Aubrey de Grey – Inflammation and Aging

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dr. Rhonda Patrick here and this
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adventure of the found my fitness
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podcast I’m in Mountain View California
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at the Sens Research Foundation and I
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have sitting here with me dr. Aubrey
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grey in the house Audrey is a biomedical
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gerontologist and he is founder of the
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sense Research Foundation and as far as
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I know the Sens Research Foundation has
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taken on quite a ambitious goal and that
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goal is to help prevent and cure aging
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what about some of the more recent
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methods for example the the CRISPR you
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know where this technology we’re now
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where I’m gonna totally oversimplify
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this for people but the ability to
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specifically target a gene and clip it
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out and replace it with another gene or
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a version of the gene that’s more active
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or less active depending on what it is
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you want i I think that these this new
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technology for music CRISPR for example
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dramatically changes a lot of things
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because I mean even if we look at for
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example centenarians semi centenarians
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which live to be about 105 or the or
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semi super centenarians litter to be 105
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and then the super centenarians which
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are about 110 plus a recent study came
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out from I think it was Tokyo and New
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Newcastle I think I don’t know if you’re
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familiar the city but essentially what
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the study did it was the largest cohort
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of the semi super super they’re sentient
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centenarians and the super centenarians
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and what they found was that they looked
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at a variety of different biomarkers so
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they looked at inflammatory biomarkers
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they looked at lipid profiles glucose
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they looked at you know senescence so
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when your immune cells no longer are
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living and dividing they basically sit
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around and they’re not dead but they’re
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doing more damage because they’re
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producing more inflammatory things that
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are damaging other cells so it’s like a
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spreading more nasty stuff around they
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looked at immuno immuno senescence and
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then they also looked at 200 links and
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then they also looked at like diseases
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and then they looked at you know organs
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like liver function kidney function and
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so
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anyways they’re correlating all these
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factors and what they found was that
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inflammation was the only thing that
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drove Aging in all the groups so
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inflammation the higher the inflammation
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the higher you know the risk of death of
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non accidents you know so you know
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age-related diseases cardiovascular
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disease cancer and this was true for all
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the groups but what was really also
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interesting was that the centenarians
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there was a positive correlation between
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between inflammation and amino
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senescence which was essentially lost in
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the super centenarian group and I don’t
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know why that is but the immuno
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senescence so essentially the
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inflammation went up and then that the
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super centenarians you know as the
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information went up to they died there
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was a positive correlation but the
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immuno senescence seemed to stay around
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the same for whatever reason so in my
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mind I think you know well we know that
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these super centenarians that’s possibly
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around a 25 to 30 percent increase in
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human lifespan so human lifespan in the
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United States is average around 79 years
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old and we could live to be a hundred
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and fifteen and live to be healthy
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that’s that’s fantastic so we know that
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it can be done with these super
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centenarians and we know that there is a
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lot of genetic factors that are playing
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a role on this I mean obviously these
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people have lower inflammation compared
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to non centenarians they also showed
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that and so an inflammation is a stream
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of a lot of damage it’s upstream of the
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damage that’s damaging DNA proteins in
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the cells lipids you know etc etc so if
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we can use CRISPR technology to go in
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and replace you know say give it more
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anti-inflammatory you know capabilities
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and this has been shown also in mice I
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don’t know if you’ve seen this study but
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NF kappa-b
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which is a gene that produces a protein
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that regulates a lot about other genes
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that are pro inflammation so they cause
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inflammation but it also has an anti
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inflammatory component to it and when
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you take away that anti inflammatory
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component and put it in mice what what
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happens is every time there’s an immune
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response every time inflammation happens
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which leads to chronic damage as you
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talked about there’s a low level
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inflammation and it drives aging
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maturely in mice all right big question
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that yes let me give a very big answer
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let me start with a very simple thing I
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will declare that inflammation is a
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double-edged sword that we need it the
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reason we have it if anything which
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physically carry that hasn’t just you
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have mutated into oblivion over
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evolutionary time it’s because it’s good
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for us it because it’s an essential
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component of how we survive infections
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however there are certain aspects of
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age-related damage accumulation which
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because they are only age-related are
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not very interesting to evolution and
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therefore evolution has not taken the
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trouble to improve the precision of the
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inflammatory response so as to
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discriminate between things that the
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inflammatory response can actually help
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with namely the elimination of
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infections and things that the
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inflammatory response actually
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exacerbates namely the accumulation of
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damage that is not an infection like
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oculars cholesterol or water so that
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means that yes it’s likely that it’s my
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surprise for us that when you look at a
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very very elite population the
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population that lives 100 510 then they
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were overwhelmingly have a weak
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inflammatory response because that is
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the only way that they will have been
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able not to succumb at the age of 80 or
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90 to atherosclerosis or Alzheimer’s
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which are definitely driven partly by
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the inflammatory response however what
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also needs to be taken into account is
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that plenty of people aged 80 and 99
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would die of infections so yes these
