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Announcer: Ladies and gentlemen, please welcome to the stage Bryan Johnson.
Bryan Johnson: This blue light is terrible for my sleep. I know it.
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Bryan Johnson: You guys it’s amazing that we’re here, look at this!
[crowd cheers]
HOST: I'm in New York City, at a giant convention center. I'm sitting in a darkened conference room, surrounded by a thousand or so people. and they are going wild as Bryan Johnson comes on stage.
Bryan Johnson: Why are we here?
Crowd: Don’t Die!
Bryan Johnson: Why are we here?
Crowd: Don’t Die!
HOST: Welcome to the Don’t Die Summit.
Bryan Johnson made a fortune in tech. But he’s become better known in recent years for plowing his wealth into a quest to slow down his aging. His health regimen ranges from a strict schedule of exercise and sleep, and a barrage of vitamins and supplements, to much more extreme and experimental measures – including getting blood transfusions from his teenage son.
Maybe you’ve seen the Netflix documentary about Johnson, called, “Don’t Die: The Man Who Wants to Live Forever." Maybe you’ve read one of the many magazine articles about him, or seen him promoting his health protocol on social media, where he has millions of followers. Johnson says he’s using all that attention to build a movement. A religion.
Bryan Johnson: From a historical perspective, what I hope this event represents is for those that exist in the 25th century, including many of us, they look back at this time in the early 21st century and they see us as the flicker. When humans began to see what was happening in this moment. That we began to imagine a new era of being human.
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HOST: The people who’ve come to the Don’t Die Summit don’t strike me like disciples of a new religion. But they are doing an awful lot to try to fight old age.
Sarah Sandnes: The pillars are, you know, sleep, workout, diet, for sure. And then, you know, I have a significant supplement stack on top of that.
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Sarah Sandnes: Omega 3 vitamin B complex. And they have the NMN. Yeah. I also take tons of other stuff like turmeric and vitamin D. I don't know, I take like 20 different things.
Carl Zimmer: 20 different things?
Sarah Sandnes: Yeah. I can't remember all of them.
Julia: We do a lot of supplements. Yes, we do.
Carl Zimmer: Vitamin therapy.
Julia: We take peptide injections. We, you know, do a lot of specialized testing to see what our current status is. What else do we do?
HOST: The popular term for what these people are doing is biohacking. There's no precise or scientific definition, but in general it refers to a wide range of behaviors to slow or stop aging – from vitamins and lifestyle changes to more drastic interventions.
And while the people at this gathering are doing a lot of biohacking, perhaps nobody does more of it than Bryan Johnson.
He reportedly spends two million dollars a year on a long list of treatments. Stem cell injections. Gene therapy. Regular sessions in a hyperbaric chamber, which is a pressurized machine that increases your oxygen intake. Price tag for a home unit? over 100 thousand dollars.
And Johnson acknowledges that all of this may not seem exactly normal.
Bryan Johnson: When we first started doing this and it went viral, people had this really strong reaction where they didn't quite know how to think about me. Typically the headlines were like eccentric billionaire Patrick Bateman, Prometheus, right? And then like vulgarity, vulgarity, vulgarity. So, we had to reframe the conversation. And I had to say, okay, so when LeBron James exercises and sleeps well and he shows up on the basketball court and he plays well, we're like, that's cool. But when someone tries to be healthy, they're weird. And we wanted to change that frame and say actually we are professional rejuvenation athletes. Like we actually are a sport. We're a discipline. So I started referring to myself as a professional rejuvenation athlete.
HOST: Johnson is doing what you’d expect from someone with a background in tech. He is gamifying longevity – trying to turn his obsession into a contest.
Bryan Johnson: But when you start playing a game, you need a leaderboard. You need some kind of point system.
HOST: He co-founded a website called the rejuvenation olympics, where longevity enthusiasts can compete to see who can slow their aging the most. How do you know who’s winning?
Bryan Johnson: Everything you do, you can test through a fitness test, the blood test, a speed of aging test.
HOST: Every three months, competitors in the rejuvenation olympics have their blood tested. A lab measures chemical changes in their cells, and uses those results to estimate how quickly they are getting old – their speed of aging.
The results then get posted on the website. and you can probably guess who is at the top of the rankings…
Bryan Johnson: I have the best biomarkers of anybody on planet Earth. I am the healthiest person alive. Now, is that true? We don't know. Has anyone else beat me? No.
