This Podcast Will Kill You - Ep 101 Immortality: This Podcast Won't Kill You

Episode Date: July 19, 2022

For what was originally going to be our 100th regular season episode, we wanted to turn the vaguely threatening title of our podcast on its head by exploring a topic that’s not about something that can kill you but rather the hows and whys of staying alive, forever. That’s right, this week we’re taking on the immense and amorphous concept of immortality, viewed primarily through the lens of biology. Why don’t humans or any other organisms live forever, evolutionarily speaking? What can the long search for an elixir of life tell us about our future prospects of life without end? How close has current technology brought us to achieving immortality in even the remotest sense of the word? This may not be your typical TPWKY episode, but we promise laughter, trivia, and existential contemplation about the meaning of life, so you’re not gonna want to miss it. See omnystudio.com/listener for privacy information.

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our 100th regular season episode. But when things with Monkey Poc started to ramp up, we decided that we wanted to make sure that we got a Monkey Pox episode out to you as quickly as possible. And that meant pushing back this immortality episode, which we had actually recorded before monkeypox. So, throughout this episode, you may hear references. to this being our 100th episode, even though it's actually episode 101, and we just wanted to explain why in advance. Okay, I think that about covers it, so let's get started. Introducing

immortality. The life that you seek, you never will find. When the gods created mankind, death they dispensed to mankind, life they kept for themselves. But you, Gilgamesh, let your belly be full, Enjoy yourself always by day and by night. Make merry each day. Dance and play, day and night. Let your clothes be clean. Let your head be washed. May you bathe in water.

Gaze on the child who holds your hand. Let your wife enjoy your repeated embrace. Still don't actually know the story of Gilgamesh? I still only know a little part of the story of Gilgamesh. So, yes, that's. was from the epic of Gilgamesh, which is one of the oldest, I think actually the considered the oldest, like surviving document or text. Wow. That's amazing. Yeah. Yeah. It's from a long time ago, like 2000 BCE, something like that. Wow. Yeah. Hi, I'm Aaron Welsh. And I'm Aaron Alman Updike.

And this is, this podcast will kill you. And today, we're not, just like reading you the story of Gilgamesh. No, that's most of what you'll hear about Gilgamesh. Today we're doing something very different in honor of our 100th episode. 100th. I mean, it is, I can't believe it. I never would have thought we could make 100 episodes of a podcast, Aaron. Me either. And okay, here's the thing is that like technically we surpassed 100 a long time ago. That's true. I forgot about that. With like all the COVID episodes and the bonus ones you've done. Yeah. Still. This is this is our like our title episode 100. Yeah. And I think in honor of that as we slowly get around to talking about what we're going to be talking about today,

we thought it would be fun to take the name of our podcast and change it up a bit, right? This podcast will kill you. Today, this podcast won't kill you. Yeah. It might make you live forever. Probably not. Give you the secrets to eternal life. Today we're going to be talking about immortality and aging, and it's definitely not going to be a comprehensive journey through the history of aging and how immortality could be achieved. But I think it's going to be a nice little taste. Yeah. And our structure is going to be a little different than usual because it's such an amorphous topic. Yeah. So I'm going to be starting out talking about the history of immortality and what that means in terms of evolution.

And then what that means in terms of like human culture. And again, it's just sort of like a brief little jump through this topic. And then I'm going to talk about I don't really know what, Aaron. Maybe like where we stand. in terms of like aging today or anti-aging research or the quest for immortality, what we know about the biology of it? I don't know. It's going to be a little bit of a conversation.

I think it's going to be really exciting and fun. Yeah. I'm just looking forward to it. Same. Same. Well, speaking of like tastes of things, what time is it? Oh, quarantini time. Still is quarantini time.

Still is always quarantini time. What are we drinking this week? Well, of course we're drinking none other than The Elyxer of Life. We are. And in The Elyxer of Life, it's a, it's a fun little drink because we've got gin, we've got lemon juice, we've got blackberries, we've got simple syrup, and then to kind of like create the fun little magical, I don't know, aura around it, We've got butterfly pea flower extract, which was sent to us by a very generous listener.

So thank you so much. It is such a cool looking drink. I'm really excited, but I want to come visit you so that I can actually taste it. Okay. Let's make that happen. Yeah. We will post the full recipe for the elixir of life, as well as the non-alcoholic placebo Verita on our website, This Podcast Will Kill You.com, as well as on all of our social media channels.

Our website, This Podcast Will Kill You.com, if you haven't been there yet, you should go and check it out. After 100 episodes, try it. We have merch, we have transcripts, we have links to our bookshop.org affiliate account. We have links to our Music, Bloodmobile. We have a goodreads list. We have all of our sources for all of our episodes. We have our Patreon. We have more than I could say in that single breath. Well, I think he did a great job. Thanks. Love it. All right. Any other business? No, Aaron. Please tell me, like, I don't know, from Gilgamesh to now, how has humanity fared on our quest for immortality? Great questions there. I will do my very best right after this break. Dinner shows up every night, whether you're prepared for it or not.

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Is immortality simply living forever? Not aging. Being invulnerable to any illness or injury. Does it mean that your name and life will be remembered hundreds of years from now? Or that your genes will be carried on in your offspring and their offspring and so on and so on down the line. There are many different ways that we can think of and have thought of immortality, and if your goal is to achieve immortality,

which definition you choose has tremendous bearing on how you go about that. And that can also be said for this episode. So how will we consider immortality today? Really, we'll at least touch on the most common concepts in a general sense, but since we're a health and science podcast, most of what we'll talk about is immortality from a biological perspective. First by talking about not what immortality is and how we can achieve it, but what stops us from being immortal in the first place.

