Daniel and Kelly’s Extraordinary Universe - Why do we age? (featuring Dr. Venki Ramakrishnan)

Episode Date: October 9, 2025

Daniel and Kelly get answers to listener questions about why we age from Dr. Venki Ramakrishnan, author of "Why We Die: The New Science of Aging and the Quest for Immortality".See omnystudio.com/listener for privacy information.

This is an I-Heart podcast. Hey, it's Ed Helms host of Snafu, my podcast about history's greatest screw-ups. On our new season, we're bringing you a new snafu every single episode. 32 lost nuclear weapons. Wait, stop? What? Yeah, it's going to be a whole lot of history, a whole lot of funny, and a whole lot of fabulous guests. Paul Shearer, Angela and Jenna, Nick Kroll, Jordan, Klepper.

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Welcome to Decoding Women's Health. I'm Dr. Elizabeth Pointer, chair of Women's Health and Gynecology at the Adria Health Institute in New York City. I'll be talking to top researchers and clinicians and bringing vital information about midlife women's health directly to you. A hundred percent of women go through menopause. Even if it's natural, why should we suffer through it? Listen to Decoding Women's Health with Dr. Elizabeth Pointer. on the iHeartRadio app, Apple Podcasts, or wherever you get your podcasts. It may look different, but native culture is alive. My name is Nicole Garcia, and on Burn Sage,

Burn Bridges, we aim to explore that culture. Somewhere along the way, it turned into this full-fledged award-winning comic shop. That's Dr. Lee Francis IV, who opened the first native comic bookshop. Explore his story along with many other native stories on the show, Burn Sage, Burn Bridges. Listen to Burn Sage Burned Bridges on the IHeart Radio app, Apple Podcasts, or wherever you get your podcasts. They say that only two things in life are certain. Death and taxes. For the lucky among us, we'll pass away quietly at an old age. But why is aging and thus death inevitable? And how do we even define aging. Yes, you can define it by the ticking of the clock, but is there a biological way to define it that gives you a better shot at really understanding how the passage of time has worn

away at your body? If two people in their 30s can mix their old cells together to make a brand new baby, then why can't those same two people just start making young cells for themselves? And shouldn't evolution favor living a really long time so we can make more babies and be around to help them grow? Aging can be a counterintuitive phenomenon, and Daniel and I get many questions from our audience, the extraordinarily, about the aging process. However, despite the furrows in my forehead that get deeper each year and that my son sometimes stares at, this biologist is not an expert in the science of aging, but lucky for us, we were able to get Dr. Venki Ramakrishnan, author of Why We Die, the new science of aging, and the science of aging, and the science of aging,

the quest for immortality to come onto the show to answer your questions. Welcome to Daniel and Kelly's extraordinarily old universe. Hi, I'm Daniel. I'm a particle physicist. I round my age up to 100. Hello, I'm Kelly Weiner Smith. I study parasites. And space. And Daniel, last time we talked, you rounded up to 50. Have you just decided that now that you're 50, you're rounding up to 100? Because that is not a helpful way to round.

I think that's totally consistent. When I was 48, I called myself 50. And now that I'm 50, I got to round up to 100. It totally makes sense. Not to me. Plus, I think I look pretty good for 100. You look great for 100. And I say, you look good for 50 too.

But like, I don't, yeah, I know that kind of rounding doesn't make sense to me. all right. All right. So here's my question for you today, Kelly. If you could take a pill that would extend your life to a thousand years or a million years, would you? Do you want to live a super crazy long life? All right. So one, okay, so selfishly, I would need to know about the quality of that life. And if the quality of my life was going to be as good it is now for all of that time, I would think about it. But to be honest, the only reason I'm thinking that I might want to say yes is that I want to live at least as long as my son lives because he's going to need care

his whole life and I don't want him to ever be alone. And so if I could live as long as he lives, 100%. So what about you? No, I see life is like a hike. You know, hikes are wonderful. There's wonderful moments. You're glad you went on them. You're also glad when they're over. Nobody wants

to be on a hike that lasts until the end of the universe. And maybe sometimes the best part of a hike is when you get to sit down at the end, you're like, oh, wow. What a nice walk. done. Especially at the end of a good hike. You're like, all right, I'm ready to be done. Exactly. And my grandpa passed away recently, and I think he had that kind of life. He, like, he hiked. It was a good trip. And at the end, he told everyone, he's like, I'm ready. And then he passed away into sleep. And I was like, man, I really hope that's in the jeans somewhere, because that's pretty solid. And I hope that listening to this podcast has improved that everybody's quality of life out there. We're making your hike through life more pleasant.

Maybe it will improve their quality of sleep, which at the end of the episode we'll discover is an important part of being healthy. So we're doing our part. You're saying that listening to the podcast could technically, scientifically, extend your lifespan. Maybe. Maybe. Listen to our prior episodes about how you evaluate scientific statements and see what you think, dear listeners. And whether you should believe people who have skin in the game, exactly. Yes.

All right. Well, so we get loads and loads. loads of questions about aging from the extraordinaries. And so I pulled them all together. We found an amazing expert to answer the questions. Amazing. Amazing. He does such a great job. How do you know this Nobel Prize in Kelly?

Oh, thanks for pitching by we both were on the short list for the Royal Society Book Prize. Yep, Why We Die is Vanky Ramakrishnan's book and a city on Mars was my book and we both made the short list for the Royal Society Prize. And you're just going to omit those

crucial piece of information that you won the prize. So Kelly is the author of a book which edged out a Nobel Prize winning nonfiction science book. I was not going to mention that. It's thank you for all of your support over the years. I appreciate it. All right. Well, this is a wonderful conversation with a deep expert who also has the unusual quality of being able to explain things clearly. Yes, and being so nice. So nice. Yeah. Anyway, So I had so much fun. I feel so lucky we got to do this interview. Before we bring on our expert who won a Nobel Prize in this area,

we asked you guys what you thought was the reason for aging. Here's what people had to say. I interested it to be oxidative pressures where new copies of things just aren't quite as good as they used to be, and there are errors throughout. Short answer, telomeres. Real answer so that there's someone to say, I wouldn't do that if I were you, to the younger generations.

It's not like the clouds are going to yell at themselves. Certain proteins that mark ourselves or do something along the lines of maintaining how our DNA gets repeated or transcripted, aggregate over time. The body forgets how to make a new body the way that it once did. We age as a consequence of too many gas station burritos, 99-cent big gulps, and betrayal by telomere. At a molecular point of view, it's in real. really hard to maintain consistency in the gazillion times molecules and the cells needs to reproduce. These errors keep stacking up until the whole body decays.

