"Roadmap to end aging" transcript, slightly more legible

18 minutes is an absolutely brutal time limit,
00:27
so I'm going to dive straight in, right at the point
00:29
where I get this thing to work.
00:31
Here we go. I'm going to talk about five different things.
00:33
I'm going to talk about why defeating aging is desirable.
00:36
I'm going to talk about why we have to get our shit together,
00:38
and actually talk about this a bit more than we do.
00:40
I'm going to talk about feasibility as well, of course.
00:42
I'm going to talk about why we are so fatalistic
00:44
about doing anything about aging.
00:46
And then I'm going spend perhaps the second half of the talk
00:48
talking about, you know, how we might actually be able to prove that fatalism is wrong,
00:53
namely, by actually doing something about it.
00:55
I'm going to do that in two steps.
00:57
The first one I'm going to talk about is
00:59
how to get from a relatively modest amount of life extension --
01:02
which I'm going to define as 30 years, applied to people
01:05
who are already in middle-age when you start --
01:07
to a point which can genuinely be called defeating aging.
01:10
Namely, essentially an elimination of the relationship between
01:14
how old you are and how likely you are to die in the next year --
01:16
or indeed, to get sick in the first place.
01:18
And of course, the last thing I'm going to talk about
01:20
is how to reach that intermediate step,
01:22
that point of maybe 30 years life extension.
01:25
So I'm going to start with why we should.
01:28
Now, I want to ask a question.
01:30
Hands up: anyone in the audience who is in favor of malaria?
01:33
That was easy. OK.
01:34
OK. Hands up: anyone in the audience
01:36
who's not sure whether malaria is a good thing or a bad thing?
01:39
OK. So we all think malaria is a bad thing.
01:41
That's very good news, because I thought that was what the answer would be.
01:43
Now the thing is, I would like to put it to you
01:45
that the main reason why we think that malaria is a bad thing
01:48
is because of a characteristic of malaria that it shares with aging.
01:52
And here is that characteristic.
01:55
The only real difference is that aging kills considerably more people than malaria does.
02:00
Now, I like in an audience, in Britain especially,
02:02
to talk about the comparison with foxhunting,
02:04
which is something that was banned after a long struggle,
02:07
by the government not very many months ago.
02:10
I mean, I know I'm with a sympathetic audience here,
02:12
but, as we know, a lot of people are not entirely persuaded by this logic.
02:15
And this is actually a rather good comparison, it seems to me.
02:18
You know, a lot of people said, "Well, you know,
02:20
city boys have no business telling us rural types what to do with our time.
02:25
It's a traditional part of the way of life,
02:27
and we should be allowed to carry on doing it.
02:29
It's ecologically sound; it stops the population explosion of foxes."
02:32
But ultimately, the government prevailed in the end,
02:34
because the majority of the British public,
02:35
and certainly the majority of members of Parliament,
02:37
came to the conclusion that it was really something
02:39
that should not be tolerated in a civilized society.
02:41
And I think that human aging shares
02:42
all of these characteristics in spades.
02:45
What part of this do people not understand?
02:47
It's not just about life, of course --
02:49
(Laughter) --
02:50
it's about healthy life, you know --
02:53
getting frail and miserable and dependent is no fun,
02:56
whether or not dying may be fun.
02:58
So really, this is how I would like to describe it.
03:00
It's a global trance.
03:02
These are the sorts of unbelievable excuses
03:04
that people give for aging.
03:06
And, I mean, OK, I'm not actually saying
03:08
that these excuses are completely valueless.
03:10
There are some good points to be made here,
03:12
things that we ought to be thinking about, forward planning
03:15
so that nothing goes too -- well, so that we minimize
03:17
the turbulence when we actually figure out how to fix aging.
03:20
But these are completely crazy, when you actually
03:23
remember your sense of proportion.
03:25
You know, these are arguments; these are things that
03:29
would be legitimate to be concerned about.
03:31
But the question is, are they so dangerous --
03:34
these risks of doing something about aging --
03:36
that they outweigh the downside of doing the opposite,
03:40
namely, leaving aging as it is?
03:42
Are these so bad that they outweigh
03:44
condemning 100,000 people a day to an unnecessarily early death?
03:50
You know, if you haven't got an argument that's that strong,
03:52
then just don't waste my time, is what I say.
