[RADIOLAB INTRO]

JAD ABUMRAD: I'm Jad Abumrad.

ROBERT KRULWICH: And I'm Robert Krulwich.

JAD: And this is Radiolab.

ROBERT: You ever wondered why it is that all living things die?

JAD: I do wonder about that, actually. It keeps me up at night.

ROBERT: Which always leads me to the next question: do we have to? Do I have to?

JAD: The topic of our show, as a matter of fact. And a natural place to begin to look for an answer is in a garage.

JAD: Here we are in your garage.

LEONARD HAYFLICK: Here we are in my garage.

JAD: The owner of this particular garage is one Leonard Hayflick. He is a biologist. He takes me to the corner where he's got this ...

JAD: Wow, so describe what we're looking at here.

LEONARD HAYFLICK: Well, what we're looking at is a barrel-shaped device made out of metal that is actually ...

JAD: It's a metal canister that is shaped kind of like a thermos, except bigger.

LEONARD HAYFLICK: So I'm opening the lid ...

JAD: He twists off the top and—whoosh!—out comes all of this smoke.

JAD: Dry ice from Halloween is what it looks like.

LEONARD HAYFLICK: Well, this liquid nitrogen is used in a lot of movies.

JAD: He reaches his hand into the liquid nitrogen fog, right into the bowels of this canister and pulls out—and this is what I'd come to see ...

LEONARD HAYFLICK: Those are the—those are what we call ...

ROBERT: What?

JAD: Some test tubes.

ROBERT: Oh.

LEONARD HAYFLICK: Tubes in which these samples are kept.

JAD: Admittedly, they're not much to look at, but if you know what's in there, it's almost holy. Each tube has millions of frozen human cells in there, and these cells have completely changed how we think about mortality, and immortality.

JAD: And you keep it in your garage?

LEONARD HAYFLICK: Yes.

JAD: Why? I mean I think it's pretty cool but why ...

LEONARD HAYFLICK: Because nobody will think of looking here.

JAD: Oh, okay. Well I won't—I certainly won't divulge your address or anything, but ...

LEONARD HAYFLICK: No, please don't tell anybody.

JAD: No, of course I wouldn't, but ...

JAD: It's in California is all I'll say.

LEONARD HAYFLICK: Well, where else would you want me to put it? In my bedroom?

JAD: No, I don't know. I mean it's—I imagine something like this, you would find it in the middle of ...

JAD: It started for Leonard Hayflick about 50 years ago. I got the backstory actually not in California, in Philly.

JAD: Soundcheck. Do you wanna tell me where we are?

LEONARD HAYFLICK: Well, we're sitting on the 12th floor of the William Penn House in Philadelphia, Pennsylvania, which happens to be my mother's apartment, who has just celebrated her 100th birthday.

JAD: Just that day, appropriately enough. In any case, let's rewind to the '50s. Biology was facing a problem, basic problem: how do you study human cells? Cells are us. It is what we are, but you can't exactly put a microscope up your wrist—well, you know, I guess you could, but ...

LEONARD HAYFLICK: I wouldn't say it's impossible, but it's certainly highly impractical.

JAD: What you can do instead, and Hayflick was among the first to perfect this, is—well, he explained it to me.

LEONARD HAYFLICK: If I take a tiny biopsy from any part of your anatomy that you're willing to surrender to me ...

JAD: Like say, a fleck of my—like, my wrist. A fleck of my wrist.

LEONARD HAYFLICK: Your wrist, your—anywhere you want. The tip of your nose, the tip of your toe, I don't care where it is, and then you raise a pyramid of skin by grabbing onto the tip of a hair, pull it up, and then with the other hand you take a sterile scalpel and whack the tip of that pyramid of skin off. And I drop it into a test tube, and I introduce an enzyme preparation called trypsin. And that material dissolves the cement that holds all the cells together. Think of your tissue as a brick wall, and once I drop that brick wall into my test tube I need to dissolve the mortar.

JAD: Right.

LEONARD HAYFLICK: And now I have your individual cells. And if I feed them and treat them nicely, they will divide. Each cell will produce two cells. Each cell will produce two cells. Two cells. Two cells. If you do the math you'll find that they'll cover the city of New York in about three weeks.

JAD: I mean, you know, that's if you had a big enough petri dish. In any case, this process, it's called "cell culturing." It is the simplest thing in the world these days. I mean, modern biologists can do it with their eyes closed, but back in Hayflick's day in the '50s, it was very fuzzy.

ROBERT: Hmm.

JAD: Because no one really understood the mechanics of it. No one knew exactly what a cell liked or what it didn't like, and so the people that were really good at getting the cells to divide, from two into four and eight into 16, whatever, they ...

ROBERT: Yes?

JAD: They—it was like they had the touch.

LEONARD HAYFLICK: They had what was called a green thumb.

JAD: There was a mystique about them. Because, you know, don't forget, this was the early days. Biology ...

LEONARD HAYFLICK: Cell biology at that time ...

JAD: ... was still kind of a black art.

LEONARD HAYFLICK: Well, I'm interested that they used the term "black art," because that attribute was given to the field by a single individual who dominated the field for about 20 or 30 years. His name was Alexis Carrel. He believed that the contamination of tissue cultures with airborne bacteria could be eliminated or prevented by maintaining sterile circumstances that in his mind included everything being painted black. Now don't ask me the rationale for that because I can't explain it.

JAD: That's so gothic, I love it!

LEONARD HAYFLICK: Exactly. All of his technicians and he himself were dressed from head to foot in black, and he had a gallery around the lab where reporters could wander to see these mystical black figures roaming the laboratory floor, doing strange things with strange implements, and ending up with cells growing.

JAD: It must have seemed like witchcraft, almost.

LEONARD HAYFLICK: It didn't seem like, they believed it was witchcraft. Especially because Alexis Carrel claimed to have kept a chick heart alive for 46 years.

JAD: A chick heart.

LEONARD HAYFLICK: Yes.

JAD: Like the heart of a baby chicken?

LEONARD HAYFLICK: It was a fragment of tissue from the chick heart.

JAD: So for 46 years the cells divided and divided every couple days?

LEONARD HAYFLICK: Right. That's what was alleged.

JAD: Now 46 years is a long time, right?

ROBERT: Yeah, I'll say.

JAD: And so scientists thought that if they've gone this long they'll probably go forever.

LEONARD HAYFLICK: Forever.

JAD: Because of Carell and a couple other scientists, it was thought that cells are immortal.

LEONARD HAYFLICK: Under the proper conditions, they'll grow indefinitely.

JAD: And Carell's little chicken heart seemed to be proof of this. It just kept spewing new cells, which he'd keep dividing into new bottles.

LEONARD HAYFLICK: As the New York Post said, "If all the cells produced by Doctor Carrel from his cultured chicken heart were kept together, they would produce a rooster that could cross the Atlantic Ocean in a single stride."

JAD: [laughs] I wish I'd come up with that myself. Now was that a quote that was made lovingly or admiringly, or was it a sort of sneering quote?

LEONARD HAYFLICK: It was made to sell the New York Post.

JAD: But people bought it, I guess is what I'm asking.