My short answer is we age due to the passage of time. I think we age because we need to die ultimately. I think it's conducive, if not crucial, to the evolution of life itself for organisms to have a finite lifespan. Every beginning has an end. So I believe I've read somewhere that the reason why we age is because there is a shortening of some kind of a protein or molecule within our cells. The ends of our DNA kind of fray and just gets left up to entropy. Aging and death are just part of the evolutionary process and processes that have brought us to where we are today. It's just a fact.

Thanks, everybody, for your speculation. on this concept. Now let's talk to the expert and find out what we know and what we don't know. Dr. Vanky Ramakrishnan was initially interested in physics, but I'm going to go ahead and give a point to biology because he transitioned to focusing more on this field. And the biology stuff worked out well for him because in 2009 he received a Nobel Prize for his work on ribosomes. He was president of the Royal Society from 2015 to 2020 and recently wrote the book, Why We Die, the new science of aging and the quest for immortality. And today we'll be talking about the science of aging.

Welcome to the show. Thank you. And thank you for having me. Yeah, we're super excited to have you. We get so many questions from our audience about aging. And every time I'm like, look, I know when you look at me, I look like the right person to ask about questions for aging. Well, they should look at me then. And there's so much discussion out there about aging and how to prevent it.

And if it's possible and so much snake oil being sold out. there. It's so important to cut to the chase. It's certainly having a moment, and I'm a little bit cynical. I think it has to do with my generation, the boomer generation, that's used to having everything it wanted in life, suddenly coming to terms with getting old. And so, you know, there's a lot of anxiety in the air. Although, having said that, you know, this fear of death and fear of aging is simply as old as humans, you know, because ever since we learned about mortality, we've fretted and worried about it. And I like to say we may be the only species that's

aware of mortality. Other animals maybe are aware of death, but they're not aware that they all have a finite lifespan and everybody's going to die. I'm not sure that other species have that understanding that we do. And when we somehow obtain that understanding, perhaps as a result of cognitive development, language, and so on, ever since then, it has become, it became a theme. And if you look at most religions, they're all about, you know, how to deal with death and what happens after we die. I don't know if it's a blessing or a curse that our species is aware of that. Yeah. I mean, many species, aren't even aware of death.

You know, it just simply happens. Yeah. Well, can I start us off with a very broad sort of philosophical question, which is, how do you define aging biologically? Because as a physicist, I might think, well, you have a clock, and it starts, and it stops, and that's your age. But we're interested in more than that, right? It's some sort of, like, decrease in the quality of life.

You're gradually moving towards death. It's this fact that you don't just, like, live for 62 years and then, poof, you're done. your body degrades. How do we define aging in a crisp way scientifically? Yeah, so it's definitely related to the chronological clock to time. But the rate is very different

not only for species, it's vastly different for species, but it's also different for individuals within a species. If you go to your high school reunion, you will immediately be aware of that, the fact that people don't age at the same rate.

And I think aging, molecular biologists would define it as the gradual accumulation of changes and damage to us over time. That can happen different rates and different individuals. And it's not just damage.

Some of it is changes that occur with time. It may occur different rates and different individuals. and these changes may have a purpose early in life, for example, modifications of our DNA, but they cause us, or at least they're strongly correlated with aging later in life. So that's how I would define it, and this accumulation of changes and damage leads to a gradual loss of function. And when that loss of function reaches some point where some critical system fails, then you have death.

And so death is a result of aging, but its exact moment can't be predicted because in a complex system, you can't predict exactly when a critical component will fail. And so aging and changes, but that must mean very different things to different. parts of your body. You're talking about your nerves or your skin or your eyes. Are there ways that we have to measure it? It happens at every level. It happens at every level, but I would say fundamentally it happens at the molecular level. And that then manifests itself in each increasing level of complexity. So you can go from molecules to collection of molecules in our cell, to components of the cell, to cells themselves. And then, entire tissues and, you know, the way cells communicate with each other, like our immune system.

So you can see that, you know, it happens at the molecular level, but it starts manifesting itself at increasingly higher levels, you know, until a point that, you know, we see aging as various forms of frailty. You know, so, in fact, a very good measure of aging is actually something called the frailty index, they'll measure things like, can you get out of bed, how fast can you walk, you know, 50 yards, what's your grip strength, how good is your eyesight, how good is your cognition, how good is your memory. So all of those things are indications of frailty at a macroscopic level, at a level that you know, you and I experience. But ultimately, the underlying causes are molecular. Okay. And is aging universal? So we're getting

to one of our first listener questions right now. One of our listeners noted that they had heard stories about immortal organisms, and they wanted to know, are they actually immortal? Yeah, I had to say there's a lot of hype. What happens is people will study an organism that ages very slowly, and suddenly they'll say, oh, this has no sign of biological mortality. So let me back up and explain what I mean by that. So in, Normal species, the likelihood of that we are going to die at any given time keeps increasing exponentially. So, for example, that chances that you'll die when you're 10 are very small, but the chances you'll die in the next year when, say, you're 95 or 100 are almost 50%.

Okay? So the chances keep going up. Now, in some organisms, it appears that... that likelihood of dying, you know, of aging events, not of being eaten by a predator or starving or anything else, those are called external causes. But, you know, aging, just dying of aging, that probability doesn't seem to go up with time. And so there are some species like a freshwater species called the hydra. There's another species called the immortal jellyfish. And these tend not to show any signs of biological aging.

That is, the likelihood it's going to die just doesn't seem to change with time. But in fact, what is happening is it's probably aging very, very slowly. So if you looked, if you simply followed a hydra in the wild, it would die of some other cause, not of old age. But if you kept it safe and followed it long enough, you will find that it too gradually ages

because no regeneration is perfect. The reason Hydra and jellyfish appear not to age is they constantly regenerate their tissue using specialized cells called stem cells. In a way, they're like plants. You know, plants have stem cells all over themselves, and that's why you can take a cutting from a plant and, you know, grow an entirely new tree with it, right?

We can't do that. But, you know, some animals regenerate like starfish, you know, it cut off an arm and it'll regenerate an arm. And, you know, some of these species can regenerate, you know, any tissue. And but it's not perfect. And so I would say to your listener that, yes, everything will die, but they die at different rates. Okay. I mean, they age at different rates. And so everything ages.

