Instant Genius - What happens in our bodies as we age? And is it possible to turn back the clock?

Episode Date: March 29, 2024

Be it biology, psychology or philosophy, ageing and death are undoubtedly two of the most difficult concepts to tackle in any field of research, so where do we even begin? In this episode I speak to Prof Sir Venki Ramakrishnan, a researcher based at Cambridge University’s MRC Laboratory of Molecular Biology, a former president of the Royal Society and recipient of the 2009 Nobel Prize in Chemistry. We talk about the fascinating discoveries he outlines in his latest book Why We Die: The New Science of Ageing and the Quest for Immortality. Learn more about your ad choices. Visit podcastchoices.com/adchoices

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master class in podcast form. Each week you'll hear world leading experts and scientists talking about the most fascinating ideas in science and technology today. I'm Jason Gugent. I'm Jason Gugendez. Commissioner, Commissioner, a BBC Science Focus. Be it biology, psychology, or philosophy, aging and death are undoubtedly two of the most difficult concepts to tackle in any field of research. So where do we even begin? In this episode, I speak to Professor Sir Benkei Ramakrishnan, a researcher based at Cambridge University's MRC,

Laboratory of Molecular Biology, a former president of the Royal Society, and recipient of the 2009 Nobel Prize in Chemistry. We talk about the fascinating discoveries he outlines in his latest book, Why We Die, the new science of aging and the quest for immortality. Okay, so first off, let's introduce you to our listeners. You've had quite an illustrious career. So could you briefly sum that up for us, please?

My name's Venki Ramakrishnan. I am a molecular biologist who works in the MRC laboratory of molecular biology in Cambridge, England. and I'm best known for my work on the ribosome, which is this large molecular complex that takes our genetic information and uses that information to make proteins. So that's what I'm mostly known for, and that's the subject of my own research. And I was also president of the Royal Society between 2015 and 2020. Great. So let's get on to the meat of our conversation then. So you're here today to talk about your book, Why We Die. So this is obviously a huge topic. So the obvious question is, what led you to tackle this?

Well, several things. First of all, the field I work in, which is how proteins are made, is a fundamental process in biology and impinges on almost every biological process, including, aging. And at the same time, the aging field was exploding, partly because all developed countries are facing an aging population. And so there is an imperative to figure out how we can age more healthily and be more productive for longer in our lives. And this has created a huge amount of research investment. It's also created a lot of private investment. Now, at the same time, because it is such a personal thing. All of us, at some level, we don't like the idea of getting old, and certainly we don't like the idea of dying. And because of that, there's a huge amount of hype in the field. So I wanted to take a sort of objective look at what is the biology of aging,

what has been the progress in the last, say, few decades, and what can we do about it? What are the most promising ways to tackle aging and try to sort of give the reader the tools to understand the basis of aging and also how to evaluate new discoveries and new claims as they come along. Speaking from a purely scientific standpoint then, what can we say about the existence of death? I mean, not by accidental disease, etc., but by aging. Why do organisms age at all? That's an interesting question. So, of course, the answer to any biological question that begins with why is because evolution

made it that way. And it's no different for aging. So when we look at life, we see species that live for a few days or a few weeks, and other species live for hundreds of years. So on one extreme, you have insects and butterflies and so on. the other extreme, you have certain species of shark or whales or large tortoises that can live several hundred years. And this gives the impression that aging is programmed, that each species has a certain program built into it that determines its lifespan. In fact, that's not the

case. Rather, aging occurs because it's an evolutionary compromise. to optimize our fitness. So first of all, what do I mean by fitness? Fitness is the ability to mature and pass on our genes. That's really what evolution selects for. And that involves a series of compromises. So let me give you an example. In mammals, lifespan is roughly related to size. So, for example, rats or mice live much shorter lives than whales or elephants and other large species. And this is because it makes no sense for biology to invest a lot of resources into preventing aging if the species is going to be eaten by predators or starve to death or die in any number of other ways. So it would rather spend resources to mature quickly and produce lots of offspring quickly

to ensure the maximum chance for passing on its genes. On the other hand, if you're a large animal, you don't have predators, maybe you have a slow metabolism, you can live quite a long time. And the longer you live, the more likely you'll have to produce more offspring. And so it's because of this trade-off between spending resources to maintain the organism so it doesn't die versus spending resources on things that allow it to mature and produce offspring. That's the trade-off that has been worked out for each species. So the optimum will be different for different species.

