Ep 101 Immortality: This Podcast Won't Kill You

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

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Episode Transcript

Speaker 1 (00:02):
Hi everyone. Aaron here you are about to listen to
a very exciting episode on immortality. And this episode is
not just exciting because of the topic, but also because
it was going to be our one hundredth regular season episode.
But when things with monkeypox started to ramp up, we

(00:23):
decided that we wanted to make sure that we got
a monkey pox's episode out to you as quickly as possible,
and that meant pushing back this immortality episode, which we
had actually recorded before monkey pocks. So throughout this episode
you may hear references to this being our one hundredth episode,
even though it's actually episode one hundred and one, and

(00:46):
we just wanted to explain why in advance. Okay, I
think that about covers it, So let's get started introducing immortality.
The life that you seek you never will find. When
the gods created mankind death, they dispensed to mankind life
they kept for themselves. But you, Gilgamesh, Let your belly

(01:10):
be full, enjoy yourself always by day and by night.
Make mary each day, dance and play day and night.
Let your clothes be clean, Let your head be washed.
May you bathe in water. Gaze on the child who
holds your hand. Let your wife enjoy your repeated embrace.

Speaker 2 (02:14):
I still don't actually know the story of Gilgamesh.

Speaker 1 (02:19):
I still only know a little part of the story
of Gilgamesh. So yes, that was from the epic of Gilgamesh,
which is one of the oldest I think actually the
considered the oldest like surviving document or text.

Speaker 2 (02:37):
Wow, that's amazing.

Speaker 1 (02:39):
Yeah, yeah, it's from a long time ago, like two
thousand BCE something like that.

Speaker 2 (02:46):
Wow.

Speaker 1 (02:47):
Yeah. Hi, I'm Aaron Welsh.

Speaker 2 (02:50):
And I'm Aaron Allman Updike.

Speaker 1 (02:53):
And this is this podcast will kill you.

Speaker 2 (02:55):
And today we're not just like reading you the story
of Gilgamesh.

Speaker 1 (03:00):
That's most of what you'll hear about Yogamesh.

Speaker 2 (03:05):
Today, we're doing something very different in honor of our
one hundredth episode.

Speaker 1 (03:11):
One hundredth I mean it is. I can't believe it.

Speaker 2 (03:15):
I never would have thought we could make one hundred
episodes of a podcast, Darin either.

Speaker 1 (03:21):
And Okay, here's the thing is that, like technically we
surpassed one hundred a long time.

Speaker 2 (03:27):
That's true. I forgot about that with.

Speaker 1 (03:29):
Like all the COVID episodes and all the bonus one
bonus episodes. Yeah, still, this is this is our like
our title episode one hundred, Yeah, and I think in
honor of that, as we slowly get around to talking
about what we're going to be talking about today, we
thought it would be fun to take the name of

(03:51):
our podcast and change it up a bit, right, this
podcast will kill you today.

Speaker 2 (03:57):
This podcast won't kill you. Yeah, it might make you
live forever, probably not give you the secrets to eternal life.

Speaker 1 (04:09):
Today, we're going to be talking about immortality and aging.
And it's definitely not going to be a comprehensive journey
through the history of aging and how immortality could be achieved,
but I think it's going to be a nice little taste.

Speaker 2 (04:25):
Yeah, And our structure is going to be a little
different than usual because it's such an amorphist topic. Yeah.

Speaker 1 (04:31):
So I'm going to be starting out talking about the
history of immortality and what that means in terms of evolution,
and then what that means in terms of like human culture,
and again it's just sort of like a brief, little
jump through, yeah topic.

Speaker 2 (04:46):
And then I'm going to talk about I don't really
know what erin maybe like where we stand in terms
of like aging today or anti aging research or the
quest for immortality, what we know about the biology of it.

Speaker 1 (05:04):
I don't know.

Speaker 2 (05:05):
It's going to be a little bit of a conversation.

Speaker 1 (05:08):
I think it's going to be really exciting and fun. Yeah,
I'm just looking.

Speaker 2 (05:12):
Forward to us same same Well, speaking of like.

Speaker 1 (05:15):
Tastes of things. What time is it?

Speaker 2 (05:18):
Oh, quarantiny time still is quarantiny time.

Speaker 1 (05:22):
Still is always quarantiny time. What are we drinking this week?

Speaker 2 (05:27):
Well, of course we're drinking none other than the Elixir
of Life.

Speaker 1 (05:31):
We are and in the Elixir of Life. It's a
it's a fun little it's a fun little drink because
we've got gin, we've got lemon juice, we've got blackberries,
we've got simple syrup. And then to kind of like
create the fun little magical I don't know aura around it,

(05:52):
we've got butterfly pea flower extract, which was sent to
us by a very generous listener, so thank you so much.
It is such a cool looking drink.

Speaker 2 (06:03):
It's a nice I'm really excited about. I want to
come visit you so that I can actually taste it.

Speaker 1 (06:09):
Okay, let's make that happen. Yeah, we will post the
full recipe for the Elixir of Life as well. As
the non alcoholic place Rita on our website This podcast
will kill You dot Com, as well as on all
of our social media channels.

Speaker 2 (06:25):
Our website This podcast will kill You dot Com. If
you haven't been there yet, you should go and check
it out. After one hundred episodes, try it. We have
merch we have transcripts. We have links to our bookshop
dot org affiliate account. We have links to our music bloodmobile.
We have a good Reads list, we have all of

(06:46):
our sources for all of our episodes. We have our Patreon.
We have more than I could say in that single breath.

Speaker 1 (06:53):
Well, I think you did a great job. Thanks, loving
all right, any other business?

Speaker 2 (06:57):
No, Aaron, please tell me, like I don't know, from
Gilgamesh to now, how has humanity fared on our quest
for immortality?

Speaker 1 (07:07):
Great questions there I will, I will do my very
best right after this break. Like we said, this is

(07:46):
definitely not our typical format. But then again, this is
not our typical episode topic. So the focus of our
episode today is immortality. But what does that mean? Not
just like what are we going to cover, but the
word or the concept itself is immortality, simply living forever,

(08:08):
not aging, being invulnerable to any illness or injury. Does
it mean that your name and life will be remembered
hundreds of years from now, or that your genes will
be carried on in your offspring and their offspring, and
so on and so on down the line. There are
many different ways that we can think of and have

(08:28):
thought of immortality. And if your goal is to achieve immortality,
which definition you choose has tremendous bearing on how you
go about that, And that can also be said for
this episode. So how will we consider immortality today? Really,
we'll at least touch on the most common concepts in

(08:49):
a general sense, but since we're a health and science podcast,
most of what we'll talk about is immortality from a
biological perspective. First by talking about not what immortality is
and how we can achieve it, but what stops us
from being immortal in the first place? Why do we die?

