Dr Bradley Elliott — physiologist, university lecturer, and a trustee and Communications Lead at the British Society for Research on Ageing — joins host Daphna for a refreshingly honest conversation about what longevity science actually knows and what we still cannot explain.

This episode cuts through the certainty. We talk about biomarkers and biological age, why many measurements may be tracking effects rather than causes, we discuss extracellular vesicles and the surprising limit of science. Dr Bradley discusses some of his papers and related research, and our conversation challenges much of the conventional wisdom in the longevity space.

What we cover:

-Why we still do not know what fundamentally causes ageing — and why every “root cause” often leads to something deeper

-What biomarkers really measure, what they can and cannot tell you, and which markers are most worth tracking right now

-Biological age vs chronological age: where the concept is useful, and where it gets overclaimed

-Why muscle is one of the most underrated “health organs” in ageing — and what it supports beyond strength

-Exercise for longevity: the evidence-based basics, plus what matters most for consistency and adherence

-“It is not too late”: what studies in very old adults suggest about strength gains later in life

-Extracellular vesicles: the hidden communication system between cells, and why it is getting so much attention

-Wearables: why they can still be useful even when the numbers are not perfectly accurate

This is a fascinating episode with someone who knows how to communicate science and make it relatable

Links to Dr Bradley Elliot:

- https://www.westminster.ac.uk/about-us/our-people/directory/elliott-bradley

- https://bsra.org.uk/bradley-elliott-2/

- https://www.bradelliott.online/

Papers & Research Referenced

• Perri et al. (2025) — Delphi review identifying 14 biomarkers of ageing for use in human research (co-authored by Dr Elliott)

' https://pubmed.ncbi.nlm.nih.gov/39708300/

• Lady V Barrios-Silva et al. — Activin subfamily peptides and prediction of age and physical function (undergraduate-led research, University of Westminster)

https://pubmed.ncbi.nlm.nih.gov/30178598/

• Dr Yvoni Kyriakidou (PhD) — Exercise-induced muscle damage in young and old men; extracellular vesicle characterisation post-exercise

https://pubmed.ncbi.nlm.nih.gov/34650440/

• Dr Niharika Duggal (University of Birmingham) — Masters athletes and immune function; older athletes vs. age-matched non-athletes

https://pubmed.ncbi.nlm.nih.gov/29517845/

• Stephen Harridge (King's College London) — Resistance training in 90+ year olds; gains in muscle strength and mass in the oldest old

https://pubmed.ncbi.nlm.nih.gov/10398199/

• Science paper on genetic contribution to longevity — updated estimate shifting genetic contribution to ~50% (noted with editorial by Dr Elliott)

https://www.science.org/doi/10.1126/science.adz1187

https://theconversation.com/what-new-twins-study-reveals-about-genes-environment-and-longevity-274763

https://www.ukbiobank.ac.uk/

If you enjoyed this episode, we'd love it if you took 60 seconds to leave us a review on Apple Podcasts or Spotify. It genuinely helps more people find the show and means we can keep bringing you honest, science-backed conversations like this one. Thank you

https://beyond-longevity.co.uk/

Chapters:

00:00 Why We Age

01:52 Meet Bradley Elliot

03:07 From Sports Science

05:32 Defining Ageing

07:03 Mechanisms And Theories

09:29 Biomarkers Explained

13:02 Delphi Biomarker List

16:59 Myostatin Study Story

21:25 Actionable Biomarkers

26:07 Wearables And Accuracy

27:38 Endocrine Fingerprints

30:11 Muscle And Healthy Ageing

33:21 Athletes And Immunity

34:26 Muscle Mass And Healthspan

36:36 Exercise Dose Guidelines

39:42 Resistance Training Plateau

40:42 Lifestyle Versus Genetics

42:42 Muscle Damage Study

44:44 Extracellular Vesicles Explained

46:49 Young Blood Controversy

50:08 Dream Research With Omics

56:55 What People Misjudge

58:43 It’s Never Too Late

01:02:41 Rapid Fire And Wrap

01:04:31 Final Takeaways

Welcome to Beyond Longevity, the podcast that explores not just how we age, but how we can build a longer, healthier future for ourselves.

Why do we age?

Joining me today on Beyond Longevity to discuss this fundamental question is Dr. Bradley Elliot, lecturer in Aging Physiology at the University of Westminster and a trustee and communications lead at the British Society for Research on Aging.

In this episode of Beyond Longevity, we get into one of the biggest questions in longevity.

What is aging?

What do we actually know about it?

And what do we still not know about it?

Because for all the progress in the field, Dr. Bradley makes a very striking point.

We still do not really know why we age or what is ultimately driving the process underneath it.

That is what makes biomarkers such an interesting debate.

We now have more and more ways to measure aging.

But what are those markers really picking up?

Are they getting to the biology causing aging, or are they just tracking the footprints aging leaves behind?

And because Dr. Bradley's main focus is muscle, this also gives us a very practical way into the conversation.

We talk about what happens to muscles as we get older, why that matters so much for health and physical function, and what it can tell us about healthy aging more broadly.

Across a range of Dr. Bradley's papers, we explore what we know, what we still do not know, why biomarkers matter, and what healthy aging really means once you move past the hype and start asking the harder questions.

So let's ask those questions.

Dr. Bradley, welcome to Beyond Longevity.

Hello, Dr. Bradley.

Thank you so much for joining us on Beyond Longevity.

Well, thank you for having me.

Defna, why don't you tell us a little bit about you, your background?

Sure.

So my day job, the reason I guess I'm here is I have an academic post at University of Westminster.

My formal grownup title is Reader in Aging Physiology.

And I've been there for about 10 years studying aging biology and especially studying how humans age.

I've got a couple of hats that I wear.

So I do lots of communication and outreach as well as my science life.

I spend a lot of time translating science, trying to get people to understand science outside of academia, talking policy, talking to corporates, talking just to general public and really fun events.

I would do a lot of work for an organization called the bsra, British Society for Research on Aging.

So I sit on their board of trustees and I'm the head of their communications as well.

What else do you need to know about me?

Background wise, I'm a pretty easygoing Kiwi guy.

I came to aging longevity relatively late in my career.

I've Been on it about 10 years now, but a bit of a mixed academic background and just doing interesting topics that I think are fun, and that's what gets me to somewhere like here today.

Tell us about some of those interesting, fun topics.

So my academic training's a bit mixed.

I was a ice hockey player growing up, and that's relevant because I wasn't scientifically very literate kid in school.

I was a nerdy kid, but I wasn't interested in science at all.

I made a deal with my father at the time that I would go to university and I did sports science because that sounded like the most fun thing to do.

Spoiler.

It was a serious, hard science and it was quite challenging, and it wasn't just running around in a field, but I actually really enjoyed exercise physiology, the physiology of how athletes work as outlier populations, as extremes of human ability.

And I got really interested in that.

But in my sports science life, I was studying how muscles grow.

And then for my master's, I did a lot of research around how muscles waste and chronic diseases and how we lose muscle into, say, older age or into disease, sarcopenia and cachexia and similar.