It's universal across organisms. do we understand why we age? Yes. Like, is it an inevitability of, like, thermodynamics or molecular copying or something, or is it an evolutionary advantage? Well, there are two ways of looking at it. One is, you know, the physicist's way would be that, you know, second law wins, and there's always increase in entropy and disorder, and eventually things sort of degrade, and, you know,

life is not a, you know, an equilibrium system. The problem with that is that life is not a closed system. And if you apply enough energy and enough resources, you can reverse damage. And in fact, that's what we do. So why is it then that we age and die? Well, I'll tell you the evolutionary argument. The evolutionary argument is resources are limited. And throughout our history, and in fact, until recently, resources were limited for humans

well. You know, we had to struggle to have enough food to live and so on. When resources are limiting, the organism has a choice to make. Does it put more of the resources into maintenance and repair, which requires energy, requires food, etc. Or should those resources be put into rapid growth and development? Now, if you take a mouse, for example, a mouse lives about two years, whereas a blue whale lives a few hundred years. So why is it that there's this vast difference? Well, the evolutionary argument is that evolution doesn't actually care how long you live. Evolution simply cares about how successful are you going to be at passing on your genes, because it's selecting for those genes. It's not really selecting for you as an individual. And so

in the case of a mouse, there's no point in spending a lot of resources getting a mouse to live to be 40 years. And the reason is that long before that, it'll be eaten or it'll die of starvation or in a drought or all of a zillion external causes. And so in the case of a mouse, it's more advantageous from an evolutionary point of view for a mouse to grow very rapidly, produce lots of offspring, and then, you know, it doesn't matter whether it dies. Whereas with larger animals, their metabolism is also slower. So they take longer to mature. Their offspring take longer to, you know, produce and grow up and mature. And so in there, it does make sense for evolution to have selected for longer lifespan in order to ensure fitness, okay, because otherwise it may not

actually have the chance to reproduce or not to reproduce enough. And it gets worse than that. It's not even that evolution doesn't care what happens to you after you've produced your offspring. Evolution also will select for traits that are advantageous early in life that will get you to maturity and reproduction, even if those exact same traits will cause you to age later in life. And there are many examples of that in my book. For example, certain mechanisms that cause us to age may have evolved as anti-cancer mechanisms. Now, of course, you want to prevent cancer early in life, but later in life, they may cause aging. And ironically, cancer itself increases as we age, the likelihood of getting cancer. But that's a different story. Can you give us an example of an anti-cancer strategy

that causes aging later? Yeah, sure. So one very classic example is, that most of the cells in our body can only divide a certain number of times, and then they reach a state called senescence. Senescent cells are these dysfunctional cells that can't divide, and they actually secrete inflammatory compounds. And as we age, we accumulate more senescent cells, and that becomes a problem, and inflammation becomes a problem. Now, why do the cells stop dividing? Well, it turns out, that our chromosomes are linear DNA molecules, and their ends are specialized structures called telomeres.

Now, the copying mechanism for DNA, every time a cell divides, the DNA has to be copied, the copying mechanism is such that our chromosomes get slightly shorter every time the cell divides, okay? And these ends have a special structure. Now, when they become too short, that structure unravels. When it unravels, the end of our chromosomes looks to the cell like a broken piece of DNA.

That the cell has evolved mechanisms that if there's a DNA break, it will either try to repair it or if it can't repair it, it will send the cell into senescence. Why? Because a cell with a defective genome is a cancer risk. because it's about, you know, it could do all kinds of abnormal things. And it's much better to send that cell off to senescence and have it be removed by the immune system than have it continue with a DNA defect or a chromosome defect, right?

So the cell has evolved as DNA response, damage response, in order to get rid of cells that are problematic in this way. But of course, that same thing is causing senescence and increase in senesin cells as we get older and causing us to age. So that's a very clear example of how something that may have evolved as an anti-cancer mechanism early in life really is a cause of aging later in life. All right, I want to hear a lot more about that, but first we have to take a break. Hey, it's Ed Helms, and welcome back to Snafoo, my podcast about history's greatest screw-ups.

On our new season, we're bringing you a new snafu every single episode. 32 lost nuclear weapons. Wait, stop? What? Ernie Shackleton sounds like a solid 70s basketball player. Who still wore knee pads? Yes. It's going to be a whole lot of history, a whole lot of funny, and a whole lot of

of guests, the great Paul Shear made me feel good. I'm like, oh, wow. Angela and Jenna, I am so psyched. You're here. What was that like for you to soft launch into the show? Sorry, Jenna, I'll be asking the questions today. I forgot whose podcast we were doing. Nick Kroll, I hope this story is good enough to get you to toss that sandwich. So let's see how it goes. Listen to season four of Snap-Foo with Ed Helms on the I-Hart Radio app.

Apple Podcasts, or wherever you get your podcasts. There's a vile sickness in Abbas Town. You must excise it. Dig into the deep earth and cut it out. The village is ravaged. Entire families have been consumed. You know how waking up from a dream? A familiar place can look completely alien.

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Radio app, Apple Podcasts, or wherever you get your podcast. Okay, we're back, and we're talking about aging. So you mentioned that as cells go on and replicate, the telomeres, you know, get shorter, but we, and this is another listener question, but we're able to, you know, combine our gametes with somebody else and make a fetus that has all new cells. And you also mentioned that starfish can, you know, regenerate an entire arm using stem cells. Yeah. So why is it inevitable that our cells will break down when we seem able to set the clock back if we want to? So we have evolved so that most of our cells have lost that ability to regenerate,

probably because you don't want all of the trillions of cells in our body to be able to keep dividing at will because that is also a cancer risk, okay, because they could acquire mutation and then they could become a cancerous. So we have specialized cells called stem cells, which can keep regenerating. They don't go into senescence. And these specialized cells,

their role is to regenerate tissue. Now, where do these stem cells come from? Well, they came from the fertilized egg, The fernalized egg is the ultimate stem cell because it's what is called a totipotent stem cell. That means it can make everything in the body, including the placenta. Then that separates off into placental cells and the cells that actually form the fetus and the body, you know, and the organism. Early in development, those cells are called pluripotent because they can make any kind of tissue. They could make kidneys, they can make lungs, they could make brain cells, they can make anything.

