'll certainly make life feel longer. But yeah, those guys showed early on that you can extend the lifespan through diet, but it's not pleasant. But now we're seeing combination drugs. There was one published last week that combination of two anti cancer drugs could extend lifespan of mice 30%. So we're approaching the same levels of extension as we saw with those early studies. But ultimately, we want to make mice live five times longer, ten times longer. Live longer.
- [49:36]
A
You think we'll get there. And I don't care about the mouse living longer. I just want some additional evidence that we move the needle.
- [49:43]
B
Yeah, well, our field has made lower organisms live 10 times longer. So what is it about mammals that's harder? I think we were just taking the wrong approach. We were saying, oh, let's try this molecule that turns on this longevity pathway or that longevity pathway. Most of these longevity pathways that we worked on starting in the 2000s with molecules to tweak them, we were just slowing aging. We weren't reversing aging. I think with this new age reversal approach and these technologies, the gene therapy and these new cocktails that we have in my lab, we have a much better chance of being able to repeatedly reverse aging and get them out to a lot. Maybe five years. And this is. I'm excited about this because, remember I said over the holiday break. Yes, within four weeks, we made them basically young mice again.
- [50:29]
A
Yes.
- [50:30]
B
We want to try this over the lifespan, and we've got a good chance, I think, of.
- [50:34]
C
Can't wait.
- [50:35]
A
When might you do that? When might you run that experiment?
- [50:38]
B
Well, as soon as we have the money to do that. Right. So let's.
- [50:41]
A
All right, we're going to talk about money in just a little bit. I do want to hit on a basic idea that I want people to understand, which is the idea of these seven sirtuin genes or these proteins and the battle between DNA repair and epigenetic Drift. Right. So if I understand from reading your book and speaking to you, what we have are these seven sirtuins that are conserved across almost all life.
- [51:15]
B
Yeah. Even bacteria.
- [51:16]
A
Yeah, even bacteria. And as they have two functions in the cell, Right. One is to repair DNA damage and one is to make sure that the right genes are on and the right genes are off. Is that basically the case?
- [51:30]
B
Yeah. Yeah.
- [51:32]
A
And as we get older, and I'm pitching this back to you because this is how I explain on stage, we're accumulating some DNA damage and of course the, you know, the sirtuins are, are going back and forth between these two functions. And as we get older, our internal NAD levels drop by as much as 50%. Right. And NAD is sort of the energy currency in the cell that powers these sirtuins. And so if they're having less energy and having to go back and forth between DNA repair and epigenetic drift, our epigenome loses and we get aging. Is that correct?
- [52:11]
B
Mostly.
- [52:12]
A
Okay, correct me, Gramoff.
- [52:14]
B
Even without the decline in nad, we have problems. And we showed this in a mouse that we published in 2023 in the journal Cell, was that even if we distracted the sirtuins from their main role of silencing genes when a mouse was young, that was enough to make them age 50% faster. And these were called the ice mice, the inducible changes to the epigenome mice. And so we created non mutagenic cuts and that distracted the sirtuins from where they were on the chromosomes. And they went elsewhere and often didn't come back to where they belonged. And that just for three weeks was enough to trigger the domino effect of aging in those animals. And they didn't just look old, they were old by every measure. Their tissues were old, their physiology was old, their DNA methylation clocks were older. And then we also did a little experiment to reverse their tissues at the end. Just for some fun.
- [53:06]
A
Just for some fun. Your lab must be a blast to work in. I wish I go back to my medical school days and come and knock on your door and volunteer. Let's talk about AI in your research, because that's new since we last really went deep, I mean, the entire the explosion of the AI field and understanding especially is applied to basic sciences. So tell me, how are you using it? What's it doing for you?
- [53:31]
B
Well, it's central to everything now. We barely run an experiment without consulting our AI agents. Let me tell you about two areas I think it'd be interesting. The first is in visualization. We've developed algorithms. It's called DASH AI. I forget what it stands for. But basically the idea is that we can visualize old and young cells using a microscope and tell very quickly, within nanoseconds, whether what age those cells are just by looking at them.
- [54:01]
A
Fascinating.
- [54:02]
B
And that's important, if we're sure. And as we are screening for genes and molecules that control and reverse aging, Measuring what matters. Yeah, yeah. And so we have a curve that stretches from 20 year old cells, or cells from 20 year old skin cells to 93 year olds. And within nanoseconds you can not you. But the computer looks at the image and can say, all right, those cells were 93 last week and now they're 20. And so we have chemicals that do that.
- [54:33]
A
So that just gives you super rapid screening of all kinds of chemicals.
- [54:37]
B
Yeah, so that's using robotics and AI visualization. That's one aspect. But really what blows me away is the other part, which is we believe we've found the four main levers to reverse aging. What do I mean by that is that there are enzymes that control the epigenome. There are four main pathways, and you want to pull back the lever. So inhibit three of those and push one. And that combination is the winning one. And so we have chemicals that do that, but they're cocktails. And we've published some of these. These cocktails work on these four levers. But what we really want is just one simple, safe molecule because it's easier to develop as a medicine that does those four things. Now, if you'd said to even a pharmaceutical company with a billion dollars, did you do that? They would have said probably five years ago, no way. Doing one of those lever pulls is hard enough.
- [55:35]
A
We're talking decades and billions of dollars.
- [55:37]
B
Yeah. Optimizing and physical screening and making the molecules by hand as chemists. But now we can just take all known molecules and virtually screen them in a couple of months against all those four targets and come up.
- [55:51]
A
And so when you say take all known molecules, we're talking about actually physically doing this in a petri dish.
- [55:59]
B
No, no. Goodness. That would take millions of years.
- [56:01]
A
So what are you actually doing?
- [56:03]
B
Yeah, well, we virtually dock them into
- [56:06]
A
the enzymes and the AI is precise enough to create an actual sort of physical model.
- [56:16]
B
Oh, for sure. Demis and his team solved all of the structures, as you know, and so that made this all possible. Now we can just do the crunch, number crunching. And so, yeah, so normally this docking would be done by hand, by a person, would take days to do. And now it's just done like this. This, this. And you can do billions, actually trillions. And there are libraries of virtual molecules, but also there are actually physical libraries. So what's happened is we've now got a set of 100 top candidates, some synthetic, some natural, and we can just order them like you would on Amazon, bring in your chemicals and put them through our AI assisted screening.
- [56:55]
A
Crazy. So earlier you said it was gonna be a cocktail of four molecules that you're trying now?
- [57:01]
B
Yeah, we published six, and we're now down to three.
- [57:05]
A
Three.
- [57:05]
B
Okay. And if we're. If I was.
- [57:07]
A
And you believe you can get it down to one?
- [57:10]
B
Well, we're testing them now, and they look good so far.
- [57:12]
A
Amazing. Amazing. I want to turn to a subject that's a bit painful and recent and very impactful about this longevity future, which is funding. It's been a travesty of the massive cuts in science, and I know you've been hit hard by it. How hard have you been hitting?
- [57:41]
B
Well, I spend more time as a psychiatrist now than a doctor than a scientist. It's tough. The poor kids in my lab who are innocent in this are really suffering.
- [57:52]
A
What percentage of your lab is funded through government grants?
- [57:57]
B
The majority is government funded. And all of those grants were terminated?
- [58:01]
A
100% of those grants were terminated?
- [58:03]
B
Yeah, they're all gone.
- [58:06]
A
Any explanation as to why Harvard's in
- [58:10]
B
the target of the federal government?
- [58:12]
A
It's not just the Doge activities, it's Harvard's being specifically.
- [58:18]
B
They're singled out for anti Semitism. But taking it out on my poor students who are like my own kids, it's rough.
- [58:26]
A
Well, they're taking it out on the rest of us, too. If the science gets delayed by a year, that just puts, you know, another percentage of the population at risk of dying.
- [58:36]
B
Well, we may never know what medicines will never exist in our lifetime because of this, unfortunately, because Harvard Medical School is the crown jewel of research in the world. And to stop all that research, I met one of my colleagues in the cafeteria last week, and he's a leading guy in his field. And I said, what are you going to do now that you've got no money? He goes, I had a good run. I'll go home. I might write a book.
- [58:58]
A
Wow.
- [58:58]
B
It's done. He's over. His career has ended. He's done. I'm not giving up. I'm going to fight. This is too important to give up, as you should.
- [59:06]
A
And I want to help you. One of the things I realized is probably the single thing that the US could do to solve the US debt is give people an extra 20 years of health.
- [59:22]
B
Yeah, absolutely. We've crunched the numbers.
- [59:24]
A
I know. So talk about that. There was a study at Harvard, London School of Business and Oxford on that. What did the study say? What was the financial implication here?
- [59:33]
B
Yeah, so I teamed up with a couple of great economists and they calculated that in the US extending healthy lifespan just by one year, by keeping people out of nursing homes and giving them back to the community and making them productive was a value to the U.S. economy of $86 trillion. That's just one year. That's doable.
- [59:55]
A
36 or 86.
- [59:57]
B
Did I say 36?
- [59:58]
A
No, you said 86. Is it. I think it's 30.
- [60:00]
B
It's 86.
- [60:01]
A
It is 86 million. 86 billion.
- [60:03]
B
No, 86 trillion. We will fact check that.
- [60:07]
A
Okay.
- [60:08]
B
And then it was 366 or 7 trillion for 10 years. Yeah, it's a lot. These numbers are staggering. This is like the defense budget.
- [60:18]
A
I mean, this is people staying active and generating in the economy and not having to pay out on healthcare costs.
- [60:26]
B
That's what it is. And then people spend money, right? They're traveling and they're buying things. I use my father as a role model. And, you know, he's on our program or whatever, he's doing well. The update on him is he's turning 86. And when most men at his age are in the ground or on the shelf, he is as young as he was when he was in his 40s. Right. He acts, moves, travels, thinks, enjoys his life like we do. And he's not slowing down at all. He still drives at night without glasses. He has to take a test because he's old, but he passes with flying colors. So think about if the population on average was like him, what kind of a world would it be? These people are valuable. Every life is valuable. You can even put dollars on every life's value. It's millions.