LEONARD HAYFLICK: You're darn right they bought it. Until it was torpedoed by me.

JAD: Right. Well, that's the story that I want to get to next.

JAD: It happened by accident. He did not set out to torpedo the rooster or the whole idea of cellular immortality, it just kind of happened. He was in the lab, it was the '50s, he was just a kid, and he becomes worried—this was an ordinary worry at the time—that his little cells would become contaminated.

LEONARD HAYFLICK: I knew at the time that if you cultured normal human tissue from adults, you might grow simultaneously unwanted viruses.

JAD: Because in adults, the viruses would sometimes sneak into the cells and hide there.

LEONARD HAYFLICK: And I didn't want, of course, my cultures to be contaminated with these viruses, so I zeroed in on human fetal tissue.

JAD: Human fetal tissue. As in from abortions.

JAD: Now sorry to ask an ignorant question but abortion at that time was—was it anything like the crazy political thornbush that it is now?

LEONARD HAYFLICK: No. Far more rational.

JAD: It was actually quite easy, he says. He just picked up the phone ...

LEONARD HAYFLICK: Called my friends at the University of Pennsylvania and said I wanted fetuses whenever they were surgically aborted. And as you might expect, when you put your order in for fetal tissue you know not when the phone will ring.

JAD: He never knew when the shipments would arrive.

LEONARD HAYFLICK: I would receive maybe one fetus one week, and then two weeks later another one.

JAD: And so to keep track of things—and this turns out to be key—he kept a log. Every time he'd get a new shipment he would jot down the arrival day and then drop the cells into the flask, watch them divide, do the whole deal. And then every couple weeks he would come check on them. And that's when it started.

LEONARD HAYFLICK: I began to realize that some of the cultures are unhappy, they stopped dividing.

JAD: At first it was just one. One batch.

JAD: What were you thinking at this point?

LEONARD HAYFLICK: I didn't know what to think.

JAD: Because it's just an observation and it was just one batch—batch A let's call it. Yeah, all right. No biggie. We'll see how it goes.

LEONARD HAYFLICK: Come back, and a month later I find out that not only A is still not doing its thing, but B and C aren't either.

JAD: Now three batches of cells had gone kaput!

LEONARD HAYFLICK: I said to myself, "Well, that's peculiar."

JAD: Peculiar because here he'd done the same with these cells as he'd done with all the others. He'd put them in the same glasses, same solutions ...

LEONARD HAYFLICK: Same conditions.

JAD: Didn't add up.

LEONARD HAYFLICK: Now I had to find out what the cause is. So I go back and look at my records.

JAD: And that is when it smacks him in the face.

ROBERT: What?

JAD: The thing that all three batches of cells had in common, and he knew this because he'd kept the logs, is that they were the oldest, so to speak. He'd received each batch of fetal tissue from the hospital ...

LEONARD HAYFLICK: I received it from the hospital ...

JAD: ... roughly ...

LEONARD HAYFLICK: ... nine months ago.

JAD: And at nine months or thereabouts, they just kind of hit a wall and they stopped dividing.

LEONARD HAYFLICK: But the ones received one month, two months, three months, four months, five months, six months ago ...

JAD: Those cells were doing just fine.

LEONARD HAYFLICK: Perfect, beautiful.

JAD: And he kept seeing this. Simultaneously, two thoughts enter his mind. Thought number one: this can't be an accident.

LEONARD HAYFLICK: If it was an accident it should be random.

JAD: Uh-uh. Thought number two: wait a second, this has to be an accident.

LEONARD HAYFLICK: Because I had been taught by experts ...

JAD: That cells are immortal.

LEONARD HAYFLICK: ... they will grow forever.

JAD: All right. Fast forward a few months, those two conflicting thoughts are still fighting it out in Hayflick's mind, and along comes the annual biology conference.

LEONARD HAYFLICK: The biggest scientific meeting in the world. That time, the meeting was held in Atlantic City.

JAD: Hayflick and a few friends decide to hop in a car and crash the meeting, because the featured speaker was a guy Hayflick really admired, a guy by the name of Ted Puck.

LEONARD HAYFLICK: Because I want to hear what he has to say and I'm gonna—if I can get enough guts, I'm gonna ask him a question.

JAD: Hmm.

LEONARD HAYFLICK: I remember it distinctly. It was a big hall, you know, like a thousand people. I'm sure it's an exaggeration, but it's huge and lots of people, and I'm somewhere in the middle, listening to his talk.

[ARCHIVE CLIP, Ted Puck: You see the methods previously developed whereby single cells ...]

LEONARD HAYFLICK: And at the end, as is customary, he asked for questions.

[ARCHIVE CLIP, Ted Puck: Are there any questions?]

LEONARD HAYFLICK: I timidly raised my hand.

[ARCHIVE CLIP, Ted Puck: Oh yes, the young fellow in the center. Yeah, you.]

LEONARD HAYFLICK: And I ask him the following question: Dr. Puck ...

[ARCHIVE CLIP, Leonard Hayflick: Have you ever found that the cells that you culture stop dividing?]

JAD: Did you want to give him a kind of a gotcha, or what were you thinking?

LEONARD HAYFLICK: No, I was ready to publish. I wanted to know whether I'm in trouble, whether I have an artifact on my hands that nobody has seen because they do it right.

JAD: I see.

LEONARD HAYFLICK: I'm still worried.

JAD: Got it.

LEONARD HAYFLICK: And so he says—he looks at me, you know, like I'm an idiot. Well, of course ...

[ARCHIVE CLIP, Ted Puck: Well of course the cells stop dividing occasionally. Of course I lose my cells occasionally. But I simply go back to the freezer and reconstitute them.]

JAD: Meaning that when the cells stop dividing, which he just admitted they do all the time, he just said, "Eh, something happened, I don't know what. I'll just go back to the freezer and get more."

ROBERT: Well, that's not right. Because if they stopped dividing they might have just died.

JAD: It's not that he was cheating, it's that he thought he had screwed up.

ROBERT: Oh.

LEONARD HAYFLICK: Then I knew it was a gotcha.

JAD: Well, he didn't yell "gotcha" right at that moment, he just sat back down. But now he knew it was real because even the brilliant Ted Puck had seen it too. But like everyone else for the past 60 years, he just hadn't recognized it for what it was.

JAD: I imagine in labs all over the country, there must have been a lot of moments when cells stopped dividing. And at every one of those moments you're saying the thought that popped into the technician's mind is "I [bleep] up."

LEONARD HAYFLICK: Absolutely.

JAD: That seems like a crazy kind of mass delusion.

LEONARD HAYFLICK: It's called dogma. Is there—you know the definition of the word dogma?

JAD: [laughs] Yeah, I've heard that word before.

LEONARD HAYFLICK: That's it. The concept of mortality was absent from people's minds.

ROBERT: Well, wait. If they didn't understand the idea of mortality, then how did the scientists explain getting older and moving towards death?

JAD: Pre-torpedoing?

ROBERT: Yeah.

JAD: Radiation.

ROBERT: What?

JAD: Radiation.

