Stress ages us on a cellular level

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1:26Regina G. Barber:This is Unexplainable. I'm Bird Pinkerton. 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. You're listening to Shortwave from NPR. Hey, Shortwavers.

2:13Regina G. Barber: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.

2:25Diana Kwon:I've reported a lot of stories in the past about the biological effects of stress.

2:30Regina G. 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.

2:46Diana Kwon: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.

2:55Regina G. Barber:She told me about a study researchers did in the early 2000s looking at stress in 58 biological mothers.

3:02Diana Kwon: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 the kind of reason that this latter group would have higher levels of stress due to having to take care of somebody with an illness.

3:18Regina G. 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.

3:29Diana Kwon:It was one of the first studies to really bring the stress and aging link to the molecular level.

3:35Regina G. Barber:So more researchers started looking for signs of psychological stress in people's DNA.

3:41Diana Kwon: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.

3:52Regina G. 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 to an increase in something called senescent, or zombie cells.

4:15Diana Kwon:As our cells age, they stop performing their regular functions and they enter this kind of sleepy, zombie-like state.

4:24Regina G. Barber:And 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,

4:38Diana Kwon:what is it about stress that's changing our cells that, you know, makes people become less healthy later in life?

4:46Regina G. 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 NPR.

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8:20Regina G. 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?

8:33Diana Kwon:Yeah, yeah. So this is a really interesting model developed by, you know, 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, you know, 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 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.

9:25Diana Kwon: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.

9:37Regina G. Barber:Yeah, it makes me think of like how older appliances like fridges, you like use more energy. They're less energy efficient, like then the newer ones that are like running well, you know? Yeah. 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?

9:58Diana Kwon: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, 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.

10:35But actually, it turns out that they're burning a lot of energy.

10:38Diana Kwon:And so, you know, 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 models, what they came up with.

10:54Regina G. Barber:And this is a pretty new hypothesis, right? Like the entire aging research community isn't completely convinced yet, right?

11:02Diana Kwon: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, you know, 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, you know, this might actually be happening.

11:42Regina G. 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?

11:51Diana Kwon: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.

12:33Diana Kwon:Also a dysfunction in mitochondria or these cellular powerhouses. This is also something that happens as we age. GDF-15 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 GDF-15 is responsible for sending the brain signals about cellular stress.

13:14Diana Kwon: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.

13:25Regina G. 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.

13:37Diana Kwon: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.

14:10Regina G. 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?

14:20Diana Kwon: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 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.