- [61:14]
A
I tell people if you're. If you're 80, but you feel like you're 50, you've got all of your relationships. Are you gonna wanna retire or are you gonna wanna just go for the next thing? I mean, the reason people retire is they're in pain, they're out of energy, or they're forced to by regulation.
- [61:33]
B
Yeah. Or you don't like your job. But there's skillbaticals. And we live in a world where you can reinvent yourself pretty quickly. And so I look forward to people like my dad who started a new career in his 80s and he was now supervising clinical trials. And he's giving back to the communities. He's living with one of my nephews who's raising my dad. My dad, at 86, nearly 86, is raising his nephew. It should be the other way around, right? But now he's so healthy, he's taking care of his grandkid. And, you know, it's better that way because imagine life the other way around, and you don't actually have to imagine it. Just go to Japan, where people our age are taking care of not just their parents, sometimes their grandparents and their kids and sometimes their grandkids. That's a huge burden on a generation to take care of both the people who are sick, older than them, and the young people who either don't have jobs or need help in other ways.
- [62:25]
A
David, how much funding did your lab lose?
- [62:28]
B
In total, it was millions. And we're just at the beginning of some of these grants. And one of the grants, by the way, was a career grant given to Kelly Rich, a postdoc who has actually been speaking out in the media as to the cruelty of these cuts to her in the lab. She was working on ALS in a race to try and help Serena's mom. And we were making good progress. We showed that these reprogramming chemicals and genes could treat neuromuscular disorders in mice. And we, not that far away with AI of having something she could take as a pill, perhaps some natural molecules. And to have the funding cut without really any explanation was more than a blow to us. And so we've lost a lot of money and also the. The spirit to go on.
- [63:15]
A
We have a lot of amazing people that watch this podcast. There are three ways that I want to invite you to join me in supporting David's research and his lab. Again, this is not a request he made. This is something I feel compelled to do because I care deeply about this work. I care deeply about having it available personally for my family and for all of us. And hopefully what you've seen here so far convinces you that there is real value that's being created. And honestly, for the small amount of money that, that you spend, it's a travesty because it does compare a few million dollars to trillions of dollars of upside, let alone lives. Lives being saved. So there is a link we're going to put in the show notes that is to donate directly to his lab at lab at Harvard. It's tax deductible. You can donate from $50 to $1,000 and welcome you to do that. And I'm sure Dave would be super grateful for it.
- [64:21]
B
So let's do it. Because the future's too important to not let it happen in our lifetime.
- [64:25]
A
Yeah, agreed. I mean, we hold two different futures in superposition, and we have to choose which one we want. Yeah.
- [64:35]
B
Let's not be in the universe where, you know, things don't happen. Let's make us get us into that universe where we're just thriving as a species.
- [64:43]
A
I love that. I love that this is a subject that just, you know, gives me such incredible hope. Right. You know, this is the most exciting time ever to be in life. And if you want more of it, we're going to make it happen right here, right now. And we all have that one thing in common right now. Aging is a disease and a common biology to solve.
- [65:04]
B
We do. We'll stay healthy for longer, but ultimately, we have to be able to reverse aging if we're going to make it for a long time. So while we work on it, let's stay healthy, but then let's just fund these research projects and make the future a reality.
- [65:17]
A
Yeah. David, I want to talk about another area, which. And then we're going to go to ama. Questions. I put out a tweet. I'm going to meet with David. What questions do you have? Like, so we picked, you know, the top 20 or so that were provocative and fun. But before we go there, I want to talk about what your longevity protocols are. So what are you doing? I mean, honestly, you look great, dude. And I appreciate the fact that you're a poster child for this industry.
- [65:45]
B
Hey, thanks.
- [65:45]
A
Yeah, I, you know, I went online and. Or at least my. My team did, and found something published@nad.com. i'm not sure how. How real it is because I don't think it's. They probably put it together from conversations you've had. I'll put the link in the show notes as well for folks, if they want to see at least what was reported. But let's run through these and tell me what's real, what's not real. Yeah. Okay. You want to see that? You want to see the list here?
- [66:17]
B
Yeah, sure.
- [66:17]
A
Okay. And what. And what's the main thing? I mean, there's a laundry list here, and I take, like, 80 supplements and meds a day.
- [66:24]
B
Yeah, well, you know, I do advise people on their longevity so that they get an insider look, but I'm happy to share some of the key things for everybody. I'm still on the standard stuff that was in Lifespan. It wasn't standard when I published Lifespan, but now it's become, you know, NMN has become a billion dollar industry now.
- [66:43]
A
Amazing. I mean, honestly, due to you. And just to clarify things, you're not backing any of these supplement companies. In fact, they use your name and their likeness without your permission, right? Yeah, yeah.
- [66:56]
B
My lawyers spend a fair amount of time and my money on stopping that. But new companies pop up all the time, especially overseas. But yeah, I don't currently sell anything. So the main things are. So let's start with the basics. Do what you do. So there's the saunas, there's the exercise. Weightlifting is important, especially for men. Or Pilates for women. A bit of weightlifting and then eating is important too. Serena is a trained nutritionist and chef and longevity expert. She came in and changed my life to four years ago, I stopped eating a lot of meat.
- [67:33]
A
Have you gone vegan completely?
- [67:35]
B
No.
- [67:35]
A
90%. What would you say?
- [67:36]
B
I'd say it's 90, 95. I eat out and sometimes I break the rules for celebration purposes, but I want to enjoy life. But I'm definitely plant focused. And a few things happened when I switched to plants as my main diet. I felt better, I could eat more, which was great because I love food and my mind cleared. And that might have also been because I gave up alcohol. Almost all of that.
- [68:02]
A
Yeah. So just another point. I have given up alcohol except for a celebration.
- [68:07]
B
Did you notice a difference?
- [68:09]
A
Yeah, I mean, I'm so sensitive to alcohol. It just makes me sleepy and, you know, weight gain if you're. If I'm. If I'm drinking too much. But I used to have like a little bit of wine. Now I'll taste some wine. Tonight is an exception. My deputy family, the Rees family, is having the bar mitzvah of their son. And so my friend is like, I've got the best bottles of wine. So I was, okay, I'm gonna drink a glass of wine tonight.
- [68:33]
B
Good. Well, you look like you're looking after your weight really well, so.
- [68:37]
A
I am.
- [68:38]
B
I think you've never looked so good. But in terms of weight, gaining weight is a bad thing. It puts our bodies into abundance mode. I've talked before about abundance mode versus adversity mode. We can have abundance mode. Occasionally you can eat a steak, you can eat a lot of food, but for the majority of the time, you want to be in adversity mode. So that's why I try not to eat more than two meals a day if I can. Sometimes One. And the plants help because the plants send a signal also to the body. They're filled with polyphenols that also give the signal of adversity.
- [69:11]
A
GLP1s. Let's just plug that in right here. What's the evidence right now in your mind as a pro? Longevity medication?
- [69:21]
B
Pretty good, actually. Certainly if you're overweight, getting your weight down.
- [69:24]
A
Yeah, for sure.
- [69:25]
B
But in addition, someone like you and me, would it have longevity benefits? I think if it's used judiciously, I wouldn't use it chronically because there are some side effects including muscle loss, but also some kidney and pancreas issues. Potentially even blindness is a risk. The disease that or the incident that we're going to treat next year with the age reversals called. Yeah, so that's non ischemic arteritic. Non arteritic ischemic optic neuropathy, Nyon. So the rates of that have doubled and tripled around the world because of these drugs. So it's not without risk. So you gotta be careful using these peptides. But I think as a way to turn the body into a more adversity mode, they're excellent. I have tried them not to lose weight, but just to see how my blood work turned out and I saw some improvements. So I think with your doctor's advice and permission and.
- [70:21]
A
And there are many of these drugs at this point, right?
- [70:24]
B
Yeah. And they're getting easier to use. So there's an oral version now.
- [70:28]
A
Yeah.
- [70:29]
B
I can see in the future that they'll be part of longevity programs. But again, I'm not endorsing them. I'm not saying you should definitely go do it.
- [70:36]
A
And I think one of the things that's important to note and I just again want to reinforce, if you're using a GLP1 to lose weight, the challenge is you lose the weight, you also lose muscle. And then when you stop the GLP one, you just put on fat again. You don't put the muscle back on,
- [70:56]
B
but there's an easy solution. Right.
- [70:57]
A
Work out. Yeah, you get working out.
- [70:59]
B
There's some effort involved, but just some sit ups, push ups and whatever lifts and weights.
- [71:05]
A
And use the GLP1 drug as a way to get into new habits. Right. Getting new habits of not eating as much or going to a. What meal do you miss if you're gonna miss a meal?
- [71:17]
B
Breakfast.
- [71:18]
A
Breakfast, yeah.
- [71:19]
B
And I have a late lunch. But the thing with GLP1s is even if you were to just fast and stop eating as much, you are going to lose muscle Mass. It's not just that the drugs are causing muscle loss, it's what happens when you don't eat as much. And so really you do have to keep the muscle mass up. And I wouldn't use testosterone alone to combat that muscle loss. It really is better to be working out to stop that. And clearly you're a good example of that.
- [71:46]
A
And amen. What source do you use? What sources are out there? Because I remember when Tony Robbins and I were writing our book Lifeforce when we looked at this, a lot of the NMN sources were not reputable out there. And then of course, a lot of companies have stopped putting NMN out for sale because of what's going on with Metro Biotech and the idea of having NMN become a medicine versus a supplement. So give us some knowledge there.
- [72:23]
B
Well, the first is about NMN as a supplement on can you trust it? And I'm not in the business of testing products. That's not what I do. But I do test NMN sources when I give it to mice. And we have a study that we're just revising showing NMN extends lifespan mostly in female mice, but it did improve frailty and a lot of health related things. So we do test NMN and we've tested a bunch of them and we find that there are things in there that you wouldn't want in there, like endotoxin, which is highly inflammatory parts of bacteria. And so if you're gonna have you published that data. No, I won't. It's only inflammatory. We might publish it actually.
- [73:06]
A
I mean, it's super useful.
- [73:09]
B
We should do that.
- [73:10]
A
I mean some, you know, somebody should be. Listen, you've made NMN a household name. I guarantee the number of people. Well, whether you like it or not, because you talked about the value of this, you didn't do it to try and sell nmn. You did this because you're talking about its impact on increasing NAD levels intracellularly.
