哈佛教授 David Sinclair 揭示逆龄科学：如何让人看起来、感觉上更年轻

Have we reached a state of age-reversal technology that truly works?

We can cure diseases and injuries that have never been cured before. Imagine that in 10 years, you just take a pill for 4 weeks and you get younger.

Why do we age?

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 we just take a supplement or do some exercise to slow down aging. Now we're talking about the ability to truly reset the body—to reset all of the cells in the body to be young again. A teenager today will live into the 22nd century.

Now, that's a moonshot, ladies and gentlemen. Today's episode is delivering 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, and author of Lifespan, one of my favorite books. We'll talk about what's next from David's authorship, as well as his work as one of the leading thinkers in the realms of age reversal, epigenetics, and longevity science. We'll discuss what's here in the near term, how you can support it, how you can be involved in it, and 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. 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 get a whole download on the state of age reversal.

David, welcome, buddy.

Hey, Peter. It's good to be back.

It's good to have you back. How are you doing?

I'm doing well. I'm having a blast. I am more focused on my health than I ever have been.

You're looking really good. I was commenting on your biceps right now.

That's why I'm wearing a jacket here, because I don't have them.

I think, and we can talk about this, that in fact muscle mass and exercise still remain one of the primary pro-longevity drugs out there.

Absolutely.

We'll get into the details of what the best state of the art is and what's coming, because eating right, sleep, diet—all of these things can only get you so far. Then the question is, can we turn back the clock of time?

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. I'm not asking for promises. I'm asking for your best guess.

I'm not shy to talk about what I think is coming. As I wrote in my book, Lifespan, I predicted a future where we would have wearables, video conferences with our doctors, and the ability to order medicines online. I thought that was going to take 15 years, and it happened in 3. Sometimes I actually underestimate what we're looking at.

Here's what I see. I sit in the front row of the future, at the bleeding edge, I would say. I want to share my thoughts with the listeners. What I'm seeing in my lab, and in labs that are competing with us or collaborating with us, is something quite remarkable. The pace of change is making my head spin. I'm an optimist, but I just can't comprehend right now how fast things are going.

Let's go back a few years, and then we'll project into the future. Going back a few years, in 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 actually proved, and published in 2020, that you can reverse most aspects of aging by reprogramming cells, which we'll talk about. That changes everything.

If my information theory of aging is correct—which is the idea that you don't just lose information as you get older, like software corruption, but you can actually reset that—then it changes everything. We've gone from the idea that we just take a supplement or 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—to reset all of the cells in the body to be young again. And not just slightly, but by 50%, 75%, 80%, or 90%.

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 it's like, “What are you talking about? How do you reverse aging?”

What we do is use a set of genes that are normally only active in embryos. We turn them on in adult tissues in mice and monkeys, and we can cure diseases and injuries that have never been cured before—even blindness. We published that in 2020.

Since then, what are we now? We're in the middle of 2025. What I see is that, with the advances of AI—and we're doing a lot of AI in my lab—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. We're virtually screening trillions of molecules, and we're coming up with alternatives to the gene therapy that we published in 2020.

So you ask me, first of all, how much might it cost?

Well, right now, the technology is going into humans next year, in January, hopefully.

This is with Life Biosciences, correct?

Life Biosciences has proven that this reversal of aging in the optic nerve works to cure a variety of ailments in the eye. We chose the eye mainly for business reasons. We're going to treat glaucoma and a stroke in the eye called NAION.

This is a gene therapy. Gene therapies typically cost $300,000 to $400,000 per treatment, or they could cost as much as $2 million for a gene therapy, for a rare disease.

Right. For a rare disease.

Yeah, it's a lot. The reason is that there are a lot of hurdles to get through to reach the market, and producing this stuff is expensive. It's costing us more than $10 million just to make the first batch to go into humans.

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, pennies on the dollar every time someone takes a pill. What we've been doing for the last 5 years is trying to bring that cost down. Using AI, we're now at a point where we've got molecules that would only cost $100 or less to make for a month's course.

For a month's course? Like $3 a day.

Yeah. We're seeing that those work really well in mouse studies to reset an old animal's physiology within just 4 weeks. This holiday season, we did a Hail Mary experiment. We gave the mice this cocktail orally. We weren't expecting anything, but we thought, “Why don't we just measure how fit and healthy they are?”

All the mice that were on the treatment, and not the controls, ended up behaving and being physiologically younger. When we tested their biological age—which you can do with real, quantitative tests—they were younger as well. That's just giving them this stuff Monday, Wednesday, and Friday for 4 weeks.

Wow.

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.

So, 2035: you're saying we will have an age-reversal therapeutic that works?

Well, that's where it's headed. If you extrapolate where we are, next year, if all goes well, we'll have shown that you can reverse aging in a human tissue safely—curing blindness. We've done this in primates already.

You've done this in primates already?

Yeah, it works in green monkeys amazingly well. Some of the data is just stunning. You can map whether you reverse the age of the optic nerve in these animals, and it looks like 95% of the age goes backward.

Wow.

It's a youthful state of the optic nerve, and it's semi-permanent. This isn't something where you have to keep the genes on. You can switch them off again, which we do. We have an on-off system that we've patented, and it works really well. You do it for about 6 to 8 weeks, then turn it off, and the eyes stay young. They're going to age again, but then you just turn it back on for a few weeks.

That's the plan. I like that plan. What type of age reversal do you see? 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?

Yeah, we can control it. The longer you leave it on, the younger the tissue gets.

It seems very safe. There are no untoward effects of this treatment so far in the monkeys, either.

Beautiful.

But here’s what I see: Within the next 10 years, we’ll have the ability to use gene therapy throughout the body. We’re already working at Life Biosciences on getting away from viral delivery, which is the current approach.

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’re basically using a virus to deliver—typically what’s called an AAV, or adeno-associated virus—a set of genes into targeted cells. But that’s expensive, and sometimes it may go off-target. You don’t get all the cells you want.

Well, that’s the big problem with AAV: Tissue distribution is tough. 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, for those who are questioning, “What about the vaccines?” maybe we won’t get into that. I know vaccines got a bad name in the last few years. This is obviously not a vaccine. You’re delivering genetic material inside these little particles, and there are some really good technologies.

There’s a company that I’m advising called Ligandal. They use AI to find proteins that you could put on the outside of these little particles and direct them anywhere you want them to go.

So, getting back to what you asked me about what the future looks like, I think we can either go into the doctor and have an injection of that genetic material, and we become transgenic humans. We can turn on these 3 youthful Yamanaka genes, as they’re called, every time we want to get rejuvenated or have an injury we need to heal quickly.

How do you do that? We’ve engineered it so you can just take an antibiotic for a few weeks. It’s doxycycline. You take a course—it’s pretty safe, actually, very safe—and you turn it on.

That’s what I can see happening with technology that’s already going into humans. But if we’re successful in what we’re doing in my lab, there are AI-generated molecules that are mimicking that.

The reason for having a molecule rather than gene therapy is that not only are they cheap, but you can just swallow them and they distribute evenly throughout the body, typically. Imagine that, in 10 years, you just take a pill for 4 weeks and you get younger. That’s what we’re headed toward, 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 toward in my lab.

I love it. I love it. I can’t wait, and I volunteer to come first.

The concept of longevity escape velocity: Ray Kurzweil, who’s been a dear friend and a mentor, predicts that we’ll reach longevity escape velocity by the end of 2030.

Longevity escape velocity, for those who haven’t heard the term—and hopefully, if they’re listening to this podcast, they’ve heard it—is 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. At that point, it basically departs, and you’re going as long as you want.

I’ve had the conversation with a 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.

Dario Amodei, the CEO of Anthropic, said at Davos that he expects we could see a doubling of the human lifespan in 10 years’ time. Those are good people to have in the same camp you’re in.

What do you think about longevity escape velocity? Is it a concept worth thinking about? When do you think we might hit that?

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 it’s feasible now.

There was a time in my career—5 years ago, maybe 10—when I thought this was so far into the future that it wasn’t worth talking about. It’s all speculation.

But now that the information theory of aging and the reset seem true, and we’re entering the clinic with these age-reversal technologies that can be used multiple times—not just once, but maybe 20 times or 100 times—I think it’s possible that, within our lifetime, we’ll see the ability to reset yourself.

I don’t think we’re going to live forever, because there’s always noise, and information is hard to preserve indefinitely. But I do believe that we could double the human lifespan.

I’m on record, and I’ve taken some flak 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 a teenager today will live into the 22nd century. We have to remember that. It’s not about today’s two 14-year-old boys; I keep telling them that.

Yeah.

Just think about what’s happened in the last 10 years. We can’t imagine what’s going to happen during their lifetimes. That’s why I think it’s quite possible that they’ll be able to live to 150 or more.

But for us, the question is: Were we born one generation too early? Those of us in our 50s—I’m 56. The answer is, actually, since I was 18, I decided, “Damn it, I don’t want to be part of the last generation to live a normal human lifespan.” That’s not right. I know it’s coming. It’s just a question of whether we can do it in time for all of us.

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 100s, because certainly by the time you and I are 90 or 100, the technology is going to be there. I mean, at this exponential pace, with what’s going on with AI—

I was with Eric Schmidt recently for our last podcast, and he said, “We will reach digital superintelligence within the decade.” This is not just AGI, whatever AGI means; this is billions of times more intelligent than a human.

Of course, the work going on right now to model a cell in silicon will get there. Then we’ll have a cell with David Sinclair’s genome or my genome, and we’ll know exactly which molecules activate that or don’t.

