Your Lifestyle Is Your Medicine
“Your Life Style Is Your Medicine” is a podcast that focuses on how a person's lifestyle can be the key to health and happiness. Routed in the principles of lifestyle medicine, Ed Paget, osteopath, and exercise scientist, interviews area-specific experts on how lifestyle impacts well-being, focusing on purpose, physical activity, nutrition, sleep, and stress, which could lead to a longer, happier life. Edward now runs immersive lifestyle medicine retreats, with the purpose of helping others take back control of their lives to live longer and healthier.
Your Lifestyle Is Your Medicine
Episode 48: Decoding Aging: Science, Healthspan, and the Future of Longevity with Dr. Matt Kaeberlein
A conversation with Dr. Matt Kaeberlein unveils the latest insights into aging, focusing on how studying dogs can illuminate human longevity. The discussion emphasizes the significant role of environmental factors in aging and the potential of interventions like rapamycin.
Dr. Matt Kaeberlein, is a world-renowned scientist and leader in the field of aging biology. He is a professor of Laboratory Medicine and Pathology at the University of Washington School of Medicine, with additional roles in Genome Sciences and Oral Health Sciences. Dr. Kaeberlein’s groundbreaking work is dedicated to unraveling the biological mechanisms of aging, paving the way for innovations that enhance healthspan and quality of life—not just for humans but also for our four-legged companions.
Dr. Kaeberlein is the founding director of the University of Washington’s Healthy Aging and Longevity Research Institute and the director of the NIH Nathan Shock Center of Excellence in the Basic Biology of Aging. Additionally, he leads the Biological Mechanisms of Healthy Aging Training Program and co-founded the Dog Aging Project, which explores how we can use scientific insights to improve the health and longevity of dogs and, by extension, humans.
Throughout his career, Dr. Kaeberlein has delved into cutting-edge research on interventions like rapamycin, NAD+ precursors, metformin, spermidine, and many others, driving conversations at the forefront of aging science.
Today we speak about:
• Understanding the role of companion animals in aging research
• The Dog Aging Project's approach to studying environmental influences
• The impact of chronic inflammation on healthspan
• Importance of lifestyle changes for longevity
• Challenges in funding for aging research
• Future possibilities with AI and epigenetic studies in the field
• Dr. Kaeberlein’s personal experience with rapamycin and its implications for aging
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Please remember, if you want my direct help, send me an email, ed at edpadget.com, or visit my website, edpadgett.com, where you can learn a little bit more about how I can help you make your lifestyle your medicine.
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Website: https://kaeberleinlab.org/ https://www.optispan.life/company
Welcome to the your Lifestyle is your Medicine podcast, where we do deep dives into topics of mind, body and spirit. Through these conversations, you'll hear practical advice and effective strategies to improve your health and ultimately add healthspan to your lifespan. I'm Ed Padgett. I'm an osteopath and exercise physiologist with a special interest in longevity. Today's guest is Dr Matt Kaeberlein, a world renowned scientist and leader in the field of aging biology. He is a professor of laboratory medicine and pathology at the University of Washington School of Medicine, with additional roles in genome sciences and oral health sciences. Dr Kaeberlein's groundbreaking work is dedicated to unraveling the biological mechanisms of aging, paving the way to innovations that enhance healthspan and quality of life. Dr Kaeberlein is the founding director of the University of Washington's Healthy Aging and Longevity Research Institute and the director of the NIH Nathan Schock Center of Excellence in the Basic Biology of Aging. Additionally, he leads the Biological Mechanisms of Healthy Aging training program and co-founded the Dog Aging Project, which explores how we can use scientific insights to improve the health and longevity of dogs and, by extension, humans.
Speaker 1:Dr Kamelan, welcome to the show, thank you. A pleasure to be here. We've got a lot to talk about today. I've mentioned some stuff in the introduction about what we're going to cover. But before we do that, I want to lay the foundation of who you are and why are you talking about this stuff. So give us a little bit of a background on who you are, please.
Speaker 2:Sure, yeah. So, matt Kaberlein, I am the CEO of a health tech startup called OptiSpan. Our goal at OptiSpan really is to create tools, technologies to enable health optimization for as many people as possible, and happy to tell you more about that. My background really is as a basic scientist, so I got my PhD from MIT in Lenny Garenti's lab 22 years ago now studying the biology of aging. So what are the mechanisms that drive the aging process and, I think, more importantly, how can we use that information to impact health and well-being for people?
Speaker 2:And I have a special interest in companion animal aging as well. So that's really been the theme of my career studying those processes in the laboratory. The theme of my career studying those processes in the laboratory. And then about 10 years ago, began studying aging in companion dogs living in the real world with their owners and have sort of made the evolution now to actually trying to impact health and longevity in people. But the theme throughout my entire career has been what can we understand about the biology of aging and how can we use that information to improve health and longevity?
Speaker 1:Okay, and you mentioned companion animals and so you're heading up something called the Dog Aging Project and that's got a lot of attention in the press and the media and so on. But what is the purpose of that project and how would it benefit us? Or is it just going to benefit the animals?
Speaker 2:Yeah, great, great question. So I'd say there's really two overarching goals of the dog aging project. So, first of all, the dog aging project is a large, what we call longitudinal study of aging in companion dogs or pet dogs living with their owners. So none of this is dogs in a captive environment in the laboratory. There are really two overarching goals. One is to understand what are the most important genetic and environmental factors that influence the aging process in companion dogs and then, secondly, to do something about it, so to actually modulate those processes to increase lifespan and health span in companion dogs and people's pets.
Speaker 2:I think there are two ways where insights gained from the Dog Aging Project will have an impact on human well-being.
Speaker 2:One is many of us love our companion animals, consider them to be part of our families, and so by increasing health span and lifespan in companion animals, that has a positive impact on quality of life for people, for the human partners.
Speaker 2:But also we know the biology of aging is largely shared or largely conserved among mammals, and so I would say the vast majority of what we learn about the aging process in companion dogs will be relevant for the aging process in people and in fact, I think one of the very powerful features of the Dog Aging Project is that it allows us to query the biology of aging not just at the genetic level but at the environmental level, and in particular we know our companion animals share very much most aspects of the human environment, maybe with the exception of diet, our pets live in the same world we live in, and that's something we can't study in laboratory animals. So this really allows us to understand a big component of human aging that is sort of a black box in the laboratory studies all of the things in our environment that impact the way we age. And we know, or at least we have estimates, that probably 70% or so of human longevity is in fact environmentally determined. So environment plays a big role in health outcomes during aging and in life expectancy.
Speaker 1:Okay, now that's interesting. You've said a lot of things there that I want to touch on. Yeah, so we'll come back to the environment as 70% factor in longevity. But just going back to the study, most people know that different breeds live different lengths of time, so how is that factored into the study, right?
