Science has revealed paradigm-breaking insights
into the workings of the human body.
(dramatic music)
There is a vast web of information networks,
just like the internet, within our bodies.
And in fact, our various internal organs
are sending out messages
and directly communicating with one another.
The latest research has also revealed
that even some unexpected body parts are playing
crucial roles within the body's inner networks.
One of these surprising players is fat.
Perhaps you'd only thought of your body fat
to be just oily deposits.
We'll also be featuring bones.
You may have just thought our skeleton is merely
a mass of calcium that supports the body.
But in fact, it's becoming increasingly clear
that both fat and bone are sending out messaging molecules
which are responsible for controlling
a variety of different organs.
And disruptions in this communication are the likely causes
of many modern day diseases that affect us today.
What was somewhat surprising was that
the hormone was made by fat tissue.
It's now very clear that adipose tissue is a very dynamic
organ and makes hormones, plays a very important role
through the production of these hormones to regulate hunger.
Fat and bone possess an incredible power,
crucial for protecting our lives.
To discover their secrets, let's go on a journey
into this remarkable world within our bodies.
We'll start with fat.
(speaking in foreign language)
Do you know what our fat tissue looks like?
This is actress Manami Hashimoto.
She is taking part in an experiment where a state-of-the-art
MRI machine is going to scan her from head to toe.
So we can visualize the actual
appearance of fat inside the body.
We're now seeing the long and convoluted intestines.
And we can see a cross-section of her stomach.
Above this, we can see a large silhouette.
It's her liver.
If we delve in deeper, we can even see her heart.
It's a complete picture of Manami's internal organs.
This image shows only the parts of her body composed of fat.
You can see that fat tissue is present everywhere,
more or less revealing the shape of the body.
The sort of fat that we're usually concerned with,
fat under our skin, looks like this.
And there's even fat in the bones, too, called marrow fat.
And visceral fat surrounds the internal organs.
The total weight of all this in Manami's body
comes to a sizeable 18 kilograms.
Relative to her total body weight
of 56 kilograms, it's roughly 1/3.
So what kind of messages are being
sent out by fat tissue like these?
This boy can tell us more.
Julian Felton, an 18-month old toddler
living in Connecticut in the United States.
Look over on this side.
For the most part,
Julian acts just like any healthy child of his age.
But Julian was born with a very rare disease.
Yeah, yeah, there.
It's called lipodystrophy,
where his body has no fat tissue at all.
One more time.
And at meal times, the symptoms
of his condition become more obvious.
Seaweed.
Trying to get it all in at once, huh?
One at a time, one.
Julian devours his favorite snack, seaweed.
He has an insatiable appetite.
Today, his lunch consists of salad.
Yogurt.
To see.
And a dish made from chicken and cabbage.
These should be enough to fill him up.
But he doesn't seem full.
This is all mine, bud.
Yeah, I know, it's mine, it's Mama's, I love you.
Muah.
(Julian wining)
He reaches out,
hoping for some of his mother's lunch too.
It's all gone.
(Julian crying)
So we noticed Julian was extra hungry
shortly after returning home from the hospital.
It's almost like he's starving.
Like if I don't get it right now, I'm going to die.
Julian constantly feels hungry.
This is actually caused by the absence
of fat cells in his body.
But fat inside our bodies aren't just made up
of sticky clumps of oily deposits.
These are electron microscope images of fat tissue
taken from multiple angles.
They were then combined to create this groundbreaking
three-dimensional image of body fat.
Take a look.
Each one of these spheres is a fat cell,
also known as an adipocyte.
Fat deposits within our bodies
are all made up of these living cells.
(gentle jazz music)
Let's take a closer look at one of them.
The red area is the cell nucleus.
The cell contains a large lipid body
which holds molecules of fat.
Sugar and fat sourced from food
are stored here as energy source.
But Julian's body has no fat cells.
So any sugar or fat in his food
must remain in the blood stream.
As his body has nowhere to store them.
