ROBBIE: It is my pleasure today
to introduce Aubrey de Grey to Google for the third
or fourth time I think. AUBREY: Fifth. ROBBIE : FIfth time that
he's talked to Google, but the first time in Cambridge. Dr. de Grey has been for the
last decade or so probably the leading proponent
of anti-aging reasearch. Originally a computer
scientist, he developed an interest in
biology and combatting aging in the 1990s and went on
to create the SENS Foundation which has the ambitious goal
of defeating biological aging, or at least, radically
extending healthy human life. So I think we have a sort of
very interesting talk ahead of us. And I would like you to join
me in welcoming Dr. de Grey. [APPLAUSE] AUBREY: All right,
yes, thanks for coming. Yes, actually while
Robbie was talking I realized I think this was the
sixth one actually that I gave. I gave I think four
in Mountain View. If there any people in
Mountain View listening who were at the talk
I gave last year, this talk will be
slightly different. I constantly try to
improve the presentation. And, of course, there are two
ways in which that can happen. One is to talk about
new data-- things that we have achieved
over the recent times. And also, of course, to
improve the persuasiveness of the argument that aging
really is humanity's worst problem and something
that is completely scandalous that so few
people actually try to solve. So the title of my talk deserves
a little bit of explanation. First of all, the
word "rejuvenation," that is carefully chosen. I use that word very
advisedly because I really mean that we are talking
about reversing aging. In other words, turning
back the biological clock, making people
biologically younger both mentally and
physically than they were before the
intervention was begun. And as you'll see
over the next 10 or 20 minutes, the first, let's
say, half of my talk, I shall be explaining
why this constitutes a kind of happy medium
between two essentially impractical and
implausible extremes that have been the major source
of all the pessimism that surrounds the feasibility
of doing anything about aging with medicine. So first of all, the
nature of the problem. This is just a randomly
chosen statistic. I've used American data here. And this is simply
the proportion of the US population
over the age of 65. The x-axis goes from 1950
through to a projection out to 2050. And in case you can't
see the screen properly, the proportion in question
goes up from 8% up to 22%. So it's pretty dramatic. And the first thing I want to
make sure that you don't forget is that this is a
cause for celebration. Ultimately the fact is that
this is a result of the fact that we are no longer seeing
all that many people dying prematurely in infancy, or
in childbirth, or whatever. And that's wonderful. But we all know the downside. We all know that pension plans
are creaking and in danger of collapsing and all
matter of other difficulties are occurring as a
result of this change. The thing, of course,
that I want to focus on is the fact that it's not the
result of the statistics shown here-- the proportion of
the population over 65. Rather, it's a result of
the fact that people over 65 tend to not be very
well, and especially over the age of 75 or 85. And that is what
I'm out to change. Ultimately this is a
little bit of a paradox if you think about it. 200 years ago the life
expectancy was very low. People used to die
of other stuff. And mostly they died of
communicable diseases-- tuberculosis and diphtheria. And we have become very good,
at least in the developed world, actually to be honest quite
good in the developing world, at stopping that from happening. Not just through medicine
like vaccines antibiotics, but just through
realizing that hygiene is a good idea and
mosquito nets work. So you might think,
well hang on, why haven't the diseases
of old age been similarly susceptible to elimination or
at least very great reduction from similar measures? And that's where I want to
spend an amount of time. And I'm going to start by
simply giving a definition. As computer scientists, you all
know that precise definitions are rather important in getting
anything done technologically. And medicine is no different. And this will do as a
pretty good hardcore definition of aging. There are loads of definitions
of aging out there. So it's quite important
to actually fix on one for the purposes of discussion. This one is first
of all mechanistic. It actually says what aging is
in terms of cause and effect. But also in other ways it's
good at orienting our thoughts around what might be
necessary in order to do something about aging. So what I'm saying here is in
a very simple nutshell-- aging is a side effect of being
alive in the first place. It is very, very
similar, in essence it's really no different
in the human body than it is in a simple man-made
machine like a car or whatever. Ultimately any machine
with moving parts is going, a simple side effect
of the laws of physics, forgot biology, to
do damage to itself as a consequence of
its normal operation. And that damage is going
to accumulate progressively until eventually it
exceeds the tolerance that the body, the machine,
is set up to manage. And once that
happens, the machine starts to work less well and
eventually not work at all. So it's just the same
in the human body as it is in a man-made machine. There is, of course,
a big, big difference between the human body and
a typical inorganic machine which is that the human body and
indeed other living organisms have a fabulous array of
built-in damage repair machinery-- machinery
that eliminates damage as fast as it is created. But you got to remember
what that means. It doesn't mean that we can't
think of the body as a machine. What it means is that our job in
extending the healthy longevity of the machine, in the
case of the human body, is easier than it otherwise
would be because we've got all this help
from the machinery that the body has
already has installed. The reason it's
harder in aggregate is, of course, that the
human body is vastly, vastly more complicated than a simple
man-made machine or even the most complicated
man-made machine. And, of course, also,
we have the misfortune of not having the plans. So it's a bit tricky
figuring out what to do. But it still means
that we ought to be able to use the same
kind of approaches against aging of
the human body as we do against aging of
a simple machine. Now the thing is that this
is not very well understood. And there's a
particular way in which it's very poorly
understood by society that has had an enormous impact
on the extent to which we have taken seriously the idea of
doing anything about aging medically. Ultimately the misunderstanding,
the misconception that exists, is that an arbitrary division
is made between whatever aging itself might be defined to
be as against the diseases and disabilities of old age--
the diseases in particular. Things like cancer
and Alzheimer's and cardiovascular disease. These diseases of old
age are, of course, enormously widespread
and staggeringly costly now that we don't have
much in the way of diseases of early life. But they are not like
infectious diseases. First of all, they
are universal. You will get Alzheimer's unless
you die of something else first. You just will. And secondly, they
are not medically curable in the strict sense. What I mean by that is
simply that we cannot, even in principle, invent a
therapy that can be applied once to the body and eliminate
a disease like Alzheimer's from the body such that the person
won't get it again unless they are reinfected in some way. We can't do that
because aging is a side effect of being
alive in the first place. And the diseases of old
age are caused by aging. So you can't cure it in
that way without curing being alive in the first
place which would rather defeated the object really. So that makes it difficult. But it does not make it
impossible to apply medicine to the disease of old age. They are still medical problems. And they are medically
preventable in principle. We just have to start
from a different point-- a different conceptual
starting point. Putting it in another
