How Dogs Are Going to Make You Live Longer – Matt Kaeberlein | 1145 | Dave Asprey

For me, food is mostly not a longevity issue. It's a health span issue.

Exercise, sleep, quality. I think the reason those things impact multiple age related diseases simultaneously is precisely because they are impacting the biology of aging. I think the way I would frame it is you can only get so far by modifying those lifestyle factors. And so you're not going to see 150, 160-year-old people in good health simply by modifying lifestyle.

Exactly. We're not gonna extend life very much. You can reduce toxins, you can probably hit your maximum lifespan, sort of genetic.

Potential without additional intervention.

Yeah. And that's lifestyle and all that, but extending it, that's stuff like the gene therapy that I just did. Maybe the guy who said, man will never fly a year before the Wright brothers flew. Maybe he was right. I'm gonna bet on us extending human lifespan, because we are. You're listening to the Human Upgrade with Dave Asprey. You're listening to the Human Upgrade with Dave Asprey. Today we're going to talk about dogs, specifically how to hack your dog to live a lot longer. Okay, maybe not quite, but maybe our guest is Matt Kaeberline, who's working on exactly that. Extending radically. Extending the lifespan of dogs and other pets as well, but starting with dogs, because dogs are better than cats, in case you were wondering. What you're going to hear here is a really fun conversation that mixes human longevity because Matt is the CEO of OptiSpan, where they're extending human life, or at least healthspan as much as they can. By the way, he's one of those guys who still says healthspan because he hasn't quite bought in on the fact that we are extending human life. And that's the goal. But I'm going to bring him over on this one, so, you know, that'll be fun. Oh, hey, Matt. Yeah, you didn't hear that right. And then we're going to also talk about packing your dog, which is what I already mentioned, and we're going to talk a lot about longevity in your pets because there's such a commonality of humans and dogs. So listen to the whole episode. You'll learn something about how to think about longevity for you and then how to translate it over to your pet. Matt's in town because it's south by Southwest here in Austin, which means it's a madhouse. How bad was the airport coming in?

You know, it was pretty crazy, but I made it, so that's all that counts.

My son is coming in. He's flying by himself. And he's probably never seen an airport at that level of chaos. So I'm kind of looking forward to his eyes rolling back in his head as he just sees what true traffic chaos is like. Now I'm giving a couple talks at south by this year. You're also giving a talk on what you're doing with pets, right?

Yeah. So there's a panel discussion on. I think it's called something like, could dogs be the key to Unraveling human longevity? Or something like that.

Well, it's neat. So you're doing the dog aging project. And dogs have this really nice space between. In longevity research that a lot of my books are based on. It all starts with yeast and roundworms and then maybe goes to mice. Right, right. And then maybe we have some other data somewhere or another, and then we start using it with humans using aging clocks.

That's what we do today. You're right.

Yeah. And aging clocks are pretty useful because before that we couldn't do anything. There's still some, like, Luddite skeptic people.

Like me.

Well, no, like Peter Attia, who says aging clocks aren't scientific. I'm like, I want to see Steve Horvath in a wrestling match with Peter Atia.

Well, I know both of those guys, and I'm pretty sure I know who would win.

Well, Peter would win, but that's because he's a meathead, not a longevity scientist is my point here. So, sorry, Peter, you need to revisit what is scientific. And maybe less time in the gym, more time in the labs. Just saying.

So I actually want to push back on that a little bit. Peter is a friend of mine, but also one of the people I. I've.

Been on stage with him.

He's not a bad guy among. Among.

He's not a believer in longevity.

No, I would disagree with that. So, look, I think. I think Peter has strongly held opinions, like all of us do, that are.

That are wrong. Yeah.

Most of the time he's right. And I would say among.

On statins and vaccines, among a lot.

Of the influencers in this space. I think Peter does a good job of doing his homework, and I think there is some nuance here. I am certainly not going to try to speak for Peter, but here's the way I would frame the aging clocks.

There you go.

I think they are very useful research tools. I think that the utility of the aging clocks in the consumer space is pretty questionable in my mind. And part of that is because we really don't have much data on how precise or reproducible these clocks are when sold by companies to consumers. And so I actually have a lot of concern that these clocks are being misused and abused in the consumer space.

Interesting.

I also think that it's important to recognize that all of the clocks that are currently in use are really only measuring one, sometimes two small aspects of biological aging. We don't really know, you know, to what extent are they capturing the entire biological aging process?

Nothing does right now. And we do know that the aging clocks and Steve Horvath's interpretation of it is the first one, but there's about a dozen others. They can predict when you're going to die within about 10 years, pretty reliably.

I think it depends on what you mean by pretty reliably. I can look at somebody and predict pretty reliably whether they're going to die in 10 years.

That's a good point. I would have to look at. I don't know if they compare it.

I've had this conversation with Steve, so I kind of know how the math plays out. They're better than just looking at somebody. They're honestly not that great.

They're better than telomeres.

Yes, but actually that's true. But the question is, is that because we don't have the tools yet to precisely measure individual telomere lengths. I actually think this is a super interesting questions, way off, way off on a tangent. But I think it is really something we don't. We don't know at this point whether the epigenetics, which is what Steve's clock is based on. Those are nice because we have huge dimensionality. There are tens of thousands of epigenetic marks we can measure and we can do it very precisely. That's very different than the telomeres, where we only have, you know, 46 or so things we can measure and we can't do it very precisely. So maybe telomeres actually are a pretty good clock if we could measure them. I think we just don't know. I actually don't believe that. I'm just saying we don't know the answer at this point.

It's true that we're discovering a lot and we know more now than we did.

Nobody could argue with that.

Every 72 days, the amount of info we have about biology doubles, right? Yeah. So it's this golden age of longevity research. And I've seen telomere numbers swing by 20 years in one week. That's either because of lab errors or because your blood is a terrible Place to telomeres.

Well, I think that's a good point. Yeah, absolutely. The tissue type that you're measuring, and blood, of course, is a complex set of cell types that you're actually measuring. So. Yeah, but this goes back to my point earlier, which is that I think that while these things can be quite useful in a research setting, because of a lot of those uncertainties about what we're actually measuring, their utility in the real world for, I think, is unclear. But I'm super enthusiastic that we're going to get there in probably the not too distant future.

