Episode 3
Professor David Weinkove, Chair of the BSRA, on C.elegans research and evidence-led longevity science
What can a tiny worm tell us about human ageing, and could gut bacteria hold the key to a longer, healthier life?
In this episode of Beyond Longevity, we sit down with Professor David Weinkove: Chair of the British Society for Research on Ageing (BSRA), Professor at Durham University, and Co-founder and CSO of Magnitude Biosciences. David's lab uses the short-lived nematode C. elegans to run fast, rigorous experiments looking for interventions that extend healthspan and lifespan, and the results are pointing in some surprising directions.
We cover how Prof David moved from physics into experimental molecular biology, how his team discovered that bacterial strains and metabolites can dramatically alter how long worms stay active, and what inhibiting bacterial folate synthesis reveals about the biology of ageing. He also explains how worm movement is a practical proxy for healthspan and why that matters for scaling up research.
The conversation gets into the thornier questions, too: when do you need mice, and when might you skip straight to human-relevant models? How do you fund prevention research when the payoff is decades away? And what are the real risks of mandatory folic acid flour fortification, a policy Prof David argues deserves more scrutiny, given potential microbiome effects we don't yet fully understand.
Prof David also unpacks what the BSRA does day-to-day: from connecting researchers and lobbying government to running small grants and building bridges with clinicians and industry, and why he thinks the longevity field's biggest enemy isn't scepticism, it's overpromising.
Plus, we discover the most extreme longevity idea he's ever come across (involving spare parts — we'll leave it there).
Links:
https://www.durham.ac.uk/staff/david-weinkove/
https://www.linkedin.com/in/david-weinkove-bab807b
In this episode:
00:00 Welcome to Beyond Longevity + Meet Prof. David Weinkove
02:40 From Physics to Bioscience: Career Origins & Model Organisms
04:29 The Breakthrough: How Bacteria (and Folate) Can Extend Worm Lifespan
09:12 Measuring Healthspan in C. elegans: Movement, Decline & New Tech
10:38 Why C. elegans? Fast Ageing, Whole-Organism Biology & Screening Power
12:19 Worms vs Mice: Similarity to Humans, Ethics, Cost & Experimental Variability
15:35 Translating Worm Findings to Humans: Microbiome Links, Exercise Paper & Next Steps
17:52 Funding the Science: UKRI, MRC vs BBSRC, and the Reality of Grant Constraints
20:52 Why Longevity Research Struggles for Support: Messaging, Hype & Prevention
28:39 BSRA’s Mission & the Five Pillars: Public Engagement, Advocacy, Fundraising, Translation
32:01 Breaking Down Silos: Making Longevity Research Useful (and Public)
34:07 Prevention Mindset: Why “Healthier for Longer” Isn’t Instant Gratification
36:15 When to Start Interventions: Metformin, Timing, and Trial Design Challenges
39:39 Why Magnitude Bioscience Exists: Fast Whole-Organism Ageing Screens
41:12 What Companies Test in Worms: From Candidate Drugs to 1,000-Compound Screens
42:48 Folic Acid Fortification & the Microbiome: A Potential Unintended Consequence
45:55 Should Government Engineer Health? Autonomy, Risk, and Public Policy Trade-offs
52:37 Ageing Demographics & the Case for Prevention-First Healthcare Investment
55:59 Making Longevity Matter to Everyday People + Rapid-Fire Q&A
01:01:47 Final Takeaways, Thanks, and Episode Wrap-Up
Transcript
Welcome to Beyond Longevity, the podcast that explores not just how we age, but how we can build a longer, healthier future for ourselves.
Speaker A:Joining me today on Beyond Longevity is Professor David Weinkove, chair of the British Society for Research on Aging and a professor at Durham University.
Speaker A:What really sets Professor David apart is the kind of longevity science he does.
Speaker A:His work is deeply rooted in experimental biology.
Speaker A:Using C. Elegans, a tiny transparent worm that lets you test aging and healthspan questions quickly and rigorously, it can help uncover how lifespan can be shaped not just by the animal itself, but by the bacteria it lives with and the metabolites and nutrients moving between them.
Speaker A:In other words, Professor Weinkove studies aging as a system where microbes, diet and metabolism can meaningfully shift outcomes.
Speaker A:Professor Weinkove is also co founder and chief scientific Officer of Magnitude Biosciences.
Speaker A:This platform enables other researchers and companies to run well designed C. Elegans aging and healthspan studies.
Speaker A:This is not only helping to advance the world of research, but it is giving Professor Weinkove a front row seat to what holds up in data and what doesn't when people test interventions.
Speaker A:As chair of the bsia, Professor Weinkove has been very clear about keeping the field evidence led.
Speaker A:Separating what is genuinely supported by data from what is just exciting storytelling.
Speaker A:Welcome, Professor David Weinkop.
Speaker A:Thank you so much for joining us today on Beyond Longevity.
Speaker A:It's a great honor and great pleasure to have you.
Speaker B:It's a pleasure to be here.
Speaker A:You are a man that wears many hats.
Speaker A:You are obviously a professor at Durham University, currently doing research work.
Speaker A:You're also chair of the bsra, the British Society on Research of Aging.
Speaker A:And you also are co founder and chief scientific researcher for the Magnitude Bioscience company.
Speaker A:Let's start at the beginning.
Speaker A:How did you become a professor and why in bioscience?
Speaker B:Hi.
Speaker B:And that's a really good question.
Speaker B:I actually went to university to study physics.
Speaker B:I didn't really like biology at school.
Speaker B:I dropped it when I was about 14 and I got back into it again at university.
Speaker B:And that's because at the time, this is in the 90s, molecular biology was really exciting and you could do so many different things and so I really wanted to do that.
Speaker B:Whereas physics was much more intangible.
Speaker B:You had to to be cosmology or quantum physics, which you couldn't really conceptualize.
Speaker B:Whereas with biosciences you can just do experiments in the bench.
Speaker B:I could just go to the lab and do something brand new that no one's ever done before.
Speaker B:And that was really exciting.
Speaker B:So that's how I got into biosciences, and then I pursued my career.
Speaker B:And I really like to combine genetics and biochemistry because they're two independent ways to look at biology.
Speaker B:So that makes it really powerful.
Speaker B:And if you find the same thing with both techniques, you're more confident of what you find.
Speaker B:So it was really good to do that and use the small model organisms.
Speaker B:So I did my PhD using the fruit fly, Drosophila.
Speaker B:And then when I became a postdoctoral scientist, first in the Netherlands and then and later on back in London, I worked with the small nematode worm C. Elegans.
Speaker B:And I've worked with that ever since.
Speaker B:And so I found a mutant of the bacteria that the worms live on that makes the worms live a lot longer.
Speaker B:And that started a whole line of research.
Speaker B:And that's what led to me coming to Durham University, where I was asked to teach biochemistry but do research on aging.
Speaker B:And so that's what we've been doing ever since, and working with this small little worm, C. Elegans.
Speaker B:And I enjoy the teaching part of my job here.
Speaker B:And the research.
Speaker A:Of course, your research work into longevity started when you realized that the bacteria side of the story mattered from the worms, or how did that relate?
Speaker B:No, I was actually working on aging long before that, because when I was doing my PhD, I was working in Drosophila on this gene called pi3kinase.
