Speaker 1: Welcome to Stuff to Blow your Mind from how Stuff
Speaker 1: Works dot com. Hey you welcome to Stuff to Blow
Speaker 1: your Mind. My name is Robert Lamb and I'm Joe McCormick,
Speaker 1: and we're back for part two of our discussion about
Speaker 1: where's my eternal youth? Why can't I be young and
Speaker 1: beautiful forever? Why do we age? I know that's the
Speaker 1: It's the question we've always wondered. It shows up in
Speaker 1: our philosophical writings, it shows up in our religion, our mythology. Uh.
Speaker 1: In researching this topic, I kept thinking back to Genesis
Speaker 1: six three. This is the King James version, and the
Speaker 1: Lord said, my spirit shall not always strive with man,
Speaker 1: for that he is also flesh. Yet his days shall
Speaker 1: be a hundred and twenty years. So there's God putting
Speaker 1: a limit on how old a human can become and
Speaker 1: saying like, here's the aging process. Uh, these are the rules.
Speaker 1: Obviously doesn't apply to Highlanders, that's right. Well, you know,
Speaker 1: maybe they're they're part of the giants in the earth
Speaker 1: or something. I don't know, Oh that could be. Yeah,
Speaker 1: I guess they're not humans. So well, the spoiler for
Speaker 1: Highlander too certain cuts they are not from Earth in
Speaker 1: the good cuts. They're not from Earth yet again, we're
Speaker 1: just trying to throw those seeds down. Highlander two episode
Speaker 1: it's coming now. Speaking of parts one and two, this
Speaker 1: episode is a part two. Yeah, so if you haven't
Speaker 1: listened to part one yet, you should go back check
Speaker 1: that out first. And that we explored the question of
Speaker 1: why we age. We look at some animals that don't
Speaker 1: really age in the same way that humans and other
Speaker 1: similar mammals do, and we look at historical explanations people
Speaker 1: have tried to come up with for why we age,
Speaker 1: and we also explored some reasons to think that those
Speaker 1: historical explanations were not correct. Today, we're going to try
Speaker 1: to get into the modern evolutionary synthesis take on why
Speaker 1: we age. What's happening and how do you solve this
Speaker 1: paradox of the fact that aging is a decline over
Speaker 1: time in our survival and reproduction fitness, and yet evolution
Speaker 1: should be constantly optimizing our survival and reproduction fitness. Why
Speaker 1: would it allow us to go into this period where
Speaker 1: we tend to die and tend to get worse at
Speaker 1: surviving and tend to not be able to reproduce anymore. Indeed,
Speaker 1: because I certainly don't want to deify natural selection and
Speaker 1: say that like natural selection produces perfect forms or ideal forms.
Speaker 1: But look at the forms that natural selection has produced,
Speaker 1: look at all the various engineering problems that that that
Speaker 1: evolution has managed to solve. Why would there be this
Speaker 1: be this huge, at least from our perspective, flaw in
Speaker 1: the design. Yeah. Now, of course, today, as we often
Speaker 1: do with evolution, just for the ease of communication, we're
Speaker 1: going to be using a lot of metaphors that offer
Speaker 1: a kind of like embodied view of evolution, as if
Speaker 1: like it's making choices. What we, of course know is
Speaker 1: that evolution is a is an optimization algorithm. It's not
Speaker 1: a person, it's not a thing. It doesn't really have
Speaker 1: desires of it of its own. It has a way
Speaker 1: that it works, and the way that it works is
Speaker 1: to optimize the success of genes that survived natural selection
Speaker 1: and reproduce. Now, one of the answers we explored in
Speaker 1: the last episode is one of the most common things
Speaker 1: people are going to turn to when they're trying to
Speaker 1: explain why we age. It's the thing that my brain
Speaker 1: and immediately went to before I read anything on this subject,
Speaker 1: I started to think, well, let's see, if everybody just
Speaker 1: lived forever and nobody naturally aged out and died, then
Speaker 1: you'd have way too much competition for resources, right, You'd
Speaker 1: have way too many people trying to live on the
Speaker 1: same landscape. You'd have too many people trying to eat
Speaker 1: from the same food sources. You'd have overpopulation, and and
Speaker 1: everybody would suffer for it. Overpopulation ties and to a
Speaker 1: number of our different dystopian views of the future, as
Speaker 1: does the possibility of immortality becoming an option at least
Speaker 1: a certain privileged people in society. You know, you get
Speaker 1: this sort of trope of the awful uh Methuselah of
Speaker 1: the future, Right, some just dreary, old, greedy individual who
Speaker 1: will not die and let go the reigns of life
Speaker 1: so that others may grasp it. Right, Well, as much
Speaker 1: as we don't personally want to grow old and die,
Speaker 1: you can sort of recognize from an impartial standpoint, if
Speaker 1: you just consider it in other people, that it seems
Speaker 1: kind of unfair that people should live forever, right, Yeah, yeah,
Speaker 1: unless it's me or someone that I'm investing, and there
Speaker 1: they should put a limit on that stuff. Yeah, So
Speaker 1: but these types of answers, while true, it is true
Speaker 1: that it's good for the species that we should age
Speaker 1: and die, and that it's good for future generations. Uh,
Speaker 1: good of the species and good of the group based
Speaker 1: explanations come under a lot of fire from evolutionary biologists.
Speaker 1: There's some biologists to endorse kind of qualified versions of
Speaker 1: of good of the group and good of the species
Speaker 1: type explanations, but there I think many more who don't.
Speaker 1: And here's an example to illustrate one of the big
Speaker 1: problems in why these good of the group explanations failed
Speaker 1: to hold up. Alright, hit me with it. Okay. Let's
Speaker 1: imagine a pack of alien space wolves. Okay, and for
Speaker 1: our Warhammer for fans out there, he's not talking about
Speaker 1: space marines here. Wait, I don't know what space will
Speaker 1: Is that a thing? Yeah, it's a faction of the
Speaker 1: space marines in the Warhammer forty K universe that are wolves.
