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Reverse Aging Now: The Latest Longevity Breakthroughs | Dr. Eric Verdin
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Coming up on this episode.
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So aging is the accumulation of disorder, and that disorder is caused by a whole series of external forces over which we have essentially no control. Think about gravity. Think about the gamma rays coming from interstellar radiation. Think about uv. Think about oxygen stress. All of these forces are there, and they're always going to be with us. And we know that they are the driving forces of the aging process.
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Welcome to Doctor's Pharmacy. I'm Dr. Mark Hyman. That's Pharmacy with an F. A place for conversations that matter. And today's conversation matters because it affects all of us and it's about how we age and perhaps how we may be able to slow down that process. And we're talking with one of the world's Experts on Aging, Dr. Eric Burden, who's the president and CEO of the Buck Institute for Research on Aging, a pioneering biomedical research institute dedicated to aging and age related disease. He's a native of Belgium. He received his MD degree there from the University of Liege and then completed his clinical research training at Harvard Medical School. And he's published over 280 scientific papers in aging and metabolism. He's the guy who knows more about aging than most people on the planet. He's worked on the molecular mechanisms of aging, mitochondrial function, inflammation, caloric restriction. He's a pioneer in so many ways, and as a very interesting, great guy, we had a deep conversation today about some really key elements that you probably heard about in the news, like mitochondria, or the role of our own healing and repair system in activating longevity pathways. We talked about how do we diagnose, in a sense, the rate of aging, how do we look at our biological age as opposed to our chronological age. We talked about some of the exciting new developments in therapies, from things like NMN nr, which help increase NAD in the body, to some of the key molecules that are being researched on reversing aging, like quercetin and fisetin. We get deep into so many topics. We literally could have talked for hours and hours and I had to cut it after a while. But I think we're head back for a round two of the podcast because we didn't get to cover all the things I want to cover. And you know, I'm very interested in this topic. So go ahead and fasten your seatbelts. This is going to be a very interesting and deep conversation. You might have to look up a few things, but we're going to put everything in the show notes and let's dive right in. Well, Eric, has been so long that I wanted to have you on the Doctor's Pharmacy podcast. Your work has been an inspiration for me. And the Buck Institute, which is basically the one of the few places in the world that's dedicated to study aging, is doing extraordinary work. And you're the president CEO of that institute that now I think is leading the way in helping us understand the biology of aging, how to measure aging, and to understand the underlying mechanisms that are driving us to age rapidly and that lead to chronic disease. So I'm so excited to have you on the podcast and to dive deep into the science around it. It might get a little geeky, everybody, but I want you to stay with us. We're going to explain everything as we go along and hopefully you'll leave understanding the whole science of aging in a much deeper way.
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Thanks for having me, Mark. Delighted to be here with you and looking forward to the next hour.
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Yeah, me too. So, okay, so let's start with high level. There's a lot of research on aging happening now, but it's not always been that way. Aging essentially was a neglected area of medicine. And in fact, you were ridiculed or dismissed if you even thought about studying aging because it was thought to be something that just happened that you couldn't do anything about. And now there's this whole field of longevity research and what called gero science, like gerontology, looking at the science of how we age. Even thinking about describing aging as a disease or what we see as typical aging, which is, I think, abnormal, aging as a disease. And so the question is really, how do we need to think differently today given the science that we have, particularly around the underlying root causes of dysfunctions that happen as we age, the hallmarks of aging, how do we need to think differently about aging and disease going into the next decade or so?
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That's a good question, actually. And the way I think about it, and it's true, about 20, this is something that's relatively recent. About 25, 30 years ago, aging was considered sort of the backwaters of biology. This Was an area that you did not go there because it was considered too messy. And the way people use was bad for your career. Bad for your career. Exactly. Well, people used to think about aging as chaos. So think about, if you have a little bit of a background in physics, entropy. So aging is the accumulation of disorder. And that disorder is caused by a whole series of external forces over which we have essentially no control. Think about gravity. Think about the gamma rays coming from interstellar radiation. Think about uv, think about oxygen, stress. All of these forces are there, and they're always going to be with us. We know that they are the driving forces of the aging process. What people had not appreciated is the degree to which we actually resist these forces. And this is where the potential is. So think about, you know, we're not going to change the fact that we're living in oxygen or that there is gravity and gamma rays surrounding us. But what had not been appreciated is the degree to which we resist the. For example, if you're lacking DNA damage repair, which is one of the consequences of gamma irradiation or UV irradiation, you're going to live to about 20 years old, and you're going to show in those 20 years a very accelerated form of aging. And so what people had not appreciated, again, is this idea of all of these repair mechanisms and how we can actually activate them. So what happened about 20, 25, 30 years ago is the identification of a whole series of mutations that could actually increase lifespan. And so this ran counter to everything we had ever thought about biology. People thought about mutation. That's typically deleterious. You get a mutation, you get a disease. And here were a number of mutations that were identified in animal models. And in C. Elegans, the little worm that we study, or in fruit flies or in mice, they could actually double your life expectancy. That really put the whole world of aging up on its head and highlighted the potential of identifying novel interventions, including lifestyle or drugs, that could actually significantly increase lifespan. Initially, of course, these findings were met with a lot of resistance. People thought, well, this is an exception. This is only applying to C. Elegans or to fruit flies or mice. But over the last 20 years, you know, the work has really shown that there are a large number of genes and proteins that you could target and interfere with that will result in an increase in lifespan and health span. And we are right now at a stage where this is slowly percolating into humans. And I Predict the next 10 to 20 years are going to be transformative in our ability to Bring all of this basic knowledge on the biology of aging to humans.