03:55
(Laughter)
03:56
Now, there is one argument
03:57
that some people do think really is that strong, and here it is.
03:59
People worry about overpopulation; they say,
04:01
"Well, if we fix aging, no one's going to die to speak of,
04:03
or at least the death toll is going to be much lower,
04:06
only from crossing St. Giles carelessly.
04:08
And therefore, we're not going to be able to have many kids,
04:10
and kids are really important to most people."
04:12
And that's true.
04:14
And you know, a lot of people try to fudge this question,
04:17
and give answers like this.
04:18
I don't agree with those answers. I think they basically don't work.
04:21
I think it's true, that we will face a dilemma in this respect.
04:24
We will have to decide whether to have a low birth rate,
04:28
or a high death rate.
04:30
A high death rate will, of course, arise from simply rejecting these therapies,
04:33
in favor of carrying on having a lot of kids.
04:37
And, I say that that's fine --
04:39
the future of humanity is entitled to make that choice.
04:42
What's not fine is for us to make that choice on behalf of the future.
04:46
If we vacillate, hesitate,
04:48
and do not actually develop these therapies,
04:51
then we are condemning a whole cohort of people --
04:55
who would have been young enough and healthy enough
04:57
to benefit from those therapies, but will not be,
04:59
because we haven't developed them as quickly as we could --
05:01
we'll be denying those people an indefinite life span,
05:03
and I consider that that is immoral.
05:05
That's my answer to the overpopulation question.
05:08
Right. So the next thing is,
05:10
now why should we get a little bit more active on this?
05:12
And the fundamental answer is that
05:14
the pro-aging trance is not as dumb as it looks.
05:17
It's actually a sensible way of coping with the inevitability of aging.
05:21
Aging is ghastly, but it's inevitable, so, you know,
05:25
we've got to find some way to put it out of our minds,
05:27
and it's rational to do anything that we might want to do, to do that.
05:31
Like, for example, making up these ridiculous reasons
05:34
why aging is actually a good thing after all.
05:36
But of course, that only works when we have both of these components.
05:40
And as soon as the inevitability bit becomes a little bit unclear --
05:43
and we might be in range of doing something about aging --
05:45
this becomes part of the problem.
05:47
This pro-aging trance is what stops us from agitating about these things.
05:51
And that's why we have to really talk about this a lot --
05:55
evangelize, I will go so far as to say, quite a lot --
05:57
in order to get people's attention, and make people realize
06:00
that they are in a trance in this regard.
06:02
So that's all I'm going to say about that.
06:04
I'm now going to talk about feasibility.
06:07
And the fundamental reason, I think, why we feel that aging is inevitable
06:11
is summed up in a definition of aging that I'm giving here.
06:14
A very simple definition.
06:15
Aging is a side effect of being alive in the first place,
06:18
which is to say, metabolism.
06:20
This is not a completely tautological statement;
06:23
it's a reasonable statement.
06:24
Aging is basically a process that happens to inanimate objects like cars,
06:28
and it also happens to us,
06:30
despite the fact that we have a lot of clever self-repair mechanisms,
06:33
because those self-repair mechanisms are not perfect.
06:35
So basically, metabolism, which is defined as
06:37
basically everything that keeps us alive from one day to the next,
06:40
has side effects.
06:42
Those side effects accumulate and eventually cause pathology.
06:44
That's a fine definition. So we can put it this way:
06:46
we can say that, you know, we have this chain of events.
06:48
And there are really two games in town,
06:50
according to most people, with regard to postponing aging.
06:53
They're what I'm calling here the "gerontology approach" and the "geriatrics approach."
06:57
The geriatrician will intervene late in the day,
06:59
when pathology is becoming evident,
07:01
and the geriatrician will try and hold back the sands of time,
07:04
and stop the accumulation of side effects
07:07
from causing the pathology quite so soon.
07:09
Of course, it's a very short-term-ist strategy; it's a losing battle,
07:12
because the things that are causing the pathology
07:15
are becoming more abundant as time goes on.
07:17
The gerontology approach looks much more promising on the surface,
07:21
because, you know, prevention is better than cure.
07:24
But unfortunately the thing is that we don't understand metabolism very well.
07:27
In fact, we have a pitifully poor understanding of how organisms work --
07:30
even cells we're not really too good on yet.