Speaker 1: Well no, they well they wear wolf skins and they're
Speaker 1: you know, genetically enhanced super soldiers. Okay, So it would
Speaker 1: really complicate them the analogy you're making here, if if
Speaker 1: we were to draw them into the discussion. Well, I
Speaker 1: was just trying to make clear that this is a hypothetical,
Speaker 1: not like real wolves on Earth. Okay, so alien space
Speaker 1: wolves living on an asteroid somewhere in hunting space here. Now,
Speaker 1: let's imagine this pack of alien space wolves has evolved
Speaker 1: genes that cause them to grow old and become infertile
Speaker 1: after about ten years of age, after which you know
Speaker 1: they usually die within a couple of years. And let's
Speaker 1: say that each female space wolf has an average of
Speaker 1: one space wolf pup every year that she remains fertile.
Speaker 1: So unless the space wolf is killed by injury or
Speaker 1: disease or a marauding space explorer, um, the average space
Speaker 1: wolf female has tin offspring in her life lifespan. Everybody's happy, right,
Speaker 1: because they don't eat too many of the space dear,
Speaker 1: they don't become overpopulated. It just works out pretty well.
Speaker 1: But then suddenly one of these space wolves acquires a
Speaker 1: mutation that allows her to stay fertile and survive for
Speaker 1: twelve years instead of ten, So she has twelve of
Speaker 1: space wolf pups, whereas all the other females in the
Speaker 1: pack are still having ten, and half of her pups
Speaker 1: carried this extended fertility and longevity gene, So those x
Speaker 1: pups each have twelve pups, while non carriers of the
Speaker 1: gene only have ten, and so on and so on
Speaker 1: down the generations, and eventually this cheater gene for extended
Speaker 1: life and extended fertility is going to proliferate, even if
Speaker 1: it might be worse off for everybody in the long run.
Speaker 1: Even if the long living, long reproducing animals have too
Speaker 1: many offspring and consume too many resources and suffer die outs,
Speaker 1: this won't really cause a reselection towards shorter lifespans, because
Speaker 1: how would it. Instead, what it would do is optimize
Speaker 1: for whatever genes are possessed by the survivors of those
Speaker 1: die outs, and that would probably be like those that
Speaker 1: store fat better, or hunt better, or can extract nutrition
Speaker 1: from space moss in addition to meat. And this is
Speaker 1: a really common type of argument against good of the
Speaker 1: group and good of the species explanations and evolution, because
Speaker 1: any mutation that cheats on the stasis you've created for
Speaker 1: the good of the group will tend to start to
Speaker 1: at an edge and then have more offspring than those
Speaker 1: who don't cheat, and eventually that new gene will become
Speaker 1: the norm. Right, Yeah, It's kind of like if you
Speaker 1: have a you know, an academic environment where everybody's cheating
Speaker 1: on the exam. Need the grading becomes that much harder
Speaker 1: each and every time. It's true. Yeah, it's great. So
Speaker 1: it's like you got a grade on a curve because
Speaker 1: everybody's cheating, so everybody's grade goes down. Um. Yeah, And
Speaker 1: so I just want to remind you, though, this doesn't
Speaker 1: mean that there is not such a thing as the
Speaker 1: good of the group and the good of the species.
Speaker 1: Those things clearly are true. And it clearly is true
Speaker 1: that it's good for the next generation that older generations
Speaker 1: age out and die. I care about the survival of
Speaker 1: the rest of my group. I care about members of
Speaker 1: my species and about future generations. But I care because
Speaker 1: I have a brain and I can recognize what's going on.
Speaker 1: Magines don't care, and your genes don't care. They just
Speaker 1: chemically proliferate themselves. They don't have a sentimental attachment or
Speaker 1: or an idea that the next generation should get resources
Speaker 1: to all right, So this just brings us back to
Speaker 1: the question, though, why have we evolved to grow old? Right?
Speaker 1: It's still unsolved. Why not live and reproduce forever, maintaining
Speaker 1: perfect youth and vigor until something extrinsic happens, until we
Speaker 1: get killed by a hemorrhagic fever or tractor accident. Alright,
Speaker 1: we're gonna take a quick break and we come back.
Speaker 1: We will answer that very question. Thank alright, we're back.
Speaker 1: Al right. So, there are a number of modern, well
Speaker 1: accepted scientific theories trying to answer the question of why
Speaker 1: we evolved to age. And here's a starting point for
Speaker 1: several of those theories. Let's go back to the wolves
Speaker 1: for a second. Imagine the space wolves. Maybe a hypothetical
Speaker 1: wolf species could breed and stay healthy until about the
Speaker 1: age of ten. Like we said, why not twenty, Why
Speaker 1: not thirty? Why not five hundred? Well, here are a
Speaker 1: few things to consider. Wolves did not evolve in zoo
Speaker 1: 's or as domestic pets, where they're guaranteed meals and
Speaker 1: protection from violence and guaranteed access to veterinary care. The
Speaker 1: landscape that created the wolf as it exists is one
Speaker 1: in which there is a constant struggle to get enough
Speaker 1: meat to survive and to not get sick and die,
Speaker 1: and to not get injured and become unable to hunt,
Speaker 1: so you starve. If you are a wolf living in
Speaker 1: the wild, and you survive the first year of your life,
Speaker 1: one of these things like injury or disease or starvation
Speaker 1: very likely will kill you before you get a chance
Speaker 1: to reach old age. These causes of death like disease
Speaker 1: and injury, or what's known as quote extrinsic causes of death,
Speaker 1: death caused by outside pressures and not by stuff that's
Speaker 1: in your genes or by old age. And so we
Speaker 1: can look at the real life example to see how
Speaker 1: common this is. The actual gray wolf Canis lupus lives
Speaker 1: somewhere around an average of six years or so in
Speaker 1: the wild, but in captivity it can live for more
Speaker 1: than fifteen years. So here's the first crucial bit to
Speaker 1: use some more metaphorical language. If there are physical processes
Speaker 1: that tend to render a wolf progressively less fit every
Speaker 1: month after it's more than ten years old, evolution almost
Speaker 1: never sees that. To put it in another metaphor, asking
Speaker 1: why evolution allows the wolf to grow old to deteriorate
Speaker 1: with old age is kind of like asking why we
Speaker 1: don't have laws against time travel. The reason isn't that
Speaker 1: our legislative bodies have considered and debated the issue of
Speaker 1: time travel and in the end they concluded that time
Speaker 1: travel is good, we better, we better allow it. That's
Speaker 1: not what happens. What happens is the issue doesn't come up. Yeah,
Speaker 1: it reminds me of some of these various programs that
Speaker 1: informs you have to do to figure out how you're
Speaker 1: saving your for your retirement, and they tend not to
Speaker 1: cover the second century of your life because it's not
Speaker 1: going to happen. That's perfect metaphor. Yeah, how come you're
Speaker 1: not saving enough money for when you're two hundred years old.
