March 30, 2019 • 48 mins
Throughout history, humans have faced the inexorable process of aging and death. We’ve dreamt up countless myths to explain why we age and what comes of seeking immortality, but what does science tell us about the process? Why do we age? What purpose does it serve in natural selection? Indeed, what can science offer us in the way of eternal youth? Robert Lamb and Joe McCormick seek to find out in this two-part Stuff to Blow Your Mind exploration. (Originally published Jan. 9, 2018)
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Episode Transcript
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Speaker 1 (00:05):
Hey, you welcome to Stuff to blow your mind. My
name is Robert Lamb and I'm Joe McCormick, and it's Saturday.
Time to go into the vault for Eternal Youth Part two.
If you checked us out last Saturday, it was Eternal
Youth Part one. This is going to be the second
part of that series. This originally published January. Should we
get right into it. Yeah, let's just belly right up
to the bar and have a drink from the Fountain
(00:27):
of Youth. Welcome to stuff to blow your mind from
how stuff weren't dot Com? Hey, you, welcome to stuff
to blow your mind. My name is Robert Lamb and
I'm Joe McCormick, and we're back for part two of
our discussion about where's my eternal youth? Why can't I
(00:50):
be young and beautiful forever? Why do we age? I
know that's the It's the question we've always wondered. It
shows up in our philosophical writings, it shows up in
our religion, our mythology. Uh. In researching this topic, I
kept thinking back to Genesis six three. This is the
King James version, and the Lord said, my spirit shall
(01:12):
not always strive with man for that he is also flesh,
yet his days shall be a hundred and twenty years.
So there's God putting a limit on how old a
human can become and saying like, here's the aging process. Uh,
these are the rules. Obviously doesn't apply to Highlanders. That's right. Well,
(01:33):
you know, maybe they're they're part of the giants in
the Earth or something. I don't know, Oh that could be. Yeah,
I guess they're not humans. So well, the spoiler for
Highlander to certain cuts, they are not from Earth right
in the good cuts from Earth. Yet again, we're just
trying to throw those seeds down. Highlander two episode it's
coming now. Speaking of parts one and two, this episode
(01:55):
is a part two. Yeah, so if you haven't listened
to part one yet, you should go back check that
out first. And that we explored the question of why
we age. We look at some animals that don't really
age in the same way that humans and other similar
mammals do, and we look at historical explanations people have
tried to come up with for why we age, and
(02:17):
we also explored some reasons to think that those historical
explanations were not correct. Today, we're going to try to
get into the modern evolutionary synthesis, take on why we age?
What's happening and how do you solve this paradox of
the fact that aging is a decline over time in
our survival and reproduction fitness, and yet evolution should be
(02:40):
constantly optimizing our survival and reproduction fitness. Why would it
allow us to go into this period where we tend
to die and tend to get worse at surviving and
tend to not be able to reproduce anymore. Indeed, because
I certainly don't want to deify natural selection and say
that like natural selection produces perfect forms or ideal forms,
(03:02):
But look at the forms the natural selection has produced,
Look at all the various engineering problems that that that
evolution has managed to solve. Why would there be this
be this huge, at least from our perspective, flaw in
the design. Yeah. Now, of course, today, as we often
do with evolution, just for the ease of communication, we're
going to be using a lot of metaphors that offer
(03:24):
a kind of like embodied view of evolution, as if
like it's making choices. What we, of course know is
that evolution is a is an optimization algorithm. It's not
a person. It's not a thing. It doesn't really have
desires of it of its own. It has a way
that it works, and the way that it works is
to optimize the success of genes that survived natural selection
(03:48):
and reproduce. Now, one of the answers we explored in
the last episode is one of the most common things
people are going to turn to when they're trying to
explain why we age. It's the thing that my brain
and immediately went to before I read anything on this subject.
I started to think, well, let's see, if everybody just
lived forever and nobody naturally aged out and died, then
(04:13):
you'd have way too much competition for resources, right, You'd
have way too many people trying to live on the
same landscape, you have too many people trying to eat
from the same food sources. You'd have overpopulation, and and
everybody would suffer for it. Overpopulation ties into a number
of our different dystopian views of the future, as does
the possibility of immortality becoming an option at least a
(04:35):
certain privileged people in society. You know, you get this
sort of trope of the awful uh Methuselah of the future. Right,
some just dreary, old, greedy individual who will not die
and let go the reins of life so that others
may grasp it. Right, Well, as much as we don't
personally want to grow old and die, you can sort
(04:57):
of recognize from an impartial standpoint, if you just consider
it in other people, that it seems kind of unfair
that people should live forever, right, Yeah, unless it's me
or someone that I'm invested, and there they should put
a limit on that stuff. Yeah. So, but these types
of answers, while true, it is true that it's good
for the species that we should age and die, and
(05:18):
that it's good for future generations. Uh, good of the
species and good of the group based explanations come under
a lot of fire from evolutionary biologists. There's some biologists
to endorse kind of qualified versions of of good of
the group and good of the species type explanations, but
there I think many more who don't. And here's an
(05:39):
example to illustrate one of the big problems in why
these good of the group explanations fail to hold up.
All right, hit me with it, Okay, Let's imagine a
pack of alien space wolves. Okay, and for our warhammer
for fans out there. He's not talking about space marines here. Wait,
I don't know what space will Is that a thing? Yeah,
it's a faction of the space Marines. In the Warhammer
(06:02):
Fort K universe, there are wolves. Well, no, they well
they wear wolf skins and they're you know, genetically enhanced
super soldiers. Okay, so it would really complicate them the
analogy you're making here, if if we were to draw
them into the discussion. Well, I was just trying to
make clear that this is a hypothetical, not like real
wolves on Earth. Okay, So alien space wolves living on
(06:23):
an asteroid somewhere in hunting space here. Now, let's imagine
this pack of alien space wolves has evolved genes that
cause them to grow old and become infertile after about
ten years of age, after which you know, they usually
die within a couple of years. And let's say that
each female space wolf has an average of one space
wolf pup every year that she remains fertile. So, unless
(06:46):
the space wolf is killed by injury or disease or
a marauding space explorer, um, the average space wolf female
has tin offspring in her life lifespan. Everybody's happy, right,
because they don't eat too many of the space dear,
they don't become overpopulated. It just works out pretty well.
But then suddenly one of these space wolves acquires a
(07:09):
mutation that allows her to stay fertile and survive for
twelve years instead of ten, so she has twelve space
wolf pups, whereas all the other females in the pack
are still having ten, and half of her pups carried
this extended fertility and longevity gene, so those six pups
each have twelve pups, while non carriers of the gene
(07:32):
only have ten, and so on and so on down
the generations, and eventually this cheater gene for extended life
and extended fertility is going to proliferate, even if it
might be worse off for everybody in the long run.
Even if the long living, long reproducing animals have too
many offspring and consume too many resources and suffer die outs,
(07:53):
this won't really cause a re selection towards shorter lifespans,
because how would it. Instead, what it would do is
optimized for whatever genes are possessed by the survivors of
those die outs, and that would probably be like those
that store fat better or hunt better, or can extract
nutrition from space moss in addition to meat. And this
(08:14):
is a really common type of argument against good of
the group and good to the species explanations and evolution,
because any mutation that cheats on the stasius you've created
for the good of the group will tend to start
to get an edge and then have more offspring than
those who don't cheat, and eventually that new gene will
become the norm. Right. Yeah, It's kind of like if
(08:36):
you have a you know, an academic environment where everybody's
cheating on the exam, the exam, the grading becomes that
much harder each and every time. It's true. Yeah, it's great.
So it's like you've got to grade on a curve
because everybody's cheating, so everybody's grade goes down. Um. Yeah.
And so I just want to remind you though, this
doesn't mean that there is not such a thing as
(08:59):
the good of the group the good of the species.
Those things clearly are true. And it clearly is true
that it's good for the next generation that older generations
age out and die. I care about the survival of
the rest of my group. I care about members of
my species and about future generations. But I care because
I have a brain and I can recognize what's going on.
(09:19):
Ma genes don't care, and your genes don't care. They
just chemically proliferate themselves. They don't have a sentimental attachment
or or an idea that the next generation should get
resources to. All right, So this just brings us back
to the question, though, why have we evolved to grow old? Right,
it's still unsolved. Why not live and reproduce forever, maintaining
(09:41):
perfect youth and vigor until something extrinsic happens, until we
get killed by a hemorrhagic fever or tractor accident. All right,
We're gonna take a quick break and we come back.
We will answer that very question. Thank alright, we're back,
all right. So there are a number of modern, well
accepted scientific theories trying to answer the question of why
(10:04):
we evolved to age. And here's a starting point for
several of those theories. Let's go back to the wolves
for a second. Imagine the space wolves. Maybe a hypothetical
wolf species could breed and stay healthy until about the
age of ten, Like we said, why not twenty, Why
not thirty? Why not five hundred? Well, here are a
few things to consider. Wolves did not evolve in zoos
(10:28):
or as domestic pets, where they're guaranteed meals and protection
from violence and guaranteed access to veterinary care. The landscape
that created the wolf as it exists is one in
which there is a constant struggle to get enough meat
to survive and to not get sick and die, and
to not get injured and become unable to hunt, so
(10:50):
you starve. If you are a wolf living in the
wild and you survived the first year of your life,
one of these things like injury or disease or star ovation,
very likely will kill you before you get a chance
to reach old age. These causes of death like disease
and injury, or what's known as quote extrinsic causes of death,
(11:12):
death caused by outside pressures and not by stuff that's
in your genes or by old age. And so we
can look at the real life example to see how
common this is. The actual gray wolf canis lupus lives
somewhere around an average of six years or so in
the wild, but in captivity it can live for more
than fifteen years. So here's the first crucial bit to use.
