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Why do some people live well into their 90s while others die decades earlier? Lifestyle clearly matters, but a new study suggests our genes may play a much bigger role than scientists once believed.

The findings could reshape how researchers approach aging, longevity, and the biology of long life, reopening questions long thought settled.

The Longstanding Debate Over Longevity

For decades, scientists have tried to answer a deceptively simple question: how much control do our genes have over how long we live?

Earlier research, largely based on historical twin studies, suggested genetics accounted for only about 20 to 30 percent of lifespan differences. Environment, behavior, and chance were believed to dominate the rest.

But that conclusion has never sat entirely comfortably with biologists, especially those studying aging in animals, where genetics often play a far larger role.

A New Estimate, A Bigger Genetic Role

A new study published this week in Science challenges those earlier assumptions. Using updated mathematical modeling and refined data analysis, researchers now estimate that genetics may explain roughly 50 percent of the variation in human lifespan.

That figure is about double what many previous studies concluded and closely aligns with results seen in laboratory animals, from worms to mice.

The research was led by Ben Shenhar, a doctoral student at the Weizmann Institute of Science in Israel, alongside systems biologist Uri Alon. Their work focuses on understanding not just whether genes matter, but how much they matter relative to everything else.

The Hidden Problem in Classic Twin Studies

Much of what scientists believed about lifespan genetics came from studies of Swedish and Danish twins born in the 19th century. These datasets were valuable, but incomplete.

Crucially, they recorded age at death, not cause of death.

That missing detail turns out to matter a lot.

If one twin lived to old age and the other died young due to an infectious disease, accident, or violence, the difference would appear genetic on paper, even if it had nothing to do with inherited biology.

Researchers refer to these external causes as extrinsic mortality, deaths driven by forces outside the body.

Why Extrinsic Mortality Skews the Data

According to Shenhar, extrinsic mortality was dramatically higher when those early twins lived. Before antibiotics and modern medicine, infectious diseases like cholera and typhus were common killers.

The study estimates that extrinsic mortality during that era was roughly ten times higher than it is today.

When those deaths are not accounted for, the genetic signal becomes buried under noise, making heredity appear weaker than it truly is.

A Mathematical Fix for an Old Blind Spot

To address this, the research team developed a mathematical framework that adjusts for extrinsic mortality. The model separates lifespan variation into two broad components: genetics and “everything else,” including environment, lifestyle, and chance.

After correcting for non-biological causes of death, the genetic contribution rose sharply, landing near the 50 percent mark.

“This is about partitioning the sources of variation,” Shenhar explained. Genetics accounts for about half, while the remaining half comes from non-genetic influences and randomness.

Newer Data Confirms the Pattern

To test whether the model reflected reality, the team analyzed more recent Swedish twin data that included crucial distinctions missing from older studies.

This dataset covered twins raised together and twins raised apart, a powerful way to separate genes from environment.

As extrinsic mortality declined in modern times, heritability estimates climbed, precisely as the model predicted.

Identical twins raised apart, who share genes but not upbringing, were especially informative in revealing the genetic signal.

Why Lifespan Is Different From Other Traits

Twin studies have long been reliable tools for measuring genetic influence on traits like height, blood pressure, or personality.

Lifespan, however, is different.

“These other traits are not affected by extrinsic mortality,” said Uri Alon. “Mean lifespan is uniquely sensitive to it.”

Because historical datasets lacked cause-of-death information, lifespan genetics were never properly corrected, until now.

Implications for Aging Research

The findings could have far-reaching consequences for how scientists study aging.

Low estimates of heritability may have discouraged funding and research into the genetics of longevity, reinforcing the idea that lifespan is mostly environmental or random.

This study suggests otherwise.

“Our work validates the search for genetic factors of longevity,” Shenhar said, noting that the genetic signal was always present but obscured by flawed data.

Genes Can Shorten or Extend Life

Genes influence lifespan in both directions.

Some inherited mutations increase the risk of early disease and premature death. Others appear to offer protection, delaying or preventing conditions commonly associated with aging.

Many centenarians, researchers note, reach age 100 without developing major age-related illnesses.

That resilience is unlikely to be accidental.

“These individuals seem to carry protective genetic variants,” Shenhar said. While some longevity-related genes have already been identified, lifespan remains a complex trait shaped by hundreds, possibly thousands, of interacting genes.

What This Means Going Forward

The study does not suggest that lifestyle choices are irrelevant. Diet, exercise, smoking, alcohol use, and environment still matter profoundly.

But it reframes the balance.

Genes may quietly set the boundaries within which those choices operate, influencing how resilient, or vulnerable, our bodies are over time.

As researchers continue to map the genetics of aging, this new perspective could accelerate efforts to understand healthy longevity, age-related disease prevention, and personalized medicine.

A Clearer View of How We Age

By revisiting old assumptions with modern tools, scientists are uncovering a more nuanced picture of human lifespan, one where biology and behavior are deeply intertwined.

Longevity, it turns out, is neither purely fate nor pure chance. It is the product of inherited code, lived experience, and the unpredictable turns in between.

(With inputs from Reuters.)

 

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