Why Scientists Can’t Agree on Aging

Summary

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Curiosity Weekly – "Why Scientists Can’t Agree on Aging"

Podcast: Curiosity Weekly (Discovery)
Host: Dr. Samantha Yammine
Guest: Dr. Paul Robbins, Professor of Aging & Metabolism, University of Minnesota
Date: January 7, 2026

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Episode Overview

This episode investigates why scientists can’t agree on a single definition or strategy for aging, dissecting the biology of aging, longevity research, and new therapeutic possibilities. Host Dr. Samantha Yammine (Sam) welcomes Dr. Paul Robbins—an expert on the biology of aging—for a nuanced conversation about what aging truly means on a cellular level, genetic factors at play, and emerging science aimed at prolonging healthy years rather than simply extending lifespan.

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Key Discussion Points & Insights

What Longevity Research Teaches Us (02:02 – 06:12)

• Supercentenarians as Research Subjects:
  Sam spotlights María Branyas Morera, who lived to 117, exemplifying “supercentenarians” (those aged 110+). Scientists built a comprehensive health profile by comparing her genetics, epigenetics, metabolites, and microbiome to others in her region.
• Findings:
  • Extreme age does not necessarily mean poor health or major diseases.
  • Short telomeres were present without disease, challenging simplistic markers.
  • Genetic “luck”—protective variants, but also healthy Mediterranean lifestyle habits.
• Lifestyle Takeaways:
  • Grounding habits like sleep, social connections, spending time with pets, reading, and walking outshine big, ambitious health trends.
  • Quote (Sam, 05:16):
    "If there’s one thing to take from Maria, it’s this: her everyday habits line up with what we always hear researchers talking about on this podcast… all the small grounding moments that rarely make it onto our big annual goal lists."

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Why Scientists Can’t Agree: Defining Aging (09:04 – 10:50)

• Cellular Definition:
  Dr. Robbins notes there’s no single definition: “You ask 100 aging researchers what is aging, you get 100 different answers.” (09:28)
• Robbins’s Preferred Definition:
  • The loss of a tissue’s ability to repair itself over time due to cellular and molecular damage; eventually, this leads to decline and death.
• Hallmarks of Aging:
  • Includes loss of stem cell function, mitochondrial dysfunction, increased reactive oxygen species, genome instability, and more.

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Learning From the Outliers: Long-lived Animal Species (10:50 – 12:43)

• Comparative Biology:
  • Studying animals like hydra, naked mole rats, lobsters, bats, and bowhead whales reveals that lifespan can vary dramatically, even within similar species.
  • Robbins (11:48):
    “Why does a species that looks similar among the different strains, why does one live much longer than another?”
  • Long-lived species provide clues, but there are still more questions than answers.

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Human Longevity: Genetics vs. Lifestyle (12:43 – 14:25)

• Centenarian Studies:
  • Humans’ maximum verified lifespan appears to be ~115 years, with strong genetic contributions to those reaching advanced ages.
  • Some centenarians defy lifestyle odds (e.g., smoking, drinking), reinforcing the central role of genetics alongside lifestyle.
  • Robbins (13:55):
    “There’s clearly a genetic component. It’s not all genetics, but it’s clearly a genetic component.”
• Exposome:
  • An individual’s cumulative exposures—environment, diet, habits—shapes how the aging process unfolds.

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The Real Goal: Healthspan over Lifespan (16:00 – 16:46)

• Compression of Morbidity:
  • The hope is not necessarily to extend lives drastically, but to extend years of healthy, active life and compress the period of disease and dependency before death.
  • Robbins (16:09):
    “What you want to do is compress that period of morbidity… you like to compress that so you don’t have as much time being sick with multiple diseases.”
• A Good Death:
  • Ideal scenario is a rapid decline at a very old age, not prolonged frailty—“105 and you can die on the golf course” (16:42).

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Genetics & Interventions: Where Can Science Help? (16:54 – 19:03)

• Pathways Across Species:
  • Aging mechanisms in worms, flies, mice, and humans share key pathways, despite varying complexity.
• Drug Development:
  • Medications for diabetes (like metformin) and certain blood sugar regulators already show promise in slowing aging processes in other animals.
  • Progress requires far-reaching clinical trials and personalized strategies since responses vary widely.

