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