E30 The Future of Aging
In this interview, biologist and aging expert Dr. Steven Austad joins host Don MacPherson to discuss how and why we age, various ways to extend human life, and ethical questions that accompany a 100-year life expectancy. They also dive into medical treatments that show signs of slowing the aging process, the impossibility of immortality, and the societal changes that will occur if we all live longer.
Season Three of the podcast is dedicated to exploring the future and how life is sure to change over the next decade. This episode provides insight into the current developments in the field of aging and the impact of longer life on culture, parenthood, lifestyle, and our careers.
Dr. Austad has dedicated his career to understanding the science of how and why we age. He is a distinguished professor and Chair of the Biology Department at the University of Alabama at Birmingham. He has also authored numerous books, academic papers, and articles on aging.
Don MacPherson:
Hello, this is Don MacPherson, your host of 12 Geniuses. For 25 years, I've been helping organizations and the leaders who run them improve performance. Now I travel the world to interview geniuses about the trends shaping the way we live and work.
Today's topic is the future of aging. Our guest is Dr. Steven Austad from the University of Alabama, Birmingham. Dr. Austad is the author of Why We Age: What Science Is Discovering About the Body's Journey Through Life. He's spent his career researching why different organisms age at different rates, and how that knowledge can be applied to humans. Dr. Austad believes that human life expectancy will continue to rise to a hundred years by the year 2150, and that the first human to live to 150 has already been born.
Dr. Austad, welcome to 12 Geniuses.
Dr. Steven Austad:
Delightful to be here. Thank you.
Don:
You have a very fascinating background, and as I was doing the research, it turns out you have been both a New York City taxi driver and a lion tamer.
Dr. Austad:
Right. Yeah. I think the more exciting of those is probably the taxi driver part.
Don:
I was wondering if one prepared you for the other.
Dr. Austad:
It may have. I drove the taxi from about four in the afternoon till two in the morning, and that's when a lot of, let's say, interesting things happened around New York City, particularly the 1970s when I was doing this. Yeah, I mean, the Lion training after that, except for the fact that I didn't know anything about it when I got into it, I'd say that taxi driving was pretty good training.
Don:
How did you get interested in animals and aging?
Dr. Austad:
Well, I've always had an interest in animals. In fact, my high school biology teacher told me I was going to be a biologist, and I thought that was the most ridiculous thing in the world because everybody in the world knew I was going to write the Great American novel at that point. But I had a series of pets. I've always been very close to animals. And then, I got into this job by accident, training big cats for the movie business. That reawakened really my interest in studying animals in some sort of formal sense. And that really convinced me to go on to graduate school to formally study animal behavior. I wanted to study lions in the wild; had no interest in aging whatsoever. Science is never a straight line. For most people, you start off working on this, and this leads to something else.
So, I never did get a chance to work on lions in the wild, but I ended up in South America working, of all things, on possums. Again, I wasn't interested, I wasn't studying aging, but what I noticed, because I had to recapture them once a month and sort of look in their pouches to see… look at their young and all. And I noticed that I would catch them, they’d be in wonderful healthy, vigorous, clear-eyed, muscular adults. And I catch them three months later and they would look ancient. They would have cataracts. They would've lost muscle mass. They would have parasites. Their gait was erratic. And I thought, “Whoa, what is going on?”
I would've thought that they aged about like a house cat, over 10 or 15 or even 20 years. But here, within a few months, they'd completely fallen apart. It was that observation that got me interested in aging.
Don:
Why do animals age, and humans, for that matter?
Dr. Austad:
The power of nature or natural selection to favor beneficial traits and to disfavor deleterious traits gradually fades out the older we get. So, selection for maintaining health and maintaining processes, an immune system, a good vision and all is very, very strong when we're young and in those prime childbearing years. But as we get older and older, and older, and our childbearing years gradually vanish, and our impact on our children gradually vanish, nature has less and less power to influence any new genetic variation that might arise. This leads to aging in two ways. First of all, if there are genes that don't affect me at all until relatively late in life, those can't be gotten rid of by natural selection, even if they're really, really bad for my health.
And many more new genetic mutations are bad for my health than are good for my health. So, over eons and eons and eons, these sorts of genes, to the extent that they exist, can accumulate in my genome. Ultimately, as I get older and older, they can start having effects.
Don:
You alluded to animals that don't age or maybe age at a very different rate. So, in the research, we discovered that clams live to 500 years old and hydro don't age at all. What's been learned from these discoveries?
