Shadowing-Übung: Can We Live Forever? – A Question of Science with Brian Cox - Englisch Sprechen Lernen mit Video

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Hello, I'm Brian Cox, and this is a question of science here at the Francis Crick Institute.

Now, I sat down to write this introduction to the first episode, and there will be at least 12 episodes,

by the way, and I hope many more, and began by listing the subjects we're going to cover.

Why do we age?

What is the state of the art in our understanding and treatment of cancer? should we be worried or excited about AI?

Actually, what is AI?

How do we ensure that in areas that have become contentious, climate science, for example, we use the best scientific advice to address the problem effectively?

And I realise that these are conversations about pretty much everything that affects us today, and everything that will shape our future as individuals,

as a society, and as a civilisation.

So the aim of these podcasts is to talk about everything,

but the twist perhaps unusually is we'll talk about everything with a panel who actually know what they're talking about

and i'd like to say something about why i think discussions like this

so scientists explaining what they do taking questions from everyone are important we live in a society

that is underpinned by science and our understanding of nature

and the technologies that rely on that understanding are becoming ever more powerful.

If access to the ever -growing library of scientific knowledge becomes restricted to fewer and fewer citizens, perhaps because it feels too difficult or too daunting,

then as one of my personal heroes

Carl Sagan once put it,

who makes the decisions about the science and technologies that are going to determine what kind of future our children live in?

It should of course be all of us, but that requires us to have access to that knowledge.

So our goal here is to throw open the doors of the library

and answer as many of your questions as we can about as many subjects as possible.

Now, today we're talking about ageing.

Are we on the brink of an ageing revolution?

Can we turn back time and halt the ravages of old age?

But before we dive into that topic, I'm joined by Sir Paul Nurse, the founding director of the Crick Institutes.

And I wanted to just, Paul, give you a chance to explain why you felt that these podcasts were necessary.

I think it's really important, Brian.

As you said, science is really at the centre of everything, all the problems and all the opportunities that we have as a society.

But we need to be able to discuss those issues in a very honest and straightforward way.

And as you say, based on a proper knowledge base of what needs to be considered.

And sometimes we get a bit gloomy when we talk about science, because we're always looking at what could go wrong,

you know, where might it go?

And these sorts of things sort of drag us down a bit.

I think we need to consider those things. But actually, we should also be optimistic about what science can bring to

society what how can science enhance our lives improve our standards of living

and do all the things that we really care about

so i see it as an optimistic series as well as a knowledgeable series

and this is a leads in beautifully to the subject

because the question we're asking the title of today's podcast is can we live forever

I suppose one of the questions is whether that is an optimistic or a pessimistic thing to do.

The first question, Brian.

Ageing is one of the few things that is a universal experience for all of us.

While some people enjoy relatively good health well into their old age,

others will experience an extended period of uncomfortable decline as they struggle with poor physical health and cognitive health.

What if decline with the growing years isn't inevitable?

So our panel today is made up of scientists who are unravelling the mysteries of ourselves,

exploring the underlying mechanisms behind ageing and developing potential interventions for healthier, long lives.

So is there a maximum age limit for humans?

And as we said, even if we could live for centuries, is that desirable?

What might be the societal and medical implications of living longer?

Joining us to help answer these questions are our panel, and they are.

Hi, my name's Lynne Cox.

I'm a biochamist at the University of Oxford, and I've been working on ageing for the past 29 years,

looking at the basic underlying biology of how we age.

And I'm also running a global programme looking at how to do it better, so -called dynamic resilience.

Well, as you've heard, my name's Paul Nurse, and I'm director of the Francis Crick Institute, in which you are sitting this afternoon.

I know nothing about ageing, so I'm the...

Just here as, well, what should I say exactly?

But I'm going to hopefully ask good questions of our three people who actually do.

I work on what controls the division of a cell from one to two.

In one discussion we'd had about this, Paul said, I'm the intelligent layperson.

I said, yeah, you got the Nobel Prize.

Anyway.

yeah hello everyone i'm linda partridge i'm from the institute of healthy aging at university college london

and unlike lynn i'm not going to tell you how long i've been working in aging research

and i'm interested in interventions so diet drugs and other things

that can compress that period of ill health at the end of life

that brian was talking about that can keep us healthier for longer before we drop off the perch.

Is that a technical answer? And I'm Andrew Steele.

I wrote a book called Ageless, The New Science of Getting Older Without Getting Old.

I actually was a scientist here at the Francis Crick Institute,

but during that time, I discovered that even a lot of scientists don't know that much about the ageing process,

so I decided I needed to go and write a book

and tell as many people as possible about this incredible science in the hope that we can do some more to,

as Linda says, keep people healthier for longer.

