How SIRT1 Works

This sounds like progress in understanding the roots of the longevity and health benefits of calorie restriction and other light stresses on the body:

Cells have evolved a particular response to stay alive in adverse conditions. When a cell starts getting too hot, too hungry or too oxygen-deprived, certain proteins migrate into the nucleus. There, they latch onto sections of DNA and cause heat-shock proteins to be produced. Heat-shock proteins - so named because they were first discovered in cells experiencing high temperatures - cruise around the cell, fixing damaged or improperly folded proteins.


Normally the repair process falls off quickly, because heat-shock proteins inhibit the proteins that grab onto the cell's DNA and summon them in the first place. But Morimoto and his colleagues found that jacking up levels of SIRT1 keeps the protein-repair process going for hours and hours.

So processes, such as calorie restriction, that increase sirtuin levels are improving the performance of repair mechanisms in your cells - assuming you are also undergoing cirumstances that will release heat shock proteins. Calorie restriction will do that nicely.

It occurs to me to wonder to what degree this particular method of improved repair is important in longevity versus others mechanisms, such as autophagy for example, also increased during the practice of calorie restriction.


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