Speaker B:And while I was doing my PhD, it was found that the age 1 mutant in C. Elegans, which was at that time one of the only mutants found that made an animal live longer, it was found that that was a disruption of the same enzyme that I was working on, the PR3 kinase.
Speaker B:So suddenly there was, like, an interest that there was some connection with aging.
Speaker B:And what we found in flies was that the PR3 kinase affected the growth of the worms and the growth of the organs of the worms, both at the cell and organ level, kind of integrating those things.
Speaker B:And so we kind of thought that that might have something to do with aging.
Speaker B:And so that started that collaboration within the Partridge and David Gems, all at University College London, which led to quite a lot of work in the aging field and the eventually the Institute for Healthy Aging.
Speaker B:So then I went to the Netherlands to learn to work with C. Elegans and did some more work on that, and then came back to the Institute of Healthy Aging and started working more on that problem of how this pi3 kinase, insulin signaling, pi3 kinase pathway, affected aging.
Speaker B:And then by accident, I found a strain of e. Coli that made the worms live longer while I was doing work on that other pathway.
Speaker B:And so I followed that up, because when you see a big result like that, you don't let it go.
Speaker B:You know, when you see a mutant worm that's long lived anyway become even more long lived, you're like, wow, we need to do something here.
Speaker B:What's going on?
Speaker B:And so I followed that up and then found, yeah, that the bacteria affected aging in the worms.
Speaker B:And in particular, what was happening in this mutant was it interrupted the synthesis of folates, which is you've probably heard of folic acid.
Speaker B:So it interrupted the synthesis of folates in the bacteria, and that was the thing that made the worms live longer.
Speaker B:And then we found out that it wasn't to do with the folates themselves.
Speaker B:It was to do with what the folates were doing in the bacteria.
Speaker B:And if we brought the folate synthesis down, the bacteria were less likely to age the animal.
Speaker B:So that's what we've been working on ever since.
Speaker B:And we also went to look for other e. Coli meters that made the worm live longer.
Speaker B:And we screened about a thousand different mutants of e. Coli with each of the different gene disrupted to see if those would also make the worms live longer.
Speaker B:And we found a few that did, Although they didn't really tell us what was happening on a molecular level, but it was really interesting.
Speaker B:But also, that also led to us designing technology, which then led to us in our company.
Speaker B:So that's a different story.
Speaker B:But, yeah, we think that the bacteria age the worms, and we think that it's likely that the bacteria age humans.
Speaker B:We just need to do some more work to find that out when we apply for a patent in this area.
Speaker B: his paper from Germany in the: Speaker B:And they found that sulfonamides might made mice, rats, and even dogs live longer in this paper.
Speaker B:And that may well be, by the same mechanism, the precursor to folates that the bacteria can use to make folates.
Speaker B:The mice didn't live long anymore.
Speaker B:So it fitted exactly with what we thought to do with bacteria, Although they didn't think about bacteria in that paper.
Speaker A:To sum it up very briefly, is the bacteria in animals or the bacteria that the animals live with can and does change their lifespan and their health span?
Speaker A:Is that correct to say that is correct?
Speaker B:Yes, we know that's happening with C. Elegans.
Speaker B:C. Elegans eat the bacteria, so it goes through their intestines.
Speaker B:They're also surrounded by the bacteria.
Speaker B:So it could be that what's going on around them.
Speaker B:But we all have bacteria inside us.
Speaker B:Some are beneficial, some aren't.
Speaker B:It depends on the context.
Speaker B:But what I think is that it may well be that the bacteria inside us are also aging us.
Speaker B:So that's what we need to work out and need to work out ways to intervene.
Speaker B:But this gave a model where the bacteria was definitely aging the animal.
Speaker B:And you can see it.
Speaker B:It's not just in terms of lifespan, but also in terms of health span.
Speaker B:The worms stay healthier for longer.
Speaker B:We can see that by looking at their movement.
Speaker B:They stay more active and so on for longer when we stop the synthesis of folate inside that bacteria with a drug.
Speaker A:You've already answered the question that I had, which was, how do you measure healthspan in worms lifespan?
Speaker A:Fair enough.
Speaker A:You know, if they live longer, you know, the lifespan's extended.
Speaker A:But so health span is purely by their physical activity, or are there any other markers?
Speaker B:You can use multiple markers to look at healthspan in the worm, if you want to look at it in depth.
Speaker B:But we wanted to find a way to look at it quite quickly and easily.
Speaker B:And when we do a lifespan experiment, when we look at the worms a week later, none or maybe a few of the worms are dead, but they all are a lot slower.
Speaker B:And you can see that by eye.
Speaker B:And everyone that does lifespan experiments sees that when they go back to their worms a week later, they're slower.
Speaker B:But actually measuring that is difficult.
Speaker B:So that's why we invented some technology to help us measure that slowdown.
Speaker B:But the slowdown is clear.
Speaker B:So what really happens is that the worms are quite active for the first three days of adulthood, and then we see a decline, a slow and steady decline that's very reproducible.
Speaker B:And so we find that interventions that increase that time of activity also increase lifespan, as far as we've seen.
Speaker B:And that's definitely true for when we inhibit folate synthesis in the bacteria.
Speaker B:We see that change.
Speaker B:We could look at healthspan in other ways, and we have a little bit.
Speaker B:But mostly it's the movement of the worm.
Speaker B:That's.
Speaker B:That's really obvious.
Speaker A:And the.
Speaker A:You're using C. Elegans mainly because the lifespan of the worm is two weeks.
Speaker B:It's a very good point, because that's the reason why C. Elegans is so powerful for aging, is because they only live two or three weeks, and they age even faster than that.
Speaker B:So it means that we can look through lots of different drugs, different concentrations of drugs, different combinations.
Speaker B:We can look at natural products, we can look at different kinds of bacteria.
Speaker B:We can do all sorts of different things very quickly and very easily within the lab.
Speaker B:And you can't really do that with any other system.
Speaker B:The closest is fruit flies, but they live about two months, so two to three months.
Speaker B:So it takes longer, a substantial difference, especially if you want to look at lots of different things.
Speaker B:So the worm is really easy like that.
Speaker B:It's also great for lots of other reasons.
Speaker B:But I could go into that.
Speaker B:I actually was a.
Speaker B:A fly person, as I told you.
Speaker B:And then.
Speaker B:Right.
Speaker B:And then I, I was converted to the worm after, after a while and saw the benefits.
Speaker B:I mean, obviously both systems have their own merits and strengths and weaknesses.
Speaker B:But, but the worm is really great for looking at whole organism.
Speaker B:You know, it has a nervous system, it has muscles, it has an intestine, there's a germ line.
Speaker B:It uses the same kind of neurotransmitters that we do.
Speaker B:We can see nearest generation, we can see muscle decay, we can see all sorts of signs of aging inside the cells, and yet we can do that all within weeks, whereas almost any other system isn't much harder.
Speaker B:And when you, you come to a mouse, for example, it takes.
Speaker B:They live for three years.
Speaker B:It takes a year to see some really significant aging, you know, so, yeah, it makes life a lot easier to work with worms.
Speaker A:Do you know, though, why still so many researchers, you know, in the longevity field, or in any field for that matter, still prefer to use mice rather than nematodes?
Speaker B:Oh, it's obviously a mouse is more similar to a human because it's a mammal, and so that's part of it.
Speaker B:Obviously, there are things that a worm doesn't have.
