SHANEE NISHRY: Hey, everyone.
Good to have you here.
You may heard of him as the man who will make you live forever,
or at least until you get hit by a car.
But here he is, Aubrey de Grey.
AUBREY DE GREY: Thank you, Shanee.
I like the way that Shanee introduces me.
It's great.
I've had the good fortune to be introduced by her twice today.
All right.
So thank you for coming.
I'm going to try and tell you all about what
we are doing at SENS Research Foundation.
I have already made my first mistake,
which to leave the clicker on my chair.
So as Shanee said, we are interested in stopping you
from getting sick as you get old.
It has been a source of frustration to me
that we get sick as we get old, for quite some time.
And an even greater source of frustration
that it isn't a sort of frustration for everybody.
So I'm trying to change that.
But also, of course, actually change the facts of the matter,
to try to actually deliver medicines
that will allow us to stay healthy.
And so I'm going to spend the next hour telling you
all about how.
First of all, the success story.
So this is, simply for illustration,
statistics from the USA showing the proportion
of the population that are over the age of 65, which
was way down at 8% or so in 1950 and it's
projected to be up around 22% in 2050, which is pretty dramatic.
And, of course, this is a cause for celebration,
because it is the consequence of a great deal of success
over the past 100 or 150 years in bearing down
on the diseases that used, historically,
to kill an awful lot of people in infancy,
or in childbirth, and so on.
And the result is that pretty much everybody
is surviving long enough to reach the age of 65 or more.
But it also has, of course, created some problems.
The economic problems are perhaps
foremost in many people's minds right now.
And again, here, I'm just showing US statistics
for illustration.
But, of course, it's the same throughout the industrialized
world.
We have this problem that even though the economy has
been growing nice and fast-- I'm going to use this one,
where you can actually see my pointer.
I've never understood why these screens can't made to actually
reflect a laser point of light, even-- whatever.
So, yes.
So this is the US economy, the red line going up
at a nice, steady rate.
And if you look at the rate of medical expenditure in the US
over the same time period, which is the last 50 years or so,
then it looks perfectly manageable really.
It doesn't look particularly scary.
But it's a great deal scarier if you
take the trouble to divide one by the other, which
is where the green line comes from.
And the green line shows obviously therefore
the proportion of the GDP that is being spent on medical care.
And it's gone up from 5%, 50 years ago,
to 18%, which is extremely scary.
And, of course, is the reason why
we have all these concerns about pension funds
running out of money, and Medicare running out
of money, and so on.
So the question is, first of all, why?
Why have we got this situation in the first place?
Putting it in starker terms, why have the diseases
and disabilities of old age, which, of course, dominant
medical expenditure today, why have they been so much more
resistant to medical intervention
than the infectious diseases that we have more or less
entirely eliminated over the past century or so?
This is actually pretty paradoxical
when you think about it.
And in order to answer this question,
the first thing I think we need to do
is to ask ourselves what is aging anyway?
What is the ultimate substrate for these age-related diseases?
So I'm going to give you a definition of aging
now, that I'm going to be using for the rest of the talk.
And this definition is specifically
geared to trying to eliminate the distractions that often
come when aging is discussed.
There are many definitions of aging out
there that really do more harm than good because they just
confuse the issue.
But this one brings it down to its essentials.
And I think it's useful.
Essentially, what I'm trying to do here
is to emphasize that the aging of living organisms
is really no different at the bottom line
from aging of inanimate subjects, like cars,
or airplanes, or whatever.
It is simply a fact of physics, never mind biology,
that machines with moving parts do
themselves damage as a side effect
of their normal operation.
And it's also a fact of physics that that damage accumulates
and, therefore, eventually it exceeds the level
that the machine is set up to tolerate.
So that's true for a car.
It's true for an airplane.
And it's true for a human being.
It's true for the human body.
The human body does a lot of different types of damage
to itself, which I'll be getting onto over the next while.
And, therefore, we are subject to a whole bunch
of different eventual failure modes,
so to speak, of the body.
And that's really all it's about.
So really what that means is that we
must address a very fundamental misconception that
is prevalent within society today concerning
the diseases of old age on which we spend
so much money, diseases like Alzheimer's, and most
cancers, and cardiovascular disease,
and type 2 diabetes, and osteoarthritis, and so on,
and so forth.
These diseases are normally viewed as diseases.
In other words, they're viewed as, in some sense,
similar to infections, and potentially amenable
to the same kind of medical interventions
that infections are amenable to.
But they're not.
They're actually all part and parcel
of one single process, the accumulation of damage
that the body does to itself in the course
of its normal operation.
So not only are they, as we all know,
widespread and staggeringly costly, but they are universal.
The only way that you will not get a particular disease
of aging is if you die beforehand of something else.
You are going to get it.
And furthermore, they not medically curable
in the strict sense of the word "curable."
What do I mean by the strict sense?
I simply mean that we cannot eliminate them from the body
in the way that we can eliminate an infection.
If you eliminate an infection, then the person
isn't going to suffer from that infection
again unless they get reinfected.
But you can't do that with things
that are a side effect of being alive in the first place,
other than by eliminating being alive in the first place, which
would kind of defeat the object.
So let's not do that.
But that does not necessarily mean
that we can't address the diseases of old age
using medicine.
It just means that we have to rethink our starting point
in designing the medical interventions that we
might be use.
I'd like to put it this way, even more starkly.
Most people think of the various causes
of ill health along the lines that I'm showing in this table.
There are various types of disease.
There's infections, communicable diseases.
And there are congenital diseases
that a small proportion of us have
because we got dodgy DNA of one sort or another one.
And then there are the chronic age-related diseases,
which are the subject of so much concern and so much
expenditure today.
And then, in most people's minds,
there is this completely separate category
called aging itself, which is composed
of these nonspecific, rather poorly defined things,
like sarcopenia, which is the decline of muscle
mass in the elderly; or a gain of fat mass;
or a decline in function of the immune system, these things
that we don't really think of diseases.
That's what most people have in their minds when
it comes to ill health.
But it's nonsense.
This is the way that we ought to be thinking about all of this.
All the columns are the same here.
It's just where the black line is that's changed.
There are diseases and then there's aging.
But the diseases of old age are part of aging.
The only difference between column three and column four
here is that column three consists
of those aspects of aging that we have taken the trouble
to give disease-like names to.
Its purely semantic and no more.
That is an absolutely fundamental thing
that I'm going to be leaning on for the rest of the talk.
So I wanted to make sure you have it in your heads
very clearly at the outset.
Now, what does this mean in economic terms?
I mean we can look at it in many terms, humanitarian of course.