- [73:30]
B
And I haven't made any money off it. In fact, I've invested a lot of money into clinical trials. No, I mean there's been like $30 million worth of my money and others to do clinical trials to test a version of NMN in humans. It's cost me a lot to try and validate NMN as a molecule.
- [73:47]
A
One of the advantages if metrobiotech has a particular crystallized NMN that they're testing in a wide range of medical conditions. Right?
- [73:59]
B
That's right. And I don't see why they can't exist in the same Universe that supplements which are not under FDA approval, usually they're not prescribed by doctors. But there's an ultra pure pharmaceutical grade crystalline stable form that has been shown to work that can be prescribed. That's been shown even for fish oil. Gsk. Actually, our friends at GSK made a fish oil thing. It's still available in the market.
- [74:26]
A
And it's a pharmaceutical, it's a drug because of its purity. But the reason I would use the Metro Biotech NMN if and when it becomes approved as a drug is because I'm assured of quality and purity.
- [74:41]
B
That's right, yeah. Yeah. And then to get to the FDA thing, you know, I see on social media people accusing me of being the one to take it off the market. That's absolutely not true. I think everybody should have access to it, otherwise why would I talk about it? I do think though that there should be some better regulation on how pure this stuff is. Because there was a study that showed that, I think it was roughly half of them didn't have what was on the label.
- [75:06]
A
And it degrades over time in the non crystalline form.
- [75:09]
B
Exactly. But what actually happened? I'll explain what actually happened, please. So Metro Biotech, it's not my company. I've invested in it. And there's a chairman and a board. And so they made the decision that they would support the FDA in looking at NMN as a supplement. And there's a law that says if you're using a molecule in clinical trials, it shouldn't be sold as a supplement to protect the $30 million investment that the people are putting in. I believe I'm on record, I'll say here that I was not in favor of that. I didn't want Metro Biotech to get involved with the fda. That was not my decision. But I don't run that company. There are very few companies that I actually have 100% control over. But I am learning that it's better to control the company that, that you're the figurehead of.
- [76:03]
A
Yeah.
- [76:04]
B
But in this case, I couldn't, couldn't stop that. But I think where we're at now is that there's some gray zone.
- [76:11]
A
I mean, I'm seeing, I'm seeing NMN for sale.
- [76:14]
B
Yeah.
- [76:14]
A
Let me clarify something. So ultimately what you're trying to do is raise your intracellular NAD plus levels. NAD levels. That's the end goal.
- [76:24]
B
And the sirtuins need that NAD to work.
- [76:26]
A
It's powerhouse.
- [76:27]
B
Yeah.
- [76:28]
A
So NMN can cross the cell membrane and inside the cell gets converted to nad, correct. Yeah.
- [76:36]
B
You know, academics will argue over everything. I don't think it's still 100% agreed upon as to how NAD is made from NMN. There's some work by Shin Amai at Washington University that there's a transporter even high up in the gut that absorbs it into cells and through the gut membrane. But there are people who say, oh, NMN has to be broken down first before it gets into nad.
- [77:00]
A
And then there's nr nicotinamide riboside, which is.
- [77:03]
B
Which is what's used to make NMN in the cell.
- [77:06]
A
Right. And so you have this sequence. So some people are arguing that you should take NR, some people are arguing to take NMN, other folks are doing NAD IVs. And am I wrong in believing that an NAD IV is not getting into your cell?
- [77:24]
B
Oh, I think that NAD drips will raise the intracellular nad, probably because it gets broken down and then gets reabsorbed. Yeah. But the unfortunate thing with NAD drips, even though they're very popular, is that we still rely on anecdotal evidence that they do something. And I would love to see some more studies on that. But what I can say about oral nmn, we have spent money studying that. And when I say we, the scientists that conducted the study, and I was one of the middle authors on that, have shown that NMN in small groups of people improves blood pressure and cholesterol and lipids, and even seems to look like it works on strength and endurance. So in terms of living up to what we saw in mice, it is looking promising. And there are at least five clinical trials at Metro Biotech now looking at whether it's efficacious in a disease state. Alzheimer's, kidney function, it's all on the website. And so with five and hopefully six shots on goal, the idea is that one of those will work. The other thing that that's interesting is there's a new molecule that they saw that.
- [78:31]
A
So MIB626 was the old molecule.
- [78:34]
B
Yeah, 626 is my birthday, by the way.
- [78:36]
A
Ah, that's where it came from. Interesting.
- [78:38]
B
And then 725, almost.
- [78:39]
A
Happy birthday.
- [78:40]
B
Thank you. So 725 is the new molecule. MIB 725. And that's the birthday of Anthony Sarvey, my great colleague, who passed away during COVID and he was at Cornell, but we miss him dearly. And so that hopefully, if that makes it onto the market, it'll be his legacy.
- [78:57]
A
Nice.
- [78:58]
C
A quick aside. You probably heard me speaking about Fountain Life before. And you're probably wishing, Peter, would you please stop talking about fountain life? And the answer is no, I won't. Because genuinely, we're living through a health care crisis. You may not know this, but 70% of heart have no precedent. No pain, no shortness of breath. And half of those people with a heart attack never wake up. You don't feel cancer until stage three or stage four until it's too late. But we have all the technology required to detect and prevent these diseases early at scale. That's why a group of us, including Tony Robbins, Bill Capp and Bob Hariri, founded Fountain Life, a one stop center to help people understand what's going on inside their bodies before. Before it's too late. And to gain access to the therapeutics to give them decades of extra health span. Learn more about what's going on inside your body from Fountain Life. Go to fountainlife.com peter and tell them Peter sent you. Okay, back to the episode.
- [79:53]
A
All right, let's run down a few of these. So fisetin, lipoic acid, epa, dha, L, taurine. Comments on those?
- [80:06]
B
Yeah, I mean, Fazetin is a molecule we actually first discovered to be a longevity molecule before it was known as a senolytic.
- [80:14]
A
Yes, Quercetin together.
- [80:17]
B
Although the people that now talk about Fazetin just ignore our research.
- [80:21]
A
But that's how is that the Australian pronunciation of it? Setin versus fisetin?
- [80:27]
B
Yeah, I think it doesn't matter what you say, etin. But we showed fisetin is a sirtuin activator just like resveratrol. And so I think it might be doing both things is to either calm down or kill senescent cells at high doses. And at low doses it activates the sirtuin enzyme, which is what we want because I think of NAD as the gas or the petrol for the enzyme. And then the accelerator petal are these polyphenols like physitin and resuratrol. And together they have a double whammy of benefit. Lipoic acid. I did a PhD on that when I was in Australia. I've always liked it. And then I started taking it about 15 years ago when I was introduced to one of my heroes, Denham Harmon, who came up with the free radical theory of aging. And he was still in the lab at 92. And I said, what's your theory? What's your secret? And he said, it's alpha lipoic acid.
- [81:23]
A
Interesting. But the, but the free radical theory of aging has really been kind of disproven hasn't it?
- [81:30]
B
Yes, but I still admire him for being in the lab at 92.
- [81:33]
A
Sure. But I mean, for those people who are thinking, oh, I need to be dealing with my free radicals, that appears not to be one of the primary reasons of aging.
- [81:43]
B
Well, indirectly it is because we know DNA breaks are going to accelerate aging.
- [81:48]
A
Sure.
- [81:49]
B
And free radicals can damage DNA, so. But it's not the Holy Grail. Taking antioxidants doesn't extend the lifespan of animals very much.
- [81:58]
A
Okay. You mentioned El Taurine. Just had a paper published on it.
- [82:03]
B
Yeah, it just came out in Science. Rafael Decabo is a very good friend of mine for 25 years and he was the one that just showed that El Taurine levels don't decline, apparently in humans or monkeys or mice.
- [82:17]
A
Because that was like, I started a year ago because of all the news about it, and now, now it doesn't
- [82:24]
B
look as promising, put it that way. And so I would say it's not going to hurt you, but I think there's less likelihood that it's going to extend your lifespan.
- [82:33]
A
By the way, nmn1 gram, that's what I take. Is there any. If you do 2 grams or 3 grams, is there a problem with going more than a gram that you know of? Well, I'm just curious.
- [82:46]
B
Well, I always.
- [82:46]
A
Because I have it in a bunch of supplements. So I'm like, you know.
- [82:50]
B
Well, it's published that both 1 gram and 2 gram have benefits and that 1 gram will double your NAD and 2 grams will roughly triple it on average. But in my personal opinion, now I don't think it makes sense to go any higher. Your body will just pee it out anyway and there's no point taking the risk. But I know 1 gram and 2 grams seem to be safe in short term human clinical trials.
- [83:14]
A
Got it. We've talked about resveratrol, spermidine, vitamin D,
- [83:19]
B
vitamin K. Yes, yes, yes.
- [83:22]
A
Okay. Low dose aspirin still.
- [83:25]
B
Yes.
- [83:25]
A
Okay.
- [83:26]
B
And that's interesting because a lot of people have heard, at least through the grapevine, that aspirin shouldn't be taken. So here's the deal. And when, you know, I actually read the papers, I don't just read Twitter. When you go into the literature. The reason that doctors are mostly against aspirin these days is that they're balancing the risk reward. Now the reward is prevention of clots and cardiovascular risk. Now the risk is that you get stomach bleeding. And based on the numbers, it wasn't clear if it was worth taking aspirin with the Risk. But that's for the average human. And there is no such thing as an average human. So really, medicine should be breaking it down as to. For you, Peter, what's good for you? Do you want an aspirin or not?
- [84:12]
A
And by the way, everything we've spoken about so far, I do take, including
- [84:16]
B
the aspirin, 81 milligrams a day.
- [84:18]
A
81 milligrams, right. Baby aspirin.
- [84:20]
B
So take a coated one.
- [84:21]
A
Yeah, I do.
- [84:22]
B
Yep. So that reduces the risk of any stomach issues. But here's the thing. That there are people at risk of cardiovascular disease, and then it does make sense for them to take an aspirin. It makes perfect sense for me to take it because I genetically have high levels of lp.
- [84:36]
A
I do, too.