And that's why we have this range of lifespins, and that's also why we die. evolution doesn't care about constantly having to correct all the accumulated defects that lead to aging and death, as long as you've lived long enough to survive and pass on your genes. So let's have a look into that idea then. So in the book, you break down in the sort of different processes that occur within an organism as it ages. And you talk about an organism having something you call a master controller. Yes. So what is this? And what role does that? that play in aging and ultimately in death? So I think the master controller is just a term I used. It's a catchy phrase. It's slightly misleading because it refers to DNA. And I don't want to give the

impression that everything we do and experience is completely controlled by our genes. In practice, it's always a mixture of genetics and environment. But fundamentally, our biological progress, program is really specified by our genes. And that's why we're different from chimpanzees and different from butterflies, for example. So our genes reside on DNA. And that's what determines the program. Now, if you damage DNA or if you modify it, then, of course, you're disrupting the program of life that's specified in our genes. And DNA gets damaged all the time, and these damages are constantly being repaired. But of course, occasionally damage escapes the repair machinery and persists. And so as we age, we accumulate damage to our machinery. The other is that when the cell senses

certain kinds of damage or too much damage, then it triggers a DNA repair resource. response, a DNA damage response. And that response itself can sometimes be the cause of aging. It's often the cause of aging. So that's what I mean by the master controller being one of the primary drivers of aging. So let's have a look at a little bit more deeply into DNA then. So one property of DNA is its ability to replicate. Yes. So what role does that play in all of this? You can think of DNA as a long set of instructions. So think of it as a complicated set of sentences that all follow one another. Now, if you start corrupting that text, then the meaning of those sentences will change. Sometimes it'll become nonsensical. Sometimes it could even mean the opposite of what it originally

intended. And so that's the analogy I like to think of. So when you have errors in your DNA, it's as if you're scrambling the text that specifies the program. And those damages occur for all sorts of reasons. They occur due to chemical environmental causes like carcinogens, chemical mutagens, radiation can cause changes in our DNA. But they also occur in the natural course of things. This is a discovery for which Thomas Lindahl, who's a world expert on DNA repair,

should get a lot of the credit because he showed that DNA actually accumulates damage even in normal aqueous environments, just sitting around that accumulates damage. And of course, because of that, the cell has evolved all sorts of repair machinaries, which check the DNA, and every time it senses damage, it repairs it.

Without that repair machinery, we simply wouldn't be alive as complex. complex beings. And in fact, every species from bacteria all the way to humans have very elaborate DNA repair machinery. Nevertheless, as I said, when the repair machinery cannot keep up, then you get an accumulation of damage. You also get sensing of damage, which can either tell the cell to commit suicide, or it can send the cell into a state called senescence, where it stops dividing, but it doesn't just stop dividing. It also starts secreting inflammatory molecules.

And there's a reason for that, because often damage occurs under stress or in wounds where the organism wants to signal that there's something wrong there and bring in other cells to repair things. So for all these reasons, DNA damage leads to symptoms of aging. There's a moment when you start to wonder,

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This podcast is sponsored by Nguyen, Name, Audio and Focal. With over 100 years of combined expertise, Name and Focal have been bringing music to listeners just as the artist intended. Since day one, this mantra has shaped every innovation in high-fi design, technology and acoustic engineering, balancing craftsmanship and tradition with pioneering thinking.

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lifespans of different animals earlier. So how about human lifespans? How have they changed over the years? That's very interesting. So a few hundred years ago, in fact, all the way up to perhaps 150 years ago, our average lifespan was only about 35 or 40 years of age. That's how long an average person could expect to live at birth. So what has changed? Now we're almost double that. Life expectancy in the West is in the 80s. Until recently, it was climbing, although it seems to have plateaued out in several countries. Now, the main reason for that is dramatically reducing infant mortality. And that's because of better sanitation, prevention of infectious disease, better treatment for infectious disease, vaccination, better nutrition. All of these things helped prevent. infant mortality. At the high end, there wasn't quite as much change, but there was some change. For example, because we're treating things like cardiovascular disease and cancer and diabetes,

much better than we used to, we have extended life a little bit at the other end as well. But even in earlier days, people did live very long lives, except there were very few of them. And so people might argue that although we've increased our average lifespan, our maximum lifespan, which is the maximum number of years a human could live, has probably not changed. And the record right now is held by a French woman, Jean Calmond, who died at the age of 122. But I should point out that no one in a verifiable manner has lived to be beyond 120, nobody else. And so there is a feeling that given our natural biology, our maximum lifespan is about 120 years. So what are the processes that could perhaps create that limit?

