The Billion-Dollar Bet: Will Humans Live to 150?

Transcript for Season 6, Episode 1: The Billion-Dollar Bet: Will Humans Live to 150?

HOST: In 1999, Dr. Steve Austad, a biologist, was invited to a conference in Los Angeles. 

[MUSIC IN]

HOST: Not too unusual for an academic. But this was a tiny gathering – of people from a field that was still pretty niche at the time: human longevity: basically the science of aging. He was there with about a dozen other experts, as well as a reporter. 

Steve Austad: And she asked a question at one point, well, when is the first person going to live to be 150 years old? And none of us there wanted to risk an answer to that because there's no way to look more foolish in science than to make long term predictions. But I was never good at waiting. And so eventually I just blurted out, “I think that person is already alive.” 

HOST: That was a pretty bold thing to say. The record for the longest lifespan at the time was held by a French woman named Jeanne Calment. She died in 1997, at the incredible age of 122 years and 164 days. Now here was Austad, saying that Calment was going to lose her title. Someone already living in the year 1999 was going to live longer. Almost three decades longer. So why did Austad, who is now a professor at the University of Alabama, feel so confident about his prediction. 

Steve Austad:  I had been doing a lot of work on dietary restriction and I knew that dietary restriction in the laboratory at least could make animals live 20 or 30% longer. And I also knew that the oldest person to that date had been 122 years. And I thought, well, 20% longer than that is around 150. So that seemed quite plausible to me.

HOST: Austad’s prediction made waves in the world of aging research. 

Jay Olshansky: So I called Steve up. I said, Come on, you can't really be serious.

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HOST: This is Dr. Jay Olshanksy. He’s a friend of Austad’s who teaches at the University of Illinois at Chicago. They are both experts in Geroscience, that’s the study of aging, but they come at it from different angles. 

Austad is a biologist who studies animals. He wants to know why some animals can live hundreds of years, while others live and die in a few weeks. He thinks the answers could have huge implications for the human lifespan. 

Olshanksy, on the other hand, is a Biodemographer. A data guy. He dives into things like census reports and databases of birth and death records looking for hidden patterns. Olshansky says those patterns hold secrets about how we get old, and how long we may be able to live. 

After two decades of studying those patterns, Olshanksy thought Austad’s claim…just didn’t add up. 

Olshansky: You know, going from 122 to 123 is not the same as going from 80 to 81. When I see the difference between 122 and 150, it's not 20%. I mean, mathematically it's 20% in terms of the absolute value. But what's required to get there is light years different than what got us to 122. Something bizarrely different would have to happen in order to get somebody up to 150.

HOST: Okay. So Steve says this bold thing, you call him up and say, that's ridiculous. You have a conversation. And what comes out of that? What's the result of this exchange? 

Jay Olshansky: Let's put our money where our mouth is. 

[MUSIC IN]

HOST: So they made a bet. Austad wagered that by the year 2150, at least one person born in or before 2000 will have lived to be 150 years old. Olshanksy said, not a chance. The stakes? 

Jay Olshansky: $150 made perfect sense. We each put $150 down.

HOST: They invested the early money well, and, years later, they added in another $150 each. And here’s the thing about a bet this long. With the right early investments and compound interest, it can turn into a lot of money. 

Jay Olshansky: By the year 2150, it will be worth at least $1 billion. 

HOST: That’s right. A billion dollar bet. Twenty five years have passed since Austad and Olshansky made that bet. Olshansky is 71 now. Austad is 78. And after all that time, neither of them has backed down. But they do agree on one thing: We are already in the middle of an unprecedented global experiment to see how far we can extend human life. 

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[MUSIC IN]

HOST: In 1900, the average life expectancy for an American was just 47 years. By 2023, it had jumped to over 77 years. On average, men live to be just under 75, while women live to be more than 80. This trend has swept across the entire world. More years have been added to our life spans in the past 120 years than in the previous 10,000 years combined. 

How much farther can we extend human life? What are the ramifications if we do? Can we hack our way back to youth? And what do we do about the problems of aging that we’re already facing, like how to fund our elder years, and the increasing threat of Alzheimer’s?

