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PROFESSOR DAVID SINCLAIR | Can Humans Live For 1000 Years?

David Sinclair is a Professor in the Department of Genetics at Harvard Medical School and co-Director of the Paul Glenn Centre for the Biological Mechanisms of Ageing. Today we hear from a scientist at the cutting edge of longevity research as Professor Sinclair gives us a fascinating insight into the world of anti-ageing. Expect to learn how and why we age, why stabilising the epigenetic landscape may enable a human to live for 1000 years, exactly what tactics Professor Sinclair is using himself to try and extend his life and how fasting, Sirtuins and NAD can be used to promote health and reduce diseases. Extra Stuff: David’s New Book - http://lifespanbook.com/ Follow David on Twitter - https://twitter.com/davidasinclair Inside Tracker - https:// www.insidetracker.com Recommended Books - https://www.amazon.co.uk/shop/modernwisdom Nick Bostrom on Sam Harris - https://podcasts.apple.com/gb/podcast/making-sense-with-sam-harris/id733163012?i=1000432217348 - Listen to all episodes online. Search "Modern Wisdom" on any Podcast App or click here: iTunes: https://apple.co/2MNqIgw Spotify: https://spoti.fi/2LSimPn Stitcher: https://www.stitcher.com/podcast/modern-wisdom - I want to hear from you!! Get in touch in the comments below or head to... Twitter: https://www.twitter.com/chriswillx Instagram: https://www.instagram.com/chriswillx Email: modernwisdompodcast@gmail.com

Chris WilliamsonhostDavid Sinclairguest
Apr 22, 20191h 14mWatch on YouTube ↗

EVERY SPOKEN WORD

  1. 0:01 – 2:12

    At Harvard: InsideTracker results and why “biological age” matters

    1. CW

      What's happening? I'm coming to you from the beautiful Harvard Medical School in Boston. I arrived last night. I've had the requisite amount of caffeine, and I'm about to go and sit down with David Sinclair, who is a biologist and a professor of genetics here at Harvard Medical School. You may have recognized him from the Joe Rogan podcast he did a couple of months ago. That was interesting and exciting to say the least. Introduced me to a lot of topics that I didn't know about before and I'm super excited to follow up on some of them today. So yeah, stay tuned. Professor David Sinclair of Harvard Medical School. How are you today?

    2. DS

      I'm doing really well, Chris.

    3. CW

      I'm very, very glad to be here. I'm, uh, off to see your friends at InsideTracker later on. Uh, I'm gonna go straight over there and have a sit down with them and go through my, uh, my results. See what, see what they've got to say.

    4. DS

      Oh, really? You've had your blood drawn?

    5. CW

      I have indeed, yeah.

    6. DS

      Uh-huh. That'll be exciting.

    7. CW

      I went to Quest Diagnostics, uh, a week and a bit ago in California, um, and I went through my results with Stacy. If it's not, if she's not called Stacy, I'm gonna be in so much bother. Um, with one of the analysts at InsideTracker, and they took me through all of my stuff earlier on actually, which was super interesting.

    8. DS

      So are you, uh, older or younger than your actual age?

    9. CW

      I am 31 in real years, and the inside of my body's 36-

    10. DS

      Oh, wow. Yeah.

    11. CW

      ... unfortunately. Um, that is because glucose being out of range-

    12. DS

      Mm-hmm.

    13. CW

      ... weighs very heavily. Um, and the only thing I've got is slightly out of range glucose, and my lipids are a tiny little bit out as well. So I need to eat soluble fiber.

    14. DS

      Yeah. You'll, you'll enjoy that. Um... (laughs)

    15. CW

      (laughs) Soluble fiber, when I was looking at the list of potential groups of foods, it was just 20 different types of beans.

    16. DS

      (laughs)

    17. CW

      And I was like, "I have-"

    18. DS

      Oh, no.

    19. CW

      "... I have no types of beans in my diet." Like, are baked beans, like does that count as a bean? Uh, I-

    20. DS

      I'm sure it does. It has the desired effect, I bet.

  2. 2:12 – 5:37

    Sinclair’s lab and the aging-research ecosystem (academia + biotech)

    1. CW

      It does indeed. So the first question I've got for you, what, what do you do here? I know we're in Harvard Medical School. (laughs) I haven't got the first idea about what it is that you do.

    2. DS

      Well, so I, I come in every day to my lab. Uh, there's about 30 to 35 people in, in my lab. Um, and I instruct them to discover really cool stuff. And that's basically my job. Uh, and they'll come to me and they'll say, "I've got an idea to discover something." And I'll say, "That sounds good, go do it." Or, "That sounds really boring, don't bother doing it. And by the way, how much is that gonna cost?" And they'll tell me, "It's gonna cost about $2 million."

    3. CW

      (laughs)

    4. DS

      So it's my job to bring in the money and let them, uh, figure it out. But the theme of my lab is focused on aging, and has been since I started the lab, uh, about 20 years ago here at Harvard. And so I, I run a center for aging research here, and we are really working, uh, not just on trying to understand why we age, but also how do we slow down and reverse that process as well.

    5. CW

      And that's all being conducted here, but also offsite at one of your multiple companies? Or is it mostly here or is it... How does it work?

    6. DS

      Well, there's a giant ecosystem. Um, this is the Menlo Park version, uh, of the ecosystem where we do the very basic discovery. We can ask fundamental questions about what is the clock of aging? Uh, can we reprogram the body? Is it safe? Uh, and can we extend lifespan? Mostly of animals we work with here. Uh, these are, um, laboratory animals. Uh, outside of the university is, uh, a network of companies, um, institutes, colleagues, collaborators, um, literally thousands of people around the globe. Uh, Europe, Asia, Australia, and others, uh, all working with us on trying to understand these questions, answers to these questions. But also what makes my lab rare, uh, and unusual is we're very innovative. So that we file patents once every few months. We spin out a company, uh, at least a couple times a year. Uh, and the reason for doing that is not because... Well, I do like starting companies, but that's not why I do it.

    7. CW

      (laughs)

    8. DS

      Uh, I do it because I'm not satisfied with just publishing work. I feel that my role on this planet, if I have one, is to try and help people with their lives. To live longer and healthier and more productively. And just making a discovery in a yeast cell or a mouse isn't doing it for me. That's just part of what I'm here for.

    9. CW

      You need to apply that as well.

    10. DS

      Exactly. So most of the companies that come out of this lab are biotech companies working on medicines, but we also do a whole range of other things. We have biosecurity, so protecting the world from pathogens and, and other nasty things that can go on. Um, we also work on bioinformatics, so trying to understand... So like InsideTracker, how do you estimate somebody's age and help them with their living and what they're eating? Um, but mostly it's molecules that we hope will be drugs one day to not just treat one particular disease of aging, say diabetes or heart disease or cancer, but to have a radical type of medicine, uh, that would actually slow down all diseases as, at once with a single pill.