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I mean, that's pretty exciting. What you're saying, and I just want to highlight something that I think is really important, is that historically we just thought that, you know, the body degrades over time and that there's no mechanisms to actually stop it or reverse it. And what you're saying is that the discovery of some of these mutations has led to an understanding that we have these built in, what I call longevity switches, which is sort of a term that I kind of came up with, but built in repair, renewal, regenerative and healing mechanisms that we have neglected, that we can learn to activate through various interventions from lifestyle to nutraceuticals to phytochemicals to prescription medications, pharmaceuticals, or maybe even hormetic interventions, stresses to the body like hot and cold therapy. There's all these ways in which the body can actually activate these processes, and there's very few of them, but they're influenced by so many things we do. So there's so many redundant mechanisms that actually can activate these longevity pathways that we're now discovering. And to me, it's one of the most exciting times in science because for the first time, we're not really looking just at the downstream diseases that we typically look at in medicine based on diagnostic codes. We're looking at the upstream causes and the mechanisms and the hallmarks of aging is sort of description that. That kind of tries to describe some of these underlying causes and mechanisms, but. But sometimes I don't think they go far enough because they. They only talk about, well, these are the things that go wrong, not what are the causes of the hallmarks. So the cause marks are the causes of aging on diseases, what are the causes of the hallmarks going awry? Right. So that's kind of an interesting inquiry. So I think this is such an exciting time. And we're going to get in during this podcast, we're going to get into discussion of some of the ways in which we can regulate these ancient preserved, conserved pathways that exist across everything from worms to humans. Right?
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Yes, it is. You're completely wrong. This is a really exciting time as a physician. And by training I went to medical school, even though I did most of my career in research. I've always. Once a physician, always a physician. So I've always been intrigued by the relevance of what we're studying in these animal models to humans. It is truly an exciting time. This idea that something that we've always thought was ineluctable and over which we had little control is becoming another tractable problem. And this is, you know, the excitement that you see in the field is a reflection of this. You know, one number that I like to remind people of is when we think about our own longevity, we, you know, many of us have a sort of a fatalistic approach to it. We think, you know, my parents didn't live very old, and therefore, you know, I might as well well have another cigarette, another glass of wine, enjoy life while it's there. But it turns out that, you know, about 93% of our longevity is determined by our lifestyle factors.
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93, that's a very specific number.
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Well, that's the result of a great study by calico looking@ancestry.com, they were able to sort of revise a number which used to be about 80%. People used to think about 80% of lifestyle was determining health span and lifespan. But the number they came up, based on millions of people and records, appears to be 93% lifestyle, 7% genetics. That's true only if you. And the only exception to this, if you have an ancestor, someone in your first degree relative who has lived above 100, then there's some likely genetic factors, most likely protect it, and you can have another cigarette.
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Well, I have Apoe 2 as one of my Apoe Elite.
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Fantastic.
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So I call that the jackpot gene.
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You're one of the lucky ones.
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Yeah. So I don't know what that means exactly, but I have APO 2 3. So I think. I don't know how far I can go. How much ice cream can I actually eat before I get into trouble? That's kind of what I want to know.
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Probably more than me. I'm E3. E3, which is already good.
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That's average. That's average.
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Good.
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Okay, so let's. Let's get into the conversation around two. Two aspects. Which one is, what are these mechanisms and pathways? Let's. And then let's talk about how we. How we. And the research at the Buck Institute is actually uncovering ways in which we regulate these. And. But before we do that, I want to go into sort of a conversation that almost is preceding that, which is how do we measure aging? How do we know if what we're doing is working? And this is the whole discussion around how do we measure biological age and how do we look at our biological clocks? And there are so many out there. I think you were on a paper that I read that listed all of the different kind of clocks and the pros and cons of Each one, which I was great. It was great because I was like, well, I don't know, this is very overwhelming, but it was really helpful for me to understand that. And, you know, personally, I did the true diagnostic DNA methylation test. I don't have any affiliation with them, but I just did it two years ago. Oh, and when I was 62, and then I implemented a whole bunch of interventions, including more aggressive lifestyle change, different nutraceuticals, analytic supplements, which we'll talk about, as well as different kinds of treatments like plasmapheresis and exosomes and stem cells. I just kind of went, I did it all. And then I also did rapamycin. And I was like, how far can I change this biomarker? And if I just throw the kitchen sink at it, which is not very scientific, I get. But I want. I'm an n of 1. So I thought it was, you know, we're trying. And I went back, even though I got two years older. Now I'm 64 on the same test I went to from 43 when I was 62 to 39 when I'm 64. So I bent back four years even though I got two years older. And so how reliable are these clocks? You know, am I just falsely enthusiastic about my own result? And one of the things we should be looking at, is it the need and pace of aging? Is it demethylation? Which, you know, what are the, what are the things that actually are worth looking at?
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Yeah, that's a. The whole idea of biomarkers of aging is going to be critical. And here's the reason we, we go through life right now sort of hoping, you know, that things are going to work out for the best. And traditional medicine essentially waits for you to get sick, to really start intervening. So there is a need, a crying need for what we call surrogate markers, markers that would be able to predict how well are you aging? And when we talk about biological aging or biological age, this is in contrast to chronological age, just for your audience, you can be 40 years old, but your body can be behaving more like the body of a typical 30 year old or like the body of a typical 50 year old, that would be your biological age. And by the way, we are also able to generate an estimate of biological age. If you've met someone who's 70 years old and you think that person looks younger, you have defined in your own head that this person is biologically younger. This, by the way, these are true variables. They're actually algorithms that will predict your Age simply based on facial recognition, just like we do. And so there's been a lot of interest in the field of generating more precise and more predictive biomarkers of biological age. The reason being not just to be able to tell you where you are on your trajectory, but also to assess the efficacy of our interventions. And you just described Your n of 1, which is critical, which is okay, you start a whole series of interventions. How do you know you're actually helping yourself versus hurting yourself? And so this is where these clocks are coming into play. Now we are right at the beginning of a whole field. So I did the same thing as you did, True Diagnostic. I don't have any affiliation with them, we collaborate with them. I think they are the best company right now in terms terms of providing a large number of assays. And I say large number I think is key. They are, right now there's a proliferation of these clocks. Many of them are epigenetic clocks. They're measuring methylation and DNA. The reason is not that these clocks are better than others, it's just that historically they were the first one. This is work pioneered by Steve Horvath and his colleague. So I did the same thing as you did. I measured all my clocks. I'm 67 years old and my clocks came between 25 and 67. And of course I look at the 25 year old clock and I say, that's a really good clock.
