Instant Genius - The science of ageing, with Dr Andrew Steele

Episode Date: December 27, 2021

Dr Andrew Steele, computational biologist and author of Ageless, explains what happens in our bodies as we get older, and why some species don’t seem to age at all.Once you’ve mastered the basics with Instant Genius, dive deeper with Instant Genius Extra, where you’ll find longer, richer discussions about the most exciting ideas in the world of science and technology. Only available on Apple Podcasts.Produced by the team behind BBC Science Focus Magazine. Visit our website: sciencefocus.com Hosted on Acast. See acast.com/privacy for more information. Learn more about your ad choices. Visit podcastchoices.com/adchoices

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I'm Sarah Rigby, online staff writer. This week, I'm joined by Dr. Andrew Steele, author of Ageless, the new science of getting older without getting old. He studied for a PhD in physics at the University of Oxford before switching fields to computational biology. He tells me everything I need to know about the science of aging, including the species that don't seem to age at all. So first of all, could you please just tell us a bit about your book?

My book's called Ageless, The New Science of Getting Old or Without Getting Old, and it's asking us to reimagine the ageing process. I think it's something that a lot of us think is just a natural, inevitable part of being alive. But in the book, I characterize it as our greatest humanitarian challenge. Now that might sound like a slightly strange thing to say. But actually, if you look at the sort of biology of this, aging is behind all of the biggest killers in the modern world, things like cancer, heart disease, stroke, dementia. These are all diseases that are essentially

caused by the aging process, if you look at the biology. And that means that by tackling, by understanding that aging process, we can potentially create medicines that could prevent or even, you know, defer these diseases all at the same time. And that's something I just find really, really exciting. And that's, I guess, why I wrote a book about it. And there are lots of different theories about what happens in the body when we age on there. So what is the, what's the main theory of what biologically causes aging? I actually think, I'm going to disagree slightly with the question there. So there have been dozens and dozens of theories. There was even a joke, which might even have been accurate back when the joke was made, that there are more

aging theories and they were researchers to study them. And that's partly because aging is just such a small field. There have been, you know, a comparatively tiny number of researchers working on this historically. But also because there is this sort of vast, burgeoning number of different theories about why we age. Is it caused by reactive molecules inside our bodies? Is it caused by damage to our DNA? Is it caused by our mitochondria, the little powerhouses inside our cells that generate all of our energy? And actually, although quite a lot of them have, either been disproven or just fallen by the wayside, I think what we've got now isn't one overarching theory as to why we age, but an understanding that it's a contribution from lots of different processes

all acting together. So in the book, I break it down into 10, what I call the hallmarks of the aging process. And these are the fundamental cellular, molecular, biological underpinnings of everything from the way that our cells age, to the way that those cells grouped together into organs, those organs age, to the way that our whole body age, its whole systems in our body. So things like the immune system deteriorating with time. And it's the combination of the these 10 hallmarks that ultimately causes to grow old. And these things are very interrelated. So, you know, something like the damage to the DNA is perhaps one of the most fundamental hallmarks. This is the instruction manual in the center of every one of our cells. But that can

then go on to cause things like the cells themselves to age. And then the aging of those cells can be partly what's behind the aging of the immune system. So all of these things are very interconnected. And what's most exciting about this is firstly, although 10 might sound like quite a big number, actually it's a tiny, tiny number when you compare it to the sheer volume of age-related diseases. There are hundreds of kinds of cancer. There are dozens and dozens of different ways your heart could go wrong, your brain can go wrong in dementia. And yet we think that this comparatively small number of underlying processes is what gives rise to everything from cancer to basically wrinkles and gray hair. All of these things are caused by the same underlying biology.

So as we understand it, hopefully we can do something about it. Right. So what is it exactly that does give rise to the outer sort of trappings of age that we see like gray hair and wrinkles? Well, it's a variety of different things. as I said, it's all of these different hallmarks acting together. I think perhaps the two most significant in terms of wrinkles. Firstly, there's DNA damage. So our skin is a place where we get an awful, awful lot of damage to that instruction manual

in the centre of our cells. And that's because unlike most of the rest of our body, which of course is encased in our skin, our skin is subject to the vagaries of the external environment. In particular, if you don't wear enough sunscreen, if you spend a lot of time on the beach, or even if you've just been alive for 70 years, so you spent quite a lot of time outdoors, the ultraviolet rays from the sun can damage that DNA inside our skin cells. And obviously the worst consequence of this, a lot of people will have heard of is cancer because that's caused by mutations, by damage to our DNA essentially getting to a point