But as the fetus, as the embryo, I should say, develops, the stem cells become more and more specialized. And then you have hematopoetic stem cells, which can make anything in the blood system. And that includes all of our immune system and our red blood cells, et cetera. Another kind can make anything in the nervous system, you know, neurons, gleeves, all of those cells. Others can make skin and hair and so on. So you get the picture. The stem cells are becoming more specialized. But those stem cells have a balancing act. They have to reproduce so that they maintain the stem cell population. But they also have to differentiate and produce more of the tissue. So there's always this switch going on. Do they reproduce more of themselves?

so you have more stem cells, or do they make the tissue keep regenerating the tissue they are? And there's always this balance. But as we get older, our stem cells get depleted because they also get defective, they also age, they also become senescent. And so you get this depletion of stem cells. You also get the remaining stem cells are not optimal.

They become what are called clones instead of having a diverse population of stem cells as when we're young, you get these clonal stem cells, which are suboptimal. They're selected for being able to reproduce rather than being effective at generating tissue. So these stem cells also decline. So that's why we can't, you know, keep going forever, you know, by regenerating tissue. Now, the other question your listener had was, you know, what about our germ cells? know, we can, you know, we keep producing babies that are age zero.

They're not, you know, in my book, I point out that a 40-year-old woman doesn't give birth to a baby that's 20 years older than a 20-year-old woman. They're both zero, right? Born at times zero. So that's a combination of two things. One is our germline cells are highly protected against damage. They have better repair mechanisms for repairing DNA damage. they're shielded against DNA damage, et cetera.

So that's one aspect. The others is a brutal selection process. You know, a female is born, a female human is born with about a million or so eggs. But, you know, if you look at the number of menstrual cycles in a woman over a lifetime, it's only maybe a few hundred. So why do you need a million eggs, you know, when you're really only going to use at the most, a few hundred, right? So that's because there's a lot of selection in the process of going from the germline's precursor

cells to the egg that's actually eventually selected for ovulation, there's a lot of selection. Sperm, of course, you know, is highly selected. I mean, you know, in each fertilization event there, you know, I don't know how many, I would hate to guess, take a guess, but maybe it's a million sperm cells or something. And out of that, only one is selected. So they have to race and they have to, you know, win the competition. So they are also selected for fitness and for health. And then after the fertilized egg is formed, you know, it is also checked.

So if the developing embryo is at all defective, there'll be spontaneous abortion. Often a woman won't even know it, you know, the very early spontaneous abortion. Later abortions are what we call miscarriages, and that's another selection. And even within the growing embryo, cells are selected against if they're defective. The embryo keeps growing, but it kills off cells that are defective, which I found remarkable. So it's this combination of selection and protection that ensures that, you know, the child that is born has its aging clock so much reset

at each generation but is it technically possible for us to reset our own clock is it just like a bad idea evolutionarily or is there something that prevents us from just like constantly being at t equals zero I don't see how you would reset your entire clock

you know in the whole organism there are people so if I were to back up just a little bit, there is an example of taking a fully grown adult cell and making a whole new animal from it. And the first time that was done was by John Gurdon, who received the Nobel Prize for it, when he cloned a frog from a skin cell. So he took a skin cell from an adult frog and implanted the nucleus of that cell into the egg of another frog and then just grew it up. And it resembled the frog from which the skin cell had been taken. So it was essentially

a clone. And then people asked, could they do it to mammals? And that made big headlines when Dolly the sheep was cloned. Now, Dolly the sheep turned out to be a very sickly sheep and died at about half the age of a normal sheep. So everybody said, aha, this is because Dolly the sheep was cloned from and fully grown adult cell, which was already kind of old and damaged and didn't go, you know, wasn't a normally produced sheep. It was done by this weird cloning procedure. But it turns out that there are many other cloned animals. And in fact, with Dolly, there were other cohorts like Daisy and Debbie. They're all females that had D names. And these sheep, though, by and large, had normal lifespans, and so that means that you could actually, you know, reset the clock

to substantial degree by erasing all the marks on the DNA. Okay? It's not perfect because the cloning itself involved lots of selection. You know, it's very, very inefficient. It only works small fraction of the time, and most of them end up in miscarriages or they don't take and so on. So at least in theory, it's possible. Now, could we do to cells in a more systematic way what Dolly the sheep or John Gurden did with his frog? Because they just treated it in various ways, but they didn't have a clear idea of what was, what was it, what were they doing to make that adult cell go back to resembling a fertilized egg and start growing a new animal? You know, it's like going backwards in time, right? And so,

So a Japanese scientist named Shinya Yamanaka asked, could you take these stem cells that are in the final stage, or even the final cells, like a skin cell or, you know, lung cell or whatever, and have them go all the way back to pluriporten stem cells so that they could then, you know, become any kind of cell? And remarkably, he found that if you take four genes, and introduce them into one of these adult cells and turn them on, you could change the genetic program of the cell

and have it go backwards all the way back to pluripotence. Now, this has created a big industry in the stem cells because stem cells are going to be useful for all kinds of things. For example, if you want to replace damaged tissue, let's say you want to replace pancreas and diabetics so that they can produce insulate. There are all kinds of things being talked about and they're, you know, cartilage in a guy like me

with very bad joints. So, or for a guy like me with, you know, very little hair, you could imagine stem cells stimulating new hair growth, okay? And that would be a billion dollar industry. Yeah, if you could develop some like gun, you pointed a part of your body and you're like, make this younger. Exactly.

So people asked, now the problem with going all the way back is that you have the risk of cancer, you know, because it's, you're taking these cells. They're not quite exactly the same as a normal embryonic development is. It's the somewhat artificial process that you're using to go backwards in development. And when they try to grow those pluriportin stem cells, they often would get these tumor-like growths called teratomas. And so there is definitely a cancer risk. But what a number of scientists asked was supposing you turn on these Yamanaka factors transiently, you know, just turn them on and then figure out a way to turn them off after a while. Then what would happen? Well, astonishingly,

they tried this in mice. And they found that the mice, you know, resembled younger animals. They suddenly had better fur and muscles, and, you know, by various markers, they seemed younger. So this idea of cellular reprogramming is a big area in the longevity field, but it's still in early stages, even though there's a lot of excitement, the idea that tomorrow you're going to go and get a treatment that will suddenly make all your cells younger, it's really not You're going to happen any time soon. And it's because there are lots of problems. One is, you know, you have to get the right dose.

You have to make sure it's safe. You have to make sure it goes to the tissues and just the right amounts. These are all big, challenging problems. And, you know, of course, a long-term cancer risk is another problem. So I think it's very exciting and promising, but it's not something that's around the corner as it's often hyped. I mean, that's my opinion. Of course, you know, people will disagree with me.