07:32
We've discovered things like, for example,
07:34
RNA interference only a few years ago,
07:37
and this is a really fundamental component of how cells work.
07:39
Basically, gerontology is a fine approach in the end,
07:42
but it is not an approach whose time has come
07:44
when we're talking about intervention.
07:46
So then, what do we do about that?
07:49
I mean, that's a fine logic, that sounds pretty convincing,
07:51
pretty ironclad, doesn't it?
07:53
But it isn't.
07:55
Before I tell you why it isn't, I'm going to go a little bit
07:58
into what I'm calling step two.
08:00
Just suppose, as I said, that we do acquire --
08:04
let's say we do it today for the sake of argument --
08:06
the ability to confer 30 extra years of healthy life
08:10
on people who are already in middle age, let's say 55.
08:13
I'm going to call that "robust human rejuvenation." OK.
08:16
What would that actually mean
08:17
for how long people of various ages today --
08:20
or equivalently, of various ages at the time that these therapies arrive --
08:24
would actually live?
08:26
In order to answer that question -- you might think it's simple,
08:28
but it's not simple.
08:29
We can't just say, "Well, if they're young enough to benefit from these therapies,
08:32
then they'll live 30 years longer."
08:33
That's the wrong answer.
08:35
And the reason it's the wrong answer is because of progress.
08:37
There are two sorts of technological progress really,
08:39
for this purpose.
08:40
There are fundamental, major breakthroughs,
08:43
and there are incremental refinements of those breakthroughs.
08:47
Now, they differ a great deal
08:49
in terms of the predictability of time frames.
08:52
Fundamental breakthroughs:
08:53
very hard to predict how long it's going to take
08:55
to make a fundamental breakthrough.
08:56
It was a very long time ago that we decided that flying would be fun,
08:59
and it took us until 1903 to actually work out how to do it.
09:02
But after that, things were pretty steady and pretty uniform.
09:06
I think this is a reasonable sequence of events that happened
09:09
in the progression of the technology of powered flight.
09:13
We can think, really, that each one is sort of
09:17
beyond the imagination of the inventor of the previous one, if you like.
09:20
The incremental advances have added up to something
09:24
which is not incremental anymore.
09:26
This is the sort of thing you see after a fundamental breakthrough.
09:29
And you see it in all sorts of technologies.
09:31
Computers: you can look at a more or less parallel time line,
09:34
happening of course a bit later.
09:35
You can look at medical care. I mean, hygiene, vaccines, antibiotics --
09:38
you know, the same sort of time frame.
09:40
So I think that actually step two, that I called a step a moment ago,
09:44
isn't a step at all.
09:45
That in fact, the people who are young enough
09:48
to benefit from these first therapies
09:50
that give this moderate amount of life extension,
09:52
even though those people are already middle-aged when the therapies arrive,
09:56
will be at some sort of cusp.
09:58
They will mostly survive long enough to receive improved treatments
10:02
that will give them a further 30 or maybe 50 years.
10:04
In other words, they will be staying ahead of the game.
10:07
The therapies will be improving faster than
10:10
the remaining imperfections in the therapies are catching up with us.
10:14
This is a very important point for me to get across.
10:16
Because, you know, most people, when they hear
10:18
that I predict that a lot of people alive today are going to live to 1,000 or more,
10:23
they think that I'm saying that we're going to invent therapies in the next few decades
10:27
that are so thoroughly eliminating aging
10:30
that those therapies will let us live to 1,000 or more.
10:33
I'm not saying that at all.
10:35
I'm saying that the rate of improvement of those therapies
10:37
will be enough.
10:38
They'll never be perfect, but we'll be able to fix the things
10:41
that 200-year-olds die of, before we have any 200-year-olds.
10:44
And the same for 300 and 400 and so on.
10:46
I decided to give this a little name,
10:49
which is "longevity escape velocity."
10:51
(Laughter)
10:53
Well, it seems to get the point across.
10:56
So, these trajectories here are basically how we would expect people to live,
11:01
in terms of remaining life expectancy,
11:03
as measured by their health,
11:05
for given ages that they were at the time that these therapies arrive.
11:08
If you're already 100, or even if you're 80 --
11:10
and an average 80-year-old,
11:12
we probably can't do a lot for you with these therapies,
11:14
because you're too close to death's door
11:16
for the really initial, experimental therapies to be good enough for you.