where the cells start dividing uncontrollably. But we actually understand that now that even if your cells don't get to the point of becoming a full cancer, they can still start to behave in ways that are detrimental to the skin overall. And another hallmark that's really, really crucial to the aging of our skin is the degradation of the proteins inside our skin. So the reason that skin when you're young is youthful, it's flexible, it's soft and supple and not wrinkly is because of proteins like collagen and elastin, which are these structural proteins. So these are molecules that hold together of the skin. They maintain its structure. They make sure it's, you know, not too stiff, not too soft, but just right for maintaining a barrier.

But unfortunately, as we get older, and one of the driving factors is, again, the UV, but there are also a number of other factors involved there. These proteins start to get lower in number. They get less effective at their job. They get damaged themselves. And so it's a combination of all these different things that cause you to get wrinkly. But actually what's really interesting, as I said, is that, you know, these external signs, there's good, reason to believe that they are, they're caused by these same biological processes, and there are two ways to think about this. The first of which is actually how old you look is a really good indicator of how old you are biologically. So there was a fascinating study that was done a few years ago where they asked people to rate how old photographs of people looked. And what they found

was that people who looked old for their age actually were old for their age biologically. They went on to get more diseases. They went on to die sooner than people who looked younger. So that really shows us that, you know, there is something a bit more fundamental about wrinkles and grey hair than you might think. They're not just cosmetic signs. And the second thing is that because these hallmarks affect both the same hallmarks effectively affect both our skin and the other parts of our body, I talked about the damage to the collagen in your skin being one of the things that drives the wrinkles as you get older. Damage to collagen is actually a fundamental driver of damage to your arteries and veins, the little vessels inside your body that carry your blood around. And so, you know, it's the stiffening of those that's one of the driving factors behind heart disease and other kinds of, you know, cardiovascular problems that we get as we get older.

And so, although I wouldn't necessarily go after these cosmetic things first, I actually wonder if some of them are going to be fixed almost as a side effect of other treatments. Because one of the researchers I was speaking to said she was obviously far more excited about having, you know, supple, youthful arteries and wrinkly skin than the other way around. But it might be that when she developed some of these therapies that can improve the quality of the collagen and our aging arteries, maybe some of those drugs will, you know, make it into our skin and improve the aged collagen there too. So, you know, you can potentially fix multiple things at the same time. And that's what we're so excited about with these anti-aging treatments.

And so you mentioned earlier that there are lots of other theories of aging that have since been disproven. Could you take us through maybe some of the more well-known ones? Because I'm sure lots of people have heard some of these. I think one of the most famous, actually one that sort of persists, staggers on to this day, even though the biology is very much disproven it, is something called the mitochondrial reactive oxygen species theory. And people might not have heard of it in quite that ridiculous biological terms. But we often hear about free radicals being something that causes aging.

This is a term that a lot of people I think have heard that might. not necessarily know the chemistry of what's going on here. The idea is that when your body is working, obviously you need to eat food, you need to breathe. Those are two of the most fundamental things. And oxygen and things like sugars in the food that we eat are some of the most reactive chemicals that we come into contact with. And they have to be reactive. They have to have a lot of energy inside them because that's how we make the energy that allows our bodies to function. But unfortunately, it means that we have got these highly reactive chemicals inside us a lot of the time. And particularly oxygen is a voraciously reactive chemical. And that means that if your body,

if your mitochondria that are generating the energy inside your cells, if they fumble one of these oxygens, they can create something called a free radical. And this is essentially a berserker chemical that goes around your cell damaging anything it comes into contact with. And for a long time, it was thought that maybe the accumulated damage of fumbled oxygens throughout our whole lifespan are one of the things that caused the aging process. Now, unfortunately, we've since discovered that really isn't the case. It's obviously a lot more complicated than that. And actually, with hindsight, that makes a lot of sense because life has been dealing with the consequences of free radicals for billions of years.

This is an thing that afflicted even the first oxygen using cells. And so accordingly, we've got lots of different ways that we use those free radicals for important processes inside the body. Actually, one of my favorite is that when your immune system comes across a bacterial invader, they might bombard that bacterium with free radicals in order to kill it. So there are loads and loads of functions. They're used for signaling. They're used for cells talking to each other.