And this is our panel.

before we start we've already raised

that question actually about the desirability of living for a very long time

so if i am if we do a show of hands

so if i chose a number out of thin air let's say 200 years

so who would like to live for 200 years raise your hands

if you would it's interesting actually for those listening

it's probably less than half the audience can i add a

supplement to the question who would say they'd like to live to 200

if they were guaranteed good health for that whole time

aha yeah oh there's a lot more people with their hands up there

so that so that's that's interesting

so the the thing is we're i suppose we're imagining that we're living to 200 with the health

outcomes of current 200 year olds

which are not great yeah negative well

i thought we'd start up with a just a top line overview to everyone on the panel um

so the question would be can we

imagine living for a very long time and let me define

that as as i said maybe a couple of hundred years right i'm a little skeptical about

that because our understanding of biology at the moment is no um as humans there are organisms

and andrew will talk about this

that um you've got sharks living in the north seas at 400 years old

so biologically we know

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that you can live to an awful old age um

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i said awful old age it might be a good old age i haven't asked a shark recently

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but um i don't think from what we know about human biology at the moment

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and what we can do with human biology at the moment we could live

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that long what would be the difference between a shark

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and a human being there in in principle

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so the metabolic level well well yeah i think i think the simplest way to try

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and answer this might be rather than in terms of metabolism in terms of statistics so

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if you think about being a human being every one of us in this audience

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we might not all necessarily have

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that much in common we've all got different you know skin colors

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and backgrounds and all kinds of things

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but the one thing I know about every single person in this room is

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that your risk of death doubles every eight years

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that means every year or

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so you're gaining about a 10 % increase in your risk of death

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so I said I'm 39

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that means my risk of death this year is about one in a thousand

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and I quite like those odds because if

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that were to continue for the rest of my life I'd live into my thousand

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and thirties on average but unfortunately if you carry on doubling

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and doubling and doubling that eventually it's an exponential function it gets very big very quickly

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and what that means is that if I'm lucky enough to live into my 90s

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but unlucky enough that we haven't had any medical breakthroughs in

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that intervening time my risk of death every year will be about one in six

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and that's life and death at the roll of a dice

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and so you can look at this as a human

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and think I'm terrified there's this exponential wall of mortality coming to get me

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or you can look at it as I did as a scientist and say you know what is it, what's going on inside our bodies,

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this fundamental ticking clock that means the increasing risk of cancer, of dementia, of heart disease, of all of these things going up with shocking synchronisation.

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And if we could uncover what that metabolomic, what that cellular, what that biological ticking clock is, maybe we could do something about it.

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And to talk briefly about those animals for a minute,

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this idea of a risk of death that changes so substantially with age is not universal in the animal kingdom.

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So there are some animals like tortoises, like salamanders, like certain kinds of fish

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and they have a risk of death that's flat it doesn't depend upon how long ago they were born

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and that means that 150 year old tortoise is basically as sprightly as it was aged 50.

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They seem to age without getting old and

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so maybe we won't be able to live an incredibly long time we don't have enough biology today

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but we could perhaps be a little bit more tortoise.

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And to bring it back to humans and you know what's happening now and in the recent past I don't know.

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Clearly, our lifespan is incredibly malleable.

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There's been a massive increase in life expectancy since the 19th century, two and a half years per decade.

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But the interesting and slightly sad thing is just at the moment, it seems to be slowing down pretty much worldwide.

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It went at a very steady rate for a very long time.

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And then just before the pandemic in Europe, for instance, it's really slowed down.

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And in the UK, it's somewhat, you know, ticked down our life expectancy.

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So in terms of reality on the ground now, I think we need new discoveries before we're thinking about these extraordinary long lives.

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I think there's a lot of questions there that we're going to cover through the scope of this discussion.

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So just as the intelligent layperson,

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this question of is it possible for a human to live to ages 200, let's say.

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Yes, I suspect not.

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If you look at the statistics, if you look, I mean, we've got experts here.

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I think we'd be doing pretty well if we had a healthy age of around 100, maybe a bit more than that.

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I don't know, but I can't see it going beyond.

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So that raises an intriguing question.

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To what extent will science reveal how long any of us or each of us might live?

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Time for our first question.

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Hello, I'm Jodal Sierra de Nacel and my question is this.

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As a Hispanic living in London, I recently did a DNA test, and it came out that I'm, like, from 1 ,100 different genetic backgrounds.

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Are there DNA or other tests that can tell me how long am I going to live?

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I mean, I'm happy to take that one.

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There's a lovely test called Grim Age, which predicts your time of death within four years.

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It's quite accurate.

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It's not the DNA itself.

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It's little chemical flags sitting on the DNA and those flags happen as a consequence of all sorts of life experiences.

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They can change according to what you eat, whether you're exposed to pollution,

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all sorts of different things and they tell genes whether they're switched on and off.

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So that's called the epigenetic clock and that's Steve Horvath's Grimmage clock.

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So we have certain ways of measuring when you're going to die which is sort of a layer above the DNA.

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We've got, I mean, I want to pass this to Linda

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because different parts of you age at different times as you've just shown in your nature paper

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there's some wonderful work that that we've built on recently

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which is going a bit beyond the dna so it expresses rna

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which encodes the proteins which do so much of the work in the body

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and you can measure the proteins

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that are present in the plasma of people you can get a sample

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and simply survey which proteins are there and what state they're in

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so that's the blood for anyone hasn't had a plasma blood the circulation

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and the fantastic finding recently is

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that you can analyze those proteins you can figure out

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which tissue in the body the kidney the lung the heart where did they come from

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and they produce a signature of how fast different organs in your body are aging not just the whole body

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so to the extent that you deviate from the protein pattern and expected for your age, if it's accelerated, then that organ's at risk,

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and you can show that people with that signature are more likely to go on and get the diseases of that organ.

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So people with fast -aging lungs are more likely to end up with respiratory problems and so on, and if there are problems in kidneys,

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it actually knocks on to multiple organs in the body.

