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

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.

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."

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.

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.

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.

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).

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.

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…”

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.”

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.”

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.”

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

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.

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

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