KATHMANDU, July 20: How long can a human being live? A new scientific study suggests that even if most major causes of aging are eliminated, the maximum human lifespan may still be limited to around 156 years due to irreversible DNA damage that accumulates in the body's cells over a lifetime.
According to the researchers, the key limiting factor is somatic mutations—permanent changes and damage to DNA that occur in the body's cells throughout life. Using a mathematical model, the study estimated the theoretical upper limit of the human lifespan if all other major drivers of aging could be controlled.
The research, conducted by scientists at Russia's Skolkovo Institute of Science and Technology (Skoltech) and the Artificial Intelligence Research Institute (AIRI), began with a fundamental question: If future medicine could eliminate all major causes of aging except somatic mutations, how long could humans theoretically live?
Scientists explained that somatic mutations gradually accumulate in the DNA of the body's cells as people age. Somatic cells include all cells in the body except reproductive cells such as sperm and eggs. Because these mutations are permanent, they progressively impair the normal functioning of tissues and organs.
To answer the question, researchers first created a hypothetical model in which humans do not biologically age and the risk of death does not increase over time. They then gradually introduced the effects of somatic mutations, cellular damage and age-related decline in organ function into the model to estimate the maximum possible lifespan.
The findings were published last week in the scientific journal NPJ Aging.
Slowing down aging
The model focused on four vital organs—the brain, heart, liver and lungs. According to the study, organs such as the liver can continually generate new cells, allowing damaged cells to be replaced and reducing the long-term effects of DNA damage. As a result, these organs could theoretically continue functioning for hundreds of years.
The brain and heart, however, present a different challenge.
The study found that neurons in the brain and cardiomyocytes—the muscle cells of the heart—have little or no ability to regenerate throughout life. As DNA damage accumulates in these non-renewable cells, the function of these organs gradually declines, eventually leading to organ failure.
Although previous studies have established that somatic mutations increase with age and damage cells, their precise role in determining the maximum human lifespan had remained unclear.
To better understand this, the researchers developed a mathematical model to quantify their impact. While medical advances may eventually slow or reverse many aspects of aging, current science is still unable to completely repair or reverse DNA damage caused by somatic mutations.
According to the researchers, this irreversible damage may represent one of the ultimate biological limits on human lifespan.
"Non-renewable neurons and heart muscle cells are the primary factors limiting human lifespan," said Evgeny Efimov, co-author of the study, in a statement released alongside the findings.
How did researchers arrive at 156 years?
The researchers first modeled a hypothetical person who does not age biologically and whose risk of death remains constant throughout life. Under those ideal conditions, the model estimated an average lifespan of 1,759 years.
However, once somatic mutations were introduced into the model, the estimated lifespan dropped dramatically to 156 years, primarily because of irreversible DNA damage accumulating in the brain and heart.
The researchers said the study is not intended to claim that humans will actually live for 156—or even 190—years.
"The purpose of this study is not to suggest that people will actually live for 156 or 190 years," Efimov said. "Rather, it aims to identify which biological processes impose the strongest limits on lifespan and help guide future anti-aging therapies toward the areas that matter most."
Current research on aging is increasingly focused on drugs that regulate biological aging, therapies that remove senescent—or worn-out—cells, and other interventions designed to slow the aging process. However, scientists have yet to discover an effective method to prevent or reverse somatic mutations.
According to the researchers, the findings suggest that human lifespan is constrained not simply by the aging of the body as a whole, but more specifically by irreversible long-term damage to the brain and heart.
The study identifies somatic mutations as one of the principal biological factors limiting human longevity. At the same time, the researchers noted that other age-related biological processes—including the gradual weakening of cells' natural defense mechanisms, declining mitochondrial energy production, disruption of protein balance within cells, and changes in gene regulation—also play important roles in aging.
The report concludes that substantially extending human lifespan will likely require therapies that address all of these biological processes simultaneously. It adds that integrating multiple mechanisms of aging into a single scientific framework could provide a clearer understanding of the true biological limits of human longevity.
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