And off the back of that, I actually ended up here in London doing a PhD at the University of Westminster, where I studied muscle loss again in altitude and low oxygen environments and diseases again.

And it's just been a really interesting career where I just followed what was interesting at the time.

And that's what led me to where I was.

And that kind of mixed background of formal training and, say, clinical research and sports science and studying outlier populations and then my PhD all led to me getting an academic post at Westminster, where I got bonkers lucky.

I got an academic job way earlier than I should have for an international audience.

I got tenured really young and I was really lucky.

But when that happened, it was almost unexpected.

And then the university just says to you, congratulations, welcome aboard.

Here's your job.

And instead of paying to train, I was being paid to do research.

All of a sudden that was a really weird moment of my life.

But they also said, and what are you going to research?

You can do whatever you want.

And I was kind of, wow.

So I sat down and thought about it for a while and really, really thought, what Have I done?

Where am I going?

And what's the biggest challenge?

And that's when I first got into aging at the tail of my PhD, at the start of my academic career, of my lectureship, was, what is aging?

And then what can I contribute actively?

And that's been a real ride for the last 10 years.

So what is aging

behind the scenes?

Whenever I do interview prep, I always think about what questions you can ask.

And everyone says, what is aging in a situation like this?

And I'm going to give a really annoying scientist answer.

I don't know.

That's really hard to say.

When I do public work, when I'm doing public outreach, people want to know clean answers.

But the honest answer is, I don't know.

And I don't think we know.

That's the point.

Science is discovery.

If we knew what it was, it'd be history, and that wouldn't be my interest.

I like the unknowns.

We know aspects of it, I guess we know it involves like a continuous decline over time.

We put criteria around it.

So I often use four criteria when I study aging.

It's intrinsic and caused by processes within us, presumably not externally.

Therefore, it takes place over time.

So it's not falling and breaking a bone, but it's bones getting weaker over time.

It's universal.

Happens to all of us.

And it does across humanity.

Absolutely.

Happens to all of us.

Maybe not some species of animals, but definitely in all humans.

It's universal and from a biologist point of view.

So studying the biology of aging, it is deleterious, it is bad for you.

So it's things that fit those criteria.

But then we get into the details and it gets messy really quickly.

So we can talk about, like, cell processes and ros and senescence and all those kind of fancy words we throw around.

But for now, I don't think we know.

And that's what makes it really cool.

But do we not know why we age, or do we not know what aging is?

What about aging do we not know?

So we know, we suspect mechanisms.

Right.

But why do we age is a really good question.

Is it like an evolutionary accident program, theories of age for people who've heard of those things, Is it a byproduct of complicated multicellular life?

So it has to happen.

It's probably a bit of both.

I think it's probably a bit of both schools of thought, but mechanistically, like, if you ask a cell biologist exactly what causes aging, we've got good ideas.

Absolutely.

But every time we get a really good hypothesis and really rigorously test it in animal models, for example, like in a C Elegant, for example, we can make it live lots longer, we can make it keep function for longer.

And that's true across lots of animal species.

And there's things we can.

Humans can do to help us age better.

Sure, we'll talk about as we go along, but every time we come up with a root cause of all of those things, senescent cells, telomere shortening, Ross accumulation, all those type of things, and we say, oh, there it is, that's it, that's the cause.

There's something underlying it, there's something causing that.

Right.

And every time we come with a really good idea, like for example, telomere theory, great idea.

And then we go and find papers or animal models where it doesn't happen, or papers like recently there was work in house mice, domestic mice, and telomeres shortening not happening in a predictable way.

And so that gets a kicking as a theory as well.

So yeah, molecularly we've got ideas, but we don't have the.

This is what causes aging.

This is what aging is.

We observe aging like a phenotype in people.

It's a collection of symptoms, if you will.

Muscle wasting, cognitive decline, eyesight, my hair getting gray, my reaction time slowing down, stumbling over a stair, all those type of real things.

But from a really core point of view, what it is, that's the really cool questions.

I think, for example, many listeners might have heard of something called the hallmarks of aging, especially if they're slightly academically inclined.

It's one of the ways we characterized aging.

And we said, okay, as a community, these are the things we kind of agree are the major factors involved in aging.

But we never said that's what aging is.

We just said these are things that seem to associate with or link to aging.

But there are ways of measuring it almost.

But what's under that?

That's the question, I guess.

So you're not contradicting yourself, I guess, by saying we don't know what aging is.

We know what chronological aging is, obviously those birthdays we have.

And so just to delve a little bit deeper into that, because I think that's a really interesting angle.

And I have to say I haven't really heard that phrase from anyone else, the way you do it, that we are not quite sure what aging really is.

Because even though you say we don't know what Aging is.

You've co authored a paper noting 14 biomarkers of aging.

So biomarkers are super interesting.

I love a biomarker.

So I study humans.

And the problem is, when you study humans is we live a long time.

That's a good thing.

You know, that's kind of the point.

The point of most medical research has been to keep us healthy and alive for longer.

But if I come up with some magical idea or some cool new hypothesis and say, oh, brilliant, someone has found a gene in worms or a process in a fly, or even a pharmaceutical like a small molecule drug that seems to make small animal models live longer, what would happen in humans?

Well, brilliant.

Let's do a clinical trial and we could put people into random groups and we could study them for 100 years.

Well, no, we can't do that, can we?

Like no trial is going to last that long.

We can do retrospective analysis, we can do observational studies, we can do spontaneously natural experiments.

But funding a trial that will take place over decades or a lifetime isn't plausible.

Controlling someone's environment in the same way that we control small animal models to make sure everyone eats the same, lives the same, exercises the same, is exposed to the same environmental pollutants or similar, has the same stresses in their day to day life is implausible.

So when we study humans and we study human aging, we can't see how long did they last.

Like longevity in an experimental trial.

We can't accurately say what someone's biological age is without using biomarkers of age.

And they're really functionally useful things.

Absolutely.

A lot of biomarkers of age measure people's health.

That's the point.

But they're markers of health.

So aging is complicated.

Spoiler.

It's the world's most best statement.

Either aging's complicated.

Thanks, Brad.

Aging is complicated.

And like you rightly say, chronological age is different to biological age.

And that's brilliant.

I like that model.

And so I spend a lot of time studying incredibly healthy people.

And the reason I do that with outlier populations, studying extremely healthy older people is we use it to stress test potential biomarkers of age.

And that's what my research focus is.

That's entirely my hypothesis.

If someone comes up with a cool idea and then we stress test it, and one of the ways we stress test a biomarker of age is, does it change with age in a predictable way in a population?

Yes.

Brilliant.

First test passed.

Does it change positively in a healthy population and negatively in an unhealthy Population, that's another marker.

So we're measuring their health.

It's a deeper question if we're measuring aging processes at that moment of time.

Like lots of biomarkers of age also measure acute events that aren't aging per se.

If someone gets an infection and then a biomarker of age shifts, you're not measuring biology of aging, you're measuring another process.

So what we did in that paper, in the Perry paper you mentioned, Peri et al.

20, 25, was we stress tested the amount of evidence behind the current biomarkers of aging.