Well, as I said, it's evolution optimizing the aging of each species to maximize fitness. So given our built-in mechanisms for repair, mechanisms for dealing, dealing with senescent cells and all the various other causes of aging that I've described in the book, our bodies are such that by the time we reach 110, 115, really we're near the very end, and we become frail and things start breaking down and we die. Now, this isn't to mean that we couldn't, in principle, try to alter those natural processes and try to extend that. that limit. And that is what some people in the aging field believe is possible. I think it is theoretically possible, but I think it's extremely difficult. So what are some ideas about how we'd

go about that? Well, there's several ideas for tackling aging, and I'll give you a few of them. So one of the main ideas behind tackling aging comes from studies on caloric restriction. This is the finding that if you reduce the number of calories that animals eat to a bare minimum, so you're giving them just enough food to survive so that they don't become malnourished. You're giving them all the essential nutrients and just enough calories to survive. It turns out those animals, many different species, live longer than animals which have an all-you-can-eat-a-all-you-can-eat. That is, they're allowed to eat as much as they want and whenever they want. Now, this has led to the idea that caloric restriction can extend lifespan.

But I should point out, there are people who would take issue with that, because they're comparing a calorically restricted animal with an all-you-can-eat animal. That is perhaps not the best comparison, because it would be like comparing a human who's very abstemious with another human who's constantly gorging on a human. an all-you-can-eat buffet. So I think one has to be careful because some people might say all it shows is that an all-you-can-eat diet is detrimental. But nevertheless, it does show a relationship between calorie intake and health and later life. And people have uncovered pathways that are

influenced by caloric restriction. One famous pathway is called a Tor pathway, which affects a number of metabolic processes, and there are inhibitors of the Tor pathway. One of them is called rapamycin. And in animal studies, rapamycin, even when given relatively late in the life of the animal, has improved its health and prolonged its life somewhat. And so people are wondering whether rapamycin or its analogs would be a way to tackle aging. Now, of course, rapamycin is not without its problems because it's an immunosuppressant and it makes you more prone to infections. It makes it more difficult for you to heal wounds. So there are a number of side effects to rapamycin. It's not clear that giving an immunosuppressant, it's one thing if you have your transplant patient and you need

that immunosuppressant. It's another thing if you're perfectly healthy and you want to take this over the long term just in order to live healthier and for a longer time. And so all these safety issues are an issue. And the question is whether you can give rapamycin at a low enough dose to see the benefits, but without seeing the unwanted side effects. And one interesting study I should point out is one organized in the U.S. on dogs, on domestic dogs. And this is where they're doing a trial, control trial of rapamycin given to large dogs. And the advantage of dogs is they're not in a sterile laboratory environment. In fact, their environment is as varied as that of their owners in terms of diet, environment, and all sorts of things. So this could tell us something. But another caution,

I would say, is that often studies in animals don't directly translate to humans. And so I think the dog study will be interesting, but it'll only be a starting point. And that's only if it's promising. So that's one aspect. Another idea is that as we age, many of our cells go into senescence. This is because of many reasons. Occasionally, it's because if our DNA has sufficient damage, the cell will often send it into the senescent state. Another is over the natural course of life, our chromosomes tend to shorten gradually because of this problem of not being able to reproduce, replicate the very ends of the chromosomes. And that's the problem called telomere shortening. And that also can lead to senescence.

But in any case, we accumulate senescent cells as we age. Now, senescent cells don't just sit there and do nothing. They actually secrete inflammatory molecules, which originally had a purpose. but when you have lots of senescent cells, create a problem of general systemic inflammation, which is one of the causes of aging and one of the symptoms of aging. And so people have asked if they can target specifically senescent cells for destruction. And this has led to some very promising results, again, in mice, where mice whose senescent cells were preferentially destroyed actually seemed to have recovered from many of the symptoms of aging.