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That's good. I'm jealous now.
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And that's glycan age for whatever reason. Yeah. But the other clocks frankly varied between 42 and 67. So the question is, you know, how do you, how do we sort through this?
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And well, you just pick the best one, don't you?
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Pick the best one. So, so I mean, there's obviously there are some significant problem with this. These are not approved clinical tests. But I still think that they have value and their value really comes back in repetitive measurement, just like you said. So, you know, first you need probably to measure many of them. The paper that you're referring to is a paper in which we did plasma pheresis on a number of patients with a company called Circulate. And we found on a global scale that most of the clocks actually went back when these patients underwent plasmapheresis. But again, there was extreme variation between the different clocks. I tell people, if you want to use the clocks, companies like Tru Diagnostic will give you many numbers. They will be all over the place. But the true value comes in looking at how they change over time. Now the Prediction is that over time we will not only have these epigenetic clocks, we will have proteomics clock, metabolomics clock, facial recognition clocks. You know, there's a proliferation of these clocks right now and they paint a pretty complex picture. And I think they will allow us to do truly preventative medicine. Some of These recent clocks, e.g. proteomics clock by Tony Whiskeray at Stanford, are able to measure organ specific aging, which is going to be really critical because of course, as we age, we are always limited by what I call the rate limiting organ. It could be your liver that's going to fail first. And you would want to know and do know an intervention that favors your liver versus your brain versus your heart and so on. So I think we're right on the cusp of a revolution in diagnostics. And these epigenetic clocks is the first, the first symptoms going in this direction.
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So basically it's all getting shaken out right now in the research like, and we're going to learn which are the best clocks and we'll learn more and get better. But in the meantime, what I hear you saying is stick to one assay and repeat it over time based on what you're doing. Because if it's off, it's off by the same amount every time. And what you're looking at is a change from the baseline, either worse or better.
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So, but interestingly, another anecdote, for example, someone did an interesting experiment where they, they measured the clocks at different times of the day in the same person and they found, they found over the 24 hour period, the clock would vary by five years.
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Because I'm older at night, I know that I feel older at night. In the morning I'm good. I'm like 25. By the time night comes, I'm 70.
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Meaning that, you know, if you're going to do this, do it every time at the same time of the day because there's obviously there are no variation in there.
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Great, okay, so now we have these clocks. Let's say we can measure these changes that happen as a result of interventions. Let's talk about some of the most exciting work at the Buck Institute looking at the sort of underlying things that really regulate aging around we call cellular senescence, which is zombie cells and cells that kind of spew out inflammation throughout the body. Are looking at our metabolism and how our nutrient sensing pathways work, which I think I want to get into fairly deeply stem cell and stem cell biology and protein, protein function. And then how do we sort of make sense of it all through bioinformatics and systems biology. And I know you've recently partnered with Leroy Hood, who's just a brilliant scientist. So I'm curious about, like, how. How you start to think about where. Where are the most leverage points that you're seeing in the data that you're looking at in the research you're doing at the Buck institute about what's working in all these different areas?
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So maybe I'll just take it one step backwards and just to alert your audience to the fact that there are no. There will be no magic pill. Aging is an incredibly complex mechanism, and you alluded to earlier in our discussion to these hallmarks of aging, which is think about it as a catalog of all of these abnormalities that happen during aging. And that includes epigenetic dysregulation, senescent cells, failed nutrient sensing, defective stem cells, and defect in mitochondrial biogenesis. There's all kinds of problems that happens during aging, by the way. They're all connected to each other. And when we think about aging and solving it, I think if you study it, you will realize how complicated or process it and that, you know, we at the back Institute, we have about 300 people working on aging. We don't take sides in a way that I cannot predict what's going to be more important. So we study pretty much every one of the hallmarks of aging. We obviously have a big emphasis on senescence because it was mostly discovered through the work of Ginny Campisi at the back. So many of us are still working on senescence, but we have people working on mitochondria, we have people working on stem cells, we have people working on metabolism and so on. So I think one of the things that is really emerging right now is the complexity.
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I think that's so important that you point that out.
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It's important because, frankly, I've sometimes been called the grumpy man of longevity research because I refuse the hype or work. I think there's a lot of really exciting things happening in aging research, But I'm not deluding myself. I don't tell people I'm going to live to 150 or 170 like some of my colleagues do. I think right now we are focusing on things that are really tangible. For example, you might be surprised to hear that most of us could live to 95 years old in good health if only we would deploy everything that we know that's already a lot better than what we have today, where most of us will live to 65 in good health. So that's an extra 30 years of healthy life. And right now we are really focused on two things at the back, on the basic biology of aging. Again, we don't take sides. We study all of these processes and how they relate to each other. The bigger aspect that is being grown at the Bach Institute is the whole human aspect. Really taking all this basic knowledge and translating into actionable interventions that I can tell you and other people this is what you should be doing if you want to live the longest possible.
