Can We Cheat Death? Nobel Prize Winner Breaks Down the Science of Living Forever

00:57:34
https://www.youtube.com/watch?v=G1hGXbx-TM8

概要

TLDRIn this podcast, the host explores the philosophical and biological aspects of mortality and aging, asking whether humans truly want to live forever. The discussion covers evolutionary reasons for death, varying lifespans among species, and the current landscape of anti-aging research. It highlights the ethical implications of extending life, particularly the potential for widening health disparities. The importance of healthy lifestyle choices is emphasized as practical measures for improving health and longevity. Overall, the conversation balances optimism for emerging longevity therapies with skepticism about their efficacy and accessibility.

収穫

  • 📅 'Momento Mori' encourages us to appreciate life.
  • 🔬 Aging results from evolutionary processes favoring survival over longevity.
  • 🦠 Different species age at varied rates due to evolutionary factors.
  • 💔 Cancer and aging are interlinked; what prevents cancer early can contribute to aging later.
  • 🧬 Aging is multi-faceted, with gene damage and cellular stress as primary contributors.
  • ⏳ Compression of morbidity aims to reduce the time spent with illness before death.
  • 💪 Diet, exercise, and sleep are critical for healthy aging.
  • ⚖️ Health disparities exist, with wealth impacting health outcomes significantly.
  • ⚠️ Ethical concerns arise in anti-aging treatments regarding accessibility and societal impact.
  • 🔍 Research offers hope for better therapies, but skepticism is essential.

タイムライン

  • 00:00:00 - 00:05:00

    The concept of 'memento mori' emphasizes the importance of recognizing our mortality to appreciate life, raising the question of whether we truly desire immortality, leading to a disconnect between individual desires and societal needs.

  • 00:05:00 - 00:10:00

    A fundamental but nuanced truth of nature is that all living things age and die, with evolutionary factors contributing to why different species exhibit varying lifespans, as evolution prioritizes reproductive success over longevity.

  • 00:10:00 - 00:15:00

    Various species have distinct lifespans, influenced by evolutionary selections that prioritize traits favoring survival and reproduction, rather than longevity, illustrated by examples like mice versus elephants.

  • 00:15:00 - 00:20:00

    Death is not a straightforward concept; many cells in our bodies die continuously, yet they do not signify the death of the individual until critical systems fail, indicating a more complex understanding of mortality.

  • 00:20:00 - 00:25:00

    Research on organ repopulation suggests that death is potentially reversible at certain levels, but reversing critical system failures and inherent aging processes remains scientifically challenging.

  • 00:25:00 - 00:30:00

    The booming interest in longevity research is fueled by advances in molecular biology, increased investments due to an aging population, and public health needs juxtaposed with desires for improved health in old age.

  • 00:30:00 - 00:35:00

    Despite some progress in anti-aging research, there exists a natural limit to human lifespan, historically around 110 to 120 years, due to evolutionary mechanisms that shape biological aging processes.

  • 00:35:00 - 00:40:00

    Research on 'compression of morbidity' suggests a shift in focus from extending lifespan to enhancing the quality of life during aging, aiming to reduce the years spent suffering from chronic illnesses.

  • 00:40:00 - 00:45:00

    Patterns derived from studies of long-lived individuals may not translate universally, with ongoing research required to identify if findings can be applied broadly across populations or remain limited due to survivor bias.

  • 00:45:00 - 00:50:00

    Technological advancements in DNA methylation research highlight age prediction markers, but reversing such biological markers raises questions about causation versus correlation in the aging process.

  • 00:50:00 - 00:57:34

    The debate on anti-aging treatments underscores an ethical tension where disparities in access to emerging therapies might exacerbate existing societal inequalities, necessitating a focus on equitable healthcare solutions.

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ビデオQ&A

  • What does 'momento mori' mean?

    It means 'remember you will die,' emphasizing the beauty and brevity of life.

  • Why do we die according to evolutionary biology?

    Evolution has not selected against death; it prioritizes fitness and the ability to pass on genes.

  • What is the relationship between aging and cancer?

    The processes that protect against cancer in youth may contribute to aging later in life.

  • What are the primary causes of aging?

    Aging is multifactorial, with factors such as DNA damage, inflammation, and cellular senescence contributing.

  • Can aging be reversed?

    Currently, there's no definitive method to reverse aging, but some treatments show promise.

  • What is 'compression of morbidity'?

    It refers to the goal of shortening the period of illness before death.

  • How do lifestyle changes impact aging?

    Diet, exercise, and sleep significantly affect health spans and can help reduce age-related diseases.

  • Is there a natural limit to human lifespan?

    Yes, humans may have a natural lifespan limit of around 110-120 years due to evolutionary factors.

  • How do rich and poor people differ in terms of health outcomes?

    There are significant disparities in health outcomes, with wealthier individuals generally living longer and healthier lives.

  • What are the main ethical concerns regarding anti-aging therapies?

    Concerns include accessibility, societal impact, and the potential widening of health disparities.