But let's just do it in terms of economics.
And here, for the moment, I'm going
to move away from medical expenditure to the expenditure
on medical research because, unfortunately, it's
the same story, perhaps in even starker terms.
And again, I'm going to use US statistics just
for illustration, because I happen to have them.
But again, this is absolutely the same
across the industrialized world.
So the NIH, the National Institute of Health,
is the counterpart of the Medical Research
Council in the UK.
It's the government body that is responsible for essentially
all public expenditure on medical research.
And it has a nice healthy budget of $30 billion a year.
But only 3% of that budget is spent
on aging, the National Institute on Aging.
That is pretty bad news given that
the vast majority of medical expenditure
and, of course, suffering caused by disease
and so on, in the US, is driven by aging.
It doesn't make sense.
But that's how it is.
That's bad.
But it's not nearly as bad as it gets.
Even within the National Institute on Aging,
only about one sixth of that budget, that $1 billion,
is spent on understanding the biology of aging.
The rest goes on specific research on Alzheimer's disease
and/or geriatric medicine, or even social gerontology,
studying how to preserve the dignity of the elderly, things
like that.
Which is all very well.
They're important stuff.
But it's not what would actually give the bang for the buck.
So it's a disgrace that it's so small.
And that's not the end of the story.
The fact is that even within the Division
of Aging Biology of the NIA, of the NIH,
the amount that's actually spent on doing something about aging
is way under the 10%.
That number, $10 million, I've got there,
is a very generous estimate.
Really, that's amazing.
Most gerontology consists of-- it's a bit like seismology.
People who study earthquakes, they
understand that what they study is bad for you,
but they're not proposing to actually do anything about it.
It's all about just getting out of the way really.
So it's a bit sad.
I mean to put it in real perspective, what we're talking
about here is that my little foundation, the SENS Research
Foundation that's been created around my work, which has only
existed for a few years, and we only
have a budge of $4 or $5 million a year,
it's on the same order as the US government.
That is fairly shocking.
So something better be done really.
And that's why I go around the world giving talks like this.
This is essentially where we are today.
If you look at the bottom of this diagram, what I'm saying
is what I told you already.
Metabolism causes damage, causes pathology.
In other words, the network of processes
that keep us alive from one day to the next,
which is what biologists call metabolism,
causes various types of molecular and cellular change
to the composition and structure of the body, which
I'm calling damage.
And that damage accumulates.
And eventually, when it exceeds a certain threshold,
it impacts the function of the body.
And that's when the diseases and disabilities of old age
begin to emerge and to progress.
And all of what we try to do today
to attenuate and alleviate the pathologies of old age
consists of what I'm calling here the geriatrics approach,
geriatric medicine.
It means, in a nutshell, completely ignoring everything
that I've told you in the last five minutes.
It means pretending that the diseases of old age
are just like infections and can be eliminated from the body.
It's obviously complete nonsense.
First of all, for the reason I've told you,
namely the damage, it's continuing to accumulate.
So obviously, anything that comes
under the geriatrics heading is going
to become progressively less effective as time goes on
and as the damage becomes more and more irresistible.
And secondly, because the pathologies of old age
are quite numerous.
You're not supposed to be able to read this slide.
Don't worry.
This is simply a nice selection of the things that go wrong
with us as we get older and that we would rather didn't.
So it's completely hopeless.
But we spent a spectacular amount of money on it.
Now, I am by no means the first person to point this out.
For the past 100 years, there have been a few people out
there trying to get people to understand that actually if we
want to do anything about aging, we
have to intervene at an earlier stage in the chain of events,
in the chain of events that I've just shown you.
And that's what has given rise to what I'm calling here
the gerontology approach, which is the approach favored
and pursued by that rare breed of people who study
the biology of aging with a view to actually doing something
about it in due course.
However, that approach has also failed completely
to deliver any kind of actual impact
on the ill health of old age.
Why should it be?
Well, what is the gerontology approach?
It consists of essentially trying to clean up metabolism,
trying to slow down the rate at which metabolism
creates damage.
And that sounds like a great idea.
Because certainly if we could do that,
it would postpone the age at which the damage reaches
a pathogenic quantity.
But there's a couple of problems with the gerontology approach
too.
The first problem is that it's only slowing down
the accumulation of damage.
So that means that the later you start the therapy,
the less benefit you're going to see.
The less time you're going to have to extend,
before the pathogenic threshold is reached.
And that's a bit of a shame because some of us
may already have the misfortune to be in middle age or older
by the time that the therapies in question are even developed.
So that's a bit of a shame.
But worse than that, the gerontology approach
suffers a problem that is rather analogous to this problem,
namely-- there we go-- this problem.
Metabolism is rather complicated.
This is a simplified diagram of a small subset
of what we know about how metabolism really works,
about how the body works.
And as you can see, it's a bit hairy.
And as engineers, or as people who work with engineers,
I'm sure you will understand that it's pretty implausible
that we would be able to, in some way,
tweak this vast network of uncommented spaghetti
code in a manner that would stop it from doing the thing we
don't want it to do, namely creating damage,
without also stopping it from doing stuff
that we do want it to do, like keeping us alive.
So it's a waste of time really.
There's no way in the world that we're
going to actually make this work.
But if that the end of my story, I wouldn't be standing here.
You knew that.
So what's the "get out?"
How do we extract ourselves from this?
Well, ultimately what we do is we go back to the analogy
that I started with some minutes ago.
This car is more than 100 years old.
And, of course, there aren't many cars like this.
But they're not all that rare.
The point I want to highlight about this car
is that it was not designed to last 100 years.
It was designed to last maybe 10 or 15 years before it would
fall apart and you go and get a new one.
And the reason it's lasted so long is understood.
We all know that the way that enthusiasts allow their cars
to live a long time is by doing really comprehensive
preventative maintenance on them,
by simply repairing the damage that the cause does
to itself as a side effect of its normal operation, a phrase
that you may recognize from a few minutes ago.
Now, that means that we can realistically
ask ourselves, well, maybe we could actually
do the same thing to the human body.
Maybe we could engage in preventative maintenance.
And if it was sufficiently comprehensive,
maybe it would have the same effect.
It would greatly extend the healthy longevity
of the machine that we call the human body beyond the longevity
that it was initially set up to be able to achieve.
This is what that means in terms of comparing and contrasting
with the other approaches.
Rather than trying to slow down the rate at which metabolism
creates damage, as the gerontology approach tries
to do, or indeed the rate at which damage creates pathology,
as the geriatrics approach tries to do,
instead the proposal is to uncouple those two processes
from each other.