Dr. Austad:
I started working on these clams because a group of oceanographers called me up one day from Wales, and they said, “We work on clams that live a very long time. Would you like to collaborate? Maybe you could learn something from them.” And I said, “I don't know. Well, what do you mean by a very long time?” I thought they were going to say 50, 60, 70 years. They said, “No, 500 years.” And I sort of looked at the telephone, and I said, “We must have a bad connection. I thought you said 500 years.” And they said, “No, no, no, we did mean 500 years. That's exactly what we said.” So, we got this collaboration going and I learned a lot about clams. I learned, for instance, that they have a beating heart, they have muscles, and they have a complex physiology.
But one of the things that I looked at was they have this very large muscle. The opens and closes the shell. And I thought, there's times when a clam absolutely has to have that shell slam closed. And there's other times, such as when it's feeding that it needs to be open. So, that's a really, really important muscle to the clam. Let's focus on that muscle and see what it is about that muscle that allows it to last 500 years. What we eventually settled on is a process of protein folding. We're finding out more and more health problems that have to do with the accumulation of misfolded proteins. So, proteins, the way they fold inside your cells, they have kind of sticky parts that are on the inside that stick to each other. But when they get damaged and they start to misfold, those sticky bits start showing up on the surface.
And when they do that, they stick the other proteins that are starting to misfold and they make these aggregates. Now, these aggregates, in Alzheimer's disease, are known as plaques and tangles. Those are the characteristic lesions of Alzheimer's disease. So, it turned out that the 500-year-old clam have evolved special proteins. What we're really looking at is not the machinery of maintaining the protein folding, but the way that clam proteins have evolved themselves. So, we actually started putting human proteins in that we know misfolds. We took the protein that's involved in the plaques in your brain in Alzheimer's disease, and we put that in the clam juice. And we tried to misfold it and make it clamp into these aggregates; and we couldn't do it.
So, there's something in those tissues that somehow stabilizes proteins and keeps them from misfolding. A potential therapy for these protein folding diseases, which we're discovering more and more of.
Don:
What are some of the other animals you're studying related to aging?
Dr. Austad:
Well, I'm studying a series of more traditional laboratory animals, meaning mice, and small worms, and fruit flies to address a couple of things that we need to know. One of the things we need to know is we've become, in recent years, we've become incredibly successful at figuring out how to make animals live longer in the laboratory. But what we really would like to know is what's the quality of that life? And you might think that while understanding the quality of a mouse's life should be pretty easy, but it's not because they lead such an unchallenging life. A mouse in a research laboratory lives in a box the size of a shoebox. And all it needs to do is walk over to the food hopper and eat, and reach up, and drink from the little sippy tube that they have.
And that's pretty much all we know about them until they get hardly able to walk around. So, we're trying to figure out, first of all, are there good ways to assess their health? And we're making quite a bit of progress with that. We're not so good at assessing how well they do cognitively. Our tests are very crude for mouse mental activity because, well, they're just not very bright, to tell you the truth. Rats are much, much smarter. We can do a lot more with them. But if you ask people what's the thing that they're really worried about most when they get older, most people will say they're worried about their mental condition. So, we're working on a bunch of metrics, not only to assess a mouse's health today, but have we got assessments today that can tell us how healthy that mouse will be a year from now?
If we had a drug, let's say that we imagine would keep it healthy twice as long, well, if we could give that drug to a six-month-old mouse until by 12 months; all right, this mouse is now going to stay healthy six months longer than a regular mouse; that's a lot more efficient way to go about things than waiting until that mouse got older and older, and older and older, and finally died. So, I'm working on ways of finding predictive tools to tell how people will be doing years from now. That's one of the things that I'm working on. I'm doing that in animals, not people.
Don:
When you work with the mice, what is the average lifespan of just a natural lab mouse without any intervention?
Dr. Austad:
About two and a half years. Two to two and a half years.
Don:
And then with some engineering, how much can their life be extended?
Dr. Austad:
The biggest so far has been an extension of about 75%.
Don:
That's incredible. That's quite impressive.
Dr. Austad:
That's a real outlier. More commonly when we find a way, it's 10% to 30% longer. But right now, being able to extend an animal's life, even a mouse is a mammal. So, it's got a lot of similarities to us. 20% that's… Like I say, there are dozens of ways in mice, hundreds of ways in these worms to do exactly that. This leads me to think that extending human life by 20% to 30%, highly feasible, probably will happen in the not-too-distant future. Extending health, I say extending life, because I assume that if we extend life 20%, we'll extend health 20%. If we could extend health 20% and not extend life at all, I'd still be very happy with that. That would still be a pretty good result.