(09:11):
Why do we decline as we get older? Are there
any organisms that don't? What do we know or think
about senescence, the decline or deterioration we experience as we
age from an evolutionary perspective, And then all turn from
that to talking about the age long quest for immortality,

(09:32):
which has roots much much older than these startups in
Silicon Valley that have been looking for modern elixirs of
life that I know you're going to be talking a
bit more about, Aaron Yeap. What patterns do we see
in the different ways that people have approached immortality through history?
And how has this past century and our ever growing

(09:53):
understanding of biology changed the targets for immortality research. And
then that's sort of where I'll hands it off to
you Erin to tell us how close we are or
probably aren't to achieving immortality and the nitty gritty of
what people are working on. Okay, okay, all right, so
let's get into it. Living things age, but they don't

(10:16):
just experience the passage of time. They also change as
time passes, first growing and developing, and then at a
certain point that growth ceases and a new kind of
change occurs, one where maybe things don't heal quite as
fast as they used to, or those aches and pains
get more frequent, and eventually recovery is no longer a possibility,

(10:41):
with death being the ultimate end. And this is generally
how it happens for every living thing. And sure, the
amount of time that you spend in each life stage
may be different, or how long you can expect to
live will vary, but death and aging are essential parts
of life, even for those supposedly immortal animals that you

(11:03):
see like click bait headlines about like lobsters or certain
jellyfish or bristle cone pines. But while senescence, the biological
decline part of aging may not be as marked as
in other creatures, those organisms are not truly immortal. They
will die eventually because nothing living is immune to death.

(11:28):
Why does this have to happen? Like, why can't we
go on living forever? Well, let's think about it in
the context of natural selection and evolutionary fitness.

Speaker 2 (11:38):
That's arh.

Speaker 1 (11:40):
Evolutionary fitness, for those who haven't heard the term before,
is essentially an individual's reproductive success how many offspring they have.
If an individual has no offspring, zero fitness. If they
don't survive long enough to reproduce, fitness is also zero.
But the individuals who do live long enough to reproduce

(12:03):
and have a lot of offspring, those are the ones
who are going to contribute the most to the next
generation's gene pool. Traits that limit your ability to reproduce
or survive through reproductive age. Those traits lower your fitness
and make it less likely for those genes to be
passed on to the next generation. And over time those

(12:24):
traits those genes will become less and less common, maybe
eventually disappearing. But traits that make you more likely to
reproduce or survive through the end of reproductive age, those
are the traits that are going to be selected for
becoming more common. So we can think of tons of
examples of this, right, like the size of a bird's beak,

(12:46):
or the rate of development of a tadpole into a frog,
or fur pattern or susceptibility to disease. But what's so
crucial about this for this discussion is not the trait themselves,
not these examples, but rather the time window when these
traits matter most, and that is the critical period from

(13:09):
basically prenatal development all the way through the end of
when you are able to reproduce. That is when selection
can act. With this in mind, what does it matter
really in terms of natural selection if you live past
reproductive age. It doesn't.

Speaker 2 (13:28):
It doesn't at all.

Speaker 1 (13:29):
It doesn't. Yeah, if there are genes that affect at
least in part your longevity. How will natural selection act
on them if they don't have any bearing on your
reproductive fitness. It won't, It won't, I mean, And there
are genes in humans that are associated with longevity, but
it's likely that those play a role in maintenance or development,

(13:53):
and they don't just switch on later in life exactly. Yeah.
So essentially, in terms of natural select it doesn't really
matter how long we live past the point when we're
no longer reproductively viable. And this is of course like
a big oversimplification, and for humans and other animals, there

(14:14):
are some very interesting hypotheses about why we humans live
long past the age we reproduce, mostly centering around grandparents,
and I'd love to get into that one day with
an episode on menopause. Oh.

Speaker 2 (14:29):
I we'll definitely do it on menopause because I love
all of the evolutionary theories behind menopause and just like aging,
and like the grandparents.

Speaker 1 (14:37):
Oh, I love the grandparent hypothesis. Oh it's so interesting.

Speaker 2 (14:41):
Yeah, I love it.

Speaker 1 (14:43):
But anyway, we humans are not unique in that we
live past the age we reproduce, nor are we unique
in the fact that our bodies and minds start to
deteriorate as we get older. And even if life past
reproduction is not part of natural selection, what makes us
and other organisms age? Like? Why do we age? And

(15:06):
we have been asking ourselves this question, probably since we
were able to form thought, but it wasn't until Charles
Darwin introduced the theory of evolution by natural selection in
the mid nineteenth century that people had a scientific framework
that they could use to try to answer this question.
Since that time, many different hypotheses have been proposed, none

(15:29):
of which seem to adequately explain sinessence for every living thing.
And I'm going to briefly go through a few of
the classical hypotheses of sinessence so that we can try
to think about possible mechanisms that could explain why aging
is universal. The first of these hypotheses was proposed in
the eighteen nineties by the German evolutionary biologist August Weismann

(15:54):
the so called germ soma theory, and so Weisman suggested
that there were two types of cell lines in an organism,
a germ line and a soma or body line, and
the germ line is made up of the cells that
are involved in reproduction and the soma line consists of
the cells that make up the rest of the body.

(16:14):
It's the sole duty of the soma cells to do
whatever it takes to keep the germ line alive and reproducing.
Beyond that, soma cells basically disposable, and the soma cell
lineage will invariably die, while the germ cell lineage can
be viewed as potentially immortal. Aging happens as the soma

(16:36):
line gets beat up by the environment while protecting the
germ line. And that's the hypothesis. Yeah, obviously it has
many shortcomings, first of them being that it doesn't really
explain why sinessence evolved, like why the soma is disposable,
and it doesn't explain sinessence in single celled organisms. But

(16:58):
it did introduce the idea that reproduction is first and
foremost the priority, and many later researchers built upon this idea,
such as the famous mathematician and eugenicist Ronald Fisher, who
in the nineteen thirties proposed a mathematical model in which
he laid out his thoughts that sinessence was the accumulation
of harmful age specific traits. A couple of decades later,

(17:22):
in the nineteen fifties, Peter Medowar, whose name you might
remember from our organ transplantation episode. He wrote a now
famous essay describing how the force of selection weakens as
we get older and past our reproductive age. He wasn't
entirely right either, For instance, his belief that animals in

(17:44):
the wild don't get old they don't siness because they
just get picked off by predators or succumb to starvation.
They actually do siness, they actually do get older. But
his essay did suggest a sort of mechanism for Sinessence,
if there are genes that do exist that shorten our lifespan,
they won't really be selected against if they only show

(18:06):
their effects later in life, and so they will continue
to appear and accumulate over generations. The quote mutation accumulation theory.

Speaker 2 (18:15):
That's I love. Sorry, I just really do love these hypotheses.

Speaker 1 (18:20):
I do too.

Speaker 2 (18:21):
I find it really fun.