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  • 00:00:00
    the Romans obviously had this phrase
  • 00:00:01
    momento Mori you know remember you're
  • 00:00:03
    going to die almost as a core to Arms to
  • 00:00:07
    acknowledge the beauty and shortness of
  • 00:00:09
    Life the question I want to ask you is
  • 00:00:11
    do we really want to live forever we all
  • 00:00:14
    accept philosophically that we're going
  • 00:00:16
    to die someday what we don't want is to
  • 00:00:18
    die tomorrow we've evolved to want to
  • 00:00:20
    live and and that is a problem what we
  • 00:00:23
    want as individuals is not necessarily
  • 00:00:25
    what's good for society let alone the
  • 00:00:28
    Earth there's a disconnection
  • 00:00:31
    there thank you thank you so much for
  • 00:00:33
    joining me on this podcast and you know
  • 00:00:35
    really we could talk for hours on the
  • 00:00:37
    subject of longevity anti-aging death
  • 00:00:40
    and how to reverse it but what I really
  • 00:00:42
    wanted to get into was you know there's
  • 00:00:45
    an inescapable fact of nature that
  • 00:00:47
    everything alive ages and then
  • 00:00:49
    everything that's alive also dies
  • 00:00:51
    eventually and that seems to be a basic
  • 00:00:54
    concept but there's some Nuance behind
  • 00:00:57
    that and I guess the real question I
  • 00:00:58
    want to ask you is why do we die we die
  • 00:01:02
    because Evolution has not selected
  • 00:01:05
    against death so you did you mentioned
  • 00:01:08
    everything dies but of course although
  • 00:01:11
    we're made all made of the same material
  • 00:01:14
    protein DNA RNA lipids species die at at
  • 00:01:20
    many different rates um for example some
  • 00:01:22
    insects only live a day and then there
  • 00:01:25
    are at the other extreme there are even
  • 00:01:27
    vertebrates like sharks and whales
  • 00:01:30
    that live for several hundred years in
  • 00:01:33
    fact I like to joke that there's a
  • 00:01:34
    Galapagos tortoise which could live for
  • 00:01:37
    up to 200 years that might still be
  • 00:01:40
    walking around but had encountered
  • 00:01:42
    Darwin 150 plus years ago so the
  • 00:01:46
    question is why why is it that different
  • 00:01:48
    species age and die have such different
  • 00:01:52
    lifespans and uh that's because
  • 00:01:55
    Evolution doesn't select for longevity
  • 00:01:59
    it doesn't care how long you live it
  • 00:02:02
    selects for your ability to pass on your
  • 00:02:04
    genes for the likelihood that you're
  • 00:02:06
    going to pass on your jeans and so it
  • 00:02:09
    selects for what biologists call Fitness
  • 00:02:12
    let's give an example if you're a mouse
  • 00:02:15
    there's no point in evolution selecting
  • 00:02:17
    for a species a mouse that would live
  • 00:02:20
    very very long because that Mouse would
  • 00:02:23
    be eaten or or die of starvation or some
  • 00:02:27
    other cause long before it gets old and
  • 00:02:29
    dies
  • 00:02:30
    so in in the case of the mouse Evolution
  • 00:02:32
    has selected for a species that puts all
  • 00:02:35
    its resources into rapid growth and
  • 00:02:38
    maturation and producing lots of
  • 00:02:40
    Offspring and the case of an elephant
  • 00:02:43
    the equation's different and with the
  • 00:02:44
    whale it's different so that in a
  • 00:02:47
    nutshell is the evolutionary argument
  • 00:02:49
    for why things die it's because
  • 00:02:52
    maintaining and repairing as an a body
  • 00:02:56
    takes resources takes you know energy
  • 00:02:59
    and and resources so they' only do that
  • 00:03:02
    if it's advantageous for the survival of
  • 00:03:05
    the species so when we say that
  • 00:03:07
    something is dead and certainly when we
  • 00:03:09
    die most of the cells in our bodies
  • 00:03:12
    aren't actually dead they're maybe aged
  • 00:03:14
    or stuck in this sort of stasis and
  • 00:03:16
    contributing towards that death process
  • 00:03:19
    so you know which is why we can do organ
  • 00:03:21
    transplants and give someone a new liver
  • 00:03:23
    and they can function again yeah no
  • 00:03:25
    that's exactly right so what is the
  • 00:03:27
    definition of death in that instance
  • 00:03:29
    then yeah so death is a peculiar concept
  • 00:03:32
    because the flip side of what you said
  • 00:03:34
    is that cells in us are dying all the
  • 00:03:37
    time we don't even notice it and in fact
  • 00:03:40
    often their death is actually required
  • 00:03:42
    for the function of the organism as a
  • 00:03:44
    whole and so what we mean by death is
  • 00:03:48
    the death of the whole organism the
  • 00:03:53
    individual and in the case of the human
  • 00:03:55
    you know the individual human being and
  • 00:03:58
    that means our inability to function as
  • 00:04:01
    a coherent whole person that happens
  • 00:04:04
    when a critical system
  • 00:04:08
    fails and then you have uh some
  • 00:04:13
    inability for the entire organism to
  • 00:04:16
    survive as a whole and typically you
  • 00:04:18
    know if a critical system like your
  • 00:04:20
    heart or your brain fails then the rest
  • 00:04:22
    of the body will eventually follow and
  • 00:04:25
    that's what we mean by death I mean
  • 00:04:27
    there was an interesting um study done
  • 00:04:29
    on reperfusion treatment on dead pigs
  • 00:04:32
    and this this was also trial on human
  • 00:04:34
    brains and this reperfusion treatment
  • 00:04:37
    allowed certain parts of the human brain
  • 00:04:39
    to you know reanimate and show some
  • 00:04:41
    evidence of function and this got people
  • 00:04:43
    excited naturally thinking that death
  • 00:04:45
    could be a reversible process I mean how
  • 00:04:48
    far are we to reversing death I think
  • 00:04:52
    you know you may be able to reverse some
  • 00:04:54
    things temporarily for example uh you
  • 00:04:57
    know 100 years ago the the typical
  • 00:05:00
    Criterion for death was when your heart
  • 00:05:02
    stopped now we don't use that Criterion
  • 00:05:05
    anymore because with
  • 00:05:07
    CPR uh we know that even after the heart
  • 00:05:10
    has stopped you can revive uh heartbeat
  • 00:05:13
    and and make the person you know survive
  • 00:05:16
    and and and be alive and so now in most
  • 00:05:20
    countries the legal definition of death
  • 00:05:22
    is uh irreversible loss of brain
  • 00:05:25
    function so now I guess what you're
  • 00:05:28
    saying is well maybe by infusion you
  • 00:05:31
    could delay loss of brain function or or
  • 00:05:35
    possibly reverse it I think you may be
  • 00:05:38
    able to do it temporarily but I think
  • 00:05:40
    it' be very hard to
  • 00:05:43
    reverse uh that kind of process
  • 00:05:46
    indefinitely because usually the
  • 00:05:48
    critical system failure is a is a
  • 00:05:50
    symptom of an underlying aging process
  • 00:05:53
    things have reached a point where
  • 00:05:55
    they're no longer functioning well I
  • 00:05:57
    mean it seems that you know throughout
  • 00:06:00
    human history the Quest for immortality
  • 00:06:03
    the Quest for extending our lifespan has
  • 00:06:07
    almost taken on this mythical type Quest
  • 00:06:09
    and it's almost the you know bordering
  • 00:06:11
    science fiction and for many many
  • 00:06:14
    decades this anti-aging longevity field
  • 00:06:17
    has been seen you know as like a
  • 00:06:19
    Backwater specialty but over the last
  • 00:06:22
    couple of decades it's really come to
  • 00:06:24
    the four with a lot of investment into
  • 00:06:26
    it now what is the reason behind that is
  • 00:06:28
    that because of our insatiable appetite
  • 00:06:30
    to live forever in the midst of rising
  • 00:06:33
    cancer rates and metabolic disease and
  • 00:06:35
    chronic disease or is it because the
  • 00:06:37
    science has finally caught up with the
  • 00:06:39
    fantasies of Science Fiction well it's
  • 00:06:41
    it's a mixture of things that the recent
  • 00:06:44
    boom in in the longevity field is due to
  • 00:06:46
    mixture of things uh we've always wanted
  • 00:06:49
    to live uh to defeat death I mean even
  • 00:06:52
    the Chinese Emperors the Pharaohs in
  • 00:06:54
    Egypt they all wanted to defeat death uh
  • 00:06:57
    but what's happened recently are two
  • 00:06:59
    things one is that molecular biology has
  • 00:07:02
    made great strides in understanding uh
  • 00:07:05
    some of the key causes of aging and it's
  • 00:07:09
    really aging that leads to the kind of
  • 00:07:11
    death we're talking about not we're not
  • 00:07:13
    talking about death by accident or some
  • 00:07:16
    serious disease or Calamity or something
  • 00:07:19
    like that we're talking about the
  • 00:07:22
    natural process of death old age and
  • 00:07:24
    death so that molecular biology is
  • 00:07:28
    coming to grips with the very ious
  • 00:07:29
    causes and it's giving people some
  • 00:07:33
    feeling that now that we understand many
  • 00:07:35
    of these processes maybe we can
  • 00:07:38
    interfere with them and slow down aging
  • 00:07:40
    and therefore at least live a healthier
  • 00:07:43
    life the more extreme view is that we
  • 00:07:45
    might be able to extend life but but the
  • 00:07:48
    majority views at least it might give us
  • 00:07:50
    Health a healthier life the other reason
  • 00:07:53
    for the big boom is that uh societies
  • 00:07:57
    all over the world are aging this is
  • 00:08:00
    because people are living longer and
  • 00:08:02
    that's largely due to Better Health and
  • 00:08:05
    better medicine at the same time
  • 00:08:07
    fertility rates are
  • 00:08:09
    dropping and this means that the
  • 00:08:11
    population on average is getting older
  • 00:08:14
    that it's being skewed more towards the