And there were really interesting way of approaching it.

It's called Adelphi Review, which was the first time I got to be involved in one of these processes where you just get a bunch of people.

I'm going to use the word experts in their field with experts and inverted quotes because the only person that ever calls a scientist an expert is an external.

I find, even though I'm not that egotistical.

But you get a bunch of experts in the field, stick them in a room and then say, okay, cool, what are some, in this case biomarkers of age that you guys think are relevant?

And we hired almost 100 people at the start and we listed hundreds of things and said, okay, cool, which ones do you think is enough evidence for this?

And you whittled down the list.

We ended up with, I think it was about 14 on that list.

And there was some peptides that you can measure in blood, like GDF 15, for example.

Like I think it was IL1 or IL6, an inflammatory marker was on the list.

And that made sense in that regard.

What I thought was cool about that paper as a sidebar was what we came up with on that list that there was enough evidence to be used in research as biomarkers of age.

About half of them were physiological, phenotypical measures.

They weren't peptides, they weren't telomeres, they weren't hormones, they were things like grip strength, they were things like muscle mass, they were things that were physical measures of people.

The point of this paper wasn't that we were researching the biology of aging.

It was saying in human trials to come, be they clinical trials or observational studies that are studying how humans age.

These are the things we should be measuring to look at how humans are doing in that regard.

They're relatively common sense.

So grip strength, an incredible marker of health, muscle mass, but also things like levels of inflammation, things like GDF15, which I really like as a peptide.

I'm doing a lot of work around at the moment.

So it always comes to my mind things that we don't 100% know what they're doing, but we know they're associated with health, and we know they change with age, and we know there's an interaction between those two.

You are saying there are biomarkers to measure aging, and yet you say we don't know what aging is.

How does that correlate?

Okay, so like as an analogy, a biomarker of age is a useful way of measuring how you are doing, but it's just, how are you doing?

If I wanted to know how fast someone could run a marathon, for example, best case scenario would be I'd make them run a marathon.

But if I couldn't do that, I might make them run a kilometer and see how fast they go.

That's the analogy here.

So it's a way of seeing how you're doing without waiting till you get to the end point and going, well, it's too late to do anything about it now because we've just measured how you can be expected to age.

They're predictive markers in a model would be a way of thinking about that.

That makes a lot of sense.

You're taking those biomarkers and you are using them as a prediction.

Yeah, that's exactly it.

Yeah.

Your GP might measure your blood pressure to see how your heart health is doing, but he's not measuring your heart directly.

He's measuring an indirect measure of it.

Now, some of those biomarkers might be involved in aging processes directly.

Some of them might just be indirect things that change.

The old correlation causation argument kicks in here, and they might just associate with aging changes.

If they're associated in a useful way, we can use them as a measure of aging.

But the important thing to bear in mind with a biomarker of age is that they're markers of a model's function.

And we use them in aging studies to see how people are doing.

We're at a point now where epigenetic aging tests, for example, aging clocks, are being sold on the high street, where people can go and get a fingertip sample and see how they're doing.

Interesting functionality for the average person.

I don't know.

Interesting across a population or a study, sure.

But interesting to think about how they could be used.

And what we're saying in that paper is these are the ones we should use going forward in research.

You also co authored a paper on activin subfamily peptides, which I think touches on exactly what you just Said the fact that myostatins or activin A could be induced by aging, but also by inflammation, and we're not sure why.

Have I phrased that correctly?

I love that paper.

It was one of my favorite ones that I ever did.

I did it a long time ago when I was starting out my academic career and just starting to learn the field and getting involved.

And it's got a really fun backstory to it in that it was done as an undergraduate research project.

Every year at my academic job, I have to pay for my life.

And so we teach students.

And that's great fun.

I love teaching.

I do.

And I supervise undergrad research students.

And I was a little bit ambitious in one of the first years I had a job and I was given 10 undergrad students to supervise.

And I didn't know what to do with them.

And so I decided I want to do a big study on the MyStand family of peptides, things that control muscle growth.

And if we age, we lose muscle.

So I thought this would be a logical way of investigating this question.

As we age, does my stand change?

And then could we extrapolate evidence from that perhaps that maybe it's involved in some way?

And so what I did is I got my 10 undergrad students, I was asked to supervise and told them to go find 10 friends and family, just 10 people each, and bring them back to our lab.

And we'll measure their grip strength, we'll measure their muscle mass.

We'll put them in a machine called a bod pod that measures their body fat.

We'll measure their walking speed on something called a six minute walking test.

And then we'll take a blood sample from them and we'll measure my stat and activate and a few other bits and pieces as well.

And because it was 10 undergrads and 10 people, even I can do that math.

And that was Suddenly we had 100 people in the study.

And then I taught my undergrads how to do some basic tests and I made sure they could do them.

And we validated and we double checked.

And then I taught them how to do something called an eliza.

And all of a sudden I had undergrad students doing proper grown up research.

In three months, we produced a paper that had a hundred people on it.

We did some very simple predictive data.

And I'd love to go back now, spoiler with modern techniques, it was more than 10 years ago, but just really simple predictive algorithms.

And for example, if we took a cluster of hormones from someone's blood, like Biomarkers of age, ironically, would they predict someone's chronological age?

Yes, they would.

That's cool.

It's an interesting party trick to take a blood sample and say, how old do you look?

But what was cooler to me, what was so much cooler?

And this actually led to the direction of my research.

Now thinking about it was the blood samples we took and the hormones we measured in that blood was a better predictor of someone's function than it was of their true age.

And if we think about grip strength being this biological age marker, a marker of your health overall and your wellbeing, then the fact that we could take a blood sample and see how strong you were and looked and in fact that was easier to do, better predictor than your true age.

Was this idea around people aging differently, perhaps heterogeneity of aging.

It also kind of introduced me this idea of biomarkers.

What was really cool about that as well.

And I'm going to name check her because she's awesome.

Is the lead author on that study, Lady Barrow Silva.

Lady's her first name, not her title.

It causes all sorts of confusion.

Lady Barras Silva is an absolute star.

And she was an undergrad student at the time and she ended up as a lead author on this paper.

She went on to do a master's, she went on to a PhD, she graduated recently and she's just doing really well.

I've been keeping an eye on her and I meet up with her once a year or so for coffee, doing really cool work in muscle and bioengineering interfaces, which is really cool.

So that was a crack at this idea of biomarkers and extrapolating information.

What I would love to do is then go back and I, for various reasons, we can't do it.

But I'd love to go back now and 10 years later take all those people and measure their function now versus their change from where they were back then, measure the function now versus where they were.

And especially look at some of those peptides, some of those hormones measured in their blood versus their change over, say a 10 year period.

That's the study I really want to do.

Because then we're not saying a blood test can predict your strength or your function.

Cool.

Then we're saying a blood test can predict where you're going, what your future holds, what your rate of aging will be.

And that would be really functional and useful and meaningful, I think, to people.

The idea that biomarkers could predict outcomes.

And we're starting to do that now with really Big population based studies, things like the UK Biobank, for example, that's where biomarkers can get really, really useful really quickly, is as indicators of people's health that they can then use, if that makes sense.

