January 9, 2018 • 47 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 and Joe seek to find out in this two-part Stuff to Blow Your Mind exploration.
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Speaker 1 (00:03):
Welcome to Stuff to Blow your Mind from how Stuff
Works 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 be young and
(00:23):
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 not always strive with man,
(00:45):
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, you know,
(01:06):
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 too certain cuts they are not from Earth in
the good cuts. They're not 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
(01:26):
episode 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,
(01:48):
and 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
(02:11):
should be 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.
(02:34):
But look at the forms that 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
(02:56):
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
(03:19):
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
(03:44):
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'd 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 and to a
number of our different dystopian views of the future, as
does the possibility of immortality becoming an option at least
(04:07):
a 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 reigns of life
so that others may grasp it. Right, Well, as much
as we don't personally want to grow old and die,
(04:28):
you can sort 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, yeah,
unless it's me or someone that I'm investing, 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
(04:49):
and die, and 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.
(05:10):
And here's an example to illustrate one of the big
problems in why these good of the group explanations failed
to hold up. Alright, 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
(05:31):
space marines in the Warhammer forty K universe that 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
(05:54):
wolves living on 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.
(06:17):
So unless 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
(06:41):
mutation that allows her to stay fertile and survive for
twelve years instead of ten, So she has twelve of
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 x
pups each have twelve pups, while non carriers of the
(07:03):
gene 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,
(07:25):
this won't really cause a reselection towards shorter lifespans, because
how would it. Instead, what it would do is optimize
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 is
(07:46):
a really common type of argument against good of the
group and good of the species explanations and evolution, because
any mutation that cheats on the stasis you've created for
the good of the group will tend to start to
at 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 you
(08:08):
have a you know, an academic environment where everybody's cheating
on the exam. Need the grading becomes that much harder
each and every time. It's true. Yeah, it's great. So
it's like you got a 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
(08:28):
mean that there is not such a thing as the
good of the group and 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.
(08:51):
Magines 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
(09:13):
perfect youth and vigor until something extrinsic happens, until we
get killed by a hemorrhagic fever or tractor accident. Alright,
we're gonna take a quick break and we come back.
We will answer that very question. Thank alright, we're back.
Al right. So, there are a number of modern, well
accepted scientific theories trying to answer the question of why
(09:36):
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 zoo
(10:00):
's 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,
(10:22):
so you starve. If you are a wolf living in
the wild, and you survive the first year of your life,
one of these things like injury or disease or starvation
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,
(10:43):
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
(11:05):
use 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
(11:28):
don't 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 reminds me of some of these various programs that
(11:49):
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 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 the situation
(12:12):
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 sinescence 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 they get
(12:32):
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 age twenty
(12:56):
or at age ten, evolution is going to be very strong,
only selecting four 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 happens
(13:17):
in old age, much less optimize it. Uh, 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
(13:38):
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
(14:01):
twenty birthday surprise gene, which means that on the day
you turn twenty, carriers of this gene suddenly transform into
a bucket of fish heads 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, So kids they have before they're
(14:23):
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
species 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 to spread in the population. Now imagine
(14:46):
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 more No,
not quite No. The problem is, well, I guess you
you might get to live somewhat forever on a shelf,
(15:06):
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 still having children at age one hundred? Almost nobody.
(15:30):
So even if you have this very unhelpful 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
can spread it to all of their children and so,
and they'll all have just as many kids and grandkids
(15:52):
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
you suddenly really excellent and talking to members of the
(16:13):
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,
if it did that, then that would probably matter. But
(16:35):
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
but then the other thing too, is that if you're
(16:56):
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 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
(17:16):
not even have that thing in it. And apparently there
are going to be genetic mutations like that. And this
was Meta Wars insight. It came to be known, as
you said, as the mutation accumulation hypothesis. Whether reproduction stops
because you die of extrinsic causes. This was a big
thing Meta where had in mind. It's like we talked about,
you know, the wolf gets injured and can't hunt, the
(17:37):
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 preventing the proliferation of
(17:59):
gene 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, something bad that happens
(18:22):
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 pool of your species simply because
(18:43):
there's nothing stopping them. So simply put it in. 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 school things
in the closet scenario. What, okay, explain, but a friend
(19:04):
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 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
(19:25):
gonna have to take that 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 it out.