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Learn more@capella.edu. feel your max with Brooks Running and the all new Ghost Max 2. They're the shoes you deserve. Designed to streamline your stride and help protect your body. Treat yourself to feel good landings on an ultra high stack of super comfy nitrogen infused cushion that takes the edge off every step every day. The Brooks Ghost Max 2. You know, technically they're a form of self care. Brooks, let's run there. Head to BrooksRunning.com to learn more. Yeah, I mean I think it's so important when you just said around the nature of nature, which is, you know, it just reminds me of a quote from John Muir who was a naturalist in the 1800s who said when one tugs at a single thing in nature, he finds it attached to the rest of the world. And essentially what I see happening often in research is the reductionism even within the science of aging where, oh, it's this hallmark, or I'm going to focus on mitochondria, or I'm going to focus on inflammation, or I'm going to focus on deregulated nutrient sensing, or I'm going to make something that's going to lengthen telomeres or kill zombie cells. And that's where things get into this reductionist mindset that doesn't understand that all these interact. They're all dynamic. It's a web of connections and interrelationships that all either positively reinforce each other or negatively reinforce each other. And so. And a lot of these ancient longevity pathways, and I think when I think of this, and I would love to hear your opinion about this, is that they there's kind of a way to kind of influence a lot of it through the same kinds of interventions. Obviously the lifestyle stuff, but when I think about, for example, the four deregulated nutrient sensing pathways that tend to go wrong, mtor, insulin signaling, AMPK and sirtuins, which I know is a lot of mumbo jumbo, will explain all that, I promise. But these are, these are what I call the longevity switches. And it seems that they, they, they're affected by what we eat, but they're also affected by various kinds of other things like exercise or various hormetic stresses or other factors and that they affect all these other hallmarks. So like mtor, mpk, all these things affect mitochondria, they affect inflammation, they affect oxidative stress, they affect your epigenetic regulation, they affect DNA repair, they affect senescent cell. I mean this is when you sort of start to dig into it. It's like it's everything's affecting everything. So what's the highest leverage point? And again, I'm not a longevity researcher, I'm just sort of a doctor trying to make sense of all this. It seems like the deregulated nutrient sensing is one of the most important almost meta hallmarks because when you address those four pathways, it downstream benefits all the others. Am I off or does that make sense to you?
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B
I agree.
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A
Oh, wow. Okay. Because I made this up. I made this up.
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B
So no, I do agree. Although there are. So when I think about the buckets in which you should invest if you want to maximize your longevity, nutrition is clearly one of the top ones. But equally important is exercise. But by the way, exercise or physical activity affects all of the same pathways that we just discussed. You know, so it's it most of the time I sort of reduce this to the fact that we dealing with energy generation and you know, so if think about exercise and nutrition have this in common. They are both profoundly dependent on your ability to generate a lot of energy and the proper energy. And there's one theory of aging that posits that one of the things that happens as we age is our ability to generate energy decreases. And since for example, the repair function that we were discussing earlier, our ability to repair DNA, to repair proteins and so on, is also incredibly dependent on energy. So as energy supplies dwindle or ability to make sufficient energy becomes limiting, then, you know, if you have the choice between repairing your DNA or actually walking, your body is going to favor the walking. And so there are lots of common threads between all of these variables. And, and I'M happy to dive into this.
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A
Yeah, yeah, let's dive into it because I think I agree with you. I think the mitochondria are central. It's really about the, the how we create and make energy, as well as how we protect, preserve and improve the number and function of our mitochondria. And I always say the sort of the difference between a two year old who's, you know, running around like crazy and can't stop moving versus a 92 year old who's just sitting in the chair, barely can move, is the health and function of their mitochondria. And a lot of your research has focused on mitochondrial function, aging, and particularly around the role of NAD and ketogenic diets, for example, and the role of the role of sirtuins in regulating mitochondrial function as well. And I think I'd love to dive into this whole topic with you a little bit more because you're such an expert in it. You know what, what have you learned about how mitochondria are regulated and how they play a role in aging? And what are the most salient things we've learned about how to improve the number and function of mitochondria from lifestyle all down to nutraceuticals and even medication. Why don't we dive into that? Because you're, you're like the world's expert here.
- [35:34]
B
Lots of drawers to open there. Yes. So when we think about energy. So let's backtrack. So, you know, our energy, we generate energy from essentially burning food in the presence of oxygen. Think about when you throw coals into a fire, if you blow air on it, you know, the fire will get more intense. So this is the same thing. We burn carbohydrates, lipids or fats and proteins in the presence of oxygen to generate energy. This process takes place at many places in the cell, but predominantly in the mitochondria, which by the way, are commensal bacteria which have become incorporated into our cells. This is something, a fusion that happens billions of years ago. Quite interesting biology. These mitochondria are generating the ATP that we use as energy, and also the nad, which we use as a form, an intermediate form of energy. And we can come back to this later. Now it turns out that mitochondria numbers dwindle with aging and their ability to generate energy dwindles with aging. And there are multiple variables that are causing this. Some are mutations in the DNA. So the mitochondria have their own DNA, which is an ancestral bacterial DNA. They accumulate mutations, their numbers Decrease the NAD levels, which is this critical intermediate dwindles as well. All of these factors lead to a progressive and worsening energy deficit as we age. And so there's a lot of interest in trying to understand how do we reverse this and how do we, how do we prevent this from occurring at the first place?
- [37:31]
A
So, so, so clearly the mitochondria are key. And the question then is what, what can we do to help our mitochondria? Because if what you're saying is true, that they're central to aging, both healthy aging as well as unhealthy aging, then it seems like they're a major target for intervention. And there's a lot of stuff floating around there in this sort of literature and also in the sort of cultural zeitgeist around interventions that help to regulate mitochondria from, you know, fasting or ketogenic diets to things like rapamycin or other phytochemicals that may be able to regulate mitochondrial function like urolithin A. And I just, you know, just wonder how you, how you sort through all the massive data and information around, around all of this and where you start guiding people practically around how to make sense of the data.
- [38:32]
B
Yeah, so you know, as I mentioned, so that there's loss of mitochondrial number, there's loss of mitochondrial function and there's loss of mitochondria, you know, key metabolites like nad. And so I think when I think about, you know, what can you do? It ranges lifestyle intervention all the way down to some of the drugs that we actually working on. So the two ways in which I think you can maximize your mitochondrial function as you age is fasting. And fasting, as I mentioned earlier, activates a process called autophagy, which means self eating. And the beauty of autophagy when you're fasting is that your body is able to sort through the garbage and the, and the well functioning mitochondria. To discard the poorly functioning mitochondria and to keep the ones that are most efficient. So that the process called mitophagy, so intermittent fasting I think is part of, you know, the ability that your body has to shift between feeding and fasting is a process that we call metabolic flexibility. And I think it is really an integral part of health. So I encourage people to, you know, to incorporate this into their daily routine. Another way in which you can, is.