Why do we die? Why do we decline as we get older? Are there any organisms that don't? What do we know or think about senescence, decline? decline or deterioration we experience as we age from an evolutionary perspective. And then I'll turn from that to talking about the age-long quest for immortality, which has roots much, much older than these startups in Silicon Valley that have been looking for modern elixirs of life that I know you're going to be talking a bit more about,

Aaron. Yeah. What patterns do we see in the different ways that people have approached immortality through history? And how has this past century and our ever-growing understanding of biology change the targets for immortality research? And then that's sort of where I'll hand it off to you, Aaron, to tell us how close we are, or probably aren't, to achieving immortality and the nitty-gritty of what people are working on. Okay. Okay. All right.

So let's get into it. Living things age, but they don't just experience the passage of time. They also change as time passes. First growing and developing, and then at a certain point, that growth ceases and a new kind of change occurs, one where maybe things don't heal quite as fast as they used to, or those aches and pains get more frequent and eventually recovery is no longer a possibility, with death being the ultimate end. And this is generally how it happens for every living thing. And sure, the amount of time that you spend in each life stage may be different or how long you can expect to live will vary. But death and aging are essential parts of life. Even for those supposedly immortal animals that you see like clickbait headlines about,

like lobsters or certain jellyfish or bristlecone pines. But while senescence, the biological decline part of aging may not be as marked as in other creatures, those organisms are not truly immortal. They will die eventually because nothing, living, is immune to death. Why does this have to happen? Like, why can't we go on living forever? Well, let's think about it in the context of natural selection and evolutionary fitness. Let's, Erin. Evolutionary fitness, for those who haven't heard the term before, is essentially an individual's reproductive success, how many offspring they have. If an individual has no offspring, zero fitness.

If they don't survive long enough to reproduce, fitness is also zero. But the individuals who do live long enough to reproduce and have a lot of offspring, those are the ones who are going to contribute the most to the next generation's gene pool. Traits that limit your ability to reproduce or survive through reproductive, age, those traits lower your fitness and make it less likely for those genes to be passed on to the next generation. And over time, those traits, those genes, will become less and less common, maybe eventually disappearing. But traits that make you more likely to reproduce or survive through the end of reproductive age, those are the traits that are going to be selected for,

becoming more common. So we can think of tons of examples of this, right? Like the size, of a bird's beak, or the rate of development of a tadpole into a frog, or fur pattern, or susceptibility to disease. But what's so crucial about this for this discussion is not the traits themselves, not these examples, but rather the time window when these traits matter most. And that is the critical period from basically prenatal development all the way through the end of when you are able to reproduce. That is when selection can act. With this in mind, what does it matter, really, in terms of natural selection if you live past reproductive age? It doesn't. It doesn't at all. It doesn't, yeah. If there are genes that affect, at least in part,

your longevity, how will natural selection act on them if they don't have any bearing on your reproductive fitness? It won't. It won't. It won't. I mean, and there are genes in humans that are associated with longevity. But it's likely that those play a role in maintenance or development and they don't just switch on later in life. Exactly. Yeah. So essentially, in terms of natural selection, it doesn't really matter how long we live past the point when we're no longer reproductively viable. And this is, of course, like a big oversimplification. And for humans and other animals, there are some very interesting hypotheses about why we humans live long

past the age we reproduce, mostly centering around grandparents. And I'd love to get into that one day with an episode on menopause. Oh, we'll definitely do it on menopause because I love all of the evolutionary theories behind menopause and just like aging and like the grandparent. Oh, I love all of that. Yes, the grandparent hypothesis. Oh, it's so interesting. Yes.

I love it. But anyway, we humans are not unique in that we live past the age we reproduce, nor are we unique in the fact that our bodies and minds start to deteriorate as we get older. And even if life past reproduction is not part of natural selection, what makes us and other organisms age? Like, why do we age? And we have been asking ourselves this question probably since we were able to form thought, but it wasn't until Charles Darwin introduced the theory of evolution by natural

selection in the mid-19th century that people had a scientific framework that they could use to try to answer this question. Since that time, many different hypotheses have been proposed, none of which seemed to adequately explain senescence for every living thing. And I'm going to briefly go through a few of the classical hypotheses of senescence so that we can try to think about possible mechanisms that could explain why aging is universal. The first of these hypotheses was proposed in the 1890s by the German evolutionary biologist August Weissman, the so-called germ soma theory. And so Weissman suggested that there were two types of cell lines in an organism, a germ line and a soma or body line. And the germ line is made up of the cells that are involved

in reproduction, and the soma line consists of the cells that make up the rest of the body. It's the sole duty of the soma cells to do whatever it takes to keep the germ line alive and reproducing. Beyond that, soma cells basically disposable, and the soma cell lineage will invariably die while the germ cell lineage can be viewed as potentially immortal. aging happens as the soma line gets beat up by the environment while protecting the germ line. And that's the hypothesis. Yeah. Obviously, it has many shortcomings, first of them being that it doesn't really explain why senescence evolved, like why the soma is disposable.

And it doesn't explain senescence in single-celled organisms. But it did introduce the idea that reproduction is first and foremost the problem. priority. And many later researchers built upon this idea, such as the famous mathematician and eugenicist Ronald Fisher, who in the 1930s proposed a mathematical model in which he laid out his thoughts that senescence was the accumulation of harmful age-specific traits. A couple of decades later, in the 1950s, Peter Medawar, whose name you might remember from our organ transplantation episode. He wrote a now famous essay describing how the force of selection weakens as we get older and

past our reproductive age. He wasn't entirely right either. For instance, his belief that animals in the wild don't get old, they don't senesce because they just get picked off by predators or succumb to starvation. They actually do senes. They actually do get older. But his essay did suggest a sort of mechanism for senescence. If there are certain genes that do exist that shorten our lifespan, they won't really be selected