Speaker 1: It's not that you've decided it's better to be broke
Speaker 1: when you're two hundred. It's just that the the situation
Speaker 1: of being two hundred does not tend to come up
Speaker 1: very often. Now, obviously it's not nearly that extreme because sometimes,
Speaker 1: in some cases animals do live to old age and
Speaker 1: they face biological sinescence under natural conditions. But for many
Speaker 1: species it's pretty rare. For species of animals that tend
Speaker 1: to die from one cause or another before they get
Speaker 1: the chance to grow old evolution doesn't have many opportunities
Speaker 1: to test what happens in old age, so it can't
Speaker 1: optimize the animal for old age very efficiently, and compare
Speaker 1: this to how strongly evolution tests and optimizes for the
Speaker 1: effects of genes that manifest in early life. If something
Speaker 1: affects how likely you are to survive at age twenty
Speaker 1: or at age ten, evolution is going to be very strong,
Speaker 1: only selecting four or against that gene. Okay, So this
Speaker 1: is one part of the landscape of explanations today. Most
Speaker 1: species that show significant aging evolved to their anatomically modern
Speaker 1: condition in a situation where mortality was high and evolution
Speaker 1: didn't get a lot of opportunities to see what happens
Speaker 1: in old age, much less optimize it. Uh, let's introduce
Speaker 1: another wrinkle into the explanation. Yeah, this one has a
Speaker 1: wonderful title. This is mutation accumulation. Right, So we go
Speaker 1: to the British biologist Peter B. Meadair. He was one
Speaker 1: of the primary evolutionary thinkers credited with working out the
Speaker 1: implications of this model of aging, where the force of
Speaker 1: selection just declines with old age. So in several works
Speaker 1: in the middle of the nineteen forties and the nineteen fifties,
Speaker 1: UH he argued, based on similar logic, that natural selection
Speaker 1: would often be blind to the effects of mutations that
Speaker 1: cause negative effects laid in life after reproduction is mostly stopped.
Speaker 1: So let's use another analogy. Imagine a mutation called the
Speaker 1: twenty birthday surprise gene, which means that on the day
Speaker 1: you turn twenty, carriers of this gene suddenly transform into
Speaker 1: a bucket of fish heads and thus lose all ability
Speaker 1: to reproduce. Now, this would mean that in order to
Speaker 1: pass on this gene, a carrier would have to reproduce
Speaker 1: before their twentieth birthday, So kids they have before they're
Speaker 1: twenty years old could still carry this gene, but they
Speaker 1: don't get the chance to have any kids after their
Speaker 1: twenty years old, when plenty of other members of the
Speaker 1: species would continue having children, All potential reproduction after twenty
Speaker 1: is canceled, thus giving people with this gene significantly fewer
Speaker 1: children on average than people without it, and so the
Speaker 1: gene is unlikely to spread in the population. Now imagine
Speaker 1: a similar gene. This is the hundredth birthday surprise gene.
Speaker 1: Carriers of this gene, upon the day of their hundredth
Speaker 1: birthday suddenly transform into a VHS copy of Highlander to
Speaker 1: the quickening okay, and and and therefore becoming more No,
Speaker 1: not quite No. The problem is, well, I guess you
Speaker 1: you might get to live somewhat forever on a shelf,
Speaker 1: but you don't. You definitely don't get to reproduce after that. Right,
Speaker 1: there's very little sexual reproduction between copies of Highlander to
Speaker 1: the quickening. But also it doesn't really matter, right because
Speaker 1: do carriers of this gene have any fewer children the
Speaker 1: non carriers of this gene? The answer is no, right,
Speaker 1: because who's still having children at age one hundred? Almost nobody.
Speaker 1: So even if you have this very unhelpful gene, you
Speaker 1: don't like it that you transform into a VHS tape
Speaker 1: on your hundredth birthday, that's not good for you. But
Speaker 1: it doesn't matter to how many children you have. It
Speaker 1: has no effect on that. So if you have this gene,
Speaker 1: you can spread it to all your children, and they
Speaker 1: can spread it to all of their children and so,
Speaker 1: and they'll all have just as many kids and grandkids
Speaker 1: as the neighbors who don't have it. You've already passed
Speaker 1: it on by the time it matters, So this would
Speaker 1: be the case. Though we we've we've used the Highlander
Speaker 1: to transformation as as an example here, but even if
Speaker 1: it were something seemingly beneficial, like say a gene made
Speaker 1: you suddenly really excellent and talking to members of the
Speaker 1: opposite sex at age one hundred, you know, like or
Speaker 1: the opposite it made you terrible at a speaking to
Speaker 1: the opposite sex at age one hundred, it would still
Speaker 1: be the same case, right, yeah, unless the basically the
Speaker 1: only thing that would matter would be if it's a
Speaker 1: gene that suddenly makes you able to reproduce again. I mean,
Speaker 1: if it did that, then that would probably matter. But
Speaker 1: as long as you're past the age of reproduction and
Speaker 1: you're not having any more children, mutations good or bad
Speaker 1: are just going to sort of accumulate randomly without having
Speaker 1: any effect Onesoever, natural selection just doesn't pay attention to
Speaker 1: them because it never gets to notice them. Well. But
Speaker 1: but then the other thing too, is that if you're
Speaker 1: talking about something that would kick in so late in
Speaker 1: life that even people with that gene might never experience it. Right.
Speaker 1: It's like if you're playing a role playing game, video
Speaker 1: game or what have you, and there's some sort of
Speaker 1: like high level ability and you look at it. It It
Speaker 1: looks great, but you know you're never going to play
Speaker 1: the game long enough to get it. Yeah, so what's
Speaker 1: the point. Yeah, the game might as well for you
Speaker 1: not even have that thing in it. And apparently there
Speaker 1: are going to be genetic mutations like that. And this
Speaker 1: was Meta Wars insight. It came to be known, as
Speaker 1: you said, as the mutation accumulation hypothesis. Whether reproduction stops
Speaker 1: because you die of extrinsic causes. This was a big
Speaker 1: thing Meta where had in mind. It's like we talked about,
Speaker 1: you know, the wolf gets injured and can't hunt, the
Speaker 1: wolf gets sick and dies, the wolf gets killed by something,
Speaker 1: whether that happens or because you age out of your
Speaker 1: reproductive stage of life for some other biological reasons. Genes
Speaker 1: that have negative effects that show up mostly after reproduction
Speaker 1: has stopped are not subject to the full force of
Speaker 1: natural selection. So there's not much preventing the proliferation of
Speaker 1: gene that harm you in old age because there's nothing
Speaker 1: to weed them out, and they accumulate in the genome
Speaker 1: over generations by what's known as genetic drift. And the
Speaker 1: genetic drift is just the random dispersing of genes that
Speaker 1: don't appear to have a very strong positive or negative effect.