- [39:50]
A
Just what you're asking is to give people a break between dinner and breakfast is essentially what you're saying.
- [39:55]
B
Well, yes, that's One way to do it actually. And right now we're at the stage where there are a whole bunch of different fasting modalities have been explored and tested. And I don't think there's clear evidence that any of them is more beneficial than another. Some people will do a deep fast every three months, some people will do some fasting every day. I think there are, we're still at the stage where these different modalities are being compared and trying to decide what is the best way. But any of them is better than none. That would be the rule that I would. And practically for me, I do a five day fast every three months and then I do sort of what people call restricted time feeding, which meaning I try not to eat for 12 to 16 hours every day so that at least have a period of fasting. There are also a number of interesting supplements that are emerging that are supplements or drugs. The interest in fasting came out of the realization that animals on calorie restriction, whose calorie intake was limited, actually showed increased lifespan. That that's pretty much universal feature. So that led to study of fasting but also led to the discovery of what we call these fasting mimicking or calorie restriction mimetics. So drugs that are fooling your body into thinking that you are under calorie restriction or fasting and those drugs, you know, some of your audience running around.
- [41:31]
A
Starving all the time.
- [41:32]
B
Exactly, exactly. So you know metformin, I'm sure you've heard about metformin or rapamycin or calorie restriction mimetic. So they fool your body to think that you're fasting and they induce parts or all of the protective response. And this is why some of these drugs are being explored for their potential anti aging effect. There are also supplements that are emerging. There's a process called mitochondrial biogenesis, which is the process by which you are making new mitochondria. And we know, you know, we know the pathways, the biological pathways that lead to this. And some of them can be activated by drugs or supplements. A supplement, for example, that activates mitochondrial function would be the urolithin A, I'm sure you've heard, product sold by I.
- [42:29]
A
Take it every day.
- [42:30]
B
Yeah, I take it every day too. And you know, it's a supplement. So it's not going through the same process that an FDA approved drug would be. But the company that commercializes this called Timeline, has a very proactive approach to testing, you know, doing clinical trials and demonstrating the efficacy of what they are claiming and we've collaborated with them, so I can attest to some of the results that we've published with them. So really interesting supplement. And the last one, I mean that I, you know, physical activity, exercise is certainly a very strong way to activate mitochondrial function in your muscle. And we know muscle mass is a very strong predictor of your life expectancy. So anything that benefits your muscle having strong mitochondria bulk, frankly also of your muscle will lead to protective effect on your brain and other organs as well. So obviously, you know, whenever we're talking about anything related to aging, the reductionist approach works for a while to try to simplify the models. But once you start thinking about anything, it's connected to everything else.
- [43:49]
A
That's right. And you know, the thing around the mitochondria also that you done research around is NAD and NAD plus. And there's a lot of, you know, controversy around this particular compound. You know, some say it's kind of the data isn't there. Some say it's God's gift to mankind and we should be all taking it. What's your kind of sort of down and dirty on the science behind NAD and taking nad either as a NMN product and our product or sub Q NAD or IV nad. I mean, this is. All these people are doing these things, including me. So I'm curious about what your perspective is someone who's actually done the research.
- [44:32]
B
Yeah, happy to talk about this because frankly, it's, it's. Once you are involved in the research and you see some of the stuff that's being sold it sometimes I shake, shake my head in disbelief. But that being said, there's like in any story, there's always an element of truth to the whole NAD story. So just a word about NAD is a molecule that allows you to shuttle energy between different parts of the cell. So this is a purely intracellular molecule. So this is not something that lives in the blood. And so, you know, this will be important because there's a whole fad right now of intravenous nad, which frankly does not make any sense to me biologically. But so NAD is an intracellular and it doesn't cross from the blood into your cells. So it just, it's, you know, it is an intracellular metabolite. Why is it important? Because it allows you to shovel energy between different parts of the cells, from the mitochondria to the cytoplasm and so on, or different, different from different molecules within the cell, more correctly. So it's also known that NAD levels decrease during aging. And that's really well established in humans and in animal models. So out of this game, the idea that maybe this is one of the reasons why we have this global energy deficit as we age, maybe we're not able to manipulate. So when I think about nad, you think about Brinkman, you know, the trucks that carry money. So think about if they all went on strike, all of a sudden, the energy of the economy, which is money, would be stuck in the supermarket, and nothing moves anymore. So this is the same thing. So I think about them as the fund carriers. So out of this came the idea, maybe we can just reestablish NAD levels. And so people will see a benefit. And in animal models, you can do this using what we call NAD precursors. And there are two of them that you're familiar with. Nicotinamide ribozide NR or nicotinamide mononucleotide and Mn. And both of them essentially do almost the same thing. Some colleagues will argue vociferously on whether one is superior to the other. At the end, they both reestablish NAD levels. They might have additional signaling properties in addition to this. But. And in animal models, they do remarkable things. So, you know, we've published. We and many other people in the field have published a number of papers showing that NAD supplementation in older animals really alleviates some of the effects of aging. It does not increase lifespan, I should say, but it certainly alleviates many of the disease complications and so on. So out of this game came the interest, well, maybe you should bring this to humans now. And a number of companies are selling NR and nmn. One significant issue is that the amounts that are being sold as supplements are much lower by a factor 10 of what we used in the laboratory setting.
- [47:56]
A
So, you know, like, most bottles are like 250 milligrams.
- [47:59]
B
Exactly.
- [48:00]
A
But you're saying you need more.
- [48:01]
B
Like, we use 2 to 3 grams exactly.