There are all kinds of different things. And on less fundamental level, we've got really, really good evidence. We've got huge trials that have involved, you know, thousands and thousands. thousands of people, taking things like vitamin C. So these are supplements that are designed to be antioxidants. They soak up these free radicals without taking damage themselves. But unfortunately, if you take these supplements, what we find, people who take vitamin supplements, unless you've got a specific vitamin deficiency and your doctor has told you to go out and take a particular supplement to correct that deficiency, these people don't live any longer. In fact, some of them

even have an increased chance of death versus people not taking the supplements. It's not a massive risk. It's not like you're just killing yourself instantly. But basically, if you take too much of an antioxidant supplement, your body's going to start compensating, producing more of these free radicals to carry on those essential processes to compensate for what you're doing, and it ends up not extending your life at all. So that's definitely one of the theories that was very, very popular, but it's fallen by the wayside. Wow. And there was another one that you mentioned in your book about number of heartbeat. And I actually saw this in a museum a few years ago about how the idea that all species have a fixed number of heartbeats. Fascinating idea, isn't it? It's one of my

favorite old theories. And actually, it's sort of in contrast to the free radical theory, it seems, seems to be really quite broadly true. It's fascinating. So the way it's often stated is that animals get a billion heartbeats and then they expire. And this works remarkably well. It's not exactly a billion. But if you look at something like a mouse, it's heart beats 500 times a minute. And yet mice live, you know, an average of two or three years. So that's obviously they've got a very fast heartbeat. They race through their billion beats in no time at all. Where the longer lived animals, something like a Galapagos tortoise, they can live to 150, maybe even 200 years old. and they've got a heart that beats just six times a minute.

So if you work through, do the maths, well, actually both of those come out at about half a billion beats. And humans, if you work through, we get about 60 beats per minute if you're relatively healthy. And that can then, you know, obviously we can live, you know, 80, 90 years or something like that. We get a substantially increased number of beats compared to some other animals. We get about 3 billion beats during our lifetime. Nonetheless, you know, a factor of, you know, three or six isn't that a huge deal in biology.

There's a surprisingly tightly constrained numbers. And I don't think we really understand exactly what the underlying process is. here. It's probably down to something that we often call in science a scaling law. So it's very well known that animals that are larger tend to live longer lives, and that's for a variety of different reasons, one of which is that they're just, you know, they're bigger so they get eaten less often, and so therefore they can afford to evolve anti-aging defenses in a way that a smaller, more threatened animal can't. And it might be that bigger animals obviously have bigger hearts, and those hearts come more slowly. And so it might just be a sort of side effect of the, that basically

the physics and the engineering of our bodies, but we haven't fully understood why this, this bizarre observation, you know, seems to persist. It's really quite, it's beguiling, isn't it? We do seem to have this fixed number of heartbeats. Species do tend to age at different rates, but are there any species that don't age at all? Yeah, there are a surprising number of species that don't age at all. And actually, the Galapagos tortoise, the reason that's on the cover of my book is it's one of these ageless species. What do we mean by ageless? Well, so if you're a human, as I guess most people listening to this podcast probably are, then what that means is that you've got a risk of death that doubles about every eight years. So to sort of put that in more concrete terms, I'm 36. That means my

risk of not making my 37th birthday, starting on my 36th birthday, was about one in a thousand. And I like those odds, right? That means that on average, I'd live into my thousand and thirties on average if I've got a way and a thousand chance of dying every year. But unfortunately, of course, that isn't what happens. My risk of death doubles about every eight years. And so if I'm lucky enough to make it into my 90s, and of course, there's no advance in medicine in the intervening time, my odds of death in one of the years in my 90s is going to be about one in six. So that's that sort of life and death at the role of a dice. And this is a very sort of visceral statistical way of encapsulating the aging process. We can say that, you know, how fast do humans age? Well, our risk of death

doubles every eight years. But if you look at something like a Galapagos tortoise, well, its risk of death doesn't double. In fact, it stays completely flat once it's reached adulthood. It's constant with time. And so in a very real biological sense, these animals don't age. And obviously, you know, we're not just interested in these abstract statistical quantities. It's also interesting to look at how healthy these animals stay. And Galafka's tortoises do remain healthy throughout their lives. What you find is that, you know, they don't get frail, they don't get any less reproductively active, they don't get any less cognitively active. They're just effectively as sprightly at 150 as they were at 50 years