So do you think there is a real world use for biomarkers or is it more sort of scientific interest?

It depends, because biomarkers is a really broad umbrella.

Like walking speed is a biomarker, heart rate is a biomarker and those are functional things that people can use right now to as indicators of their health.

Like I wear a heart rate monitor sometimes, but I'm a nerdy physiologist, but I know lots of people have them nowadays and they have them on their watches or their phones and that's brilliant and really cool.

Blood pressure is a biomarker and that's crossing the Rubicon into clinical data.

But epigenetic clocks, specific hormone profiles, those are biomarkers as well.

And we're getting towards probably more research functional now.

As you go to that end of the spectrum, that could translate into day to day useful measures that could translate into population based medicine.

If you go to your GP in the UK right now, whilst you're waiting to see your doctor, you're asked to measure your height and your weight and your blood pressure.

And now we have population based biomarkers of health and you can see a future where you can use them like that, or you can see futures where they have become individualized tools.

And I'm seeing that already that companies are starting to offer biomarker profiles so people can do long term monitoring of their health.

I know of startups doing this and I know of companies active at the moment doing exactly that.

Will it work?

Probably.

Will it work today?

I don't know.

So do you think today there are any biomarkers that are actually useful to determine your biological age or do you just think they just give you an idea, but they're not really factual?

I think it's a really fair question and a really good one to think about is what biomarkers are and aren't useful for someone listening to this.

And we came down to physiological and phenotypical measures.

So measures of strength, measures of function, measures of body composition, they came up on our radar just as Much as fancy blood samples and peptides and molecular evidence over here.

So for the average person listening to this, people interested in their health, or people who are interested in longevity as a sector and want to say, what can I do?

Absolutely.

I think those are brilliant biomarkers.

I think they're amazing and those are really functional ones.

But you can even take that down at a level again, you like cycling.

You have a regular route.

How do you feel cycling up that one hill?

Or if you go for a run, what time do you do your run in regularly?

And if you clock simple things like that and you see change over time, well, that's now a measure of functionality.

Right?

So you can integrate this into relatively simple things.

If you go to the gym and lift weights regularly, how much do you lift, for example?

That's only one step away from a laboratory validated biomarker test of grip strength, for example.

So those types of biomarkers are fantastic right now.

So which biomarkers do you think are research biomarkers versus actionable biomarkers?

Oof, that's a big one.

Yeah, I guess I opened myself up to that question when I say that, didn't I?

I saw Steve Horvitz speak recently talking about aging clocks, and he kind of got up and said, and I'm gonna misquote him slightly, I'm gonna paraphrase what he said, but he got up in front of an active audience and said, come on, guys, stop using my aging clock because I did that 10 years ago.

Take it and make it better.

Epigenetic clocks are fantastic.

One of the ways we look at their accuracy is say, how well do they predict people's chronological age.

But a lot of these clocks are rapidly moving and they're clusters of thousands and thousands of epigenetic markers.

And complicated algorithms like that mean that the way we use them changes rapidly.

And so the problem with taking a research tool like that and sticking it into day to day life and saying, okay, I'm going to measure this thing for the next 10 years and see how my health changes, is every year we might change slightly how that thing works.

Every year we might change slightly how we measure it.

Where a measure like heart rate, for example, or grip strength, we measure it how we measure it, and it's not going to change rapidly.

So some of the more complicated biomarker tests that we're using in research, I don't think are quite ready for day to day use.

That doesn't mean people won't do them.

Absolutely they will.

It's A growth market longevity sector is amazing.

And if people want to measure themselves, more power to them.

I got no problem with that.

I like data and I like collecting data on myself.

Which one's more functional for your overall health or which one do you care about more?

What my epigenetic clock shows or how much my body fat percentage is, for example?

That's what I would think about that sector.

Wearables are a big hype at the moment.

What are your thoughts on those?

I like wearable data.

I do, I'm a big fan.

But I like using it in research because it gives me lots of data.

They've become incredibly ubiquitous and that's brilliant.

So resting heart rate is a fantastic marker of people using them for sleep tracking.

Fantastic.

And even if the data is not superbly accurate, I did a sidebar.

I did a study about three or four or five years ago for a friend of mine.

Part of the study was wearing four different step count tracking devices for a couple of days.

Some were wrist mounted, some were on your waist, one was on my phone and different brands and that kind of thing.

And I'm not going to name you and call them out.

The data was wildly variable.

Wildly variable.

I've got two step counting apps on my phone at the moment, and every day one of them is almost exactly double the other one.

And I'd love to know what's going on there.

But one of the things that I think is really interesting about wearables is broadly speaking, they might not be the most accurate in the world.

Some of them are more accurate than others, and that's fine.

They all have their own underlying algorithms.

But if you're using the same one over time, with the caveat that as long as I don't change the underlying algorithm, the data is consistent and good.

And so even if your step count's over counting or under counting, as long as it trends in the right direction, as long as you use it in the right motivational way, that's a useful use of it.

And I like that idea of people using data as a positive influence.

It doesn't work for everyone, it's not everyone's jam.

But if that's a thing that positively changes your life and your behavior, that's brilliant.

Which endocrine signals interest you the most?

The endocrine systems.

I'm most interested in probably around the growth and differentiation factors, the GDF family.

That's probably my bias as a researcher and that I started in GDF8, otherwise known as myostatin.

And I spent some time on GDF11.

GDF15 is very hot right now.

Being touted as a aging biomarker of everything, it seems to respond to every possible stimuli.

I think it might be more of a stress marker than anything else because it responds to acute exercise, it responds to different nutritional stimuli, it responds to getting sick, for example, with diseases.

But it's really interesting to me what exactly is going on with it and why.

And again, spoiler, I don't know.

That's why I do it.

Inflammatory markers are of course super useful and anti inflammatory in the aging sector.

You have to think about inflammatory markers with inflammatory theories of aging.

And so they're cool to think about, but both sides of that table as well.

People often think about pro inflammatory factors, things that cause inflammation.

We measure lots of markers at high resolution.

They can be useful in clinical panels or in data and research.

But even among research scientists, we forget to measure the other side of the table, the anti inflammatory factors as well.

Pro resolution factors we call them.

Inflammation being a two stage process, inflammation goes up, then hopefully inflammation comes back down again.

And it's the balance between those two things that is an outcome that matters.

So measuring both sides of that is quite useful.

So I think those are my two endocrine families I'm most interested in at the moment.

Do you think we're close to an endocrine fingerprint to determine aging?

Yeah, I mean, to a degree.

We can almost already do that.

Not with the same, say, accuracy as maybe an epigenetic clock can some of the modern clocks.

But like for example, 10 years ago I did a really simple paper with five or six peptides on it, and we were predicting age with a high degree of accuracy and we're predicting function with a high degree of accuracy.

So yeah, we could be using it.

Endocrine markers can be really useful.

Absolutely.

One of the interesting things and one of the reasons I focus on the endocrine system more than other molecular biomarkers of age is I think it's the most translatable quickly and to clinical practice one day when someone can take it from me and run with it into a future clinical trial or a future drug development.