- [84:37]
B
Yeah.
- [84:37]
A
By the way, I'm so excited about the new drug that's coming out for LP.
- [84:40]
B
Yeah, it looks promising. It just. It's in phase three.
- [84:43]
A
It should be coming out in, like, the next 12 months.
- [84:45]
B
Yeah.
- [84:46]
A
I mean, because right now, you know, it's. There's very little that moves the needle there.
- [84:51]
B
Yeah. It's really hard to bring it down. I know from experience.
- [84:54]
A
Yeah. You and I are in the same boat. Trimethylglycine.
- [84:58]
B
I don't take that.
- [84:59]
A
Neither do I.
- [85:00]
B
No. Okay. There's this unfounded claim that NMN and NAD boosters deplete your methyls and that you need to take this to supplement it. That's just based on wild speculation. There's no evidence from anything we've done that that's true.
- [85:15]
A
So I stopped taking Metformin. Are you on it still?
- [85:19]
B
Occasionally.
- [85:20]
A
Occasionally.
- [85:21]
B
Okay.
- [85:22]
A
I'm on berberine instead.
- [85:23]
B
Me, too.
- [85:23]
A
Yeah?
- [85:24]
B
Yeah. Now, I found that metformin was really rough on my stomach, and the older I get, I find it's rougher. But Berberine seems to be great. And so I do that.
- [85:32]
A
I stop Metformin mostly for the focus on muscle growth.
- [85:37]
B
Yeah, there's that. But also, I want to speak about that, please, because I find that most people don't read the papers. And if you do. What you see is that this claim, even from some doctors who talk about this, is that it blunts muscle growth. When you actually dive into the data, you see that the graph was misrepresented.
- [85:58]
A
Wow. Guilty as charged. Yeah.
- [86:00]
B
Well, the one thing you should never do as a scientist is cut the Y axis off and exaggerate the difference. But that's what they did. It's only a 5%. Why? Just looks better.
- [86:11]
A
All right, let's go to the next one. Rapamycin. So huge claims. I mean, many of the longevity experts said, okay, if there's one drug that probably has longevity impact, it's rapamycin. And I've been tracking that, I've been reading on it, and it's enough up and down where I stopped taking rapamycin. I have a very low senile cell count. How about you? What do you think about rapamycin?
- [86:43]
B
I'm less excited about was the darling because it works really well on inbred animals and seemingly might even work in dogs, but in humans. There was a study that came out, it was probably six months ago, that compared the effect on the epigenetic age of people in different clinical trials. And while some things worked really well, like caloric restriction, what else was important? I think acarbose worked really well. Metformin looked better than I thought it would. Rapamycin had no effect on the age of the epigenome. And so that combined with the known potential risks of downregulating the immune system, and let me explain later why I think that that's bad. I decided only to take it rarely.
- [87:32]
A
What occasion would you take it on?
- [87:33]
B
I'd probably take it four times a year.
- [87:35]
A
Okay. So it just pulsed?
- [87:36]
B
Yeah. And I'm monitoring myself, so I know if it has benefits or not. And I do see some.
- [87:41]
A
Are you monitoring your immune system? You're monitoring everything?
- [87:44]
B
Yeah, I monitor my immune system. I'm counting the cells that I have, the different types and cytokines, inflammatory cytokines. And I wanna keep those as low as possible, keep down inflammation inflammaging. So I wanna talk about why downregulating your immune system might be bad.
- [88:00]
A
Yes.
- [88:00]
B
Now, you wanna down regulate your inflammation, but you wanna have really active immune system when it comes to cancer.
- [88:06]
A
Sure.
- [88:06]
B
And viruses. And those two things are real risks as we get older.
- [88:11]
A
Sure.
- [88:12]
B
There are endogenous viruses that come out like cmv, and there's a. CMV is pernicious.
- [88:19]
A
And it's an epidemic out there. I mean, one thing that people don't realize is there's something called immuno exhaustion. Right. Where your immune system is fighting all these battles against herpes, against cmv, against how many different viruses do you think are endemic in the human being?
- [88:36]
B
On average, it's approaching a thousand now when you do deep sequencing.
- [88:42]
A
Incredible. And if they're fighting those viruses, your innate system is not there to fight cancer.
- [88:49]
B
Yes, there's that. And the other issue is that these viruses like cmv, they lead to autoimmune disorders. Potentially, like CMV is linked to multiple sclerosis now.
- [89:00]
A
Interesting.
- [89:01]
B
And so you do not want CMV circulating, and for that reason, I don't want chronic downregulation of my immune system.
- [89:07]
A
Yeah, yeah, that's important to note. Okay, let's jump into a few other elements here. So thank you for that. Is there anything else that we didn't talk about that's high in your supplement med list?
- [89:21]
B
Oh, there's lots, but let's leave it for the friends.
- [89:23]
A
So maybe the friends of Sinclair Lab will have a deeper dive.
- [89:26]
B
Book two.
- [89:27]
A
And book two. Okay. By the way, for those who are fans of David's first book, Lifespan, which I probably recommend more than my books, his next one, coming out in 2026, is called lifespan Survival, so can't wait.
- [89:44]
B
Thanks.
- [89:45]
A
All right, so are there any special supplements or additions for women that you want to call out?
- [89:52]
B
Oh, gee, well, that's a whole separate category. And Serena, my partner, is an expert in that. I usually defer to her. And I don't want to claim to be an expert on female hormone therapy, but I do believe that hormone therapy is anti aging. We see that in the literature. And also there are some ways to delay menopause and perhaps even reverse it. And I talk about that in my book as well. So I think mostly for women, it's hormonal, but there's other things like iron, protein that they need certain times of the month as well.
- [90:23]
A
Do you know Jennifer Garrison at the Buck? Sure. Yeah. So Jennifer is another. Another place that Tony and I have supported her research, and she put forward. She was at XPRIZE Visioneering last October, and that's where we compete all these X Prize ideas. And her work in what was being called the double X prize for women's longevity and particularly ovarian longevity, won the competition. So we're in the middle of designing that X Prize, which will be super cool.
- [90:55]
B
Well, she's great. I have a superstar in my lab who, by the way, needs our support. Maria, she's such a superstar. This morning she gave live meetings. So our live meetings go for three hours on Friday mornings. And she outlined her project to use these age reversal breakthroughs on women's fertility.
- [91:17]
A
Well, we need to get her either competing for the prize or helping to design the prize. For sure.
- [91:21]
B
Yeah. She's also, by the way, using menstrual fluid as a biological clock and diagnostic factor, which is a great idea.
- [91:29]
A
Amazing, Amazing. So sauna. Do you sauna?
- [91:34]
B
As much as I can, yeah.
- [91:36]
A
You know, I just purchased something called the Healing Sauna. It is a deep infrared sauna. It's relatively small, about, you know, about yay big. It's got a chair in the middle and it zips up around you with your head sticking out the top and you have two arm slots. So I get, in the morning, I'm on my computer doing my email and I'm like, you know, in about 30 minutes, I get a great sweat. And you don't want to sweat too much. You want to sweat enough to get the toxins out, but not so much that you start losing other vital.
- [92:11]
B
Right. And turn on the heat shock proteins in your skin and maybe deeper. Yeah, that's all important. And the science for sauna now is irrefutable.
- [92:19]
A
It is. It's a couple of thousand dollars for this thing and it fits anywhere. So if you want to increase your. It's super easy. And I actually, I love it.
- [92:29]
B
I might look into that because often the problem is we don't have space in our houses.
- [92:34]
A
So this and this actually it is. It's like the size of this table. It's no bigger and it collapses. And again, you sit in a folding chair inside and the elements are inside. And you basically zip this thing around your neck. It's got a frame and it works.
- [92:51]
B
Does it get hot enough?
- [92:51]
A
Yeah, I mean, I get a really great sweat going in 30 minutes. It's not like instantly like 10 minutes, but I enjoy my 30 minutes. I'm meditating or I'm watching a video or listening to a book.
- [93:04]
B
What's it called again?
- [93:05]
A
It's called Healing Sauna.
- [93:06]
B
Healing Sauna.
- [93:07]
A
Yeah, I think it's just healingsana.com okay, so one big question is fasting, and fasting mimicking diet? So when I looked into it, there was a lot of confusion about whether fasting actually moved the needle for humans. What do you think about it?
- [93:28]
B
I know a lot about it. In particular, I was just recording my next podcast and it is on fasting and caloric restriction. And there's 80 pages of notes. Show notes.
- [93:37]
A
Wow.
- [93:38]
B
So, yeah, so you have to do fasting the right way with all these diets. If you do it the wrong way, it can harm you. Right. But you need to be educated. You need to make sure you're not overdoing it and you're supplying yourself with enough vitamins, minerals and protein. And so yeah, I do it, but I do it in a scientific way. And that's part of the challenge. If you don't do it without having regular blood tests at least once every Few months. I think it's probably somewhat risky. But in general, fasting has been shown for forever since humans were sure.
- [94:13]
A
In fact, religions have built in fasting into their annual clock.
- [94:19]
B
Yeah. So I still believe in the science of fasting and it just has to be done the right way. And actually there are some papers that show that if you do a vegan diet, this is just separate. But in a good example, a vegan unhealthy diet will make you live shorter, but a vegan healthy diet will make you live longer. You just gotta make sure you're eating the right things. And the same with fasting, you gotta time it with your circadian rhythms. You gotta eat the right food at the right time. You can't just eat French fries once a day and hope that's gonna make you live longer.
- [94:50]
A
So I'm very vocal about the notion that sugar is a poison.
- [94:54]
B
Me too. I regard it as a poison.
- [94:57]
A
Yeah, I just want to echo, I mean, so a couple of data points here, right. We are eating in our diet today. If you look at the numbers on the order of 10 times more sugar than we did a couple hundred years ago. And one of the things, we just are getting ready to publish this data at Fountain Life. Right. So everybody coming through Fountain Life, we upload them, we get 200 gigabytes of data. It's like one of the most complete data uploads you can possibly do in five hours. Full body mri, brain, brain vasculature, a coronary CT looking for soft plaque, not calcified plaque. Right. Soft plaque is what kills you these days. And if you have a high calcium score, it doesn't mean much unless the calcium's blocking your coronary artery. If it's cement on the side of the walls, it's stable, but it's the soft plaque that could evulse in the middle of night, block your artery and you don't wake up. We do low dose lung CT, we do DEXA scan, metabolomics, 140 blood biomarkers, your gut, microbiome, retinal scan, skin scan, all of that.