Speaker 1 (18:22):
It was it was so interesting because I have never
even though I said, humans have probably asked themselves this
question forever, and I've probably asked myself this question too,
but not in like a okay, but why what is
the actual evolutionary mechanism behind it?

Speaker 2 (18:39):
I feel like I only ever thought about another hypothesis.
I think you're probably going to talk about next in
the context of the evolution of human health class that
I ta' for. So that was like a very specific
subset of time that I was thinking about it.

Speaker 1 (18:54):
Yeah, it is. It's so fun to think about. Okay,
so there are there are a few more.

Speaker 2 (18:59):
Yeah.

Speaker 1 (18:59):
So. Years after Metowar's essay, George Williams added on to
this by suggesting that in addition to these mutations appearing,
it's also possible that those genes that are helpful early
in life, like in development and during reproduction, could also
be bad or have negative effects later in life. Like,
for instance, let's think about cell growth. If your cells

(19:23):
grow super fast, that's potentially great when you're developing right,
you get larger faster and can be independent faster. But
later on that could mean uncontrolled cell growth aka cancer.

Speaker 2 (19:40):
Yep.

Speaker 1 (19:41):
And this is something that's called antagonistic pliotropy.

Speaker 2 (19:44):
It's one of my favorite concepts and I love it.

Speaker 1 (19:46):
It's so it's I mean, and it like the thing
they all make sense, And the thing that I like
too about them is that none of them are really
mutually exclusive.

Speaker 2 (19:56):
Exactly like you have, you can easily we have mutations
that accumulate as well as have genes that are beneficial
early in life and maybe have a detriment later in life.
So like these mutation, accumulation, antagonistic piotropy, these hypotheses really
do work together to explain aging in a way that
I think is just fascinating.

Speaker 1 (20:17):
Yep, yeah, exactly. And also what really helped things along
in this in this field was when in nineteen sixty
six William Hamilton combined some of these existing ideas on
the evolution of aging into a mathematical model, which, like,
maybe that doesn't sound very exciting, but it really is.

(20:38):
It was, and it's still today is super impactful because
it laid out a framework for why aging happens, and
it also showed that the strength of selection on traits
that keep you alive it becomes weaker over time in
anything that ages and doesn't reproduce via fission. Yeah. Really,
Also what it did was create a math model for

(20:59):
people to be able to to test ideas about aging.
The last of the classical hypotheses of sinessence I'm going
to talk about is the quote disposable soma theory. Proposed
by Thomas Kirkwood in nineteen seventy seven, which says that
over time and organism cells accumulate harmful genetic mutations. Mutations

(21:20):
in your DNA happen randomly all the time because of
environmental factors or mistakes in DNA replication, and it gets
increasingly costly to repair the damage from these mutations, and
at a certain point, the benefit of repairing the damage
is outweighed by the cost repair and maintenance is always
going to favor the germline. Okay, so these are just

(21:44):
a few of the most impactful hypotheses to explain why
sinessence evolved, but there are certainly others, and no single
hypothesis at this point seems to be able to explain
aging for all organisms. There's no unifying hypothesis, probably because
like there's tremendous diversity in life, no is there.

Speaker 2 (22:08):
Really are I mean that like a bristle combe pine
is not the same thing as a plenariat.

Speaker 1 (22:13):
It might not be, and even some of the fundamental
assumptions about aging have been challenged. It's an extraordinarily complicated
thing to study. You have to capture both how different
environments and different genes impact aging. You have to consider

(22:35):
ecological factors, determine whether aging in the lab is different
or the same as aging in the wild, evaluate whether
closely related species age more similarly than distantly related ones.
And the biggest thing in my eyes is that we've
really only begun looking at this within the past one
hundred and thirty years or so, which is shorter than

(22:58):
the average lifespan of some organs. That could give us
really valuable insight into longevity.

Speaker 2 (23:04):
Good point, So, like, how do you how do.

Speaker 1 (23:06):
You create a data set? Yeah, for giant tortoise?

Speaker 2 (23:11):
Right, well, even studying human aging, like we live a
really long time, right, and.

Speaker 1 (23:17):
There have been really cool like census records and especially
in certain countries or certain regions that keep really good
track of like people through time, but we still don't
have all the bits of information there, right.

Speaker 2 (23:30):
Yeah.

Speaker 1 (23:31):
So it's it's in a way we've been thinking about
it for a long time, but it seems like we're
definitely in the infancy of having data to be able
to test these hypotheses.

Speaker 2 (23:43):
Aaron, you just summed up my whole section.

Speaker 1 (23:50):
It's it was it was really interesting to read through
this also because I don't think I realized just how
huge of a field of study this, And I guess
I should have because there are like, you know, entire
journals and entire textbooks at entire companies and everything, but
like it is, it is really hard to do it justice. Yeah, yeah,

(24:14):
so yeah, So I just kind of wanted to like
wander through some of these ideas and kind of fell
and build a baseline for thinking about aging in an
evolutionary context, especially when it comes to like natural selection
and wouldn't it be great if we lived forever but
we don't really need to, yeah, in terms of our DNA.

Speaker 2 (24:38):
Getting passed on, Yeah, exactly.

Speaker 1 (24:40):
Yeah, And I also thought it was important to think
about these things like why we age before we start
exploring some of the ways that we've tried and continue
to try to stop or slow that process. So, if
they're there is anything that humans are good at, it's

(25:02):
searching for the key to immortality. We're really good at
searching for it, but we are terrible at finding it. Yeah,
because we've not found it. Yeah, spoilers, we don't have it. Spoilers,
we don't have it. We may not have it ever.
Immortality narratives are central to every culture and religion, like

(25:28):
the Epic of Gilgamesh, the oldest known written document. So
the reason that I included Gilgamesh in the beginning, I'm
like now calling back to it is that a big
part of the story is about the quest for immortality.
So King Gilgamesh's best friend dies and in response, Gilgamesh

(25:49):
vows to find eternal life. Spoilers he does not. And
I'm sure between the two of us we can think
of dozens and dozens more books or movies or poems
or songs about the search for eternal life. But it's
not just like one of my favorite books growing up.
Let's talk Everlasting and for a long time you have

(26:14):
you read talk ever Lasting?

Speaker 2 (26:15):
Rush. I didn't even know it was a book. I
thought it was a movie, but I've never seen.

Speaker 1 (26:21):
It, okay, or read it. Basically, it's about this family
that is trying to find like a home. They're like homesteading,
and they stumble across this water. They all drink from it,
including the horse, I think, and it happens to be
like an immortality.

Speaker 2 (26:38):
Spring.

Speaker 1 (26:39):
And then then there's like a girl who stumbles across
his family and then she's like, do I drink it?
Do I? Not drink it, blah blah blah, And as
a kid, I was like, drink it, obviously.

Speaker 2 (26:49):
Drink ever, don't drink it.