Don:
Can we go back to the mouse again?
Dr. Austad:
Yeah.
Don:
When you're extending their life, what is the most effective intervention? Is it gene manipulation? Is it some sort of dietary manipulation? What have you found to be the single most effective way of extending life?
Dr. Austad:
Well, for years, this dietary intervention where you simply feed them less, you feed them about 40% less than they would eat, if you gave them all the food that they wanted, that typically will extend life 20% to 30%. We've known that for years and years, and years, and years. What's worked better than that? And this is really the only thing that's worked much better than that is to knock out the activity of growth hormone in the mouse. And that's when you find the really long-lived mice. The first report of this reported about a 50% increase in male mouse longevity and about a 60% increase in female longevity. Then I said our biggest success is about 75% increase in longevity. That was when you took the same mice and then also reduced their diet. But these mice had some characteristics that probably most people could live without.
First of all, we don't know if this is true in people or not. People have growth hormone. So, it could be, but think about this; out there in the popular mind, growth hormone is a youth preserving hormone. But what I just told you was by taking away the activity of growth hormone that was keeping these mice alive longer. Now, it had some side effects that even if it worked in people, a lot of us might not like, for one thing, they're about the one third the size of a normal mouse. If a bunch of two-foot-high people were living 50% longer, I'm not sure what the trade-off would be there, right?
Don:
Yeah. It gets back to the quality-of-life conversation.
Dr. Austad:
Exactly. I think it was this discovery which was so dramatic that really got us thinking about we need to know more about health and quality of life because people definitely would not like this. These mice also tend to have pretty poor muscle mass. They move around pretty slowly. They tend to get fat. They have a lot of things that really wouldn't translate well, I don't think, to human biology. So, we've done diets, we've manipulated genes. Now, I should say about manipulating the genes, turning off genes, souping up certain genes and all, almost nobody is in favor of that as any kind of human therapy. There are a few French people who think all we need to do is knock out this gene in people and to live a lot longer or we need to soup up the expression of this gene.
Most, everybody in the field, thinks there are serious ethical issues with that. I certainly do. But we have discovered, in the last 10 to 12 years, a whole variety of drugs that seem to have remarkable effects on preserving health and longevity in mice now, and some of these drugs are getting ready for human trials. But here's an interesting feature of all of those drugs. Almost every one of them affects one sex but not the other. Or if it affects both sexes, affects one sex much differently than the other. Now, this was a shocking finding to me. Because for the one thing that we had for years and years, and years is food restriction. That doesn't work like that. That works pretty much the same in both sexes. So, we were always thinking, well, if we start discovering drugs that mimic some of these effects, which is how we tried to look for some of the drugs, just saying, “Well, what does eating less, what genes does it turn on, and what biochemical pathways, and can we intervene in that with drugs?”
Nobody expected that these drugs would only work in females or only work in males. But yet that's what we found. I've gotten really, really interested in that because it was so unexpected. And what it suggests to me is that, first of all, we're probably missing some big stories in human biology because we haven't really looked at this in the past. We do some really strange things in human medicine. We don't think about giving different drugs to males and females typically unless it's something that has to do with, say, fertility. We don't even do different doses, for the most part. If you have a 300-milligram pill, well, you'll give it to a 280-pound man and you'll give the same pill to a hundred-pound woman. And my wife's a veterinarian; they don't do that in animals if they have a great day. And they give it a lot different dose of some drug than if they have a chihuahua.
But I'm thinking there's a real avenue here for reevaluating our drugs and how they work in men versus how they work in women.
Don:
Now, that's really a fascinating finding. I would think that most people would say women live longer than men because men take greater risks, or they're involved in work that's a little bit risky, or they have higher levels of stress, or things like that. But what you're talking about is really changing the paradigm of treatment between the different genders or sexes.
Dr. Austad:
You're right. That's exactly the sort of vision that people have. But interestingly, women die at lower rates of all of the top 10 causes of death with one exception. So, they die of cancer less, they die of heart disease less, kidney disease, diabetes. The one outlier here is Alzheimer's disease. And this is not because they live longer. There are ways to factor age out of the equation here. And so, with age factored out, they die at about 70% higher rate of Alzheimer's disease. But why do they die of cancer at a lower rate? Why do they die of heart disease, infectious disease? Recently, with the COVID-19 outbreak, there's been a lot of attention to how men are dying, higher rate than women of this. But to me, I would've been shocked if it was anything else because the same thing happens with any infectious disease; influenza, pneumonia, pretty much any infectious disease that we know about, men are more susceptible to be killed by it than women.