- [96:02]
B
When am I gonna get a scan?
- [96:03]
A
Dude, please come. Please.
- [96:05]
B
I'm just teasing.
- [96:06]
A
No, I'm serious. No, please come. I'd love to try it. And as my, as my guest, we're opening up LA here in 1Q26. And of course, we're operational in Dallas today. We're opening up Houston before the end of this year. We have New York going Orlando and Naples going and opening up Miami. So we've got.
- [96:29]
B
Congratulations.
- [96:30]
A
Thank you. Yeah. Really?
- [96:31]
B
I remember when you were just talking
- [96:32]
A
about it, we looked at what correlates highest with heart disease and it wasn't Lp or triglycerides or LDL or HDL. It was your hemoglobin A1C. Right. And I mean, it's like you can control that.
- [96:50]
B
Well, you can. And it starts with good diet and lifestyle and exercise for sure. But the drugs now that are available, you can either prevent the absorption with a carbos, you can pee it out with SGLT2 inhibitors, you can take metformin or berberine.
- [97:08]
A
Yeah.
- [97:08]
B
And then there's others. And so, yeah, if you've got a good physician, you should be able to control your blood glucose these days. Of course, the GLP one's we shouldn't forget.
- [97:17]
A
It's crazy. Okay, one or two more subjects I want to go into the ama. We have so many fans of yours that have written out questions here. I just got back from Hong Kong and one of the things that I was speaking about there was the notion that a breakthrough in China works in Chicago, a breakthrough in Boston works in Beijing. We all share, all 8 billion of us share the same fundamentals of longevity. And so unlike AI, which is a battle sort of winner take all, the idea of being able to give people longevity is something that is a rising tide for everybody. I'm curious where. So when I run my platinum longevity trips, we're currently doing them one year on even years were in San Francisco and San Diego, which is sort of a cluster for longevity. And then on odd years like this year, we'll be visiting you and George and a number of other incredible people in Boston, Cambridge and Dean Kamens in New Hampshire, which is another cluster, if you would. What's going on in the rest of the world? What's hot? Where do the clusters of longevity work?
- [98:38]
B
Well, there are nations that have stood up and said, we're going to invest in this. And so in Asia, it's Singapore. In the Middle east, pretty much all the countries but Saudi Arabia, UAE and now Qatar are big on longevity. And then, and then it's just distant 3rd and 4th and 5th. The Western world is not really getting into it. Besides the us, it's a little bit in the uk, a little bit in Australia, but other than that it's just pockets of really good labs, but not really an industry yet.
- [99:13]
A
I wish that in the same way we just saw a couple of trillion dollars put into AI by the Middle east that they would get longevity religion. I mean, it's you know, and start pouring trillions into this space. And I hope we can get there. Hoping get there. Because I do fundamentally believe this is. You know, you've spoken about this. You've been really the first person to speak out that aging is a disease that when we're able to cure and reverse this, it is going to uplift every society. And God knows that South Korea, Japan, China, Italy, most of Western Europe need longevity. They're disappearing as nations.
- [100:03]
B
Yeah, well, that's the other thing. It used to be that we're gonna overcrowd the planet if we slow down aging. But we need those, need the current existing people to stay healthy and productive. Cause they're running out of people.
- [100:15]
A
Are we seeing good work coming out of China as an area? Do you know that? Are there scientists? I'm just, I'm curious what's going on there?
- [100:25]
B
They are more than a decade behind the US Right now. But we're ceding to them right now. We're cutting our science by more than half.
- [100:33]
A
And yeah.
- [100:33]
B
Oh, my God, all that stuff. So I think China's laughing all the way to the IP Patent office. And we really risk our lead in this area. And while AI is neck and neck, we have a big lead in longevity. But we could lose that.
- [100:49]
A
Yeah, for sure. All right, let's jump into questions from your fans. All right, so the first one was, what role is AI playing in your search to reverse aging? We. We heard about that already. A very big, big role. Yeah, a big role. When did it start becoming a big role in your. In your lab?
- [101:08]
B
We started using it about three years ago, but now we. We don't go a day.
- [101:14]
A
Can't live without it.
- [101:15]
B
Exactly. And think about this. That what we do now in two months would have taken thousands of years to do. Yeah, you can say it, but just let that sink in. The predictions that I made five years ago are out the window because of AI Now I'm much more optimistic.
- [101:34]
A
So the new book is going to update those predictions.
- [101:35]
B
Exactly.
- [101:36]
A
Yes. Okay, fantastic. Afia 3000 says, is there a role for epigenetic reprogramming to end ovarian aging and restore ovarian function?
- [101:47]
B
So Maria will answer that in my lab. PhD student. So, yes, we do believe that we can reverse ovarian aging. We already were the first group with our Australian offshoot to show that you can reverse infertility in old mice. That was a shocker because people said, oh, mammals run out of eggs. Right. But we took 16 month old mice, which had become infertile six months earlier and reversed them and made them produce pups again.
- [102:13]
A
Wow.
- [102:14]
B
I know. It's possible. Even with nmn, it worked. Wow. So we're going to try the even better technology, the stronger technology, the epigenetic reprogramming.
- [102:24]
A
Incredible. And, you know, most men are very ignorant about ovarian aging and. Yeah, I mean, just to pass along some facts for folks, something like only five or six species on the planet go through menopause. You know, it's three species of whales, narwhal, and humans go, which is crazy. You'd imagine everybody does. But, no, that's not the case. And if you're a guy, the age at which your sister went through menopause actually correlates with how long you'll live. Right.
- [103:00]
B
It's really a good, good indicator of longevity.
- [103:04]
A
Fascinating. All right, Glenn, Origin asks, how close are we to making partial cellular reprogramming safe and scalable for human use? What's your current stance on NAD boosters? Are nmn, NR and IV NAD still viable, or is there a next evolutionary evolution emerging? Is gene therapy still your most promising delivery method for Yamanakas? We've sort of covered many of those. I don't know if you want to add anything on there.
- [103:31]
B
That was a very long question.
- [103:33]
A
Yeah, but it's testing your memory.
- [103:35]
B
Yeah, it really is. I think we're very close. We'll go into our first humans. Hopefully by this time next year, we might know if it works. From then on, it's probably a year or two before we do whole body rejuvenation. If that works. Imagine.
- [103:49]
A
I mean, it feels like it's science fiction. It feels like it's the future. It's like we're living in the Star Trek universe with, you know, AI at this level and talking about whole body rejuvenation. I mean, what an extraordinary time to be alive.
- [104:03]
B
It is. It is. The future looks so bright. We have to make it happen.
- [104:09]
A
Yeah, we absolutely have to. Sornald asks, when can we expect results on human trials of OSK Yamanaka factors? I think you've answered that. We're going to see human trials. This is the Life Biosciences work starting in January. January.
- [104:30]
B
Yep.
- [104:31]
A
Okay. Icksing wants to know when is your next book coming out? We shared that. So it's 2026, and it's called Lifespan Survival.
- [104:42]
B
I'll tell you what it's about.
- [104:43]
A
Please. Yeah, I love that.
- [104:44]
B
So Lifespan was more of a textbook. It was, why do we age? And how does this all work? And what will happen to the planet when this happens. Book two is really answering all the questions that I've been getting since. And so think of Lifespan 2, the book as the guidebook. How do we optimize our bodies? Looking at our evolution, the genes that we all carry, how do we individualize our lifestyle? Supplements, medicines to maximize our longevity. And then what do we do for the next 10, 20 years going forward? And I look at it from the individual perspective at the molecular level, all the way through to society.
- [105:20]
A
Fantastic. Annabrilliant writes. What's your exercise routine? How much protein do you eat?
- [105:29]
B
Okay. Her name was brilliant. I like that. So the routine is whenever I can I get to the gym and often I'm on planes. So it's hard to work out on planes. But I think it's very important a few times a week to get to the gym or at least at home have something, some weights you can lift and then walk around on a treadmill moving, moving, moving and keeping. Especially after the age of 50, you gotta keep lifting weights otherwise you're gonna lose it.
- [105:55]
A
Smoking is the new, I mean sitting is the new smoking, as I like to say. And for me the tricks are I have a stationary bike. I take my zoom meetings on my stationary bike. It works well.
- [106:08]
B
Yeah. So if you've ever been on a zoom meeting with me, it looks like I'm in space because I'm standing but I'm moving all the time. And so yeah, I don't sit down during the day. I try not to at least. So that's one trick. Protein. I eat a lot of protein, but it's mostly plant based.
- [106:25]
A
Sure. So you know, for me I put on 10 pounds of muscle mass about two years ago, 18 months ago. And my job is keep it on now. And it was creatine. Do you take creatine as a supplement?
- [106:36]
B
No, but I'm considering it.
- [106:38]
A
Yeah. I mean it looks like all upside, no downside for me. So I do 5 grams of creatine and it was 1 gram of protein per pound of body weight. And there's a lot of debate on how much protein our friend down the street here is at UCLA is not liking so much protein.
- [107:01]
B
Well, I tend to Valter Longo. Yeah, there's Valter. And also Dudley Lamming is my ex student, he's now a professor and he's done some of the most work on looking at amino acids and how they affect longevity. And there are some really good amino acids and there are some that will reduce your lifespan and there are what's called branch chain amino acids. Leucine, isoleucine, valine, that are the bad ones. And you get a lot of that from meat, so I try not to eat a lot of meat. Plants have less of these amino acids.
- [107:28]
A
What's your favorite protein source from plants?
- [107:30]
B
Oh, gee. Lentils.
- [107:32]
A
Lentils. Love lentils. Yes. Okay. Aoko Nova one asks Dr. David Sinclair, what single experiment would you definitely falsify your epigenetic noise? Okay. What experiment would falsify your epigenetic noise theory of aging? Is there something that if you ran it would disprove that theory?