Speaker 2:So different breeds do have different life expectancies. And I would say even more important than breed is body size. So body size is actually the greatest determinant of longevity in dogs. The same thing is probably true in people. It's just that the variation in body size is so much larger in dogs that we can see it. So big dogs age faster, live shorter than small dogs do, age faster, live shorter than small dogs do.
Speaker 2:The way that we study that in the dog aging project is by being open to dogs of all shapes, sizes, genetic backgrounds. So really the project wants to capture as much diversity as we possibly can. So all breeds are part of the dog aging project, as well as mixed breed dogs. Any dog is eligible, any age, any genetic background, the one limitation being that the dog has to live in the United States. So so far I would love to see the Dog Aging Project become an international project, but for now it's limited to the United States, but otherwise we take all comers, and so we really want to capture that diversity to try to understand how does breed, how do other genetic factors as well as environment, which I've already talked about, influence not just lifespan but also which diseases are most prevalent.
Speaker 2:What does quality of life look like, health span another way to say that and what are the factors that are most strongly correlated with that? Now, I did mention another goal in the Dog Aging Project is to do something about it, and the way you do something about it are actually mechanistic studies, so clinical trials. So we have one clinical trial right now of a drug called rapamycin. Everything other than the clinical trial is observational. We're not asking the owners to do anything different In the clinical trial. We're actually testing whether rapamycin can impact lifespan and healthspan in dogs. I'm sure we'll talk more about rapamycin, but I just wanted to mention that there is that piece of the dog aging project as well.
Speaker 1:Yeah, so there's two arms to it. Okay, so I want to get into rapamycin for sure, but let's go back to the 70%. Of longevity is determined by the environment. Can you expand on that?
Speaker 2:Sure, and I should say that's just an estimate. So what we have learned and by we I don't mean me, I mean the field as a whole there are other people who have done these studies in humans have looked at what is the relative contribution of genetics to longevity. There are a variety of ways you can do this, but probably the easiest to understand are either twin studies or studies where people look at centenarians so those are people who live to be at least 100 years old and then ask the question if you compare, for example, the longevity of children of centenarians to the longevity of those children's spouses who are not related to the centenarians, what is the likelihood that the children are going to live longer, all other things being equal than the spouses? And so from those kinds of studies people have come to estimates that human longevity is somewhere and again it's a little bit squishy, but I would say somewhere between 60% and 80% environmentally determined and 20% to 40% genetically determined. So that's where those numbers come from.
Speaker 2:But again, I think it's important to appreciate that environments change and so the impact of a particular genetic background on longevity may be different today than it was a hundred years ago. The factors that influence what people die from, how they age, are very different today than they were even 50 years ago, and so it's sort of a moving target. Some of the genetic factors truly impact the biology of aging. Some of them impact the way we interact with our environment and, of course, the environment is changing over time.
Speaker 1:Didn't you have a personal experience with rapamycin that maybe changed your view on it or led you into researching it slightly differently?
Speaker 2:Yeah, so I did, and I would say I don't think the experience changed my view of the molecule itself or the pathway that it targets the biological pathway but it certainly changed my view of what we would call off-label use of prescription medications for health span and, potentially, longevity effects. So, to take people back, this was 2020. So, beginning of the pandemic, I started and I'd been studying rapamycin at that point for more than a decade. So in fact, I first started thinking about rapamycin back in 2004, when we pulled the target of rapamycin that's actually what the protein is called, target of rapamycin, or TOR out of a genetic screen for longevity, and so I'd been thinking about rapamycin. We started studying it in mice in my lab right around 2010. And I already mentioned we had a clinical trial in dogs that had been started by that point as well. So I'd been doing a lot of research in the kind of the basic sciences on rapamycin. I knew it could slow aging in laboratory animals, increase lifespan, affect a bunch of different healthspan metrics.
Speaker 2:And then, in 2020, I started experiencing actually quite a bit of severe pain in my right shoulder and it was sort of gradual. I first noticed it. I have done resistance training for many years weightlifting. I first started noticing it when I was lifting weights or trying to throw a ball with my son, and it gradually got worse over a period of a couple of months to the point where I really I couldn't sleep. And I think you know this is a stereotype, but I fit into many stereotypes of middle-aged men. Like many middle-aged men, I was like I'm not going to go to the doctor, I'm going to work through it, it'll be fine. But it got to the point where I had trouble sleeping. And then one day I vividly remember my son and I went across the street there's a park across the street from our house and I tried to throw a football with him and I just couldn't make this motion. I just couldn't do it. It hurt so much, and so I had to be like gosh, I'm really sorry, but I just can't throw the ball. And I mean, for me that was actually a kind of a psychologically traumatic experience. It was really the first time I'd ever experienced that aspect of getting older, and so that was the precipitating event that caused me to finally go see my primary care doc.
Speaker 2:And so I go in there. I've convinced myself. I had a torn rotator cuff. I knew that's what it was. So I go in there and I'm like, doc, I gotta go see a specialist, I gotta have surgery, get this fixed. And he's like no, I want you to go to physical therapy first. So I did that for a few weeks. That actually made it worse.
Speaker 2:So I went back to him and I said, okay, I tried it your way. Give me the referral to a specialist. And within about 15 minutes, the specialist you know. He had me like move my arms in different directions and do different things. He's like okay, you don't have a torn rotator cuff, you have something called adhesive capsulitis. And I was like, what is that? I'd never heard of it before.
Speaker 2:And so he explains it's also called frozen shoulder, that it's inflammation of the shoulder capsule, not uncommon. It's more common in women than in men, but not uncommon in people in their early fifties. So, anyways, he's like you know I could give you a shot into the joint, but I don't like to do that. That can. That can degrade cartilage. I want you to go back to physical therapy. And he literally said this to me he's like it might go away in a year. And I was like, oh my God, I cannot do this for a year.
Speaker 2:So I I'm out in my car after the appointment, depressed, angry, and I start thinking to myself okay, I study this drug that, at least in laboratory animals, is really good at blunting age-related inflammation. I've got this age-related inflammatory condition. I know lots of people who are taking the drug off label because they think it's going to help them increase their longevity. So maybe I'll just give it a try. And so I designed this sort of self-experiment where I was going to do six milligrams once a week for 12 weeks and then reevaluate. So that's what I did. And again, I'm fortunate that I had access to physicians who were savvy in this space and willing to do this with me. And within a couple of weeks, um, I had a noticeable improvement in range of motion and I perceived less pain and by the end of 10 weeks, I mean, it was 95% gone.
Speaker 2:I really like and again, I'm enough of a scientist to say, okay, there's a placebo effect, it's real, it's possible, it could be placebo effect.
Speaker 2:But this was, um, this's a placebo effect, it's real, it's possible, it could be placebo effect.