against if they only show their effects later in life. And so they will continue to appear and accumulate over generations, the quote, mutation accumulation theory. That's, I love, sorry, I just really do love these hypotheses. I do too. I find it really fun. It was so interesting, because I have never, even though I said humans have probably asked them themselves as question forever. And I've probably asked myself this question too, but not in like

a, okay, but why? What is the actual evolutionary mechanism behind it? I feel like I only ever thought about another hypothesis I think you're probably going to talk about next in the context of the evolution of human health class that I TA'd for. So that was like a very specific subset of time that I was thinking about it. Yeah, it is, it's so fun to think about. Okay, so there are a few more. Yeah. So a few years after Medawar's essay, George Williams added on to this by suggesting that in addition to these mutations appearing, it's also possible that those genes that are helpful early in life, like in development and during reproduction, could also be bad or have negative effects later in life. Like, for instance, let's think about cell growth. If your cells grow super fast, that's potentially great when you're developing, right? You, get larger faster and can be independent faster. But later on, that could mean uncontrolled cell growth, aka cancer. And this is something that's called antagonistic pliotropy. It's one of my favorite concepts, and I love it. It's so, it's, I mean, and it like the thing, they all make sense. And

the thing that I like too about them is that none of them are really mutually exclusive. Exactly. Like you have, you can easily have mutations that accumulate as well as have genes that are beneficial early in life and maybe have a detriment later in life. So like these mutation accumulation, antagonistic pliotropy, these hypotheses really do work together to explain aging in a way that I think is just fascinating. Yeah. Yeah, exactly. And also what really helped things along in this, in this field was when in 166, William Hamilton combined some of these existing ideas on the evolution of aging into a mathematical model, which like, maybe that doesn't sound very exciting, but it really, it was. And it still today is super impactful because it laid out a framework for why aging happens. And it also showed that the strength of selection on traits that keep you alive, it becomes weaker over time in anything that ages and doesn't reproduce via fission. Yeah.

Really, also, what it did was create a math model for people to be able to test ideas about aging. The last of the classical hypotheses of senescence I'm going to talk about is the, quote, disposable soma theory proposed by Thomas Kirkwood in 1977, which says that over time an organism cells accumulate harmful genetic mutations. mutations. Mutations in your DNA happen randomly all the time because of environmental factors or mistakes in DNA replication, and it gets increasingly costly to repair the damage from these mutations. And at a certain point, the benefit of repairing the damage is outweighed by the cost. Repair and maintenance is always going to favor the germline. Okay, so these are just a few of the most impactful hypotheses to explain why senescence evolved. But there are certainly others, and no single hypothesis at this point seems to be able to explain aging for all organisms. There's no unifying hypothesis, probably because, like, there's tremendous diversity in life. No, is there really, Aaron?

I'm telling me that, like, a bristlecone pine is not the same thing as a plenarian? It might not be. And even some of the fundamental assumptions about aging have been challenged. It's an extraordinarily complicated thing to study. You have to capture both how different environments and different genes impact aging. You have to consider ecological factors, determine whether aging in the lab is different or the same as aging in the wild, evaluate whether closely related species age more similarly than distantly related ones. And the biggest thing in my eyes is that we've really only begun looking at this within the past

130 years or so, which is shorter than the average lifespan of some organisms that could give us really valuable insight into longevity. Good point. So like how do you create a data set for giant tortoises? Right. Well, even studying human aging. Like, we live a really long time. Right. That's hard. And there have been really cool, like, census records and especially in certain countries or certain regions that keep really good track of, like, people through time. But we still don't have all the bits of information there. Right. Yeah. So it's, it's in a way we've been thinking about it for a long time, but it seems like we're definitely in the infancy of, of having data to be able to test these hypotheses. Erin, you just summed up my whole section. It's, it was really interesting to read through this also because I don't think I realized

just how huge of a field of study this is. And I guess I should have because there are like, you know, entire journals and entire textbooks and entire companies and everything. But like it is it is really hard to do it justice. Yeah. Yeah. So yeah. So I just kind of wanted to like wander through some of these ideas and kind of feel and build a baseline for thinking about aging in an evolutionary context, especially when it comes to like natural selection.

Yeah. And wouldn't it be great if we lived forever? But we don't really need to. Yeah. In terms of our like DNA. getting passed on. Yeah. Exactly. Yeah. And I also thought it was important to think about these things, like why we age, before we start exploring some of the ways that we've tried and continue to try to stop or slow that process. So if there's anything that humans are good at, it's searching for the key to immortality. We're really good at searching for it, but we are terrible at finding it.

Yeah. Because we've not found it. Yeah. Spoilers. We don't have it. Spoilers. We don't have it. We may not have it.

Ever. Immortality narratives are central to every culture and religion, like the epic of Gilgamesh, the oldest known written document. So the reason that I included Gilgamesh, in the beginning, I'm like now calling back to it, is that a big part of this story is about the quest for immortality. So King Gilgamesh's best friend dies, and in response, Gilgamesh vows to find eternal life. Spoilers, he does not. And I'm sure between the two of us, we can think of dozens and dozens more books or movies or poems or songs about the search for eternal life.

But it's not just like one of my favorite books growing up was Talk Everlasting. And for a long time, have you read Talk Everlasting or Worship? No, I didn't even know it was a book. I thought it was a movie, but I've never seen it or read it. Basically, it's about this family that is trying to find like a home, they're like homesteading and they stumble across this water. They all drink from it, including the horse, I think. and it happens to be like an immortality spring. And then there's like a girl who stumbles across his family and then she's like, do I drink it?

Do I not drink it? Blah, blah, blah. And as a kid, I was like, drink it, obviously. Don't drink it. Don't drink it. And yeah. Anyway, but it's a really interesting contemplation about immortality and life. Yeah.

