More than half of your lifespan is shaped by genetics

Why do some people live much longer than others? For decades, most explanations have focused on external factors: lifestyle, disease, wealth, even luck. But new research published this week challenges that view, giving the genes we inherit from our parents a far more central role than previously believed.

According to the study, led by molecular biologist Uri Alon from the Weizmann Institute of Science in Israel, up to 55% of the variation in human lifespan is determined by genetic factors, after accounting for the effects of external causes of death, such as accidents or infections. This rate is more than double previous estimates, which placed the heritability of human lifespan between 6% and 33%.

The research, published in Science, argues that the true genetic contribution to the variation in human lifespan has been masked. A genetic contribution of 55% aligns far more closely with what has been observed in laboratory mice and other animals, as well as with the known influence of other human physiological traits.

A key element of the study is the idea that not all deaths reflect the same underlying biology of aging. The researchers distinguish between extrinsic mortality — deaths caused by external factors such as accidents, violence, infections or environmental toxins — and intrinsic mortality, which stems from internal biological deterioration and the aging process itself.

The authors of the study note that much of the earlier research on this topic relied on cohorts of people who lived and died in the 19th century or the first half of the 20th. Those studies often failed to specify causes of death. They also reflect a period in which deaths from infections and other external factors were far more common than today — a distortion that, according to the new paper, has not been adequately corrected in subsequent analyses.

Alon’s team built mathematical models to reassess large datasets of twins — both identical, who share 100% of their DNA, and fraternal, who share about 50% — drawn mainly from major Danish and Swedish cohorts. They also incorporated data from twins raised apart, to remove the influence of a shared environment, as well as from siblings of U.S. centenarians, which helped confirm that the findings are not limited to Scandinavian populations. In total, the dataset covers nearly 16,000 related pairs, including about 14,000 twins and more than 2,000 sibling pairs.

Once extrinsic mortality is statistically removed, the heritability of longevity rises steadily until it levels off at around 55%. The study also shows that the contribution of external causes of death declines across the periods covered by the three major datasets examined (1870–1935). Today, these external causes are 10 times less common.

Until now, the prevailing view held that genetics might account for as little as 6% of a person’s total lifespan. That idea reinforced the misleading notion that most of one’s longevity was essentially self‑determined: by avoiding risky behaviors, steering clear of proven harms such as tobacco or alcohol, and maintaining a healthy lifestyle, one could significantly extend life. The new estimate reduces that degree of control, but it also makes clear that roughly 50% still depends on external factors that are, at least in part, modifiable — including diet and physical activity.

The study also examined how genetic inheritance influences different causes of death. For cancer, the genetic component was roughly 30% and did not vary with age. Cardiovascular deaths showed a higher degree of heritability — around 50% at younger ages. Dementia‑related deaths displayed the strongest genetic influence, reaching about 70% at age 80 before stabilizing between 40% and 50% at more advanced ages.

Nir Barzilai, one of the world’s leading experts on genetics and longevity, who was not involved in the research, praised the study’s significance. “It’s a very revealing piece of work and will help shift the current dogma,” he told EL PAÍS. Barzilai, director of the Institute for Aging Research at the Albert Einstein College of Medicine in the United States, notes that earlier studies underestimated the role of genetics because they relied solely on twin data without distinguishing whether deaths were caused by intrinsic or extrinsic factors. “Cases of people who die young should not be included in studies on the contribution of genetics to longevity,” he added.

The scientist has spent years studying centenarians in search of the genetic factors that determine their exceptional longevity. “In a study of 750 centenarians and their families [the Genes of Longevity trial], genetics explains between 80% and 100% of the chances of reaching such advanced ages,” explained Barzilai. “If both your parents are centenarians, your life will be 24% longer than that of the rest of the population to which you belong; 13% longer if only one of your parents is a centenarian; and 7% longer if you have a grandparent who lived to these ages. This means that you are likely to live past the age of 100, 93, and 85, respectively, considering an average life expectancy of 80 years.”

In a commentary in Science, Daniela Bakula and Morten Scheibye-Knudsen, from the Department of Molecular and Cellular Medicine at the University of Copenhagen in Denmark, argue the study “has important consequences for aging research.” “A substantial genetic contribution strengthens the rationale for large-scale efforts to identify longevity-associated variants, refine polygenic risk scores, and link genetic differences to specific biological pathways that regulate aging,” they wrote.

Bakula and Scheibye-Knudsen point out that this 55% figure aligns far more closely with what is known about the genetic contribution to other complex human traits: “Perhaps this means that intrinsic rates of aging are tightly optimized through evolution, in line with other traits such as cognitive function and metabolism.”

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