Speaker 2:But this was going from such a severe in what I would call debilitation because I couldn't do what I wanted to do to being almost back to normal in a 10 week period. I think it was probably a real effect of the drug and it's biologically plausible. Again, given what we know about rapamycin and how it works, it's pretty reasonable to think that it specifically targeted this age-related inflammatory process to kind of blunt that inflammation. And I've since cycled rapamycin multiple times. So this again was going on three or four years ago now and I usually do 10 or 12 week cycles. I've gone as long as six months and then I take some time off and I have to say in the subsequent cycles there's been nothing this profound Like I have this sort of perception of decreased joint pain when I'm lifting weights and things like that. But I have to admit that could be placebo effect. I'm pretty confident this attenuation or reversal of the frozen shoulder was probably a real effect of the drug.
Speaker 1:That sounds amazing. I mean, I've treated people with frozen shoulder and it's a pretty tough diagnosis and it just doesn't budge quickly.
Speaker 2:You know, the one thing I would say is, in all my studies of rapamycin and I'm not an immunologist, I've tried multiple times to become an expert in immunology and it's just really, really complicated and hard. But at my sort of crude level of understanding of immunology it seems as though rapamycin is particularly effective at blunting inflammation, so chronic, what we would call sterile inflammation. So when the immune system is responding to self in some way or some signal that it is inappropriate for it to be responding to that type of inflammation, rapamycin seems particularly good at blunting, at least at the doses that people are using it at off-label. Now, many people may know that rapamycin is also it was first FDA approved as an organ transplant drug. There it's given at higher doses a different dosing schedule, so usually daily, and I suspect that it is more of a broad spectrum immune suppressant when used in that context, especially when used with other true immunosuppressants, than it is in somebody who's not taking those other drugs relatively healthy taking it in a sort of once weekly dosing schedule. But it's not in my experience. This is anecdotal now, just talking to lots of people. We've collected some data by survey. It's my impression that there are a variety of age-related chronic inflammatory conditions where at least a subset of people can get pretty significant relief from a fairly short-term treatment with rapamycin. Again, we're talking on the order of a few months rather than a year or more.
Speaker 2:One of the reasons why I bring that up is the reason why I settled on 12 weeks to start with is because we had done experiments in the lab in my lab in mice, and other people had done experiments where we had seen that somewhere between six and 12 weeks in mice is long enough to knock down inflammation in a bunch of different tissues and you can actually see functional improvements in at least a few different tissues and you can actually see functional improvements in at least a few different tissues and organs.
Speaker 2:So people had shown that you could see rejuvenation of the heart in eight weeks. You could see rejuvenation of immune function as measured by a vaccine response in six weeks. We had shown that you could reverse periodontal disease and increase lifespan from a single eight to 12 week treatment in mice. So I kind of knew that timeframe in mice was long enough to knock down the inflammation, and so that's what led me to think, okay, well, given that what we're talking about is an anti-inflammatory effect. You might see similar outcomes in humans in that same sort of timeframe and I think what we've learned since then is that seems right. It seems like you can get fairly potent anti-inflammatory effects maybe not broad spectrum anti-inflammatory but more targeted anti-inflammatory effects in that framework of six to 12 weeks of treatment time.
Speaker 1:I want to put this into context for people, because you've mentioned age-related inflammation, and I think in the public eye there is inflammation that happens from an injury, maybe even an illness, but we're talking about inflammation that happens as you just get older. Is that correct?
Speaker 2:Yes, that's correct, and I think we don't completely understand all of the different types of inflammation that go along with aging or all of the different causes. We know about some of the causes at the molecular level, which I think is very informative. We could certainly talk about that if you want to, but I think it's just important to appreciate that there are a variety of reasons why, with age, we see an increase in chronic inflammation. Now, I do this too. Not all of it is what we call sterile inflammation, but most of it is, and again, by that I mean it's the immune system responding to signals that it normally would ignore. It's in many ways very similar, if not identical, to autoimmunity, and there are a variety of different types of autoimmune disorders, but they all involve the immune system targeting the body itself, and I think, to some extent, it's not unreasonable to think of aging as an acquired autoimmune condition. And so we see that there's this broad increase in chronic inflammation with aging, but it's individual, it's very individual.
Speaker 2:Some people have a lot of chronic inflammation, some people have less. It's strongly influenced by lifestyle, so we're going to talk about lifestyle. So I think again, this is my speculation that the people who I've talked to who take rapamycin and they're like, oh my God, I feel so much better. Those are the people who have a very high burden of chronic inflammation and what they're feeling is that reduction in chronic inflammation. The other thing I think it's important to say is there are other ways to reduce chronic inflammation. Fasting is a great example. Cleaning up your diet, exercising regularly, right All of those things will to some extent affect your health, decrease chronic, sterile inflammation that goes along with aging.
Speaker 1:Some people are saying that most diseases of aging are to do with inflammation, and my audience here is hearing about rapamycin and they might be like what is this? Do I need it? But I guess what you're saying is it's been shown to be useful, but there's other things to do as well. But what, in your opinion, would be the most useful intervention for someone to do to decrease this age-related information?
Speaker 2:I mean, I think again, it very much depends on the individual right. And there are some people where if they're eating a low-quality diet and they go to eating a high-quality diet and maybe reducing the amount of calories they're taking in, whether that's through fasting or some other form of caloric restriction will have great relief from chronic inflammation. Other people, that doesn't actually move the needle for them and we don't, I think, have a great understanding why, other than I would speculate it has to do with what the underlying cause of that chronic inflammation is. So I think for some people just focusing on lifestyle will be enough to really have a very large impact. For other people they may need other types of interventions and again, I have to be honest, I'm speculating a lot about rapamycin. I can tell you my own experience and how I interpret it and I've talked to lots of people. But what we don't have, unfortunately, are the definitive clinical trials showing who and where and how much rapamycin is beneficial. But I do think for some people they need that extra bit that can come potentially from rapamycin or from other types of therapies to help alleviate whatever is driving their chronic inflammation.
Speaker 2:I do want to double click a little bit on this idea that aging is all about inflammation or only inflammation.
Speaker 2:I think that's almost certainly an oversimplification, but I do think a lot of the conditions that limit quality of life and potentially quantity of life do have chronic inflammation as a major component. And again, I don't know how much you want to get into the hallmarks of aging, but I'll just say there are these 12 hallmarks of aging that the community has kind of settled on are a big part of the biology of aging. These are molecular cellular processes that we think drive biological aging. Inflammation, chronic inflammation is one of the 12, but many of the others can cause inflammation, and so I think it's just important to appreciate aging is really this complicated systems, biology or network interaction, and chronic inflammation is one of the key, maybe nodes in that network, and it's one of the levers we have that can have a big impact. But I would not want to suggest that even if we could fix chronic inflammation a hundred percent, that people would then stop aging. That's not true we. There are other things happening that contribute to the biology of aging as well.