To actually go in and periodically repair the damage
so that the damage, even though it's still being created,
never actually reaches the pathogenic threshold.
What I'm going to be trying to persuade you of today,
in the rest of the talk, is that this approach is very much more
favorable than the other two.
That we have a realistic chance of pulling it off
within the foreseeable future.
So in order to go on to that, I'm
going to now start talking about actual biology.
I'm not going to get too technical, obviously.
But I'm going to try to give you a feel for what this is all
about.
The first thing we have to do is to define
the problem in concrete terms, in down-to-earth, actual
biological terms.
And that is what this table does.
Here we have a list of seven types
of damage, seven categories of damage.
And as you can see, each of these things
is a genuine, bona fide, physical, biological thing.
Cell loss simply means cells dying and not
being automatically replaced by the division
of other cells, a very simple concept.
And this is a classification which
I have been using for this purpose for quite some time.
Now, you may have a couple of questions
about this classification.
And I want to answer them right at the outset.
The first question you may have is, well, hang on,
what's so useful about this classification?
You recognize, as I've already, in fact, highlighted,
that there's an awful lot of things
that happen during aging.
There are, indeed, an awful lot of different types of damage
that gone on.
So a thousand things can be classified, can be grouped,
into seven different categories in many different ways.
What's so useful about this one, you may be asking yourself?
The answer is that within each of these categories
there is a particular generic type of intervention that
exemplifies, that illustrates, the maintenance approach.
That within each category there may many examples.
But all of them can be, in principle anyway,
addressed by, broadly speaking, the same therapy,
differing only in details from one example to another.
That's the absolutely fundamental thing
that you're looking for in any kind of classification
of a problem into subproblems.
So that's what this classification is all about.
The second question you may have is, well, hang on,
how do we know that this is exhaustive?
How do we know that there isn't an eighth category
and a ninth one?
And, of course, we can't absolutely know.
But the good news is that we have
at least a good circumstantial argument that it probably
is an exhaustive classification.
What is that circumstantial argument?
Here it is.
It's been the same classification
for more than 30 years.
All of these things have been major topics
of research and discussion within gerontology
since at least the early 1980s.
Now, one could say, well, that's not really a fair argument
because people weren't really looking
to classify damage in this way back then.
And that's kind of true.
But it's increasingly not true because the fact
is I've been out there, making a nuisance of myself
and challenging people to actually
come up with other categories to add
to this list for more than a decade now.
And I do seem to be getting away with it.
I am like, you know, getting away with it.
So that's pretty good news.
I mean it's a circumstantial argument.
But it's quite compelling really.
Now, I'm going to spend a few minutes now highlighting
the relationship between damage and pathology.
And this is really important because ultimately it's
where the rubber hits the road.
At the end of the day, we need to actually convince ourselves
that if we could repair all of these types of damage,
we genuinely would have this effect
on the various pathologies of old age.
What I want to emphasize to you here
is that the relationship between damage and pathology
is, in some cases, quite complex, but it is established.
It is well known.
The stuff I'm going to be talking
about in this particular section,
for the next couple of minutes, is not innovative ideas
without portfolio, that SENS Research Foundation
has put forward.
These are things that no one working in these field
would dispute.
So let's start with cancer.
Cancer is the simplest example.
Because in this case, it's pretty much a one to one
relationship between the pathology and the damage.
There's this one category of damage
that I define as division-obsessed cells,
in other words, having too many cells because there are cells
which are dividing when they're not supposed to.
That's pretty much the definition of cancer.
So it's a nice, straightforward one to one
relationship between a type of damage
and a type of age-related disease.
But, in general, it's not quite like that.
So the heart is a good example.
The heart is an organ that can go
wrong in a whole bunch of different ways in old age.
And it turns out that the different ways it can go wrong
are driven by different types of damage.
So let's first of all take atherosclerosis,
the accumulation of fatty deposits
in the major arteries, which leads, of course,
to heart attacks and strokes, and therefore
to the major killers, the number one
killer of the Western world.
That comes down, at the end of the day, to this thing here,
I'm calling intracellular junk, molecular garbage
that accumulates within cells.
In particular, what happens here is
that there are a type of white blood cell,
called a macrophage, which goes into the artery
wall for the purpose of clearing up detritus.
And it's very good at it.
But the macrophage gets poisoned by contaminants
in that detritus, which eventually
cause it to become more of a problem than a solution.
And I will come back to that at some length
later on because we've done some quite important work
in addressing that over the past few years.
The second type of way that the heart can go wrong
during old age is arteriosclerosis,
which is the stiffening of the major arteries.
This is something that is very important in terms of pathology
because it leads to increased blood pressure in the elderly,
and therefore to things like kidney failure.
And the ultimate molecular driver of arteriosclerosis
is this thing at the bottom, in pink, the stiffening
of this lattice of proteins called the extracellular
matrix, which essentially gives each of our organs
their shape and physical properties that it has.
And, in particular, the extracellular matrix
of the major arteries is extremely essential in terms
of giving them the elasticity that they
need to dampen the pulsation of the heart, of the heart beat,
and thereby protect the more fragile capillaries and smaller
parts of the circulation from the blood pressure.
So that's arteriosclerosis.
The extracellular matrix becomes less
elastic as a result of chemical modifications.
And we need to fix that.
Then there's amyloidosis, which actually
has been discovered quite recently
to be a major killer of the really elderly.
People who live more than 105, 110, it
turns out that most of them, certainly half of them,
die of a disease called senile cardiac amyloidosis, which
is essentially the accumulation of molecular garbage
outside the cell, that thing I wrote in blue here.
That's all about a type of protein
that gets into this kind of fibers that essentially
weaken the joints between the various muscle cells that
make the heart up and weaken its ability to beat.
So that's rather bad for you, eventually, of course.
And then finally there is cell loss.
The heart actually does not beat on its own.
It only beats when the brain tells it to.
And the cells in the heart that mediate that signal,
they're called pacemaker cells.
And it turns out that they don't maintain their numbers
during age.
They die progressively.
And eventually, you haven't got enough of them
and the heart stops listening to the brain.
And it just doesn't beat anymore.
So that's another way that the heart can stop.
So, as you can see, the relationship here,
between damage and this particular type of pathology,
is quite a complicated one, a many to one
relationship for sure.
But, like I said earlier, it's really well understood.
And that's the important thing I want to get across.
The same with Alzheimer's disease.
Alzheimer's disease was defined about 100 years ago or more,
as the combination of these two things
here, a type of junk inside neurons
called tangles and another type outside called plaques.
And now, of course, we also know that there's
a lot of cell death in Alzheimer's disease.
So again, a complex relationship, but a well
understood one.
