Aging is an intrinsic part of life. But it may turn out to be just a historical accident on our evolutionary path.
This is the story of how aging came to be, and why it doesn’t have to be this way.
This is the story of the beginning of the end of aging.
I’m Dr. David Benaron, a Harvard and MIT trained physician scientist, and former professor at Stanford. And I’ll be your narrator as we explore Aging Different.
Age Different podcast 1: The end of aging.
People had thought of aging as a slow decline, with damage accumulated over a lifetime. Dolly, a 1996 cloned sheep, shocked scientists by showing us this wasn’t the case at all. Before Dolly people believed that DNA took in more and more damage over time, and that's how and why we inevitably grow old. But Dolly was made from older skin cells, and her old cell DNA was in fact actually perfect. It begged revisiting the question: Why do we age?
It took us a while to get started studying aging. For a long time, the study of life extension had a very bad rep. The public sees the subject as merely modern snake oil, a revisiting of Ponce de Leon and his ill-advised quest for immortality. Doctors are no different. Even today, the US FDA only approves treatments for diseases, and since everyone gets old the FDA doesn't consider age a disease. So there was no product research that got funded, no start ups that addressed it, and no marketed treatments. Only con men and carnival barkers claimed cures for growing old.
But while Dolly got us thinking, but it was the human genome project that kicked this into high gear. By the year 2000 DNA was cheaply sequenced, so labs searched for magic genes that let you live longer, matching lifespan to gene-set. Surprisingly, the answer wasn't there, inherited genes contributed less than 1/3 to your lifespan. The rest? It was set by your lifestyle.
But how does lifestyle influence aging, and how can it even do that?
I’m Dr. David Benaron. Join me for the next podcast in the Age Different series: the Basis of Aging.
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