  • 00:08:16
    older end so that creates a real
  • 00:08:19
    imperative to make sure that this aging
  • 00:08:23
    population remains healthy and
  • 00:08:26
    preferably independent and productive
  • 00:08:28
    that means trying to understand the
  • 00:08:30
    causes of aging and seeing if we can do
  • 00:08:33
    something about it so governments are
  • 00:08:35
    investing a lot in aging research and of
  • 00:08:38
    course there's a huge interest from
  • 00:08:40
    industry because you know people are
  • 00:08:43
    aging they naturally want to be
  • 00:08:45
    healthier they're susceptible to wanting
  • 00:08:47
    to try all kinds of things and there's
  • 00:08:50
    money to be made there are about 700
  • 00:08:53
    startups with many tens of billions of
  • 00:08:55
    dollars invested in longevity research
  • 00:08:59
    and it ranges from what I would call
  • 00:09:01
    quite
  • 00:09:02
    mainstream uh unobjectionable uh
  • 00:09:06
    research to uh really some dubious
  • 00:09:09
    practices and claims it's interesting
  • 00:09:12
    that over the last few decades we've not
  • 00:09:14
    really seen that age barrier crossed I
  • 00:09:17
    mean I think the the oldest person
  • 00:09:18
    recorded to have ever lived was 122 uh
  • 00:09:21
    back in the 1970s and you know 50 years
  • 00:09:24
    on we haven't crossed that threshold so
  • 00:09:26
    going back to your earlier Point saying
  • 00:09:28
    that evolution select for Fitness do you
  • 00:09:31
    think there is an evolutionary barrier a
  • 00:09:33
    ceiling set for humans at the 115 120
  • 00:09:36
    Mark and is there a reason why Evolution
  • 00:09:39
    wouldn't make it possible to live
  • 00:09:41
    forever both are true I think the way
  • 00:09:43
    Evolution has acted on our
  • 00:09:46
    species it is selected for a species
  • 00:09:49
    that whose natural limit is about 110 or
  • 00:09:52
    so there are very very few outliers who
  • 00:09:55
    go past 110 and even fewer past 115 and
  • 00:09:59
    only one past
  • 00:10:01
    120 and so that suggests that there is a
  • 00:10:04
    natural limit to our species and we have
  • 00:10:07
    evolved so that all of our repair
  • 00:10:10
    mechanisms and wear and you know
  • 00:10:12
    maintenance mechanisms simply sort of
  • 00:10:15
    give up around that point so that is
  • 00:10:19
    true but there's no physical or chemical
  • 00:10:22
    law saying that if we were to interfere
  • 00:10:25
    with the processes of Aging themselves
  • 00:10:27
    which are the result of evolution in in
  • 00:10:29
    our case so if we were to be able to
  • 00:10:32
    interfere with that uh then we might be
  • 00:10:35
    able to extend it so but I think it'd be
  • 00:10:37
    very very hard I think it'd be easier I
  • 00:10:41
    think to
  • 00:10:43
    improve health uh in our old age I'm
  • 00:10:47
    talking about say our 80s or 90s that I
  • 00:10:50
    think is more feasible than really
  • 00:10:52
    pushing it Beyond 120 I think that would
  • 00:10:56
    require a number of things to work in
  • 00:10:58
    concert although the more optimistic
  • 00:11:01
    people claim oh it could happen any day
  • 00:11:04
    now but but I'm I'm more skeptical about
  • 00:11:06
    it so I guess that refers to you know
  • 00:11:09
    quite a interesting point you made in
  • 00:11:11
    your book why we die about the
  • 00:11:12
    compression of morbidity so that maybe
  • 00:11:15
    you know in the sort of pursuit of
  • 00:11:17
    increasing our health span we need to
  • 00:11:20
    potentially Focus Less on the reversing
  • 00:11:23
    biological aging and focus more on
  • 00:11:26
    shrinking the number of Life years we
  • 00:11:28
    have where we're sort of boted with
  • 00:11:31
    chronic disease like hypertension
  • 00:11:33
    diabetes and other cardiovascular
  • 00:11:35
    insults and various other chronic
  • 00:11:36
    diseases like that yeah and then an
  • 00:11:38
    important one you you didn't mention was
  • 00:11:40
    dementia which I think uh is going to be
  • 00:11:43
    an
  • 00:11:44
    increasingly prevalent disease in old
  • 00:11:46
    age because it's the one that's hardest
  • 00:11:48
    to tackle um so you raised a very
  • 00:11:51
    important point which is all of the
  • 00:11:54
    conventional aging research communi
  • 00:11:57
    talking about compression of morbidity
  • 00:11:59
    for example the head scientist of altto
  • 00:12:03
    labs a big billion dooll investment by
  • 00:12:06
    Tech billionaires in California but but
  • 00:12:08
    there's a branch right here in Cambridge
  • 00:12:11
    he he said our goal is is not to extend
  • 00:12:15
    life but our goal is for everybody to
  • 00:12:17
    Die Young after a long time now what it
  • 00:12:20
    means is that you stay healthy and then
  • 00:12:22
    suddenly you die and that concept where
  • 00:12:27
    the period in which you have diseases
  • 00:12:30
    and disabilities where you need
  • 00:12:32
    extensive care and you're generally
  • 00:12:35
    speaking not a very happy person in
  • 00:12:37
    terms of health um that period that want
  • 00:12:41
    to compress and that's called
  • 00:12:43
    compression of morbidity now there is
  • 00:12:46
    there isn't really very good evidence
  • 00:12:49
    that it's possible for example all of
  • 00:12:51
    the advances that have extended Health
  • 00:12:55
    in in the past for example by treating
  • 00:12:57
    cancer heart disease diabetes they've
  • 00:13:00
    all extend increased our health but
  • 00:13:02
    they've also extended our lifespan and
  • 00:13:05
    so the result is that the period we're
  • 00:13:07
    going that we have with disabilities has
  • 00:13:10
    not actually decreased it's in fact if
  • 00:13:13
    anything it's increased because as a
  • 00:13:15
    fraction of our life it's about the same
  • 00:13:19
    and so there is a danger that as we
  • 00:13:21
    improve uh health and aging by
  • 00:13:25
    interfering with the process of Aging
  • 00:13:27
    you may Simply Be postponing the this
  • 00:13:29
    long slow decline to a later time so you
  • 00:13:32
    may actually be extending your lifespan
  • 00:13:34
    and having long period maybe even a
  • 00:13:37
    longer period of of of morbidity that's
  • 00:13:40
    not entirely clear the one counter
  • 00:13:44
    example I would say is studies of
  • 00:13:48
    supercentenarians people who live to be
  • 00:13:50
    110 or so those people seem to have
  • 00:13:54
    extraordinarily healthy lives and then
  • 00:13:57
    go through a rapid Decline and die so in
  • 00:14:00
    their case at least they've somehow
  • 00:14:03
    managed that compression of morbidity
  • 00:14:06
    but I'm not sure how translatable that
  • 00:14:09
    is to the general population because
  • 00:14:11
    when you look at these people who live
  • 00:14:13
    over 110 they're very few so we may be
  • 00:14:16
    looking at some kind of Survivor bias
  • 00:14:19
    these are simply the people who lucked
  • 00:14:21
    out either by their genes or some
  • 00:14:25
    combination of Lifestyle life history
  • 00:14:28
    they managed to dodge various bullets
  • 00:14:29
    along the way and and and survived so
  • 00:14:33
    it's not clear that what they have is
  • 00:14:37
    something that could be adopted for the
  • 00:14:40
    rest of the population but that's that's
  • 00:14:42
    an active area of research and people
  • 00:14:44
    are looking into both their genetics and
  • 00:14:48
    their life history to see if there's
  • 00:14:50
    something that we could learn from it
  • 00:14:52
    yeah I mean I guess if we had a
  • 00:14:54
    blueprint to look at for healthy aging
  • 00:14:57
    and improving our lifespan it would be
  • 00:14:59
    these super centenarians and people who
  • 00:15:00
    are regularly living beyond 100 and I
  • 00:15:03
    guess one my rebuttal to that would be
  • 00:15:06
    unfortunately it seems that there's a
  • 00:15:07
    lot of poor bureaucracy and datae
  • 00:15:09
    keeping which potentially undermines
  • 00:15:11
    some of that research because I think uh
  • 00:15:14
    there was a scientist that I had on this
  • 00:15:15
    podcast recently who won the IG Nobel
  • 00:15:17
    Prize for exposing the blue zones a
  • 00:15:20
    great piece of work lot of fraud in that
  • 00:15:23
    industry and a lot of um you know sort
  • 00:15:26
    of pension fraud and tax fraud and
  • 00:15:28
    people basically lying about their birth
  • 00:15:30
    and death uh date so I guess that sort
  • 00:15:33
    of undermines our ability to look at
  • 00:15:35
    these people and actually take
  • 00:15:37
    actionables from them that that's true I
  • 00:15:39
    mean there is uh you know a lot of the
  • 00:15:41
    Blue Zone effect goes away when you
  • 00:15:44
    really restrict it to only those people
  • 00:15:46
    with very good recordkeeping but quite
  • 00:15:49
    apart from that there is this question
  • 00:15:51
    that I raised which is it's simply maybe
  • 00:15:54
    Survivor bias you know you're looking at
  • 00:15:57
    just the ones that happen to be lucky
  • 00:15:59
    and survived and there there might not
  • 00:16:01
    be General lessons for us but I think
  • 00:16:04
    that's something that only time will
  • 00:16:05
    tell if you if you look at the process
  • 00:16:08
    of Aging I guess it's wrong for us to
  • 00:16:10
    think that there is one singular cause
  • 00:16:13
    for aging it's multifactorial there's
  • 00:16:15
    not just a single Gene for aging it's an
  • 00:16:18
    accumulation of errors and insults and
  • 00:16:20
    DNA mutations and inflammation over our
  • 00:16:23
    lives so is there anything in the
  • 00:16:27
    current research and science going on
  • 00:16:29
    right now that's sort of pointing Us in
  • 00:16:30
    the direction of reversing that aging on
  • 00:16:33
    a cellular level there are several
