30,000 years ago, a man lies dead. But
who or what could have killed him?
There was no sign of blood. He hasn't
fallen from a great height or been
crushed by falling debris. There are,
however, some scars on his scalp.
Perhaps he was killed by a heavy blow.
But wait, these scars are old. Healed
wounds from a long time ago. He has a
slightly shortened forearm and a crooked
foot, perhaps from a fall. But again,
these happened months, maybe years
before. These are all healed memories of
damage. Things that aided this man,
perhaps slowed him down on his final
journey across the ancient plane. But
none of these injuries killed him. These
scars, if anything, are a mark of
endurance. Proof that he fought, bled,
and survived throughout his life. And so
what was it that killed him? This
ancient man, the ancestor of many humans
alive today, was not killed by violence
or hunger. His body shows no sign of
starvation or predators claws. No, he
was stalked by an enemy he could not
defeat through fighting skill or speed,
nor evade with intelligence. This killer
was a spectre, one that had followed him
throughout his life, growing as the
years passed, stalking him from within,
written into his DNA. Evolution had
allowed this killer to exist, and it had
actually kept him alive, protecting him
against other causes of death until it
killed him.
From the hours of life experienced by a
mayfly to the centuries long endurance
of a sequoia tree, all living things
come to an end. Despite the long process
of evolution producing an array of
astonishing ways to survive and thrive,
regeneration, hibernation, reproduction,
aging remains inevitable. But if
evolution truly is the survival of the
fittest, why should living things age at
all? What purpose, if any, does aging
serve in the grand scheme of natural
selection? Evolution clearly has
increased the complexity of living
things and extended their lifespans. And
so, why hasn't it solved the great
problem of death?
Why don't we live forever?
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Buried beneath layers of dolommitic
limestone in South Africa's cradle of
humankind, intombed in the dust of a
cave that collapsed untold numbers of
years ago, was a fossil. And when
researchers cleared away the final
grains of sediment, a fragment of bone
emerged from the stone, smooth,
unmistakably humanlike, but between 1.6
and 1.8 million years old. This was
SK7923,
a partial left fifth metatarsal, a
footbone recovered from the Swatran's
cave site. Though not identified, the
fossil comes from an area that has also
yielded fossils attributed to Homoagasta
and Paranthropus Robustus. But what
makes SK7923
unique is that X-ray microtomography
showed evidence of malignant
osteocaroma, a type of bone cancer,
making it the earliest known case of
cancer in a hominin. But the question is
why? This fossil is ancient to us, but
it's as old as yesterday when viewed on
an evolutionary scale. Around 4 billion
years of life had existed on Earth
before this homminin had cancer. And in
all that time of evolutionary trial and
error of survival of the fittest, life
has not eradicated aging and death.
In May 1848, Henry Walter Bates reached
the Amazon rainforest on a trip that
would reveal much about the survival of
the fittest. Bates caught the tropical
butterflies of the Amazon with nets,
examined them in the dim light of his
hut, and mounted them carefully on pins.
And slowly, through patient observation,
he began to notice something strange.
Some butterflies, he had learned, were
dangerous for birds to eat. Their
caterpillars had fed on plants toxic to
bird life, and as a result, the birds
had learned to view their colors as a
warning. Eat me and regret it. But
flying among these toxic butterflies
were entirely unrelated species that
looked almost identical with the same
bold red stripes or yellow bands.
Predators could not tell the difference
and so avoided them, too. The imposters,
he realized, survived because of their
resemblance to the real thing. When
Bates returned to England, he read the
work of one Charles Darwin and
recognized that he had seen natural
selection at work.
Natural selection is the engine that
drives evolution, not through intention
or design, but through persistence,
trial, and error. Within every
population, no two individuals are
exactly alike. Those with traits that
give them an advantage in a given
environment, making them fitter in an
evolutionary sense are more likely to
live longer and have the opportunity to
produce more young. Those young then
inherit those useful traits via their
genes, and so those useful traits spread
and populations change. Indeed, this is
why Bates's butterflies seem to mimic
each other. The individuals that
resembled the toxic model most closely
would live while those that did not
would be eaten. And indeed, this process
of selection can happen even more
rapidly than we may think. Before Mosamb
beek civil war, 18.5% of female
elephants in Gorangosa National Park
were naturally tuskless. But among those
born since the early 1990s, the figure
has risen to 33%.
Why? Because tusked elephants were
targeted by poachers during this chaotic
period, while tuskless elephants were
spared. The tus elephants were more
likely to survive and pass on the trait.
Selection can be remarkably efficient.
And yet this efficiency creates a
paradox. If natural selection so
effectively eliminates disadvantages,
why is it not eliminated the biggest
threat to life of all, aging? If natural
selection favors organisms that survive,
why after so many millennia of evolution
to any organisms die at all?