Speaker 1:You've mentioned about the, the, the cells, that, um, there's a word that I've heard the popular press zombie cells, essentially cells that don't do anything, and in a younger body they would have been taken out by the immune system. But, somehow they've become invisible to the immune system. And they're there and they're not doing any good. But why is our body clearing those out anymore?
Speaker 2:Yeah, so those are called senescent cells and, yes, some people call them zombie cells, and so I think there's a couple of things going on here. So one is, as you suggested, when we're youthful, our immune system is functioning what we would call in homeostasis. Right, it's functioning the way it's supposed to. As we age, at least in part because of this chronic inflammation. And again from a simplistic perspective, people can think of inflammation as activation of the immune system. Right, that's what inflammation is. But what happens with age is you get this chronic inflammation where the immune system is activated towards things it shouldn't be targeting, and what that means is it can't target the things it should be targeting, like pathogens, viruses, bacteria or these senescent cells or maybe more importantly, cancer cells. So that's part of the reason why we see an exponential increase in cancer with age is because the immune system is too busy over here, causing frozen shoulder or whatever else it's doing and not doing what it's supposed to do. So these senescent cells normally would be cleared, as you said, and they're actually important for certain things like wound healing, for causing inflammation, to do what it's supposed to do. But with age we accumulate more of these senescent cells. We know something about the types of damage that cause cells to become senescent.
Speaker 2:Going back to the hallmarks of aging, cellular senescence is one of the 12 hallmarks, and it's sort of this vicious cycle, because these zombie cells it's not only that, they're sitting around doing nothing. So there's a little bit of a problem, because the cells normally have a job and they stop doing their job. But it's worse than that, because they're like workers in a factory who stopped doing their job, but then they go around. They're rabble rousers that get other cells to stop doing their job, and that's what the real problem is. These senescent cells give off inflammatory signals that create more chronic inflammation, and so it's sort of like this vicious cycle where you get the immune system being driven more and more in the wrong direction, and these senescent cells are contributing to that.
Speaker 2:And so one of the strategies that people have thought about and are trying to develop drugs to target are drugs that specifically kill these senescent cells. These are called senolytics, and the hypothesis is that if you could do that effectively, you would increase lifespan, improve healthspan, reduce chronic inflammation. There's some evidence to support that in laboratory animals. We don't yet have evidence in humans, but there are people studying these drugs, and there are both pharmaceuticals and natural products that people claim have senolytic properties, and so I think it's. My personal opinion is it's pretty early days with the senolytics. None of them are very potent, None of them are specific for senescent cells, but I do think conceptually and theoretically, it should be possible to develop newer, better therapies that are more specific and more effective at targeting senescent cells, and there's the potential there to have a pretty significant impact on a variety of different age-related conditions.
Speaker 1:It reminds me of a study where they connected the vascular system of a old rat to a younger rat and then they tested. I think it was a genetic test for the age of the older rat, but it somehow got younger. Was that to do with senescent cells?
Speaker 2:Probably it has more to do with circulating factors that accumulate or decrease with age. So the experimental paradigm you're referring to is called heterochronic parabiosis. So the parabiosis means the shared circulatory system. Heterochronic means different age. So they surgically connect an old mouse to a young mouse so they have the same circulatory system and the observation is that the old mouse actually does better in a variety of tissues and organs, actually lives a little bit longer, it seems, than it would if it wasn't connected to a young mouse, but the young mouse actually does worse. So that suggests that there are both factors in the young mouse that benefit the old mouse and factors in the old mouse that are detrimental to the young mouse. Now, are those factors senescent cells? It's possible that has a little bit to do with it, but more likely I think there are other circulating factors, probably hormonal factors, maybe hormonal peptides and other components.
Speaker 2:This fraction of the blood called epizomes or exosomes has RNAs in it or other metabolites or proteins. So I think we don't know what the specific components are. Some people have hypothesized specific factors, but I don't think anybody yet has convincingly been able to narrow it down to one or a few and most likely it's going to be in the order of tens or dozens of different factors that mediate this effect, but I think it seems clear that the effect is real. I also think there is some evidence that just diluting out old blood can be beneficial, and there are therapeutic ways to do that that people are studying. Even just donating blood may have some benefits in that context, because you're just sort of diluting out some of the stuff that has accumulated and then re-synthesizing new macromolecules. So I think that's yet another component of this complicated puzzle that is biological aging.
Speaker 1:So this field of research seems to be relatively new compared to some other fields of research with health and wellness. So the medical models that I grew up with in the UK and you in the US the doctors there are mainly about treating disease, whereas trying to prevent the disease may be better for us in the long run, but it's where do you put that intervention in is the big question. We're pretty clear on exercise, diet and sleep, but there's other things we're not clear on. My question to you is this if there could be a big cash injection into research, how do you think this field would benefit from it?
Speaker 2:Yeah. So there's a few things I would say about this. So one is I think it's useful to look at the relative investment in individual disease-focused research versus research on the biology of aging, but also it's useful to appreciate what the possible benefits that could accrue to society are. So I don't think most people understand the math here. So first of all, one thing to say that's really important at the individual level if somebody has a disease, it's really important to that person and their loved ones to cure that disease. If somebody I loved had cancer, I'd want that cancer cured right away. At the population level, though, curing individual diseases in isolation is probably the least effective way to approach population level health, for a couple of reasons. One is when you cure one disease you don't do anything about the other diseases, so you don't actually increase health span by very much. The other is that the actual magnitude of effect in terms of longevity is very small.
Speaker 2:So a demographer named JL Shansky, a really, really sharp guy, did an analysis several years ago where he asked a pretty simple question. You think about a typical 50-year-old woman in the United States and we just assume that we had a therapy that cured all forms of cancer. Today a magic pill. What would the impact be on life expectancy for that 50-year-old woman? And it turns out it's about three years, and that's pretty easy to calculate because the CDC is very good at keeping track of what people die from. So you just take out all the deaths due to cancer, it's three years. You cure all forms of heart disease, it's three years and a couple of months. You cure both of them, you get closer to seven years, and so that's not insignificant, but I think it's smaller than most people would expect, given that we've had a war on cancer for 50 years, and 50 years ago it was the number two cause of death in the United States. And guess what? It is today Still the number two cause of death in the United States. So even if we could cure cancer, if we could win the war on cancer, it's not a huge impact on average life expectancy. Now, if we compare that to what is now pretty routine in laboratory animals by using something like rapamycin, you get a much larger increase in life expectancy, probably close to two to two and a half decades for that 50-year-old woman. But you also get the added value that those years are predicted to be spent in relatively good health because you've slowed all of the functional declines of aging, not just one disease of aging. So the potential payoff is much greater.