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Senotherapeutics: Targeting Aging at the Cellular Level (19:03 – 25:13)

• Senescent Cells:

  • Cells enter “senescence” under stress/damage, stop dividing, secrete inflammatory signals to call immune cells to clear them; effective when young, less so with age.
  • The buildup of senescent cells triggers chronic inflammation and spreads malfunction to neighboring cells—likened to “one bad apple spoiling the bunch.”

• Therapeutics:

  • Senolytics: Drugs that target and remove senescent cells.
  • Senomorphics: Compounds that suppress the inflammation released by senescent cells.
  • Many are adapted from anti-cancer drugs, given similarities in cell biology.

• Clinical Trials:

  • Promising results in animal studies, mixed results and need for better targeting in humans.
  • Trials for Alzheimer’s, diabetes, age-related muscle loss, and macular degeneration.

• Memorable Analogy (Robbins, 23:02):
  “I show a bushel of apples and you have one bad apple in the bushel... That’s the way if you look at the liver in an aging person with senescent cells, we see senescence spreading to adjacent cells.”

• Personalized Treatment:

  • Effectiveness depends on identifying who has high “senescent cell burden”—not a one-size-fits-all therapy.
  • Robbins (25:05):
    “If you don’t have an increase in senescent cell burden, senotherapeutics will have no benefit…”

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Longevity Hacking & Supplements: Sorting Science from Hype (25:13 – 28:15)

• Popular Trends:
  • From intermittent fasting to bean-heavy diets, supplements, and more—much remains unproven or highly individual.
• Individualized Effects:
  • What works for one may not work for another, due to genetics and exposome.
• Supplements and Overlap:
  • Some supplements show efficacy (e.g., stress resistance, killing senescent cells), but combinations could cancel each other out or diminish effectiveness.
  • Cautious Optimism:
    • Robbins does not recommend blanket supplement regimens; research is ongoing.
    • Robbins (27:45):
      “It’s not that the more you take, you see additive effects… In animal model systems that some of these have—not necessarily adverse effects, but—they don’t provide the benefit because they cancel each other out.”

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New Research: Mitochondrial 'Recharging' & The Nanoflower Method (31:02 – 34:46)

• Background:
  • Cellular aging ties closely to loss of mitochondrial function, causing systemic fallout.
• New Approach:
  • Texas A&M study uses “nanoflower” particles to boost stem cells’ ability to manufacture and transfer mitochondria to damaged cells.
  • This rejuvenation helps tissues recover energy capacity, even under stressors like chemotherapy.
• Potential:
  • Could target not just classical aging but diseases like muscular dystrophy, heart disease, and neurodegeneration.
• Quote (paraphrased, 33:30):
  “It’s like training healthy cells to share their spare batteries with those that are running low.”

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Notable Quotes & Memorable Moments

• On Defining Aging (Dr. Robbins, 09:28):
  “You ask 100 aging researchers what is aging, you get 100 different answers.”

• On Genetic vs. Lifestyle Factors (Dr. Robbins, 13:55):
  “There’s clearly a genetic component. It’s not all genetics, but it’s clearly a genetic component.”

• On The Goal of Aging Research (Dr. Robbins, 16:09):
  “What you want to do is compress that period of morbidity… so you don’t have as much time being sick.”

• On Senescent Cells (Dr. Robbins, 23:02):
  “I show a bushel of apples... one bad apple... That’s the way if you look at the liver in an aging person with senescent cells, we see senescence spreading to adjacent cells.”

• On Supplements and Hype (Dr. Robbins, 27:45):
  “It’s not that the more you take, you see additive effects… some of these cancel each other out.”