These are some of the questions we’ll be asking in season six of The World As You’ll Know It: The Future of Aging.  

I’m Carl Zimmer, your host this season. I’m the science columnist for the New York Times and the author of fifteen books, including my latest: Air-Borne: The Hidden History of the Life We Breathe. 

In this podcast, we’re going to take a broad look at aging: where we are now, how we got here, and where we’re headed. I’ve been keeping tabs on the science of aging since the 1990s, when it was still a small field. And over the years, I’ve watched more and more scientists join Austad and Olshanksy in the quest to understand what causes us to get old and what we might do to extend our life expectancy even further. 

Scientists have found some crucial clues, and billions of dollars have flooded the field, along with a lot of companies looking to cash in. Which has led to claims about how immortality is just around the corner. But there are still some big gaps in our understanding of the aging process. 

That’s why we’re starting the story here- with Austad and Olshanksy. Because their bet is about more than two guys doing a little recreational gambling. 

It reveals two competing ways of understanding the human lifespan: are we locked into a hard limit established by centuries of data, as Olshansky argues? Or, like Austad believes, could a scientific breakthrough push us far beyond it?

[MUSIC OUT]

In order to figure out who might win this bet, we first need to talk about Austad and Olshansky’s work before the bet. How did two scientists in the same field end up on such different sides?

Carl Zimmer: So, Steve, let's start with you. You study animals, and as I understand it, your working relationship with animals kind of goes back a long way, even before you were a scientist. 

Steve Austad: Yes. I did a stint as a Hollywood animal trainer for the movies, working mostly with big cats. 

Carl Zimmer: You mean you don't mean like large house cats, right? 

Steve Austad: No, no, no. I mean big cats. Like African lions and tigers and mountain lions. That kind of big cat. 

Carl Zimmer: So how do you, how do you figure out how to wrangle a lion in Hollywood? 

Steve Austad: What you really need to do is you need to convince them that you're the dominant animal, you're the number one lion or tiger. 

HOST: One day, Austad was taking a three hundred pound lion named Orville for a walk when a duck darted out in front of them. Orville lunged at it. So Austad, as the number one lion, slapped him on the head. 

Orville didn’t take it well. He knocked Austad over and sank his teeth into his knee. Austad knew that if he struggled to get free, Orville might go for his neck next. So Austad just…lay there. For fifteen minutes. Until finally another trainer sprayed Orville with a fire extinguisher, and the lion let go. 

Austad spent six days in the hospital. But after he got out, he still couldn’t go back to work. 

Steve Austad: Lions and other predators are so good at picking up cues about weakness, I couldn't go back to work until I had no trace of a limp. So I had a lot of time off to think about my future. And I thought, I really enjoy trying to figure out what animals are thinking. But maybe I could do this in a more systematic and professional way by becoming a scientist who studies animals.

Host: Austad went on to get his PH.D. in biology, thinking he’d get back to working with lions. Instead, he ended up working with a slightly less deadly animal: the opossum. He was in Venezuela studying these marsupials when he discovered something surprising. You see, in general, little species of mammals live fast and die young. Bigger ones tend to live longer. But opossums broke this rule. 

Steve Austad: I assumed that an opossum, which is about the same size as a housecat, would live about the same length of time as a house cat, maybe 10 or 15 years.  And in doing that study, I discovered by accident that opossums in the wild don't live any longer than mice do. 

Carl Zimmer: So like how long?

Steve Austad: About two years. 

[MUSIC IN]

Steve Austad: And not only did they live a short time, but the project I was doing, I would recapture them once a month. And what I did, I'd see within a very short time, within a few months a very healthy looking opossum, I would recapture them. They'd have cataracts. They would have lost all kinds of muscle, but be parasitized, basically turn into an old opossum from a young, vigorous opossum in a matter of months. And that observation kind of haunted me. I have to figure this out. 

HOST: So Austad discovered his obsession with longevity in a rain forest. Olshansky discovered his in a college library. He was a graduate student in demography at the University of Chicago, and one of his classes was taught by an expert in the psychology of aging, Bernice Neugarten. Neugarten explained to the class that some people can be healthy in their old age, while other people are unhealthy while they’re still young. 