But remember, a lot of these people have quite a lot of skin in the game. They have financial interests. They've founded companies and so on. So you have to slightly take what they say with a pinch of salt. So you've mentioned that one of the reasons that we age and die is because it has something to do with resources and... With evolutionary choice, basically. Yeah.

So now many humans like me live in an environment where there are too many resources maybe and we should take in fewer resources. And we live in an environment where we're getting better and better at being able to treat cancer because it seems like we keep coming up across, you know, cancer as the thing that's holding us back. So if we were in a high resource environment and we could figure out how to cure cancer, do you think we might be able to get our lifespans up 100 years or something? Well, somebody did a calculation, a demographer named Jay Olshanski from Chicago, who's a leading expert in this area. He did a calculation a number of years ago, maybe 25, 30 years ago, which suggested that if there are four major causes of major diseases of old age that cause death. One, you mentioned cancer. The other one is diabetes. A third one is heart disease.

and the fourth one is dementia, neurodegenerative diseases. And of course, the neurodegenerative diseases are among the hardest to treat. But let's say you could eliminate all four of them. The suggestion is you would only gain about 15 years of lifespan if you eliminated all of these four causes. And the reason is that they will not affect the normal process of aging, you know, which leads to frailty of, you know, system-wide frailty. And there's always this argument, it's aging a disease.

And people say, well, you know, all of these major things like diabetes, cancer, etc., the risk goes up with age. In fact, the biggest risk factor is age. The older you are, the more likely you are to get one of these things or several of them. But the other argument is that, well, these diseases don't happen to, everybody. Not everybody dies of cancer. Not everybody has heart disease. And also young people get cancer. So it's not directly related. And aging, on the other hand, is something that happens to every single person and it's inevitable. So how can it call something that's both ubiquitous and

inevitable a disease? It's simply a process of life. And I tend to agree with that. But the reason they want to call it a disease is because then it's easier to get approval for clinical trials. Well, I think they ought to try some other thing. For example, they can choose a target, a disease target that's strongly correlated with aging. For example, osteoarthritis or loss of various functions and so on. And then they could use that as the measure of success of their drug. So there are ways to get around it. But I don't think that just eliminating these diseases will increase lifespan that much.

And in fact, even people in the aging field who have bet. So Olshansky was on one side of a bet with another gerontologist named Stephen Ostad. Stephen Ostad made a bet with him that the person who lives to be 150 has already been born. And that bet was made some time ago. And they bet it so that in 150 years, you know, the amount would be worth, I don't know, a billion dollars or something. Of course, you know, maybe it'll cost a billion dollars to buy a sandwich, but by that time. But anyway, but they made this bet. Now, Stephen Ostad also doesn't believe that it's just going to be because of eliminating disease.

Rather, what he thinks is that we're making progress in slowing down or arresting aging itself. and that's the reason why we may end up living longer. And for example, you know, there is a drug called rapamycin, which is somewhat related to caloric restriction, which also allows animals to live longer. That, for example, can increase lifespan in mice by, you know, 20 or 30%. Well, if we live, you know, 90 years, you know, 30% of that would already get us to, 120 or so, you see. So maybe he's counting on things like that. I tend to be on the Olshansky side.

I think that really fundamentally increasing lifespan and especially healthy lifespan is not going to be as easy, as they say, because it's highly multifactorial. There's so many things going on. Well, how do we know you're not just a shell for big death? You know, are you being paid by The death industry. All right, well, take a break. And when we get back, we'll talk more about aging. Hey, it's Ed Helms, and welcome back to Snafu, my podcast about history's greatest screw-ups. On our new season, we're bringing you a new snafu every single episode.

32 lost nuclear weapons. You're like, wait, stop? What? Yeah. Ernie Shackleton sounds like a solid 70s basketball player. Who still wore knee pads. Yes. It's going to be a whole lot of history, a whole lot of funny, and a whole lot of guests.

The great Paul Shear made me feel good. I'm like, oh, wow. Angela and Jenna, I am so psyched. You're here. What was that like for you to soft launch into the show? Sorry, Jenna, I'll be asking the questions today. I forgot who's podcast. we were doing.

Nick Kroll. I hope this story is good enough to get you to toss that sandwich. So let's see how it goes. Listen to season four of Snap-Fu with Ed Helms on the IHeart Radio app, Apple Podcasts, or wherever you get your podcasts.

There's a vile sickness in Abbas Town. You must excise it. Dig into the deep earth and cut it out. The village is ravined. Entired families have been consumed. You know how waking up from a dream?

A familiar place can look completely alien? Get back, everyone. He's going to next. And if you see the devil walking around inside of another man, you must cut out the very heart of him. Burn his body and scatter the ashes in the furthest corner of this town as a warning. From IHeart Podcasts and Grimm and Mild from Aaron Manky, this is Havoc Town.

A new fiction podcast sets in the Bridgewater Audio Universe, starring Jewel State and Ray Wise. Listen to Havoc Town on the IHeart Radio app, Apple Podcasts, or wherever you get your podcasts. The Devil Walks in Aberstown. It may look different, but native culture is very alive. My name is Nicole Garcia, and on Burn Sage, Burn Bridges, we aim to explore that culture. It was a huge honor to become a television writer. because it does feel oddly, like, very traditional. It feels like Bob Dylan going electric,

that this is something we've been doing for the hundreds of years. You carry with you a sense of purpose and confidence. That's Sierra Taylor Ornellis, who with Rutherford Falls became the first native showrunner in television history. On the podcast, Burn Sage, Burn Bridges, we explore her story, along with other native stories, such as the creation of the first Native Comic-Con or the importance of reservation basketball.

Every day, native people are striving to keep traditions alive while navigating the modern world, influencing and bringing our culture into the mainstream. Listen to Burn Sageburn Bridges on the IHeart Radio app, Apple Podcasts, or wherever you get your podcasts. But the humility in knowing that life is this classroom that we should never graduate for is what is going to keep you growing. And that's all that matters. World Mental Health Day is around the corner. And on my podcast, Just Heal with Dr. Jay, I dive into what it really means to care for your mind, body, and spirit from breaking generational patterns to building emotional capacity. Healing is a journey and wholeness is the destination.

I'm going to walk away feeling very healed and feeling like, yes, I'm going to continue my healing journey and I'm going to get some keys from you. Listen to Jess Hilbert, Dr. Jay, from the Black Effect Podcast Network on the iHeart Radio app, Apple Podcasts, or wherever you get your podcasts. because by then, when you're old, you've basically seen everything. It is true that immune systems are exposed to more things as we age, but immune systems are essentially a collection of cells, and the cells themselves age, and so they don't respond as well as they do when we're younger or when we're in our prime.