The big thing to take into account here and to emphasize
is that these nonspecific aspects
of aging, that we don't give disease-like names to, the same
applies.
Most of these things-- pretty much everything
except division-obsessed cells-- ultimately
can be linked causally to various types of decline
in function, like loss of muscle,
or loss of immune function, and such like.
So this is really good news.
We have a very clear idea of this linkage.
All right then, enough about the problem.
Let's go to the solution.
So what is the preventative maintenance approach?
It falls into these four types of approach,
replace stuff that's gone missing;
remove stuff that has accumulated,
that you don't want; sometimes in situ repair
of stuff that you don't want to remove or to replace;
and sometimes reinforcement.
That means essentially breaking the link between damage
and pathology, somehow doing something to the body.
That means that the damage can still accumulate,
but it no longer actually has any pathogenic effects.
And when we come down to specifics, it's all about this.
So I won't go through this in detail.
I'm going to touch on a couple of the examples
here in a moment, to look at the details of the pathologies.
But essentially what I'm showing here
is that we know exactly how to do this in principal.
Some of this, much more than in principle.
Lets take cell loss.
The main way-- the generic way to restore cellularity, cell
number, to a given tissue is, of course, stem cell therapy.
That's true for cell loss during aging,
just as it is in terms of any kind of acute trauma
or injury for which stem cell therapy may originally
have been developed.
Parkinson's disease is a great example of this.
It's a disease in which cells in one particular part
of the brain die unusually rapidly.
And stem cell therapies for Parkinson's, they
were first attempted nearly 20 years ago,
when we really didn't know what we were doing with stem cells.
But even then, they sometimes worked really, really well.
And now, there's a great deal of resurgence
of interest in this and new clinical trials going on.
And I think there's quite a good chance, at least 50%,
that within as little as 10 years from now,
we will be able to say that Parkinson's disease has
been cured.
So I won't go on to the others now because I'm
going to touch on some of them in detail.
What I'm going to do is talk about how far
advanced they are.
And I'm going to start with the ones that are most advanced.
So I'll just mention clinical trials for stem cell therapy.
These are already in progress, in certain cases.
And that's great.
That's wonderful.
And actually, it's the main reason
why SENS Research Foundation doesn't do anything
to speak of, hardly anything, in the whole area,
because our contribution would be a drop in the ocean.
Another case that I want to highlight
in a little more detail consists of this business
of molecular garbage outside the cell, which in general comes
down to this thing called amyloid.
Amyloid, as I mentioned earlier, accumulates in the heart and it
also accumulates in the brain during Alzheimer's.
That's what female plaques are.
And 15 years ago, or so, it was determined, at least in mice,
that one could get rid of this stuff just by immunization.
Essentially, one could trigger the immune system
to engulf the material, get it inside the cell,
inside phagocytic cells.
And this was enough to get rid of it, to remove it,
because the machinery for breaking things down
inside the cell is much more powerful
than what exists outside.
And this moved, in the case of Alzheimer's disease,
very rapidly to clinical trials.
And those clinical trials got to phase III
and reported just a year ago.
And the reaction was frustrating.
The trials did not achieve their clinical endpoints.
That isn't what was frustrating.
I would have been absolutely amazed
if people, given these treatments to get rid
of plaques, had actually exhibited
any significant restoration of cognitive function.
Why?
Because it's not the whole of Alzheimer's, dummy.
I mean Alzheimer's is these three things that happen.
It's not just amyloid accumulating.
It's also tangles accumulating inside the cell, which
was not targeted by the therapy.
And so there was no reason why we
would expect them to go away.
And similarly, the cells that had
gone missing, that had died, were not being replaced.
There's no clear chain of causation.
It's not as if we already had any reason
to believe that if you remove plaques
then the tangles would go away on their own
or the cells would somehow regenerate.
I think it's a bit like what I'm saying at the bottom there.
It's a bit like saying let's take a car apart and put
the individual components out in a line.
And then let's pour burning petrol over them
and we'll expect to see some kind of motion.
It wouldn't happen really.
So it's frustrating that medical researchers and scientists
are often rather careless in their evaluation of how
technology is supposed to work, especially divide and conquer
technology of this kind.
Let me talk about another case.
And here I'm going to emphasize the role of the private sector
and especially the role called of venture capital.
Because obviously in the IT world,
you guys are quite tuned into all of that.
And you may be wondering already why
does a nonprofit, such as SENS Research Foundation,
really need to exist, if all of this is so clear?
So I'm going to talk about this case
because it's an interesting, kind
of intermediate, transitional case.
It concerns death-resistant cells,
which is a category that I've defined,
that simply means "the other way of having too many cells."
You can have too many cells because cells
are dividing when they're not supposed to.
That's what cancer is, as I mentioned a moment ago.
Or you can have too many cells because cells are not
dying when they are supposed to.
People often overlook that because they think, well, cells
are not supposed to die, right?
But that's not true.
It turns out of there are certain parts
of the body in which cells are absolutely
required to die in order for the whole system to function.
So we'd like to be able to get rid of these things.
And for a long time now, I've been
saying that the way to do this is with something
called suicide gene therapy, where
you use engineered viruses to introduce
a toxic gene into cells.
This gene creates a protein that will actually kill the cell.
And the way you do it is by ensuring that the protein is
only synthesized within the cell,
in the case where the cell has got into this bad state, where
you'd like to get rid of it.
So this is something that is routine in the lab,
in mouse experiments.
But it's very dangerous and so it
hasn't got to prime time for the clinic yet.
But it will.
It will.
So that was the thing I was interested in making happen.
And the good news is that a couple of years ago,
a group at a very prestigious institution called the Mayo
Clinic, actually had a go at pretty much that.
What they did was, since they were working in mice,
they didn't actually need to resort to this engineered virus
business of suicide gene therapy.
They just introduced the suicide gene transgenetically
so that it was in every cell in the mouse
from the time the mouse was conceived.
And what they did was they made a combination of two things.
First of all, they introduced a second mutation
into these mice, a different mutation,
which caused these death-resistant cells
to accumulate much, much more rapidly
than they normally would.
But which did not cause any other aspect
of aging to be accelerated.
So these mice basically died of having too many death-resistant
cells.
And they died pretty quickly.
They died at less than half the normal age.
This mouse at the bottom here is such a mouse.
It's less than a year old.
And it's only got about a month to live, if it's lucky.
And you can see, it's very unhealthy already.
So what they did was, this research group,
they engineered this suicide gene into these mice.
And they engineered this in what we call a drug inducible way.
In other words, in such a manner that they could
activate that gene, but only, of course,
in the cells that they wanted to kill,
by giving the mice some simple drug in their drinking water.