In the late 1800s, German biologist
August Viceman thought he had the
answer. He trained as a physician before
turning fully to zoology. Drawn to the
puzzles of heredity and evolution,
Viceman saw age as a negative trait
evolutionarily speaking. Elderly people
could not hunt, gather, or fight as
effectively, and if the old lingered too
long, he suggested they would even
compete with the young for scarce
resources. Programmed death in this view
was adaptive. It cleared the way for new
generations serving the survival of the
lineage. Yet objections to this idea
included Alfred Russell Wallace who
argued that natural selection acts on
individuals not species and of course no
individual benefits from its own demise.
Viceman would go on to ultimately revise
his position, but his idea of programmed
death sparked debate around the
relationship between evolution and
aging, with a more promising theory
arriving a few decades later.
It is the 1920s at University College
London. A man sits alone in a specially
designed chamber. The door is closed and
tightly sealed. The air tastes strange.
He tries to continue writing numbers and
short words, but the blood pounds in his
head and he begins to wobble on his
stool. Still, he tries to keep the
pencil moving, but his hand shakes.
Everything begins to blur as the pain
intensifies in his head until the door
cracks open and new air spills in cool
and sharp. The man's father appears,
smiling, and John Burden Salison Haldane
smiles back, his vision steadying. Now
the chamber is not filled with 7% carbon
dioxide.
Haldane did not have the most
conventional of upbringings. Indeed, his
physiologist father had no qums about
bringing his son into his experiments.
At 13, he was sent deep sea diving to
work out how to avoid the bends and took
a trip down a coal mine to experience
the effects of harmful gases deep below
the earth. And he perhaps it is no
wonder that he developed such a ponchant
for risk within his own work. He went on
to drink acid, sat in decompression
chambers to the point of suffering
crushed vertebrae and burst eardrums,
and reported that the 7% carbon dioxide
room gives one a rather violent
headache. Palane risked both injury and
death by participating directly in his
experiments, but eventually would become
a towering figure of early evolutionary
biology by investigating the mystery of
death itself.
Hulane wanted to understand why certain
diseases such as Huntingtons persisted
in populations even though they were
deadly. Why hadn't they been selected
out? The reason for terrible diseases
emerging in older age, he suggested was
timing. Indeed, Huntingtons typically
emerges in middle age after most
individuals have already had children.
Haldane argued that natural selection
cannot eliminate a disease that strikes
only after our genes have been passed
on. And in this sense, he said, the
later in life a trait appears, the less
visible it is to selection. Haldane
worked on this concept with Peter
Medawir in the 1940s and called this
idea of decreasing evolutionary pressure
over an individual's lifetime the
selection shadow. And so he saw that
evolution matters most in the period
where individuals are reproducing.
Beyond that, the strength of selection
fades into shadow. Death might not be
programmed, as Viceman once suggested,
but it was clear that past a certain
point, it could simply be ignored.
This idea of the indifference of
evolution would be expanded on in a way
that would capture the public
imagination many decades later by
Richard Dawkins in his book the selfish
gene.
Natural selection he argued does not
operate for the good of the group. It
operates at the level of genes which in
a sense use bodies as vehicles for
replication. And so from this
perspective, what really matters is not
whether an organism lives a long and
comfortable life, but whether its genes
are successfully passed on. Once
reproduction has occurred, the fate of
the body is of little consequence to the
force of evolution. And it is this that
has affected our ancestors for millions
of years. Today, humans experience a
relatively long puberty compared to
other species with full sexual maturity
around 13 to 17 in girls and 15 to 18 in
boys. But
our early homminin relatives living
around 4 to2 million years ago, likely
matured far earlier than that, at around
8 to 10 years old, much like chimpanzees
do. Homoerectus, however, a member of
our own genus, perhaps reached adulthood
closer to modern humans. The famous
Turkana boy fossil, a particularly
complete skeleton of Homoerectus youth
dated to around 1 and a half million
years ago, appears to be not yet fully
grown at potentially around 8 to 12
years of age, suggesting a longer
childhood than earlier prehuman
ancestors. And so it seems likely that
the selection shadow has been drifting
later over our evolutionary journey. But
how exactly is this shadow built? Is it
just specific diseases such as
Huntingtons that natural selection lets
through the net of its protection later
in life? Or does the selection shadow
involve much more than that?
To answer this, we must return to
University College London in 1951 and to
a lecture with a mysterious title by
Haldane's colleague Peter Medawir, an
unsolved problem of biology.
Addressing his audience that day of
other esteemed scientists, students and
members of the public, Medawir began,
"The problem I propose to discuss is
that of the origin and evolution of what
is commonly spoken of as aging." In this
revolutionary lecture, Medawa would
illustrate in concrete and mechanical
terms the extent of the selection shadow
and how it can be built within a human
body. All living things accumulate
cellular damage. Sometimes as a result
of this damage they lose their ability
to divide or their repair systems fail.
This accumulation leads to organs
functioning less well and the body
becomes prone to disease or infection.