old. Just to say, obviously, they're not running around kicking a football, they are tortoises. But nonetheless, this lack of a decline, you know, lack of increase of risk of death, lack of increase of risk of frailty, lack of increase of risk of diseases, this is very much something we as humans could aspire to. And the fact that there are, in fact, quite a few animals out there that seem to display this property, which is called negligible senescence, is really encouraging to suggest this isn't a biological impossibility. This is something that we as humans could strive for. So is there something from the biological angle that we can learn from Galapagos tortoises and apply it to humans, or is it just that it's innate to these sort of immortal species?

I think the first thing to say is that it's going to be very, very tough. Because say we were to try and directly port whatever longevity hacks, because the Galapagos tortoise has into humans. The way we'd do that is, you know, we might observe their genes are a bit different to ours and maybe, you know, in some future, or we've got gene therapy, we could start applying some of those genetic changes to ourselves. Ultimately, though, we're going to end up, you know, closer and closer and until eventually we become tortoises. You know, they've obviously got a set of adaptations that work very well as a tortoise, but might not necessarily work so well in the context of a human, you know, we're warm

blooded, we're a very different kind of animal. However, I think what's really cool about these things, firstly, they are a proof of principle. And secondly, there are some things that we can learn from them, and particularly, I think, from the longer lived and, in fact, some negligibly senescent mammal species. So there's an animal called a naked mole rat, and these are very strange-looking little creatures that they're relatively closely related to rats and mice, their rodents just like they are, but they live in burrows underground at these enormous colonies, so they're quite a strange species. And they look like, I think they look a little bit like a penis with teeth, to be perfectly honest. They're not those beautiful creatures.

But these wrinkly little sausages, they've got this incredible property that they can live to about 30 years old. So, you know, as I said, a mouse lives about two or three years. A rat sort of the same amount of time. This very closely related species lives substantially longer. And again, they seem to be negligibly senescent. They don't get any more frail. They carry on being reproductively active. They scurry around these little burrows just as quickly right up until their very final years. And so perhaps, you know, these animals that are a bit closer to us, we can start to understand. I think the other thing is that by looking at these creatures that do age more slowly, we can learn more general things about the biology of aging. So it's the

case that these 10 hallmarks I talked about. The sort of clock that these hallmarks provide effectively ticks more slowly in animals that are negligibly senescent. And that gives us some confidence that these hallmarks are genuine, sort of universal aspects of the aging process and not just weird quirks of biology we've happened across. And what about at the other end of the spectrum, species like the may fly that live for a very, very short amount of time? I think that's, yeah, we can certainly try and avoid whatever biological problems they have. I think some of them, some of these species that live for a very short period of time, they often do it for very strange reasons that aren't necessarily that applicable to human biology. For example, there are some insects that live in incredibly short time and literally don't have a mouth, which means they're unable to feed themselves so they can just end up dying of starvation. And I think what this tells us more broadly actually is about the evolutionary history of aging.

So, you know, people often think this is strange because evolution is survival of the fittest. What evolution tries to do as it builds an organism is build organisms that are the best, the fastest, the strongest, you know, the fittest for their environment. So what on earth could be fittest about a process of progressive regeneration with time or on earth could be fittest about, you know, living for a couple of hours or a couple of days. and having this sort of big bang of reproduction and then dying, as in the case of an animal like a mayfly. And I think what's really important is to look at the evolutionary context in which these arose. So I've already mentioned this in terms of the size of animals.

Animals that are bigger tend to live for longer. And one of the reasons for that is because they're less predated upon, they're less eaten. And actually, you know, let's think about the mice versus another animal, this is another very long-lived but closely related to animal, the bat. A mouse, it can live two or three years, I already mentioned in the lab. But actually, they probably live more like six months to a year in the wild. And that's because mice, you know,

there are lots of cats out to eat them with, you know, sharp claws. There are lots of diseases that can kill them. They're also just tiny little animals so they can die of exposure. They can just get so cold that they just end up dying effectively of that. And so that means there are loads of natural ways that a mouse can come to an end that are sort of external to its body. So imagine your evolution trying to put together the perfect mouse. You're not going to bother investing in incredible, perfect anti-cancer defenses that would allow the mouse to live to 30 with not a trace of cancer because the mouse is going to be dead at six months anyway because it's going to have been eaten. And so what evolution does in the case of something like a mouse is it prioritizing.

