Question for you: what if you could slow down, stop or even reverse your aging process? What if you could live, not just longer, but better? Extending and even potentially expanding your physical and mental health and well-being. Staving off decline or illness. Is any of that really possible, and what does cutting-edge science have to say?
That is what we are talking about with today’s guest. David Sinclair. David is a worldwide leader in aging research. He is a Professor in the Department of Genetics and co-Director of the Paul F. Glenn Center for Biology of Aging Research at Harvard Medical School.
He’s best known for his work on genes and small molecules that delay aging, including the sirtuin genes and resveratrol and its precursors, which we get into. He’s published over 170 scientific studies, is the co-inventor on over 50 patents, has co-founded 14 biotechnology companies in the area of aging vaccines, diabetes, fertility Cancer Biodefense. His book Lifespan, Why We Age, and Why We Don’t Have To explores what we get wrong about aging and how to approach it differently. And, his podcast, Lifespan, explores healthy aging and how to live not just longer, but better, too.
So excited to share this Best Of conversation with you.
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Jonathan Fields: Okay, so question for you. What if you could slow down time? What if you could stop or even reverse the aging process? What if you could live not just longer, but better, extending, and even potentially expanding your physical and mental Health and well-being staving off decline or illness? Is any of that really possible? And what does the latest science have to say about it? That is what we’re talking about with today’s guest, David Sinclair. So David, as a worldwide leader in aging research, he’s a professor in the Department of genetics and co-director of the Paul F. Glenn center for biology of aging research at Harvard Medical School. And he’s best known for his work on genes and small molecules that delay aging, including certain genes and resveratrol and its precursors. And we get into all of this in a lot of detail. He’s published over one hundred and seventy scientific studies is the co-inventor of over fifty patents and co-founded. Fourteen biotech companies in the area of aging, diabetes, fertility Cancer Biodefense, his book lifespan, why we age, and why we don’t have to explore is what we get wrong about aging and how to approach it differently. And his podcast lifespan also explores healthy aging. And how to live not just longer, but more well as well. So excited to share this best of conversation with you. I’m Jonathan Fields and this is Good Life Project.
Jonathan Fields: I’m curious about a number of different things and I figure we’ll touch down in a few different areas. I guess one of my early fascinations is I’m always curious about people’s personal choices about how they want to invest their energy in a body of work for their life. And so I’m curious about you, when you could have taken any number of paths when you decide to enter medicine. Why aging?
David Sinclair: While I like a challenge, I tend to go the opposite direction of anyone else. If everyone’s going off and studying computer science, I’ll avoid that. And it seemed to me that trying to figure out why people don’t live longer than they do was something No one else was really doing in a rigorous way. But really it goes back to when I was four years old, my grandmother was telling me the truth. She was a very honest and brutal person who raised me. And she said, David, your cat’s going to die. I think I was asking about my cat’s Health. Yeah, it’s going to die and I die. What does that mean? I was gone forever. You’ll never see it again. Really? Yeah, this can happen to your parents, can happen to me. It’s going to happen to you; for a four year old. That’s a real shock because I’d been raised on Disney movies and no one dies in Disney movie. And I think that happens to everybody around the age of four or five. But by the age of about seven to nine, we forget about it. And we have to because if we are constantly worried about dying, it’s pretty stressful. So we’ve evolved coping mechanisms and we typically don’t think about aging until much later in life. Fifty sixty, we start to see the end of life and we see our parents, grandparents pass away. But I’ve, since I think thanks to my grandmother, I’ve been unable to get that out of my mind. And I’m not so much worried about my own mortality. Some people think I’m, I’m worried about dying. Anyone who’s seen me drive, my Tesla knows, I’m not really worried about that. But I am worried about not doing the best I can for humanity. I’m a real fan of humans. And I want to leave this World a better place than I found it.
Jonathan Fields: When you start to go down this road. I mean, it’s interesting because to a certain extent, also you choose a focus, an area of focus that I think a lot of people actually don’t consider a problem, but rather just a fact. And that is Largely unchangeable. I think like a lot of the old paradigm is, well, this is what happens. We get old systems fail, you know, like things start to melt down. It seems like, you know, you hear, you know, well, no, they died of old age. Yeah. And it’s just kind of saying that that’s just the state of things, it’s not a disease to be fixed or cured. That’s just what happens.
David Sinclair: Well, we used to say that about cancer and heart disease and we don’t accept those things anymore. Cancer is just as natural as aging. So why do we rail against cancer and infectious disease? We’re trying to combat that right now. Why don’t we say, oh, that’s natural let, let nature take its course the same with aging. I think the world is in a stupor. That doesn’t understand that what’s causing most diseases on the planet from heart disease to cancer, to alzheimer’s is aging itself. Now, doctors are trained to treat diseases so they don’t think about really what’s causing them. Typically, they treat the symptoms. But the driver of what’s pushing us off the cliff is really the aging process. If turns out if we stay young and healthy and resilient, we wouldn’t get these diseases in the first place.
Jonathan Fields: Describe for me when we talk about aging, what’s the current understanding? What sort of like the current slash old model for understanding what this is?
David Sinclair: Oh, the old model or the current model
Jonathan Fields: Well, tell me what the distinction is.
David Sinclair: The reason I wrote the book mainly is that the science has gone through massive leaps and bounds to a point where we think we understand what’s driving aging. And the good news is we can actually do something about it. Now if you can’t do anything about it, like people two hundred years ago when it came to an infection, they basically accepted it. Go home, pack your things, you’re going to die, cut them off, maybe That’ll help. Once you can do something about it, then you can actually contemplate addressing it same with aging. The science is at a point now that we understand, we think what, not just how to slow it down, but actually totally reset the body to be young again. And if you’ve seen the kind of data that I’ve seen from Labs around the World and including my own at Harvard, you have this new sense of optimism that we can actually do something about this process. Not that we’re going to live forever or even two hundred years, but we are entering a World where we don’t have to accept aging as natural. And the other thing that we’ve seen, which is really empowering, is that only twenty percent of our lifespan is genetic. And the rest is up to how we live our lives.
Jonathan Fields: Deconstruct that a little bit.
