For decades, the standard recipe for a long life was simple: eat your greens, hit the gym, and skip the cigarettes. But what if the most influential factor in your longevity was decided before you were even born? A groundbreaking study is shifting the conversation from the treadmill to the double helix, suggesting that our DNA may play a much larger role in our expiration date than we ever imagined.
Researchers reached this conclusion by studying twins and separating deaths caused by external factors like accidents or infections, from deaths tied to internal aging, such as chronic disease or natural health decline.
By doing this, they said they were able to get a clearer picture of the relationship between genetics and longevity.
“The number that we got is not out of nowhere,” lead author Ben Shenhar, who studies aging at the Weizmann Institute of Science in Israel, told NBC News. “If you look at twin studies on pretty much anything in humans, you get this 50 percent. If you look at the heritability of age of onset at menopause, which is an age-related decline, that is also around 50 percent.”
Another expert, Morten Scheibye-Knudsen of the University of Copenhagen, said this approach helped remove what he called “outside noise” to better understand aging.
“We live [a maximum of] 120 years, and a yeast cell lives 13 days, and bowhead whales live 200 years,” Scheibye-Knudsen told NBC News. “So we already know our genes have set a limit to our lifespan, as it is now. I think people should have thought a little bit more about that because it cannot only be our behavior.”
But Dr. Eric Verdin, CEO of the Buck Institute for Research on Aging in California, said some deaths counted as “external” (such as those from infections like COVID) may still be influenced by genetics.
“We know that your genes play an enormous role in how you respond to infection,” Verdin explained.
Even so, Shenhar said his team rechecked the data while accounting for rising health risks with age, and genetics still explained about 50 percent of life expectancy.
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“It’s clear that these people are not just clawing their way to 100,” Shenhar added. “No, they have protective genes that protect against the harms of age.”
So far, only a few genes — FOXO3, APOE and SIRT6 — have been linked to longevity. Verdin said lifespan is likely dictated by many genes working together, not just one.
If genetics explains 55 percent, that leaves 45 percent affected by things like diet, exercise and habits, Shenhar explained.
“The depressing thing about this is that it makes people be fatalistic,” Verdin added. “‘It doesn’t matter what I do. Why should I try to live better and not drink and do sport if it’s determined by genes basically?’ ”
But Shenhar pushed back.
“The message of our paper is not that lifestyle, exercise and diet are not important,” he said. “That is not our message, not at all. Even if your genetics gives you a particular potential or range for what your natural lifespan would be, depending on lifestyle, that might shift slightly one way or another. So it’s still important.”
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