- [107:55]
B
Oh, yeah. It's easy to disprove a theory. It's much harder to prove it. Lots of things could disprove it. For example, the ice mice. If we had accelerated the epigenome aging, so changing the methylation pattern, the gene expression, and those mice were normal and didn't look old, then I would have thrown out the theory. But they did look old. And that was the reason that I thought it's likely to be true, because the chances that it would fail were 99%. But that 1%, it worked.
- [108:26]
A
Wow. All right. Oodtothinkwith asks what AI advancement would be the most useful for your research?
- [108:34]
B
Oh, that's great. I would love if AI could tell me who the observer is, where the observer is. We've been working on that, but would love it if they said we just analyzed all the world's data and it's gotta be this result that would help. Sure. That's my dream is before I die, to figure out has the cell rejuvenated
- [108:54]
A
and have the AI publish the paper
- [108:57]
B
for you as well, well, that's almost doable now. But I think that also being able to do drug development even better than we do now. So to be able to say this one molecule is your candidate for going into humans would be amazing.
- [109:12]
A
Wow.
- [109:12]
B
We're not there yet. You know, it says top hundred, but going down to one. And like you said, having a digital twin and being able to simulate the interaction with all the proteins in the body and say, okay, that one's probably going to be toxic, but this one will work. That would be. We're probably only a few years away from that. And eventually you'll just do it on your phone. We'll talk about, oh, let's cure whatever disease on your phone by the time you get home, it's told you how to do that.
- [109:36]
A
Yeah, I love that. I have a question that pops in mind here. There's a crazy statistic about the non Reproducibility of research data. I mean, is it like half of the research out there? I'm not sure if it's that high, but can't be reproduced. Well, what's going on there?
- [109:55]
B
Yeah, that number is an exaggeration. We sometimes struggle to reproduce people's data and it's because you're using a different cell line, different water supply, it's different handler. The mice don't behave the same way. So it's not that the people are faking it. It's more that science is complicated and variable and depends on where and how you do it. And some labs rejoice in disproving things. I don't do that. I always assume I'm the one that it's not working. The reason it's not working. But there are labs that thrive on not reproducing people's data and it's super easy to not reproduce someone's result. Sure, I could easily do it. Just change one thing and it's not going to work. So there's that category. But of course there's a lot of research that isn't done rigorously like this Turing paper. It might have been due to just inherent variability taking one time point, but when you look over the lifespan of longitudinal same humans, you do see it. So sometimes there's some bad science, but I think that number is exaggerated. I'm very happy to say that none of our papers have ever been disproved or had to be retracted or change their conclusions. I stand behind my scientific record and we work really hard to make sure that everything we do is very reproducible. In fact, we don't publish something unless our lab and another lab can reproduce it.
- [111:07]
A
That's super high standards. Okay, Obertzx writes, what one area do you want to see more innovative startups tackling? Is there something that in longevity or. I assume so, in the biotech longevity world is.
- [111:23]
B
I would love more labs to be working on finding new ways to reverse aging. Right now we have three genes that we know work. That's our technology. And we have some small molecules we're working on. But then it's all white space for people to get into. We do have some competition, right? We've got Altos and the others. But I think that this area is similar to AI. There's just that there's so much that can be done and it's not like one company is going to win everything. If you're talking about potentially being able to treat and or cure most diseases, you could have Hundreds of companies being very successful in this area and I would like to see more jump in.
- [112:07]
A
One of our mutual friends, Dr. Zaboronkoff from Insilico Medicine, has built an amazing lab that is AI and robotic driven. So the AI proposes the experiment, the robots run the experiment overnight, get the data, iterate on the theory and so forth. Does anything like that exist in, in Boston right now?
- [112:30]
B
I am not aware of it, but that sounds, that's the future for sure. Alex is onto it. Yeah, I think that humans will just play a minor supervisory role in the future of drug development. Now, right now, we humans are more creative than AI. We can imagine things that AI cannot. But that is only a few years from being superseded by AI that can have an imagination just like ours. I, by the way, actually I believe that we're going to see consciousness in these machines. And I just tweeted out because I just finished listening to a book about the evolution of intelligence, which Max Bennett, I think is the author and it's a great book and he talks about how we evolved our intelligence. And it starts with language, by the way, which now we're doing LLM. So we're early stages of human evolution over the last million years. But there's not that many steps that between once you've got language to becoming sentient. Almost a given.
- [113:28]
A
Wow. I'm about to go on a two week vacation to Alaska with my family and I was looking for a book to read. I think you just found it for me. You remember the title of it?
- [113:36]
B
I think it is the Evolution of Intelligence.
- [113:38]
A
Fantastic.
- [113:38]
B
Oh, it might be A Brief History of Intelligence.
- [113:41]
C
Every day I get the strangest compliment. Someone will stop me and say, peter, you have such nice skin. Honestly, I never thought I'd hear that from anyone. And honestly, I can't take the full credit. All I do is use something called One Skin OS one twice a day, every day. The company is built by four brilliant PhD women who've identified a peptide that effectively reverses the age of your skin. I love it. And again, I use this twice a day, every day. You can go to Oneskin Co and write Peter at checkout for a discount on the same product I use. That's Oneskin Co and use the code Peter at checkout. All right, back to the episode.
- [114:20]
A
Jared Michaels writes, when will poor people be able to extend their lifespan? You know, so one of the things that we get critique on all the time is the expectation that it's going to be super expensive.
- [114:35]
B
And it is. Initially, the gene therapy is not Cheap. But as I've said today, we're working on making it as cheap as possible.
- [114:42]
A
Dollars a dose.
- [114:42]
B
I could see it being a dollar or less a dose eventually. Oh, and by the way, patents run out. So even if the company recoups its money, it'll eventually be like aspirin.
- [114:52]
A
I mean, you know, Moderna's COVID vaccine was between a dollar to $2 a dose. When you're providing something to a billion people, it gets really cheap.
- [115:03]
B
Yeah. And actually, based on what my lab is doing now, I see for a few cents a day, everybody could afford a longevity pill.
- [115:10]
A
Yeah, I mean, it's a beautiful vision. All right, let's see. V or Vladimir Adelnor asks, what is the difference between the current longevity metrics and actually being young, I can at age 22, go and get in a fight, get drunk, do an overnight while still operating. Many high skill work at perfection. Whereas longevity folks can't do any of that.
- [115:39]
B
We can.
- [115:40]
A
I don't know. I feel like I can do anything like that. But listen, I'm not gonna put all nighters like I did in my 20s. Right.
- [115:48]
B
Well, our organs are not optimized still their gene expression. So the epigenome has degraded. You and I have lost some of that information. So our liver cells are not pristine anymore. They are behaving a little bit more like a nerve cell or a skin cell. They're more like a melange of cells. So we need to reboot them so that they know how to be perfectly liver cells again. So that's why I think you and I cannot do an all nighter now and get away with it. But that doesn't mean we can't. I mean, I now look at an old person. I don't see them as an old person. I just see someone who needs a reboot.
- [116:21]
A
I love that. I love that. Hey, you want to reboot? Come on over here. All right. Kingsley says, what are the second and third order effects once aging has been cured? Does life have more meaning before it's because it's finite. So this is. It gets in the philosophical conversation here. And I love your thoughts on this. I definitely have opinions.
- [116:47]
B
Please, we may share them. I am not enjoying this conversation because I'm worried about dying. Yeah, I'm enjoying it because the moment is fantastic. And I don't think if the fact that I'm gonna die one day makes this any more enjoyable. I believe every day is a joy. It's a gift and you make the most of it. And whether I'm gonna live 80, 200, 400 years. I'm gonna enjoy this moment just as much.
- [117:13]
A
You know, I remind people, listen, the average age for most of human history was like 30. Are you enjoying life now less because we've increased it two and a half or threefold? I don't think so. I'm having a blast. I want to see as much of it as I can. The impact of AI on purpose is going to be interesting. I think that that's something important to do in this world of extraordinary abundance and cognitive superpowers, can we continue to keep ourselves engaged and excited about the future? There is another thing. When I have my longevity platinum trip, one of the first exercises I do with people is I say, okay, I want you to write down on a piece of paper what you would do with 20 extra healthy years. Write it down. And most people can. Most people can sort of think about 20 extra healthy years. Now. I say, what would you do with 50 extra healthy years? And people's minds start to break. It becomes much more difficult for them to do that. What would you do with 50 years?
- [118:21]
B
What would I do?
- [118:22]
A
Yeah.
- [118:22]
B
Oh, I'd keep researching and get us into new places. I had somebody ask me once, why don't I work on climate change? And I figure if we solve aging, that'll just work on something else. I love research. I love knowing things for the first time in human history. I'll keep doing science as science for as long as I am funded and can do it. I love life, too. It's just. It's so much better than the alternative. But if you look at my father, you know, I didn't expect my father to live beyond 80. Nor did he, by the way. And he is loving life like you wouldn't believe. He's out every night with different people, and a lot of them are good friends and women, and they're younger than him. It turns out when you're 85, 86,
- [119:05]
A
most people are younger than you.
- [119:06]
B
There's that. And if you're a man, there's not a lot of competition at that age. But yet, look at him. He would not say, I wish I died at 80, like some people say he wants every day. And he wouldn't mind another 20 years. I think what we may have to do as a society is do what Sweden did, which is they recently pegged their longevity to their retirement age. And so as longevity goes up, you work longer. It makes sense. We can't just all sit around drinking cocktails.
- [119:37]
A
Yeah. And we'll have a revolt when that happens. But it makes sense.
- [119:41]
B
But it'll slowly inch up. Let's say longevity goes up by a year in the country you work for next year. Again, what's the alternative? Do you want to just die young?
- [119:48]
A
But I think, again, if you feel great, if you've got the energy, if you've got the cognitive clarity, if you've got the mobility, you're going to want to do stuff. Yeah.
- [119:57]
B
And maybe there's a world where we've got AI and androids where we don't have to work for.
- [120:01]
A
Yeah. We have some version of ubi, but health is still going to be. Is the most valuable asset we have.
- [120:06]
B
Yeah.