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Timestamps for Key Segments

• [02:02] – Supercentenarian research & lifestyle lessons
• [09:27] – Definition and hallmarks of aging
• [10:50] – Lessons from animals with extreme longevity
• [12:43] – Why some humans live to 100: genetics vs. environment
• [16:00] – Healthspan, the real target
• [19:03] – Targeting cellular senescence & senotherapeutics
• [25:13] – Sorting through longevity hacks and supplement hype
• [31:02] – Mitochondrial rejuvenation and “nanoflower” technology

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Closing Thoughts

Despite the explosion of interest in longevity, there is no universal solution or agreement among scientists about exactly what aging is and how to “cure” it. The message is clear: genetics is powerful, but healthy lifestyle basics and social connections offer real, science-backed value. New therapeutic avenues, like senolytics and mitochondrial transfer, are promising but will require meticulous science and targeted approaches before becoming mainstream.

For listeners, the takeaway isn’t a secret pill—but a renewed appreciation for sleep, connection, and moderation while watching the frontiers of aging research unfold.

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Guest Info:
Dr. Paul Robbins—Professor and Co-Director, Masonic Institute on the Biology of Aging & Metabolism, University of Minnesota

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Produced by: Wheelhouse DNA
Senior Producer: Teresa Carey
Producer: Kiara Noni
Audio Engineer: Nick Kimi
Head of Production: Cassie Berman
Host: Dr. Samantha Yammine

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Transcript

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[Dr. Paul Robbins]

Foreign.

[Dr. Samantha Amin]

It'S the New year and with it comes the annual onslaught of New Year's resolutions. Whether you're working on your posture or trying to decrease your screen time, or even trying to spend more time with friends, these goals have a way of showing us our priorities. The most popular New Year's resolutions are often centered on money, getting fit, or aging in a healthier way. So let's talk about it. The science of aging isn't just about living longer, but adding more healthy years to our lives. And it's surprisingly complicated. So I'll be speaking to Dr. Paul Robbins to discuss how scientists are currently looking at aging and how we can all use their knowledge to better take care of ourselves, whether we're 25 or 85. But first, I'll dig into what we can learn from a study of a woman who lived to be 117 years old. And then finally, we'll talk about cellular aging and some new research on how mitochondria methods be able to slow that process down. So Happy New Year. My name is Dr. Samantha Amin and this is Curiosity Weekly from Discovery. Researchers look for the secrets to longevity by studying people who reach extreme ages. One of them was Maria Branas Moreira, who lived to be 117 before her passing on August 19, 2024. She's what's called a supercentenarian, someone who lives beyond the age of 110. According to verified records from Guinness World Records and the Gerontology Research Group, Maria is the 8th oldest person ever, with the absolute oldest clocking in at 122. To learn more about how Maria may have lived so long, researchers met with her multiple times to collect urine, blood and stool samples and also interview her about her lifestyle. With this data, they were able to build a robust profile of her health, characterizing her genetics, epigenetics, the proteins and metabolites in her blood, and even her gut microbiome. They compared her profile with those of the women living in the same Catalonia region of Spain and published the results in Cell Reports Medicine. They found something I thought was pretty surprising. Extreme age and poor health don't necessarily go hand in hand. Maria showed the expected signs of advanced age, but she didn't have the major diseases often associated with it, like cancer or neurodegeneration. Her telomeres were short below the 20th percentile, which is common in older adults and often linked with disease risk. But in her case, short telomeres didn't reflect any underlying disease. This subtlety suggests that age related markers aren't automatically indicators of illness and that living to an extreme age doesn't mean disease is inevitable, which is something I've always wondered about. She had some genetic variants that are known to protect against cardiovascular disease, cognitive loss and diabetes, but none that increase the risk for conditions like Alzheimer's. She also had some variations in genes where the equivalents in other animals are linked to longer lifespans. The researchers believe it wasn't just any single variant that did the trick, but probably the combination. So there was some element of what you might call genetic luck. But her active lifestyle and healthy Mediterranean diet probably played a big role, too. If there's one thing to take from Maria, it's this. Her everyday habits line up with what we always hear researchers talking about on this podcast. The things that matter are good sleep, strong social connections, time with pets, reading, gardening, walking, playing piano, all the small grounding moments that rarely make it onto our big annual goal lists. And with that, let me just text my mom to make some plans.

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[Dr. Paul Robbins]

Me.