Because we know how to target hormones in your bloodstream, we know how to use that as a druggable component.

So if we find causation from these associations and correlations we're doing at the moment, that's the way we'll go forward quickly, I think with interventional studies.

Let's move on to a slightly different topic that I know you've been studying muscle.

Why is muscle so central to healthy aging?

I've always studied muscle tissue.

That's probably a bias of coming out of a sports science background and studying muscle growth before I studied muscle loss.

Muscle loss is such a central component of aging.

If you talk to average people and say, what are you most worried about with age?

What are you most scared of with aging?

What are your biggest concerns?

People typically cite two things depending on the audience.

One of the others comes out first and then second.

But it's cognitive aging, loss of my brain's function and the physical frailty with age, the loss of my ability to do things.

And those are really scary aspects of aging for most people.

And so I think it's important to understand from that point of view a loss of muscle mass.

I'm noticing this already.

I'm only in my early 40s, but where I am now, relative to my 30s or my 20s even.

And then looking at trajectories ahead from my own data, I know what's involved and I know best case scenarios.

When you age over decades, you will lose muscle mass.

And the best case scenario optimized, you will.

And I've got data from high level athletes across populations that show this not just in the average normal person, but in people who train frequently, who optimize their diet, who compete at the highest levels nationally and internationally into their 40s, 50s and 60s.

You lose function with age.

And again, I'll come back to that point I said earlier.

I don't know why, you know, if we can optimize everything in our environment, our lifestyle, you still show a loss of function with age.

And that's true of all systems.

But it happens to be that I think muscle's the most important for me.

And that's what I study as a specialty.

And that's one of the ways I've focused in on it.

Besides just simple function of movement, muscle is of course really important for more than just that.

It's involved in metabolism.

It's a metabolic sink for our diets, for glucose in our diets.

It's important for thermogenesis, keeping us warm and active.

It's involved in health in ways that I don't think we really understand beyond just typical muscle functions.

Muscle's an endocrine organ.

When I was an undergrad student a long time ago, we would study all the tissues one by one and we say, okay, this is the brain, this is the skeletal system, this is your muscles.

And then we'd have a something towards the end of this Mess.

And these are endocrine organs, the things that make hormones.

And there was a handful of them.

We know what they are.

We know about your thyroid, for example, we know about parathyroid, we know about the things that make hormones.

And one of the things that's happened in my lifetime is we've become much more aware of the fact that every tissue releases hormones systemically and is involved in systemic endocrine signaling.

So muscle's a big endocrine organ.

It releases a lot of the peptides.

I studied myokines, muscle specific cytokines.

And it's involved in wider health beyond just that.

Again, a friend of mine up at Birmingham near Harika Dugal, she did an amazing study looking at master's athletes.

So people who were in their 60s, but were still highly active and competitive versus younger individuals and versus society, representative, normal older people in their 60s.

And one of the things we know when you get older is function declines.

And so we see that, of course, and one of the things we know as well is that your immune system's function declines.

So as you get older, you're more likely to get sick from a bacteria or a virus and the outcome's more likely to be more severe.

But what seems to be the case is older athletes don't show that.

And what she showed in her data is these older athletes actually had immune systems that looked at every level, more like younger people's than older peoples.

And there's like an interaction going on here between high levels of activity, between, I'm gonna say with optimal body composition, between maintaining lowish fat mass and highish muscle mass and high levels of physiological function and high levels of immune cell function that interacts in some way, that's really cool.

So I think muscle tissue has effects on wider tissues outside of just itself, not just itself in the skeletal system keeping your bones strong, for example, but across all sorts of systems, it's more integrated than just this system acts by itself.

So sarcopenia is the decline and the wasting away of muscles.

It's a really grim thought that you are going to die.

Like there's an outcome here from this ride that we're on.

There's only one exit, and something will take you out at the end.

Now, if you know that over the course of the of decades of your life, from about 35 to 40 years of age, everything gets worse with time, until the point where the complicated system that is your body completely fails.

And that's what death is.

Essentially.

It's a complex system failure, keeping each aspect as Functional as possible for as long as possible is an aim.

And that's basically what healthspan is, right?

Trying to keep everything functional for as long as possible.

Muscle mass seems to have, in my humble opinion, a higher contribution to that than other tissues.

So being active throughout your life helps you into older age, be functional, keep muscle mass for longer and keep it functionally for longer.

So knowing that you will decline with age, the question becomes a rate of change with time.

And people who are highly active over the course of their lives show slower rates of change, are functional for longer, but most importantly are healthier for longer as well.

Not just muscle healthier, like a better grip strength in the lab or a better body composition scan or something like that, or just beach muscles.

But their wider physiological systems show improvements.

They show better immune system function, they show better cognitive time decision processing, for example.

Things on average are better overall.

Now of course everything gets worse, but everything gets worse.

Slower rate of change.

And if you can do that in a way that delays something like sarcopenia for as long as possible, where your muscle function dips below a critical threshold of independence and functionality, that's brilliant.

But at the moment the only thing we really have for maintaining muscle mass a long period of time is nutrition and diets.

But if you can maintain muscle mass and muscle function above a sarcopenic level, not only are you going to stay physically functional independent for longer, but overall your health will stay, is more likely to be better for longer.

How much exercise is involved in keeping muscles above sarcopenia level?

Such a good question.

And one of those questions that sounds like it's really easy to answer and it's really not like all things in science, right?

One of the problems with asking a scientist to question it so immediately weasel out of it and say, well, you know, here there NHS guidelines at the moment, it's for good health, is do about 150 minutes of moderate intensity exercise most days of the week and do strength training about twice a week for about half an hour each I think it is.

Now that sounds really simple because 150 minutes most days is the idea being it's about 30ish minutes a day of walking, running, cycling, moderate activity, things that get your heart rate up and get your breath up and maybe cause a little bit of sweat and then do muscle building or resistance exercise about twice a week.

Those relatively simple sounding guidelines have a bonkers amount of evidence behind them.

And every time we stress test them, they stand up.

One of the big debates around physical activity is like from population Based measures from observational studies.

And don't ask scientists.

If you want to know about longevity, ask insurance people.

From insurance data, is physical activity moving more?

On a population basis, more tends to be better.

Aerobic style exercise, walking, running, cycling, that type of thing.

Within reason, on a population basis, more is better.

So for example, one insurance company gives people Fitbits or Apple watches step count.

And if you are more active, you get better insurance rates.

That makes sense because you're more likely to stay healthier and you're more likely to live longer because of that.

And that saves them money.

Now win, win.

I choose health over not, don't get me wrong.

But they're not doing it for positive reason.

They're doing it to save themselves money.

That's fine.

Things like resistance training, the current guidelines are about twice a week and that seems to be about optimal.

So there's been a handful of meta analyses, studies that look at large numbers of studies and condense data down and they show this kind of interesting trend where the biggest gain for health of populations is about twice a week, about one to one and a half hours of exercise, about a grip strength that's slightly above society average, but would be what you get out of doing a few resistance training sessions a week.

And after that you don't see as much returns.