David Sinclair: Well, there’s a study that was done in Denmark on twins, identical twins, and these twins were leading to very different lifestyles. You know, one’s smoking and eating hamburgers and the other one’s eating a plant based diet and exercising, to take extreme, extreme examples. And those twins were living dramatically different lives. So clearly it’s not all in the genes and that the number is twenty percent genetic and eighty percent, something else. And what I’ve put forth in the book is a new theory on why we age, and that is, it’s called the information theory of aging. And what we lose over time is actually information that we’re given as youngsters. It’s called epigenetic information. And we lose that over time if we don’t take care of our body. If we don’t do all the right things, which I list in my book on page three hundred and four, if people are interested, then we lose that information. Now you might be saying, Jonathan, you’re looking at me like, what’s this information? The information isn’t what you might think the information is in two forms in the body. One is genetic and that’s surprisingly largely intact in our bodies. Even when we’re all genetic, the DNA information is there. It’s this other type of information that reads the DNA that tells the cell you should be a nerve cell, you should be a liver. So that’s the epigenetic information. Much in the same way that a DVD to use an old device would be the genome and the reader of the DVD would be the epigenome or another way to think of it would be the genome is the piano and the pianist is the epigenome playing the notes and that aging is a simply a demented pianist. And what I’m excited about is that we can keep the pianist playing beautiful music for longer doing just the right things in our life. But also we’ve just discovered & we’re just about to publish that you can bring in a new pianist and reset the system like a, a software reboot. And if that’s true, then you know all bets are off, then we may be able to do things that we’ve only dreamed of. We already know there are animals on the planet that can regenerate whole limbs and even be immortal, like a jellyfish. And I think we’re finally tapping into those mechanisms for our own body.
Jonathan Fields: It’s the Holy Grail, right? And Yet at the same time, that’s the Holy Grail. And then, and I want actually to like, go into that more with you. But zooming the lens out, you know, there are also these sort of bigger ethical and moral questions about, well, what if humans actually could live? Maybe not indefinitely. I read somewhere once in the study that even if you, your body actually could stay the same age at somewhere around three hundred years old. Your likelihood of death is one hundred percent through accidental means. So this sort of like this cut off almost anybody like you’re going to get. Yeah, like something’s going to happen here. But, you know, if, if, in fact, we can do this, if we can expand lifespan, double it, maybe what is then the effect on society was the effect on the planet, you know, and all these sort of like bigger conversations. Yeah.
David Sinclair: So the last third of my book covers this, because if I’m going to work on this, I have to think about its implications. That’s my responsibility. The good news is that this isn’t going to happen tomorrow. We cannot stop aging tomorrow. You know, I’m optimistic but I’m not that optimistic. And society will evolve similar to how we adapted to kids not dying in, you know, childbirth with their mothers and limbs not being amputated anymore. We adapt and I use the analogy of old London in eighteen thirty, where people were dying in droves from cholera. And in those days, London was overpopulated. A lot of pollution. Fast forward now to the city where there’s three times as many people and people are living utopian dreams in that city with restaurants and shops and no disease except for maybe recently. That is the future that I think we will have, which is that if we live longer and relatively free of disease, let’s say we can all make it to one hundred. Even let’s say one hundred and fifty. You know, if we really dream without getting Cancer and heart disease, we’re going to live in a World where, yeah, it will be different. We can’t retire at sixty five anymore. That’s just not enough young people to take care of. You know, the bank accounts of the older, but it’s a tradeoff, right? Would you rather get cancer at seventy and die a horrible death over the next ten years? Or would you rather have a world where you would have to be more conservative with resources and take, you know, a greater care of the world around us in exchange not worry about getting these diseases until much later?
Jonathan Fields: Well, hopefully we reach a point where we get to grapple with that. Yeah, when we’re talking about aging also, so you talk about the loss of information. How does that manifest physically in the process of what actually unfolds in the body?
David Sinclair: Yes, so we, we typically use mice to check this out. They don’t live as long as humans, so we can go a bit faster. And we can create aging, we can speed it up. We can also slow it down and reverse it. And we’ve been able to disrupt the epigenome in a way that speeds up the aging process in older tissues, gray hair, wrinkles, skin and all the good stuff that comes with aging. Those mice become fragile. But we can also now reset the system and get the epigenome to go back to the way it was. There’s information, there’s a backup of that information some way we haven’t found exactly where it is, but we know how to tap it in using a special gene therapy that we’ve discovered. And when we do that, we get us amazing. Some amazing things. So we can take old mice that have just aged naturally and become blind like a human would. And we can give the gene therapy in their eye and they get their vision back just like they’re young again. Now those sorts of things give me, well, a lot of optimism, but also some pause to think what is the future going to look like if we can do that to the eye? Can we reset the body, the epigenome of the entire body? And how many times can we do that? Now we’ve done it once in a mouse, it looks to be very safe. We haven’t seen any evidence of increased cancer or illness. These mice are quite happy, especially even if we give it in whole body. It doesn’t hurt them, and of course safety first, right? We don’t want to cause harm. But imagine if you could reset more than once you, you reset your body and go back twenty years. And then you age out twenty years and go back and reset again. That would be an incredible future, but also one that’s kind of scary because we’re not used to thinking about life that way.
Jonathan Fields: Yeah, I mean all the times that you’ve said, if I had only known what I know now when I was twenty or thirty and be able to sort of like, have that physical and emotional capacity at this. Yeah. Like at this age and you’re effectively saying that there may be a future where you can more or less do that.
David Sinclair: Yeah, and it raises really interesting questions about biology. So one question would be if you reset the age of the entire brain. So we’ve just done the optic nerve, but the brain is very similar stuff. What happens to the brain? Does alzheimer’s go away? If you make the brain young again? I’m betting that it will, but what happens to memories? Do you retain memories and wisdom or do you lose it? And I’m hypothesizing, betting, as a scientist that you will retain your memories. In fact, you may even recover lost memories because your nerves will now function better.
Jonathan Fields: And it is an interesting question, right? Because if, if memory is stored in some massive complex, you know, like neuronal set of connections and, and in some way, shape or form, the reset has a risk of altering that in some way.
David Sinclair: Right, right, we’ll see maybe your, your emotions will go back to being immature. We don’t know, but we’re testing that right now.
Jonathan Fields: Yeah, I mean, because some of sure there’s some, there’s some things that you would like to get back, but also there’s a, there’s a seasoning. There’s a wisdom, there’s all these things that took time to develop that. You don’t want to reset. Yeah. Along with it. And it’s fascinating when we talk about aging at how are we, how do we measure that these days? Because I think, you know, people think chronological age, you know, I’m fifty four. So that’s my age. But in fact, it’s much more nuance and maybe in fact there are much better markers for this.