Don:
We've alluded to this a little bit, the research that you're doing on animals and how it can apply to humans, but what are some of the other ways that this research can be applied to humans? And then I want to get into what the future of aging is for humans, how much longer we can live, etc.
Dr. Austad:
The other big surprise is how late they could be started and still have a measurable impact on health and longevity. The first one of these that was discovered was a drug called rapamycin. And it's a drug that's already used in human medicine, but only in sick, sick, very sick people. But what happened in that is the way they do these studies is rather than stressing a mouse out by plucking it out of its cage and giving it an injection every couple of days, they wanted to put it in the food. They had some real problems with it degrading when they were putting it in the food. Well, it took them almost two years to figure out how to solve that problem. They'd set aside these mice, in the meantime, for this study. And in this whole time, the mice were getting older and older, and older, and older.
And by the time they'd figured it out and were ready to start the experiment, the mice were 20 months old, which is about 60 years old in human years. And they turned out that in these 60 year equivalent mice, when they started taking these drugs, the females lived 38% longer on the drug than the ones — this is from the time they started getting it from the age of 60 — than the ones that were not getting the drugs. And the difference in males was about 28%. So, that was a shocker. And there have been other studies since then; that's been confirmed. They've tried it in even older mice and still had a substantial effect. So, the implications of this for humans are enormous. I mean, it does a ton of things. It doesn't just make the mice live longer. It does almost all the things that you think would happen if you've got something that really slows the aging rate.
Don:
How many humans are taking rapamycin now?
Dr. Austad:
I hope very few because there are some side effects. So, there's a cocktail that people take when they've had a kidney transplant to try to prevent rejection of the transplant. And rapamycin is part of that cocktail. But it's at a very high dose. Interestingly, it has a reputation as an immunosuppressant because of this. But there also are both mouse and human studies that show that if you give rapamycin for a few weeks to older people before they get a flu vaccination, you get a much more youthful response to the vaccine. That's about the only clinical trial, but those are way lower doses than the cancer chemotherapy dose. There are some trials going on with not rapamycin, and I hate to sound too cynical, but the reason they're not going on with rapamycin is rapamycin is off patent, and really, nobody's going to make a great deal of money on it.
But if you tweak it a little, as some of the pharmaceutical companies do, add a little relatively meaningless chemical here or there, then you can call it something else and you can patent it and then you can do research on it. With some of these rapalogs, as we call them, there are human trials going on now; not for longevity, but for other things; for certain diseases. Resistance to infectious diseases is one of them. One of the things that we did in mice early on is we actually introduced them to this bacteria that causes pneumonia in older people. It's the number one infectious disease killer of older people before the current pandemic. And we found out that a dose of rapamycin actually protected them against this.
Don:
What are some of the other drugs that are showing some promise in combating aging in humans?
Dr. Austad:
There are whole series of drugs that they call senolytics. And some of these are cancer drugs and some of them are supplements. There is a supplement called fisetin that seems to show; again, this is in mice, seems to show pretty dramatic effects at preserving the health and certain tissues. There's another drug called quercetin, which in combination with a cancer chemotherapeutic drug has shown some promise. There's a drug called 17 Alfatradiol. So, there's a number. There’s another one called Acarbose. And then the one that I think is closest to a human trial for actual aging is a drug called metformin, which millions of people already take because it's the most common drug in the world that people get for type 2 diabetes.
Don:
What are you seeing with metformin since it is such a widely used drug?
Dr. Austad:
A group of us got together in this castle in the middle of nowhere in Spain, in this 15th century castle a few years back with the idea of locking ourselves in there; and at the end of it, coming out with an idea of how to do an experiment for the first drug that will slow aging in humans. I went in pretty much advocating for rapamycin and I came out convinced that the best way to go was with the metformin first. There were two reasons. First of all, there's a lot of information on metformin. People taking metformin tend to get fewer cancers than people not. Now, these typically are compared to other diabetics that are taking other drugs. They get less dementia; they get less heart disease. But these are all observational studies. But there was one study in England also that took about 80,000 people, and those 80,000 people were taking metformin because they had diabetes, and they compared them… They went through medical records and found people that weren't diabetic, that matched them for age, and weight, and as many things as they could.