I would say that aging clocks are extremely scientific and early days. And so the idea that, well, there's no way we're going to extend human life and there's no way to measure how old you are biologically, which is kind of a summation of Peter's work, which is why I'm like, let's go to the A4M. Let's go to the people who are actually looking at extending life with something besides exercise and statins, because, well, I think those have been tried for a while and no one's living longer. That's why I'm.

But you believe it?

Well, 20 minutes.

You can tell by looking at you.

20 minutes a week of exercise is all I do, and I do it with AI and that upgrade labs. I believe that most people way over exercise, including Peter. Right. Because it turns out it's not the area under the curve, it's the slope of the curve up and most importantly, the slope of the curve down, and then the nutrient and protein availability.

So I'm going to push back a little bit and suggest, by the way.

Peter could kick my ass.

Just to be really clear, most people are. Don't. Don't over exercise. Maybe people in the optimization world over exercise.

People who exercise every day, usually over exercise. And almost everyone doesn't move enough. Right. So there's a lot going on there. And it's funny because, you know, we're here to talk about dogs, but we're talking about humans, because I think dogs are the bridge between the research from mice and yeast and the little creatures. And, hey, if they can live longer, there's pretty good evidence that some of that stuff will help us, but it doesn't always. Right. And so. Well, what's in the middle? Well, dogs are a lot closer to people than they are yeast, but they're still pretty far away.

Yeah. Yeah. And I mean, so, first of all, I love the way you sort of frame that because. Because my career path has Followed that trajectory. I started in yeast as a graduate student, then worked in nematode worms as a postdoc. And when I started my own lab, we started doing stuff in mice because I believed that there were aspects of aging biology that were, in fact, shared across this broad evolutionary distance. Turns out that's right. And then about 10 years ago, it occurred to me that, as you suggested, dogs are this really powerful bridge between the laboratory studies and humans, not only because they're closer to humans in a biological sense, but there's this huge environmental component that we can't or choose not to study in the laboratory that's really important for human aging. And because dogs share so much of the human environment, at least companion dogs or pet dogs do, we can capture that environmental component and really understand, you know, not only what are the most important genetic factors that influence longevity, but what are the most important environmental factors. And then there's this huge other piece which is what I'm most interested in, is we can actually test whether interventions affect lifespan and health span metrics in dogs, which would be great for giving us confidence about people. But I'm a dog person, so what I really care about is making my dog and other people's dogs live longer, healthier lives.

The number of people in the longevity enthusiast field, whether you work in the field or you're just someone like me who's. Who's spent decades. I guess I do work in the field, come to think of it, but I didn't used to. So the number of us who have pets who are not on longevity regimens is very low. All of us know, huh? The things that work for me, like red lights, and we know what it does with mitochondria and cell folding and all that stuff. Maybe I should shine it at the dog when the dog hurts and then the dog stops hurting, and it probably affects longevity and maybe not feeding them the pet equivalent of chicken nuggets will also affect longevity. Right. So we all kind of do that. Whereas it's still very common. People go to the store and they buy big things of pet food that are made out of euthanized dogs. Maybe your dog shouldn't eat that. There's some really bad stuff happening.

I mean, there's some really interesting and in many ways unfortunate parallels between what most human beings eat, or at least the quality of the diet that most human beings eat and the quality of the diet that most human beings give to their companion animals. And there's complicated reasons for that, obviously, but, you know, I think you're Right. I think the people who are on this path towards improving their own health span trajectory often recognize that the same thing is true for their pets and take a healthier approach to their pets.

So you're a, you're a PhD and actually a very well studied one because you, I guess published 250 studies, something like that, you founded research centers and you're in the American Aging association. And so you talk like the best PhD ever. But I think what I heard you say in that was that humans and dogs shouldn't eat kibble. Did I get that right?

Well, certainly, I think humans probably should not eat kibble. I think again, the quality of the food itself. Right. In the general food supply is really problematic, both for dogs and for people.

Yeah. So we've got to fix food. And for me, food is mostly not a longevity issue, it's a health span issue.

I don't know. I understand that perspective. I would say I'm a little bit less certain. I certainly believe to some extent that the reason quality diet, exercise, appropriate amount of exercise, whatever that is. I think we're still figuring that out. Exercise, sleep, quality. I think the reason those things impact multiple age related diseases simultaneously is precisely because they are impacting the biology of aging. I think the way I would frame it is I. You can only get so far by modifying those lifestyle factors. And so you're not going to see 150, 160 year old people in good health simply by modifying lifestyle.

Exactly. We're not going to extend life very much. You can reduce toxins, you can probably hit your maximum, your maximum lifespan sort.

Of genetic potential without additional intervention.

Yeah. And that's lifestyle and all that.

Right.

But extending it, that's stuff like the gene therapy that I just did and I maybe.

We'll see.

We'll see. Of course. Right. And for all of history, it's always been a we'll see for all the things we're doing on things like that. We just have better tools now to do it. And hey, maybe the guy who said, you know, man will never fly a year before the Wright brothers flew, maybe he was right. I'm going to bet on us extending human lifespan because we are. I mean, you talk, no doubt, you see all the research being done.

I have no doubt that it's possible. Right. Of course, I think, you know, the questions in my mind more revolve around how long is it going to take before we can actually demonstrate that these things work. And this is where, going back to the aging clocks, I think once the aging clocks evolve to the point where there's confidence that they are in fact predicting future mortality, future disease risk with high precision. Then you have a real opportunity. It's still not going to be proof until you actually see somebody live that long. But you can be pretty darn confident that these things are having the effect that you wanted them to have. Then the last question is, is there some long term consequence that we don't know about that's going to offset that? Right. Because it only takes, only takes one mortality event to keep you from living a long time. So that's an unknown. And we're not going to know until we get there.

One of my big longevity strategies is to drive a heavy vehicle.

Right. Avoid dying, I think, is rule number one of longevity. Yeah.

You use physics.

Necessary but not sufficient.

Yeah, sorry. If you're in the Prius, I want to be in the Suburban. And you know, it's not to say that I think I'm more important than you. I'm just allocating my resources in a way where physics protects me. And it's something I think is not looked at enough in the field of longevity is just, you know, don't fall down and break yourself. Don't blow out your spine on hitting a new PR when you're 60. It's probably not worth it, right?

Yeah, absolutely. I mean, we kind of think about four movements at Optisman as we're trying to communicate some of these ideas to people. And one of them is staying alive. Right. You got to avoid risky behaviors and there's a lot of luck. There's a lot of probability in life, but you can change the probabilities in your favor, like you're saying, by taking steps to reduce your likelihood of dying.