David Sinclair: There are and there brand new systems. So the epigenome is directed in part by what are called DNA methylation. So that’s just a complex way of saying chemicals that get added to your DNA, and we can read those with a machine that’s as big as a Snickers bar in the lab. It’s not that complicated sounds, but it’s not any high School student can do this. So I could take, Dorothy, I could take your DNA today, a swab of your mouth and in a couple of days, come back and tell you exactly how old you are. Not how old you are based on birthday candles, but biologically, are you above or below the average human for your age? And if you’ve taken care of yourself, then you should be under that line and younger and vice versa. If you’ve smoked and not exercised and eating a bunch of fat and become obese, you are typically older than your actual age for an average human. And that’s good and bad news. The bad news is that you might be older than you think you are. But the good news is that aging, as I mentioned, is malleable. You can take your age and slow it down and possibly even reverse aspects of your age, just by changing certain things in the lifestyle which we should talk about. And these are changes that I’ve made in my life and my family. We do special things to try to prolong health. But the fact that you can get a mathematical now read out of your true age is, is revolutionary. It tells us, first of all that the epigenome probably is linked to aging and this information theory is probably right. Not proven, but indicated. And it also says that we can much more quickly test interventions. In other words, instead of waiting forty years to see if taking supplement, X works, why don’t we just test it for a year or two and see if your clock goes back. And now we’re at that point.
Jonathan Fields: A lot of folks have been speaking to our have been focusing on telomeres, measuring Telomere length. And based on the assumption that they start to shrink as you age and that if they are longer than the average person, your age, that in fact, you know, similarly you’re actually sort of like, by Telomere. You know, like measurement younger than your chronological age. How is that right? Is that not? Is that being replaced by this new metric?
David Sinclair: Well, so the information theory of aging attempts to explain all of the changes that occur with, with age, including Telomere shortening. So there are about eight or nine, depending on who you ask, what we call hallmarks of aging. Telomere shortening is one of those. So others, people might be curious, are things like loss of stem cells, mitochondrial dysfunction, nutrient regulation, proteostasis is your ability to renew your proteins. These hallmarks of aging are considered separate entities. Right now they’re drawn as a pie chart by scientists. But what I’m proposing is that there’s a unifying cause that leads to all of these, including Telomere shortening. And it turns out that the proteins that we study, they have a name called sirtuins. That’s seven different flavors of them, types in the body. At least two of them are protecting the ends of chromosomes, the telomeres. And so in my theory, I can explain how this is all linked together and the loss of information in the body includes the shortening of the telomeres.
Jonathan Fields: So that’s basically one contributor, one component is different things and this is so it’s almost like your measure becomes the meta marker.
David Sinclair: Yeah, that’s exactly right. And telomeres are an okay measure of your age, but it turns out they’re Much more variable and they can get longer, they can get shorter. We’ve actually learned that they’re not as accurate as the actual DNA methylation clock that I was describing, which is also known as the Horvath clock, named after my friend Steve Horvath, who discovered it
Jonathan Fields: You also you brought up is one of those components. Mitochondria Mitochondrial function, which, you know, immediately, my brain goes back to middle School, the power plant of the cell. And this is where we get our energy. This is where ATP is, you know, goes out into the body. And but, but it seems like there’s also been a lot of focus on that, similar to telomeres on Mitochondria and their dysfunction over time as a real contributor to, to every element of aging. So it, if it folds into this mean a marker is, I guess I’m curious, am I getting it right in the way I’m describing Mitochondria. And I’m curious, yes. About how that really contributes to the experience of aging.
David Sinclair: Yeah, no doubt Mitochondria declines with aging. And what we’ve discovered is that the reason they decline mainly is that the epigenome isn’t, isn’t preserved, the inflammation in the body to turn on the right genes isn’t preserved. And what we’ve discovered, actually in my lab is that it’s very easy to reverse Mitochondrial dysfunction. And decay during aging. We published a paper a few years ago just by triggering a pathway that we work on getting these sirtuins to work better. The Mitochondria could be totally rejuvenated. So if again we take a mouse, it’s old. It’s got Mitochondria that are producing Much less energy, less ATP by the old idea about aging, which is, it’s all about free, radical damage, and mutations that should be irreversible, right? As you lose inflammation of your DNA, you’re not going to get it back. Like if you break off a piece of a DVD, it’s not going to come back, you smash a piano, it’s not going to play music. But I’m saying no, the piano is intact, the DVD is still there, you just need to read it again. So in our treatment in our paper we showed that within just a few days, we can rejuvenate the Mitochondria back to being young again just by tweaking the epigenome. And that tells me that the, the DNA is intact. Largely, it’s just the cells, forgetting how to read that DNA.
Jonathan Fields: So it’s not so much that the CD is scratched, it’s the reader that’s having trouble.
David Sinclair: Well, it’s both they both have the same effect. I think a scratched CD is a good analogy actually that if you can just polish the CD, you’ll be able to read the music underneath. And that’s what our, our methods are doing. Actually, it’s just allowing that laser beam to hit the right pits in the, the silver lining of a CD for any young people listening, CDs of these things. We used to put music on and you could fit about three photos on there. That’s really amazing technology.
Jonathan Fields: Once upon a time they replaced floppy disks and computers.
Jonathan Fields: It’s interesting and you know, epigenetics first came into my orbit when I and they were described as okay, so you have your DNA, which essentially is like that the code which is relatively fixed except for damage that can happen to it over time, which degrades it. But then there’s this, you know, is, are they, is, there’s the expression of it, which actually is what affects us
David Sinclair: And that’s the epigenome.
Jonathan Fields: Right. And then, you know, whether they’re turned on or turned off, or whatever the state is effectively is that overlay,
David Sinclair: That’s the, the actually, the most important information in our bodies is how to read the right genes the right time. And make sure the cells are functional. And so what we’ve found actually is that if you can reset the epigenome cells that are dysfunctional and causing disease such as blindness, the body heals itself, comes back and also resets all of those defects. So Mitochondria, rejuvenated the telomeres, come back in their length. All of those things that we think are actual causes of aging, we think are stemming from this loss of the epigenetic information that allows the genes to be read. I mean, we should have known this a long time ago, really if you look at the evidence ever since the first frog was cloned from, from a tadpole. And now we have dogs and sheep and cats that live normal lifespans, Barbra Streisand, cloned her two dogs. These animals are healthy, so what that says is that adult cells have all the information to be immortal. You just need to tell the cells how to read those genes again.
Jonathan Fields: So I guess what’s popping into my head also then is, why do we lose this information?
David Sinclair: Well, that’s been what we’ve been working on for twenty years now. And what we think is going on is that the proteins that control which genes should be on and off, become distracted by other things. One of the main distractions that causes them to leave their posts. So I don’t know if I want to get into how genes are regulated, but essentially there are proteins that sit on DNA and tell it to either be shut off, which is what we study this or twins are gene silencing proteins. They’re also proteins that turn genes on, okay? And part of that process is DNA packaging. If you bundle up DNA really tightly, like a hose reel, it doesn’t get turned on. Whereas if you open it up, pull out the hose reel. Now the genes tend to come on, those proteins are very important because they, they tell genes whether they’re on or off. But those proteins have other functions. For instance, the sirtuins that we work on. Three of them, at least out of seven, need to repair broken DNA. So if you break a DNA, which is happening all the time in our body, a trillion times in our bodies, the day, those proteins get distracted, they have to go off and they repair the DNA. But they also have to find their way back to where they came from to gene X from one earlier, similar to when Hurricane Sandy destroyed the South and the Army Corps of engineers had to go off and repair those things. But they had to find their way back home and pay bills and mow the lawn and whatever. And if that game, call it a game of ping pong of moving things out, coming back. What I’m saying is that over time, that doesn’t reset.