Indeed, this is the process of aging in
concrete terms. And so with diseases
like Huntington's, this accumulation of
damage matters little to our
evolutionary success if genes have
already been passed on. Aging,
therefore, Medawa argued, was simply the
byproduct of survival beyond the age of
evolutionary concern.
Meet's theory of mutation accumulation
expanded the scope of the selection
shadow concept beyond disease to include
the small unperceivable buildup of
damage within our bodies. And this
theory still stands as one of the
primary causes of aging and why it would
still exist today. And so the work of
Haldane and Medawir showed that aging is
a consequence of evolution prioritizing
youth and fertility. Past our
reproductive prime selection pressure
lessons and the accumulation of
mutations and deletions are no longer
getting in the way of passing on our
genes. Our body's job is done, so to
speak, and can slide into disrepair.
And so it was with the dead man on the
plane 30,000 years ago. His hair
thinning on his head has been supplied
by less melanin from the follicle,
turning it a whitish gray. The cell
turnover in his nails is decreased,
making them rigid. And the keratin that
makes the nail plate has lost moisture
and oil over time, leaving them brittle.
And his skin has been producing less
collagen, leading to a loss of
elasticity that leaves wrinkles near the
corners of his eyes and the slightest
sag from under his chin. And so we can
see that he'd clearly lived well into
the selection shadow. His life was long
enough that he'd seen his genes passed
on to not one but two generations.
Cellular damage, therefore, would have
been long accumulating in his body. And
so was it simply this that killed him?
Or is there more to discover? For there
is another possibility. Could it be that
whatever killed him was not simply
ignored due to selection shadow, but
instead was something that was actively
selected for? Could natural selection
have actually chosen the trait that
would kill him?
An old stooped homo sapiens climbs a
rocky path slow and uneven, leaning on a
branch as a support. Each step sends
pain through her knees and hips. Her
fingers can barely close around the
stick. She stops often breathing hard,
but she keeps going, one foot ahead of
the other, grimacing through the pain.
Once she was strong, able to run and
hunt and swim and climb. Now her joints
swell and her body aches. We might think
of arthritis as a price paid for modern
longevity, but the fossil record shows
it was a harsh reality for our ancestors
50,000 years ago, too. This arthritic
pain will be with the ancient female
until she dies. And indeed, the lack of
mobility it causes makes her vulnerable
to the many dangers of the prehistoric
world. She is stalked by a cave lion and
will have no chance of outrunning it.
But of course, she is old, her genes
long passed on, and so there has been no
drive for the forces of natural
selection to spare her from this tragic
fate. But what if it goes further than
that? What if she has lived this long in
part due to the exact genes that now
give her this pain and vulnerability?
What if her DNA contained a genetic
jackal and hide?
The fossil record reveals examples of
the ailments of old age existing even
tens of thousands of years ago in both
ancient Homo sapiens and our Neanderal
cousins. Indeed, perhaps the most famous
example is the old man of Le Chappelle
saw discovered in 1908 in France. This
neanderal male was around 50 to 60 years
old at his death and his bones revealed
severe arthritis had deformed his spine,
hips, and shoulders, restricting his
mobility. His remains made it clear that
age- related conditions like arthritis
have existed for at least 60,000 years,
confirming they're not just a modern
ailment encountered too recently for
natural selection to have addressed
them. And so, what if there is in fact a
reason that they are there? What if the
genes that cause the diseases of aging
like arthritis are selected four?
The sky had turned a hazy color of rust.
Sirens wailed throughout the valley and
the Paradise California wildfire had
burnt outside for hours. And in one
house, a manuscript begins to cinder an
autobiography by George C. Williams that
would be lost to the fire in his son's
house.
The details of the book were doubtlessly
a great loss. Williams, a biology
professor, was a character. Some
described him as something of a commod,
but others loved his directness. Indeed,
he wrote all his notes in Icelandic
despite not being Icelandic himself. His
collaborator Randolph Ness said he had a
fascination with aspects of bodies and
minds that just didn't seem to make
sense in evolutionary terms. He is seen
today as the father of evolutionary
medicine. The idea of viewing disease
and searching for their causes through
the lens of evolution.
Williams would die at 84. The disease
that killed him was Alzheimer's. A
common disease of old age and in this
case an ironic one. Indeed, it was
diseases like Alzheimer's that so
fascinated Williams. Why have such
diseases at all? Why should they exist
within us? The solution Williams came up
with would influence evolutionary
biologists forever after. For in 1957,
at the age of just 31, Williams
published a paper that changed how
scientists thought about aging titled
pleotropy, natural selection, and the
evolution of scinessence. It argued a
controversial idea that aging is not the
result of forgotten biology, but the
logical outcome of how genes are
selected. He like hold in this new era
of DNA, genes and the fundamental basis
of natural selection. Williams saw aging
as not the forgotten byproduct of a
reproducing animal, but as collateral
damage. He worked off Haldane and
Medoir's principles that the key driver
of evolution is reproductive fitness,
not health or comfort or longevity for
its own sake. Therefore, he argued if a
gene improves fertility early in life,
it will be favored by natural selection
even if it carries damaging consequences
later. So, genes with multiple effects
or geneticists call pllyotropy can
create trade-offs where the effects are
opposite in different life stages.