I want to go to a basic question, which I think is important for everybody to understand, and I’d like to understand how you express the answer. Why do we age in the first place?

We have the Greenland shark and the bowhead whale, which lives to 200 years old. The Greenland shark lives to 500 years old and has pups at 200 years old. We make it to 100 on a relatively regular basis. But why do we age? And why were there no factors selecting for us to live longer than that?

The first answer to the second question is that there was no need. Evolution doesn’t build things that there’s no need for. On the savannah, we were likely to die from war, 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 has been gathering for 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. It’s all about information and entropy.

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. Those 2 elements of information get lost over time due to noise.

We’ve identified some of the causes of that noise. DNA breaks in chromosomes are part of that noise. Stress on a cell is another. If you crush a nerve cell, it will accelerate its aging. We showed that in the 2020 Nature paper.

I think of the body not as a lump of meat, but like a computer. The software gets corrupted over time. The great news is that we found there’s a backup copy of that software that can be reset.

Amazing. You haven’t done any podcasts in the last few years, so I’m super happy to have you here. I really want to go into what you’ve learned.

You published the information theory of aging as part of your book Lifespan. TIME did an amazing piece on you and the information theory of aging. I was so happy that Marc Benioff’s TIME did that. I was like, “Yes, it’s good to get the exposure for this.”

Let’s take it a step further in explaining what the information theory of aging means, and have you had any new proof points supporting that in the lab?

Yeah, we’ve come a long way since 2020. Just to set things up, you get 3.2 billion letters from your mom and 3.2 billion letters from your dad. That’s your genome. It doesn’t change over the course of your life.

I like to ask people, “Why do you look different at 20 and 100? Why don’t you look the same?” That genome codes for—what’s the current estimate?—22,000 genes.

Thereabouts. So, epigenetics is effectively which genes are on and which genes are off. As you age, if I have this right, the wrong genes turn on, and the wrong genes might turn off, and that’s causing some of this aging effect.

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. Book 2, hopefully, will come out next year. It was a risk putting the 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 stands up.

What have we learned since?

We're trying to figure out how it's possible to reset a cell and get back the original structures of the epigenome. If we were to dive into the cell—let's say we're going to pierce the membrane and go inside a cell—then you swim down and see the nucleus. There's another membrane, and there are little pores in the membrane that you can swim through. Now we can see the chromosomes, and that's really the epigenome.

If we unwrap those chromosomes, what we would see is the 6 feet of DNA that's in every cell. The DNA is wrapped up in proteins, and that wrapping is important for 2 reasons. One is that's how you fit 6 feet into a microscopic cell. But also, whether it's wrapped tightly or not determines whether a gene is on or off.

If it's tightly bundled, we call that silent chromatin, or heterochromatin. 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 and loops of DNA, and when it's bundled tightly, it can't be read.

It can't be transcribed because it's hidden.

Exactly. It's tightly bundled. One of the big clues that this was relevant to aging came when I was in the lab of Lenny Guarente as a 25-year-old postdoc. As a team, we uncovered these silent information regulator genes called the sirtuins. Their job is to bundle up DNA, and at the time we were 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. That's why information has been key to my research ever since.

Getting back to what happens during aging, these bundles and loops change over time, in part because the cell loses the ability to bundle them and these loops open up. But also, 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.

I could take one of your cells and clone you, and even though your cells are old, we can start new life with those.

I love that. I know one set of experiments took cells from 23 sequentially cloned mice. 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. 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.

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, so you can start life again. But the good news is we figured out a way to safely reset that without having to clone yourself.

Mhm.

Think of it as resetting the system, like going through conception without having to be reborn.

Amazing. So, the control of the epigenome—I know, for example, skin has a multitude of different proteins, including collagen molecules. As you grow older, one of the reasons your skin ages is that the genes for those collagen molecules get silenced. One could imagine unsilencing them.

We do that in the lab all the time. We have a skin project, so you don't have to imagine it. I'll show you.

Okay. I can't wait for the product to come out.

We think skin is a good model. It also may help some people with wound healing and how they look. We actually grow bundles of human skin and hair in the lab. For those of you who are queasy, you may not want to hear this, but we open up that organoid of human tissue that we grow.

These are engineered to be able to drive aging forwards and backwards, so we can study that. We put them in the backs of mice, and it's pretty funny. You can see them, and the mice give them the blood supply and keep them alive.

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 then test if we can reverse it. So far, it looks good.

If you can do that, I think you have another huge winner. I'll never forget at the Abundance Summit, where I've had you speak a couple of times, and you're going to be back in 2026. Thank you for that.

Sure.

Eric Schmidt will be our opener, and you'll be our closer that year. That'll be fun. I remember I had a biotech longevity scientist on stage, and he was talking about his technology—how it could cure cancer, increase the health of particular organs, and do this entire list of things. Then he says, “And it can grow hair,” and the crowd erupts in applause.

Yeah, I remember that.

People do care about skin and hair.

But we're also learning the fundamentals about what makes cells old and how we reverse that, and skin is just one example.

The original data set that helps the cell remember its original state—have you found out where that lives?

The answer is probably. I'm going to wait to reveal that in detail, but I have some very good students working on it 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.

Basically, what we need for this to be real is a memory of youth in every old cell. What is that memory? It's probably got to be something physical. It could be a chemical modification of the DNA, chemical modifications of the proteins, like methylation. It could be something else. It 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.

I figure people would have seen this by now.

People have bumped into this and ignored it because they didn't think it was important.

I read through all of your tweets as we got ready for this, and I love one of them: “Your cells remember how to be young. We just need to remind them.”

Exactly. My students are great.

They are. I came to your lab a month ago, and I met many of them. They are brilliant.

Yeah, they're like my children. Actually, on some days, I love them more than my own children.

We'll talk about the insanity of funding cuts in a little bit, and the importance of the work that you're doing. Is there anything else you want to add on the information theory? Do you have experiments planned that will just nail this down? When does a theory become accepted gospel?

I think it happens at one funeral at a time. I've been very pleasantly surprised that the theory, which is called information theory of aging, or iT for short, is being well accepted by the community. There's more and more evidence every few weeks about this.

I think what will really convince people is when we disrupt the observer, as we call it. This backup copy is based on Claude Shannon. I'm a big fan of his, and you know that.

For those of you who don't know about Claude Shannon, he was a scientist at MIT and Bell Labs who figured out the information theory of communication. The reason we have the internet is because of him. I poached the same mathematics and concepts and used them for aging.

The information theory of aging is all about the preservation of information and having a backup copy, which at the time he called the observer. We still talk in my lab about finding the observer. The observer keeps a backup copy of the original signal, and if you lose it by the time it gets to the receiver, you can go back and retrieve what's missing from the observer.

What we think is that the observer has a physical state, as I mentioned. It's got information there. We think we found that information; it's novel biology. If we show that breaking that system prevents age reversal from happening, then I think the community will believe us.

Love it. Love it. We just launched, about 18 months ago, something called the $101 million Healthspan XPRIZE.

Thank you.

Absolutely. I think you're in the process of registering for that competition.

We are registered.

Oh, you're registered. Fantastic. We've had about 625 teams from around the world. For those who haven't heard me speak about it before, this is one of our largest XPRIZEs. We raised $157 million. GSK is a big sponsor of it as well.

Our primary 2 sponsors are Chip Wilson, the founder of lululemon, who has a form of muscular dystrophy called FSHD, and he put in $36 million. Then there's a group out of Saudi Arabia called Hevolution—think health and evolution—and they put in $40 million. I'm a multimillion-dollar donor. We have a lot of incredible people who are supporting this.

The goal is, can we get the smartest people in the world, including you, working on reversing the loss of cognition, immune function, and muscle? I'm amazed by the variety of different approaches, and I'm excited that your lab will be participating. We're seeing a huge range.

I mean, from cellular medicines to gene therapies. So I want to ask you, beyond your own work, about the state of the union for age reversal and longevity. Is it still an uphill battle in the scientific world and the funding world? It used to be a stigma if you said you were doing age-reversal work. It was like, “Oh, this person’s insane.” Has that gotten better?

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 you work on longevity isn’t a stigma. 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 medicine.

Yeah. The interesting thing is that a lot of the funding is coming from the crypto community. There’s a great alignment between people who believe in crypto’s long-term vision for capital, like Bitcoin, and longevity. We’ve seen Jeff Bezos and Yuri Milner back Altos. We’ve seen Brian Armstrong back NewLimit, and Sam Altman back Retro Biosciences. So it’s good to see some of these multibillionaires backing these things. I, for one, if I had that level of capital, would be backing all of them.

Well, one or more of these companies could dominate pharmaceuticals in the 21st century. I mean, it is a multitrillion-dollar marketplace.

Yeah. I’m on stages, and perhaps you are too, and I ask, “Okay, you’re 70 or 80 years old. This is a room of family offices and wealthy individuals, and you’re slowly degrading, as people do, in the last decades. 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, but like where you were in your 50s. How much of your wealth would you give for that?’”

If they’re honest, it would be the vast majority—80-plus percent. When I think about that, that is tens of trillions of dollars. I’m hopeful that we’ll see a lot more funding coming in, both philanthropically and investment-wise.

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. The years you have are worth everything to you—more than money.

Agreed. Agreed.

What else are you seeing out there that could be a viable age-reversal therapeutic? Are you seeing any particular approaches, without necessarily naming labs or anything?

Well, there are a few. I work on epigenetic reprogramming at Life Biosciences, and these companies you just mentioned are also chasing us. We started a little earlier than they did, but they’re trying to catch up. That’s a big area, and it’s why I’m hopeful that one or more of us is going to succeed. For me, that’s the most promising. That’s why I’m putting my own money into it as well.