(19:46):
It would be completely irrelevant. So it can accumulate forever,
just like these deleterious Janes 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 roam wild
(20:09):
by sort of the careless shepherd of natural selection. What
if they're positively selected for in some way, and that's
what we'll explore when we come back from this break.
Thank thank all right, we're back. So now it's time
to talk about antagonistic pleotropy. In a paper in N
seven and the journal Evolution, the American evolutionary biologist George C.
(20:32):
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 came to be known,
as I said, as antagonistic pleotropy. And what this means
(20:55):
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 the behavior. So
if you had one gene that both gave you black
(21:18):
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. 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
(21:39):
frizzle chickens? Who? I don't know. I've seen some pretty
funny looking chickens before 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 a lot of extra feathers around their their
talents and all. The frizzle gene is is a gene
in chicken that causes the feathers to curl up instead
(22:02):
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
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
(22:24):
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
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
(22:48):
quick in cats, did you know about cats with white
fur and blue eyes are also deaf? I have heard
this one, yes, yeah, odd. So pleotropy can be like that.
It can come and it 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
(23:11):
a situation where appearance has has has a survival advantage.
Yeah exactly. So pleotropy can go both ways. 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
(23:33):
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, 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
(23:58):
to have more healthy children than the average member of
their species would also spread. So it's not optimizing for
like you to have a long life, for you to
have a fun life. It's optimizing for a number of
offspring and the success of those offspring. Now, William's theory
of antagonistic pleotropy picks up from this fact. He hypothesizes
(24:19):
that some of the genes that cause aging are selected
for because they have other separate effects that maximize fitness
and reproduction earlier in life, which, like metair showed, is
more strongly selected for in 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
(24:42):
you're young. So here's a really broad example. How about
genes that control the rate of cell division. Yeah, 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 he wounds and
grow faster when you're young. But the same gene that
(25:04):
causes prolific cell division could potentially be a problem later
in life because what happens when cells are prone to
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 Hadross or example that
(25:24):
we touched on earlier. Yeah, back in the first episode,
or you can think about something going exactly the reverse.
You could have a gene that could increase apoptosis signaling,
and apoptosis is programmed cell death, so a gene that
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
(25:48):
because it would select against organisms that get cancer when
they're young and can't reproduce much. But the exact same
gene would 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.
(26:10):
The P fifty three gene has been implicated in antagonistic pleotropy,
and it's thought that P fifty three protects young animals,
including humans, 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
(26:31):
of interrupting the proliferation of normal, non cancerous cells, like
stem cells, which are the cells the body uses to
rejuvenate tissues over time. So the same gene that plays
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
(26:53):
cells and rejuvenating your tissues and detaining eternal youth. So
the takeaway from this obviously 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 not that
hard to imagine when you think about all the various
(27:14):
uh uh side effects and caveats that come with eternal
youth in most of our myths and legends. Right well,
I mean, yeah, you've got uh. I guess it's not
applicable in the Tiffannas story because he doesn't get eternal youth.
He wants to live forever. But you imagine the equivalent
of the Tiffanas story where you ask for eternal youth.
So Tiffanus asked for eternal life, or he doesn't ask
Aos asked for eternal life. For Tithness. He gets eternal life,
(27:37):
but not eternal youth. So it's the monkeys Paul coming
back to bite him. In this story. You would ask
for eternal youth and they say, okay, here's 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
(27:59):
increase answer risk. Now here's another example of a potential
antagonistic pleotropy inflammation. So I want to cite one paper
from two thousand eight in Bioscience Trends by Makoto Godo,
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
(28:22):
mechanism for the body. It helps you survive the redness,
the swelling. It's not pleasant, 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,
(28:45):
from type two diabetes to rheumatoid arthritis. As the kind
of military reaction to invasion that is helpful for the
young organism can be a detriment to the older or
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.