Williams called it antagonistic
pleotropy, the genetic jackal and hide.
Imagine
a young homo sapiens male. He stands at
the edge of a river, breath steaming in
the cold dawn. He picks up a rock, hulls
it across the water to feel the strength
of his throwing arm. He is strong and
growing stronger through hunting and
through butchering and hauling his
prizes home. However, his strength has
not gone unnoticed. Other males have
admired his skills and sought alliances
with him. A number of females have made
their intentions clear, too. Years pass.
The group has moved many times, and his
children have grown tall and strong. His
hair is beginning to gray, but the
muscles of his body, although slightly
diminished, are still impressive.
However, his biology has made him
destined to burn bright and fast.
For the testosterone that made him so
successful will betray him. He stands at
the side of a new river, picks up a
stone, and feels a tightening in his
chest.
High levels of testosterone are
associated with greater fertility,
higher libido, and social dominance in
young men. All traits that historically
would have translated into more
children, and more chance of passing on
genes. But later in life, the same
hormonal profile is linked to higher
risks of prostate cancer, cardiovascular
disease, and shortened life. And so
clearly, the benefits come when it
matters for evolution. And the price is
paid when it no longer matters. The
lineage is already secured. And it was a
similar trade-off for the old man of
Lashappelle. Certain genes can promote a
strong inflammatory response that might
have been beneficial for surviving
infections in ancient environments. Can
also increase the risk of age- related
inflammatory diseases like rheumatoid
arthritis. This can also be seen in BRCA
genes. Today they are known as massively
raising the risk of breast and ovarian
cancer, often striking in a woman's 30s
and 40s. Yet some evidence suggests that
they might once have conferred a slight
immune advantage or even higher
fertility, keeping them in circulation
despite their dangers. And so Williams
theory was a breakthrough that allowed
other scientists to push the idea
further, even down to the cellular
level.
In 1977, British biologist Tom Kirkwood
proposed a theory that many consider
alongside mutation accumulation and
antagonistic pleotropy to be the third
great theory of aging. Disposable soma
theory. The soma is the body, the mass
of cells and organs that carry out
genes. Kirkwood argued that evolution
forces a budgetary choice. Energy is
finite and an organism can spend it on
reproduction or on long-term repair and
maintenance, but not both at full speed.
Natural selection channels resources
towards reproduction, gearing cells to
undertake actions that help fertility
and child rearing like sperm production.
However, less energy is spent on
repairing cells as they accumulate
damage. This means that bodies are
maintained just long enough to ensure
reproductive success after which
maintenance inevitably declines. In a
sense, this is not a design flaw. This
is the design. Different species show
the principle in extreme forms. The
Pacific salmon expends itself entirely
in a single spawning run. It hulls
itself upstream, mates, and then dies,
collapsing under the strain. Mayflies
are even more extreme. Some live as
adults for less than a day. Their only
purpose to mate before they fall to
their deaths. Then there are creatures
like the boowhead whale which invests
heavily in cellular repair and can live
for more than two centuries. But of
course, even these are not immortal.
Every living body carries a trade-off
between maintenance and reproduction.
Humans fall somewhere in the middle. Our
repair systems sustain us through
several decades of fertility, but then
maintenance falters. DNA errors
accumulate leading to cancers and immune
systems weaken. And so in a sense, death
in this view is not a catastrophic
failure, but the gradual exhaustion of a
maintenance budget. We do not die
because evolution wants us to, but
because evolution has driven our bodies
to prioritize our younger, fertile
years. even when that directly
negatively impacts our later ones.
And so we now return to our cold case on
the ancient plane.
It's time to look past the wrinkles of
his skin and delve beneath inside his
body. What does this network of organs
and arteries and veins tell us? Is there
a sign of a heart attack? antagonistic
pleotropy at work. It doesn't appear so.
Neither are there tumors or infections
or arthritis or Parkinson's. And so we
can look deeper at the microscopic
elements of his body. What do his cells
tell us? Did they simply run out of
energy? His body having spent its
resources on survival rather than
repair. A slow degradation.
There is damage, but nothing
catastrophic. Wear and tear on the
fringes of his organs. Yet still the
killer is unclear. It's only when we
return to the outside of his body that
we see it. Not a wound or a bruise, but
the shape of his body itself. His body
is narrow, the limbs thin and drawn, the
muscle wasted not by famine, but by a
long, subtle, unseen process. It is
clear that the answer lies deeper than
flesh or bone, deeper even than the
cell. To find it, we must look into what
wrote the blueprint of this body before
it ever began to live. And in journeying
towards this answer, we must also settle
something else. Why do old people even
exist?