11:20
You won't be able to withstand them.
11:21
But if you're only 50, then there's a chance
11:23
that you might be able to pull out of the dive and, you know --
11:26
(Laughter) --
11:27
eventually get through this
11:30
and start becoming biologically younger in a meaningful sense,
11:33
in terms of your youthfulness, both physical and mental,
11:35
and in terms of your risk of death from age-related causes.
11:37
And of course, if you're a bit younger than that,
11:39
then you're never really even going
11:41
to get near to being fragile enough to die of age-related causes.
11:44
So this is a genuine conclusion that I come to, that the first 150-year-old --
11:49
we don't know how old that person is today,
11:51
because we don't know how long it's going to take
11:53
to get these first-generation therapies.
11:55
But irrespective of that age,
11:57
I'm claiming that the first person to live to 1,000 --
12:01
subject of course, to, you know, global catastrophes --
12:04
is actually, probably, only about 10 years younger than the first 150-year-old.
12:08
And that's quite a thought.
12:10
Alright, so finally I'm going to spend the rest of the talk,
12:13
my last seven-and-a-half minutes, on step one;
12:16
namely, how do we actually get to this moderate amount of life extension
12:21
that will allow us to get to escape velocity?
12:24
And in order to do that, I need to talk about mice a little bit.
12:28
I have a corresponding milestone to robust human rejuvenation.
12:31
I'm calling it "robust mouse rejuvenation," not very imaginatively.
12:34
And this is what it is.
12:36
I say we're going to take a long-lived strain of mouse,
12:38
which basically means mice that live about three years on average.
12:41
We do exactly nothing to them until they're already two years old.
12:44
And then we do a whole bunch of stuff to them,
12:46
and with those therapies, we get them to live,
12:48
on average, to their fifth birthday.
12:50
So, in other words, we add two years --
12:52
we treble their remaining lifespan,
12:54
starting from the point that we started the therapies.
12:56
The question then is, what would that actually mean for the time frame
12:59
until we get to the milestone I talked about earlier for humans?
13:02
Which we can now, as I've explained,
13:04
equivalently call either robust human rejuvenation or longevity escape velocity.
13:08
Secondly, what does it mean for the public's perception
13:11
of how long it's going to take for us to get to those things,
13:13
starting from the time we get the mice?
13:15
And thirdly, the question is, what will it do
13:17
to actually how much people want it?
13:19
And it seems to me that the first question
13:21
is entirely a biology question,
13:22
and it's extremely hard to answer.
13:24
One has to be very speculative,
13:26
and many of my colleagues would say that we should not do this speculation,
13:29
that we should simply keep our counsel until we know more.
13:33
I say that's nonsense.
13:34
I say we absolutely are irresponsible if we stay silent on this.
13:37
We need to give our best guess as to the time frame,
13:40
in order to give people a sense of proportion
13:43
so that they can assess their priorities.
13:45
So, I say that we have a 50/50 chance
13:48
of reaching this RHR milestone,
13:50
robust human rejuvenation, within 15 years from the point
13:53
that we get to robust mouse rejuvenation.
13:55
15 years from the robust mouse.
13:58
The public's perception will probably be somewhat better than that.
14:01
The public tends to underestimate how difficult scientific things are.
14:03
So they'll probably think it's five years away.
14:05
They'll be wrong, but that actually won't matter too much.
14:07
And finally, of course, I think it's fair to say
14:10
that a large part of the reason why the public is so ambivalent about aging now
14:14
is the global trance I spoke about earlier, the coping strategy.
14:16
That will be history at this point,
14:18
because it will no longer be possible to believe that aging is inevitable in humans,
14:21
since it's been postponed so very effectively in mice.
14:24
So we're likely to end up with a very strong change in people's attitudes,
14:28
and of course that has enormous implications.
14:31
So in order to tell you now how we're going to get these mice,
14:34
I'm going to add a little bit to my description of aging.
14:36
I'm going to use this word "damage"
14:38
to denote these intermediate things that are caused by metabolism
14:42
and that eventually cause pathology.
14:44
Because the critical thing about this
14:46
is that even though the damage only eventually causes pathology,
14:48
the damage itself is caused ongoing-ly throughout life, starting before we're born.
14:53
But it is not part of metabolism itself.
14:56
And this turns out to be useful.
14:57
Because we can re-draw our original diagram this way.