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people got genetically lucky because
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they didn’t get an excessive immune
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response response to those age-related
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problems but they also got
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environmentally lucky in that they
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didn’t die of infection or maybe they
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just had a really strong adaptive immune
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system that compensated for the wicked’
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advantage but I thought so you know
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there’s a real trade-off here and what
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this adds up to is that we cannot
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conclude that it would necessarily be a
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good idea to take people in there let’s
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say 60 or 70
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and that down there inflammatory
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response what about bump up there anti
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inflammatory response muscle ascend
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thing if we’re talking about the
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strength of the inflammatory response as
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opposed to the strength of other aspects
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of the immune system like mm b-cells
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then we are engaging in a change of a
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trade-off we are giving people less we
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were different it was risk of rate of
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well likely rate of progression of
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atherosclerosis and up famines and such
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like but we were also increasing their
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risk of dying pneumonia simple as that
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and the best way to deal with this is to
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find the best of both worlds solution to
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let people have the strong inflammatory
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response that they need in order to be
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protected well against infections but to
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fix the problem of miss snow of
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maladaptive activation of the immune
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response and what we’re kind of doing
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exactly that
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not by changing the inflammatory
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response itself but rather by changing
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the targets ultimately what’s happening
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in atherosclerosis is that the
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inflammatory response is being activated
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by the accumulation of indigestible
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waste products specifically oxidized
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cholesterol in macrophages in the artery
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wall which turn into firm cells and
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generally make cells around them angry
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if we could if they didn’t happen if we
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could get rid of that oxidized
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cholesterol then it wouldn’t matter in
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or how strong your inflammatory response
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was you would not get atherosclerosis
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same for Alzheimer’s ultimately up
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families has an inflammatory response
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because the stuff it’s reacting to its
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amyloid and turn on so we can get rid of
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those materials stop them from
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accumulating to a pro-inflammatory
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inflammation triggering level then we
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won’t get inflammatory response even in
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people with a strong inflammatory
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genetic I’m something else you know
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talking about this damage and you know
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you and I both agree that I mean I think
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the damage the accumulation of damage
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intracellular so inside the cell outside
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of cells on cell membranes proteins DNA
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on and on I mean I think that is a
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driver of Aging and essentially causes
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aging
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I would think yeah and I focus more on
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the an easier solution which is the
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nutritional aspects of preventing or
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allowing your body to you know
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metabolize and produce energy the best
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it can and even though you’re still
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going to age like even if you’re at the
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optimal amount I mean even if you have
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the optimum ount of you know
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micronutrients you have these minerals
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and vitamins that are essential to run
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your metabolism they’re essential to run
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enzymes that repair damage you know so
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on
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the fact is you will still age this the
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question is you know ha so yeah exactly
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the questions are much better and I’m
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all for all of that work you know life I
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love why Bruce and I became friends a
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long time ago was because I absolutely
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endorse the idea that we need to do the
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best we can for the population to get
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them to an average level of nutrition
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but I think the critical thing to
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understand is average if you ask about
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the difference in terms of health
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expectancy and life expectancy between
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let’s say the middle 10% of the
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population and the bottom 10% it’s a
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large difference and that’s the
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difference that we’re talking about here
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the difference the Bruce is trying to do
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something about by making sure that if
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the poor won’t eat fruit then that we
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found multivitamins and so on but if you
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look at the opposite end of the spectrum
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if you look at the difference between
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the middle 10% and the top 10% in terms
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of health expectancy and life expectancy
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it’s basically nil of course I’m
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factoring out genetics here I’m talking
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about less time talking about things
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that we can modify and that’s really
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important to remember because it’s so
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easy from the popular press and so on to
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get the impression that if you just do
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what your mother told you to do it
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really well you know you we don’t really
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get diet and you get a lot of exercising
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you never drink anything you never
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smoked it so and then you’re actually
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going to live 20 years longer than you
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otherwise would well in fact the message
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of all of the data we have
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epidemiological or anything is that it’s
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probably closer to two years if that you
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know I mean an example I like to give is
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just a very simple one
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looking at national life expectancies so
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people laugh at the USA a great deal
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because of the fact that it’s it’s that
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number something like forty five in the
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league table of longevity among the
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industrialized world despite the fact
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that you guys spend far more per head on
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medical care then than anybody else but
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if you look at the absolute numbers and
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you look at the actual difference in
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number of years in life expectancy
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between the USA and the number one big
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country namely Japan it’s only for you
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only for you
Full Video: https://goo.gl/2jvhQg Website: http://sens.org YouTube: https://www.youtube.com/user/SENSFVideo Facebook: https://www.facebook.com/sensf Aubrey de Grey: https://en.wikipedia.org/wiki/Aubrey_… Dr. Aubrey de Grey is a biomedical gerontologist and the founder of the SENS research foundation which aims to find technologies that can repair the various types of damage that occur during the aging process. In this episode Rhonda and Aubrey discuss the types of damage that cause aging, how aging results in a decrease in the capacity to repair damage, what role epigenetics play in aging, how people age at different rates, chronic inflammation as a driver of aging, factors that are in young blood that repair damage, the role of nutrition in aging, and recent technologies such as CRISPR, induced pluripotent stem cells that will advance anti-aging research and more. You can find Aubrey on twitter at @aubreydegrey, and his foundation at http://www.sens.org. Facebook: https://www.facebook.com/agingreversed Tumblr: http://agingreversed.tumblr.com

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