Longevity by luck, dementia vaccines and how fame ages you
Professor Brian Cox takes a deeper dive into the science of ageing, answering more of your questions with two returning experts.
How do men and women age differently? Why is it healthy to forget things? What’s the latest research on regenerating old cells?
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More Questions of Science gives you extra episodes that continue the conversations started in A Question of Science.
From his home studio, Professor Brian Cox catches up with expert panellists from earlier in the series. Together, they tackle your follow-up questions, explore new angles and go deeper into the topics that sparked your curiosity.
Brian: Hello and welcome to a bonus episode of A Question of Science, the show where we tackle your questions on everything from climate change to curing cancer with the help of a panel of leading experts. Now, the original debates were recorded in front of an audience at the Francis Crick Institute in London. But this show is a chance to hear some of your feedback and answer some extra questions that we didn't have time for. And today we're returning to the question of whether we can live forever - or to be more specific - how can science and technological advances help us stay healthy for longer?
Joining me are Professor Linda Patridge from the Institute of Healthy Ageing at University College London and Andrew Steele, author of Ageless: The New Science of Getting Older Without Getting Old. Thank you both for coming back.
We learned a lot in the original debate about why we age, and what we can do to stave off diseases that might kill us. And it seems that while our underlying genetics do play a role, our environment is also very important. Things like pollution, smoking, and diet. So, I wanted to expand on this idea a bit with a question from Chris Griffiths who asked, how is it possible that lifelong hell raisers are still going strong in their late seventies and eighties after a lifetime of drinking, smoking, and drug taking, while people who've lived much more sedate and wholesome lives die a lot earlier of natural causes? So, Linda, maybe there's an element of luck to this.
Linda: I think there is, it's a very interesting question. I think it's important to point out straight away that hell raising is generally not advised if you want to lead a long and healthy life. I mean, mostly hell raisers do tend to die young. But the same's true of the general population, there's huge variation in age at death despite rather similar lifestyles.
And there's no indication, I think that, you know, centenarians and super centenarians have particularly healthy lifestyles. Genetics probably plays a role, I think, we don't know how big a one, but you know, maybe 20%, something like that. And it's also become really clear that events very early in life, so even in utero and shortly after birth, that's a very sensitive time in life where minor environmental insults, you know, the nutrition of the mother, accidental traumas of a quite minor kind have very long-term effects. So it's possible that I think that these people with terrible lifestyles who nonetheless live a very long time, were a particularly tough bunch to start with, either for genetic or environmental kinds of reasons.
There's one quote I love, from a baseball player, called Mickey Mantle. He made it to a hundred and said, "If I knew I was going to live this long, I'd have taken better care of myself." So, you know, it's quite a mystery and I think there is an element of luck involved.
Brian: I was wondering, Andrew, whether, Chris is trying to get permission to live a slightly less sedate and wholesome life?
Andrew: Yeah and I'm afraid, I'm gonna back up Linda on this one. Hell raising is not recommended. I looked up, some statistics on this and there has actually been a study on musicians to see how much longer or shorter they live than the general population and the most interesting result, I thought, was that, they compared famous musicians, so musicians that had achieved that sort of rock and roll fame versus less famous people doing the same job.
And what they found was the famous ones lived three or four years less long. Now it's very interesting to speculate as to why that might be. Maybe unlocking that fame means you suddenly get fame, fortune, wealth, and you can start living that rock and roll lifestyle, drinking, smoking, taking drugs, whatever that might be, or it might be that there are pressures that come along with the fame all that public scrutiny that cause stress, which we also know is something that can accelerate ageing.
So it's actually, you know, although there are these, these sort of isolated examples, I think they're probably a case of, you know, what's called survivorship bias. So that means we, we look at the ones that survive and we don't see the sort of, of musicians who are already in their graves by their sixties, seventies, eighties.