Speaker B:It doesn't have an adaptive immune system, it doesn't have a cardiovascular system.
Speaker B:It doesn't have all the things that we think about.
Speaker B:And also when we talk about developing drugs and then you're looking at preclinical stages that you need to get approval, go to humans.
Speaker B:You need to show something in an approved model, and that is a mouse, you know, so that's why people prefer to use mice.
Speaker B:But actually, if you want to try and do aging experiments in mice, it takes you several years.
Speaker B:It takes a lot of money because you have to keep those mice going all the time.
Speaker B:You know, nothing can go wrong.
Speaker B:You're also getting ethical approval is difficult.
Speaker B:Even studying the lifespan of a mouse is difficult because if a mouse starts to get sick at a certain point, you have to sacrifice that mouse.
Speaker B:That's.
Speaker B:Those are the rules.
Speaker B:So that means you can't necessarily look at the full lifespan of a mouse.
Speaker B:So, of course, mouse experiments are powerful, but I think if you can do as much as possible in C. Elegans before you go to mice, it allows you to do much, much more.
Speaker B:I think we could work together.
Speaker B:There's definitely things that I think we can do.
Speaker B:I mean, I'm actually on the scientific advisory board of the National Mouse Genetics Network in the uk, because I'm trying to see if the mice and the C. Elegans and other model organism communities can work together to help each other out.
Speaker B:In terms of understanding what's the best way to do experiments.
Speaker B:With C. Elegans, for example, what's really interesting is that we might do a lifespan with 100 animals for one each condition.
Speaker B:And these animals are genetically identical and they're in effectively identical conditions, and yet you see a big variation in aging and lifespan.
Speaker B:So the first worm will die around eight days of adulthood, and the last worm will die at 24 days of adulthood, about three times longer.
Speaker B:And that is just through intrinsic variability.
Speaker B:And that's the reason why you need to do that experiment with 100 animals.
Speaker B:If you did it with 10 animals, you don't get a very good result.
Speaker B:So when it comes to mouse experiments, I'm always advising use as many animals as possible, because the variation could be even greater in the mouse potentially.
Speaker B:So that's what we need to do.
Speaker B:That's just the reality of how aging works.
Speaker B:You have variability, you need large numbers, it takes time, so it needs a lot of resource.
Speaker B:There's something that I've been talking about in one of my other roles of the chair of the British Society for Research on Aging, is to get people to understand how much resource is needed for aging research and what we need to do.
Speaker B:And of course, doing experiments in mice is brilliant and we should do that.
Speaker B:It's just that it's difficult to do and expensive and we need the funding and the support.
Speaker B:And when a researcher comes to a funding agency and says, okay, I want to do a lifespan experiment in mice and it's going to cost me a million pounds and it's going to take four or five years, it's competing with other projects that they're going to do so many other different things that it's difficult to compete.
Speaker A:How do you make the step from the worms to the Human, does it need the testing on mice or other mammals?
Speaker A:How removed in reality is the testing on worms to effects in the human?
Speaker B:That's a good question.
Speaker B:I don't think you always need to go via mice.
Speaker B:I think there's many situations where you can go directly to human to test things.
Speaker B:For example, we're looking at bacteria and we can look at bacteria that have come directly from humans.
Speaker B:So we did a collaborative project with Professor Li Ping Zhao at Shanghai Jiao Tong University where we looked at bacteria that he had isolated from obese humans.
Speaker B:And we put C. Elegans on there and we could see, see what happened to the worms.
Speaker B:And so there's finding from that that we could apply directly to humans.
Speaker B:And we would like to be able to do some work to try inhibiting fertilizens in people.
Speaker B:And I don't think we necessarily need the mouse data to be able to do that.
Speaker B:It's just what we need to do is show that the folate levels in bacteria are important for health and try and correlate that.
Speaker B:And that's what we've been thinking about, working with clinicians to try and make that happen, where we can find ways to measure folate levels in bacteria and see if there's a connection going back to mice for a little bit.
Speaker B:There was a really interesting paper that came out in October where they were showing that exercise in a mouse made them better at fighting a tumor in a cancer model.
Speaker B:And they found that that exercise effect depended on the microbiome.
Speaker B:The interesting thing was the folate levels in the bacteria went down after exercise.
Speaker B:So maybe there's a connection there.
Speaker B:They also showed a connection to formate, which was a byproduct of the folate cycle.
Speaker B:So there might be a.
Speaker B:And they had a whole lot of mechanistic work there.
Speaker B:There's tantalizing things to suggest that there is a difference between folate levels in bacteria and health that I think can be explored in humans without necessarily doing mouse work.
Speaker B:We're trying to get funding for that and make that happen.
Speaker A:Where do you go for funding?
Speaker B:It's a very good question.
Speaker B:Our first port of call is usually the ukri.
Speaker B:So I've had quite a lot of funding for this project from the.
Speaker B:From the bbsrc, which is the Biology and Biotechnological Research Council.
Speaker B:And UKRI also has other, as you know, you know, this Innovate uk, which we've had funding from before for our company and the Medical Research Council and the nihr, which is the National Institute for Health research.
Speaker B:There is a little bit of an issue actually between the MRC and the bbsrc because the MRC is about disease and whereas the aging falls under the BBSRC remit.
Speaker B:But I think there's a very, a lot of links between aging and disease, which we can talk about later.
Speaker B:But yeah, BBSRC is the first protocol for us.
Speaker B:But there are other funding bodies out there, there's charitable funding bodies and so on.
Speaker A:How restricted are you in your research or angle of research when you take those funding monies?
Speaker B:You have to put together a project and it's peer reviewed, so it has to pass that quite stringent test and it's competitive with lots of other projects.
Speaker B:So it's quite difficult.
Speaker B:But you basically have to put a project together and do what you said you will do in the project.
Speaker B:So it's restrictive in that, that you have to follow that project and also you have to come up with a project that your peers will think is a good project, but it's not too bad, you know, in that respect.
Speaker B:The problem is, is that the continuity can be challenging because projects usually come in short periods of time.
Speaker B:Between one to three years of funding is typical.
Speaker B:And so that often isn't enough.
Speaker B:And you want to continue your expertise in your research group.
Speaker B:And that can be difficult when you've only got small amounts of funding.
Speaker B:I think almost everyone that's working on aging in the UK is restricted by funding.
Speaker B:There's a lot more science out there that could be done that isn't done because of funding.
Speaker B:And we find that from the members of the BSRA.
Speaker B:So there's about over 300 people that are members of the BSRA across the country that are working on aging across 50 different institutions.
Speaker B:And if you ask all of them, I would say funding is their number one challenge because there's so much more research that could be done.
Speaker B:And it's kind of interesting that there's so much interest in aging nowadays, more than they used to be.
Speaker B:You know, your podcast is a testament to that.
Speaker B:But there is real limits in the research we can do.
Speaker B:And I think a lot of the interest has come from the advances that have been made in basic research and that has led to a kind of consumer led movement.
Speaker B:And following the consumers are the companies that make products for those consumers.
Speaker B:And then there's a lot of journalists and social media influencers that are getting interested in this and there's a huge amount of activity in that sphere.
Speaker B:But we're not getting the funding that you would think would Come back and then help grow more research and make more advances.
Speaker B:So I think that is a major issue that I'm trying to address.
Speaker A:In the US you have maybe not a lot, but you do have a certain number of private individuals that fund various longevity research.