If you had to pick one thing, not exercising or eating just the worst possible fast food diet for the rest of your life, which one would you pick?

I would.

Oh, God. If you want to exercise, I don't.

Think I could eat the worst fast food diet. I'd have to choose not exercise. That would kind of suck for me, but I could. Yeah. I mean, again, as somebody who ate a pretty crappy diet, like many people, for a big chunk of my life.

I think we're about the same age.

Now that I'm out of that world, like I. It just is repulsive to me to think about going back to it.

I will never go back to eating food that makes me feel crappy. And I am willing to die on that. And this is what the regulators who think we're going to live on crickets and grain. I can't live on that and I won't. And I'll eat a politician before I'll eat a cricket. And I'm just okay with that. Right. They're made out of meat. It's not, not my ideal source of meat.

But I actually think this is pretty interesting. Cause I've talked to a fair number of other people who kind of share that. Not so much about eating politicians, but the sort of revulsion at the idea of going back to this standard American diet. Right. And it's hard sometimes for people who aren't already in this place to understand that. But I think it's just worth emphasizing. Right. It's really about building habits. And if you can get out of the habits that you're in, that society and culture pushes you towards and get to a better place in terms of the quality of your diet, you will, I can almost guarantee you will agree that there's just no way you want to go back to that once you get out of it.

And also, it's not the same for everyone.

This is true. Absolutely.

There are people who just feel great on chicken. I am a beef guy and I've tested everything. I would eat gravel if I could, but beef is what works for me. And you try and take away my beef with a regulatory thing, it's like, no, you've taken away my oxygen. We are not going to be okay with this.

So here's the way I think about it. I think there are multiple types of high quality diet. A one size fits all. I completely agree with that and I think that, that. But I also think that there is a high quality diet that can fit almost everybody. So in other words, I, I don't believe that there, that there are people who will just thrive or if there are, they are the way outliers who will just thrive on, on garbage.

And you know, there are some. I, I know people who do, at least for a while. And I also know a couple people who thrive on a vegan diet. It's just their kids and their grandkids who are paying for it because it matters. In fact, if you look at the health of vegan offspring and things like that, it's not pretty, the placental health. So you might get away with it, but you're actually paying for it in future generations. It's a big experiment.

Yeah. I mean, I'm less opinionated about vegan diets. I'm not a vegan, but I'm certainly not a vegan basher.

I Was a devout vegan for a couple years and it trashed my health like in a big way. I'm a food supporter. I absolutely love the vegan philosophy. Like you want to take care of your health, you want to take care of the planet and you want to reduce animal suffering and death. The problem is the vegan diet doesn't do any of those three things. And I believed it did.

And so, yeah, and I think the way I sort of also think about this, but I struggle a lot with the nutrition literature. I mean, honestly, I mean, look, these are, these are good scientists trying, trying to do good science, but it's really hard to do high quality, definitive science in human nutrition.

Oh yeah.

And so I really struggle with a lot of the epidemiology. And so I personally, you know, I'm very slow to come to strong conclusions about what is the optimal diet, what isn't, and what are the long term consequences to some of these dietary, different dietary approaches people take. I think, you know, again, the way, the way I sort of align is there are some things that we can be almost certain are not good to have in your diet. Right. Highly processed foods, a lot of simple sugars. Right. Low, low quality fats. So I think those are the things that, that most people should agree if they're knowledgeable. You want to get out of your.

Diet and all the flavorings and coloring.

Yeah, right.

The.

Yeah.

And those are bad for dogs, they're bad for people. And from there, you know what, what plant toxins can your body tolerate versus mine? You know, 28% of rheumatoid arthritis is caused by nightshades. If you have the genetics. But for, if you don't have the genetics, you can eat them all day long. Right.

And this really actually ties in, in an interesting way to the biology of aging because I think a lot of what's driving that is our own individual immune response.

Right.

So the reaction of the immune system to molecules that we're getting in our diet and other places in the environment that drive chronic inflammation. Some people are just much more prone to that sort of hyper inflammatory state. And that leads to a lot of the conditions that you're talking about.

I'm certainly one of those, being £300 and all the health stuff I've gone through when I was younger. So I recognize I'm coming from behind in my goal to live to at least 180. Well, did I try? I'm fine with that. I just want to do 50%.

Well, the nice thing is this is pretty Cool. One of the things that has has emerged from the literature in my academic career is that it doesn't seem like there's a point where it's too late unless you've got a disease, where the pathology of the disease has sort of outpaced the biology of aging. So we now know, and we didn't know this when I started, but now we know you can start intervening in middle age and still get pretty big effects on both longevity and health span.

It's funny, if you start before pregnancy, the three months before your mother was pregnant with you and you have a really healthy pregnancy, you get the most leverage on longevity.

That's all the epigenetic effects, right?

Yeah. That was why my first book was on fertility. And what do you do before you get pregnant? And then it's sort of, you get less and less leverage the longer you wait to do longevity interventions. I'm just like in my 20s, I learned from people in their 80s, all this longevity stuff in Palo Alto.

I wonder though, because that's sort of the mindset I think people had before 2009, when the first study on rapamycin in mice was done where they kind of accidentally started the treatment in a 60 year old equivalent mouse. But I think what we've learned is that at least with some interventions, you can get most of the benefit even starting late in life with some of them.

You can, yeah.

And I think as these tools to kind of reset the epigenome evolve, we might actually be able to get closer to that sort of initial epigenetic state that you were talking about.

It may not even matter. At a certain point in the world that I see coming, you'll be able to edit your mitochondrial DNA so it more closely works with your nuclear DNA. And these are all editable settings in your hardware. The biggest challenge will be if you make too big of a change, is just causing systems integration to work between all the differences.

Yeah, it's interesting. I don't know how far. I mean, again, I agree, theoretically that's all possible. I think the challenge that I see, and this is where, you know, it'll be interesting to see how effective the sort of evolution of AI tools is at disentangling the complexity of the biology. Look, I'm in this field deep and I recognize how little we actually understand.

Half what we think we know is just wrong. And the AI believes it. That's one of them.

So it'll be interesting to see. But I do agree all of that's on the table. I just don't know how long it's going to take to get there.