  • 00:16:36
    aspects to that so it is true that there
  • 00:16:39
    isn't a single cause of Aging but the
  • 00:16:42
    causes are somewhat related for example
  • 00:16:45
    one primary cause is damage to our
  • 00:16:47
    genome and that could be DNA damage or
  • 00:16:50
    damage to the ends of our chromosomes
  • 00:16:52
    getting which get shorter or
  • 00:16:55
    modification of our DNA which changes
  • 00:16:57
    the program of genes that are expressed
  • 00:17:00
    as we age so that then has a KnockOn
  • 00:17:05
    effect it affects the program of what
  • 00:17:07
    proteins we make and these proteins
  • 00:17:10
    actually carry out all of the functions
  • 00:17:12
    in the cell and then that of of course
  • 00:17:15
    affects the cellular
  • 00:17:17
    compartments like these organel in our
  • 00:17:20
    cells called mitochondria which are
  • 00:17:23
    essentially where energy production is
  • 00:17:25
    carried out in a lot of
  • 00:17:27
    metabolism it's a big metabolism H Hub
  • 00:17:30
    in the cell and then that affects of
  • 00:17:33
    course our cell's ability to function
  • 00:17:37
    and communicate with other cells which
  • 00:17:39
    affects our tissues and our immune
  • 00:17:41
    system so you can see they're all sort
  • 00:17:42
    of related even though uh you could
  • 00:17:46
    think of them as having different levels
  • 00:17:48
    of complexity the molecules at the very
  • 00:17:50
    basic level of complexity then going
  • 00:17:53
    into collections of molecules then to
  • 00:17:56
    organel then to cells and then to
  • 00:17:58
    tissues and then the entire uh animal or
  • 00:18:02
    or person and so it is true it's
  • 00:18:05
    multifactorial uh but they're sort of
  • 00:18:07
    connected okay and they're they they're
  • 00:18:10
    connected in the sense that each level
  • 00:18:12
    affects the level not just above it but
  • 00:18:14
    also even the ones below it you know so
  • 00:18:16
    it's not even a strict hierarchy if we
  • 00:18:20
    look at some of the factors which uh
  • 00:18:22
    potentially contribute to aging so for
  • 00:18:25
    example for the average person listening
  • 00:18:27
    right now they may not know but the ends
  • 00:18:30
    of the DNA we have these little caps
  • 00:18:32
    called the tiir and the tiir shortening
  • 00:18:34
    obviously contributes to that aging
  • 00:18:37
    process so if we try to stop the
  • 00:18:40
    shortening of those tiir we could induce
  • 00:18:44
    or increase the risk of cancer formation
  • 00:18:46
    similarly if we you know try to you know
  • 00:18:51
    reprogram cells by making them kind of
  • 00:18:54
    baby cells or stem cells again from
  • 00:18:55
    their adult cells we could reverse aging
  • 00:18:58
    but also increase a risk of cancer so
  • 00:19:00
    there seems to be this sort of you know
  • 00:19:02
    mismatch between aging or Balancing Act
  • 00:19:05
    between aging and cancer if we try to
  • 00:19:07
    reverse aging we might increase the risk
  • 00:19:09
    of cancer so that's a that's a very very
  • 00:19:11
    good and very general point and you know
  • 00:19:14
    you remember I mentioned about Evolution
  • 00:19:16
    not selecting for longevity but it it's
  • 00:19:19
    actually more interesting than that
  • 00:19:21
    Evolution will often select for traits
  • 00:19:25
    that are advantageous when you're young
  • 00:19:28
    for example
  • 00:19:29
    uh growth so growth hormone pathway
  • 00:19:33
    helps you grow and mature and things
  • 00:19:35
    like that but that very same pathway
  • 00:19:38
    causes problems with aging later in life
  • 00:19:41
    and the the interplay between Cancer and
  • 00:19:43
    aging is something that we see time and
  • 00:19:46
    again you mentioned about the shortening
  • 00:19:49
    of telr well what happens is when the
  • 00:19:52
    telar which are the ends of our
  • 00:19:55
    chromosomes which contain our DNA when
  • 00:19:58
    they become
  • 00:19:59
    short they unravel then the cell thinks
  • 00:20:03
    of it as a break in the DNA it thinks of
  • 00:20:05
    it as damaged DNA and so it sends the
  • 00:20:08
    cell into a state called syence where it
  • 00:20:11
    can't function normally and it secretes
  • 00:20:14
    inflammatory chemicals so the immune
  • 00:20:16
    system can come and clear it away and
  • 00:20:18
    repair the damage no you can see why
  • 00:20:21
    that evolved because early in life a
  • 00:20:24
    cell with breaks in the DNA is a cancer
  • 00:20:26
    risk and so it it evolved a DNA damage
  • 00:20:30
    response which senses the DNA damage and
  • 00:20:33
    and gets that cell out of Harm's Way
  • 00:20:35
    doesn't let it survive and and
  • 00:20:38
    reproduce uh but that same process later
  • 00:20:42
    in life causes us to age because many
  • 00:20:46
    cells start suffering various kinds of
  • 00:20:48
    stress and damage and go into syence and
  • 00:20:51
    so we have an overpopulation of ccent
  • 00:20:55
    cells and inflam just systemic
  • 00:20:57
    inflammation which actually almost feeds
  • 00:21:00
    back and creates and and you get this
  • 00:21:03
    feedback loop where you get more and
  • 00:21:04
    more uh ccent cells being formed and so
  • 00:21:08
    again you have this interplay between
  • 00:21:10
    something that prevented cancer early in
  • 00:21:12
    life becomes a problem later in life I
  • 00:21:16
    mean over the years when I've been
  • 00:21:18
    working in the hospital and particularly
  • 00:21:19
    when I've been operating on patients as
  • 00:21:21
    well I've learned to almost ignore the
  • 00:21:25
    discreet chronological age that people
  • 00:21:27
    have been given because I can see two
  • 00:21:29
    60-year-old men who will be completely
  • 00:21:32
    different in their physiology the only
  • 00:21:34
    common denominator will be their age
  • 00:21:35
    which is 60 and maybe their ethnicity
  • 00:21:38
    and one can be really fit with a good
  • 00:21:40
    Baseline walking miles and miles a day
  • 00:21:43
    and the other will have multiple
  • 00:21:44
    cilities and maybe get short of breath
  • 00:21:45
    climbing a flight of stairs and I guess
  • 00:21:48
    the the sort of the link between the two
  • 00:21:51
    would be how can we how can you have two
  • 00:21:54
    people who are the essentially the same
  • 00:21:55
    age but so different um you know I guess
  • 00:21:59
    in their you know phenotype in their
  • 00:22:01
    life and it comes to this point of DNA
  • 00:22:03
    methylation this accumulation of these
  • 00:22:05
    chemical tags on their DNA maybe the
  • 00:22:07
    person who isn't so fit has lots of this
  • 00:22:10
    methylation tags which is you know
  • 00:22:12
    resulting in them being more
  • 00:22:14
    physiologically more you know geriatric
  • 00:22:16
    or age compared to the fit 60-year old
  • 00:22:18
    so I guess if we're using DNA
  • 00:22:21
    methylation as a marker of aging on a
  • 00:22:24
    you know microscopic level is there any
  • 00:22:26
    way to remove that tag and make someone
  • 00:22:30
    healthier or deage someone based on that
  • 00:22:32
    there is a lot of work in this area so
  • 00:22:35
    the the one thing we do know is that the
  • 00:22:38
    methylation patterns are laid down as we
  • 00:22:41
    age and they're laid down at different
  • 00:22:44
    rates in different people but
  • 00:22:46
    interestingly they're even laid down at
  • 00:22:47
    different rates in different tissues in
  • 00:22:49
    the same individual so it's almost
  • 00:22:51
    incorrect to talk about someone's
  • 00:22:54
    biological age as a single number
  • 00:22:57
    because you may have an older liver but
  • 00:23:00
    your kidney might not be quite as old
  • 00:23:02
    for example uh but that's shown to be
  • 00:23:05
    true that the methylation pattern is
  • 00:23:08
    almost a better
  • 00:23:09
    predictor of How likely it is you're
  • 00:23:12
    going to die uh in the next you know
  • 00:23:15
    coming years uh compared to
  • 00:23:17
    chronological age it's a better
  • 00:23:19
    predictor of what they call
  • 00:23:22
    mortality and so people say it's a
  • 00:23:24
    better marker for the so-called
  • 00:23:27
    biological age although as I said it's
  • 00:23:29
    biological age I I don't agree that it's
  • 00:23:31
    a single number anyway that's true what
  • 00:23:36
    isn't so clear is if they reverse the
  • 00:23:39
    methylation marks that they're going to
  • 00:23:41
    suddenly also reverse your age uh that
  • 00:23:46
    there are people who claim they've done
  • 00:23:50
    experiments along those lines but that's
  • 00:23:53
    more controversial because what we don't
  • 00:23:55
    know about this methylation is is is it
  • 00:23:58
    causation is it the methylation that's
  • 00:24:00
    causing the Aging or is it simply
  • 00:24:03
    correlated with aging that as you age if
  • 00:24:06
    you age faster you you lay down these
  • 00:24:08
    methylation marks more so do you think
  • 00:24:11
    actually when we're moving towards an
  • 00:24:14
    era of personalized or hyper
  • 00:24:16
    personalized health care and treatment
  • 00:24:18
    for people we should move away from
  • 00:24:21
    biological aging as a discrete number
  • 00:24:23
    and actually look to age specific organs
  • 00:24:26
    so we can actually Target treatment and
  • 00:24:28
    make bespoke treatment for individual
  • 00:24:31
    patients yeah I I would be more
  • 00:24:33
    enthusiastic if I if there were actually
  • 00:24:36
    treatments that would improve a
  • 00:24:38
    particular organ I I we're not I don't
  • 00:24:40
    think we're there or anywhere near there
  • 00:24:43
    uh yet and I personally am somewhat
  • 00:24:47
    skeptical there are lots and lots of
  • 00:24:49
    companies now that have sprung up that