  3. 5:37 – 6:49

    Is there an “anti-aging pill”? Why slowing aging may be easier than curing cancer

    1. CW

      Is it likely that there is a, I don't know whether panacea is the right word, but a out there, a particular way to manipulate molecules, which will be, uh, the equivalent of an aging panacea?

    2. DS

      Uh, well, there certainly will be. Uh, a lot of people who hear that we're close to finding something that'll slow down aging, um, they're right to be skeptical because-

    3. CW

      It sounds like turning back time, right?... like, literally feels like, "Oh, you're slowing down aging? Yeah, cool. And can I go and get in a DeLorean at the same time, please? Is that all right?"

    4. DS

      Right. But actually figuring out how to slow down aging or reverse time is, is a lot easier than building a time machine.

    5. CW

      (laughs)

    6. DS

      And I think it's gonna be easier than curing cancer. Uh, it's not that hard. We actually understand as a field over the last 20 years what controls aging. We have genes in our body called longevity genes that slow the process down. And in recent breakthroughs, just in the last couple of years, uh, the field and my lab have discovered that you can reprogram the body and reset the body's clock to be young again. And when I say body, I mean it's still in the l- in the lab. But we hope that within a couple of years, we'll be actually be doing human clinical trials to literally reverse aging in cells.

  4. 6:49 – 8:23

    Three intervention strategies: defenses, senescent cells, and partial reprogramming

    1. CW

      What's the mechanism that this works on? Can you take us through it?

    2. DS

      Yeah. Well, there are three main approaches that we're taking, um, and I'll just summarize them. The first that we've been doing for a long time is activating the body's defenses against aging. So normally, you have to be hungry or exercise to do that. We found genes and molecules that you can give to animals and to people actually that slow down the effects of aging. So that's one. So that, think of that as activating the body's natural defenses against deterioration and disease. That, we've been doing for 20 years at least. The second is to delete cells that are actually causing the problem. So there are cells called senescent cells that you might think of as zombie cells, and those zombie cells are causing havoc, and you can actually get rid of them. And when you do that in a mouse, it'll live longer and be healthier. Then the third approach, which is much more recent but much more powerful than any of those, is called partial cellular reprogramming. And, uh, my lab and some others have actually shown, just a few others around the world, that currently, if you put a combination of resetting genes into cells in the dish and actually in an animal, you can quite literally reverse the age of those cells so that they become young again. And in mice, what we're discovering, we're writing these papers up now, is that you can drive aging forward and accelerate it with this technology, and you can reverse it just as easily and make cells behave as though they're almost embryonic.

  5. 8:23 – 10:06

    Optic-nerve regeneration in mice: reversing age to restore function

    1. DS

      I'll give you an example.

    2. CW

      Yes.

    3. DS

      When we're, when we're born, one of the first things that ages in our body is our, is our spinal cord and our central nervous system. And you, you might say, "Well, David, why do you say it's aging?" Well, a young neuron will be able to repair itself and regrow. But we know that if we damage our eye, our optic nerve, or our spine, we're never gonna walk again or see again. But if you're young or if you're a salamander, you can actually regrow the, the central nervous system. So we've got ways now of reprogramming those cells or an entire mouse to make it ostensibly younger again, and they regrow their optic nerves so that they can see again.

    4. CW

      That sounds like science fiction.

    5. DS

      I thought so too. Um, but in May this past year, 2018, um, one of my students who was working on this, Juan Cheng, he thought it was never gonna work, but he thought he'd try it anyway. So he injected this gene combination into the eye of a mouse, and he damaged the optic nerve so that it was all dying-

    6. CW

      Mm-hmm.

    7. DS

      ... turned on the system, and it grew back. And he texted me the picture and said, "I cannot believe this is working." And I said, "You know what? I can see the future right now." And, uh, he's since tested it on glaucoma, which is damage due to eye pressure. He's tested on, on just on regular old mice that don't have good vision. You know, I'm f- almost 50, and I can already tell my retina's not as good as it used to be. Uh, we can actually treat old mice and get them to see like a young mouse within just a few weeks.

  6. 10:06 – 14:23

    The epigenetic clock and the “tennis game” model of aging (information loss)

    1. CW

      (sighs) I, to me, aging feels a little bit like the passage of time. So it feels like something that you are along for the ride with, and it would appear that that's not quite the case and that... I think I'm a good avatar for the layperson. Um, I understand that cells regenerate, and I think that your entire body, every cell is redone within a particularly... not a hugely long window of time. Um, but for some reason, the concept of them actually growing or getting younger just seems at odds. It feels like we would be going back in time.

    2. DS

      Well, we're going back in age. Uh, and you can disconnect biological age from chronological age. The... one of the main reasons I believe we age is that, uh, we have a... we, we have what's called an epigenetic clock that ticks over as we get older due to time, but also how we treat our bodies. If we smoke, we don't exercise, or we're obese, the clock will tick faster. But now that we understand what the clock is, we're finding that we can actually revert that age and get the biological clock to go backward, not just slow it down. And so those nerve cells that I was talking about regenerating, we do literally make them biologically young again. And how that actually happens is on the cutting edge of science right now. But we have some clues as to how the cell is accessing the youthful information that is locked away inside it.

    3. CW

      Can you explain how that works?

    4. DS

      I can to the very extent of what is known to science right now.

    5. CW

      Yes. Your best, your best idea. Is it what's on this whiteboard? Is that it?

    6. DS

      Some of it. That's a messy diagram that I drew trying to explain it. Uh-

    7. CW

      It looks like bunches of grapes. Those are some mice running towards other mice. That's a little boat at sea.

    8. DS

      (laughs)

    9. CW

      Um, that is... that's a cloud. That's a cloud with birds coming out of it.

    10. DS

      That's exactly right.

    11. CW

      Cricket-

    12. DS

      You've solved it.

    13. CW

      Cricket balls there at the top.

    14. DS

      Yep, yep. Actually, that's a tennis game within our cells literally.

    15. CW

      (laughs)

    16. DS

      Maybe not, not literally, we don't have tennis balls.

    17. CW

      (laughs)

    18. DS

      But what we do have are proteins that act like tennis balls that bounce around inside the cells going from one thing to another, and that's a tennis game. And what we've discovered is that normally those tennis balls, those proteins will sit on parts of the genome to tell a cell it's a liver cell, or it's a brain cell, muscle cell.

    19. CW

      So it doesn't regenerate the wrong thing?

    20. DS

      Right.

    21. CW

      Okay.

    22. DS

      Right. And those are laid down, those structures in the cells are laid down when we're born. So a l- muscle cell is not gonna give rise to two liver cells, it's gonna give rise to more muscle cells.

    23. CW

      Yes.

