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#036 Judith Campisi, Ph.D. on Cellular Senescence, Mitochondrial Dysfunction, Cancer & Aging
Apr 28, 2017
Dr. Judith Campisi, a leading authority on cellular senescence and a professor at the Buck Institute for Research on Aging, dives into the intricate dance between aging, cancer, and cellular health. She discusses how DNA damage and mitochondrial dysfunction contribute to senescence. The conversation highlights why healthspan is more crucial than lifespan and the rejuvenating effects of prolonged fasting and exercise. Listeners also learn about potential interventions for combating senescence and the importance of NAD+ boosters in promoting longevity.
01:08:20
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Quick takeaways
- Cellular senescence, while a protective mechanism against cancer, contributes to aging-related diseases through chronic inflammation and tissue damage.
- Interventions such as prolonged fasting and regular exercise can effectively reduce senescent cell accumulation and promote overall healthspan.
Deep dives
The Role of Cellular Senescence in Aging and Cancer
Cellular senescence plays a crucial role in both the aging process and the development of cancer, acting as a stress response to cellular damage. As cells accumulate damage over time, they can either die, cease to divide while remaining metabolically active, or become cancerous. The implications of senescence are significant; while it prevents potentially malignant cells from proliferating, the accumulation of senescent cells contributes to various aging-related pathologies and chronic inflammation. This inflammation can lead to further damage to surrounding tissues, creating a feedback loop that exacerbates cellular senescence and age-related diseases.
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