The reason why I'm saying this is not to boast. Okay, that's not true. I'm boasting. Also, but it's basically meant to say if you want to pop in the conversation on health and wellness, if you want to be an expert, if you want to be taken seriously, post your biomarkers. Share your data. Like actually put it to the test.
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HOST: Okay, reality check. Johnson talks a lot about things like epigenetics and exosomes, but he’s not a medical doctor.
And that speed of aging test? It's a real test, but it’s purely experimental. It hasn't been approved by the fda, or clinically validated for any diagnostic purpose.
Like a lot of the big names in the biohacking world, Johnson is financially invested in the stuff he’s promoting. He has a company that sells the supplements he uses – and it has a big booth at the Don’t Sie summit.
But the FDA hasn’t evaluated the company’s products. And their lead doctor resigned last year, reportedly over concerns about the products’ safety and efficacy.
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HOST: When it comes to aging, it can be hard to tell the difference between hype and fact. As you heard in our last episode, aging experts are making solid progress in understanding the molecular basis of aging. They've run experiments on animals to boost longevity. And those animals have lived longer.
But whether we will see those same effects in humans is still a big question.
There is real science behind biohacking. There is also a lot of snake oil. I'm Carl Zimmer. And in this episode of The World As You’ll Know It: The Future of Aging, we’re going to find out the difference.
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Venki Ramakrishnan: Aging research has gone from a somewhat not disreputable but unfashionable backwater to really mainstream biological research attracting really top scientists.
Dr. Venki Ramakrishnan is the Nobel Prize winner who gave us an intro course on the biology of aging in the last episode.
But that's also resulted in a lot of private money going into it. Lots of biotech companies are people selling various products which range from plausible to really quite dubious. And it's just generated an excessive amount of hype.
HOST: In his book, Why We Die, Ramakrishnan unpacks how aging occurs. He also explores the various methods people have used to try to stop it. I asked him to walk me through the most prominent ones.
Carl Zimmer: I suppose the oldest of these is maybe the simplest, which is just to eat less calories.
Venki Ramakrishnan: So this idea of caloric restriction has been around in many different cultures. In fact, nearly all religions encourage fasting at various times. Gluttony, as you know, in Western religions, is considered a vice. So I think people were aware that overeating is not a good thing.
The real experiments, I would say, were done a few decades ago when people looked at animals that had been calorically restricted. And I should define what calorically restricted means, it means to have just the bare minimum calories to live healthily. That is, they're not starving. They're not losing weight. They're not sickly. Versus animals that had an all you can eat diet. When they did this comparison, they found that the calorically restricted animals resembled much younger animals in terms of many of the markers in their blood and and their system, but also in terms of their movement, their hair, their skin, you know, all these just they just looked younger.
Carl Zimmer: So, if an animal doesn't eat very much, you're saying that things are going to change in their bodies? What happens?
Venki Ramakrishnan: So if you eat a lot, it turns on protein synthesis and our ability to grow. If you're restricted, you turn off that ability to make lots of proteins and turns off that sort of growth signals. And at the same time it turns on signals, which I call the garbage disposal signals of the cell. And this is called autophagy. Now, autophagy is a process where any components that are defective in the cell are taken to these recycling centers, where they are broken down and recycled. So think of all the junk you accumulate. And if you accumulate too much junk in your office or in your house, you just won't be able to function properly. And so you need a clean out and you have to just take it all and take it to your local recycling center or your garbage dump. And that's what the cell does all the time.
Carl Zimmer: It kind of sounds like, boom, we've found it like, let's just cut our calories down in half.
Venki Ramakrishnan: So something like caloric restriction can help with some aspects of aging and indeed it can have a broadly beneficial effect. But it can't abolish aging because it'll still happen from other causes.
HOST: Caloric restriction may clear out damaged proteins from our cells. but it can’t fix DNA that has mutated. It can’t undo tissue damage or stop old cells from malfunctioning.
And it comes with some side effects.
Carl Zimmer: I suppose another thing about caloric restriction is that it wouldn't really be a whole lot of fun to be going around every day having annoying hunger inside of you. And so it'd be much more appealing to just pop a pill that could shortcut around being hungry all the time.
Venki Ramakrishnan: Absolutely. And in fact, you've hit on a very big area of aging research, which is caloric restriction mimics. As you say, Nobody likes to be hungry, but you also feel cold. You have more trouble healing wounds. There are a bunch of side effects of caloric restriction that occur to varying degrees. So the idea is, could we have a pill that mimics caloric restriction? And there are a number of candidates.