    24. DS

      And we understand pretty much how that works. These proteins that sit on the DNA, they control which genes are on and which are off at any one time.

    25. CW

      Okay.

    26. DS

      But those balls actually get distracted. And so th- here's where the tennis analogy comes in. We can distract those proteins by doing things to the cell. One really great way of distracting them is to break a chromosome, and then those proteins, they panic and the cell pulls them to the break to help repair the broken chromosome, leaving those genes at, to, to wreak havoc for a short period. But then once the repair is complete, they'll go back and reestablish that program again, so that the liver cell stays a liver cell. The problem is with the tennis analogy, if you keep whacking balls back and forth over 70 or 80 years, you're gonna lose balls. You're gonna not hit them back to where they came from, and it ends up being a huge mess. And so there's balls scattered all over the court-

    27. CW

      Mm-hmm.

    28. DS

      ... or in this case, the, those proteins that were once laid down in the right place to turn the cell, the s- the genes on at the right time are now scattered all over the, the cell, the nucleus and the cell loses its identity. So a liver cell is ... an old liver cell is more like other cells in the body, and actually they forget to be liver cells.

    29. CW

      Okay. So can you explain the difference between what would look like a young cell and what would look like an old cell? Or what is, (phone ringing) what categorizes that? That's someone who needs to know what a young liver and an old liver cell look like. That's what that person is.

    30. DS

      Well, I can pretty much guarantee you that it's someone calling me to find out how much of a certain molecule they should ingest.

  7. 14:23 – 24:29

    Public interest, long-form science, and fear of death as a driver

    1. CW

      Is that really what you're getting at the moment?

    2. DS

      Uh, hundreds of emails a day, yeah.

    3. CW

      Really?

    4. DS

      It's a lot. Um-

    5. CW

      I mean, this is the Joe Rogan effect, isn't it?

    6. DS

      Well, it's always been a lot, but yeah, Joe, uh, did, uh, increase the level-

    7. CW

      Orders of magnitude.

    8. DS

      ... of interest, for sure. Uh, also, you know, um, um, fairly rare as a scientist, I talk about research as it's happening.

    9. CW

      Mm-hmm.

    10. DS

      And it's, it sparked people's imagination.

    11. CW

      To segue briefly here, um, one of my friends who spends a fair bit of time on Reddit, uh, mentioned that him and some of his buddies loved the episode that you'd done with Joe. And that they were part of the, uh, r/longevity, uh, thread, uh, on Reddit. And, uh, he just decided that he would post, um, "One of my buddies is going to go and do a podcast with Professor David Sinclair. Does anyone have any questions?" And I thought it would be like, I don't know, th- sh- "How many, how many pieces of fruit and veg should I eat a day?" Or, uh, "How long is the optimal window of a fast? Like, you know, 16:8 or should I be doing like a, a, a 18:6?" Or whatever it might be. And the list of questions that I had to try and translate, I've not even ... uh, they're in Evernote, but they're just staying there because I can't pronounce half of the words that are in there.

    12. DS

      (laughs)

    13. CW

      But I think one of the things that it definitely did identify to me is that-

    14. DS

      Yeah.

    15. CW

      ... uh, longevity at the moment appears to be a very emerging field within kind of the, the general public or becoming more of a, a general public concern.

    16. DS

      Yeah.

    17. CW

      Um, I mean, everyone's aging, right?

    18. DS

      Right. Well, we've always been aging as a species for ... ever since we were, you know, primordial cells in the soup four billion years ago. Uh, and we've always been conscious of our mortality. But I think there are two things happening, Chris. One is that the science is mature, and it's no longer an if, it's just a when. We have the technology. We understand how to slow down aging, maybe even reverse it. And the other is that the world I see is bifurcating into two types of people. Uh, those that wanna understand a topic in detail, so your listeners are those type of people, and God bless them. Um, this is the level of detail that typically members of the public would never know about. Uh, and then the rest of the world watches cats playing pianos and stuff. But-

    19. CW

      (laughs)

    20. DS

      ... thank goodness there are people who really care about the world and what's happening and, and wanna learn in detail beyond what, uh, typically a newspaper used to tell people.

    21. CW

      I agree. Uh, I think that we've emancipated the ability for people to, uh, to learn, uh, in as much detail as they want. And there is a, there is a horse for every course, uh, with regards to what people want to learn. Um, you're totally right, that for myself, I ... w- we get comments all the time on the, on the YouTube videos and stuff, like a too long, didn't read, like, "Can someone do a TL;DR of this particular podcast?" And I'm like, "I- i- if you want a shortened version of this, there's someone ... or if you want to watch something which is short, YouTube is awash with three and four-minute videos. Like, feel free to go and watch that." I particularly, and I know that the listeners do as well, they enjoy the nuance and the subtlety and the detail and, and deconstructing things down to its component parts over the course of one, two hours. That's what I think is important. And it definitely sounds like that's helping people to buy into more difficult topics potentially like this.

    22. DS

      Oh, for sure. Uh, because when a newspaper reporter, not all of them, but many of them over the, my career, which now spans 25, 30 years, uh, they latch onto this, and it's always hyped. "Oh, we're gonna live forever. You should drink more red wine." Blah, blah, blah.

    23. CW

      (laughs)

    24. DS

      And I can tell you as a scientist who's spent his career working on the cutting edge of research at Harvard Medical School, publishing in the world's best scientific journals, it's really frustrating. And it, it's actually taken a lot of willpower to make it through those times, because the nu- almost every time what I say comes out-... changed, misshapen-

    25. CW

      And you get a bastardized version of whatever it is that you've said.

    26. DS

      And no wonder the public says, "Yeah, this is another stupid story-

    27. CW

      Mm-hmm.

    28. DS

      ... it can't be true." But if you listen to two hours of someone like me talking, uh, you really do realize that the science is way more advanced than people ever knew about. And as a scientist, I, I just, you know, thank heaven, thank people like you-

    29. CW

      (laughs)

    30. DS

      ... who can actually allow people like me to, to reach many people at a level that never was possible before.

  8. 24:29 – 30:21

    Ethics and safety: CRISPR babies, consent, and “enhancement” slippery slopes

    1. DS

      Um, where I think people get uncomfortable with this technology is, um, so we now understand that there are genes that control how long we live. There's one, for example, called FOXO, which is turned on in whales and longer-lived animals than us. There are even human variants. Uh, my children were lucky enough, two of them out of three, to inherit two really good copies of, of this longevity gene. And so they're probably gonna live a lot longer than, than my wife and I will. Um, so we, we know a lot about that. So, why does this get weird? Well, now that we can CRISPR engineer babies, what's gonna happen when the world's most, uh, intent helicopter parent wants a kid that can live to 120? That's probably doable right now. Whether or not we should is another question.

    2. CW

      Whose job is it to work out whether or not we should?