Unless his food intake is controlled,
his blood sugar will rocket
to 1 1/2 times that of a healthy person.
And the amount of fat in his blood can reach
more than 20 times greater than normal.
And this puts his health at great risk.
Up until now, the expected lifespan of patients
with this syndrome was only about 30 years.
This is because there's no way to effectively control
their appetite in order to protect them
from severe diabetes and heart disease.
This raises the question, why does
a lack of fat cells cause constant hunger?
The answer to this was identified by one of the world's
leading authorities on appetite, Dr. Jeffrey Friedman.
He made a startling discovery.
Fat cells release a molecule
that actually inhibits appetite.
This signaling molecule is a hormone called leptin.
It's about a millionth of a grain of sand,
a very tiny speck.
This very small molecule, however, packs a punch.
Looking at a juicy piece of steak
should activate a certain part of your brain.
Let's take a look.
These regions are the brain's appetite centers.
Normally, increased activity in these areas
subsides after eating.
But in a patient with lipodystrophy,
the brain's appetite centers
remain active even after eating.
However, when the brain receives a dose of leptin,
this activity recedes.
Leptin is suppressing that insatiable appetite.
What was somewhat surprising was that
the hormone was made by fat tissue.
It's now very clear that adipose tissue is a very dynamic
organ and makes hormones, plays a very important role
through the production of these hormones to regulate hunger.
As a result of this discovery,
new drugs are being rapidly developed
trying to overcome lipodystrophy.
(Julian crying) You're okay.
It's okay, it's alright.
I know, I know.
Yeah, I got that one. -: Okay.
I can put (mumbles) so we're gonna take.
But how exactly are these tiny,
minuscule signaling molecules manipulating the brain?
High-resolution computer imagery created based
on the latest research can help us understand this process.
Let's go and explore the world within our bodies.
We are surrounded by spherical fat cells.
These cells are about 0.1 millimeters across.
Something seems to be leaking from that blood vessel.
These are sugar and fat molecules that have come from food.
They will be stored inside the fat cells
in the large lipid body.
At which point a dramatic change takes place.
Let's dive into one of these fat cells.
There are tiny particles contained in capsules.
These are the signaling molecules leptin.
Leptin sends messages from the fat cells
to the rest of the body.
(light music)
And its message says that there's
ample energy stored here, so stop eating.
As the amount of stored lipids increase,
more leptin is released into the body by the fat cells.
Let's follow the leptin as it travels through the body.
It's headed for a blood vessel.
Now it's being along the bloodstream.
Our blood vascular system serves as the information highway
for the exchanges between our body organs.
Some of these leptin molecules are headed for the brain.
They reach the brain's hypothalamus,
which regulates our instinctive needs.
The hypothalamus is a mass of countless neurons.
Now the leptin molecules are passing through
the blood vessels and into the brain.
They finally reach the surface of these neurons.
There are special receptors which respond only to leptin.
This is the moment where the brain
receives the message from fat cells.
The brain then decides that no more food is needed
and suppresses appetite.
Every day, these tiny molecules
from our fat are working away quietly,
regulating our appetite.
We now know that the way the body communicates
nutritional information is in part
by the production of this hormone, leptin.
So in a sense what the fat is telling the rest of the body
is either my nutrition is okay or I'm starving
or I'm too fat and in each case
the body responds in a different way.
Apart from leptin,
many more signaling molecules that are released
from fat tissue have been discovered.
Around 600 different types have been found so far.
Fat sends messages not only to our brain,
but to many different places that include
our bones, blood vessels, and immune cells.
It's thought that fat cells monitor
the levels of energy stored within our body
and optimize our energy intake and consumption.
So now, fat is beginning to be seen in a new light,
as a driving force operating behind the scenes,
controlling our body's energy balance.
Let's continue onto our next topic, bones.
Chunks of strong calcium that support the body.
But such a simplistic idea is being rewritten.
And it's now attracting a huge amount of attention.
The latest studies have revealed that our bones too send out
messages and that the messages work to keep us young.