(29:09):
They're good for you when you're young. They help you
survive young adulthood and childhood, 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.
(29:31):
So one more theory that is pretty similar to these
ones we've just discussed. We've got 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
(29:52):
some of the things that cause negative effects later in
life are positively selected for because those negative effects later
are much outweighed by positive of 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
(30:14):
by the English biologist Thomas Kirkwood. And this 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
(30:35):
youth and maintaining body tissues. And so if you've 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,
(30:56):
if you live in a scenario where you don't tend
to live to you know, your natural end of life age,
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
(31:18):
way more in those earlier stages in maximizing reproduction early on.
And so, drawing on metal war, evolution is going to
tend 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
(31:39):
sounds kind of silly, but basically like, should the body
spend its precious limited energy resources keeping your artery walls
from 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 it when we discussed
(32:00):
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 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
(32:22):
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 in
a way that benefits the short 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
(32:44):
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, And that's the equivalent here
that this is to say that you can't even be
guaranteed that it will matter or whether you've got a
gene that optimizes against atherosclerosis or not. But if you
(33:05):
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. 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. Burn the candle at both ends.
(33:27):
That was combining the two there, you know. Or burn
it like you stole it, really like it's hot it
It behooves you to go ahead and burn it so
that they don't figure out you 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.
(33:48):
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 sticker, though. You 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
(34:08):
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 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.
(34:28):
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 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,
(34:51):
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 search is uniform
universally funded by mortals, right who and many of them
are are interested and possibly having more life to live
(35:13):
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 based on things like fruit fly research
are actually known. But unfortunately they're not the kind of
(35:33):
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 and high juvenile mortality if you get a bunch
(35:54):
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
flies increases over generations of evolution. And this kind of
(36:17):
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 delay aging, and they will become
more successful. Normally, evolution wouldn't care about those types of
genes very much. But of course we can't do this
(36:40):
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 rate for younger people, such as
during wars. Uh, it's still I don't think there's any
(37:03):
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 that's a whole different area of study,
like the effects of war on reproduction and the health
(37:24):
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 we can't predict other complicating factors
(37:45):
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, end up on an island where
you don't have many predators or diseases, you will probably
(38:07):
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 old adults can just keep on breeding.
And they probably have, you know, a fair amount of moisture.
(38:28):
I think 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, are there things researchers are working
(38:49):
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 of people working
on it. One example, of course, is the gerontologist and
author Aubrey de Gray. He's made a whole career out
(39:11):
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 this big wizard's beard and he's resput and yeah,
he shows up in all sorts of he doesn't hate respute.
He shows up in various documentaries about this topic all
(39:33):
the time. Uh. And his his basic argument is, I think,
rather than genius, it's instead of viewing aging and death
as this unbeatable war, you know, this this unbeatable um
um problem, it's like, break it up into smaller battles,
smaller problems that you can win. You can solve. Yeah,
And I think this is the key appeal of his approach.
(39:56):
He says, aging is not one thing, it's maybe seven things. Us.
For instance, the problem might be cells die off and
are naturally replaced in the heart or in the brain,
and he says, well, use stem cell replacement for dying cells.
Or another example would be the body undergoes a proliferation
of unwanted cells, such as fat cells that replace muscle
and lead to diabetes. He says, we'll trick the problem
(40:17):
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, genetic engineering, etcetera. Now, for
people who are interested in avoiding aging, obviously this message
is very appealing, Yes, but there are also we should
(40:40):
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 essentially immortality into a number of
different treatment options that are available, then then who are
they available to who has access to these treatments. And
(41:04):
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 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
(41:26):
to make them available to everyone. Then again, you do
have that intrinsic question of whether it's actually good to
allow any member of a species to be biologically immortal, uh,
to keep on living and 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
(41:48):
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 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 yea um. But then again, yeah,
(42:09):
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, not necessarily that it's a bad idea,
but that you you can't extend aging or not extend.
