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Could a drug prevent depression and PTSD?

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    This is a tuberculosis ward,
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    and at the time this picture was taken
    in the late 1800s,
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    one in seven of all people
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    died from tuberculosis.
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    We had no idea
    what was causing this disease.
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    The hypothesis was actually
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    it was your constitution
    that made you susceptible.
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    And it was a highly romanticized disease.
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    It was also called consumption,
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    and it was the disorder of poets
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    and artists and intellectuals.
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    And some people actually thought
    it gave you heightened sensitivity
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    and conferred creative genius.
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    By the 1950s,
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    we instead knew
    that tuberculosis was caused
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    by a highly contagious
    bacterial infection,
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    which is slightly less romantic,
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    but that had the upside
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    of us being able to maybe
    develop drugs to treat it.
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    So doctors had discovered
    a new drug, iproniazid,
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    that they were optimistic
    might cure tuberculosis,
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    and they gave it to patients,
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    and patients were elated.
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    They were more social, more energetic.
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    One medical report actually says
    they were "dancing in the halls."
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    And unfortunately,
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    this was not necessarily
    because they were getting better.
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    A lot of them were still dying.
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    Another medical report describes them
    as being "inappropriately happy."
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    And that is how the first
    antidepressant was discovered.
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    So accidental discovery
    is not uncommon in science,
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    but it requires more
    than just a happy accident.
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    You have to be able to recognize it
    for discovery to occur.
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    As a neuroscientist,
    I'm going to talk to you a little bit
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    about my firsthand experience
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    with whatever you want to call
    the opposite of dumb luck --
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    let's call it smart luck.
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    But first, a bit more background.
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    Thankfully, since the 1950s,
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    we've developed some other drugs
    and we can actually now cure tuberculosis.
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    And at least in the United States,
    though not necessarily in other countries,
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    we have closed our sanitoriums
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    and probably most of you
    are not too worried about TB.
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    But a lot of what was true
    in the early 1900s
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    about infectious disease,
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    we can say now
    about psychiatric disorders.
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    We are in the middle
    of an epidemic of mood disorders
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    like depression and post-traumatic
    stress disorder, or PTSD.
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    One in four of all adults
    in the United States
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    suffers from mental illness,
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    which means that if you haven't
    experienced it personally
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    or someone in your family hasn't,
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    it's still very likely
    that someone you know has,
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    though they may not talk about it.
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    Depression has actually now surpassed
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    HIV/AIDS, malaria, diabetes and war
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    as the leading cause
    of disability worldwide.
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    And also, like tuberculosis in the 1950s,
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    we don't know what causes it.
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    Once it's developed, it's chronic,
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    lasts a lifetime,
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    and there are no known cures.
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    The second antidepressant we discovered,
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    also by accident, in the 1950s,
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    from an antihistamine
    that was making people manic,
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    imipramine.
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    And in both the case of the tuberculosis
    ward and the antihistamine,
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    someone had to be able to recognize
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    that a drug that was designed
    to do one thing --
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    treat tuberculosis
    or suppress allergies --
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    could be used to do
    something very different --
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    treat depression.
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    And this sort of repurposing
    is actually quite challenging.
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    When doctors first saw
    this mood-enhancing effect of iproniazid,
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    they didn't really recognize
    what they saw.
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    They were so used to thinking about it
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    from the framework
    of being a tuberculosis drug
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    that they actually just listed it
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    as a side effect, an adverse side effect.
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    As you can see here,
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    a lot of these patients in 1954
    are experiencing severe euphoria.
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    And they were worried
    that this might somehow interfere
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    with their recovering from tuberculosis.
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    So they recommended that iproniazid
    only be used in cases of extreme TB
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    and in patients that were
    highly emotionally stable,
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    which is of course the exact opposite
    of how we use it as an antidepressant.
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    They were so used to looking at it
    from the perspective of this one disease,
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    they could not see the larger implications
    for another disease.
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    And to be fair,
    it's not entirely their fault.
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    Functional fixedness
    is a bias that affects all of us.
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    It's a tendency to only
    be able to think of an object
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    in terms of its traditional
    use or function.
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    And mental set is another thing. Right?
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    That's sort of this preconceived framework
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    with which we approach problems.
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    And that actually makes repurposing
    pretty hard for all of us,
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    which is, I guess, why they gave
    a TV show to the guy who was,
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    like, really great at repurposing.
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    (Laughter)
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    So the effects in both the case
    of iproniazid and imipramine,
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    they were so strong --
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    there was mania,
    or people dancing in the halls.