In order to study such features of bones.
Three, two, one.
Main engines up and running and liftoff
of the Falcon Nine to the space station.
Cleared the tower.
We have to go up into space.
It's been known for some time
that astronauts lose significant bone mass
while up in space during a long mission.
Zero gravity in space is thought to be the best place
to study the effects of gravity on bones in the human body.
Being cultured in this bag are some components
of bone marrow from human bones.
You might think that bones
are all dry and rough on the inside.
But living bone looks very different
and contains gelatinous tissue within them.
This is bone marrow, and it contains various types of cells.
We're now inside our skeleton.
Let's explore this microscopic world
inhabited by these living cells.
We can see big columns made up of calcium.
And these red strands are blood vessels.
Look at this cell clinging to the surface of the bone.
It's called an osteoclast.
A cell that breaks down bone.
Osteoclasts dissolve the calcic surface of the bone
and discharge the dissolved bone debris.
But it can't be a good thing to leave bones like these
with potholes all over them, right?
But you needn't worry.
There's another type of cell that fixes the bone.
These little round cells are multiplying quickly.
They're called osteoblasts, and they build bones.
They cram into the big cavity in the bone
and release a viscous liquid.
It hardens like cement and forms fresh bone tissue.
This process of erosion and rebuilding keeps the bone strong
and replaces your entire skeleton every five years.
Besides building bones, osteoblasts have other tasks.
The latest research is starting to reveal that they send
crucial messages to keep our bodies in a youthful state.
Dr. Gerard Karsenty is a leading researcher
of signaling molecules sent out by bones.
He discovered a molecule which is released from osteoblasts
that works on the brain.
It's called osteocalcin, a tiny particle
which is not even 1/100 of a millimeter across.
But it plays a critical role
in directing our memory ability.
Dr. Karsenty conducted experiments on mice
which were genetically incapable of producing osteocalcin.
(mysterious music)
A mouse was placed in a tank of water
to see whether it can swim to safety.
And the time it takes to get to the island is measured.
In the first trial, both mice without osteocalcin
and normal mice took about the same time.
It took them about 80 to 90 seconds.
But in subsequent trials,
(stopwatch ticking)
the normal mice were eventually able
to swim to the island in just four seconds.
(stopwatch ticking)
But the mice that can not produce osteocalcin
never did much better than 90 seconds.
No matter how many times they've tried it before.
Normal mice complete the test faster with more experience.
But mice without osteocalcin gain
almost no benefit from previous tries at all.
To find out precisely why that was,
Dr. Karsenty closely examined the brains of these mice.
And he discovered something remarkable.
In mice unable to produce osteocalcin,
the hippocampus had actually shrunk.
This is an area of the brain
that's responsible for forming new memories.
Without osteocalcin from the bones,
the hippocampus declines in function.
Dr. Karsenty believes this is why the mice could not
remember the location of the island in the tank.
In essence, osteocalcin carries a message
that says, boost memory power.
Through the bloodstream,
this message is delivered to the brain.
Osteocalcin arrives at the hippocampus,
which is packed with neurons.
Neurons have special receptors for osteocalcin.
The message is received.
In turn,
the brain responds by revving up its ability to memorize.
The affect of osteocalcin on memory was unexpected.
And when we saw it, it was extremely surprising.
Organs need to speak to each other.
And that there is more to understand physiology
than single cell or single organs.
But the messaging powers of our bones
aren't just limited to memory.
This is Dr. Hartmut Geiger, who specializes
in studying the mechanism of aging.
Dr. Geiger discovered that in elderly mice,
the bones were releasing far fewer levels
of a molecule called osteopontin.
Could this molecule contain the messages
that are are connected to the process of aging?
Dr. Geiger set up an experiment using two sets of mice
and gave osteopontin to one group.
Five months later, we can now see a marked difference
in the mice which were given osteopontin.
Their immune cells, which fight off viruses
and infections in the body, had almost doubled in number.
So the message from osteopontin
is essentially to boost immunity.
