Stress ages us on a cellular level

Summary

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Podcast Summary: Unexplainable – "Stress ages us on a cellular level"

Date: February 23, 2026
Host: Regina Barber (Shortwave, featured on Unexplainable)
Guest: Diana Kwan, Science Journalist

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Episode Overview

This episode explores the scientific connection between psychological stress and biological aging at the cellular level. Host Regina Barber and science journalist Diana Kwan discuss new research on how chronic stress manifests in our bodies, focusing specifically on molecular changes—particularly shortened telomeres and "zombie" (senescent) cells—that are linked to aging. They also introduce a novel hypothesis: the brain-body energy conservation model, which could explain how the brain shifts resources in response to cellular damage. The discussion ends on a hopeful note, emphasizing the possibility of reversing some stress-related aging effects.

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Key Discussion Points & Insights

1. The Link Between Stress and Aging

• Regina shares her personal experience with work-related stress, highlighting its bodily effects (02:00).
  • “When I'm stressed, I can definitely feel it in my body. Which science journalist Diana Kwan says makes sense.” – Regina Barber (02:15)
• Diana Kwan introduces the foundational research on stress and biological aging:
  • An early 2000s study observed that mothers caring for chronically ill children (more stressed group) had noticeably shorter telomeres than those with healthy children, signaling accelerated cellular aging (02:47–03:43).
  • “It was one of the first studies to really bring the stress and aging link to…the molecular level.” – Diana Kwan (03:21)

2. Senescent ("Zombie") Cells and Aging

• Chronic stress is shown to promote the emergence of senescent, or so-called ‘zombie’ cells—cells that no longer function or divide but remain in tissue, potentially harming overall health (04:06).
• These cells stop dividing and may siphon resources from healthy cells, contributing to bodily decline with age (04:16–04:30).
• Key research question:
  • “What is it about stress that’s changing our cells that makes people become less healthy later in life?” – Diana Kwan (04:30)

3. The Brain-Body Energy Conservation Model

• Hypothesis Overview:
  • Developed by a small group of aging researchers, though not yet widely accepted (09:08–09:35).
  • Energy Demand Hypothesis: As damaged or zombie-like cells proliferate, the brain reallocates energy from less critical functions (like muscle maintenance or hair pigmentation) toward cellular damage control, leading to visible signs of aging (09:08–10:11).
  • Analogy: Older appliances use more energy; inefficient older cells do the same (10:11).
  • Lab study at Columbia (2022): Senescent cells consume roughly double the energy of younger cells—contradictory to previous assumptions (10:31–11:27).

4. GDF15: The Messenger Molecule

• Growth Differentiation Factor 15 (GDF15):
  • Identified as a potential signaling molecule that may mediate communication between the body and brain about cellular stress (12:16–13:59).
  • Produced by many organs, but receptors are only in the brain—a unique pathway.
  • Associated with senescence, mitochondrial dysfunction, Alzheimer’s, and other chronic conditions.
  • “Maybe GDF15 is responsible for sending the brain signals about cellular stress.” – Diana Kwan (13:40)

5. Rethinking Clinical Trials in Aging Research

• The field largely overlooked the role of chronic stress in aging interventions. Now, researchers argue clinical trials for anti-aging therapies must account for subjects' stress levels, as it could drastically impact efficacy (14:11–14:44).

6. Is Stress-Aged Biology Reversible?

• Hopeful Take on Stress and Aging:
  • Some cellular changes driven by stress can be reversed, as shown in a monkey study: when moved to less stressful environments, their immune cells began to appear biologically younger (15:27).
  • “These changes are not irreversible. These are things that we can affect in our daily lives to some extent.” – Diana Kwan (16:12)
  • Discussion counters the “stress about stress” anxiety, empowering listeners to take action against chronic stress.

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Notable Quotes & Memorable Moments

• On telomeres and stress:
  “More stressed parents with shorter telomeres equals biologically older parents.” – Regina Barber (03:43)
• On zombie cells:
  “They stop dividing like normal cells do... researchers are starting to think these zombie cells are sucking up resources…which ultimately results in aging.” – Regina Barber (04:16)
• On the new hypothesis:
  “The researchers I spoke to who hadn’t developed this hypothesis…thought it was really intriguing. It brings the brain and body together in aging—that hasn’t really been done before.” – Diana Kwan (11:35)
• On GDF15:
  “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…is only found in one place in the body and that’s in the brain.” – Diana Kwan (13:30)
• On reversibility:
  “When they switched up [the monkeys'] conditions and put them in less stressful situations, all of a sudden the cells bore…reduced signs of accelerated aging.” – Diana Kwan (15:33)

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Timestamps for Key Segments

• 02:00 – 03:43: Effects of stress on the body; telomeres and the early study on stressed parents
• 04:06 – 04:30: Introduction of senescent/zombie cells and their role in aging
• 09:08 – 10:11: The brain-body energy conservation model explained
• 10:31 – 11:27: Columbia study on zombie cell energy demands
• 12:16 – 13:59: The "messenger" molecule GDF15’s possible centrality in linking stress, aging, and the brain
• 14:11 – 14:44: Why anti-aging trials must consider participants’ stress levels
• 15:27 – 16:12: Evidence that stress-driven cellular aging can be reversed

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Tone and Style Notes

• Approachable, conversational, and optimistic:
  The episode balances scientific details with relatable analogies (e.g., fridges using more energy as they age), and maintains a sense of hopefulness about our power to slow or reverse some aging effects by managing stress.
• Encouraging message:
  The main takeaway is not to become stressed about stress, but to recognize the difference science can make as it better understands these deep cellular processes.