And it turns out the people that were diabetic, taking metformin, lives longer than the people who were non-diabetic. All of that said, okay, there's a lot of weak evidence, because I consider all this observational stuff when you're not doing a real experiment, to be weak evidence. There's a lot of weak evidence that suggests that metformin in people now, not in mice, but in people, has broad benefits with respect to aging. On top of that, it's been used by millions of people for 60 years. So, we know it's side effects really well, and they're minor, and they don't hit a lot of people. We're not going to accidentally kill 3% of the people taking them because of things we didn't know. The other thing we thought, because we wanted to get FDA approval for this, is it's dirt-cheap. A bottle of metformin, it's cheaper than aspirin. So, the safety, the lack of the profit motive, and a lot of observational indications suggest that this was the way to go.
Don:
What do you predict the upper ends of human aging to be?
Dr. Austad:
I just wrote an editorial where I said, for the Wall Street Journal, where I said that I thought that life expectancy for people born in the 21st century is going to be a hundred years or more. I think that's a pretty reasonable projection.
Don:
And 150 years is not unattainable.
Dr. Austad:
Well, I would say, if life expectancy is a hundred years, there will be a handful of people that reach 150 years; just like life expectancy is roughly 80 now, but we have people that live to about 120 occasionally, very rarely. One hundred and fifty-year life expectancy, I think, is highly unlikely, but having a handful…
Don:
A couple outliers.
Dr. Austad:
Yeah, that strikes me as perfectly reasonable. In fact, I have this large wager on that, that you probably know about.
Don:
I've heard about this.
Dr. Austad:
Yeah. But for me to win that bet, the life expectancy would almost have to be a hundred years, around a hundred years. Because what I did is I calculated this well, if life expectancy now is 80 years, and the oldest person lived to be 120 years, it's actually 122, how long would the average people have to live to reach 150? It came up to about 100, 102. But again, some demographic projections suggest that, and I like to tell that to my college students now when I'm teaching on the biology of aging, because, of course, they were all born in the 21st century. So, I get a very receptive audience.
Don:
There are some who have predicted, one person in particular, who's predicted that humans could live to 1,000 years. Is that just a way to get attention or is there something there?
Dr. Austad:
No, there's nothing there whatsoever.
Don:
Okay [laughing].
Dr. Austad:
It is a way to get attention. But you do read these outlandish claims like that. I'm sympathetic to the wish. I also think they betray a great deal of fear and wish fulfillment. People are welcome to the fantasies that they want. That just strikes me as ridiculous.
Don:
Look, I know when people say outrageous things; a lot of that is just to get the attention. So, that was my assumption. What are two or three things that people should be doing right now to extend their life?
Dr. Austad:
The most important things that we know right now, we're finding more and more and more benefits of exercise and cognitive benefits; things that you would've never expected a few years ago. It's a good Alzheimer's preventative for one thing. I would say the best things that you can do right now are lifestyle things. Don't smoke, for sure. Get lots of exercise. Don't eat too much. Drink with moderation. I mean, these are boring things, and things we've done a long time, but the other thing that I would say is keep an eye on what's going on. My guess is if you came back and we were having this conversation 10 years from now, I might also, say, take 350 milligrams of metformin every day, or I might have something else. But right now, I think it's sort of the tried and true lifestyle factors.
There was a famous study on metformin that compared diabetics who basically were not taking any drugs but were trying just to eat right and all, and then there was a lifestyle group trying to eat right and exercise, and then there was a group taking metformin. This was a huge study that showed how beneficial metformin was, not just for people with diabetes, but even for people with pre-diabetes, people who were on the road to diabetes. But interestingly enough, the group that had the best result was the exercise group, the lifestyle group, the group that watched their diet and did the exercise. At least for now, until a little bit more science comes out, and when I say a little bit, I'm talking a little bit because a lot of these things are just poised to go into human trials.
Don:
It feels like we are on the verge of a breakthrough.
Dr. Austad:
I think we are. I think we are, but people shouldn't jump the gun. I had somebody say to me once, “I'm a stock broker, I can afford anything. Where can I get some rapamycin?” And I said, “Whoa, whoa, whoa, whoa. Way too early on that. Wait for the science to get done.” The same thing that's happening with COVID-19 pandemic is that people are so desperate to find something that they're lurching into trying things that you really shouldn't be trying because they could have really bad side effects, particularly in certain people that we don't know about yet.