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[Dr. Paul Robbins]

Let's go, grandpa. Wait, you did? Yep, on Carvana.

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[Dr. Paul Robbins]

You don't say.

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[Dr. Paul Robbins]

Wow.

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Ah, forget about it.

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Until Carvana makes one, I'm not interested.

[Dr. Samantha Amin]

Car selling made easy on Carvana. Pick up these mantly. Longevity seems to be the latest rebrand for anti aging. Something that as a woman I've been pressured to think about from way too young an age. While it used to be about dying gray hairs, now botox fillers and avoiding a different food every day, those are all the latest attempts in staying young for longer. And I think it's great to optimize our health and get to spend more years with a high quality of life. But with the conflicting advice and self experiments by billionaires, I wanted to talk to an actual expert on the biology of aging to learn more about what we actually know so far so we can better sniff out the hype. We're chatting with Dr. Paul Robbins, a professor and co director of the Masonic Institute on the biology of aging and metabolism at the University of Minnesota who also has several clinical trials related to aging based on his discoveries. Welcome to the show, Paul.

[Dr. Paul Robbins]

Great, thanks for having me, Sam. Very pleased to be here.

[Dr. Samantha Amin]

Thrilled to talk to you about this very hot topic that we see everywhere. I am no more than three scrolls away from something, some sort of hype about longevity. So very relevant to our everyday lives. I think a lot of people know what aging looks like. We depending on our age may start to feel some of its effects. But on a cellular level, what is aging actually?

[Dr. Paul Robbins]

Yeah, you know, it's actually, it sounds like a very simple question, but it's very complicated. There was a paper published where somebody asked 100 ag researchers what is aging? We got 100 different answers. So the definition that I use is really the loss of the ability of tissues to repair itself with time. So as we age, our tissues start to lose the ability to repair the damage that occurs and eventually that damage catches up with us. And we go to this period of rapid decline and eventually mortality. But there are many different definitions, including when you look in the mirror, you know what aging looks like. But at the molecular level, it's even more complicated. So what the field has done is broken out aging into what they call the hallmarks of aging. So these are things that can go wrong in the cell over time with aging. And these include things like loss of stem cell function. Mitochondria, which are the powerhouses of the cells, start to become dysfunctional, there's an increase in reactive oxygen species, there's dn genome is affected. So all of these things contribute to driving aging and loss of the ability of a tissue or an organism to repair itself over time.

[Dr. Samantha Amin]

How do animals who don't seem to age, like certain jellyfish, Hydra, naked mole rats, lobsters, do you look to those to kind of inform an understanding of aging, or are we very focused on mammalian or human biology?

[Dr. Paul Robbins]

Well, I think you gave a lot of examples, and I would argue they don't all live forever. Hydra and others have been shown that least live for an extended period of time, although predators eventually take them out. Naked mole rats probably have a finite lifespan. It's just not something we've defined in the laboratory. But they do age. And it's just intriguing that some organisms, even within the species. So I'll use the example of bats, that's a talk I just heard recently. But some bats live two years and some live 50 years. And the question is, why does a species that looks similar among the different strains, why does one live much longer than another? Another example would be sea urchins. There are sea urchins you might eat at a nice restaurant in Japan that are hundreds of years old as compared to others that live only one to two years. And so why does something that really looks the same have this huge difference in lifespan? And it's an intriguing question. And so we're looking at different organisms to know why one may live much longer than. There was a lot of publicity just recently about a study in the bowhead whale, which lives at least 211 years, because they found a harpoon in one that was 211 years old. They probably live longer, but they identify some pathways in the boed whale that may contribute to longevity. Studying different species is, I think, a very fruitful area in the aging research space, hasn't answered all the questions, but it does provide insight into changes that can allow one organism live 200 years and other women live two years.

[Dr. Samantha Amin]

You mentioned different Organisms within the same species live for different lengths of time. And that's kind of also true for humans. And so I know you've done some studies in centenarians, people who have lived to 100 or more. I'm curious, are there common genetic or even lifestyle characteristics for people who reach that age or beyond? What's the constraint in humans?

