For decades, scientists believed that how long we live was largely shaped by environment, lifestyle, and sheer chance, with genetics playing only a modest role. But a new study published in Science by researchers at the Weizmann Institute of Science overturns that assumption, suggesting that genes may account for around 50 per cent of human lifespan, more than double previous estimates.
The research, led by Ben Shenhar in the lab of Uri Alon, addresses a long-standing puzzle in ageing science: how much of longevity is inherited. Earlier studies had placed the heritability of lifespan at just 20 to 25 per cent, with some large datasets suggesting it could be as low as 6 to 10 per cent.
“For many years, lifespan was attributed mainly to non-genetic factors,” Shenhar notes, quoted by Weizmann Institute publication, a belief that “fueled skepticism about genetic determinants of longevity.”
The new study challenges that scepticism by rethinking how lifespan data has traditionally been analysed. The researchers examined extensive twin datasets from Sweden and Denmark, including, for the first time in such research, twins who were raised apart. This allowed them to better isolate genetic influences from shared environmental factors.
A key innovation of the study lies in its distinction between intrinsic and extrinsic mortality. Intrinsic mortality refers to deaths caused by biological ageing and genetic factors, while extrinsic mortality includes deaths due to accidents, infections, violence, or environmental hazards.
“Earlier heritability estimates were masked by high levels of extrinsic mortality,” the researchers explain. In historical populations, particularly those born in the late 19th and early 20th centuries, such external causes of death were far more common. Because older datasets did not record causes of death in detail, it was “impossible” to filter out these factors using conventional methods.
To overcome this, Shenhar and his colleagues developed an “innovative framework” that used mathematical modelling and simulations of “virtual twins” to separate intrinsic from extrinsic causes of death. This allowed them to reconstruct a more accurate picture of how genetics influences lifespan.
The result was striking: once extrinsic mortality was accounted for, the heritability of lifespan rose to over 50 per cent, bringing it in line with other complex human traits.
The findings also align with evidence from animal studies, strengthening the case that genetics plays a central role in determining longevity. “If heritability is high, as we have shown,” Shenhar says, “this creates an incentive to search for gene variants that extend lifespan, in order to understand the biology of ageing and, potentially, to address it therapeutically.”
The implications of this shift are far-reaching. For years, the assumption that genes played only a minor role had dampened efforts to identify specific “longevity genes.” With stronger evidence of genetic influence, researchers may now intensify the search for biological pathways that regulate ageing.
The study also sheds light on disease-specific risks. For example, the researchers found that up to age 80, the risk of dying from dementia shows a heritability of about 70 per cent, significantly higher than that of cancer or heart disease.
At a broader level, the findings challenge the widely held view that lifestyle interventions alone can dramatically extend lifespan. While factors such as diet, exercise, and healthcare remain critical, the study suggests that genetic predisposition may set more rigid boundaries than previously thought.
Still, the researchers do not dismiss the role of environment. Instead, their work highlights the complex interplay between genes and external factors, and the need to account for both in longevity research.
This story is done in collaboration with First Check, which is the health journalism vertical of DataLEADS