  • 00:24:51
    will uh sell you a kit to determine your
  • 00:24:56
    so-called biological age for a few
  • 00:24:57
    hundred quid a pop and uh that's great
  • 00:25:01
    you know they'll they'll take your
  • 00:25:03
    sample and they will analyze either your
  • 00:25:05
    DNA methylation or there's another uh
  • 00:25:08
    way which is to look at your blood
  • 00:25:10
    enzymes or how much sugar has been added
  • 00:25:13
    to your proteins that also changes with
  • 00:25:16
    age each of them will claim that their
  • 00:25:18
    marker is better some of them will sell
  • 00:25:20
    you a combination of markers and the
  • 00:25:23
    question is what will you do with that
  • 00:25:25
    with that number and and currently
  • 00:25:27
    there's not much you can do that you
  • 00:25:29
    shouldn't be doing anyway I mean you
  • 00:25:31
    should be exercising and doing all the
  • 00:25:34
    things that keep you healthy uh
  • 00:25:37
    regardless of uh what this number from
  • 00:25:40
    some kit tells you so I'm fairly
  • 00:25:43
    skeptical about these efforts but but as
  • 00:25:46
    as I say there are a lot of there's a
  • 00:25:49
    lot of capitalizing on people's fears of
  • 00:25:53
    growing old and we are reaching a stage
  • 00:25:56
    where the boomer generation that's used
  • 00:25:58
    to and I'm one of them so I can be
  • 00:26:01
    critical uh the boomer generation is has
  • 00:26:03
    been used to having its way all its life
  • 00:26:07
    things worked out very well they've
  • 00:26:09
    ridden the wave and now they're getting
  • 00:26:11
    older and they don't like it and so
  • 00:26:14
    that's also driving a lot of this market
  • 00:26:17
    so VY if these atome tests work to
  • 00:26:20
    analyze someone's biological age what
  • 00:26:24
    metrics can they use in their daily life
  • 00:26:26
    to then say I've actually improved my
  • 00:26:28
    biological age for example my V2 Max is
  • 00:26:30
    better my blood pressure is better my
  • 00:26:33
    hba1c is better are there any markers
  • 00:26:36
    that someone could say that they've
  • 00:26:37
    improved their biological age with oh I
  • 00:26:39
    think uh all of those things that you
  • 00:26:41
    mentioned uh are worth uh looking at for
  • 00:26:45
    example let's say they have biological
  • 00:26:47
    markers like methylation or
  • 00:26:50
    glycosilation which is adding sugars to
  • 00:26:53
    your proteins uh there's a rate at which
  • 00:26:55
    that happens and let's say they take
  • 00:26:58
    measures to be healthier then if that
  • 00:27:01
    rate goes down it means they've somehow
  • 00:27:04
    slowed down possibly the process of
  • 00:27:08
    Aging but apart from that there's things
  • 00:27:12
    like V2 Max uh another thing that's
  • 00:27:15
    highly correlated with healthy aging is
  • 00:27:18
    grip strength and ability uh your
  • 00:27:21
    ability to walk distances in in a in a
  • 00:27:25
    short amount of time so there are number
  • 00:27:27
    of uh markers for fitness and as well as
  • 00:27:31
    biochemical markers and you could assess
  • 00:27:34
    that and see if your interventions are
  • 00:27:38
    actually either keeping you healthy or
  • 00:27:40
    at least slowing down uh your your aging
  • 00:27:44
    process uh I'm not sure how personalized
  • 00:27:48
    this is because I I think that these
  • 00:27:51
    measures are not going to be based on
  • 00:27:54
    your particular genome and your
  • 00:27:56
    particular result I think the the
  • 00:27:58
    measures are going to be very general
  • 00:28:00
    because anything that uh improves uh
  • 00:28:04
    healthy aging is going to be do it for
  • 00:28:07
    almost everybody so I'm a little
  • 00:28:09
    skeptical about the whole personalized
  • 00:28:12
    aspect of it but I I realize there's a
  • 00:28:15
    lot of money in the business yeah I mean
  • 00:28:18
    you mentioned before that there's
  • 00:28:20
    differences in the lifespans of various
  • 00:28:23
    animals uh you know you can have sharks
  • 00:28:25
    and whales and elephants who live you
  • 00:28:28
    you know a number of years of magnitude
  • 00:28:30
    more than humans and then you've got
  • 00:28:32
    rabbits rats mice Flies who are living
  • 00:28:35
    you know significantly shorter lives
  • 00:28:37
    than humans what is it about these
  • 00:28:40
    different creatures that we can maybe
  • 00:28:41
    learn from and apply to human science to
  • 00:28:45
    reverse aging to some degree because for
  • 00:28:47
    example a common question that people uh
  • 00:28:50
    ask in pop science is you know why don't
  • 00:28:52
    elephants get cancer despite them having
  • 00:28:55
    so many more cells than you know humans
  • 00:28:57
    they get uh cancer in a very
  • 00:29:00
    astonishingly small frequency so is
  • 00:29:03
    there things that we can apply from
  • 00:29:05
    these animals from nature and translate
  • 00:29:08
    that into human research that we're
  • 00:29:10
    doing it it'll be hard and and I think
  • 00:29:13
    part of the reason is that uh species
  • 00:29:16
    have evolved a complex balance in their
  • 00:29:20
    metab metabolism in their
  • 00:29:23
    physiology that uh is a balance between
  • 00:29:26
    repair and maintenance and growth and
  • 00:29:29
    maturation and and and various other
  • 00:29:32
    things and that's what determines
  • 00:29:34
    lifespan as I mentioned so you mentioned
  • 00:29:36
    the case of elephants that's a it's a
  • 00:29:38
    paradox known as Pito Paradox after the
  • 00:29:41
    person who first formulated it which is
  • 00:29:43
    the idea is if you have lots of cells if
  • 00:29:46
    you have many more cells the odds that
  • 00:29:48
    one of them becomes cancerous is much
  • 00:29:50
    higher so that animals should be more
  • 00:29:53
    prone to cancer in the case of elephants
  • 00:29:56
    it turns out they have 20 Copp iies of a
  • 00:29:59
    DNA repair protein uh whereas mice and
  • 00:30:02
    we only have two and so they clearly are
  • 00:30:07
    better in some ways at DNA repair uh and
  • 00:30:10
    so they're preventing cancer from
  • 00:30:13
    developing early uh in in their species
  • 00:30:17
    and uh if you look similarly at very
  • 00:30:19
    longlived whales it turns out they have
  • 00:30:22
    all sorts of repair DNA repair
  • 00:30:25
    mechanisms uh that are not the same same
  • 00:30:28
    as ours and certainly not the same as in
  • 00:30:30
    mice so you can see how in those species
  • 00:30:34
    Nature has chosen to put more effort
  • 00:30:37
    more resources into repair and
  • 00:30:40
    maintenance now the question you asked
  • 00:30:42
    is can we learn from that we can learn
  • 00:30:45
    biology from it but I don't I don't
  • 00:30:48
    quite know and I don't think anybody
  • 00:30:50
    does how to translate that to something
  • 00:30:53
    beneficial to humans I mean what are we
  • 00:30:55
    going to do create trans genic humans
  • 00:30:59
    where we've cloned in multiple copies of
  • 00:31:01
    DNA repair genes we don't even know what
  • 00:31:03
    that'll do uh to our physiology so so I
  • 00:31:07
    think it's it's it's quite complex and
  • 00:31:11
    not so E I think we learn a lot and from
  • 00:31:13
    the
  • 00:31:14
    general understanding of the biology
  • 00:31:16
    we'll be able to then apply it in in in
  • 00:31:20
    a broad but indirect way to our own
  • 00:31:22
    biology but I'm not sure we can directly
  • 00:31:25
    take information from some other species
  • 00:31:28
    and say oh this species does it this way
  • 00:31:30
    so let's engineer that into humans
  • 00:31:32
    that's I think asking for quite a lot I
  • 00:31:36
    think something you said there was
  • 00:31:37
    really interesting because you know the
  • 00:31:40
    the unknowns and you know what the
  • 00:31:42
    KnockOn effects of certain things are
  • 00:31:44
    and I see this anti-aging longevity
  • 00:31:46
    space as a spectrum you've got obviously
  • 00:31:48
    on one end the sort of sane end of
  • 00:31:49
    research and you've got you know
  • 00:31:51
    mainstream research and then you've got
  • 00:31:53
    the what I like to refer to them as the
  • 00:31:55
    gerona Nots you know these kind of uh
  • 00:31:57
    longevity astronauts trying to really
  • 00:31:59
    push the boundaries and take that leap
  • 00:32:01
    sometimes doing any equals one science
  • 00:32:03
    which you know if they want to fall off
  • 00:32:05
    the cliff first so other people can
  • 00:32:07
    learn lessons so be it and there's a lot
  • 00:32:09
    of people who you know self-medicate
  • 00:32:12
    with these things to biohack their
  • 00:32:13
    biology in some way and I guess
  • 00:32:16
    including I should say many sort of many
  • 00:32:19
    respected scientists who work in
  • 00:32:21
    longevity are are quietly taking all
  • 00:32:24
    kinds of things on the side I guess the
  • 00:32:27
    the question then comes back to the
  • 00:32:29
    point you raised whilst there may be
  • 00:32:31
    some mechanistic understanding of some
  • 00:32:34
    novel medication providing some degree
  • 00:32:38
    of benefit on a cellular level so for
  • 00:32:40
    example maybe metformin or Rapa seems to
  • 00:32:43
    be the the trending substance these days
  • 00:32:46
    I guess we don't have any idea of the
  • 00:32:50
    sort of knock on or offsite or
  • 00:32:51
    unintended effects of that thing because
  • 00:32:53
    these are all very complex metabolic and
  • 00:32:56
    biological pathway so whilst it may show
  • 00:32:58
    on the surface hey this can reverse
  • 00:33:00
    aging from a cellular level or at least
  • 00:33:02
    decrease inessence and cellular aging we
  • 00:33:05
    don't know what it does 20 streams that
  • 00:33:08
    way in terms of your biology and
  • 00:33:10