Speaker 2:Now if we look at the amount that's been invested again just to give people a flavor. So still today I don't know this fiscal year what the exact numbers are, but it's in the ballpark of $6 to $8 billion from the National Institutes of Health goes to cancer, to the National Cancer Institute About $300 million goes to the biology of aging. If you look at the whole NIH budget, it's one half of 1% of the NIH budget goes to the biology of aging, and the biology of aging is the single greatest risk factor for nine out of 10 of the top causes of death in the United States. So there's a huge misalignment and misallocation of resources. In my opinion that has gone on for the past 50 years. Now I think you can make a legitimate argument that 50 years ago the science of aging was not mature enough to justify the same level of investment that we put towards cancer or kidney disease or heart disease. That argument hasn't been justifiable for the past 20 years, and so in my view, really at a minimum I would say the biology of aging should get at least the same amount of resources that we put towards cancer, and I think you can make an argument given that it is the leading risk factor for nine of the 10 causes of death in the United States, there should be the same amount of resources going to target aging as there is those other nine things, and it's just. It's completely misaligned currently. Hopefully that will change. I think we're starting to see some hints that policymakers are recognizing the potential of keeping people healthy rather than keeping people sick the other.
Speaker 2:The last thing I'll say on this. I know I've gone on for a little bit, but I think the last thing that's useful to understand is this isn't just a federal government funding challenge. It's a whole sort of biomedical community research all the way through to clinical practice cultural issue that we have. I, in my view, we have to change. We, for the past hundred years, have been very disease oriented. We focus on individual diseases in isolation and we've been very reactive. We typically wait until people are sick before we try to do something about their health. I think that whole picture needs to change. That's been true in basic research, but it's also true in biotechnology. It's also true in pharmaceutical drug development. It's also true in the way most physicians practice medicine, and I think we need to change that whole paradigm to focus on keeping people healthy rather than focusing on keeping people sick, and I think targeting the biology of aging is an important part of that, but it's not the only part of that change in paradigm.
Speaker 1:Are there some countries that are doing a better job, or at least looking at this more than the US?
Speaker 2:I mean, I think certainly one way you can look at this is the economic investment in healthcare and the outcomes. I think if you look at it that way, almost every developed country is doing better than the US. So, saudi Arabia there was a royal decree, this is my understanding to create something called the Hevolution Foundation and invest ultimately I think it's on the order of a billion dollars a year to aging research. Now I don't know if they're up to that level of investment yet, it's sort of a rolling increase. But they have started to release grants to researchers in the field and if they get to that level, that will be obviously a significant increase in resources allocated to this area of research.
Speaker 2:Again, if we go back to the numbers I gave before, about 300, 350 million from the U S federal government and we're talking about a billion from Saudi Arabia into the field so it's a threefold ish increase in investment in the field, which is great. That's. That would be fantastic if and when that happens. But if we still look at that relative to what the U S government invests in cancer or infectious disease again, by the way, the leading risk factor for death from infectious disease at least things like COVID-19 and influenza is aging, it's still a drop in the bucket. So again, probably $12, $13 billion a year to cancer and infectious disease, not even a third of a billion to aging biology.
Speaker 1:Okay. So we've got an overriding philosophical problem in the medical care system. That's saying, well, aging may be just inevitable. There's no point researching that, because we're all going to die.
Speaker 2:I think historically I think that's been part of it and again, you know, I think, to be fair to the establishment right, I think it is valid to say that that has been the perception. Again, I don't think that perception has been valid for 20 plus years Like we have. The science has clearly shown that aging is modifiable. It's under genetic control, it's under environmental control. We know a lot about the mechanisms. We still have a lot to learn, don't get me wrong, but we know a lot about the mechanism. So there's really no excuse for anybody who's informed to take the view that aging is not modifiable, that it's not a genetically and environmentally determined trait. But yes, I think that's part of it.
Speaker 2:I also think there has been the perception and this is not completely unearned that the field is populated with low quality science and charlatans and unfortunately, I think the majority of scientists in the field like I know most of these people they're my colleagues and many of them are my friends are really good scientists doing top notch work. I would say, oftentimes better quality science than in infectious disease or cancer. But there are some high-profile cases of just really bad behavior, really low-quality science and certainly lots and lots of people trying to make a buck by selling snake oil. So I think that has also made it more challenging for serious people policymakers, funders to really take the field seriously, because there is a history of charlatanism and snake oil in the field and you know, as is often the case, a small number, a minority of bad actors can have a negative impact on sort of a larger system.
Speaker 1:I've heard you talk about scientists sometimes not publishing the studies that don't fit with their prevailing paradigm. The nine studies show this thing doesn't work and one study does, and they publish that one it exists in every field yes, absolutely, but it's not unique to aging.
Speaker 2:It exists in every field yes, absolutely, but it's not unique to aging. I think this is fit a very simple, straightforward model and still most scientists do it the right way, but it only takes a small number taking the shortcuts that can have a very large impact on the quality of science overall. And one of the more insidious aspects to this is so certainly, people get promoted, they become famous, they can start companies and get wealthy doing that. But the more insidious part of this is that bad models get in the literature and it just takes a really, really, really long time for that stuff to get cleaned up. And again, that's not unique to the aging field, like I know some of the dirty skeletons in the closet of the aging field. But this is true in every field. There's a bunch of that in the Alzheimer's field. You know high profile stuff where you know just bad science became dogma and it took a really, really long time for the community to come around to recognize that it was bad science and to discredit it. So unfortunately, it just is really hard. Once something becomes accepted, it's really hard to clean that up and it eventually happens. So the scientific approach eventually gets it right, but it takes a really long time.
Speaker 2:Any result in the longevity or biology of aging, I want to see it replicated independently, at least once and again. I know almost everybody in the field so I know who I trust and if I see it replicated by somebody I trust I'm going to give that more credit than by somebody I don't trust. But I always want to even stuff from my own lab. I wanted to see somebody else replicate it before. I was like, okay, yeah, that is rock solid for sure, and I think that's kind of the minimum that should be. The minimum standard is independent replication by you know somebody else, not by the same lab. What you often see is one lab that goes on and they publish three, four, five cell science, nature papers on the same topic and then we find out 10 years later it was all wrong, right, because it was only one lab that did all that work.
Speaker 1:What are the most exciting interventions evidence-based interventions for promoting healthy aging that are available today?
Speaker 2:Yeah, I mean again. I think part of me feels almost silly saying this but the most obvious things are healthy diet, regular exercise, and we can get into the more nuanced aspect of that. But then it starts to get very individual in terms of what does that mean? A healthy diet, I think in general, you know, cutting out simple sugars, right, cutting out processed foods as much as possible, maintaining a healthy body weight. So healthy diet, regular exercise, high sleep quality.