ROBERT: What—what do you mean? [laughs]

JAD: No, seriously. I mean, it was this idea that, like, stuff was happening outside the cell, that the radiation is bombarding the cell, like gamma rays and alpha rays and these kind of things, and that that somehow ages the cell.

ROBERT: So the trigger is outside the being not inside the cell.

JAD: Right.

LEONARD HAYFLICK: And so my discovery—and I pointed it out in that first paper—was to indicate that it's in the cell, not outside the cell. That's where the action is.

JAD: Hayflick argued that somewhere in the cell there's a counter. There's gotta be, because something in the cell is keeping track. Because after about nine months of happy dividing in a petri dish, when a cell gets to 50 divisions, sometimes it's a few ticks more, a few ticks less, but 50 is the average. And when it reaches 50, a little counter inside the cell says ...

["Stop!"]

JAD: 50 is the magic number.

JAD: Where did this number 50 come from?

LEONARD HAYFLICK: You'll have to ask God that question.

JAD: Nonetheless, Hayflick, not God, has his name forever attached to that number, because it's become known as the "Hayflick limit." Now one of the interesting things Hayflick told me while we looked at his secret stash of fetal cells in his garage is that there is a way to tinker with the cellular counter. If you lower the temperature by, say, putting the cells in liquid nitrogen as he has, the dividing will get slower and slower and slower until it stops. At 250 degrees below zero the cells will not divide, and they won't die. They'll just wait for as long as you keep them frozen.

LEONARD HAYFLICK: The cells I have in my freezer have been frozen for 44 years.

JAD: Does that make them the longest ...

LEONARD HAYFLICK: These cells are the longest frozen, normal human cells in the world.

JAD: The fetal cells he's talking about, incidentally, are the ones that he used to discover the Hayflick limit. He calls it WI-38.

JAD: What do we know about the mother of the fetus that created WI-38?

LEONARD HAYFLICK: She was a Swedish woman, and she wanted an abortion because she had many children and was very poor. Her husband was not a good father, and that's where this tissue came from.

JAD: Here's the kicker: after the Hayflick limit experiments, these cells, this particular strain was used to incubate and produce vaccines, all different kinds.

LEONARD HAYFLICK: Polio, German measles, measles, mumps, rabies ...

JAD: And anybody born in the last 50 years who's had any of these vaccines has had these cells in their body.

LEONARD HAYFLICK: The numbers of people who have benefited from these vaccines now exceed one billion people.

JAD: That's billion with a B.

LEONARD HAYFLICK: That's a billion with a B.

JAD: Wow.

JAD: One aborted child creates a fleet of cells that vaccinate a billion people. Think about that for a second.

JAD: And is it true that you have a cell line from—is it your daughter?

LEONARD HAYFLICK: Yes. I also have cells in there from the amnion of my daughter, Susan Hayflick.

JAD: And do you keep them for purely scientific reasons? Or is it sort of like stamp collecting? You have them as ...

LEONARD HAYFLICK: Well, it would be—she's a scientist now herself, and so I'll probably give the ampules to her so she can do with them what she wishes.

JAD: But you keep them because it's your daughter mostly.

LEONARD HAYFLICK: Yes, mostly. Yeah, sure.

JAD: Aww, that's really sweet!

LEONARD HAYFLICK: [laughs]

JAD: Here's the interesting thing, scientifically: if you were to warm these cells up, give them some food, they'd start to divide again. And not only that, they'd pick up right where they left off. And even if you froze them again—let's say the 16th doubling—and kept them that way for a thousand million years, wouldn't matter. Because as soon as you unfroze them, off they'd go on their way to 50 without missing a beat.

LEONARD HAYFLICK: What does that tell you? Tells you that cells remember. They have a memory.

JAD: Somehow the cell always remembers where it is in the count to 50.

ROBERT: Cells can't count. How do they do that?

JAD: Well, that's—that was the next big question.

LEONARD HAYFLICK: So we set about to do a number of experiments.

JAD: However, the next big breakthrough came in 1971 and not by Hayflick. While he was doing his experiments in Philly, halfway across the world at the very same moment ...

LEONARD HAYFLICK: A Russian named Alexey Olovnikov ...

JAD: ... was attending a lecture ...

LEONARD HAYFLICK: ... heard a lecture ...

JAD: ... about Hayflick's research. And he left the lecture puzzled by this question that you asked: how do the cells remember?

LEONARD HAYFLICK: And when he—have you ever been to Moscow?

JAD: Mm-mm.

LEONARD HAYFLICK: Well anyhow, so he entered a Moscow subway station, went down to the railroad platform, and suddenly he had an insight. He had a brilliant insight when he looked at the railroad track.

JAD: First thing he thought was: those tracks look a lot like DNA.

LEONARD HAYFLICK: If you take railroad tracks and you twist them ...

JAD: You twist them, yeah.

LEONARD HAYFLICK: You've got DNA.

JAD: Okay, say you had some DNA, and that DNA's job is to count to 50 and then yell ...

["Stop!"]

JAD: Well, we know part of the DNA has the job of yelling, but the other stuff, the rest of it, what if it's just ...

LEONARD HAYFLICK: A long sequence of nonsense.

JAD: ... nonsense? What if every time that cellular copier comes along to copy the cell, you lose one little piece of it. The nonsense, I mean. Well, if you had, say, 50 pieces of nonsense as a buffer around the sense part, the switch, well then it would take 50 copies to snip away all the nonsense until you're left with the switch which would turn on and tell the cell to stop dividing. Back in Philadelphia, as we were wrapping up that first interview, a question occurred to me: if we kind of understand how that off switch works ...

JAD: Shouldn't we theoretically be able to figure out how to tinker with when the switch gets switched?

LEONARD HAYFLICK: In theory, I suppose you could. Yeah, sure.

JAD: And wouldn't that allow us to have a longer amount of cell divisions?

LEONARD HAYFLICK: Well, that certainly doesn't violate any knowledge about this system, of course.

JAD: And wouldn't that theoretically give us something, whether it be extended life or something?

LEONARD HAYFLICK: Yes. Certainly.

JAD: Hayflick had clearly been asked this question a million times. And he patiently explained to me that there is a way right now that we can tinker with the timing of the switch. You take an enzyme called telomerase ...

LEONARD HAYFLICK: Telomerase.

JAD: ... throw it into the mix, and every time that cell gets copied and loses pieces of track, the telomerase enzyme comes along ...

LEONARD HAYFLICK: And it adds them back on. And maintains the length constant.

JAD: That way the track is always long, the stop switch never gets switched, and the cell can keep going and going and going.

LEONARD HAYFLICK: That's how they become immortal. So you're not gonna tell me, "Well, let's inoculate everybody with telomerase."

JAD: Yeah. And?

LEONARD HAYFLICK: [laughs] Well, if you volunteer we'll have a shot at it. Are you ready?

JAD: There—there must be—if I were to go out and shout from your balcony right here ...

LEONARD HAYFLICK: You have to remember this.

JAD: ... I'm sure I'd get a hundred people who would want to try.

LEONARD HAYFLICK: Really? Not after I tell you what you still don't know.

JAD: What's that?