Until that time, even the bad cells
would not actually die because they would not
express the suicide gene.
So what they did was they waited until, let's say, halfway
through these mice's lifespan before giving them the drug
and activating the suicide gene, so that a whole bunch
of these cells would already be in existence.
And the result was very nice.
The top mouse there is one like that,
same age as the bottom one.
And as you can see, it's perfectly healthy,
doing very fine.
And they measured the relative health of these mice
in all manner of different ways.
This graph on the right is just one of the dozen things
they did.
It's to do with muscle mass.
So this was all very good news.
Now, here's the interesting thing.
They did this in an academic institution.
But they decided to go out and start a startup company.
And they got VC money really pretty fast.
Why is that interesting?
The reason it's interesting is because the experiment
was extraordinary preliminary.
First of all, it was in mice.
And we all know that stuff that's in mice often
takes quite a long time to translate to the clinic.
Second of all, they were working in this artificial system
where they had accelerated one aspect of aging very, very
dramatically.
So there's no evidence from this experiment showing
that the senescent cells, these death-resistant cells,
are actually all that bad for you in a normal mouse,
in a normal lifespan.
So this was really a bit of a leap of faith.
The third thing that was very preliminary
about this experiment was that it was a transgenic experiment,
where they introduced this gene into the mice that allowed them
to kill the relevant cells at a point of their choosing.
Now, tells us absolutely nothing about what
the actual plausibility is of the company's business
plan, which is to create an actual pharmaceutical,
a small molecule drug that would do the same thing.
There's absolutely no way that there's
any evidence from this experiment
that that is even possible.
And the fourth thing is that even if you forget all this
and you just presume investors were stupid or at least
they thought that their eventual customers would be stupid,
that they might be going for some kind of very
superficial bottom line, that bottom line would be longevity.
There's one thing I haven't told you about this experiment
so far.
You probably think that these mice at the top, right,
probably lived a normal life, like 2 and 1/2 years,
as it gained certainly a year for the mouse at the bottom.
That turns out not to be true.
It's actually the case that the mice at the top
died after a year, same as the mice at the bottom.
Because it turned out that was something else
than the gene did, that the mutation did,
that caused the accelerated accumulation
of death-resistant cells, that was not
to do with death-resistant cells.
It just basically made the heart unhappy
and so they died anyway.
So on every single measure that you could think of,
this is a massively preliminary experiment.
But they got their money.
How did they do it?
I think that the answer is a very encouraging answer.
Namely, that investors, smart investors,
who are looking at things to do with the eventual delivery
and development of anti-aging medicine that actually works,
have been paying attention to the numbers.
They've started paying attention to the fact
that the real anti-aging industry to come,
the anti-aging industry consisting of therapies that
work, is going to be the biggest industry
ever, by a very large margin.
It's going to be the industry of all time.
So that, of course, means that if you
want to get into it, if you want make money, then
your calculations of decisions about whether to go for it
or not will use different numbers.
You will be willing to accept higher risk.
You will be willing to accept a longer time-frame
before access, all those things.
That seems to be happening now.
That's why this kind of thing is actually occurring.
And it's very heartening, indeed.
All right.
So you may think, well, OK, that's great.
So even something really preliminary
is getting funded by the private sector.
Why does SENS Research Foundation
need to exist as a nonprofit, funded by philanthropy?
Well, I'm afraid the answer is that even
though some things are moving forward nicely like this,
and they are in the position also being able to get money
out of venture capital, a lot of things that need to be done
are still at an earlier stage than that.
At early enough that I don't think
the calculations are going to fly for a while.
The mission statement of SENS Research Foundation
is that we want to create a rejuvenation biotechnology
industry.
Don't get me wrong.
We definitely want that to happen.
But there are some things where it's not ready for prime time
yet in the private sector.
And I'm going to give you an example here because it's
a good example of the stuff that we've been doing.
It's showing very good proof of concept.
But it still has a little way to go.
And it's do with this thing, molecular garbage
inside the cell.
And it comes back to the number one killer
in the Western world, atherosclerosis.
Atherosclerosis, as I mentioned earlier,
starts with white blood cells, a particular type
of white blood cell called a macrophage-- excuse
me-- going into the artery wall and clearing up garbage,
clearing up detritus.
And it's very good at it.
It basically recycles various materials
and exports them back out for reuse.
But there are certain contaminants
in that detritus which the macrophage is not
equipped to handle.
And those contaminants poison the macrophage.
And eventually, it doesn't work.
The particular part of the macrophages that stops working
is this thing called the lysosome, which
is kind of the garbage disposal machinery of the cell.
And it's really an important part.
So when the lysosome stops working,
the cell stops being able to do things
that it used to be able to do.
And eventually it turns into this kind
of undead thing called a foam cell, which
is what we have showing here.
This is the first visible stage in atherosclerosis.
And actually, all of us have foam cells
in our major arteries, even as young kids.
But we don't have very many of them.
And when we don't have very many of them, lo and behold,
they're not harmful.
But eventually there's too many.
And the environment, the other cells around,
start to get a little angry.
They get inflamed and bad things start happening.
More white blood cells pile in, in an attempt
to solve the problem.
But they got poisoned as well, so they
become part of the problem.
And the plaque grows and grows.
And eventually you end up with the plaque bursting.
And that's when you got heart attacks and strokes.
So what could we do about this?
Well, about 15 years ago I proposed
that what we really need to do to stop this kind of thing
happening-- and a similar kind of thing
happens with different toxic molecules in, for example,
macular degeneration, the number one
cause of blindness in the elderly.
The thing we need to do is simply
equip the relevant cells that are being poisoned
with additional machinery for breaking things down.
So that, in particular, they can break down
the things that are poisoning them.
And it turns out that that's not so hard as all that.
In the case of atherosclerosis, there
is just one particular compound.
It's called 7-Ketocholesterol, which
appears to be responsible for at least most of the problem.
It's not by any means the only thing
that accumulates in macrophages over time.
But it does seem to be the most important
in terms of its abundance and its toxicity.
And what we decided to do was to take a leaf out
of the book of environmental decontamination, not even
a biomedical field at all.
So, of course, no one working in gerontology
knew anything about this.
But what we did was we simply used the idea
that you might be able to find bacteria in the environment,
in the soil, that could break down the material that
is poisoning these macrophages, this compound
7-Ketocholesterol.
Now our idea was not, I should emphasize,
that having found such bacteria, we
would inject them into the body.
I have to think that might have side effects.
But what we decided to do instead
was, once we found such bacteria,
we would identify the genetic basis for that capability,
the genes and enzymes that they had,
that allowed them to break down these compounds.
