Lifespan: The Revolutionary Science of Why We Age—and Why We Don't Have To

by David A. Sinclair

he found two chemicals that, rather than inhibiting SIRT1, stimulated or “activated” it, making it work ten times as fast. That was a serendipitous discovery, not only because he was expecting to find inhibitors but because activators are very rare in nature. They are so rare, in fact, that most drug companies don’t even bother following up when one is discovered, figuring it must be a mistake. The first SIRT1-activating compound, or STAC, was a polyphenol called fisetin, which helps gives plants such as strawberries and persimmons their color and is now known to also kill senescent cells. The second was a molecule called butein, which can be found in numerous flowering plants as well as a toxic plant known as the Chinese lacquer tree. Both had a significant effect on SIRT1, though not the sort of pedal-to-themetal reaction that might make them ripe for further research.

The three main pathways: mtor, ampk and sirt