way, it's like this. This is the conventional
way that we partition, that we classify, the
various sources of ill health that humanity is susceptible to. We have communicable diseases. We have congenital diseases
that occasionally people are born with because of
mistakes in their DNA. And we have the diseases
of old age-- the intrinsic, chronic, progressive things
that predominantly affect people who were born a long time ago. And then completely separate
from all these three, we think of this over
here-- this miscellaneous, kind of diffuse, nonspecific
phenomena like sarcopenia. That means lots of muscle mass. Or immunosenescence,
the decline in function of the immune system,
which we think of as part of aging itself. That is the way that most
people think of ill health. But it's completely wrong. The correct way
to think about it is to put that big black
line there instead. That actually these are
diseases in the sense that they can actually be
cured, whether by a vaccine or whatever, or by some
kind of gene therapy maybe. And these ones over
here are parts of aging. The only difference
between the third column and the fourth column is
that these things over here are things that we've taken
the trouble to give names to. That really is all it is. It's terminological, semantic. It's not a biological
difference at all. And once we understand that,
that the diseases of old age are part and parcel of
aging, we have a chance of getting somewhere
with both of them. This is the tragedy
of not getting to grips with that concept. At the moment, if we start
with my definition of aging down here, that
metabolism in other words, being alive in the first
place, the normal operation of the human body
throughout life causes a variety of different
molecular and cellular changes to occur in the body
that eventually once they get a abundant
enough, contribute to the ill health of old age. That definition
leads to a variety of different
potential approaches to postponing the ill
health of old age. And pretty much everything
we have in the clinic today consists of this up
here-- geriatric medicine. That is a real tragedy because
the whole idea underpinning geriatric medicine, in
other words, the attacking the pathologies of old age,
is to ignore everything that I just told you in
the past few minutes. It is to pretend that
the disease of old age can be cured just
like an infection-- to bash away at the symptoms
and hope for the best. And it's never going to
work because the precursors of these pathologies,
this damage done here, is obviously still
continuing to accumulate while the person is still alive. And therefore the pressure
against these therapies-- the pressure to make pathology
happen anyway is increasing-- and the therapies are
inevitably, inevitably going to get less and less
effective as someone gets older and older. So of course geriatric medicine
is better than nothing. I'm not saying it isn't . But it's only a little
bit better than nothing, and it only ever will be a
little bit better than nothing. Now, I'm not the first person
to realize that by any means. For the best part of
a century some people have been pointing this
out and saying well, prevention is better than cure. Maybe we should try to
intervene at an earlier stage in the chain of events
because this definition of aging is perfectly
uncontroversial. You know? I may be saying it in a
slightly different way, but ultimately, this is what
people-- people wouldn't have argued with that definition
of aging even a century ago. So as people have said well,
let's go in to up here. Let's call the problem
the problem of metabolism. Let's try to clean up
the way the body works and thereby slow down the rate
at which it creates damage. It sounds like a fine idea. It would postpone the age
at which the damage reaches this pathogenic threshold. And that unfortunately
has not succeeded. No real medicine has emerged
that substantially postpones the disease of old
age by slowing down the accumulation of damage. Why not? There's a very simple reason. It's called complexity. Just as the pathologies of
old age are rather complex. You don't have to
read this slide. This is just a small
subset of the things that go wrong with you late in life. Similarly,
unfortunately, metabolism is also a rather complicated. This is a simplified
diagram of a small subset of what we know about
how the body works. And as you can tell, it's
a bit of a mess really. And any software
engineer can easily understand that this
is like spaghetti code with no comments. There's no way that you're going
to be able to go in and tweak this thing to make it not do the
thing you don't want it to do, namely create
damage in this case, without having side effects
that do more harm than good. It's just not going to happen. The gerontology approach,
as I am calling it, is not doomed in principle the
way the geriatric approach is. But we would need to understand
this massively complex network of processes almost infinitely--
astronomically better than we actually
do today-- in order to have a prayer of
implementing what I'm calling the
gerontology approach. Of course I'm actually
understating the problem. The problem is not really that
this is a simplified diagram of a small subset of what we
know about how the body works. The problem is that this
is a simplified diagram of a small subset of what we
know about how the body works which is completely
dwarfed by the completely astronomical amount that
we don't know about how the body works, even ignoring
all the stuff that we don't even know that we don't know. So you know waste of time. Not going to happen
any time soon. So that is in a nutshell
why the world has become, when I say "the world" here
I am not talking of course about people who have thought
about biology and aging, has become so fatalistic
and pessimistic about applying medicine
to this problem. But luckily that's not
the end of the story. Let me come back to
cars for a minute. This, of course,
is a success story. This car here is
perhaps 100 years old. And it was definitely not
designed to last 100 years. It was probably designed
to last 10 or 20. So we must ask
ourselves how has it succeeded in lasting so long. And we all know the answer. The answer is that it's
been very, very, very well maintained. If you maintain your car
only as well as the law requires, then sure enough
it lasts only about as long as its manufacturer
is expected to wait until they could
sell you a new one. But this car, somehow
or other its owners fell in love with
it, and they did an unusually and
necessarily comprehensive amount of maintenance on
it, and that was the trick. Maintenance really works if
it's comprehensive enough. And we don't have any
200-year-old cars. But the only reason for
that is because cars had not been invented 200 years ago. We certainly will have
200-year-old cars. So if we come back and
ask what that analogy means for the problem
at hand, the human body. It mean this. It means that rather than
trying to go in and slow down or eliminate this process
whereby metabolism creates damage or go in and
interfere with this process where damage creates pathology. Instead we just uncouple those
processes from each other. We dive in and separate them
by periodically repairing the damage that's been
created already by the way the body works, and
thereby, even though it's continuing to be
created, preventing it from reaching this pathogenic
threshold-- very simple idea. It's an idea whose
proof of concept is all around us in
well-maintained machines. It's the way that we're
actually going to defeat aging. So what does that
mean in practice. Of course you or I,
anyway, certainly can't go out and keep a
car going for 100 years because we don't
have the expertise. So what I need to do is
summarize now for you, and I realize, of
course, that most of you will not very much biology. So I won't go into
too much detail. What I need to
summarized now for you is what it means in practice
to actually do the maintenance approach. And the big first
step in addressing a really complex problem
like this is often, I am sure you agree,
to break it down into sub-problems, preferably
a manageable number of sub-problems. So that was the first step that