    3. DS

      Well, right now there's a worldwide debate amongst scientists about whether we should come out against it. Uh, interestingly, when, when human stem cells were first discovered, uh, and that you could reprogram cells and clone animals, there was a, a much greater backlash. Uh, you probably remember the, the Blair Bush days where there were all these in- these committees set up and it was banned here in the US, blah, blah, blah. We had something just as big happen, uh, last year, was that a Chinese researcher, a professor, he had a couple of, uh ... well, engineered a couple of twins, twin girls who were res- are resistant, going to be resistant to HIV infection, and he engino- engineered those genetically. Now, there was a little bit of upset. Lot of scientists got upset because this was announced without any warning at a scientific conference. There was no oversight, there was no consultation with governments or other scientists. So, the shock really took us all by surprise. But there was no major backlash. There hasn't been yet. There hasn't been any outlawing. You certainly don't hear a lot of backlash at the higher levels of government over here in the US, at least. Um, I think that's healthy. I think that what we've got is a very rational debate and that we shouldn't just overreact just because something feels weird or isn't, has never been done before.

    4. CW

      Mm-hmm.

    5. DS

      Now, we need to discuss, uh, not just the ethics but is it safe? And that, I think safety is more important than, than ethics actually. Um, and what I mean by that is someone's ethics might be different than yours. I mean, usually, uh, I come down on the side of freedom to, to do things as long as they're safe and that they're beneficial, um, and there's some consent. Um, but in this case, what's tricky is the ch- your children don't have consent. So, that's why I think-

    6. CW

      Mm-hmm.

    7. DS

      ... it's, it's a hard one. But what if your child was definitely going to get, say, a dominant genetic disease and there was no way to get around it except, um, either have new parents-

    8. CW

      Mm-hmm.

    9. DS

      ... or don't breed, um, or to, uh, have an abortion?

    10. CW

      What would be an example of a dominant genetic disease?

    11. DS

      Uh, so Huntingdon's for example. If both parents have Huntingdon's, you can ... or even one, you can have a, a child with Huntingdon's. Um, I mean, you can always select the embryo, but maybe you don't wanna kill embryos, so maybe you could create, uh, an embryo that you go in with this CRISPR editing system and chop out the bad Huntingdon's gene and create a healthy child. That should be doable.

    12. CW

      There's a big ethical question there, isn't there?

    13. DS

      Uh, well, the- there is, though i- if you're making people healthier and not suffer, I always say that that's what we humans have always done. That's why we invented aspirin and antibiotics. We're just going into a new era where we can really have a big effect because it's not just on one person's life, it's generations forever-

    14. CW

      Mm-hmm.

    15. DS

      ... beyond that person.

    16. CW

      What's the second order, third order, fourth order effect of this particular decision?

    17. DS

      Yeah.

    18. CW

      I guess the, the more subtle, the more subtle question is, between Huntingdon's disease and a, a healthy, uh, human baby, the line appears to be quite clear, uh, as what is preferable. But as the fidelity of that becomes, "Well, I've got two ginger parents and my dad got bullied at school for being ginger, like, I don't wanna have a ginger child," uh, you know, where do we begin to draw the line here? Because in essence all we're talking about at the lowest or the highest resolution is preference.

    19. DS

      It is, and then it gets really crazy when parents say, "I want the smartest kid I can have," uh, or, "The best-looking kid."

    20. CW

      Can we identify the, uh, contributing factors to that?

    21. DS

      Well, there, there was a gene published last year that is thought to contribute to, to human intelligence and speech-

    22. CW

      Mm-hmm.

    23. DS

      ... uh, that differentiate, differentiates us from the chimps. And perhaps having more copies of that gene could make us smarter. We don't know that yet. So, I think that that's still in science, the realm of science fiction. But, you know, looking ahead 30 years from now, you could probably engineer your child to have these traits of-

    24. CW

      Mm-hmm.

    25. DS

      ... certainly height, disease resistance, we can protect against cardiovascular disease. Um, and what about intelligence and longevity? Um, and then we also, it gets into a crazy zone where imagine a hundred years from now that you can have a- an army of clones or of people who are robust, who heal better, don't bleed out, they don't get diseases.

    26. CW

      Super soldiers.

    27. DS

      Yeah. I mean, this is not beyond possibility in terms of technology today-

    28. CW

      Mm-hmm.

    29. DS

      ... here in the, uh, the second decade of the 21st century. 22nd century, it's gonna be quite something to see. And biology, getting back to the iPhone, I think biology is gonna really make a much bigger difference to our lives than any electronic technology.

    30. CW

      Wikipedia.

  9. 30:21 – 32:58

    Chimeras, organ supply, and the real-world tradeoffs of bioengineering

    1. CW

      I do love Wikipedia. Um, did you listen to Alex Jones on Joe Rogan, the most recent one?

    2. DS

      I did, yeah.

    3. CW

      Um, I mean, I don't really even know where to start with that. But the, the-... trans human-animal hybrids in the flesh farms, wherever it is. Like, is, is, that the sort of thing that's doable at the moment with current technology?

    4. DS

      Oh, (sighs) yeah, we, we do create, uh, chime- chimeric animals, uh, in the lab.

    5. CW

      Right. Yeah.

    6. DS

      Uh, and so-

    7. CW

      What's-

    8. DS

      ... that, the Island of Dr. More-

    9. CW

      Can you define chime- chimeric, please?

    10. DS

      Well, admit to, it's a, an organism that's comprised of cells with different genomes. And, uh, so it's a, it's a mixed organism. And yeah, we, we could do that but, uh, I mean, that, that to me seems highly unethical and even unnecessary.

    11. CW

      Well, I, I think everyone would, would agree that that's the case. But it doesn't necessarily stop the technology from occurring. And I suppose the line between how do you... What if you had to do a lot of iterations of chimera, um, proliferation, and X number of years from then you would develop this unbelievable new, uh, solution to something you've been looking to work on? Does the cost-

    12. DS

      Yeah.

    13. CW

      ... outweigh the, the benefit?

    14. DS

      Right. Well, I think we all, we all have personal views on that. Um, one area that I think is really interesting in this building right here at Harvard Medical School is, uh, whether or not you think it's okay to use animal organs for humans. And so one of the reasons we don't use pig, uh, livers for transplant is they're full of pig viruses. But George Church in his, uh, spin-out company are actually removing those viruses, cutting them out of the pig genome so that these livers might be useful. Um, and you might say, "Well, we, we shouldn't be breeding pigs to, to have transplants." But if we're eating the rest of the animal and throwing away the livers, why not?

    15. CW

      That's a very good question. I'll be interested to hear what the listeners think about that particular ethical dilemma about, I suppose, the vegans and the vegetarians might be firmly on one side of that already. They don't need-

    16. DS

      (laughs)

    17. CW

      It doesn't matter whether or not the liver's going into someone's body. I think they, they've already made their stance on that.