It is the early 1950s and America is
waking up to the Today Show. The camera
pans across a sleek New York studio. The
audience begins to clap and onto the
stage waddles a small chimpanzee dressed
in human clothes. He claps his hands,
grins, and leaps onto the desk. The host
offers him a cup of coffee, which he
pretends to sip before spitting
dramatically into a bin. The audience
laugh and cheer. This chimp was J. Fred
Mugs, one of the most famous animal
celebrities. Born in Cameroon, but
brought to New York as an infant, Mugs
became a regular part of the Today Show,
getting up to various antics like
playing the drums and mimicking his
human colleagues. But perhaps just as
astonishing as his career is his
longevity.
Born in 1952, Jay Fred Mugs lived to
over 70 years old.
However, this is a special case and
makes him one of the oldest living
chimpanzees in history. Wild chimpanzees
rarely live beyond their 30s and life
expectancy at birth is around 19 years,
highlighting the dangers of living in
the natural world. And so were the lives
of our homminin ancestors once as short
as wild chimpanzees? And if so, when and
why did this change?
To begin with, what do lifespan and life
expectancy really mean? Lifespan is
often given as a maximum age, the
longest amount of time a particular
species has been observed to or could
potentially live. The term life
expectancy, however, usually refers to
the average number of years a newborn
can expect to live given their
environment. The life expectancy of
someone born in the USA today is very
different to someone born in medieval
Germany or even someone born in many
other countries. But averages can
mislead. The life expectancy of someone
born today in Chad, for example, is just
59. But when you look at the life
expectancy of someone in Chad who has
made it to their fifth birthday, that
figure jumps to 66. Why? Because they've
made it past one of the hardest parts of
life. And indeed, human life is full of
hard parts. These hard parts are
scientifically called mortality risks
and they can be extrinsic or intrinsic.
Extrinsic mortality refers to risks that
come from the outside world. for
example, predators, accidents,
infections, violence, or famine. Whereas
intrinsic mortality refers to the body's
internal processes. For example, risks
from genetic disease, cancer, and
gradual cellular decline. And it is
really the balance between these two
things that has shaped the story of
human life expectancy. Extrinsic risks
are particularly high at different times
for different people. But for all of us,
the very first years of our life are
probably the most dangerous. Indeed,
preodern medicine, human babies faced a
difficult time staying alive. In
medieval Europe, it is estimated from
records that almost a third of infants
died before their first birthday. Babies
today are more likely to survive. But
still, in some of the poorest countries
in the world, babies dying in their
first year is not uncommon. For example,
in Afghanistan, around 10% of all
infants die in their first year of life.
Of course, humans in our infancy, and in
particular, our very first days are
incredibly vulnerable. We are born
entirely dependent on our carers with
immature immune systems and weak
thermorreulation.
Diseases like diarrhea, pneumonia, and
sepsis regularly claimed infant lives
before modern medicine. And even deeper
in our evolutionary history, we would
also have been at greater risk from the
world around us, exposed to the elements
and predators of the natural world.
The tongue child of fossil of
Oralopythecus Africanis was only 3 years
old when they died. Their skull is
scored by talon marks in its eye
sockets, marks similar to those left on
modern monkeys attacked by African
crowned eagles. It looks like this child
from 2.8 8 million years ago was
attacked and possibly snatched by a
great eagle. Another Oralopythecus child
skull from South Africa known as SK54
shows puncture marks from leopard's
teeth. And yet to survive childhood was
not the end. It meant facing new
challenges. For example, for our
ancestors, if they were female, they
would potentially face the risks of
pregnancy and childbirth. Before modern
obstetrics, labor and immediate weeks
after delivery carried around six times
the normal risk of death. Hemorrhage,
sepsis, obstructed labor, all were
deadly in the absence of medical
intervention. And for men, the danger
was different, but no less present.
Anthropologists studying huntergatherer
groups find that adolescence and young
adulthood are highly perilous. Young men
take on hunting roles, risking injuries
from prey and predators and fight rival
clans for territory. Male mortality
spikes in those years in huntergatherer
societies, just as maternal mortality
spikes in reproductive age for women.
These different risks created an uneven
landscape of survival, but the pattern
is clear. Get through childhood, dodge
the hazards of early adulthood, and your
chance of reaching old age raises
significantly.
And older people do appear in the fossil
record. [ __ ] man, who lived in
Australia around 40,000 years ago, was
so well preserved that scientists were
able to age him to around 50 at the time
of his death. Similar to the estimated
age of Neanderal specimens, Lafarasi 1
and Shannadar 5, both dated to around
50,000 years ago. And indeed, older
specimens aren't limited to only the
time of our species. The oldest evidence
of which is around 300,000 years old.