So I have a pretty good track record of, you know, seeing things before they happen. I'm the first guy to sell anything over the Internet. Before E Commerce had a name, it was a T shirt that said caffeine. My drug of choice. And I sold out in my dorm room. I was in the Miami Herald and like the first data center company. So I've. I've picked reliably. I also have a track record of thinking it's going to happen before it does. But now I'm wise because I have some age on me now. So I would have said, oh, it'll be three years before we get there. If I was 20, I'm going to say 10 years before we get there. Mostly because of advances in AI subject to two things. One, that governments don't succeed in basically destroying our access to these things or to breaking AI. I don't think they can, but they might. And two, that a comet doesn't hit the planet. But otherwise I'm pretty confident on it because we have a hard time conceptualizing this is even beyond exponential rates of growth in AI. So I think we're going to get there. As long as we train the AI to care about it, then it'll do it. But if we train the AI to be really good at killing people, it might not care much about making us live longer. So this is.

Yeah, it'd be interesting to see. We should sit down and come up with a bet about like, what are the actual. What do we actually want to bet on? I'm less optimistic, but in part that's because. And again, this is where the exponential equation can fool you. But I look back at where we were 10 years ago in this field and I don't see 10 years from now as getting to that point. So we'll see.

Oh, not everyone will get there. Well, the first couple people will get there in 10 years.

Well, yes, there may be people who are. There's already people who are editing their genome. So sure.

I mean, I've had the gene therapy, but it wasn't my. My inheritable genome.

Which gene therapy?

I did the follistatin gene therapy with mini circles, just plasmid level stuff. And I'm impressed. And I'll be in the first trial for clobal.

The biology is real. I mean, no question about it, it works, right?

And now the fact that, you know, nine years comes off your aging clock, for that you can say, well, that doesn't really matter. Very much. I'm like, yeah, but the bone density increase in the increase in muscle and the decrease in fat works.

Yeah, it's super intriguing. That's one of the spaces I'm watching pretty closely.

It's funny because, you know, in your day job you're at Optispan, you're working on extending human lifespan for high end clients. And then in your night job you're saying, well, let's do the same thing for dogs.

Yeah. Although let me clarify. So it's not for high end clients only. What is Optispan? So what I would say is our mission at Optispan is really to enable the transition from reactive disease care to proactive health care for as many people as possible. Right.

I like it.

So, and I think there are lots of ways you can do that. There are lots of smart people working on this, but I think we have an opportunity to contribute. And so we're really looking right now at two lanes. One is sort of high end concierge medicine, because that's the place where you can do the most expensive, most sophisticated sort of approaches here. But we're also working in the corporate wellness space and trying to say, what can we do in this proactive science based healthcare for, you know, 1500 $2000 a year? Something employers might be willing to put towards employee health recruitment, retention, things like that. So we really are trying to democratize this as much as possible, recognizing that as a for profit company, you know, you also have to be able to make revenue.

Absolutely. If you run a business that doesn't make any money ever, it's probably not a very good business. Unless you're Amazon or Tesla. Oh, wait, sometimes you can have external funding, but I'm with you. I believe that the best way you can change the world is as an entrepreneur, not as a donor. Right. And I also have donated meaningful amounts of money to projects I believe in. But end of the day, if the money makes more money to support the cause.

Now start the flywheel.

You've got a movement versus you've got a one time flash.

People will throw the word superfood around like it means something and they'll apply it to almost anything. I'm waiting to see superfood kibble for humans. But there are real superfoods, and there's one that I've been researching for years with so many health benefits you almost wouldn't believe it. I first started using it for gut health and then I figured out that it supports metabolism, hair growth, healthy skin immunity, and even athletic performance. I'M talking about Colostrum. Colostrum is the first nutrition we receive in life and has all the essential nutrients that your body needs to thrive and grow. To get those nutrients, it's important to properly source your colostrum. And that's why I use Armra. Colostrum Armor is a bovine colostrum concentrate that's natural, sustainable and third party tested for purity and efficacy. Armor's process preserves the integrity of 400 bioactive nutrients. Since I started taking Armor Colostrum, I've noticed a difference in my energy, my fitness, my skin, my gut, especially when I travel. And I like it that I can take one or two or three scoops and I could just take it in my mouth or I can drink it with water and it tastes mild and it really does change the state of my body. It's a potent anti aging substance. Go to tryarmra.com T R-Y-A R M R A.com use code Dave they'll give you a 15% off your first order. People are talking about this a lot online. I've been a fan of Colostrum for years. I just couldn't find one that consistently worked. Armor really makes me happy because it does.

We've talked about human aging a little bit here, and there's a lot we don't know and we're making great progress. Now we also know small dogs live longer than big dogs. Does this mean that small humans live longer than big humans?

Yeah, actually there's some evidence to support that. So this is something where people have a lot of confusion. There's this idea that large animals live longer than small animals. And that's true if you look across species. So if you look across the animal kingdom, larger animals do in fact live longer than small animals like elephants and whales. Yeah. But when you look within a species in general, at least in mammals, smaller individuals tend to live longer than larger individuals. And that's true in people. It's complicated in people by the fact that there is a social component to being tall. And so you have to kind of take that into consideration. Dogs are interesting because the body size difference is so much bigger when you look across the dog species that we can really see that difference in aging rate.

I've had six dachshunds over the course of my life, including when I was a kid, and all of them lived 15, 16, 17 years old. But the last two were when I knew the most about nutrition and longevity. And I applied those things. Merlin, who was the last dog that I had Passed away and he was 15 and a half or something, but he got a krill oil every day and he got a little bit of collagen. And he ate mostly raw grass fed beef and some egg yolks on occasion and very small amounts of vegetable matter. And when he was young, I gave him things like the barf diet, you know, bones and raw food. And I don't think dogs are supposed to eat huge amounts of celery and carrots. It didn't work so well. But he ended up with a dog that just didn't have pain in his body, didn't have a lot of the debilitating things. No lipomas and good fur. And it was pretty incredible, actually.

Yeah. And I mean, I think this goes back a little bit to what we touched on earlier about how a lot of the components of the diet for dogs as well are pro inflammatory. In other words, they're not things that the canine body has evolved to see. So there's an immune response against some of these factors and that gives you this chronic inflammatory state which drives a lot of diseases of aging. A lot of the pain that you mentioned, one of the things that's challenging in dogs is there's much less data on the long term effects of different diet in dogs. So there's a lot of strong opinions out there and not a lot of good data. So one of the things we want to do at the Dog Aging Project is actually collect that data so we can actually start to understand and be able to draw strong conclusions that yes, in fact, a particular diet does seem to be associated with much longer health span. There's that word. And lifespan.