    18. DS

      Yeah, I, I would charge the, the listeners with the following thought. What if it was your mother or your child who needed a liver transplant and there were none available, would you sacrifice a pig?

    19. CW

      That is a difficult question to answer, isn't it?

    20. DS

      Mm-hmm.

  10. 32:58 – 36:59

    What you can do now: eat less, fast, and trigger longevity pathways

    1. CW

      So moving back onto the, uh, questions that you get all of the time ringing through the phone. What are the, um... What would you say are the foundational, uh, strategies that people right now should be looking to incorporate into their lives to improve longevity?

    2. DS

      Right. Well, one of the, the reasons that this field is, is taking off also is because there are things that people can do right now that we've learned are actually helpful for turning on these longevity genetic pathways. Uh, if I could give one piece of advice, only one, uh, and I will give more, but if I could only give one, the most important thing would be eat less. Eating less has been shown for, for centuries, but also in labs for the last 70, 80 years to be extremely effective in extending lifespan of everything from yeast cells, to worms, to flies, to mice, to monkeys. And if humans don't live longer for fasting and calorie restriction, then, then we'd be the exception on the planet. And I don't believe that we're an exceptional species, biologically speaking. Um, so eat less. What does that mean? Well, nobody knows what the perfect diet is. I get a lot of those questions.

    3. CW

      What should I eat?

    4. DS

      What should I... Well, what you eat is important, but when you eat and how much you eat are just as important as well. Uh, so why don't I, I give you an example of what I do as, as... You know, I do a fair bit of research and I've come up with my own best practices. Um, so I do intermittent fasting. And now there are a variety of those, and I think many of your listeners probably know them by name. But there, there's fast every other day, there's fast, uh, two days out of five, there's, uh, skip breakfast and perhaps have a late lunch and don't have a late dinner as well. Uh, that's the one that I prefer. I find it easier to skip breakfast and have a late lunch than to really go through days of, of being hungry. I can't tolerate it for too long. But I don't mind hunger pains for a few hours. Um, on top of that, uh, I take a, a drug called Metformin, which is prescribed for diabe- diabetics, type 2 diabetics, age-associated diabetes, which has two main effects. First of all, obviously, it low- lowers blood glucose. That's what it's prescribed for, for, for patients. Uh, but it also is, is quite rough on people's stomach, and I find that it actually stopped me from being hungry.

    5. CW

      It curbs the hunger pangs.

    6. DS

      Yeah, it really is effective. And so I have the kind of biology, uh, and so does my son, uh, that we like to eat. We feel hunger s- more strongly apparently than other people. We're kind of like Labradors of the human world. Uh, but we also gain weight, uh, rapidly. We put on muscle, but we also gain weight pretty quickly. And so I would... If I was allowed to eat what I wanted to without a lot of mental power and a little bit of help from Metformin, I would be quite an obese person. And, and my son, uh, God bless him, he hopefully is not listening to this podcast, he's put on a lot of weight. Uh, he's 11 years old and we go into the gym, but, uh, you can see that it's, it's pretty hard for people with our genotype to, uh, keep the weight off. And so-

    7. CW

      His body's raring at the, chomping at the bit to get bigger?

    8. DS

      Well, it is, it is. And so he's, he's getting strong, but he's also covered in a layer of fat. And so my point is that if I can do it, and you know, I'm, I've got a BMI of about 21, 22.

    9. CW

      Mm-hmm.

    10. DS

      If I can do it, anyone can.

    11. CW

      'Cause you are genetically predisposed to have a, a poor thin person, uh, body type?

    12. DS

      Yeah. Well, you know, my, my father, uh, it- was prone to obesity. He has di- he has diabetes. And his grandmother, well, my grandmother, his mother, had a stroke in her 30s and-... had type 2 diabetes. So my, I, I have half Ashkenazi Jew genetics-

    13. CW

      Mm-hmm.

    14. DS

      ... coming out of Hungary. Sinclair is not my real family name. It's Szigeti. Uh, those genes are pretty crap when it comes to longevity and, uh, so we're fighting it, my, my father, my son, myself, trying to live at least a normal lifespan.

  11. 36:59 – 49:09

    Mechanisms: sirtuins, NAD, mTOR/AMPK, and the survival tradeoff

    1. CW

      I understand. So you mentioned that fasting is effective due to calorie restriction. What's the mechanism that that works on?

    2. DS

      Right. So we didn't know how calorie restriction worked until recently, and it's exciting we understand it. So how does it work? Well, this is partly what we've discovered in my lab. There's many others in the world as well, but we can put a little brick in the wall for that. We showed that there are longevity genes. Uh, they've got the name sirtuin. Um, actually named after a ye- yeast gene called SIR2. And that gene controls which genes are switched on and which genes are switched off. It's called a silent information regulator. That's what SIR2 stands for. And this gene really gets back to that clock of aging that I started talking about earlier. It controls which genes should be off to maintain youth, but over time, it actually gets distracted and goes to other places to repair broken chromosomes, for example, and ends up causing a yeast cell to lose its identity. It actually bec- loses its sexual identity, becomes sterile, and that's a hallmark of yeast aging. So what that tells us is that there are genes in a yeast cell that control its longevity. Turns out if you give a yeast cell more SIR2 genes or more copies of SIR2, it'll live longer. Um, take it away, it'll live shorter. Okay, so that's the fundamental knowledge that you need to understand what I'm about to tell you. SIR2 makes a protein that controls these, the epigenome, these genes, but it, it doesn't work well unless it has a molecule in the cell called NAD. The long-term... The long, uh, word for that is nicotinamide, uh, adenine dinucleotide, but let's call it NAD.

    3. CW

      NAD is much better, yeah.

    4. DS

      Yeah, NAD or nad, some people call it, but it should be called NAD.

    5. CW

      Let's not call it nad. I'm British.

    6. DS

      Don't call it nad.

    7. CW

      I'm British and nads are not, not what I want to be taking.

    8. DS

      No, it... Well, you know, some people want larger nads.

    9. CW

      That's true (laughs) .

