ABOUT THE SPEAKER
Elizabeth Blackburn - Molecular biologist
Elizabeth Blackburn won a Nobel Prize for her pioneering work on telomeres and telomerase, which may play central roles in how we age. She is president of the Salk Institute and author of the New York Times Best Seller, "The Telomere Effect."

Why you should listen

Dr. Blackburn is the president of the Salk Institute and a pioneering molecular biologist. She received the Nobel Prize in Physiology or Medicine in 2009 for discovering the molecular nature of telomeres, the ends of chromosomes that serve as protective caps essential for preserving genetic information, and for co-discovering telomerase, an enzyme that maintains telomere ends. Both telomeres and telomerase are thought to play central roles in aging and diseases such as cancer, and her work helped launch entire new fields of research in these areas.

In addition to the Nobel Prize, Blackburn has received nearly every major scientific award including the Lasker, Gruber, and Gairdner prizes. She has served as president of the American Association of Cancer Research and the American Society for Cell Biology, and on editorial boards of scientific journals including Cell and Science. She coauthored the best-selling book The Telomere Effect: A Revolutionary Approach to Living Younger, Healthier, Longer.

More profile about the speaker
Elizabeth Blackburn | Speaker | TED.com
TED2017

Elizabeth Blackburn: The science of cells that never get old

Filmed:
1,957,519 views

What makes our bodies age ... our skin wrinkle, our hair turn white, our immune systems weaken? Biologist Elizabeth Blackburn shares a Nobel Prize for her work finding out the answer, with the discovery of telomerase: an enzyme that replenishes the caps at the end of chromosomes, which break down when cells divide. Learn more about Blackburn's groundbreaking research -- including how we might have more control over aging than we think.
- Molecular biologist
Elizabeth Blackburn won a Nobel Prize for her pioneering work on telomeres and telomerase, which may play central roles in how we age. She is president of the Salk Institute and author of the New York Times Best Seller, "The Telomere Effect." Full bio

Double-click the English transcript below to play the video.