This is a phenomenon that's actually talked about beyond longevity. You know, we talk about it in the stock market, we talk about it in all kinds of different parts of life, but obviously it's very literally the case, looking at lifespan that some people. And there, I think there is just a huge element of luck.
I think this is often neglected, even identical twins die on average about seven years apart, which means they've got identical genetics, they had identical conditions in utero. They probably grew up in quite a similar environment, but in spite of all of those similarities, they still don't die on the same day, which I guess is a relief to any identical twins listening. but it shows us, you know, that there was just this huge degree of randomness involved here.
Brian: So, so I suppose the, the message is that, you increase your personal chance of living longer by looking after yourself. Is that the, would that be a reasonable summary, Linda?
Linda: Yes, but it's no guarantee.
Brian: Yeah, of course.
Andrew: That's exactly why Linda and I are so excited about trying to develop these medicines that can, you know, improve the ageing process and give people a bigger chance of living healthier for longer.
Linda: Yeah.
Andrew: Because the fact is there is such a massive luck component involved here. Wouldn't it be nice if we could sort of level the playing field by allowing everyone to have some of that sort of luck, in pill form?
Brian: Well, specifically in terms of diet and alcohol, Tomoko Uemura had a question about, else we're often told is good for us, which is mindfulness and meditation. And Tomoko to know if there's any evidence that this kind of practice can help us live longer or at least stay healthy for longer. Andrew?
Andrew: I think this is a really tough one. I mean, what, what you'd really want to do to find out the answer to this question is get a bunch of people, let's say in their sixties, randomize half of them to do mindfulness meditation, the other half not, and then watch them for, you know, potentially decades to try and tease out whether the people who were meditating got sick later or lived a little bit longer. Of course, unfortunately, we don't have that perfect randomized data, and what that means is we're left looking at observational data. We have to look at people you know, out there in the population who are meditating and compare them to those who aren't. And obviously there are lots of systematic differences.
If you are fortunate enough to have the time, you know, just to sit down and meditate for 10 minutes, for half an hour in a given day, that probably means you're wealthier. It probably means you have a less stressful, you know, time intensive job. It probably means you don't have childcare or other caring commitments.
So there are loads of differences between these populations that make it very hard to tease out. I think to be sort of optimistic about its potential, we have got some evidence that people who meditate have longer telomeres. And I think we're gonna, a spoiler alert, come to what telomeres are a bit later in the, in the show.
But this is an indication that they might be ageing a bit more slowly, but it's very, very hard to tease out the sort of cause and effect here. I think we also know that people who experience a lot of stress during their lives do indeed age more quickly in various ways. So again, that would sort of point in the direction of perhaps meditation and at least generally low stress being helpful. The real question on my mind is if I had a spare half hour a day, and as a new dad, I don't really have that spare half hour, but perhaps in a few years time when I do, you know, would I rather devote that to meditating or going out for a run? And I think in terms of evidence, the evidence for exercise is just a lot, lot stronger.
Brian: We have a question now from Christine Hinton who's asking about the difference between men and women. So do men and women age differently? If so, how? And what conditions are more likely to affect each? So that's a very, a very big question, and maybe, maybe Linda, you'd like to start?
Linda: That's a huge question. I think all over the world, women outlive men. So men do have shorter lifespans, and while the big increase in life expectancy's been happening over the last couple of hundred years, we've seen the increase in longevity, but also an increase in the unhealthy period at the end of life.
So what we'd love to see is that as people live longer, we see a compression of the bad period at the end of life, but the opposites happen. It's expanded and expanded, particularly in women. So women have a longer unhealthy period at the end of life than men do. So that that is a real problem associated with what otherwise is something to be celebrated.
We've kept ourselves healthy, so for a given age we're less likely to die, which is quite an accomplishment of civilization, and I mean, causes of death differ slightly between the sexes and men are more likely to get cancer than women are, they're also more likely to get cardiovascular disease, but women are much more likely to suffer from dementia. So there, there are big sex differences there, and most of the evidence for the kind of mechanisms involved actually has come from animal studies, rather than humans. And there are very big differences between the sexes, for instance, associated, with great difference in reproductive strategies.
