'Zombie' cells could explain aging — and help scientists slow it

Summary

Podcast Summary: "Short Wave" Episode – 'Zombie' Cells Could Explain Aging — and Help Scientists Slow It

Release Date: August 5, 2025

Hosts: Emily Kwong and Regina Barber

In this enlightening episode of NPR's "Short Wave," host Regina Barber delves into the intricate relationship between stress and aging, exploring groundbreaking research that connects psychological stress to cellular changes in the body. Joined by science journalist Diana Kwan, the discussion unravels how "zombie" cells, or senescent cells, contribute to the aging process and what this means for future scientific interventions.

---

Understanding the Link Between Stress and Aging

Regina Barber opens the conversation by sharing her personal experiences with stress and its physical manifestations, setting the stage for a deeper exploration into the science behind stress and aging.

Regina Barber [00:34]:
"Stress can really take a physical toll, but I don't think I realized just how much of a toll until this episode when I called her to discuss the link between stress and aging."

Diana Kwan confirms the extensive research linking stress to biological aging, explaining that various disorders and diseases accelerate the aging process.

Diana Kwan [00:55]:
"There’s a whole body of research on this very topic."

Early Studies: Stress and Telomere Shortening

The discussion shifts to a seminal study from the early 2000s that examined stress levels in 58 biological mothers, divided between those with healthy children and those caring for children with chronic illnesses.

Regina Barber [01:05]:
"She told me about a study researchers did in the early 2000s looking at stress in 58 biological mothers."

Diana highlights the study's unique approach of linking psychological stress to molecular indicators of aging, specifically telomere length.

Diana Kwan [01:38]:
"It was one of the first studies to really bring the stress and aging link to, like, the molecular level."

Findings revealed that mothers under higher stress—those caring for chronically ill children—had shorter telomeres, the protective caps on chromosomes associated with cellular aging.

Regina Barber [02:01]:
"Telomeres are the protective caps on the ends of chromosomes. And overall, their shortening is associated with aging. So more stressed parents with shorter telomeres equals biologically older parents."

Senescent Cells: The Zombie Cells Hypothesis

Expanding on molecular mechanisms, Kwan introduces the concept of senescent or "zombie" cells, which cease to divide and begin to consume cellular resources, potentially accelerating the aging process.

Diana Kwan [02:24]:
"As our cells age, they stop performing their regular functions and they enter this kind of sleepy zombie-like state."

Regina likens these cellular changes to older appliances becoming less energy-efficient, enhancing the listener's understanding of the biological processes at play.

Regina Barber [05:38]:
"It makes me think of like how older appliances like fridges, you know, use more energy. They're less energy efficient, like, than the new ones that are, like, running well."

Brain-Body Energy Conservation Model

Kwan discusses a novel hypothesis—the brain-body energy conservation model—which posits that as cells accumulate damage, the brain reallocates energy to manage this damage, resulting in visible signs of aging.

Diana Kwan [04:34]:
"So the brain... senses that, okay, there's a bunch of cells out there that need energy. And so we're going to take energy away from other processes to fuel this damage control."

This model is still emerging and not yet widely accepted, but it offers a unified perspective on how different bodily systems interact during the aging process.

Diana Kwan [07:03]:
"One can kind of think of it in that way, but in a lot of ways, a lot of pieces of this puzzle are untested."

GDF15: A Central Molecule in Aging Research

A significant portion of the episode focuses on Growth Differentiation Factor 15 (GDF15), a molecule that appears to play a pivotal role in mediating the relationship between cellular stress and brain signaling in the context of aging.

Regina Barber [07:42]:
"Yet one of these things that has come up in these studies is this molecule called GDF15. Why is this important in this research?"

Diana Kwan [07:51]:
"GDF15 is a cellular messenger... It’s been linked to a bunch of different aging related processes."

GDF15 is unique in that it is secreted by multiple organs but interacts with receptors exclusively in the brain, suggesting a targeted communication pathway about cellular stress.

Diana Kwan [08:55]:
"All of these things together have made researchers think... maybe GDF15 is responsible for sending the brain signals about cellular stress."

Implications for Clinical Trials and Future Research

The conversation transitions to the practical implications of this research, particularly how it could influence the design and effectiveness of clinical trials aimed at slowing aging.

Regina Barber [09:26]:
"With this new hypothesis, how are scientists going to maybe think differently about clinical trials?"

