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cover of episode #333 ‒ Longevity roundtable — the science of aging, geroprotective molecules, lifestyle interventions, challenges in research, and more | Steven Austad, Matt Kaeberlein, Richard Miller

#333 ‒ Longevity roundtable — the science of aging, geroprotective molecules, lifestyle interventions, challenges in research, and more | Steven Austad, Matt Kaeberlein, Richard Miller

2025/1/27
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Steven Austad: 我对长寿研究的公众关注度激增感到惊讶,因为我们过去一直试图避免使用“长寿”这个词,因为它让人联想到延长虚弱老年人的寿命,而不是延长健康寿命。现在公众关注度提高,可能是因为特定年龄段的人开始思考自己的长寿问题,以及新一代科技企业家认为这是可以让他们健康生活更长时间的问题。 我们过去一直专注于健康寿命,而不是长寿本身,因为我们担心人们会误解长寿的含义。 现在,情况有所改变,一部分原因是特定年龄段的人开始关注自己的长寿问题,另一部分原因是新一代科技企业家认为长寿研究可以帮助他们健康生活更长时间。 总的来说,我对长寿研究的公众关注度激增感到惊讶,但这可能是因为特定年龄段的人开始思考自己的长寿问题,以及新一代科技企业家认为这是可以让他们健康生活更长时间的问题。 Richard Miller: 公众对长寿研究的兴趣激增,一部分原因是90年代的科学发现表明延长健康寿命是可能的,近20年来,有证据表明至少在小鼠身上可以通过药物实现。另一部分原因是,一些公司通过销售未经验证或无效的产品来牟利,利用公众对长寿的渴望。此外,长期以来人们错误地认为健康寿命和寿命是此消彼长的,但实际上延长寿命的干预措施通常是通过延缓疾病来实现的。 我认为公众对长寿的兴趣由来已久,但直到90年代的科学发现才证明延长健康寿命是可能的。近20年来,我们发现至少在小鼠身上可以通过药物延长寿命。这自然会让人们猜测,是否可以通过药物来延长人类的健康寿命。 然而,也有一些公司利用公众对长寿的渴望,销售未经验证或无效的产品来牟利。 此外,长期以来存在一个误解,即健康寿命和寿命是此消彼长的。但实际上,延长寿命的干预措施通常是通过延缓疾病来实现的。 Matt Kaeberlein: 长寿研究进入主流,是科学进步、大众媒体宣传(包括一些不够严谨的网红的影响)以及科技企业家参与的共同作用结果。 我认为长寿研究进入主流是多种因素共同作用的结果,包括科学的进步、大众媒体的宣传以及科技企业家的参与。 科学的进步使得更多人相信我们可以调节衰老的生物学过程。大众媒体的宣传,包括一些网红的影响,也促进了人们对生物衰老概念的了解。科技企业家的参与也为长寿研究带来了更多的资金和资源。 然而,长寿研究进入主流的速度仍然很慢,这可能是因为科学研究本身的进展速度以及这些概念渗透到公众领域的速度都比较慢。

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In this special episode of The Drive, Peter introduces a brand-new roundtable format. Joined by three renowned experts in longevity science—Steven Austad, Richard Miller, and Matt Kaeberlein—the group explores the rapidly evolving field of geroscience. Together, they dive deep into topics like the relationship between healthspan and lifespan, evaluating interventions like rapamycin and senolytics, the role of epigenetic changes in aging, and whether GLP-1 receptor agonists hold geroprotective potential. They also tackle major challenges in funding and public acceptance of longevity research including how geroprotective interventions might be tested in humans. Packed with nuanced debate, humor, and groundbreaking insights, this episode is a must-listen for anyone fascinated by the science of aging.

We discuss:

  • The recent rise in public interest in longevity, misconceptions, and the link between healthspan and lifespan [3:45];
  • Redefining healthspan, the US healthcare paradox, and separating longevity science from commercial hype [12:30];
  • The need to redirect medical research from disease-specific models to aging-focused approaches [21:30];
  • Proactive healthcare: rethinking health, disease, and the role of aging [30:00];
  • Biologic age versus chronologic age, and the limitations and potential of epigenetic clocks [35:00];
  • The utility and drawbacks of the “hallmarks of aging” as a framework for research and funding [49:30];
  • The role of epigenetic changes in aging and the challenges of proving causality [56:45];
  • The translational challenges of moving aging research from preclinical studies to human applications [1:03:45];
  • Distinguishing between a biomarker of aging and aging rate indicators [1:17:15];
  • The difficulties of translating longevity research in mice to humans, and the difficulties of testing interventions in humans [1:21:15];
  • Exercise, aging, and healthspan: does exercise slow aging? [1:35:45];
  • Are GLP-1 receptor agonists geroprotective beyond caloric restriction effects? [1:41:00];
  • The role of senescent cells in aging, challenges with reproducibility in studies, and differing views on the value of current research approaches [1:46:15];
  • How funding challenges and leadership in NIH and other institutes impact the advancement of aging-related research [2:00:15];
  • Metformin: geroprotective potential, mechanisms, and unanswered questions [2:02:30];
  • Canagliflozin and rapamycin as geroprotective molecules: mechanisms, dosing strategies, and longevity potential [2:10:45];
  • Resveratrol and NAD precursors—a lack of evidence for anti-aging effects [2:22:45];
  • The potential of parabiosis and plasmapheresis to slow aging, the challenges in translating mouse studies to humans, and possible design for human studies [2:29:45]; and
  • More.

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