I loved it. And that's just one of like hundreds, dozens, thousands, I mean, an unbelievable number. But it's not just in these fictional stories that people have been on the hunt for a way to live forever. The quest for immortality is a very real thing that takes many different forms. And I want to talk a bit about these forms before focusing on a couple that are more in line with this episode. While researching for this episode, I came across a book titled Immortality. the quest to live forever and how it drives civilization. And in this book, the author, philosopher Stephen Cave, groups the search for immortality into four different themes.

The first two deal with the physical side of things. First, there's living forever. You as an individual stopping aging or aging but not dying, living indefinitely. And then there's resurrection, being brought back to life after death. think Jesus. Third is the soul, the idea that a part of you, but not the physical you, lives on after you die. And finally, there's legacy, which can mean living on through memories or fame, as in you're only truly dead when your name is no longer said. Coco.

Or also offspring, the idea that your genes achieve immortality by being passed on. And I wanted to explore some of the ways we've sought to. to achieve immortality throughout human history, focusing on those that fall into the first two of these themes, staying alive and resurrection. Because in terms of targets for biological research into immortality, all of those projects can be lumped into those themes. Yeah.

And after going through some of these adventures in immortality, I want to end by reflecting on what these stories tell us about human nature. We humans may be, unique in our ability to recognize our own mortality, that one day each and every one of us will die. And the knowledge of our own inevitable death, yet the simultaneous inability to actually imagine what it will be like, has driven us to find any way around it, either by delaying it, undoing it, or preventing it entirely. In ancient Egypt, there was an entire, industry devoted to preserving the body after death so it could be magically revived. And of course,

pyramids and other monuments were built as a testament to the person's life, immortality through legacy. Ancient papyri describe not just preparation for the afterlife or resurrection, but also ointments and elixirs that were meant to extend life and slow aging. The search for an elixir of life or a fountain of youth is similarly old. There are countless stories of emperors and kings searching in vain for a way to escape death. Like the first emperor of China, who lived around the 200s BCE,

he became obsessed with the idea of living forever and searched high and low for someone who could reveal the secret to him. He did find someone, probably one of the oldest known swindlers, who promised it all, delivered nothing and just ran away with his reward. Of course. Ultimately, the emperor died young, only 49, likely from either arsenic or lead or mercury poisoning, all of which were likely

ingredients in his daily, quote, life-extending vitamins. Oh, gosh, that's just such a bummer. I know. But he did achieve immortality in a way. I mean, we're still talking about him. We are. Through legacy. He, the terracotta army. Have you heard of the terracotta army? Oh, yeah. Yep. That's him. That's him. Huh. Mm-hmm. All right. The elixir of life wasn't always viewed as just a potion or something you ingest. At various points, it was thought to be a plant or a series of exercises or a special object like the philosopher's stone, which was one of the mythical substances famous in alchemy. Alchemy was a kind of pre-science, practiced by philosophers and early chemists, the goal of which was to transform one metal into another, typically gold, and to find the elixir of immortality or a cure-all for any disease. It was practiced all over the world, from ancient times, all the way up through the 18th century, when it declined after the rise of more rigorous scientific thinking. Although it might be more accurate to say that alchemy didn't decline, but rather it was repackaged,

primarily into the field of chemistry. Nor did people grow tired of looking for the elixir of immortality. Instead, the development of each new field or new scientific discovery was applied to that quest. For instance, electricity. So if you think back to our electricity episode, you may remember me telling the story of Galvani and his metal wires and the frog's legs jumping. Oh, yeah. Uh-huh.

So his nephew took a page out of his book and held public demonstrations where he reanimated corpses of freshly hanged murderers. Oh, my. Okay. Yeah. And his demonstrations may have been the inspiration for Mary Shelley's Frankenstein. Oh, my goodness. I know.

Connections. And this pattern continues to be repeated. In the mid-20th century, advancements in cellular technology, allowed researchers to use previously frozen sperm for insemination, resulting in three pregnancies, which was revolutionary. And that soon turned into whole-body freezing plans. As we've learned more about genes linked to aging, thanks to genomic sequencing technologies, those inevitably became our targets for modern-day immortality projects. And the amazing thing, in my eyes, is that despite humanity's continuous and innumerable attempts to achieve immortality over thousands and thousands

of years, we have not been remotely successful. And we probably never will be. Maybe you'll change my mind. Yeah, we'll see, Aaron. Over the past couple hundred years or so, the average age a person can expect to reach has been greatly extended, largely due to vaccines, antibiotics, and many other small things, especially a better understanding of disease overall. But this has not been an extension of our inherent lifespan. Humans have been able to live to 80 years old, 90 years old, for thousands of years. But were prevented from commonly achieving old age because of extrinsic factors, like insert any vaccine preventable disease here.

We're also taking, like, mercury in our... arsenic as a vitamin. Just like that too. But from what I've read, there's not a single anti-aging serum, pill, potion, whatever that has been shown to actually slow aging or reverse or stop it. There is some evidence that diet and exercise may play a role. Longivity and aging are both such incredibly multifaceted processes that are nearly impossible to predict. And I'm not saying at all that I don't think this research should be done. Some of these projects have uncovered knowledge that has had huge implications for improving quality of life and treating diseases that primarily manifest later in life. I guess I'm just expressing my skepticism that a meaningful extension

of both lifespan and quality of life alongside that will be achieved in the near or even kind of near future. The section definitely came out differently than I had planned. When I started it, I thought I'd take us through the history of the search for the elixer of life or the beginnings of cryonics. And those stories are fascinating and worth telling. But I think that overwhelmingly, while doing the research for this part and while going through it just now, I think that what sticks out to me most,

is how so many things have not changed. We will continue to keep looking for ways to live forever, to upload our brains or slow our aging, to reanimate frozen bodies, or download our memories into a cloned body. And if any of those technologies are successful, you can also be sure that the select few, the richest and most powerful,

will be the only ones to benefit from them, which is also how it has been throughout history. But would it truly be a benefit to live forever? Would it be something you want? I've talked about a few stories about people who have searched for a way to live forever. Now let's think of some where they achieved immortality. How did those stories end? Never well.

