Why interventions such as calorie restriction and rapamycin slow the aging process: slowing cellular noise

Extract from the video at The Sheekey Science Show

What if aging weren’t programmed, but simply the result of random cellular noise? In this interview, Dr. David Meyer, an aging researcher and bioinformatician at the University of Cologne, reveals why our best “aging clocks” actually measure the accumulation of random changes in our cells.
We delve into:

  • How DNA methylation and transcriptomic clocks actually work
  • The DREAM complex and its role as a master regulator of DNA repair
  • Why interventions like calorie restriction and rapamycin slow the aging process
  • Groundbreaking findings on cellular reprogramming and the potential for rejuvenation
  • The future of aging research and what scientists might be overlooking.

Timestamps:
0:00 – Introduction
1:30 – What are aging clocks? How do they work and why are they important?
7:00 – Do aging clocks measure causation or correlation?
13:30 – Stochastic aging: Noise accumulation vs. programmed aging
17:30 – The DREAM complex: DNA repair, lifespan, and master regulators
24:00 – Interventions: Calorie restriction, rapamycin, and slowing cellular noise
29:00 – Rejuvenation: How cellular reprogramming can reset biological age
36:00 – The future of aging research: What’s next and what’s being overlooked?

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