Speaker 1 (26:52):
And yeah, anyway, but it's a really interesting contemplation about
immortality and and life. I loved it. And that's just
one of like hundreds, dozens, thousands, an unbelievable number. But
it's not just in these fictional stories that people have
been on the hunt for a way to live forever.

(27:15):
The quest for immortality is a very real thing that
takes many different forms, and I want to talk a
bit about these forms before focusing on a couple that
are more in line with this episode. While researching for
this episode, I came across a book titled Immortality, The
Quest to Live Forever and How It Drives Civilization. And

(27:37):
in this book, the author philosopher Stephen Cave, groups the
search for immortality into four different themes. The first two
deal with the physical side of things. First, there's living forever,
you as an individual, stopping aging or aging but not dying,
living indefinitely. And then there's resurrection, being brought back to

(28:00):
life after death, think Jesus. Third is the soul, the
idea that a part of you, but not the physical
you lives on after you die. And finally, there's legacy,
which can mean living on through memories or fame, as
in your only truly dead when your name is no
longer said Coco, or also offspring the idea that your

(28:25):
genes achieve immortality by being passed on. And I wanted
to explore some of the ways we've sought to achieve
immortality throughout human history, focusing on those that fall into
the first two of these themes, staying alive and resurrection,
because in terms of targets for biological research into immortality,

(28:45):
all of those projects can be lumped into those themes. Yeah,
And after going through some of these adventures and immortality,
I want to end by reflecting on what these stories
tell us about human nature. Here. Humans may be unique
in our ability to recognize our own mortality that one day,

(29:07):
each and every one of us will die, and the
knowledge of our own inevitable death, Yet the simultaneous inability
to actually imagine what it will be like has driven
us to find any way around it, either by delaying it,
undoing it, or preventing it entirely. In ancient Egypt, there

(29:30):
was an entire industry devoted to preserving the body after
death so it could be magically revived, and of course,
pyramids and other monuments were built as a testament to
the person's life immortality through legacy. Ancient papyri describe not
just preparation for the afterlife or resurrection, but also ointments

(29:52):
and elixirs that were meant to extend life and slow aging.
The search for an elixir of life or a fountain
of youth is similarly old. There are countless stories of
emperors and kings searching in vain for a way to
escape death, like the first Emperor of China, who lived
around the two hundreds BCE. He became obsessed with the

(30:15):
idea of living forever and searched high and low for
someone who could reveal the secret to him. He did
find someone, probably one of the oldest known swindlers, who
promised it all but delivered nothing and just ran away
with his reward. Of course, ultimately the emperor died young,
only forty nine, likely from either arsenic or lead or

(30:40):
mercury poisoning, all of which were likely ingredients in his
daily life. Extending vitamins.

Speaker 2 (30:46):
Oh gosh, that's just such a Bomber.

Speaker 1 (30:49):
I know, but he did achieve immortality. And what I mean,
we're still talking about him. We are through his through legacy.
He the terra Cotta Army. Have you heard of the Terracota? Yeah, yep,
that's him.

Speaker 2 (31:01):
That's him. Huh, all right.

Speaker 1 (31:04):
The elixir of life wasn't always viewed as just a
potion or something you ingest. At various points, it was
thought to be a plant, or a series of exercises,
or a special object like the Philosopher's stone, which was
one of the mythical substances famous in alchemy. Alchemy was
a kind of prescience practiced by philosophers and early chemists,

(31:27):
the goal of which was to transform one metal into another,
typically gold, and to find the elixir of immortality or
a cure all for any disease. It was practiced all
over the world from ancient times all the way up
through the eighteenth century, when it declined after the rise
of more rigorous scientific thinking, although it might be more

(31:50):
accurate to say that alchemy didn't decline, but rather it
was repackaged primarily into the field of chemistry. Nor did
people grow tired of looking for the elae of immortality. Instead,
the development of each new field or new scientific discovery
was applied to that quest, For instance, electricity. So if

(32:12):
you think back to our electricity episode, you may remember
me telling the story of Galvani and his metal wires
and the frog's legs jumping. So his nephew took a
page out of his book and held public demonstrations where
he reanimated corpses of freshly hanged murderers.

Speaker 2 (32:31):
Oh my, okay, yeah.

Speaker 1 (32:35):
And his demonstrations may have been the inspiration for Mary
Shelley's Frankenstein.

Speaker 2 (32:39):
Oh my goodness.

Speaker 1 (32:41):
I know connections, and this pattern continues to be repeated.
In the mid twentieth century, advancements in cellular technology allowed
researchers to use previously frozen sperm for insemination, resulting in
three pregnancies, which was revolutionary and that soon turned into

(33:02):
whole body freezing plans. As we've learned more about genes
linked to aging thanks to genomic sequencing technologies, those inevitably
became our targets for modern day immortality projects. And the
amazing thing in my eyes is that despite humanity's continuous

(33:22):
and innumerable attempts to achieve immortality, over thousands and thousands
of years, we have not been remotely successful, and we
probably never will be. Maybe it'll change my mind.

Speaker 2 (33:36):
Yeah, we'll see erin.

Speaker 1 (33:39):
Over the past couple hundred years or so, the average
age a person can expect to reach has been greatly extended,
largely due to vaccines, antibiotics, and many other small things,
especially a better understanding of disease overall. But this has
not been an extension of our inherent life span. Humans

(34:01):
have been able to live to eighty years old ninety
years old for thousands of years, but were prevented from
commonly achieving old age because of extrinsic factors like insert
any vaccine preventable disease here.

Speaker 2 (34:18):
We're also taking like mercury and arsenic as a as
a vitamin, just like that too.

Speaker 1 (34:25):
But from what I've read, there's not a single anti
aging serum, pill, potion, whatever that has been shown to
actually slow aging or reverse or stop it. There is
some evidence that diet and exercise may play a role.
Longevity and aging are both such incredibly multifaceted processes that

(34:48):
are nearly impossible to predict, and I'm not saying at
all that I don't think this research should be done.
Some of these projects have uncovered knowledge that has had
huge implications, who are improving quality of life and treating
diseases that primarily manifest later in life. I guess I'm
just expressing my skepticism that a meaningful extension of both

(35:11):
lifespan and quality of life alongside that will be achieved
in the near or even kind of near future. The
section definitely came out differently than I had planned when
I started it. I thought I'd take us through the
history of the search for the elixir of life or
the beginnings of cryonics, and those stories are fascinating and

(35:35):
worth telling. But I think that overwhelmingly while doing the
research for this part, and while going through it just now,
I think that what sticks out to me most is
how so many things have not changed. We will continue
to keep looking for ways to live forever, to upload

(35:56):
our brains or slow our aging, to reanimate form and bodies,
or download our memories into a cloned body, and if
any of those technologies are successful, you can also be
sure that the select few, the richest, and most powerful
will be the only ones to benefit from them, which
is also how it has been throughout history. But would

(36:19):
it truly be a benefit to live forever? Would it
be something you want? I've talked about a few stories
about people who have searched for a way to live forever.
Now let's think of some where they achieved immortality. How
did those stories end?