Diana Kwan [09:38]:
"They should really think about how much stress the people who are taking these drugs... are exposed to. Because that might have a huge impact on how well these interventions work."

Acknowledging that stress management may become a critical factor in the success of anti-aging therapies, Kwan emphasizes the need for holistic approaches in future research.

Hope for Reversible Aging Changes

Concluding the episode on an optimistic note, Kwan shares studies suggesting that some stress-induced aging markers are reversible, offering hope that interventions could mitigate the negative effects of stress on aging.

Diana Kwan [10:54]:
"These changes are not irreversible. These are things that we can affect in our daily lives to some extent."

She cites experiments with monkeys that demonstrated reduced signs of accelerated aging when stress conditions were alleviated, reinforcing the potential for lifestyle modifications to influence biological aging.

Diana Kwan [11:20]:
"It's a hopeful view of the future where we will have a toolbox of things that may help us stay healthy for longer."

Personal Reflections and Takeaways

Regina Barber reflects on the newfound understanding of the stress-aging connection, expressing hope and a positive outlook towards managing stress to influence aging outcomes.

Regina Barber [10:11]:
"When you were doing this story... did you come away thinking differently about aging, about stress?"

Diana Kwan [10:20]:
"I thought it was really cool that this research seems to be entering a kind of new era where, you know, hopefully it'll start to make a big difference in people's lives."

---

This episode of "Short Wave" effectively bridges personal experiences with cutting-edge scientific research, providing listeners with a comprehensive understanding of how stress impacts aging at a cellular level. By introducing complex concepts like senescent cells and the brain-body energy conservation model in an accessible manner, Regina Barber and Diana Kwan deliver a thought-provoking exploration of potential avenues to slow or even reverse aspects of the aging process.

Transcript

[Ad Sponsor]

This message comes from Mint Mobile. Mint Mobile took what's wrong with wireless and made it right. They offer premium wireless plans for less, and all plans include high speed data, unlimited talk and text, and nationwide coverage. See for [e-mail] Switch.

[Regina Barber]

You're listening to Shortwave from NPR. Hey, shortwavers. I love my job, but I'm going to be honest, sometimes it's stressful, and when I'm stressed, I can definitely feel it in my body. Which science journalist Diana Kwan says makes sense.

[Diana Kwan]

I've reported a lot of stories in the past about the biological effects of stress.

[Regina Barber]

Stress can really take a physical toll, but I don't think I realized just how much of a toll until this episode when I called her to discuss the link between stress and aging. And she told me, yep, Gina, there's a whole body of research on this very topic.

[Diana Kwan]

It just kind of made a lot of sense that stress would affect aging as well, because, you know, things like various disorders and diseases, you know, these all affect how quickly we age.

[Regina Barber]

She told me about a study researchers did in the early 2000s looking at stress in 58 biological mothers.

[Diana Kwan]

About a third or a bit more than a third who had a healthy child and two thirds who had a child with a chronic illness. And they kind of reasoned that this latter group would have higher levels of stress due to having to take care of somebody with an illness.

[Regina Barber]

Part of the study included asking those parents about their stress levels, which were higher for the caretakers of kids with an illness. But Diana says this study also did something pretty unique.

[Diana Kwan]

It was one of the first studies to really bring the stress and aging link to, like, the molecular level.

[Regina Barber]

So more researchers started looking for signs of psychological stress in people's DNA.

[Diana Kwan]

You know, not only did this group of people with a chronically ill child report having higher levels of stress, they also had shorter telomeres.

[Regina Barber]

Telomeres are the protective caps on the ends of chromosomes. And overall, their shortening is associated with aging. So more stressed parents with shorter telomeres equals biologically older parents. Since then, other studies have found other clues to how stress affects the body. On the molecular level, they link to chronic stress and to an increase in something called senescent or zombie cells.

[Diana Kwan]

As our cells age, they stop performing their regular functions and they enter this kind of sleepy zombie like state and.

[Regina Barber]

They stop dividing like normal cells do. Some researchers are starting to think that these zombie cells are sucking up resources from the rest of our body, which ultimately results in aging and could ultimately help researchers answer the question, what Is.

[Diana Kwan]

It about stress that's changing our cells that makes people become less healthy later in life?

[Regina Barber]

Today on the show, a new hypothesis for how the brain handles these aging zombie like cells may help researchers understand aging on the molecular level, plus what science could do about it. I'm Regina Barber and you're listening to Shortwave, the science podcast from.