So that's another approach. A third approach, which comes from a very slightly bizarre set of studies where a young mouse was connected to an old mouse so that they shared their blood, they shared their circulatory system. And what they found is that the blood from the young mouse made the older mouse healthier in some sense it rejuvenated it. And in the other flip side of the coin was that the old blood also caused problems to the young mouse.

This means that there are factors in young blood as well as in old blood that needs studying. And so we could ask, what are these factors in young blood that help keep the organism healthy and not so aged? And the flip side is what goes wrong in old blood that causes problems. And scientists are busy trying to isolate factors and then trying to understand what effect they have. Perhaps some of them may be involved in regenerating stem cells. These are cells that are responsible for regenerating all of our tissues. And we lose stem cells as we age. And that stem cell depletion means that we don't regenerate our tissues as well.

It also leads to frailty. it's a major cause of aging. And so ability to regenerate those cells could help. And so maybe there are factors in blood that will help. And the final thing is perhaps the most exciting, but also I would say maybe the most difficult as well. And this is called cellular reprogramming, and it's created a lot of excitement in the field.

And this comes from the fact that Yamanaka, a scientist who was working on this, showed that just three or four factors could make a cell go backwards in development. So what do I mean by that? Well, we all start off as a fertilized egg, but as the egg develops, the cells become more, more specialized. So some cells become skin cells, other become liver cells, other become precursors of our blood cells, and others become neurons, etc. you also need to regenerate many of those tissues. For example, our blood cells need to be constantly regenerated as to our liver and skin cells. And our neurons regenerate much more slowly. So as we age, this becomes a problem because, as I said, we deplete stem cells. So could we perhaps

coax some of those specialized cells to go backwards in development by the introduction of these factors, and then, you know, you'd be able to perhaps restart the process and regenerate these tissues. So that's the promise, and that's the reason for so much excitement. But as always, there are problems. For one thing, these Yamanaka factors, when induced all the way back and allowed the cells to develop, they can cause tumors called teratomas, which are a form of cancer. And we also don't know what the systemic cancer risk is. over the long term. And so I think people are thinking, well, maybe we won't take cells all the way back to what are called pluripotent cells, that is cells which can develop into any kind of tissue.

But we'll take them just a little way back and then turn them off so that we minimize all these risks, and then they'll still be like the precursor for that particular tissue, and then we'll be able to regenerate healthier tissue. And people have tried this, and there are some promising results in mice. But again, you know, mice, first of all, don't live as long. And secondly, we don't know what the consequence of doing this will be over the long term. But if it can be made to work, it's one of the few things that can actually sort of make the clock go backwards. There's certainly big practical difficulties to doing that. So we're talking about cells there and the aging of cells. And we also mentioned that the population as a whole is growing older.

And this has led to an increase in the incidence of cognitive conditions such as Alzheimer's disease. So what's going on there? You know, aging in the brain, what's happening there? So I think a lot of aging diseases are due to our own proteins misbehaving. So when we make our ensemble of proteins, each protein is made, as I'm, mentioned earlier by translating genetic information that codes for that protein. And initially, we have a lot of checks on the proteins we make. We have quality control checks to make sure that the protein is correct, that it's folded properly, that it's functional, et cetera. And we also have mechanisms. So if a protein is misfolded or unfolds later in its lifetime, the cell has ways to

get rid of it. Now, when these systems start breaking down, which is themselves a result of age, then what happens is you get aberrant proteins accumulating in the cell. And these proteins can form tangles. For example, in many dementias, you have different types of tangles. Some of them come from a protein called beta amyloid. Others come from a protein called tau. And both of those are implicated in these diseases of dementia. So it's not entirely clear how the formation of these aggregates or these tangles leads to cell death, but there's no question that they're involved for two reasons. One is mutations in these proteins, which perhaps might cause them to aggregate more easily,

lead to early onset of many of these diseases. So that's one reason we know that. And a second reason comes from the structural work of my colleagues here at the MRC lab of molecular biology like Michelle Goddart and George Sherriss. And what they've found is something that was quite unexpected, which is that these tangles are not random aggregates, but rather the way that these tangles are formed, the interactions that makes these tangles, is very specific. for each disease. So someone having Alzheimer's will have a particular type of tango. Others,