HOST: Turns out, these mimic pills do exist. And it’s worth looking at how the first one was developed, because the story illustrates why we don’t yet have a panacea for aging.
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HOST: In 1964, a team of scientists sailed from Canada to Easter Island – that’s the remote patch of land in the Pacific known for its giant stone heads. They wanted to study the indigenous people there. and as a side project, they scooped up some soil for future study.
Years later, a microbiologist named Suren Sehgal was studying the dirt for possible medical compounds. That's not a surprise – some of our best antibiotics come from soil bacteria.
In 1975, Sehgal discovered that the Easter Island bacteria make an antifungal compound. The compound worked by stopping fungal cells from growing. Sehgal discovered that it could also stop certain cancer cells from growing. and immune cells, too.
He named this new drug Rapamycin, in honor of the indigenous name of Easter Island, rapa nui. And in 1999 — almost 25 years later — Rapamycin won FDA approval as an immunosuppressant.
Venki Ramakrishnan: The reason for that is when you get a graft, if you get an organ transplant, your immune system recognizes it as foreign and wants to reject the graft. So if you want to live happily with your graft, you have to take immunosuppressive drugs. And Rapamycin was one of those drugs.
HOST: But Sehgal couldn’t say how Rapamycin worked – just that it did.
It wasn't until the 1990s that a scientist named Michael Hall solved that mystery. And in the process, he discovered Rapamycin’s potential for anti-aging.
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Hall learned that Rapamycin grabs onto a special protein inside cells. That protein acts as a switch for cell growth. When a cell senses nutrients are around, it flicks the switch one way, prompting growth.
If nutrients disappear, the cell flicks the switch the other way. It stops growing, and instead starts cleaning the house – with autophagy. Rapamycin turns that switch off. That's how it can stop an immune cell or a cancer cell from growing.
Venki Ramakrishnan: So then the idea was that, well, okay, then maybe Rapamycin might have similar effects to loss of nutrients or in other words, caloric restriction.
Carl Zimmer: And maybe if you just take this antifungal drug, you might actually slow down the aging process. That’s the idea?
Venki Ramakrishnan: Absolutely, that is the logic. And so when they tried it with mice, they did find exactly that effect. The mice resembled calorically restricted mice. They lived significantly longer, 30% or so. And their biological markers, again, started to resemble younger animals. And so Rapamycin has become the darling of some of the anti-aging community, including researchers. Now you could ask, what’s the problem?
Carl Zimmer: Sure, what's the problem? I mean if I’m like a mouse, I could get an extra 20 years by taking this drug that's been shown to be safe and then… and I’ll also be healthier…
Venki Ramakrishnan: Ah, you’re jumping the gun there.
Carl Zimmer: What!
Venki Ramakrishnan: Shown to be safe.
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HOST: Remember, Rapamycin was first approved to suppress the immune system. That's good if you get a kidney transplant. But Rapamycin can potentially prevent the immune system from doing things you do want it to do – like fighting infections and attacking cancer cells.
Venki Ramakrishnan: Now, advocates of Rapamycin would say, well, we can actually adjust the dosage so that we get the benefits without the side effects. We don't have to use these very high doses that you have for immunosuppression. And that's ongoing work. But it hasn't prevented people, including serious scientists, from jumping the gun and just advocating taking it. And many of them are taking Rapamycin on the side. This is a general problem with the anti-aging field. Everybody feels the clock is ticking and they don't want to wait for the clinical trials and proper experiments to come out.
Carl Zimmer: So science scientists themselves are not immune from, you know, a fear of aging?
Venki Ramakrishnan: Oh, I always say, science is great. Science is rational. Scientists are not rational, okay? We're humans like everybody else. We have our prejudices and so on. It's the scientific system and the method that keeps the whole enterprise honest. You know, you do something shady, your fellow scientists will call you on it.
HOST: Over the past 20 years, scientists have carried out a number of small clinical trials to see if it can improve people’s health.
A few of them produced promising changes in people’s skin, their hearts, and their immune systems. But no trial has yet shown that Rapamycin makes people live longer.
And some trials have also shown side effects, ranging from increased infections to an increase in cholesterol.
Bryan Johnson has said that he took Rapamycin for 5 years. Then he decided to drop it. On a post on his website in early 2025, Johnson said, “the benefits of lifelong dosing of Rapamycin do not justify the hefty side-effects.”