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Our next questioner, Caroline Stanton, has sent her question in,

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and she wants to dig into the whys of ageing research good afternoon my name is caroline stanton

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and this is my question

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what is the research into aging aiming to achieve surely we need to halt the progressive degenerative conditions

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and improve people's quality of life before we extend life thank you

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couldn't agree more exactly i think you'll find universal agreement with

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that on this panel what we're about is trying to keep people healthier for longer

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if it's a side effect of that they live longer well

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and good although an ethical discussion could be had around that

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but the important thing and the thing

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that really people really care about for themselves is their health how much of that so

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that aim depends on us understanding the mechanisms of aging

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you can treat heart disease with heart disease drugs you can treat cancer with anti -cancer agents

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but you're treating a disease that's already there

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and you're treating in essence almost the symptoms of the disease

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if we could actually get in there before these diseases manifested then you will improve people's quality of life

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and these basic biological processes are called hallmarks of aging and linda So.. was on the key paper that changed the field.

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So I think the real breakthrough discovery in recent years has been of these hallmarks of ageing.

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So the fundamental things that happen at the molecular level, what goes wrong with gene expression, what goes wrong in cells,

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how do they lose control of their protein domain, how do they become senescent, I'll come back to that in a minute.

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So stem cells do very strange things during ageing.

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They sometimes differentiate into cells when they shouldn't or fail to renew the tissue when they should.

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Different tissues talk to each other.

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There's a lot going on in the systemic environment.

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So it's a complicated process, but we really understand what its essentials are.

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And many of them can be targeted genetically with mutants or with drugs.

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And what we find is that we can often go for one mechanism of aging,

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but then the organism is protected against multiple things in different tissues

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that go wrong later this is the geroscience idea target one thing often with a single drug

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and you can have a preventative effect on lots of the things

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that happen later and i think that's the approach

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that we would all like to see come in to medicine preventative

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but also the idea

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that you can prevent multiple things simultaneously well i think that's it's a good example isn't it of the

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so the crick institute a multidisciplinary institute institute studying biological sciences at life

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but as we've seen with what we've been discussing that it's

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so complex research into one area can have a profound influence on research in another area

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so is that that's the case

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when we talk about aging we're talking about all of biology essentially yes

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so we don't have a sort of aging initiative

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but what we what we do have is 120 research groups here with no discipline boundaries

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and that is extremely unusual

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so what this means is we mix up different scientists from different disciplines

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and don't have departments that tend to fight with each other for resource and power and money.

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We have a structure, but it is not discipline -based, and that is very unusual.

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Now, for a topic like ageing, as we've just been hearing, which is clearly multidisciplinary, that sort of approach is, I think, important.

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And I wondered if I could extend and ask a question of my experts.

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I think what you're saying is that we have,

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and I'm perhaps oversimplifying this we have a series of different sort of systems let's call them organ systems

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and that there are common reasons for death

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which involve I don't know four five six seven of these

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which are probably aging them each one of them

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and what Linda has just said and what you just said is

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that we can now test which ones and where they've gone

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so is it now possible for us to sort of think about it in terms of these different organ systems

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and targeting each of those in some sort of separate way that we could actually try and combine together

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but at least taking an individual what is the most vulnerable one?

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I think that's going to be the big wave in the next few years is understanding

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if we know we're looking at someone who's got problems with their lungs

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they're aging too fast even though they're completely subclinical at the

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moment what preventative interventions can we do to protect them from

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that vulnerability so

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that their lungs manage to keep up with the rest of

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them can i chip in there with an example very specific example linda's mentioned cell aging um

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it's also known as cell senescence and

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if you think of cancer normal cells in the body go weird they behave badly

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and they cause a disease as we get older our cells

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accumulate damage damage to their dna damage to other parts of them

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and if they're essential to you being you they don't die they hang around

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but they're different so we call them sometimes zombie cells

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and our zombie cells change in really weird ways

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so mine are currently kicking out enzymes that are degrading the collagen the structures

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that support my skin so if you ever look in the mirror

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and see the crow's feet coming on that is your senescent cells accumulating and eating away the tissue structures in you.

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So senescent cells can be quite harmful, and we know that they're harmful in multiple different parts of the body.

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If you inject senescent cells just into the abdomen of a mouse, it gets old across the whole body.

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If your immune system is old, you get old across all your different organs.

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So there's some really cool research now showing that

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if you actually get rid of senescent cells in a middle -aged or even an old mouse that mouse

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shows improvement across multiple domains

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so better cognitive function its brain works better it's stronger

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it has more energy its fur is better its behavior it's less anxious

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and if it gets cancer it has a much better rate of cancer survival

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so removing senescent cells from old mice looks really promising

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and that's now in clinical trials in people

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so for diseases where we know senescent cells are a key

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driver like a geopathic pulmonary fibrosis where your lungs just fill up with senescent cells

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so there are some really exciting developments in the field where we know some of the mechanisms there are drugs

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that can do something about it and they're being tested

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so i i would say optimistically we have therapeutics

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that can get in there that have an early preventative effect across the board

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and i would definitely recommend if you go home and search the internet for pictures of the mice,

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sort of before and after photos with these senolytic drugs.

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I was a computational biologist back when I worked at the Crick, so I didn't deal with mice at all in my day job.

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You do not need to be an expert to see the difference.