(11:34):
Some more metaphorical language. If there are physical processes that
tend to render a wolf progressively less fit every month
after it's more than ten years old, evolution almost never
sees that. To put it in another metaphor, asking why
evolution allows the wolf to grow old to deteriorate with
old age is kind of like asking why we don't
(11:57):
have laws against time travel. The reason isn't that our
legislative bodies have considered and debated the issue of time travel,
and in the end they concluded that time travel is good,
we better, we better allow it. That's not what happens.
What happens is the issue doesn't come up. Yeah. It.
It reminds me of some of these various programs that
(12:18):
informs you have to do to figure out how you're
saving your for your retirement, and they tend not to
cover the second century of your life because it's not
going to happen. That's a perfect metaphor. Yeah, how come
you're not saving enough money for when you're two hundred
years old. It's not that you've decided it's better to
be broke when you're two hundred. It's just that the
(12:39):
the situation of being two hundred does not tend to
come up very often. Now, obviously it's not nearly that extreme,
because sometimes in some cases animals do live to old
age and they face biological siniscence under natural conditions. But
for many species it's pretty rare. For species of animals
that tend to die from one cause or another before
(13:00):
they get the chance to grow old evolution doesn't have
many opportunities to test what happens in old age, so
it can't optimize the animal for old age very efficiently.
And compare this to how strongly evolution tests and optimizes
for the effects of genes that manifest in early life.
If something affects how likely you are to survive at
(13:22):
age twenty or at age ten, evolution is going to
be very strongly selecting for or against that gene. Okay,
so this is one part of the landscape of explanations today.
Most species that show significant aging evolved to their anatomically
modern condition in a situation where mortality was high and
evolution didn't get a lot of opportunities to see what
(13:45):
happens in old age, much less optimize it. Let's introduce
another wrinkle into the explanation. Yeah, this one has a
wonderful title. This is mutation accumulation, right, So we go
to the British biologist Peter B. Meadair. He was one
of the primary evolutionary thinkers credited with working out the
implications of this model of aging, where the force of
(14:06):
selection just declines with old age. So in several works
in the middle of the nineteen forties and the nineteen fifties,
uh he argued, based on similar logic, that natural selection
would often be blind to the effects of mutations that
cause negative effects laid in life after reproduction is mostly stopped.
So let's use another analogy. Imagine a mutation called the
(14:29):
twenty birthday surprise gene, which means that on the day
you turn twenty, carriers of this gene suddenly transform into
a bucket of fishheads and thus lose all ability to reproduce. Now,
this would mean that in order to pass on this gene,
a carrier would have to reproduce before their twentieth birthday.
(14:50):
So kids they have before they're twenty years old could
still carry this gene, but they don't get the chance
to have any kids after their twenty years old, when
plenty of other members of the piece these would continue
having children, all potential reproduction after twenty is canceled, thus
giving people with this gene significantly fewer children on average
than people without it, and so the gene is unlikely
(15:11):
to spread in the population. Now imagine a similar gene.
This is the hundredth birthday surprise gene. Carriers of this gene,
upon the day of their hundredth birthday, suddenly transform into
a VHS copy of Highlander to the Quickening. Okay, and
and and therefore becoming immortal. No, not quite No. The
problem is, well, I guess you you might get to
(15:33):
live somewhat forever on a shelf, but you don't. You
definitely don't get to reproduce after that, right, there's very
little sexual reproduction between copies of Highlander to the Quickening.
But also it doesn't really matter, right because do carriers
of this gene have any fewer children the non carriers
of this gene. The answer is no, right, because who's
(15:54):
still having children at age one hundred Almost nobody. So
even if you have this very unhel helpful gene, you
don't like it that you transform into a VHS tape
on your hundredth birthday. That's not good for you, but
it doesn't matter to how many children you have. It
has no effect on that. So if you have this gene,
you can spread it to all your children, and they
(16:14):
can spread it to all of their children and so,
and they'll all have just as many kids and grandkids
as the neighbors who don't have it. You've already passed
it on by the time it matters. So this would
be the case. Though we we've we've used the Highlander
to transformation as as an example here. But even if
it were something seemingly beneficial, like say a gene made
(16:37):
you suddenly really excellent and talking to members of the
opposite sex at age one hundred, you know, like or
the opposite it made you terrible at a speaking to
the opposite sex at age one hundred, it would still
be the same case, right, yeah, unless the basically the
only thing that would matter would be if it's a
gene that suddenly makes you able to reproduce again. I mean,
(17:00):
if it did that, then that would probably matter. But
as long as you're past the age of reproduction and
you're not having any more children, mutations good or bad
are just going to sort of accumulate randomly without having
any effect Onesoever, natural selection just doesn't pay attention to
them because it never gets to notice them. Well. But
(17:22):
then the other thing too, is that if you're talking
about something that would kick in so late in life
that even people with that gene might never experience it. Right.
It's like if you're playing a role playing game, video
game or what have you, and there's some sort of
like high level ability and you look at it. It
looks great, but you know you're never going to play
the game long enough to get it. Yeah, so what's
the point. Yeah, the game might as well for you
(17:44):
not even have that thing in it. And apparently there
are going to be genetic mutations like that. And this
was Meta WIRs insight. It came to be known, as
you said, as the mutation accumulation hypothesis. Whether reproduction stops
because you die of extra ends it causes. This was
a big thing Meta or had in mind. It's like
we talked about, you know, the wolf gets injured and
(18:05):
can't hunt, the wolf gets sick and dies, the wolf
gets killed by something, whether that happens or because you
age out of your reproductive stage of life for some
other biological reasons. Genes that have negative effects that show
up mostly after reproduction has stopped, are not subject to
the full force of natural selection. So there's not much
(18:26):
preventing the proliferation of genes that harm you in old
age because there's nothing to weed them out, and they
accumulate in the genome over generations by what's known as
genetic drift. And the genetic drift is just the random
dispersing of genes that don't appear to have a very
strong positive or negative effect. So if you've got a
mutation that you acquire for a nasty surprise in old age,
(18:49):
something bad that happens to your body, and you could
look at the process of aging like this, it's just
a large plethora of genetic mutations that cause bad things
to happen to your body. Later on, you can still
pass it on to your kids because you're you've had
all your kids by the time it starts affecting you.
And so these genes can become common in the gene
(19:10):
pool of your species simply because there's nothing stopping them.
So simply put it, the force of selection declines with age.
Mutations that are neutral early in life when selection is strong,
but negative later on, they could accumulate in the population.
I like to think of this as the sack of
kitty litter scoopings in the closet scenario. Okay, explain. But
(19:31):
a friend of mine, when I first met her, she
had a cat box, and then she would scoop the
cat box and it would accumulate in a garbage bag
in the closet. Accumulate me, you mean accumulate as and
she would dump it, yes, in a garbage bag in
the close. And it was. It was a lot cleaner
than this makes it sound, but it was. It was
very much a sort of kicking the can down a
road scenario, like eventually you're gonna have to take that
(19:54):
bag of of of of litter scoopings out, but you're not.
The whole situation is not built on what you're going
to have to do tomorrow. It's about what's happening to today.
But what if you're looking at that closet and you're saying, oh,
there's enough space in here that I could keep scooping
it into the closet until I die of some of
their cause, and then I would never have to take
(20:14):
it out. It would be completely irrelevant. So it can
accumulate forever, just like these deleterious genes can. Okay, So
that's clearly one part of the answer. One part is
that stuff that affects you late in life is just
less likely to get weeded out by natural selection. But
what if there's something more than that. What if maladaptive
genes that manifest in old age aren't just allowed to
(20:36):
roam wild by sort of the careless shepherd of a
natural selection. What if they're positively selected four in some way.
And that's what we'll explore when we come back from
this break than all right, we're back, So now it's
time to talk about antagonistic pleotropy. In a paper in
(20:57):
seven and the journal Evolution, the American Evolutionary by alllogist
George C. Williams had a breakthrough that made metoirs original
hypothesis even stronger and sort of complimented it. And so
this was a paper that I mentioned in part one.
Actually it's the paper called pleotropy, Natural Selection and the
Evolution of sinescence. Williams hypothesis for the evolution of aging
(21:19):
came to be known, as I said, as antagonistic pleotropy.
And what this means is that well. Pleotropy. The word
comes from the Greek roots meaning multiple turns or many effects.
Pleotropy happens when a single gene codes for multiple different
phenotypic effects, meaning effects on the body or effects on
(21:41):
the behavior. So if you had one gene that both
gave you black hair and gave you an extremely long,
pinky fingernail, that would be pleotropy. Or if you had
a gene that made you really tall and also made
you better at learning multiple languages, that would be pleotropy.
(22:01):
And there are lots of examples of this in animals
in the real world. Here's one in chickens. Robert, have
you ever seen the frizzle chickens? Who? I don't know.
I've seen some pretty funny looking chickens before. I've seen
a frizzle chicken. I mean the ones that have like
the curly vegas outfits. Uh yeah, well yeah, I have
seen some of these. These these chickens that have like
(22:22):
a lot of extra feathers around their their talons and all.
The frizzle gene is is a gene in chickens that
causes the feathers to curl up instead of lying flat,
so you get these crazy looking like awesome, beautiful, regal
puffy chickens and they look really cool. But it turns
out this gene also controls several other phenotypic effects. So
(22:43):
if you are a chicken with the frizzle gene, you'll
also have a different metabolic rate and different body temperature
and lay a different number of eggs than the chickens
who don't have this gene. So if you want the
gene for the magnificent curl, you're going to be laying
fewer eggs, among other things. And these are examples where
the situation it feels more like a trade off and
(23:05):
probably has more in common with some of our our myths, right,
because the gift of the god often comes with some
sort of consequence. Yeah, exactly. So another one, just real quick.