I took back nearly 15 years ago now. These are the seven
sub-problems-- seven types of damage-- changes in the body
at the cellular or molecular level which continue throughout
life as side effects of being alive-- side effects of the
body's normal operation. And which eventually
accumulate to a point where they contribute to
one or another or more of the diseases and
disabilities of old age. And as you can see, these
are very clearly down to earth, concrete,
biological phenomena. They are very broad categories,
and that's a good thing because it means we don't
need so many of them. But the point is that
they are clearly defined and within each
category-- this is the reason why this
particular classification is useful-- within
each category there is a generic therapy, a type
of approach to implementing the maintenance concept
that can be applied to every example
within the category, not necessarily identically. Certain minor changes
might be required. And we'll come to
those things later on. But basically, there's
one generic therapy, which means that this
classification is useful. So lets go through it briefly. Cell loss-- what does that mean? It just means
cells dying and not being automatically replaced
by the division of other cells. Simple enough-- cells die,
they are not replaced, the number of cells goes
down, eventually the organ of which the cells
were a part is going to not have enough
cells to do its job. So you can understand that
that would be a part of aging. You can have too many cells. It turns out that there
are two very different ways in which you could
have too many cells. And the reason they are
different for my purposes is precisely because
the way in which we would go about
addressing the problem is different in the two cases. The first one is
having too many cells because they are
dividing when they're not supposed to, in
other words, cancer. And the other one is
having too many cells because they are not dying
when they are supposed to. That's something that
a lot of people ignore. But it's quite
important, it turns out, in certain parts of aging. Possibly the most conspicuous
is the immune system in which cell death and
the-- and cell death is really important as a way
of making room for rapid cell division later on. So those are the three that are
related to the number of cells. Down here we've got things
that the molecular level. Two of them inside cells
and two of them outside. The ones that are
inside-- the first one is mitochondrial mutation. So I guess most of you
know what mitochondria are, but just to recap. They are the part
of the cell that does the chemistry
of breathing-- the combining of oxygen with
nutrients to extract energy from the nutrients that is then
used by the rest of the body. And unlike any other
part of the cell, mitochondria have
their own DNA-- a very small amount--
only encodes 13 proteins, but still very essential. And it just turns out that
mitochondrial DNA accumulates mutations far far faster
than the nuclear DNA. So that's really important. The second one is
garbage-- waste products-- just waste products--
things that the cell makes as a side effect of
was it's normally doing, but which for whatever
reason, the cell does not have the machinery either
to break down or to excrete. And so, of course,
it accumulates. And just as your
kitchen works every bit as well after a week's
worth of garbage has accumulated in the garbage
can as it did the moment you took the garbage out. Similarly, the cell
works just as well with a manageable
amount of garbage. But just as your
kitchen doesn't work so well if you don't take
the garbage out for a month, the cell doesn't work
so well in old age because it's got too
much of this stuff. The other two are
things that's happen outside the cell in the
spaces between cells and they're also
really important. First one is, again,
waste products. There's a question over there
which I will take in a moment. Extracellular
junk-- this is stuff like the amyloid that form
plaques in Alzheimer's disease. And this is important
in the same kind of way that molecular garbage
inside the cell is important. But again I list it
separately because the way we're going to address it is
different than for the stuff inside. And finally then, molecular
changes that are not garbage but rather changes of structure
that cause loss of elasticity of the lattice of proteins that
gives our tissue it's-- gives our tissues their shape and
their stretchiness which is important in things
like the major arteries. So the question was? AUDIENCE: You mentioned that-- AUBREY: I am sorry shout please. AUDIENCE: You mentioned the
mutation rate in nuclear DNA is much lower than
mitochondrial, and that makes sense. But there is still mutational
damage to nuclear DNA. That eventually is going
to be a problem, right? AUBREY: Right, so
great question. I'll repeat it because it
may not have been heard. So the question is
OK, hang on, we've got mitochondrial
mutations here. Even if nuclear mutations
accumulate much more slowly than mitochondria, it's
still non-zero rate, surely we're going
to have to fix it. And I agree. We are going to have to fix it. The question really
is are we going to have to fix it in
anything like a currently normal lifetime. And it turns out that it
looks as though we probably aren't going to have to
except in one indirect way. So without going
into too many details the essential answer is that
there's one particular problem that mutations in the nucleus
can cause that is so much more serious so much more
quickly than any other that is the thing that
has driven evolution to make the quality of
our DNA repair machinery and made the machinery
as good as it is. And that thing is
cancer which is in my list in a different place
that doesn't talk about DNA. So that's basically the
answer to your question. We believe, or I believe anyway,
that the effect of mutations which do not affect
the cell cycle, do not actually cause
cancer, is non-zero, but it is so rare as
to be non-pathogenic until we have lived
very much longer than we have any danger
of living so far. All right so to go on. So these are the damage types. This is a great start, but of
course, we need to know more. First of all, we need
to know a little bit about how this type of damage
translates into pathology. And here I want to
stop for a moment and emphasize perhaps
a philosophical point, a conceptual point, but a
really, really important one that underpins the whole
logic of what I'm saying here. We would like to know
as much as we can about how metabolism creates
these various types of damage. And we would like to
know as much as we can about how these types of damage
cause the various pathologies and diseases of old age. But we don't need to know all
that much about those things. Really it's just a
case of reassurance to know these things because
at the end of the day given that metabolism causes damage
and damage causes pathology, if we can actually implement the
maintenance approach properly-- repair the damage--
in other words restore the molecular and
cellular structure of the body to how it was at a younger age
within a good approximation, then we have solved our problem. We do not need to know
how it got that way, or how it's going to get worse. We just need to-- we can
just rely on the fact that since the human
body is a machine, its function is determined
by its structure. So if we can restore
the structure, we will restore the function,
including the remaining longevity. This kind of side
stepping of our ignorance is absolutely fundamental to
why this whole approach feasible in the foreseeable future. One thing, however, that
it is important to try to get a grip on is a reason why
we can be reasonably confident that this classification
is exhaustive-- that it really does
cover everything. We haven't got number eight
and nine hiding out there to be found. Now, I can make a biological
argument for that. You can start by saying
well OK, damage can only accumulate throughout
life in structures that persist throughout life--
long-lived structures. If a cell, or indeed a molecule,
is created and maybe gets damaged and then it's