Jonathan Fields: So effectively a bit, there’s too Much work to do for too few of these things too few. So they become overwhelmed and you lose. You either lose adequate DNA repair or the sort of like the epigenetic effect of keeping things young and healthy.
David Sinclair: Exactly. That’s what’s going on, and that’s why if we stimulate the sirtuins, if we make more of them by leading a healthy lifestyle, or eating the right foods, or even taking some supplements that we think might help. Then what happens is we give the sirtuins enough energy to do both activities at the same time.
Jonathan Fields: What is it? So you said, and you know, there’s DNA damage going on in our body trying times day. What’s that caused by in the first place? I mean, you know, if, you know, on the one hand, yes let’s, let’s supercharge our so to, and so that they can actually do both jobs, what’s actually leading to the DNA damage. And is there a way to lessen that or slow it down, that would also help the entire situation?
David Sinclair: Well, the good news is the sirtuins are sensing the cellular environment. When they think that the body is under threat of survival, they’ll be more active. And you can do that a few ways. You can encourage the body to make more protein. So too, and protein. And you can do that by being hungry or exercising. And there are two other ways to turn on sirtuins. One is to give them more fuel, they actually their enzymes, they need fuel to maintain the epigenome. And that fuel comes in the form of little molecule called NAD, which our body makes, but actually makes less as we get older. And then the third way is that there are molecules produced by our body or in our food that we eat. That also are like the accelerator on the sirtuins and rev them up.
Jonathan Fields: Let’s walk through some of those. But first you also mentioned, I guess food and exercise and I slipped in there. But, but food in particular, and I guess this has been a really hot trend over the last couple of years is the idea of fasting or intermittent fasting. There are all these different variations of these things, and I know people have pointed to different Mechanisms why they think it’s helping in different ways, whether it’s weight loss, reducing inflammation. But you’re kind of suggesting something different happening in relation to that.
David Sinclair: Again, it’s putting the body in a state of fear, fear that food is going to run out. And now you don’t want to starve. You don’t want to have malnutrition. But if you are hungry for part of the day or part of the week, your body biologically says, Holy crap, I could run out of food here. I need to build survival mechanisms and so it ends up doing that. And one of the ways it does that is through these sirtuin enzymes that preserve the epigenome but also help repair things or repair DNA fix the proteins. Now when you, when you’re hungry, a few things happen that are really good. In the short run, you will raise your energy levels, so sirtuins have more fuel. You’ll make more sirtuins themselves, so there’s more enzymes around to do the job. You’ll also break down fat. And what we’ve just learned, thanks to another lab that published this a month ago, is that the breakdown of fat produces oleic acid, which is a monounsaturated fatty acid. Like acid is an activator one of these accelerator pedals. All of this or to him. Like I said, may be familiar to people who study food. You get it also from guess what? Olive oil, avocados, all the things that we’ve learned seem to correlate with Better Health. So what I’m saying is, when you’re hungry, you’re activating your CO2 in defenses against aging and disease in many different ways.
Jonathan Fields: So maybe that’s actually, maybe not like the entirety of the underlying mechanism, but a healthy part of it. When people talk about the benefits of some version of fasting,
David Sinclair: Well, it’s a large part of it, and some of the evidence comes from work that we’ve done where we can take molecules that accelerate this sirtuins. So one is resveratrol from red wine, which most people have heard our lab work on. Now if we, if we give a mouse that’s on a Western diet its obese, it’s going to live a short lifespan like a lot of us tend to do with our lives. And we just give it resveratrol. That’s the only thing we’ve changed in its diet, makes it only the food. Their bodies are as healthy and as long lived as a mouse that eats a healthy lean diet. What does that tell me? It tells me that with a small intervention just by activating the sirtuins, you can mimic fasting. And it’s probably true, and this is now more speculation because we haven’t done the experiment. But when you eat Olive oil or take like acid in your mimicking fasting, as though your body is degrading your fat and it, it perfectly explains why this Mediterranean diet is so healthy. Now, I’m not saying it’s everything, of course. There’s no such thing as one thing does everything. But I think a large part of it is correct is that when you’re fasting, it’s not that you have less inflammation and that’s all it happens even less free radicals. What’s happening is that you’re turning on these defenses in your body, partly through these sartiuns, and you get less inflammation because of these defenses. If we knock out the sirt1 gene or some of these sartiuns genes which we can do in a mouse, and then we fast them or give them caloric restriction, then the benefits go away. You need these genes for it to work.
Jonathan Fields: So clearly then that is a huge part of the mechanism if not the mechanism, right?
David Sinclair: So I get a little frustrated, but I’m a little too busy to get too frustrated with this anti-oxidant idea that if we just take these molecules that are antioxidants, that’s the whole story. That’s nineteen eighty science, we’ve moved beyond all of that.
Jonathan Fields: Well, I mean, because I think a lot of people still do use the word anyhow accident and think about it. You know, that was, you know, your body. I think it has a lot of the original theory on aging. Your body’s experiencing Oxidative stress, you’re essentially rusting from the inside out. And there are these things that will stop the process or fight it. And battle free radicals, but you’re saying that’s really not the paradigm.
David Sinclair: No, no, I mean there’s a lot of attempts to use antioxidants to mop up free radicals and extend the lifespan of live animals. And almost all of those have been failures. It’s a real disappointment. We learnt that in the nineteen nineties, but I think the whole antioxidant story is a good marketing ploy. Billions of dollars of drinks and food sold under that premise. But it’s not true. We actually need free radicals for a lot of biology for the immune system. And there’s a theory, I guess it’s kind of not theory anymore. It’s called my toe or missus, which is that Mitochondria need to produce free radicals for longevity, benefits. We study in the field, these nematode worms because they only live for a few weeks. If you make a worm long lived by knocking out say it’s insulin signaling pathway. If you then give it a free radical quencher of an antioxidant, it live shorter.
Jonathan Fields: Hmm.
David Sinclair: An exercise needs free radicals. If you mop up free radicals, you’re not going to have the benefits as much of exercise. So really and oh, and the other thing I want to tell Jonathan is that if you take resveratrol, which some people call a quote unquote antioxidant. It’s a very weekend toxin and by the way, we can chemically modify resveratrol, so it’s not an antioxidant, but it still activates sertuin genes, enzymes. Then it still gives the Health benefits even though it’s no longer an antioxidant.