Speaker A:I don't think that's so much the case in Europe.
Speaker A:Any idea why that is?
Speaker B:The one that comes to mind is Jim Mellon, who's a British billionaire who funds some research.
Speaker B:But you're right, there isn't so much of that kind of funding.
Speaker B:But I think that just it's a cultural thing in that in America, you know, I think a lot of people feel that it's important to fund research in a charitable way.
Speaker B:And maybe that isn't so much in the uk but also I think aging research has a bit of a communication problem compared to something like cancer research.
Speaker B:It's much harder to put that across.
Speaker B:And some people have tried to put that across have ended up appearing like they're a little bit crazy, I think is the right word.
Speaker B:Because you almost need to build up some sort of hype to make people value it.
Speaker B:Because it's much harder thing to sell than cancer research.
Speaker B:Because when someone donates to cancer research, the unwritten message is that that money will go towards curing cancer.
Speaker B:And usually people that contribute to cancer research are people that have relatives or had.
Speaker B:Had relatives that have suffered from cancer or die from cancer.
Speaker B:And they can see that and they want to do something about it.
Speaker B:And so it's a very clear idea.
Speaker B:Even though in reality maybe we haven't got as far as we would like in terms of treating cancer.
Speaker B:But there's a clear narrative.
Speaker B:Whereas when it comes to aging research, there's two issues.
Speaker B:One is, even though we've had made a lot of advances, we're not going to stop aging.
Speaker B:So you're not going to say, okay, we're going to cure aging.
Speaker B:We might make way to slow aging.
Speaker B:So it's difficult to say that.
Speaker B:And then secondly, what does research mean?
Speaker B:Actually, research isn't necessarily about finding a cure.
Speaker B:Research is understanding something.
Speaker B:Right.
Speaker B:And so aging research isn't so much geared towards aging in the way that cancer research is geared towards cancer.
Speaker B:It's still valuable.
Speaker B:And I would say it's even more valuable because I would say what we need to do is think about preventing those diseases.
Speaker B:Aging is the major risk factor for cancer and lots of other diseases, lots of terrible diseases such as Alzheimer's and on.
Speaker B:So we can harness aging to prevent people having those diseases.
Speaker B:Then that's even better than curing the diseases once you've got them, even though it's, it's much more apparent that someone has something like cancer and it's very tragic, but it wouldn't be much wider not have that in the first place.
Speaker B:I think that's the point behind aging research.
Speaker B:But conveying that message to the general public or to the research rich donors that maybe want to support that is harder.
Speaker A:Yes, David, I do agree with you that the spotlight is not really on longevity research, but rather on illnesses like cancer.
Speaker A:And people like you said, are aware there's a terminality to cancer, whereas longevity I think people still see as a luxury.
Speaker A:You know, we all live, we all die and all we do is sort of live a little bit longer.
Speaker A:And I do think the marketing, if we can call it that on longevity, needs to change that.
Speaker A:It's not about living longer, but it's about, as you mentioned, eradicating all these illnesses.
Speaker A:And I don't say that lightly, but that can easily be avoided by the longevity research that's going on at the moment already.
Speaker A:And that is tangible, not some future sort of fantasy.
Speaker A:But I do think, as you said, it's the longevity research still has a bad rep. What can be done about it?
Speaker B:Well, I think it's important for people to understand that what the research is behind that.
Speaker B:I mean, I often say it's important for scientists to be heard, but it's also important for scientists as well not to be easily tempted into over promising and under delivering and being honest about the challenges because it isn't easy to do this kind of work.
Speaker B:It will take time and resource.
Speaker B:But the amount of time and resource might seem a lot to us.
Speaker B:But compared to what's spent on other things, like the kind of investments we've seen recently in AI for example, the amounts aren't astronomical, but we do need to have time and patience to work that out.
Speaker B:So I think that's part of it.
Speaker B:And it's also important for us to spell out what we're trying to achieve and how we're trying to get there.
Speaker B:So I think trying to get people to think about their lives and thinking about where are they in their life, what do they value?
Speaker B:And then they get them to think ahead a bit, 10, 20 years time, where do they want to be and how do they want to be in that space.
Speaker B:So my first goal is to stay alive long enough my daughter to be, be an adult and be independent.
Speaker B:Right.
Speaker B:That's the first thing.
Speaker B:Ideally I'd love to be Alive long enough to see the grandchildren if they appear, you know, and then hang out with them.
Speaker B:I mean, my mother is healthy and 80 and she hangs out with her granddaughter.
Speaker B:And that's, that's lovely to see.
Speaker B:So that's what I want, you know, and so people often aren't thinking about that.
Speaker B:They're not thinking about where they're going to be in certain time frames.
Speaker B:I think we need to understand what people think on one and try and understand that.
Speaker B:And I think there is a lot of interest in aging as people.
Speaker B:I think people do worry about their health and that's why there is this interest in aging.
Speaker B:But at the same time, they have to kind of realize that we, the research needs time, it needs resource, and we can get there.
Speaker B:And we are not all crazy.
Speaker A:Well, we hope not.
Speaker B:And also, I think when people start talking about living for hundreds of years or thousands of years, it just puts people off.
Speaker B:Because first of all, maybe we can increase lifespan.
Speaker B:It's not impossible.
Speaker B:I'm not saying it's impossible, but let's try and get there bit by bit in what we know.
Speaker B:Because at the moment, no one, apart from one individual, which some people have put into doubt, no one's lived more than 120 years.
Speaker B:There's only a handful of people that have made it to 115.
Speaker B:So we have to like, keep it in proportion.
Speaker B:But what we really want is for the majority of people to live a long, healthy life and not have too many years of illness.
Speaker B:You know, my grandmother lived till 96 and she lived independently till 94, then a year or so of ill health.
Speaker B:And that's what I would love.
Speaker B:You know, I think most people would, would be happy for that, you know, So I think that's what we need to focus on and focus on the, on the research.
Speaker B:And it is a difficult thing to convey.
Speaker B:And we're working on that.
Speaker B:We really are working hard on that.
Speaker B:We're reaching out to people to understand what people are thinking and seeing how we can fit with that rather than sort of just standing here as scientists saying our thing.
Speaker B:You know, it's important to engage with people at all different levels, all different social groups and ethnicities and so on, and just really understand what's important to them.
Speaker B:What's important to you.
Speaker B:Daphne, in terms of aging, it's exactly
Speaker A:what you said, that it's the living as healthy for as long as possible.
Speaker A: ke you were saying, to get to: Speaker A:But it's just to live healthily for longer.
Speaker A:But should that not be the job of the BSIA to communicate that to the wider public?
Speaker A:Shouldn't that be one of its PR jobs for longevity?
Speaker B:Absolutely.
Speaker B:We're trying to do that.
Speaker B:We're only a volunteer run organization.
Speaker B:We're all mostly academics and volunteers that are working and we have very limited resources.
Speaker B:We do.
Speaker B:Our money only comes from our members and from a few donors and Trusts.
Speaker B:But you're 100% right.
Speaker B:That is what we're trying to do.
Speaker B:We have.
Speaker B:So our vision is to help people live longer, healthier lives.
Speaker B:And the five pillars are.
Speaker B:One of our major roles is bringing scientists together that work on aging from different disciplines, which is, and that's what we have our annual conference and we have our online seminars to connect scientists together.