- [48:05]
A
Of the precursors.
- [48:06]
B
Yes, we used a lot more. And those of us who take NMN or NR typically take a lot more than the 200 milligrams a day.
- [48:15]
A
What would you say take, 2 grams or 1 gram?
- [48:17]
B
Well, I take a gram most of the time. Now, obviously, what we need is more clinical data in humans. And a lot of noise has been made about a couple of initial studies that failed. And, you know, and that's, you know, that's true, Peter. TIA is highly skeptical. And there are, you know, there are really good reasons to be skeptical about some of the claims that have been made for NMN and nr. But I think my argument is, let's not throw the baby with the Batwoman. And there is. There's enough compelling evidence in model systems that NMN and NR actually are having interesting effect to pursue the studies and to conduct the clinical trials. Now, one of the biggest problems I have is why is asking the question, and something my lab has been working on, why are NAD levels decreasing during aging? That really has not been studied by many people except us and Eduardo Chini, who is a male Mayo Clinic. And what we both found is that the reason why NAD levels decrease during aging is because there's another molecule called CD38 which is activated during aging for reasons that are not entirely clear, but in part because of a senescent cell burden. So the CD38 is itself as NAD hydrolase. It chews up NAD. And so when you give an RNA.
- [49:55]
A
Enzyme like PAC man, that kind of eats up your nad.
- [49:58]
B
Exactly. So think about your NAD pool like water in a sink. The problem that we're having is a leaky sink. So there's something that's chewing up the nad. And when you give NMN or nr, you're essentially filling up more water in the leaky sink. And so which is not a very satisfying way to solve a problem. So the way we are going about it, and a growing number of companies are doing this as well, is to actually identify small molecule inhibitors of CD38. And so I have a startup called Napa Therapeutics, which has a large number of these novel molecules. We're testing them. Some of these inhibitors, not ours, but others, have been shown to increase lifespan and to correct some of the aging associated energy deficits much more sort of efficiently than the precursors. So my prediction is that if you think about NAD defect in the future, in the long run, we probably will be looking for these CD38 inhibitors rather than filling up the tank with more water.
- [51:11]
A
Interesting. So it's essentially stopping the breakdown of NAD rather than just taking more precursors of nad.
- [51:18]
B
Exactly.
- [51:19]
A
Hole in the bucket. You can keep filling the bucket faster, but at some point it's kind of diminishing returns. Better to just put the hole in the bucket.
- [51:26]
B
You got it. You got it. And, you know, one, one reason, you know, for doing this is, and this is, speaks also to the importance. A lot of people are taking a lot of supplements these days, and they're not being followed appropriately by physician. As I was taking a lot of nmn, I was always concerned because we know that NMN as it's being, if you take a large amount of it will consume your one carbon, your methyl groups. And so as I was doing this, I was always following my homocysteine levels and actually I found it to rise significantly in the presence of a large amount of NMN intake. And you know, and if I, if it goes too high, I stop NMN for a while. So speaking to the fact that all of these processes are connected and I'm somewhat worried about, you know, the proliferation of supplements that are being touted and sold to somewhat naive public, hoping, you know, this is going to increase my lifespan. There are a lot of, you know, there are very few molecules that have absolutely no consequence. And I think, you know, if you're going to go down this route, do it with someone you know, that knows, understands the biochemistry and can follow you appropriately.
- [52:52]
A
It's interesting, I mean, basically just to summarize what you said is that the precursors, NR and nmn, which are available, and we don't talk about which companies produce the best ones, but let's just assume you're getting the best one, will actually lead to an increase in NAD levels. But if you do intravenous or subcutaneous nad, it won't. And that you might be wasting your money.
- [53:14]
B
Yes, you are. You know, a typical NAD infusion costs about $700. There are studies showing what happens when you inject NAD intravenously. It goes to your liver and it is cleaved into nicotinamide and ADP ribose. Now the nicotinamide is essentially niacin. You know, you can buy this for, you know, 20 cents or whatever. So this $700 injection, I really have no idea. Actually no one has any idea what happens to it. Most of it is likely very quickly degraded.
- [53:52]
A
And that's why you feel that kind of weird flushing feeling when you get.
- [53:55]
B
Yes, well, niacin, as you know, will activate these flushing receptors. This was one of the limiting use of niacin as a drug, but a cholesterol lowering. A few decades ago, people had some flushing issues. It's the same thing that you're feeling when you're taking intravenous nicotinamide.
- [54:19]
A
There's an anecdote and I don't know what to make of it. I did a retreat on longevity and one of the local companies was in Turkey, offered NAD as part of this. And there was a woman who had Parkinson's who was quite severely affected. And we know that Parkinson's is a mitochondrial disease. And her response was pretty remarkable. Her tremor stopped, her gait improved immediately. It was an immediate shift like Someone taking L dopa. And I was like, well, that's interesting. And I don't know, I don't, it's just an anecdote, but I imagine it's doing something. And yeah, it's a, it's not a fun way to take it, you know, intravenously, subcutaneously. You can also do it, same thing. It seems like it would lead to the same kind of result. But this is fascinating data. So what you're saying about nad, is it in the precursor, essentially is it doesn't necessarily extend lifespan, but it improves quality of life and health span. Would that be accurate?
- [55:24]
B
That's the prediction and that's what we, Although, you know, there's evidence that CD38 inhibition or deletion actually increases lifespan. So that might be one way to put back this whole pathway in the context of longevity.
- [55:43]
A
Wow. And that's what Napa Therapeutics is working on, right? This.
- [55:46]
B
Yes, yes. Absolutely.
- [55:47]
A
Incredible. Amazing. The, the. God. I mean, I, I feel like we need to go have another one of these podcasts. I might do this in two parts because anytime.
- [55:58]
B
Happy to come back.