[Dr. Paul Robbins]

Well, it's a great question. You know, the data, which has been maybe slightly controversial, but the data suggests that the maximum lifespan in humans is around 115 years of age at this point. There may be one or two examples living a little bit older, although there have been questions about their birth certificates, if they're really that old. So that's their maximum lifespan. And some people have a genetic or their genetic makeup seems to allow them to live longer. They seem to be more resilient, their immune function's better. They don't have these hallmarks of aging progressing at the same rate as in non centenarians. But there's not necessarily a lifestyle choice. I mean, obviously a Mediterranean diet has been at least linked to longevity. But many of these centenarians, they smoke, they drink, they do everything that we're not supposed to be doing, but yet they live to be 105 years old, as are their sister, brother, you know, other relatives showing there's a genetic component. So, you know, but not all of us have centenarians in our family. And so many of us are not going to make it to 100 unless we develop ways to intervene either with lifestyle choices or by developing drugs that may target some of these pathways of aging.

[Dr. Samantha Amin]

And what do we understand about why it's, let's say 115 years? Like is it just that cells have accumulated too much damage and those other hallmarks you described, that they can no longer function for everyday activities?

[Dr. Paul Robbins]

Yeah, and I think that's the current concept. Although what happens with you, you're still very young, so you don't have to worry about this yet. But you know, some people, maybe their mitochondria that start to show defects, other people may be losing stem cell function, other people may have more DNA damage which may lead to cancer. You know, what drives aging in one person may not be identical to another because of their genetic makeup and their environment, the food they've eaten, what's called now kind of a buzzwords, the exposome, what are you exposed to in your environment that may contribute to either you living healthier or not? And these all contribute to our lifespan. But when it comes to centenarians, there's clearly a genetic component. It's not all genetics, but it's clearly a genetic component. And if we can identify those genetic change and try to mimic them with other therapeutic approaches, such as find a drug that mimics the effect of that centenarian variant, I think will help all of us live a little bit longer. Maybe they're not all going to be centenarians, but will help us all live a little bit longer and healthier, which is really the goal. The goal is not to keep us alive for longer. The goal is to keep us alive healthier because we don't want to live longer in a nursing home.

[Dr. Samantha Amin]

I think it's a good distinction that optimizing quality of life is different than optimizing length of life outright.

[Dr. Paul Robbins]

And a lot of people have the kind of the. I think the misconception that those of us in aging research are all focused on living longer. Living longer may be a byproduct of living healthier. And so we'll take it. But what you want to do is compress that period of morbidity. There's that period when everything starts to fail and that leads to people going to nursing homes. You like to compress that so you don't have as much time. Being sick with multiple diseases, it's a very rapid decline at the end when you're hopefully 100 years old or 105 and you can die on the golf course of a heart attack or such. But that's kind of the goal.

[Dr. Samantha Amin]

Is that the goal?

[Dr. Paul Robbins]

I'm not a golfer, but for some people it would be. Maybe it's a tennis court or some other activity, but yes.

[Dr. Samantha Amin]

Yeah, sleep on a beach would be nice. Exactly. So when it comes to genetics, are there certain pathways that we know are critical and high level? What are they doing in.

[Dr. Paul Robbins]

Right. So I think both the genetics of centenarians, but going all the way down kind of the model organism scale. I mean, studies done in worms, which C. Elegans is the model system used in the lab, these worms live two weeks, but we can manipulate them or treat them with certain drugs that will extend their lifespan and health span. And the pathways we've identified in worms are actually conserved in humans. They're just more complicated. We have more genes, more contributors to these pathways. But these same pathways seem to be popping up across all species. So we have a good idea where to start. And there are drugs being developed that can mimic the changes we think which will allow us to live healthier longer. And clinical trials have started. But these are pathways that May regulate your blood sugar levels. It seems like many things that treat diabetes actually seem to allow model organisms to live longer. I think there's a number of drugs, such as metformin, SGLT2 inhibitors, all across these species. They've been shown to have positive effects on lifespan. So I think these pathways, we're identifying them and we're now identifying interventions which can mimic the effects of what we're seeing in centenarians or in long lived species. So I think the future is very, we're very optimistic about the ability to keep people healthier for longer. It just doesn't happen overnight. It's going to take a lot of clinical studies, not just phase one, phase two, but large scale studies, because it may vary. We have to identify the people that will respond to a certain intervention and not another. So I think there's going to be a lot of research, a lot of clinical studies that are needed. But I think eventually we'll identify approaches that will mimic what we're seeing in these different model organisms.

