

Genes and Longevity
Los Angeleño George Smith celebrates his 104th birthday in 2002.
Los Angeleño George Smith celebrates his 104th birthday in 2002.
David McNew/Getty Images


­The hypotheses from the Harvard and MIT studies aren't the only theories floating around the aging research field that attempt to explain this type of longevity. Nor is SIRT1 the only candidate for what will surely be called the Ponce de Leon gene. In fact, studies have concluded that other genes may be responsible for preternatural longevity among humans. This is not to say that geneticists and biologists have abandoned the decades-old findings concerning calorie-restricted diets. Quite the contrary -- they accept as fact that near-starvation leads to longevity. However, it remains a mystery exactly how cellular processes and the genes responsible for regulating them manage to continue despite this starvation.

In 2007, the gene FOXO3A was shown to have a proven effect on worms' life spans. Researchers turned the gene on and off by adding compounds to some of the worms' food that targeted and shut down other specific genes in their bodies. When the gene was switched on, the worms lived longer. By 2009, FOXO3A had begun to establish itself as the de facto gene for creating longevity in humans after studies emerged that showed elderly Japanese people (Japan has the highest per capita ration of centenarians of any nation) shared active FOXO3A genes [source: Okinawa Centenarian Study]. Active FOXO3A genes have also been found in elderly Germans, suggesting that the gene is not racially specific in humans.

Still another group of researchers believe that the key to longevity lies in the gene responsible for regulating insulin production. After studying a population of centenarian Ashkenazi Jews, researchers at the Albert Einstein College of Medicine in New York concluded in 2008 that a mutation on the insulin-like growth factor (IGF-1) gene is responsible for very long life in humans. The group found that women in the population who were centenarians or the children of centenarians were more likely to feature this genetic mutation, which impedes the production of insulin. This could explain a lack of cancer in centenarians, since insulin is related to growth hormones, which can aid in the development of cancerous cells.

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