Jonathan Fields: Yeah, so clearly that’s not the pathway there. I mean, what’s fascinating about the idea of taking something on the one hand, it, it makes it so much easier and accessible to a lot of people because we’ve all been told for generations. You know, it’s like watch what you eat and, and move your body like exercise is the healthiest thing that you can do. It’s like the best medicine out there. And, and in fact, I think when you look at a lot of the research, you see a tremendous benefit from staying active on a regular basis. Have this sort of like mixed feeling going on where it’s like on the one hand, if part of the research you’re showing now is saying that we can get nearly identical benefits from essentially taking something that we can from exercise and from fasting. Which a lot of people experience as not pleasant and huge compliance issue. So on the one hand, yes, it solves that. But on the other hand, are there also some benefits of things like, you know, like reasons to continue to do those things. And does that essentially give people permission to just never move their body again?
David Sinclair: It, it doesn’t. And that’s the reason that even though I take resveratrol, I’m still exercising. What we find in our studies is that the? Yeah, you get some benefits for exercise. You get benefits from fasting, you get benefits from taking resveratrol and Raising your energy levels. If you’re a mouse, probably a human too. But when you combine them all, that’s when you get the biggest bang for the buck. So it’s, it’s not an excuse to just sit around and pop a pill at all. In fact, if you want to be healthy in ninety your nineties, you’ve got to do all those things I think, or at least many of them, for instance. So we can raise NAD levels in a mouse, an old mouse, and it can run like a young mouse. But if we take that same mouse and we exercise it and raise NAD, then it’s double the effect. And so I’m, I’m not trying to say it’s an excuse to just sit around and watch movies and eat popcorn all day. Not at all.
Jonathan Fields: Right. So does it have the potential to reverse that part of the aging, you know, experience is a sort of a progressive loss of muscle mass and bone density. It will, it act on a level where it actually has a potential to, to stop and even reverse those.
David Sinclair: Well, so it was pretty easy to reverse the loss of blood flow in the muscle and the energy in the muscle, so that ATP goes back up. We haven’t found that it’s easy to reverse muscle loss. That’s been a struggle for a lot of scientists. We can a little bit. And so we’re working with NASA funding actually to try and preserve muscle mass and mimic exercise for astronauts so they don’t have to spend three hours on a treadmill every day. But it’s really hard. That aspect is harder than pretty Much everything except maybe hair loss and hair growing as the two tough ones. But, but here’s the, the good news is that it doesn’t take Much to preserve muscle mass actually. So I spend an hour working out a week. I’d like to do more, but I don’t have time. And that for me is maintaining my muscle mass. I’m now in my fifties, which it’s extremely important. I can’t emphasize enough to people who are listening. Please work out, please make sure that your legs, your hips, stay strong, especially after fifty because the number of people who die from a fall is, is it, it’s really scary. Not every ninety minutes, an American falls over and breaks a bone in their old age. And they don’t recover and that leads to to death. Eventually my grandmother had the same thing. She tripped on a carpet in her eighties and never recovered. So please keep the strength up. You’ve got to do that. And then also it’s, it’s very important to do high intensity exercise, not a lot. You don’t have to run marathons just fifteen minutes a week is certainly better than nothing. I’ve also now I’ve got a standing desk which has helped maintain my strength of my hips too. And I’m writing this book took a couple of years of sitting down. And by the end of it, I’ll tell you, I could not walk properly. I couldn’t run. I had what’s called a poor performance muscle cramps syndrome. It’s that muscle that runs through the hole in your hips. I. It took me a year to recover from that and I’m never going to go back to that. So I’m going to stand up whenever I write.
Jonathan Fields: Yeah, it’s funny, I’ve sort of been altering a lot of things. Also I go back and forth between standing desk and sitting because I spent a lot of time writing also. And I had to start into the whole new project and, and just like you have, have felt the profound and negative effect of doing that. And I think it gets, I feel like it gets harder and harder to recover from that. The older you get now maybe if I’m actually supplementing differently, behaving differently, but even so I think, you know, just the physical activity part of it, it takes longer to sort of like recoup what I’ve lost in terms of mobility and muscle mass and loss of pain that I’m really curious about this idea though that you are able to effectively reactivate so many of these contributors to the what we would call an aging. But muscle loss is still so elusive. Well, I’m just curious like why, what’s going on there?
David Sinclair: Well, we haven’t reset the epigenome in the muscle Yet. We’re going to do that. That’s one experiment that’s ongoing in my lab. My suspicion is that once we reactivate that and reset those cells, then they’ll respond exercise and walking and rebuild those muscles. But until we do that, I think that that’s, that’s the obstacle, right? So I’ve got a couple of different approaches in my toolbox. One is molecules that turn on the body’s defences and reverse some aspects of ageing. Mitochondrial function, blood flow, all of that was pretty easy. The hard part is you’re still dealing with cells that don’t read the CD properly. And so you know, it’s not perfect and it still scratches there. So my second thing in my toolbox, just in the last couple of years, which I talk about in the book. And actually I wrote the book while we’re making these discoveries. So the readers get the feeling of what it’s like to make them resetting the epigenome I think it changes everything. It means that those cells won’t just feel young, they’ll actually be young literally. And if I go in and measure the biological age of those cells, I won’t be able to tell that they’re old anymore. And then they will, I predict build muscle like, you know, your twelve year old again.
Jonathan Fields: I mean, what I mean, powerful in the context of just reversing the loss that we’ve always assumed is just kind of like what happens, you know, like you hit your mid years and then every year you, you know, the average person I think loses a half pound of muscle mass or something like that. But also in the context of the zooming the lens out to diseases that in some way involve muscle loss and muscle wasting. If there’s a need, I realized that some of those diseases also are neurological in basis. And it’s, you know, it’s the circuitry that actually stops the contraction of muscle which leads to accelerated living. But if you could potentially reverse all of that, I mean, the implications are pretty stunning, not just to aging, but to that. Things like that as well.
David Sinclair: Mm hmm. Yeah, so I was excited when we were able to make old mice run on a treadmill. Fifty percent further. In fact, they ran so far, the treadmill stopped working because mice weren’t supposed to run that far. What that led me to think was that the big problem with frailty in the elderly is that they stop exercising a. They don’t get the gains from it, but B, they don’t feel like they’ve got the energy. And often it’s too late once you become frail, but if you could reverse that and get people out of their chairs and out of their beds to move again, you know, get the benefits of exercise again. But that does remind me to say that you don’t want to get to that point if you can help it. You know, it’s all coming, but you can put it on. My father has to exercise three times a week to maintain what I can do with one bout of exercise, and he’s eighty. So to your point, it gets hotter and hotter as you get older. So start early so that you don’t have to try to regain it. You just want to maintain it at least.