Speaker 1: So if you've got a mutation that you acquire for
Speaker 1: a nasty surprise in old age, something bad that happens
Speaker 1: to your body. And you could look at the process
Speaker 1: of aging like this. It's just a large plethora of
Speaker 1: genetic mutations that cause bad things to happen to your body.
Speaker 1: Later on, you can still pass it on to your kids,
Speaker 1: because you're you've had all your kids by the time
Speaker 1: it starts affecting you. And so these genes can become
Speaker 1: common in the gene pool of your species simply because
Speaker 1: there's nothing stopping them. So simply put it in. The
Speaker 1: force of selection declines with age. Mutations that are neutral
Speaker 1: early in life when selection is strong, but negative later on,
Speaker 1: they could accumulate in the population. I like to think
Speaker 1: of this as the sack of kitty litter school things
Speaker 1: in the closet scenario. What, okay, explain, but a friend
Speaker 1: of mine, when I first met her, she had a
Speaker 1: cat box, and then she would scoop the cat box
Speaker 1: and it would accumulate in a garbage bag in the closet.
Speaker 1: Accumulate me, you mean accumulate as and she would dump
Speaker 1: it in a garbage bag in the close and it
Speaker 1: was it was a lot cleaner than this makes it sound,
Speaker 1: but it was. It was very much a sort of
Speaker 1: kicking the can down a road scenario, like eventually you're
Speaker 1: gonna have to take that bag of of of of
Speaker 1: litter scoopings out, but you're not. The whole situation is
Speaker 1: not built on what you're going to have to do tomorrow.
Speaker 1: It's about what's happening to today. But what if you're
Speaker 1: looking at that closet and you're saying, Oh, there's enough
Speaker 1: space in here that I could keep scooping it into
Speaker 1: the closet until I die of some of their cause,
Speaker 1: and then I would never have to take it out.
Speaker 1: It would be completely irrelevant. So it can accumulate forever,
Speaker 1: just like these deleterious Janes can. Okay, So that's clearly
Speaker 1: one part of the answer. One part is that stuff
Speaker 1: that affects you late in life is just less likely
Speaker 1: to get weeded out by natural selection. But what if
Speaker 1: there's something more than that. What if maladaptive genes that
Speaker 1: manifest in old age aren't just allowed to roam wild
Speaker 1: by sort of the careless shepherd of natural selection. What
Speaker 1: if they're positively selected for in some way, and that's
Speaker 1: what we'll explore when we come back from this break.
Speaker 1: Thank thank all right, we're back. So now it's time
Speaker 1: to talk about antagonistic pleotropy. In a paper in N
Speaker 1: seven and the journal Evolution, the American evolutionary biologist George C.
Speaker 1: Williams had a breakthrough that made metoirs original hypothesis even
Speaker 1: stronger and sort of complimented it. And so this was
Speaker 1: a paper that I mentioned in part one. Actually it's
Speaker 1: the paper called pleotropy, Natural Selection and the Evolution of sinescence.
Speaker 1: Williams hypothesis for the evolution of aging came to be known,
Speaker 1: as I said, as antagonistic pleotropy. And what this means
Speaker 1: is that, well, pleotropy, the word comes from the Greek
Speaker 1: roots meaning multiple turns or many effects. Pleotropy happens when
Speaker 1: a single gene codes for multiple different phenotypic effects, meaning
Speaker 1: effects on the body or effects on the behavior. So
Speaker 1: if you had one gene that both gave you black
Speaker 1: hair and gave you an extremely long, pinky fingernail, that
Speaker 1: would be pleotropy. Or if you had a gene that
Speaker 1: made you really tall and also made you better at
Speaker 1: learning multiple languages, that would be pleotropy. And there are
Speaker 1: lots of examples of this in animals in the real world.
Speaker 1: Here's one in chickens. Robert, have you ever seen the
Speaker 1: frizzle chickens? Who? I don't know. I've seen some pretty
Speaker 1: funny looking chickens before chicken. I mean the ones that
Speaker 1: have like the curly vegas outfits. Uh yeah, well yeah,
Speaker 1: I have seen some of these. These these chickens that
Speaker 1: have like a lot of extra feathers around their their
Speaker 1: talents and all. The frizzle gene is is a gene
Speaker 1: in chicken that causes the feathers to curl up instead
Speaker 1: of lying flat. So you get these crazy looking, like awesome, beautiful, regal,
Speaker 1: puffy chickens and they look really cool. But it turns
Speaker 1: out this gene also controls several other phenotypic effects. So
Speaker 1: if you are a chicken with the frizzle gene, you'll
Speaker 1: also have a different metabolic rate and different body temperature
Speaker 1: and lay a different number of eggs than the chickens
Speaker 1: who don't have this gene. So if you want the
Speaker 1: gene for the magnificent curl, you're going to be laying
Speaker 1: fewer eggs, among other things. And these are examples where
Speaker 1: the situation. It feels more like a trade off and
Speaker 1: probably has more in common with some of our our myths, right,
Speaker 1: because the gift of the god often comes with some
Speaker 1: sort of consequence. Yeah exactly. So another one, just real
Speaker 1: quick in cats, did you know about cats with white
Speaker 1: fur and blue eyes are also deaf? I have heard
Speaker 1: this one, yes, yeah, odd. So pleotropy can be like that.
Speaker 1: It can come and it kind of mixed blessing form,
Speaker 1: though I guess I don't actually know if blue eyes
Speaker 1: are good for the cat. Maybe that's double bad. But
Speaker 1: uh well you I mean, certainly, when you get into
Speaker 1: the selective breeding of of a species, you get into
Speaker 1: a situation where appearance has has has a survival advantage.