Speaker 2:The one a lot of people don't talk as much about, I would say, is sort of mindfulness and human connection, human relationships. But I think that probably is equal, if not more important for at least for quality of life, and and we now have evidence that human relationships and I would also put companion animal relationships in that same bucket are actually pretty important for quantity of life as well. So I kind of think of those as what I would call the pillars of lifestyle or the pillars of healthspan, and I think one thing that I like to emphasize is there's a reason why the pillars of healthsp span impact not just one disease of aging, but apparently most, if not all, of them. It's because they impact the biology of aging. That's why lifespan is so potent or sorry, lifestyle is so potent at modifying health is because we now know some of those connections through which healthy diet, exercise, sleep, relationships at the molecular cellular level can impact the hallmarks of aging. So it's just important for people to understand. Yeah, I mean, everybody knows about lifestyle but not everybody understands that these lifestyle factors actually seem to influence the rate at which you're aging or the quality of your aging process. So again, we can talk about, like what I think is is are some of the important pieces of those but, but I would put those buckets out there. And then, when you get beyond um, beyond the pillars, I think there's a few things that I really try to to incorporate myself and that we're we're working on at OptiSpan, and this is less in the biology of aging and more in how do we figure out where individuals are at and help them get on a better health span trajectory.
Speaker 2:So I think there's a really big component of preventative healthcare, preventative medicine, and I would put in that bucket early screening tools, repeated biomarker assessments, and again there's a pretty long list that we could go through. For what are the at least in my view, the biomarkers that are more informative, less informative, but it goes. It kind of runs the gamut from stuff that I think everybody should be doing. So regular, comprehensive blood work, as an example and by comprehensive I mean way more than what most people get at their primary care physician Looking in detail at vitamins, nutrients, toxins, inflammatory markers, hormones, right, I think all of those things are kind of low-hanging fruit that as a society, at least in the United States, we do a terrible job of actually monitoring and helping people with. There are pretty easy, non-invasive imaging modalities, so ultrasound, dexa, even MRI, I think is valuable. There are some interesting sort of advanced cancer screening tools that are coming online, the liquid biopsy tests like the Grail test from Gallery. Again, that's not right for everybody, but I think those are the kinds of things where you can often detect problems early, before they become disease, and help people get on a better trajectory, hopefully to avoid the disease, done in an appropriate way as part of an overall educational program.
Speaker 2:Continuous glucose monitoring is one of the stickiest tools for lifestyle modification, right? When you educate people about how their body actually responds to the food they're putting in it in real time, or to the exercise that they're getting or to their sleep quality, you can't unlearn that, and I think it has a long-term sort of behavior modifying effect that a lot of these other approaches people try to take to lifestyle are less effective at modifying behavior. So those are the kinds of things I think about that would be in that preventative bucket and also somewhat personalizable, and then we can talk about this more experimental stuff. So rapamycin I would put in the experimental bucket, I think for some people, as I've already mentioned, I know many people who have had pretty significant improvements in quality of life. We have no idea if it's going to be a quantity of life intervention at this point. Um, uh, I you know you can think about things like metformin. Metformin is interesting. I don't personally think metformin is a great choice for people who don't have, who are metabolically healthy, I'll put it that way but for people who are metabolically challenged, I think it's a fantastic drug and it works really well. Um, I think we can. We can talk about you know.
Speaker 2:I know there's a lot of interest in peptides not a lot of data yet one way or the other, but I think there's definitely biological potency there. I think the question is what's the risk reward profile look like with some of these peptides? I put stem cell therapies in that bucket as well. I think what I would say about those kinds of things is what I would really like to see, as much as I really don't like a lot of how the FDA operates is what I would really like to see. As much as I really don't like a lot of how the FDA operates, I think I would really like to see a little bit more regulation so that we can actually get data from these experimental therapies to evaluate. When do they work, how do they work, who do they work for? I think right now, there's a lot of enthusiasm and not much data to back up the enthusiasm and I'm as enthusiastic as anybody, but I would really like to see the data.
Speaker 1:You didn't mention resveratrol as well. There's something in there that people seem to get very excited about that, because it's a compound in red wine, but in order to take it into a dose that might have a clinical effect, you have to take a lot of it, but you have an interesting opinion on that.
Speaker 2:Yeah, well, and I would also put resveratrol in the entire supplement bucket. So I think there's this question of supplements in general, right, and then we could talk about specific supplements. So I think supplements in general also, for me, often fall in that very challenging to evaluate category, because we usually don't get the really solid, you know, clinical trial type of data for supplements, unfortunately, and I think the industry is massively corrupt, unfortunately, and so there's a lot of bad stuff out there. Having said that resveratrol but that's not to say that supplements don't work. These molecules do have biological activity. Usually they're not particularly bioavailable. So I would say this is a generalization, but for many supplements, the doses people are taking are not bioavailable enough to actually have the desired biological effect, and I think resveratrol may fall in that bucket. As you alluded to, the challenge with resveratrol in the case of longevity is that the original data that was published, suggesting that resveratrol could impact the biology of aging, turns out to be all wrong, sorry, um, or at least mostly wrong, uh, so it's just not reproducible. So I I think I I sort of have characterized resveratrol as the most debunked longevity drug in the world, because when you look at the meta-analysis of all the studies that have ever been done in any organism testing whether resveratrol affects lifespan, the net result is zero, which means that there were lots of studies where it shortened lifespan. So we were talking about replication before. This is now looking at, you know, a hundred plus different scientific studies testing this molecule and the net effect is zero. So I think it's pretty safe to say resveratrol is not a longevity drug at any dose, um, at least in laboratory animals Again, I'm a scientist.
Speaker 2:I can't say for sure in people, but you know there's no reason to think it impacts the biology of aging in a potent way. Uh, but that doesn't mean it couldn't have biological effects that are positive or negative on humans. Um, but I just, you know, sort of fall into the the camp that unless there's a really good reason to believe that something you're putting in your body is going to be helpful, I would tend to err on the side of not putting it in your body. And one of the reasons why I sort of I have a relatively high bar, which is some people are going to be like this, is the guy taking rapamycin and he's saying he's got a high bar. But but I think I I tend to have a pretty high bar before I add anything to my supplement stack, which is like four things.
Speaker 2:It's tiny, um, uh, is because I think we don't, we haven't we.
Speaker 2:It's tiny is because I think we have a limited understanding of interaction effects, right, when we start to combine a bunch of stuff.
Speaker 2:And my view on this is the human body is one of the most complex pieces of biological machinery out there, and if you think about any other complicated machinery that you can possibly think of and you go around and you just start mucking around in there and moving screws and bolts around, the likelihood you're going to make that machine function better is really, really small.
Speaker 2:And so I think when you start doing 10, 20, 30, 50 different supplements, none of which or few of which we actually know is going to have a positive effect, the likelihood you're going to get a net benefit versus a deficit to me airs on the side of deficit. So I want to be careful, relatively, I want to have at least a reasonable feeling in my own mind of the risk reward being on the reward side before I start adding stuff to my supplement stack. And I say this because I know a lot of people take a different view, which is that well, if it might help, I should just add it, because these things are perfectly safe. I think people have a fundamental misunderstanding of how supplements are, and are not, regulated. The FDA has pulled a whole lot of supplements off the market after they found out that people got sick and died from those things, so it's not the case that everything that you can buy on Amazon is perfectly safe for you.