destroyed, then the damage is gone along with the
molecule or the cell. So that's not accumulating. So we can say OK, what is
long lived in the body? DNA-- certain types of
protein that don't get destroyed-- cells that
don't divide-- and so on. And that kind of-- kind of
give you this list that way. But actually there's
a quite persuasive circumstantial argument
as well, a very simple circumstantial
argument that says this list is probably complete. Here it is. It's been the same list
for more than 30 years. All of these things
have been major topics of study and discussion
in gerontology since at least the 1980s and
in many cases a lot longer. And you kind of
would have expected that the list would
have got longer by now. We've come a long way
in biology in that time. Now one argument that might be
considered a rebuttal of this is that well hang
on, maybe people weren't looking for
a classification. And that's kind of
true, they weren't. But that argument is going away
as well because the fact is I've been challenging
people to extend this list for more
than a decade now and I seem to be
getting away with it. This seems-- this
really does seem to be standing the test of time. So that's quite encouraging. And it gets progressively more
encouraging as time goes on. All right, so now I do a little
bit just to concentrate mind, so to speak, with how this
translates into the initiation and progression of the
various major diseases and disabilities of old age. This is something that--
especially people when I am talking to donors--
they really care about this. Someone's decided that they
are predisposed to getting Parkinson's at an early age. You know who I am talking about. Someone may have found that
their mother's got cancer or whatever. So they'll have specific
things that they care about. They'll give eight-digit
sums to the charity that is working on Parkinson's
disease which they hadn't done the year before because they
only were triggered to do so when they realize that they
personally had a problem. This is a personal thing. I think that's a shame. I think it would be much
better if the bulk of humanity cared more about each other. But I work with this. So let's look at those
pathologies, the linkage between the damage
and the pathology. Sometimes it's really simple. It's a one-to-one
relationship here. Division obsessed
cells-- cells that are dividing when they
are not supposed to. That's basically the
definition of cancer. Usually though, it's a
lot more complicated. So there are a lot of things
that can go wrong with the hear during old age. Atherosclerosis, the
number one cause of death in the Western world--
the cause of heart attack-- the cause of strokes. That's this down here. It starts out with cells in
the artery wall being poisoned by stuff that gets inside
them that they can't process. And I'll talk more about
that later because it happens to be something that we've had
some good success on recently. Arteriosclerosis, stiffening
of the arteries, which causes hypertension
and of course, all the knock on effects
like in kidney failure. That's this bottom
one down here-- molecular bonds being
formed between the proteins that make up the artery wall
and that give it its elasticity. And those bonds just stiffen
it, they make it less elastic, and that's what causes
high blood pressure. Molecular garbage outside
the cell-- there's something called senile
cardiac amyloidosis which is now known to be the
number one killer of people who get over the
age of about 105. It seems to be the number one. It took a long time to
figure that out simply because not many people that
old have autopsies done on them. But now we've got
enough data, it's pretty clear that
that's the case. And then finally, there's
cells in the heart called pacemaker cells which are
responsible for actually responding to signals
from the brain and causing the heart
to actually beat. And those cells die, and
they're not naturally replaced over time, not
adequately anyway, so eventually we haven't
got very many in the heart. And even though nothing
else may be wrong with it, the heart just stops
listening to the brain and it can't be bothered to
beat anymore and you die. So that's this one up here. So heart disease is complicated. Alzheimer's is another
really complicated one. This is a disease that was
defined more than a century ago as the combination
of these two things down here-- molecular
garbage inside neurons called tangles-- molecular junk
outside neurons called plaques. We now know that the sharp end
of Alzheimer's is cell loss. Neurons dying initially
in certain parts of the brain like the
hippocampus-- and then more broadly-- and causing
loss of cognitive function. So again we've got to fix all of
these things in order to really get a cure for Alzheimer's. Frailty-- let me call just
like non-specific decrepitude. This is pretty much everything. Maybe cancer doesn't
come into that. But pretty much all
the rest you can point to certain
aspects of frailty that are driven by each
of these types of damage. So you see the
linkage is very clear. It's inextricable the
linkage between damage and pathology-- the relationship
between aging itself, whatever you mean by that,
and the diseases of old age. And if society could just
get that into its thick head, then there would be
a very great deal more money spent on doing
something about aging. And we wouldn't be making
such slow progress. All right, let's get
on to the solutions. We've only talked about
the problem so far. So the maintenance
approach breaks down itself into a variety of
different strategies. They all begin with r--
replacement, removal, repair, and reinforcement. And that-- well they say it that
way, but to be more specific, they work like this. So you all have heard of
stem cell therapy, of course. Stem cell therapy is
the maintenance approach to address this
problem-- cell loss. That's what it's all about. We put cells into the body that
can divide and differentiate to replace cells that the body
is not replacing on its own when they die. And of course, stem cell
therapy by and large has been developed to do things,
to treat problems that are not related to aging, things
like spinal cord trauma. But the fact is it is just
as applicable to certain of the pathologies of old age. And it now increasingly
in clinical trials being actually applied
to such problems. Perhaps the most
conspicuous and best example is, well, the simplest anyway,
is Parkinson's disease, which has historically
been treated in rather primitive ways
by injecting compounds such as precursors of
dopamine-- the chemical whose shortfall is the main
driver of Parkinson's disease. But the holy grail of treatment
for Parkinson's disease without the faintest doubt is
the introduction of stem cells into the relevant
part of the brain, to substantia nigra which
will divide and differentiate into the type of neuron
that makes dopamine. And we are now getting there. This was first tried
about 15 years ago. And it was sometimes successful. Sometimes patients got better. Sometimes they didn't. When it did work, it
worked spectacularly. There are people out
there now who have not had any symptoms of Parkinson's
disease for well over a decade. And despite having been treated
once with stem cells and not had any other treatment since. That's how well it
works when it works. But because it
usually didn't work, there was an enormous amount
of pessimism in the field. And it was pretty much
given up on for a long time. Now if you think about that,
you have to ask well, OK, was that actually
the right decision or was it driven by
short-termist, political, or other motivations? Ultimately, if you
think about it, it's so obvious
why it didn't work. I mean this was
already known-- namely that they were just not quite
good enough at getting the stem cells into the right states,
the right type of stem cell, that it was a shame
that they gave up. But they did give up. They were just not making
dopaminergic neurons sometimes. And now that has finally--
the circle has finally closed, and clinical trials are now
being pursued with great vigor. And I think that we're in a
very, very strong position to have a proper cure