What else is important?

Well, I think there are factors from the blood. We know that plasmapheresis—exchanging your plasma—has some benefits, and it’s looking better all the time.

Like therapeutic plasma exchange.

That’s right.

Yeah. I’ve done that 5 times now.

Right. 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, so stay tuned for that, because it’ll be easier than a machine for an hour.

But that sounds promising, right? There’s something in our blood that’s keeping us old, or something that comes in and makes us young.

There are some factors that companies are already working on, but I think there might be a few really good ones that you could take as a drip and rejuvenate.

There was a promise of GDF11 years ago. I mean, the problem is that a lot of these companies get funded with seed capital, but being a biology or medical company is expensive, and they run out of capital.

Yeah, it is. I think there’s something we haven’t found yet that’s going to be more rejuvenative. We’re screening these proteins in the blood and genes that do epigenetic reprogramming. You could imagine that there’s a peptide, perhaps, or a protein circulating in the blood, and when it circulates, it triggers these genes that give rejuvenation. So, we’re looking for that.

Stem cells have been a bit slow, but we’re starting to see a resurgence of stem-cell interest and approval. The FDA now approves certain types of stem-cell therapy.

Yeah. We’ve just seen states begin to become much more lenient. Florida is in the process of passing regulations to allow you to do stem-cell treatments in-state. I think Utah is already there, along with other places, which is great, because before this, you’d go to Panama, Costa Rica, or Antigua to do it. That’s fine, except you don’t have your medical team around you and you’re operating ex-U.S., right? So presumably Fountain Life is going to get into that.

Fountain Life has 2 centers right now, in Naples and Orlando, and we’re opening up Miami. Those will all hopefully have the most advanced stem-cell therapeutics available, as well as other cellular medicines, like NK-cell supplementation.

Yeah, which kill cancer cells. Natural killer cells, your innate immune system, kill cancers. We’re always developing cancers, and we depend on our immune system to find and kill them. The same NK cells also hunt down virally infected cells.

Well, we’re working on a new type of stem cell, a very rare type.

Okay. We should talk, because there’s a stem cell that actually turns into the tissue that it lands in. That’s different from current stem cells.

Oh, interesting. Okay. I think that area has promise too.

Senescent-cell-killing chemicals are somewhat promising. I saw Altos bought a company, or is merging with a company, that works on that.

Mm-hm. It’s been a little slow and a little disappointing with Unity Biotechnology.

Yeah, I was so surprised. Unity Biotechnology went public, and then its data came back and the stock crashed. It’s slowly eating its way back. It wasn’t a complete failure; they just didn’t reach the endpoint. So there’s a lot of variability.

That’s part of the issue. But I think they’ll keep pushing on and 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.

Can you use epigenetic reprogramming to move senescent cells back to normal, healthy cells?

We have a project in my lab on that, and so far it looks like, yes, we can do both: rejuvenate senescent cells so that they don’t cause havoc. They normally cause a lot of inflammation and even cancer. We can stop that with reprogramming, but in some cases we can even rejuvenate them so they grow again. Normally, they’re sitting there and don’t grow.

For folks, there’s something called the Hayflick limit, right? It’s about 50 cell replications, thereabouts—that a cell should replicate 50 times and then have the decency to die. If it doesn’t, it can become a cancer cell or a senescent cell, which is pumping out these inflammatory factors.

Yeah. So you can either kill them or cure them. 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 somebody might be asking—or you might be asking—if you reprogram a cancer cell, what happens?

Oh, yeah, fascinating. I have good news on that front. 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 cancer are killed by reprogramming, which is interesting if you think about it.

So, you have a cancer cell. It’s growing. You’ve discovered it at stage 3 or stage 4, and it’s spread through different parts of the body. You hit it with an epigenetic-reprogramming cocktail, and it has the decency to die.

Well, I think it freaks out and realizes—or wakes up from—its zombie-like state and says, “Oh my goodness, my chromosomes are messed up. I better kill myself.” One of the hallmarks of becoming a cancer cell is ignoring its DNA damage. They’re filled with DNA damage.

Yeah.

If you wake up a normal cell, it goes back and gets younger. But if you wake up a cancer cell, it looks like it realizes it should kill itself, and it does.

Amazing. That’s crazy amazing. All right, I want to dive into a couple of your companies that I’m tracking.

Life Biosciences and MetroBiotech are 2 very cool companies. Let’s talk about each of those. Should we start with Life Biosciences? This is the more recent one.

This was founded in 2017–2018. They’re the ones that have shown in monkeys that you can basically cure blindness and get vision back. The first studies will be in January, if all goes well. So you’ve gone originally from mice to monkeys, so nonhuman primates, and it worked as expected in both cases. It worked better than expected, actually.

So far, there’s no sign 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. Hopefully, by this time next year, we’ll know if it’s working because the studies go straight into patients.

And is it a single injection? What is it?

Good question. It’s a single injection. With macular degeneration, it’s very common to get 1 injection or more. You don’t feel it; it’s nothing bad. What this virus does—the AAV you mentioned—goes into the nerves at the back of the eye, and we just turn it on by giving the patient the antibiotic doxycycline.

That, by the way, is just the trigger that turns on that segment of DNA. We put in those 3 genes as 1 inside the virus. We normally have these genes; we’re not changing the genome. But by putting these 3 genes in the virus, we can control them better, and now they’re what’s called doxycycline-inducible.

We could have used any chemical; it doesn’t have to be doxycycline. But doxycycline is such a safe, easy way, and it’s been in research for decades, so we chose that. By this time next year, we should know if it can improve vision in people who have gone blind, either from a stroke in their eye or from glaucoma.

How big will your phase 1 be? You think it’s a small study, right? You start with 1, then 2, then 10.

We’re just raising money to go into our phase 2 study already.

Awesome. Are there any other elements of Life Biosciences besides that specific program?

Some of it is confidential, but I can say in general that the company has—let’s call it stage 1, not to confuse it with clinical trials. Stage 1 is proof of concept in the eye. Does it work? 2 shots on goal, 2 diseases.

Stage 2 for the company, which is already underway, is using AI to convert it into chemicals, so you have a pill instead, or an LNP, which is a lipid nanoparticle, so you don’t use viruses. That’s whole-body rejuvenation. They’re already doing that. Stage 3 would be going into multiple diseases and eventually whole-body rejuvenation.

All right. Let’s pause right there and focus in on this. I think one of the realizations is that for those who develop a disease when you’re older, you didn’t have the disease when you were younger. So if you’re able to actually induce some type of age reversal, does that cure the disease?

In mice, it’s working great. For instance, glaucoma is an age-related disease. You make the eye young again in the animal, and the disease goes away. The body can heal itself, and that’s really not been the approach of medicine as we know it.

Medicine, as you know—you’re a trained doctor—is, “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 have to grow new tails. It’s a similar process. We just turn on these embryonic genes, and now we get youth, and the body can heal itself.

So besides vision, what else have we tried?

In my lab, we’ve done Alzheimer’s disease—cured. Some muscle diseases—cured. ALS, pretty much cured. That’s important because in my partner’s family, we have ALS, so we’re rushing to fix that one.

We published with a collaborator that we could alleviate multiple sclerosis with this as well. So far, we have not seen a disease or an injury that could not be effectively treated with this therapy. That 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.

Finally, now we’re treating what’s really underlying most diseases, which is the universal aging process itself.

The challenge is that today’s medical system is built all around just treating the symptoms. It’s built around keeping you alive and treating what’s possible, but not curing you. It’s really quite insane.

With whole-body rejuvenation, again, by taking a set of pills, we don’t see 1 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, muscle, or hepatic tissue—it’s going to hit all tissues, all organs.

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 were collaborating with George. You know George; 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 to inject the virus not just into the eye, but into the vein of a mouse. If we’re right, the mice should live longer. Even though this was a Hail Mary experiment, not optimized, those old mice that they treated lived another 109% longer.

I have to ask you this question at this point. We talk about mice. Mice are the most common lab animals; everything is experimented on them. A typical lab mouse lives how long? 24 months? 36 months?

Yeah, 20 to 28 months.

28 months. Okay. Why aren’t we seeing mice that are living not 2 years but 10 years at this point? What’s going on there?

Because I think we were taking the wrong approach. What happened to the field, unfortunately, is that we were trying to slow aging. And, by the way, just for reference, in June of 1982, Richard Weindruch and Roy Walford at UCLA showed that life extension of 30% to 40% was possible through calorie restriction, getting a mouse to what is currently the record of 53 months.

You just have to starve the mouse, and you can almost double its lifespan, which I don’t think anybody here wants to do. Those guys showed early on that you can extend the lifespan through diet, but it’s not pleasant.

No, it’ll certainly make life feel longer.

Now we’re seeing combination drugs. There was one published last week showing that a combination of 2 anticancer drugs could extend the lifespan of mice by 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 10 times longer.

You think we’ll get there? I don’t care about the mouse living longer; I just want some additional evidence that we’ve moved the needle.

Yeah. 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, “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, 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 longer, maybe 5 years.

When might you run that experiment?

As soon as we have the money to do that.

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 7 sirtuin genes, or these proteins, and the battle between DNA repair and epigenetic drift.

If I understand from reading your book and speaking to you, what we have are these 7 sirtuins that are conserved across almost all life—even bacteria. They have 2 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?

Yeah, even bacteria. They have 2 functions in the cell.