Speaker B:Another one is we engage with the public, which is we have public lectures and discussions and online and in person we're working on this communication question, as you say.
Speaker B:We're working with various people in the PR communications world to try and work on this.
Speaker B:But we know we're very quite strapped for resources there.
Speaker B:The third thing is we are advocating to government to try and increase more funding to research and wrote a paper asked by Lord Kakar, who's the chair of the Office for Strategic Coordination of Health Research.
Speaker B:I wrote a paper on the barriers to translation of Asian research and that went to the heads of some of the research councils and trying to find ways to influence government to support Asian research more.
Speaker B:The fourth thing is we do fund small amounts of research from our resources, but our resources are small.
Speaker B:So we fundraise.
Speaker B: for: Speaker B:And so we are, we are raising money for that.
Speaker B:Every small amount helps is a very small amount of money.
Speaker B:So we'd be grateful for any of your listeners would, would be interested in, in, in supporting us.
Speaker B:And then finally it's really important that we translate the research.
Speaker B:It's not that it's just publish a paper, but actually something concrete comes out of this research.
Speaker B:And so that involves working with both industry and clinicians to try and find ways to use that research into real world outcomes.
Speaker B:One of the things I really think is important is that people working on research and aging work together with People working on prevention of specific diseases, because there is work, for example, on the prevention of cancer.
Speaker B:And what they're doing is very similar to what people work on aging are doing.
Speaker B:So we need to have more interactions there.
Speaker B:So it's very important that those things are supported and translated.
Speaker B:And we invite industry and clinicians to our conference.
Speaker B:And we also support our early career researchers to think about commercialization and translation of their research.
Speaker B:So there are lots of activities that we're doing to try and make this happen, but we don't have a lot of resource.
Speaker B:So the more resources we have, the more we can do.
Speaker A:So the BSRA is doing dual work in the sense that you're connecting researchers and people within the field, but you're also announcing to the public or sharing with the public what research is being done.
Speaker A:Is that correct?
Speaker B:That's absolutely correct.
Speaker B:And as well as that, we're trying to make sure that the research gets used.
Speaker B:That comes in your first category of connecting people.
Speaker B:But we're advocating for the research and we're communicating it to the public as much as we can.
Speaker B:Obviously, there are other ways that science gets communicated to the general public.
Speaker B:We do what we can and we have a great membership that spans different things.
Speaker B:So as people work on aging from a very kind of molecular point of view, a lot of people working on cell biology, people working on aging on more physiological grounds, people working on the evolution of aging and human aging, so there's all sorts of scientists working together and want to harness all those great minds and get them to make aging research happen.
Speaker B:I think that's the way real solid research can progress.
Speaker A:Yes, absolutely.
Speaker A:The research shouldn't be siloed, which I think is less and less happening at the moment.
Speaker A:I think it used to be very siloed a few years ago, but I do think now there is some overlap and some research that is coming together.
Speaker A:And I think that is where you've seen the greatest progress is when different research groups have come together and move forward together.
Speaker A:But I think it's very important, as you said, to educate the general public.
Speaker A:And for example, people that are listening to this podcast, they are already aware of the field of longevity, be it as an investor, be it as a researcher, be it as a clinician.
Speaker A:But the vast majority of people, the general public, I don't think really has an idea of what exactly is meant by the term longevity.
Speaker A:And I think there is a lot of public work that needs to be done in order to further the whole field and also to make it more factual.
Speaker A:Rather than fiction.
Speaker A:I know that you, in your work with the bsra, you're very field evidence based and I think that's the way forward.
Speaker A:What is your ultimate goal?
Speaker B:I think you're right that the general public don't really understand what we do and what all this interest in longevity really means.
Speaker B:Because I suppose people are looking for things to improve their health and they, and they're often looking for things that improve their health kind of immediately or within, in a short space of time.
Speaker B:Whereas actually, if we think about the longer term picture, what you're looking for is something that will keep you healthier for longer.
Speaker B:It won't necessarily make you feel better within a few months.
Speaker B:And it's kind of interesting because if you talk to people in the health and nutrition world, which we've worked with quite a lot through our company, is that in that world they, people are looking for things that make them feel better within a couple of months.
Speaker B:You know, that's what they're looking for.
Speaker B:A good analogy that I like to think about is like there are preventative measures in medicine that we have already, for example, controlling blood pressure.
Speaker B:If you have high blood pressure, then you are given tablets to control that.
Speaker B:And high blood itself doesn't really have symptoms.
Speaker B:And taking those tablets doesn't necessarily do anything to you in the short term, but it will prevent you having a heart disease and probably prevent a lot of other things happening to you as well, you know, bad things happening to you.
Speaker B:So, so there is a kind of paradigm for that.
Speaker B:It's kind of a bit boring, right, because you know, you're just taking something to prevent something happening is a hard thing to, to get people to engage with.
Speaker B:But it is something that I think we need to look at.
Speaker B:Trying to find other ways to prevent people getting ill or even aging and something that you might take regularly or do regularly.
Speaker B:We know that things like diet and exercise already have an effect in that respect.
Speaker B:So I think we want to make people understand that this is a much better route than always seeing healthcare as something that you, you only turn to once you're really unwell.
Speaker B:And actually healthcare should really be about keeping you healthy and not just patching up when things go wrong.
Speaker A:And a lot of the longevity interventions, I think from what we understand now need to be started when we're relatively young.
Speaker A:So you've mentioned before Metformin, a drug that costs pennies nowadays.
Speaker A:I read a research paper that if you start metformin in your 60s, it's not really effective.
Speaker A:Whereas when you started earlier your 30s or 40s, it's very effective for all the sort of health span and longevity benefits.
Speaker A:I guess it's hard trying to convince someone in their 30s or 40s that Healthspan and longevity is something they should consider.
Speaker A:Is that your finding?
Speaker B:Well, I can't comment on the metformin data because I'm not aware of that difference.
Speaker B:But there's still a lot to be done to understand metformin's effect on us.
Speaker B:But the more general point that you, you may, you know, an intervention, once it's been shown to work, may need to occur earlier, I think is very possible.
Speaker B:I mean, given from the work that we've done with model organisms, we tend to give these drugs early and we know that aging starts relatively early.
Speaker B:I mean, aging's always happening, but the older you are, the faster you age.
Speaker B:And there seems to be from evolutionary theory and general observation that aging really starts getting going near the end of the kind of reproductive period.
Speaker B:Right.
Speaker B:So whether you look at a worm or you look at a human, so that kind of fits with the 30s and 40s timeframe.
Speaker B:Right?
Speaker B:So yeah, it might be.
Speaker B:The problem about it is it's very difficult to get a drug approved under those circumstances because you're talking about giving someone a drug for a long, long time to healthy people.
Speaker B:So it's got, the safety has to be really amazing and you have to be able to show that it has that preventative effect.
Speaker B:So that means if you, you know, someone in their 30s or 40s, wouldn't ordinarily, most people, if they're 40s, are unlikely to get chronic illnesses until they're in their 50s or 60s or later.
Speaker B:So that means you have to prove that it's working.
Speaker B:You have to do a study that's about 30, 40 years long, which is almost impossible, you know, so a lot of the studies in aging will work with people that are older because if you have healthy people, 70 year old healthy people, then there's relatively high chance that some of them will get ill in the next few years.
Speaker B:And so then you can see whether your drug prevents that or prevents some other sort of decline within a few years.