[Ad Sponsor]

This message comes from Charles Schwab. When it comes to managing your wealth, Schwab gives you more choices like full service, wealth management and advice when you need it. You can also invest on your own and trade on thinkorswim. Visit schwab.com to learn more. This message comes from NPR sponsor State Farm. If you're a small business owner, it's your life. State Farm agents are small business owners too, so they can help you choose personalized policies. Like a good neighbor, State Farm is there. Talk to your local agent today. Support for this podcast and the following message come from Prolon. Want to look and feel your best this summer? Don't just think skin deep, think cell deep. The goal of Prolon's five day nutrition program is to rejuvenate you at the cellular level with boxes labeled by day so you know exactly what to eat. Based on their clinical study, Prolon aims to trigger a fasting state while you eat procedure. Prolon is the future of Nutrition. Get 15% off when you [e-mail] NPR.

[Regina Barber]

Okay, Diana, so these researchers that are like studying aging, they've developed this hypothesis called the brain body energy conservation model. As a physicist, I love any energy conservation model actually. How does this work? Yeah, yeah.

[Diana Kwan]

So this is a really interesting model developed by a small group of aging researchers. So it's by no means a well established, widely accepted model. Yet basically, as our cells get older, they accumulate energetically costly forms of damage. So these are things like becoming zombie like or senescent or accumulating DNA damage or inflammation. All of these things are those telomere shortening. Exactly. So all of these things require energy to fix. And so the brain, through various signaling molecules that are coming through, the body senses that, okay, there's a bunch of cells out there that need energy. And so we're going to take energy away from other processes to fuel this damage control. And so this ultimately results in the outward signs of aging that we're all familiar with. Things like graying hair or reduction in muscle mass that are less essential than keeping ourselves alive.

[Regina Barber]

Yeah. It makes me think of like how older appliances like fridges, you like, use more energy. They're less Energy efficient, like, than the new ones that are, like, running well, you know.

[Diana Kwan]

Yeah.

[Regina Barber]

So in your piece, you write about an experiment these researchers did, the ones who came up with this model a couple years back, to look at how these zombie cells use energy. Can you tell me more about that?

[Diana Kwan]

Yeah. So this was back in, I think, 2022, where a bunch of researchers at Columbia took human skin cells and cultured them in a laboratory dish, and they observed them over a short period of time. And they found that they, the cells that had stopped dividing and entered this zombie like, state were using about double the energy that younger cells were. And this kind of flew in the face of what researchers had thought about these zombie cells because, you know, a lot of people thought, okay, a cell doesn't divide anymore. Cell division requires a lot of energy. You know, these cells must not need a lot of energy. But actually it turns out that they're burning a lot of energy. And so the researchers went and kind of looked at the literature and found, oh, wait, there's like, all of these other damage processes that are happening, and these are all costly. You know, we should put this into a model. And, you know, the brain body energy conservation model is what they came up with.

[Regina Barber]

And this is a pretty new hypothesis, right? Like, the entire aging research community isn't completely convinced yet, right?

[Diana Kwan]

Yeah, it's absolutely a new hypothesis. They only came up with it, you know, in the last couple of years. And the researchers I spoke to who hadn't developed this hypothesis, a lot of people thought it was really intriguing. And I think what a lot of people like about it is that it kind of brings the brain and body together in aging. And that's something that hasn't really been done before, this kind of unified hypothesis of aging. One can kind of think of it in that way, but in a lot of ways, a lot of pieces of this puzzle are untested, even though there are some really compelling hints or pieces of evidence that this might actually be happening.

[Regina Barber]

Right. Yet one of these things that has come up in these studies is this molecule called GDF15. Why is this important in this research?

[Diana Kwan]

Yeah. So GDF15, or growth differentiation factor 15, which is a bit of a mouthful. So I think this was one of the most fascinating pieces of the brain body aging model puzzle. So basically, GDF15 is a cellular messenger, and researchers think it might play a really central role in mediating the link between the body and brain in aging. And this molecule has also come up in aging research, sort of not related to the brain either. So it's been linked to a bunch of different aging related processes. Once again, cellular senescence or a zombie like state. So this molecule is found to be linked to that process, also a dysfunction in mitochondria or the cellular powerhouses. This is also something that happens as we age. GDF15 is also linked to aging related diseases like Alzheimer's and a bunch of chronic physical and mental illnesses too. And so one thing that's really interesting about this molecule is that it's secreted by many, if not all of our organs. But the receptor for this molecule is only found in one particular place in the body, and that's in the brain. And so all of these things together have made researchers think, okay, maybe GDF15 is responsible for sending the brain signals about cellular stress. So this is kind of a working hypothesis at the moment, but a really fascinating molecule that might play a really important role or be a really important piece of this whole puzzle.