[Dr. Samantha Amin]

You're part of the team that was the first to identify xenotherapeutic compounds, these drugs that can slow down aging or increase lifespan, Even if that's not their explicit or sole goal. Some work by killing these aging cells or senescent cells, and others target cell signaling pathways involved in aging. Can you tell us a little bit more about that concept of these xenotherapeutics?

[Dr. Paul Robbins]

Right, so senescence or cellular senescence is one of the hallmarks of aging. And that's what happens. This process of cellular senescence is what happens to a cell when it acquires damage or stress. So an example of stress to a cell would be if you were taking chemotherapy to kill a tumor. Many of these cause DNA damage that stress on the cell can drive into a state of cel. And we've evolved this system thought to actually prevent cancer. So another way to induce senescence is if you start, the cell starts to divide in an uncontrolled manner. This pathway of senescence kicks on, the cell stops growing and it starts to release inflammatory factors that tell the immune system, this cell is damaged. This cell is precancerous. Come clear it and your immune system comes in and kills that cell. So when you're young, like you are Sam, your immune, clearing these damaged cells very efficiently as you age and you start to accumulate more damage, your immune system is not as effective. These cells aren't cleared. And so they're releasing inflammatory factors that tell the immune system come clear them. The immune system is not so they accumulate, they drive chronic inflammation. That inflammation can affect immune responses, it can affect stem cell function, it can affect a variety of other hallmarks of aging. So it's not the end rid of these senescent cells, but we've shown, at least in model organisms, that getting rid of them extends health span. It doesn't necessarily extend lifespan dramatically, but it seems to extend the period of healthy aging. So we've developed drugs, as you refer to, which we call senotherapeutics that either will kill a senescent cell or suppress the inflammation driven by the senescent cell. And those we call senomorphics. So we have senolytics that kill senescent cells, senomorphics that suppress it. And. But what's interesting is these drugs, many of them are anti cancer drugs because these senescent cells have many of the same hallmarks of a precancerous cell. So many things that will kill a tumor cell seem to be able to kill these senescent cells. And clinical trials have started, and so there are some positive results coming out. But what we realize is we have to know who has more senescent cells than another. So when we go back and look at some of the readouts from the clinical trials, we realize that those that have higher senescent cell burd. So in future trials, we can hopefully identify that subset that the third or the half of the population that should be getting senolytics, those are the ones that are enrolled in the trials. And those that do not have an increase in senescence, but may have mitochondrial dysfunction, may have other things going wrong. They would need a different class of drugs to suppress those changes. So we are very excited about the future of senotherapeutics, but it's going to require a lot of testing and identifying the right population that needs senotherapeutics. If you don't have an increase in senescent cell burden, senotherapeutics will have no benefit. So we have to identify that right subset.

[Dr. Samantha Amin]

And then, I mean, that's almost surprising to me that just targeting those senescent cells could have this overall bigger effect, like you're just removing, I guess, the product. But I guess because they're so central in this whole cascade, it slows things down a bit. Is that the logic behind it?

[Dr. Paul Robbins]