Speaker B:But if you start with people that are in their 30s, you're going to be waiting a long time to see that, that change in decline that, I mean, it's kind of like analogous to what we're doing with the worms, right?
Speaker B:We, we see this decline of worms after three days.
Speaker B:Three days is when they kind of stop reproducing.
Speaker B:We see this decline and we can see interventions that stop them declining.
Speaker B:Right.
Speaker B:That would be potentially something you could do.
Speaker B:But the decline in your 30s and 40s is quite small, variable, depending on different things.
Speaker B:So it's much more difficult to measure than later on.
Speaker B:There's a kind of, you might be right that we need to start taking metformin in our 30s, but it'd be very difficult to do that experiment to give healthy people metformin from their 30s onwards and to justify that as an.
Speaker B:As an experiment, unless you had really good evidence.
Speaker B:So there are challenges there.
Speaker A:Yeah.
Speaker A: In: Speaker A:From my understanding, it helps companies run de elegant studies for aging healthspan screening.
Speaker A:When you started that company, what gap were you trying to fill?
Speaker B:While we were trying to fill the gap that you can't look at aging quickly and easily?
Speaker B:Because a lot of research that's done in early drug discovery is done on cell lines from tissue culture cells from disease models.
Speaker B:And those cell lines you don't see aging unless you take a primary cell line.
Speaker B:And you go through many passages, but most cell based essays, you can't see aging quickly.
Speaker B:And as we discussed already, mice take a long time to age.
Speaker B:So we needed the whole organism model to look at aging where we could go through a lot of different compounds quickly.
Speaker B:And that's where we thought we could do that.
Speaker B:And the other thing that the company provides is that C. Elegans expertise.
Speaker B:So there are a few companies around the world, not many that have their own internal C. Elegans labs, but to set up a C. Elegance lab takes a lot of resource expertise and so on.
Speaker B:So we were kind of offering ourselves as a C. Elegans lab that we could work with for other people so they wouldn't have to do all that and they could test their compounds, their products, their drugs and that kind of thing quite quickly and get results fast about whether it worked in that whole organism model.
Speaker A:So what do companies typically want to know when they come to work with Magnitude bioscience?
Speaker A:Is it does this product work or not?
Speaker A:Or is it more the research stage and what can be best answered by those worms?
Speaker B:Yeah, so it's a mixture of things.
Speaker B:So sometimes they might be working on some candidate drugs and they want to know which one's the best one, you know, which one's most likely to work for aging or for some sort of disease.
Speaker B:We can make disease models as well, like kind of things related to Alzheimer's or other models.
Speaker B:So they can want to See which one worked, which was most likely to work with to help them decide internally which ones to follow on.
Speaker B:Sometimes they have products already or drugs already and they want to see, well, okay, does this really have an effect on aging?
Speaker B:Because they've just looked at some papers and have things that are theoretically involved in aging, but they haven't really been able to show it works in aging in humans, as we've discussed, it's very difficult.
Speaker B:So they want to have some aging model where they can test for actual effect on aging.
Speaker B:So they come to us to look at that.
Speaker B:And more recently we've had companies coming to us because we've got more of a high throughput platform now who might have want to screen libraries of thousands of compounds and say, well, okay, we've got all these compounds.
Speaker B:Do any of them slow aging?
Speaker B:And the chances are that some of them will.
Speaker B:They've never been able to tell because they've got never had a system to test that.
Speaker B:You can't take a thousand mice and do them all for three years and see which ones work on aging.
Speaker B:Well, you could, but it would take cost you billions to do that.
Speaker A:Is there anything you're most excited about right now that you've seen in other people's research or your own, or any insider info you can give us on what's coming up?
Speaker B:At the moment, I'm really focusing on some of my our own research and we're really excited to look at can we apply this idea of bringing down folate levels of bacteria in humans in a way that's safe?
Speaker B:We are a little bit concerned because later this year it's going to be mandatory to fortify flour with folic acid.
Speaker B:And that's been done to prevent neural tube defects because if a mother is folate deficient, there's much higher chance of neural tube defects.
Speaker B:And so obviously that's a good thing for that group.
Speaker B:But what we are worried about is that it might affect other groups, for example, older people or people with some problems with their gut microbiome.
Speaker B:And what we found was that the folic acid has a breakdown product and that breakdown product can't be used by humans, but it can be used by certain bacteria to make more folate, which we have shown is potentially harmful.
Speaker B:So we're worried about that.
Speaker B:It hasn't really been considered.
Speaker B:And so we're trying to work with clinicians at King's College London to try and see if that has an effect and if there's a way we can counteract that effect.
Speaker B:Folic Acid is actually put in the flower in many countries, including the U.S. so it's something that I think should be looked into a bit more, but I'm excited about also.
Speaker B:The other side of the coin is if we can understand this.
Speaker B:Like I was talking to you about that study about exercise causing the reduction of bacterial folate levels in that paper that I talked to you about, maybe this is a pathway in, to making this cupulus healthy.
Speaker B:I like to think about things from an evolutionary point of view.
Speaker B:And animals evolve much later than bacteria.
Speaker B:Bacteria were around for like a billion years before any animal showed up.
Speaker B:And so we've always had to deal with bacteria and microbes.
Speaker B:There's always been a battle between the animals and the microbes.
Speaker B:What we've done is managed to contain those microbes in our intestines and put them to good use.
Speaker B:And that allows us get more nutrients from our food and so on, help us digest our food.
Speaker B:A worm doesn't do that.
Speaker B:A worm has to go to a rotting apple and let the bacteria digest the apple and then eat the bacteria.
Speaker B:When we eat an apple, we.
Speaker B:We can eat a nice fresh apple and let our microbes get the nutrients out of it later.
Speaker B:So we've got this kind of like cauldron of microbes inside us, and we control that in a way that's beneficial to us.
Speaker B:But as we get older, everything about aging is about losing control, you know, losing that balance.
Speaker B:And homeostasis is what happens with aging.
Speaker B:Right.
Speaker B:So that's also going to happen with our microbes is always going to be a.
Speaker B:We're going to have.
Speaker B:Make it harder to keep them under control.
Speaker B:And so I think if we can find ways to.
Speaker B:To manipulate the system to maintain that control for longer, that would be a really great way and I think kind of obvious way to try and keep us healthy for longer.
Speaker B:Excited about that and working together with people that work in humans, with microbiologists and all sorts of people to try and make that happen.
Speaker A:The folate discussion is an interesting one.
Speaker A:I know there are many people uproar about it.
Speaker A:And here comes the question also a little bit, and I don't know if you have any strong opinions on that, is how much should the government be involved in making sure the society stays healthy or as healthy as possible?
Speaker A:You know, I know the sugar tax, and that's all fine, but putting folate into food, folic acid might be a step too far.
Speaker A:Apparently it's only in plain flour, not in whole wheat flours where it needs to be added.
Speaker A:But Is that taking away the responsibility and the autonomy of the population?
Speaker A:And there is a quite, you know, a number of people that are allergic to folate and don't react well to it.
Speaker B:Yeah, there's a really good question of how much that intervention should be there.
Speaker B:And also I think there's about 200 neural tube babies born with neural tube defects a year.
Speaker B:And it's thought that this intervention will prevent about half of them.
Speaker B:So we're preventing 100 kids a year being born with neural defects, which is a great thing.