for Parkinson's disease within 10 years. That's a strong
statement I know. But I really think it's true
because we're now good enough at getting stem cells
into a state that is a dopaminergic
precursor, as it's called, and thereby restoring
dopaminergic capacity to the substantia nigra
by stem cell therapy. So in one talk I
don't have time to go through all of these in detail. If you go back into the
Google Tech Talk archive, you'll find talks from me back
in 2005, 2006 on three or four of these things just
dedicated to each one of them. So that's where you want
the detail from back then. If you want more detail,
obviously go to our website or read the book that I gather
we have plenty of copies of outside at the back
which we'll give away later. But I'm going to just highlight
a couple of these later on. First of all though,
I want to emphasize what this means in
terms of the sociology and the politics of medicine
and medical research. At the moment, as I have
probably already said a bit too often, the problem
is that we are simply not addressing aging
as the precursor of age-related disease
in the way we should be. We have to reorganize medical
research in recognition of the fact that there is no
difference between treating aging and preventing
age-related disease. Preventative medicine for
the diseases of old age is the treatment
aging-- it just is. Now this is beginning to change. For the longest
time, I was basically the only person
saying this and maybe I just wasn't saying
it well enough. I don't know. But now I'm by no
means the only one. There are mainstream people,
especially influential people at the National
Institutes of Health, who are beginning to
get this message out. However, I'm not exactly
holding my breath. The fact is it's the government. It doesn't tend
to move very fast. There's an enormous amount of
vested interest in the status quo in keeping
things how they are. So I honestly don't know whether
this is really going anywhere. I think that the progress
that needs to occur is going to rely
predominantly on people with independent means for
quite a long time to come. We shall see. However, in the end
what we're going to have is medicine that actually
works against the disease and disabilities of old age. And they are going to
be the medicines that dominate medical
practice in the future. Medical practice
is going to be all about what I'm calling here
"preventative geriatrics" because ultimately that is
the major threat that people in the developed world
anyway, and increasingly in the developing world, face
in terms of their health. And in the long term,
it's very simple. Just as today nobody
gets tuberculosis, nobody gets polio, it's
going to be like this. Nobody will get Alzheimer's
or heart attacks, or macular degeneration
or all these other things. And there will be dramatic
consequences for health. If we're not getting those,
and we're also not getting tuberculosis and so on, then
we're going to stay the way the people in this room are
today however long we live. And that is a very,
very different world. Now, I'll talk about
life span a bit later on. But I want to emphasize
that what we work on is not life span. We don't work on longevity. We work on health. Longevity is a side effect. It's a consequence of
keeping people healthy. Now, in terms of
credibility, I think it's important to emphasize that
it's not just me saying this. I'm still, as Robbie mentioned
at the beginning, probably the primary and most
prominent, and most vocal advocate of all of this. But that's just because I've
been doing it for a long time. There's quite a lot
of people out there who have come very
enthusiastically around to the point of view that
I'm putting out to you today. This is just by
way of illustration a research advisory board. There are 25 people here
who are extreme luminaries, world leaders in their
various research fields. Any of you know a bit
of biology will probably have heard of some
of these people. Here's George Church
whom I actually had coffee with this morning. He's one of the pioneers of
next-generation sequencing among other things. He's a really,
really important guy. Let's see, this
is Bill Haseltine who invented the term
"regenerative medicine." This is Mike West who started
Geron and then advanced cell technology. He is a really important guy. This is Maria Blasco who
runs the Spanish equivalent of the NIH. Tanya Tyler who runs the world's
biggest regenerative medicine institute. You know, these are
quite important people. And they have signed up
very, very unambiguously to a hard-hitting statement
of endorsement of the approach that I've been
describing to you today. So you might ask, well
hang on, what role does a nonprofit have? If this is getting so
credible, then surely it must be getting attention
from the private sector. People must realize that
there's a fair amount of money to be made in this area. And those of you who
listen to the news probably know that
this is indeed true. There is actually an
increasing interest from the private sector
in a very big way. Six or eight months ago
Larry Page, in particular, and Google in general,
announced that there was going to be a new
company called Calico working on the problem of aging
as a medical problem. And they hired one of the most
successful biotech leaders of our time, Art Levinson, who
ran Genentech for a long time, to run it. Now Art Levinson has
the enormous advantage that he is not a card-carrying,
lifelong gerontologist, so he is not in danger
of being encumbered by conventional wisdom. He also has the
enormous advantage of being extremely smart
and a careful thinker, and he has the third
extraordinary advantage of having a humongous
budget courtesy of Google. So he is in a position to
make an enormous difference. And I have very high
hopes he will do so. Much more recently,
just two weeks ago, the person who sequenced the
human genome, Craig Venter, together with the
person who founded the X Prize and Singularity
University, Peter Diamandis, got together and
announced a new company named Human
Longevity Inc., which is working on the same problem
in a rather narrow way, focusing on genome
sequencing which is no surprise given
Venter's involvement. But again, this shows that the
credibility issue is beginning to go away, and
it's about time too. However, the fact is that
human longevity is working on low-hanging
fruit and does not, honestly, claim to be
working on the problem in a comprehensive manner. I'm hoping first
for sure that Calico will be working on this problem
in a comprehensive manner. But while their precise
plans remain somewhat opaque, I'm not relying on it. Ultimately, I believe
that for quite a while to come we're going to need a
nonprofit participation in this that is essentially the
guardian of the things that other people might be
in danger of neglecting. And that's what SENS
Research Foundation is. We don't work much on this top
line-- on stem cell therapy. And the reason we don't is
precisely what I just said. There's a lot of
people out there doing exactly that already. And our money, our
very limited budget of something in the region of $4
million or so dollars per year, is better spent making more
of a difference elsewhere. All of these things down
here are correspondingly much more neglected, especially
the ones with two exclamation marks. Pretty much nobody else
is working on them, and that is a tragedy. But it does mean that
someone, namely us, needs to be around to do it. I am going to talk about
this one for a little longer just to give you a
proper feel for what we do. And make sure you understand
that we aren't just talk, we actually get lab work done. This is the beginning
of atherosclerosis when a white blood cell, a
macrophage, in the artery wall becomes poisoned by
contaminants, oxidized cholesterol to be
precise, contaminants of the material that
it is processing. It becomes this thing
called a foam cell, a kind of undead,
inflammatory thing. And it gets full of
lipids as you can see. And this is something
that progresses. These cells don't go away. More and more of them
pile into the plaque and eventually the plaque
gets big enough to burst. And that's when you get a