And when this message reaches the cells
that give rise to various immune cells,
more numbers of immune cells are created, thereby improving
the body's overall immunity and the source.
Furthermore, the messages from our bones can affect
the testes in men to improve reproductive capabilities.
And they also work on our muscles to help increase stamina.
These are all crucial factors in keeping us young.
Scientists are now beginning to think that our bones
are actually responsible for our body's youthfulness.
Fat and bones.
Both are exchanging messages with other organs
to control energy and vigor of our bodies.
But first of all, why have our bodies
been set up in such a complex manner?
This is thought to be related to when
human ancestors started walking on two legs.
The Hadza, the hunter-gatherer tribe of East Africa,
still live in a traditional way today,
unchanged from ancient times.
(men shouting)
They travel as much
as 30 kilometers a day pursuing their prey.
And sometimes they end up with little
to show for it, despite running all day.
Human ancestors also lived in a time
where access to food was unpredictable.
And so their bodies developed a way
to store precious fat whenever food was available.
These rare microscopic images show fat cells
taking in sugar and lipid molecules.
Humans in particular have an excellent ability to store fat.
For instance, chimpanzees have three to 5% body fat.
But the Hazda people's body fat percentage
is between 10 to 25%.
So they are able to store a lot of fat.
Our bodies are configured for moving across vast distances
and living in a world where access to food is limited.
But in the modern world,
food is always available and plenty.
And even walking might be a rarity.
So our modern lifestyle causes disruptions
in our body's mechanism as it works
through messages sent from our fat and bones.
It's becoming clearer that this situation could be
the cause of many of our serious modern-day diseases.
One such disease is obesity.
The number of patients suffering from diseases
caused by obesity has continued to surge.
About 2.8 million people die each year
as a result of being obese.
Brenda Ote lives in the state of Missouri in the U.S.
Due to her advanced obesity,
she has been diagnosed with metabolic syndrome.
Alrighty, we're gonna go into room two.
When she was 35,
she suffered thre eheart attacks in succession
and had to have emergency operations.
But there's.
According to her doctor, Brenda is at risk
not only of heart attacks, but also stroke,
diabetes, kidney disease, and hypertension.
She takes 15 different medications
every day to stave off these diseases.
This is what I have to take tonight.
But this is what it looks like, all the pills I take.
Why does obesity lead to so many diseases?
Up until now, it had been thought that eating
too much fat caused a buildup in our blood vessels,
and blocking the flow of blood would go on
to cause strokes and myocardial infarctions.
But new research is shedding light on yet another cause.
Adipose tissue underneath.
Dr. Gokhan Hotamisligil.
He's a world-famous authority on obesity-related diseases.
He points to an unexpected culprit.
When you are constantly exposed to energy and nutrients
and fat cells actually start producing
many immune mediators.
The immune system is the body's defense system
against pathogens and other harmful invaders.
Here, we see immune cells consuming bacteria,
which appear as blue rods.
So what does the immune system have to do with obesity?
Let's travel into the body of an obese person
to observe this serious situation on a microscopic scale.
We are inside the visceral fat of an obese person.
What appears like smoke floats all around us.
These are excess sugar and lipid molecules.
Fat cells have become swollen to the brim with lipids.
Let's zoom into the surface of the cell.
Lipid molecules are bouncing off them.
(tones buzzing)
Then, the lipid molecules are mistaken for bacteria
or some other invader, and the cells
begin to release a different signaling molecule.
According to Dr. Hotamisligil,
the molecules are carrying the message, intruder alert.
A red alert message is relayed,
despite there being no intruder.
The signaling molecules rush throughout the body.
Their message is received by immune cells,
the body's defense forces.
Immune cells that have received
this message begin to change shape.
They have been spurred into combat mode,
mobilized to defend the body.
The immune cells also begin to divide rapidly
and release their own signaling molecules,
further spreading this false alarm.
The immune system is now running amok,
and it's this runaway immune response
that makes obesity dangerous.