Jay Olshansky: And I raised my hand and I was 24 years old, completely naive. And I said, aren't all old people the same? And Bernice looked at me with these puzzled eyes.

Jay Olshansky: She said, I've got an assignment for you. 

Host: Neugarten sent Olshansky off to learn about aging. 

Jay Olshansky: So I went to the library. And began reading books on this, and I became absolutely enthralled with the question of how long we can live.

Carl Zimmer: What was so enthralling about it? 

Jay Olshansky: The uncertainty. There were so many people historically who said, yeah, we could live, you know. For thousands of years, we could live forever. But, but we don't. So I got hooked and I've never left. 

[MUSIC OUT]

HOST: Olshansky became an expert at analyzing data on human health and using it to calculate what’s known as the death rate. The death rate tells you how likely it is that someone is going to die in a given period of time, like in the next year, based on their demographics. Olshansky found that death rates have changed over time, but especially in the last 100 years or so. Remember, in the 20th century, life expectancy for Americans increased by about 30 years.

In 1900, children died at a shocking rate. In some American cities, up to 30 percent of infants died before reaching their first birthday.

Then came vaccines. And clean water. And pasteurized milk. And antibiotics. Rates of childhood mortality plummeted. 

Childbirth also became safer, so young mothers were less likely to die. 

Jay Olshansky: The only reason life expectancy rose so dramatically in the 20th century and where we're at today is because we saved the young. We were exceptionally good at reducing early age mortality, maternal mortality. 

HOST: But old people?

Jay Olshansky: Look, even in 1900, when life expectancy was 50 or when it was 40 or below in centuries prior to that, we still had old individuals. We still had people make it out into their 70s, 80s and 90s and. And guess what? They were old. 

HOST: While the death rate for younger people fell dramatically during the 20th century, the death rate for old people stayed pretty much the same. More people were reaching advanced ages, but once they got there, they still had a significant chance of dying. And the higher the age, the higher the death rate. 

This is a big reason why Olshansky is so confident in his bet. There just aren’t enough people living extremely long lives for a single outlier to reach 150 years.

Jay Olshansky: Once you get out past 100, you're getting death rates close to about 50%. You'd have to have billions of people make it out to 100 just to have one person break Jeanne Calment’s record. Mathematically, it doesn't work out. There aren't enough humans that exist today that would allow for that to happen.

HOST: But what if we could do what we did for the young, and wipe out diseases that affect old people? What if we could get rid of heart disease, for example, the leading cause of death in the U.S. for people 65 and older. Wouldn't that dramatically affect the death rate?

Olshansky had already been thinking along these lines, even before he made the bet. In 1990, he and his colleagues did the math for a paper in the journal science. They calculated that, even if no American died of heart disease ever again, the average life expectancy would only go up by three years. 

They also hypothesized that the average human life expectancy would max out at around 85 years. But that was more than three decades ago. And a lot can change in 30 years.

HOST: So Jay, you recently decided to go back to your original arguments about life expectancy and test them. What did you find? 

Jay Olshansky: We looked at the longest lived populations in the world and the United States, which isn’t one of the longest lived populations in the world. And what we found exactly what we had predicted in 1990, which is that the rise in life expectancy must decelerate. What we observed was that in the last 30 years, advances in life extending technologies accelerated dramatically, but the rate of improvement in life expectancy slowed down. It's not that we're not living longer. We are. It's just that the rate of improvement has slowed down. That's exactly what we predicted in 1990. And now we've provided what we consider to be definitive evidence that this is going to continue. And it means that we probably shouldn't all plan on living to 100. We've now demonstrated that that's highly implausible. 

HOST:  This is something else the pair agrees on. We’ve already attacked the primary causes of low life expectancy: things like Tuberculosis, Typhoid, maternal infections during childbirth. If we’re going to extend our lives further, we have to look for something else, something beyond getting rid of diseases one by one. 

Carl Zimmer: Steve, what do you think of this new study? 