is really rapid reproduction. You want to grow up fast. You want to pop out as many kids as you can in that first six months to a year in order that your genes get passed on. As if you imagine you're an animal like a bat, now the obvious difference between bats and mice is that bats can fly. And it isn't the sort of pure joy of aerial living that means bats can then live to 30 or 40 years old. It's the fact that because they're up in the air, they're at much less risk of predators. And that means they've had time to evolve those evolutionary defenses. It's worth evolution, putting some effort into building their bodies carefully in such a way to avoid heart disease or cancer or whatever it is that goes on to kill them. And that means that because they're killed less by external sources, they can afford to invest in those anti-aging defences. I think understanding that aging isn't some evolutionary adaptation, it's not something that evolution has chosen for us. It's just sort of a screw up because animals that are killed more easily by other means lose those adaptations that allow them to live longer. I think that again gives us some optimism. This isn't something we're going to have to be clever than evolution in order to solve. We just need to fix some of the mistakes that evolution is introduced because we can get

killed by other things. And so back to humans now, as you mentioned earlier, different people age at different rates, and how much of that is genetic and how much of it is environmental? It's a great question, and it's a very hard question. This is a little bit of controversy about answering this. But I think what might be surprising to a lot of people is how little of the contribution is genetic. The controversy is basically how small is that genetic contribution. And depending on exactly how you do the maths, you can say this contribution is anywhere between maybe 5 and 25%, this is a very small amount of what's called the variance in human longevity is driven by the age of your parents. Now, there's an optimistic note on this for most of us,

which is that how long your parents lived, you know, you needn't see that as a ceiling on your own lifespan if your parents live to 70 or 80. And there's a huge amount of that is within your own control, because even on the largest genetic contribution I just mentioned, 75% of how long you live is down to lifestyle and obviously unfortunately luck, which not, you know, none of us can do anything about. The place where this ceases to be the case is in people who live an incredibly long time. So if you look at people like centenarians, so that's people who make it to a hundred, suddenly there does seem to be a much larger genetic contribution. If you've got a grandfather or a grandmother who lived to 100, then, you know, you should start getting a little bit

excited because that does seem to run in families. And if you've got a parent or a sibling who makes it to 100, you've got about a 10 times greater chance than someone in the rest of the population of doing the same. So there clearly is some potential for us to mind the genetics of these incredibly, you know, super old, super fit, healthy people in order to try and understand what allowed than to get to those incredibly advanced stages. We often talk about people dying of old age. Is there an actual biological thing that is dying of old age? I think this is a bit of a myth that's been perpetuated for,

because for many, many years, this was actually a perfectly legitimate thing to write on a death certificate as a doctor. You know, if someone got to 80 and they just died in their sleep, they wouldn't bother investigating exactly what had killed them. But I think what we've come to understand is that, you know, although there is a sense in which 90% of people in the rich world die of old age, you know, that's the percentage of deaths that are caused by aging. That's one of the reasons that I call it our greatest humanitarian challenge,

because it's the single largest cause of death around the world. Actually, you know, what goes on to kill you is that as you get older, you get at higher risk of these diseases because of all these changing hallmarks in your body. You get a high risk of cancer, high risk of heart disease, higher risk of dementia. These diseases can take years to develop, but eventually one of them becomes severe enough that it can take your life. And so ultimately everyone does die off some specific disease.

It's just that that disease will probably have been made substantially more likely by the aging process. Is there a biological limit to how old humans can be? I think this is another fascinating and controversial question. I really think it depends what you mean by it. So I think in the sense that current humans, if I could give you the absolutely optimal diet, lifestyle, you know, the perfect, you could be lucky enough to have the perfect genetics and so on. There probably is some kind of limit as to how long you can live. Because, you know, humans evolved in a certain environment. There'd be absolutely no need for a free historic human to make it to 122, which is the current human lifespan record. So clearly there is sort of an evolutionary, you know, time are built into all