You can't extend youth forever. They're just gonna be hard
physical limits that you're gonna hit within the human body.
(42:32):
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 Competition and the Inevitability of Multicellular Agent. So this
study was conducted by UH scientists Joanna Massel and Paul Nelson,
and Massel and Nelson use mathematical models to argue that essentially,
(42:56):
no matter what you do, you will be faced with
one facet of aging or another, and the main tension
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.
(43:17):
You get the body breaking down. If you find a
way to rejuvenate tissues, beef them up, make them youthful again,
you get cancer. Age is gonna get you one way
or another. It's like we're in that trolley car, right.
We have the tracks diverging to two unwanted fates in
a sense equally unwanted fates, and we have to try
(43:37):
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,
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
(43:58):
your fate with one or the other. Uh I like that? Yeah,
this is this is where our modern day gods can
jump in and and provide us the story to make
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 whole doom talk, because
(44:20):
I mean, ultimately, I guess here's the here's the silver lining. Uh, Aging,
even dying, everybody does it. It couldn't be. It couldn't
be that much to it, right, look at the people
who do it. It It couldn't be. It couldn't be that difficult,
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.
(44:41):
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
bears reminding 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,
(45:03):
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, and I think that's
what it was. Well, then that's the other side too,
is like you're gonna grow ahold, 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
(45:23):
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
of like pure unsweetened chocolate. Uh yeah, I mean it's
it's always couched and 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
(45:44):
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 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,
(46:05):
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 on my my quickening science.
I don't know. We'll 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?
All right, well there you go. Uh again, this was
(46:27):
a two parter. If somehow you made it through all
of part 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
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to Blow your Mind dot Com, you will also find
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(46:50):
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us at blow the Mind at how stuff Works dot
(47:11):
com for more on this and thousands of other topics.
Does it how stuff works dot Com
Welcome to Stuff to Blow your Mind from how Stuff
Works 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 be young and
(00:23):
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 not always strive with man,
(00:45):
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, you know,
(01:06):
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 too certain cuts they are not from Earth in
the good cuts. They're not 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
(01:26):
episode 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,
(01:48):
and 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
(02:11):
should be 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.
(02:34):
But look at the forms that 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
(02:56):
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
(03:19):
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
(03:44):
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'd 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 and to a
number of our different dystopian views of the future, as
does the possibility of immortality becoming an option at least
(04:07):
a 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 reigns of life
so that others may grasp it. Right, Well, as much
as we don't personally want to grow old and die,
(04:28):
you can sort 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, yeah,
unless it's me or someone that I'm investing, 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
(04:49):
and die, and 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.
(05:10):
And here's an example to illustrate one of the big
problems in why these good of the group explanations failed
to hold up. Alright, 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
(05:31):
space marines in the Warhammer forty K universe that 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
(05:54):
wolves living on 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.
(06:17):
So unless 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
(06:41):
mutation that allows her to stay fertile and survive for
twelve years instead of ten, So she has twelve of
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 x
pups each have twelve pups, while non carriers of the
(07:03):
gene 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,
(07:25):
this won't really cause a reselection towards shorter lifespans, because
how would it. Instead, what it would do is optimize
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 is
(07:46):
a really common type of argument against good of the
group and good of the species explanations and evolution, because
any mutation that cheats on the stasis you've created for
the good of the group will tend to start to
at 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 you
(08:08):
have a you know, an academic environment where everybody's cheating
on the exam. Need the grading becomes that much harder
each and every time. It's true. Yeah, it's great. So
it's like you got a 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
(08:28):
mean that there is not such a thing as the
good of the group and 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.