And then we would introduce those genes and enzymes
into human cells, thereby augmenting
the capacity of those cells to break things down.
So here's the first step.
And as you can see, this paper came out in 2008.
It was actually the first paper that
was published out of work funded by us.
And it went very nicely.
We found bacteria that did the job.
What you're seeing here is what's
called an enrichment culture, where
we take a whole bunch of different bacterial strains
and we give them this stuff, 7-Ketocholesterol.
And we don't give them anything else to live on.
The idea here is that if they can break down 7KC,
then they can grow because they can extract energy from it.
And if they can't, they can't.
So most of these strains can't.
They just there like lemons, doing exactly nothing.
But a couple of them are doing very fine.
You've got a couple of strains there which after only 10 days,
have consumed the entire material.
So that's great.
Then we're got to, as I say, find the genes and enzymes
that they're using.
And that turned out not to be too hard.
This is one way the way we did it.
It's called mass spectrometry.
We essentially identified the breakdown products
that the bacteria are creating in the process of breaking down
the original substance.
And that allows us to infer what enzymatic reaction is occurring
and used by informatics to identify candidate genes.
There are other approaches.
We also used expression analysis to find
which genes were being activated when we gave them the 7KC,
and so on.
All these methods seemed to work pretty well.
The long and short of it was we had a few candidate
genes by about 2010.
That's when things started getting tricky.
Step three in this process is the hard one,
which is to actually get these enzymes to work
in a human cell.
The reason that's hard is because humans cells
are very different from bacteria.
Bacteria doesn't even have lysosomes.
But we managed it.
First of all, we actually had to do the localization.
We have to get our enzymes to go to the lysosome.
And this shows that we could do that.
The red on the left is a stain for the lysosome in cells.
The middle one is our engineered protein.
And the fact that they're overlapping reasonably well
shows us that plenty of our enzyme
is going to the right place.
So that's all good.
But at the end of the day, we also
had to show that it worked.
And that was what we were able to show maybe 18 months ago.
This graph is a summary of the results.
Essentially what it says is that if you give cells
a completely insupportable amount of 7KC,
on the right-hand end here, then it
doesn't matter what you've done to them in terms
of giving them extra enzymes.
They die anyway.
But if you give them a relatively modest amount
of this toxic molecule, then the fact
that the right-hand bar of each of these groups
is higher than the other bars, that basically says
that the cells which have the enzyme
seem to be targeted to the right part of the cell,
the lysosomes are projected.
They survive better than other negative control cells, cells
that don't have an enzyme, or they have the wrong enzyme,
or they have the enzyme not targeted to the right place.
So this is a extremely good proof of concept.
We're very happy about it.
We have a couple more steps to go
before we think we would be able to take this
to the private sector.
First of all, we would need to get
this working in a different cell type.
We did this in fibroblasts, which
happened to be easy to work with.
But we need to get it to work in macrophages.
Then we need to move to mouse models
of cardiovascular disease and show
that it's protective there as well.
But we're well on our way.
I think I can probably trust you to understand that this really
is a very effective proof of concept.
And we learned a lot more.
We only have $4 million a year, or thereabouts.
But we are spending it very efficiently.
We have a headquarters in Mountain View, California,
just a couple of miles from the Googleplex,
that has a few thousand square feet of lab space, where
we do three of our major projects.
And we have more than a dozen other project
at various universities around the world.
That one I just described to you happens
at Rice University in Houston.
We also have an educational arm, which I always
like to mention because I think it's
very important to understand that we're trying to grow
the next generation of rejuvenation biotechnologists.
So that's something that you can read
about at the website, of course.
Now, I thought I should mention a little bit about credibility.
Because maybe 10 years ago-- some of you
have already come across me-- it was actually
pretty tough to sell this concept.
I think you already got the idea from my early remarks
that the whole maintenance approach is
a big departure from what people had previously been thinking.
People who were working in gerontology
viewed this whole idea of damage repair as a complete solution,
as a very, very implausible idea.
It was as far away from the historical thinking
as the geriatric medicine approach was.
So I had to do a lot of education.
And it took a while.
But the good news is that it really has been very effective.
We are now in the very heartening position
of having this kind of research advisory board, of very
obviously explicit endorsers of our approach.
Every single one of these people are really, really prestigious
dignitaries in their various biological disciplines.
Now, there are obviously still a few people out there
who just refuse to be educated about this.
But by and large, the credibility barrier
has been breached, which is very nice to know.
But still, we're got to do more.
One thing we have to do, of course, is publish.
We have to demonstrate the validity of what we're
doing in the traditional manner.
And that's, of course, what we're doing.
So these are just a small selection of the papers
that we've published recently.
That one at the top is the one I've just mentioned, of course,
the rescue of cells from 7-Ketocholesterol.
But we've done a lot more than that.
A couple months ago, we had a lovely paper
in a very prestigious journal, "The Journal of Biological
Chemistry," showing that we could address
senile cardiac amyloidosis using antibodies
that would break the stuff down.
A couple of other examples there.
So things are going nicely.
But, of course, there's still a very long way to go.
I'm pretty much done.
And I'm just going to spend a few minutes on other matters.
The first thing I'm going to tell you
is what I'm not going to tell you.
In other words, I don't really do
the sociological considerations.
I do have to.
Some of you probably know that I do a brutal amount of media.
I do probably 100 interviews a year.
And the bulk of my time in those interviews
is spend answering questions along the lines of, oh, dear,
where are we going to put all the people,
or won't dictators live forever, or won't we all get bored?
Shall we say, I have become a little bit
bored myself of these questions.
I regard them as being ultimately founded
on a degree of myopia with regard
to the importance of this work, a degree of ability
to put out of one's mind the fact that we have
quite a bad problem today with aging,
namely a problem of 100,000 people every single day
dying of it.
That's 2/3 of all deaths.
In the developed world, it's something
like 90% of all deaths.
And, of course, it's not just the death.
It's also all the suffering that most people
have for a long period of time before they die of aging.
So it's fairly obvious that this is not really the right way
to think about it.
We shouldn't be thinking about these problems.
We should be thinking about this, that if we were actually
to move to a post-aging world, we
would have no age-related ill health.
People's health would not be a function
of how long ago they were born.
The elderly would still be contributing wealth to society,
so these therapies would pay for themselves.
The elderly would not be a burden on their kids anymore.
This is obviously something that a lot of the elderly
worry about a great deal.
So that's kind of the way I think.
All right then, so the final point, call to action.
What can you guys do?