Well, we all want healthspan. So it's a great goal. It's just not a big goal. I want healthspan twice as long. Yeah, that's a big goal.

I agree. So I hear what you're saying. Here's the way I would think about it. And this is easier to talk about in humans than it is in dogs. Again, because we have the data. At an individual level, I agree completely. At a population level, healthspan in the United States sucks.

Right?

So 60% of people have a chronic disease. Average lifespan in the United States is 38.1 years. That means that if you define healthspan as the period of life without a chronic disease or disability, healthspan ends for most people before they're 38 years old. Life expectancy is in the mid-70s. So if we could, if we could push that healthspan curve out, that's a Big deal at the population.

It's just, it's a very easy goal. It's mostly.

It's easy to talk about.

It's harder to accomplish behavior change. We don't need to know more to do that. We just need to do more to do that. You can move it out 20 years with what we know today.

I think that's true. I think it's more than behavior change, though. I think there's policy factors, there's all sorts of other stuff that goes into that. But I hear what you're saying.

You have to clean out the big food agencies that control the government agencies that tell us what to eat. That might be part of it. And, and maybe change some tax incentives, but those are all ultimately behavioral.

It's doable.

Yeah. It's not like we have to crack the atom in order to do this.

This is true. Right.

And what we're looking to do in the doubling of human lifespan is the equivalent of a Manhattan Project level undertaking.

I agree. I mean, look, the best that people have been able to do in a mouse beyond genetic intervention through development is about 60% increase in lifespan. So we've still got a long ways to go.

But what about the 95% from carbon 60?

Right. So you have to be careful about short lived controls. So percent change is numerator over denominator. If your denominator is much smaller than it should be, your percent change gets dramatically overinflated.

So then you're saying you get mice that are engineered to die in 90 days. You make a move of 180, or.

Because of poor experimental conditions, they were exposed to toxins or pathogens or whatever that shortened their lifespan. So I guess I should reframe that. The largest effect that has been reproducible in a quality experiment is about 60%.

Okay, there you go. I like that. And it's funny, my 180 number, we have humans who are 120. I just want to do 50% better.

Hey, I think that would be. That's a fantastic goal.

Yeah, that's, that's where 180 comes from for me. And I know I might not make it, but I don't think it's a crazy goal. I think it's a big goal. Right?

I would agree. Yeah.

And that's, and that's why I keep talking about it. It's so many people. Like, that's crazy. Like, I don't think it is. It might not happen in my life, but I'm going to bet on it. Right. And what else am I going to do with all this time. All right.

And it's fun to talk about, right?

It totally is. One of my questions about dogs is, and you're trying to control what they eat and all this sort of stuff. I have taken my dogs to a dog park. They eat poop. How do you control for poop intake?

So you believe it or not, that is one of the questions on the survey. So the Dog Aging Project longitudinal study actually has a very comprehensive survey tool that we use to collect a lot of data about the dog's environment, health history. So indeed, at least one of the questions, there may be more than one, addresses whether or not your dog consumes feces. Also asks about time spent at the dog park, time with other animals. So we really do try to capture that. It's not quantitative. We don't ask how much feces does your dog consume?

But you have to get a scale.

But believe it or not, I mean, there are. There are you. I'm sure you know this, right? There are certain dogs that absolutely love to eat poop from other dogs. And then there are other dogs that won't touch it. They might eat rocks or something. Right. So there's a genetic predisposition here as well.

Is there a certain breed that's more of a poop eater? Because I don't probably, but I don't.

I don't know the answer.

I don't want a poop eater breed.

So, yeah, we had a Kazon or some people call them quiche hounds. That was a poop eater and boy, you had to watch her like a hawk.

You're like, don't kiss me, don't kiss me.

Oh, and Kazons love to kiss you as well. Yeah, it's a bad mix.

The other thing that's a great crossover is that people who own dogs live longer than people who don't. Is that from emotional support, energetic support, or like some bacterial thing in the microbiome?

It's a good question. Yeah. I mean, I think there could certainly be biological, like you're talking about the microbiome, those kind of biological interactions. My intuition is that it really more is comes from the sort of connection that a lot of people get from their dogs. So we all, we all know that that human connection is really important for happiness and that people who have strong human connection also tend to live longer. And I absolutely believe that many people can get at least some of that connection from their companion animals. There's also really good data that interacting with a dog or a cat, believe it or not can have impacts on the physiology of the person in terms of reducing stress hormones, reducing anxiety. So that certainly could play a role as well.

So you don't think that the toxoplasmosis from cat owners that causes the crazy cat lady thing is real Again, there's.

Probably a genetic predisposition there.

That was the best PhD answer ever. That was like the worst loaded question I've ever asked a guest and you dodged it like a pro. So, Matt, congratulations. The other difference between dogs and cats is that if you were to pass away unexpectedly, the dog will sit next to you and starve to death guarding you, and the cow will eat your eyeballs. Just saying.

I have no direct experience with that.

I like cats. I just, you know, if I had a choice, I would pick the dog. So, guys, I know that if you have a cat right now, you're just.

Really trying hard to go after the cat.

Maybe we can do a crossover study with vegans. What do you think of vegan cat food and vegan dog food for longevity?

Personally, I wouldn't use that as a PhD.

Who knows?

Yeah, I wouldn't personally feed that to my dog.

Yeah. What about feeding people food to dogs?

It depends on the people food. Right. So feeding Big Macs and fries to your dog on a regular basis, probably a bad idea.

So I go back to my childhood. We didn't know much. In fact, we were in the days of get rid of butter and use squeeze margarine brand muffins. And it's fine to go get a Big Mac. And we would boil hot dogs and just boil them and make hot dogs at home. And we would give the hot dog water to the dogs and they would drink it until they were so bloated, like little stuffed sausages, you could, like flick their sides and they would make weird, you know, watery sounds. And I look back and like, that was the worst thing I ever could have done to my poor dogs. But, well, they like it and it's food and I'm willing to eat it. And I was just entirely ignorant of the effect of the food on my biology, which was Jack.

Sure, right.