    10. DS

      We, we have, we have nad boosters in the lab. That's what, that's what my dad takes. So these nad, NAD boosters, the relevance of that is that these SIR2 proteins, these sirtuins in, in our body, they don't work well unless they have a lot of NAD in the cell. Uh, as we get older, and even as yeast cells get older, they lose their NAD so that by the time you're 50 years old, uh, like me, you have about half the levels of NAD that you had when you were 20. Without the NAD, the sirtuins are lazy. They don't control the genes of youth well, and they don't repair broken DNA well, and that leads to aging in organisms, we believe, among other things. But that's one of the main causes. So what does calorie restriction and fasting have to do with it? By fasting and calorie restricting, we actually boost the levels of NAD in the cell so that those repair genes and those protectors of the, of the genome sirtuins are more active. That's one of the explanations for calorie restriction. There are other genes that control aging. There's one called mTOR. There's one called AMP kinase. And all of these longevity pathways that I'm telling you about are boosted by fasting. And so we think that by being hungry, what you're really doing in a general sense is telling the body, "I'm under threat. I might be dead in a month from now. My food supply is running out. I'm gonna hunker down. I'm gonna build a stronger body. I'm gonna survive. I'm gonna breed less." Remember, the yeast cells become sterile. We become less fertile if we're starving as well, by the way.

    11. CW

      (laughs)

    12. DS

      Especially women. Um, and that's a survival response that we kick into action just by being hungry or by exercising for that matter.

    13. CW

      Is that one of the reasons why bodybuilders when they diet down for a show and they're at super low body fat will have trouble with, uh, maintaining erections and, and sex drive and things like that? Is that likely to be the same pathway?

    14. DS

      Well, so I didn't know that for a fact. Uh, but it perfectly makes sense that it's a balance between growth and reproduction and hunkering down and surviving. And we call this the disposable soma theory. So this is actually a, a Brit, uh, Tom Kirkwood dis- pro- proposed this back in the 1970s. And the idea is that species as a whole and individuals also are exercising a trade-off between growing fast and reproducing and hunkering down and building a body that lasts a long time. So by stimulating growth and reproduction, so if you take a lot of testosterone, that triggers a lot of growth, take a lot of protein, amino acids, it's great. Bodybuilding, you'll repair things better, but it's probably at the expense of building a long-lasting body eventually-

    15. CW

      Mm-hmm.

    16. DS

      ... that, that may run out. So you might wanna pulse between growth and reproduction and then shut it down a little bit by fasting. And so testosterone is one of those molecules that tells the body, "Grow muscle."

    17. CW

      Mm-hmm.

    18. DS

      Which is shut down by being hungry, so you'd survive.

    19. CW

      So the, the actual hunger itself, is it the sensation of being hungry that causes this beneficial effect? Or is it the fact that the blood glucose is lower? Is it- what's the actual mechanism that it's working on?

    20. DS

      Well, it, it's actually thought to be both based on mouse experiments. If you cut back on calories, but still fill the stomach with cellulose, that is sufficient to extend lifespan. So part of it is the, the biochemical response to low calories and low amino acid.

    21. CW

      Okay.

    22. DS

      But it's not everything. Uh, so the, the-... uh, uh, th- 'cause you can be full, uh, and you can still get the benefits of low calories.

    23. CW

      That's interesting.

    24. DS

      Right? But on the other hand, some people have done the opposite, which is, uh, give a lot of calories but stimulate hunger. And you can do that by tweaking the brain in, in ways.

    25. CW

      Like in- i- increasing ghrelin release and stuff like that.

    26. DS

      Exactly. Uh, and w- people can also tweak the hypothalamus, uh, which, uh, in itself can extend the lifespan of an animal.

    27. CW

      True. I mean, tweaking the hypothalamus sounds-

    28. DS

      (laughs)

    29. CW

      ... like a terrifying (laughs) thing to do. It's not taking your car in to get the MOT done or have a service. It's like poking your brain.

    30. DS

      Right, it's changing glucocorticoids which signal to the body that it's hungry or it needs to grow, uh, and that also extends lifespan. Uh-

  12. 49:09 – 55:28

    Practical stack and cautions: exercise, metformin, NAD boosters, resveratrol, hormones

    1. DS

      Sure. Well, what I do is I, uh, besides intermittent fasting, uh, I also exercise. Uh, exercise is the other thing that raises NAD and boosts these longevity pathways. And we've also known, uh, for centuries that this is healthy, right? Uh, so we're not discovering anything that new other than what types of exercise seem to activate these longevity pathways the best. And what seems to work best is the high-intensity interval training, is to get the body stressed. So just as intermittent fasting tricks the body into thinking your food's running out, exercise is tricking the body into thinking-

    2. CW

      Something's chasing after it.

    3. DS

      ... "I might have to run a-a marathon," or yeah, exactly, there's a saber-toothed tiger in town, um, or cat. So that- that's exactly right. So the- the high intensity seems to really stimulate the body's defense networks even more than just a- a long walk or- or a- a- a steady long run.

    4. CW

      Mm-hmm.

    5. DS

      It's all about varying it, right? The high, the low. So intermittent fasting, it's- it's food, no food, and intensity training is running, stop, running, stop, hypoxia, ox- oxygen, hypoxia. And it's that up and down that seems to work really well. That's why whatever you're doing, do something different and get your body into shock. So the- the thing to think about is... The concept is called hormesis, but really it- the c- concept of hormesis is just whatever doesn't kill you makes you stronger and longer lived, by the way.

    6. CW

      (laughs)

    7. DS

      So keep your body on edge.

    8. CW

      It sounds like all of the things that are good for you are really uncomfortable or a lot of the things that are good for you.

    9. DS

      Yeah. Well, that's the say- I think people say, "Oh, why is cake taste so- why does it taste so good?" And why doesn't sitting on the couch feel good?

    10. CW

      (laughs)

    11. DS

      Uh, no, other way around, "Why doesn't exercise feel good?"

    12. CW

      Yeah.

    13. DS

      "And why is sitting on the couch bad for you?" Um, I mean, that's exactly the reason, is that you've got to put your body in the- this slight painful experience to get it to react. Otherwise, it becomes complacent and your body just falls apart.

    14. CW

      It'd be nice if cake extended your life though, wouldn't it? It'd be fantastic if that was the case. Um, so what (laughs) what else- what else is it that- that you're doing?

    15. DS

      What else? Well, so I mentioned metformin. That's been a- a recent change, uh-

    16. CW

      Is that-

    17. DS

      ... an addition.

    18. CW

      Some of this- some of this is, uh, available without prescription, but I think metformin is something which you do need a prescription for, is that right?

    19. DS

      In Western countries, yeah.

    20. CW

      Okay.

    21. DS

      In Eastern countries less so.

    22. CW

      Over the counter?

    23. DS

      Well, yes, in Thailand.

    24. CW

      You can get everything in Thailand over the counter.

    25. DS

      Yeah. You can, and- and actually it's smart of them, I think, because they- they have rampant diabetes like we do, and metformin is one of the safest drugs in the world. Uh, you'll get an upset stomach. It's extremely rare that there's anything more serious than that. Um, it's not perfectly safe. No drug is. Um, but in terms of drugs, this one's pretty safe. It's a derivative of a molecule from the French lilac. It's an- basically a version of a plant molecule. Uh, so anyway, so I take metformin, uh, every morning. Uh, sometimes I vary it, you know, I'm not strict with everything, but sometimes it's half a gram, sometimes it- it's a gram.