So how much exercise kind of comes down to another question of what type of exercise.

And in that when people ask me those types of questions, I typically say, look, physical activity is brilliant, more than merrier.

I cycled here today because the tube was delayed and city bikes are brilliant for that.

In London, for example, I walk to work some days even though it takes me twice as long because it's a nice way to start the day, but also incidental physical activity.

I tend to take stairs, not elevators, if I can.

We took the stairs today, those types of things and then some resistance training mixed in.

That's my stock standard answer for what and how much.

But did I understand you correctly that more is not always more?

In the breakdown of that from a physical activity into aerobic exercise, it seems to be that some is good and more is better.

Simply put, with an obvious caveat at the end, that there's overtraining, et cetera, and modern people with their wearables and their heart rate monitors might know about these things and recovery.

But being physically active is good for you and more tends to be better with resistance training.

At the moment, the data seems to suggest that after about two to three sessions a week, you end up with a plateauing of effects and more might not necessarily, from a health and longevity point of view, be necessarily better.

That's not saying that going to the gym more will not make you stronger.

Of course, someone who goes to the gym, say four to five times a week versus once to twice a week will see larger gains in muscle mass over time and bigger training outcome.

But in terms of longevity and health span measures over decades, there might be a plateauing of effects.

When we look at large numbers of studies condensed down and where do people

overestimate or underestimate exercise?

Exercise is one component that you can affect for healthy aging.

Some aspects of aging must be intrinsic and independent of your lifestyle and your environment.

But the aspects that you can control, exercise is one of them.

And it's one of the ones I think people most recognize.

If you ask people what affects their long term health, they will say physical activity, they'll say nutrition, and then they might not think about it.

But sleep's on that list as well as a major contributor.

And this is stepping outside of my remit expertise wise.

But physical activity, nutrition, sleep and stress, social environments, social cues, those types of things have massive effects on our physical health.

Emotional stress has physical effects upon us, physiologically speaking, I think I would argue that exercise is the biggest contributor from those four.

Now, I know sleep researchers, I know one that will listen to this later who will tell me that sleep's more important.

And I know plenty of nutrition and exercise scientists who say you can't outrun a bad diet.

And those are fair components.

But it's almost a moot argument.

Like if let's say one has 20% effect versus 40%, what does it really matter?

If you know a thing as a variable that you can control and it's within your ability to control it, then why not control it To a similar parallel, People often ask me how much is controllable, how much is genetics and how much is environment.

And again, the argument's relatively moot at the moment because there was a big Nature paper recently on contribution of genetics to longevity.

I think I wrote an editorial for someone about it and it was genetics shifted back up in that prediction of these authors from about 20 to 30% to about 50% predictor of longevity.

Brilliant.

Interesting scientifically, but that means that components of that healthy aging and longevity that you can affect would shift down.

The argument is relatively moot.

These are things we can control, so we can control them.

Things we can't control, we can't control them.

For now.

You co authored work on exercise induced muscle Damage in young and old men.

What did you find?

Oh, that was an interesting one.

I have to try and recall off the top of my head now.

It was a really cool cluster of work done by one of my PhD students, Vani Kirigato.

She was a stunning PhD student and then she ended up working for me as a postdoc for a while on that work.

And she was interested in exercise induced muscle damage.

And we studied that at first.

So just for people listening, that is when you do novel, especially resistance training, maybe it's a run, or maybe it's even just going for a long walk with lots of changes in altitude, especially walking down slopes or stairs.

Or maybe it's resistance training for the first time and then afterwards you feel okay, but then the next day, 24 hours later, and 48 hours later is the worst delayed onset muscle soreness, or doms, if you've heard that term before.

And Ivani was really interested in what exactly was going on there and is there any simple nutritional or simple countermeasures we can use?

And part of that work we looked at was whether or not aging affects response.

And what we did is we looked at inflammatory markers, so changes in inflammation.

We looked at changes in function, so how people recovered so their strength goes down the next day and then recovers over 48, 72 hours.

And we looked at young and old groups and we didn't find a huge amount of difference between them, to be honest, from memory.

So of course younger people were stronger than older people, but the outcomes were very similar in that both groups lost function, increased pain, who knew?

And then recovered over a few days.

We did some really cool work around extracellular vesicles, These little things that are involved in endocrine signaling, but they're not traditional peptide hormones or steroid hormones.

They're cargo containing carriers that move from cell to cell.

And we started to characterize that.

But I have to admit it's been a few years, so I don't recall all those results off the top of my head.

So just to explain it to people who might not know it, and please correct me if I'm wrong, because obviously I'm not an expertise in that.

Extracellular vesicles are little carriers that go from cell to cell and sort of transmit information.

And if things go wrong and we age, they transmit faulty or wrong information and thus damage the cells and make us what we call age.

Is that as we collectively, not me, but we scientists figured out over the last few years or so is so cells shed these little Tiny blips that will split off from a cell.

And they what we call extracellular vesicles.

So they come off a cell and they're containers.

And they carry components from inside that cell.

So they can carry peptides, they can carry small signaling RNAs, they can carry mitochondria, even between cells.

And that means they will communicate information between cells, and they can communicate information from one cell to another.

Now they circulate in your blood so they can move systemically.

People are interested in them in terms of cancer biology, in terms of cancer cells transmitting information from the body, whether or not they have metabolic or functional signaling, whether or not they carry information from cell to cell and then change the destination ce.

And we're even starting to figure out now how we can measure where they come from.

So can you say what tissue it came off of based on unique proteins around it?

Do they have functionality?

Do they carry information in functional ways?

And they do, in really interesting ways.

And so they've become like another endocrine system.

Not just hormones, but these things will blurb around, bind to a future cell, release their cargo into it, and then affect that cell's function.

That's what extracellular vesicle is, a whole other system we didn't know about.

And then we're just like, oh, we've got this endocrine thing down.

Oh, wait, what are these?

What are they doing?

Oh, they have an effect.

Awesome.

Now we've added a layer of complexity on top of that.

What do these extracellular vesicles tell us about aging and adaptation?

Do they tell us anything about aging and adaptation?

This comes full circle into what we don't know, I think.

But there was a cool study I did a few years ago that got a lot of attention at the time around young blood.

So one of the studies we did was we took blood samples from younger and older people, but we didn't characterize the hormones in the blood so much.

Instead, we used it as a growth media for cells from a different source in vitro, outside of their bodies.

And what was really cool is we noticed that cells grown in a young, like environment and the plasma from younger people grew differently and respond to injury differently than the cells growing from blood from older people.

And there was a controversial outcome from that a couple years ago, and some other people found similar things and interesting ways.

And so there was a while where certain people thought, oh, we'll just infuse young blood into people and we'll be grand.

And people started doing that, which was a interesting moment in History.

And the FDA had to come out and say, please don't do this now.

Well, the reason I mentioned that is at the time we thought, oh, brilliant, there's some peptide hormones going on and that's affecting these cells.

But what we've come to think about now after that work with extracellular vesicles and aging, is maybe it wasn't hormones per se.