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The mice just look younger.

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They look fantastic.

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They should be on the cover of Vogue.

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So, you know, obviously that's a really visually striking thing, but what we know is these hallmarks of ageing,

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not only do they cause the crow's feet around your eyes, not only do they make your hair go grey,

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they're actually causing those same kinds of processes in your arteries and your blood vessels.

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They're causing the risk of cancer to increase

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and those things are much harder to see of course

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but since they're driven by those same hallmarks

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if things look good on the outside they often look better on the inside too

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and that shows that we're keeping those mice healthy

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and really almost every way for longer

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you mentioned removing the senescent cells what do we know about why they become senescent

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or behave like that in the first place well i it's an evolutionary mechanism

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so um most things that happen in biology have either been selected for

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or against over evolutionary time and we need senescent cells so

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when you're young you fall off your bike you cut your knee you have a wound

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and that wound has to signal to the rest of the body look come

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and heal me so it's sending out signals to the immune system to come along

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and remodel the tissue around the wound and fix the wound

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so we know that senescent cells are part of

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that all these nasty chemicals that they're kicking out when we get older are actually beneficial chemicals when you're young.

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So senescent cells are good for wound healing.

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They're also a way of stopping cells from becoming cancerous, which is an incredibly important thing to do.

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And of course, those things are before the evolutionary cutoff.

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Once you've stopped having babies, then you're in the evolutionary shadow.

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And so the selective pressures against accumulation of senescent cells may not happen.

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So these things just build up over time and

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because your immune system gets a bit with age sorry

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that's the technical term your immune system is less good at coming

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and finding the senescent cells and weeding them out you just accumulate with age

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so you get more and more and more of them

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and then they do harm as they accumulate

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and just coming back to the interventions you were asking about you know the anti -senalytic cells

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and so on there are lots of drugs

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that already target the network I've just talked about

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because it's very important in metabolic disease and in cancer

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so there are drugs there already and it turns out that

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if you use these drugs at low doses in animal models mice for instance

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you can actually produce a very broad spectrum improvement in their health during aging the kind of geroscience

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that I was talking about earlier

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but we're facing a real problem in the field there are lots of these drugs out there we know

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or we strongly suspect that

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if we repurpose them to be used at lower doses they would have a great preventative effect on health

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or loss of health in old age in people

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but these are drugs that have been off patent for years

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and you would have to have a completely fresh set of clinical trials

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if you were going to use them preventatively for the diseases

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of old age rather than to treat a disease at the time

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so there's a problem there we really need a lot more public funding coming into looking at these drugs

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and repurposing them I think that's really important the point

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you just said there we keep

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we always think in this context of commercial development of drugs

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commercial development of drugs is driven by profit the health of society in the nation is driven by different things

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and we have to start thinking more about um public private

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partnerships where the public um engagement in these activities is looking

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at the um what is good for society rather than good for the profits of the company absolutely

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i mean the behavior of the farmers is completely understandable

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that you know that's their business model

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but then they're not going to touch these drugs

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because there's absolutely nothing in it for them

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and the business model of the public is completely different yes

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and and likely I mean there are huge inequalities in health during aging

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and these drugs I think are likely to be particularly beneficial to people who are not ageing healthily?

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I think this is something that we could really do well in the UK because of the NHS, because we have this national health system.

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And in fact, the same with the clinical trials we were just talking about.

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There was a fantastic clinical trial in the UK called Recovery, which happened during the pandemic,

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where everyone who went into intensive care for COVID was randomised.

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They were given a different drug at random because we didn't know what was going to work.

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And we could do this with these so -called geroprotective, these sort of real anti -ageing drugs.

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It could be that every time you go into your GP, if you're over the age of 60 or 65,

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a little light flashes up on their computer

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and they say would you like to be involved in this trial

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and they might randomize you to one of these drugs

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that we think has an anti -aging effect and we can see

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if people do stay healthier for longer as a result

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and this is something there's a drug called metformin

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which is often spoken about it's a diabetes drug

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there are probably a lot of you in the audience taking this

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because it's the first line therapy for diabetes

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and there are some indications

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it might slow down the aging process the problem is just as linda said

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it's out of patent i think the nhs can get it for a few pence per pill

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so no one's going to make a huge amount of money

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if this trial turns out to be successful but

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that means the nhs is in a fantastic position to hand out

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this incredibly cheap medication to a large number of people

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and potentially save the health system a huge amount of money okay

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i like this next question it is a bit left field

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but let's see what our panel thinks hello i'm akima fashion you

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and my question is could the age regression ability of the immortal jellyfish be adapted for humans to achieve a similar effect.

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Thank you.

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Someone describe the immortal jellyfish.

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The immortal jellyfish.

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Well, this jellyfish is not technically immortal.

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It can still get eaten.

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It can still get a disease, but it's what we call biologically immortal.

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And that is this property that I talked about earlier, where you have a risk of death that doesn't change depending on how old you are.

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But the way this jellyfish does it is really unusual.

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It starts out as what's called a polyp.

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That's how all jellyfish start their lives.

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And then it grows up into an adult jellyfish.

