For most of human history, aging has been treated as an unavoidable condition of being alive: something that might be delayed, endured, or softened, but never fundamentally reversed. A new generation of researchers is challenging that assumption through approaches such as cellular reprogramming, which aims to restore aged cells to a more youthful functional state by altering patterns of gene activity. The science remains experimental, but it has now crossed an important threshold as researchers begin testing reprogramming therapies in humans. Public opinion, however, is considerably more cautious than the ambitions of the field. In a July 2026 National Geographic survey of 1,000 U.S. adults, 59 percent said aging is a natural process and that medicine should focus on treating individual age-related diseases, while only 9 percent considered aging itself a disease that should be treated or reversed.
That tension runs through journalist D.T. Max’s recent National Geographic feature on the emerging race to rejuvenate the human body (“Are We on the Brink of Ending Aging?“). His reporting moves from David Sinclair’s first-in-human glaucoma trial to the laboratories of Juan Carlos Izpisua Belmonte and the billionaire-backed companies betting that age-related decline may eventually become treatable. The public appears intrigued by that possibility, but more interested in remaining healthy than simply remaining alive. Thirty-six percent of survey respondents said they would prefer to extend the number of years they remain in optimum health without necessarily extending their total lifespan, while another 33 percent wanted both longer life and longer health. Sixty-four percent said they would actually accept a shorter life if their remaining years were entirely free from physical and mental decline.
Those hopes coexist with deep unease about how far longevity science should go and who might benefit from it. Forty-two percent of respondents said they would take an FDA-approved cellular reprogramming pill, despite 39 percent saying they currently know nothing about the technology. At the same time, 72 percent expressed concern about the risks of emerging life-extension technologies, 68 percent worried that such treatments would be affordable only to the extremely wealthy, and nearly half said human trials should proceed only with extreme caution once risks such as uncontrolled cell growth and cancer were considered. In the following conversation, Max discusses what drew him to the science, the gap between evidence and the grander promises of the longevity movement, the unusual role of private capital in driving the research, and a human desire to outrun mortality that stretches from The Epic of Gilgamesh to today’s biotechnology laboratories.
MARC LANDAS: What drew you to this story initially? Obviously, as your background shows, you’ve written about David Foster Wallace. This is some distance from David Foster Wallace. What drew you to the story, and at what point did you realize there was a lot going on here?
D.T. MAX: It’s true that I wrote a book on David Foster Wallace, but my first book, The Family That Couldn’t Sleep, is a medical book. It’s about prion diseases and fatal insomnia. So I actually do a lot of science journalism. I’d say it’s one of the two or three areas at The New Yorker where I typically work the most.
This is actually a story that, in various forms, I’ve been chasing in a lot of different ways over the years. I’ve looked at some of the people who are dosing themselves with peptides or going to other countries to undergo treatments that aren’t approved yet. I’ve been in touch with a bunch of them and thought about doing stories about them, but I never felt that any of that stuff was really going to affect us. These were sort of outliers.
I had also been following the hard science involving the Yamanaka factors and so on. When I heard there was an actual FDA trial, it seemed like the time was ripe to look at this in a more serious way than anyone I knew of had looked at it before.
MARC LANDAS: Your article begins with a patient receiving the glaucoma treatment ER-100. You also make clear very early on that David Sinclair sees that almost as a proving ground for something much bigger and more ambitious: reversing aging. How difficult was it to separate what’s actually being tested from what Sinclair believes could eventually happen?
D.T. MAX: I should make a distinction between what he believes can happen and what I believe can happen. The overlap isn’t 100 percent. He’s an apostle for this field, and he’s the leader of that wing of the field. Whereas I’m a journalist. I’m always interested and always skeptical. I’m not dismissive—I thought there was a lot going on here, and I wanted to see it.
We’re a long way from a treatment. There’s a moment in the piece where David says he thinks we’re maybe 20 years away from something you could get in the drugstore. I’m paraphrasing there. I don’t know. Twenty years passes pretty fast in the world.
The glaucoma treatment itself is only in a safety trial right now. In theory, you’re not even looking at whether it works. In reality, of course, they look at whether it works. Why would you do a trial and not look at whether it works? But in theory, all they’re going to know at the end is whether this injection hurts people.
There’s a lot that has to be proven in this field before we’re going to see this in more general medical use. But I do think it’s at least possible, maybe even probable, that some of this will wind up in actual medical use.
That’s different from saying there’ll be a pill you can take that brings your cells back to where they were when you were five. That’s a different discussion. But could this be used to treat certain diseases that are particularly age-related? I think that’s a possibility, maybe as one of a number of treatments given at the same time.
With glaucoma, the idea is that the disease is progressive and age-related. If you can take those particular nerves back to an earlier state, you might remove or reverse the glaucoma. When you think about it, it’s a whole different approach to disease.
The book I wrote was about prion diseases, which affect people in late middle age. You have the gene from the beginning, but the gene creates proteins, and those proteins only become malformed when you reach a certain age. That’s another age-related disease. You could look at Alzheimer’s that way, too. There are many diseases where we don’t necessarily say, “That’s an age-related disease.” Instead, we talk about the particular mechanism.