And this has to do with molecular damage, affecting higher levels like the cell and communication between cells. And so for all kinds of reasons, our immune system as a result of this accumulated damage doesn't function optimally. So it's got a lot more wisdom, but like less energy and effectiveness? Yeah, and actually it doesn't function as well. For example, it responds in an aberrant way. It's not as well regulated.

you know, the immune system always has to be very finely regulated because you don't want to react against yourself or against harmless things. You only want to react against truly dangerous entities. So that fine balance is disrupted and so you get essentially a dysfunctional immune system and you also get a lot of inflammation as a result. So, for example, I mentioned those senescent cells. the reason those senescent cells secrete inflammatory compounds is as a signal to the immune system that, hey, there's something wrong here, come and clear it up. And so the immune system will come there. It may be the site of a wound or an infection or some other stress, and it will deal with it. But as we get older, and not only do the number of senescent cells increase, but the immune system doesn't respond as well to the signals.

And so you get this sort of autocatalytic or, you know, you get this essentially this explosion in the growth of senescent cells and inflammation. And is this something that's understood across species? One of the listeners asked why cats and dogs have the same age-related diseases that we do, but they appear at a younger age, maybe a small number of years. That's simply the fact that this allocation of repair. to maintenance and repair to growth and reproduction. That balance is different for different species. You know, you could ask, why do whales live so long? Well, one reason is they have a slower metabolism than, say, an animal like a mouse.

But the other reason also is that they have a large number of repair enzymes. You know, if you look at just DNA repair enzymes, they have many different repair enzymes when they sequence the genome of some of these species. And elephants, for example, have many more copies of a DNA repair enzyme than mice do. Because they live longer, so they need more repairs. Yeah, and they have to maintain that. And also, there is a paradox. They have many more cells.

And so the chance that one of their cells could become cancerous and kill the whole animal is much higher in a larger animal than in a small animal. than in a small animal. But paradoxically, its mice get cancer more often than elephants. And that's because

the elephants do have this additional capacity to repair. So it's all evolution really just optimizing for fitness.

Remember, evolution does not optimize for long life. It doesn't care about long life. It cares about survival of genes because that's what

it selects for. This might be a little too far off topic, but I've seen articles that say like, green sharks never get cancer. Are there actually species that never get cancer or it just takes them away and we don't see it often? It is almost entirely that we don't observe them long enough. Okay. So for example, I'll give you an example, Galapagos tortoises, right? You know, they live to be 200 years old and I like to joke that there's probably a Galapagos tortoise wandering around now that might have actually met Darwin. Oh,

Oh, that's a cool thought. Right, but anyway. Let's have them on the podcast. Exactly. So, you know, if they could talk, they might be able to tell you quite a bit. But anyway, no, it was thought for a while that these things, these tortoises don't age. Well, actually, they do age. If you look at old tortoises, they have terrible eyesight and, you know, they're slow-moving, their skins, you know, old.

You know, they have all these. They don't know how to use the V. Exactly. They have all of the same problems. And it's just that it happens more slowly. Okay. And I got to say, Daniel, I think the VCR joke aged you more than anything. Well, the fact that you laughed at it aged you. Oh, you got me. That's true. That's true. So let's jump back, if that's okay, to another example of folks trying to extend lifespan. So I've heard of examples of like taking blood from young mice and giving it to old mice. And then I think there's a guy, Brian Johnson, who, trying to limit aging by using his son's blood.

Is there any evidence that that's anything other than nuts? That's an excellent question. And it is true that when they connected an old rat to a young rat, the old rat benefited by the exchange of blood. And the young rat actually suffered. And then they were wondering whether it was really due to the blood itself or maybe the young rat had better liver and kidneys to detoxify. the blood. And so it wasn't just the blood, but it was just that it had better organs to clean up

blood. So they separated them and simply gave them transfusions. And they found that, in fact, the effect was still there, but it was more that the old rat had things in it that were harmful to the young rat. That was more the case than that the young blood was beneficial to the old rat. But it did, but there was some effect both ways. Now, this is true. And when the people discovered it, they caught all sorts of creepy phone calls from rich people asking, you know, whether they could get young blood and so on. And in fact, companies... Where do I buy babies, this kind of stuff.

Exactly. And in fact, companies sprouted up. And as you can imagine, mostly in California, I think. What? That's what I would have guessed. You mean the center of innovation and forward thinking and creativity. That's why you said California. Anyway, somehow obsessed with youth.

But anyway, some of these companies would get blood from young donors and sell them at a huge markup to rich people who wanted them. And in one case, the FDA actually tried to shut a company down and then it opened up under a different name. And in one case, the CEO said, well, look, our people simply don't have the time to wait for clinical trials, you know? Oh, my goodness. And it was really bizarre coming from, you know, a CEO of a, you know, a health-based company. But you're saying that there are real benefits to having transfusions of blood from young people?

Well, there certainly seem to be in animals. And so there's a big body of research. to find out what is changing in blood as we get older? And what do these factors do? You know, if they're harmful in old age, what do they do? Maybe we can inhibit them. Or if they're beneficial in early life, maybe we can take advantage of that

and introduce them into older people. So I think that's a very legitimate and broad area of research and lots of very, you know, top scientists from very well-known university, are actually working on that. But, you know, this idea that you should just take transfusions, you know, it's not really going to help that much at this point. And Brian Johnson, whom you mentioned, actually did this experiment of keeping it all in the family.

He took blood from his son and gave his blood to his dad. But he's also, I mean, to give him some credit, he's obsessed with aging, you know, or not aging, to be more precise. He spends like a couple of million dollars a year on all kinds of longevity treatments and measurements and, you know, probably has, you know, fitness programs and all sorts of things. Okay. Well, the thing that fascinates me about Brian Johnson is that he does take a lot of data, right? He is focused on these metrics, right? He's focused on metrics. But he doesn't look young. Like, even though he says he has all these metrics, which are equivalent to an 18, year old, he still looks like a vampire.

So he sort of captures this like... Well, I would say, no, no, I'll give him credit. He's in late 40s. He looks pretty good for late 40s. But I'll tell you, my son is in his late 40s. Does none of this stuff. Yeah. Okay. But he runs regularly and eats well. And he looks just as good as Brian Johnson. And I'm not just being biased. You could look him up online. He's a cellist.