In cats, did you know about fort of cats with
white fur and blue eyes are also deaf? I have
heard this one, yes, yeah, odd, So pleotropy can be
(23:26):
like that. It can come in and kind of mixed
blessing form, though I guess I don't actually know if
blue eyes are good for the cat. Maybe that's double bad.
But uh well, you I mean, certainly when you get
into the selective breeding of of a species, you get
into a situation where appearance has has a has a
survival advantage. Yeah, exactly. So pleotropy can go both ways.
(23:47):
One effect of a gene could be good while the
other effect could be bad. And here's where we get
the idea of quote antagonistic pleotropy. A pleotropy that's pulling
in both directions, but usually it'll pull a bit stronger
in one direction than another. So if the good effect
outweighs the bad effect, the gene will spread through the
gene pool. But if the bad effect outweighs the good effect,
(24:09):
the gene will tend to go extinct. That we should
be clear again what's meant by good and bad genes here, Because,
for example, a gene that caused the carrier to experience
intense pain and misery throughout life, but somehow also caused
the carrier to have more healthy children than the average
member of their species would also spread. So it's not
(24:32):
optimizing for like you to have a long life, for
you to have a fun life. It's optimizing for number
of offspring and the success of those offspring. Now, William's
theory of antagonistic pleotropy picks up from this fact, he
hypothesizes that some of the genes that cause aging are
selected for because they have other separate effects that maximize
(24:54):
fitness and reproduction earlier in life, which, like Metawir showed,
is more strongly select did foreign nature. The same genes
that make your skin sag and give you heart disease
in old age might also make you extremely reproductively competitive
when you're young. So here's a really broad example. How
about genes that control the rate of cell division. Yeah,
(25:18):
so a hypothetical gene might be selected for because it
makes cells divide more efficiently. And if cells divide more efficiently,
it means you can rejuvenate tissues and heal wounds and
grow faster when you're young. But the same gene that
causes prolific cell division could potentially be a problem later
in life, because what happens when cells are prone to
(25:39):
divide a whole lot you could be prone to cancer
cancer is runaway cell division. Cells that are not useful
for the body are suddenly being created in great abundance,
which brings us back to the hydrosaur example that we
touched on earlier. Yeah, back in the first episode. Or
you could think about something going exactly the reverse. You
could have a gene that could increase apoptosis signaling, and
(26:02):
apoptosis is programmed cell death, so a gene that causes
cell lines to die off more frequently, and this would
help prevent runaway cell lines from turning into cancer while
you're young. Natural selection obviously would love this because it
would select against organisms that get cancer when they're young
and can't reproduce much. But the exact same gene would
(26:24):
cause tissues to deteriorate more with age because they undergo
more and earlier cell death. And in fact, something like
what I just described has actually been studied. The example
would be the gene at P fifty three. The P
fifty three gene has been implicated in antagonistic pleotropy, and
it's thought that P fifty three protects young animals, including humans,
(26:46):
but I think it's mostly been researched in mice. It
protects these young animals against cancer by interrupting cell proliferation.
It says, now, don't cells don't divide too much now,
But in doing this it can also have the effect
of erupting the proliferation of normal, non cancerous cells like
stem cells, which are the cells the body uses to
(27:06):
rejuvenate tissues over time. So the same gene that play
some role in helping protect against cancer when you're young
also helps play some role in the physical deterioration of
the body with age by preventing it from making new
cells and rejuvenating your tissues and detaining eternal youth. So
(27:26):
the takeaway from this, obviously is that anytime you see
a story about eternal youth in fiction or in a
movie or something like that, imagine these these characters who
are eternally youthful riddled with cancer. It's not really nothing
hard to imagine when you think about all the various
uh uh side effects and caveats that come with eternal
youth in most of our myths and legends, right well,
(27:49):
I mean, yeah, you've got uh. I guess it's not
applicable in the tiffan A story because he doesn't get
eternal youth. He wants to live forever. But you imagine
the equivalent of the tiffan A story where you ask
for eternal youth. So Tiffannus ask for eternal life, or
he doesn't ask Aos ask for eternal life for Titness,
he gets eternal life, but not eternal youth. So it's
the monkeys Paul coming back to bite him. In this story,
(28:10):
you would ask for eternal youth and they say, okay,
here is your eternal youth. But you get lots of
cancer with it. And I think actually have read in
the past that some of these experimental youth extension techniques
that people do research on initially look promising but sometimes
turn out to appear to increase cancer risk. Now here's
another example of a potential antagonistic pleotropy inflammation. So I
(28:34):
want to cite one paper from two thou eight in
Bioscience Trends by Makoto Goto, And in this paper, the
author explores the idea that a lot of the signs
of physical deterioration associated with aging are driven by inflammation.
But inflammation is a defense mechanism for the body. It
helps you survive the redness, the swelling. It's not pleasant,
(28:55):
but all that's part of a primitive immune system response
that protects you against antigens and parasites. So inflammation responses
can help you survive when you're young, but later in life,
inflammation related aging effects cause widespread damage to the body,
including all kinds of diseases from type two diabetes to
rheumatoid arthritis. Also, the kind of military reaction to invasion
(29:22):
that is helpful for the young organism can be a
detriment to the older organism. Correct, exactly right, And so
it's believed now by scientists that there are tons of
things like this in the body. There are genes that
have these antagonistic pleotropy effects. They're good for you when
you're young. They help you survive young adulthood and childhood
(29:42):
and help you have more children early on. But the same,
very same genes having the very same effects also cause
you to age and become sick and reduce your fitness
later on in life, when, as we established earlier, the
force of selection is diminished. So one theory that is
pretty similar to these ones we've just discussed, we've got
(30:04):
metairs mutation accumulation hypothesis, which says, you know, uh, natural
selection doesn't pay much attention to what happens later in life,
so negative mutations can kind of just hang out there
without really being weeded out. Then you've got antagonistic pleotropy,
which says that some of the things that cause negative
effects later in life are positively selected for because those
(30:25):
negative effects later are much outweighed by positive effects early
in life and uh enhancing reproductive fitness early on. So
there's a very similar theory along the same lines called
the disposable soma theory, And this is a theory on
the evolution of aging that was put forward in nineteen
seventy seven by the English biologist Thomas Kirkwood. And this
(30:46):
reframes it as a question of resource investment in the body.
Here's the basic premise. The body has a finite amount
of resources that it can spend on various projects. And
these projects would include things like speeding up reproduction in
the youth and maintaining body tissues. And so if you've
(31:08):
got both of these things and you've got a limited
budget to spend on them, you're gonna need to make choices, right,
how much goes to each one, and indeed which one
is the most important for the biological mission at hand. Right.
And so, drawing on the same logic we looked at earlier,
if you live in a scenario where you don't tend
to live to you know, your natural end of life age,
(31:32):
you tend to get weeded out by things happening to
you in the wild, you know, predation or starvation or
or a disease or injury, anything like that, It will
obviously look to your body like you need to invest
way more in those earlier stages in maximizing reproduction early on,
and so drawing on metawar evolution is going to tend
(31:53):
to favor pouring finite resources into early reproduction optimization instead
of maintaining tissues for an infinite natural lifespan. So I'm
trying to think of a human equivalent. Uh, it sounds
kind of silly, but basically like, should the body spend
its precious limited energy resources keeping your artery walls from
(32:16):
thickening over time or spending them on making you super sexy? Well,
you know, I God knows. I am not an economist,
but I find that when we discussed life cycles of organisms,
or or life cycles of of stars, even I think
of companies and how they work. So it comes down
to a question as as say that the CEO or
(32:38):
even the founder of a company, are you running the
company like you want to retire from it and watch
it continue to prosper as you in your retirement, or
are you running the company like you intend to sell it?
You know or we know what the answer is. In
most cases, yeah, you're you. In many cases you're running
the company because in a way that benefits the short
(33:02):
term sale of the company, or you're leaving this company
for another company. Yeah. I mean people like to have,
you know, sort of like long term investment type rhetoric.
But a lot of people have realized that the smart
strategy for themselves is grab and go, you know, optimize
whatever you can get out of a system for yourself
as soon as possible, and then be on your way.
(33:23):
And that's the equivalent here that this is to say
that you can't even meet guaranteed that it will matter
whether you've got a gene that optimizes against atherosclerosis or not.
But if you can optimize for being real sexy and
having lots of successful reproductive strategies early on in life,
you're pretty much guaranteed a better chance at having more children.
(33:44):
And we have so many different adages that back up
this kind of like personal philosophy and life. Right, you know,
burn it like you've stole it, I believe, not burn
it like you still drive it, like you sto it.
Burn the candle at both ends of his combining the
two there, you know, or burn it like you stole it.
Really you like it's hot, do it? It behooves you
to go ahead and burn it so that they don't
(34:04):
figure out who stole it. Yeah, sees the day. Spend
like there's no tomorrow exactly because sometimes well sometimes there isn't,
or there's there's a finite amount of tomorrow. Sometimes a
leopard will bite your face off. You should just operate
on the assumption that a leopard might bite your face off.
So spend what you've got today. Well, that's good. I
don't know if we'll fit that on a bumper stick
(34:25):
or Now. What we've described so far are I think
what's known as the classical theories of aging. And in
recent years, we should point out some scientists have proposed
various kinds of updates to accommodate new experimental findings. Maybe
in the future we could come back to this topic
again and and explore the most recent developments in in
aging theory. But these are basically I would say, these
(34:48):
classical theories are still pretty much intact. There. You know,
you might need to modify them in some ways to
to update them for newest experimental findings. But for example,
an antagonistic pleotropy. People still basically think that this is
a good explanation for why a lot of the aging
effects we experience take place, and it gives us room
(35:09):
on which to build uh further analysis, Yeah, of course,
and it gives us room to say, if we understand
how a process happens and why it happens, I wonder
if it could be reversed or undone. And of course
there's a lot of that. There's a lot of interest
in this, given that medical research is uniform universally funded
(35:32):
by mortals who and many of them are are interested
and possibly having more life to live or if possible,
you know, an infinite amount, right, So, of course, because
we don't want to age and grow old and sag
and wrinkle and and eventually die, scientists are always working
on ways to beat aging, and some broad evolutionary mechanisms
(35:56):
based on things like fruit fly research are actually known.