Steve Austad: For people who watch these things and I watch some very, very careful, it's been quite clear that since 2010, there's been limited improvement. To make Jay's point more vividly, perhaps if you account for age, heart attack and stroke deaths since 2000 have declined by over 30% and cancer deaths have declined by 20%. Yet we're talking about just a handful of aging years of increase in life expectancy. Which really emphasizes why we need to have research that targets the biology of aging rather than going after cancer or Alzheimer's disease or heart disease one at a time. 

HOST: The biology of aging itself. What if all those diseases of old age aren’t the cause of aging, but the symptoms? What if we could prevent those diseases by slowing or stopping aging altogether? 

In order to do that, we’d need to understand – on a molecular level – what it really means to get old and die. 

[MUSIC SWELL]

Venki Ramakrishnan: What we mean by death is the loss of our ability to function as a coherent individual and in our case, as a conscious individual. And if it weren't for that consciousness and self-awareness, we wouldn't even be worried about death. It would just happen, you know, plants die. I'm sure they're not really aware of it. It just happens. And many animals probably it just happens. So we're in that peculiar position. This self-awareness means that aging and death have obsessed humans ever since we discovered our mortality. 

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HOST: This is Dr. Venki Ramakrishnan. He's a structural biologist who’s been at the forefront of some incredible discoveries about how our cells work. This research has revolutionized our understanding of life – and death. In 2009, he won the Nobel Prize for his insight into the ribosome, the cell’s factory for using our genetic code to manufacture proteins.

Venki Ramakrishnan: Everybody thinks they know what genes are, they think of them as things we inherit or pass on. But actually, what a lot of genes are are units of information for how to make the thousands of proteins in our bodies that actually make us work. In fact, all life forms require proteins to work, and what the ribosome does is it acts like a giant translating machine. It latches on to the genetic message, and uses the genetic instructions to make a particular protein. And it does this for the thousands of proteins in our cell. 

HOST: It’s an incredible feat when you think about it. It’s like a speed Lego competition. A ribosome can connect half a dozen building blocks together every second, and keep going until it’s assembled a protein that is thousands of building blocks long. The protein then folds into a complicated shape, and then goes off to do its job. Maybe it carries oxygen from our lungs. Maybe it’s a hormone that tells our bodies to grow. 

Through his research, Ramakrishnan saw how impressive ribosomes can be. But he also saw them mess up. They sometimes grab the wrong building block, creating a defective protein. And when that happens, the protein might not be able to do its job. It can even become toxic, damaging the cell that made it.

Molecular failures like this are what drive aging, Ramakrishan says. He wrote a book in 2024 called Why We Die where he lays out how those failures happen, and what they mean for our bodies.

Venki Ramakrishnan: My own field, which is protein synthesis, is actually central to aging, because the proteins in our body in every cell have to work together. They have to work like an orchestra. They have to come in at the right time, leave at the right time. They can’t be dysfunctional.

Carl Zimmer: Maybe I should ask you a really basic question. I mean, what is aging? 

Venki Ramakrishnan: Well, aging in a broad sense is the accumulation with time of changes and damage that causes the system to become more and more dysfunctional. Let's start at the very fundamental level of the molecule that somewhat, it sets the program. 

Carl Zimmer: We're talking about DNA?

Venki Ramakrishnan: I'm talking about DNA. So the molecule contains all of the instructions, not just on how to make the gene products, but also on when to make them, how much to make them and when to shut them off. All those things exist in DNA. So think of DNA as lots of sentences. If you start corrupting those sentences, well, you could tolerate a few typos here and there. Some typos can change the sense completely. For example, if you change hire with fire, like why don't you hire him versus why don't you fire him? They would have completely opposite meanings, just an H to an F change. And the same thing could happen with DNA as well. So some changes are harmless, but other changes can have dramatic consequences. So these kinds of things not only can cause the cell to not function well, that itself can be a cause of aging, but they trigger something called a DNA damage response. 

HOST: A cell can sense when some of its DNA is damaged. And it responds by making special proteins that can swoop in and fix the problem. They may reconnect a broken strand of DNA. Or they may rewrite a faulty sequence in a gene. 