And on the dogs. But those dogs still live 17 years. They had a bunch of lipomas and like their final couple of years maybe weren't that comfortable compared to later in life. But it seems like food quality in humans from 25 years ago and now there's something different that maybe is worse for pets and worse for humans. Do you think there's been a change?

Well, there's clearly Been a change. I think there's no question that the composition that the typical person is eating in their diet is obesogenic. Right. And I mean, that's just, that's just using a fancy word to say something we all know, right. Which is that what people are eating now drive us towards obesity. And all you have to do is look at pictures from 30, 40 years ago of people and this is obvious. So exactly what those mechanisms are, I think we're starting to learn. I think there's been a lot of engineering of the food to get people to eat it faster, to get people to eat it more, eat more. And that's intentional. Like that is intentional engineering. I understand why the food companies did it. But then there's this additional factor there, which I don't know whether it was intentional or not, that it's not satiating. So then people are hungry again, so they eat faster and eat more. And there's this cycle that drives obesity. So absolutely there have been changes.

Okay. I think that's a big part of it too. There are some compounds that I've written about that a lot of people in the longevity field are paying attention to, like rapamycin. Can you talk about rapamycin? What is it? And should we give it to our dogs?

Right, so rapamycin is a small molecule that was found on Easter island, which also goes by the name Rapa Nui. That's where the drug gets its name. It's actually produced by bacteria there in the soil. And rapamycin has this super cool backstory. So if anybody's interested, you can Google it and find it.

Tim Ferriss went to the island to go discover it or something along with.

Your buddy Peter at the Attia. Oh yeah, and my real buddy Peter Attia.

No, I've been on stage at a 4m with Peter. It's just weird to have someone on stage saying you can't extend human life. I'm like, what is wrong with that?

This is one of my bucket list items is to get to Rapa Nui and see where it all started. But regardless, that's where rapamycin was first discovered. And it was initially attempted to be developed as an antifungal anti cancer agent. But the way it actually was developed clinically was for organ transplant patients because it is a potent anti inflammatory and what people call anti proliferative drug. In other words, it slows down the cell cycle. And so in an organ transplant patient who's got a transplanted organ, you want to target the immune system to prevent it from reacting to that organ. So it was clinically approved as an organ transplant drug, and it's called an immunosuppressant, and that's how it's been used clinically. So there's a lot of data in human use there. But I think we have to recognize those are in people who there's a reason why they had an organ transplant. They're taking high doses of rapamycin and they're taking a bunch of other true immunosuppressants. So it does have some side effects in that context, but it's sort of got a bad reputation clinically because of how it was used and developed. Now in parallel, really, around the 2000, early 2000s, several labs independently discovered that you could treat yeast, worms, flies, like we were talking about, with rapamycin and increase lifespan. And so people started studying what's the mechanism there. And it turns out rapamycin is an inhibitor of a protein called mtor, mechanistic target of rapamycin. And we now know from studies over the last 20 years that MTOR is, if not the most potent, one of the most potent knobs that we can turn to regulate the rate of aging in laboratory animals. And as we alluded to earlier, there was a study, I think, that really changed the game for rapamycin in the longevity field in 2009, from the interventions testing program, where they showed that you could start treating mice at 20 months of age, which is about the mouse equivalent of a 60 year old person, with rapamycin, still get significant effects on lifespan. And then since then, lots of labs have shown not only can you increase lifespan when you start treatment in middle age, but you can actually improve pretty much every metric of aging that people look at in pretty much every tissue and organ where people study it. So it really seems as though rapamycin modifies the biology of aging in a way that can increase both lifespan and health span, again, at least in laboratory animals. And you can get the benefits starting in middle age.

MTOR is an interesting compound because of that research. Back in 2009, when I first started the biohacking movement and I wrote one of my early posts was how to triple down on mtor because it works. I mean, you're a PhD, you can say if any of this is wrong, but the picture I have in my head from reading all the papers is that it kind of works like a spring. You want to suppress it, but when the more you suppress it, the more it's going to spike when you unsuppress it so the three big things I could find back then that were going to suppress MTOR temporarily were fasting, coffee and weight bearing, exercise. So I went, well, that's funny. Drink coffee during your fast, lift at the end of the fast, and then eat a meal with protein and carbs because carbs raise mtor like 10 times more than protein. Right. Insulinic carbs.

Right. So I actually think this is where there's a lot of confusion out there. So most people would say it's the protein that I think it's the carbs.

Do you think it's the carbs?

Because I don't actually, I don't know the answer to that. Right. And I think it depends on where you look is the honest, honest answer. I think it depends on the tissue that you're looking in. But it is absolutely massively over simplistic to say that it's, that it's only amino acids that activate mtor. But you'll see, you see that all the time.

It's something that I'll say. I, I probably went 50% too far in that direction in my longevity book because I wrote about, you know, 0.6 grams of protein per pound of body weight and there's a bunch of studies that support that, but most of them are because of methionine and tryptophan and other things that increase mtor. But if you want to look good, you need MTOR because that's how muscles build and you don't want sarcopenia and you don't want bone loss. I have absurdly dense bones and a relatively high amount of skeletal muscle mass when I look at all my quantified stuff. So if I drop my MTOR too much, the only thing I could eat would be fat because carbs raise it and protein raises it from animals. But I could eat brown rice protein full of arsenic and stuff, but its biological availability is so low I need twice as much of it. So I would be eating industrial processed plant proteins, huge amounts of them, farting all the time and having all the.

There's no way there's a quality of life issue there.

It seems like you can't do it. So where did you end up on the Protege?

So, again, so. So I think those are actually two different questions because I think mtor. First of all, you. I'm not convinced that, that getting MTOR as low as you possibly can is the right answer. Right. There's an optimum to everything. But I also think that we need to recognize that MTOR cycles like many other molecules in our body in terms of activity. And there are natural cycles of MTOR activity that are different in different tissues, different organs. And the optimal level of MTOR is probably going to be different in different tissues and organs. You talked about muscle. We know that in order to build new muscle you need to activate mtor. Right. So the optimal level of MTOR in your skeletal muscle may be different than the optimal level of MTOR in your kidney or your brain. And we just don't know. I think this gets back to how little we know. So here's the way I think about it. I think we know dietary protein. Again, this is challenging because it depends on what else you eat.

It depends on what kind of dietary protein.