And as we get older—and I’m pitching this back to you because this is how I explain it onstage—we’re accumulating some DNA damage. The sirtuins are going back and forth between these 2 functions. As we get older, our internal NAD levels drop by as much as 50%, right?

NAD is sort of the energy currency in the cell that powers these sirtuins. 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?

Mostly. Even without the decline in NAD, we have problems. We showed this in a mouse that we published in 2023 in the journal Cell: even if we distracted the sirtuins from their main role of silencing genes when a mouse was young, that was enough to make it age 50% faster.

And these were called the ICE mice: inducible changes to the epigenome mice. We created non-mutagenic cuts that distracted the sirtuins from where they were on the chromosomes. They went elsewhere and often didn’t come back to where they belonged, and that just for 3 weeks was enough to trigger the domino effect of aging in those animals. They didn’t just look old; they were old by every measure. Their tissues were old, their physiology was old, and their DNA methylation clocks were older. Then we also did a little experiment to reverse their tissues at the end, just for some fun.

Just for some fun. Your lab must be a blast to work in. I wish I could go back to my medical school days, 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. The entire explosion of the AI field, especially its application to the basic sciences—tell me, how are you using it? What’s it doing for you?

Well, it’s central to everything now. We barely run an experiment without consulting our AI agents. Let me tell you about 2 areas that I think would be interesting.

The first is visualization. We’ve developed algorithms 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, what age those cells are just by looking at them.

Fascinating. That’s important if we’re—as we are—screening for genes and molecules that control and reverse aging, measuring what matters.

Yeah. We have a curve that stretches from 20-year-old cells, or skin cells from 20-year-olds, to 93-year-olds. Within nanoseconds, the computer looks at the image and can say, “All right, those cells were 93 last week, and now they’re 20.”

We have chemicals that do that, so that gives you super-rapid screening of all kinds of chemicals.

So that’s using robotics and AI visualization. That’s 1 aspect.

Yeah. But what really blows me away is the other part. We believe we’ve found the 4 main levers to reverse aging. What I mean by that is that there are enzymes that control the epigenome. There are 4 main pathways, and you want to pull back the lever: inhibit 3 of those and push 1. That combination is the winning one.

We have chemicals that do that, but they’re cocktails. We’ve published some of these cocktails. They work on these 4 levers, but what we really want is just 1 simple, safe molecule, because it’s easier to develop as a medicine, that does those 4 things.

Now, if you’d said to even a pharmaceutical company with $1 billion, “Could you do that?”

They would have said, probably 5 years ago, “No way.”

Yeah, right.

Doing 1 of those lever pulls is hard enough. We’re talking decades and billions of dollars, optimizing and physically screening and making the molecules by hand as chemists. But now we can take all known molecules and virtually screen them in a couple of months against all 4 targets and come up with candidates.

When you say “take all known molecules,” are we talking about actually physically doing this in a Petri dish?

No. Goodness.

So what are you actually doing?

We virtually dock them into the enzymes, and the AI is precise enough to create an actual physical model. Demis and his team solved all of the structures, as you know, and that made this all possible. Now we can just do the number crunching.

So normally, this docking would be done by hand by a person and would take days to do, and now it’s just done like this?

And you can do billions—actually, trillions. There are libraries of virtual molecules, but there are also physical libraries. What’s happened is we’ve now got a set of 100 top candidates, some synthetic and some natural, and we can just order them like you would on Amazon, bring in the chemicals, and put them through our AI-assisted screening.

Crazy. Earlier, you said it was going to be a cocktail of 4 molecules that you’re trying now.

Yeah, we published 6, and we’re now down to 3.

Three.

And we believe we can get it down to 1. We’re testing them now, and they look good so far.

Amazing. I want to turn to a subject that’s a bit painful, recent, and very impactful about this longevity future, which is funding. It’s been a travesty—the massive cuts in science—and I know you’ve been hit hard by it. How hard have you been hit?

Well, I spend more time as a psychiatrist now than as a scientist. It’s tough. The poor kids in my lab who are innocent in this are really suffering.

What percentage of your lab is funded through government grants?

The majority is government-funded, and all of those grants were terminated. One hundred percent of those grants were terminated. They’re all gone.

Any explanation as to why?

Harvard is in this—the target of the federal government.

Oh, it’s not just the DOGE activities.

Harvard is being specifically singled out for “antisemitism,” but they’re taking it out on my poor students, who are like my own kids. It’s rough.

Well, they’re taking it out on the rest of us, too.

If the science gets delayed by a year, that just puts another percentage of the population at risk of dying. We may never know what medicines will never exist in our lifetime because of this, unfortunately, because Harvard Medical School is a crown jewel of research in the world.

And to stop all that research, I met 1 of my colleagues in the cafeteria last week. 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.”

Wow.

It’s done. He’s over. His career is ended. He’s done. So I’m not giving up. I’m going to fight.

Yeah, it’s too important to give up, as you should, 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.

There was a study at Harvard, London Business School, and Oxford on that. What was the financial implication? What did the study say?

Yeah. I teamed up with a couple of great economists, and they calculated that in the US, extending healthy lifespan by just 1 year—by keeping people out of nursing homes, giving them back to the community, and making them productive—was a value to the US economy of $86 trillion. That’s just 1 year.

That’s doable. Thirty-six or 86? Did I say 36?

No, no, you said 86. Is it? I think it’s 86.

It is $86 million. $86 billion. No, $86 trillion. Wait, we’ll fact-check that.

And then it was $367 trillion for 10 years.

Yeah. Yeah. It’s a lot. These numbers are staggering. This is like the defense budget.

I mean, this is people staying active and generating in the economy and not having to pay out on health care costs. That’s what it is. And then people spend money, right? They’re traveling and buying things.

I use my father as a role model. He’s on our program, or whatever he’s doing, and he’s doing well. The update on him is that 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. He acts, moves, travels, thinks, and enjoys his life like we do. He’s not slowing down at all. He still drives at night without glasses, and he has to take a test because he’s old, but he passes with flying colors.

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.

I tell people, if you’re 80 but you feel like you’re 50, and you’ve got all of your relationships, are you going to want to retire, or are you going to want to go for the next thing? The reason people retire is that they’re in pain, they’re out of energy, or they’re forced to by regulation. Or you don’t like your job, but there are skill sabbaticals, and we live in a world where you can reinvent yourself pretty quickly.

I look forward to people like my dad, who started a new career in his 80s. He was supervising clinical trials and giving back to the community. He’s living with 1 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.

It’s better that way, because imagine life the other way around. And you don’t actually have to imagine it. Go to Japan, where people our age are taking care of not just their parents, but sometimes their grandparents and their kids, and sometimes their grandkids. That’s a huge burden on a generation: taking care of both the people who are sick and older than them and the young people who either don’t have jobs or need help in other ways.

David, how much funding did your lab lose in total?

It was millions, and we’re just at the beginning of some of these grants. 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 about the cruelty of these cuts to her and the lab. She was working on ALS in a race to try and help Serena’s mom.

We were making good progress. We showed that these reprogramming chemicals and genes could treat neuromuscular disorders in mice.

And we're not that far away with AI from having something that she could take as a pill, perhaps some natural molecules. 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 spirit to go on.

We hold 2 different futures in superposition, and we have to choose which one we want.

Let's not be in the universe where things don't happen. Let's get us into that universe where we're just thriving as a species.

I love that. This is a subject that gives me such incredible hope. This is the most exciting time ever to be alive. 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 as a disease and a common biology to solve.

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.

Yeah, David, I want to talk about another area, and then we're going to go to AMA questions. I put out a tweet: I'm going to do an AMA with David. What questions do you have? We picked 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. What are you doing? Honestly, you look great, dude, and I appreciate the fact that you're a poster child for this industry.

Hey, thanks. I went online—or at least my team did—and found something published at NAD.com. I'm not sure how real it is. I think 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 and what's not real.

Okay. You want to see the list here?

Yeah, sure. Okay, and what's the main thing? There's a laundry list here.

I take like 80 supplements and medications a day. 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 standard. Do you know NMN has become a billion-dollar industry now? Honestly, that's due to you.

And just to clarify, you're not backing any of these supplement companies. In fact, they use your name and your likeness without your permission.

Right. My lawyers spend a fair amount of time and my money on stopping that. New companies pop up all the time, especially overseas, but I don't currently sell anything.

So, the main things are—let's start with the basics. Do what you do. 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 4 years ago. I stopped eating a lot of meat.

You've gone vegan completely, or 90%? What would you say?

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. 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. My mind cleared, and that might have also been because I gave up alcohol almost entirely.

Yeah. Just another point: I have given up alcohol except for a celebration.

I'm so sensitive to alcohol. It just makes me sleepy, and I gain weight if I'm drinking too much. I used to have a little bit of wine. Now I'll taste some wine.

Tonight is an exception. My buddy's family, the Reese family, is having the bar mitzvah for their son. My friend is like, “I've got the best bottles of wine.” So, I said, “Okay, I'm going to drink a glass of wine tonight.”

Good. Well, you look like you're looking after your weight really well. I think you've never looked so good.

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.

That's why I try not to eat more than 2 meals a day if I can, sometimes 1. The plants help because they also send a signal to the body. They're filled with polyphenols that give the signal of adversity.

GLP-1s, let's just plug that in right here. What's the evidence right now in your mind as a prolongevity medication?

Pretty good, actually. Certainly, if you're overweight, getting your weight down is beneficial.

But in addition, for 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 or incident that we're going to treat next year with age reversal is called nonarteritic anterior ischemic optic neuropathy, or NAION. The rates of that have doubled and tripled around the world because of these drugs, so it's not without risk. You've got to be careful using these peptides.