You know, women have to invest much more anabolically in producing children than men do. They actually have to make the fetus that's going to be born, and that can have quite a dramatic effect on their health and in ways that you wouldn't expect. So for instance, the intestine expands enormously during pregnancy and that means that the kind of, intestinal sicknesses that women get are different from the ones that men get later in life.
Brian: Well, that, that raises a question right at the start of the introduction. We talked about the length of life. it. Is there a difference between length of healthy life and length of life in terms of the span or the timescale that we can expect? I mean, obviously you said they are separate, but is there a, physical reason why they may be very different? So the healthy lifespan and the actual lifespan.
Andrew: I think that, part of the reason is actually the way that we do medicine these days, which is that we wait until you're sick and then when you are sick, we try and treat that individual disease. So, for example, if you, you know, come down with cancer, unfortunately you are gonna go to your doctor, you'll get radiotherapy, you'll get chemotherapy, and that cancer is very much treated in isolation. And that means this is all happening while the rest of your body is kind of falling apart. Even though, you know, in nature you might have died of that cancer, you might have died of something else beforehand. but we're sort of very good at keeping people alive with diseases, but we aren't very good at treating the sort of broad things that happen as we get older.
And I think that's what's very exciting about this idea of longevity science because we're trying to come up with medical interventions, with lifestyle, stuff we can do that allow us to extend that healthy period longer. And I think something that's often lost in this discussion, I do get people saying to me, you know, why do we wanna extend lifespan?
Isn't health span the sort of period of life in good health the most important? I think the kinds of interventions we develop through longevity science are very likely to increase both of those things in tandem. And that's because, you know, fundamentally it's being old, it's being unwell, it's being frail. That's what kills you.
And so if we can extend that period of health span, lifespan is gonna increase kind of as a side effect. But the most important thing is we're gonna have a larger period in good health and a larger fraction of our lives in good health if we can get this stuff right.
Linda: And it's very clear that we know, we know the underlying mechanisms of ageing. We know what goes wrong at the molecular level, cellular level, whole organism. And it's clear from the way that different diseases develop, that these mechanisms of ageing say, you know, loss of, respiratory function cause the mitochondria go down during ageing.
The diseases associated with that mitochondrial design are more likely to occur together in individual patients. We know that these mechanisms of ageing can account for multi-morbidity, the presence of more than one disease in a single individual. So there's a very strong implication that if we could tackle them directly, we could actually delay or prevent groups of diseases.
That's really important because we're starting to tackle the whole ageing process rather than waiting for one disease to occur. And I think the other very important point is that it's going to be a particularly powerful approach for neurodegenerative diseases, 'cause dementia particularly is proving extremely intractable and it's becoming clear that we need to tackle it much earlier in the disease process if we're going to succeed.
Brian: That that links beautifully onto a question from Regis Julia,about the ageing brain. And Regis asks, can mRNA vaccine technology help prevent the brain ageing badly? And if yes, how might that work?
Linda: There's some absolutely fabulous work going on on that at the moment. It, it's really, cutting edge stuff. So the clinical trials that have been done is for a brain cancer called glioblastoma, so you can get the mRNA vaccines into the brain, using lipid nanoparticles. So it, it's possible to get the vaccines in there and for them to then enter immune cells in the brain or other classes of cells.
Brian: You, you take that orally, do you?
Linda: No, they have to be injected. Although I think eventually, it will be possible to do things that cross the blood-brain barrier. In fact, I think some of this is not my area of expertise, but I think some of the, nanoparticle approaches can actually be done orally. And what they found is-
Andrew: The interesting one actually is that you can spray them up your nose because the way that your sensory neurons work in your nose, the way that you smell is they're basically a direct connection to the brain. And so there are experiments being done trying to give people vaccines or gene therapies or all kinds of therapies by spraying them up into the nasal cavity
Linda: Brilliant.