Speaker 1: Yeah exactly. So pleotropy can go both ways. One effect
Speaker 1: of a gene could be good while the other effect
Speaker 1: could be bad. And here's where we get the idea
Speaker 1: of quote antagonistic pleotropy, a pleotropy that's pulling in both directions,
Speaker 1: but usually it'll pull a bit stronger in one direction
Speaker 1: than another. So if the good effect outweighs the bad effect,
Speaker 1: the gene will spread through the gene pool. But if
Speaker 1: the bad effect outweighs the good effect, the gene will
Speaker 1: tend to go extinct. That we should be clear again
Speaker 1: what's meant by good and bad genes here, Because, for example,
Speaker 1: a gene that caused the carrier to experience intense pain
Speaker 1: and misery throughout life, but somehow also caused the carrier
Speaker 1: to have more healthy children than the average member of
Speaker 1: their species would also spread. So it's not optimizing for
Speaker 1: like you to have a long life, for you to
Speaker 1: have a fun life. It's optimizing for a number of
Speaker 1: offspring and the success of those offspring. Now, William's theory
Speaker 1: of antagonistic pleotropy picks up from this fact. He hypothesizes
Speaker 1: that some of the genes that cause aging are selected
Speaker 1: for because they have other separate effects that maximize fitness
Speaker 1: and reproduction earlier in life, which, like metair showed, is
Speaker 1: more strongly selected for in nature. The same genes that
Speaker 1: make your skin sag and give you heart disease in
Speaker 1: old age might also make you extremely reproductively competitive when
Speaker 1: you're young. So here's a really broad example. How about
Speaker 1: genes that control the rate of cell division. Yeah, so
Speaker 1: a hypothetical gene might be selected for because it makes
Speaker 1: cells divide more efficiently. And if cells divide more efficiently,
Speaker 1: it means you can rejuvenate tissues and he wounds and
Speaker 1: grow faster when you're young. But the same gene that
Speaker 1: causes prolific cell division could potentially be a problem later
Speaker 1: in life because what happens when cells are prone to
Speaker 1: divide a whole lot you could be prone to cancer
Speaker 1: cancer is runaway cell division. Cells that are not useful
Speaker 1: for the body are suddenly being created in great abundance,
Speaker 1: which brings us back to the Hadross or example that
Speaker 1: we touched on earlier. Yeah, back in the first episode,
Speaker 1: or you can think about something going exactly the reverse.
Speaker 1: You could have a gene that could increase apoptosis signaling,
Speaker 1: and apoptosis is programmed cell death, so a gene that
Speaker 1: that causes cell lines to die off more frequently, and
Speaker 1: this would help prevent runaway cell lines from turning into
Speaker 1: cancer while you're young. Natural selection obviously would love this
Speaker 1: because it would select against organisms that get cancer when
Speaker 1: they're young and can't reproduce much. But the exact same
Speaker 1: gene would cause tissues to deteriorate more with age because
Speaker 1: they undergo more and earlier cell death, and in fact,
Speaker 1: something like what I just described has actually been studied.
Speaker 1: The example would be the gene at P fifty three.
Speaker 1: The P fifty three gene has been implicated in antagonistic pleotropy,
Speaker 1: and it's thought that P fifty three protects young animals,
Speaker 1: including humans, but I think it's mostly been researched in mice.
Speaker 1: It protects these young animals against cancer by interrupting cell proliferation.
Speaker 1: It says, now, don't cells, don't divide too much now,
Speaker 1: But in doing this it can also have the effect
Speaker 1: of interrupting the proliferation of normal, non cancerous cells, like
Speaker 1: stem cells, which are the cells the body uses to
Speaker 1: rejuvenate tissues over time. So the same gene that plays
Speaker 1: some role in helping protect against cancer when you're young
Speaker 1: also helps play some role in the physical deterioration of
Speaker 1: the body with age by preventing it from making new
Speaker 1: cells and rejuvenating your tissues and detaining eternal youth. So
Speaker 1: the takeaway from this obviously that anytime you see a
Speaker 1: story about eternal youth in fiction or in a movie
Speaker 1: or something like that, imagine these these characters who are
Speaker 1: eternally youthful, riddled with cancer. It's not really not that
Speaker 1: hard to imagine when you think about all the various
Speaker 1: uh uh side effects and caveats that come with eternal
Speaker 1: youth in most of our myths and legends. Right well,
Speaker 1: I mean, yeah, you've got uh. I guess it's not
Speaker 1: applicable in the Tiffannas story because he doesn't get eternal youth.
Speaker 1: He wants to live forever. But you imagine the equivalent
Speaker 1: of the Tiffanas story where you ask for eternal youth.
Speaker 1: So Tiffanus asked for eternal life, or he doesn't ask
Speaker 1: Aos asked for eternal life. For Tithness. He gets eternal life,
Speaker 1: but not eternal youth. So it's the monkeys Paul coming
Speaker 1: back to bite him. In this story. You would ask
Speaker 1: for eternal youth and they say, okay, here's your eternal youth,
Speaker 1: but you get lots of cancer with it. And I
Speaker 1: think actually have read in the past that some of
Speaker 1: these experimental youth extension techniques that people do research on
Speaker 1: initially look promising but sometimes turn out to appear to
Speaker 1: increase answer risk. Now here's another example of a potential
Speaker 1: antagonistic pleotropy inflammation. So I want to cite one paper
Speaker 1: from two thousand eight in Bioscience Trends by Makoto Godo,
Speaker 1: and in this paper, the author explores the idea that
Speaker 1: a lot of the signs of physical deterioration associated with
Speaker 1: aging are driven by inflammation. But inflammation is a defense
Speaker 1: mechanism for the body. It helps you survive the redness,
Speaker 1: the swelling. It's not pleasant, but all that's part of
Speaker 1: a primitive immune system response that protects you against antigens
Speaker 1: and parasites. So inflammation responses can help you survive when
Speaker 1: you're young, but later in life, inflammation related aging effects
Speaker 1: cause widespread damage to the body, including all kinds of diseases,
Speaker 1: from type two diabetes to rheumatoid arthritis. As the kind
Speaker 1: of military reaction to invasion that is helpful for the
Speaker 1: young organism can be a detriment to the older or
Speaker 1: organism correct exactly right, And so it's believed now by
Speaker 1: scientists that there are tons of things like this in
Speaker 1: the body. There are genes that have these antagonistic pleotropy effects.
Speaker 1: They're good for you when you're young. They help you
Speaker 1: survive young adulthood and childhood, and help you have more
Speaker 1: children early on. But the same very same genes having
Speaker 1: the very same effects also cause you to age and
Speaker 1: become sick and reduce your fitness later on in life, when,
Speaker 1: as we established earlier, the force of selection is diminished.