But unfortunately they're not the kind of simple medical fixes
that could like be ethically applied to humans. They're they're
evolutionary fixes that you couldn't really implement on purpose. I
mean you could in fruit flies, and researchers have so
what are they, Well, one would be low adult mortality
(36:19):
and high juvenile mortality. If you get a bunch of
fruit flies and you create a scenario such that adults
tend to survive longer than they would in the wild,
while juveniles die very often. What actually happens is that
the life span and the reproductive lifespan of the fruit
(36:41):
flies increases over generations of evolution. And this kind of
makes sense, right if the if the mating pool is
limited to older individuals, genes that favor fitness in later
life will be selected for, and thus these would be
genes that prevent or lay aging, and they'll become more successful. Normally,
(37:03):
evolution wouldn't care about those types of genes very much.
But of course we can't do this to stop human
aging unless we're prepared to like implement a policy that
only people over a certain age can have children and
then keep pushing the minimum age upwards. Obviously we don't
want to do that. Well, even in scenarios like you know,
periods of history in which there is a high mortality
(37:26):
rate for younger people, such as during wars, uh, it's
still I don't think there's any data to back of
the idea. That this would definitely interfere with reproduction because
obviously there there are children that grow up in the
in the wake of war. Now perhaps the father is
not there anymore, but reproduction has been initiated. But then
(37:47):
that's a whole different area of study, like the effects
of war on reproduction and the health of the resulting
offspring um, something we've touched on before on the show,
and we could easily revisit. Oh yeah, that's all interesting stuff.
Another thing to point out about what I just mentioned
about low adult mortality and high juvenile mortality contributing to
extended lifespans. We know this works in fruit flies, but
(38:10):
we can't predict other complicating factors that might stop this
from working another species. Though it does appear to be
pretty general that species that have lower extrinsic mortality evolve
longer lifespans. Like if you've got good defense mechanisms against
predators and disease, or if you just happen to, say,
(38:30):
end up on an island where you don't have many
predators or diseases, you will probably evolve over a long
period of time to breed longer and live longer. Think
about the Great Wizzen tortoises of the Galapagos. They've got
a shell, they don't have really natural predators, and they've
got these long, long lifespans because the adults and the
(38:51):
old adults can just keep on breeding. And they probably
had a fair amount of moisture. I think Aristotle would
Aristotle was onto something. Yeah, No, they don't have moisture
at all. They look so dry. Those tortoises are like
the driest looking creatures I can think of, But they
live in a moist environment. Maybe that's it. That is true,
But okay, So looking at more like potentially ethical medical fixes,
(39:15):
are there things researchers are working on in order to
beat aging and humans? Well, the answer is obviously yes.
There are plenty of questions about whether these projects are
actually a good idea, and even if they are a
good idea, whether they could be successful in principle, but
there are plenty people working on it. One example, of course,
(39:36):
is the gerontologist and author Aubrey de Gray. He's made
a whole career out of the idea, going around promoting
that we can and should be trying to completely defeat
the process of aging, and that we can do it
within the next few decades. Yeah, he's everyone's probably seen
images of de Gray before he has his big wizard's beard,
and he's resputant. Yeah, he shows up in all sorts
(39:57):
of He doesn't hate respute if he shows up in
very it's a documentary is about this topic all the time. Uh.
And his his basic argument is, I think rather ingenious.
It's instead of viewing aging and death as this unbeatable war,
you know, this this unbeatable um problem, it's like, break
it up into smaller battles, smaller problems that you can win,
(40:19):
that you can solve. Yeah, and I think this is
the key appeal of his approach. He says, aging is
not one thing, it's maybe seven things. Yes. For instance,
the problem might be cells die off and are naturally
replaced in the heart or in the brain, and he says, well,
you stem cell replacement for dying cells. Or another example
would be the body undergoes a proliferation of unwanted cells,
(40:41):
such as fat cells that replace muscle and lead to diabetes.
He says, we'll trick the problem cells into self destruction
through suicide, gene therapy, this sort of thing. So it's
it's taking taking the overall problem breaking it down into
little individual problems that you could potentially solve through medical
intervention and genetic engineering, etcetera. Now, for people who are
(41:02):
interested in avoiding aging, obviously this message is very appealing. Yes,
but there are also we should mention many researchers who
find degrees program unrealistic. Like he has plenty of critics. Well,
on one level, it's kind of the basic trans anti
transhumanist argument, right like if okay, if you break down
(41:23):
essentially immortality into a number of different treatment options that
are available, than then who are they available to? Who
has access to these treatments? And then it becomes this, uh,
this this inequality situation where you have the very dystopian
idea of the super rich individuals who can afford all
of the various treatments that that keep their unnatural lives
(41:44):
going while the rest of us simply live and die
as always. I would say the answer to that critique
is not that you shouldn't develop the medical technologies, but
that you should find ways to make them available to everyone.
Then again, you do have that intrinsic question of whether
it's actual good to allow any member of a species
to be biologically immortal. Uh, to keep on living in
(42:05):
consuming resources beyond what would what would normally be allotted
to them in a normal lifespan, because, as we talked
about earlier on, there's this whole good of the species argument.
Your genes might not care about the good of the species,
but you should, right, we should. Well, it's an easy
argument for for for us to make. But then again,
we're not a hundred and fifty years old and hooked
(42:26):
up to the immortality machine. Right. Well, once your time comes,
you will probably change your tune. Right, It's like, no,
give me a little more. I just need a little more,
one more year. Um. But then again, yeah, so that's
like the question of whether we should be trying to
achieve biological immortality. There's also this question that many scientists
have have brought up, which is that his program is unrealistic,
(42:48):
not necessarily that it's a bad idea, but that you
you can't extend aging for or not extend. You can't
extend youth forever. They're just gonna be hard physical limits
that you're going to hit within the human body. Just
one example of that strain of thinking as a paper
that came out earlier this year in published by the
Proceedings of the National Academy of Science is called Intercellular
(43:11):
Competition and the Inevitability of Multicellular Aging. So this study
was conducted by scientists Joanna Massel and Paul Nelson, and
Massel and Nelson use mathematical models to argue that essentially,
no matter what you do, you will be faced with
one facet of aging or another, and the main tension
(43:32):
they highlight is tissue deterioration or cancer, one or the other.
It's a mathematical inevitability. They say. If you find a
way to prevent cancer, tissues deteriorate and cells become less efficient,
you get the body breaking down. If you find a
way to rejuvenate tissues, beef them up, make them youthful again,
(43:52):
you get cancer. Age is going to get you one
way or another. It's like we're in that trolley car, right.
We have attracts diverging to two unwanted fates in a
sense equally unwanted fates, and we have to try and
figure out, well, which way we're gonna go, What are
we going to plow into. I feel like this should
be reimagined as a myth, like going back to Tiffanus,
(44:13):
like I want the gods gods that represent one represents
cancer and one represents the deterioration of body tissues. And
they're like at war and you have to choose between
your fate with one or the other. Yeah. I like that. Yeah,
this is this is where our modern day gods can
jump in and and provide us the story to make
(44:35):
sense of our our doom. Okay, well, I guess that
wraps it up for for part two of this episode
about why we age and why we can't have eternal youth. Yeah. Well,
and I don't want to leave it on too dark
of a note there with the doom talk, because I mean, ultimately,
I guess here's the here's the silver lining. Uh, Aging,
even dying, everybody does it. It can be. It couldn't
(44:58):
be that much to it, right, look at the people
who do it. It It couldn't be. It couldn't be that difficult,
It couldn't be that hard to go through. Well, I mean,
it's easy to get down when you spend a lot
of time thinking about the inevitability of aging and death.
But um, I mean the thing to think about is, yeah,
it comes to everybody. It's a part of life, and
there's a lot of life to love. Yeah, and it
(45:18):
bears your minding that there is a lot of stuff
you can do in the in the near future to
make your your far future a little more easy going.
You know, you can look after the body you have.
You can uh, you know, exercise and try to eat right.
I think I saw a study saying you need to
eat a bunch of chocolate to make it. I think
that's what it was. Well, then that's the other side too,
(45:41):
is like you're gonna grow a hold, You're going to die.
You can't just spend your whole time worrying over that inevitability,
So you might as well have some chocolate, you might
as Oh no, I mean I was joking about those
articles that actually say chocolate will make you live longer.
Oh okay, not just the ones where there's like a
new study out that points to uh some beneficial quality
(46:02):
of like pure unsweetened chocolate. Uh yeah, I mean it's
it's always couched in, like eat chocolate to be healthier. Well,
if it's not couched in it, That's how I think
sometimes we interpret it. We read the study and we're like, well, good,
I like chocolate, or I like red wine or I
like coffee, and now I can just continue to enjoy
the things that make my life more bearable and uh,
(46:22):
and not worry about what they might be doing too.
Anytime you read an article about the one silver bullet
thing to eat or to drink that will make you
live forever, don't believe it. I agree, unless that one
silver bullet thing is the quickening which will work? Can
the quickening be transferred to another though I'm a little
shaky on my my quickening science. I don't know. We'll
(46:45):
have to come back to that. What's the quickening conversion rate?
I don't know. I think you just have to be
from the planet's ice, right remember? Hold? All right, Well
there you go. Uh again, this was a two parter.
If somehow you made it through all the parts two
without listening to part one, go back and listen to
part one. You will find it in all other episodes
of Stuff to Blow your Mind at Stuff to Blow
your Mind dot Com, and you'll get our moisture jokes.