    26. CW

      Mm-hmm.

    27. DS

      A typical diabetic will take somewhere between a gram and two grams, so it's a bit below that.

    28. CW

      Mm-hmm.

    29. DS

      Uh, what else do I do? Let's get this all on the table.

    30. CW

      Throw it out there, come on.

  13. 55:28 – 1:00:31

    When to start longevity interventions: aging begins before birth, but start early after adulthood

    1. CW

      Um, one question that did come out of the Reddit furor, which I think was actually pretty pertinent, was when do you think that people should begin thinking about longevity? Obviously, we think about health our whole lives. Like, we don't just let the kids go loose on a b- uh, like a bag of sugar. But is there... you know, should people be taking NAD at 18 years old?

    2. DS

      I love that question because, uh, I have new answers to that based on new research, partly in this lab.

    3. CW

      Unleash it. Unleash it on the world, Dave.

    4. DS

      So, so here-

    5. CW

      The internet is waiting.

    6. DS

      Here is something that almost f- no scientist, let alone in the public, understands. The clock of aging, the epigenetic clock that we measure and other scientists have published now just a few months ago, begins even before birth. We are aging constantly.

    7. CW

      Oh, shit.

    8. DS

      Yep.

    9. CW

      Okay. (laughs)

    10. DS

      Uh, and it actually tracks with development. Girls who go through puberty early have a faster aging clock that's ticking.

    11. CW

      So they're old- older?

    12. DS

      They're older. They're literally older. So even though you think you look old, you're actually getting older. And you might age faster than others. It'll show up later in your life, but it's pretty scary, right? So the other thing that we know is that if your mother, while you were in her uterus, ate certain foods, you can be predisposed either to obesity and diabetes or to health and longer life, which is crazy. So you might... one answer could be the earlier, the better. Even before you're born, you should be working on this. (laughs)

    13. CW

      (laughs) Give you NAD as an embryo.

    14. DS

      Yeah, right.

    15. CW

      (laughs)

    16. DS

      If you've got, you know, helicopter parents who'll genetically engineer you-

    17. CW

      Yeah. Yeah.

    18. DS

      ... and feed you the right food and... anyway. But I... the other, the other answer is, um, and this is a, a really important one, is that in, in animal studies, in mouse studies particularly, the earlier we start, after development of course, we're not gonna, uh, calorie restrict or interfere with these pathways before an animal reaches adulthood.

    19. CW

      Mm-hmm.

    20. DS

      Let alone a person. But after adulthood, say 24, 25, uh, equivalent of a mouse-

    21. CW

      Mm-hmm.

    22. DS

      ... we put them on these regimes of molecules or genes and that's where you get the biggest bang for your buck. Start early.

    23. CW

      Mm-hmm.

    24. DS

      Uh, if we start mid-life, let's say on a 50-year-old equivalent of a mouse, you get about half the effect of, of when you start early. Uh, and that's why actually, uh, I've been... I started way early compared to my peers-

    25. CW

      Mm-hmm.

    26. DS

      ... my scientific peers. I started resveratrol when I was in my early 30s.

    27. CW

      Mm-hmm.

    28. DS

      And I probably would've started earlier knowing now, if I knew then what I know now.

    29. CW

      Well, I guess when you're talking maybe 10, 20 years ago it's this experimental drug, no one really knows what the effects are and you're just like, "Ah, fuck it. Might make me live longer, I better just take it."

    30. DS

      Exactly.

  14. 1:00:31 – 1:04:48

    Big-picture mission: aging as disease, funding urgency, economics, and population fears

    1. DS

      Yes. Uh, there's no question that I wake up every, up every day, and most days, uh, I pinch myself that I'm in this position. Uh, it hasn't been easy and it's been not just hard work, I don't mind working hard, I love what I do. But it's been, uh, there's been criticism, there's been ups and downs, um, getting to-

    2. CW

      There was nearly a bankrupt company at one point, wasn't there, and you took a big risk at some point. I think there was a...

    3. DS

      Ah, sure. I mean-There's been so many things. So I've helped build about 15 companies and they all go through strife and running out of money. And a lot, most of the money that I make, I pour back into companies.

    4. CW

      Mm-hmm.

    5. DS

      Um, you know, I've made more money than I would ever know what to do with. But what I want to do with that is, is pour it back in. And so my wife chews her fingernails because, you know, we're, we're multi- multimillionaires for about a month until I find a way to get rid of it.

    6. CW

      (laughs) The next, the next

    7. NA

      cool thing comes along.

    8. DS

      I don't want the money. I want to see that humanity progresses. I wanna see what the future holds. I want us to get to the future faster and that's my way of doing it. But anyway, the adversity, all scientists get criticized if they stick their neck out to do something that's different, whether it's discovering a longevity gene or saying that we could live longer or saying that aging is a disease, which I truly believe it is. All of those things have been tough. But fortunately I, I'm very stubborn and I, I'm not taking my eye off, off the prize in the end, which is that we all get to live ... Hopefully all of us get to live longer, more productive lives. And when we do that, uh, we'll look back at today and think, "What were we thinking? Why weren't we doing a, um, Manhattan Project," or maybe, maybe I should call it the, a moon shot on this, because it's so important. Um, one of the things I truly believe is that we look at all the problems on the planet; it's global warming, there's, um, poverty, uh, there's bankruptcy for countries, or at least economic burden of people being sick. All of these are real problems. Social security, um, welfare in, uh, around the world. I think the, the biggest solution to that, um, and admittedly I'm somewhat biased but I do crunch the numbers on this, is if we can solve people's health and make them more productive for another 10 years, maybe even longer, but 10 years would be enough to save trillions of dollars every year across the planet. Even in the US it would be a saving in the tens of trillions of dollars. This is money that can be put to work saving the economy and working on other big problems that we need to solve, like the, saving the environment, saving species, uh, preventing global warming.

    9. CW

      Would there be an issue of over-population with that?

    10. DS

      Yeah, good question. It, it ... There's no question that if people aren't dying as fast as they, they would, there will be more people. But it's not as many as you might think. If we stopped everybody dying today, uh, and which we can't do that, but if nobody died again, the rate of population growth would be less than the rate of immigration here in the US, which, um, you know, the government's trying to limit that as well.

    11. CW

      Yeah.

    12. DS

      Uh, but it's, it's not as though suddenly there's, there's five times as many people. Uh, and the good news is that, that we're not gonna stop aging any time soon, we're just going to hopefully live another five to 10 years. What that means is, though, that, uh, we'll probably plateau around 10 billion, maybe up to 13 billion. But most of that problem is not driven by people living longer, it's driven by the birth rate. And over the last decade we've seen an extraordinary change in our birth rate as a species and it's going down all the time and going to plateau. The World Health Organization and the UN have agreed, and Bill Gates has given a wonderful podcast on this, that we're gonna plateau out over the next 30 years and we're not gonna be overrun with humans. In fact, places like Europe and Asia are, especially Japan, are struggling with not enough-

    13. CW

      Need some more humans.