    completely screwing your body no that's
  • 00:33:13
    that's an excellent point and you raised
  • 00:33:14
    two very interesting chemicals so
  • 00:33:16
    metformin and
  • 00:33:17
    rapamycin now both of those are in some
  • 00:33:20
    ways related to the general idea of
  • 00:33:23
    caloric restriction which I I think is
  • 00:33:27
    certainly something that seems to work
  • 00:33:28
    and this is the idea that if you
  • 00:33:30
    restrict the number of calories in your
  • 00:33:33
    diet then it improves your health an old
  • 00:33:36
    age and people have shown that in many
  • 00:33:38
    different species from flies and worms
  • 00:33:41
    to mice and uh not not in humans but but
  • 00:33:45
    in chimpanzees as well or or monkeys
  • 00:33:47
    anyway the idea is that of course what
  • 00:33:50
    they're doing is they're comparing
  • 00:33:52
    animals that are fed in all you can eat
  • 00:33:54
    diet very rich all you can eat diet with
  • 00:33:58
    a an animal that has just the sufficient
  • 00:34:00
    just sufficient number of calories to
  • 00:34:02
    live but not to starve so it's not
  • 00:34:05
    losing weight and and and starving so
  • 00:34:08
    when they do that they find the
  • 00:34:10
    calorically restricted animals tend to
  • 00:34:12
    resemble younger animals and they they
  • 00:34:14
    seem to be healthier now some people
  • 00:34:16
    have argued all it's saying is that an
  • 00:34:19
    all you can eat Rich diet is very bad
  • 00:34:22
    for you you know and that's true so they
  • 00:34:24
    haven't done quite the proper uh
  • 00:34:27
    comparison but nevertheless you know if
  • 00:34:29
    you don't overeat and eat a modest
  • 00:34:32
    number of calories that seems to be
  • 00:34:34
    beneficial and they've shown that
  • 00:34:37
    caloric restriction affects certain
  • 00:34:39
    Pathways we don't know all of the
  • 00:34:41
    pathways probably but at least two of
  • 00:34:43
    the pathways involve these drugs
  • 00:34:46
    metformin and rapamycin now metformin is
  • 00:34:50
    interesting because it's a widely
  • 00:34:52
    approved drug for diabetes so there are
  • 00:34:55
    millions of people already taking
  • 00:34:56
    metformin
  • 00:34:58
    but the question of whether it benefits
  • 00:35:01
    healthy people is controversial there
  • 00:35:03
    was some indication that it did
  • 00:35:06
    originally uh but that other other
  • 00:35:08
    studies showed uh that it didn't and so
  • 00:35:11
    there are some large-scale trials which
  • 00:35:13
    are underway to ask what is the effect
  • 00:35:16
    of Metformin on healthy people and and
  • 00:35:19
    although the trials have been going on
  • 00:35:20
    or maybe at least were proposed for
  • 00:35:23
    quite some time I haven't seen any
  • 00:35:25
    results emerging yet that are that are
  • 00:35:28
    definitive now Romy is a an interesting
  • 00:35:31
    thing because it's a drug approved for
  • 00:35:35
    organ transplant recipients to prevent
  • 00:35:38
    rejection of their transplant and the
  • 00:35:41
    reason is it's an
  • 00:35:43
    immunosuppressant that's great if you're
  • 00:35:45
    an organ transplant recipient you you
  • 00:35:47
    want to live and not reject your organ
  • 00:35:49
    and so of course you have to take it but
  • 00:35:52
    to ask healthy people to take an
  • 00:35:55
    immunosuppressant over a long period
  • 00:35:58
    when you know it'll make you not only
  • 00:36:00
    more prone to infections but also have
  • 00:36:02
    all kinds of other side effects that's a
  • 00:36:04
    a tall order and yet on the basis of
  • 00:36:08
    studies in mice that show that
  • 00:36:11
    Rapa mimics some of the effects of
  • 00:36:14
    caloric restriction there are people who
  • 00:36:17
    in this field who who are quietly
  • 00:36:19
    popping
  • 00:36:20
    Romy uh on the side and I guess that
  • 00:36:24
    just shows that scientists are like
  • 00:36:25
    everybody else you know they're not
  • 00:36:27
    completely rational when it comes to
  • 00:36:29
    their own lives because rationally the
  • 00:36:31
    thing to do would be to wait for proper
  • 00:36:34
    long-term trials in humans now what they
  • 00:36:37
    would argue is that you could adjust the
  • 00:36:39
    dose that you could give rapamycin in
  • 00:36:42
    lower doses so it doesn't have the the
  • 00:36:45
    bad side effects of immunosuppression
  • 00:36:47
    Etc but maybe still has uh The
  • 00:36:50
    Beneficial effects but I'm not sure
  • 00:36:52
    that's possible because maybe the two
  • 00:36:54
    are related the the very fact that it's
  • 00:36:56
    immunos impressive is related to why
  • 00:36:59
    it's uh having its effect on on Aging
  • 00:37:03
    there's an interesting trial that's
  • 00:37:05
    that's been proposed for Ramy see that
  • 00:37:08
    normally they people do this in in in
  • 00:37:10
    laboratory animals like rats or mice
  • 00:37:12
    which are kept in sterile cages and
  • 00:37:15
    they're genetically uniform and so on so
  • 00:37:18
    it's not a real life environment so they
  • 00:37:20
    thought well we should maybe give it to
  • 00:37:22
    dogs domestic dogs dogs have a much
  • 00:37:26
    shorter lifespan than than we do and and
  • 00:37:28
    medium-sized dogs or large dogs tend to
  • 00:37:32
    have a shorter lifespan and so they
  • 00:37:33
    thought they they'd do it to medium and
  • 00:37:35
    large-sized dogs and the idea is that
  • 00:37:38
    dogs are not in a sterile environment in
  • 00:37:40
    fact they're in a whole variety of
  • 00:37:42
    environments that mimic humans because
  • 00:37:45
    they're as as varied as their owners and
  • 00:37:48
    so that would be a great trial I think
  • 00:37:51
    and then you could see do these dogs get
  • 00:37:53
    infections do they have other problems
  • 00:37:56
    or do they actually uh live a longer and
  • 00:37:58
    happier life I guess to your point about
  • 00:38:01
    a lot of these scientists in Industry
  • 00:38:03
    quietly popping Rapa and you know novel
  • 00:38:06
    medication which may or may not provide
  • 00:38:08
    any benefit to them at all I guess there
  • 00:38:10
    is something to be said about you know
  • 00:38:12
    the sort of uh very idiosyncratic
  • 00:38:15
    scientists actually providing the first
  • 00:38:17
    breakthroughs like I can think back to
  • 00:38:19
    Dr Barry Marshall a gastroenterologist
  • 00:38:21
    who also won the Nobel Prize like
  • 00:38:23
    yourself who you know swallowed H pylori
  • 00:38:26
    bacteria and proved that that was the
  • 00:38:28
    cause of stomach ulcers and then you
  • 00:38:30
    know led to the sort of treatment of
  • 00:38:33
    hpylori so I guess some of this testing
  • 00:38:36
    that we have we we sometimes need these
  • 00:38:39
    slightly crazy cooky people to really
  • 00:38:41
    push the barriers because I I I agree
  • 00:38:43
    with some of that but I I will push back
  • 00:38:46
    a little in that by the time Barry
  • 00:38:48
    Marshall swallowed H pylori and then
  • 00:38:51
    treated himself with antibiotics he had
  • 00:38:54
    very very strong evidence from animals
  • 00:38:57
    that that was actually the cause of
  • 00:38:59
    ulcers and so he he really uh I think
  • 00:39:04
    wasn't taking as much of a leap the
  • 00:39:06
    problem with anti-aging medicine is is
  • 00:39:10
    the following you know if you have a
  • 00:39:11
    serious disease even ulcers but let's
  • 00:39:13
    say you have serious disease like cancer
  • 00:39:16
    or diabetes or high arterial obstruction
  • 00:39:21
    or things like that then the and
  • 00:39:24
    especially cancer if it's a life or
  • 00:39:26
    death situation you'll be willing to
  • 00:39:27
    take all kinds of nasty chemicals to
  • 00:39:30
    eliminate the cancer because the
  • 00:39:32
    alternative is you're going to die okay
  • 00:39:35
    but if you're asking should I take this
  • 00:39:39
    medication for the next 10 or 20 years
  • 00:39:42
    in the hope that at the end it'll give
  • 00:39:44
    me another 10 years of healthy life uh
  • 00:39:48
    that's a that's a completely different
  • 00:39:50
    balance of risk and benefit so I I I
  • 00:39:55
    think aging anti-aging Therapeutics has
  • 00:39:58
    a problem it has a higher bar to
  • 00:40:01
    overcome before it's sort of generally
  • 00:40:04
    acceptable uh for for long-term
  • 00:40:07
    treatment now we do take long-term
  • 00:40:09
    treatments which are which are almost
  • 00:40:11
    anti-aging in in some respect for
  • 00:40:13
    example I take a Statin uh and I take
  • 00:40:16
    blood pressure medicines and both of
  • 00:40:18
    those are really about keeping me
  • 00:40:21
    healthier as I age but the fact is those
  • 00:40:25
    who' been tested yeah in millions of
  • 00:40:28
    patients of extensive clinical trials
  • 00:40:31
    before they were approved in the uh
  • 00:40:34
    Marketplace so it's rational to to take
  • 00:40:37
    them uh and that's what's needed I for
  • 00:40:40
    anti-aging medicines yeah absolutely and
  • 00:40:43
    I guess you know on top of that the some
  • 00:40:46
    of the drugs you mentioned blood
  • 00:40:47
    pressure medication statins for
  • 00:40:49
    cholesterol they have become so widely
  • 00:40:52
    tested and they have been proven to work
  • 00:40:54
    for over such a long period of time that
  • 00:40:57
    the cost is accessible usually to the
  • 00:40:59
    average person not just The Preserve of
  • 00:41:01
    the alter rich or the tech billionaires
  • 00:41:04
    and unfortunately the anti-aging space
  • 00:41:06
    is dogged by the fact that a lot of
  • 00:41:09
    these novel therapies some that do work
  • 00:41:11
    some that don't all of them are
  • 00:41:13
    relegated to that Ultra .1% of society
  • 00:41:18
    that you know can afford these things so
  • 00:41:20