Carl Zimmer: So, our DNA, you're saying, is building up damage, but our cells just aren't standing back and letting it happen. I mean, they are really trying to get rid of this damage as much as they can. I mean, that's an important part of our existence. 

Venki Ramakrishnan: Absolutely. 

Host: Most of the time, the fix works. Our cells repair little bits of DNA damage thousands of times a day. 

But sometimes the damage is too much for a cell to repair. And it can be really dangerous to just let a cell continue existing with this damaged DNA. It may start multiplying out of control.  

Venki Ramakrishnan: Many cancers occur due to DNA damage. And as a result, a cell has evolved very sophisticated mechanisms to take cells that have DNA damage and send them off to either to commit suicide or to send them in a into a state called senescence. 

[MUSIC] 

HOST: Senescence is kind of like suspended animation for a cell. The cell is still alive, but it can’t grow. And it can’t divide. And that means it can’t turn into a tumor. 

Venki Ramakrishnan: What the senescent cell does is it can't divide. It's no longer functional, but it secretes inflammatory compounds. And these inflammatory compounds are actually signals to the immune system to come to the site, get rid of the senescent cell, but also repair the site because the damage may be due to some kind of stress like a wound or due to an infection. So senescent cells play a very important role early in life. But as we age, this accumulation of senescent cells is a problem because we have too many of them. They’re causing inflammation throughout, the inflammation is making more cells dysfunctional and so there’s a general acceleration of aging due to inflammation.

Carl Zimmer: It sounds, it sounds like there's, you know, there's kind of no free lunch. I mean, you know, in order to keep the damage at bay when we're young, we're kind of making things even worse once we get even older. 

Venki Ramakrishnan: Yeah.

HOST: So aging happens at many levels all at once. 

It happens on the genetic level as our DNA builds up damage. it happens on the level of cells as they malfunction and become senescent. 

[MUSIC OUT]

It happens at the level of our whole immune system, which responds by producing inflammation. and that inflammation can damage organs throughout our bodies. 

In our lungs, for example, it can scar the delicate tissues we need to breathe properly. And that means that they can’t deliver as much oxygen to our cells– making conditions even harder for them.

Aging burdens the entire body – until the body breaks.

Venki Ramakrishnan: Aging, of course, eventually leads to death. And that's because when enough defects build up in any complex system, then you have a critical system failure. So imagine you have lots of defects building up and then suddenly your heart fails or your kidneys fail or your brain fails. Then the body can no longer function as a coherent whole. 

Carl Zimmer: And so then there's all this research on these different animals and people where scientists have been looking for ways to play around with that schedule and, you know, maybe lengthen life. 

But this is, this is also big business. And I was surprised in your book you said that there are 700 biotech companies focused on aging and longevity with a market cap of at least $30 billion. There’s huge money in this. What do you think about that?

Venki Ramakrishnan: Many of these companies are built around some legitimate research. And what they want to do is use that research to develop something that can be used in humans, and that's fine. But some fraction of them are built on rather flimsy evidence and heavily marketed. And it's because none of us wants to get old and die, you know, it's just, you know, we fear that loss of existence. I think that's what plays on a lot of this. 

And so I think it's inevitable.

[MUSIC IN]

Carl Zimmer: When you look ahead, what would you foresee? I mean do you think none of this is ever going to work? Do you think like, oh we might have drugs to live to 150? Like what's, what's the future as you see it? 

Venki Ramakrishnan: You can put it into different categories. I think drugs that might improve our health in old age are much closer, possibly in the next ten years. We might have drugs on the market which are proven to improve health in old age. I can see that as a real potential. In terms of expanding our lifespan, as you know, the oldest person on record is 122. And since she died 30 years ago, nobody has lived past 120. So that seems to be about our natural limit. And that involves probably a lot of luck and genetics and lifestyle. So I'm not sure we'll be able to break that without fundamentally having breakthroughs and stopping the aging process itself. That might take a bit longer.  I wouldn’t say, I wouldn't say it's impossible, but I think it will require major breakthroughs.

[MUSIC OUT]

HOST: All this research on aging, it makes Steve Austad hopeful. We just need to figure out how to fight the damage that ages our cells — and by extension, our bodies and minds —  on a molecular level. 

