A new analysis of the Swedish Adoption/Twin Study of Aging, published in Science, estimates that inherited factors explain about 50% of lifespan variation after adjusting for changing external causes of death. This estimate is higher than many prior studies, which typically placed heritability in the 6%–33% range. The authors validated their model with Danish and U.S. data but caution that cohorts were largely white and relatively affluent. Heritability applies to specific populations and times, and environmental factors still offer substantial room for intervention.
Twin Study Reassesses Role Of Genes In Lifespan — Estimates About 50% Genetic Influence
New Research Provides More Insight on How Much Genes Impact Longevity
Why do some people reach 100 while a sibling dies decades earlier? Is it chance, lifestyle, or something written in our DNA? A new analysis of historical twin data argues that inherited factors may explain roughly half of the variation in human lifespan — a larger share than many earlier studies reported.
What The Study Did
The paper, published in Science, reanalyzed data from the Swedish Adoption/Twin Study of Aging, which uniquely includes monozygotic (identical) twins raised apart. By focusing on twins born between 1900 and 1935 and explicitly correcting for changing external causes of death (such as improvements in sanitation, infectious disease control and accident rates), the authors estimated that genetics account for about 50% of lifespan differences in those cohorts.
How This Differs From Earlier Work
Many previous large-population studies reported more modest heritability estimates — typically in the mid-20s to low-30s percent, and in some cases as low as 6%–16%. The new analysis shows that if you do not correct for shifting external mortality influences, heritability estimates fall back into that lower range. The authors validated their approach using Danish and U.S. datasets, but note those cohorts are largely white and relatively affluent.
Biology, Environment And What It Means
Experimental biology has long shown that single-gene changes can dramatically extend lifespan in short-lived organisms: for example, a 1993 discovery found that a mutation affecting insulin signalling doubled lifespan in nematode worms. However, single-gene effects generally weaken in longer-lived species, and the gene changes observed so far tend to mimic metabolic effects similar to calorie restriction or exercise.
Crucially, lifespan is a complex trait shaped by many genes plus environment. Under the study’s interpretation, roughly half of an individual’s potential lifespan is influenced by inherited genetic factors, and the other half is shaped by environmental and lifestyle factors such as exercise, nutrition, sleep, stress, pollution and exposure to infectious disease.
“Heritability is a statistic that applies to a particular population in a particular environment at a particular time.”
That caveat matters: heritability estimates can change with different populations, historical periods and environments. The current estimate is the largest recent figure for genetic contribution to human longevity, but it does not imply fixed destiny — environmental changes and personal choices remain important.
Limitations: The cohorts analyzed are historically and demographically narrow (largely European, white and relatively affluent). More diverse, contemporary datasets will be needed to confirm how widely the ~50% estimate applies.
Takeaway: This reanalysis strengthens the evidence that genetics play a substantial role in lifespan in some historical populations, but it also underscores that environment and behavior collectively account for a large, modifiable share.
Bradley Elliott is a researcher in aging philosophy at the University of Westminster. This article was republished from The Conversation under a Creative Commons license. The original piece first appeared on Katie Couric Media.
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