Andrew: And it can sort of work its way up into the brain. So again, not my area of expertise, but I'm, watching that sort of stuff excitedly.
Linda: But the fantastic thing about these glioblastoma trials is that they've, shrinking the tumors and increasing the lifespan of the patients. It's really working, which is absolutely fantastic. And there's, there's further back work going on preclinical rather than clinical trial. Trying to, tackle Amyloid Beta, which is the critical thing that accumulates clump proteins in the brain during the early stages of dementia. And again, they're getting positive results that they can start to, this is mainly in animal studies at the moment that they can, start to shrink those Amyloid Beta clumps. So I think it could be an extremely powerful approach over the coming years.
And of course, it it can be done preventatively. So at the moment we wait for somebody to show mild cognitive impairment and then try to do something about it. But the lovely thing about a vaccine is that it could almost be a public health measure that it, it prevents the Amyloid Beta accumulating in the first place. I mean, that's, you know, gazing into the future and guessing, but it would be fantastic if they could be developed in that way.
Andrew: I've just got a couple of things to add. firstly, I think these mRNA vaccines could help, at least slow cognitive decline, maybe prevent dementia directly by their work as vaccines. 'Cause there's this increasing evidence that, various different infectious agents are often found in the brains of people with dementia or might be able to accelerate that dementia. There's a herpes virus, the thing that causes cold sores, seems to have some connection with dementia. also have seen increasing evidence in the last few years that people who get the shingles vaccine, as they get older, and that's the virus that causes chickenpox, hides out in your body for the rest of your life after you've had a chickenpox infection.
Getting that shingles vaccine seems to delay the onset of dementia. So it really does seem as though, you know, if we can develop better vaccines for some of these diseases, perhaps through mRNA technology, that could have a direct effect. And the other thing is that although we think of this mRNA platform under lipid nanoparticles that Linda referred to as vaccine in, 'cause that's, you know, how we were all introduced to them through the COVID vaccine. Actually, they can also deliver a huge range of different things. One of the things you can even do is gene editing.
So you can put the instructions to do some gene editing into that mRNA rather than instructions to build a coronavirus spike protein, which is what all of us have been having over the last few years. And it can then go in and do that gene edit in your cells. So there are a couple of ideas that could actually slow down dementia. One of them is a PCSK-9 gene edit, which is something that goes in and dramatically reduces cholesterol, by looking at looking at where it's produced in your liver. That can have effects on dementia potentially down the line. And people are also looking into editing a gene called APOE-4, which we know increases your risk of dementia substantially.
And actually what's fascinating about that is it's a single genetic letter. So, you know, there this gene is thousands and thousands of, of As Ts, Cs and Gs Long. But by changing just one letter, we could potentially dramatically reduce people's risk of dementia. So there's some really exciting stuff going on by changing what that mRNA codes for and the things that it can do in your body.
Linda: Just thinking about ageing more broadly as opposed to specific diseases. There's also been a really interesting discovery very recently that there are some autoimmune cells, T cells, they're called, and normally we think of autoimmunity as a really bad thing because it causes the immune system to attack the patient's own body and, and leads to various diseases. But it turns out there's a subgroup of them that are really important in, regenerating nerve cells in the brain. And again, if a vaccine could be used to boost those, then we might be able to improve brain health really broadly, as opposed to just tackling a risk factor for a specific disease. So again, that, you know, it's it, it's future gazing, but it would be wonderful if that turned out to work.
Brian: There's a wonderful question about, I like this. As a physicist, it's really about information storage, I suppose, but it's a Therell Gonzaga said. a nurse working in a dementia unit, I see firsthand how memory loss affects people as they age. So if humans could live forever or for a very long time, how would our brains handle unlimited memories? Would we need to forget things to make space, or could our cognitive capacity expand essentially indefinitely? Linda.