Don:
If somebody was to address aging, let's say there's some breakthrough with rapamycin or metformin, and people say, “Okay, if you start taking this, it's going to address aging or suspend your biological aging,” do they just freeze in place or is there a way to kind of go back?
Dr. Austad:
The answer to both of those is no, you don't freeze in place.
Don:
Damn it.
Dr. Austad:
You continue to get worse, but you just get worse at a slower rate.
Don:
Slower rate. Okay.
Dr. Austad:
So, it may take you 20 years to get 10 years older. I think most of us would take that.
Don:
For sure.
Dr. Austad:
Going backwards, I mean, there's ways to make certain tissues healthier, but that's not really going back because all other tissues are going… You can't put used toothpaste back in the tube. Once it's out, it's out. But I think this idea of slowing the rate, and of course, if you combine them with lifestyle factors, that's the thing we haven't talked about; if you're doing this, but you're also combining lifestyle factors, we don't know how that will work. It certainly, it's not going to stop aging. That's another one of these wish fulfillment fantasies that people have. But it could slow it substantially.
Don:
One thing that we didn't talk about is addressing the telomere. Are these drugs addressing that? Or maybe you could talk for a moment about what that is and how that could potentially extend or reduce aging.
Dr. Austad:
This will come as a surprise to most people, I think, because telomeres have gotten a great deal of press. But in modern aging biology, there's scarcely a mention of telomeres, and I'll tell you why. The telomeres, of course, are the tips of the chromosomes that need to be protected to keep your chromosomes from sticking together and causing very, very bad diseases. And the idea was that every time a cell divides, these telomeres shorten a little bit, and when they get too short, they cause all kinds of problems. So, there's a lot of work on finding ways to keep those telomeres long. The reason that this hasn't really become a major player in the aging field is that it turns out that when telomeres get too short, your cells go into the state they call senescence. And it turns out that you don't need short telomeres for your cells to do that.
There's lots of things that make your cells do that. Short telomeres may be one of the least common ways that cells do that. So, there's lots of other reasons, but getting rid of these senescent cells that can be caused by shortened telomeres, but also can be caused, and much more commonly are caused by a lot of other things, it's getting rid of those cells turns out to be what some of these drugs are doing. But the telomeres themselves, I think that's a fascinating biology. I think for cancer biology, they're going to turn out to be quite important. But for aging biology now, if you went to a 21st century aging conference, it should be unlikely to hear any talks about telomeres.
Don:
What about the ethics of this? If we were able to cure aging or really extend life to average lifespan of 100 years old, does that affect our sense of urgency? Does it change our relationship to work? What are the ethical conversations around this?
Dr. Austad:
Well, it changes everything. It changes the whole trajectory of our lives. I think we could easily think about having serial careers, delaying having our kids; or having our kids, let them grow up, changing careers. It would change everything. Now, there are ethical considerations that I've thought a lot about. The main ethical concern that people seem to have when they come and ask me about this is they seem to be worried about various kinds of research resource shortages. It's a Malthusian idea that if we slow aging, the population will grow to be even bigger than it is. We’ll pollute the environment. Tenured college professors will never retire. A whole lot of things that they see as really, really, really bad. And my response to that is these are problems that we're facing today and are going to get worse; that we're going to need to do something about whether we do anything about aging or not.
And I'd much rather have an aged population that's energetic and vigorous and cognitively intact to try to help us deal with some of these issues. The idea that by doing this we're just going to overload nursing homes to capacity makes an assumption that what we're really doing is tacking on a few decades at the end of life where people are even more frail than they are now. But that's not what we're after and that's not what the animal work suggests is going to happen. We're keeping people healthy longer so they don't end up in the nursing homes.
Don:
Dr. Austad, this has been a very engaging conversation. I appreciate you taking the time with me. Sorry I couldn't be there in person in Birmingham today. Thank you for sharing your knowledge and wisdom with us, and thank you for being a genius.
Dr. Austad:
Thank you.
Don:
Thank you for listening to 12 Geniuses. Our upcoming episodes include The Future of Reproduction, the Future of Faith, and the Future of Transportation. Devin McGrath is our production assistant; Brian Bierbaum is our research and historical consultant; Toby, Tony, Jay, and the rest of the team at GL Productions in London make sure the sound and editing are phenomenal. To subscribe to 12 Geniuses, please go to 12geniuses.com. If someone you know would benefit from the information in this episode, please feel free to share it with them. Thanks for listening, and thank you for being a genius.