Jeanne Calment of France died in 1997 at the age of 122 years and 164 days. Guinness World Records verified it, and nobody has come close since. For nearly three decades, many researchers have treated her as something near the ceiling for the species.
A new modeling study argues the ceiling could sit higher, and it names an unlikely culprit for what finally stops us. Researchers at the Skolkovo Institute of Science and Technology in Russia, working with co-authors from the AI Research Institute, posed a blunt question: if every reversible driver of aging were removed, what would still kill a person? Their answer, published in npj Aging, is somatic mutations. These are random copying errors in DNA that arise in body cells after conception. They are not inherited, but they pile up over a lifetime.
One mechanism, switched on alone
The team built a multistage model that turns aging mechanisms on one at a time. They left only somatic mutations running and measured how long a population would survive.
Organs fared very differently. The liver replaces worn-out cells, so in the model it keeps working for thousands of years. Neurons and heart muscle cells cannot be replaced. For those cells, mutations cut median lifespan from a theoretical no-aging baseline of 1,759 years to 156 years. Combine all the organs and the model lands on a median lifespan of 146 to 194 years, about twice what people reach today.
The authors are careful about what that number means. The work is computational, not experimental, and it does not suggest anyone is near such ages. Lead author Dmitrii Kriukov, a computational biologist at Skoltech and the AI Research Institute, put it this way: “Our study shows that somatic mutations contribute significantly to aging, but they cannot by themselves explain the observed mortality.”
Where the damage falls
Dr. Jordan Weiss of NYU Grossman School of Medicine told Newsweek that dementia and heart failure “fall heavily on precisely the tissues that cannot regenerate.” Worldwide, 55.2 million people were living with dementia in 2019, according to data published in the Journal of the American Heart Association, and the estimate for 2030 is 78 million.
Not everyone thinks mutations are the place to aim. Michael Leone, also of NYU Grossman, called somatic mutations “likely among the highest-hanging fruit in targetable geroscience.” In his view, lower-hanging targets, “such as inhibiting mTOR with rapamycin or clearing senescent cells, are far more logical interventions to prioritize.”
The Skoltech group says this is only a first step. Next they plan to add mitochondrial dysfunction, loss of proteostasis, telomere shortening and epigenetic changes to the model. Consult your doctor for medical advice.