(08:51):
Magines 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
(09:13):
perfect youth and vigor until something extrinsic happens, until we
get killed by a hemorrhagic fever or tractor accident. Alright,
we're gonna take a quick break and we come back.
We will answer that very question. Thank alright, we're back.
Al right. So, there are a number of modern, well
accepted scientific theories trying to answer the question of why
(09:36):
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 zoo
(10:00):
's 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,
(10:22):
so you starve. If you are a wolf living in
the wild, and you survive the first year of your life,
one of these things like injury or disease or starvation
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,
(10:43):
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
(11:05):
use 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
(11:28):
don't 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 reminds me of some of these various programs that
(11:49):
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 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 the situation
(12:12):
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 sinescence 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 they get
(12:32):
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 age twenty
(12:56):
or at age ten, evolution is going to be very strong,
only selecting four 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 happens
(13:17):
in old age, much less optimize it. Uh, 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
(13:38):
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
(14:01):
twenty birthday surprise gene, which means that on the day
you turn twenty, carriers of this gene suddenly transform into
a bucket of fish heads 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, So kids they have before they're
(14:23):
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
species 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 to spread in the population. Now imagine
(14:46):
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 more No,
not quite No. The problem is, well, I guess you
you might get to live somewhat forever on a shelf,
(15:06):
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 still having children at age one hundred? Almost nobody.
(15:30):
So even if you have this very unhelpful 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
can spread it to all of their children and so,
and they'll all have just as many kids and grandkids
(15:52):
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
you suddenly really excellent and talking to members of the
(16:13):
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,
if it did that, then that would probably matter. But
(16:35):
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
but then the other thing too, is that if you're
(16:56):
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 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
(17:16):
not even have that thing in it. And apparently there
are going to be genetic mutations like that. And this
was Meta Wars insight. It came to be known, as
you said, as the mutation accumulation hypothesis. Whether reproduction stops
because you die of extrinsic causes. This was a big
thing Meta where had in mind. It's like we talked about,
you know, the wolf gets injured and can't hunt, the
(17:37):
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 preventing the proliferation of
(17:59):
gene 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, something bad that happens
(18:22):
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 pool of your species simply because
(18:43):
there's nothing stopping them. So simply put it in. 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 school things
in the closet scenario. What, okay, explain, but a friend
(19:04):
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 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
(19:25):
gonna have to take that 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 it out.
(19:46):
It would be completely irrelevant. So it can accumulate forever,
just like these deleterious Janes 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 roam wild
(20:09):
by sort of the careless shepherd of natural selection. What
if they're positively selected for in some way, and that's
what we'll explore when we come back from this break.
Thank thank all right, we're back. So now it's time
to talk about antagonistic pleotropy. In a paper in N
seven and the journal Evolution, the American evolutionary biologist George C.
(20:32):
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 came to be known,
as I said, as antagonistic pleotropy. And what this means
(20:55):
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 the behavior. So
if you had one gene that both gave you black
(21:18):
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. 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
(21:39):
frizzle chickens? Who? I don't know. I've seen some pretty
funny looking chickens before 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 a lot of extra feathers around their their
talents and all. The frizzle gene is is a gene
in chicken that causes the feathers to curl up instead
(22:02):
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
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
(22:24):
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
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
(22:48):
quick in cats, did you know about cats with white
fur and blue eyes are also deaf? I have heard
this one, yes, yeah, odd. So pleotropy can be like that.
It can come and it 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
(23:11):
a situation where appearance has has has a survival advantage.