15:00
We can say that, fundamentally, the difference between gerontology and geriatrics
15:03
is that gerontology tries to inhibit the rate
15:05
at which metabolism lays down this damage.
15:07
And I'm going to explain exactly what damage is
15:09
in concrete biological terms in a moment.
15:12
And geriatricians try to hold back the sands of time
15:14
by stopping the damage converting into pathology.
15:16
And the reason it's a losing battle
15:18
is because the damage is continuing to accumulate.
15:20
So there's a third approach, if we look at it this way.
15:23
We can call it the "engineering approach,"
15:25
and I claim that the engineering approach is within range.
15:28
The engineering approach does not intervene in any processes.
15:31
It does not intervene in this process or this one.
15:33
And that's good because it means that it's not a losing battle,
15:36
and it's something that we are within range of being able to do,
15:39
because it doesn't involve improving on evolution.
15:42
The engineering approach simply says,
15:44
"Let's go and periodically repair all of these various types of damage --
15:48
not necessarily repair them completely, but repair them quite a lot,
15:52
so that we keep the level of damage down below the threshold
15:55
that must exist, that causes it to be pathogenic."
15:58
We know that this threshold exists,
16:00
because we don't get age-related diseases until we're in middle age,
16:03
even though the damage has been accumulating since before we were born.
16:06
Why do I say that we're in range? Well, this is basically it.
16:10
The point about this slide is actually the bottom.
16:13
If we try to say which bits of metabolism are important for aging,
16:16
we will be here all night, because basically all of metabolism
16:19
is important for aging in one way or another.
16:21
This list is just for illustration; it is incomplete.
16:24
The list on the right is also incomplete.
16:26
It's a list of types of pathology that are age-related,
16:29
and it's just an incomplete list.
16:31
But I would like to claim to you that this list in the middle is actually complete --
16:34
this is the list of types of thing that qualify as damage,
16:37
side effects of metabolism that cause pathology in the end,
16:40
or that might cause pathology.
16:42
And there are only seven of them.
16:45
They're categories of things, of course, but there's only seven of them.
16:48
Cell loss, mutations in chromosomes, mutations in the mitochondria and so on.
16:53
First of all, I'd like to give you an argument for why that list is complete.
16:58
Of course one can make a biological argument.
17:00
One can say, "OK, what are we made of?"
17:02
We're made of cells and stuff between cells.
17:04
What can damage accumulate in?
17:07
The answer is: long-lived molecules,
17:09
because if a short-lived molecule undergoes damage, but then the molecule is destroyed --
17:12
like by a protein being destroyed by proteolysis -- then the damage is gone, too.
17:16
It's got to be long-lived molecules.
17:18
So, these seven things were all under discussion in gerontology a long time ago
17:21
and that is pretty good news, because it means that,
17:25
you know, we've come a long way in biology in these 20 years,
17:27
so the fact that we haven't extended this list
17:29
is a pretty good indication that there's no extension to be done.
17:33
However, it's better than that; we actually know how to fix them all,
17:35
in mice, in principle -- and what I mean by in principle is,
17:38
we probably can actually implement these fixes within a decade.
17:41
Some of them are partially implemented already, the ones at the top.
17:45
I haven't got time to go through them at all, but
17:48
my conclusion is that, if we can actually get suitable funding for this,
17:52
then we can probably develop robust mouse rejuvenation in only 10 years,
17:56
but we do need to get serious about it.
17:59
We do need to really start trying.
18:01
So of course, there are some biologists in the audience,
18:04
and I want to give some answers to some of the questions that you may have.
18:07
You may have been dissatisfied with this talk,
18:09
but fundamentally you have to go and read this stuff.
18:11
I've published a great deal on this;
18:13
I cite the experimental work on which my optimism is based,
18:16
and there's quite a lot of detail there.
18:18
The detail is what makes me confident
18:20
of my rather aggressive time frames that I'm predicting here.
18:22
So if you think that I'm wrong,
18:24
you'd better damn well go and find out why you think I'm wrong.
18:28
And of course the main thing is that you shouldn't trust people
18:31
who call themselves gerontologists because,
18:33
as with any radical departure from previous thinking within a particular field,
18:37
you know, you expect people in the mainstream to be a bit resistant
18:41
and not really to take it seriously.
18:43
So, you know, you've got to actually do your homework,
18:45
in order to understand whether this is true.