00:13
Where does the end begin?
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Well, for me, it all began
with this little fellow.
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This adorable organism --
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well, I think it's adorable --
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is called Tetrahymena
and it's a single-celled creature.
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It's also been known as pond scum.
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So that's right, my career
started with pond scum.
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Now, it was no surprise
I became a scientist.
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Growing up far away from here,
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as a little girl I was deadly curious
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about everything alive.
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I used to pick up lethally poisonous
stinging jellyfish and sing to them.
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And so starting my career,
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I was deadly curious
about fundamental mysteries
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of the most basic building blocks of life,
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and I was fortunate to live in a society
where that curiosity was valued.
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Now, for me, this little
pond scum critter Tetrahymena
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was a great way to study
the fundamental mystery
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I was most curious about:
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those bundles of DNA
in our cells called chromosomes.
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And it was because I was curious
about the very ends of chromosomes,
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known as telomeres.
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Now, when I started my quest,
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all we knew was that they helped
protect the ends of chromosomes.
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It was important when cells divide.
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It was really important,
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but I wanted to find out
what telomeres consisted of,
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and for that, I needed a lot of them.
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And it so happens
that cute little Tetrahymena
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has a lot of short linear chromosomes,
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around 20,000,
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so lots of telomeres.
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And I discovered that telomeres
consisted of special segments
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of noncoding DNA right
at the very ends of chromosomes.
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But here's a problem.
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Now, we all start life as a single cell.
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It multiples to two.
Two becomes four. Four becomes eight,
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and on and on to form
the 200 million billion cells
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that make up our adult body.
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And some of those cells
have to divide thousands of times.
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In fact, even as I stand here before you,
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all throughout my body,
cells are furiously replenishing
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to, well, keep me
standing here before you.
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So every time a cell divides,
all of its DNA has to be copied,
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all of the coding DNA
inside of those chromosomes,
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because that carries
the vital operating instructions
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that keep our cells in good working order,
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so my heart cells can keep a steady beat,
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which I assure you
they're not doing right now,
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and my immune cells
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can fight off bacteria and viruses,
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and our brain cells
can save the memory of our first kiss
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and keep on learning throughout life.
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But there is a glitch
in the way DNA is copied.
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It is just one of those facts of life.
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Every time the cell divides
and the DNA is copied,
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some of that DNA from the ends
gets worn down and shortened,
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some of that telomere DNA.
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And think about it
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like the protective caps
at the ends of your shoelace.
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And those keep the shoelace,
or the chromosome, from fraying,
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and when that tip
gets too short, it falls off,
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and that worn down telomere
sends a signal to the cells.
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"The DNA is no longer being protected."
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It sends a signal. Time to die.
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So, end of story.
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Well, sorry, not so fast.
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It can't be the end of the story,
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because life hasn't died
off the face of the earth.
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So I was curious:
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if such wear and tear is inevitable,
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how on earth does Mother Nature make sure
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we can keep our chromosomes intact?
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Now, remember that little
pond scum critter Tetrahymena?
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The craziest thing was,
Tetrahymena cells never got old and died.
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Their telomeres weren't shortening
as time marched on.
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Sometimes they even got longer.
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Something else was at work,
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and believe me, that something
was not in any textbook.
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So working in my lab with
my extraordinary student Carol Greider --
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and Carol and I shared
the Nobel Prize for this work --
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we began running experiments
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and we discovered
cells do have something else.
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It was a previously undreamed-of enzyme
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that could replenish,
make longer, telomeres,
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and we named it telomerase.
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And when we removed
our pond scum's telomerase,
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their telomeres ran down and they died.
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So it was thanks
to their plentiful telomerase
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that our pond scum critters never got old.
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OK, now, that's
an incredibly hopeful message
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for us humans to be
receiving from pond scum,
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because it turns out
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that as we humans age,
our telomeres do shorten,
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and remarkably,
that shortening is aging us.
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Generally speaking,
the longer your telomeres,
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the better off you are.
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It's the overshortening of telomeres
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that leads us to feel and see
signs of aging.
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My skin cells start to die
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and I start to see fine lines, wrinkles.
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Hair pigment cells die.
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You start to see gray.
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Immune system cells die.
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You increase your risks of getting sick.
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In fact, the cumulative research
from the last 20 years
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has made clear that telomere attrition
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is contributing to our risks
of getting cardiovascular diseases,
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Alzheimer's, some cancers and diabetes,
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the very conditions many of us die of.
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And so we have to think about this.