LEONARD HAYFLICK: 95 percent of all tumors contain telomerase, which normal cells do not contain. The single most distinguishing criteria between normal and cancer cells known today is that fact.

JAD: So the tradeoff for cellular immortality, at least in this case, is cancer. But here's the weird thing: if you look around, you'll see that our Hayflick limit of 50 is not the only one.

LEONARD HAYFLICK: We do know that if you look at the normal cells of a Galapagos tortoise, which has been reported in the literature, they undergo about 125 doublings if I remember correctly.

JAD: So their Hayflick number is 125 and ours is 50?

LEONARD HAYFLICK: Apparently, yes.

JAD: Does that correlate to the Galapagos turtle living twice as long?

LEONARD HAYFLICK: Well, it seems to, but that comparison may be anecdotal and not universal.

JAD: That's what Hayflick is up to these days. He's become fascinated by animals who age differently than us, who might have a doubling limit of, you know, 200, 500, or no limit at all!

LEONARD HAYFLICK: There are a whole class of animals that don't age.

JAD: Well, like what?

LEONARD HAYFLICK: The American lobster.

JAD: The lobster doesn't age?

LEONARD HAYFLICK: It either does not age, or the rate is so slow we can't measure it.

JAD: I don't even know how to imagine that. What does that mean, is that it doesn't ...?

LEONARD HAYFLICK: Well, what it means is that the animal gets bigger and bigger.

JAD: Just grows?

LEONARD HAYFLICK: Yes. There are lobsters that have been found—recently I read about one that's over 50 pounds.

ROBERT: I looked it up. The largest lobster ever reported was close to, yes, 50 pounds. Found in the 1950s, just off the coast of New Jersey.

JAD: Hey, New Jersey!

ROBERT: Yep.

JAD: How old is a—how old is a 50-pound lobster? Who knows?

ROBERT: The one indication it was wearing a Grover Cleveland for President button. So it was very old.

JAD: [laughs] I'm Jad Abumrad.

ROBERT: I'm Robert Krulwich.

JAD: This is Radiolab.

ROBERT: We'll be right back.

[LISTENER: My name is Ayusha Srivaskava, and I'm calling from the University of Chicago. Radiolab is supported in part by the National Science Foundation and by the Alfred P. Sloan Foundation, enhancing public understanding of science and technology in the modern world. More information about Sloan at www.sloan.org.]

JAD: Ready?

ROBERT: But what am I supposed to do? I don't have to do anything, right?

JAD: This is Radiolab. I'm Jad Abumrad.

ROBERT: And I'm Robert Krulwich.

JAD: And today we're talking about aging.

ROBERT: Yup.

JAD: Do you ever wonder why it is that human beings live like—well, how long do we live?

ROBERT: About 70-ish, something like that.

JAD: Roughly?

ROBERT: Something like that.

JAD: Yeah, so why 70?

ROBERT: As opposed to?

JAD: Seven? Or, like, 700? Why that number?

ROBERT: Well, that's—you know, that's a good question because apparently every creature has for some reason a sort of natural range. So you want to hear a very cool one? How about a rat. Got a rat in your head?

JAD: Yeah.

ROBERT: [laughs] And a squirrel.

CYNTHIA KENYON: The rat and the squirrel. Here you have two animals people call—I have friends who call squirrels "tree rats."

ROBERT: That's Cynthia Kenyon from the University of California-San Francisco. I recently paid her a visit.

CYNTHIA KENYON: You know, they—so in other words they're very similar to each other. They're rodents. But a rat has a three-year lifespan, whereas a squirrel has a 25-year lifespan. And no one knows why really. There are theories, but no one really knows why. I got the idea that maybe somehow lifespan was evolvable in the sense that there might be genes in the animal which when changed allow big leaps in lifespan to take place.

ROBERT: So you figured you could just hunt the genes down?

CYNTHIA KENYON: Exactly.

ROBERT: And this is exactly what she seems to have done. But not with rats and squirrels.

JAD: With what?

CYNTHIA KENYON: Why don't I show you the incubator, where we keep all the worms?

ROBERT: With worms.

CYNTHIA KENYON: Come with me. Little round worms, yes. Called C. elegans. Actually, you can't see them with the naked eye. They're just a little speck, but when you put them under a microscope you see how beautiful they are. So first, I'm showing you here a normal worm when it's a young adult. and what you can see is it's very active, and it's healthy looking. It's moving around.

ROBERT: So we're looking at this dish, and in the dish is this worm moving back and—it's a wiggler.

CYNTHIA KENYON: Moves really nicely. Okay, now let's fast forward two weeks.

ROBERT: Then she showed us a different set of worms in a different dish. These worms were 13 days old.

CYNTHIA KENYON: Day 13 of adulthood.

ROBERT: They only live to 14, so ...

CYNTHIA KENYON: Just live two weeks.

ROBERT: They're at the very, very end of their lives.

CYNTHIA KENYON: And what we see here is a dead one, so one has already died. And another one that's clearly in the nursing home, just lying still, not moving at all. And you can tell immediately that it's old. It looks kind of wrinkled and lethargic, and even if you've never seen a worm ever, you can tell that one is old.

ROBERT: So there you have it. You have a young worm, you have an old worm, and essentially what Cynthia Kenyon is trying to do is she's trying to hunt down the gene that could turn that old worm backwards in time and make it look like a young worm.

CYNTHIA KENYON: The worms have about 20,000 genes. So the idea is really simple: you just go and change genes at random one by one.

ROBERT: One at a time.

CYNTHIA KENYON: And see whether any of these gene changes can extend lifespan.

ROBERT: How long did it take you to bump into a good one?

CYNTHIA KENYON: Well, we actually were really lucky to find a gene pretty quickly. And we found that if we change this one gene called DAF-2, if we change this one gene called DAF-2 then the worms live twice as long as they normally would.

ROBERT: Just like that. And pretty much by sheer luck, she'd taken this worm and stretched its lifespan from 14 days all the way out to about 28 days.

JAD: Just 28?

ROBERT: Yeah, it doesn't sound like a lot to you, but to a worm that's double!

ROBERT: Can you tell me—like, when you ran into it did you do, like, a little war dance around the lab? Were you ...

CYNTHIA KENYON: Yeah, it was amazing. I mean it was incredible. I had a person in my lab who said, "DAF-2 is magic." And she's right. Okay, I'm gonna show you these magic worms, which are exactly the same as the normal worms except that we've changed one gene, the DAF-2 gene.

ROBERT: So remember that old wrinkly worm that we saw before?

JAD: Yeah.

ROBERT: The worm she's about to show me is the same age as a 13-day-old, really old worm ...

CYNTHIA KENYON: Okay, and it's bolting out of its—bolting into the picture here. It looks young, it's moving, it's very healthy, it's active. And actually, if you take a microscope and you look at the tissues, what you see is the tissues of the worm look young. If you just look at that, you just sit there and you just look at it and look at it and look at it, and just let it sink in what it means, it's really amazing. It's really very deep and fundamental. You're looking at something that I guess wasn't supposed to happen in some funny way. They were supposed to die.

JAD: So what exactly is this gene doing to make them live longer?