    I guess one of my fears would be as we
  • 00:41:23
    progress in our science of longevity and
  • 00:41:26
    we do come up with more therapies that
  • 00:41:28
    may prove beneficial whether it's to
  • 00:41:30
    treat chronic disease or even for
  • 00:41:33
    longevity and reverse aging to some
  • 00:41:35
    degree that will continue to widen the
  • 00:41:37
    health inequalities and disparities
  • 00:41:39
    between you know in society that we have
  • 00:41:42
    where you maybe have the ultra Rich
  • 00:41:44
    living a decade maybe two decades longer
  • 00:41:47
    than you know people in a lower socio
  • 00:41:49
    economic status and that's quite
  • 00:41:50
    worrying yeah it's it it is a very
  • 00:41:53
    serious point and it's something I've
  • 00:41:55
    I've uh talked about uh fairly
  • 00:41:57
    extensively it turns out that even today
  • 00:42:01
    uh even in the UK which has a National
  • 00:42:03
    Health Service and there and therefore
  • 00:42:05
    Health Care accessible to to all the
  • 00:42:08
    richest 10% live about 10 years longer
  • 00:42:12
    than the poorest 10% and in the US it's
  • 00:42:15
    about 15 years but it's worse than that
  • 00:42:18
    it turns out that the health span the
  • 00:42:20
    number of healthy years is almost double
  • 00:42:23
    the difference is almost double so so
  • 00:42:25
    the difference between the healthy life
  • 00:42:27
    of a poor person healthy life of a rich
  • 00:42:29
    person's 20 years and not just 10 years
  • 00:42:31
    and in the US it may be even more so the
  • 00:42:35
    question is if we now uh have specific
  • 00:42:38
    anti-aging medicine will it increase
  • 00:42:41
    this disparity and it very well could
  • 00:42:45
    depending on the nature of the therapy
  • 00:42:47
    so if you have very
  • 00:42:50
    sophisticated stem cell therapy for
  • 00:42:52
    example uh that might only be accessible
  • 00:42:55
    to very rich people unless they have
  • 00:42:57
    insurance or unless the NHS pays for it
  • 00:42:59
    and so on and by by and large I would
  • 00:43:01
    expect rich people to be the first to
  • 00:43:04
    take advantage of that uh on the other
  • 00:43:06
    hand if you have something that's a very
  • 00:43:09
    inexpensive pill let's say something
  • 00:43:12
    like a Ramy analog or metformin analog
  • 00:43:17
    or uh maybe chemicals that might attack
  • 00:43:20
    senescent cells and there they can be
  • 00:43:24
    cheaply produced and they can eventually
  • 00:43:27
    become as widespread as stattin or blood
  • 00:43:29
    pressure medicines uh then of course uh
  • 00:43:32
    that's a benefit that uh perhaps
  • 00:43:34
    everybody uh could Avail themselves of I
  • 00:43:37
    guess another ethical conundrum of
  • 00:43:40
    anti-aging research and the consequen of
  • 00:43:42
    that if we have a large volume of people
  • 00:43:45
    living longer as you see in Japan for
  • 00:43:48
    example and we've seen the social and
  • 00:43:50
    economic consequences of that how do we
  • 00:43:53
    plan for that now it's going to be hard
  • 00:43:56
    um because as I said it's not even just
  • 00:43:59
    that people are living longer but
  • 00:44:01
    they're also fertility rates are also
  • 00:44:04
    going down and they're going down for a
  • 00:44:05
    variety of reasons uh at least I think
  • 00:44:09
    the ma major reason sociological women
  • 00:44:12
    are now empowered and uh it's quite
  • 00:44:15
    understandable that they don't want to
  • 00:44:17
    sacrifice their career and uh so on by
  • 00:44:20
    having several children and and so even
  • 00:44:23
    in places like India fertility India is
  • 00:44:26
    now almost replacement rate and many
  • 00:44:28
    states in India are below replacement
  • 00:44:30
    rate and so what you are going to have
  • 00:44:33
    is more and more older people and if now
  • 00:44:37
    they start living even
  • 00:44:38
    longer uh then you have a situation
  • 00:44:41
    where you have first of all a smaller
  • 00:44:44
    fraction of younger people in the
  • 00:44:46
    workforce uh that will have to support
  • 00:44:49
    an increasing population of older people
  • 00:44:52
    but even if you keep figure out ways to
  • 00:44:55
    keep older people healthy and productive
  • 00:44:57
    there is this problem that you then have
  • 00:44:59
    a society which has very low turnover
  • 00:45:03
    and so as people age they tend to
  • 00:45:06
    typically accumulate wealth power
  • 00:45:09
    influence and so on and so what you'll
  • 00:45:13
    have is a society I think that is
  • 00:45:15
    that'll have less turnover of ideas of
  • 00:45:19
    power uh in general a less vibrant uh
  • 00:45:23
    Society a less creative Society I think
  • 00:45:25
    people also uh forget that in many
  • 00:45:28
    fields people are more creative when
  • 00:45:31
    they're young than when they're old and
  • 00:45:33
    this has to do with a number of things
  • 00:45:34
    not just cognitive decline which is of
  • 00:45:37
    course a real fact uh but also the fact
  • 00:45:41
    that when we're young we uh are seeing
  • 00:45:44
    things fresh for the first time and
  • 00:45:46
    we're we've accumulated less bias over a
  • 00:45:50
    long lifetime so we're more open-minded
  • 00:45:52
    and that leads to to creativity so I I I
  • 00:45:56
    think it will create a different kind of
  • 00:45:59
    society and something that we don't talk
  • 00:46:01
    about and we're not really uh prepared
  • 00:46:04
    for I wonder with all the billions being
  • 00:46:06
    poured into anti-aging research are we
  • 00:46:09
    leaving simple lwh hanging fruits on the
  • 00:46:11
    table for example you know on the topic
  • 00:46:13
    of India air pollution is you know
  • 00:46:15
    abysmal in India and we're leaving life
  • 00:46:18
    table SP a few weeks there yeah well I
  • 00:46:20
    hope you I hope you masked up I I I I we
  • 00:46:23
    did Mask up sometimes but it's it's so
  • 00:46:25
    also uncomfortable because it's warm and
  • 00:46:27
    sometimes humid and uh I I do have to
  • 00:46:31
    say what I noticed was that the well off
  • 00:46:33
    in India this again has to do with this
  • 00:46:35
    health disparity you just mentioned the
  • 00:46:38
    well off in India have essentially
  • 00:46:40
    seceded from India they they live in
  • 00:46:42
    their air conditioned homes with air
  • 00:46:45
    purifiers they go in their air
  • 00:46:47
    conditioned cars to visit their friends
  • 00:46:49
    or their offices or clubs and the 95% of
  • 00:46:52
    the people who can't afford this have to
  • 00:46:55
    face the consequences of all this
  • 00:46:57
    horrible uh air pollution and so on and
  • 00:47:01
    yes I think that is you know certainly
  • 00:47:03
    if I were a public health official in
  • 00:47:05
    India I would put far more money in
  • 00:47:08
    improving air quality and public health
  • 00:47:11
    and sanitation you know clean water and
  • 00:47:14
    and uh public toilets and so on I would
  • 00:47:16
    put far more money into those than I
  • 00:47:18
    would put into anti-aging and Longevity
  • 00:47:21
    research uh that's much more pressing
  • 00:47:24
    but uh and of course infectious disease
  • 00:47:27
    which we didn't touch on but I think in
  • 00:47:31
    well-off countries it's not often an
  • 00:47:33
    either or
  • 00:47:35
    situation uh because people do want to
  • 00:47:39
    uh tackle existing diseases and public
  • 00:47:41
    health and so on but but they also do
  • 00:47:44
    have this growing population of older
  • 00:47:46
    people and they want to ensure Health in
  • 00:47:48
    old age so that has become a an
  • 00:47:51
    imperative you know the the Romans
  • 00:47:53
    obviously had this phrase momento Mory
  • 00:47:55
    you know remember you're going to die
  • 00:47:56
    die almost as a core to Arms to
  • 00:47:59
    acknowledge the beauty and shortness of
  • 00:48:02
    life so you can make more of the limited
  • 00:48:04
    time you have you know in in life and I
  • 00:48:07
    guess the question I want to ask you is
  • 00:48:09
    do we really want to live forever and if
  • 00:48:11
    someone were to live to 200 would that
  • 00:48:15
    in some way blunt their drive to be
  • 00:48:18
    creative to be Innovative to kind of
  • 00:48:20
    seek New Heights because they know I've
  • 00:48:23
    got 200 years to live rather than 80 I I
  • 00:48:26
    agree with that I I'm not sure everybody
  • 00:48:28
    does certainly many of these longevity
  • 00:48:31
    Advocates would disagree with me for
  • 00:48:33
    example uh what they would say to me is
  • 00:48:35
    that look a 100 years ago or 150 years
  • 00:48:38
    ago on average life expectancy was about
  • 00:48:42
    half of what it is today and so would
  • 00:48:44
    you want to go back uh to that time or
  • 00:48:48
    and if we increased it by a factor of
  • 00:48:50
    two what's wrong with increasing it by
  • 00:48:52
    another factor of two well there are a
  • 00:48:54
    couple of things wrong with that those
  • 00:48:56
    early
  • 00:48:57
    uh advances were about reducing infant
  • 00:49:01
    mortality and untimely death they didn't
  • 00:49:04
    actually extend our the limits of our
  • 00:49:07
    biological lifespan because even in the
  • 00:49:10
    even in olden times people like
  • 00:49:12
    Michelangelo lived to be almost 90 I
  • 00:49:15
    think he died at the age of 89 so it's
  • 00:49:17
    not that nobody lived for a very long
  • 00:49:20
    time in olden times it's just more
  • 00:49:22
    people were dying of disease and
  • 00:49:25
    avoidable scenarios and what we're
  • 00:49:27
    trying to do now is tackle things which
  • 00:49:29
    are essentially inevitable and trying to
  • 00:49:32
    uh to avoid those so there is a
  • 00:49:35
    fundamental difference the other is you