However, toothware studies do show that
homo sapiens and neanderal populations
sustained a larger share of older adults
than the homminins and even the earlier
species of homo that came before them.
Early hominins such as sahalanthropus
chidensis andolopythecus apherenis
likely shared short precarious life
expectancy similar to modern chimps.
Their bodies show rapid growth and early
maturity, a pattern more like nonhuman
apes than humans. Indeed, the work of
American professor Caleb E. Finch has
not only found a doubling of life
expectancy since the year 1800. Perhaps
not surprising when we consider modern
medicine, diet, and living standards,
but also another more ancient increase.
He found that across the roughly 300,000
generations between 1800 and the last
common ancestor of humans and
chimpanzees, our ancestors life
expectancy had already doubled once
before. But what is the cause of this
increased life expectancy? One obvious
reason is reduced extrinsic mortality
due to the development of technology and
cooperation. The leopard, for example,
that killed Oralopythecus SK-54 is less
dangerous to a group of hominins armed
with stone weapons, fire, and housed in
some form of shelter. If this group can
communicate, share a knowledge of
potential leopards and how to avoid
them, its members are at much less risk,
increasing their life expectancy
further. But does this explain
everything? Was it simply that our
advanced tools and intelligence became a
trump card protecting us well into the
selection shadow of our lives? Or are
there different reasons for old people
to exist?
An old woman sits at the entrance of a
crude shelter made of wood and hides
silver hair, wrinkled skin, wiry frame.
Two small children play beside her,
tapping sticks together and rolling
pebbles along the ground. She keeps them
close. Every so often, she offers them a
little food or swipes at their feet to
admonish them for bad behavior. She
starts preparing something for the
children to eat, hacking at some fruit
with a roughly human blade. Her joints
ache, but she flexes her fingers to ease
the pain. However, these are not the old
woman's children. These are her
grandchildren. Her own daughter is out
foraging, armed with the knowledge her
mother can continue to give her into her
adult life. She's known many droughts,
many lean times, many storms, and now
her skills and knowledge can also be
passed down to new generations, allowing
her to contribute to the evolutionary
success of her genes long after
reproductive age.
And so grandmothers may have been some
of the most important parts of our
evolutionary history and a driver of our
longer life as shown by the uniqueness
of human life after menopause.
Menopause marks the end of reproductive
life in women and is almost unique to
humans. While some female animals in
captivity can survive for a while after
the end of their reproductive period, it
is only human women and a handful of
whale species that show universal
menopause with a long post-reroductive
stage. And so, if natural selection only
cares about reproductive health, why
does menopause exist? And this long
period of life after the end of
menstruation?
One suggestion is known as the
grandmother hypothesis. Anthropologist
Christine Hawks was observing older
Hanza women in northern Tanzania dig for
tubers when she found herself asking why
do women live so long after they stopped
bearing children. The answer hawks
advanced along with colleagues James O'
Connell and Nicholas Bluren Jones was
that they lived because they were
useful. Older women, far from being
evolutionarily spent, improved the
survival of their grandchildren by
providing food and care in addition to
their parents and also allowing parents
more time to generate food and other
necessities for them and the wider
group. By taking on some parenting
responsibilities, the hypothesis went,
grandmothers freed up mothers to have
more children, increasing the number of
their surviving descendants and carrying
on the genes that supported longevity
beyond reproduction. And indeed,
ethnographic data from the Hanza of
Tanzania did seem to support the idea.
Children with grandmothers nearby were
more likely to survive into adulthood.
And indeed, it's not only the transfer
of knowledge and skills that older
people can provide, but also some other
more active roles can be best filled by
those with experience.
For example,
hunting.
Various studies have shown that while
the success of foraging and fishing
activities can peak by the age of 20,
men's hunting success peaks in the age
range of 35 to 50, long after many of
these men in huntergatherer societies
are grandfathers. And so it would appear
that older humans were not simply
protected from the risks of extrinsic
mortality by the technology of their
species, but were key players in the
knowledge and use of this technology. As
generations passed, our ancestors gained
a larger variety of skills to be passed
on, woven into an ever more complex web
of culture. A 2004 study by Rachel
Kaspari and Sanghi Lee pinpointed a
specific window within the history of
homminins where life expectancy
increased. They analyzed 768 human
fossils dating back 3 million years. And
after aging them, an astonishing
statistic emerged. After entering the
upper Paleolithic period around 30,000
years ago, there was a five-fold
increase in the number of individuals
surviving into old age. Kaspari said in
an interview, "In the upper Paleolithic,
the proportion just skyrocketed. It was
unbelievable. We didn't expect that."
They would go on to suggest that older
adulthood is a critical demographic
factor in the development of human
culture. In their paper, the old become
common. Elders could become cultural
libraries, passing on useful knowledge
and skills that kept their direct
descendants alive and able to pass on
the long life genes they had inherited.
