A team of researchers has unveiled a new mathematical model suggesting humans could theoretically live up to 156 years if every reversible hallmark of aging were eliminated except one. The finding offers the first quantitative ceiling on human longevity based solely on somatic mutations—the irreversible DNA errors that accumulate in our cells over time.
The work affects both aging science and future therapeutic strategy, signaling that even the most advanced anti-aging interventions may hit a hard biological limit unless genomic damage can be controlled.
According to the study’s authors, the tissues that cannot regenerate—the brain and the heart—are the ones that ultimately set that limit.
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The research, published in npj Aging, uses a multistage model to “switch on” aging mechanisms one by one and measure how long a human could live if all but somatic mutations—a DNA change that arises in any non‑reproductive cell after conception, meaning it affects the body’s tissues but cannot be passed to offspring—were cured.
The authors found that eliminating every other aging process still leaves a median lifespan capped between 146 and 194 years, with neurons and cardiomyocytes acting as the bottlenecks. “Neurons and cardiomyocytes, which lack the ability to divide, turned out to be the main limiting factors,” said co-author Evgeniy Efimov in a statement.
Newsweek has reached out to the study’s corresponding author Dmitrii Kriukov via email for comment.
Somatic Mutations as the Final Barrier
Unlike other hallmarks of aging—such as mitochondrial decline, epigenetic drift, or loss of proteostasis—somatic mutations cannot be reversed with any existing therapy. They accumulate slowly but relentlessly, and in tissues that cannot replace their cells, the damage becomes permanent. The model shows:
Liver and other renewing organs can withstand thousands of years of mutation accumulation thanks to continuous cell turnover.Brain and heart cells, which do not divide, cannot dilute their damage and eventually fail.
This asymmetry explains why diseases such as dementia and heart failure dominate late‑life morbidity: they strike precisely the tissues that cannot regenerate.
Assistant Professor Jordan Weiss, who studies health span and population‑level aging at NYU Grossman School of Medicine, said the model’s tissue‑specific insight mirrors real‑world patterns.
“The conditions that cost people their independent, healthy years—such as dementia and heart failure—fall heavily on precisely the tissues that cannot regenerate,” he told Newsweek. “So the gap between how long people live and how long they stay well is not one general breakdown of the body. It is concentrated in the organs that have no way to replace worn‑out cells.”
Why the Limit Is 156 Years
The researchers began with a hypothetical “non-aging human” whose mortality risk never increases with age. In that scenario, the median lifespan would be 1,759 years. Once somatic mutations were added back into the model, the lifespan collapsed to 156 years, entirely due to the vulnerability of non-renewing tissues.
Even when all other aging processes were removed, the model’s ceiling barely budged. That suggests somatic mutations contribute roughly half of the gap between theoretical immortality and real-world human lifespan.
Pharmacist and regenerative‑medicine researcher Egle Pavyde said the study’s value lies in quantifying what scientists have long suspected. “It proves that DNA damage accumulating in our cells is one of the reasons we cannot live indefinitely but also shows that our bodies are complex systems and that it is only one piece of a much larger puzzle,” she said.
What This Means for Aging Research
The study’s authors and outside experts agree somatic mutations are likely the “highest‑hanging” fruit in geroscience. They are difficult to prevent, nearly impossible to reverse, and lack a single druggable pathway.
As Michael Leone, Assistant Professor in the Division of Precision Medicine at NYU Grossman School of Medicine, told Newsweek: “Somatic mutations are likely among the highest-hanging fruit in targetable geroscience … lower-hanging targets—such as inhibiting mTOR with rapamycin or clearing senescent cells—are far more logical interventions to prioritize.”
The model does not claim humans will live to 190. Instead, it provides a ranking system for aging mechanisms, showing which ones shorten life the most and where interventions might matter most.
Pavyde echoed that sentiment, noting that aging is “more like a machine wearing out in several ways at once,” with mitochondrial dysfunction, protein‑quality decline, epigenetic changes and other processes contributing together.
The Brain and Heart as Longevity Bottlenecks
The strongest insight from the model is that longevity is not limited by the whole body, but by two specific tissues:
These cells cannot divide, cannot replace themselves, and cannot dilute DNA damage. Their failure sets the upper bound on human lifespan—even in a world where every other aging process is cured.
Weiss said this framing offers a more precise way to think about healthy aging: “If renewable organs already tolerate decades of DNA damage without much trouble, there is little to gain from protecting them further. The harder and more valuable problem is preserving the DNA of brain and heart cells.”
What Happens Next
The researchers plan to expand their model to include other hallmarks of aging, such as:
mitochondrial dysfunctionepigenetic drifttelomere shorteningloss of proteostasis
Their goal is a comprehensive quantitative theory of aging—one that can rank every mechanism by how much it shortens life and guide future therapeutic priorities.
“The takeaway is not that people might live to 190. It is that researchers now have a way to set priorities,” said Weiss.