Jonathan Fields: Yeah. But I’ve actually long agreed with you about this idea of the sort of like that. The exercise cart before the frailty horse, you know, it sort of, you know, does the fact that we become old, you know, like stop us from being able to move our body or the fact that we stop moving our body actually accelerate the process of being old which accelerates the process of muscle loss which accelerates us, not being able to move and it’s actually and then just Becomes this destructive cycle. That Becomes, I guess, I would imagine a certain point. Well, actually let me not imagine this before this conversation, I would imagine a certain point like the, the average person in that spin cycle would hit a tipping point where you really can’t go back. Is that true? And if so, do you think the work that you’re doing and other people are doing the work may in fact change that
David Sinclair: Yeah, it’ll certainly help get people back on the cycle, figuratively and literally. But I’ve seen some incredible things on social media where elderly old frail, obese, elderly people, male and female, have changed their lives and lost the weight and gone to the gym and become essentially fit happy people again. So I would say it’s almost never too late, but the longer you leave it, the harder it is.
Jonathan Fields: I want to jump back to, you reference resveratrol a number of times and you’re doing a lot of research on this and it sounds like it’s an incredible. There’s also research out there, at least that I’ve seen, and I’d love your lens on this that shows that. And maybe I’m not reading this, right. It’s not always beneficial that there’s a sort of a timed dose effect where it can be incredibly beneficial, but also consumed the wrong way. Becomes destructive Pro. Oxidative leads to, to the increase of cancer cells rather than the decrease of them is. So it seems like it’s not, you know.. am I reading that right?
David Sinclair: Well, so resveratrol isn’t known to cause Cancer. There’s a theory out there that raising an NAD could promote cancer. Okay. And that came out of a misinterpreted study from University of Washington. Unfortunately, the misinterpretation went viral and Scientific American wrote about it. And I guess now that we’re down that rabbit hole, the study showed that if you knock down the NAD levels in Cancer cells, they don’t grow as well. There’s a brain cancer in a mouse, which means that Cancer cells need NAD. It doesn’t mean if you raise an NAD, cancer cells are going to grow more. It’s like saying, if you take the wheels off a car it won’t move, but if you put tiny wheels on a car, it’ll go faster. That’s ridiculous. So I, I’ve done a lot of work both in mouse and Human studies. Now I wouldn’t say I know everything, we have much more work to do, but haven’t seen anything that makes me concerned that what I’m doing or my father is doing would cause cancer. Obviously, I wouldn’t do it if I thought that. But again, I’m not saying it’s all risk free either. We’re still learning. We’re all born probably one or two generations too early for us to know everything. But if we wait another one or two generations, we’re all dead. So you’ve got to take some risks and you know, it’s a calculated risk. Raising NAD does seem to actually slow down Cancer. We found in at least in mouse models. And the fact that we’re now in humans and done a lot of safety studies. And these are, these are separate groups from me, in hospitals. They’ve reviewed all the literature. If they’re allowing these trials to go forward, I think for now, there isn’t reason to panic about it.
Jonathan Fields: Yeah. Are you seeing now that you’ve made the jump from mass transit to human trials? Are you seeing the outcomes translate in a pretty linear way? Are they, are you seeing really similar things happen in humans that you saw in mouse?
David Sinclair: Well, what I can say is we’re seeing that it’s possible to raise the NAD levels in humans, a lot, two fold or more, which is what you’d get if you were a marathon runner or something like that. But we don’t, don’t know Yet if we can recapitulate, these other things like improvements in endurance and Mitochondrial activity. So that we should know by the end of this year allows those.
Jonathan Fields: Wow, it’s going quickly the research.
David Sinclair: Yeah, we just got FDA approval to go into patients to actually test whether they work or not. And but actually we’re not only testing older people, we’re also testing rare diseases. For instance, friedreich’s ataxia is a, is a Mitochondrial related disease.
Jonathan Fields: We recently had somebody on the podcast who has lived with that .
David Sinclair: Really? Yeah. Okay.
David Sinclair: Yeah. So that’s the other thing about aging research is that often we underestimate the value of the research. I know aging is important. No question, but also we’re talking about boosting the body’s defenses against frailty and injury in diseases beyond typical ones, which I say,friedreich’s ataxia is a good example. Viral infections. If you can boost the body’s immunity, then you can survive that as well
Jonathan Fields: In this day and age obviously big benefits there.
David Sinclair: Yeah, yeah. I mean it’s mostly the frail and the elderly that are succumbing to coronavirus. If we could magically, or even pharmaceutically, make old people young even temporarily while they were sick, then they wouldn’t die and we wouldn’t have this crisis.
Jonathan Fields: hmm.
Jonathan Fields: As you’re speaking, I’m noticing also you’re waving around your hand and there’s a little silver ring on it. And I have the stealth version of what I think is the same thing, is that an ora sleep ring?
David Sinclair: It is
Jonathan Fields: Which, which makes me curious also about the contribution of sleep to everything that we’re talking about.
David Sinclair: Yeah, so NAD and sirtuins also control the sleep wake cycle. That was, it’s well proven. And so your NAD levels go up and down throughout the day and if you take an energy boost or late at night, you probably won’t sleep very well. Conversely, as we get older, we have less energy and our sleep wake cycle gets disturbed. So all elderly people don’t sleep well. And jetlag is not good for us either. As we think of longevity and age and sleep as being intimately connected through this mechanism that I’m talking about. And if you’re not going to sleep well, then you’re not going to defend your body against aging long term. If you disrupt the sleep of a rat for a couple of weeks it’ll get diabetes. It’s that potent, oh wow. Yeah. So it’s very important to get a good night’s sleep, particularly the deep sleep.
Jonathan Fields: Yeah. And so, and you’re saying, NAD it potentially plays a role in the, in the quality of your sleep.
David Sinclair: Yeah, that’s, that’s agreed upon by scientists and there was a discovery about ten years ago. And so actually I find that anecdotally though, that if I take an NAD boosting molecule, when I arrive in Australia, I don’t get jetlag.
Jonathan Fields: So interesting too, because as you reference, you know, if the average person gets less and less sleep and you know, with every decade of their life and at the same time there’s a fairly similar relationship to reduction of NAD over that same window. I guess maybe there’s not research to prove it, but there’s an interesting correlation there. You know, whether it’s causation or not.