Never well. Almost universally, they end in profound loneliness, sadness, and regret. Not at first, maybe, but over time, as their mortal friends and family grow older and die, as days pass and time becomes meaningless. Granted, all of those stories have been imagined by mortal humans, so perhaps these endings are just consolation for not being able to live forever. But I don't know. Personally, I don't think so. I think too often we decide we want to live forever without considering what that could truly look like. I want to end this section with a quote by Stephen Cave that I think puts it nicely.

Quote, the deep problem is this. The value of a thing is related to its scarcity. People conscious of their mortality value their time and aim to spend it wisely because they know their days are numbered. But if our days were not numbered, this incentive would disappear. Given infinity, time would lose its worth. and once time is worthless, it becomes impossible to make rational decisions about how to spend it. The consequences of this for an individual would be bad enough. For a civilization of such dithers, it would be disastrous.

Yeah. Yeah. And with that, Erin, I'll turn it over to you to tell me how close we are to such consequences. Oh my goodness, Erin. This episode turned out so different than we expected. I'm going to need a break. Okay, yeah. And then I'll dive in to what's happening today.

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Nibbles would have loved you like a brother. Connecting homeowners with skilled pros for over 30 years. Angie, the one you trust, to find the ones you trust. Find pros for all your home projects at Angie.com. So when I first started trying to research for this episode, I had a really hard time because I wasn't sure how to really approach this question. I actually wasn't sure what my question was. I normally do the biology section of whatever disease or thing we're talking about. And then I talk about the current status. Where do we stand today?

So what was my question for immortality? Is it how close are we to immortality? Is it, are we still pursuing this quest? Which, spoilers, you already told us. And the answer is, yes. We still are. Oh, yeah. Was the question, have we learned anything from these thousands of years of futility so far? I don't know what question I'm answering out of those, but I did a lot of reading. And I read a lot about the various, you know, Silicon Valley startups that exist. The number of companies, the number of billionaires and millionaires and the amount of dollars that are going in to try to solve this quote problem of aging or the problem of death. It kills me the problem of aging or death. It's really, really interesting. And I think I got a little bit overwhelmed and also maybe a little

cynical by the end of it. Oh, for sure I got cynical by the end of it. Yeah, but it's not to say, like what you said, Aaron, it's not that what any of these researchers are doing is unimpressive or unimportant. It's just that we remain in the very early stages of this research. So let's kind of go through the way that I at least tried to frame thinking about this. If we're talking about immortality, like you said, Aaron, at the top, then we're kind of talking about the idea of anti-aging, or we're talking about increasing our lifespan. And if we're talking about halting aging to the point of halting death, then for me, the way to get there logically is to answer a series of four different questions.

The first question, you kind of answered, Aaron, and that is why do we age? I think that you provided a lot of evolutionary perspective on the idea of why we as humans and we as living organisms on the planet Earth age evolutionarily. But we still don't fully necessarily know. We at least have a lot of hypotheses. But a very closely related question to why do we age is how do we age? Like fundamentally what governs the process of how our cells senesce and how is this process related to those evolutionary reasons of why we age? Because if we could answer those two questions really well, then we could ask the next question, must we age? Are those processes, like we said, from an evolutionary perspective, necessary for life?

And are they immutable? And if the answer to that question is no, they're not immutable. And if we can figure that out by virtue of figuring out the answers to the first two questions. Then we can ask the final question. If we don't have to age, do we have to die? So at least to me, those seem like the four fundamental questions that have to be answered if we have any hope of answering this riddle of immortality. And suffice to say, those four questions are massive. And I think the biggest issue for me in talking specifically about immortality.

mortality is the leap between those last two questions. Must we age and must we die? Right. Because while there are in nature and in the laboratory, many, many examples, be they plant or worm or lobster, that live a very long time that seem to be immortal, nothing is invincible, right? Right. If you take one of these invincible planarians out of their worm juices, they're going to die. They're not invincible. And so that's, I think, one of the biggest issues I see with even just entertaining this idea of true immortality. Oh, yeah. Right? Immortality is not invincibility. Exactly. Yeah. Okay. But so is that what people are working on? Are people working on immortality? Or are people really working on the first few questions, but selling it, packaging it,

as the idea of immortality. Maybe that's more accurate. So what do we actually know about these first couple of questions, especially how we age and must we age? There has been, like you said, Aaron, without a doubt, huge increases in the estimated life expectancy for humans globally, and there is a lot of variation in estimated life expectancy, between countries, between genders, et cetera.

And most of that increase is, like you mentioned, credited to early life advancements, things like antibiotics, vaccines. Basically, we know for sure that we've had huge reductions in early life mortality because of scientific and biomedical achievements over the last 50 to 100 years. However, there has also been a decline in late life mortality. So the fraction of each birth cohort that reaches old age has been increasing year after year. Or at least it had been until about the 1980s. And since then, it's actually been very stagnant despite increasing overall life expectancy.

But the maximum reported age at death has plateaued. You may have heard of Jean Calmey, who was a fullerable. who was a French woman who died in 1997 at the ripe age of 122 years and five months. She still holds the verified longevity record by a lot, by a couple of years. And while there are over 500,000 centenarians alive worldwide, at least that's what the UN estimated in 2020, Wow. 500,000 people over 100. That number is 20 times higher than 50 years prior.