heart attack and a stroke, and we don't want that. So what have we got now
to do anything about that? What we've got is surgery--
stents and such like. That as you probably know
doesn't really work very well and plus surgery
is really invasive. Also we've got statins. Statins are preventative. It sounds good, doesn't it? But they are too preventative. They are an example of the,
what I would call a moment ago, the gerontology approach. They attack the
problem by attacking the aspects of our
desirable metabolism that cause the problem. In other words,
in this case they reduce the rate at which
we synthesize cholesterol. Now cholesterol itself is an
absolutely vital molecule. And it's only oxidized
cholesterol that's bad for you. So that means that if we
diminished oxidized cholesterol by diminishing
cholesterol, we have a very serious
therapeutic index problem. But there's only
so far we can go before we start to do
more harm than good. That's why statins ultimately
are not the solution. What we're doing at
SENS Research Foundation is attacking the oxidized
cholesterol directly. In particular we're
attacking a particular type of oxidized cholesterol,
7-Ketocholesterol, which has been well
established by other people to be public enemy
number one here-- the most toxic and
the most abundant. First thing we did
we found bacteria that were able to break it down. You do something called
an enrichment culture. You take a bunch of
different bacteria. You give them this stuff to eat. You don't give
them anything else. The ones that can't eat it
just sit there like lemons. The ones that can, grow. And of course, the
stuff goes away. And that's very straightforward. Then rather than proposing
to inject lots of bacteria into the body to eat the stuff,
which would probably have side effects, we instead
figure out the genetics. We figure out how they do this. We do mass spectrometry
which is a way of identifying the breakdown
products and inferring the enzymatic activity. We could also do
expression analysis to figure out which genes are
being activated by the thing that this thing
is breaking down. And the result is
quite some time ago back in 2008--
no 2009 maybe 2010-- we had got our hands on
some genes and enzymes which were able to break
down 7-Ketocholesterol. Then we started on
the hard part which was to get those genes
working in human cells. That's tough
because bacteria are very different from human cells
in lots of different ways. But we finally did it. And first of all,
we had to make sure that our engineered gene--
engineered protein-- went to the right part of the cell. This just shows
that we can do that. You have to go to the lysosome
which is sustained by red. This is our engineered protein. This is overlap. But then we had to
actually make it work. And this basically is what
shows that we succeeded. If you have an absolutely
supportable amount of 7-Ketocholesterol
in the medium of cells that are trying to grow, then
they die, whatever happens, but if you have a more
modest amount than the fact that this bar on the right is
always taller than the ones before it is an illustration
that the engineered gene is protective. It's protective because
it creates an enzyme that breaks down 7-Ketocholesterol
and the enzyme is targeted to the
right part of the cell. These various negative
controls, either they don't have an enzyme, or
they have the wrong enzyme, or the enzyme is not
targeted to the lysosome. So this was a pretty
impressive result. It's only about a
year-and-a-half old. And we're now working
to extend that to make it work in the cells that really
necessary-- not macrophages. And then of course we'll
move to mass models. AUDIENCE: Sorry just wanted
to know which of those bars is control, ie, no
change, it's the same. AUBREY: OK, so the
sets of bars here. Right? So each of these sets is
a different concentration of the toxin so-- AUDIENCE: I got that. And the one on the far
right is with your enzyme. AUBREY: That's right. AUDIENCE: So what's
the one that has nothing cutting the cells off? AUBREY: That's the black one. AUDIENCE: OK, thanks. AUBREY: Right, so let's go
on to longevity for a minute. So the first
question is how much extra life do we expect to get? And the first thing I
want to mention of course is to reemphasize the fact that
this will all be healthy life. We will be keeping alive only
by keeping people healthy. That's really just
an extension of what we have seen historically over
the past, let's say, 50 years. The reason why life
expectancy is now maybe 10 or 12 years greater
than it was in the 1960s is because people
aged, let's say, 70, are about as healthy
as people work in the 1960s who
were aged only 58. That is a really important
thing to understand. But it's not the whole story. So the therapies that I've been
outlining to you today I think have a good chance of getting
about 30 years onto our life. They will add 30 years. And because they are
rejuvenation therapies that repair damage. What that means is that we'll
be taking people who already, let's say 60, and fixing them
up well enough that they won't be biologically 60 again,
either mentally or physically, until they are
chronologically 90. So that's the key
thing that we're doing. Not just slowing aging
down, but reversing it. Now you may ask,
well OK, why only 90? Why doesn't this
work indefinitely? And the answer is because these
therapies won't be perfect. They are pretty good. I think they're going to work
on most of the types of damage that we've got. Certainly, they're going to
work on most of the examples within each of the
categories of damage. But they are still
going to be stuff that is a little bit harder. They won't be perfect. So then what? Well the thing is
that 30 years is a hell of a long
time in technology, including medical technology. And essentially we've
bought that time. So bearing in mind
what I told you earlier about the
very high likelihood that these categories are indeed
an exhaustive classification, notwithstanding what
the first question I mentioned about the possibility
that in a very distant future we may have to worry about other
effects of nuclear mutations. We're talking about a seriously
interesting situation. We're talking about the
possibility that by the time these people who are
rejuvenated come back as 90-year-olds who
are biologically 60, we will have improved these
therapies enough, still not perfectly, but enough that
we can re-rejuvenate them even though the
problems of rejuvenation is a bit harder than it used
to be so that they won't be biologically 60 for a third
time until they are 150. And I don't know whether
by the age of 500 we're going to be
able to figure out how to solve the problem
of nuclear mutations that don't lead to cancer
well enough as well. But I certainly think
it's quite likely. So we're talking
about the possibility of kicking the ball up the road
faster than time is passing pretty much as for
as long as we like. That's what I've called
longevity escape velocity-- the minimum rate
at which we need to improve the comprehensiveness
of the therapies in order to stay one step
ahead of the problem. And I think we've got a very
good chance of maintaining longevity escape velocity once
we get that first generation set of therapies
that give 30 years. That's quite an important
thing to understand. So we're talking about
very long longevity-- people just don't tend to
die when they are healthy. So that's quite nice to know. The next question, therefore,
which you're probably all thinking about
now, is well how soon are these therapies,
these first generation therapies, likely to arrive. And I want to answer
that in two ways. First of all, I want to
tell you a direct answer, and then I want to tell you
the answer that matters. The direct answer is of
course we don't know. Like any other
pioneering technology, the time frame is
extremely speculative. But I would say,
going out on a limb, that we have a 50/50
chance of getting there within 20 or 25
years just so long as within the next 5 or 10
years the rate of progress is not seriously slowed
down by lack of funding. I would say it is
currently being slowed down by at least a factor of three. So we're in a bad way--