[Regina Barber]

There's so many unknowns still, but scientists are already trying to create medicines like to slow down aging. So with this new hypothesis, how are scientists going to maybe think differently about clinical trials?

[Diana Kwan]

Yeah, I think both with this new hypothesis and the kind of growing body of research that shows that stress plays a really important role in these aging related processes, what a lot of the stress researchers or the stress and aging researchers that I spoke to said is that this field of aging, which traditionally hasn't really thought about the effects of stress, should really think about how much stress the people who are taking these drugs, or you know, will be taking these drugs in the future are exposed to. Because that might have a huge impact on how well these interventions work.

[Regina Barber]

When you were doing this story, at the very end, when you've done all this reporting, did you come away thinking differently about aging, about stress?

[Diana Kwan]

I guess yes and no. No, in that, you know, I wasn't necessarily surprised that stress, which affects so parts of our body, affects aging as well. But I guess yes, in that for such a long time it was kind of this like woo woo connection. Oh, you know, stress causes aging, but you know, how without a mechanism. So I thought it was really cool that this research seems to be entering a kind of new era where, you know, hopefully it'll start to make a big difference in people's lives.

[Regina Barber]

Yeah, I mean, this actually does make me feel like more hopeful as well about stress and aging.

[Diana Kwan]

Yeah, absolutely. And that makes me think of, you know, there's actually been some experiments where scientists have found that some of these stress related aging changes in our Cells are reversible. So there were researchers who did a study in monkeys where they found that monkeys that were stressed out had these changes in their immune cells that were linked to accelerated aging. But they found that when they switched up their conditions and put them in less stressful situations, you know, all of a sudden the cells or less or reduce signs of accelerated aging. So I think that's a really positive thing because I think the this kind of stress may be linked to aging or cause aging at some level. It can be a really negative message and it can stress people out to think that stress is going to age you because, you know, stress is one of these things. You're like stress. You're telling yourself you're stressed about stress. Exactly. Yeah. But no, these changes are not irreversible. These are things that we can affect in our daily lives to some extent. It's kind of more hopeful, in my view. It's a hopeful view of the future where we will have a toolbox of things that may help us stay healthy for longer. Yeah.

[Regina Barber]

And less stressed.

[Diana Kwan]

Yeah.

[Regina Barber]

Diana, thank you so much for talking to me today about aging. It makes me think about aging, you know, more because I always think about it.

[Diana Kwan]

Don't we all? Thanks so much for having me.

[Regina Barber]

Shortwavers, thank you for listening. If you want to help us out, share this episode with a friend. We want to grow as we age and reach even more science curious people. And that's one of the best ways to do it, by word of mouth from you to your friends. And why not follow us on the NPR app or whatever other podcast app you use. This episode was Produced by Burleigh McCoy, edited by showrunner Rebecca Ramirez, and fact checked by Tyler Jones. The audio engineer was Jimmy Keeley. Beth Donovan is our senior director, and Colin Campbell is our senior vice president of podcasting strategy. I'm Regina Barber. Thank you for listening to short wave from NPR.

[Ad Sponsor]

This message comes from LinkedIn ads. One of the hardest parts about B2B marketing is reaching the right audience. That's why you need LinkedIn ads. You can target your buyers by job title, company role, seniority, and skills. All the professionals you need to reach in one place to get a $100 credit on your next campaign. So you can try it yourself. Just go to LinkedIn.com results. That's LinkedIn.com results. Terms and conditions apply only on LinkedIn ads.

[Regina Barber]

This message comes from NPR sponsor Rosetta Stone, an expert in language learning for 30 years. Right now, NPR listeners can get Rosetta stone membership to 25 different languages for 50% off. Learn more at Rosetta Stone.com NPR this.

[Ad Sponsor]

Message comes from Bombas. Socks, underwear and T shirts are the top three requested clothing items by people experiencing homelessness. Bombas makes all three and donates one item for every item purchased. Go to bombas.com NPR and use code NPR for 20% off.