But the average age at death for these centenarians has not increased since 1968. So there is a lot of research and mathematical modeling, like you mentioned, Erin, as far back as the 1800s, that really suggests that there may be a true upper limit to the human life space. And while this idea is still a little bit controversial, there are people who don't like to agree with the idea that there is a limit to human life expectancy. A lot of studies that have used various methods and are to varying degrees controversial have converged around this idea that perhaps between 120 and 150 years might be the maximum human lifespan that one could expect. So could we even live forever? It seems highly unlikely. Yeah. But there is another piece to this puzzle.

Besides actual lifespan is like you mentioned, Aaron, quality of life. This is often called health span. So if lifespan is the length of your life, health span is often defined as the period of your life that is free from disease. I personally will take slight issue with this definition because health is, of course, a lot more than merely the absence of disease. But this is generally how health span is defined. So we'll go with it for the purposes of this episode. Okay. And if we look worldwide, despite how much lifespan has increased, chronic diseases are the leading cause of morbidity

and mortality worldwide, and many of these, cardiovascular disease, cancer, dementia, these are often considered diseases of aging. And an estimated 58% of chronic disease-related mortality happens in people over age 70. So if we look at the discrepan between health span and lifespan, there's an estimated gap right now in the world of nine years. So there's a nine-year gap where you are still alive, but you are no longer, quote, free from disease. And a lot of the field of what is called gerontology research isn't truly focused on the idea of immortality, at least not overtly. Or in a lot of cases, they're not even focused on the idea of increasing our lifespan, but rather they're focused on increasing health span. So they talk instead about the idea of compressing our morbidity to the end of life,

such that we live healthier lives for longer and can either avoid or prolong the onset of these various age-related diseases. And this, I think, sits as both a more palatable goal. For sure. I would agree with that. But I also think that it's closer to what seems maybe feasible. Yes. Although I do stress that we're not there yet. It's so interesting because I think that like given the past 150 years of scientific research,

we tend to view things as science will always progress at an increasing rate. Yeah. Right? Like we make bigger leaps and bounds in our understanding and in our technology and so on. And it doesn't, that's not necessarily the case, I think. with every field. Yeah. It is really, really interesting to read a lot of this research and then also read the media

reports about this research or about the companies that are funding this research. I bet. Because it's very different, right? Yeah. This is where reading between the lines of popular news articles is tricky. It's tricky and where there's like have a heavy dose of skepticism and go to the original text. Yeah, definitely.

But there are, I will say, a lot of researchers out there that are trying to really get into the nitty-gritty of answering those first couple of questions that I posed. How and why do we age? And can we alter this process? So while we don't have a single answer, I will link to a couple of different papers that go into a lot more detail on these mechanisms. But we can define, based on what we know so far, about nine different flavors or nine different targets that are related to aging and potentially modifiable, at least in cell culture and

or in animal models, or maybe just theoretically modifiable. So I'll mention all of these, but spoiler alert, reading some of the papers that go into detail on this, I had a very difficult time following through. But let's at least look at what we know about aging, because it turns out we know a lot more than you might think. So when we look at the mechanisms of aging, one of them, Aaron, you mentioned already. And that is damage to our DNA, be that nuclear DNA, our mitochondrial DNA. Basically, over time, insults, to our bodies result in the inability of our bodies to properly repair damage to our DNA the way that it is supposed to. And there are a lot of different potential genes involved in this and specific

mechanisms that researchers have altered in flies or in worms or just in cells. But essentially, this genomic instability does play a really big part in the process of aging. So if there was a way to make our DNA more easily able to repair itself, that could then delay that process of aging. And we know delay a lot of the age-related diseases that are related to this like cancers, like maybe heart disease. There's also telomere damage. Telemere's, I think they talked about in our HPV episode. Was that right? You talked about it in some episode, but can you do a refresher? Of course. I'd love to. So telomeres got a lot of press in age. a while back, but basically they're the end caps of our DNA. They're these strings of repeat DNA

that sit at the ends of our chromosomes. And in a lot of cases, they don't get completely copied over when our cells divide. So over time, telomeres can become shortened. And this process of telomere shortening or telomere exhaustion then leads to a decline in the regenerative capacity of tissues and therefore accelerated aging. So in mice models and in other animal studies, telomere length has been shown to be associated with lifespan. In humans, it's not quite that simple, but this is at least another potential target. What do you mean it's not quite that simple? It's not like the length of your telomeres determines how long you're going to live. It's not a one-to-one association. So just adding on to our

telomeres doesn't necessarily mean that we're going to increase our lifespan or our health span because this is one of nine processes related to the aging process. Nine that we know of so far. Okay, there's more. Lots and lots of research right now, especially by some of these big biotech companies, into epigenetic modifications. Epigenetics, we've only ever briefly mentioned,

but I actually think I talked a bit about it in our folate episode. It was kind of fun. I was thinking that. Yeah, yeah. Basically, epigenetics are changes to DNA patterns that are not within the DNA itself, so not within a gene, but it's changes to things like methyl groups that are attached to our DNA. It's changes to things like histones, which are like the proteins that our DNA wraps itself around. It can be changes to how our DNA is stored. Any of these changes are considered part of the of epigenetics and changes in a number of different things, from methylation to histone proteins, have been shown to be associated with aging. There is a family of enzymes called sertoin's, I think that's how you pronounce it, that are involved in DNA methylation and got a lot of press because in yeast and in worms, when these enzymes are manipulated, then you can increase lifespan by significant amounts in a worm. Again, in humans, we don't have any data to show that

as of yet. But that's at least the idea that epigenetics likely plays a big role in the process of aging. So if this is something that we could target, we could maybe affect it. Yet another target would be proteostasis. So basically, our cells are both DNA and proteins, right? So, So as we age, our cells become less able to maintain proteins in the correct stable configurations and correct functionality. If you think of something like Alzheimer's disease, this is largely a disease of protein misfolding. So there are a lot of studies in cells, in yeast, and I think at least some in worms and flies,