ROBERT: Well, maybe we should ask the question a different way, because the worms that lived longer, they didn't actually have this working gene.

CYNTHIA KENYON: Right. When we make a mutation in the DAF-2 gene we damage it. That actually causes it not to work as well. So that actually is kind of profound. That tells you right away that the worm has a gene in it that's shortening the worm's lifespan.

ROBERT: Which is why she calls it the grim reaper gene.

CYNTHIA KENYON: The grim reaper gene.

ROBERT: It's the gene that makes you die.

JAD: If you're a worm.

ROBERT: Right. So by damaging this gene, Cynthia and her team essentially are taking the Grim Reaper and knocking his knees out.

[Grim Reaper voiceover: Ow, no! Stop that! Ow!]

CYNTHIA KENYON: Okay, so the question is what exactly is the DAF-2 doing to make the cell age more quickly?

ROBERT: Here's where the story gets a little weird.

CYNTHIA KENYON: Well, we found another gene whose name is also DAF, but it's a different DAF. It's called DAF-16, and this is a gene whose normal function is to keep you young. It's like a fountain of youth gene.

JAD: So wait, there was a grim reaper gene before.

ROBERT: Right.

JAD: And now there's a fountain of youth gene?

ROBERT: That's what she discovered. And inside the worms, these genes are struggling with each other. Here's how it works when a worm ages normally.

CYNTHIA KENYON: The DAF-2 receptor kind of squashes the activity of DAF-16. It turns it down.

[Grim Reaper voiceover: Silence!]

ROBERT: And so the worm ages.

CYNTHIA KENYON: Okay? So when you come along and you inhibit the activity of the DAF-2 receptor now you liberate DAF-16. It's free, it springs into action and it activates about 100 genes in the DNA. These 100 genes, each do a little tiny good thing for the cell, and altogether it makes the cell live twice as long.

ROBERT: So let me just back up here. So there's the bad gene, the gene that says "All right, everybody die." But the way that it tells everybody to die is it goes particularly over to this little guy over in the corner who's the good guy, who's repairing and protecting and fighting disease, and it says—it conks it on the head like some kind of Three Stooges thing and says, "You shut up!"

CYNTHIA KENYON: Exactly.

ROBERT: So if that good guy can stay vibrant, then we're in the ballgame for a little while longer.

CYNTHIA KENYON: Exactly. Very good. And you can get a lifespan that may increase, say, 100 percent like the one I mentioned. Even longer. Even threefold.

ROBERT: Threefold! How'd you do that?

CYNTHIA KENYON: Well, we found that the signals from the reproductive system affect aging, it turns out.

ROBERT: Kenyon and her team found that if you steal away some of the worm's baby-making powers, that alone makes them live longer. If you do that, and if you cripple the grim reaper gene, and if you strengthen the fountain of youth gene ...

CYNTHIA KENYON: The best possible change we knew how to make.

ROBERT: ... well, now we're talking!

CYNTHIA KENYON: We get incredibly healthy animals that are—live to be six times as long on average. Which would be like 500 years for a human. And they're so healthy it's incredible.

ROBERT: Five hundred! So that would be like Ben Franklin still being around playing golf.

CYNTHIA KENYON: It's—yeah, it just blows your mind to think about it. Which by the way, that doesn't mean it will ever be possible in humans.

ROBERT: Then why do we turn—why are we listening to this program? No, she kind of has to say that because she's a scientist. She doesn't know yet whether it affects us. On the other hand, she has started a company.

CYNTHIA KENYON: Yes, Elixir.

ROBERT: And the company is making a pill, and it's a pill for people, interestingly.

ROBERT: Have you any notion of how much you could slow down the process?

CYNTHIA KENYON: Well, we don't know. You know, we're just hoping that we can slow it down at all.

ROBERT: But just imagine!

CYNTHIA KENYON: Used to be people would talk about that, but it's the world of fairy tales and fantasy. And now it sort of reopens the quest for the fountain of youth in a new molecular way.

JAD: But wait a second, though. What happens if she, dare I say it, succeeds with this little pill of hers? Do we necessarily want a lot of 500-year-old golfers hanging around, you know, not getting out of the way?

ROBERT: Well, we're already there in some places in the world. In Germany and in Japan, the population of older people has grown to the point where you—if you're a middle-aged or a younger person, you feel the oppression of having so many people to support.

JAD: Well, can we talk about Japan for a second?

ROBERT: Mm-hmm.

JAD: Japan might be a canary in the coal mine as it were. Sort of a glimpse of where we're all headed. Jocelyn Ford, a reporter, has been looking at aging societies in Asia, and recently took a trip back to Japan where she used to live to see how they're dealing with things.

JOCELYN FORD: When I arrived in Japan, it was immediately obvious that there was something different here. I went into the closest little town to the airport and there was a festival, a street festival going on. I thought, great. Went down the street, and what really surprised me is I think of street fairs and kids playing and, you know, "Let's go out with the family," but everyone sitting around listening to the music was—I mean, there were a lot of gray heads. I met a guy who was like 90 years old and he was on a bicycle. And when he cycled off I thought, "It's a different society."

HIRO OGAWA: Bottom line is this: in Japan, aging is very fast. The fastest ever in the entire world.

JOCELYN FORD: This guy banging the chalkboard?

JAD: Yeah?

JOCELYN FORD: That's Hiro Ogawa.

HIRO OGAWA: Hiro Ogawa. I'm a demographer at the Nihon University Population Research Institute.

JAD: Where is that, by the way?

JOCELYN FORD: Nihon.

JAD: Is that in Tokyo?

JOCELYN FORD: In Tokyo, yup. And he said that the reason that Japan looks so old all of a sudden is because, in part, people are living longer, but that's not the big reason. The big reason is that the birthrate is falling.

HIRO OGAWA: Look, I mean, Japanese population is shrinking.

JAD: They're not having as many kids?

JOCELYN FORD: That's exactly it. And this is something that's happening all over the developed world: people are having smaller families, and as a result, there are fewer young people, more older people.

HIRO OGAWA: Right now in fact, the proportion of the elderly, I mean 65 and over is more than 21 percent, which is the highest in the entire world.

JOCELYN FORD: 21 percent elderly. Can you imagine what that looks like?

JAD: No, help me.

JOCELYN FORD: Just think Florida. What do you think of when you think of Florida?

JAD: Florida. I think of beaches and I—well, that's where a lot of old folks go to retire, so I think it's a lot of you know, 70 and 80 year olds.

JOCELYN FORD: Florida is the oldest state in the United States, but compared to Japan it's young. It's only 17 percent over 65 and Japan is 21 percent.

JAD: Whoa!

JOCELYN FORD: So imagine that all of Japan looks like Florida—just older. And Ogawa expects that percentage to double in 40 years.

HIRO OGAWA: Right now I mean, we cannot really picture the future scenario, but it's gonna change.

JOCELYN FORD: Well, I got some insight into that change back at the street fair. I went to get some tea and rice crackers, and in that shop there was a 103-year-old granny. I tried to talk to her, but she couldn't really communicate. She didn't really know what was going on. Her daughter who's in her 60s is the main caretaker.