- [120:07]
A
All right. So, you know, second and third order effects. One other thing that people ask is, oh, my God. Overpopulation of the planet from people living longer. And of course, I think everybody listening to here in the moonshots knows the numbers here. Right. The replacement number of children per family is 2.1. Almost every country on the planet is below that. Some dramatically. Right. South Korea is like 0.7 children per family. Japan is not far from that. Italy is evaporating. Most of Europe, the US is.
- [120:43]
B
Those economies are screwed, by the way, unless they do something seriously.
- [120:47]
A
Well, longevity is critical, and robotics and AI are gonna be critical. And somehow incentivizing people to build family, I think is critical.
- [120:58]
B
Yeah. Or extend the fertility age of women. Because a lot of women these days leave it till too late.
- [121:04]
A
Yep. I mean, it's not fair to them. You know, I had kids at 50. Right. I'm 64 now. You're a young man.
- [121:14]
B
You're 64.
- [121:15]
A
Yeah.
- [121:15]
B
You're looking great.
- [121:16]
A
Thank you. I feel great. And my kids are 50. And I keep on telling them, yes, when you're 50, I'll be 100 and I'll still kick your butt. Yeah.
- [121:25]
B
Well, I think we men, we tend to take it for granted that we can be fertile and fit for most of our lifespan. But for women, it's not fair. And sometimes These careers take 40 years. As a scientist, you're not mature until you're 40.
- [121:41]
A
And Hollywood paints all these pictures of women in their 40s having kids, but that's a struggle. That's a struggle. And it's through in vitro fertilization or egg donors, and it just is not communicated.
- [121:55]
B
And after 30, it's a precipitous drop in fertility. So if you're a woman in your 20s, look at those numbers and realize that after 30, it's going to go down dramatically and try to make life's plan until we figure out a solution.
- [122:08]
A
Freeze eggs.
- [122:09]
B
Is that. Yes. Freeze fertilized eggs if you can, and follow these protocols. Is every indication that we can delay infertility by delaying aging?
- [122:18]
A
Yeah. All right. Mad scientist asks, if aging is fixed and we all live for 500 years, what will happen next? What are all of the pros and cons of life past 150 years of age? I, you know, listen, I revert to Star Trek. It's like there's a lot of universe out there. I just want to see it all. I also imagine, you know, uploading. I think we'll get there. We just mapped the connectome of a Drosophila. Did you see that work? Yeah, yeah, it's amazing. And I had on stage at my abundance summit last year a gentleman, Michael Andreg, who is working on mapping a mouse and he wants to. He believes the technology now exists to map a human brain fully and upload it. The problem is it's destructive in process.
- [123:10]
B
Yeah, that's a slight downside.
- [123:14]
A
I'm going to have my AI up on the cloud over the speakers that will say, hey, Peter, you've successfully uploaded. You can kill yourselves now.
- [123:21]
B
It's like, yeah, there's a good Black Mirror episode on that.
- [123:25]
A
You know, listen, I'm gonna hit this for a second. I am pissed off at Black Mirror. I'm pissed off at Hollywood. Because we humans need a positive vision of the future to aim for. You know, we need a story that is, that is compelling and abundant and hopefully. And we don't have many of those. I mean, Star Trek was the one that really lit me on fire. We need more of those.
- [123:55]
B
Yeah, I couldn't agree more. And especially when it comes to longevity, it's usually, oh, something's gone horribly wrong.
- [124:01]
A
Yes. Yeah, exactly. Aronbank says maybe ask about longevity's economic impact. Keep it insightful. So I want to drill down more into the Harvard London School of Business Oxford paper because I want to understand how we get to tens of trillions of dollars from one year of additional healthy life. Because that's what it's saying. I mean, the global economy is $110 trillion. Was this for the US or was this for the globe? Do you remember?
- [124:39]
B
It was just us for one year extra. It's the value to the economy. And the value is the key word. The value is how much are people willing to pay? It's called the willingness to pay. Wtp. And the way economists use this number is they say, what's it worth to you to have an extra year of life. And the reason that the number balloons out astronomically is that there's a positive feedback, is that for every extra year that somebody lives, that it turns out they want more of that and they're willing to pay for more of that. Yeah. And that's one of the main reasons. And then of course, you can take away a lot of the healthcare issues. The longer somebody lives, the less burdened they are on the economy. And that also factors in. But healthcare is expensive. As somebody who's got dementia or als like my mother in law, this is super expensive. That's just one person costing tens of thousands a day to be looked after. If she was still healthy at 76, she'd be still earning, she'd be looking
- [125:44]
A
after, she'd be spending. Yeah. So this is what Gemini says. Research published in nature aging in 2021. You were an author on this paper, right?
- [125:53]
B
Yeah.
- [125:54]
A
By a team including Harvard and Oxford economists, showed that a slowdown in aging, that increased life expectancy by one year is worth an estimated $38 trillion to the global economy. So again, I find those numbers crazy. I wish I'd been able to feed that information to Elon at the beginning of his like, spend the government money solving aging and then I don't have to worry about any of this other stuff. Yeah, that would have been much better. Cassinova says what are the most effective over the counter modalities available today for under $1,000. So we talked about some of those supplements. I don't think any of them are expensive. Exercise, you know, is probably, I would think exercise, like the most important modality. How do you feel about that?
- [126:48]
B
I think yes, what you eat and exercise, those are the two big ones. Relatively easy. It's a little bit more technical to get your supplements. Right. Because it's tailored to you for cardiovascular disease. There's something that I've been taking for a couple of years now and that actually has been shown in studies to reverse cardiovascular disease.
- [127:10]
A
Removes plaque. What is it?
- [127:11]
B
It's called nattokinase.
- [127:13]
A
Oh, yeah. I take nattokinase as well. Great. Yeah.
- [127:15]
B
So maybe I take it for, you
- [127:17]
A
know, post Covid on airplane flights, just reducing clotting potentially.
- [127:21]
B
Oh. So that's the short term. But the long term benefit was there was a study with I think 10, 86 people, a Chinese study, but it was very well powered and they showed that up to 95% of plaque got removed in one year.
- [127:35]
A
Wow.
- [127:36]
B
Just by taking. But you need at least 12 units a day. They're called FU units, but not FU, but fibrolytic units. So I've been doing that, and it's been so far, great. I measure my carotid with ultrasound, and there's no. No plaque buildup there at all. So it's hard to reduce that. But I do take it as prevention.
- [128:00]
A
Let me see where I am on nattokinase.
- [128:02]
B
Nattokinase is an enzyme that digests fibrin, which is part.
- [128:05]
A
I'm on 100 milligrams of your block. I'm on 100 milligams of Nattokaine. So I don't know how many units that translates to.
- [128:12]
B
Yeah, I would say if you don't want to take a lot of pills, at least 6,000 units would be a good start. And then work up from there. But, of course, do this with the knowledge of your physician. You don't want to.
- [128:21]
A
I have an army of doctors I hire. I have 30 of them that are working for me at Fountain Lifestyle.
- [128:27]
B
That's true, but not everyone can do that. But still, just in general, just as a warning, if you do change your lifestyle and supplements, just make sure your doctor knows for sure.
- [128:36]
A
One of the things I really so desperately want is. And there was a question about what people should build. I want an AI model that will take in my genetics, take in my recent blood work, take in my goals. Like, I want higher cognitive clarity. I want more muscle. I want more longevity. Whatever your goals are, you prioritize them and then how many pills a day you're willing to take. And it should spit out a prioritized list, because right now, you go to one doctor, you'll get one set. You listen to you or me, you'll get another set. You listen to another person, another set. There is an optimal. There truly is.
- [129:13]
B
And so it wouldn't be that hard
- [129:15]
A
actually, to make it. No, it wouldn't be. The data's out there.
- [129:17]
B
We're working on that. But you go to doctors, and most doctors would say, what's nattokinase? They can't keep up with the literature. It's just too much. But AI can.
- [129:25]
A
AI can. Let's talk about something that you and I might differ on. I'm curious. Sleep.
- [129:31]
B
I suck at it. How do you do?
- [129:35]
A
I got a 92 last night, which I was very happy about on my OURA ring.
- [129:39]
C
I got.
- [129:40]
A
I won't tell you what I got. I will tell you, because I got to look right now. Last night was awful. I mean, I'm usually very proud of my of my sleep last night, I got a 64. It's the lowest I've gotten in like a year. And I think it was. I've been so going 247 this week, getting ready for being gone for two weeks and whatever it was. But I made up for it today. Definitely.
- [130:08]
B
Good. Well, I try my best, but I love him traveling.
- [130:12]
A
You said to me once you think you can get away with less sleep.
- [130:15]
B
I have figured out how to do that.
- [130:17]
A
Okay. Pray tell.
- [130:18]
B
It's about the amount of deep sleep that you get.
- [130:21]
A
Sure.
- [130:21]
B
And so I've got a.
- [130:22]
A
Which is the most important thing, a
- [130:24]
B
supplement that I take that puts me straight into deep sleep.
- [130:27]
A
Is it Adora drug? Is it.
- [130:29]
B
Serena makes it. Serena sells it.
- [130:31]
A
Actually, I'm happy you're not promoting her, but I can. What is it?
- [130:36]
B
It's called Sweet Dreams and it's changed a lot of lives. It's a mixture of very low dose melatonin, five HTPs, L thionine. It's magical.
- [130:47]
A
And where would I find it? What website?
- [130:48]
B
Even if she wasn't my partner, I would say that's what I take because I used to have insomnia really badly. And I'm off Ambien now.
- [130:55]
A
Oh, yeah, Ambien's just terrible.
- [130:56]
B
You just get it on her website, serenaloves.com.
- [130:59]
A
okay, fantastic.
- [131:00]
B
Oh, thanks, Peter.
- [131:01]
A
Yeah.
- [131:01]
B
No, again, I'm not here to promote it.
- [131:03]
A
No, I get it. But, you know, we share what we know. That works for us, and that's all we can do. Yeah.
- [131:11]
B
Another disclaimer. Just want to make sure everyone knows that my thoughts, my opinions, and even what I just said have nothing to do with Harvard Medical School. They're just my employer.
- [131:21]
A
And they're not medical advice.
- [131:22]
B
No.
- [131:23]
A
Okay. Sam Rankenma asks, what are the top 10 practical longevity tips? Top three for each organ. And which five longevity gadgets do you recommend? So let's go with the last part.
