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The science of cells that never get old

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    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.
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    On the other hand,
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    if you typically see something stressful
    as a challenge to be tackled,
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    then blood flows to your heart
    and to your brain,
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    and you experience a brief
    but energizing spike of cortisol.
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    And thanks to that habitual
    "bring it on" attitude,
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    your telomeres do just fine.
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    So ...
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    What is all of this telling us?
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    Your telomeres do just fine.
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    You really do have power
    to change what is happening
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    to your own telomeres.
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    But our curiosity
    just got more and more intense,
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    because we started to wonder,
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    what about factors outside our own skin?
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    Could they impact
    our telomere maintenance as well?
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    You know, we humans
    are intensely social beings.
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    Was it even possible
    that our telomeres were social as well?
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    And the results have been startling.
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    As early as childhood,
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    emotional neglect, exposure to violence,
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    bullying and racism
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    all impact your telomeres,
    and the effects are long-term.
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    Can you imagine the impact on children
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    of living years in a war zone?
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    People who can't trust their neighbors
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    and who don't feel safe
    in their neighborhoods
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    consistently have shorter telomeres.
  • 16:43 - 16:46
    So your home address
    matters for telomeres as well.
  • 16:46 - 16:47
    On the flip side,
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    tight-knit communities,
    being in a marriage long-term,
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    and lifelong friendships, even,
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    all improve telomere maintenance.
  • 16:58 - 17:02
    So what is all this telling us?
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    It's telling us that I have the power
    to impact my own telomeres,
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    and I also have the power to impact yours.
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    Telomere science has told us
    just how interconnected we all are.
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    But I'm still curious.
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    I do wonder
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    what legacy all of us
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    will leave for the next generation?
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    Will we invest
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    in the next young woman or man
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    peering through a microscope
    at the next little critter,
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    the next bit of pond scum,
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    curious about a question
    we don't even know today is a question?
  • 17:44 - 17:47
    It could be a great question
    that could impact all the world.
  • 17:47 - 17:51
    And maybe, maybe you're curious about you.
  • 17:52 - 17:54
    Now that you know
    how to protect your telomeres,
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    are you curious what are you going to do
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    with all those decades
    of brimming good health?
  • 17:59 - 18:03
    And now that you know you could impact
    the telomeres of others,
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    are you curious
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    how will you make a difference?
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    And now that you know the power
    of curiosity to change the world,
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    how will you make sure
    that the world invests in curiosity
  • 18:20 - 18:25
    for the sake of the generations
    that will come after us?
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    Thank you.
  • 18:28 - 18:33
    (Applause)
Title:
The science of cells that never get old
Speaker:
Elizabeth Blackburn
Description:

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.

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Video Language:
English
Team:
closed TED
Project:
TEDTalks
Duration:
18:46

English subtitles

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