David Sinclair: Yeah, well again, it’s one of these negative feedback, horrible cycles that you don’t want to get on. We know that if we disrupt the certain gene, number one for two, and one, the mice will have disrupted sleep cycles and they’ll get premature aspects of aging. So it’s very clearly linked together. But yeah, it could be that, that the loss of NAD leads to the lack of sleep, which makes things worse. So yeah, you just don’t want to go anywhere near that stage if you can help it.
Jonathan Fields: Yeah, and so many people listening to this right now are thinking to themselves. But that’s just my life.
David Sinclair: You know, it used to be my life. I was an insomniac was horrible. I’m almost suicidal. It was that bad. You can, you can change your life, at least I’ve found, I have, by looking at the ring, changing things before I go to sleep during sleep, how I sleep, what I wear during sleep. I’ve been able to get a good night’s sleep most nights. And I’ll give you some of the, some of the ideas. If you want the cheat sheet, go to page 304 of the book. But some things that, you know, blue light blocking is important. Don’t be reading your emails too late or watching TV without those blue light blocking glasses. What else? I don’t drink a lot of alcohol straight before sleep or a large meal, especially meat. It’s hard to sleep with that in your stomach. I do take melatonin, a little bit of melatonin, and there’s l-theanine, which has helped me as well.
Jonathan Fields: It’s interesting also there’s a familiar with those. And I’ve also looked at over over the years, the relationship between exercise and sleep quality. And it seems like the exercise, the relationship there is really mixed. And also may really depend on the nature of exercise the time of day and be specific to gender.
David Sinclair: Yeah, well I find if I exercise late, I don’t sleep.
Jonathan Fields: Yeah, I’m pretty much just the same way I’ve experimented. There’s another chemical molecule that you reference that that is really interesting and NMN, I’m not, I’m not going to, I can’t remember what that actually stands for. Tell me more about this.
David Sinclair: Yes, so this is a nicotinamide mono nucleotide and it’s what the body uses to make NAD. So you can force your body to make youthful amounts of NAD by eating. I take about a gram of it per day and so I haven’t measured my NAD, but I know from looking at other people, my NAD levels might be about two times normal. And that is giving me fuel for chemical reactions in the body. And particularly the sertuin defenses that’s one of the molecules that we gave to mice to reverse aspects of aging. That was what gave them more endurance. And so I take that in the hopes, expectation that my body is fighting aging and will not get is old. And will preserve the epigenetic information. So these sirtuins are the epigenetic regulators and we’ll have to see, I want to measure my Horvath clock. I haven’t done that Yet. A Lot of people want me to do that. And I will, it’s just been a matter of these tests haven’t been really available till recently.
Jonathan Fields: Yeah, I mean if you’re taking resveratrol and NMN simultaneously and they both increase the levels of need, then it also, I mean, wouldn’t it also become sort of like confounding variables, you know, like it’s difficult to figure out which of these is actually having an effect or does it really matter?
David Sinclair: It does matter for me because I’m a scientist, right. What I do is different than most people, though anyone can do it. I subscribed to a company that gives me blood biomarker, readouts. I’ve been doing that for about twelve years now. You mind if I mention the company I don’t have to, it’s called inside tracker. And in full disclosure I advised that company. But I do so because I believe in it. And what they do is that they, unlike your regular doctor, they can graph all of your biomarkers, they measure a whole bunch, thirty four or so. And what I can see in my body is first of all how it’s been changing over time. And when things go out of the range of optimal, knowing your disease, but even just slightly yellow from Green, I bring them back into the Green Zone. And the second thing that inside tracker does, which we found is quite beneficial and as effective as the best medicine for diabetes. Type two diabetes is the Health recommendation. So they tell you primarily what to eat, to correct imbalances and it works for me. And so whenever I get high cholesterol or just trending up, I can bring it back down with their recommendations. And to your question, when I take a new supplement, I’m monitoring what happens. I’m not taking them all at once and hoping for the best, which is what typically we do. I know what happens to my body and if nothing happens, I’ll know. And if something good happens, I’ll know. And if something good happens, I keep taking it until otherwise informed.
Jonathan Fields: It’s fascinating to me. The availability, you know, to sort of on a consumer basis to track, I mean we both reference this ring that we’re both wearing, which we actually, I haven’t said what it is, but we’re wearing a ring that essentially is a little computer that tracks the quality of sleep and also heart rate, heart rate availability and things like that. So you can kind of monitor and graph it over time and it gives you a lot of interesting information. And then you know, the ability to then do bloodwork and actually track biomarkers over time. You know, essentially, I think it’s become so Much more available. I know a number of different companies that let you do that. My sense is, but for the weirdoes who call themselves biohackers or scientists and just a really fascinated by this stuff. A lot of people don’t, don’t take advantage of any of that. I’m. I’m in a weird place in that, you know, like, we’re in New York City right now in New York is actually the only state in the country that doesn’t allow you access to any sort of independent Labs. So I’m, I’m waiting for that. Hopefully to change one day, but the entire rest of the country and I think a lot of the World does. And I love the fact that that we are gaining the ability to do it literally every month if we want check in and not just, you know, say well how am I feeling, but actually look at the data and see what’s actually happening here.
David Sinclair: Right. We are empowered, we can look at our DNA, we can look at our biological age, we can look at our biomarkers that’s important, because we don’t know if anything’s working. And the analogy I put in the book is we have over one hundred and fifty sensors in our cars. And we wouldn’t think of driving a car without a dashboard or an alert if something was going wrong. But we know nothing about our bodies the best we get is we go to the doctor for an annual checkup if we’re not sick. And you know, these, these old crappy printouts of the doctors look out. And there’s an asterisk, if it’s out of range and the doctor will say, well, you’re out of range, we’ll give you this medicine or whatever. That’s primitive, that’s nineteen sixties, nineteen seventies stuff. We can now move our own. Well, I wouldn’t say therapies, but our own knowledge into the twenty first century with these companies that are accelerating our own ability to to know our bodies, the way we know our cars. And I think in the future we’re going to think how crazy was it that we went for an annual checkup. And our doctors had no idea during the year if we, if we really had developed a tumor or Cancer, or high blood pressure or diabetes. Now kids in the future will our kids already think it’s crazy that, that we only go to the doctor once a year. And with the ability to now measure Cancer years before it actually develops where the blood tests are, we’re going to be alerted within a few days of developing a tumor. There’s something wrong and that will prevent what happens now as you go to the doctor and it’s often too late.
Jonathan Fields: Yeah, it feels like we’re on the edge of a real sea change in the way that we understand what’s happening ourselves, the speed at which we have information and our ability to respond to it. Especially with so many conditions and diseases that dramatically limit or end life. A lot of them the earlier you identify it and can work with it, the better the outcome. So this gives you a lot of that. So we’ve talked about resveratrol, we’ve talked about NMN in the context of NMN. That’s all I mean, dissimilar to resveratrol. It’s from what I understand, a pretty shelf unstable substance.
