Mads TangChristensen The brain science of obesity TED
Transcriber:
Have you ever wondered
why a pair of siblings
living in the same house
with the same parents,
with the same food,
sometimes end up in opposite sides
of the weight spectrum?
My name is Mads
and for the last 25 years,
I’ve been studying what we eat,
when we eat and how much we eat.
And probably more importantly,
I’ve been studying
how each of our unique bodies
responds differently to the same food
and the same environment.
To be more precise, I study obesity.
During my training as an MD, PhD,
I was very fascinated by a series
of experiments done by Barry Levin.
He took 100 rats and subjected
them to high-fat feeding.
After months of feeding,
he ended up with a bell-shaped curve
and a weight distribution
with some skinny rats and some obese rats
and some in the middle.
What he then did
was to take the skinny rats
and breed them among themselves,
and the heavy rats.
And he bred those among themselves.
And after rounds of breeding,
he ended up with two distinct populations:
a diet-resistant rat
and an obesity-prone rat.
And here’s the really interesting part.
Then he took the skinny or the obese,
and either massively
over- or underfed them.
And their weight would,
of course, go up and down
depending on the dietary regimen.
But it was as if the little bodies would
remember the same old weight trajectory.
So once the dietary regimen was stopped,
the rats went right back
to the initial weight trajectory.
It was like as if you could
dress up the obese rat
in a skinny sheep’s clothing.
But the obese rat nature
was still scratching to get out.
The same thing applies to humans.
If you take a thousand kids
and weigh them,
their weight will also be distributed
in a bell-shaped curve.
Some skinny, some in the middle
and some heavy.
We know that some of the skinny kids
will remain skinny throughout life,
and some of the obese kids
will stay obese throughout life.
You could argue that their weight,
to some degree, has been predetermined.
You could also argue
that obesity is a disease.
Wait, did I just say
that obesity a disease?
Yes.
There’s actually data
and science that shows that.
And I’ve made it my audacious life goal
to come up with a solution
to prevent, treat or even cure obesity.
Let me explain.
In the early 1980s and 1990s,
obesity was considered
a potential global problem,
a global problem of a magnitude
that led WHO in the end of 1990s
to declare obesity a global pandemic.
And I probably don’t have to tell you why.
Higher rates of diabetes, hypertension,
cardiovascular disease, even some cancers,
osteoarthritis and a clear link
to mental conditions such as depression.
So as the number
of obese individuals grew,
so did the number of people
suffering from these diseases.
Today, more than 50 percent
of the US adult population
are living with obesity or overweight.
From a health perspective,
that is devastating.
But it’s not only a US problem.
The obesity surge has made obesity
a global health problem.
Many inside and outside
the medical community
believe obesity is not a disease.
They believe that obesity is a condition,
a condition brought about
by too much eating
and too little exercise.
As a matter of fact, a lot of people
living with obesity think that too.
They believe that their weight
is 100 percent their own fault,
which can lead to self-blame
and low self-esteem,
and perhaps even shame or stress eating,
which is both heartbreaking,
as well as counterproductive.
But where is the scientific proof
that obesity is a disease?
Well, medically speaking,
there’s many ways to define disease,
but let me give you just three examples.
As a process that impairs
your functionality
and reduces life expectancy
– obesity, check.
You can define disease as a process
that leaves you more susceptible
to other diseases or causes disease.
Obesity, check.
Or you can define disease
as a genetic impairment
that leads to functional impairment,
like, for instance,
a duplication of genes on chromosomes.
There is clear evidence
that a single gene mutation
can lead to obesity,
such as, for instance,
leptin deficiency and POMC deficiency.
We also have two-three genes
leading to obesity.
And it’s my prediction that we,
by the year 2030,
will be able to explain most obesity
by the genetic makeup of the individual.
So obesity as a disease
by this measure, check.
Let me be clear.
We humans have had
the same genes for decades.
And just recently,
obesity has become a bigger problem.
How do we then explain that?
One obvious thing is actually food,
especially calorie-rich food,
which is much more readily available.
It’s relatively easy
and also relatively cheap
to eat your entire daily need of calories
by a fast food or big soft drinks.
So genes do play a role,
but the environment
also plays a huge role.
The overabundance of calories
in certain communities
is a relatively new thing,
and our genes haven’t quite adapted yet.
In the history of feast and famine,
genetic selection has prepared us
much better for famine,
and for good reason.
Starvation is bad,
but you could also argue obesity is bad.
And if obesity is a disease,
how do we then prevent,
treat or even cure it?
I believe that the brain holds the key.
I have always been fascinated
with how small electrical signals
in discrete parts of the brain
lead to big behavioral changes.
And my study of the brain
led me to Glucagon-Like Peptide 1,
or GLP-1 for short.
GLP-1 is a hormone and a signal molecule
that is produced
both in the gut and in the brain.
The brain speaks to the gut
and the gut speaks to the brain.
Yes, that’s right.
Your belly and your brain
are literally connected.
Our research led us to see
that GLP-1 has an effect on nerve cells
sitting in areas that control
whether we eat or not.
So, for instance,
if we increase the level of GLP-1,
the body’s desire to eat
or overeat food gets turned off.
GLP-1 serves as the full signal
in your car’s gas tank.
I’ve spent years and decades
mapping the circuitry of GLP-1
and how GLP-1 interacts
with other signal molecules and hormones.
All of these things go together
and control food intake,
body weight and the control
of eating behavior.
And what does that all mean?
Well, today, we have engineered
and studied the molecule,
so we now have a molecule
that can lead to
a significant weight loss.
Obviously, GLP-1 is not the whole answer.
We and others have discovered
numerous hormones
and other signal molecules
that are also pivotal for the regulation
of food intake and body weight.
And it may end up
that these signal molecules and hormones
are even more important than GLP-1.
So …
There’s plenty for us to do.
There’s still plenty for us to explore.
So this is not the end.
It’s not even the beginning to the end.
But perhaps this may be
the end to the beginning.
We may have a massive weight crisis
on the planet today,
but the good news is
we are on the right path.
We now have solutions
for people living with obesity,
and the next steps will be
to understand even better
the problems people
living with obesity are facing.
To understand even better
how genes and environment play together.
And understand, finally,
how all these things come together
and determine our body weight.
Then, and maybe just then,
we will be able
to come up with a prevention,
a treatment or even a cure
for people living with obesity,
like we strive for
with any other chronic disease.
And this – this still remains
our audacious life’s goal.
Thank you.