And indeed, it is clear the dead man on
the ancient plane lived just such a
life. For he lived not only long enough
to pass on his genes, but to ensure
their success by passing on his
knowledge to multiple generations. His
crooked foot was an injury sustained
whilst hunting many decades into his
life. He would have passed on this
knowledge to younger hunters whilst also
ensuring the success of many hunts that
would feed his community. But what was
it that caused his body to finally
become frail? What was it that brought
this long successful life to an end?
This man lived right in the period of
the five-fold increase of old age
individuals in our history. A boom in
life expectancy that actually would
decline just after the close of the
upper Paleolithic. The transition to the
Neolithic, when people settled and began
farming, should have been a time of
plenty. But at first, we faced new
challenges. Living in larger, denser
communities, increased exposure to
infectious disease. While reliance on
crops before storage and preserving
technologies had developed meant
vulnerability to famine, archaeological
evidence shows that in early farming
societies, lifespans fell compared to
hunter gatherers. Malnutrition,
epidemics, and social inequality cut
lives short. It was only much later with
improvements in sanitation and
eventually medicine that lifespans began
to climb again.
And of course, the greatest improvement
came in the 20th century, a time of
massive medical advancement. Today,
humans live longer than ever before in
our history. As we've seen before, this
longevity lies partly in our genes.
Perhaps meddling with those genes could
halt the aging process altogether.
Indeed, advances in gene therapy make
this idea seem not entirely fictional.
Could the future be one in which we can
live forever?
Deep beneath the Arctic ice, a Greenland
shark glides slowly through the dark. It
hasn't noticed in its slow traversing of
the deep sea. But this shark has lived
through the time of the English Civil
War, the birth of modern science, the
industrial revolution, and both World
Wars. It was already ancient when humans
first landed on the moon. It has lived
through four centuries.
Using radiocarbon dating of proteins in
28 sharks eye lenses, scientists have
found that these slow growing predators
likely reach sexual maturity only after
around 150 years. Indeed, one female was
perhaps born in the early 17th century
and was still swimming when the study
was published. The Greenland shark is
the longest lived vertebrae known with
lifespans estimated at up to 390 years.
Its secret is partly its environment.
Cold waters slow metabolism, delaying
aging. But it also tells us something.
What counts as a long time is relative.
Whales, turtles, and sharks live longer
than even the longest lived human. And
so why can some animals delay the
inevitable for so long?
To understand this, it's useful to look
at PTO's paradox
named after epidemiologist Richard Pto.
The paradox arises from a simple
observation. Cancer, one of the biggest
killers of those who live to an older
age, is caused by mutations in cells.
The more cells an organism has and the
longer it lives, the more opportunities
there are for mutations to accumulate.
And so by that logic, large, long-ived
animals should be riddled with cancer. A
blue whale has a thousand times more
cells than a mouse and lives decades
longer. So it should be a cancer
factory. And yet elephants, despite
their size and long lives, have far
lower cancer rates than humans. Why?
Scientists believe it is because they
carry multiple copies of a genome
protector called TP53.
Sometimes called the guardian of the
genome, this gene acts as a vigilant
quality control officer, scanning DNA
for damage and halting cells from
dividing when their code goes wrong. If
the flaws can be repaired, TP53
coordinates the fix. If not, it orders
the cells to self-destruct. The gene
itself is ancient, far older than our
own species. Variants of TP53 appear
more than a billion years ago, long
before animals, plants, or fungi took
their modern forms. In the microbial
world of early Earth, where radiation,
ultraviolet light, and reactive oxygen
molecules constantly bombarded living
cells, DNA damage was inevitable. The
first TP53- like proteins evolved in
single-sellled organisms as rudimentary
guards. molecular systems that detected
errors in genetic material and paused
the cell cycle long enough for repair.
As multisellular life evolved, this role
became much more important. As cells
began cooperating, passing chemicals
between one another, they became
vulnerable. A single mutation could now
endanger not just one cell, but the
integrity of an entire organism, like a
single brick falling and taking the
entire wall with it. More cells meant
more divisions, more mutations, and more
chances for a cell to start reproducing
out of control, the cause of tumors. And
so in this new multisellular world, TP53
acted as the control center, halting
replication, summoning repair enzymes,
and if the damage couldn't be fixed,
triggering apoptosis, programmed death
of the cell to prevent a tumor from ever
forming.
The role of TP53 mirrors the complexity
of the organism it protects.
In humans, it coordinates hundreds of
genes involved in DNA repair, cell cycle
controls, metabolism, and immune
response. It can even influence how
cells respond to stress, starvation, or
viral infection. But like any complex
system, it has weak points. For when
TP53 itself is damaged, the consequences
are profound. Roughly half of all human
cancers contain mutations that silence
or corrupt this gene, stripping cells of
their ability to protect themselves. And
so TP53 may have evolved primarily to
protect us through the years of
fertility, ensuring survival long enough
to reproduce, but it continues to defend
us long after that evolutionary mandate
has been met. It is a relic of life's
earliest struggles, still performing the
same essential task to hold the line
against cancer for as long as possible.