Speaker B:Right.
Speaker B:But we're also supplementing millions of people and we don't know what's going to happen.
Speaker B:I mean, it might be totally fine.
Speaker B:We don't actually know.
Speaker B:And that's the thing.
Speaker B:We have to hold up our hands.
Speaker B:We don't know.
Speaker B:But shouldn't we know that before we start doing it?
Speaker B:We should know what's going to happen to those other people.
Speaker B:And I suppose there have been studies looking at this, but sometimes, for example, there were studies showing that folic acid caused the increase in colon cancer, and then there were other studies that showed that it didn't.
Speaker B:So overall, when they did the meta analysis, the meta analysis concluded that actually, no, there isn't an effect.
Speaker B:But maybe we don't know why in some studies they saw effects and why.
Speaker B:So they didn't.
Speaker B:Maybe the ones that, where they did see an effect, there was something about their microbiome which was different from the ones where they didn't see effect.
Speaker B:That may be a plausible explanation.
Speaker B:So, yeah, it's a bit worrying that, that we do that.
Speaker B:Whether or not, I mean, it's a whole.
Speaker B:It's almost like a.
Speaker B:It's a political decision about how much the government should be involved in health.
Speaker B:I mean, from one perspective, you say, well, should there be a.
Speaker B:If you were like completely against that kind of intervention, you would say, well, we should be able to drive around without wearing seatbelts and go as fast as we like.
Speaker B:Right.
Speaker B:But most people would disagree with that.
Speaker B:Right.
Speaker B:Think that seatbelts are a good idea.
Speaker B:But on the other hand, I do take your point that there are some interventions that might be too far.
Speaker B:If you wanted to have white bread and not folic acid, it's going to be very difficult to do that.
Speaker B:Right.
Speaker B:It's kind of restricting something that doesn't seem.
Speaker B:It's not harming anybody else to take.
Speaker B:So maybe you could say speeding, for example.
Speaker B:That's a clear one.
Speaker B:It shouldn't speed, because it's not just that.
Speaker B:Yourself, you might actually Harm other people seat belts.
Speaker B:Well, you may be not harming someone else, but at the same time you don't want people to dying in accidents.
Speaker B:But not having folic acid in the flour, it's not harming, especially if you're not a woman of childbearing age.
Speaker B:Basically, if you're outside of the target group, then why should you have to have folic acid in there?
Speaker B:So yeah, I think it's a tricky
Speaker A:one, which is the majority of the population, let's not forget that, you know, and, and it's an easy supplement to give to women who want to become pregnant or are pregnant.
Speaker B:Well, I think the problem has been, is that it's actually the neural tube defects are much more common in areas of lower economic.
Speaker B:Social economic groups.
Speaker B:So.
Speaker B:And those people probably wouldn't take folic acid normally.
Speaker B:So that.
Speaker B:And then.
Speaker B:And it's because their diet isn't good enough.
Speaker B:Because actually for most people, they don't really need to take folic acid.
Speaker B:They, their diets should provide enough folate anyway.
Speaker B:So that's another question.
Speaker B:Right.
Speaker B:So if you live in the areas of the lowest social economic group, you live shorter and you have more years of ill health.
Speaker B:Right.
Speaker B:So really we should try and address that maybe more than the consequences of that.
Speaker A:Does it all come down to money?
Speaker A:Because if you look at it in a very objective way, one of the most damaging things to human beings in general is sugar.
Speaker A:Whether you're old or young, you know, rich or poor.
Speaker A:Sugar, I think we can all agree on, has no benefit to the human being other than give pleasure while you're eating it.
Speaker A:Do you think though that the sugar lobby, for example, is so strong that the government would never interfere in really heavily regulating it other than maybe adding a sugar tax to it?
Speaker A:Do you think the government picks an easy battle to say, okay, we'll add folic acid?
Speaker A:Tick.
Speaker A:We've done something for society rather than really looking at real life benefit.
Speaker B:I mean, I spoke to somebody who said that if the government really wanted us to live and eat healthy, they could, because you can arrange things in a way that makes it more advantageous for people to eat healthily and so on.
Speaker B:Yes, but then again, it's a difficult one because the level intervention that you might not want to have sugar, for example, I would say a bit of sugar is not that bad.
Speaker B:It's just that having too much sugar, you know, it's not like it's a poison just in itself, like taking a spoonful of sugar is going to kill you.
Speaker B:Right.
Speaker B:It's like it's just the equation of quantity.
Speaker B:Right.
Speaker B:So it's the same kind of question.
Speaker B:If someone wants to eat a sugary snack, should we stop them?
Speaker B:You know, I don't know how to get around that.
Speaker B:It'd be much better if they kind of understood that the sugar isn't great, so it might be better to do something else.
Speaker B:But at the same time, you know, sugary snacks are cheap forms of calories.
Speaker B:Right.
Speaker B:So if you're hungry, you eat a sugary snack.
Speaker B:Right?
Speaker B:So I think you have to provide a affordable alternative.
Speaker B:It's no good saying to people, oh, you've got to eat these other things if it's not within their reach.
Speaker A:No, no, absolutely you're quite right.
Speaker A:But I'm not saying the government should or shouldn't.
Speaker A:I just want to understand sort of what your view is on with regards to longevity as a whole.
Speaker A:What is the direction the government should take and maybe people as a whole should take?
Speaker B:Well, I think for a lot of these things I always come back to what we know, what we don't know.
Speaker B:Right.
Speaker B:So we still.
Speaker B:So even like the folic acid question, we don't know whether folic acid is harmful or not.
Speaker B:We're just hypothesizing from stuff that we've done in C. Elegans.
Speaker B:So we don't know if it's true in human.
Speaker B:But I think we should find these things out.
Speaker B:I think we need to do more research to understand these things.
Speaker B:We can do anything about it.
Speaker B:I mean, I think, although I also think that the evidence is crystal clear that being better off makes you healthier.
Speaker B:So you could argue, well, maybe the government should try and look after people a bit more.
Speaker B:The other problem that we have is affecting the government and affecting what the government can do is the fact that we have an aging population.
Speaker B:So that aging population puts much more pressure on our economic system on, on our health service.
Speaker B:When I came Back to, to UCL 20 years ago from the Netherlands, I heard people who work on this subject predicting that in 20 years time we're going to have problems with inflation and economic issues and health service issues and those that has come to pass and purely from the demographics, purely from the fact that we've got an aging population, our population is continuing to age and we're having trouble because the baby boomers now, the people that were born after the Second World War are now in their mid to late 70s and that's causing a problem.
Speaker B:But their children, the Gen X's who are now in their 50s, 50s and 60s, when they get to that age, then we're really going to have a problem.
Speaker B:So even though we're suffering the problems of our aging population now, it's going to get worse in the next 10, 20 years.
Speaker B:That means that we have to try and find ways to keep those people healthy.
Speaker B:And we have to think about prevention rather than treatment when it comes to disease.
Speaker B:Like I went to this conference on prevention of cancer and there was someone talking about the World Cancer Atlas and the map that made a huge impression on me was a map of how many radiotherapy machines there are per country across the world.
Speaker B:And there's something like 47 countries in the world that don't have a single radiotherapy machine and 30 something countries that have only 1 per million people.
Speaker B:And in those countries, surgery is also not an option.
Speaker B:So in actually most of the world, treatment for cancer isn't really an option or very limited in most places, prevention is all you've got.