you know, Parkinson's or Picks disease, they'll have different ones. So I think, you know, we're beginning to understand the process. There's a lot of work on understanding how these formation of these aggregates actually leads to disease, whether it's the tangles themselves or the cells response to the tangles. But nevertheless, we're trying to get a handle on, we, meaning the science community, is trying to get a handle on that. And so there isn't much you can do about Alzheimer's today, unfortunately. There have been some studies of antibodies to these tangles showing a very modest effect. And if it weren't such a dire field, there wouldn't be that much excitement about such a modest effect. But the very fact that we have something at all is what

created a lot of news reports about those discoveries. But I think today we really don't have a real cure. And as you mentioned, the brain doesn't regenerate very much. I mean, most of our neurons, the ones we're born with, there is some, unlike what people thought earlier, we do regenerate some neurons, but it's at a very slow rate compared to, say, skin or blood. And so it's very hard to know how to deal with this problem. It's also hard to get things into the brain because of the blood brain barrier. So, you know, getting drugs into the brain or especially getting large molecules into the brain is also problematic. So I would say that this is a very difficult problem and it's going to be an increasingly worrying problem because as we try to

alleviate all the other causes of aging, as we grow older, one of the paradoxes, that as we live longer, we're increasing our chances of getting dementia in our old age. And, you know, it's already the UK's largest cause of death. I believe it overtook the others recently. And it's only going to get worse unless we figure out how to solve it. So we've talked about the aging population there. And sort of coming alongside this is an increase in the number of centenarians. So what do we know about centenarians? Do they have any common characteristics that contribute to their longevity? So somebody named Tom Pearls, who's in Boston and runs the New England Centinarian

study, has done quite a bit of work on Centenarians. So he's a physician scientist, so he actually sees them as a doctor, but he also studies them. And he has tried to understand what these people have in common. And of course, he's also busy trying to sequence their genomes, to see them. if they have any genetics in common and so on. And only a limited amount of genetic information has emerged. And it's hard to imagine what is common about their lifestyle.

Of course, you know, many of them have some things in common. And in fact, there's a website called Livingto100.com that he's got, which you can go to and you can enter all sorts of information about your life. And it'll sort of give you an estimate for how long it thinks you have to. live. You should take that with a little grain of salt, although it does tell you something about the factors involved in aging. There are a large number of them, some of which are quite unusual. One factor was flossing your teeth, which I thought wouldn't be a major factor. But anyway, one interesting thing he's told me is that the number of centenarians has been steadily growing

because of advances in health and medicine. So people are living to their 80s longer, so therefore a larger number of them are surviving to beyond 100. But one surprising thing he pointed out to me is that the number of people over 110 is not actually growing much, if at all. And so his feeling is that beyond 110, there's not much we can do. It's down to genetics and our natural sort of biological makeup. The other very interesting thing he found is those people who live to be 105 or 110, were extremely healthy for nearly all their lives.

So unlike most people who by the time they're 60 or 70 start accumulating various ailments, these people were almost entirely healthy until very late in life. And then they had a rapid decline and then eventually died. So, you know, since we're talking about trying to increase the fraction of our lives that's healthy, I think studying these so-called super centenarians might give us some clues about what's going on in order to remain healthy for as long as possible and shorten that period called morbidity. So the idea of shortening that morbid period is called compression of morbidity.

And that's one of the goals of the aging community. So would you say then the key really is not living as long as possible, but remaining healthy for as long as possible. but remaining healthy for as long as possible. I think that's true. However, I also think it's not a straightforward problem. So in the past, every measure that we've done to improve health, for example, tackling diabetes, tackling heart disease with statins or blood pressure medication, every one of those has also extended our overall lives.