Right. So senescent cells with this inflammatory, all the inflammatory factors they release, what it does is it affects adjacent cells. So the example I use when talking to the lay public is I show a bushel of apples and you have one bad apple in the bushel and it releases things, non inflammatory factors, but other factors that lead to kind of all the other apples in the bushel becoming bad. And that's the way if you look at the liver in an aging person with senescent cells, we see senes spreading to adjacent cells. So one or two or three bad cells in an area can lead to hundreds of bad cells, which lead to thousands. And that can lead to loss of ability of a tissue to function appropriately, whether it's the brain or liver or kidney or muscle, et cetera. So this spreads. It's not the only thing that goes wrong with aging, but it's one of the things. And in animal models, clearing these cells has a tremendous benefit. It. But we'll have to see in humans, we'll have to see, like I said, we have to identify the right patient population. These trials haven't been done for aging, they've been done for diseases. So they're trials for Alzheimer's, they're trials for diabetes. There was a trial for just muscle skeletal health, but there are trials for a variety of different conditions. Because if you're doing aging, that takes years to see changes. But here they can see, you know, responses much faster. At least that's the thought. There was a trial done for macular degeneration in the eye. So they actually injected in the back of the eye these sendotherapeutics and the trial just missed its primary endpoint. But if you look at those that have the most senescence in the eye, they responded the best. So when they redo the trial, I think it's going to be very significant. So we're learning. If you look at what's been done in cancer or in other areas, it's took decades to really develop these drugs that are used in cancer studies and identify which patients to be enrolled in those studies. So, you know, we're just scratching the surface, but very optimistic about the future.

[Dr. Samantha Amin]

Now longevity hacking is a very hot topic. There's some advice that seems reasonable, like getting enough sleep, eating a balanced diet, getting regular exercise, wearing sunscreen. And there are things that are a little more creative. Daily saunas, avoiding seed oils, intermittent fasting, eating lots of beans, ultra processed foods. The list goes on. And it gets worse or more fringe, perhaps I should say what's actually, what actually has scientific evidence behind it. What are the things that you see that are, are like big no no's or big yes?

[Dr. Paul Robbins]

Well, I, I can't say. I, I can't say they're big no no's out there. The question is whether does the supplements you're taking or your lifestyle choice actually work? And I think the data might suggest that for one person it does work. For another person because of just their whole exposome, their genetics, it may not work. So that's what we don't know. If you did intermittent fasting, you may not see the benefit. For example, if you take 100 different strains of mice, some live longer on caloric restriction, other ones do not. So the genetic makeup really influences how you respond to these. So that's what we don't know. So people are trying a variety of things. I do think some of the supplements that people are using do have benefits. The question is we just don't know for which person is going to respond to those supplements. I mean, we have shown there are supplements that will kill senescent cells, there's supplements that will improve stress resistance, there's supplements which will have other pos effects. We just don't know which person will respond most effectively to these supplements. So people are taking a handful of supplements every day. It's hard to say is that really providing a benefit to them or not. Once we can sort out who really needs what supplement or drug, then we can see big changes. And in animal model systems we see that supplements can cancel each other out. Don't know if this is true in humans, but it may be one supplement suppresses a pathway that's the target for another supplement. So it's not that the more you take, you see additive effects. We actually have shown in model organisms that some of these have not necessarily adverse effects, but they don't provide the benefit because they cancel each other out. So what supplements, how often, how much? These are things we don't know know. And that's the reason I don't advise people to take handfuls of supplements because we just don't know. So I think we're just scratching the surface. In the next decade is going to be an amazing time in aging research. There's going to be a lot of supplements, new FDA approved drugs coming on the market that will have positive effects on your health.

[Dr. Samantha Amin]

That's fantastic. That's Dr. Paul Robbins, professor and co director of the Masonic Institute on the Biology of Aging and Metabolism at the University of Minnesota. Thank you so much, Paul for being on our show.

[Dr. Paul Robbins]

Thanks Sam. It was a pleasure talking with you.

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[Dr. Samantha Amin]

Stand clear of the closing doors please. Stuck on your commute again. Bad wifi, no signal, nothing to do. Time to make your ride a lot more fun with Royal Kingdom. It's a puzzle game that's relaxing, challenging and works perfectly offline. With no ads and amazing graphics. Every level feels fresh and satisfying. Each round only takes a few minutes. Ideal for a daily commute or wherever you have a little bit of time.

[Dr. Paul Robbins]

Time.