(47:07):
That's right, and hey, while you're stuff to Blow your
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(47:27):
Alex Williams and Tory Harrison are excellent audio producers, and
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the Mind at how stuff works dot com for moralness
(47:50):
and thousands of other topics. Does it how stuff works
dot com, The busy, many past four foot fo
Hey, you welcome to Stuff to blow your mind. My
name is Robert Lamb and I'm Joe McCormick, and it's Saturday.
Time to go into the vault for Eternal Youth Part two.
If you checked us out last Saturday, it was Eternal
Youth Part one. This is going to be the second
part of that series. This originally published January. Should we
get right into it. Yeah, let's just belly right up
to the bar and have a drink from the Fountain
(00:27):
of Youth. Welcome to stuff to blow your mind from
how stuff weren't dot Com? Hey, you, welcome to stuff
to blow your mind. My name is Robert Lamb and
I'm Joe McCormick, and we're back for part two of
our discussion about where's my eternal youth? Why can't I
(00:50):
be young and beautiful forever? Why do we age? I
know that's the It's the question we've always wondered. It
shows up in our philosophical writings, it shows up in
our religion, our mythology. Uh. In researching this topic, I
kept thinking back to Genesis six three. This is the
King James version, and the Lord said, my spirit shall
(01:12):
not always strive with man for that he is also flesh,
yet his days shall be a hundred and twenty years.
So there's God putting a limit on how old a
human can become and saying like, here's the aging process. Uh,
these are the rules. Obviously doesn't apply to Highlanders. That's right. Well,
(01:33):
you know, maybe they're they're part of the giants in
the Earth or something. I don't know, Oh that could be. Yeah,
I guess they're not humans. So well, the spoiler for
Highlander to certain cuts, they are not from Earth right
in the good cuts from Earth. Yet again, we're just
trying to throw those seeds down. Highlander two episode it's
coming now. Speaking of parts one and two, this episode
(01:55):
is a part two. Yeah, so if you haven't listened
to part one yet, you should go back check that
out first. And that we explored the question of why
we age. We look at some animals that don't really
age in the same way that humans and other similar
mammals do, and we look at historical explanations people have
tried to come up with for why we age, and
(02:17):
we also explored some reasons to think that those historical
explanations were not correct. Today, we're going to try to
get into the modern evolutionary synthesis, take on why we age?
What's happening and how do you solve this paradox of
the fact that aging is a decline over time in
our survival and reproduction fitness, and yet evolution should be
(02:40):
constantly optimizing our survival and reproduction fitness. Why would it
allow us to go into this period where we tend
to die and tend to get worse at surviving and
tend to not be able to reproduce anymore. Indeed, because
I certainly don't want to deify natural selection and say
that like natural selection produces perfect forms or ideal forms,
(03:02):
But look at the forms the natural selection has produced,
Look at all the various engineering problems that that that
evolution has managed to solve. Why would there be this
be this huge, at least from our perspective, flaw in
the design. Yeah. Now, of course, today, as we often
do with evolution, just for the ease of communication, we're
going to be using a lot of metaphors that offer
(03:24):
a kind of like embodied view of evolution, as if
like it's making choices. What we, of course know is
that evolution is a is an optimization algorithm. It's not
a person. It's not a thing. It doesn't really have
desires of it of its own. It has a way
that it works, and the way that it works is
to optimize the success of genes that survived natural selection
(03:48):
and reproduce. Now, one of the answers we explored in
the last episode is one of the most common things
people are going to turn to when they're trying to
explain why we age. It's the thing that my brain
and immediately went to before I read anything on this subject.
I started to think, well, let's see, if everybody just
lived forever and nobody naturally aged out and died, then
(04:13):
you'd have way too much competition for resources, right, You'd
have way too many people trying to live on the
same landscape, you have too many people trying to eat
from the same food sources. You'd have overpopulation, and and
everybody would suffer for it. Overpopulation ties into a number
of our different dystopian views of the future, as does
the possibility of immortality becoming an option at least a
(04:35):
certain privileged people in society. You know, you get this
sort of trope of the awful uh Methuselah of the future. Right,
some just dreary, old, greedy individual who will not die
and let go the reins of life so that others
may grasp it. Right, Well, as much as we don't
personally want to grow old and die, you can sort
(04:57):
of recognize from an impartial standpoint, if you just consider
it in other people, that it seems kind of unfair
that people should live forever, right, Yeah, unless it's me
or someone that I'm invested, and there they should put
a limit on that stuff. Yeah. So, but these types
of answers, while true, it is true that it's good
for the species that we should age and die, and
(05:18):
that it's good for future generations. Uh, good of the
species and good of the group based explanations come under
a lot of fire from evolutionary biologists. There's some biologists
to endorse kind of qualified versions of of good of
the group and good of the species type explanations, but
there I think many more who don't. And here's an
(05:39):
example to illustrate one of the big problems in why
these good of the group explanations fail to hold up.
All right, hit me with it, Okay, Let's imagine a
pack of alien space wolves. Okay, and for our warhammer
for fans out there. He's not talking about space marines here. Wait,
I don't know what space will Is that a thing? Yeah,
it's a faction of the space Marines. In the Warhammer
(06:02):
Fort K universe, there are wolves. Well, no, they well
they wear wolf skins and they're you know, genetically enhanced
super soldiers. Okay, so it would really complicate them the
analogy you're making here, if if we were to draw
them into the discussion. Well, I was just trying to
make clear that this is a hypothetical, not like real
wolves on Earth. Okay, So alien space wolves living on
(06:23):
an asteroid somewhere in hunting space here. Now, let's imagine
this pack of alien space wolves has evolved genes that
cause them to grow old and become infertile after about
ten years of age, after which you know, they usually
die within a couple of years. And let's say that
each female space wolf has an average of one space
wolf pup every year that she remains fertile. So, unless
(06:46):
the space wolf is killed by injury or disease or
a marauding space explorer, um, the average space wolf female
has tin offspring in her life lifespan. Everybody's happy, right,
because they don't eat too many of the space dear,
they don't become overpopulated. It just works out pretty well.
But then suddenly one of these space wolves acquires a
(07:09):
mutation that allows her to stay fertile and survive for
twelve years instead of ten, so she has twelve space
wolf pups, whereas all the other females in the pack
are still having ten, and half of her pups carried
this extended fertility and longevity gene, so those six pups
each have twelve pups, while non carriers of the gene
(07:32):
only have ten, and so on and so on down
the generations, and eventually this cheater gene for extended life
and extended fertility is going to proliferate, even if it
might be worse off for everybody in the long run.
Even if the long living, long reproducing animals have too
many offspring and consume too many resources and suffer die outs,
(07:53):
this won't really cause a re selection towards shorter lifespans,
because how would it. Instead, what it would do is
optimized for whatever genes are possessed by the survivors of
those die outs, and that would probably be like those
that store fat better or hunt better, or can extract
nutrition from space moss in addition to meat. And this
(08:14):
is a really common type of argument against good of
the group and good to the species explanations and evolution,
because any mutation that cheats on the stasius you've created
for the good of the group will tend to start
to get an edge and then have more offspring than
those who don't cheat, and eventually that new gene will
become the norm. Right. Yeah, It's kind of like if
(08:36):
you have a you know, an academic environment where everybody's
cheating on the exam, the exam, the grading becomes that
much harder each and every time. It's true. Yeah, it's great.
So it's like you've got to grade on a curve
because everybody's cheating, so everybody's grade goes down. Um. Yeah.
And so I just want to remind you though, this
doesn't mean that there is not such a thing as
(08:59):
the good of the group the good of the species.
Those things clearly are true. And it clearly is true
that it's good for the next generation that older generations
age out and die. I care about the survival of
the rest of my group. I care about members of
my species and about future generations. But I care because
I have a brain and I can recognize what's going on.
(09:19):
Ma genes don't care, and your genes don't care. They
just chemically proliferate themselves. They don't have a sentimental attachment
or or an idea that the next generation should get
resources to. All right, So this just brings us back
to the question, though, why have we evolved to grow old? Right,
it's still unsolved. Why not live and reproduce forever, maintaining
(09:41):
perfect youth and vigor until something extrinsic happens, until we
get killed by a hemorrhagic fever or tractor accident. All right,
We're gonna take a quick break and we come back.
We will answer that very question. Thank alright, we're back,
all right. So there are a number of modern, well
accepted scientific theories trying to answer the question of why
(10:04):
we evolved to age. And here's a starting point for
several of those theories. Let's go back to the wolves
for a second. Imagine the space wolves. Maybe a hypothetical
wolf species could breed and stay healthy until about the
age of ten, Like we said, why not twenty, Why
not thirty? Why not five hundred? Well, here are a
few things to consider. Wolves did not evolve in zoos
(10:28):
or as domestic pets, where they're guaranteed meals and protection
from violence and guaranteed access to veterinary care. The landscape
that created the wolf as it exists is one in
which there is a constant struggle to get enough meat
to survive and to not get sick and die, and
to not get injured and become unable to hunt, so
(10:50):
you starve. If you are a wolf living in the
wild and you survived the first year of your life,
one of these things like injury or disease or star ovation,
very likely will kill you before you get a chance
to reach old age. These causes of death like disease
and injury, or what's known as quote extrinsic causes of death,
(11:12):
death caused by outside pressures and not by stuff that's
in your genes or by old age. And so we
can look at the real life example to see how
common this is. The actual gray wolf canis lupus lives
somewhere around an average of six years or so in
the wild, but in captivity it can live for more
than fifteen years. So here's the first crucial bit to use.