Well, you're definitely biased. But I don't, I don't not believe you. But, you know, I think it raises a deeper question, which is, like, is it possible to be young biologically by all of these metrics, as you say, you know, you're measuring the damage to whatever molecular mechanisms, but still somehow not be young in the sort of social sense. That's a very good question. You know, so, you know, I mentioned the high school reunion and how we all look different. Yeah. So that's led to this quest for biological markers of age, okay? Yeah. Because you want to know, your birthday may have been, you know, 40 years ago, but how old are you really in biological terms, right?

So the people have come up with different clocks, you know. So one clock is this so-called DNA methylation clock. So these are little tags that get attached to our DNA from the time we're conceived, okay? It happens even in utero. We're aging even in utero. Okay. And that's apparently better correlated with mortality than chronological age. So chances that you're going to die are more correlated with your DNA methylation than they are with your date of birth.

So that's, you know, used as a clock. But does that suggest that if you could somehow adjust that, you would extend your life? I mean, is it causal or is it correlated? That's the real question. You know, we don't know the extent of causality. The other case is that as we age, extra sugar groups get added to our proteins. This is called glycation.

And so you can measure this, you know, addition of sugar groups to our proteins. And when that happens to our proteins of our immune system, it also doesn't work as well. So people think that it has some connection with this, you know, decay. of the immune system. But anyway, that's another clock.

Now, people will sell you kits. They'll tell you a DNA methylation kit or a glycation kit or a full blood, you know, library, you know, they'll just analyze a bunch of stuff in your blood to give you a sort of biological age. And each one will say, this is our thing is the most accurate, okay? Now, I think these are all very useful research tools because if you have a longevity intervention,

like an anti-aging intervention, you can see, are these markers changing more slowly or are they changing at the same rate? Okay. They'll give you a good idea of, you know, are you aging faster or not. But people need to come together and agree on a panel.

You know, I don't think a single clock is going to tell you the whole story. Yeah. Okay. I think they need to agree on a panel and then say, okay, here's a panel, and this is what it represents, and it might be a complex thing. There's no point in talking about your biological age because your liver may not be the same age as your kidney or your lung. You can imagine if you're an alcoholic, your liver might be older than other parts of your bodies. So I think people need to have a more complex view of aging.

biological age. But don't we also need to unravel this question of causality? I mean, if you identify a marker, even or even a complex panel that indicates biological age, adjusting those results doesn't necessarily make you younger. It's like I can turn back the clock literally and it will read a different number. Doesn't make me younger. And if I just comment one more thing, which is one of my favorite mechanisms that Brian Johnson keeps track of is that, and I love that he's so transparent about his data, is that he measures his, erection quality during the night, and he posts this data online, which I think is hilarious. But, you know, just as an easy example, if the guy took a Viagra every night when he went to bed,

he probably would have, like, glorious erections all night long. It wouldn't make him any younger, right? That's true. But, you know, let's take DNA methylation. You know, so one of the things about those reprogrammed cells is that they have changed the methylation pattern as well. You know, so, I mean, one of the distinct things about going back to an early embryonic state is that the methylation pattern is different. So there may be some element of causality, because methylation does change the program of our gene expression. So if you're going back to an earlier state, you're maybe you're going back to an earlier program.

But I agree that, you know, causality, you know, needs to be established by careful experiments, you know, is it sufficient to reverse methylation and would that cause automatically cause something to look younger? There are some scientists who claim that they have reversed aging just by this process, but it's highly controversial. So I imagine our listeners are going to want to know as an expert in aging who doesn't believe, you know, that there's a me. pill out there that's going to give us an extra 50 to 100 years, what do you do to slow the aging process? Yeah. Yeah, I should say, you know, there's no theoretical reason why we couldn't all start living to be 150 eventually, okay?

The thing that I'm, what I'm saying is that we don't know how to do that at this point. And more importantly, we don't know how long it's going to take. And that's where I differ with some of the more extreme optimists that the field is full of. Okay. But what we can do right now, before then, I wanted to address one question. If you ask most aging researchers, they would say, oh, we're not interested in an extending lifespan. We're really interested in extending health span. Okay.

And this whole thing is based on an idea called compression of morbidity. So as we get older, we start accumulating various morbidities. You know, you could say diabetes is one or heart disease or dementia, cancer, et cetera, you know, frailty of various kinds or morbidities. And the ideal life would be that you're extremely healthy and then suddenly undergo a rapid decline, okay? This is called compression of that morbidity into a very short space of time, span of time. So that's the goal. The question is, is that even possible? Well, in the last

few decades, we are all living healthier as a result of improvements in health, but it's also extended our lives so that our period of morbidity has not changed. Okay. So it's just postponed it. And in fact, you know, we're living more years and it sort of decline than, you know, whereas before we might have died brutally quickly. Okay. As soon as something went wrong, you know, would collapse and die. Now we're sort of prolonging it and have a long period of morbidity. So it's not clear that as we improve things, we're going to somehow keep healthy and reach some fixed limit and then collapse, it may simply be that we'll live a bit longer

and still have that inevitable period of decline. That's an unsolved question, no matter what people will actually say. The one exception to this are supercentenarians. These are people who live to be over 110 and even over 105. They tend to be extremely healthy. Many of them have never seen a doctor

until they're a hundred or so. And then they suddenly go into a decline and die. Now, you could ask, why is that? Well, it could be that they're selected, and there's a selection bias there. First of all, they may be lucky in the combination of genes that they have, but each combination, there's no fixed combination.

They may be different in each individual, but somehow these combinations give them that edge. Another is that they may simply have been lucky in avoiding various diseases and cancer and accidents and so on. And you're looking at the survivors, okay? And so this, it's not something that's translatable to the rest of the population necessarily. So that's still debating. And people are studying centenarians, which I think is a great idea and trying to find out more about their lifestyle and their genome and also their methylation patterns and so on. Now, you asked, what could we do? Well, I advocate the trio of diet, exercise, and sleep. It's been known in

many species that caloric restriction improves lifespan and improves health in old age. And, of course, caloric restriction is extreme. It means you're consuming just the bare minimum number of calories required to have a steady state. In other words, you're not losing weight and starving, but you're just steady. But that will leave you hungry and cold and loss of libido and all sorts of side effects, which maybe not worth it. Not worth it. It reminds me of that joke about the doctor who said, you know, if you do these things,

you'll live longer. And the patient said, really? He said, well, I'm not sure, but it'll feel like it. So anyway, but you could have a moderate diet, you know, and it is true that a healthy and moderate diet will help. And exercise has all kinds of things, including, by the way, those regenerative ability, regenerating muscle and even regenerating mitochondria,