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That's the thing with the stingers on

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that you know undoubtedly you've dodged at the beach at some point

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and if it finds itself in a stressful situation it can turn back the biological clock it can revert to

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that early polyp stage now we wouldn't want to do this directly for humans

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because what that would mean is you turn all of your cells back into being stem cells

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and then you'd re -differentiate with any luck back into an adult

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and that would mean your brain would turn into a stem cell based mush

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and everything that was important about your personality would disappear during this process

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so that's not a great idea but we can do this in the lab

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if we're a little bit more subtle about how we do it.

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So back in 2007, 2006 I think actually, a guy called Shinya Yamanaka and his team identified a series of genes

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which are now called the Yamanaka factors that can turn back the clock inside cells.

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And if we put these genes into mice, if we leave them turned on permanently, it's very bad news for the mice.

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They get a lot of these stem cells.

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Stem cells are very powerful in terms of being able to become any cell in the body,

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but they're very, very bad at being a liver cell and detoxifying your blood or being a heart cell and beating.

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And so what that means is if these genes are constantly active, the mice die of organ failure, very sadly.

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But they found that if they give these genes in a special form where they can be activated with a drug,

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and they turned on these genes effectively at weekends, they turned them on two days a week and then five days off,

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they found that they could rejuvenate the cells in the mice and keep them healthier,

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but without having them turning all back into stem cells and losing their cell identity.

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And actually, this is one of the hottest areas of aging biology at the moment.

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Some of you might have heard of Altos Labs, which is a $3 billion quote -unquote startup.

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I'm not sure with that kind of endowment, you can call it a start -up, but it's backed by a number of people,

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including Jeff Bezos, obviously the guy who founded Amazon.

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And hopefully $3 billion is enough to have a serious go at turning this from something

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which works in mice in the lab to something that maybe we could use to treat diseases in people.

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Could I ask a question to the panel based on the jellyfish?

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What are the good models for looking at ageing and why?

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Well, I think currently we're very limited in the way

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that we use models in science like it's exactly the same as the models

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that you know colleagues in any part of biology would use it's yeast it's worms it's flies it's mice

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but the problem with a lot of these species is they're very short -lived

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but there's another animal about the same size as a mouse

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called a naked mole rat looks a bit like a penis with teeth they're not the most beautiful creatures

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but these animals they're the same size as a mouse

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but they can live up to 30 years old

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and they seem to be essentially immune to a lot of age -related diseases

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they have very low rates of cancer very low rates of neurodegeneration

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and so maybe as a field we should be turning our attention to some of these incredibly long -lived species

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that live a really long time for their age finding out what naked mole rats have

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that mice don't and whether we can bottle that

425

and give it to human beings and the bowhead whale

426

so there's there's some people doing comparative evolutionary biology looking at animals

427

that live a long time and looking at their genes and

428

which genes they have either more copies of or switched on more highly

429

and there's one particular gene called cert 6

430

which is a dna repair gene that is um at high levels in animals

431

that live an awful long time and then you take it back to humans

432

and you look at centenarians and we've all got this gene called cert 6

433

but centenarians have five different letters in the alphabet of

434

that gene and

435

if you make a copy of the gene with those five differences the centenarian version it's much much better at repairing DNA,

436

then genes that most of us have got.

437

So we can learn from super long -lived animals, we can learn from super long -lived people and we can actually make a difference.

438

We can understand the biology by starting to turn these clocks back.

439

The next question turns to lifestyle choices in shaping human ageing.

440

Hello, my name is Anjna Ketuchakaria and my question is,

441

what is special about people who live long lives is there a link between diet

442

and long life and is it true that there is evidence

443

that fasting can extend your life thank you yeah well can i kick start

444

that with some studies on centenarians in japan um they we're not just human

445

and people tend to forget that that we are made of human cells

446

but we're also colonized by billions of bacteria and viruses

447

and fungi that live in us and on us

448

and the Japanese team were looking at the microbiome in the gut

449

so all the bacteria that live in the gut and they showed that super centenarians people over 110 115

450

had a different composition of bacteria in their gut

451

so they had all the normal bugs that we've got

452

but some other ones as well

453

and then they narrowed it down to a couple of species of bacteria

454

that were making a chemical it's it's called a bile acid

455

but it makes a chemical in the gut that kills off harmful bacteria

456

so you can take that chemical

457

and you can put it on nasty disease causing bacteria like c difficile it kills them

458

so these people are actually making their own antibiotics in their gut

459

which is a phenomenal finding and that microbiome is japanese specific

460

and of course people in japan tend to have an incredibly healthy diet i felt like i was on detox

461

when i went over there i felt just

462

so much more alive um natto fermented soybean has components in something called spermidine

463

which is actually we know triggers a process of waste removal within the body autophagy

464

so what they're eating is very good for them

465

and it also supports a very healthy microbiome i think we can also learn a lot from just you know straightforward

466

inequalities in life expectancy in different social contexts so within the uk

467

if you just look even over quite short distances between different parts of cities

468

you can get a 10 year difference in life expectancy

469

and it's really tied up with socioeconomic factors so

470

if I was going to advise people on the one thing

471

that's really important to be healthy during aging it would be exercise

472

but you need to have the kind of lifestyle where you can factor in the time

473

and the opportunity to get exercise healthy diet also very important

474

but again eating healthily is actually more expensive than eating unhealthily

475

so i think we need to tackle these basic socioeconomic things almost first i mean super centenarians are very interesting