Yeah, absolutely. But I think if you look at people who are eating a high quality diet, I think in general, this is my perspective of the literature as it exists now, a higher relative amount of dietary protein in combination with resistance training is a very good strategy for maintaining and growing muscle mass as you get older. And bone density. I'm glad you actually mentioned that because a lot of people only think about muscle, but if your bones are crap, it's not going to matter how much muscle you've got. So I think this is actually really, really important. And I worry that this again, you get some people out there who simplistically think about mtor and they're like, well, just don't eat any protein. Low protein's good. I worry we're misleading people.

It's destructive to be on low protein.

Hey, biohacker. So you've heard of stem cells. You know they're powerful and maybe you wonder about stem cell therapy, but the process seems kind of a dense.

But because it is.

Well, there's a new company called Stem Regen that I've been working with. The founder, Christian Dropo, is a stem cell scientist. He's traveled the world in search of unknown plant extracts that can stimulate the release of your body's own stem cells right from your bone marrow. His discoveries led to an amazing breakthrough in stem cell therapy. Stim Regen is the world's first, first stem cell enhancer. Just two capsules will release 10 million of your own stem cells into circulation. Those stem cells migrate throughout your body and help your body naturally repair and renew itself. This is a new, powerful and very cost effective way to get the benefits of stem cells without having to hop on an airplane. And how about 20% off? Now go to Stemregen Co Dave. That's Stemregen Co Slash, Dave.

Over the last about three years now I've tested the 0.6 to 0.8 grams and said, you know, I think it has to be nonsense because of this carbs versus protein thing. So I've been doing reliably one gram per pound of body weight or a little bit more. And I also looked at my aging clock and the last, at the end of my 0.6 to 0.8 kind of things, based on my longevity book, I was at 0.69 for my rate of aging. And you know, we say, are you those matter? Do those not? That would be.

This is the Dunedin pace.

Yeah, exactly. Dunedin pace. It's part of the True age. My audience, most of them heard the episode on the True age test. So just to figure out, it's like, hey, I need a metric. It's better than telomeres. And they have about 20 other metrics for aging that I'm tracking. I'm going to do a big post on that that I've done things like pulse wave and P300D. Like there's all kinds of things that are like correlated with age. They don't cause it, but they show is the ultimate output of your system like a young person or an old person. So looking at all that, after three years of absurdly high 200 grams of animal protein every day, my rate of aging is 0.72, which is the same as Brian Johnson's on his non vegan diet because he's eating 20 grams of collagen protein every day, which comes from cows.

I have no idea what Brian Johnson said. I completely ignore that whole thing.

I actually, I interviewed him. He's a very fun person to talk with because he's so unusual. Yeah, right. I don't agree with him and I'm.

Not trying to bash him. Look, I like the fact that he is making his data available to people. I think that's great.

I do too.

There's a lot of noise.

Well, there's a lot of noise and also we're all biologically unique. And so like for me, I haven't published my list of 150 supplements that I take. Right? And the reason for that is that I don't want people copying me. I have people who worship the ground I walk on and guys, could you stop? I'm a knowledgeable guy and I'm inspirational, all that stuff. But you didn't used to weigh 300 pounds, have autoimmune conditions and all the weird stuff that I did. And you don't need excessive amounts of B6 and zinc and biotin genetically the way I do. So if you do what I do, you'll probably at best shit your pants, and at worst, you'll feel like crap for a couple weeks. So we have to customize this to you. And I'm working on tools for you. And you must see this in your optispan, because some people come in and this person just needs a couple things. So I don't want to do what a guru does. I want to do the things the guru does for the reasons the guru does them.

Yeah. And one of the things that I like to emphasize is whenever possible, I think biomarkers are where it's at for sure. And whenever possible, measure, intervene, and measure again. In other words, you want to know where you're at. You want to know whether whatever the intervention is that you're doing is working. And you want to get yourself into what we think is the optimal range. And too many people, I think, just start randomly doing stuff they don't ever measure in the first place. And I think that's something that can be okay, but can also get you in trouble.

It can. And I'll say, look, if you have very little money taking, you know, vitamin D, A, K and E, it's probably better than not doing anything, even if you don't have a blood test.

Sure. But the blood tests are not that expensive. So, again, this is, I think.

Hold on. Half of households in the US don't have a thousand dollars to spend on emergency expenses right now. Like, Biden has stripped our currency by just printing a lot of dollars. So for some people, a $50 vitamin D test really is a lot.

Sure.

And so if. And a lot of people listening are in that situation right now, and they're. They're saying, well, how many supplements versus the quality of my beef? So it's like, if you're there, don't get the test and do the lowest cost thing that's likely to move the needle and hope. But I sure want you to get the test.

I think that's fair. Look, I think we could go down a whole rabbit hole on healthcare, disparities of which there are many, and they are real, and it sucks. That's the reality of the world we live in. Yes. If you absolutely cannot afford the test, you're probably better off being probabilistic and saying, there's a chance, a good chance I'm deficient. Take the supplement. I think a lot of people who claim they can't afford the test actually don't know how much the test Cost and could stop going to Starbucks and getting their $10 coffee every day.

Yeah, just skip two drinks one night a week and you'll be fine. I agree with you people. Allocate things different.

Okay, so anyways, we were talking about.

Rapamycin in dogs, but that's because you're a broad spectrum, knowledgeable longevity guy. So I'm having fun with you. Talk to me about triad.

Yeah. So rapamycin, we know from the preclinical literature in laboratory animals, it seems to affect biological aging across the evolutionary spectrum. And it occurred to me, again, this was probably 2013, 2014, that, that there were actually several things we knew could increase lifespan and health span in mice, and those things almost certainly would work in dogs. And I've been a dog person my entire life, and I suddenly realized, holy crap, I could probably extend the lifespan of my dog and other people's dogs, but we need a way to actually test it. And so that's how TRIAD evolved was as really an effort to do a rigorous double blind, placebo controlled clinical trial in dogs to answer the question, does rapamycin increase lifespan and improve healthspan metrics in dogs? And so we designed the trial. It took about five years to get funding to actually do that trial. And then we started enrolling dogs, and it's happening right now.

Any preliminary data you can share?