So one of the next studies we want to do, and we're trying to find exactly how to do this, and there's a few ways of doing it, is take blood samples from people, spin them down and separate them.

So we separate off the plasma or the serum where the hormones are found, but we can also separate them in a way.

We separate that from where the extracellular vesicles are found.

And then we can do the same thing again and grow cells in the endocrine hormone environment only, the extracellular vesicle environment only, and then absent of both them, and combine with both of them, and then we can start to track back what happens because that shows what the environment does to the cell.

That would be an interesting experiment to do, and I haven't done it yet.

So if someone's out there who thinks that's a cool idea, do that.

And if someone's out there, this real, real corny science moment, look out for this.

But if you've got any money wants to give it to me, I'll do it.

Brilliant.

Because most of my job nowadays is fundraising.

Right.

But it's a relatively simple experiment to do.

I think that there's some complexities around it as well, and devil's in the details, one of them is what exactly is having that effect?

So let's say we took extracellular vesicles from younger people and older people and we showed there was an age like effect.

And when exposed to old extracellular vesicles, cells didn't respond as well.

It's cool.

Now we've got another mechanism of aging, one more for the list, one more hallmark to add to that.

But then we don't know what's behind that again.

So is it one of the cargo features within it?

So is it a circulating rna?

Is it a mitochondrial thing?

Because mitochondria love to affect their environment.

Is it some peptide hormone?

Is it all of them acting together?

So then we go a layer deeper.

Then we go a layer deeper.

There's some really cool interest in the market at the moment about using this as a method of treatment.

And it's possible that we'll end up with like synthetic vesicles that contain cargoes one day and that makes sense, or farming them or use them in some way.

And there's a cool ideas in there for drug delivery that have been done at the moment, vesicleization of things because they bind to cells and tissues.

So maybe we can use them to target specific tissues in the future and then deliver a drug or a cargo to a specific cell.

Again, it's massively outside of my remit, but some ideas being like what if we could target them to say, specific cancer cell lines, for example?

Then we could deliver drugs that have side effects only to the right location.

Really cool emerging areas.

Just so interesting.

Continuing down that line, if money was not an object, what research would you love to do?

Oh, that's such a good question.

Because we're always saying give me more money and I'll solve the world.

All right, here's the untapped check.

Go for it.

One of my favorite approaches to research is the antithesis of which I teach my students sometimes, which is hypothesis free research.

We don't know what we don't know.

So as a really small example of this, I did a study recently on only a handful of people.

I think it was about 18 people, some younger, some older, some trained, some untrained.

And we went in and did quite a simple proteomic array.

So that's a thing where we go and we take a blood sample from them and Instead of measuring one hormone like you mentioned Actovins or GDF15, or some inflammatory marker like IL1 or IL6, instead we go in and we measure everything we can in this array.

We measure a thousand things.

I probably know what a hundred of those things are.

And there's 900 things I've never heard of before on that list.

But what's really cool about that is we can use that in a way to uncover what we didn't know about hypothesis free research.

So if I had an unlimited check right now, I'd recruit back in the envelope calculation.

50 to 100 ish people per group, younger, older, highly trained or comically healthy.

Older versus society normal.

And then another group of saying aging poorly, multiple disorders, non communicable diseases of aging for example.

And then younger as well, same thing.

So young but not healthy.

Young society, normal and young, but extremely healthy.

Your outliers on either side of the normal distribution curve of what we can be use what's called a multi omics approach.

So proteomics, metabolomics, RNA seq and measure everything, just everything possible on that sample.

And then from that dive into that data and just spend.

I did this recently.

It was so much fun.

Just spend days just looking at the data and seeing what you don't know about, like what's changed.

And we don't know why, because you start to pull data off of these type of studies and you say, okay, cool, that goes up, that makes sense, that goes down, that makes sense.

But you know, that goes up and I don't know why.

And that's hypothesis generating.

That's what we need to do.

And specifically in humans, we need to that in human populations.

Lots of my colleagues do work in flies and worms and even mice and rats.

And that's brilliant and it gives us hypotheses for the human work.

But spoiler, you are not a fly, you're not a worm.

And humans physiology is different in important ways.

We age differently.

And so studying these things in humans is the best way for now.

I think that we can that observational study that we can understand what human aging looks like.

So if I understand that correctly, you want to do research into things that we don't know yet and the outcome would be even more things we don't know yet.

That's a really good way of saying, what are you doing, dude?

I'm a professional nerd.

I am incredibly lucky and I have a career studying a thing that we might not be able to understand in my lifetime.

And there's lots of tools we can use and we've come so far so fast and we'll probably keep going and things will change.

But yeah, there's a very real chance that we're not seeing the full picture right now.

Of course we aren't.

We started with what is aging?

I said I don't know.

And that's the point.

You asked about extracellular vesicles.

Until recently, we didn't really know about them.

And there's a whole nother endocrine system.

There's probably massive components of aging that we've got no idea about right now.

And so we have to keep trying to understand the complex system.

And lots of disciplines of all sciences sometimes get held up by technology or ability or methods at the moment we've got these cool omics techniques where we can produce more data than we've ever had before.

And then we put it together in ways we've never been able to do before.

But we're generating data that's becoming really difficult to understand.

And this was true of physics 20 or 30 years ago.

They were generating more data than they could analyze.

So we need to do things where we can't easily predict the outcomes.

I guess we need to generate new hypotheses.

One of the problems with that is that's not immediately translatable.

So I come along to someone, I say, all right, you give me a chunk of money and I'll do this and I'll do exactly what you just said.

I'll find out some things we didn't know.

Brilliant.

How do we use that to make money for my company or how does the government use that to help people?

Oh, no idea.

But I can tell you that the things we're doing now successfully came out of basic science.

We had no idea about 10 or 20 years ago.

And in 10 or 20 years time, we need to have basic science now that produces the new knowledge so we can translate into future things.

And it might not immediately pay off, but we have to do it.

We have to try and find the things we don't know.

So how did you put it?

So we know what we didn't know and we don't know what's behind that because we have to keep going down that rabbit hole.

We have identified a lot of things that might be mechanisms involved in aging.

And we're currently at a point now where we're producing interventions, drugs that are targeting some of them.

Senolytics is a great example of this.

Senescent cells producing the secretory phenotype, the hard to pronounce acronym, sasp, if you're saying it in front of people, the senescence associated secretory phenotype, or just spitting out bad things like pro inflammatory cytokines and such that cause cells around them to age phenotypically.

And so someone came up with the idea of senolytics and that seems to work.

And that's brilliant.

Absolutely.

And so we could see a future where they can be used in humans coming up clinically.

But they came out of a basic science idea.

I don't know if we've answered everything at the moment, but we've got really cool approaches that are coming out of that.

And we'll have more coming up.

We'll have ideas that might have sounded insane 10 years ago, like microbiome targeting things or immune modulators or I don't know, the metformin trial might then finally pay off or something like that or something similar.

But rapamycin, we might get some data for that one day, something functional.

These are complex clinical trials that sit above me, for example.

I won't be the guy to do them.

And that's okay, I'll be the guy hopefully over here saying, that's a cool observation in mice or rats or worms.