JAD: In her 60s. Wow.

JOCELYN FORD: In her 60s. And she has to—the granny can no longer get out of her wheelchair by herself. She can't take a bath. She's completely dependent on her daughter like a baby. But she's a lot heavier than a baby, and her daughter had really strained her back and hurt herself. I mean, it's the elder looking after the aged, basically. And that's probably the biggest—the biggest problem.

HIRO OGAWA: The problem is that the caregivers, the primary age of the caregivers is about 40s and 50s, so we are sort of short on caregivers.

JAD: That never occurred to me that from society's perspective, the reason kids are good, are useful, is so that they take care of the old people.

JOCELYN FORD: Yeah. A government spokesman I spoke with, Mr. Tamaguchi, he was quite concerned about that.

1. TAMAGUCHI: There's going to be a shortage of labor as society ages, and someone has got to fill the void.

JOCELYN FORD: In countries like the United States, we might import foreign labor.

JAD: Sure, yeah.

JOCELYN FORD: Bring in immigrants to care for the elderly, you know? But in Japan ...

1. TAMAGUCHI: It'll happen only reluctantly ...

JOCELYN FORD: ... it's not so simple.

1. TAMAGUCHI: ... because this society is still debating whether it's gonna be a good thing or not to increase the number of immigrants.

NISHIMURA YASUTOSHI: We have decided to open our labor market to some extent.

JOCELYN FORD: Nishimura Yasutoshi. He's another government spokesman.

NISHIMURA YASUTOSHI: First we start ...

JOCELYN FORD: He said the government has decided they can allow 100 Filipino caregivers to come into the country.

JAD: Just 100?

JOCELYN FORD: Just 100.

JAD: Huh.

JOCELYN FORD: I know what you're thinking.

JOCELYN FORD: Is it basically because Japan is xenophobic?

HIRO OGAWA: Well, let's put it this way: Japanese people tend to have this island concept. Having more international workers in our neighborhood might dilute that kind of tradition. I think that's what the Japanese people might be worried about.

JOCELYN FORD: What's wrong with that? Things change.

HIRO OGAWA: I think basically communication. Particularly when you're sick, I mean, when you're bedridden, if the nurses are foreigners you have to communicate and it's very difficult.

JOCELYN FORD: You know, some people might think that's xenophobic, that people don't want to deal with foreigners, but that's not really what it's about. People don't want to be a burden to anybody. They don't want to depend on anybody.

1. SUGA: I don't want to—how you say, burden?

JOCELYN FORD: This is Mr. Suga. He's a demographic researcher.

JOCELYN FORD: You just don't want to be a burden.

1. SUGA: No.

JOCELYN FORD: This feeling that you shouldn't be a burden, it runs very deep.

JOCELYN FORD: Physically, psychologically?

1. SUGA: Both of them. I just prefer I will be helped not by any other people.

JOCELYN FORD: Why is that?

1. SUGA: Just a feeling. It might cause problem with them, with other people.

JOCELYN FORD: So you'd be more comfortable knowing that you're not putting anyone else—causing them trouble?

1. SUGA: Yep. Yep. Yep. So if I would need some help from other people, I might want to kill myself.

JOCELYN FORD: That's how extreme it gets. This is a young man who's 30. He said, "I would rather commit suicide than be taken care of by somebody who doesn't want to take care of me, who—who I'd be a burden on."

1. SUGA: You know, there is a culture like 200-300 years ago in Japan. If the old woman is alive and you're, like, 70 years old, then the family take this old mother to a mountain and stay there, make the mother stay there.

JOCELYN FORD: There is a very long tradition in Japan of…They call it Ubasute.

JAD: Ubasute.

JOCELYN FORD: Ubasute. And 'Uba' means grandma, and 'sute' means to throw away.

JAD: You're serious.

JOCELYN FORD: They have whole movies about this in Japan. There's one called The Ballad of Narayama. It's set in a very poor, rural village about a hundred years ago. It tells the story of a son taking his old mother up the mountain. On the way up they pass by another son literally throwing his father off of a cliff.

1. SUGA: It makes a family happier.

JOCELYN FORD: So grandma stays in the mountain and starves to death.

1. SUGA: Yup. Yup.

JOCELYN FORD: And the family is happier because there's less of a burden.

1. SUGA: Right.

JOCELYN FORD: It was understood among all the generations that this is the way the problem was solved.

JAD: Not anymore, obviously.

JOCELYN FORD: Right. Right. Japan is really quite socialist these days, they look after everyone in society. But that idea is still out there. So what do you do today? You don't want your kids to take care of you, you don't want foreigners to take care of you. Who's left? One solution is instead of having people do these jobs, have machines.

JAD: Machines?

JOCELYN FORD: Robots.

JAD: Robots? [laughs] Are you joking?

HIRO OGAWA: It's not actually a joke. Panasonic and others are manufacturing robots as caregivers.

JOCELYN FORD: When you think about it, it sort of makes sense. Why don't we automate the heavy duty work?

[ARCHIVE CLIP: Welcome to Miricon.]

JOCELYN FORD: I visited a bunch of labs and met with some scientists.

SCIENTIST: This robot is connected to here.

JOCELYN FORD: Can I ask what that is?

JOCELYN FORD: They've got robots that will ...

JOCELYN FORD: It looks like a dentist chair.

JOCELYN FORD: ... tell your wheelchair where to go.

JOCELYN FORD: I wonder how fast this is going?

JOCELYN FORD: There's a special pair of trousers that you can put on, and if your legs are weak and you can't walk, well, it will help you walk. There's a washing machine robot.

JOCELYN FORD: It looks like it's got a fancy handle.

JOCELYN FORD: It's actually for washing people.

JOCELYN FORD: Are any of these in actual use?

SCIENTIST: Yes they are.

JOCELYN FORD: People do not want to have to ask somebody to clean their diapers, to wash their bum.

JAD: Right.

JOCELYN FORD: I think for anybody in any society ...

JAD: Absolutely.

JOCELYN FORD: ... that is a difficult thing to have to ask somebody.

HIRO OGAWA: Robots help more. I mean you don't have to talk, you just press a button.

JOCELYN FORD: Now this is where I start to get weirded out [laughs]. I went to a nursing home about an hour and a half outside of Tokyo.

JOCELYN FORD: Big room with lots of people mostly sitting around. There's a television. About three people are watching the TV. One is looking out the window.

JOCELYN FORD: I walked in, and there were a lot of old people just sitting around, each keeping mostly to themselves, sitting very quietly, not talking. It was sort of sad. In steps PARO the seal. PARO is one of the world's first therapy robots. Get it?

JAD: No, what does that mean? [laughs]

JOCELYN FORD: [laughs] What they've done is they've made this sort of like a large stuffed animal—white, furry, long eyelashes. And it flutters them at you, and it squeals!

[PARO squeals.]

GRANDMOTHER: Konnichiwa!

JOCELYN FORD: When PARO came out, one of the grannies just lit up. Got so excited. She peered into the seal's eyes and she tried to talk to it.