Speaker 1: So one more theory that is pretty similar to these
Speaker 1: ones we've just discussed. We've got metairs mutation accumulation hypothesis,
Speaker 1: which says, you know, uh, natural selection doesn't pay much
Speaker 1: attention to what happens later in life, so negative mutations
Speaker 1: can kind of just hang out there without really being
Speaker 1: weeded out. Then you've got antagonistic pleotropy, which says that
Speaker 1: some of the things that cause negative effects later in
Speaker 1: life are positively selected for because those negative effects later
Speaker 1: are much outweighed by positive of effects early in life
Speaker 1: and uh, enhancing reproductive fitness early on. So there's a
Speaker 1: very similar theory along the same lines called the disposable
Speaker 1: soma theory, And this is a theory on the evolution
Speaker 1: of aging that was put forward in nineteen seventy seven
Speaker 1: by the English biologist Thomas Kirkwood. And this reframes it
Speaker 1: as a question of resource investment in the body. Here's
Speaker 1: the basic premise. The body has a finite amount of
Speaker 1: resources that it can spend on various projects. And these
Speaker 1: projects would include things like speeding up reproduction in the
Speaker 1: youth and maintaining body tissues. And so if you've got
Speaker 1: both of these things and you've got a limited budget
Speaker 1: to spend on them, you're gonna need to make choices, right,
Speaker 1: how much goes to each one, and indeed which one
Speaker 1: is the most important for the biological mission at hand, right,
Speaker 1: And so, drawing on the same logic we looked at earlier,
Speaker 1: if you live in a scenario where you don't tend
Speaker 1: to live to you know, your natural end of life age,
Speaker 1: you tend to get weeded out by things happening to
Speaker 1: you in the wild, you know, predation or starvation or
Speaker 1: or a disease or injury, anything like that, it will
Speaker 1: obviously look to your body like you need to invest
Speaker 1: way more in those earlier stages in maximizing reproduction early on.
Speaker 1: And so, drawing on metal war, evolution is going to
Speaker 1: tend to favor pouring finite resources into early reproduction optimization
Speaker 1: instead of maintaining tissues for an infinite natural lifespan. So
Speaker 1: I'm trying to think of a human equivalent. Uh, it
Speaker 1: sounds kind of silly, but basically like, should the body
Speaker 1: spend its precious limited energy resources keeping your artery walls
Speaker 1: from thickening over time or spending them on making you
Speaker 1: super sexy? Well, you know, I God knows. I am
Speaker 1: not an economist, but I find it when we discussed
Speaker 1: cycles of organisms, or or life cycles of of stars,
Speaker 1: even I think of companies and how they work. So
Speaker 1: it comes down to a question as as say that
Speaker 1: the CEO or even the founder of a company, are
Speaker 1: you running the company like you want to retire from
Speaker 1: it and watch it continue to prosper as you in
Speaker 1: your retirement or are you running the company like you
Speaker 1: intend to sell it? You know or we know what
Speaker 1: the answer is. In most cases, yeah, you're you. In
Speaker 1: many cases, you're running the company because in a in
Speaker 1: a way that benefits the short term sale of the company,
Speaker 1: or you're leaving this company for another company. Yeah. I
Speaker 1: mean people like to have, you know, sort of like
Speaker 1: long term investment type rhetoric. But a lot of people
Speaker 1: have realized that the smart strategy for themselves is grab
Speaker 1: and go, you know, optimize whatever you can get out
Speaker 1: of a system for yourself as soon as possible, and
Speaker 1: then be on your way, And that's the equivalent here
Speaker 1: that this is to say that you can't even be
Speaker 1: guaranteed that it will matter or whether you've got a
Speaker 1: gene that optimizes against atherosclerosis or not. But if you
Speaker 1: can optimize for being real sexy and having lots of
Speaker 1: successful reproductive strategies early on in life, you're pretty much
Speaker 1: guaranteed a better chance at having more children. And we
Speaker 1: have so many different adages that back up this kind
Speaker 1: of like personal philosophy and life. Right, you know, burn
Speaker 1: it like you've stole it, I believe, not burn it
Speaker 1: like you still drive it. Burn the candle at both ends.
Speaker 1: That was combining the two there, you know. Or burn
Speaker 1: it like you stole it, really like it's hot it
Speaker 1: It behooves you to go ahead and burn it so
Speaker 1: that they don't figure out you stole it. Yeah, sees
Speaker 1: the day spend like there's no tomorrow exactly because sometimes
Speaker 1: well sometimes there isn't, or there's there's a finite amount
Speaker 1: of tomorrow. Sometimes a leopard will bite your face off.
Speaker 1: You should just operate on the assumption that a leopard
Speaker 1: might bite your face off, So spend what you've got today. Well,
Speaker 1: that's good. I don't know if we'll fit that on
Speaker 1: a bumper sticker, though. You now, what we've described so
Speaker 1: far are I think, what's known as the classical theories
Speaker 1: of aging. And in recent years we should point out
Speaker 1: some scientists have proposed various kinds of updates to accommodate
Speaker 1: new experimental findings. Maybe in the future we could come
Speaker 1: back to this topic again and and explore the most
Speaker 1: recent developments in in aging theory. But these are basically,
Speaker 1: I would say, these classical theories are still pretty much
Speaker 1: intact there. You know, you might need to modify them
Speaker 1: in some ways to to update them for newest experimental findings.
Speaker 1: But for example, an antagonistic pleotropy, people still basically think
Speaker 1: that this is a good explanation for why a lot
Speaker 1: of the aging effects we experience take place, and it
Speaker 1: gives us room on which to build uh further analysis, Yeah,
Speaker 1: of course, and it gives us room to say, if
Speaker 1: we understand how a process happens and why it happens,
Speaker 1: I wonder if it could be reversed or undone. And
Speaker 1: of course there's a lot of that. There's a lot
Speaker 1: of interest in this given that medical search is uniform
Speaker 1: universally funded by mortals, right who and many of them
Speaker 1: are are interested and possibly having more life to live
Speaker 1: or if possible, you know, an infinite amount, right. So,
Speaker 1: of course, because we don't want to age and grow
Speaker 1: old and sag and wrinkle and and eventually die, scientists
Speaker 1: are always working on ways to beat aging, and some
Speaker 1: broad evolutionary mechanisms based on things like fruit fly research
Speaker 1: are actually known. But unfortunately they're not the kind of
Speaker 1: simple medical fixes that could like be ethically applied to humans.