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, they can be useful.

And there are many of these drugs at this point, right?

Yeah, and they're getting easier to use. There's an oral version now.

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.

One of the things that's important to note—and I just want to reinforce this—is that if you're using a GLP-1 to lose weight, the challenge is that you lose the weight and also lose muscle. When you stop the GLP-1, you just put on fat again; you don't put the muscle back on.

But there's an easy solution, right? Work out.

Yeah. There's some effort involved, but just some sit-ups, push-ups, and whatever. Use the GLP-1 drug as a way to get into new habits, right? Get into the habit of not eating as much. What meal do you miss if you're going to miss a meal?

Breakfast. I have a late lunch.

The thing with GLP-1s is that even if you were to just fast and stop eating as much, you're 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.

So, really, you do have to keep the muscle mass up. I wouldn't use testosterone alone to combat that muscle loss. It really is better to be working out to stop that. Clearly, you're a good example of that.

And then, what source do you use? What sources are out there? I remember when Tony Robbins and I were writing our book, Life Force, when we looked at this, a lot of the NMN sources out there were not reputable.

Of course, a lot of companies have stopped putting NMN out for sale because of what's going on with MetroBiotech and the idea of having NMN become a medicine versus a supplement. So, give us some knowledge there.

The first question is about NMN as a supplement: can you trust it? I'm not in the business of testing products. That's not what I do. But I do test NMN sources when I give them to mice, and we have a study that we're just revising showing that NMN extends lifespan, mostly in female mice. It did improve frailty and a lot of health-related things.

We do test NMN, and we've tested a bunch of them. We find that there are things in there that you wouldn't want in there, like endotoxin, which is highly inflammatory and comes from parts of bacteria.

Are you going to publish that data?

No, I won't. It's only inflammatory. We might publish it. It's super useful to have.

We should do that. Somebody should be listening. You've made NMN a household name, whether you like it or not, because you talked about the value of it.

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.

And I haven't made any money off it. In fact, I've invested a lot of money in clinical trials. [laughter] No, I mean, there's been like $30 million worth of my money and others' money to do clinical trials to test a version of NMN in humans. It does cost me a lot to try and validate NMN as a molecule.

One of the advantages is that MetroBiotech has a particular crystallized NMN that they're testing in a wide range of medical conditions, right?

That's right. And I don't see why they can't exist in the same universe: supplements, which are not under FDA approval and usually aren't prescribed by doctors, and an ultrapure, pharmaceutical-grade, crystalline, stable form that has been shown to work, which can be prescribed. That's been shown even for fish oil. GSK, actually, our friends at GSK, made a fish oil that I think is still available on the market. It's a pharmaceutical; it's a drug.

Yeah, because of its purity.

Yeah. And so, the reason I would use the MetroBiotech NMN, if and when it becomes approved as a drug, is because I'm assured of quality and purity.

That's right.

Yeah. And then, to get to the FDA thing, 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, which is a problem. And it degrades over time in the noncrystalline form.

Yeah. Exactly, in the noncrystalline form.

Exactly. But what actually happened—I'll explain what actually happened, please. MetroBiotech—it's not my company. I've invested in it, and there's a chairman and a board. They made the decision that they would support the FDA in looking at NMN as a supplement. 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 people are putting in.

I believe I'm on record, but I'll say here that I was not in favor of that. I didn't want MetroBiotech 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 have control of a company that you're the figurehead of.

Yeah.

But in this case, I couldn't stop that. But I think where we're at now is that there's some gray zone about—you can sell it now.

I'm seeing NMN for sale.

Let me clarify something. Ultimately, what you're trying to do is raise your intracellular NAD+ levels—NAD levels. That's the end goal.

And the sirtuins need that NAD to work. It's the powerhouse.

Yeah. So NMN can cross the cell membrane, and inside the cell gets converted to NAD.

Correct. Yeah. And then there's NR, nicotinamide riboside, which is what's used to make NMN in the cell, right? So you have this sequence. Some people are arguing that you should take NR. Some people are arguing to take NMN. Other folks are doing NAD IVs. Am I wrong in believing that an NAD IV is not getting into your cell?

Oh, I think that NAD drips will raise intracellular NAD, probably because it gets broken down and then gets reabsorbed. 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 more studies on that.

But what I can say about oral NMN is that we have spent money studying that, and we've—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, cholesterol, and lipids, and even seems 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 5 clinical trials at MetroBiotech now looking at whether it's efficacious in a disease state—Alzheimer's, kidney function; it's all on the website. And so, with 5, and hopefully 6, shots on goal, the idea is that 1 of those will work.

The other thing that's interesting is there's a new molecule.

I saw that.

So MAB 626 was the old molecule.

Yeah. 626 is my birthday, by the way.

Ah, that's where it came from. Interesting.

And then 725—almost happy birthday.

Thank you. So 725 is the new molecule, MB 725, and that's the birthday of Anthony Sauve, my great colleague who passed away during COVID. He was at Cornell, but we miss him dearly. And so, hopefully, if that makes it onto the market, it'll be his legacy.

Nice.

All right, let's run down a few of these. Fisetin, lipoic acid, EPA, DHA, taurine. Comments on those?

Yeah. I mean, fisetin is a molecule we actually first discovered to be a longevity molecule before it was known as a senolytic. The people who now talk about fisetin just ignore our research.

Is that the Australian pronunciation of fisetin versus fisetin?

I think it doesn't matter what you say—fisetin—but we showed fisetin is a sirtuin activator, just like resveratrol, and I think it might be doing both things: either calming down or killing senescent cells at high doses, and at lower doses it activates the sirtuin enzyme, which is what we want. I think of NAD as the gas, or the petrol, for the enzyme, and then the accelerator pedal is these polyphenols, like fisetin and resveratrol, and together they have a double-whammy benefit.

Alpha-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 Harman, who came up with the free radical theory of aging, and he was still in the lab at 92. I said, “What's your theory? What's your secret?” And he said, “It's alpha-lipoic acid.”

Interesting. But the free radical theory of aging has really been kind of disproven, hasn't it? 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 for aging.

Yes. But I still admire him for being in the lab at 92.

Sure. But I mean—

Well, indirectly it is, because we know DNA breaks are going to accelerate aging. And free radicals can damage DNA, but it's not the holy grail. Taking antioxidants doesn't extend the lifespan of animals very much.

Okay. You mentioned taurine; it just had a paper published on it.

Yeah. It just came out in Science. Rafael de Cabo is a very good friend of mine for 25 years, and he was the one who just showed that taurine levels don't decline, apparently, in humans or monkeys or mice. I started taking it a year ago because of all the news about it, and now it doesn't look as promising, put it that way. 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.

By the way, NMN—1 gram; that's what I take. Is there any problem with going more than a gram, if you do 2 grams or 3 grams, that you know of? I'm just curious. I have it in a bunch of supplements, so I'm like—

It's been published that both 1 gram and 2 grams 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.

Got it. We've talked about resveratrol, spermidine, vitamin D, vitamin K.

Yes, yes, yes.

Low-dose aspirin still?

Yes.

And that's interesting, because a lot of people have heard, at least through the grapevine, that aspirin shouldn't be taken.

Here's the deal. 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. The risk is that you get stomach bleeding, and based on the numbers, it wasn’t clear if it was worth taking aspirin. But that’s for the average human, and there is no such thing as an average human. Medicine really should be breaking it down as to, for you, Peter, what’s good for you. Do you want an aspirin or not? And, by the way, everything we’ve spoken about so far I do take, including the aspirin: 81 milligrams a day.

81 milligrams, right? Baby aspirin. So, take a coated aspirin?

Yeah, I do. That reduces the risk of any stomach issues. But here’s the thing: there are people at risk of cardiovascular disease, and 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(a).

I do, too. By the way, I’m so excited about the new drug that’s coming out for Lp(a).

Yeah, it looks promising. It’s in Phase 3, and it should be coming out in the next 12 months.

Yeah, because right now, there’s very little that moves the needle there. It’s really hard to bring it down. I know from experience.

You and I are in the same boat.

Trimethylglycine.

I don’t take that.

Neither do I. There’s this unfounded claim that NMN and NAD boosters deplete your methyls and that you need to take trimethylglycine to supplement them.

That’s just based on wild speculation. There’s no evidence from anything we’ve done that it’s true. So, I stopped taking metformin. Are you on it still?

Occasionally.

I’m on berberine instead.

Me, too. I found that metformin was really rough on my stomach, and the older I get, the rougher it gets. Berberine seems to be great, so I do that.

I stopped metformin mostly because of the focus on muscle growth.

Yeah, there’s that. But I want to speak about that.

Please.

I find that most people don’t read the papers. If you do, what you see is that the claim, even from some doctors who talk about this, is that metformin blunts muscle growth. When you actually dive into the data, you see that the graph was misrepresented.

Guilty as charged.

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 5%.

It just looks better.

All right, let’s go to the next one: rapamycin. There have been huge claims. Many of the longevity experts said, “If there’s 1 drug that probably has a longevity impact, it’s rapamycin.” I’ve been tracking that and reading about it, and it’s enough up and down that I stopped taking rapamycin. I have a very low senescent cell count. How about you? What do you think about rapamycin?

I’m less excited about it. It was the darling because it works really well in inbred animals and seemingly might even work in dogs. But in humans, there was a study that came out probably 6 months ago that compared the effect on the epigenetic age of people in different clinical trials. While some things worked really well, like caloric restriction—I think acarbose worked really well, too—and metformin looked better than I thought it would, rapamycin had no effect on the age of the epigenome.

Yeah.