Linda: Well, speaking as somebody trying to learn Spanish for the first time late in life, I struggle and I don't know whether that's 'cause I've learned several other languages previously or not, but I think one thing that's clear is that you know, the brain isn't a hard disc. It, it, it's not a thing with a fixed storage capacity that will eventually overflow it.
It's not how it works and it's not how memory formation works, so forgetting is a very important process and, things that aren't rehearsed, whether the memory isn't recalled quite quickly after it's formed and that are neglected, are basically lost and pushed out the back. So there's a very effective process for getting rid of pointless memories and the ones that are retained really well with age are the ones that are used all the time, the things that have been learned and, and get rehearsed as time goes by. But the way that memory's distributed in the brain, it's rather hard to put into words. It's extremely complicated. It's not that there's a little group of neurons and memory, there's a memory in there.
It's distributed across the brain in little modules, and quite often a new memory will pull in existing bits of previous memories to form the new one. It's a big connectivity problem or or connectivity process, and that has huge capacity because of the ability to actually use old memories to form new ones.
So I think yes, the brain does get less effective at forming memories with age, but that may be much more just to do with general deterioration in blood supply, neuron function, and so on, rather than because the brain is stuffed with memories already.
Andrew: the, the, the way I answer this is just to sort of think about my own life. I think about, you know, how detailed are my memories, even if, you know quite major events of getting married of my first day at school, like as I recede further and further into the past, I get hazier. There's a lot of very interesting research about how merely recalling a memory can actually, you know, sort of change that memory.
Um, it change the way it's stored. So I think we don't have necessarily as strong a grasp on the past as we sometimes think we do. But actually that's probably a good thing. Like if I could remember exactly why I had for lunch on, you know, a Tuesday in January in 2023, I think I'd probably be crushed by the weight of all that pointless information.
So I think our brains already do a very good job of sort of editing the highlights reel of our life and I imagine that would continue even if we lived for, you know, hundreds of years.
Brian: We, we discussed earlier, Andrew mentioned it actually I think, telomeres. We said we, we'd get back to it. So these are sequences of DNA located on the end of chromosomes. So I wonder if you could expand a bit more on that. We, we had a, a question from Leslie Thelwall who was curious about how we can keep those telomeres, her language was, how can we keep them in an optimal state?
So maybe Linda, you could the scene on these things. So, first of all, what are telomeres.
Linda: Well telomeres were a Nobel Prize-winning piece of molecular machinery. They're the, the caps on the end of chromosomes. So we've got the genetic materials stored in the chromosomes in our cells, and at the end of those chromosomes, there are telomeres. So there they're multiple repeats of short DNA motifs, a few bases long, and there's a great string of them.
On the end of the chromosomes, the length of that string varies a lot between different species. So for instance, mice have enormously long telomeres and humans are rather shorter ones. And every time a cell divides, those telomeres are replicated along with the rest of the chromosome, but they're not completely replicated.
Just because of the way the molecular mechanism works, it can't replicate the very last few bases at the end. So gradually a cell division proceeds the telomeres get shorter and shorter and shorter. They get nibbled at, and if they get nibbled at too often.
Then it actually starts to eat into the chromosome itself and the genes at the end of the chromosomes. And so that, that is now outright DNA damage. We need that DNA. And so there's a DNA damage response and the cell goes into something called senescence, so it becomes unable to divide. it actually usually becomes resistant to cell death, and those cells can. Be a real nuisance in tissues because they're rather biologically active. They secrete, molecules that can damage the cells near them and also act as a, a distance to increase inflammation in the whole body. So serious telomere shortening is pathological and you don't want it. So basically what that's saying is you don't want your cells that do divide to have to divide too often or there's going to be a problem.