18:46
And we'll just end with a few things.
18:48
One thing is, you know, you'll be hearing from a guy in the next session
18:51
who said some time ago that he could sequence the human genome in half no time,
18:55
and everyone said, "Well, it's obviously impossible."
18:57
And you know what happened.
18:58
So, you know, this does happen.
19:02
We have various strategies -- there's the Methuselah Mouse Prize,
19:04
which is basically an incentive to innovate,
19:07
and to do what you think is going to work,
19:10
and you get money for it if you win.
19:13
There's a proposal to actually put together an institute.
19:16
This is what's going to take a bit of money.
19:18
But, I mean, look -- how long does it take to spend that on the war in Iraq?
19:21
Not very long. OK.
19:22
(Laughter)
19:23
It's got to be philanthropic, because profits distract biotech,
19:26
but it's basically got a 90 percent chance, I think, of succeeding in this.
19:30
And I think we know how to do it. And I'll stop there.
19:33
Thank you.
19:34
(Applause)
19:39
Chris Anderson: OK. I don't know if there's going to be any questions
19:42
but I thought I would give people the chance.
19:44
Audience: Since you've been talking about aging and trying to defeat it,
19:48
why is it that you make yourself appear like an old man?
19:52
(Laughter)
19:56
AG: Because I am an old man. I am actually 158.
19:59
(Laughter)
20:00
(Applause)
20:03
Audience: Species on this planet have evolved with immune systems
20:07
to fight off all the diseases so that individuals live long enough to procreate.
20:11
However, as far as I know, all the species have evolved to actually die,
20:16
so when cells divide, the telomerase get shorter, and eventually species die.
20:21
So, why does -- evolution has -- seems to have selected against immortality,
20:26
when it is so advantageous, or is evolution just incomplete?
20:30
AG: Brilliant. Thank you for asking a question
20:32
that I can answer with an uncontroversial answer.
20:34
I'm going to tell you the genuine mainstream answer to your question,
20:37
which I happen to agree with,
20:39
which is that, no, aging is not a product of selection, evolution;
20:42
[aging] is simply a product of evolutionary neglect.
20:45
In other words, we have aging because it's hard work not to have aging;
20:50
you need more genetic pathways, more sophistication in your genes
20:52
in order to age more slowly,
20:54
and that carries on being true the longer you push it out.
20:57
So, to the extent that evolution doesn't matter,
21:02
doesn't care whether genes are passed on by individuals,
21:04
living a long time or by procreation,
21:07
there's a certain amount of modulation of that,
21:09
which is why different species have different lifespans,
21:12
but that's why there are no immortal species.
21:15
CA: The genes don't care but we do?
21:17
AG: That's right.
21:19
Audience: Hello. I read somewhere that in the last 20 years,
21:24
the average lifespan of basically anyone on the planet has grown by 10 years.
21:29
If I project that, that would make me think
21:32
that I would live until 120 if I don't crash on my motorbike.
21:37
That means that I'm one of your subjects to become a 1,000-year-old?
21:42
AG: If you lose a bit of weight.
21:44
(Laughter)
21:47
Your numbers are a bit out.
21:50
The standard numbers are that lifespans
21:53
have been growing at between one and two years per decade.
21:56
So, it's not quite as good as you might think, you might hope.
22:00
But I intend to move it up to one year per year as soon as possible.
22:03
Audience: I was told that many of the brain cells we have as adults
22:06
are actually in the human embryo,
22:08
and that the brain cells last 80 years or so.
22:10
If that is indeed true,
22:12
biologically are there implications in the world of rejuvenation?
22:15
If there are cells in my body that live all 80 years,
22:18
as opposed to a typical, you know, couple of months?
22:20
AG: There are technical implications certainly.
22:22
Basically what we need to do is replace cells
22:26
in those few areas of the brain that lose cells at a respectable rate,
22:29
especially neurons, but we don't want to replace them
22:32
any faster than that -- or not much faster anyway,
22:34
because replacing them too fast would degrade cognitive function.
22:38
What I said about there being no non-aging species earlier on
22:41
was a little bit of an oversimplification.
22:43
There are species that have no aging -- Hydra for example --
22:47
but they do it by not having a nervous system --
22:49
and not having any tissues in fact that rely for their function
22:51
on very long-lived cells.