That, combined with the known potential risks of downregulating the immune system—and I’ll explain later why I think that’s bad—led me to decide to take it only rarely.

What occasion would you take it on?

I’d probably take it 4 times a year.

Okay, so it’s just pulsed.

Yeah, and I’m monitoring myself, so I know if it has benefits or not. I do see some.

You’re monitoring your immune system. You’re monitoring everything.

Yeah, I monitor my immune system. I’m counting the cells that I have, the different types, and cytokines—inflammatory cytokines—and I want to keep those as low as possible to keep down inflammation, or inflammaging. So, I want to talk about why downregulating your immune system might be bad.

Yes.

You want to downregulate your inflammation, but you want to have a really active immune system when it comes to cancer and viruses. Those 2 things are real risks as we get older. There are endogenous viruses that come out, like CMV. CMV is pernicious; it’s an epidemic out there. One thing that people don’t realize is that there’s something called immune exhaustion, where your immune system is fighting all these battles against herpes and CMV. How many different viruses do you think are endemic in the human being, on average?

It’s approaching 1,000 now when you do deep sequencing.

Incredible. If they’re fighting those viruses, your innate system isn’t there to fight cancer.

Yes, there’s that.

The other issue is that viruses like CMV can potentially lead to autoimmune disorders. CMV is linked to multiple sclerosis. You do not want CMV circulating, and for that reason I don’t want chronic downregulation of my immune system.

Yeah. That’s important to note. Okay, let’s jump into a few other elements here. Is there anything else that we didn’t talk about that’s high on your supplement and medication list?

There’s a lot, but let’s leave that for the fans.

Are there any special supplements or additions for women that you want to call out?

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. There are also some ways to delay menopause and perhaps even reverse it, and I talk about that in my book as well. Mostly, for women, it’s hormonal, but there are other things, like iron and protein, that they need at certain times of the month.

Do you know Jennifer Garrison at the Buck?

Sure.

Jennifer is another person whose research Tony and I have supported. She was at XPRIZE Visioneering last October, where we compete with all these XPRIZE ideas. Her work, which was being called the XX Prize for women’s longevity, particularly ovarian longevity, won the competition. We’re in the middle of designing that XPRIZE, which will be super cool.

She’s great. I have a superstar in my lab who needs our support. Maria is such a superstar. This morning, she gave a lab meeting. Our lab meetings go for 3 hours on Friday mornings, and she outlined her project to use these age-reversal breakthroughs on women’s fertility.

We need to get her either competing for the prize or helping to design the prize.

For sure. She’s also using menstrual fluid as a biological clock and diagnostic factor, which is a great idea.

Amazing. So, sauna. Do you sauna?

As much as I can. I get a great sweat in about 30 minutes. 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 vitals. You also want to 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.

It is.

The problem is that we often don’t have space in our houses.

I purchased a relatively small one, about the size of this table, and it collapses. You sit in a folding chair inside, and it works. It gets hot enough that I get a really great sweat going in 30 minutes. It’s not instant, like 10 minutes, but I enjoy my 30 minutes. I’m meditating, watching a video, or listening to a book.

One big question is fasting and the fasting-mimicking diet. 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?

I know a lot about it. In particular, I was just recording my next podcast on fasting and caloric restriction, and there are 80 pages of notes and show notes. You have to do fasting the right way; with all these diets, if you do it the wrong way, it can harm you. You need to be educated, make sure you’re not overdoing it, and supply yourself with enough vitamins, minerals, and protein. I do it, but I do it in a scientific way, and that’s part of the challenge. If you don’t do it with regular blood tests at least once every few months, I think it’s probably somewhat risky.

But in general, fasting has been shown forever, since humans were around.

Sure. In fact, religions have built fasting into their annual clock.

Yeah. So I still believe in the science of fasting; it just has to be done the right way. There are some papers that show that if you do a vegan diet—and this is a separate point—a vegan unhealthy diet will make you live shorter, but a vegan healthy diet will make you live longer. You just have to make sure you're eating the right things.

The same is true with fasting. You have to time it with your circadian rhythms, and you have to eat the right food at the right time. You can't just eat French fries once a day and hope that's going to make you live longer. So I'm very vocal about the notion that sugar is a poison.

Me too. I regard it as a poison. I just want to echo that with a couple of data points. We are eating, in our diet today, on the order of 10 times more sugar than we did a couple hundred years ago.

One of the things we're getting ready to publish this data at Fountain Life: everybody coming through Fountain Life, we upload them. We get 200 gigabytes of data. It's one of the most complete data uploads you can possibly do in 5 hours: full-body MRI, brain MRI, brain vasculature, a coronary CT looking for soft plaque—not calcified plaque. Soft plaque is what kills you these days.

If you have a high calcium score, it doesn't mean much unless the calcium is 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 evolve in the middle of the night, block your artery, and you don't wake up. We do low-dose lung CT. We do a DEXA scan, metabolomics, 140 blood biomarkers, your gut microbiome, retinal scan, skin scan—all of that.

When am I going to get a scan?

Dude, please come. Please.

No, I'm serious.

No, please come. I'd love to have you try it as my guest. We're opening up Los Angeles here in the first quarter of 2026. 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 we're opening up Miami.

Congratulations.

Thank you. I remember when you were just talking about it. We looked at what correlates highest with heart disease, and it wasn't Lp(a), triglycerides, LDL, or HDL. It was your hemoglobin A1C. You can control that.

Well, you can, and it starts with a good diet and lifestyle and exercise, for sure. But the drugs that are now available are effective. You can either prevent the absorption with acarbose, pee it out with SGLT2 inhibitors, or take metformin or berberine. Then there are others. So, if you've got a good physician, you should be able to control your blood glucose these days. Of course, you shouldn't forget the GLP-1s.

It's crazy. Okay, one or two more subjects, and then I want to go into the AMA. We have so many fans of yours who have written out questions here.

I just got back from Hong Kong, and one of the things I was speaking about there was the notion that a breakthrough in China works in Chicago. A breakthrough in Boston works in Beijing. All 8 billion of us share the same fundamentals of longevity. Unlike AI, which is a sort of winner-take-all battle, the idea of being able to give people longevity is a rising tide for everybody.

I'm curious: when I run my Platinum Longevity trips—we're currently doing them every other year—on even years, we're in San Francisco and San Diego, which is sort of a cluster for longevity. On odd years, like this year, we'll be visiting you and George and a number of other incredible people in Boston and Cambridge, and Dean Kamen is in New Hampshire, which is another cluster.

But what's going on in the rest of the world? Who's hot? Where are the clusters of longevity work?

There are nations that have stood up and said, "We're going to invest in this." In Asia, it's Singapore. In the Middle East, pretty much all the countries are involved, but Saudi Arabia, the UAE, and now Qatar are big on longevity.

Then the Western world is a distant third, fourth, and fifth. It's not really getting into it besides the United States. There's a little bit in the UK, a little bit in Australia, but other than that, it's just pockets of really good labs—not really an industry yet.

I wish that, in the same way we just saw a couple of trillion dollars put into AI by the Middle East, they would get longevity religion and start pouring trillions into this space. I hope we can get there.

Yeah, I hope we can get there.

I firmly believe this is—​you've spoken about this. You've been really the first person to speak out that aging is a disease, and that when we're able to cure and reverse this, it is going to uplift every society. God knows that South Korea, Japan, China, Italy, and most of Western Europe need longevity. They're disappearing as nations.

Well, that's the other thing. It used to be that we were going to overcrowd the planet if we slowed down aging, but we need the existing people to stay healthy and productive because they're running out of people.

Are we seeing good work coming out of China? Are there scientists there? I'm just curious what's going on.

They are more than a decade behind the United States right now, but we're ceding to them right now. We're cutting our science by more than half and all that stuff, so I think China is laughing all the way to the IP patent office. We really risk our lead in this area. While AI is neck and neck, we have a big lead in longevity, but we could lose that.

Yeah, for sure. All right, let's jump into questions from your fans. The first one was, "What role is AI playing in your search to reverse aging?"

We heard about that already. A very big role. A big role.

When did it start becoming a big role in your lab?

We started using it about 3 years ago, but now we don't go a day without it.

Exactly.

Think about this: what we do now in 2 months would have taken thousands of years to do. You can say it, but just let that sink in. The predictions that I made 5 years ago are out the window because of AI.

Now you're much more optimistic. So the new book's going to update those predictions?

Exactly. Yes.

Okay, fantastic. Safia 3000 says, "Is there a role for epigenetic reprogramming to end ovarian aging and restore ovarian function?"

Maria will answer that. She's a PhD student in my lab. So yes, we do believe that we can reverse ovarian aging. We were already the first group, with our Australian offshoot, to show that you can reverse infertility in old mice.

That was a shocker because people said, "Mammals run out of eggs." But we took 16-month-old mice, which had become infertile 6 months earlier, reversed them, and made them produce pups again.

Wow.

I know it's possible. Even with NMN, it worked. So we're going to try the even better technology—the stronger technology of epigenetic reprogramming.

Incredible. Most men are very ignorant about ovarian aging. Just to pass along some facts for folks, only 5 or 6 species on the planet go through menopause. There are 3 species of whales, the narwhal, and humans, which is crazy. You'd imagine everybody does, but that's not the case.

If you're a guy, the age at which your sister went through menopause actually correlates with how long you'll live. It's a really good indicator of longevity.

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 evolution emerging? Is gene therapy still your most promising delivery method for Yamanaka factors?"

We've sort of covered many of those. I don't know if you want to add anything on there.

That was a very long question.

Yeah, testing your memory.