Andrew: There's a really interesting story here, which is the sort of, the waves of hype, then anti hype about telomerase, which is this enzyme that can actually extend your telomeres. That was, discovered in the 1990s. and what, what scientists thought was, oh wow, you know, we've got this incredible way to extend these things that we know get shorter with life. Isn't that a way to make animals live a lot longer? And I actually remember watching a Horizon documentary back when I was at school about how we're all gonna live forever 'cause we discovered this telomerase and it was gonna extend the telomeres and all our cells. But scientists tried inserting telomeres into mice and what they found was it caused massive cancer risk, basically because, one of the thing, you know, what is cancer? Cancer is a cell that can divide infinitely many times, and one of the things it often does to do that is activates the telomerase gene and that allows it to keep those telomeres nice and long.
It means it can carry on dividing and dividing and dividing without this senescence mechanism that Linda just mentioned, putting the brakes on and stopping that division. So we think that telomeres evolved partly as a cancer protection mechanism. Which means it slams on the brakes if a cell's divided too many times, it's looking a bit suspicious, looks a bit cancery. So that kind of, you know, put the tin lid on it for a lot of scientists, I think. But actually since then, there have been some results that have shown us that, you know, maybe we shouldn't be quite so pessimistic about telomere extension as a way to maintain healthy life. There was a paper that came out in 2008, under a scientist called Maria Blasco in Spain, and she showed that by giving mice telomerase, but not just telomerase, also a trio of three anti-cancer genes that would try and basically kill cells that looked as though they were becoming cancerous.
Those mice actually live longer and healthier. So, you know, by doing a really naive gene edit by just throwing in some telomerase, you do break things, but by doing a slightly more intelligent one, it seems that we can, you know, optimize for lifespan in a way that evolution hasn't necessarily done and that same group has since shown that we can give a temporary telomerase boost.
I mean, you could even actually imagine doing this with an mRNA vaccine where you put in a temporary copy of that telomerase gene, it extends the telomeres. And because that telomerase isn't actually active, that doesn't help cancer, but the telomeres are a bit longer. And again, mice in these experiments seem to live longer. And I think that, some of these drugs are now being tried for people who have diseases where we know that short telomeres are a problem. There's a disease called lung fibrosis, which is kind of scarring of lung tissue that often happens as you get older, and we haven't really got any particularly promising treatments for that at the moment.
Apart from they are trying both senescent cell killing, treatments and also these sort of telomere extending treatments as well. So, I think it's an exciting time for telomere science. I'm just a bit frustrated that more attention hasn't gone into this. I think, you know, a lot of people saw those early results where basically loads of mice got cancer in the early two thousands and have dismissed the whole field.
But actually I think it's a bit more exciting than that sort of, sort of naive summary would suggest.
Linda: I think there is that very positive side to it. We do have to be aware that, you know, natural cancers in humans usually do reactivate telomerase. So it is a very important enabling process for cancers to, you know, become really dangerous. So I think any intervention's always going to have to keep that in mind, the danger that it's going to induce some form of carcinogenesis.
Brian: We're coming towards the end actually. We've got, one more question, which is where this research is leading. so Andrew Erskine wrote in and said there's been a lot of focus recently on Bryan Johnson in his attempts to defy ageing. So, are his activities useful in a scientific sense, either through the value of the research itself, or because they increase awareness of this area of science? Or do you think there's a danger that it could be distracting from other potentially more rigorous research taking place? Maybe, maybe Andrew first for the, for the listeners, and I'm one of them actually 'cause I don't pay much attention to this area. You may explain who Bryan Johnson is.
Andrew: Bryan Johnson, quite a few years ago now, sold his company for $400 million and has since been doing a variety of different activities. One of which is that he's got this personal project he calls his blueprint to try and well essentially live forever. He believes that if he can live long enough, he can merge with ai and then that.