Speaker 1:Okay, I think people listening to this will want to know what is in your supplement stack and then, after you tell us that I'm going to share with you what I take and I want you just a quick fire yes, no, and a couple of reasons why. So what's in your supplement stack and why?
Speaker 2:So right now mine is pretty limited. So I do take a multivitamin. Really I think of that as an insurance policy. I'm not convinced that there's a ton of benefit from a multivitamin, but there's also very limited risk in my view. I take vitamin D because I know I live first of all I live in Seattle area, so I don't get a lot of natural vitamin D and I know I'm deficient. I like vitamin D because I can measure it, take the supplement and see a change in my measurement. So I take vitamin D. I take omega-3, same reason, take B12. That's about it. I used to take creatine and I actually stopped taking creatine about three, four months ago, not for any particular reason other than I just wanted to kind of see if I felt any different. And I haven't noticed any difference. But that's about it. And then periodically I take rapamycin.
Speaker 1:My supplement stack is similar. Occasionally it's a multivitamin, a sort of phase in and out. Creatine I had a creatine expert on the show convinced me that we got to get that into our body when we can. Omega oils I had Dr Bill Harris on the show, really interesting guy and then some B vitamins as well. So I know you've done a little bit of research into niacin and NAD precursors and that kind of thing. Can you just expand on that slightly and why you don't take that?
Speaker 2:Sure, yeah, nad is one of the most common molecules in all of our cells. Every cell in nature has NAD. It's what's called a cofactor that is involved in thousands of different metabolic reactions in our cells. It's very important for what's called mitochondrial function, which is the production of energy in our cells, but it's also involved in a whole bunch of other processes, including DNA damage response. And people got interested in NAD in the context of aging because it is a requirement for the activity of a family of enzymes called sirtuin. More broadly speaking, there is a belief that NAD levels decline with age, and if you could boost NAD levels then that would be beneficial for aging. There are other people, like Charles Brenner, who are skeptical of the aging link but who believe that NAD levels are important for a variety of different age-related diseases and so, again, boosting NAD in that context would be beneficial. So there are multiple molecules niacin, nicotinamide, nicotinamide, riboside, nicotinamide, mononucleotide and even NAD that are sold as orally bioavailable supplements. Turns out NAD itself is not orally bioavailable. I don't know why anybody would buy that pill and take it, but you can buy it. But the others do seem to be orally bioavailable and probably can all increase circulating NAD levels and at least NAD levels in the liver. They all also probably get broken down to niacin by the gut microbiome or nicotinamide. So the reason why people would pay 10 or 100 times more for nicotinamide riboside or nicotinamide mononucleotide I don't know, but people do and I think we have almost no evidence that taking NAD precursors is actually beneficial for the average person.
Speaker 2:There have been a few small clinical trials. Some of them show no effect. Some of them show potentially beneficial effects in certain populations. I think Parkinson's disease is one place where it's kind of there's kind of some interesting preliminary data. So I would say it's not that there's no evidence, but there's not a lot of evidence that these molecules are beneficial for human health at this point and there's a little bit of reason to maybe be cautious.
Speaker 2:So there's one study in mice showing that oral supplementation with nicotinamide mononucleotide led to apparently beneficial effects in heart and I think liver as well in the context of aging, but led to pathological effects in the kidney and maybe actually limited the life of those mice due to pathological effects in the kidney. So is it possible that NAD precursors in people predisposed to kidney disease could exacerbate that condition? Yeah, it's possible and, as far as I know, predisposed to kidney disease, could exacerbate that condition. Yeah, it's possible and as far as I know nobody's really studied that yet. So in my mind that falls in the category of you know, maybe there's a benefit for some people, maybe there's a benefit for a lot of people, but also maybe some risk, and it just hasn't pinged my radar as something that rises to that threshold that I want to start taking NAD boosters as a supplement.
Speaker 1:We're getting close to the end of our time here and I think we can talk forever about this stuff. But I want to have a look to the future now and just mention to the listeners that there was some interesting research in stem cells by a doctor called Yamanaka and Gordon. They actually got the Nobel Prize for this and they managed to take a stem cell and reprogram it to become a pluripotent stem cell. That's effectively reversing the aging process, and one of the exciting areas in this longevity medicine is this research into stem cells and how we can possibly reverse the aging process on a genetic level.
Speaker 2:Yeah, so what you're referring to is called epigenetic reprogramming, so it's not actually reversing aging genetically. In other words, what I mean by that is, when we talk about genetically, we're talking about genetic changes with age, we're talking about mutations, chromosomal rearrangements, but on top of the DNA there are these epigenetic marks that control which genes get turned up or turned down, and that's what can be modified by the Yamanaka factors in epigenetic reprogramming. And there's a growing body of evidence that epigenetic dysregulation or changes in the epigenome with age drive at least a subset of age-related phenotypes diseases, functional declines. Again go back to the 12 hallmarks of aging. Epigenetic dysregulation is one of the 12 hallmarks, so it's not everything. But many people believe that it might be sort of a proximal driver of other hallmarks of aging. And if that's the case, then if you could reverse those epigenetic changes, you could have an outsized impact on the biological aging process, and the Yamanaka factors provide an opportunity to do that.
Speaker 2:Now there's a couple of things that make it challenging to reprogram in the context of aging without causing catastrophic problems. So one is if you reprogram all the way, if you de-differentiate all the way, you basically become a bag of stem cells like a jellyfish right. So that's not good for a complex animal like a human being. So you want to avoid fully reprogramming and it turns out that if you reprogram too much or at the wrong time you can induce cancers, which also is problematic if your goal is to increase lifespan and health span. So the technology is pretty challenging to really dial this in, and so what I would say is, given those technological challenges, what people have been able to show is that through partial epigenetic reprogramming and maybe show is that through partial epigenetic reprogramming and maybe even multiple rounds of partial epigenetic reprogramming, it does seem to be the case that you can improve function in a few different tissues and organs and probably increase lifespan by maybe the same amount as rapamycin, maybe not quite as much as rapamycin. So I would put it in the intriguing but not sort of a game-changing category at this point.
Speaker 2:Having said that, if people can get the technology really dialed in to do this optimally, is it possible? You could do a lot better than rapamycin or even better than caloric restriction in terms of magnitude of effect. Yeah, it's possible, and I think that's where a lot of the enthusiasm comes from. And again, maybe it's useful just to give people numbers that they can appreciate. So a lot of people like to look at percent effect on lifespan. So you talk about caloric restriction can increase lifespan by 50%. That's fine. But that is a little bit problematic because the percent increase is dependent both on the numerator and the denominator. In other words, the effect of caloric restriction and the effect of the controls is what determines the percent increase. Many times the largest percent increases in the literature don't come because the intervention was that effective. It comes because the controls were short-lived.