[Dr. Samantha Amin]

So download Royal Kingdom now on Google Play or App Store. Cellular Aging. It's that process where our cells slowly lose their normal functions, which can take a toll on tissue health and how well our bodies perform. But what if I told you that there's a way for a cell to recharge its aging parts using the body's own built in tools? Well, a team of researchers from Texas A and M University may have found a new method to do just that. At the heart of this research are the mitochondria. They're the kidney bean shaped structures often called the powerhouses of our cells because they turn energy from our food into fuel that cells can actually use. The fuel is called ATP and it powers everything in our bodies from muscle contractions to digestion and even brain cells firing. These tiny structures are so important for energy production that a lot of diseases like Alzheimer's and heart diseases are associated with them not working as well as Same thing for aging. As we get older or deal with illnesses or take treatments like chemotherapy, our body takes a toll and the number of mitochondria can drop. That makes it tough for our cells to do their jobs. Enter this new research published in the Proceedings of the National Academy of Sciences. The researchers developed a new way to swap out worn out mitochondria with fresh ones to keep our cells energized and functioning at their best. The team's method takes advantage of the fact that some stem cells can naturally transfer their mitochondria. But it's usually pretty inefficient and doesn't necessarily happen when and where you'd want it to. So they mix those stem cells with some pretty cool tiny flower shaped particles called nanoflowers. Think of these nanoflowers as little energy boosters. They turn the stem cells into mitochondria factories, making twice the usual amount of mitochondria. That makes them much faster at replacing worn out or aging mitochondria in nearby cells. It's like giving aging cells a second chance at youth. Dr. Gaharwar led the study. He said in a press release that it's like training healthy cells to share their spare batteries with those that are running low. The nanoflower boosted stem cells can transfer two to four times more mitochondria than untreated ones. This energy handoff helps revive damaged cells, allowing them to kick into gear and even resist resist cell death even when a chemotherapy drug was added to the dish. Given how essential mitochondria are for our cells, there's a big need for ways to improve their function, whether it's in diseases or aging. Other methods to replace. Damaged mitochondria are out there, but they typically come with some drawbacks, like needing frequent doses. Whereas these nanoflowers stick around inside the stem cells, giving mitochondrial production and replacement a longer lasting boost, potentially requiring just monthly administration. There's also potential for things beyond aging too. These stem cells are really mobile and so they're good at getting to a bunch of different tissues, meaning that this approach could also apply to illnesses spanning from muscular dystrophy to heart disease. For Warner Bros. Discovery, Curiosity Weekly is produced by the team at Wheelhouse DNA. The senior producer and editorial creator correspondent is Teresa Carey. Our producer is Kiara Noni, our audio engineer is Nick Kimi and head of Production for Wheelhouse DNA is Cassie Berman. And I'm Dr. Samantha Yuin. Thanks for listening.

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[Capital One Announcer]

With no fees or minimums on checking accounts, it's no wonder the Capital One bank guy is so passionate about banking with Capital One. If he were here, he wouldn't just tell you about no fees or minimums. He'd also talk about how most Capital One cafes are open seven days a week to assist with your banking needs. Yep, even on weekends, it's pretty much all he talks about. In a good way. What's in your wallet? Terms apply. See capitalone.com bank capital1na member FDIC.

[Dr. Paul Robbins]

Hey Sal.

[Dr. Samantha Amin]

Hank.

[Dr. Paul Robbins]

What's going on? We haven't worked a case in years. I just bought my car at Carvana and it was so easy.

[Dr. Samantha Amin]

Too easy.

[Dr. Paul Robbins]

Think something's up? You tell me. They got thousands of options, found a.

[Dr. Samantha Amin]

Great car at a great price, and.

[Dr. Paul Robbins]

It got delivered the next day. It sounds like Carvana just makes it easy to buy your car, Hank. Yeah, you're right. Case closed.

[Dr. Samantha Amin]

Buy your car today on Carvana. Delivery fees may apply. Save over $200 when you book weekly. Stays with VRBA this winter. If you need to work, why not work from a chalet? If you haven't seen your college besties since, well, college. You need a week to fully catch up in a snowy cabin, and if you have to stay in a remote place with your in laws, you should save over $200 a week. That's the least we can do. So you might as well start digging out the long johns because saving over $200 on a week long snowcation rental is in the cards book [e-mail].