Can I find a parallel in humans or doing a human study that produces that idea for that next one?

Wow.

We've gone through quite a lot and I have to say it's a very different angle and discussion than what I've had with most people, because most people that I speak to have a very clear idea of what they understand when we use the word aging.

And I love the fact that you've sort of thrown it all up in the air and said we actually don't know what aging is.

What do you think the general population most underestimates about aging physiology?

It's a really interesting question, I think, what do people underestimate the most?

So people are relatively familiar with what aging looks like.

So everyone has an auntie or an uncle or a grandparents that they've seen the stereotypical characteristics of age or are going through it themselves.

Like we're all studying aging just incredibly slowly.

Case study of one right here studying aging as I experience it.

People misunderstand risk.

I think trying to think how to better put that.

The cliche would be smokers saying, oh, but yeah, I won't be the one to get cancer.

Or people make bad decisions and don't predict the risk of it happening to them.

So despite seeing all the aspects of aging in the world around us, despite seeing immobility or cognitive decline into dementias, for example, despite knowing full well that poor diet over long periods of time, that physical activity over long periods of time is bad for you, not extrapolating that to specifically these are the risks.

To me, it is an abstract idea, right, that what I do in my 20s and 30s and 40s will substantially affect how I am in my 50s and 60s.

Because we're not forward planners as a species.

It's not who we are.

I can't right now say this is exactly the risk.

If you increase your activity by this much, you'll be this much less likely.

We have the data.

I could pull off of populations, that is.

But I think people misinterpret those risks and they all have that innate it won't happen to me or I'll be okay.

Which is probably the biggest one.

Can we make up for bad behavior in our youth?

Yes.

Simply put, can you completely make up for it?

No.

But will it help?

Yes.

So the 60 year old who quits smoking or takes up exercise or changes their diet will see positive changes.

I've got data lying around from 90 year olds starting resistance training and then ending up after a period of time in a gym lifting weights and showing increases in muscle mass and showing health outcomes improve.

Yes.

At any point in your life, positive changes like increasing physical activity will have positive outcomes on your health and your future health.

Absolutely.

We also know of course that positive influences in your 20s will have influences decades later.

And there's kind of some really cool evidence emerging that suggests that things you do in your 20s and 30s, even if you stop them in your 40s and return to them in your 50s, you see greater gains in later life from early life activities.

So despite all the phenotypical things like muscle mass or body composition going away, you can get them back quicker and be more responsive years to decades later, I think, which is really cool.

The less complicated way of saying all of that is it's all good and do something.

Whatever it is that you do, do something.

I think the follow up question to that is always what should I do?

And we kind of touched on that earlier.

So I'm going to put a question in your mouth because people always say, what type of exercise should I do, Brad?

I don't know, what do you like doing?

I'm not going to say you should run for half an hour every single day.

If you hate running, don't do that.

Do the thing that in 10 years time you'll most likely still be doing.

And that's the best thing I can suggest to people listening to this is what activities are you going to maintain for years to decades?

I love cycling.

Being on my bike is my happy place.

So I cycle.

I hate running.

I hate it with a passion.

Every time I go for a run I think, well, if I was on my bike I'd be there by now.

And I do run occasionally and these must.

But it's not the regular thing that I do for physical fitness.

So it's good to know that there is such a thing as muscle memory.

Yeah, the muscle memory quote's a great one and it is really cool.

Is it epigenetic?

Is it some cellular change or something?

There's some cool evidence from some animal models, but it does seem to absolutely be a thing.

So if you did something and then stopped, you know, if that's motivation to pick it up again, brilliant.

The simple answer is do something, do something.

And just to be very clear, because you really are the expert in that field, if you are older and have never done exercise, it's never too late to start it and it's never not beneficial.

Absolutely Yeah, I think that's a very clear statement that should be made as loudly as possible.

Quite a few years ago now, the American Medical association put out a statement and it was a really as clear as possible in the most litigious science society possible, American hospitals.

They specifically said that increasing physical activity in patients as quickly as possible was the best case scenario.

The quote was something along the lines of risk of falls in immobile older patients was not to be used as a prevention for increasing physical activity.

But the benefits outweighed the risks.

Stephen Harridge, professor of aging physiology at King's here in London, he did some really cool work.

An older woman between 90 and 100, I think the oldest one was 102 many, many years ago.

And they were almost essentially chair or bedbound.

And they did resistance training and they showed increases in muscle strength and muscle mass in their legs.

And so even at one end of the spectrum completely and the frailest, oldest people possible, they still showed positive outcomes from simple training.

Wow.

Really cool study that ends this conversation on a high note here.

You know, it's never too late.

Thanks, Brad.

This is so insightful.

We all think we know a lot about muscles, but I think you've really brought a very interesting angle to the whole aspect.

Not just muscles obviously, but of aging in general and how we ought to look at it, how we should look at it, and how we are looking at it.

At the end.

I always ask my guest five rapid fire questions.

Oh, great.

Just for our Excel, what's the single

best piece of advice you would give your younger self?

I was going to make a joke and say you're not going to make it as a professional hockey player.

I love it.

But all the exercise you're doing will pay off in the long run.

Anyway.

Name one habit everyone should adopt for a longer, healthier life.

Exercise.

That was a given, right?

Sorry, shouldn't have asked you that question.

If you weren't in longevity science, what career would you have chosen?

Split answer.

Failed ice hockey player.

Wrong country to be an astronaut.

But that was my aim growing up.

I wanted to be an astronaut.

Aim for the stars.

Why not?

Still eligible to apply.

There you go.

Look out.

What microdose habit, sort of five minute routine or small daily action yields outsized longevity benefits.

I'm getting the same answer.

Exercise and physical activity.

Sorry.

Toothbrush, squats, standing up in ad breaks, anything.

Taking the stairs one or two flights a day instead of taking the lift just all the time.

Absolutely.

What's the craziest longevity myth you've encountered.

And is there any truth to it?

I'm going to go with the youngblood one because that was part of my work.

So there's probably some truth to it, but that doesn't mean you should be stealing your son's blood and infusing it into yourself.

There's possibly something to it, and we just got to figure out what it was in those young blood samples.

Is it EVs?

Is it hormones?

Is it something like that?

Dr. Bradley, thank you so much for coming on Beyond Longevity.

What an insightful and interesting conversation.

Thank you.

Oh, anytime.

Be an absolute pleasure.

And I'll always talk about science with interested people.

Fabulous.

Thank you.

What a conversation.

What I took away most from this conversation is how honest it was.

For all the progress in longevity science, we still cannot fully explain why we age.

We now have more and more ways to measure aging, but the question underneath all of it is what are these markers really picking up?

Are they pointing to the biology driving aging, or are they mostly tracking the footprints aging leaves behind?

We talked about so much in today's episode, yet didn't even scratch the surface of Dr. Bradley's research work on muscle and working with aging athletes and other outliers.

So we simply have no choice but to ask Dr. Bradley to come back on Beyond Longevity for another episode to talk about how he stress tests elite athletes and what this all means for us normal people trying to live longer, healthier lives.

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