Speaker 2 (36:35):
Never well?

Speaker 1 (36:37):
Never well? Almost universally, they end in profound loneliness, sadness,
and regret. Not at first maybe, but over time, as
their mortal friends and family grow older and die, as
days pass and time becomes meaningless. Granted, all of those
stories have been imagined by mortal humans. These endings are

(37:00):
just consolation for not being able to live forever. But
I don't know. Personally, I don't think so. I think
too often we decide we want to live forever without
considering what that could truly look like. I want to
end this section with a quote by Stephen Cave that
I think puts it nicely. Quote The deep problem is this,

(37:23):
The value of a thing is related to its scarcity.
People conscious of their mortality value their time and aim
to spend it wisely because they know their days are numbered.
But if our days were not numbered, this incentive would disappear.
Given infinity, time would lose its worth, and once time
is worthless it becomes impossible to make rational decisions about

(37:45):
how to spend it. The consequences of this for an
individual would be bad enough. For a civilization of such ditherers,
it would be disastrous.

Speaker 2 (37:56):
Yeah.

Speaker 1 (37:57):
Yeah, And with that, Aaron, oh gosh, I'll turn it
over to you to tell me how close we are
to such consequences.

Speaker 2 (38:05):
Oh my goodness, Arin, this episode turned out so different
than we expected. I'm going to need a break, okay, Yeah,
and then I'll dive in to what's happening today. So

(38:41):
when I first started trying to research for this episode,
I had a really hard time because I wasn't sure
how to really approach this question. And I actually wasn't
sure what my question was. I normally do the biology
sect of whatever disease or thing we're talking about, and

(39:04):
then I talk about the current status. Where do we
stand today? So what was my question for immortality? Is it?
How close are we to immortality? Is it? Are we
still pursuing this quest? Which spoilers you already told us
And the answer is yes, we still are. Oh was
the question have we learned anything from these thousands of

(39:26):
years of futility so far? I don't know what question
I'm answering out of those. But I did a lot
of reading, and I read a lot about the various
you know, Silicon Valley startups that exist, the number of companies,
the number of billionaires and millionaires, and the amount of

(39:49):
dollars that are going in to try to solve this
quote problem of aging or the problem of death.

Speaker 1 (39:57):
It kills me, the problem of aging, or it's really
really interesting, and I think I got a little.

Speaker 2 (40:07):
Bit overwhelmed and also maybe a little cynical by the
end of it.

Speaker 1 (40:12):
Oh, for sure, I got cynical by the end of
the day.

Speaker 2 (40:14):
Yeah. But it's not to say, like what you said, Erin,
It's not that what any of these researchers are doing
is unimpressive or unimportant. It's just that we remain in
the very early stages of this research. So let's kind
of go through the way that I at least tried
to frame thinking about this. If we're talking about immortality,

(40:39):
like you said Erin at the top, then we're kind
of talking about the idea of anti aging, or we're
talking about increasing our lifespan. And if we're talking about
halting aging to the point of halting death, then for me,
the way to get there, logically is to answer a
series of four different questions. The first question you kind

(41:04):
of answered, Aaron, and that is why do we age?
I think that you provided a lot of evolutionary perspective
on the idea of why we as humans and we
as living organisms on the planet Earth age evolutionarily, but
we still don't fully necessarily know. We at least have

(41:24):
a lot of hypotheses. But a very closely related question
to why do we age is how do we age?
Like fundamentally, what governs the process of how our selves siness?
And how is this process related to those evolutionary reasons
of why we age? Because if we could answer those

(41:47):
two questions really well, then we could ask the next question,
must we age? Are those processes, like we said, from
an evolutionary perspective, necessary for life? And are they immutable?
And if the answer to that question is no, they're

(42:07):
not immutable. And if we can figure that out by
virtue of figuring out the answers to the first two questions,
then we can ask the final question, if we don't
have to age, do we have to die? So, at
least to me, those seem like the four fundamental questions

(42:29):
that have to be answered if we have any hope
of answering this riddle of immortality. And suffice to say,
those four questions are massive, and I think the biggest
issue for me in talking specifically about immortality is the
leap between those last two questions, must we age and

(42:51):
must we die? Right? Because while there are in nature
and in the laboratory many many examples be they plant
or worm or lobster that live a very long time
that seem to be immortal, nothing is invincible, right, right.
If you take one of these invincible planarians out of

(43:14):
their worm juices, they're going to die. They're not invincible.
And so that's I think one of the biggest issues
I see with even just entertaining this idea of true immortality.

Speaker 1 (43:27):
Oh yeah, right, immortality is not invincibility exactly.

Speaker 2 (43:31):
Yeah, okay, But so is that what people are working on.
Are people working on immortality or are people really working
on the first few questions but selling it packaging it
as the idea of immortality. Maybe that's more accurate. So

(43:52):
what do we actually know about these first couple of questions,
especially how we age and must we age? There has
been like you said, Aaron, without a doubt huge increases
in the estimated life expectancy for humans globally, and there
is a lot of variation in estimated life expectancy between countries,

(44:16):
between genders, et cetera. And most of that increase is,
like you mentioned, credited to early life advancements, things like antibiotics, vaccines. Basically,
we know for sure that we've had huge reductions in
early life mortality because of scientific and biomedical achievements over
the last fifty twoe hundred years. However, there has also

(44:40):
been a decline in late life mortality. So the fraction
of each birth cohort that reaches old age has been
increasing year after year, or at least it had been
until about the nineteen eighties, and since then it's actually
been very stagnant despite increasing overall life expectancy, but the

(45:04):
maximum reported age at death has plateaued. You may have
heard of Jean Calmeat, who was a French woman who
died in nineteen ninety seven at the ripe age of
one hundred, twenty two years and five months. She still
holds the verified longevity record by a lot, by a

(45:24):
couple of years. And while there are over five hundred
thousand centenarians alive worldwide, at least that's what the UN
estimated in twenty twenty wow, five hundred thousand people over
one hundred. That number is twenty times higher than fifty
years prior. But the average age at death for these

(45:48):
centenarians has not increased since nineteen sixty eight. So there
is a lot of research and mathematical modeling like you
mentioned erin as far back as the eighteen hundreds, that
really suggest that there may be a true upper limit
to the human life span. And while this idea is

(46:10):
still a little bit controversial, there are people who don't
like to agree with the idea that there is a
limit to human life expectancy. A lot of studies that
have used various methods and are to varying degrees controversial,
have converged around this idea that perhaps between one hundred
and twenty and one hundred and fifty years might be

(46:32):
the maximum human lifespan that one could expect. So could
we even live forever? It seems highly unlikely. Yeah, But
there is another piece to this puzzle besides actual lifespan is,
like you mentioned Aaron, quality of life. This is often