Speaker 1: They're they're evolutionary fixes that you couldn't really implement on purpose.
Speaker 1: I mean you could in fruit flies, and researchers have,
Speaker 1: so what are they Well, one would be low adult
Speaker 1: mortality and high juvenile mortality if you get a bunch
Speaker 1: of fruit flies and you create a scenario such that
Speaker 1: adults tend to survive longer than they would in the wild,
Speaker 1: while juveniles die very often. What actually happens is that
Speaker 1: the life span and the reproductive lifespan of the fruit
Speaker 1: flies increases over generations of evolution. And this kind of
Speaker 1: makes sense, right if the if the mating pool is
Speaker 1: limited to older individuals, genes that favor fitness in later
Speaker 1: life will be selected for, and thus these would be
Speaker 1: genes that prevent or delay aging, and they will become
Speaker 1: more successful. Normally, evolution wouldn't care about those types of
Speaker 1: genes very much. But of course we can't do this
Speaker 1: to stop human aging unless we're prepared to like implement
Speaker 1: a policy that only people over a certain age can
Speaker 1: have children and then keep pushing the minimum age upwards.
Speaker 1: Obviously we don't want to do that. Well, even in
Speaker 1: scenarios like you know, periods of history in which there
Speaker 1: is a high mortality rate for younger people, such as
Speaker 1: during wars. Uh, it's still I don't think there's any
Speaker 1: data to back of the idea that this would definitely
Speaker 1: interfere with reproduction, because obviously there there are children that
Speaker 1: grow up in the in the wake of war. Now
Speaker 1: perhaps the father is not there anymore, but reproduction has
Speaker 1: been initiated. But then that's a whole different area of study,
Speaker 1: like the effects of war on reproduction and the health
Speaker 1: of the resulting offspring. Um something we've touched on before
Speaker 1: on the show, and we could easily revisit. Oh yeah,
Speaker 1: that's all interesting stuff. Another thing to point out about
Speaker 1: what I just mentioned about low adult mortality and high
Speaker 1: juvenile mortality contributing to extended lifespans. We know this works
Speaker 1: in fruit flies, but we can't predict other complicating factors
Speaker 1: that might stop this from working another species. Though it
Speaker 1: does appear to be pretty general that species that have
Speaker 1: lower extrinsic mortality evolve longer lifespans. Like if you've got
Speaker 1: good defense mechanisms against predators and disease, or if you
Speaker 1: just happen to, say, end up on an island where
Speaker 1: you don't have many predators or diseases, you will probably
Speaker 1: evolve over a long period of time to breed longer
Speaker 1: and live longer. Think about the great Wizzen tortoises of
Speaker 1: the Galapagos. They've got a shell, they don't have really
Speaker 1: natural predators, and they've got these long, long lifespans because
Speaker 1: the adults and the old adults can just keep on breeding.
Speaker 1: And they probably have, you know, a fair amount of moisture.
Speaker 1: I think Aristotle was onto something. Yeah, no, they don't
Speaker 1: have moisture at all. They look so dry. Those tortoises
Speaker 1: are like the driest looking creatures I can think of,
Speaker 1: But they live in a moist environment. Maybe that's it,
Speaker 1: that is true, But okay, so looking at more like
Speaker 1: potentially ethical medical fixes, are there things researchers are working
Speaker 1: on in order to beat aging and humans? Well, the
Speaker 1: answer is obviously yes. There are plenty of questions about
Speaker 1: whether these projects are actually a good idea, and even
Speaker 1: if they are a good idea, whether they could be
Speaker 1: successful in principle, But there are plenty of people working
Speaker 1: on it. One example, of course, is the gerontologist and
Speaker 1: author Aubrey de Gray. He's made a whole career out
Speaker 1: of the idea, going around promoting that we can and
Speaker 1: should be trying to completely defeat the process of aging,
Speaker 1: and that we can do it within the next few decades. Yeah,
Speaker 1: he's everyone's probably seen images of de Gray before. He
Speaker 1: has this big wizard's beard and he's resput and yeah,
Speaker 1: he shows up in all sorts of he doesn't hate respute.
Speaker 1: He shows up in various documentaries about this topic all
Speaker 1: the time. Uh. And his his basic argument is, I think,
Speaker 1: rather than genius, it's instead of viewing aging and death
Speaker 1: as this unbeatable war, you know, this this unbeatable um
Speaker 1: um problem, it's like, break it up into smaller battles,
Speaker 1: smaller problems that you can win. You can solve. Yeah,
Speaker 1: And I think this is the key appeal of his approach.
Speaker 1: He says, aging is not one thing, it's maybe seven things. Us.
Speaker 1: For instance, the problem might be cells die off and
Speaker 1: are naturally replaced in the heart or in the brain,
Speaker 1: and he says, well, use stem cell replacement for dying cells.
Speaker 1: Or another example would be the body undergoes a proliferation
Speaker 1: of unwanted cells, such as fat cells that replace muscle
Speaker 1: and lead to diabetes. He says, we'll trick the problem
Speaker 1: cells into self destruction through suicide, gene therapy, this sort
Speaker 1: of thing. So it's it's taking taking the overall problem,
Speaker 1: breaking it down into little individual problems that you could
Speaker 1: potentially solve through medical intervention, genetic engineering, etcetera. Now, for
Speaker 1: people who are interested in avoiding aging, obviously this message
Speaker 1: is very appealing, Yes, but there are also we should
Speaker 1: mention many researchers who find degrees program unrealistic, Like he
Speaker 1: has plenty of critics. Well, on one level, it's kind
Speaker 1: of the basic trans anti transhumanist argument, right like if okay,
Speaker 1: if you break down essentially immortality into a number of
Speaker 1: different treatment options that are available, then then who are
Speaker 1: they available to who has access to these treatments. And
Speaker 1: then it becomes this, uh, this this inequality situation where
Speaker 1: you have the very dystopian idea of the super rich
Speaker 1: individuals who can afford all of the various treatments that
Speaker 1: that keep their unnatural lives going while the rest of
Speaker 1: us simply live and die as always. I would say
Speaker 1: the answer to that critique is not that you shouldn't
Speaker 1: develop the medical technologies, but that you should find ways
Speaker 1: to make them available to everyone. Then again, you do
Speaker 1: have that intrinsic question of whether it's actually good to
Speaker 1: allow any member of a species to be biologically immortal, uh,
Speaker 1: to keep on living and consuming resources beyond what would
Speaker 1: what would normally be allotted to them in a normal lifespan, Because,
Speaker 1: as we talked about earlier on, there's this whole good
Speaker 1: of the species argument. Your genes might not care about
Speaker 1: the good of the species, but you should, right, we should. Well,
Speaker 1: it's an easy argument for for for us to make.