    14. DS

      ... babies. Exactly, more humans. But what you wanna do is also preserve the productivity of the older people. So when we look at a, a 70-year-old now we think, "That's an old person." 10 years from now, 20 years from now, 70 will be middle-aged, uh, well, we certainly see that happening already. Look at Tom Cruise. He's ... What's he now? In his mid-50s, he's riding motorcycles.

    15. CW

      He's, he's easily 105 and he looks-

    16. DS

      Looks great.

    17. CW

      ... fantastic. Straight out of Cocktail-

    18. DS

      Right.

  15. 1:04:48 – 1:14:39

    Can humans live 1000 years? Rejuvenation cycles via reprogramming and “longevity escape velocity”

    1. CW

      ... Top Gun. And I couldn't agree more. That, that was the question that I wanted to finish on, was, um, well, two parts. Firstly, would it be possible to make someone live for a really inordinate amount of time, like a thousand years? Is that possible? Presuming they don't, you know, get shot or one of the easier ways of, uh, of killing someone that we identified earlier on. Is there, is there a realistic upper limit on the amount of time that a organism could live?

    2. DS

      Well, we know that there, there isn't. There are immortal organisms on the planet. There are trees that live for thousands of years. There are jellyfish that go on hydra, these little jellyfish-like things, they live for, for seemingly immor- immort- uh, go for immortality. The, the mistake that, that most people have is that they think that there is a biological limit to humans. And they look at human history and they say, "Looking back in time, there's never been anyone who, as far as we know, has lived beyond 122." And even that's doubtful.

    3. CW

      Mm-hmm.

    4. DS

      That's been, that's been challenged.

    5. CW

      I was in the Guinness Book of World Records, uh, store on Hollywood Boulevard a couple of days ago and they had the photo of the guy that was 120 that was the oldest certified, I think. But I mean, I'm going to guess-

    6. DS

      Yeah.

    7. CW

      ... that the standards to which you hold your research may be a little bit higher than that, that the Guinness Book of Records does.

    8. DS

      Well, whether or not, uh, Jeanne Calment in France lived to 120 or not doesn't matter. Um, there are still plenty of people who make it to 115, 117. So let's say that's the, the current limit. But looking backwards doesn't tell you the, the future when it comes to technology. When you looked at the Wright Brothers, looking backwards from 1902 doesn't really tell you that we're gonna go to the moon within 60 years. Uh, so that actually happened. Um, so what I, I think is that there is no biological limit to human lifespan. We are living things. We fix ourselves, we repair ourselves. Uh, we succumb to entropy, no question. We, we lose information over time. But what we've discovered with this reprogramming stuff is that we can regain information that-... is still there as we get older. We just need to access it. Those genes are still there to make us young. We just need to tell the cell to read the right genes at the right time and we can reverse aging. Um, um, we don't know how many times you can reverse aging. But it's possible you could. Uh, so let me tell you a s- a bit of a story but it's based on results in the lab. You know how I was telling you we can reprogram neurons to grow again? We can actually use that same virus to infect an entire mouse and turn on these reprogramming genes and get the mouse, we think, to, to be younger. That's what we're working on. So imagine a future where you could have your genome changed so that you have these reprogramming factors injected. So I'll, I'll come along, Chris, today. We can go to my lab. If we wanted to, literally, I could take a vial of the virus. I could get, give you an injection and it would be compatible with your body and you would be genetically modified to be able to be reprogrammed. Now, we've engineered that virus, literally, we have done this, to be turned on by an antibiotic called doxycycline which you can go get from your doctor.

    9. CW

      I've been on it for a while. I've been on and off it for the last few years, yeah. It's used as a, a ... Doxytetracycline is used as a acne drug.

    10. DS

      Yes, or anti-malarial or if you have Lyme disease here in the US. It's pretty safe. I mean, you wouldn't wanna take a long time-

    11. CW

      Be careful you don't accidentally take that when you've got this super gene that's potentially active inside of you.

    12. DS

      Well, he- so here's the thing. We ... Imagine a future where you now have this virus in your body and it's switched off. You've ... nothing's happening to you. But you start to, uh, experience aging. Let's say you're starting to build up cardiovascular disease in your, in your veins or you're losing your memory. How about you just take antibiotic for a few weeks, your reprogramming factors come on, your body gets rejuvenated, it finds the youthful information, your nerve cells remember how to be nerve cells again and you get rejuvenated. You go back another decade. You don't go, don't go too far. You stop taking the antibiotic before it causes a tumor or something really bad. Um, and you get reset and then you wait another 20 years and you turn it back on and you get rejuvenated time and time again. And maybe that's the path to, to living for a thousand years. But for the first time in my career I can actually see how it would be possible to do that.

    13. CW

      It was just conjecture before whereas now there's, there's an actual mechanism, there's a pathway?

    14. DS

      It wasn't even conjecture. It was insanity to think that it was possible.

    15. CW

      (laughs)

    16. DS

      And anyone who would say that we could live a thousand years was considered crazy. And I, I'm on record saying that the first person who's born today could live to 150. Uh, and I get criticized by a lot of people for saying that 'cause it sounds outrageous. Um, and I don't know if that's true but I do know that someone who's born today is most likely going to make it to the year, what, 2220 at least?

    17. CW

      Mm-hmm.

    18. DS

      What kind of technologies will they have then?

    19. CW

      You're totally right and I suppose as well if, as you've suggested today, aging is a ... not only something which can be paused at its current point, uh, and kind of held where it is, but can also be reversed, it means that as soon as sufficiently sophisticated technology becomes available, everyone who is alive at that time is potentially brought back to wherever they need to be.

    20. DS

      Right. And actually the longer you live, the longer you get to live.

    21. CW

      Yeah. (laughs) Yeah, which is very bizarre.

    22. DS

      Yeah.

    23. CW

      So everybody should be working on not getting shot and not stepping out into open traffic and not eating cake, not sitting on a couch.

    24. DS

      Yeah.

    25. CW

      Because the longer that you live is the potential that you'll get towards being around when we do have this particular solution.

    26. DS

      Yeah, I th- I think the number is every year you live, you get another three months extra of life. Uh-

    27. CW

      That's so crazy. (laughs)

    28. DS

      Yeah. Uh, it gets kind of weird when you, when you get to technology where every year you live you get another year to live.

    29. CW

      Wow. That's like the, um, uh ... It's not Dunbar's number, but what's the one that talks about, uh, processing power doubling every three years?

    30. DS

      Mm-hmm.

Episode duration: 1:14:39

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