(46:55):
called health span. So if life span is the length
of your life. Health Span is often defined as the
period of your life that is free from disease. I
personally will take slight issue with this definition, because health
is of course a lot more than merely the absence

(47:15):
of disease, but this is generally how health span is defined,
so we'll go with it for the purposes of this episode. Okay,
And if we look worldwide, despite how much lifespan has increased,
chronic diseases are the leading cause of morbidity and mortality worldwide,
and many of these cardiovascular disease, cancer, dementia. These are

(47:39):
often considered diseases of aging, and an estimated fifty eight
percent of chronic disease related mortality happens in people over
age seventy. So if we look at the discrepancy between
health span and lifespan, there's an estimated gap right now

(47:59):
in the world of nine years. So there's a nine
year gap where you are still alive, but you are
no longer quote free from disease. And a lot of
the field of what is called gerontology research isn't truly
focused on the idea of immortality, at least not overtly

(48:22):
or in a lot of cases, they're not even focused
on the idea of increasing our lifespan, but rather they're
focused on increasing health span. So they talk instead about
the idea of compressing our morbidity to the end of life,
such that we live healthier lives for longer and can
either avoid or prolong the onset of these various age

(48:45):
related diseases. And this I think sits as both a
more palatable goal. For sure, I would agree with that,
but I also think that it's closer to what seems
maybe yes, although I do stress that we're not there yet.

Speaker 1 (49:05):
It's it's so interesting because I think that, like, given
the past one hundred and fifty years of scientific research,
we tend to view things as science will always progress
at an increasing rate. Yeah, right, like we make bigger
leaps and bounds in our understanding and in our technology
and so on, and it doesn't. That's not necessarily the case,

(49:30):
I think with every field.

Speaker 2 (49:33):
Yeah, it is really really interesting to read a lot
of this research and then also read the media reports
about this research or about the companies that are funding this.

Speaker 1 (49:43):
Research, I bet, because.

Speaker 2 (49:46):
It's very different, right.

Speaker 1 (49:48):
Yeah, This is where reading between the lines of popular
news articles is tricky. It's tricky, and where there's like
have a heavy dose of skepticism and go to the
original text.

Speaker 2 (50:00):
Yeah, definitely, But there are I will say a lot
of researchers out there that are trying to really get
into the nitty gritty of answering those first couple of
questions that I posed, How and why do we age?
And can we alter this process? So while we don't

(50:23):
have a single answer, I will link to a couple
of different papers that go into a lot more detail
on these mechanisms. But we can define, based on what
we know so far, about nine different flavors or nine
different targets that are related to aging and potentially modifiable

(50:44):
at least in cell culture and or in animal models,
or maybe just theoretically modifiable. So I'll mention all of these,
but spoiler alert. Reading some of the papers that go
into detail on this, I had a very difficult time

(51:06):
following through. But let's at least look at what we
know about aging, because it turns out we know a
lot more than you might think. So when we look
at the mechanisms of aging, one of them Aaron you
mentioned already, and that is damage to our DNA be
that nuclear DNA or mitochondrial DNA. Basically, over time, insults

(51:31):
to our bodies result in the inability of our bodies
to properly repair damage to our DNA the way that
it is supposed to. And there are a lot of
different potential genes involved in this and specific mechanisms that
researchers have altered in flies or in worms, or just
in cells. But essentially this genomic instability does play a

(51:56):
really big part in the process of aging. So if
there was a way to make our DNA more easily
able to repair itself, that could then delay that process
of aging, and we know delay a lot of the
age related diseases that are related to this, like cancers,
like maybe heart disease. There's also telomere damage telomere's I

(52:19):
think we talked about in our HPV episode. Was that right?

Speaker 1 (52:23):
You talked about it in some episode, but can you
do a refresher?

Speaker 2 (52:26):
Of course, I'd love to so. Telomere's got a lot
of press in aging a while back. But basically, they
are the end caps of our DNA. They are these
strings of repeat DNA that sit at the ends of
our chromosomes and in a lot of cases, they don't
get completely copied over when our cells divide, so over time,

(52:46):
telomeres can become shortened, and this process of telomere shortening
or telomere exhaustion then leads to a decline in the
regenerative capacity of tissues and therefore accelerated aging. So in
mice models and in other animal studies, telomere length has
been shown to be associated with lifespan in humans. It's

(53:09):
not quite that simple, but this is at least another
potential target.

Speaker 1 (53:14):
What do you mean, it's not quite that simple.

Speaker 2 (53:16):
It's not like the length of your telomeres determines how
long you're going to live. It's not a one to
one association. So just adding on to our telomeres doesn't
necessarily mean that we're going to increase our lifespan or
our health span, because this is one of nine processes
related to the aging process, nine that we know of

(53:37):
so far. Okay, there's more lots and lots of research
right now, especially by some of these big biotech companies
into epigenetic modifications. Epigenetics we've only ever briefly mentioned, but
I actually think I talked a bit about it in
our full late episode. It's kind of fun.

Speaker 1 (54:00):
I was a thinking that, yeah, yeah.

Speaker 2 (54:02):
But basically, epigenetics are changes to DNA patterns that are
not within the DNA itself, so not within a gene.
But it's changes to things like methyl groups that are
attached to our DNA. It's changes to things like histones,
which are like the proteins that are DNA wraps itself around.

(54:22):
It can be changes to how our DNA is stored.
Any of these changes are considered part of epigenetics, and
changes in a number of different things from methylation to
histone proteins have been shown to be associated with aging.
There is a family of enzymes called sirtuins I think

(54:44):
that's how you pronounce it, that are involved in DNA
methylation and got a lot of press because in yeast
and in worms, when these enzymes are manipulated, then you
can increase lifespan by significant in a worm. Again in humans,
we don't have any data to show that as of yet,

(55:09):
but that's at least the idea that epigenetics likely plays
a big role in the process of aging. So if
this is something that we could target, we could maybe
affect it. Yet another target would be proteastasis, so Basically,
our cells are both DNA and proteins, right, So as

(55:30):
we age, our cells become less able to maintain proteins
in the correct stable configurations and correct functionality. If you
think of something like Alzheimer's disease, this is largely a
disease of protein misfolding. So there are a lot of
studies in cells in yeast, and I think at least

(55:51):
some in worms and flies that if you mess with
some of the genes related to protein stability, then you
can precipitate aging make them age faster. So that suggests
that these systems are directly involved in the process of aging,
and thus if they could be manipulated in the opposite way,
could perhaps promote longevity or reverse aging.

Speaker 1 (56:15):
Reverse aging. Interesting, say, yeah.

