How long could humans live if we cured aging? People might live to 200 years before DNA damage kills them

How long would humans live if we cured aging? Not merely slowing it but preventing the gradual breakdown that causes muscles to weaken, organs to deteriorate and diseases such as dementia and heart failure to become more common. A new study offers a provocative answer. Even under that almost unimaginably optimistic scenario, most people might not live much beyond 200.

The reason lies inside every cell. Throughout life, our DNA picks up random errors known as somatic mutations. They arise when cells copy their genetic material or repair everyday damage. Most do nothing noticeable, but some kill cells or prevent them from working properly. Unlike many other changes associated with aging, these mutations cannot simply be reset once they have accumulated.

Researchers at the Skolkovo Institute of Science and Technology modeled what would happen if scientists eliminated every other major cause of aging while allowing these mutations to continue. Depending on their assumptions, they calculated a median human lifespan of 146 to 194 years — somewhere about 156 years. Perhaps in extreme cases, one person in 100,000 might live to a “maximum” of 470 years, although the researchers used a statistical definition of a “maximum” lifespan, rather than a hard limit beyond which nobody could live.

“This is a mathematical estimate (though careful), not experimental data,” said Dmitrii Kriukov, a computational biologist at the Skoltech Biomed Technologies Center in Russia and study co-author.

The longest living person in recorded history is Jeanne Calment of France, who lived to 122 years and 164 days before dying in 1997.

The Lifespan Without Aging

Somatic mutations are DNA changes acquired after conception in ordinary body cells. They cannot pass to children. Most appear harmless, but some can disable an essential gene, promote cancer or leave a cell unable to function. Every time your cells divide, there’s a small risk of mutation during the DNA copying process.

The researchers combined measurements from single-cell sequencing studies with estimates of how many mutations arise each year in five cell types: neurons, heart muscle cells, liver cells, liver progenitor cells and airway basal cells. They then estimated how often a mutation would disable a gene essential to that cell, how many cells an organ could lose before failing and how much those quantities vary from person to person.

Essentially, they treated the body like an engineered system whose survival depends on every critical component continuing to work. They also froze all other mortality at the level of a 30-year-old in Switzerland, the lowest young-adult risk among the long-running national datasets they examined. With that risk held constant and aging removed, the model produced the fantastical median lifespan of 1,759 years. This is the mathematical baseline from which the authors measured mutation’s effect.

Systems Built (or Not Built) to Last

The theoretical lifespan results depended largely on whether an organ could replace cells lost to mutations.

The brain and heart had the greatest difficulty. Most neurons and heart muscle cells do not regularly divide to create replacements. As harmful mutations accumulated and killed some of these long-lived cells, the losses became permanent. In the model, damage to neurons alone reduced the median lifespan to 194 years. Damage to heart muscle cells reduced it to 208 years.

The liver proved far more resilient because it can regenerate. When mutations killed liver cells, other cells could divide and replace them. With additional support from liver progenitor cells — reserve cells that help rebuild damaged tissue — none of the simulated livers failed during the model’s 100,000-year window. Cells lining the airways also replaced themselves effectively, although their ability to keep dividing eventually ran out after several thousand years.

“Our study shows that somatic mutations contribute significantly to aging, but they cannot by themselves explain the observed mortality,” Kriukov said.

A New Number in an Old Argument

Scientists have debated the somatic mutation theory of aging for a long time. A major piece of recent evidence came from a 2022 Nature study of 16 mammal species. It found that species with longer lifespans accumulated mutations more slowly each year in intestinal crypt cells, while those cells reached surprisingly similar mutation burdens near the end of life. The pattern supported a role for mutations in aging, but it did not establish how much they matter. The new study tries to turn that association into a quantitative survival model.

Its lifespan range also resembles a 2021 Nature Communications estimate, which placed a possible human limit around 120 to 150 years by estimating the age-related loss of physiological resilience from blood tests and activity data. The numerical overlap is striking, but the studies measure different things. One models mutation-driven cell loss after other aging processes vanish. Meanwhile, the other projects when the body may lose its ability to recover from stress.

The new model leaves out much of real aging, which is incredibly unrealistic. It covers only four organs, treats mutations as causing immediate cell death, and largely excludes cancer, organ-to-organ signaling, impaired but living cells and the expansion of mutant cell clones. It also assumes no transplant, no therapy that slows mutation accumulation and perfect removal of every other age-related process. Those omissions make its numbers upper bounds, the authors argue, because adding more routes to failure should generally shorten life.

“The maximum lifespans calculated are ‘not a verdict of inevitability’,” Kriukov said, “but it does highlight that somatic mutations, while surprisingly weak as a standalone aging driver, may become critical when combined with other mechanisms”.

The study’s more durable contribution may therefore be not the age 156, but the accounting system behind it. Researchers could add mitochondrial failure, disrupted protein maintenance and other mechanisms one at a time, then compare how sharply each one pulls the survival curve downward.

“We can now not just say that mutations are harmful, but quantify exactly how much they shorten life and compare their contribution with other aging processes,” said Ekaterina Khrameeva, the study’s principal investigator.

The results appeared in the journal npj Aging.

This story originally appeared on ZME Science. Want to get smarter every day? Subscribe to our newsletter and stay ahead with the latest science news.