- [55:59]
A
I, I, I, there's so much more I want to get into around inflammation, around nutrition, around the microbiome and aging and many, many other topics. But I, I would love to kind of just finish up for the last few minutes on two topics. One is what are the all star molecules for longevity? And I have a list that I want to sort of get your thumbs up, thumbs down on. And two, what do you do not as a scientific kind of, kind of clear scientific protocol, but as your own self care based on what, you know, as someone who's an insider, like it's almost like insider stock trading, right? Like, what are you doing? So the, the molecules that I, I think, you know, seem to me to be the most promising are around the rapamycin molecule, which is a drug that we've talked about in the podcast before. Essentially is inhibits mtor, which is one of these longevity switches that regulates everything from muscle protein synthesis to autophagy to inflammation, to mitochondrial function to DNA repair. That's one. Then there, you know, the metformin question, which I think is a little, probably a little longer than we have to get into, but I'm a little dubious about it. And I don't know if we're going to get to the tame trial now, which is a randomized trial that's going to give us the answer, unfortunately. And then there's all the sort of phytochemicals, like quercetin fisetin, curcumin, green tea extractor, epigalactocatechin, gallate, berberine, and some of these molecules that seem to be sort of promising as both. And your lithium A, which you mentioned, which is sort of a mitochondrial supporting phytochemical that can be derived from pomegranate among all these sort of players, you know, which are ready for prime time, which have sort of low risk potential benefit, which should be really careful with like how do we think about this?
- [57:58]
B
It's a tough one. I tell people, you know, if you.
- [58:01]
A
Want to in five minutes or less.
- [58:04]
B
Okay, so I'll start first. I think before taking any supplement, I think people should optimize the rest of their lifespan because there's nothing, you know, if you have a wound that's affected with a bacteria, you don't put a bandaid on it, you start getting.
- [58:26]
A
So let's assume everybody's exercising, eating perfectly, sleeping great, managing stress and removing toxins from their life. Okay, we've done all that.
- [58:34]
B
Now very few people do this. So the next step would be to have, once you've optimized all of this the best you can. And I think about them as buckets.
- [58:45]
A
And I agree with you, by the way, I agree with you.
- [58:46]
B
You can make it. Because a lot of people will go to the supplements, they don't want to do any of the other things and they're missing the really powerful stuff. This is where the reason I'm bringing, I'm making this point so strongly is that we do not have and will not have for the next 20 years an anti aging medicine or supplement that is better than physical activity. And mark my words, for 20 years, in 20 years we will still not have something that works as well as physical activity.
- [59:19]
A
It's called a miracle drug.
- [59:21]
B
It is the miracle drug. And so if you are sort of not paying attention to that one, well, you can sort of put a bandaid on some issues but you never really get to the core problems. Now thinking about the rest first for me is blood draw. You know, are you balanced in terms of vitamin D, vitamin B12? This would be the first big ones. And I'm surprised how many people tell me, friends and colleagues, no, I don't know when my vitamin D is very. So that's number one. Number two, there are by the way.
- [59:52]
A
That'S why I saw, I started Function Health which was to give people access to their own data, including all the things we talked about, inflammatory markers, the inflammation markers that we talked about as well. As vitamin D and methylonic acid and homocysteine. All the things that we want to know, right?
- [60:08]
B
Exactly. You're also, you're, you know, I don't know if you're measuring this, but you're omega fatty acid.
- [60:13]
A
We're measuring omega 3 fats, 100%, we're measuring omega 3 fats, insulin, lipid fractionation, all the things that you should be measuring to see what your metabolic health is and your mitochondrial health critical.
- [60:23]
B
So, you know, there are a few supplements that have documented efficacy. One of them is omega fatty acids. And especially if you are like most people in the western world and you are, you don't have access to enough of them. So omega fatty acid would be one of the top ones for me, for everyone to take every morning and every night if you're exercising. Carnitine is really one of the well recognized supplement that people take. Now we talked about a whole variety of flavonoids, quercetin, curcumin, fisetin, all of those. The problem with many of those is bioavailability. So much of what has been shown about their efficacy is based on studies where the chemicals are added directly to cell. The problem is before the chemicals get to your cells, they have to go through the gut and have to be absorbed and all this. Most of those have extremely low bioavailability. Now some companies are trying to remedy this by making them into phytosomes and all this, but most of the time the data is just not there, that these things are getting absorbed to a significant level. So I have, you know, you take.
- [61:42]
A
The pill and then your blood levels.
- [61:44]
B
Don'T reflect, don't change the pill, it just goes through. So there are, you know, for example, one thing you didn't talk about, which I think is really critical is fiber and probiotics, which I think for me, I'm a fervent believer in the whole gut health being a critical determinant of your health and brain function. And so optimizing your bacteria in your gut, not by eating the bacteria but by eating the fibers that feed them is really a critical part. So I have a special concoction of prebiotics that I make myself and I think that to me is really one of the central components of having a healthy digestive system which will determine your immune system and so on. As I told you earlier, I believe in urolithin A. That's one of the few well documented supplements that has been shown to have an increase, an effect on your VO2 max on other immune Function we published on the effect on immune function. I don't know any other ones that I forgot the list of all the compounds that you mentioned. One thing that I want to mention also is the whole concept of, as a physician, you know about polypharmacy, the idea of polypharm. Well, people, you know, polypharmacy is the idea that once you start, you start with one compound, you have a series of positive effects, but you also have a series of side effects. The idea of polypharmacy is when you start adding things on top of each other, you generate responses that are unpredictable and not always beneficial. And I, I do worry about the tendency in the field of what people call stacks where you're taking 5, 10, 20 supplements together and hoping that all of this magically is going to work together. I can tell you one experiment that some colleagues have done in the lab. So in C Elegance, the little worm that we study, we can identify readily small molecules that increase the lifespan. So this experiment was done, it generated to a whole series of molecules that increase lifespan. So let's say we have 10 compounds that all increase lifespan. So what they did then, okay, so take combine each of these 10 compounds pair wise, and what you find is they were actually able to identify a number of pairs that actually had synergistic effect where the, the lifespan effect was bigger than the sum of the two drugs. So very exciting. Then they took these pairs and then screened again the whole library to see, okay, what can we add. And what they found is that when you actually. So they had these pairs with two drugs that increases lifespan. Whenever they added another drug that also increased lifespan, all of the effects went away. So that's not good. And I hear about Brian Johnson taking 120 supplements and I'm thinking it cannot be good. What's happening at this mixture of all of these drugs, all of this byproduct? I don't know. It worries me in general. And I tell people, so how do you solve this problem? One way would be to do sequencing. So you would go, for example, for three months on this compound and then another three months on this other compound. So I think we are right at the beginning of, of a, of a new land that we do not understand.
