A study in Science estimates that about 50% of human lifespan may be genetic after removing external causes of death from the analysis. Researchers built a statistical model to separate intrinsic aging processes from extrinsic events like accidents and treatable infections, then applied it to twin cohorts from Sweden, Denmark and the U.S. (birth years 1870–1935). Results were consistent across datasets, but limitations include reliance on Northern European cohorts and incomplete cause-of-death records. Authors stress that genetics confer propensity, not certainty, and lifestyle remains important.
New Study Suggests Genetics May Account for About Half of Human Lifespan
A new study suggests genetics may play a pretty big role in determining how long a person lives, although environmental factors still have influence. . | Credit: Elena Pejchinova via Getty Images
A study published Jan. 29 in the journal Science estimates that roughly 50% of an individual’s lifespan may be attributable to genetics after accounting for external causes of death. The researchers developed a statistical model to separate intrinsic biological drivers of aging from extrinsic factors—such as accidents and treatable infections—and applied it to multiple twin cohorts.
Study Design and Key Findings
The research team used a mathematical model that explicitly accounts for extrinsic mortality even when cause-of-death records are incomplete. They applied this approach to twin datasets from Sweden, Denmark and the United States covering people born between 1870 and 1935. Each dataset returned a consistent heritability estimate of about 50% for lifespan, substantially higher than earlier twin-study estimates of 6%–25%.
Joris Deelen, a geneticist at Leiden University and co-author, explained that the model helps remove environmental "noise"—such as accidents or treatable infections—to better reveal the genetic contribution to longevity.
Why This Differs From Previous Estimates
Classical twin-study approaches typically use all-cause mortality, which can conflate intrinsic and extrinsic causes of death and underestimate genetic effects. By modeling and removing extrinsic mortality, the authors argue, the genetic component becomes clearer. The new estimate aligns better with heritability values for lifespan in other mammals and with genetic links to age-related diseases.
Limitations
The authors acknowledge important caveats. The model was tested primarily on people of Northern European ancestry because comparable twin data from other regions are scarce. The ideal dataset would record verified causes of death so intrinsic and extrinsic causes could be classified directly rather than modeled—data that largely do not exist for the historical cohorts used.
Implications
Identifying genetic markers and biological pathways that influence lifespan and health span could inform geriatric medicine and targeted interventions to promote healthier aging. However, the authors and outside experts emphasize that a 50% heritability estimate is not deterministic: genes confer a propensity, not a guarantee. Environmental factors and lifestyle choices remain crucial modifiable determinants of individual outcomes.
Luke Pilling, a geneticist at the University of Exeter (not involved in the study), noted that better modern recordkeeping and more diverse datasets could test whether this estimate holds across populations and time.
Bottom line: The study suggests genetics may play a larger role in human longevity than previously estimated, but broader data and direct cause-of-death records are needed to confirm and generalize the finding.
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