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Rapamycin isn’t the only drug that people are taking in hopes of slowing aging.
In 1994 the FDA approved a drug called Metformin for diabetes. But it had already been in use for hundreds of years.
Venki Ramakrishnan: Metformin was actually discovered almost by accident. It was from a plant that was used by monks to treat disorders like diabetes. And then the key ingredient was isolated and called metformin. And then it became a drug for treating type two diabetes. And its one advantage is, because it's been clinically tested for safety, etc, it's been widely prescribed.
HOST: Around 2013, researchers studying Metformin’s impact on longevity discovered that mice taking the drug lived longer than control mice. And when they looked at people on metformin for diabetes, they saw something similar.
Venki Ramakrishnan: There was one finding which suggested that diabetics on metformin lived longer lives than even non diabetics.
Carl Zimmer: Wow.
Venki Ramakrishnan: And that's unusual because diabetes itself is a real risk factor.
Carl Zimmer: You would not expect that!
Venki Ramakrishnan: You would not expect that. And so there's a great deal of interest.
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HOST: So it’s not crazy to think that an intervention like a pill could help people live longer and enjoy a healthier old age. But, despite all the excitement about various drugs, it’s not clear if they work at all for people. and they may have side effects in humans that don’t show up in experiments on animals.
So how can researchers prove that something will make us live longer? Do they have to wait decades to see how long volunteers in clinical trials live?
Or could there be a faster way to measure efficacy?
Dan Belsky: My name is Dan Belsky. I am an associate professor of epidemiology at Columbia University's Mailman School of Public Health. Do you want me to say something about, like, what I actually do?
Carl Zimmer: That would be good.
Dan Belsky: Okay. Our lab studies human aging as a process that we think we can modify to prevent or delay the onset of many different aging related diseases. And our particular work in that space has focused on the development of methods to quantify how fast or slow people are aging relative to the norm in the population, as well as to identify environments and behaviors that might contribute to faster or slower aging.
Remember the speed of aging test that Bryan Johnson uses? Belsky and his colleagues created it.
But they didn’t make it with the rejuvenation olympics in mind. The idea came to Belsky when he was studying how our experiences early in life influence how we age later in life.
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Dan Belsky: So I was interested in how the conditions of early development led some kids to lead long, healthy lives and other kids to get sick and die younger. And as I moved forward in that work, what I encountered were lots of studies focused on the development of disease A or disease B or disease C. But they all had the same finding. They all found that people who have more difficult lives, lives that are characterized by more environmental toxicants like air pollution, water pollution, as well as social toxicants, like victimization, bullying, discrimination, they get not one of these diseases, but all of them earlier and more severely than people who grow up under more favorable early life conditions.
HOST: It looked to Belsky as if poverty and other stresses early in life were speeding up the aging process. But he needed to test that idea.
And it just so happened that other scientists were starting to invent tools to measure aging. They called them epigenetic clocks.
Much of the pioneering work was done in the late 2000s, led by Dr. Steve Horvath, a biostatistician at UCLA. Horvath took advantage of the fact that our DNA is studded with millions of tiny molecular knobs.
He found that most people have the same pattern of knobs on their DNA when they are young. but over time that pattern changes. Enzymes chop off knob after knob. They also add new knobs. This process is called DNA methylation.
Horvath discovered that by reading the pattern of knobs, he could predict a person’s age – surprisingly well.
Daniel Belsky: Steve developed an algorithm that could predict how old a person was with an error of just a few years. And in fact what was remarkable about Steve's approach, was that he couldn't just do this in one type of cell. He could do it in essentially any cell from the human body. We think about our bodies as, you know, having been with us for a long time. So the fact that a cell in my body knows how old I am is maybe not as surprising as, in fact, it should be. My blood cells are at most three weeks old. So the fact that they carry within them – each of them – my birth date, is biologically extraordinary and still a mystery in terms of how that information is captured, recorded and then reproduced across generations of cells.
Carl Zimmer: Woah. Yeah, when you put it that way, that is pretty remarkable.
HOST: This was a huge breakthrough. and it led Horvath and other scientists to another insight: some people age faster than others.
In some people, the pattern of knobs on their DNA looks like it belongs to an older person. and these people often have health problems that are more common at older ages. In other words, a 40-year-old could have the cells of a 50-year-old.