476

but there's something much more important straight in front of us

477

that we need to deal with but the diet

478

and the fasting was raised as well yes

479

and um we know it comes up a lot doesn't it yeah intermittent fasting

480

or lowering your calorie intake and these ideas i mean from the 1930s we knew that

481

if you gave rats 30 less food than they would normally choose to eat then they lived a lot longer and

482

so caloric restriction has been shown to be true in all species

483

that's being looked at were they happy were they happy

484

well as linda will tell you you can have dietary restriction without malnutrition

485

there is a running joke in aging biology

486

that maybe uh fasting won't make you live longer

487

but it'll certainly feel like so we know that caloric restriction can work

488

and we know that intermittent fasting can work i have one caveat with

489

that that a lot of people are saying oh just fast

490

the studies in mice have shown that if you're young

491

and middle age fasting can actually increase your life expectancy

492

if you're old it can increase your risk of mortality old people are very vulnerable to any changes

493

and it can just push them over

494

that edge of not being able to cope metabolically

495

so linda's done a lot of work on dietary restriction

496

which linda's described the whole thing brilliantly

497

but the other thing about older people is

498

that they probably need a higher protein diet it's not just the amount they eat

499

but what they eat so sarcopenia you know muscle wasting is a real problem in older people

500

and to some extent it can be combated by increasing the amount of protein in the diet

501

so there are composition issues as well as and also

502

when you eat is very important there have been some very nice studies in mice now that they've developed automatic feeders,

503

showing that they're much healthier if they're doing the eating that they do.

504

during the wake period

505

if you feed them during their night period they develop really bad metabolic problems they haven't looked at lifespan

506

but it's clear from the metabolic changes that it would probably be shortened

507

and that may be one of the reasons

508

that shift work in humans is associated with ill health

509

it's partly eating during what should be the rest period the night period right

510

so if we imagine

511

that we do all live longer lives our next questioner wants to know about the societal implications of

512

that hello i'm richard goody and my question is what are the societal impacts

513

that the panel envisage

514

we would need to tackle arising from an increasing population of super elderly thank you who would like to take

515

that i can start you look at japan

516

and 30 of the population already are over the age of 65

517

and they're having major problems with the dependency ratio

518

so the number of people in work who are earning money to pay for

519

and look after the people who are over 65 generally in poor health who need looking after

520

so they're developing robotics to change people's adult nappies

521

they are doing all sorts of things there aren't enough young people to look after the older people

522

and this is a major major problem in intergenerational fairness

523

i struggle with looking at societies where all of us are getting old

524

and we're expecting fewer

525

and fewer young people to just keep working for longer to keep us in our pensions

526

and our health care so the only way to tackle

527

that really is to keep people healthy

528

and economically active until a lot longer we're going to restructure society

529

because it's not tenable the way we're doing it at the moment it's interesting isn't it

530

because i think many of us think

531

when we say we'd to live longer healthier lives you think longer retirement

532

but what you're essentially saying there is that does not follow

533

but retirement isn't necessarily good for you

534

because there are a lot of studies suggesting

535

that as soon as people hit retirement their health deteriorates

536

and the sense of purpose is one of the things

537

that keeps people healthy the psychoneuromology there's a lot of being positive

538

and optimistic and knowing that you're doing something useful that keeps you going.

539

The original idea behind retirement, I think it was Bismarck first introduced them,

540

was that they were really a safety net for people who'd had industrial injuries

541

or were in bad shape after a lifetime of manual work.

542

And the vast majority of people never live long enough to collect a pension.

543

So this idea of a long retirement is very much a modern thing.

544

I think the other point is

545

that the dependency ratio also depends very much on fertility rates

546

so things are really bad in the far east at the moment

547

because fertility is also so low actually if the whole thing equilibrates

548

so the population is a replacement

549

but with everybody living longer than they do at the moment the problem would be a lot less acute

550

so it's a complicated issue actually

551

because i mean um the uh the natural um consequence of this is

552

that we retire at older ages

553

but then we have to consider what we're capable of doing at the older ages

554

and you know we're sitting here with sort of white collar jobs

555

and it really could be quite different

556

if you're digging in the road to have a certain age sounds very sensible and fair but actually it probably isn't

557

We do have a question actually from the audience that feeds into what you said about extending your healthy lifespan

558

Hi, my name is Andrea Giusti, and my question is, what are three to five things humans can do to help increase our health span?

559

Three to five.

560

Well, we've touched on a few of them.

561

So, decent diet.

562

So, particularly plant -based diets are looking extremely important because they support a healthy microbiome.

563

Exercise, as Linda has pointed out, there's some really beautiful data about what exercise does to us.

564

So there's a study in London and Birmingham looking at super cyclists, so people who are on their bikes cycling over 100 miles a week.

565

And their levels of inflammation, nasty chemicals floating around in your blood, are way lower.

566

So these are people in their 70s or 80s.

567

Their inflammatory levels are down what you would expect for a normal 40 -year -old.

568

So the exercise is damping down all the nasties, keeping you healthy

569

so exercise is helping you metabolically it's preventing inflammation

570

which can can drive all sorts of damage to your tissues

571

and organs so diet exercise sleep and that's something

572

that we're really bad at in the west we don't get enough

573

it's not just enough sleep it's the right sleep and as linda has pointed out the social inequalities

574

Don't live somewhere that's got loads of pollution.

575

Don't live somewhere where you're so stressed to walk on the streets.

576

Don't live in somewhere where you experience racism.