Speaker 2 (56:17):
Yeah, there's more. I'm only on number four of nine.
I don't have goodness as much detail on all of them.
Let me tell you. There's also the idea, and I
think this one has gotten probably the most press very recently,
or at least maybe just the most press of the
press that I read. But it's this idea of as

(56:38):
we age, we have a deregulated ability to do nutrient sensing. Basically,
our bodies are not able to tell as we age
if we have an abundance of food or if we
have not enough food. And this goes along with a
lot of data in mice and in some primates of

(57:02):
caloric restriction. So having less food for a portion of
your life increases lifespan in a lot of animal models.
So there are a lot of different host factors that
are implicated as a possibility in this. Some of them
are things you've definitely heard of, like insulin right or
IGF one insulin growth factor one. There are a lot

(57:25):
of others like m tour amp K sirtuins are in
amp K. These are all various fancy names for factors
that our body uses to help signal to our brain
when there is food that needs to be digested versus
when our nutrients stash is very low, so we need
to engage in catabolism like break down our own stores

(57:47):
instead of building a bunch of muscle in fat. So
there's evidence to suggest that states of anabolic signaling that
is our body saying, hey, we've got a lot of food,
we need to build up stores. That process accelerates aging,
at least in mice and so manipulating this signaling so
that a mouse's metabolism thinks it's living underlimited nutrients. By

(58:11):
manipulating some of these factors can extend longevity.

Speaker 1 (58:17):
Interesting, So that's that's what is meant by caloric restriction,
is manipulating the factors, not straight up chloric restriction.

Speaker 2 (58:25):
So straight up coloric restriction means straight up coloric restriction.

Speaker 1 (58:28):
Okay.

Speaker 2 (58:28):
This is trying to get out a way of can
we trick our bodies into thinking that we're living colorically restricted,
but we don't want to live calorically restricted?

Speaker 1 (58:38):
What is the mechanism for chloric restriction increasing longevity? And
what does chloric restriction mean?

Speaker 2 (58:46):
Great questions. So caloric restriction in animal models means reducing
an animal's nutrient intake to about thirty to forty percent
of what is typically considered necessary for like, you know,
the amount of calories that a mouse needs. So it's
very very restricted. I want to be extremely clear on
here that I am not by any means recommending this

(59:08):
for human beings. This could be very dangerous, okay, but
in mice, restricting them to that very small amount of
calories thirty to forty percent of what would normally be needed,
does increase lifespan, and it also increases the age at
which animals are able to reproduce, if that makes sense.

Speaker 1 (59:30):
It increases how long you are reproductively viable.

Speaker 2 (59:33):
Well, no, because these animals tend to not be able
to reproduce while they're living under caloric restriction. But then
they get to an age where normally, like a normal
mouse at say this many months of life would no
longer be able to reproduce. This mouse who's been calorically
restricted now can reproduce if you start feeding them.

Speaker 1 (59:53):
Okay, butzing if the mouse is only consuming thirty to
forty percent of what is considered neces necessary for it
to live, how is it living well?

Speaker 2 (01:00:04):
So that is the idea behind all of these factors. Basically,
the thought is that in so doing, in restricting these calories,
you're altering the way that the body is metabolizing everything
in a way that is promoting catabolism. So that breaking
down of our own body stores rather than anabolism, the
building up of our muscles, the building up.

Speaker 1 (01:00:26):
Of fat stores. Right.

Speaker 2 (01:00:28):
So that's the idea behind why caloric restriction works. We
know from animal model studies from a long long time
ago that restricting animals diets makes them live a longer time.
These genes and these factors and these hormones that have
been identified seem to be the possible mechanistic way that

(01:00:52):
caloric restriction manifests. So if we could directly affect those
mTOR or insulin or what have you, so then we
could trick our bodies into breaking down stores rather than
building fat, and that might make us live longer. That's
the theoretical idea behind it.

Speaker 1 (01:01:12):
Interesting. Yeah, it kind of it reminds me of going
back to the evolutionary hypotheses, the germ soma theory, where
it's like the germ line is always favored, but maybe
here's the exception where if the soma line can't support
the germ line, then the soma line has to be favored. Yes, first, exactly.

Speaker 2 (01:01:33):
I think that that is a good way to kind
of yeah, pieces together.

Speaker 1 (01:01:37):
Interesting.

Speaker 2 (01:01:38):
Okay, there's a few more, but I will say I'm
not going to go into quite as much detail because
from what I read, the topics that I've already covered
are maybe the ones where we are a little bit
farther along in that we have data from animal models
and from cell models to show that manipulating these various things,

(01:02:01):
be they nutrient sensing or you know, protein stability can
affect aging. The other ones are a bit more theoretical still,
at least from what I read. And apologies. If someone
has some great data that I didn't see on these
last few.

Speaker 1 (01:02:17):
Topics, send it our way, ye if you do, I.

Speaker 2 (01:02:20):
Would love to read it. So another possibility is the
idea of mitochondrial dysfunction. So our mitochondria are often called
the powerhouse of our cells. They do a lot for
our bodies, and the idea is that over time, just
like our DNA in our nucleus, these mitochondria can just

(01:02:41):
sort of not function as well anymore. This is thought
to be very related to things like oxidative stress over time.
That's all I got for you on mitochondrial dysfunction related
likely to the process of aging. Okay, there's also just
the idea of cellular sinescence in general, cells going quiescent

(01:03:05):
over time. A lot of our cells in our body
are not dead, but they no longer divide, they're no
longer active. So there's a large thought that just this
entire process of cells kind of turning off a lot
of their activity then relates to aging, and it's likely

(01:03:25):
protective to write, like, reduce the amount of DNA damage
that might occur through the process of replicating cells that
don't need to be replicated, et cetera. So this might
be something that's more related to protection against aging rather
than involved in the process of aging, like protective against it.

Speaker 1 (01:03:45):
Yeah, yeah, Okay.

Speaker 2 (01:03:47):
Then there's the idea of stem cell exhaustion, which I
again didn't get that much into detail of, but the
idea that our stem cells are the ones that aren't
able to keep up the way that they need to
to be able to produce more cells correctly, like the
basal layer of our skin. Cells are stem cells that

(01:04:08):
can become any various type of cell. But as insults
occur to these stem cells, then hence the process of
aging AI yeah.

Speaker 1 (01:04:16):
Yeah.

Speaker 2 (01:04:18):
And finally, there is also this thought of defective or
diminished cell to cell communication. And there's a lot that
probably goes into this one that I think is interesting
and I didn't I will full disclosure, actually read any
papers by him, but I watched a TED talk of
this researcher named Michael Levin, who is a researcher at

(01:04:41):
Tufts University and does really interesting research on cell cell
communication from a bioelectric field perspective. Right, it's very very interesting.
But there's also a lot of other ways that our
cells communicate with each other besides potentially a bioelectric field.
But I will link to that Ted talk because it's
fascinating and it's likely that this process over time also

(01:05:04):
becomes defective and is involved in the process of aging.
That was like a very fast speed through and I
know that I left a lot of detail out. I
will cite a couple of papers, one from twenty thirteen
that's a few years old now, but another that is
a summary of a twenty twenty one symposium of gerontologists

(01:05:26):
that has a lot more detail on these nine different
processes and where we kind of stand in terms of
in vitro cell data, animal model data, and human data.
But the thing is, I think it's very clear just
for going over all those various processes that these are
all very interconnected, right, especially when we talk about humans.