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    It's actually not that surprising
    they were caught.
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    But it does make you wonder
    what else we've missed.
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    So iproniazid and imipramine,
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    they're more than just
    a case study in repurposing.
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    They have two other things in common
    that are really important.
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    One, they have terrible side effects.
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    That includes liver toxicity,
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    weight gain of over 50 pounds,
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    suicidality.
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    And two, they both
    increase levels of serotonin,
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    which is a chemical signal in the brain,
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    or a neurotransmitter.
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    And those two things together,
    right, one or the two,
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    may not have been that important,
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    but the two together meant
    that we had to develop safer drugs,
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    and that serotonin seemed
    like a pretty good place to start.
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    So we developed drugs
    to more specifically focus on serotonin,
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    the selective serotonin
    reuptake inhibitors, so the SSRIs,
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    the most famous of which is Prozac.
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    And that was 30 years ago,
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    and since then we have mostly
    just worked on optimizing those drugs.
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    And the SSRIs, they are better
    than the drugs that came before them,
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    but they still have a lot of side effects,
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    including weight gain, insomnia,
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    suicidality --
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    and they take a really long time to work,
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    something like four to six weeks
    in a lot of patients.
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    And that's in the patients
    where they do work.
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    There are a lot of patients
    where these drugs don't work.
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    And that means now, in 2016,
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    we still have no cures
    for any mood disorders,
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    just drugs that suppress symptoms,
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    which is kind of the difference between
    taking a painkiller for an infection
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    versus an antibiotic.
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    A painkiller will make you feel better,
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    but is not going to do anything
    to treat that underlying disease.
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    And it was this flexibility
    in our thinking
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    that let us recognize
    that iproniazid and imipramine
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    could be repurposed in this way,
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    which led us to the serotonin hypothesis,
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    which we then, ironically, fixated on.
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    This is brain signaling, serotonin,
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    from an SSRI commercial.
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    In case you're not clear,
    this is a dramatization.
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    And in science, we try
    and remove our bias, right,
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    by running double-blinded experiments
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    or being statistically agnostic
    as to what our results will be.
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    But bias creeps in more insidiously
    in what we choose to study
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    and how we choose to study it.
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    So we've focused on serotonin now
    for the past 30 years,
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    often to the exclusion of other things.
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    We still have no cures,
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    and what if serotonin
    isn't all there is to depression?
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    What if it's not even the key part of it?
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    That means no matter how much time
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    or money or effort we put into it,
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    it will never lead to a cure.
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    In the past few years,
    doctors have discovered
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    probably what is the first truly new
    antidepressant since the SSRIs,
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    Calypsol,
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    and this drug works very quickly,
    within a few hours or a day,
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    and it doesn't work on serotonin.
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    It works on glutamate,
    which is another neurotransmitter.
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    And it's also repurposed.
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    It was traditionally used
    as anesthesia in surgery.
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    But unlike those other drugs,
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    which were recognized pretty quickly,
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    it took us 20 years
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    to realize that Calypsol
    was an antidepressant,
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    despite the fact that it's actually
    a better antidepressant,
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    probably, than those other drugs.
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    It's actually probably because of the fact
    that it's a better antidepressant
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    that it was harder for us to recognize.
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    There was no mania to signal its effects.
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    So in 2013, up at Columbia University,
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    I was working with my colleague,
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    Dr. Christine Ann Denny,
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    and we were studying Calypsol
    as an antidepressant in mice.
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    And Calypsol has, like,
    a really short half-life,
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    which means it's out of your body
    within a few hours.
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    And we were just piloting.
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    So we would give an injection to mice,
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    and then we'd wait a week,
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    and then we'd run
    another experiment to save money.
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    And one of the experiments I was running,
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    we would stress the mice,
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    and we used that as a model of depression.
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    And at first it kind of just looked
    like it didn't really work at all.
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    So we could have stopped there.
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    But I have run this model
    of depression for years,
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    and the data just looked kind of weird.
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    It didn't really look right to me.
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    So I went back,
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    and we reanalyzed it
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    based on whether or not they had gotten
    that one injection of Calypsol
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    a week beforehand.
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    And it looked kind of like this.
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    So if you look at the far left,
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    if you put a mouse in a new space,
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    this is the box, it's very exciting,
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    a mouse will walk around and explore,
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    and you can see that pink line
    is actually the measure of them walking.
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    And we also give it
    another mouse in a pencil cup
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    that it can decide to interact with.