577

There's one really shocking study from King's College London

578

that black women who experience racism during pregnancy give birth to children with short telomeres.

579

Now, your telomeres tell yourselves how old they are.

580

So these babies who are born to mothers who experience racism are actually older than they should be.

581

Now, that's incredibly shocking that those psychosocial things impact our rate of ageing.

582

So one final thing on that, optimism.

583

Andrew is optimistic.

584

Beautiful study of nuns entering a convent.

585

They live the same lives.

586

They have the same amount of exercise, same diet, same amount of sleep.

587

All those things are controlled.

588

But what's not controlled is their personality before they went in

589

and the ones who wrote letters home who are optimistic lived

590

on average 10 years longer than the ones who are pessimistic

591

so those would be my points can i give what i

592

think is the single most important piece of unconventional health advice

593

because i suspect a lot of people know they should diet exercise

594

and sleep and if you're already trying to do most of the right things

595

and fortunate enough to live in a nice neighborhood the single most important thing

596

you can do not just for your health

597

but for the health of everyone around the world is to campaign for more funding for aging biology research

598

because and bear in mind i'm not a scientist i'm not getting these grants

599

because what that means is we can develop some of these treatments

600

that will help people even if they are living in poor neighborhoods even

601

if they don't have time for exercise to stay healthy for longer

602

so i think getting people's attention spreading the word about this science getting politicians to know

603

that you know

604

if they invest in aging biology

605

you will vote for them could be the single best thing you can do for your health

606

so we have a question actually which was from from the audience from sally horton

607

which feeds into what we've been talking about which is

608

which has more impact on aging genetics or environment

609

or is it a complex interaction between the two i i think the answer to

610

that is pretty clear actually it's much more environment it's interesting

611

because it varies by age doesn't it yes once you're a hundred then genetics becomes more important exactly

612

but up till that point for the vast majority of ill health and death

613

You're looking at environmental factors, lifestyle factors, what you're exposed to.

614

It goes back to what you mentioned earlier, Linda, about the fact that it may be it's

615

socioeconomic interventions that may have as big an effect as generating new knowledge on the biology.

616

Well, it's a big public health issue.

617

Can I make the case for biology in the Francis Crick Institute of Biology?

618

I think the reason that I'm really so excited about the medicine is because public health is really, really hard.

619

And I don't think we should give up on public health.

620

I think it's super important.

621

But I've got a three -month -old baby at home.

622

I know I need to exercise.

623

I just don't have any time.

624

And I know that a lot of people are in the same position.

625

And if I had some drug, I'm not saying to replace exercise,

626

but to help me keep my health good at a time when I'm finding it really, really hard, I think that would be hugely beneficial.

627

I think there are so many people around society in that position.

628

They're trying to earn a living, trying to make their rent, trying to cook food for their three kids.

629

People need help with some of this public health stuff.

630

And we should be doing that at the same time

631

but i think

632

if we could develop some of these medicines

633

it would be a really good adjunct to support those public health measures

634

i say we need different interventions across the life course

635

we need the biomedical interventions right now for the people suffering age -related diseases

636

we need those preventative interventions for the people in their 40s

637

and 50s at high risk of getting them

638

but we also need the socio -economic stuff that's going to prevent any of those risk factors occurring

639

so i think we need a completely holistic approach across society

640

and public health definitely early on

641

and we've shown the doubling in life expectancy over the past hundred years has been soap

642

and sanitation that's public and vaccination uh public health interventions

643

that really really work but those were the low hanging fruit

644

and now we've got to be a bit more creative about those interventions

645

so i think just if i was actually to summarize i mean it seems to me

646

that this the aging we've chosen something that cuts across everything it's about fundamental biology it's about health,

647

it's about economics, it's about society as a whole.

648

So it's probably the most complex subject we could have chosen.

649

Well, thank you very much.

650

That is all we've got time for today.

651

So thank you all to our wonderful panel.

652

Professor Lynn Cox, Professor Sir Paul Nurse, Professor Dame Linda Partridge, and Dr Andrew Steele.

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Wortschatz und Sprechhinweise zu dieser Lektion

Diese Sprechübung basiert auf dem Video „Can We Live Forever? – A Question of Science with Brian Cox“. Dieses Video enthält 475 Sätze und 8246 Wörter zum Nachsprechen. Der gesprochene Teil dauert 44:28. Der Sprecher spricht schnell, etwa 185 Wörter pro Minute – rechne mit verbundenen und verkürzten Lauten. 84 % der Wörter gehören zu den 3.000 häufigsten im Englischen; den Rest solltest du dir vor dem Üben ansehen.