Horvath and other scientists used this information to create a second type of clock. Instead of telling you the age you are, these clocks tell you the age your body is most similar to. The scientists call this number your “biological age.”
But Daniel Belsky wanted to use these clocks to do something a little different. He wanted to measure how quickly people age.
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Dan Belsky: The metaphor of the car traveling down the road is a good one in this case. You can think about your biological age as the readout on your odometer. That's awfully important. You know, you need to know how many miles there are on the car. But in the course of the trip, if you want to know when you're likely to get to your destination, the thing that's most informative is going to be your speedometer.
HOST: In order to build their speedometer, Belsky and his colleagues took advantage of a remarkable long-term medical study in New Zealand. Nearly all the babies born at one hospital in the city of Dunedin between 1972 and 1973 were enrolled in the study. Three years later, doctors gave them a clinical examination—all one thousand and thirty-seven of them. And to this day, doctors have continued to examine those kids every few years—except now they’re middle-aged adults.
Belsky and his colleagues compared the results of the exams at ages 26, 32 and 38.
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Dan Belsky: They gave blood, they did an exercise test, they did a lung function test, they got a dental exam. Altogether there were 18 different measurements taken that could be measured in parallel at each of those three time points. And so for each of those measurements and for each of those study members, we measured how fast they changed over the 12 years of follow up from 26 to 38.
HOST: They found that these biomarkers changed faster in some people in the Dunedin study than in others.
The researchers then examined the DNA methylation in these fast and slow agers – they looked at those knobs on the subjects’ DNA. And the pattern of knobs reflected how fast people were aging.
They used these patterns to develop a score. One is the average speed of aging. Higher than one means you’re aging faster, and lower than one means you are aging slower.
The researchers named this test Dunedin Pace, which stands for “pace of aging calculated from the epigenome.” They've gone on to use it to study the speed of aging in thousands of people.
Carl Zimmer: So now that the Dunedin Pace clock is in use. What do you think are the important things that you and others have learned? I mean, what is your clock telling us about aging?
Dan Belsky: So people who the clock measures to be aging faster experience an earlier onset of heart disease, diabetes. They become physically disabled earlier in life. They experience more rapid cognitive decline as they grow older and are at increased risk for dementia. They develop the kinds of problems that we expect should come with accelerated aging. So things that we know lead people to get sick and die younger tend to make their pace of aging faster, at least in observational studies.
HOST: Belsky is encouraged by these results, because they suggest that the Dunedin pace clock really works. It's not approved by the FDA – at least not yet. But someday clocks like this one could become widely used in medicine and public health.
Carl Zimmer: In an ideal world, how would you want people to use this clock that you and your colleagues have created?
Dan Belsky: Biggest picture, I think about this as a technology that we can use to surveil the population. The federal government fields these big studies to kind of give the country an annual physical to evaluate the prevalence of health problems, what might be some new risk factors in the general population. So an epigenetic clock would allow the government to ask how fast is our population aging? Are they aging faster in some places than others? Are policies, programs, allocations of health care resources influential of that population-level pace of aging? So that can inform public policy and public health in the same way that the kind of measurements that we're used to seeing, like the prevalence of hypertension or the prevalence of diabetes.
The second application gets into the ways in which we interact with the health care system. So when I come in to get my annual physical, the doctor takes a blood sample. They measure a couple of dozen things and they'll tell me about maybe how they're related to one disease or another or, you know, what I can do. But it's pretty abstract. There's a lot of numbers and they don't have any inherent meaning to people. If your doctor gave you an epigenetic clock test, though, everybody intuitively understands what it means if their blood test says they're five years older than their birth certificate does, like that's not good news. And similarly, I think they can understand whether they're aging fast or slow. And that then provides a point of communication for the doctor to talk to the patient about how changes they might make in their lifestyle, behavior or interventions that they might get in the clinic could alter their pace of aging.
Carl Zimmer: Do you think, oh in 10 or 20 years it'll be in your doctor's office and be reliable for you? Or do you think that that's just off the table?
Dan Belsky: No, I think I think we're less than that. I think within five years I would expect that we will have measurement tools that patients should be interested in and that clinicians might consider including in the battery of services that they offer. And just to be clear, there are doctors who are already giving these tests to their patients. And there are people who are already giving these tests to themselves.
HOST: Researchers can get a free license to use the Dunedin-Pace clock from Duke University and the University of Otago.
But the universities have also signed an exclusive agreement with a company called Trudiagnostic, which sells the dunedin-pace clock to consumers at about $500 a pop.