we're losing a lot of lives-- but the fact is that's
a reasonable time frame. I think there's at
least a 10% chance that it will take 100
years if we hit problems that we haven't thought of yet. But still you know a 50%
chance is quite enough to be worth fighting for. So that's what I'm going for. But here's the answer that
you need to be thinking about is this down here. Eventually, at some
point before then, we're going to have sufficiently
dramatic and impressive progress in the lab,
typically with mice, to convince people that
it's only a matter of time before we get this sort
of thing happening. And that is when the shit is
really going to hit the fan. It's going to be
complete pandemonium. And you'd better be ready. I think the sooner that
happens the better. And I believe that one
thing I'm achieving by giving so much
publicity to this research is softening the world
up-- getting people to understand the
feasibility and indeed the desirability of doing
something serious about aging in the clinic and
thereby diminishing how dramatic the
progress in the lab needs to be to
achieve this tipping point of public opinion. That's what I want
to try and achieve. So I am just going to close
in the last minute or two by highlighting the
sociological implications-- the social context. I spend my entire life
answering questions like this. Oh, dear where we
put all the people? Won't it be only for the rich? Won't dictators live forever? Won't we just get bored? Wouldn't it be so
boring not having Alzheimer's and being able to
remember everything you did? And how will we
pay the pensions? Now look, why do we pay people? Why do we pay people
quite a lot of money to do nothing from
the age of 65? Any ideas? I'll tell you why. It's because we're
very sorry for them. And the reason we're
very sorry for them is because there are
about to get sick and die. And I'd prefer that
not to be the case. You know it will be a
whole new social contract, yes, but the fact is,
it's the only reason. So these are not
very good reasons, and I'm not even going to bother
going any further with saying, why not? This is what we ought to
be thinking about when we come to the sociological
considerations. Not having ill health in
old age is quite important. You know it was a massive,
massive shock to me when I discovered in
the age of about 30 that most people, certainly
even most biologists, don't really regard
aging as a particularly interesting or particularly
important problem. And the reason it
was a shock was because I had never
considered that anyone could think any differently. It's like you don't consider
the color of the sky. I mean it's so completely clear
that ill health is the number one source of
suffering in the world and that aging is the number
one source of ill health. So obviously it's the
world's biggest problem. Dear me. When it comes to the
economics, obviously you have to consider the fact
that the elderly will be able to contribute
wealth to society rather than just
consuming wealth. And that they won't get bored
because they'll have the energy and vitality to explore
novelty the way you and I do. And they can take-- they
can retire temporarily for 20 years. And then go back
and retrain and be a rock for the next 40 years. And above all, the thing that
the elderly get the most scared of is that they will become
a burden on their kids, on the people that
they used to support. And they are really
scared of that-- it's not going to
happen anymore. So that's what we need
to be thinking about. This is the book I mentioned. It was written in
2007 so you might think it might be
a bit out of date. It isn't really out of date yet. And the reason it's not
is not because there's been no progress. There has been
masses of progress. The reason, the very
heartening reason, is that the progress
has overwhelmingly been the sort of progress
that we said would happen. So again, this idea, this
concept, this paradigm, is really standing
the test of time. And I'll stop there. And I hope there's time
for some questions. [APPLAUSE] AUBREY: Go ahead. Please. AUDIENCE: So one thought
that occurs to me. We talked earlier about
how this is easier because the body already has
all these self-repair systems. But the question that
comes to my mind for that is a little bit of a Pollyannish
[INAUDIBLE] question. Is the synergy between the
systems that you mentioned and whether or not recruitments
in one of those systems would buy that synergy
from the other systems. I specifically thinking
of mitochondria producing mitochondria, but it's
a general question. Do you think there's
a possibility of that? Do you see that? AUBREY: So very
interesting question-- so it's so interesting
that I'm even going to take the
trouble to repeat it. So the question is
really supposing we just fixed one of
these things really well. But we didn't actually
fix anything else. Would that not have kind of
knock-on secondary effects that would somewhat alleviate
the pathologies that were being predominantly caused
by the other types of problem, even if those other types
of problems themselves were not being
directly addressed? I'm absolutely sure that
there would be such an effect. The thing that is much,
much harder to ask is how much effect? And furthermore I
think we can certainly say that if you fixed
one of these things, the overall effect
will certainly not be so substantial as to give
let's say, a decade of life. I think we can certainly put
pretty confident upper bounds. Now you mentioned
mitochondria mutations at a particular candidate,
and it's a great candidate to choose. I think that is the one about
which the range of uncertainty is the greatest partly at
the bottom end actually. The mitochondrial
mutations are the one case where we can't point to any
particular pathology of old age for which that type of
damage is the major driver. But looking at it the other
way around, what we can say is that if mitochondrial
mutations matter at all, then they probably
matter very ubiquitously. So actually, my very first
book, which was purely for an academic
audience back in 1999-- that was the book for
which I got my Ph.D.-- that was written precisely
about that and I said that maybe we've got a 10% chance of
doubling a lifespan just like that. Any more? AUDIENCE: Do you
still think that? AUBREY: Yeah, 10%. Good. AUDIENCE: So I suspect
this is another one of your boring
questions, but you didn't have it on your list. You say that aging is
the biggest problem. How about hunger and
poverty as things that cause a lot of
suffering in the world today? AUBREY: Yeah, just
do the numbers. How many people are hungry? How many people have the
diseases and disabilities of old age? Just do the numbers. Yep. AUDIENCE: You may not
be able to answer this, but if you were
going to estimate. Say you wanted to get all this
accomplished in the next 25 years, what do you
think that it would cost in today's economics? AUBREY: The glorious
news is that the money is ridiculously small. So we need to
divide it in phases. The money certainly gets
much bigger at later stages just as for any
medical research when we get into clinical trials. But I don't even bother
thinking about that because I know, as I
mentioned in I think the second-to-last
slide, that once we get sufficiently dramatic
results in mice, game over. Money will be no object. People will just get it. And it will be straightforward
to get money in the door. So the question
then is how much is the money we need now
to really get this done. When I say "we"
here I am not just talking about SENS Research
Foundation, of course, I'm talking about overall. I think we're talking
about really small money like $100 million dollars per
year for as little as 10 years would do it. And we're already up
in the SENS Foundation itself like $4 or
$5 million dollars. So It's only an order of
magnitude we're talking about. It's pitifully small. And when we look back on how
long it took for that money to be forthcoming,
we are going to be very ashamed as a species. AUDIENCE: Are there parts of
the body that are not really designed to be rejuvenated? Like teeth and
[INAUDIBLE] maybe? AUBREY: The parts