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    This is also a dramatization,
    in case that's not clear.
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    And a normal mouse will explore.
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    It will be social.
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    Check out what's going on.
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    If you stress a mouse
    in this depression model,
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    which is the middle box,
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    they aren't social, they don't explore.
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    They mostly just kind of hide
    in that back corner, behind a cup.
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    Yet the mice that had gotten
    that one injection of Calypsol,
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    here on your right,
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    they were exploring, they were social.
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    They looked like they
    had never been stressed at all,
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    which is impossible.
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    So we could have just stopped there,
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    but Christine had also used
    Calypsol before as anesthesia,
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    and a few years ago she had seen
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    that it seemed to have
    some weird effects on cells
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    and some other behavior
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    that also seemed to last
    long after the drug,
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    maybe a few weeks.
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    So we were like, OK,
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    maybe this is not completely impossible,
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    but we were really skeptical.
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    So we did what you do in science
    when you're not sure,
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    and we ran it again.
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    And I remember being in the animal room,
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    moving mice from box to box
    to test them,
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    and Christine was actually sitting
    on the floor with the computer in her lap
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    so the mice couldn't see her,
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    and she was analyzing
    the data in real time.
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    And I remember us yelling,
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    which you're not supposed to do
    in an animal room where you're testing,
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    because it had worked.
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    It seemed like these mice
    were protected against stress,
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    or they were inappropriately happy,
    however you want to call it.
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    And we were really excited.
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    And then we were really skeptical,
    because it was too good to be true.
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    So we ran it again.
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    And then we ran it again in a PTSD model,
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    and we ran it again
    in a physiological model,
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    where all we did was give stress hormones.
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    And we had our undergrads run it.
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    And then we had our collaborators
    halfway across the world in France run it.
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    And every time someone ran it,
    they confirmed the same thing.
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    It seemed like
    this one injection of Calypsol
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    was somehow protecting
    against stress for weeks.
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    And we only published this a year ago,
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    but since then other labs
    have independently confirmed this effect.
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    So we don't know what causes depression,
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    but we do know that stress
    is the initial trigger
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    in 80 percent of cases,
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    and depression and PTSD
    are different diseases,
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    but this is something
    they share in common.
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    Right? It is traumatic stress
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    like active combat or natural disasters
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    or community violence or sexual assault
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    that causes post-traumatic
    stress disorder,
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    and not everyone that is exposed to stress
    develops a mood disorder.
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    And this ability to experience
    stress and be resilient
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    and bounce back and not develop
    depression or PTSD
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    is known as stress resilience,
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    and it varies between people.
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    And we have always thought of it
    as just sort of this passive property.
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    It's the absence of susceptibility factors
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    and risk factors for these disorders.
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    But what if it were active?
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    Maybe we could enhance it,
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    sort of akin to putting on armor.
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    We had accidentally discovered
    the first resilience-enhancing drug.
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    And like I said, we only gave
    a tiny amount of the drug,
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    and it lasted for weeks,
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    and that's not like anything
    you see with antidepressants.
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    But it is actually kind of similar
    to what you see in immune vaccines.
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    So in immune vaccines,
    you'll get your shots,
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    and then weeks, months, years later,
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    when you're actually exposed to bacteria,
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    it's not the vaccine in your body
    that protects you.
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    It's your own immune system
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    that's developed resistance and resilience
    to this bacteria that fights it off,
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    and you actually never get the infection,
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    which is very different
    from, say, our treatments. Right?
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    In that case, you get the infection,
    you're exposed to the bacteria,
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    you're sick, and then you take,
    say, an antibiotic which cures it,
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    and those drugs are actually working
    to kill the bacteria.
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    Or similar to as I said before,
    with this palliative,
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    you'll take something
    that will suppress the symptoms,
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    but it won't treat
    the underlying infection,
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    and you'll only feel better
    during the time in which you're taking it,
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    which is why you have to keep taking it.
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    And in depression and PTSD --
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    here we have your stress exposure --
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    we only have palliative care.
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    Antidepressants only suppress symptoms,
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    and that is why you basically
    have to keep taking them
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    for the life of the disease,
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    which is often
    the length of your own life.
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    So we're calling our resilience-enhancing
    drugs "paravaccines,"
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    which means vaccine-like,
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    because it seems
    like they might have the potential
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    to protect against stress
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    and prevent mice from developing
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    depression and post-traumatic
    stress disorder.
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    Also, not all antidepressants
    are also paravaccines.
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    We tried Prozac as well,
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    and that had no effect.