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. It feels like science fiction. It feels like the future. It's like we're living in the Star Trek universe, with AI at this level and talking about whole-body rejuvenation. What an extraordinary time to be alive.

The future looks so bright. We have to make it happen.

Yeah, we absolutely have to. Ethor Arnolds asks, "When can we expect results from 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. Yep.

Okay. Atnik Singh wants to know, "When is your next book coming out?" We shared that. It's 2026, and it's called Lifespan Survival.

I'll tell you what it's about.

Please. Yeah, I love that.

Lifespan was more of a textbook. It was: Why do we age? How does this all work? What will happen to the planet when this happens?

Book 2 is really answering all the questions that I've been getting since. Think of Lifespan 2, the book, as the guidebook: How do we optimize our bodies? Looking at our evolution and the genes that we all carry, how do we individualize our lifestyles, supplements, and medicines to maximize our longevity?

Then what do we do for the next 10 or 20 years going forward? I look at it from the individual perspective, at the molecular level, all the way through to society.

Fantastic. Dana Brilliant writes, “What’s your exercise routine? How much protein do you eat?” Her name is Brilliant. I like that.

The routine is, whenever I can, I get to the gym. 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 have something at home—some weights you can lift—and then walk or run on a treadmill.

Moving, moving, moving, and keeping—especially after the age of 50, you’ve got to keep lifting weights, otherwise you’re going to lose it. Sitting is the new smoking, as I like to say. For me, the trick is that I have a stationary bike. I take my Zoom meetings on my stationary bike. It works well.

Sure. So, for me, I put on 10 pounds of muscle mass about 2 years ago, 18 months ago, and my job is to keep it on now. It was creatine. Do you take creatine as a supplement?

No, but I’m considering it.

Yeah. It looks like all upside, no downside, for me. I do 5 grams of creatine, and it was 1 gram of protein per pound of body weight. There’s a lot of debate on how much protein. Our friend down the street here at USC is not liking so much protein.

There’s Valter Longo, 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. There are some really good amino acids, and there are some that will reduce your lifespan.

There are what are called branched-chain amino acids—leucine, isoleucine, and valine—that are the bad ones, and you get a lot of those from meat. I try not to eat a lot of meat. Plants have fewer of these amino acids. What’s your favorite protein source from plants?

Lentils. I love lentils.

Aoko asks, “Dr. David Sinclair, what single experiment would definitely falsify your epigenetic noise theory of aging? What experiment would falsify your epigenetic noise theory of aging? Is there something that, if you ran it, would disprove that theory?”

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 epigenome aging by changing the methylation pattern and 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. That was the reason I thought it was likely to be true, because the chances that it would fail were 99%. But that 1%—it worked.

At Good Thinking With asks, “What AI advancement would be the most useful for your research?”

That’s great. I would love it if AI could tell me who the observer is, where the observer is. We’ve been working on that, but I would love it if it said, “We just analyzed all the world’s data, and it’s got to be this result.” That would help.

That’s my dream: before I die, to figure out how the cell rejuvenates and have the AI publish the paper for you as well.

Well, that’s almost doable now.

I think that also being able to do drug development even better than we do now—to be able to say, “This one molecule is your candidate for going into humans”—would be amazing.

Wow. We’re not there yet. It says “top 100,” but going down to 1 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 amazing. We’re probably only a few years away from that.

Eventually, you’ll just do it on your phone. You’ll say, “Oh, let’s cure whatever disease,” on your phone. By the time you get home, it will have told you how to do that.

I have a question that pops into mind here. There’s a crazy statistic about the nonreproducibility of research data. Is it half of the research out there? I’m not sure if it’s that high, but it can’t be reproduced. What’s going on there?

That number is an exaggeration. We sometimes struggle to reproduce people’s data, and it’s because you’re using a different cell line, a different water supply, or a different handler. The mice don’t behave the same way. It’s not that the people are faking it. It’s more that science is complicated and variable, and it depends on where and how you do it.

Some labs rejoice in disproving things. I don’t do that. I always assume I’m the reason it’s not working. But there are labs that thrive on not reproducing people’s data, and it’s super easy not to reproduce someone’s result. I could easily do it. Just change one thing, and it’s not going to work.

There’s that category. But, of course, there’s a lot of research that isn’t done rigorously, like this taurine paper. It might have been due to just inherent variability from taking 1 time point, but when you look over the lifespan of longitudinally observed 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, had to be retracted, or changed 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.

That’s a super-high standard. Robertz ZX writes, “What one area do you want to see more innovative startups tackling? Is there something in longevity—or, I assume, in the biotech and longevity world?”

I would love for more labs to be working on finding new ways to reverse aging. Right now, we have 3 genes that we know work. That’s our technology, and we have some small molecules we’re working on, but it’s all white space for people to get into.

We do have some competition. We’ve got Altos and the others. But I think that this area is similar to AI. There’s so much that can be done, and it’s not like 1 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. I would like to see more jump in.

One of our mutual friends, Dr. Alex Zhavoronkov from Insilico Medicine, has built an amazing AI- and robotics-driven lab. 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 Boston right now?

I’m not aware of it, but that sounds like 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. 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.

By the way, I actually believe that we’re going to see consciousness in these machines. I just tweeted this out because I finished listening to a book about the evolution of intelligence. Max S. Bennett, I think, is the author, and it’s a great book. He talks about how we evolved our intelligence, and it starts with language. Now we’re doing large language models, so we’re in the early stages of human evolution over the last million years.

There aren’t that many steps between once you’ve got language and becoming sentient. It’s almost a given.

Wow. I’m about to go on a 2-week vacation to Alaska with my family, and I was looking for a book to read. I think you just found it for me. Do you remember the title?

I think it’s the evolution of intelligence. Oh, it might be A Brief History of Intelligence.

Jared Michaels writes, “When will poor people be able to extend their lifespan?”

One of the things that we get critiqued on all the time is the expectation that it’s going to be super expensive. 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. 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. Moderna’s COVID vaccine was between $1 and $2 a dose. When you’re providing something to a billion people, it gets really cheap.

Yeah. And actually, based on what my lab is doing now, I see no reason why, for a few cents a day, everybody could afford a longevity pill.

Yeah, I mean, it’s a beautiful vision. All right. Vladimir Adelor asks, “What is the difference between the current longevity metrics and actually being young?”

At age 22, I can get in a fight, get drunk, do an all-nighter, and still perform many high-skill tasks to perfection.

Whereas longevity folks can't do any of that. We can—I don't know. I feel like I can do anything like that. But listen, I'm not going to pull all-nighters like I did in my 20s.

Yeah, right. Well, our organs still aren't optimized. Their gene expression—the epigenome—has degraded. You and I have lost some of that information, so our liver cells are not pristine anymore. They're behaving a little bit more like a nerve cell or a skin cell. They're more like a mélange of cells.

So we need to reboot them so that they know how to be perfectly liver cells again. That's why I think you and I cannot do an all-nighter now and get away with it.

Yeah, but that doesn't mean we can't. I now look at an old person and I don't see them as an old person. I just see someone who needs a reboot.

I love that. I love that. Hey, you want a reboot? Come on over here.

All right. J. Kingsley asks, “What are the second- and third-order effects once aging has been cured? Does life have more meaning because it's finite?”

This gets into the philosophical conversation here, and I love your thoughts on this. I definitely have opinions.

Please.

We may share them.

I'm enjoying this conversation not because I'm worried about dying. I'm enjoying it because the moment is fantastic. I don't think the fact that I'm going to 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. Whether I'm going to live 80, 200, or 400 years, I'm going to enjoy this moment just as much.

I remind people, listen, the average age for most of human history was around 30. Are you enjoying life now less because we've increased it 2.5 or 3-fold? 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'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.” Right? Write it down. Most people can sort of think about 20 extra healthy years. Now I say, “What would you do with 50 extra healthy years?”

People's minds start to break. It becomes much more difficult for them to do that. What would you do with 50 years?

What would I do? 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, they'll work on something else.

I love research. I love knowing things for the first time in human history. I'll keep doing science for as long as I am funded and can do it. I love life, too. It's just so much better than the alternative. [laughter]

If you look at my father, I didn't expect my father to live beyond 80. Nor did he, by the way. 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 or 86, most people are younger than you. [laughter] There's that, and if you're a man, there's not a lot of competition at that age. [laughter] But 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. So, as longevity goes up, you work longer. It makes sense. You can't just all sit around drinking cocktails.

Yeah, and we'll have a revolt when that happens. But it makes sense. It'll slowly inch up. Let's say longevity goes up by a year in the country; you work for the next year again. What's the alternative? Do you want to just die young?

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. And maybe there's a world where we've got AI and androids, where we don't have to work.

Yeah. We have some version of UBI, but health is still going to be the most valuable asset we have.

All right. So, 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 Moonshots knows the numbers here, right? The replacement-rate number of children per family is 2.1. Almost every country on the planet is below that, some dramatically. South Korea is like 0.7 children per family. Japan is not far from that. Italy is evaporating. Most of Europe and the US—those economies are screwed, by the way, unless they do something serious.

Well, longevity is critical, and robotics and AI are going to be critical. Somehow incentivizing people to build families, I think, is critical.

Or extend the fertility age of women, because a lot of women these days leave it until too late.

Yep. And 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. You're 64. You're looking great.

Thank you. I feel great. My kids are 15 and 10, and I keep telling them, “Yes, when you're 50, I'll be 100 and I'll still kick your butt.” [laughter]

Well, I think we men 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. Sometimes these careers take 40 years. As a scientist, you're not mature until you're 40. 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.