It's gonna lead to an indefinite, glorious future ahead of him. He claims he spends $2 million a year trying to optimize his health. He says he's got a team of doctors. He does every single, you know, test under the sun. He does every single, takes hundreds of supplements every single day.
He does, you know, very intense diet exercise interventions. He tries to get absolutely perfect sleep scores all the time. he's become a real thing on social media. This was first covered a couple of years ago in the press, and he's since exploded on, you know, Instagram, on YouTube. He's, he's all over the place constantly talking about his slogan, don't die.
Brian: It's good advice, isn't it, if you want, you want to live to an old age, don't die is probably.
Andrew: I mean, it's good advice. That's the, you know, perhaps, perhaps one place that he and I agree, but. I'd been blocked by him on Twitter, back when it was called Twitter, and the reason for that is that I suggested, you know, given he sold his company for $400 million, I don't know exactly how much of that he personally kept, but he's clearly quite a wealthy guy. And he could be using some of that money to invest in longevity research. And I think that, you know, the way to contrast this, and the reason he blocked me actually, is I suggested that he invested in something called the TAME Trial. Now, the TAME trial is a trial of a drug called Metformin, and the sort of principle of this is get a few thousand people, have half of them, Metformin, you give half of them a placebo.
And we want to know if Metformin slows down the ageing process. So have to watch them for maybe three to five years, see if the people taking the drug get fewer diseases, if they get, if obviously if they die later, that's a good sign you're slowing down ageing too. And this, this experiment's probably gonna cost about $70 to $100 million dollars but actually they've already got some of the funding in hand. I think they're waiting for about $20 million and have been for, for a number of years now. So this would be a hugely important study, and it would tell us, you know, whether Metformin slows down the ageing process, but it could also provide a template for other drugs.
So I suggested, you know, maybe Brian would like to fund that study and essentially after a bit more of an exchange, he reached for the block button. And I think that the sort of contrast between those two things. Really shows you, you know, why what he's doing isn't that scientifically useful? The idea of Tame is that we get thousands of people, get lots of people taking exactly the same predefined intervention, we watch them for a very long time. What he's doing is there's one of him and he's taking hundreds of different interventions.
So, all of these interventions together in one person, it's impossible to tell what, if any of them are having an effect. I actually worry he might be shortening his own life because of all these different things interacting together in some complicated way that, you know, current biology doesn't really understand.
Linda: Completely agree, I'm always amazed at what people will swallow. You know, you go to the average drug store and there's always a huge pile of shelves of unproven supplements where there's been no clinical trial at all, and I would never, ever take something that hadn't been through a clinical trial. I can't understand why anyone would do that. And, from what I can see, just looking at the web, you know, Bryan Johnson is taking all sorts of things for which there's no evidence at all, and it could be really dangerous. So I certainly think that, you know, if that leads to others following the example, it's actually quite harmful.
Brian: Yeah, I think my favorite trial on myself is the first question, which is just do rock and roll and see what happens. That's my approach, but anyway. It's probably irresponsible.
Andrew: Get 3000 people to do rock and roll and 3000 people not to,
Brian: Yeah
Andrew: then we can do a real randomized trial and see if you live longer or shorter
Brian: I wanna be the rock and roll sample
Linda: Go for it.
Brian: You're not allowed to choose which bit of the randomized trial you're in though, are you? That's the problem.
Andrew: Yeah, that's the issue. Imagine being forced to be a rock and roll star, I'm sure a lot of people would like it, but there must be another subset who wouldn't enjoy it so much.
Brian: Thank you With that, we've run out of time that I should say that's not the advice of the panel, but yeah, that it, just to summarize what you said, the way to acquire know reliable knowledge about this area is to do science, a large part of which are randomized trials and so on, not to just experiment on yourself, I suppose is what you would say.
Andrew: Say so, yeah.
Brian: Well, well thank, thank you very much. thank you to Linda Patridge, Andrew Steele for coming back to answer more questions of science. Goodbye.