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Summary Takeaway

Chronic psychological stress doesn’t just make us feel older—it literally accelerates cellular aging, as shown by research on telomeres and senescent cells. A novel hypothesis—the brain-body energy conservation model—suggests our brains shift energy to coping with damaged, energy-hungry cells, resulting in the familiar symptoms of aging. Central to this process may be the molecule GDF15, which could be the key communicator between stressed cells and the brain. Importantly, while stress can speed up aging, evidence suggests some changes are reversible, giving reason for hope and motivation to manage stress for better aging outcomes.

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Transcript

[Bird Pinkerton]

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[Unexplainable Host]

Support for the show comes from Anthropic, the team behind Claude. They say that Claude is the collaborator that actually understands your entire workflow. So for developers that looks like Claude code, it runs in your terminal, reads your code base, and can apparently take on things like writing tests, refactoring or debugging without you hand holding it through every step. Anthropic committed to not running ads in Claude. So when you are deep in something that matters to you, they say the answer you get is shaped by your question, not by an advertiser's agenda. Ready to tackle bigger problems? Get started with Claude today at Claude. AI Unexplainable. This is unexplainable. I am Bird Pinkerton and and today on the show, I am very excited to bring you an episode of a show that I really enjoy, NPR's shortwave. I have been listening to shortwave pretty much from the beginning. I find the show funny. I find the people on it friendly. I love how they tackle science news. And so they're going to tell us a story about stress, specifically about some research on how stress shows up in our bodies and what it might have to do with, quote, unquote, zombie like cells. So without further ado, here's the show.

[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 sort of faked 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 linked 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?

[Diana Kwan]

What is 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 N.

[Unexplainable Host]

Support for Unexplainable comes from Shopify. Every worthwhile journey starts with a handful of granola and a brain full of dreams. Dreams like what if I discover a new species or a new genus? Dreams like what if I paint a masterpiece that whispers some eternal truth to everyone who sees it? Dreams of winning the big race car trophy with your big fast race car? Or dreams of building your own thriving business? That last one is a dream Shopify can help you with. Shopify is the commerce platform behind millions of businesses around the world, and according to their data, at least 10% of all E commerce in the United States. Start with your own design studio and choose from hundreds of ready to use templates to create to make your online store. You can use their AI tools to help you with copywriting and glamming up your product photos, and then use the platform to build a marketing campaign. You can turn those what ifs into a thriving business with Shopify today. Sign up for your $1 per month trial today at shopify.com unexplainable go to shopify.com unexplainable that is shopify.com unexplainable. Support for the show comes from 1Password Are you small and are you also a business? Or probably more likely, do you work at a small business? Well, I'm not trying to freak you out, but cyber villains might be trying to get you Cyber evildoers know that small businesses often lack the resources to prevent or respond to breaches, but the good News is that 1Password provides simple security that can help small teams tackle the number one risk that cyber malefactors weak passwords 1Password provides centralized management to make sure your company's logins are secure. They provide turnkey solutions that can be rolled out in hours whether you have dedicated it staff or not. And 1Password is built to grow with your company. However complex your security needs may get, 1Password will stay with you every step of the way. You can take the first step to better security by securing your team's credentials. Find out [e-mail] unexplainable and start securing every login. Support for the show comes from Anthropic, the team behind Claude. If you are the kind of person who goes down a rack rabbit hole and then stays there, or who keeps pulling at a question until it clicks, they say Claude was built for that kind of thinking. For developers, that looks like Claude code. It runs in your terminal, reads your code base, and can apparently take on things like writing tests, refactoring or debugging without you handholding it through every step. I texted my friend who uses Claude and told him I was making an ad about Claude and asked why I should use Claude and or Claude code. It's just really good at coding. Lol. He said what does that mean? I said with it I can build things. I wouldn't have time for myself or ability for myself in many cases. He said nice. I said Anthropic says they are committed to not running ads in Claude. So when you are deep in something that matters to you, they say the answer you get is shaped by your question, not by someone else's advertisement taking you out of the deep work ready to tackle bigger problems. Try Claude for free at claude AI unexplainable. And see why some problem solvers choose Claude as their thinking partner.

[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, but 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. You know, all of these things are those telomere shortening. Exactly. So all of these things require energy to fix. And so the brain, through, you know, 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. Yeah.

[Regina Barber]

It makes me think of, like, how older appliances, like fridges, you, like, use more energy. They're less energy efficient, like, than the newer 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 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 a lot of people thought, okay, a cell doesn't divide anymore. Cell division requires a lot of energy. 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 all of these other damage processes that are happening, and these are all costly. We should put this into a model. And 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.

[Diana Kwan]

Right? Yeah, it's absolutely a new hypothesis. They only came up with it 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.

[Diana Kwan]

Yeah.

[Regina Barber]

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 and aging. And this molecule has also come up in aging research, not related to the brain either. So it's been linked to a bunch different agent 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 these 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 place in the body and that's in the brain. And so all of these things together. Yeah. 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 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 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 many 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 hopefully it'll start to make a big difference in people's lives. Yeah.

[Regina Barber]

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

[Diana Kwan]

Yeah, absolutely. And that makes me think of. 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, all of a sudden the cells bore less or reduced signs of accelerated aging. So I think that's a really positive thing because I think 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 stress is one. Cause you're like you're stressed about stress. Exactly. 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.

[Unexplainable Host]

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]

Short wavers. 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 a 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 N.