  • 00:49:38
    asked whether would we want to live that
  • 00:49:40
    long and that's goes back to an old joke
  • 00:49:43
    which is uh you ask somebody who would
  • 00:49:46
    want to live to be a 100 and the answer
  • 00:49:49
    is somebody who's 99 and and the problem
  • 00:49:52
    is we all accept philosophically that
  • 00:49:55
    we're going to die someday you know
  • 00:49:57
    momento Mory as you said but what we
  • 00:50:00
    don't want is to die tomorrow or the
  • 00:50:02
    next week or the next year or even the
  • 00:50:04
    next decade and so if somebody were to
  • 00:50:07
    come to you and say Here's a pel that'll
  • 00:50:11
    give you an extra 10 years of healthy
  • 00:50:13
    life you know very few of us would not
  • 00:50:16
    take it in fact the reason I'm taking
  • 00:50:18
    Statin and blood pressure medicines is
  • 00:50:20
    precisely because I want to stay healthy
  • 00:50:22
    for for longer and and so I think human
  • 00:50:26
    nature we've evolved to want to live and
  • 00:50:30
    and that is a problem what's good for
  • 00:50:33
    what we want as individuals is not
  • 00:50:35
    necessarily what's good for society let
  • 00:50:37
    alone the Earth there's a disconnect
  • 00:50:40
    there and I don't know I mean I don't
  • 00:50:44
    think that's a easily solvable problem
  • 00:50:47
    the other issue of course is if we live
  • 00:50:50
    to be 200 we'd be wondering about why
  • 00:50:53
    aren't we living to 400 so I think it's
  • 00:50:55
    a sort of NeverEnding
  • 00:50:57
    uh your goal this immortality it's it's
  • 00:51:00
    a almost a meaningless Quest and then
  • 00:51:03
    the final thing you asked about Drive I
  • 00:51:06
    do think our mortality is what gives us
  • 00:51:08
    drive there an old Jo old saying I think
  • 00:51:11
    one of Parkinson's laws that work
  • 00:51:14
    expands to fill available time yeah you
  • 00:51:16
    know if somebody gives you six months to
  • 00:51:18
    do something you'll take six months and
  • 00:51:20
    if they say you have to do it in six
  • 00:51:21
    weeks you'll do it in six weeks and so
  • 00:51:24
    if you have a very long time will be the
  • 00:51:27
    tendency oh I can do it tomorrow I've
  • 00:51:28
    got lots of time but the our finite life
  • 00:51:31
    gives us some urgency and you can see
  • 00:51:34
    that in the creativity and output of
  • 00:51:36
    writers
  • 00:51:38
    musicians uh scientists you know you
  • 00:51:40
    look at the old scientist gaus or Newton
  • 00:51:43
    they were no less productive than modern
  • 00:51:45
    scientists even though they lived on
  • 00:51:47
    average uh shorter lives and you know
  • 00:51:50
    all those great musicians who died in
  • 00:51:53
    their 30s and and and 40s and 50s even B
  • 00:51:57
    he died in his 50s which would be young
  • 00:51:59
    considered young today so I don't see
  • 00:52:01
    that modern composers are doing more
  • 00:52:04
    with their longer lives than uh people
  • 00:52:07
    like Beethoven or Mozart so I I do think
  • 00:52:11
    that you do get a sense of urgency and
  • 00:52:13
    drive from having a finite life I mean I
  • 00:52:16
    I look at people like Brian Johnson
  • 00:52:18
    who's obviously you know made it to the
  • 00:52:20
    forfront or is the poster child of the
  • 00:52:22
    anti-aging uh movement and whilst I
  • 00:52:26
    admire and commend his diligence for n
  • 00:52:29
    equals one science and you know pushing
  • 00:52:31
    the packet out there to see what works
  • 00:52:33
    and what doesn't obviously he's got the
  • 00:52:35
    financial resources to do such things
  • 00:52:38
    from an external point of view looking
  • 00:52:40
    at what he does in his supplements and
  • 00:52:41
    regimes it seems very stressful to adere
  • 00:52:44
    to such a strict protocol where you
  • 00:52:46
    can't you know ER away from the you know
  • 00:52:50
    discrete number of calories to consume
  • 00:52:52
    these supplements the testing so I guess
  • 00:52:55
    you know the stress in life is also you
  • 00:52:59
    know an aging accelerant oh I think um
  • 00:53:03
    you know I I was slightly down on Brian
  • 00:53:06
    Johnson until I watched some of his
  • 00:53:08
    videos yeah and to me he seems like a
  • 00:53:10
    very nice guy and enthusiastic about uh
  • 00:53:13
    what he's doing but I think he's got
  • 00:53:15
    this weird Obsession about aging and
  • 00:53:18
    death which is preventing him I think
  • 00:53:21
    from actually making the most of life
  • 00:53:24
    because he's spending all his time or a
  • 00:53:26
    good fraction of his life on longevity
  • 00:53:29
    extension longevity treatments and
  • 00:53:32
    measuring various parameters about
  • 00:53:34
    himself when he should be out yeah to
  • 00:53:37
    end creating and enjoying life and and
  • 00:53:40
    doing you know what he finds enjoyable
  • 00:53:42
    well maybe he finds this enjoyable but I
  • 00:53:44
    I find it rather strange I think you
  • 00:53:47
    know ultimately at the end of this
  • 00:53:49
    conversation we've spoken about this
  • 00:53:51
    kind of fantastic research that's being
  • 00:53:53
    done in longevity but I think the the
  • 00:53:55
    boring UNS sexy truth is that sleep diet
  • 00:53:59
    movement less stress all those things
  • 00:54:02
    are are the boring routine things that
  • 00:54:04
    will still extend your lifespan and
  • 00:54:06
    health span as well probably yeah the
  • 00:54:09
    thing I like to say is that the research
  • 00:54:11
    has not been in vain for
  • 00:54:13
    example uh we now although these these
  • 00:54:16
    kinds of measures like Diet exercise and
  • 00:54:19
    sleep they've been advocated you know
  • 00:54:20
    our grandmothers would probably have
  • 00:54:21
    told us that but what what we do know
  • 00:54:24
    now is exactly why they work for example
  • 00:54:28
    what is it that sleep does and what is
  • 00:54:30
    it that exercise does to our
  • 00:54:33
    biochemistry and our physiology that
  • 00:54:35
    causes its beneficial effects and same
  • 00:54:37
    thing with moderate diet which has to do
  • 00:54:40
    with these caloric uh restriction
  • 00:54:42
    Pathways so we understand much better
  • 00:54:45
    why they work and and that gives us
  • 00:54:47
    confidence that actually these things
  • 00:54:49
    are really worth doing because they they
  • 00:54:53
    work and they have knock on effects for
  • 00:54:54
    example stress is a driver of Aging but
  • 00:54:57
    of course if you exercise well you sleep
  • 00:55:00
    better and the combination then also
  • 00:55:02
    reduces your stress and the same thing
  • 00:55:04
    with and helps you improve your diet so
  • 00:55:06
    these things are all synergistic and to
  • 00:55:09
    the things you you mentioned I would add
  • 00:55:12
    very inexpensive things like getting a
  • 00:55:14
    test for high blood pressure for
  • 00:55:17
    diabetes for cholesterol because these
  • 00:55:19
    are easily detectable and very cheaply
  • 00:55:23
    and efficiently treatable and they too
  • 00:55:25
    will improve health Health in old age
  • 00:55:28
    and there are a couple of sociological
  • 00:55:30
    things that I ought to mention and that
  • 00:55:33
    is it's shown that people who tend to
  • 00:55:36
    have good social networks and don't
  • 00:55:39
    isolate themselves in old age tend to
  • 00:55:41
    live longer now again this could be
  • 00:55:44
    correlation rather than causation but
  • 00:55:46
    there is a feeling that isolation is bad
  • 00:55:49
    for you it increases mortality maybe it
  • 00:55:52
    increases depression and stress uh for
  • 00:55:55
    whatever reason and the other is that
  • 00:55:57
    oddly enough people with a sense of
  • 00:56:00
    purpose tend to have lower
  • 00:56:02
    mortality and this is an argument that
  • 00:56:04
    when you're older maybe you should
  • 00:56:06
    become involved in projects perhaps in
  • 00:56:09
    community projects in altruism in in in
  • 00:56:13
    volunteer work uh so all these things
  • 00:56:16
    can help and these are not things that
  • 00:56:20
    uh you know cost a lot although I will
  • 00:56:22
    point out all of these things are harder
  • 00:56:24
    for poor people to do for for example we
  • 00:56:27
    talk about health diet and exercise as
  • 00:56:29
    if it was free you know sorry sleep diet
  • 00:56:32
    and exercise a poor person will have to
  • 00:56:35
    grab whatever food they can find on the
  • 00:56:37
    go they may be working multiple jobs or
  • 00:56:40
    long hours so they won't have time to
  • 00:56:42
    exercise their sleep pattern may be uh
  • 00:56:45
    not as good so all these things that we
  • 00:56:47
    who who are well off can take for
  • 00:56:49
    granted is also harder uh for poor
  • 00:56:52
    people and that's part of the reason you
  • 00:56:54
    also have health disparities
  • 00:56:56
    really fascinating discussion because
  • 00:56:58
    there's obviously lots of interest in
  • 00:57:00
    the longevity space but there's also a
  • 00:57:02
    lot of skepticism that's needed and uh
  • 00:57:05
    hopefully people listening to this can
  • 00:57:07
    go forth into this anti-aging world with
  • 00:57:10
    a healthy dose of skepticism so thank
  • 00:57:12
    you very much thanky thank you and and I
  • 00:57:14
    should add there is a lot of really good
  • 00:57:17
    research and and I am hopeful that in
  • 00:57:19
    the end uh we will get uh really good
  • 00:57:23
    therapy that will at least keep us
  • 00:57:25
    healthier uh for longer but in the
  • 00:57:27
    meantime there are things we certainly
  • 00:57:29
    can do ourselves thank you thank you
タグ
  • longevity
  • aging
  • mortality
  • evolution
  • anti-aging
  • health disparities
  • lifestyle
  • compression of morbidity
  • ethics
  • society