As far as I'm concerned, this is really
where I want to place emphasis because whenever
I give a talk like this, or an interview,
I feel I do get people inside.
I do get people to understand that, yes, this
is a really important problem, and yes, we
do have a respectable chance to actually solve it.
But I need to actually make sure that we solve it
faster than we otherwise would.
And at the end of the day, it all comes down to these things.
The first thing is, ultimately it all costs money.
10 years ago, 15 years ago, when I started out,
I had three problems to solve.
I need a plan for how to solve aging,
and that's what I've been telling you today.
I needed people.
I needed the world's best experts
in the various scientific areas to be
enthusiastic about working on this.
And that, I have demonstrated.
We already have now, very much.
But, at the end of the day, these people
are still, by and large, sitting on their hands,
waiting for the resources to actually get on with it.
Because we only have perhaps one tenth of the budget
that we would need to be able to fund everything
that really needs to be funded.
And that is absolutely the number one problem right now.
Obviously, I'd like you to learn more.
I've only had an hour.
That's not nearly enough time to do justice to all that we do.
Anyone who wants to get involved in terms of actually learning
more about it through our educational initiative,
please go and have a look at that at the website,
at sens.org.
But ultimately, it's all about advocacy.
Hands up.
Anyone here who doesn't know anyone
who's richer than you are?
All right.
So it's all about changing people's minds, right?
It's all about changing people's minds.
The more people we have on-side, who
understand about the importance of this mission,
the faster it's going to happen.
And I spent a lot of my time getting people
to understand how important this is.
If the people that I were able to bring on-side,
were to go out and bring other people on-side,
and so on and so forth, we would solve
this problem a great deal faster.
I wrote this book several years ago.
It's very comprehensive.
I call it semi-technical.
What that basically means is you don't
have to be a trained biologist to understand it,
but you probably won't be reading it in one sitting.
It's quite dense.
It doesn't cut any corners at all on the science.
And it was written several years ago.
But it's still fairly up to date.
That is not because there has been
inadequate progress in the meantime.
The progress has been wonderful.
But what it is is because the progress
has been pretty much the type of progress that we predicted
would happen.
In other words, this is, again, another piece of evidence
that the SENS paradigm is standing the test of time.
So that's all very heartening.
I think I should also mention this.
Incidentally, if any of you are going be in California
a few weeks from now-- but I guess you probably
have friends who are-- and anyone that you might want
to recommend to come to our conference,
I would very much encourage you to do that.
This conference is happening just-- maybe 10 miles south
of the Googleplex, August 21st to 23rd.
And, of course, it will cover all
of the science of what we're doing,
of rejuvenation biotechnology.
But also we'll have extensive participation
from industry, from regulatory people,
from policymakers, and so on.
So it's going to be quite a gathering.
And, of course, lots of laypeople there as well.
And I very much encourage you to encourage other people
to do that.
I'll stop there.
And I think there's probably a bit of time for questions.
Thank you very much.
[APPLAUSE]
AUDIENCE: Hi.
So in the field of cancer, we see
that there are some cancers that have been very-- well, have
been tackled extremely well in the last 100 years,
others that become very resistant and very
difficult to deal with.
Do you see the same things likely to happen when we tackle
aging more generally, in that some diseases will be
eradicated quickly and others will take a much
longer time to get rid of, and a long tail.
AUBREY DE GREY: Yeah.
That's a really great question.
So first of all, let me give you my take on where cancer sits
within the whole universe of problems of aging.
My view is that concept is by far the hardest
aspect of aging to fix.
It's the one that has natural selection on its side.
And that makes it-- any cancer that's
big enough to be clinically relevant has
a trillion different individual engines of genetic creativity
in it.
It's really a tough nut to crack.
Now a lot of people, because of largely the kind of evidence
that you described, they don't like
to think of cancer as a single disease anymore.
They like to think of it as family of diseases
that we just happen to give some collective name to.
But the fact is that's not really fair.
Because there are some things that cancers have in common.
And in particular, there's one thing
that absolutely all cancers have in common, namely
the fact that they need to figure out a way
to grow the ends of their chromosomes.
Chromosomes get shorter when a cell divides
and there needs to be a way to compensate for that.
There's only two ways that cancers ever use to do that.
And we're well on our way to being
able to stop that from happening.
So that's essentially the way that we're going about it.
In general when you talk about the relative degree
of difficulty of coping with aspects of aging,
I think you're right.
There are definitely things that are harder than others.
And actually, the last part of the reason-- well,
in fact, most of the reason why SENS Research Foundation was
set up, was precisely to mitigate that problem.
To ensure that we work on the hottest things
and that they don't get left behind
and we just fix the easy things and end up where we were.
AUDIENCE: Thank you.
AUDIENCE: If you had like a crystal ball,
how long do you think it will take until you've got something
that you say actually we'll be able to live for 100 years?
AUBREY DE GREY: Yeah.
You ask that question in exactly the way
that an engineer should ask it.
In other words, I haven't the slightest fucking clue
because it's a long way away.
But, of course, you want an estimate.
And actually you're quite right to ask the question.
Because a lot of gerontologists would just refuse to answer.
They would say it's irresponsible to get people's
hopes up, or something like that.
And I say, on the contrary, it's irresponsible
not to give an estimate because however bad my estimate is
going to be, yours is going to be even worse, right?
And therefore, I'm got to give as good an estimate as I can.
So my estimate is this.
I think we have at least 50/50 chance
of getting the technologies that I described today
working reasonably well within the next 20 to 25 years.
AUDIENCE: Yes.
AUBREY DE GREY: Right.
And the technologies that I describe today I think
will probably give about 30 additional years
of healthy life.
And, of course, they will give those years
to people who are already in middle age or older, 60, 70,
or even maybe 80, at the time that the therapies arrive.
So that means most people in this room
have a relatively good chance of benefiting.
Two caveats.
The first caveat, everything I just said
is only going to be true if research in the next five
or 10 years goes a lot faster than it's currently going.
The funding limitation that exists at the moment,
I estimate is slowing things down
by roughly a factor of three.
In other words, over the past 10 years, the amount of progress
we've made towards getting proof of concept of these things
in the lab and so on, has probably only advanced
by about three years relative to where
it could have gone if only science had been limiting.
The second caveat is the probabilities.
So I can tell you the 50-50 estimates.
But I want to tell you right now the variance is high.
I think there's at least a 10% chance
that we won't get there for 100 years.
But who cares?
A 50% chance is perfectly enough to be worth fighting for.
AUDIENCE: Yeah.
Thank you.
AUDIENCE: Thank you very much for this very interesting talk.
AUBREY DE GREY: Thank you.
