Restrict nutrient access, remove a couple of genes and one lives 5-fold longer than normal. This is not science fiction, this is the cutting edge science. But, of course, I am not talking about humans here. The research was done on a unicellular organism, yeast. In the paper published this month in Cell the authors state that they have created conditions that "causes one of the longest chronological lifespan extensions reported for any organism".

Interestingly, the gene, called Sir2, that the scientists have removed to create the record longevity in yeast, is the same gene that was previously shown to extend longevity if its activity is INCREASED! Yes, Sir2, when overactivated, has been known to cause a longer life span in different organisms, from yeast to flies. How to reconcile these two opposite observations? It appears that Sir2 can play different roles in different cells. In the cells that are actively dividing extra Sir2 activity extends their capacity to divide. While in the cells that have stopped dividing, extra Sir2 activity appears to be harmful.

If Sir2 can have two opposite effects on life span depending on the cell state, which of the roles could be critical for human longevity? The most likely answer is "both". Human body is made of billions of cells. Some of them are capable of dividing, the others are not, but we need them both. Therefore, provided that the human Sir2 similarly has dual function like its counterpart from yeast, simply turning Sir2 on or off may not be enough to extend our life span. If too much Sir2 is not good for dividing cells, while too little is not good for the post-mitotic ones, could it be that we have just the right amount?

Reference:
Cell. 2005 Nov 18;123(4):655-67.
Sir2 blocks extreme life-span extension.
Fabrizio P, Gattazzo C, Battistella L, Wei M, Cheng C, McGrew K, Longo VD.