This remarkable microscopic footage
shows immune cells that have become active in this way.
Around these bloated fat cells, immune cells, which appear
in white, are prowling around, looking for intruders.
Immune cells usually attack bacteria
and other intruders to protect our bodies.
But when immune cells run amok,
they create a terrifying situation.
They slip inside the wall of a blood vessel.
And there, they find excess lipid molecules.
The immune cells start gobbling them up.
Lipids are now their targets that require removal.
But the sheer quantity of lipids is too great.
The immune cells become engorged, and finally, burst.
As they burst, they release the harmful substances
they had been using for their attacks.
And these toxic bursts harm the blood vessel walls.
Immune cells running riot like this can cause damage
to numerous places around the body.
In doing so, they can bring on life-threatening diseases
like heart attacks and strokes,
kidney disease, and diabetes.
The problem with obesity is not just about the way we look.
In the body of an obese person,
this dangerous disruption of the interaction
among organs can cause fatal damage to the body.
So understanding the workings of these signaling molecules
have revealed previously unknown threats from obesity.
Modern-day lifestyles which are disturbing our signaling
molecules are also occurring in other organs, too.
A serious situation is also appearing in our bones.
One such consequence is osteoporosis.
Because of an extremely low bone mass,
patients with osteoporosis become very weak
and highly susceptible to breakage.
Osteoporosis had mainly been thought
of a problem in elderly women.
But today, regardless of gender,
younger people seem to be becoming more liable
to this disease in greater numbers.
Moreover, it is now known that bone loss
can bring on far more serious issues than we can imagine.
Shocking data shows that 20 to 25%
of elderly people with osteoporosis
who fracture a thigh bone die within one year.
And messages from our bones seem deeply implicated in this.
What's happening within our bones?
Let's try to find clues from these two men,
whose fates are deeply influenced by their skeletons.
Blake Caldwell now,
instigating just a little bit,
throwing another (mumbles)
Blake Caldwell is showing us
that he is the future of American cycling.
This summer during the Tour de France.
This is Blake Caldwell,
a former leading American cyclist.
He is 33 years old.
Live from here 200 times.
They would probably win.
I'm in the center there, goosebumps on my skin.
(announcer speaking incoherently)
He became a professional racer
and won numerous awards.
He was runner-up in the 2008 U.S. pro championships.
However, at the height of his career,
Caldwell was diagnosed with bone issues
and was forced to retire from professional cycling.
His disease was turned out when he suffered a fracture
to the head of his femoral bone by the groin.
He was examined and the results showed
that he had osteoporosis and extremely low bone mass,
though he was only 25 years old.
This is right after the accident.
In 2009 when I was still in Spain.
For my age, it would be more normal
for if I was 70 or 80, but not for 25.
It was so severe, when I'd actually,
I felt like I was a normal, healthy person in their mid-20s.
What's unique about my case, so there's more questions
and a little, it brought unease and anxiety to me, for sure.
How could a top athlete lose
so much bone mass at such a young age?
(ethereal music)
A clue to this issue came from South Africa,
from the study of an incurable disease.
This is Timothy Dreyer, age 27.
He suffers from a rare bone-related disease too.
He has sclerosteosis.
It's a disease where bones cannot stop growing.
(speaking in foreign language)
On the left is Timothy's skull.
On the right is a healthy skull.
The bone is indicated in light green.
The difference in thickness is quite startling.
As the skull continues to thicken,
this applies undue pressure to the brain,
which leads to impaired hearing and vision.
Timothy has to have surgery every four years,
where the back of his skull is temporarily removed
and excess bone is carved away.
As an eight-year-old,
my surgery was really, really daunting.
When they did the back part, you would wake up with tubes
from your nose, going down the way all here,
so you can't speak or anything.
And those are the kinds of things that you actually
do remember and you don't want to go back.
It's a sign of everything that I went through.
And I mean I made it. (laughs)
Why did Timothy's bones grow out of control?