of the body that don't have very much in the way
of intrinsic, built-in repair capacity are actually tending
to be the easiest ones to fix because they're the
ones that don't need repair very much. So teeth is a great example. Teeth have some repair. Some species have more than two
sets of teeth in their life, and actually the work
that's going on in that area is precisely along those lines,
organizing for stem cells to regrow a new set of teeth. That is relatively
on the simple side. Yep, in the back. AUDIENCE: At the
beginning you said that damage was the
main cause of aging, and yet we haven't had a lot of
success moving out maximum life spans in different
creatures, which makes it seem that
maybe there are other mechanisms
besides just damage. AUBREY: OK, so we've done
pretty well with maximum life. First of all it depends
how you define maximum. So the technical
definition that is conventional within gerontology
which can be used conveniently for populations like 7 billion
or populations like 100 like you have with
mice in the lab. They normally use
the life span-- the number after which 5
or 10% of the population is still alive. So If we use that
definition, then yes we've actually been pretty
successful in moving things out. But not because of
progress against aging. What has predominantly happened
over the postwar period is that people seem
to be benefiting from what are called cohort
affects, which essentially means they were born younger, or
at least they were-- they spent most of their lives younger. And we understand
a bit about that. Prenatal nutrition has
made an enormous difference to lifelong health. AUDIENCE: Actually I
meant maximum as maximum. AUBREY: OK, so I was
going to get onto that. AUDIENCE: So the
model organism would be pushed out to the maximum. AUBREY: Right, so yeah, so in
the case of model organisms, no question, we've
actually got-- I mean the world record mouse
lifespan is like five years and like 20 years ago it wasn't. It was like three years--
or three and a half. So that's happened, but
that's small populations. So that's why I wanted to
give that earlier answer. If we look at huge
populations, like human race, then things get a
bit more interesting. It is rather curious what's
been happening there. The world record lifespan
is 122, and the person who reached that
age died in 1997 which is quite long time ago. In the time between
then and now, the number of people
who reached 100 has gone up worldwide by a
factor of several, right? So it's bizarre that-- in fact
no one is anywhere near this. The current world record
living person is 116. Well, what's going on? That is a big paradox. Nobody has much idea. It could be cohort effect again. It could be that
there were periods of particularly good nutrition
and such like in the 1870s or whatever. But it's a major research topic. We really don't know
the answer to that. Yep. AUDIENCE: Do you do anything
with nanorobots and things like that. Do you think that's
going to play in this? AUBREY: Will nanobots and
such like play a big part? Well, my view in
general-- let me answer a slightly
more general question. My view in general is that
non-biological solutions to medical problems which
already play a minor role with things like cochlear
implants, or indeed spectacles, right? They do actually have
a very good prospect of playing an increasing
role as time goes on. And certainly the
miniaturization of non-biological solutions
such as nanobots or things on the way to that--
millibots, microbots-- will accelerate that process. However, I'm pretty sure that
they won't play a dominant role until well after we've got
this stuff working well enough to get to
longevity escape velocity. Yep. AUDIENCE: Do you think
that on the whole our genes and
genetic program are kind of indifferent to whether
the elderly live longer. Or are there sort of mechanisms
within the genetic code that are actively
reducing life span because it would be adaptive to
have non-reproducing organisms sort of not be taking it? AUBREY: So the three-word
summary of your question is-- is aging programmed? That's the way it's
normally stated. So the consensus answer to
this in the field which I agree is that no aging
is not programmed. A long time ago,
however, in fact for probably 60 or
70 years starting in the 1880s it was
firmly believed that aging is programmed because
everything must be programmed because evolution
is clever, right? And people came up
with clever reasons why it would be programmed
like it would improve the signal-to-noise ratio
of natural selection by eliminating these
useless, old organisms. At the beginning of
the 1950s the people started to point out that
very few organisms in the wild are actually old enough
to suffer any real functional decline because
predation, and starvation, and hypothermia, and so on take
such a rapid toll that you've just got nothing
left by that time. Now originally that
argument was oversimplified. You do indeed need some
non-negligible amount of death from aging in the wild in
order to maintain selection for our antiaging machinery
that I spoke about earlier. Otherwise that
machinery will just degrade through
spontaneous mutations in the germline from one
generation to the next. But there isn't very much. And certainly when you look at
questions like how rapidly does the rate of aging change in a
population when you put them into a different environment
where the selective pressure is sharply divergent
from how it was, then it turns out that
the rate of change is really slow, so slow
that it can be ascribed only to selection from
spontaneous mutations rather than any kind of
changing in the input environmental parameters
to any kind of program. AUDIENCE: Metabolism
reduction is one of the things that people try to use for
[INAUDIBLE] without-- it doesn't seem like it's very
sure how it's going to work out. How does it lead
to the degradation? AUBREY: OK, so
first of all I want to make sure that
everyone understands the way I'm using the
word "metabolism." There's a phrase in
biology, metabolic rate, which refers specifically to the
rate of consumption of oxygen. So that's in other words, the
rate of oxygen metabolism. But I am using the word
metabolism in the way that biologists use
it strictly which means everything that
goes in the body-- all of the processes that
keep us alive from one day to the next,
whether they have oxygen involved
or anything else. Now, your question refers
to calorie restriction, essentially eating less,
and it turns out, yes, it was discovered way back in the
1930s that if you feed a mouse or rat less than
it wants then it lives a bit longer--
that's cool. Other than that it
seems not to work very well for
longer-lived species. It works much
better, conversely, for really short-lived
spaces like nematodes. You can get the nematodes to
live three or four times longer than they otherwise would
just by starving them at the right time
in their life cycle. Why is this? Why it turns out to be
fairly straightforward. It all comes down to the
strength of natural selection. Long famines are less
common than short famines and therefore the
reason, the need, to live longer
so-to-speak is less. So we have less good machinery,
less efficient, less impressive machinery to respond to
nutrient deprivation in this way than a short-lived
organism does. Thank you very much. [APPLAUSE]
I can't wait to see what this guy can do. He's a hero, and I don't say that about people.
A modern day warrior. A fighter OF and FOR humanity! http://en.wikipedia.org/wiki/Aubrey_de_Grey
Once you get past the speech impediment (which is not hard, it's mild) this guy is extremely well spoken. Not in the emotionally compelling way many TED speakers are, but in a technically excellent and relatable way.
Good talk, although nothing really new.
So ... why has there been no research publication from SENS for over a year?
The research blog is just slowly publishing chapters of a report written mid-last year, describing research performed mainly the year before or earlier.
Is there just a research pipeline that is about to burst open? I can't imagine the research is going so poorly as to stall in dozens of different places all at once.