Speaker B:And I think that's going to happen to more of the world.
Speaker B:There's going to be a point where actually the health service, we know we already say it with the NHS is really struggling.
Speaker B:And I think there's going to be a case where prevention is going to be the only way to get out of that problem is to keep people healthy, keep people out of hospitals in the first place.
Speaker B:But that's just going to take time and investment.
Speaker B:So we need to start investing now.
Speaker B:It's bad now, but in 20 years time it's going to be worse.
Speaker B:So we have to really invest in this.
Speaker B:And I think the way to do it is not just to invest in aging research, but invest in aging research working together with prevention of specific diseases.
Speaker B:Because that's kind of how we're going to unlock, block this.
Speaker B:You know, we were discussing earlier, get people in their 30s to start taking interventions to slow their aging.
Speaker B:In reality that that's very hard to get through trials.
Speaker B:But what is easy to get through trials is to look at risk groups.
Speaker B:If you look at a risk group for a particular disease and then prevent them from getting the disease, then if that works in the risk group, then you can bring it back and make it to a wider population to work backwards, if that makes sense.
Speaker B:So I think we need to do that in a serious manner.
Speaker B:And that's what I've argued before and I want to continue to argue that case.
Speaker A:I think that's an incredibly valid point you are making.
Speaker A:How do we get there?
Speaker B:I don't know.
Speaker B:That's why I think Working with the general public is important because until the public understand the value, they won't be putting pressure on the politicians to make a difference.
Speaker B:And politicians, the main thing they care about is getting reelected.
Speaker B:And if they put in Asian research and prevention of the design disease now, even if they put billions of pounds into it, they're not going to see the results to that until 10, 20 years time or more, in which case the electorals, they're no longer in power, the electoral cycle is finished.
Speaker B:So that is the challenge.
Speaker B:But I think if it became important to people, there will be some, at least some political pressure and some political action there.
Speaker B:We are trying to do that.
Speaker B:And I do think it is possible to frame this in a way that people can understand and we can, and we can get to.
Speaker B:And I think we got to.
Speaker B:To be honest, I think a lot of the longevity of people are appealing to the egos of the super egocentric people.
Speaker B:Right.
Speaker B:We have to start appealing to what everyday people care and think about, which is usually the their families, their day to day life and what their aspirations are and what their aspirations are for their towns and villages.
Speaker B:So I think we have to make more of a connection to a broader group of people.
Speaker A:Absolutely.
Speaker A:To sum it all up, do you see the future of longevity in research work as much as in educating the public about what's available already, as well as, you know, preventative care?
Speaker B:I think all of those, because I think we need to do so much more research.
Speaker B:We've only just scratched the surface of understanding aging, so we need to do so much more research.
Speaker B:But we also need people to be aware of what we know now.
Speaker B:And some of the stuff is quite straightforward and we need to think about prevention as an important thing in life.
Speaker B:Especially difficult to think of prevention.
Speaker B:It's almost like biblical, right?
Speaker B:Because and I'm not a religious person and I don't really know anything about this, but you know, I did see the musical Joseph and his amazing Technicolor Dreamco.
Speaker B:And the message of Joseph, which is the beginning of Genesis in the Bible, is that you have to store stuff because there will be times when you need that the corn, when there's.
Speaker B:The things are bad.
Speaker B:Right now if you think about it, that's prevention, isn't it?
Speaker B:It's preventing something that's not happening.
Speaker B:And it's also a kind of saving for a rainy day.
Speaker B:It's a bit like not going for the chocolate cake, but holding back a little bit.
Speaker B:Right.
Speaker B:So looking at prevention is something that takes that kind of high Level of thinking.
Speaker B:Okay, I'm going to store something, I'm going to keep myself healthy.
Speaker B:If you're taking blood pressure tablets, none of those blood pressure tablets are going to make you feel better.
Speaker B:But you're doing it because you want to stop yourself getting a heart attack in 10 years time, you know, so it's almost like a whole way of thinking, a whole culture of thinking which isn't as glamorous as, as the kind of things that the social media influences talk about, but is important.
Speaker A:Nitin, I could talk to you for hours on end.
Speaker A:It's so interesting, your views and your thoughts and, and all the research you've done.
Speaker A:But we have to come to an end.
Speaker A:I always ask my guests five rapid fire questions.
Speaker A:What's the single best piece of advice you would give your younger self?
Speaker B:Believe in yourself.
Speaker A:Name one habit everyone should adopt for a longer, healthier life.
Speaker B:I would say stay active every day in some form or another.
Speaker A:If you weren't in bioscience, the longevity science, what career would you have chosen?
Speaker B:As I said before, I went to university, originally wanted to study physics and I really enjoyed it.
Speaker B:So I think something like that.
Speaker B:But also a designer or engineer, that kind of thing.
Speaker A:You're kind of designing and engineering right now, right?
Speaker B:I suppose I'm doing that anyway.
Speaker B:Yeah, I suppose I am.
Speaker A:What microdose habits A five minute routine or small daily action here yields outsized longevity benefits.
Speaker B:Cleaning your teeth.
Speaker B: In the: Speaker B:And I think there are potential links between oral microbes and Alzheimer's.
Speaker B:Teeth cleaning is really important, I think.
Speaker A:Last but not least, what's the craziest longevity myth you've encountered and is there any truth to it?
Speaker B:Oh man, I've encountered a lot of longevity myths.
Speaker B:Well, I don't know if it's a myth, but I've come across people that want to grow humans for spare parts basically and they were serious about it and they were asking me if they knew anyone.
Speaker B:They were saying, oh yeah, they come from California and they're all very conservative.
Speaker B:Is there people in England that are maybe a little bit more outgoing that might want to invest in this?
Speaker B:And I said no.
Speaker B:So that was out there.
Speaker A:Gosh, you leave us hanging there on a shocker.
Speaker A:That's food for thought.
Speaker B:There is some crazy stuff out there.
Speaker B:There really is.
Speaker B:And people are not holding back.
Speaker B:They will do anything.
Speaker B:I mean, and it is a little bit scary to be honest, but we'll see.
Speaker A:Wow.
Speaker A:I've had various answers to this question, but I think this one is way out there.
Speaker A:Way out there.
Speaker A:Thank you so so much for coming on the podcast.
Speaker A:I really appreciate your time and all the work that you're doing to make us live longer and healthier and better overall.
Speaker A:So thank you so so much.
Speaker A:I really appreciate it.
Speaker B:It's been a pleasure been lovely talking to you.
Speaker A:This was a very grounded conversation with Professor Weinkopf diving into the real experimental biology what the data can genuinely support, what still needs work, and where the field has to stay disciplined.
Speaker A:We have learned so much from C. Elegans over the years.
Speaker A:It's tiny, but it has been an incredibly effective way to stress test ideas about aging and healthspan.
Speaker A:It lets us test cause and effect at speed, quickly and properly, including how the bacteria it lives with and the metabolites moving between them can meaningful shift aging outcomes.
Speaker A:Professor Weinkove is championing an evidence led approach by keeping the focus on what is real, measurable and reproducible.
Speaker A:If you enjoyed this episode of Beyond Longevity, please subscribe and share it with your friends, family and colleagues.
Speaker A:For more information and links, have a look at the show.
Speaker A:Notes let's redefine what it means to live longer, to live healthier.
