What if today’s human lifespan is nowhere near biology’s true limit? In a remarkable new study published in npj Aging, researchers Evgeniy Efimov, Vlad Fedotov, Leonid Malaev, Ekaterina E. Khrameeva, and Dmitrii Kriukov constructed a mathematical model of the human body to answer that question.
When they combined the brain, heart, liver, and lungs into a single model, they estimated that if every reversible aspect of aging could someday be eliminated, the median human lifespan could reach about 156 years, with a plausible range of 146 to 194 years.
Under their assumptions, the luckiest individuals might live roughly 470 years.
Even more astonishing, before adding aging back into the equation, their theoretical baseline suggested a possible lifespan of 1,759 years. The study is not a prediction that humans will someday live nearly two millennia. Instead, it reveals just how much of our current lifespan is determined by aging itself.
The key to the entire study is something called a somatic mutation. Every cell in the human body contains DNA, the genetic instructions that tell the cell how to function. Throughout life, that DNA gradually accumulates tiny copying errors and damage.
These changes, known as somatic mutations, are not inherited from our parents and are not passed on to our children. They simply accumulate in the cells of our bodies as we age. Because these mutations permanently erase or alter biological information, the researchers describe them as an entropic process, a gradual increase in disorder that cannot simply be reversed by repairing damaged tissues.
To estimate how much these mutations limit human life, the researchers combined several enormous sources of data. They analyzed single-cell genome sequencing studies that measured how quickly mutations accumulate in different organs. They incorporated CRISPR gene-editing research that identifies which genes are essential for cell survival.
They used modern life expectancy data from the Human Life-Table Database to establish normal mortality rates. Finally, they built a mathematical model using reliability theory, the same branch of engineering used to predict when aircraft, power plants, and other complex systems are likely to fail. In their model, the human body is treated as a collection of vital organs. If enough cells are lost in one critical organ, the entire system eventually fails.
The Thought Experiment
The researchers began with a thought experiment. Imagine a healthy 30-year-old whose body never biologically ages. This person could still die in a car accident, from an infection, or from any of the ordinary risks of life, but their chances of dying from those causes would never increase with age. Using that constant risk as a starting point, the model produced a median lifespan of approximately 1,759 years. That enormous figure is not meant to describe reality. It is simply the mathematical horizon before any aging mechanisms are added back into the model.
The picture changes dramatically once somatic mutations are introduced.
The study found that not every organ ages in the same way. The liver, for example, constantly replaces damaged cells with new ones. Because of this remarkable regenerative ability, the model predicts that the liver could continue functioning for tens of thousands of years under mutation pressure alone. In some simulations, liver failure never occurred even after 100,000 years.
The brain and heart are another story entirely.
Most neurons in the brain and cardiomyocytes in the heart are not routinely replaced. Every time one of these cells dies from accumulated mutations, it is effectively gone forever. Over centuries, enough of these irreplaceable cells disappear that the organ can no longer perform its job. In the researchers’ model, these two organs become the ultimate bottlenecks that limit human longevity. When all four organs were combined, the theoretical median lifespan fell from 1,759 years to approximately 156 years.
One of the most important conclusions is that somatic mutations cannot fully explain why humans age today. Even if every other major hallmark of aging could somehow be eliminated, mutation-driven damage would still limit lifespan, but not nearly enough to explain why most people die before reaching 100. The study concludes that other aging processes contribute roughly as much as somatic mutations themselves.
Perhaps the most fascinating implication lies just beyond the paper’s own conclusions. The model demonstrates that organs capable of continuous regeneration, such as the liver, become extraordinarily resistant to mutation-driven aging. The true obstacles are organs that cannot easily replace lost cells. This suggests that the future of longevity research may depend less on slowing aging and more on learning how to regenerate the brain and heart. If medicine someday achieves that goal, today’s estimates may prove to be only another stepping stone toward an even more distant horizon.
The authors are careful to point out that their work is a mathematical model, not a forecast. It assumes no organ transplantation, no whole-body cell replacement, and no future technologies capable of removing accumulated mutations themselves. It also examines only four organs and simplifies many biological interactions that occur in real people. Nevertheless, the study offers something profoundly valuable. It provides one of the clearest quantitative pictures yet of how different aging mechanisms shape the limits of human life.
For centuries, people have asked whether there is a fixed ceiling on human longevity. This research suggests a different question may be more important. Rather than asking how long humans can live today, we may someday ask which biological barriers still remain. If the first theoretical horizon is 156 years, and the mathematical horizon without aging stretches to 1,759 years, then humanity’s journey toward longer life may have only just begun.