After 30, there'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.

Freeze eggs?

Is that it?

Yes. Fertilized eggs if you can. And follow these protocols. There's every indication that we can delay infertility by delaying aging.

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 revert to Star Trek. There's a lot of universe out there. I just want to see it all. I also imagine 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.

I had on stage at my Abundance Summit last year a gentleman, Michael Andre, who is working on mapping a mouse. He believes the technology now exists to map a human brain fully and upload it. The problem is it's destructive in the process.

Yeah. That's a slight downside.

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.”

Yeah, there's a good Black Mirror episode on that.

Oh, you know, listen, I'm pissed off at Black Mirror. I'm pissed off at Hollywood because we humans need a positive vision of the future to aim for. We need a story that is compelling, abundant, and hopeful, and we don't have many of those. Star Trek was the one that really lit me on fire. We need more of those.

Yeah, I couldn't agree more. Especially when it comes to longevity, it's usually, “Oh, something's gone horribly wrong.”

Yes. Exactly.

Sharon Bank asks, “Maybe ask about longevity's economic impact. Keep it insightful.” So, I want to drill down more into the Harvard, London Business School, and Oxford paper because I want to understand how we get to tens of trillions of dollars from 1 year of additional healthy life, because that's what it's saying.

Yeah. I mean, the global economy is $110 trillion. Was this for the US or was this for the globe? Do you remember?

It was just the US, for 1 year of extra life. It's the value to the economy.

The value is the key word. The value is how much are people willing to pay? It's called the willingness to pay, WTP.

The way economists use this number is they say, “What's it worth to you to have an extra year of life?” The reason that the number balloons out astronomically is that there's positive feedback: for every extra year that somebody lives, it turns out they want more of that, and they're willing to pay for more of that. That's one of the main reasons.

Then, of course, you can take away a lot of the health care issues. The longer somebody lives, the less burden they are on the economy, and that also factors in. But health care is expensive. If you know 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 were still healthy at 76, she'd still be earning, she'd be looking after people, 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?—by a team including Harvard and Oxford economists showed that a slowdown in aging that increased life expectancy by 1 year is worth an estimated $38 trillion to the global economy.

Again, I find those numbers crazy.

I wish I'd been able to feed that information to Elon at the beginning. It's like: spend government money solving aging, and then not have to worry about this other stuff.

Yeah, that would have been much better.

Cassie Nova asks, “What are the most effective over-the-counter modalities available today for under $1,000?” We talked about some of those supplements, and I don't think any of them are expensive. Exercise—I would think exercise is the most important modality. How do you feel about that?

I think, yes, what you eat and exercise are the 2 big ones. They're relatively easy. It's a little more technical to get your supplements right because you've got to tailor them to you.

For cardiovascular disease, there's something that I've been taking for a couple of years now that has actually been shown in studies to reverse cardiovascular disease—to remove plaque.

What is it?

It's called nattokinase.

Oh, yeah, I take nattokinase as well.

Great. Yeah.

I take it for post-COVID travel on airplane flights, just potentially reducing clotting.

That's the short-term benefit, but the long-term benefit is that there was a study with, I think, 1,086 people—a Chinese study, but it was very well-powered—and they showed that up to 95% of plaque was removed in 1 year just by taking it. You need at least 12,000 fibrinolytic units a day.

I've been doing that, and so far it's been great. I measure my carotid with ultrasound, and there's no plaque buildup there at all.

Sure. It's hard to reduce that, but I do take it as prevention. Let me see where I am on nattokinase. Nattokinase is an enzyme that digests fibrin, which is part of blood clots. I'm on 100 milligrams of nattokinase. I don't know how many units that translates to.

I would say if you don't want to take a lot of pills, at least 6,000 FU would be a good start, and then work up from there. But of course, do this with the knowledge of your physician.

I have an army of doctors I hire. I have 30 of them working for me at Fountain Life, so that's true. But not everyone can do that.

Still, just in general, as a warning, if you change your lifestyle or start taking supplements, make sure your doctor knows.

Yeah, for sure.

One of the things I so desperately want—and there was a question about what people should build—is an AI model that will take in my genetics, my recent blood work, and my goals. Maybe I want higher cognitive clarity, more muscle, or more longevity. Whatever your goals are, you prioritize them, and then say how many pills a day you're willing to take.

It should spit out a prioritized list, because right now you go to 1 doctor and you'll get 1 set. You listen to you or me, you'll get another set. You listen to another person, you'll get another set. There is an optimal approach. There truly is, and it wouldn't be that hard, actually, to—

No, it wouldn't be. The data is out there. 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.

Yeah, it can.

Let's talk about something you and I might differ on. I'm curious about sleep. I suck at it. How do you do?

I got a 92 last night, which I was very happy about, on my Oura Ring.

I won't tell you what I got. I will tell you, because I've got to look right now. Last night was awful. I'm usually very proud of my sleep. Last night I got a 64. It's the lowest I've gotten in about a year.

I think I've been going 24/7 this week, getting ready to be gone for 2 weeks, or whatever it was. But I made up for it today, definitely.

Good.

I try my best. I'm traveling. You said to me once that you think you can get away with less sleep. I have figured out how to do that.

Okay, pray tell.

It's about the amount of deep sleep that you get. I've got a supplement that puts me straight into deep sleep.

Is it a drug?

It's a mixture of very low-dose melatonin, 5-HTP, and L-theanine. It's magical. I used to have insomnia really badly, but I'm off Ambien now.

Oh, yeah. Ambien's just terrible.

We share what we know that works for us, and that's all we can do.

Sam Renkema asks, “What are the top 10 practical longevity tips—top 3 for each organ? And which 5 longevity gadgets do you recommend?”

Let's go with the last part. We can go with gadgets. What are you using for gadgets?

In our home, we have a red-light bed. It's a big one.

You have the THOR, the lie-down one. I have panels right now that I use—a panel, I think it is.

Yeah, it's a big thing with a lid that looks like a tanning bed, but it's not. I love that. I do red light as many mornings as I possibly can.

The other thing I've been doing is using a portable red light. I put it outside the shower, shining in, so as I'm in the shower, I'm getting red-light therapy, too. It's also a steam shower, which is nice.

I use that on my head as well.

Yeah, I have a red-light cap for hair-growth stimulation. It's doing okay. It's working.

I still can't believe you're 65.

Is that 64? Sorry, I didn't mean to age myself.

No, that's okay.

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. For me, that is a call to action to remain at the highest health status for as long as possible, because we have incredible technology coming our way, and I want to intercept that longevity escape velocity.

Well, you're also a role model. I feel like I'm 28 or 29. That's my internal age—that's my internal number for myself.

Physically, you look like you'd be in your 30s or 40s, and you move just like you were in your 30s or 40s, I bet.

Yeah. And, by the way, my father is stronger, fitter, and more flexible than I am, with better balance, and he's 86. So it's very doable.

On my birthday a few weeks ago, I pumped out 100 push-ups in a row. When I was in my 20s, the most I could do was 40, and I got to 50. I've increased it from there. I'm not saying that to brag. I'm just saying I use that as a measure for how I'm doing.

In my longevity guidebook, I put my measurements that I've been tracking over the last few years in terms of squats, push-ups, planks, and such. It's important for you to measure yourself. Of course, you get a lot of data from your DEXA scans, MRIs, and so forth. The data does matter. Obviously, you have an Oura Ring on, too.

I have a ring, and I don't say what type it is.

Okay, fair enough. Do you use a CGM?

I do. Not every week, but when I feel like it's probably useful—maybe 5 times a year or something. Different brands are better than others, but you want to try them and research what works.

Monitoring your glucose—I've seen some doctors say it's irresponsible for people to have access to that data, that it should be for doctors.

Yeah. You'll look online, and 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, and that I'm not educated enough to understand this? A lot of the people out there are just as educated about glucose as their own doctors.

I'm definitely in the camp that we have a right to know our own genetics, our own epigenetics, and our own glucose levels. Information is power. As long as you're telling your doctor what you're doing and talking to them about it, and you've 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.”

One thing I'm curious about is 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?

If I'm of sound mind, or if my family agrees, why can't I? Is it called “right to test,” “right to use,” or “right to try”?

Right to Try is getting going, but 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 supervision, so your physician makes the decision with you.

The idea that it might be an uneducated decision is not true. It's the same with euthanasia. You have to go overseas now if you want to do that. If you're in agony every day, who are we to say that you shouldn't do what you want with your life?

And that raises a question I'm curious about: How long do you want to live? When I'm on stage, I ask people in the room, “How long do you think you're going to live?” You have a number in your brain. Where'd you get that number from, and why do you believe it? I find it fascinating that this mindset people have—that they have this number—can have implications, right? Your mind is a very powerful force in determining how long you'll live.

But you're asking me those questions. I'm asking you: How long do you want to live, and why? And why is the important part, right? If you're willing.

No, it's fine. I think it's a better question to ask: When do you want to die? As long as I'm healthy and I have friends, I find there will never be a day when I want to die. I think that's true for just about everybody. If you're sick, frail, lonely, or 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—who, if they're healthy and have friends and family, would say, “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. I think it's pretty boring.

Yeah. David, I truly love what you do. I consider you a dear friend, and I'm grateful for you in my life.

Buddy, listen, this was fun. I enjoyed this. I really, really did. It was great to catch up again. I'm going to see you in Boston at the end of September. I'm excited to spend the weekend with you.

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, and thank God you exist, because 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.

Yeah, I hope so. I look forward to partnering with you on that. Thank you, my friend.

All right, buddy. Be well.

You, too.