Speaker 1: But then again, we're not a hundred and fifty years
Speaker 1: old and hooked up to the immortality machine. Right. Well,
Speaker 1: once your time comes, you will probably change your tune. Right,
Speaker 1: It's like, no, give me a little more. I just
Speaker 1: need a little more one more yea um. But then again, yeah,
Speaker 1: so that's like the question of whether we should be
Speaker 1: trying to achieve biological immortality. There's also this question that
Speaker 1: many scientists have have brought up, which is that his
Speaker 1: program is unrealistic, not necessarily that it's a bad idea,
Speaker 1: but that you you can't extend aging or not extend.
Speaker 1: You can't extend youth forever. They're just gonna be hard
Speaker 1: physical limits that you're gonna hit within the human body.
Speaker 1: Just one example of that strain of thinking as a
Speaker 1: paper that came out earlier this year in published by
Speaker 1: the Proceedings of the National Academy of Science is called
Speaker 1: Intercellular Competition and the Inevitability of Multicellular Agent. So this
Speaker 1: study was conducted by UH scientists Joanna Massel and Paul Nelson,
Speaker 1: and Massel and Nelson use mathematical models to argue that essentially,
Speaker 1: no matter what you do, you will be faced with
Speaker 1: one facet of aging or another, and the main tension
Speaker 1: they highlight is tissue deterioration or cancer one or the other.
Speaker 1: It's a mathematical inevitability. They say, if you find a
Speaker 1: way to prevent cancer. Tissues deteriorate and cells become less efficient.
Speaker 1: You get the body breaking down. If you find a
Speaker 1: way to rejuvenate tissues, beef them up, make them youthful again,
Speaker 1: you get cancer. Age is gonna get you one way
Speaker 1: or another. It's like we're in that trolley car, right.
Speaker 1: We have the tracks diverging to two unwanted fates in
Speaker 1: a sense equally unwanted fates, and we have to try
Speaker 1: and figure out, well, which way we're gonna go? What
Speaker 1: are we going to plow into? I feel like this
Speaker 1: should be reimagined as a myth, like going back to Tiffanus,
Speaker 1: Like I want the gods gods that represent one represents
Speaker 1: cancer and one represents the deterioration of body tissues, and
Speaker 1: they're like at war and you have to choose between
Speaker 1: your fate with one or the other. Uh I like that? Yeah,
Speaker 1: this is this is where our modern day gods can
Speaker 1: jump in and and provide us the story to make
Speaker 1: sense of our our doom. Okay, well, I guess that
Speaker 1: wraps it up for for part two of this episode
Speaker 1: about why we age and why we can't have eternal youth. Yeah. Well,
Speaker 1: and I don't want to leave it on too dark
Speaker 1: of a note there with the whole doom talk, because
Speaker 1: I mean, ultimately, I guess here's the here's the silver lining. Uh, Aging,
Speaker 1: even dying, everybody does it. It couldn't be. It couldn't
Speaker 1: be that much to it, right, look at the people
Speaker 1: who do it. It It couldn't be. It couldn't be that difficult,
Speaker 1: couldn't be that hard to go through. Well, I mean
Speaker 1: it's easy to get down when you spend a lot
Speaker 1: of time thinking about the inevitability of aging and death.
Speaker 1: But um, I mean the thing to think about is, Yeah,
Speaker 1: it comes to everybody. It's a part of life, and
Speaker 1: there's a lot of life to love. Yeah, And it
Speaker 1: bears reminding that there is a lot of stuff you
Speaker 1: can do in the in the near future to make
Speaker 1: your your far future a little more easy going. You know,
Speaker 1: you can look after the body you have. You can uh,
Speaker 1: you know, exercise and try to eat right. I think
Speaker 1: I saw a study saying you need to eat a
Speaker 1: bunch of chocolate to make it, and I think that's
Speaker 1: what it was. Well, then that's the other side too,
Speaker 1: is like you're gonna grow ahold, You're going to die.
Speaker 1: You can't just spend your whole time worrying over that inevitability.
Speaker 1: So you might as well have some chocolate. You might
Speaker 1: as Oh no, I mean I was joking about those
Speaker 1: articles that actually say chocolate will make you live longer.
Speaker 1: Oh okay, not just the ones where there's like a
Speaker 1: new study out that points to uh some beneficial quality
Speaker 1: of like pure unsweetened chocolate. Uh yeah, I mean it's
Speaker 1: it's always couched and like eat chocolate to be healthier.
Speaker 1: Well if it's not couched in it. That's how I
Speaker 1: think sometimes we interpret it. We read the study and
Speaker 1: we're like, well, good, I like chocolate, or I like
Speaker 1: red wine, or I like coffee, And now I can
Speaker 1: just continue to enjoy the things that make my life
Speaker 1: more bearable and uh and not worry about what they
Speaker 1: might be doing too. Anytime you read an article about
Speaker 1: the one silver bullet thing to eat or to drink
Speaker 1: that will make you live forever, don't believe it. I agree,
Speaker 1: unless that one silver bullet thing is the quickening which
Speaker 1: will work. Can the quickening be transferred to another though
Speaker 1: I'm a little shaky on on my my quickening science.
Speaker 1: I don't know. We'll have to come back to that
Speaker 1: what's the quickening conversion rate? I don't know. I think
Speaker 1: you just have to be from the planet's ice, right remember?
Speaker 1: All right, well there you go. Uh again, this was
Speaker 1: a two parter. If somehow you made it through all
Speaker 1: of part two without listening to part one, go back
Speaker 1: and listen to part one. You will find it in
Speaker 1: all other episodes of Stuff to Blow Your Mind at
Speaker 1: Stuff to Blow your Mind dot Com, and you'll get
Speaker 1: our moisture jokes. That's right. And hey, while you're stuff
Speaker 1: to Blow your Mind dot Com, you will also find
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