Wichtiger Wortschatz in diesem Video

15 lernenswerte Wörter aus dem Video, mit Aussprache und Bedeutung:

Wort	Aussprache	Bedeutung
mouse Substantiv	/maʊs/	Maus, Muus
biology Substantiv	/baɪˈɑ.lə.d͡ʒi/	Biologie
gene Substantiv	/d͡ʒiːn/	Gen
intervention Substantiv	/ɪntɚˈvɛnʃən/	Intervention, Eingriff
organ Substantiv	/ˈɔːɡən/	Organ
incredibly Adverb	/ɪŋˈkɹɛdɪbli/	unglaublich
tissue Substantiv	/ˈtɪʃ.(j)u/	Gewebe
immortal Adjektiv	/ɪˈmɔɹtəl/	unsterblich
clock Substantiv	/klɑk/	Tacho, Tachometer
stem Substantiv	/stɛm/	Geschlecht, Stamm
optimistic Adjektiv	/ˌɒptɪˈmɪstɪk/	optimistisch
mechanism Substantiv	/ˈmɛk.ə.nɪ.zəm/	Mechanismus
immune Adjektiv	/ɪˈmjuːn/	immun
evolutionary Adjektiv	/ˌiː.vəˈluː.ʃən.ɛɹ.i/	evolutionär
biological Adjektiv	/ˌbaɪ.əˈlɑ.d͡ʒɪ.kəl/	biologisch

Phrasal Verbs, die du hören wirst

Wort	Aussprache	Bedeutung
slow down Verb		verlangsamen
kick out Verb		rauswerfen, rausschmeißen
point out Verb		hinweisen
come along Verb		mitgehen
come out Verb	/ˌkʌm ˈaʊt/	herauskommen
come up Verb		erscheinen
drop off Verb		wegtreten, wegdämmern
eat away Verb	/it‿əˈweɪ/	aufzehren, fressen

Sätze zum Wiederholen

Kurze, vollständige Sätze aus dem Video, die du im Alltag wiederverwenden kannst:

Why do we age?
Are we on the brink of an ageing revolution?
Can we turn back time and halt the ravages of old age?
What if decline with the growing years isn't inevitable?
I haven't asked a shark recently.

Grammatik in diesem Video

Die Strukturen, die der Sprecher am häufigsten verwendet, mit den genauen Worten aus dem Video:

Struktur	Im Video
Present Perfect Continuous have/has been + -ing – eine Handlung, die früher begann und noch andauert	I've been working · we've been discussing · we've just been hearing
Present Perfect have/has + Partizip Perfekt – eine vergangene Handlung, die jetzt noch wichtig ist	have become · you've heard · we've already raised
Passiv be + Partizip Perfekt – wichtig ist, was geschieht, nicht wer es tut	is underpinned · be considered · is made
Relativsätze who / which + Satz – eine Zusatzinformation über eine Person oder Sache	people who actually · die which is · hearing, which is

Aussprache, auf die du achten solltest

Der Sprecher verwendet 178 Kurzformen und abgeschwächte Formen, zum Beispiel I'm, they're, we're. Sprich sie in der kurzen Form, so wie du sie hörst.

Die Laute „sh“ und „zh“: intervention /ɪntɚˈvɛnʃən/, tissue /ˈtɪʃ.(j)u/, evolutionary /ˌiː.vəˈluː.ʃən.ɛɹ.i/, restriction /ɹɪˈstɹɪkʃən/, shock /ʃɔk/
Lange Wörter – auf die Betonung achten: biology /baɪˈɑ.lə.d͡ʒi/, intervention /ɪntɚˈvɛnʃən/, incredibly /ɪŋˈkɹɛdɪbli/, optimistic /ˌɒptɪˈmɪstɪk/, mechanism /ˈmɛk.ə.nɪ.zəm/

Laute, die Deutschsprachigen schwerfallen:

/w/ — mit runden Lippen, nicht wie das deutsche „w“ (/v/): inequality /ˌɪn.ɪˈkwɑ.lɪ.ti/, consequence /ˈkɑn.sɪ.kwəns/, straightforward /ˌstɹeɪtˈfɔː(ɹ)wə(ɹ)d/
Stimmhafter Auslaut — /b/, /d/, /g/, /z/, /v/ am Wortende nicht verhärten: extend /ɛkˈstɛnd/, complicated /ˈkɑm.plɪˌkeɪ.tɪd/, naked /ˈneɪkɪd/, diabetes /ˌdaɪəˈbiːtiːz/, cognitive /ˈkɑɡ.nɪ.tɪv/
/æ/ — offener als „ä“: nasty /ˈnæs.ti/, rat /ɹæt/, tackle /ˈtækəl/, vast /væst/, podcast /ˈpɑdˌkæst/

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Höre dir das ganze Video einmal an, ohne zu sprechen, und notiere die Wörter, die du nicht kennst.
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Was ist die Shadowing-Technik?

Shadowing ist eine wissenschaftlich fundierte Sprachlerntechnik, die ursprünglich für die professionelle Dolmetscherausbildung entwickelt und durch den Polyglotten Dr. Alexander Arguelles populär gemacht wurde. Die Methode ist einfach aber wirkungsvoll: Du hörst englisches Audio von Muttersprachlern und wiederholst es sofort laut — wie ein Schatten, der dem Sprecher mit nur 1–2 Sekunden Verzögerung folgt. Anders als passives Hören oder Grammatikübungen zwingt Shadowing dein Gehirn und deine Mundmuskulatur, gleichzeitig echte Sprachmuster zu verarbeiten und zu reproduzieren. Studien zeigen, dass es Aussprachegenauigkeit, Intonation, Rhythmus, verbundene Sprache, Hörverständnis und Sprechflüssigkeit signifikant verbessert — was es zu einer der effektivsten Methoden für die IELTS Speaking-Vorbereitung und reale englische Kommunikation macht.

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Wichtiger Wortschatz in diesem Video

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Sätze zum Wiederholen

Grammatik in diesem Video

Aussprache, auf die du achten solltest

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