A new analysis suggests genetics may play a much bigger role in how long people live than many earlier studies estimated, once deaths from outside causes are separated out. Researchers report that, after accounting for “extrinsic” deaths such as accidents and infectious disease, the genetic contribution to human lifespan rises to roughly half—around 50% to about 55% in their analyses.
The work, published Jan. 29 in Science, challenges a common view that lifespan is driven mostly by lifestyle and environment. The researchers argue that external causes of death can mask genetic signals tied to aging and internal biological decline, leading earlier estimates to look much lower.
What the study found
Using mathematical modeling alongside large twin-cohort datasets, the researchers estimate that lifespan heritability is consistently high—around 55%—when external deaths are properly accounted for. That figure is roughly double what many previous population studies have estimated, which often put lifespan heritability around 20% to 25%, with some estimates as low as 6%. The new analysis reframes lifespan as more similar to many other human traits that often show about 50% heritability in twin studies.
The authors also report that this higher estimate lines up more closely with what scientists have found in laboratory animals such as mice and flies, where lifespan appears more heritable. In the Science News report, the study’s lead author, Ben Shenhar of the Weizmann Institute of Science, says the findings represent a shift in how lifespan fits alongside other complex traits.
How researchers re-estimated heritability
The team compiled mortality data from Swedish, Danish, and U.S. databases and combined them with datasets from three studies of Danish and Swedish twins, plus a study involving siblings of U.S. centenarians. Because the historical datasets lacked detailed cause-of-death information, the researchers used mathematical methods to estimate and separate the impact of deaths driven by external factors.
Science News describes the approach as using a known population pattern: overall mortality tends to rise with age, but many populations show a mortality “plateau” between ages 20 and 40, linked to a dip in extrinsic mortality during those years. The researchers used the value of that plateau to help calculate extrinsic mortality and then estimate heritability with and without those external effects included.
In a simplified “controlled environment” thought experiment, Shenhar describes the central question as how much genes would matter if environments and lifestyles were held constant. Applying the model to twin datasets, the team reports the higher heritability estimate for lifespan once extrinsic mortality is separated out.
Why “extrinsic” deaths matter
EurekAlert’s summary of the analysis argues that extrinsic mortality—deaths from outside causes—systematically lowers measured heritability in historical populations, effectively diluting the genetic contribution that primarily shapes “intrinsic” mortality related to aging and internal biological decline. In other words, if many people die for reasons unrelated to aging biology, the remaining data can make genes look less important than they are for aging-driven lifespan differences.
This helps explain why earlier studies could reach widely varying conclusions about how heritable lifespan is, and why some researchers became skeptical about the value of genetic studies of longevity. The new calculations aim to remove that confounding effect, producing estimates that the authors say better reflect genetic influence on lifespan under conditions where external hazards are reduced.
What it could mean for aging research
A related Perspective cited in the EurekAlert release says the results have important implications for aging research and that a substantial genetic contribution supports large efforts to identify longevity-associated genetic variants, improve polygenic risk scores, and connect genetic differences to biological pathways that regulate aging. Science News similarly notes that estimating the genetic role in lifespan matters for broader aging research, and it highlights the idea that identifying why some people live exceptionally long could eventually inform interventions or medicine.
The Science News report also includes outside commentary from biostatistician Paola Sebastiani of the Tufts Clinical and Translational Science Institute, who says the new results are closer to what she and colleagues estimated for the heritability of extreme longevity—living past 100. Sebastiani suggests that removing extrinsic deaths in genetic studies could help improve the ability to detect genetic factors linked to lifespan.
Finally, Shenhar tells Science News he wants to focus next on the non-genetic side of the equation, including how much lifespan variation reflects randomness versus lifestyle. That framing keeps the study from claiming genes are destiny, even while arguing genetics may matter more than many earlier estimates suggested.