that if you mess with some of the genes related to protein stability, then you can precipitate aging, make them age faster. So that suggests that these systems are directly involved in the process of aging and thus, if they could be manipulated in the opposite way, could perhaps promote longevity or reverse aging. Reverse aging. Interesting. Yeah. Yeah. There's more. I'm only on number four of nine. I don't have as much detail on all of them. Let me tell you. There's also the idea, and I think this one has gotten probably the most press very recently, or at least maybe just the most press of the press that I read. But it's this idea of as we age,

we have a deregulated ability to do nutrient sensing. Basically, our bodies are not able to tell as we age if we have an abundance of food or if we have not enough food. And this goes along with a lot of, lot of data in mice and in some primates of caloric restriction. So having less food for a portion of your life increases lifespan in a lot of animal models. So there are a lot of different host factors that are implicated as a possibility in this. Some of them are things you've definitely heard of like insulin, right? Or IGF1, insulin growth factor one. There are a lot of

others like mTOR, amp K, Sertuans are in amp K. These are all various fancy names for factors that our body uses to help signal to our brain when there is food that needs to be digested versus when our nutrient stash is very low, so we need to engage in catabolism, like break down our own stores instead of building a bunch of muscle and fat. So there's evidence to suggest that states of anabolic signaling, that is our body saying, hey, we've got a lot of food, we need to build up stores. That process accelerates aging, at least in mice. And so manipulating this signaling so that a mouse's metabolism thinks it's living under limited nutrients by manipulating some of these factors can extend longevity. Interesting. So that's what is meant by caloric restriction,

is manipulating the factors, not straight up caloric restriction? No, straight up caloric restriction means straight up caloric restriction. Okay. This is trying to get out a way of can we trick our bodies into thinking that we're living caloricly restricted, but we don't want to live caloricly restricted. What is the mechanism for caloric restriction increasing longevity? And what is and what does caloric restriction mean? Great questions.

So caloric restriction in animal models means reducing an animal. animal's nutrient intake to about 30 to 40% of what is typically considered necessary for, like, you know, the amount of calories that a mouse needs. So it's very, very restricted. I want to be extremely clear on here that I am not by any means recommending this for human beings. This could be very dangerous. Okay. But in mice, restricting them to that very small amount of calories, 30 to 40% of what would normally be needed, does increase lifespan. And it also increases the age at which animals are able to reproduce, if that makes sense. It increases how long you are reproductively viable?

Well, no, because these animals tend to not be able to reproduce while they're living under caloric restriction. But then they get to an age where normally, like a normal mouse at, say, this many months of life would no longer be able to reproduce. this mouse who's been calorically restricted now can reproduce if you start feeding them. Okay. But if the mouse is only consuming 30 to 40 percent of what is considered necessary for it to live, how is it living? Well, so that is the idea behind all of these factors. Basically, the thought is that in so doing, in restricting these calories,

you're altering the way that the body is metabolizing everything in a way that is promoting catabolism so that breaking down of our own body stores rather than anabolism, the building up of our muscles, the building up of fat stores, right? So that's the idea behind why caloric restriction works. We know from animal model studies from a long, long time ago that restricting animals' diets makes them live a longer time. These genes and these factors and these hormones that have been identified seem to be the possible mechanistic way that caloric restriction manifests. So if we could directly affect those mTOR or insulin or what have you, then we could trick our bodies into breaking down stores rather than building fat and that might make us live longer. That's the

theoretical idea behind it. Interesting. Yeah. It kind of, it reminds me of going back to the evolutionary hypotheses, the germ soma theory where it's like the germ line is always favored, but maybe here's the exception where if the soma line can't support the germ line, then the soma line has to be favored first. Yes, exactly. I think that that is a good way to kind of, yeah, piece those together. Interesting. Okay. There's a few more, but I will say I'm not going to go into quite as much detail because from what I read, the topics that I've already covered are maybe the ones where we're a little bit farther along in that we have data from animal models and from cell models to show that manipulating these various things,

be they nutrient sensing or protein stability, can affect aging. The other ones are a bit more theoretical still, at least from what I read. And apologies if someone has some great data that I didn't see on these last few topics. Send it our way if you do. I would love to read it. So another possibility is the idea of mitochondrial dysfunction. So our mitochondria are often called the powerhouse of our cells. They do a lot for our bodies. And the idea is that over time, just like our DNA in our nucleus, these mitochondria can just sort of not function as well anymore. This is thought to be very related to things like oxidative stress over time. That's all I got for you on mitochondrial dysfunction, related likely to the process of aging.

Okay. There's also just the idea of cellular senescence in general. Cells going quiescent over time. A lot of our cells in our body are not dead. but they no longer divide. They're no longer active. So there's a large thought that just this entire process of cells kind of turning off a lot of their activity then relates to aging. And it's likely protective to reduce the amount of DNA damage that might occur through the process of replicating cells that don't need to be replicated, etc.

So this might be something that's more related to protect. against aging rather than involved in the process of aging, like protective against it. Yeah, yeah. Okay. Then there's the idea of stem cell exhaustion, which I, again, didn't get that much into detail of, but the idea that our stem cells are the ones that aren't able to keep up the way that they need to to be able to produce more cells correctly. Like the basal layer of our skin cells are stem cells that can become any various type of cell. But as insults occur to these stem cells, then hence the process of aging. And finally, there is also this thought of defective or

diminished cell-to-cell communication. And there's a lot that probably goes into this. One that I think is interesting. And I didn't, I will full disclosure, actually read any papers by him, but I watched a TED talk. of this researcher named Michael Levin, who is a researcher at Tufts University and does really interesting research on cell-cell communication from a bioelectric field perspective. Ooh. Right? It's very, very interesting. But there's also a lot of other ways that our cells communicate with each other besides

potentially a bioelectric field, but I will link to that TED Talk because it's fascinating. And it's likely that this process over time also becomes defective and is involved in the process of aging. That was like a very fast speed through. And I know that I left a lot of detail out. I will cite a couple of papers, one from 2013 that's a few years old now, but another that is a summary of a 2021 symposium of gerontologists that has a lot more detail on these nine different processes and where we kind of stand in terms of in vitro cell data, animal model data, and human data. But the thing is, I think it's very clear just by going over all those various processes

that these are all very interconnected. Right. Especially when we talk about humans, it's not one single piece. All of these processes are likely at play, and we are not at a point where we can say that we have an answer or a drug or an intervention at all that can. can prolong our life in any meaningful way. We don't even have one that could likely prolong our health, at least not yet. So really, for me, what it comes down to is that forever is a very, very long time.