(01:05:51):
It's not one single piece. All of these processes are
likely at play, and we are not at a point
where we can say that we have an answer or
a drug or an intervention at all. That can prolong
our life in any meaningful way. We don't even have

(01:06:11):
one that could likely prolong our health, at least not yet.
So really, for me, what it comes down to is
that forever it is a very very long time. So
do I think it's possible that humans will ever unlock
the many locks between us and immortality? No, I will say, no, Yeah,

(01:06:38):
it doesn't seem likely. It doesn't. Do I think that
it could be theoretically possible this concept of immortality kind
I kind of don't, Aron, do you know?

Speaker 1 (01:06:53):
No, But I will say that Also what occurred to
me while you know, listening to you and while thinking
about the part that I went through, is that maybe,
you know, this is one of those things where in
the future, in the distant future, if anyone ever stumbles
across this podcast and they'll just laugh, I know how

(01:07:15):
naive we were and how unbelieving we were.

Speaker 2 (01:07:18):
Yeah, I maybe maybe I similarly doubt it.

Speaker 1 (01:07:24):
I mean, and I think that's the other thing too,
is that immortality is not what people are working on exactly,
it's how it's being sold.

Speaker 2 (01:07:34):
Yes, And one of the things that I think is
really interesting in reading from the gerontology perspective is that
I do think that a lot of the research into
these questions of like how does aging happen and can
we manipulate those processes? This research can be used to

(01:07:57):
improve the lives of humans, and I do think that
it could potentially increase our health span and delay the
onset of all these various aging related diseases. But what's
interesting is that we tend to study all of these
various age related diseases, cardiovascular disease, cancer, Alzheimer's disease. We

(01:08:20):
study these diseases in isolation.

Speaker 1 (01:08:22):
Ooh, that's such a good point.

Speaker 2 (01:08:24):
And aging itself is not considered a disease, so you
cannot study it from a like applying for nih Grant's perspective,
or from a drug development perspective. You cannot study it
in the same way that you can study diseases.

Speaker 1 (01:08:39):
Oh, that is very interesting.

Speaker 2 (01:08:42):
It really is, because it also means that the funding
is not actually being directed towards aging. The funding from
the government is being directed towards addressing these diseases that
we think maybe could be preventable. Right, But if we
think that these are inter related diseases that are all
part of the process of aging, then wouldn't it make

(01:09:05):
more sense to address them from a wider perspective by
addressing these underlying mechanisms rather than addressing cardiovascular disease or
diabetes itself and cancer itself. Let's think about these things
that underpin both of those or all of those. And
so I think that that's kind of the argument of
a lot of the people who do this type of research,

(01:09:26):
and I think it's really valid. And maybe that's the
gap that some of these biotech companies are filling by
directing their funding to address that. I don't know, maybe
that's an optimistic view, but maybe that is.

Speaker 1 (01:09:45):
That's a really good point. And I mean, I know
that like a lot of epidemiological studies will look at
all of these things together, but it just there are
so many different avetus of research.

Speaker 2 (01:09:58):
Yeah, and but it.

Speaker 1 (01:10:00):
Does seem like aging is super multifactorial. A lot of
these diseases are super multifactorial, but some of the factor
like that they are like siloed diseases exactly. That's yeah.

Speaker 2 (01:10:18):
I also think it's important to point out, like you mentioned, Aaron,
there are a lot of other in my mind, ethical
and moral concerns related to this idea of pursuing an
increased lifespan or health span in thinking about the state
of our planet and climate change and how we've impacted

(01:10:42):
our planet with the lifespans that we currently have, and
also in like you said, where is this development and
technology going to go? Who is going to benefit from it?
Because the increase in life span that we've seen in
the last fifty to one hundred years hasn't been even
across the board, and people who are wealthy live much
longer than people who are not wealthy, and so that

(01:11:06):
is likely going to continue to be true, especially if
all of the research being done on this is from
a capitalistic perspective of companies trying to make money off
of it.

Speaker 1 (01:11:20):
I don't know. I mean, anti aging is one of
the world's biggest industries.

Speaker 2 (01:11:26):
Yeah, definitely, it really is.

Speaker 1 (01:11:28):
And like, and I'll repeat again, not a single anti
aging product has been shown to actually slow stop or
reverse aging in any capacity.

Speaker 2 (01:11:39):
Yeah, diet and exercise, erin diet and exercise. Yeah, listeners,
do you think you'd want to live forever? I'm curious.

Speaker 1 (01:11:52):
I'm curious, and if so.

Speaker 2 (01:11:56):
Why or why not?

Speaker 1 (01:12:02):
Or why not?

Speaker 2 (01:12:03):
Yeah?

Speaker 1 (01:12:04):
Should we do sources? Yeah? I have a bunch, but
I'm going to shout out two books in particular that
I found really helpful. So in terms of the evolution
of sinessence and the evolution of aging. There is a
book by Jefferson at All or a bunch of editors
titled The Evolution of Sinessence in the Tree of Life,

(01:12:26):
and that's from twenty seventeen. And then the book that
I already mentioned by Stephen Cave Immortality the Quest to
Live Forever and how it drives Civilization, and those are
both really I just really enjoyed the Stephen Cave book
as an interesting way to look at immortality.

Speaker 2 (01:12:46):
I had a couple that I enjoyed. Those two that
focused on the various hows of aging were a paper
from Cell in twenty thirteen titled the Hallmarks of Aging,
as well as a symposium report from the Annals of

(01:13:06):
the New York Academy of Sciences from twenty twenty two
titled Extending Human Lifespan and Longevity a symposium report. I
also thought an important one to mention is a paper
from twenty twenty one called Longevity Leap Mind the Health
Span Gap. And then there was there's a bunch more
so I'll link to them on our website, This podcast

(01:13:26):
will kill You dot com under the episodes TAT.

Speaker 1 (01:13:31):
Thank you to Bloodmobile for providing the music for this
episode and all of our episodes.

Speaker 2 (01:13:37):
Thank you to the Exactly Right Network, of whom we're
proud to be a part.

Speaker 1 (01:13:41):
And thank you to you listeners. I really hoped that
you liked this one.

Speaker 2 (01:13:47):
Yeah yeah, I hope so too. And a special thank
you to our patrons as always, thank you so much
for supporting us.

Speaker 1 (01:13:55):
Yeah well erin Happy one hundred, Happy one hundred and
until next time, wash your hands.

Speaker 2 (01:14:03):
You filled the animals m