(11:34):
Some more metaphorical language. If there are physical processes that
tend to render a wolf progressively less fit every month
after it's more than ten years old, evolution almost never
sees that. To put it in another metaphor, asking why
evolution allows the wolf to grow old to deteriorate with
old age is kind of like asking why we don't
(11:57):
have laws against time travel. The reason isn't that our
legislative bodies have considered and debated the issue of time travel,
and in the end they concluded that time travel is good,
we better, we better allow it. That's not what happens.
What happens is the issue doesn't come up. Yeah. It.
It reminds me of some of these various programs that
(12:18):
informs you have to do to figure out how you're
saving your for your retirement, and they tend not to
cover the second century of your life because it's not
going to happen. That's a perfect metaphor. Yeah, how come
you're not saving enough money for when you're two hundred
years old. It's not that you've decided it's better to
be broke when you're two hundred. It's just that the
(12:39):
the situation of being two hundred does not tend to
come up very often. Now, obviously it's not nearly that extreme,
because sometimes in some cases animals do live to old
age and they face biological siniscence under natural conditions. But
for many species it's pretty rare. For species of animals
that tend to die from one cause or another before
(13:00):
they get the chance to grow old evolution doesn't have
many opportunities to test what happens in old age, so
it can't optimize the animal for old age very efficiently.
And compare this to how strongly evolution tests and optimizes
for the effects of genes that manifest in early life.
If something affects how likely you are to survive at
(13:22):
age twenty or at age ten, evolution is going to
be very strongly selecting for or against that gene. Okay,
so this is one part of the landscape of explanations today.
Most species that show significant aging evolved to their anatomically
modern condition in a situation where mortality was high and
evolution didn't get a lot of opportunities to see what
(13:45):
happens in old age, much less optimize it. Let's introduce
another wrinkle into the explanation. Yeah, this one has a
wonderful title. This is mutation accumulation, right, So we go
to the British biologist Peter B. Meadair. He was one
of the primary evolutionary thinkers credited with working out the
implications of this model of aging, where the force of
(14:06):
selection just declines with old age. So in several works
in the middle of the nineteen forties and the nineteen fifties,
uh he argued, based on similar logic, that natural selection
would often be blind to the effects of mutations that
cause negative effects laid in life after reproduction is mostly stopped.
So let's use another analogy. Imagine a mutation called the
(14:29):
twenty birthday surprise gene, which means that on the day
you turn twenty, carriers of this gene suddenly transform into
a bucket of fishheads and thus lose all ability to reproduce. Now,
this would mean that in order to pass on this gene,
a carrier would have to reproduce before their twentieth birthday.
(14:50):
So kids they have before they're twenty years old could
still carry this gene, but they don't get the chance
to have any kids after their twenty years old, when
plenty of other members of the piece these would continue
having children, all potential reproduction after twenty is canceled, thus
giving people with this gene significantly fewer children on average
than people without it, and so the gene is unlikely
(15:11):
to spread in the population. Now imagine a similar gene.
This is the hundredth birthday surprise gene. Carriers of this gene,
upon the day of their hundredth birthday, suddenly transform into
a VHS copy of Highlander to the Quickening. Okay, and
and and therefore becoming immortal. No, not quite No. The
problem is, well, I guess you you might get to
(15:33):
live somewhat forever on a shelf, but you don't. You
definitely don't get to reproduce after that, right, there's very
little sexual reproduction between copies of Highlander to the Quickening.
But also it doesn't really matter, right because do carriers
of this gene have any fewer children the non carriers
of this gene. The answer is no, right, because who's
(15:54):
still having children at age one hundred Almost nobody. So
even if you have this very unhel helpful gene, you
don't like it that you transform into a VHS tape
on your hundredth birthday. That's not good for you, but
it doesn't matter to how many children you have. It
has no effect on that. So if you have this gene,
you can spread it to all your children, and they
(16:14):
can spread it to all of their children and so,
and they'll all have just as many kids and grandkids
as the neighbors who don't have it. You've already passed
it on by the time it matters. So this would
be the case. Though we we've we've used the Highlander
to transformation as as an example here. But even if
it were something seemingly beneficial, like say a gene made
(16:37):
you suddenly really excellent and talking to members of the
opposite sex at age one hundred, you know, like or
the opposite it made you terrible at a speaking to
the opposite sex at age one hundred, it would still
be the same case, right, yeah, unless the basically the
only thing that would matter would be if it's a
gene that suddenly makes you able to reproduce again. I mean,
(17:00):
if it did that, then that would probably matter. But
as long as you're past the age of reproduction and
you're not having any more children, mutations good or bad
are just going to sort of accumulate randomly without having
any effect Onesoever, natural selection just doesn't pay attention to
them because it never gets to notice them. Well. But
(17:22):
then the other thing too, is that if you're talking
about something that would kick in so late in life
that even people with that gene might never experience it. Right.
It's like if you're playing a role playing game, video
game or what have you, and there's some sort of
like high level ability and you look at it. It
looks great, but you know you're never going to play
the game long enough to get it. Yeah, so what's
the point. Yeah, the game might as well for you
(17:44):
not even have that thing in it. And apparently there
are going to be genetic mutations like that. And this
was Meta WIRs insight. It came to be known, as
you said, as the mutation accumulation hypothesis. Whether reproduction stops
because you die of extra ends it causes. This was
a big thing Meta or had in mind. It's like
we talked about, you know, the wolf gets injured and
(18:05):
can't hunt, the wolf gets sick and dies, the wolf
gets killed by something, whether that happens or because you
age out of your reproductive stage of life for some
other biological reasons. Genes that have negative effects that show
up mostly after reproduction has stopped, are not subject to
the full force of natural selection. So there's not much
(18:26):
preventing the proliferation of genes that harm you in old
age because there's nothing to weed them out, and they
accumulate in the genome over generations by what's known as
genetic drift. And the genetic drift is just the random
dispersing of genes that don't appear to have a very
strong positive or negative effect. So if you've got a
mutation that you acquire for a nasty surprise in old age,
(18:49):
something bad that happens to your body, and you could
look at the process of aging like this, it's just
a large plethora of genetic mutations that cause bad things
to happen to your body. Later on, you can still
pass it on to your kids because you're you've had
all your kids by the time it starts affecting you.
And so these genes can become common in the gene
(19:10):
pool of your species simply because there's nothing stopping them.
So simply put it, the force of selection declines with age.
Mutations that are neutral early in life when selection is strong,
but negative later on, they could accumulate in the population.
I like to think of this as the sack of
kitty litter scoopings in the closet scenario. Okay, explain. But
(19:31):
a friend of mine, when I first met her, she
had a cat box, and then she would scoop the
cat box and it would accumulate in a garbage bag
in the closet. Accumulate me, you mean accumulate as and
she would dump it, yes, in a garbage bag in
the close. And it was. It was a lot cleaner
than this makes it sound, but it was. It was
very much a sort of kicking the can down a
road scenario, like eventually you're gonna have to take that
(19:54):
bag of of of of litter scoopings out, but you're not.
The whole situation is not built on what you're going
to have to do tomorrow. It's about what's happening to today.
But what if you're looking at that closet and you're saying, oh,
there's enough space in here that I could keep scooping
it into the closet until I die of some of
their cause, and then I would never have to take
(20:14):
it out. It would be completely irrelevant. So it can
accumulate forever, just like these deleterious genes can. Okay, So
that's clearly one part of the answer. One part is
that stuff that affects you late in life is just
less likely to get weeded out by natural selection. But
what if there's something more than that. What if maladaptive
genes that manifest in old age aren't just allowed to
(20:36):
roam wild by sort of the careless shepherd of a
natural selection. What if they're positively selected four in some way.
And that's what we'll explore when we come back from
this break than all right, we're back, So now it's
time to talk about antagonistic pleotropy. In a paper in
(20:57):
seven and the journal Evolution, the American Evolutionary by alllogist
George C. Williams had a breakthrough that made metoirs original
hypothesis even stronger and sort of complimented it. And so
this was a paper that I mentioned in part one.
Actually it's the paper called pleotropy, Natural Selection and the
Evolution of sinescence. Williams hypothesis for the evolution of aging
(21:19):
came to be known, as I said, as antagonistic pleotropy.
And what this means is that well. Pleotropy. The word
comes from the Greek roots meaning multiple turns or many effects.
Pleotropy happens when a single gene codes for multiple different
phenotypic effects, meaning effects on the body or effects on
(21:41):
the behavior. So if you had one gene that both
gave you black hair and gave you an extremely long,
pinky fingernail, that would be pleotropy. Or if you had
a gene that made you really tall and also made
you better at learning multiple languages, that would be pleotropy.
(22:01):
And there are lots of examples of this in animals
in the real world. Here's one in chickens. Robert, have
you ever seen the frizzle chickens? Who? I don't know.
I've seen some pretty funny looking chickens before. I've seen
a frizzle chicken. I mean the ones that have like
the curly vegas outfits. Uh yeah, well yeah, I have
seen some of these. These these chickens that have like
(22:22):
a lot of extra feathers around their their talons and all.
The frizzle gene is is a gene in chickens that
causes the feathers to curl up instead of lying flat,
so you get these crazy looking like awesome, beautiful, regal
puffy chickens and they look really cool. But it turns
out this gene also controls several other phenotypic effects. So
(22:43):
if you are a chicken with the frizzle gene, you'll
also have a different metabolic rate and different body temperature
and lay a different number of eggs than the chickens
who don't have this gene. So if you want the
gene for the magnificent curl, you're going to be laying
fewer eggs, among other things. And these are examples where
the situation it feels more like a trade off and
(23:05):
probably has more in common with some of our our myths, right,
because the gift of the god often comes with some
sort of consequence. Yeah, exactly. So another one, just real quick.
In cats, did you know about fort of cats with
white fur and blue eyes are also deaf? I have
heard this one, yes, yeah, odd, So pleotropy can be
(23:26):
like that. It can come in and kind of mixed
blessing form, though I guess I don't actually know if
blue eyes are good for the cat. Maybe that's double bad.