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    So if this were to translate into humans,
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    we might be able to protect people
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    who are predictably at risk
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    against stress-induced disorders
    like depression and PTSD.
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    So that's first responders
    and firefighters,
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    refugees, prisoners and prison guards,
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    soldiers, you name it.
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    And to give you a sense
    of the scale of these diseases,
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    in 2010, the global burden of disease
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    was estimated at 2.5 trillion dollars,
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    and since they are chronic,
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    that cost is compounding
    and is therefore expected to rise
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    up to six trillion dollars
    in just the next 15 years.
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    As I mentioned before,
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    repurposing can be challenging
    because of our prior biases.
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    Calypsol has another name,
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    ketamine,
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    which also goes by another name,
  • 15:45 - 15:47
    Special K,
  • 15:47 - 15:49
    which is a club drug and drug of abuse.
  • 15:51 - 15:54
    It's still used across the world
    as an anesthetic.
  • 15:54 - 15:57
    It's used in children.
    We use it on the battlefield.
  • 15:57 - 16:00
    It's actually the drug of choice
    in a lot of developing nations,
  • 16:00 - 16:01
    because it doesn't affect breathing.
  • 16:01 - 16:06
    It is on the World Health Organization
    list of most essential medicines.
  • 16:07 - 16:10
    If we had discovered ketamine
    as a paravaccine first,
  • 16:11 - 16:14
    it'd be pretty easy for us to develop it,
  • 16:14 - 16:18
    but as is, we have to compete
    with our functional fixedness
  • 16:18 - 16:20
    and mental set that kind of interfere.
  • 16:22 - 16:26
    Fortunately, it's not
    the only compound we have discovered
  • 16:26 - 16:29
    that has these prophylactic,
    paravaccine qualities,
  • 16:30 - 16:32
    but all of the other drugs
    we've discovered,
  • 16:33 - 16:35
    or compounds if you will,
    they're totally new,
  • 16:35 - 16:39
    they have to go through
    the entire FDA approval process --
  • 16:39 - 16:42
    if they make it before
    they can ever be used in humans.
  • 16:42 - 16:44
    And that will be years.
  • 16:44 - 16:46
    So if we wanted something sooner,
  • 16:46 - 16:49
    ketamine is already FDA-approved.
  • 16:49 - 16:51
    It's generic, it's available.
  • 16:51 - 16:55
    We could develop it for a fraction
    of the price and a fraction of the time.
  • 16:56 - 17:01
    But actually, beyond
    functional fixedness and mental set,
  • 17:01 - 17:04
    there's a real other challenge
    to repurposing drugs,
  • 17:04 - 17:06
    which is policy.
  • 17:06 - 17:08
    There are no incentives in place
  • 17:08 - 17:12
    once a drug is generic and off patent
    and no longer exclusive
  • 17:12 - 17:15
    to encourage pharma companies
    to develop them,
  • 17:15 - 17:16
    because they don't make money.
  • 17:16 - 17:20
    And that's not true for just ketamine.
    That is true for all drugs.
  • 17:21 - 17:26
    Regardless, the idea itself
    is completely novel in psychiatry,
  • 17:26 - 17:30
    to use drugs to prevent mental illness
  • 17:30 - 17:32
    as opposed to just treat it.
  • 17:33 - 17:38
    It is possible that 20, 50,
    100 years from now,
  • 17:38 - 17:42
    we will look back now
    at depression and PTSD
  • 17:42 - 17:45
    the way we look back
    at tuberculosis sanitoriums
  • 17:45 - 17:46
    as a thing of the past.
  • 17:47 - 17:52
    This could be the beginning of the end
    of the mental health epidemic.
  • 17:53 - 17:57
    But as a great scientist once said,
  • 17:58 - 18:00
    "Only a fool is sure of anything.
  • 18:00 - 18:02
    A wise man keeps on guessing."
  • 18:04 - 18:05
    Thank you, guys.
  • 18:06 - 18:10
    (Applause)
Title:
Could a drug prevent depression and PTSD?
Speaker:
Rebecca Brachman
Description:

The path to better medicine is paved with accidental yet revolutionary discoveries. In this well-told tale of how science happens, neuroscientist Rebecca Brachman shares news of a serendipitous breakthrough treatment that may prevent mental disorders like depression and PTSD from ever developing. And listen for an unexpected -- and controversial -- twist.

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Video Language:
English
Team:
TED
Project:
TEDTalks
Duration:
18:23

English subtitles

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