And we can already do it in animals. Scientists have run experiments showing that interventions can dramatically extend the lives of worms, flies, and other species.

Steve Austad: We've come up with dozens and dozens of ways to keep animals healthy. And make them live 20% longer. There's a dozen drugs now that we know that do that. There are different dietary strategies. There are blood transfusions that are keeping animals healthy longer. There are new things, new molecular techniques, partial reprogramming of cells to make them younger. All of these things, I think at least one of those is going to translate to humans and it's going to change our aging trajectory dramatically. 

HOST: Here's just one example of the many studies that make austad sure he’s going to win the bet.

A team of scientists raised hundreds of genetically identical mice until they were nine months old. For us, that would be like reaching your thirties.  

Then the scientists fed some of the mice a drug called Rapamycin. In 2014 the scientists reported that the males on Rapamycin lived about 23 percent longer. The females lived about 26 percent longer. 

It’s important to note here that while Rapamycin has been tested in humans, don’t go trying it at home just yet. We'll tell you why in the next episode. 

But, to Austad’s point, scientists have found a number of compounds with this sort of effect on animals. And they’ll very likely find more. So does that mean it’s just a matter of time before people can take pills that extend their lives for decades?

Carl Zimmer: So Jay, in a world where GeroScience is able to provide preventive treatments that slow the aging process. What would that world look like in terms of how long people would be living and what would those older years be like?

Jay Olshansky: So I'm going to give you the three word answer that I teach my students, which is the most important answer as a scientist, which is: I don't know. We don't really know how much longer we would live with a successful Gero Therapeutic. And I'm actually less interested in the answer to that question about how much longer we would live. The question that I'm much more interested in is how much longer can we live healthy? How much can we extend the period of healthy life? And I'm very optimistic that we can extend the period of healthy life. 

Steve Austad: So I do, I do think that we do have some idea about what this might look like, because if we look at the healthiest people at older ages now, they’re really quite remarkable, they don't live 150 years. But there I mean, there's now a world record for the marathon by 100 year olds, Carl. 

[MUSIC IN]

You know, who would have thought in the year 2000 that there would be a 100-year-old that ran a marathon in any length of time? 

Carl Zimmer: When I hear the two of you talk about the future of aging and research on aging, it seems like you're both pretty much on the same page about how science and medicine are going to continue to make improvements in how we age. So why do you, is there still this gap between the two of you? You know, that you still both think that you're going to win the bet? 

Steve Austad: So I know how I would explain our differences. I'm a biologist. Jay's a demographer. I am hearing all the successes before they're published. Demographers, as you can tell from listening to Jay, demographers think about long swaths of the future. You know, my thought is if you can detect a difference in molecular aging rate across five years, you can assume that you're going to get a change in the slope. Jay wants to wait until, you know, everybody taking the drug is dead and then say, “okay, they lived longer or not.” I think that's really why there is the gap.

Jay Olshansky: It's numbers. It's a numbers game. You can't get enough people to get one person to make it out to 150. And even if there were enough people, you have to get this drug into the right person. You have to find a needle in a haystack. Just giving it to everyone in a population isn't going to do it. You got to find the right person to give it to. And I'm skeptical– that person may already be dead. For all we know, the person that could have made it to 150 died in a car accident. So, um yeah, we don't–

Steve Austad: I'd like to thank Jay for proving my point. 

[LAUGHTER]

HOST: We’re still a long way from 2150. But we don’t have to wait till then to see why this bet matters. As we will discover in future episodes, this bet matters today. because right now, there are people claiming that science is going to let them live for centuries. Right now, we face a staggering epidemic of Alzheimer's. And right now we are trying to make sense of a world where people have gained decades of extra life. 

[MUSIC OUT]

[MUSIC IN]

HOST: On the next episode of The World As You’ll Know It: The Future of Aging…

Bryan Johnson: Why are we here? 

Crowd: Don’t Die!

Venki Ramakrishnan: Aging research has gone from a somewhat unfashionable backwater to really mainstream biological research attracting really top scientists. And it's just generated an excessive amount of hype.

Dan Belsky: 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. 

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.