It's not that our lifespan stayed fixed and then we would simply have. healthier for a longer fraction. So the slightly worrying thing is that the fraction of our lives that we spend in poor health has not actually gone down. And so the number of years we spend in poor health has actually even gone up slightly as we live longer because of fraction. And it's not surprising. All over the west, you can see it's increasingly full of care homes and where older people need around the clock care. So that's a real problem. And one problem is, if we increased health throughout old age,

the question is, why would we suddenly collapse? You know, so of course these supercentenarians do that, so they might offer some clue. But in general, you know, it's not clear why somebody who's in perfect health should suddenly decline and die, right? So the idea of shortening that period of morbidity, it isn't really clear how you could accomplish that, although that is the goal of the aging research community. So having mentioned those goals then, at the end of the book, you look at some of the possible repercussions that extending lifespans can have. And it raises a lot of questions and even potential problems, the aging workforce, people perhaps having to work longer, widening health inequality, overpopulation, and things like that.

sort of by way of closing, what are your thoughts on the benefits and the drawbacks of living longer? Well, we're all programmed to want to live, and none of us really wants to die. That's how we're programmed to survive. And so if somebody came to you and said, here's a pill that will make you live an extra 10 years in good health, you know, most of us would take it. And I myself take anti-aging medicines every day. I take medicines for my blood pressure and I take a statin for my cholesterol. These are essentially life extension drugs.

They're allowing me to live healthier and longer so that I don't die of a stroke or cardiovascular disease or something. So I think there is a problem there. And as we get older, there are two problems. One is, if these treatments are very expensive, it could really exacerbate inequalities. I want to point out that even today, the richest 10% live over a decade longer than the poorest 10%, even in rich countries, even in a country like the UK, which has a national health service. And if you look at the fraction of life spent healthy, that disparity is even great. which means that the poor not only live shorter lives, but they live a greater fraction of their

lives unhealthy. And so this is a real problem. And now if we have very sophisticated anti-aging solutions, which are expensive, well, guess who's going to benefit first? It's going to be the very wealthy who can afford very fancy treatments. And if it's not the wealthy within a country, it'll be wealthy countries versus poor countries. So both within countries and globally, it has a real potential to exacerbate inequalities. And unlike many other inequalities, this is a perpetuating inequality. If you live longer,

you will accumulate more wealth and you will pass on more wealth to your children. They'll in turn be wealthy. They'll live longer. So you can see how, you know, you could have a divergence of people who are well-off, long-lived, versus, you know, the rest. So I think we need to really be aware of it. I'm not saying aging research is a bad thing. Of course it's not. But I think we need to be aware of how the benefits will be distributed. The other problem is that if you have people living a very long time, then you run the risk of overpopulation because they'll be around longer, you know, and they won't be dying off as fast. And so they'll just stick around while new generations keep being born.

And so you will just get an overpopulation unless you also reduce either the fertility rate or the interval between generations. Now, the interval between generations, there's an upper limit, which is because of menopause. We don't know what to do about menopause. So unless that problem is solved, we can't space out children, much more than we already have. I mean, the average age of first child has steadily climbed in the West. It used to be around 20 or so or even less. And now in the West it's gone up into the, I believe, upper 20s or even around 30. But there's a limit to that. And so you do run the risk of either

overpopulation or the thing is that you stop having very many children or you have long gaps between generations. And what this means is that you'll have a population with a very slow turnover. And I think this could lead to a stagnant society, because society regenerates culturally and intellectually with every generation. New generations bring in fresh ideas. In fact, we're at our most creative when we're young. And so I think this would not be such a great thing for society.

who think that, oh, we'll continue to be creative, even if we're healthy, even if we live very long, I'm afraid it's not clear that'll happen. I think a lot of creativity is because we're facing life fresh for the first time. So things are new. We come to it without biases and from a fresh viewpoint. And so I think there are a number of social issues with extending lifespan that people are not talking about or they haven't really thought through. Thank you for listening to this episode of Instant Genius, brought to you from the team behind BBC Science Focus.

That was Professor Servenki Ramakrishin. To discover more about the topics we've just discussed, check out his latest book, Why We Die, The New Science of Aging and The Quest for Immortality. If you liked what you just heard, please consider subscribing to Instant Genius on your preferred podcast platform. The current issue of BBC Science Focus,

magazine is out now. Pick up a copy wherever you buy your favourite magazines or download a copy on your app store of choice. You can also find us online at sciencefocus.com. This podcast is sponsored by Name, Audio and Focal. The texture and emotional depth of music can be lost through digital sources or poor signal. Name audio believes you can have digital precision with analog warmth. Alongside French acoustic specialist Focal, Name creates high-end audio systems combining innovation with craftsmanship, so you can listen to music, just as the artist intended. Discover more at name audio.com.