David Sinclair: It is. now it’s not going to hurt being on your kitchen shelf for a few weeks, but long term. I know if I test the NMN in the lab, that’s sitting on the shelf. It’s starting to degrade into nicotinamide
Jonathan Fields: Which is not a good thing.
David Sinclair: No, no we showed years ago twenty three that nicotinamide inhibits the sirtuins. It’s a, it’s a negative.
Jonathan Fields: So you’re doing the exact opposite of what you want to do.
David Sinclair: Right? Right. So I don’t believe in taking high doses of nicotinamide some people do. I’m not sure why vitamin B3, but nicotinic acid is okay. And if you have NMN or NR, the NR is a, is a version of NMN. I would keep it in the freezer or for long term and in the fridge for a shorter time,
Jonathan Fields: So that will help preserve it if you end up going down that road right.
Jonathan Fields: Looking forward, you know, we’ve identified these two substances. Their relationship with solutions and ideas and that potential effect on the body. And you’re doing some really exciting research now, which you can start to potentially show. Can we demonstrate sort of the more granular manifestations than what you showed in mouses, in human beings? Are there other molecules or substances that you’re exploring right now that you’re really excited about?
David Sinclair: Yeah, there is. So Metformin had a big effect on my body now? I come from Ashkenazi Jew ancestry. So men in my family typically die from heart disease in their sixties and seventies. And as I mentioned, my father is now a vigorous eighty year old with with no ailments and Super strong Metformin, I think, is part of the reason that we’re doing fine. You’ve got to keep your blood sugar in check and Metformin is, is one way of doing that. If you get type two diabetes, the first thing your doctor will put you on is Metformin it’s, it’s a slightly chemically modified version of a, an extract from plants. The, the goat’s roux, or I think it’s called hellebore. It’s a, it’s basically a modified plant extract. It’s nothing really amazing in terms of foreign synthetic stuff. But what it does is it seems to trick the body into thinking that there’s not enough energy around. And so the body makes more Mitochondria and we know that’s good, but it also improves the ability of the body to take up blood sugar from the bloodstream. That’s all good. But here’s the thing about Metformin, which is a strange situation. You need to have that asterisk on your printout at your doctor for them to prescribe it. Because, you know, according to the old rules, you don’t get a drug until you’re sick,
Jonathan Fields: Asterisk being type two diabetes?
David Sinclair: Right? So they measure what’s called hba1c, which is glycated, hemoglobin, glycosylated hemoglobin. And that depends on how much blood sugar you’ve had for the last month or so. But why wait till you’ve become diabetic to get a medicine that’s very cheap and relatively safe? It’s on the list of World Health organization’s essential medicines for humanity. It’s very rare that anyone ever has any serious adverse events as one in ten thousand or something. It also seems to by looking at tens of thousands of patients protect those patients against cancer, heart disease, frailty, and Alzheimer’s. This is as close as proof that we’ve got that a molecule can slow down aging and diseases of aging. Yet if you go to your doctor, they’re going to say, if you don’t have type two diabetes, you can’t have your Metformin come back when you’ve got diabetes, which is the wrong way of thinking about it.
Jonathan Fields: Hmm. So it also sounds like it has a lot of similar effects as the two other substances we talked about is that through but, but through a different mechanism.
David Sinclair: Yeah. So there are three main pillars of, of longevity mechanisms. I’ve talked about the sirtuins, which there are seven. There’s two others. One is called activated protein kinase or ampk, which Metformin will stimulate. And then the third one is called mtor, which is stimulated by low amounts of protein. And that’s why people think a plant based diet might be healthy in part, Besides the molecules you get from them.
Jonathan Fields: Curious to, I mean, as we start to come full circle a bit, I want to jump back into the nutrition side of things like we talked about these things, which are really interesting substances to you know, follow, potentially explore. I want also be careful when we talk about things like this and we have like a large number of people listening in right now who all have their own unique Health situations, lifestyle circumstances. And you know, they’re saying, wow, this is fascinating. This is amazing. Maybe it’s right for me. I’m always hesitant, you know, like I think always, you know, talk to a qualified Health Care provider. And at the same time, part of what you’re saying is a lot of qualified Health Care providers aren’t actually familiar with a lot of what we’re talking about. So how do people do that dance of wanting to be safe, wanting to be intelligent, wanting to work with somebody who, who knows their Health knows their history and can help guide their journey and at the same time, be educated and explore. Really the next generation of what may be coming.
David Sinclair: Well, I’m glad you said that because I’m not advocating to just take your Health and join hands. It has to be done with monitoring and with Health Care professional who knows your body and everyone’s different. So what I’m saying works for me, you know, you might have a terrible reaction to tomorrow night, for example, who knows, you might have a tumor that, that, that is benefited by, by what I’m saying in, you know, a growth of a tumor. So you have to be very careful. Now, I also have to be careful that I’m not recommending anything, but what I am doing is trying to educate the public about what the cutting edge of science is saying. And in my book, actually everything is referenced. So you can look up the data or show that data to your doctor if your doctor’s willing to look at that. But let me just emphasize that we don’t know everything that there is a risk that for that particular person, especially if they’re already taking medicines. They could be, they could interfere with medicines, could be blood thinning, extra blood thinning is not good for example. So you want to be able to talk to your doctor, talk about what you, what you’re taking. So I’m always honest with my doctor. I tell him that I’m taking resveratrol, I’m taking in a man. What do you think? And he also, you know, typically he’ll say, I need to look that up. But you know, these are smart people. They’ve gone through Medical School, they know a lot. And you need to have that conversation with them in case there’s something that is particular to you that could be dangerous. Yeah.
Jonathan Fields: So as we sit here in this container, the Good Life Project coming full circle. If I offer out the phrase to live a good life, what comes up?
David Sinclair: The way I look at life is this. I imagine my funeral actually, you know, maybe a little bit before my funeral on my deathbed. What do I, what would make me happy? That’s really what I work towards. It’s how I lived a good life. I’m always testing myself every day. So, what I’m trying to do is to maximize my contribution. It’s almost to be relevant. This is a good life. So how can you do that? Well, you can do it the way I’m doing, which is trying to do improve human knowledge and Health. But not everyone can be a scientist. So I would say that if you boil it down, everyone should want to leave the World a better place. So how do you do that? Besides being a scientist, you can, you can have children who take care of leave them to take care of the World. You can make people happy or you can go to nursing homes and help those people as long as you’ve helped people or even helped animals or help the environment as long as you’ve done something good in your life. And it all hasn’t just been about being selfish. I think that’s what a good life is about.
Jonathan Fields: Thank you.