Timothy's primary care physician, Dr. Herman Hamersma,
has worked for almost 50 years
to get to the bottom of this rare disease.
He discovered that people with sclerosteosis,
like Timothy, lack a certain signaling molecule.
It is sclerostin, a signaling molecule
which is released from bone cells.
This is an image from inside our bone, a world first,
captured with a microscope using a special technique.
Take a good look at the area marked by a square.
These little green specks are believed to be sclerostin.
The message from bones, which says, stop building.
So sclerostin is responsible for regulating bone density.
The sclerostin discovery, that molecule is the (mumbles)
There was no treatment developed or thought about.
When this message is sent out,
the number of osteoblasts,
the cells that build bone, starts to shrink.
The bone construction activities then cease.
So sclerostin acts as a break,
regulating bone growth.
Timothy Dreyer's body is utterly
unable to produce sclerostin.
So in his body, the bones don't send out
this message to stop, and so his bones
don't stop growing when they should.
And in the case of Blake Caldwell, in contrast,
this message stopping the bone construction process
is in overdrive, so this could be
why he keeps losing bone mass.
Once sclerostin is overproduced,
the number of osteoblasts reduces greatly.
And this can further trigger more serious matters.
A reduced number of osteoblasts means that the messages
from them to those that keep us youthful also decline.
As a consequence, the body's aging process
accelerates very rapidly.
More and more of such chain reactions
caused by the messaging disruptions
from our bones have been elucidated today.
(dramatic music)
As latest advances in medicine have been revealing
the impacts of disturbances in these messages
from our body tissue like fat and bone,
crucial discoveries in this field are now opening doors
to entirely new revolutionary treatments.
One such discovery has been made by this researcher.
Dr. Bente Pedersen.
She's been doing research on mitigating
an overactive immune system caused by obesity
by harnessing messages from muscle tissue.
And can you move the leg?
I'll touch. -: That works.
And then back again.
She analyzed the signaling molecules
released from leg muscles when they are being used.
And she found that exercise stimulated muscles
to release large amounts
of a signaling molecule called IL-6.
So what role does IL-6 play in the body?
To find out, she gave a dose of IL-6 to eight subjects.
The amount equal to what would be produced after exercise.
The results were astonishing.
Remember what happens in obese people.
Cells and fat tissue release large amounts of erroneous
signaling molecules, which make the immune system run wild.
But administering IL-6 reduced the amount
of those molecules by more than 50%.
When you exercise, your muscles release
the signaling molecule IL-6.
It travels through the bloodstream
into every part of your body.
And is received by immune cells that are running wild.
IL-6 delivers them a message to stop their attacks.
And are receiving it.
The immune cells stand down.
Now, immune cells stop releasing
the signaling molecules for red alert.
Dr. Pedersen believes this is why exercise
can suppress excessive immune responses.
In an evolutionary perspective,
it's relatively short period, only a few decades,
where we'll be extremely inactive.
So our body is built to move.
And when we then stop moving, then it's crucial for us,
because muscle was developed
to produce all these important factors.
you know that you have to exercise
in order not to become fat.
But you have to exercise in order not to be sick.
Is there anything we can do
to prevent bone density loss and help
our bones to keep our bodies young?
For our bones too, exercise may be effective.
This is Dr. Pamela Hinton's conclusion.
She has been conducting fascinating research
on how different types of exercise affect bone density.
We asked her to analyze the bones
of the former professional cyclist Blake Caldwell for us.
And she pointed out a surprising cause of his bone loss.
I think in Blake Caldwell's case, his osteoporosis
is probably largely attributable to his cycling
and beginning cycling from such a young age.
Blake started cycling at age seven,
with dreams of becoming professional.
He avoided any exercise other than cycling
to prevent gaining extra muscle
that would increase his body weight.
This highly specialized exercise machine
may have actually led to his abnormal condition.
Dr. Hinton's research on the relationship
between exercise and bone
revealed something surprising. Okay, so let's take a look.
She assessed the bone density
of men aged in their 20s to 50s.