Yeah exactly. So pleotropy can go both ways. 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
(23:33):
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, 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
(23:58):
to have more healthy children than the average member of
their species would also spread. So it's not optimizing for
like you to have a long life, for you to
have a fun life. It's optimizing for a number of
offspring and the success of those offspring. Now, William's theory
of antagonistic pleotropy picks up from this fact. He hypothesizes
(24:19):
that some of the genes that cause aging are selected
for because they have other separate effects that maximize fitness
and reproduction earlier in life, which, like metair showed, is
more strongly selected for in 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
(24:42):
you're young. So here's a really broad example. How about
genes that control the rate of cell division. Yeah, 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 he wounds and
grow faster when you're young. But the same gene that
(25:04):
causes prolific cell division could potentially be a problem later
in life because what happens when cells are prone to
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 Hadross or example that
(25:24):
we touched on earlier. Yeah, back in the first episode,
or you can think about something going exactly the reverse.
You could have a gene that could increase apoptosis signaling,
and apoptosis is programmed cell death, so a gene that
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
(25:48):
because it would select against organisms that get cancer when
they're young and can't reproduce much. But the exact same
gene would 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.
(26:10):
The P fifty three gene has been implicated in antagonistic pleotropy,
and it's thought that P fifty three protects young animals,
including humans, 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
(26:31):
of interrupting the proliferation of normal, non cancerous cells, like
stem cells, which are the cells the body uses to
rejuvenate tissues over time. So the same gene that plays
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
(26:53):
cells and rejuvenating your tissues and detaining eternal youth. So
the takeaway from this obviously 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 not that
hard to imagine when you think about all the various
(27:14):
uh uh side effects and caveats that come with eternal
youth in most of our myths and legends. Right well,
I mean, yeah, you've got uh. I guess it's not
applicable in the Tiffannas story because he doesn't get eternal youth.
He wants to live forever. But you imagine the equivalent
of the Tiffanas story where you ask for eternal youth.
So Tiffanus asked for eternal life, or he doesn't ask
Aos asked for eternal life. For Tithness. He gets eternal life,
(27:37):
but not eternal youth. So it's the monkeys Paul coming
back to bite him. In this story. You would ask
for eternal youth and they say, okay, here's 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
(27:59):
increase answer risk. Now here's another example of a potential
antagonistic pleotropy inflammation. So I want to cite one paper
from two thousand eight in Bioscience Trends by Makoto Godo,
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
(28:22):
mechanism for the body. It helps you survive the redness,
the swelling. It's not pleasant, 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,
(28:45):
from type two diabetes to rheumatoid arthritis. As the kind
of military reaction to invasion that is helpful for the
young organism can be a detriment to the older or
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.
(29:09):
They're good for you when you're young. They help you
survive young adulthood and childhood, 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.
(29:31):
So one more theory that is pretty similar to these
ones we've just discussed. We've got 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
(29:52):
some of the things that cause negative effects later in
life are positively selected for because those negative effects later
are much outweighed by positive of 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
(30:14):
by the English biologist Thomas Kirkwood. And this 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
(30:35):
youth and maintaining body tissues. And so if you've 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,
(30:56):
if you live in a scenario where you don't tend
to live to you know, your natural end of life age,
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
(31:18):
way more in those earlier stages in maximizing reproduction early on.
And so, drawing on metal war, evolution is going to
tend 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
(31:39):
sounds kind of silly, but basically like, should the body
spend its precious limited energy resources keeping your artery walls
from 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 it when we discussed
(32:00):
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 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
(32:22):
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 in
a way that benefits the short 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
(32:44):
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, And that's the equivalent here
that this is to say that you can't even be
guaranteed that it will matter or whether you've got a
gene that optimizes against atherosclerosis or not. But if you
(33:05):
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. 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. Burn the candle at both ends.
(33:27):
That was combining the two there, you know. Or burn
it like you stole it, really like it's hot it
It behooves you to go ahead and burn it so
that they don't figure out you 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.
(33:48):
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 sticker, though. You 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
(34:08):
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 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.