- [65:38]
A
Do you think that the advent of our understanding of systems medicine, biology with AI is going to help us sort through this?
- [65:46]
B
Absolutely, absolutely. And you know, the whole area that we are pursuing is the whole idea of phenomics. This is the idea of deploying to the clinic these tests that allows us to measure tens of thousands of variables instead of a hundred. And so the buck right now, you know, has a whole program with Lihood and Nathan Price called phenomics, which is really going to the next frontier in terms of measuring, you know, typical medicine, as you mentioned, relies on 100, 200.
- [66:20]
A
Not even, not even annual checkups, like 20 or 30 biomarkers, your CBC, chem screen, cholesterol, and a urinalysis.
- [66:28]
B
Exactly. And if you take all of the tests that medicine can today conduct, maybe it's 100 or 200 in one of these samples, we can measure 5,000 proteins, and we can measure 10,000 metabolites, and we can measure ten thousand transcripts and 20 million CPG sites. So really, the idea is not to use artificial intelligence and these deep, deep phenotyping essays and try to extract all of the information that we can get on. How do these drugs work? What pathways are they activating? This is the next frontier, and I think we're tremendously excited by this. It's not for direct consumption for the public, but it's important for people to know that this is where medicine is going. It's ramping up to next stage data gathering and processing.
- [67:26]
A
I think that's really a good place to end, which is the future of medicine is something we can't even imagine right now. And the level of data we can get on each individual is, you know, orders of magnitude more than we've ever been able to get in a way that we haven't been able to apply clinically. But now, given the advent of one, the capacity to measure omics at every level. I mean, there's a hundred thousand petabytes of data just in our microbiome.
- [67:57]
B
Yes, exactly.
- [67:58]
A
But I don't even know what a petabyte is, to be honest with you. But it sounds like a lot of data. And that's just one part of our biology. And the complexity of those interactions, the dynamics, the dynamic way they interact, how they actually are affected by various inputs from lifestyle, from nutraceuticals, from drugs. We're in the most, to me, the most exciting era. It's almost like we finally figured out, like, how to look at the stars and, you know, look at what's going on in the universe in a way we never could before. And I, I'm just so excited. And I, you know, even though I'm like 65 almost, I'm gonna be 65 this year, I just feel like a kid in a candy store, and I just can't wait to see what's going to happen. And I'm going to try to keep myself alive long enough so I can actually take advantage of it all.
- [68:46]
B
That's the whole philosophy that I tell people. The reason why you should optimize your health plan today using everything that we know is that first there's 35 years of extra healthy life for you to be gathered using this. And 30 years from now, God knows where we will be in terms of our ability to interfere in these pathways and to keep you healthy even longer. So the key is, while we're working at gathering all of this data and defining what are the safest and most effective lifestyle changes or drug and so on, just keep yourself healthy and you will reap the benefits now and in the future.
- [69:32]
A
That's so exciting. Well, thank you for your work, for pioneering all this data and science. It's really tremendous. And you know, there's not that many people working at the level you're working. And it's just to hear what you're saying, to understand the implications of it, to know that you, you've come to the same conclusions that someone in the clinic working with real patients has come to. It's just very heartening. So I'm very excited. I'm definitely going to make it out to the bucket. I promise I'll get there and absolutely, we'll see. I'll see you around the next morning and I'm going to have you back because I didn't get to ask like at least half of what I wanted to ask you. So we'll find another another time and have part two.
- [70:08]
B
Take care. Bye bye.
- [70:11]
A
Thanks for listening today. If you love this podcast, please share it with your friends and family. Leave a comment on your own best practices on how you upgrade your health and subscribe wherever you get your podcasts and follow me on all social media channels at Dr. Mark Hyman and we'll see you next time on the Doctor's Pharmacy. I'm always getting questions about my favorite books, podcasts, gadgets, supplements, recipes and lots more. And now you can have access to all of this information by signing up for my free Marks picks newsletter@Dr.hyman.com markspicks I promise I'll only email you once a week on Fridays and I'll never share your email address or send you anything else besides my recommendations. These are the things that have helped me on my health journey and I hope they'll help you too. Again, that's Dr. Hyman.commandsp Thank you again and we'll see you next time on the Doctor's Pharmacy. This podcast is separate from my clinical practice at the Ultra Wellness center and my work at Cleveland Clinic and Function Health, where I'm the Chief Medical Officer. This podcast represents my opinions and my guest opinions, and neither myself nor the podcast endorses the views or statements of my guests. This podcast is for educational purposes only. This podcast is not a substitute for professional professional care by a doctor or other qualified medical professional. This podcast is provided on the understanding that it does not constitute medical or other professional advice or services. Now, if you're looking for your help in your journey, seek out a qualified medical practitioner. You can come see us at the Ultra Wellness center in Lenox, Massachusetts. Just go to ultrawellnesscenter.com if you're looking for a functional medicine practitioner near you, you can visit ifm.org and search find a practitioner database. It's important that you have someone in your corner who is trained, who's a licensed healthcare practitioner, and can help you make changes, especially when it comes to your health. Keeping this podcast free is part of my mission to bring practical ways of improving health to the general public. In keeping with that theme, I'd like to express gratitude to the sponsors that made today's podcast possible.