which are these organelles in our cells. So exercise has huge benefits that are only now, becoming clear. And then the third, which I think Americans need to take more note off. And by the way, I am an American who lives in Britain, although I'm now also a British citizen. So Americans particularly ignore sleep. Okay. And sleep is really important because that is when a lot of the repair and maintenance mechanism of the cell, the clearing out garbage, you know, repairing damage, et cetera, much of that occurs when we sleep. And there's actually a very nice book called Why We Sleep by Matthew Walker, which talks about all of the things about

sleep. So that trio is extremely helpful. Now, things like stress cause, you know, accelerate aging, but, you know, if you exercise and sleep, you will also be less stressed. And if you exercise, you'll sleep better. If you sleep better, you're less likely to overeat and you know, snack and so on. So there's, it's like a three-legged stool that help, you know, each one helps the other two. But then let me ask you about that specifically because it feels like as we get older, it's harder to sleep longer, to sleep well. And yet you're telling me that sleep is crucial for old age. And so it seems like a death spiral there. Exactly. And that's why if you exercise and eat well, you're more likely to sleep well. And then it's a, it's a kind of

virtue cycle. They help each other. Each leg helps the other two. And then there are social things. For example, again, Daniel, you mentioned causation versus correlation. But there's strong evidence that people who are socially well-networked in old age. For example, they have circles of friends, family, and they're socially involved, tend to have lower mortality rates. And people with a sense a purpose in life, independently of the social network. They have a sense of purpose in life also tend to live longer. And so this would argue for being socially involved and perhaps, you know, contributing, you know, maybe volunteering and having some sort of purpose just beyond watching your Netflix

queue, although that some people would argue that's a purpose too. So, but anyway, but having a real purpose in life might help. Now, again, you might say, well, people who are healthier and, you know, not aging as fast may be more inclined to do these things. So there is this correlation causation issue. But I think it's well worth considering. Is it time for the alien question, Daniel? I think it is. So we often wonder on this podcast, not just about the scientific mysteries here on Earth, but scientific mysteries more broadly in the galaxy.

And so since we're in this moment where we, you know, maybe on the cusp of discovering aliens on the other planets in the next decade or whatever, do you think that... I'm very agnostic about that, by the way. Asma, I sure, though enthusiastic. But say that we're there. You're an astrobiologist. You're on a mission. You're landing on the planet. Do you expect that life cycles on alien planets will also have the same sort of aging patterns that we see here on Earth?

I think so because I think natural selection. is a universal process. You know, if you think of life as essentially ability to reproduce, self-replicate, and evolve, those are two essential characteristics of life. So if you have that, you will have natural selection. And so it will inevitably have these trade-offs of resource versus maintenance and repair.

And, of course, if it's carbon-based, then, you know, it's more likely even to have that. And ultimately, ultimately, the laws of physics, which, you know, result in chemistry, which results in damage, that's not going to change, you know, somewhere else. So everywhere across the galaxy, there are grumpy old aliens telling those young kids to get off their lawn. I would bet on that if I had to. But I'm somewhat skeptical about, I think we don't know what the probability of life here is. And until we know that, we have no idea whether life elsewhere is very likely or whether we're alone or somewhere in between.

We just don't know. I should say some of the enthusiasm for extending lifespan to very, very long lifespan is by people who want to do extragalactic travel. You know, there are people who feel that we may be the only intelligent species, and we should go off and colonize, not just Mars, which you guys have pointed out is extremely hard anyway. But, you know, even other galaxies. And so they figure, well, if we have to do that, then we have to be able to survive the voyage, you know, and so we should, you know, we need to start working on longevity. So it seems like a crazy idea. But anyway, that's how it is. I think for a lot of people, it's like, you know, they'll say, oh, I want humanity to do it. But what they mean is that I want to be the one who does it in particular. Oh, yeah, yeah, yeah.

No, absolutely. Yeah. All right. Well, thank you so much for being on the show. This was fascinating. I'm sure our listeners are going to be thrilled with all of the answers. And thank you for your time. Thank you.

It's been a real pleasure chatting with both of you. And by the way, I really enjoyed your book. Oh, thanks. I loved your book. Daniel and Kelly's Extraordinary Universe is produced by IHeart Radio. We would love to hear from you. We really would. We want to know what questions you have about this extraordinary universe.

We want to know your thoughts on recent shows, suggestions for future shows. If you contact us, we will get back to you. We really mean it. We answer every message. Email us at Questions at Daniel and Kelly.org. Or you can find us on social media. We have accounts on X, Instagram, Blue Sky, and Our On all of those platforms, you can find us at D and K Universe.

Don't be shy. Write to us. Hey, it's Ed Helms host of Snafu, my podcast about history's greatest screw-ups. On our new season, we're bringing you a new snafu every single episode. 32 lost nuclear weapons. Wait, stop? What? Yeah, it's going to be a whole lot of history, a whole lot of funny, and a whole lot of fabulous guests.

Paul Shearer, Angela and Jenna. Nick Kroll. Jordan, Clepper, listen to Season 4 of Snafu with Ed Helms on the IHeart Radio app, Apple Podcasts, or wherever you get your podcasts. There's a vile sickness in Abbas Town. You must excise it. Dig into the deep earth and cut it out. From IHeart Podcasts and Grim and Mild from Aaron Manky, this is Havoc Town.

A new fiction podcast sets in the Bridgewater, audio universe, starring Jewel State and Ray Wise. Listen to Havoc Town on the IHeart Radio app, Apple podcasts, or wherever you get your podcasts. Welcome to Decoding Women's Health. I'm Dr. Elizabeth Pointer, chair of Women's Health and Gynecology at the Atria Health Institute in New York City. I'll be talking to top researchers and clinicians and bringing vital information about midlife women's health directly to you. A hundred percent of women go through menopause. Even if it's natural, why should we suffer through it? Listen to Decoding Women's Help with Dr. Elizabeth Pointer

on the IHeartRadio app, Apple Podcasts, or wherever you get your podcasts. It may look different, but Native Culture is alive. My name is Nicole Garcia, and on Burn Sage, Burn Bridges, we aim to explore that culture. Somewhere along the way, it turned into this full-fledged award-winning comic shop.

That's Dr. Lee Francis IV, who opened the first Native comic bookshop. Explore his story along with many other native stories on the show, Burn Sage Burn Bridges. Listen to Burn Sage Burn Bridges on the IHeart Radio app, Apple Podcasts, or wherever you get your podcasts. This is an IHeart podcast.