SCIENTIST: She said "I'm happy to come to PARO." It's the same feeling of when her family comes here.

JOCELYN FORD: I was taken back. I mean, it's not much more than a moving stuffed animal. And how could you look at it and see company, see something alive, see something comforting?

JOCELYN FORD: It feels a little bit warm. Is PARO warm?

TAKANORI SHIBATA: Yes, PARO has a kind of temperature control.

JOCELYN FORD: I spoke to the developer, Mr. Shibata.

JOCELYN FORD: So you're warm-blooded, huh?

JOCELYN FORD: He said yeah, they wanted a creature that would give them positive feedback but also sort of needed them.

TAKANORI SHIBATA: For example, being stroked is good for PARO, so PARO tries to be stroked by the owner.

JOCELYN FORD: Like you're doing right now?

TAKANORI SHIBATA: Yeah.

JOCELYN FORD: Did you program him to want to be held?

TAKANORI SHIBATA: Yeah.

JOCELYN FORD: He also programmed him to respond to different names.

TAKANORI SHIBATA: Yeah. So for example, I call him PARO. If you give new name like John or something ...

JOCELYN FORD: Or like Kokochan.

GRANDMOTHER: Kokochan!

TAKANORI SHIBATA: ... and call the new name again ...

GRANDMOTHER: Kokochan! Kokochan!

TAKANORI SHIBATA: ... PARO gradually learns the new name and starts to respond.

GRANDMOTHER: Kokochan!

JAD: So it's learning?

JOCELYN FORD: Put you down carefully because we don't want to hurt you. Oh, you want to be held again, huh?

JOCELYN FORD: They learn from their environment. Now these are really rudimentary, you know, beginning baby robots. But it worked, Jad. It worked. They adored it. They were loving it, and it was loving them in their minds. I started to think maybe this is a solution. People might actually be able to engineer compassion and engineer companionship. But then I started asking a lot of people around me, took an informal straw poll: would you feel comfortable with a robot taking care of you? And most people said, "No, not really." Like this woman Kako Sugi. She actually came up with a brilliant idea which seems like a no-brainer. She has a nursing home which is together with a preschool.

KAKO SUGI: So I would like you to take a tour.

JOCELYN FORD: You walk into the room, and you are bombarded by these little bodies ...

JOCELYN FORD: Screaming and flying around and ...

JOCELYN FORD: The vitality ...

JOCELYN FORD: Man!

JOCELYN FORD: ... is just over the top. And it's infectious. You know, and if you're an old person in that environment, you have no time whatsoever to dwell on the idea that you are dying. The kids are—they demand your attention, they need you. They're needed again.

JAD: But—but the first thing that you told us at the very beginning was that there are more old folks, less kids. So what happens when these kids we're listening to right now, when they dwindle?

JOCELYN FORD: Mm-hmm.

JAD: There's just a bunch of old people around, and there's gonna be one kid left and they all go to visit that one kid. I mean that—that can't work.

JOCELYN FORD: You expect me to have an answer?

JAD: [laughs] I don't know.

JOCELYN FORD: Maybe we should import kids, I don't know!

JAD: No. I mean, you're joking obviously, but I guess what I'm asking is like, are we left at the end to think that a society cannot support all of its members getting old? That somehow the old have to step out of the way?

JOCELYN FORD: Jad I think your thinking is basically old fashioned.

JAD: [laughs]

JOCELYN FORD: There will be more old people and fewer young people. That's a fact. You're not gonna turn the clock back on this. Societies do change, people do come up with new ideas, and right now hey, they're stabbing in the dark after them. But one day they'll come up with a solution, so learn to deal with it.

JAD: Damn, you just bitch-slapped me!

JOCELYN FORD: [laughs] Well, what do you expect? You called me all the way across the Pacific Ocean, across a whole continent.

JAD: Whew! We gotta go to break now 'cause I gotta sort of pick up my ego here.

JOCELYN FORD: [laughs]

JAD: Radiolab will continue in a moment.

[LISTENER: This is Casey calling from Ft. Myers Beach, Florida. Radiolab is supported in part by the National Science Foundation and by the Alfred P. Sloan Foundation, enhancing public understanding of science and technology in the modern world. More information about Sloan at www.sloan.org.]

JAD: This is Radiolab. I'm Jad Abumrad.

ROBERT: And I'm Robert Krulwich.

JAD: And in this hour we've been talking about aging mostly, but now we're gonna turn our attention to the end of that aging process.

ROBERT: You're talking about dying?

JAD: Yes.

ROBERT: Mm-hmm.

JAD: Maybe we've avoided that topic because that's generally how people deal with death, which is to avoid it.

ROBERT: To deny it, yeah. Well, this next piece is about actually a different way of dealing with death. I should say before we begin it that it does contain some graphic descriptions of the normal bodily process of aging, but if you have someone in the room who is squeamish or you don't think should hear these things—and it's nothing terrible, it's just—it's actually quite ...

JAD: Nasty.

ROBERT: Yeah.

JAD: It's nasty.

ROBERT: It's nasty. Then maybe this is time to shoo them out of the room.

JAD: This piece was produced by Lu Olkowski. It's about one family, three generations.

JEREMIAH ZAGAR: Introduce myself?

JAD: This is Jeremiah, the youngest.

JEREMIAH ZAGAR: I'm Jeremiah Zagar.

JAD: He's a filmmaker.

JEREMIAH ZAGAR: Son of Isaiah Zagar.

JAD: His dad, Isaiah, is a muralist. And his grandfather ...

JEREMIAH ZAGAR: I'm the grandson of Asher Zagar.

JAD: ... Asher Zagar is a health nut.

[ARCHIVE CLIP, Asher Zagar: 16, 17, 18, 19, 20.]

JAD: This is a video of him that Jeremiah shot of Asher doing his daily exercise routine. He's in his 90s, he's jumping on a trampoline and counting each jump.

[ARCHIVE CLIP, Jeremiah Zagar: How old are you now?]

[ARCHIVE CLIP, Asher Zagar: Me? I'm 90.]

[ARCHIVE CLIP, Jeremiah Zagar: 90?]

[ARCHIVE CLIP, Asher Zagar: Yeah.]

[ARCHIVE CLIP, Jeremiah Zagar: You're a healthy man for 90.]

[ARCHIVE CLIP, Asher Zagar: Yes. And I'll be still healthy when I'm 91, 92. The great great grandfather that I'm named after lived to 102.]

[ARCHIVE CLIP, Jeremiah Zagar: So you're gonna live to 102.]

[ARCHIVE CLIP, Asher Zagar: I don't know, but maybe.]

JAD: At the age of 93, Asher began to decline quickly.

JEREMIAH ZAGAR: How do you deal with a man dying in your house? How do you deal with that? Well, you know, my father starts taking photos of him.

ISAIAH ZAGAR: One of my modes of understanding was either drawing or photographing.

JEREMIAH ZAGAR: He was always taking pictures of my grandfather.

ISAIAH ZAGAR: Just to see ...

JEREMIAH ZAGAR: Thousands of slides. Thousands.

JAD: And that's how it went for a while. Isaiah, the dad, would take care of his dad and take some photos, while the grandson Jeremiah basically looked the other way.