It’s important to note that Belsky does get some royalties from those sales.
And that’s how Bryan Johnson wound up using Belsky’s clock for his rejuvenation olympics.
Carl Zimmer: How do you feel about that? It's your clock.
Dan Belsky: Yeah. So as a researcher who builds these things, it always makes me a little anxious when I hear about people making decisions about their own health and behavior based on the results of your tool. I think that in general, people should have access to information. I don't think we should be restricting access to these things just because they're in beta testing. I do hope that the physicians and the individuals who are generating these data are interpreting them with a grain of salt. They appreciate that any single result may have some error in it. And in the same way that when you get back a clinical lab, sometimes your doctor looks at it and says, ‘oh that's not right. Let's retest that or let's look at something else’. So I think that in some sense, it's great to bring attention to aging as a modifiable cause of disease, not something that has to happen in the same way for everybody.
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HOST: Perhaps the most important revelation from belsky’s research isn’t about pills or behaviors that can reverse an individual person’s aging. It's about the social conditions that are making some groups of people age faster.
Carl Zimmer: So, if someone is affluent. Sure, they can spend $300 or $400 on a test like this. Maybe they'll spend $1,000 to buy a ticket to go to a longevity festival but you know, your work and what brought you into this field to begin with was looking at those stresses that lead to poor health, particularly in people who can’t afford that. How do you think that those people can benefit from what you're learning about these aging clocks?
Dan Belsky: I mean, I think the principal public health benefit from these tools that we’re developing to measure aging will come from applications to discover new therapies, to refine therapeutic regimens that are already in place in clinical settings. And to surveil populations in ways that inform us about the kinds of programs and policies that are most effective in building healthy lifespan. And in all of those applications, the benefits accrue to everyone.
Now at any given point in the life span, people who are living in some kind of poverty or poverty-related circumstance are aging, you know, between maybe it's 2% faster per year to 10% faster per year. And those estimates are not very precise yet, but that's substantial when we relate it to differences in risk for the incidence of disease or death.
Personally, a hope that I have for this kind of work, is that we can build an evidence base for more effective programs and policies that ultimately address some of these health inequalities. Not least because they will show us what the economic returns to intervening on poverty, for example, might be. Poverty is really costly, both in terms of the productivity loss of the individual to the economy, but also in terms of the health care costs that they incur.
So if you can run trials that demonstrate through mitigating poverty, whether it's by a employment program or a cash transfer program or an education program, you also slow the pace of aging. That becomes part of the cost benefit analysis that determines whether this thing is paying for itself or not. And so I have a hope that these tools will contribute to population health as well as through their acceleration of the discovery of novel interventions.
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HOST: On the next episode of the World As You’ll Know It: The Future of Aging…
Rachel Wu: adults are actually better learners than kids, because as long as we don't get in our way, we can actually learn quite efficiently, because we know ourselves better than kids do
HOST: What is the secret of people who are aging more successfully, who are still having a higher cognitive level?
Cindy Lustig: You can think about things like the knowledge that you have built up over time. Maybe if you can't immediately solve a problem in the moment, maybe you don't have to because you have the experience and you're just able to rely on that experience.
Richard Nisbett: I was always skeptical as to whether people got wiser when they got older. I was never blown away by someone's wisdom who was older.I was wrong, but that was my skepticism.
HOST: The World As You’ll Know It is brought to you by Aventine, a non-profit research institute creating and sharing work that explores how today’s decisions could affect the future. The views expressed don’t necessarily reflect those of Aventine, its employees or affiliates.
For a transcript of the episode and more resources related to what you've just heard, please visit aventine dot org slash podcast.
Danielle Mattoon is the Executive Director at Aventine. Bruce Headlam is the Editorial Director at Aventine.
Our Producer is Emerald O’Brien. Our Associate Producer is Marialexa Kavanaugh.
Our Editor is Joel Lovell. Kamilah Kashanie is our Managing Producer.
Original music by Davy Sumner with additional music from epidemic sound.
This episode was mixed by Marina Paiz.
Our head of sound and engineering is Raj Makhija. Our Senior Recording Engineers are Marina Paiz and Pedro Alvira.
Fact Checking by Will Tavlin.
Music licensing by Extreme Music and Epidemic Sound.
Our executive producer is Asha Saluja.
I'm your host, Carl Zimmer.
Make sure to listen to us on the Audacy app or wherever you get your podcasts.