But uh well, you I mean, certainly when you get
into the selective breeding of of a species, you get
into a situation where appearance has has a has a
survival advantage. Yeah, exactly. So pleotropy can go both ways.
(23:47):
One effect of a gene could be good while the
other effect could be bad. And here's where we get
the idea of quote antagonistic pleotropy. A pleotropy that's pulling
in both directions, but usually it'll pull a bit stronger
in one direction than another. So if the good effect
outweighs the bad effect, the gene will spread through the
gene pool. But if the bad effect outweighs the good effect,
(24:09):
the gene will tend to go extinct. That we should
be clear again what's meant by good and bad genes here, Because,
for example, a gene that caused the carrier to experience
intense pain and misery throughout life, but somehow also caused
the carrier to have more healthy children than the average
member of their species would also spread. So it's not
(24:32):
optimizing for like you to have a long life, for
you to have a fun life. It's optimizing for number
of offspring and the success of those offspring. Now, William's
theory of antagonistic pleotropy picks up from this fact, he
hypothesizes that some of the genes that cause aging are
selected for because they have other separate effects that maximize
(24:54):
fitness and reproduction earlier in life, which, like Metawir showed,
is more strongly select did foreign nature. The same genes
that make your skin sag and give you heart disease
in old age might also make you extremely reproductively competitive
when you're young. So here's a really broad example. How
about genes that control the rate of cell division. Yeah,
(25:18):
so a hypothetical gene might be selected for because it
makes cells divide more efficiently. And if cells divide more efficiently,
it means you can rejuvenate tissues and heal wounds and
grow faster when you're young. But the same gene that
causes prolific cell division could potentially be a problem later
in life, because what happens when cells are prone to
(25:39):
divide a whole lot you could be prone to cancer
cancer is runaway cell division. Cells that are not useful
for the body are suddenly being created in great abundance,
which brings us back to the hydrosaur example that we
touched on earlier. Yeah, back in the first episode. Or
you could think about something going exactly the reverse. You
could have a gene that could increase apoptosis signaling, and
(26:02):
apoptosis is programmed cell death, so a gene that causes
cell lines to die off more frequently, and this would
help prevent runaway cell lines from turning into cancer while
you're young. Natural selection obviously would love this because it
would select against organisms that get cancer when they're young
and can't reproduce much. But the exact same gene would
(26:24):
cause tissues to deteriorate more with age because they undergo
more and earlier cell death. And in fact, something like
what I just described has actually been studied. The example
would be the gene at P fifty three. The P
fifty three gene has been implicated in antagonistic pleotropy, and
it's thought that P fifty three protects young animals, including humans,
(26:46):
but I think it's mostly been researched in mice. It
protects these young animals against cancer by interrupting cell proliferation.
It says, now, don't cells don't divide too much now,
But in doing this it can also have the effect
of erupting the proliferation of normal, non cancerous cells like
stem cells, which are the cells the body uses to
(27:06):
rejuvenate tissues over time. So the same gene that play
some role in helping protect against cancer when you're young
also helps play some role in the physical deterioration of
the body with age by preventing it from making new
cells and rejuvenating your tissues and detaining eternal youth. So
(27:26):
the takeaway from this, obviously is that anytime you see
a story about eternal youth in fiction or in a
movie or something like that, imagine these these characters who
are eternally youthful riddled with cancer. It's not really nothing
hard to imagine when you think about all the various
uh uh side effects and caveats that come with eternal
youth in most of our myths and legends, right well,
(27:49):
I mean, yeah, you've got uh. I guess it's not
applicable in the tiffan A story because he doesn't get
eternal youth. He wants to live forever. But you imagine
the equivalent of the tiffan A story where you ask
for eternal youth. So Tiffannus ask for eternal life, or
he doesn't ask Aos ask for eternal life for Titness,
he gets eternal life, but not eternal youth. So it's
the monkeys Paul coming back to bite him. In this story,
(28:10):
you would ask for eternal youth and they say, okay,
here is your eternal youth. But you get lots of
cancer with it. And I think actually have read in
the past that some of these experimental youth extension techniques
that people do research on initially look promising but sometimes
turn out to appear to increase cancer risk. Now here's
another example of a potential antagonistic pleotropy inflammation. So I
(28:34):
want to cite one paper from two thou eight in
Bioscience Trends by Makoto Goto, And in this paper, the
author explores the idea that a lot of the signs
of physical deterioration associated with aging are driven by inflammation.
But inflammation is a defense mechanism for the body. It
helps you survive the redness, the swelling. It's not pleasant,
(28:55):
but all that's part of a primitive immune system response
that protects you against antigens and parasites. So inflammation responses
can help you survive when you're young, but later in life,
inflammation related aging effects cause widespread damage to the body,
including all kinds of diseases from type two diabetes to
rheumatoid arthritis. Also, the kind of military reaction to invasion
(29:22):
that is helpful for the young organism can be a
detriment to the older organism. Correct, exactly right, And so
it's believed now by scientists that there are tons of
things like this in the body. There are genes that
have these antagonistic pleotropy effects. They're good for you when
you're young. They help you survive young adulthood and childhood
(29:42):
and help you have more children early on. But the same,
very same genes having the very same effects also cause
you to age and become sick and reduce your fitness
later on in life, when, as we established earlier, the
force of selection is diminished. So one theory that is
pretty similar to these ones we've just discussed, we've got
(30:04):
metairs mutation accumulation hypothesis, which says, you know, uh, natural
selection doesn't pay much attention to what happens later in life,
so negative mutations can kind of just hang out there
without really being weeded out. Then you've got antagonistic pleotropy,
which says that some of the things that cause negative
effects later in life are positively selected for because those
(30:25):
negative effects later are much outweighed by positive effects early
in life and uh enhancing reproductive fitness early on. So
there's a very similar theory along the same lines called
the disposable soma theory, And this is a theory on
the evolution of aging that was put forward in nineteen
seventy seven by the English biologist Thomas Kirkwood. And this
(30:46):
reframes it as a question of resource investment in the body.
Here's the basic premise. The body has a finite amount
of resources that it can spend on various projects. And
these projects would include things like speeding up reproduction in
the youth and maintaining body tissues. And so if you've
(31:08):
got both of these things and you've got a limited
budget to spend on them, you're gonna need to make choices, right,
how much goes to each one, and indeed which one
is the most important for the biological mission at hand. Right.
And so, drawing on the same logic we looked at earlier,
if you live in a scenario where you don't tend
to live to you know, your natural end of life age,
(31:32):
you tend to get weeded out by things happening to
you in the wild, you know, predation or starvation or
or a disease or injury, anything like that, It will
obviously look to your body like you need to invest
way more in those earlier stages in maximizing reproduction early on,
and so drawing on metawar evolution is going to tend
(31:53):
to favor pouring finite resources into early reproduction optimization instead
of maintaining tissues for an infinite natural lifespan. So I'm
trying to think of a human equivalent. Uh, it sounds
kind of silly, but basically like, should the body spend
its precious limited energy resources keeping your artery walls from
(32:16):
thickening over time or spending them on making you super sexy? Well,
you know, I God knows. I am not an economist,
but I find that when we discussed life cycles of organisms,
or or life cycles of of stars, even I think
of companies and how they work. So it comes down
to a question as as say that the CEO or
(32:38):
even the founder of a company, are you running the
company like you want to retire from it and watch
it continue to prosper as you in your retirement, or
are you running the company like you intend to sell it?
You know or we know what the answer is. In
most cases, yeah, you're you. In many cases you're running
the company because in a way that benefits the short
(33:02):
term sale of the company, or you're leaving this company
for another company. Yeah. I mean people like to have,
you know, sort of like long term investment type rhetoric.
But a lot of people have realized that the smart
strategy for themselves is grab and go, you know, optimize
whatever you can get out of a system for yourself
as soon as possible, and then be on your way.
(33:23):
And that's the equivalent here that this is to say
that you can't even meet guaranteed that it will matter
whether you've got a gene that optimizes against atherosclerosis or not.
But if you can optimize for being real sexy and
having lots of successful reproductive strategies early on in life,
you're pretty much guaranteed a better chance at having more children.
(33:44):
And we have so many different adages that back up
this kind of like personal philosophy and life. Right, you know,
burn it like you've stole it, I believe, not burn
it like you still drive it, like you sto it.
Burn the candle at both ends of his combining the
two there, you know, or burn it like you stole it.
Really you like it's hot, do it? It behooves you
to go ahead and burn it so that they don't
(34:04):
figure out who stole it. Yeah, sees the day. Spend
like there's no tomorrow exactly because sometimes well sometimes there isn't,
or there's there's a finite amount of tomorrow. Sometimes a
leopard will bite your face off. You should just operate
on the assumption that a leopard might bite your face off.
So spend what you've got today. Well, that's good. I
don't know if we'll fit that on a bumper stick
(34:25):
or Now. What we've described so far are I think
what's known as the classical theories of aging. And in
recent years, we should point out some scientists have proposed
various kinds of updates to accommodate new experimental findings. Maybe
in the future we could come back to this topic
again and and explore the most recent developments in in
aging theory. But these are basically I would say, these
(34:48):
classical theories are still pretty much intact. There. You know,
you might need to modify them in some ways to
to update them for newest experimental findings. But for example,
an antagonistic pleotropy. People still basically think that this is
a good explanation for why a lot of the aging
effects we experience take place, and it gives us room
(35:09):
on which to build uh further analysis, Yeah, of course,
and it gives us room to say, if we understand
how a process happens and why it happens, I wonder
if it could be reversed or undone. And of course
there's a lot of that. There's a lot of interest
in this, given that medical research is uniform universally funded
(35:32):
by mortals who and many of them are are interested
and possibly having more life to live or if possible,
you know, an infinite amount, right, So, of course, because
we don't want to age and grow old and sag
and wrinkle and and eventually die, scientists are always working
on ways to beat aging, and some broad evolutionary mechanisms
(35:56):
based on things like fruit fly research are actually known.