JEREMIAH ZAGAR: Well, I never really knew my grandfather.

JAD: But then Isaiah got an idea.

ISAIAH ZAGAR: I thought to myself, "Challenge this young boy to this duel: who can take the most objective photographs of a dying man?"

JEREMIAH ZAGAR: It wasn't like we threw down and, like, I pulled my camera out of my holster and he pulled his camera out of his holster, you know? It wasn't like that. He was involved in my grandfather's death and I wasn't, and so he said this is how I get involved. It's my senior year of high school, and I was a busboy in this restaurant down the street, and I loved it. And I would bus tables 'til two or three in the morning and then I would get drunk with the people after work, and then I would come back and I would take care of my grandpa.

JEREMIAH ZAGAR: And so I would lift him up and change his sheets, because otherwise his bedsore would burn more. And he had this horrible bedsore—you can see it in the photographs—and he would hit me while I lifted him up. And then I would photograph him, because I would want to sit with him, because you want to calm him down. And the way you sit with him—I mean, my father was right. You have a camera. I mean, that's how you cope. Otherwise you're sitting with him and he's just looking at you.

JAD: During the contest, dad and son shared duties of taking care of grandpa, and at night they'd sit at the kitchen table and compare photos.

JEREMIAH ZAGAR: As soon as I took the first pictures, you knew mine were better than my father's because my father's were from far away, and they were snapshots, and mine were like, specific. Like, I was fascinated with him dying. I wanted to know what it looked like.

JAD: And this went on for about a month, during which time even Jeremiah's friends ...

ISAIAH ZAGAR: All of his friends ...

JAD: ... got involved.

ISAIAH ZAGAR: ... in the wee hours of the night, I would wake up and I would see that there, surrounding my father, were four or five young people. Sure, they were drinking beer and they were joking around, but they were there. They were there while he was there. What I remember most was you and your friends changing his sheets and lifting him and moving him around.

JEREMIAH ZAGAR: Yeah. Gabrielle did it with me once.

ISAIAH ZAGAR: Who else did it with you?

JEREMIAH ZAGAR: John. Lincoln.

ISAIAH ZAGAR: They all became initiated into the most problematic event in our lives. It was an amazingly rare scene to see these teenagers attending to death.

ISAIAH ZAGAR: Well, this is a book of photographs of my father, your grandfather's last week of life, in this very room. So the contest was a month long. Smart guy I am, huh?

JEREMIAH ZAGAR: You're good. You know how to make a contest.

ISAIAH ZAGAR: I kept it going for one month.

JEREMIAH ZAGAR: Good job.

LU OLKOWSKI: Isaiah, can you describe this one for me?

ISAIAH ZAGAR: Well, the feet look like they're—they were out in the desert, that they've been baked and cracked and they're dry, dry, dried out.

JEREMIAH ZAGAR: I mean, look at them. They look like—I mean, look at the nail, the nail is wild. But I mean, everything. It's like, "What the ...?"

ISAIAH ZAGAR: I have these same legs.

JEREMIAH ZAGAR: Stop touching the photos.

ISAIAH ZAGAR: Well, I can almost feel him by feeling them. I'll feel you instead.

JEREMIAH ZAGAR: There. That's the bedsore. That's what happens.

ISAIAH ZAGAR: Oh, it's awful. Awful. All awful. Awful, awful, awful. A man who prided himself on his health, look what happened. How does one describe that?

JEREMIAH ZAGAR: It looks like rotting meat.

ISAIAH ZAGAR: I mean, they're just open wounds, and you move him around, move him around, but still it was impossible.

JEREMIAH ZAGAR: It's crazy to look at the colors too. Pink and then white and then green and then brown where it's rotting.

ISAIAH ZAGAR: Well the white is the muscle, isn't it?

JEREMIAH ZAGAR: I took these photos in color because in black and white you'd never get it. You know, you'd never get how painful this must've been. His anus is all red. I mean, like, really red. And you can see that parts of it have broken and there's just blood gushing out, and it's dried. I mean, the blood is dried. I think this is the last photo. Oof, this one's tough. You can see, like, the cognition is gone, mouth is agape, he's buried in his pillow.

ISAIAH ZAGAR: He knew it was over. It was just a matter of time now.

JEREMIAH ZAGAR: That's it. That's the closest I got to him dying.

ISAIAH ZAGAR: He wanted to live forever. The fix was in from the beginning.

JEREMIAH ZAGAR: [laughs] The fix was in? I was supposed to win?

ISAIAH ZAGAR: Sure, sure. How could it be any other way?

JEREMIAH ZAGAR: I don't know, I could have taken—I could have given up. You wanted me to win?

ISAIAH ZAGAR: It was a subterfuge to get you to be with your grandfather as much as possible.

JEREMIAH ZAGAR: I thought it was a fair fight. It wasn't. Oh, you knew all along.

ISAIAH ZAGAR: Can there ever be—can there ever be a fair fight?

JEREMIAH ZAGAR: You knew all along that you couldn't take a good picture.

ISAIAH ZAGAR: When a person is dying, it's very important that they're surrounded, they're surrounded by the light of life, and you don't go into the place of oblivion alone.

JEREMIAH ZAGAR: You want me to be there?

ISAIAH ZAGAR: I don't know. At this point I don't know. I'm not—I'm not at that place yet. Well, what does that mean with the camera? I mean, just be with me. Be with me, be close to me, be soft with me.

JEREMIAH ZAGAR: Yeah, I guess that's what it's about, really.

ISAIAH ZAGAR: Mm-hmm. Be soft with me.

JAD: Thanks to Lu Olkowski for that story. And to Isaiah and Jeremiah Zagar. Well, we've come to the end of our hour. I guess we should wrap.

ROBERT: Mm-hmm. We should mention the website.

JAD: Yes. Radiolab.org is the address. And also if you want to sign up for our podcast ...

ROBERT: How do you do that?

JAD: Well, you go to Radiolab.org or to iTunes directly. And if you want to send us an email, Robert?

ROBERT: If you want to send us an email, you should really write us to our email address.

JAD: [laughs] Which you can never remember.

ROBERT: [laughs]

JAD: Radiolab@wnyc.org is our email address. I'm Jad Abumrad.

ROBERT: And I'm Robert Krulwich.

JAD: We'll see you later.

[CHILD: Radiolab is produced by Jad Abumrad, Ellen Horne, Lulu Miller, Dean ...]

[MAN: Cappello.]

[CHILD: Cappello.]

[ISAIAH ZAGAR: Hi, this is Isaiah Zagar. Production support by Sarah Pellegrini, Mark Phillips, Scott Goldberg, Sam Lavender, Avir Mitra, Ryan Sciamo and Jacob Weinberg. Special thanks to Jocelyn Ford, Sam Dingman, Leonard Lopez, Josh Kain.]

[JEREMIAH ZAGAR: This is Jeremiah Zagar. I want to thank you for listening. Radiolab is supported by a grant by the Alfred P. Sloan Foundation. Radiolab is produced by WNYC—New York Public Radio, and distributed by NPR—National Public Radio.]

 

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