MARC LANDAS: For the lay reader, treating glaucoma—even reversing aging in nerve cells—still seems like a far leap from reversing aging itself. Can you explain how someone like Sinclair makes that leap?
D.T. MAX: We’re not even where you’re saying we are. We’re just doing a safety trial. This trial isn’t even about whether it works. It’s about whether it hurts somebody to get this injection.
MARC LANDAS: Right. It’s a safety trial, but Sinclair’s larger hope is still there. The idea is working in the background.
D.T. MAX: More than that. The reason they’re doing the safety trial is to then have the efficacy trial. Obviously, when they’re done with this, you and I might be having an identical conversation.
The basic idea is that your DNA ages, and when it ages, it’s less efficient at doing what it does. It’s supposed to create proteins, but the proteins it creates may be damaged or otherwise impaired. So if we can somehow clean up your DNA—shine it up so it’s like Marc’s DNA when he was newborn—your body would be doing a better job at everything. That’s the basic idea.
How do you get from that to reversing aging? Well, in effect, that is reversing aging. I know old age is just a number, but actually old age is more than a number. It’s a million qualities in your body that are no longer functioning as well as they once did: your eyesight, your cardiovascular system, your brain—you name it.
At least in theory, if you can continuously reverse somebody’s aging, they’re not going to die from natural aging. Obviously, if somebody conks you on the head with a baseball bat, I’m not sure any amount of epigenetic reprogramming is going to save you. But with natural aging, the idea is that you could potentially reverse it perpetually.
MARC LANDAS: One of the most common phrases you hear among longevity people is that aging is a disease that simply needs to be cured. Eventually, if we cure that disease, we’ll cure aging. Obviously, it’s a sound bite, but the logic has always struck me as a little reductive. After spending so much time reporting on this field, what do you think of that idea?
D.T. MAX: I have mixed feelings. If there’s such a thing as an immortalist, I’m not an immortalist. I’m suspicious of it for a number of reasons.
One is that it’s selfish. Part of what we do when we die is make room for a later generation and a different generation. If 10 generations ago they had discovered this science, would we still believe the sun revolves around the Earth? Knowledge and change come from the succession of generations. That’s one issue. And then there are all the questions of overpopulation and everything else.
The part of it I like is the idea that when we speak about old age, we’re basically speaking about decrepitude—a decline of function, often a very radical decline of function, that can end with a person who is still alive but has lost so much.
The idea that you could have an old age that wasn’t so far inferior to your younger years seems to me much more within the realm of what we can and should do, if we can do it.
Do I think we should all look like we’re 25 forever? To me, that’s kind of a triviality. But I had a father, for instance, who had early cardiovascular problems. Those problems were somewhat age-related and also related to his lifestyle. But he lost something, and I lost something from that. We all did. So there I feel I’m on firmer ground.
I should also say that if we’re far away from reversing aging, we’re even further away from immortality. There’s something slightly unclear to my mind about the idea that if we reverse aging, we live forever. David Sinclair says that, but I’m not sure it makes exact biological sense. Maybe we’ll find out one day. There are a lot of things that happen in aging. Are we really going to reverse all of them?
MARC LANDAS: Your article points out a number of interesting tensions, but one that jumped out at me is that researchers are already developing therapies even though our understanding of the underlying biology isn’t complete. Are they jumping the gun, or is this simply the usual scientific messiness—the sausage-making people don’t normally see?
D.T. MAX: I don’t think it’s exactly that. I think it’s connected to the fact that this is private science.
Private science moves faster, makes more mistakes, and is willing to take chances, whereas the normal grant-making process is conservative. The labs I write about in the National Geographic article are funded in a way that is not historically typical. They’re so well funded that they don’t have to go anywhere else for money. And they have investors.
So you have a chance to go really fast and hit a home run in a way that you wouldn’t necessarily do in academia. The motives are different. The milieu is different. The incentives are different.
I think two things about it. First, you’re obviously much more likely to have outright failures. Failure here is complicated because we do have a basic mechanism that works. We know now that you can, in a sense, reverse the aging of genes by diminishing the epigenetic material around them. That’s something no one’s going to take away from us.
But then the questions immediately become: Can you do it locally? Can you do it without causing harm? Can you do it perpetually? Can you do it in particular cells? Can you do it across all kinds of cells? Those are the things that aren’t really nailed down yet.
We’re so early in this process that we’ve almost only just realized there’s a way to use these Yamanaka factors without killing the cell. That’s early in science. That was one of the breakthrough moments when the billionaires came out of the woodwork and said, “Let’s fund this.”
MARC LANDAS: That reminds me of the Silicon Valley saying, “Move fast and break things.” A lot of the backing for this field comes from Silicon Valley. But you can’t bring that ethos into biomedical research in quite the same way, because the things you might “break” are people.
With alternative funding models, there’s also the possibility of abuse or inadequate oversight. Is there a particular risk here because so much of this research is privately funded?