But unfortunately they're not the kind of simple medical fixes
that could like be ethically applied to humans. They're they're
evolutionary fixes that you couldn't really implement on purpose. I
mean you could in fruit flies, and researchers have so
what are they, Well, one would be low adult mortality
(36:19):
and high juvenile mortality. If you get a bunch of
fruit flies and you create a scenario such that adults
tend to survive longer than they would in the wild,
while juveniles die very often. What actually happens is that
the life span and the reproductive lifespan of the fruit
(36:41):
flies increases over generations of evolution. And this kind of
makes sense, right if the if the mating pool is
limited to older individuals, genes that favor fitness in later
life will be selected for, and thus these would be
genes that prevent or lay aging, and they'll become more successful. Normally,
(37:03):
evolution wouldn't care about those types of genes very much.
But of course we can't do this to stop human
aging unless we're prepared to like implement a policy that
only people over a certain age can have children and
then keep pushing the minimum age upwards. Obviously we don't
want to do that. Well, even in scenarios like you know,
periods of history in which there is a high mortality
(37:26):
rate for younger people, such as during wars, uh, it's
still I don't think there's any data to back of
the idea. That this would definitely interfere with reproduction because
obviously there there are children that grow up in the
in the wake of war. Now perhaps the father is
not there anymore, but reproduction has been initiated. But then
(37:47):
that's a whole different area of study, like the effects
of war on reproduction and the health of the resulting
offspring um, something we've touched on before on the show,
and we could easily revisit. Oh yeah, that's all interesting stuff.
Another thing to point out about what I just mentioned
about low adult mortality and high juvenile mortality contributing to
extended lifespans. We know this works in fruit flies, but
(38:10):
we can't predict other complicating factors that might stop this
from working another species. Though it does appear to be
pretty general that species that have lower extrinsic mortality evolve
longer lifespans. Like if you've got good defense mechanisms against
predators and disease, or if you just happen to, say,
(38:30):
end up on an island where you don't have many
predators or diseases, you will probably evolve over a long
period of time to breed longer and live longer. Think
about the Great Wizzen tortoises of the Galapagos. They've got
a shell, they don't have really natural predators, and they've
got these long, long lifespans because the adults and the
(38:51):
old adults can just keep on breeding. And they probably
had a fair amount of moisture. I think Aristotle would
Aristotle was onto something. Yeah, No, they don't have moisture
at all. They look so dry. Those tortoises are like
the driest looking creatures I can think of, But they
live in a moist environment. Maybe that's it. That is true,
But okay, So looking at more like potentially ethical medical fixes,
(39:15):
are there things researchers are working on in order to
beat aging and humans? Well, the answer is obviously yes.
There are plenty of questions about whether these projects are
actually a good idea, and even if they are a
good idea, whether they could be successful in principle, but
there are plenty people working on it. One example, of course,
(39:36):
is the gerontologist and author Aubrey de Gray. He's made
a whole career out of the idea, going around promoting
that we can and should be trying to completely defeat
the process of aging, and that we can do it
within the next few decades. Yeah, he's everyone's probably seen
images of de Gray before he has his big wizard's beard,
and he's resputant. Yeah, he shows up in all sorts
(39:57):
of He doesn't hate respute if he shows up in
very it's a documentary is about this topic all the time. Uh.
And his his basic argument is, I think rather ingenious.
It's instead of viewing aging and death as this unbeatable war,
you know, this this unbeatable um problem, it's like, break
it up into smaller battles, smaller problems that you can win,
(40:19):
that you can solve. Yeah, and I think this is
the key appeal of his approach. He says, aging is
not one thing, it's maybe seven things. Yes. For instance,
the problem might be cells die off and are naturally
replaced in the heart or in the brain, and he says, well,
you stem cell replacement for dying cells. Or another example
would be the body undergoes a proliferation of unwanted cells,
(40:41):
such as fat cells that replace muscle and lead to diabetes.
He says, we'll trick the problem cells into self destruction
through suicide, gene therapy, this sort of thing. So it's
it's taking taking the overall problem breaking it down into
little individual problems that you could potentially solve through medical
intervention and genetic engineering, etcetera. Now, for people who are
(41:02):
interested in avoiding aging, obviously this message is very appealing. Yes,
but there are also we should mention many researchers who
find degrees program unrealistic. Like he has plenty of critics. Well,
on one level, it's kind of the basic trans anti
transhumanist argument, right like if okay, if you break down
(41:23):
essentially immortality into a number of different treatment options that
are available, than then who are they available to? Who
has access to these treatments? And then it becomes this, uh,
this this inequality situation where you have the very dystopian
idea of the super rich individuals who can afford all
of the various treatments that that keep their unnatural lives
(41:44):
going while the rest of us simply live and die
as always. I would say the answer to that critique
is not that you shouldn't develop the medical technologies, but
that you should find ways to make them available to everyone.
Then again, you do have that intrinsic question of whether
it's actual good to allow any member of a species
to be biologically immortal. Uh, to keep on living in
(42:05):
consuming resources beyond what would what would normally be allotted
to them in a normal lifespan, because, as we talked
about earlier on, there's this whole good of the species argument.
Your genes might not care about the good of the species,
but you should, right, we should. Well, it's an easy
argument for for for us to make. But then again,
we're not a hundred and fifty years old and hooked
(42:26):
up to the immortality machine. Right. Well, once your time comes,
you will probably change your tune. Right, It's like, no,
give me a little more. I just need a little more,
one more year. Um. But then again, yeah, so that's
like the question of whether we should be trying to
achieve biological immortality. There's also this question that many scientists
have have brought up, which is that his program is unrealistic,
(42:48):
not necessarily that it's a bad idea, but that you
you can't extend aging for or not extend. You can't
extend youth forever. They're just gonna be hard physical limits
that you're going to hit within the human body. Just
one example of that strain of thinking as a paper
that came out earlier this year in published by the
Proceedings of the National Academy of Science is called Intercellular
(43:11):
Competition and the Inevitability of Multicellular Aging. So this study
was conducted by scientists Joanna Massel and Paul Nelson, and
Massel and Nelson use mathematical models to argue that essentially,
no matter what you do, you will be faced with
one facet of aging or another, and the main tension
(43:32):
they highlight is tissue deterioration or cancer, one or the other.
It's a mathematical inevitability. They say. If you find a
way to prevent cancer, tissues deteriorate and cells become less efficient,
you get the body breaking down. If you find a
way to rejuvenate tissues, beef them up, make them youthful again,
(43:52):
you get cancer. Age is going to get you one
way or another. It's like we're in that trolley car, right.
We have attracts diverging to two unwanted fates in a
sense equally unwanted fates, and we have to try and
figure out, well, which way we're gonna go, What are
we going to plow into. I feel like this should
be reimagined as a myth, like going back to Tiffanus,
(44:13):
like I want the gods gods that represent one represents
cancer and one represents the deterioration of body tissues. And
they're like at war and you have to choose between
your fate with one or the other. Yeah. I like that. Yeah,
this is this is where our modern day gods can
jump in and and provide us the story to make
(44:35):
sense of our our doom. Okay, well, I guess that
wraps it up for for part two of this episode
about why we age and why we can't have eternal youth. Yeah. Well,
and I don't want to leave it on too dark
of a note there with the doom talk, because I mean, ultimately,
I guess here's the here's the silver lining. Uh, Aging,
even dying, everybody does it. It can be. It couldn't
(44:58):
be that much to it, right, look at the people
who do it. It It couldn't be. It couldn't be that difficult,
It couldn't be that hard to go through. Well, I mean,
it's easy to get down when you spend a lot
of time thinking about the inevitability of aging and death.
But um, I mean the thing to think about is, yeah,
it comes to everybody. It's a part of life, and
there's a lot of life to love. Yeah, and it
(45:18):
bears your minding that there is a lot of stuff
you can do in the in the near future to
make your your far future a little more easy going.
You know, you can look after the body you have.
You can uh, you know, exercise and try to eat right.
I think I saw a study saying you need to
eat a bunch of chocolate to make it. I think
that's what it was. Well, then that's the other side too,
(45:41):
is like you're gonna grow a hold, You're going to die.
You can't just spend your whole time worrying over that inevitability,
So you might as well have some chocolate, you might
as Oh no, I mean I was joking about those
articles that actually say chocolate will make you live longer.
Oh okay, not just the ones where there's like a
new study out that points to uh some beneficial quality
(46:02):
of like pure unsweetened chocolate. Uh yeah, I mean it's
it's always couched in, like eat chocolate to be healthier. Well,
if it's not couched in it, That's how I think
sometimes we interpret it. We read the study and we're like, well, good,
I like chocolate, or I like red wine or I
like coffee, and now I can just continue to enjoy
the things that make my life more bearable and uh,
(46:22):
and not worry about what they might be doing too.
Anytime you read an article about the one silver bullet
thing to eat or to drink that will make you
live forever, don't believe it. I agree, unless that one
silver bullet thing is the quickening which will work? Can
the quickening be transferred to another though I'm a little
shaky on my my quickening science. I don't know. We'll
(46:45):
have to come back to that. What's the quickening conversion rate?
I don't know. I think you just have to be
from the planet's ice, right remember? Hold? All right, Well
there you go. Uh again, this was a two parter.
If somehow you made it through all the parts two
without listening to part one, go back and listen to
part one. You will find it in all other episodes
of Stuff to Blow your Mind at Stuff to Blow
your Mind dot Com, and you'll get our moisture jokes.
(47:07):
That's right, and hey, while you're stuff to Blow your
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(47:27):
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(47:50):
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