So do I think it's possible that humans will ever unlock the many locks between us and immortality? No, I will say no. Yeah. It doesn't seem likely. It doesn't. Do I think that it could be theoretically possible, this concept of immortality? I kind of don't, Erin. Do you? No, but I will say that also what occurred to me while, you know, listening to you and while thinking about the part that I went through is that maybe, you know, this is one of those things where in the future, in the distant future, if anyone ever stumbles across this podcast, and they'll just laugh at how naive we were and how unbelieving we were.

Yeah. I, maybe. Maybe. I similarly doubt it. I mean, and I think that's another thing, too, is that immortality is not what people are working on. Exactly. It's how it's being sold.

Yes. And one of the things that I think is really interesting, in reading from the gerontology perspective is that I do think that a lot of the research into these questions of like, how does aging happen and can we manipulate those processes? This research can be used to improve the lives of humans. And I do think that it could potentially increase our health span and delay the onset of all these various aging-related diseases. But what's interesting is that we tend to study all of these various age-related diseases, cardiovascular disease, cancer, Alzheimer's disease. We study these

diseases in isolation. Ooh, that's such a good point. And aging itself is not considered a disease. So you cannot study it from a like applying for NIH grants perspective or from a drug development perspective, you cannot study it in the same way that you can study diseases. Oh, that is very interesting. It really is. Because it also means that the funding is not actually being directed towards aging. The funding from the government is being directed towards addressing these diseases that we think maybe could be preventable, right? But if we think that these are interrelated diseases that are all part of the process of aging, then wouldn't it make more sense to address them from a wider perspective by addressing these underlying

mechanisms rather than addressing cardiovascular disease or diabetes itself and cancer itself, let's think about these things that underpin both of those or all of those. And so I think that that's kind of the argument of a lot of the people who do this type of research. And I think it's really valid. And maybe that's the gap that some of these biotech companies are filling by directing their funding to address that. I don't know. Maybe that's an optimistic view, but maybe. That is, that's a really good point. And I mean, I know that like a lot of epidemiological studies will look at all of these things together. But it just, there are so many different avenues of research. Yeah. And it does seem like aging is super multifactorial. A lot of these diseases

are super multifactorial, but some of the factor, like they are like siloed diseases. Exactly. That's, yeah. I also think it's important to point out, like you mentioned, Erin, there are a lot of other, in my mind, ethical and moral concerns related to this idea of pursuing an increased lifespan or health span in thinking about the state of our planet and climate change and how we've impacted our planet with the lifespans that we currently have and also in, like you said, where is this development and technology going to go? Who is going to benefit from it? Because the increase in lifespan that we've seen in the last 50 to 100 years hasn't been even across the board.

And people who are wealthy live much longer than people who are not wealthy. And so that is likely going to continue to be true, especially if all of the research being done on this is from a capitalistic perspective. of companies trying to make money off of it. I don't know. Yeah. I mean, anti-aging is one of the world's biggest industries. Yeah, definitely. It really is.

And I'll repeat again, not a single anti-aging product has been shown to actually slow, stop, or reverse aging in any capacity. Yeah. Diet and exercise, Aaron. Diet and exercise. Yeah. Listeners, do you think you'd want to live forever? I'm curious. I'm curious.

And if so, why? Why? Or why not? Or why not? Yeah. Should we do sources? Yeah. I have a bunch, but I'm going to shout out two books in particular that I found really

helpful. So in terms of the evolution of senescence and the evolution of aging, there is a book by Shefferson et al, or a bunch of editors, titled The Evolution of Sinescence in the Tree of Life, and that's from 2017. And then the book that I already mentioned by Stephen Cave, Immortality, The Quest to Live Forever, and How It Drives Civilization. And those are both really, I just really enjoyed the Stephen Cave book as an interesting way to look at immortality. I had a couple that I enjoyed. Those two that focused on the various howls of aging were a paper from cell in 2013 titled The Hallmarks of Aging, as well as a symposium report from the Annals of the New York Academy of sciences from 2022 titled Extending Human Lifespan and Longevity, a Symposium Report.

I also thought an important one to mention is a paper from 2021 called Longevity Leap Mind, the Health Span Gap. And then there was, there's a bunch more. So I'll link to them on our website. This podcast will kill you.com under the episodes tab. Thank you to Bloodmobile for providing the music for this episode and all of our episodes. Thank you to the Exactly Right Network of whom we're proud to be a part. And thank you to you, listeners.

I really hoped that you liked this one. Yeah. Yeah, I hope so too. And a special thank you to our patrons, as always. Thank you so much for supporting us. Yeah. Well, Erin, happy 100. Happy 100.

And until next time, wash your hands. You filthy animals. This is Bethany, Friends. from Just Be with Bethany Frankel. Listen, I have a bone to pick with these dog food brands calling themselves fresh, natural, healthy. Sounds great, but a lot of these, quote-unquote, fresh dog foods in your fridge are not even 100% human-grade, which is why feed your babies just food for dogs. It's good enough for big and smalls, my precious babies, so it's good enough for your babies.

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