And TP53 is the key to why big animals
can outlive smaller ones. Mice have only
one copy of the gene while elephants
have 20. Bigger animals have simply
evolved better in cancer defenses.
The presence of TP53 raises an obvious
question. If some animals have evolved
ways to suppress cancer and extend their
lifespans, why don't all animals do the
same? Why have humans not loaded up
their genome with TP53 copies and other
protective mechanisms, thus creating
bodies that could maintain themselves
indefinitely?
Well, the answer comes back to George C.
Williams and antagonistic pleotropy the
principle where a single gene affects
multiple traits with one trait being
beneficial in earlier life and another
being detrimental in latter life. TP53
helps protect us from cancer by stopping
damaged cells from growing. However, it
is ironically particularly prone to
mutation. This means the more copies of
the gene we have, the more chances there
are for one of them to mutate. And if a
mutation happens in a way that disrupts
TP53's protective function, it can
actually increase cancer risk rather
than reduce it. If a harmful TP53
mutation causes cancer in early life, it
may kill you before you can reproduce.
And as we know, evolution always favors
reproductive fitness. And yet still,
some species have developed
extraordinary ways to keep going.
Galapagus tortoises, for example, can
live more than a century. But what about
true biological immortality? Is there
any creature on Earth that truly never
dies? For that, we have to turn to the
sea and not the Greenland shark, we have
to go to much more temperate waters and
find the so-called immortal jellyfish,
Terratopsis Dorni.
This incredible organism can rejuvenate
essentially indefinitely. When stressed
or injured, its adult body, the medusa
stage, collapses and transforms into a
tiny blob-like mass, which then attaches
to a surface like a rock or a piece of
coral, and becomes a polip, the same
form it had as a juvenile. From this
polip, new jellyfish buds grow,
genetically identical to the original,
like a little factory line of clones.
In essence, it reprograms its body back
to youth, restarting its life cycle
without reproducing sexually. It would
be like a human shrinking back to a
fetus. And in principle, it can repeat
this process indefinitely, dodging death
by becoming young again. and other
organisms also almost reach immortality,
but in different ways. Hydra, tiny
freshwater animals, continually
regenerate their cells and show no signs
of aging under laboratory conditions.
Some clams live for centuries simply by
keeping their metabolism extraordinarily
slow. Tardigrades can dehydrate
themselves into little dry husks and
remain dormant for hundreds of years
before reanimating at the touch of
water. But of course, these creatures
are relatively simple compared to us.
Complexity makes immortality much
harder. A jellyfish can reset because it
has no brain to preserve, no complex
tissues to coordinate. But humans cannot
turn back into embryos.
And yet, surprisingly, there is hope for
those among us who do wish to live
forever. For in theory, nothing in
biology rules out reaching human
immortality through technological means.
Aging is after all simply a buildup of
failures. DNA mutations, telmir
shortening, protein misfolding. If each
of those could be fixed, in principle,
aging could be stopped or reversed.
Already scientists are experimenting
with gene editing to mimic the extra
TP53 copies of elephants drugs to boost
DNA repair and stem cell therapies to
rejuvenate tissues. Anti-aging research
is a fast growing field with
billionaires funding labs that promise
to cure aging and people biohacking
their own bodies in an attempt to extend
their life. Who knows what the future
may bring?
And so though TP53 has been called the
guardian of the genome, it is still not
safe from the jackal and hide effects of
antagonistic pleotropy. Thus, we finally
find the killer of the man lying on the
plane 30,000 years ago. He was not
killed in a fight with a man or a beast.
Despite his high testosterone, he didn't
suffer a heart attack. He did not
develop cancer protected by the TP53
within his genome. In the end, TP53, the
gene that helps complex animals escape
cancer, hunting down damaged cells and
destroying them, became a victim of its
own success. Year after year, in this
man's body, TP53 was shutting down
cells, reducing the reserves of healthy
stem cells, inhibiting the repair of
tissue damage. By the end, the very gene
that kept him alive became part of the
machinery of aging, tipping the man
towards frailty. and finally an end. But
of course, not before the many
beginnings of the new generations he
oversaw.
Lifespan and life expectancy have
changed dramatically since the time of
our ancestors through many millennia of
evolution. From the beginnings of
hominins, perhaps living only as long as
wild chimpanzees, through to the
explosion of old age humans 30,000 years
ago, and all the way up to today, where
our lives are the longest they've ever
been. Indeed, our lives are long enough
to raise children, grandchildren,
sometimes even great grandchildren, and
give them the skills they need for their
lifetimes. Human lives are long enough
to build cultures like nothing ever seen
before on our planet. And so our lives
might be short compared to the long
history of our species, but they are
long enough to live a life that matters.
for watching and we'll see you next
time.