AUDIENCE: Actually about a year ago,
we set up this company called Calico, the California Life
Company.
And we set it to up work independently.
And I was just wondering, first of all,
how do you view this development?
And secondly, if you already had the chance
to work with them so far?
AUBREY DE GREY: Yeah.
Actually, I was very surprised that no one
at the talk I gave at lunchtime asked about Calico.
But, yes, Calico was, as you say,
set up my Larry and Sergey about a year ago.
Well, my view of that development
was expressed in "Time" magazine, which
was where the thing was announced.
"Time" got me to write the reaction piece, so to speak.
And I was pretty effusive.
I was overjoyed.
And I am still am.
I think there is a very respectable chance that they
will make a really big difference, but only a chance.
It just remains to be seen.
They are taking their own really good time
to decide exactly where they're going
to be prioritizing their efforts.
And in a way, that's a good thing.
The worst thing that could possibly
would have been a repeat of what happened 15 years ago when
another very wealthy individual, Larry Ellison,
decides to do essentially the same thing,
albeit in a foundation, rather than a company.
He basically went out and promptly hired
a veteran gerontologist from the NIA.
And the result was completely predictable.
15 years and $400 million later, absolutely nothing
had been done that wouldn't have been done anyway.
And he's given up now.
So Calico is potentially a really good thing.
They've got people at the top who are, by and large,
not trained gerontologists.
And therefore, they know what they don't know.
They're making their own decisions.
They're not talking to us nearly as much as we'd like them to
and as we think they should be.
But that may change.
So I'm hopeful.
AUDIENCE: Thank you.
AUDIENCE: Hey, Aubrey.
If, as you describe, this might become
one of the biggest industries ever--
AUBREY DE GREY: The very biggest.
AUDIENCE: And if, as you describe,
you've done a great job of convincing people
that it is worthwhile fighting for it, what
are, in your opinion, the three main obstacles to actually get
the necessary funding going, which
seems to be one of the biggest problems on the way?
AUBREY DE GREY: Yeah.
I will actually just stick with one main obstacle, which
is something that I historically used
to call the pro-aging trance.
But my marketing people tell me that that's too derogatory.
So I'm not allowed to say that anymore.
Essentially it's fear.
It's a combination of two types of fear.
Number one, fear of the unknown, recognition
that a post-aging world would be very, very, very, very
different.
And therefore, maybe we ought to stick to what we know.
Kind of essentially the same as what
happened to resistance to the Industrial Revolution.
And secondly, fear of getting their hopes up.
People just are not willing to reengage this battle.
People, in general, have made the peace with aging.
They have accepted defeat.
And when you've accepted defeat, the last thing you want to do
is go through all that stress again.
So that's basically what it's all about.
People who are otherwise perfectly well educated
and perfectly rational in absolutely every other walk
of life, will say things and think things
that they would be embarrassed to say to a small child
to shut them up, when it comes to this particular topic.
And, of course, the problem is that I
don't get to talk to everybody.
Time and time again, I will be in the company of people
who are not only get it, but say they get it.
And they will tell other people that they get it
and that things are good.
But do they actually run me a check, not as such.
Why do they not write me a check,
probably because their wife doesn't want them to.
AUDIENCE: Hi.
The cost of gene sequencing has decreased kind of massively
over the last 10 years.
And I've seen various depictions of people
saying that in five years' time, we'll
all be getting our gene sequenced for the cost of $10,
or whatever.
Do you think it's a high chance that we
might find genetic causes for all these problems,
like Alzheimer's, before we find solutions
that involve damage limitation?
AUBREY DE GREY: Yeah.
Great question.
So I'm going to answer it in a slightly complicated way
with two definitions of the word "solution."
There will be the possibility of identifying
genetic factors that are responsible for the age
of onset of certain age-related conditions,
whether it be Alzheimer's or anything else.
And then also the possibility of genetic conditions
that are simply responsible for it in a binary way,
for it happening or not happening.
So what I can tell you is that it's very likely
that we will find the former.
Albeit, it's not nearly as easy as people
were thinking maybe 20 years ago,
when [INAUDIBLE] was discovered.
And it looks like it will involve
a lot of different genes combining
in different people, each individual one of which
only makes a small contribution.
However, we can say definitively at this point
that the answer to the latter question is no.
That the aspects of metabolism that ultimately
drive the accumulation of these various types of damage.
And therefore the eventual arrival of these pathologies,
are non-negotiable.
Now, the number one worse thing that we have,
that drives all these things, is breathing.
Breathing is really bad for you.
But there's not a lot of choice that we have about it.
AUDIENCE: Thanks.
AUDIENCE: Hi.
You talked a lot about sort of funding
and where you get it from and also
bringing in the private market narrows
the diversity of the research.
So at what stage do you go to the private markets
and the venture capitalists?
AUBREY DE GREY: Yeah, a great question.
I'm not really sure about narrowing of diversity.
I mean in a sense the continued existence
of nonprofit participation in all of this
is a good protection against that.
So individual components of the range
of things that need to be done might
go into the private sector, without necessarily restricting
the ability of other components to continue being developed
in the philanthropic sector, so to speak.
That's kind of how it going.
I think we may be done.
More?
AUDIENCE: Hi.
This may not be of interest to you at all.
But sticking you with your car analogy, if you take a car
and you drive it on a smooth road,
and you keep it away from Sun, and you put in the right stuff
that it needs in the engine and what's in everything,
it probably accumulates less damage.
If we look at that for a human being,
in the meantime, before your research is going to save us
all, what can we be doing to damage limit?
AUBREY DE GREY: That's an absolutely excellent question
and an absolutely excellent way of expressing the question.
Because you're absolutely right, in the case
of simple man-made machines like cars, lifestyle matters a lot.
You can drive a car carefully and well and it will last a lot
longer-- quite a lot longer than if you don't.
The unfortunate fact is that it's not
quite like that for the human body.
When I mentioned a moment ago that breathing
is really bad for you, breathing and
the other non-negotiable aspects of being alive,
like eating-- eating anything, not just eating badly--
are the overwhelming majority of the drivers
of the accumulation of damage.
Of course, there are things that you can do that are obviously
bad for you, like smoking or getting seriously overweight,
but nothing you mother didn't tell you.
If you're basically averaging healthy,
then the amount of additional postponement
of age-related ill health that you
can achieve by any kind of lifestyle, or diet,
or exercise modifications, or whatever,
is, as far as we can tell, really tiny.
And therefore, there's only one way
out of this, which is to hasten the development of therapies
that we don't yet have.
In other words, give me large amounts of money.
[LAUGHTER]
Thanks very much everybody.
[APPLAUSE]