Speaker 2:So I'm gonna give absolute numbers for average lifespan or let's say maximum lifespan. So we know that for a typical laboratory mouse strain that we're talking about, average lifespan, let's say, is 900 days. That's kind of my gold standard. I want to see a control strain live 900 days. So rapamycin we showed in my lab 12 weeks with rapamycin would take you to 1,050 days, reasonably large effect on lifespan. Weindrich and Walford published back in the 1990s that maybe it was 1980s that 60% caloric restriction could get mice up to like 1,400 days. So huge effect on average lifespan. Epigenetic reprogramming is like, maybe comparable to rapamycin 1050 days. And the reason I give those numbers is I want people to appreciate the bar is pretty high, and so, for all the enthusiasm that people are out there jumping up and down talking about reversing aging, they haven't even done as well as rapamycin. So to me it's like let's actually show me the data before you start really hyping this thing. That hasn't happened yet.
Speaker 1:What else is out there in the possible future? Is there anything with AI that could be interesting for us to know about?
Speaker 2:Yeah, again, I think the idea that AI is going to solve aging is very optimistic. Part of the reason why I say that not because I question the utility of AI. I think AI tools are going to be immensely powerful, but I think our understanding of biological aging is still fairly rudimentary. And so, you know, ai can only act on the information that we give it, and if we're giving it a very crappy training set, the output is going to be crappy. So I think we need to learn a lot more about the biology of aging before AI is going to really live up to its potential. There are a couple areas where I do see potential for AI to be quite powerful. I think one is in disentangling these really, really large, complicated data sets. So we can collect very, very large amounts of data on epigenome, transcriptome, proteome, metabolome, microbiome, and we don't really know what to do with all of that data. And we can do that in people as they're aging and the same person over time. I think AI will be very useful in bringing out signatures that are hypothesis generating for future experiments and potentially giving us tools that we can use to evaluate interventions in people in real time. That's kind of the promise of these biological aging clocks. We're not there yet, but I think that's the hope. The other place AI can be useful but we don't have the data yet is in predicting which interventions are going to be most effective, first at the population level, but then at the individual level. The reason why I say we don't have the training set yet for AI to be able to do that is we really haven't tested that many interventions. If you look at all of the data, in all of the literature, in every organism that's ever been studied there's a database called DrugAge which is publicly available only has I don't know it's like less than 1,500 compounds that have ever been tested for lifespan period. That's ridiculous. We should have tested 15 million interventions by now. So I think AI can be really powerful once we have a training set. That's very powerful. I think right now our training set is so tiny we can't really use AI in any meaningful way. To say, based on what we know about these 1,500 molecules, we can predict with high confidence what other molecules out there are going to have robust effects. So that's an area that I've been interested in and working on, and we developed some technology in my lab to do very high throughput, sort of massively high throughput longevity, drug discovery. And again, I think if we can get to a database of 500,000, a million interventions, then you can really start to apply these AI tools in a predictive way to identify new combinations, new interventions of very large effect size. At least that's the hope. Maybe.
Speaker 2:The one thing I would like to leave people with is a sense of optimism, right? I mean, I do think that the field has made quite significant progress over the last 20 years. So look, I started studying the biology of aging in 1998 as a graduate student first year graduate student at MIT. So I've been in this field for 26 years. I've seen a lot and the quality of the science and our understanding of the biology of aging has increased dramatically in that time period, despite being underfunded, at minuscule levels compared to other fields. And what's most exciting, one of the things that's most exciting for me is to now see so much interest in going out of the laboratory and actually applying some of these lessons in the clinical space, both in companion animals and in humans. So I'm very optimistic that in the next decade we'll see the first FDA approved intervention to target the biology of aging. We will see drugs being developed and brought to market some already probably on market, like rapamycin generics that can have an impact on the biology of aging and improve healthspan in people. I hope that we will also see greater investment, a continued growing recognition of the importance of this type of science, and that that will also translate through to a shift in the way that the healthcare community thinks about health. I think there's movement in that direction and that's a big part of what I'm doing now with OptiSpan is trying to help continue that shift and promote that have come online in the last couple of years.
Speaker 2:Particularly the generative AI tools have the potential to have a big impact on healthcare disparities, and this is something I actually think about a lot. So our program at OptiSpan so we have several programs, but one of them is a very, very sophisticated health optimization program. It's the kind of clinical program that, frankly, only rich people can afford. I mean, that's just the reality of the situation. I think these AI tools, depending on how the regulatory environment evolves, actually have the potential to bring that level of care, or something close to that, to a much, much greater fraction of the population. Now, obviously, there's going to be all sorts of questions around when are people going to feel comfortable with AI in healthcare and data privacy concerns? Those are all real and valid. Feel comfortable with AI in healthcare and data privacy concerns? Those are all real and valid, but I do think that there is a real opportunity to address healthcare disparities that have seemed unaddressable for economic reasons in the past with these AI tools, and I'm pretty optimistic that we have the potential to get there.
Speaker 1:This is an exciting space and I'm looking forward to the future. Where can people read a little bit more about you, a little bit more about OptiSpan? Where would you direct them?
Speaker 2:Sure. So I'd say the best place to go is our YouTube channel. We have a podcast, the OptiSpan podcast, and check it out. I talk about all sorts of different topics and have, hopefully, interesting guests. I think they're interesting, at least on there. And then our website is Opti-spanlife. Uh, the other place I'd point people to is the dog aging project, dogagingprojectorg, and there is a 501c3 nonprofit that, uh, myself, daniel Promislo, kate Creevey created to support research into companion animals. Um, and in particular, the dog aging project called the Dog Aging Institute. That's dogaginginstituteorg. I'm also on X, formerly known as Twitter, at MK Berline, although, to be honest with you, I'm not on X very much anymore. I've just, you know, honestly, it's energy draining more than it's energy producing for me, so I go on like maybe once every three weeks. I probably shouldn't have said that, but that's the reality.
Speaker 1:Well, Matt, thanks very much for coming on the show. I really appreciate your time.
Speaker 2:My pleasure, thank you.
Speaker 1:Thank you for joining me in my conversation with Dr Matt Kaeberlein. If you have enjoyed listening to and learning from this podcast, please leave a comment, and also you can leave a suggestion for a future podcast guest that you would like us to feature. If you're on Apple, you can leave us a comment, a five-star review, if you can pretty. Please Remember, if you want my direct help, send me an email, ed at edpadgettcom, or visit my website, edpadgettcom, where you can learn a little bit more about how I can help you make your lifestyle your medicine.