I had noticed that yeast cells fed with lower amounts of sugar were not just living longer, but their rDNA was exceptionally compact — significantly … - David A. Sinclair

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I had noticed that yeast cells fed with lower amounts of sugar were not just living longer, but their rDNA was exceptionally compact — significantly delaying the inevitable ERC accumulation, catastrophic numbers of DNA breaks, nucleolar explosion, sterility, and death. Why was that happening? THE

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Alternative Names: David Andrew Sinclair Dr. David Sinclair David A Sinclair David Sinclair

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Here's the important point: there are plenty of stressors that will activate longevity genes without damaging the cell, including certain types of exercise, intermittent fasting, low-protein diets, and exposure to hot and cold temperatures (I discuss this in chapter 4). That's called hormesis.28 Hormesis is generally good for organisms, especially when it can be induced without causing any lasting damage. When hormesis happens, all is well. And, in fact, all is better than well, because the little bit of stress that occurs when the genes are activated prompts the rest of the system to hunker down, to conserve, to survive a little longer. That's the start of longevity.

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DELETING THE ZOMBIE SENESCENT CELLS IN OLD TISSUES. Thanks to the primordial survival circuit we've inherited from our ancestors, our cells eventually lose their identities and cease to divide, in some cases sitting in our tissues for decades. Zombie cells secrete factors that accelerate cancer, inflammation, and help turn other cells into zombies. Senescent cells are hard to reverse aging in, so the best thing to do is to kill them off. Drugs called senolytics are in development to do just that, and they could rapidly rejuvenate us.

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