- [131:42]
B
We can go for gadgets.
- [131:43]
A
Gadgets, yeah. What are you using for gadgets?
- [131:45]
B
In our home, we have a red light bed. It's a big one.
- [131:48]
A
You have the Thor, the lie down one. I have panels right now that I use a panel from.
- [131:52]
B
I think it is. But yeah, it's a big thing with a lid that looks like a tanning bed, but it's not.
- [131:58]
A
Yeah, I love that. So I. I do red light many mornings as I possibly can. Yeah.
- [132:04]
B
The other thing I've been doing is I have a red light portable and I put it outside the shower, shining in. And so as I'm in the shower. I'm getting red light therapy too. And it's also a steam shower, which is nice. So that's one red light. I use that on my head as well.
- [132:18]
A
Yeah, I have a head red eye cap for hair growth stimulation. It's doing okay.
- [132:22]
B
It's working. I still can't believe you're 65. Sorry, I didn't mean to age me.
- [132:28]
A
No, that's okay. It's fine. You know, I've gotten to a point where I'm stating my age with pride versus hiding it because I am 64 and that's it. And I'm just like, for me, that is a call to action to remain at highest health status for as long as possible because we have incredible tech coming our way and I want to intercept that longevity escape velocity.
- [132:54]
B
Well, you're also a role model. And, you know, I feel like, I
- [132:59]
A
feel like I'm 28 or 29. That's my internal age. That's my internal number for myself.
- [133:04]
B
Yeah, I would say physically you look like you'd be in 30s, 40s, and, and you move just like you were in your 30s, 40s, I bet.
- [133:11]
A
Yeah.
- [133:12]
B
And by the way, my father is stronger, fitter, and more flexible than I am with better balance, and he's at 86, so it's very doable.
- [133:18]
A
I, I, you know, on my birthday a few weeks ago, and I pumped out a hundred push ups in a row, which was when I was in my 20s, the most I could do was 40 and I got to 50, and I've increased it from there. And I'm not saying that to brag. I'm just saying I use that as a measure for how I'm doing. In fact, in my longevity guidebook, I put my measurements that I've been measuring over the last few years in terms of squats and pushups and all of the plank pose and such. And it's important for you to measure yourself. Of course. You get a lot of data from your, your DEXA scans and your MRIs and so forth. The data, the data does matter. Obviously, you have an aura ring on too.
- [134:00]
B
I have a ring and I don't say what type it is.
- [134:02]
A
Okay, fair enough. Do you use. I don't have my, my CGM on. Do you use a cgm? I do, yeah.
- [134:10]
B
Yeah. Not every week, but, you know, when I, when I feel like it's probably five times a year or something and different brands are better than others. So you want to try what and research what works. But monitoring your glucose A lot of doctors, maybe not a lot of doctors, but I've seen some doctors say it's. It's irresponsible for people to have access to that data. For doctors. Yeah. You'll look online. There are some doctors who are dead against CGMs, unless you've got diabetes, and even then, which I'm dead against. First of all, who are you to say that I can't know about my own body. Right. And that I'm not educated enough to understand this? I would say a lot of the people out there are just as educated about glucose than their own doctors. So I'm definitely in the camp of we have a right to know our own genetics, our own epigenetics, our own glucose levels, and information is power. As long as you're telling your doctor what you're doing and talking to them about it, you got doctor supervision, it's fine. When I talk to my doctors, they say, can we see the data? We'd love to see it.
- [135:12]
A
One thing that is, I'm curious about your thought here. I hate the notion that the government prohibits me from participating actively in experimental treatments. If I'm at the end of life and my option is death in some number of months, why do I have to leave the country to go and try an experimental treatment? Why? If I'm of sound mind or if my family agrees, you know, right to. What is it called? Right to test, right to use, right to try. Right to try is getting going. But.
- [135:55]
B
And it's done under doctor supervision. You don't just. I mean, you're a doctor, but most people don't just say, I want to try this. Give it to me. It's done under doctor's supervision. So your physician makes the decision with you. So just the idea that, oh, it might be uneducated decision is not true. Same with euthanasia. You know, you have to go overseas now if you want to do that and if you're in agony every day, I mean, who are we to say that you shouldn't do what you want with your life?
- [136:22]
A
All right. Entropy asks a question I'm curious about. How long do you want to live? So there's interesting. When I'm on stage, I'll ask people in the room here, how long do you think you're going to live? You have a number in your brain, and where do you get that number from? And why do you believe it? And I find it fascinating that this mindset that people have, this number can make has implications. Right? Your mind is a very powerful Force on how long you'll live.
- [137:02]
B
So you're asking me those questions?
- [137:04]
A
I'm asking you, how long do you want to live and why? And why? Is the important part right? If you're willing.
- [137:12]
B
No, it's fine. I think it's a better question to ask, when do you want to die? And as long as I'm healthy and I have friends, I find that there will never be a day when I want to die. And I think that's true for just about everybody. You know, if you're sick, frail, lonely, depressed, that's when those thoughts come in. But I don't know anybody. And I've talked to thousands and thousands of people in big crowds like you. If you're healthy and have friends and family, do you want to die tomorrow? No one ever says, yeah, take me out. But when do I want to die? Never. I don't like the idea of being dead. Yeah, I think it's pretty boring, but it doesn't mean I believe I'm going to live forever. But I also don't think that if I'm staying healthy and active and having fun, why would I want to die? Why would anybody want to die?
- [138:04]
A
David, I truly love what you do. I consider you a dear friend and I'm grateful for you in my life. Let me recap a couple of things for listeners at home. David's new book, Lifespan Survival, is coming out in 2026. A number of you asked, when is his podcast coming back? Well, David's podcast is coming back. It's coming back this fall. What's it called?
- [138:30]
B
Lifespan with David Sinclair.
- [138:32]
A
Awesome. And I asked earlier your producer, and if you want to get on his list to get access to it when it comes out, go to davidacinclair.com what's the a stand for, by the way?
- [138:46]
B
Andrew.
- [138:46]
A
Andrew.
- [138:46]
B
That's my dad. Yeah.
- [138:47]
A
All right, go to David A. Sinclair. Mine is Peter H.D. amandis and Harry is my dad's name, too. I sort of honor him with that. So, David A Sirclair.com and you'll see a subscribe button there. Please do. I will. A couple of other things. Please join me in supporting David's research and his extraordinary team at his lab. In the show notes, you'll see a link to be able to donate at a 50k to thousand k. A thousand k. 50k to a thousand dollar level through Harvard Medical School. It's tax deductible. We'll put up once again here the QR code for the Coinbase wallet, where those of you can donate either Stablecoin, Ethereum or Bitcoin. I hope you'll join me. And I would love to get like a massive surprise from somebody who comes in and says, you know, listen, we're going to match your $2 million budget. Here's some bitcoin. Yeah.
- [139:50]
B
So my Lab runs on 3 million a year.
- [139:52]
A
3 million a year. Okay. So $3 million budget.
- [139:54]
B
If someone does that, then I'll give them my entire protocol, Give them everything.
- [139:58]
A
I mean, what's it worth in success? This is a micro investment for the impact on humanity.
- [140:04]
B
Yeah. And there'll be spin outs too.
- [140:06]
A
Yeah.
- [140:06]
B
And oh, by the way, you were there when at Steve Aoki's thing. So we were at an auction and
- [140:13]
A
we were the auctions.
- [140:14]
B
We were. I forget what you offered, but for mine it was a tour of my lab and that went for 100k. So all the friends are welcome to have that as a bonus to come by my lab and see what we're up to.
- [140:26]
A
And the third approach is joining David and myself as 50k level donors for Friends of Sinclair Lab. Just send an email to fosldiamandis.com and then we'll connect you back to a site where you can tell us about yourself. And if you're serious about joining Francis Claire Lab, you'll see David and I once a quarter and we'll talk about what's the latest and greatest what's going on in your lab, what the investment opportunities are, what the breakthroughs are. When we'll see it, it'll be super secret direct access.
- [141:04]
B
Yeah. And we'll do at least one dinner, maybe more.
- [141:07]
A
Yeah. So David, where do we find you on Twitter?
- [141:11]
B
That is David A. Sinclair. And then on Instagram It's David Sinclair, PhD.
- [141:16]
A
Okay, fantastic, buddy. Listen, this was fun. I enjoyed this. I really, really did.
- [141:21]
B
It was really great to catch up again.
- [141:23]
A
I'm gonna see you in in Boston at the end of September. And by the way, if you want more information to join me for my five day, five star longevity platinum trip, it's capped at 60 people. We spend five days together with the most extraordinary scientists in the world, like David, like George Church, like Dean Kamen. Go deep for those days. You can go to abundance360.com longevity and learn more information about it. Excited to spend the weekend with you and then in March at the Abundance Summit again. It's been a few years since you were there and so much progress in this age of AI. It's awesome.
- [142:08]
B
It is, yeah. And every year it just gets better and better. And I also want to speak on behalf of everyone listening. I think we all feel the same way about you. You're a unique individual on the planet.
- [142:17]
A
Thank you.
- [142:18]
B
And thank you God. You exist because, yeah, you make things happen that otherwise would never be in history. And you've already shown that you've done that. So maybe with longevity, that'll be your legacy too.
- [142:28]
A
Yeah, I hope so. I look forward to partnering with you on that.
- [142:30]
B
Thank you, my friend.
- [142:31]
A
All right, buddy, be well.
- [142:32]
B
You too.
- [142:33]
C
If you could have had a 10 year head start on the dot com boom back in the 2000s, would you have taken it? Every week I track the major tech meta trends. These are massive game changing shifts that will play out over the decade ahead. From humanoid robotics to AGI, quantum computing, energy breakthroughs and longevity. I cut through the noise and deliver only what matters to our lives and our careers. I send out a Metatrend newsletter twice a week as a quick two minute read over email. It's entirely free. These insights are Read by founders, CEOs and investors behind some of the world's most disruptive companies.
- [143:09]
B
Why?
- [143:10]
C
Because acting early is everything. This is for you. If you want to see the future before it arrives and profit from it. Sign up@dmagnus.com metatrends and be ahead of the next tech bubble. That's dmagnus.com metatrendS.