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What is going on?
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This attrition,
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we look and we feel older, yeah.
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Our telomeres are losing
the war of attrition faster.
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And those of us who feel youthful longer,
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it turns out our telomeres
are staying longer
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for longer periods of time,
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extending our feelings of youthfulness
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and reducing the risks
of all we most dread
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as the birthdays go by.
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OK,
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seems like a no-brainer.
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Now, if my telomeres are connected
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to how quickly
I'm going to feel and get old,
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if my telomeres can be
renewed by my telomerase,
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then all I have to do to reverse
the signs and symptoms of aging
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is figure out where to buy
that Costco-sized bottle
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of grade A organic
fair trade telomerase, right?
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Great! Problem solved.
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(Applause)
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Not so fast, I'm sorry.
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Alas, that's not the case.
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OK. And why?
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It's because human genetics has taught us
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that when it comes to our telomerase,
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we humans live on a knife edge.
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OK, simply put,
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yes, nudging up telomerase
does decrease the risks of some diseases,
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but it also increases the risks
of certain and rather nasty cancers.
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So even if you could buy
that Costco-sized bottle of telomerase,
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and there are many websites
marketing such dubious products,
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the problem is you could
nudge up your risks of cancers.
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And we don't want that.
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Now, don't worry,
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and because, while I think
it's kind of funny that right now,
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you know, many of us may be thinking,
well, I'd rather be like pond scum.
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(Laughter)
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There is something for us humans
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in the story of telomeres
and their maintenance.
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But I want to get one thing clear.
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It isn't about enormously
extending human lifespan
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or immortality.
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It's about health span.
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Now, health span is the number
of years of your life
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when you're free of disease,
you're healthy, you're productive,
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you're zestfully enjoying life.
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Disease span, the opposite of health span,
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is the time of your life
spent feeling old and sick and dying.
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So the real question becomes,
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OK, if I can't guzzle telomerase,
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do I have control
over my telomeres' length
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and hence my well-being, my health,
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without those downsides of cancer risks?
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OK?
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So, it's the year 2000.
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Now, I've been minutely scrutinizing
little teeny tiny telomeres
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very happily for many years,
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when into my lab walks
a psychologist named Elissa Epel.
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Now, Elissa's expertise is in the effects
of severe, chronic psychological stress
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on our mind's and our body's health.
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And there she was standing in my lab,
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which ironically overlooked
the entrance to a mortuary, and --
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(Laughter)
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And she had a life-and-death
question for me.
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"What happens to telomeres
in people who are chronically stressed?"
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she asked me.
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You see, she'd been studying caregivers,
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and specifically mothers of children
with a chronic condition,
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be it gut disorder,
be it autism, you name it --
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a group obviously under enormous
and prolonged psychological stress.
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I have to say, her question
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changed me profoundly.
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See, all this time
I had been thinking of telomeres
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as those miniscule
molecular structures that they are,
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and the genes that control telomeres.
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And when Elissa asked me
about studying caregivers,
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I suddenly saw telomeres
in a whole new light.
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I saw beyond the genes and the chromosomes
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into the lives of the real people
we were studying.
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And I'm a mom myself,
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and at that moment,
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I was struck by the image of these women
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dealing with a child with a condition
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very difficult to deal with,
often without help.
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And such women, simply,
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often look worn down.
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So was it possible their telomeres
were worn down as well?
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So our collective curiosity
went into overdrive.
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Elissa selected for our first study
a group of such caregiving mothers,
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and we wanted to ask:
What's the length of their telomeres
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compared with the number of years
that they have been caregiving
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for their child with a chronic condition?
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So four years go by
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and the day comes
when all the results are in,
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and Elissa looked down
at our first scatterplot
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and literally gasped,
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because there was a pattern to the data,
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and it was the exact gradient
that we most feared might exist.
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It was right there on the page.
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The longer, the more years that is,
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the mother had been
in this caregiving situation,
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no matter her age,
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the shorter were her telomeres.
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And the more she perceived
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her situation as being more stressful,
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the lower was her telomerase
and the shorter were her telomeres.
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So we had discovered something unheard of:
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the more chronic stress you are under,
the shorter your telomeres,
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meaning the more likely you were
to fall victim to an early disease span
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and perhaps untimely death.
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Our findings meant
that people's life events
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and the way we respond to these events