One group spent at least six hours
per week running for fitness.
Only 19% of this group showed a decline in bone density.
The other group cycled for fitness.
A startling 63% of this group
showed a decline in bone density.
That is triple the rate of the running group.
Why would people who spend a lot of time cycling
experience loss of bone density?
Dr. Hinton believes that it's because
of the difference in forces exerted on the bones.
The osteocytes were sensing the mechanical loading
of the resistance training or the jumping and reducing
the amount of the sclerostin they're making,
allowing increased bone formation.
So cycling is an activity that we call weight-supported.
That means your body weight
is being supported by the bicycle.
Sitting on the couch is another weight-supported activity.
And those would then allow an increase in sclerostin.
If our bones don't feel an impact,
then sclerostin levels continue to rise.
The bones won't get built.
Dr. Hinton conducted a further experiment
to demonstrate this effect.
She had people suffering from low bone density
do jumping exercises that would impact the bone.
They did so three days a week,
30 minutes a day, for one year.
The results were extraordinary.
18 of the 19 participants in the study
experienced an increase in bone mass.
Their sclerostin levels had fallen.
It meant that impacts do increase bone mass.
And in addition, researchers say that impacts
through exercise should have a further effect.
They think that exercise also awakens
the bones' power to keep our bodies young.
So what happens inside our bones
after they experience impacts?
Let's have a look.
The shocks through bone are detected by osteocytes.
As we saw, these cells produced sclerostin.
And they also function as our body's impact sensors.
These are images of real osteocytes
under a powerful microscope.
Tens of billions of them spread
throughout our whole skeleton.
An astonishing number.
They form a highly sensitive
body-wide shock detection network.
When they sense an impact, osteocytes reduce
their output of sclerostin, the signaling molecule
that puts the breaks on bone building.
Instead, they send a message that says, build more bone.
This message works to boost production
of osteoblasts that create new bones.
As well as send messages that help
to keep the body's youthfulness.
To sum it up, the more active we are,
the more osteoblasts we have.
And the more messages they send,
the younger our body will stay.
Most of people think that there is a discontinuity
between the ambulatory function of bone
and the endocrine function of bone.
In a revolutionary context, there is no such a discontinuity
because bone ambulatory function is a survival tool.
Bone is a gatekeeper of aging in the sense
that as long as bone is in optimal health,
we can have muscle function, memory, and so forth.
Today, we are living in affluent society.
Where levels of our physical activity keep declining.
This should be causing disruptions
in the healthy workings of our body's inner networks,
the features of our human ancestors acquired through
the course of their long evolutionary history.
But if we can fully harness the power
of the messages our internal organs are sending out,
we may be able to regain health and vigor.
We are all born to have an extraordinary system
within our bodies that can help us revert back.
Our bodies' internal networks themselves
are the fountains of health.
We're catching up with Julian again,
who's battling a rare condition
where his body has no fat cells.
Since there was no cure, many patients of the disease
did not live beyond 30 in the past.
But discoveries on the workings
of signaling molecules are offering a new hope.
(Julian laughing)
Hi, hi.
In the U.S., treatment using leptin
is signaling molecule for the release
from fat cells received approval in 2014.
This is Alani, a three-year-old patient
with the same symptoms as Julian.
This new drug was able to wane in her insatiable appetite
and has prevented her from developing
diabetes and other conditions.
One, two, three.
Happy birthday to you.
Since leptin, her behavior
and her hunger has improved tremendously.
She's happier.
She's healthier, you can tell.
I'm very thankful for leptin.
It's changed everything.
Julian is due to begin leptin treatment soon.
Insights and a better understanding
of the body's internal networks
is a beacon of hope for these precious young lives.
Ah!
Go get it, go.
In the past, body fat and bones had not even
been considered as endocrine organs, but just a tissue.
We're only barely beginning
to understand their hidden powers.
Every moment reaching across to every part of our body,
they are sending out silent, yet very powerful messages
which are serving to keep us alive and healthy.
(dramatic music)