Why Getting Old Isn’t What it Used to Be

Nautilus

Biologist Eric Verdin considers aging a disease.

His research group famously discovered several enzymes, including sirtuins, that play an important role in how our mitochondria—the powerhouses of our cells—age. His studies in mice have shown that the stress caused by calorie restriction activates sirtuins, increasing mitochondrial activity and slowing aging. In other words, in the lab, calorie restriction in mice allows them to live longer. His work has inspired many mitochondrial hacks—diets, supplements, and episodic fasting plans—but there is not yet evidence that these findings translate to humans.

Last year, Verdin was appointed President and Chief Executive Officer of the Buck Institute for Research on Aging, the largest independent research institute devoted to aging research. The Buck, founded in 1999 by Marin County philanthropists Leonard and Beryl Hamilton Buck, includes more than 250 researchers working across disciplines to slow aging. Verdin, originally trained as a physician in his native Belgium, is eager to translate findings from the lab work done over the past 20 years in worms and mice to humans. “Aging without illness is our overarching goal!” he wrote when he began at the Buck.

In a recent Nautilus interview, Verdin was optimistic about the future. He thinks we’ll continue to live longer and age better. But to live better longer, he says, requires research but also rethinking doctors’ visits.

Why is there so much energy and excitement surrounding aging research right now?

Something happened in the ’90s. There were three groups that did an experiment that was really unexplained. Those groups, Tom Johnson, at the University of Colorado, Boulder, he actually was the first one; Lenny Guarente [at MIT]; and Sue [Cynthia] Kenyon who was at the University of California, San Francisco, all identified unique mutations that could actually increase lifespan. At that time, it was a quite astute observation in the way they completely turned upside down our conception of what aging was.

The whole idea of aging was sort of an entropy problem where everything falls apart like your car rusting, but what these papers showed is that you can make a single change in one whole organism like C. elegans with a 100 million base pair [genome], and you can double its lifespan. Caenorhabditis elegans is a worm that’s often used as a model organism. That by itself was mindboggling for a lot of people and suggested there might be pathways to regulate aging, and if there are pathways that means there are proteins, and that means you can eventually develop drugs.

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