Yeah. So we've done two what we really thought of as safety trials. So these were shorter term. So the first one was 10 weeks, the second one was six months. Again, randomized double blind placebo controlled. So a few things I can say with certainty. So we did not see any significant adverse events in any of the trials to date. So we're pretty confident that rapamycin, at least at the doses we're testing, can be used safely in dogs. We found statistically significant improvements in two measures of age related heart function, both left ventricular function, that was done by echocardiogram. And in the rapamycin treated dogs compared to placebo. And in both trials, there were increases in owner reported activity. So little bit weaker kind of data because this was owner reported. But again, the owners were blinded. They didn't know if their dog was getting rapamycin or placebo. So I think we, again, we can be pretty confident about safety and there's some evidence for improvements. I don't know anything about the outcomes from the big trial now from triad, because that trial is still blinded.

It looks like you guys designed it to detect a 9% change in lifespan.

Yeah. So it was originally Designed to detect a 15% change in lifespan. That was 230 dogs. And then a few years ago, a group of donors came together. Peter Attia actually put this together.

Cool.

Along with Tim Ferriss and a couple of others to increase the size of the study to 580 dogs. Which gives us the 9%.

Yep. So 40 to 110 pounds. You basically want big dogs at least seven years old. What about guys who like little dogs who think they're big?

Yeah. So this gets back to the idea that big dogs age faster than small dogs do. So in order to have that statistical power, we needed to have dogs that were aging more rapidly and already in middle age in order to be able to see an effect on lifespan within the three year window of the trial.

All right. And humans taking rapamycin, I mean I've done it on and off. Do you take it?

I am right now, yeah. So often I tend to cycle rapamycin. I've done typically 10 or 12 week cycles and I'm honestly pretty non scientific about it. I take it when I feel like it or when things in my life are lining up. But I've, I've done 6 milligrams a week, 10 milligrams a week, 8 milligrams a week. So sort of in that range. The first time I ever took rapamycin was because I was having some very severe shoulder pain and after a long drawn out process got it diagnosed as frozen shoulder or, or adhesive capsulitis. So inflammation in the shoulder capsule. The doc really said there wasn't much that he wanted to do. So much you can do, go back to, go back to physical therapy and it might go away any year. And I was just, you know, I was horrified by that because I couldn't sleep, couldn't throw a ball with my kid. And I started thinking, you know, I know about something that is really good at knocking down age related inflammation. So I set up my own N of one experiment, 6 milligrams a week. And I had, you know, I planned from the very beginning that I would give it 10 weeks and see what happens. And within a couple weeks there was a very significant reduction in pain. And by the end of the 10 weeks, I'd say 95% range of motion, almost no pain and hasn't come back. So for me it was a very important kind of quality of life changing experience.

It drives me nuts because as a biohacker and I see that like, well, have they tried shockwave? Have they hit it with ozone which is very cheap, 150, 200 bucks. And surprising evidence for that. And then have they done hydrodissection? Have they done all the stem cell things you could do or just exosomes? And there's all these things that don't take a year that affect quality of life. But all of those, except maybe ozone, are more expensive than rapamycin. So if you can knock it down with a pill, I'm all over that. I noticed when I went above six that I tended, because it's immunosuppressant, I tended to get more colds and things like that. I typically don't get them very often. I'm very robust now. I used to get them all the time when I was younger. So I guess that there's a dance there that you have to do. Based on the state's of your mast cells, whether you have long Covid or your mold exposure like I do.

I think there's a lot of individual variation just in both uptake of rapamycin and the rate at which it is cleared. So we know that rapamycin is metabolized by something called the cytochrome P450 family, which is also involved in a lot of drug metabolism. So some people are just faster metabolizers than others. So I think there's a very. And this is where unfortunately we just don't have much good data on individual sort of responses to off label use of rapamycin.

I have a question about the dog study that just popped into my head. Are you tracking whether the owner of the dog is a couple versus a man versus a woman?

That's a good question. So I think the answer is yes, but indirectly. So we do get information about number of people in the household.

Okay.

So we get both number of adults, number of kids and other animals. I don't think we ask ever about, you know, spousal relationship or anything like that in any of our, our data.

It's more what sex are the people I'm thinking about.

Oh, yeah, we get that.

Yeah. It's, it'd be interesting to look at whether there's, there's any information in that. Because you might have seen the studies that show when a woman feeds the lab mice, they get an entirely different stress response than men.

Absolutely. There's the spare mom thing going on. Yeah, super, super, super interesting there. Yeah.

For that matter too, if a woman in the house with a dog is on birth control versus not on birth control, we would know what's going on with the confounding variables. We just don't know about AI. Should solve that for us in about three years.

Again, you're very optimistic.

Well, it's that my field is computer science. Right. And understanding exponential growth. We still don't think of it well as humans, but this isn't exponential. This is an exponential of an exponential right now. So when you go really deep on that stuff, you just realize the world's gonna look really different every year going forward. Yeah, I'm pretty sure we'll both have jobs, and I'm pretty sure that next year we'll both be sitting at home and it'll look like we're in an interview right here. I mean, the stuff that's coming down is crazy. I'm in the very late stages of creating an AI that has every word I've ever spoken, every. Every research paper I've ever used, and all of my books. And this is 1200 interviews on my show and probably another thousand on other people's shows, along with a bunch of other research. So that when people come in and say, I want to do what Dave does, I'm like, no, no, no. Do what Dave would recommend. Right. Based on all of these interviews, what would Dave's guests recommend? And then it's even down to the point of saying, well, how much energy do you have to invest? How much suffering are you willing to endure? Because some things are harder than others. Are you going to tap into your bone marrow the way I did a couple times? Probably not. And then how much time and how much money are you willing to put in? And what is your goal? So that's ultimately where health span and life extension end up. If your goal is a healthy health span and you want to look a certain way, your recommendations are going to be different than someone who says, I don't care how I look. Make me live twice as long. Right. Or I want to be, you know, I want to be the brain from Pinky and the brain. Okay. Like, totally different set of supplements and totally. I think we're there with our knowledge, but our ability to filter and sort the knowledge you've studied for 20 plus years.

I think you've got more confidence in the quality of the data that's out there than. Than I do. I have done enough scientific research in a lab and seen enough data from other people to be pretty skeptical about the quality of a lot of the data that we've got. And so my worry is that, yes, an AI could come to answers based on those data, but are they going to be the right answers or not?

So we actually agree violently on that one. The was it the chief of the British Medical Journal just said we've reached a crisis point. You cannot reproduce most of the studies that are out there because of corruption.

Yeah, I don't know that it's because of corruption that I would push back.

On, probably ad libbing that part. But he says because of special interests.

I think there's all sorts of reasons.