A recent controversy in China also comes to mind, involving an experimental gene therapy that resulted in the death of a child. The treatment was partly financed by the family, who reportedly contributed nearly $1 million to the laboratory, and concerns were later raised that the work had not gone through appropriate oversight despite the researcher’s university affiliation. When privately funded biomedical research can move outside conventional institutional checks, is there a risk that the pressure to move quickly can come at the expense of patient safety?
D.T. MAX: Right. Is there a risk when you say, “Move fast and break things,” if the things are people? Is that something we’re going to accept?
One thing that attracted me to the story—and that is both a reason for caution and a reason to check back in a few years—is that this is being done in the United States under FDA protocols. It’s not like they can do anything they want.
Take the idea of this safety trial. In a world where there were no FDA, would a company with a promising remedy really want to lose five years on a safety trial if it could go right to an efficacy-and-safety trial? Almost certainly not.
But we should know after those years—and probably sooner—whether this treatment hurts people. We really don’t know. It’s never been given to a human before. So in that sense, no matter what the Silicon Valley ethos is, there are guardrails if the science is being done in the United States or Europe.
I don’t know enough about Chinese regulation to comment confidently on whether the same would be true there. My general impression is that if we go slowly here and the Chinese government sees an opportunity to go fast, they’ll take that opportunity. I don’t know much about what’s going on with this kind of treatment in China at the moment, but I would be very surprised if nobody were paying attention to it. It seems like exactly the kind of thing they would pay attention to, and they certainly have the scientific skills to do it.
MARC LANDAS: Your article shifts the language from extending lifespan to extending healthspan. First, can you explain what healthspan is? And do you think there’s been a genuine change in the scientific objective, or is something else going on?
D.T. MAX: Healthspan is what we were talking about before. There’s a huge number of people who are going to turn 80 in the coming years. At 85, you can have a great life or you can have a very limited life. Healthspan is about the difference between those two things.
Do I think these companies have really changed their objectives? When all this first began, Google set up Calico Labs, and Time ran a cover along the lines of “Google versus death.” The truth is that all of them still have in their hearts this idea that they’re going to conquer death, not that they’re going to conquer glaucoma. “Google versus glaucoma” wouldn’t have been much of a headline.
These are profit-making, or potentially profit-making, enterprises. The money is in healthspan. The low-hanging fruit and the middle-hanging fruit are in healthspan, not lifespan.
These are investors. I don’t think they’re investors who expect quarterly reports on revenue, but I also don’t think they put this money in for charity, any more than SpaceX was funded for charity. These moonshot-type companies are still monitored for profitability by the people who invest in them.
So I think there are two conversations going on. One is the conversation you and I hear. The other is the kind of conversation we don’t hear, which is probably still more focused on immortality and the idea that we’re doing something that’s never been done before in the history of humanity.
MARC LANDAS: I share your interest in longevity and, more broadly, human enhancement. I actually recently read The Epic of Gilgamesh for the first time for exactly that reason—to understand that very early treatment of longevity and mortality.
So, with one eye on the science today and one eye on Gilgamesh, because in some ways they’re pursuing the same thing, how do you see this larger story? Is Gilgamesh a cautionary tale, or is there something in that quest that we should still strive for?
D.T. MAX: Gilgamesh is a great story. I’m not really super up on Gilgamesh. My memory is that it’s potentially two different stories fused at the waist, but you might know better than me at this point.
MARC LANDAS: But he never gets immortality. Is it cautionary in the sense that you can do whatever you want, but ultimately we’re all heading to the same place? Or is there something more to the quest?
D.T. MAX: I would answer more from my own point of view, because Gilgamesh isn’t unique. This is an ancient, core part of humanity: the idea of the stunning unfairness that you do all these things and then you drop dead. What do you have to show for it?
I can only imagine that from almost the beginning—certainly from the beginning of writing—the idea that we could try to escape this was one of the very first things we thought about.
I also think the better and richer your quality of life, the more unfair you think death is. So there’s a reason billionaires are first in line for these treatments. There’s that joke that we used to practice medicine on primates, and now we practice it on billionaires.
I think we’re going to get part of it. I believe—and again, I have no more data on this than you do—that something is going to come out of this. I think it’s probably going to be less than immortality.
And I suspect what’s going to happen is that these things become complicated when you get into the details. The basic idea of epigenetic reprogramming is stunningly simple and really persuasive, almost like a magic key. But there have been other magic keys in science.
Over and over, once you get into the details, you encounter the real questions: How do you deliver it? What are the side effects? Which cells does it improve? Which cells does it damage? Who can’t tolerate it? Look at how many times we’ve “cured” cancer.
So is Gilgamesh a cautionary tale? I think almost all of literature basically tells you that you can’t do this.
There’s a wonderful poem by Tennyson, “Tithonus,” where Tithonus—a lover of a goddess in ancient Greek mythology—is given immortality by the goddess but forgets to ask for immortal youth. He just languishes forever and essentially says, “Boy, did I make a mistake.”
That’s another possible outcome here.
IMAGE CREDIT: Yuancheng Ryan Lu, Sinclair Laboratory, Harvard Medical School.
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