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can change how you
maintain your telomeres.
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So telomere length wasn't
just a matter of age counted in years.
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Elissa's question to me,
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back when she first came to my lab,
indeed had been a life-and-death question.
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Now, luckily, hidden
in that data there was hope.
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We noticed that some mothers,
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despite having been carefully caring
for their children for many years,
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had been able to maintain their telomeres.
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So studying these women closely revealed
that they were resilient to stress.
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Somehow they were able
to experience their circumstances
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not as a threat day in and day out
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but as a challenge,
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and this has led to a very important
insight for all of us:
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we have control over the way we age
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all the way down into our cells.
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OK, now our initial curiosity
became infectious.
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Thousands of scientists
from different fields
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added their expertise
to telomere research,
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and the findings have poured in.
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It's up to over 10,000
scientific papers and counting.
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So several studies
rapidly confirmed our initial finding
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that yes, chronic stress
is bad for telomeres.
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And now many are revealing
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that we have more control
over this particular aging process
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than any of us could ever have imagined.
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A few examples:
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a study from the University
of California, Los Angeles
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of people who are caring
for a relative with dementia, long-term,
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and looked at their caregiver's
telomere maintenance capacity
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and found that it was improved
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by them practicing a form of meditation
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for as little as 12 minutes
a day for two months.
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Attitude matters.
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If you're habitually a negative thinker,
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you typically see a stressful situation
with a threat stress response,
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meaning if your boss wants to see you,
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you automatically think,
"I'm about to be fired,"
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and your blood vessels constrict,
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and your level of the stress
hormone cortisol creeps up,
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and then it stays up,
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and over time, that persistently
high level of the cortisol
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actually damps down your telomerase.
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Not good for your telomeres.
265
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1760
15:14
On the other hand,
266
902200
1256
15:15
if you typically see something stressful
as a challenge to be tackled,
267
903480
5976
15:21
then blood flows to your heart
and to your brain,
268
909480
3456
15:24
and you experience a brief
but energizing spike of cortisol.
269
912960
4696
15:29
And thanks to that habitual
"bring it on" attitude,
270
917680
2536
15:32
your telomeres do just fine.
271
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3040
15:37
So ...
272
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1200
15:40
What is all of this telling us?
273
928160
2840
15:45
Your telomeres do just fine.
274
933480
1936
15:47
You really do have power
to change what is happening
275
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5976
15:53
to your own telomeres.
276
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2360
15:56
But our curiosity
just got more and more intense,
277
944480
5040
16:02
because we started to wonder,
278
950520
2416
16:04
what about factors outside our own skin?
279
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3216
16:08
Could they impact
our telomere maintenance as well?
280
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3920
16:12
You know, we humans
are intensely social beings.
281
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3336
16:16
Was it even possible
that our telomeres were social as well?
282
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4000
16:21
And the results have been startling.
283
969440
1720
16:24
As early as childhood,
284
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1680
16:28
emotional neglect, exposure to violence,
285
976360
3176
16:31
bullying and racism
286
979560
2016
16:33
all impact your telomeres,
and the effects are long-term.
287
981600
4440
16:39
Can you imagine the impact on children
288
987800
2296
16:42
of living years in a war zone?
289
990120
1920
16:46
People who can't trust their neighbors
290
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1856
16:48
and who don't feel safe
in their neighborhoods
291
996120
3136
16:51
consistently have shorter telomeres.
292
999280
2080
16:54
So your home address
matters for telomeres as well.
293
1002600
2976
16:57
On the flip side,
294
1005600
1200
17:00
tight-knit communities,
being in a marriage long-term,
295
1008200
3296
17:03
and lifelong friendships, even,
296
1011520
2936
17:06
all improve telomere maintenance.
297
1014480
2920
17:10
So what is all this telling us?
298
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3456
17:13
It's telling us that I have the power
to impact my own telomeres,
299
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4496
17:18
and I also have the power to impact yours.
300
1026359
3297
17:21
Telomere science has told us
just how interconnected we all are.
301
1029680
5800
17:29
But I'm still curious.
302
1037520
1200
17:31
I do wonder
303
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2240
17:35
what legacy all of us
304
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2200
17:38
will leave for the next generation?
305
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1759
17:40
Will we invest
306
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1576
17:42
in the next young woman or man
307
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3016
17:45
peering through a microscope
at the next little critter,
308
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4216
17:49
the next bit of pond scum,
309
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2656
17:52
curious about a question
we don't even know today is a question?
310
1060520
3776
17:56
It could be a great question
that could impact all the world.
311
1064320
2896
17:59
And maybe, maybe you're curious about you.
312
1067240
3680
18:04
Now that you know
how to protect your telomeres,
313
1072080
2256
18:06
are you curious what are you going to do
314
1074360
1905
18:08
with all those decades
of brimming good health?
315
1076289
2480
18:11
And now that you know you could impact
the telomeres of others,
316
1079200
3880
18:16
are you curious
317
1084040
1200
18:18
how will you make a difference?
318
1086040
1960
18:21
And now that you know the power
of curiosity to change the world,
319
1089880
4096
18:26
how will you make sure
that the world invests in curiosity
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6216
18:32
for the sake of the generations
that will come after us?
321
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4560
18:38
Thank you.
322
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1216
18:39
(Applause)
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5400

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ABOUT THE SPEAKER
Elizabeth Blackburn - Molecular biologist
Elizabeth Blackburn won a Nobel Prize for her pioneering work on telomeres and telomerase, which may play central roles in how we age. She is president of the Salk Institute and author of the New York Times Best Seller, "The Telomere Effect."

Why you should listen

Dr. Blackburn is the president of the Salk Institute and a pioneering molecular biologist. She received the Nobel Prize in Physiology or Medicine in 2009 for discovering the molecular nature of telomeres, the ends of chromosomes that serve as protective caps essential for preserving genetic information, and for co-discovering telomerase, an enzyme that maintains telomere ends. Both telomeres and telomerase are thought to play central roles in aging and diseases such as cancer, and her work helped launch entire new fields of research in these areas.

In addition to the Nobel Prize, Blackburn has received nearly every major scientific award including the Lasker, Gruber, and Gairdner prizes. She has served as president of the American Association of Cancer Research and the American Society for Cell Biology, and on editorial boards of scientific journals including Cell and Science. She coauthored the best-selling book The Telomere Effect: A Revolutionary Approach to Living Younger, Healthier, Longer.

More profile about the speaker
Elizabeth Blackburn | Speaker | TED.com

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