of us that's going to eventually cause our bodies to wear out. However, what I'm really optimistic about is that we can start to sidestep some of these things. We can start to make some tweaks some of the evolution wasn't able to make because there were no, you know, 100-year-old humans to optimise in the evolutionary environment and because they'd all reproduced long, long ago, they'd passed on their genes long ago. So there was no sort of scope for evolution to try and tweak those people. And I think that by, you know, coming up with therapies that can reduce some of these hallmarks and defer these diseases later and later into the future. I don't know how long we're going to live because it depends how fast some of these therapies are developed, but I don't really

think there is a fundamental limit on human lifespan. And you know, you can get that idea by looking at the Galapagos tortoises again. All these negligibly senescent animals, their risk of death doesn't change with time. And so although it's very hard to predict when we could get to that kind of state for humans, it's not something that's biologically impossible. It's just a question of how clever we can be and how quickly and lucky we can get, you know, developing these therapies. So is it a case that we age because we evolved to age or we aged because we haven't evolved not to age? I think it's more the latter, to be honest, because you find with these negligibly senescent species or species that just live a long time, they're in an environment or they're in a situation where it's necessary for them to, or where it's okay for them to live a long time.

They're not going to get killed by external factors or it's really, really important that they stay alive at older ages. And I think a really good example actually of this is fish. So there are some species of fish that are negligibly senescent. They've got a risk of death that doesn't change with time. And it's probably the case that this is because of their reproductive strategy. So in a lot of animals, the way that reproduction is done is, you know, and this is true in humans as well. It's primarily done by the youthful members of the species. But in fish, you get fish get bigger and bigger and bigger as they get older.

And actually, it's the biggest, oldest female fish that are the most important contributors to the reproductive system in those species. They're actually called boffs, which stands for big, big, old, fat, fertile female fish. I think I've got that right. There's a lot of Fs in there. And these massive matriarchs, they can put out, you know, dozens of times more eggs than a young female. The eggs are often more successful. So, you know, it's more likely that they're going to grow up into healthy young fish as well. And so they've just got a very different population structure to something like, you know, humans or, you know, rats or mice or whatever living on land. And that means suddenly evolution has a huge incentive to keep these pinnacles of reproductive fitness alive. They want to keep them alive as long as possible. And that's probably why evolution is invested in the defenses that allow those. fish to carry on living and carry on reproducing into a very, very old age. Whereas a human, you know, by the time you're 30 in prehistoric times, you're probably reproduced and you're basically on the scrap heap as far as evolution's concerned, because you've passed on your genes. And so it doesn't bother investing in those defences that, you know, I guess in the modern world,

all of us wish it would put a little bit more time into. And finally, what three things do you think we all should know about the science of aging? I think the three most important things are, firstly, what I started out by saying, that this is our biggest humanitarian challenge. Two-thirds of deaths around the world are caused by diseases that are caused by aging, essentially. And that means it's the single biggest cause of death. I'd also argue the single biggest cause of suffering for our species, and therefore it is our biggest humanitarian challenge, and it's vital that we do something about it. The second thing is that we understand, or are certainly beginning to understand in quite a lot of detail how it is that we age. We've got this idea of the ten hallmarks. There are

a few different theories we're converging upon, and that means that we've got the biological understanding to start to think about doing something about it. And thirdly, that these are treatments that are very much on the horizon. We've already got treatments in clinical trials in several cases for particular hallmarks. And the idea is that by reversing these hallmarks, by slowing down the rate at which certain things accumulate and so on, we can defer or potentially prevent a whole range of these age-related diseases. So this is a really exciting time. This isn't sci-fi. And I just think this is something we all need to know a lot more about in order that we can spread the word, get investment to the level it's needed and try and get some of these therapies

into humans as quickly as possible. Thank you for listening to this episode of Instant Genius. That was Dr Andrew Steele. If you want to know more about aging, check out his book, Ageless. Or, to hear him tell me about the exciting treatments that could stop us from getting old altogether, head over to Instant Genius Extra, available only on Apple Podcasts. The new year issue of BBC Science Focus magazine is on sale this week. Pick up a copy in store or visit ScienceFocus.com. This podcast is sponsored by name, audio and focal.

The texture and emotional depth of music. can be lost through digital sources or poor signal. Name Audio believes you can have digital precision with analog warmth. Alongside French acoustic specialist vocal, Name creates high-end audio systems, combining innovation with craftsmanship, so you can listen to music, just as the artist intended. Discover more at name audio.com. Ambition comes in all shapes and sizes.

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