(34:28):
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 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,
(34:51):
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 search is uniform
universally funded by mortals, right who and many of them
are are interested and possibly having more life to live
(35:13):
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 based on things like fruit fly research
are actually known. But unfortunately they're not the kind of
(35:33):
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 and high juvenile mortality if you get a bunch
(35:54):
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
flies increases over generations of evolution. And this kind of
(36:17):
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 delay aging, and they will become
more successful. Normally, evolution wouldn't care about those types of
genes very much. But of course we can't do this
(36:40):
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 rate for younger people, such as
during wars. Uh, it's still I don't think there's any
(37:03):
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 that's a whole different area of study,
like the effects of war on reproduction and the health
(37:24):
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 we can't predict other complicating factors
(37:45):
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, end up on an island where
you don't have many predators or diseases, you will probably
(38:07):
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 old adults can just keep on breeding.
And they probably have, you know, a fair amount of moisture.
(38:28):
I think 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, are there things researchers are working
(38:49):
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 of people working
on it. One example, of course, is the gerontologist and
author Aubrey de Gray. He's made a whole career out
(39:11):
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 this big wizard's beard and he's resput and yeah,
he shows up in all sorts of he doesn't hate respute.
He shows up in various documentaries about this topic all
(39:33):
the time. Uh. And his his basic argument is, I think,
rather than genius, it's instead of viewing aging and death
as this unbeatable war, you know, this this unbeatable um
um problem, it's like, break it up into smaller battles,
smaller problems that you can win. You can solve. Yeah,
And I think this is the key appeal of his approach.
(39:56):
He says, aging is not one thing, it's maybe seven things. Us.
For instance, the problem might be cells die off and
are naturally replaced in the heart or in the brain,
and he says, well, use stem cell replacement for dying cells.
Or another example would be the body undergoes a proliferation
of unwanted cells, such as fat cells that replace muscle
and lead to diabetes. He says, we'll trick the problem
(40:17):
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, genetic engineering, etcetera. Now, for
people who are interested in avoiding aging, obviously this message
is very appealing, Yes, but there are also we should
(40:40):
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 essentially immortality into a number of
different treatment options that are available, then then who are
they available to who has access to these treatments. And
(41:04):
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 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
(41:26):
to make them available to everyone. Then again, you do
have that intrinsic question of whether it's actually good to
allow any member of a species to be biologically immortal, uh,
to keep on living and 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
(41:48):
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 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 yea um. But then again, yeah,
(42:09):
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, not necessarily that it's a bad idea,
but that you you can't extend aging or not extend.
You can't extend youth forever. They're just gonna be hard
physical limits that you're gonna hit within the human body.
(42:32):
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 Competition and the Inevitability of Multicellular Agent. So this
study was conducted by UH scientists Joanna Massel and Paul Nelson,
and Massel and Nelson use mathematical models to argue that essentially,
(42:56):
no matter what you do, you will be faced with
one facet of aging or another, and the main tension
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.
(43:17):
You get the body breaking down. If you find a
way to rejuvenate tissues, beef them up, make them youthful again,
you get cancer. Age is gonna get you one way
or another. It's like we're in that trolley car, right.
We have the tracks diverging to two unwanted fates in
a sense equally unwanted fates, and we have to try
(43:37):
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,
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
(43:58):
your fate with one or the other. Uh I like that? Yeah,
this is this is where our modern day gods can
jump in and and provide us the story to make
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 whole doom talk, because
(44:20):
I mean, ultimately, I guess here's the here's the silver lining. Uh, Aging,
even dying, everybody does it. It couldn't be. It couldn't
be that much to it, right, look at the people
who do it. It It couldn't be. It couldn't be that difficult,
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.
(44:41):
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
bears reminding 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,
(45:03):
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, and I think that's
what it was. Well, then that's the other side too,
is like you're gonna grow ahold, 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
(45:23):
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
of like pure unsweetened chocolate. Uh yeah, I mean it's
it's always couched and 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
(45:44):
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 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,
(46:05):
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 on my my quickening science.
I don't know. We'll 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?
All right, well there you go. Uh again, this was
(46:27):
a two parter. If somehow you made it through all
of part 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
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to Blow your Mind dot Com, you will also find
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(46:50):
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(47:11):
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