Yes. Even though genes influence lifespan, research consistently shows that lifestyle factors such as diet, exercise, sleep, and metabolic health play a major role in determining life expectancy and healthy aging.
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A new Science paper is making waves in the longevity world with a bold claim: about 50% of human lifespan may be genetic.
If true, that would mean our genes play a much larger role in determining how long we live than many researchers previously believed.
But the idea that lifespan is genetic isn’t new—and neither is the debate around it.
For decades, aging researchers have been asking the same fundamental question: how much of a person’s lifespan is determined by genetics, and how much is shaped by environment and lifestyle?
The answer has never been simple.
Most of what we know about lifespan heritability comes from twin studies and large population datasets.
By comparing how long identical twins live relative to fraternal twins, researchers can estimate the genetic contribution to human lifespan.
Across many studies, the results have been surprisingly consistent: genes matter, but not as much as people might think.
Most previous estimates placed lifespan heritability somewhere between about 15% and 30%.
Later work suggested it may be even lower. One widely discussed study found that when researchers carefully controlled for something called assortative mating—the tendency for people to partner with others who share similar lifestyles, education, and health behaviors—the genetic contribution could drop to around 7%.
In other words, environmental and lifestyle factors appeared to dominate.
The new analysis, published in Science by various researchers, including those affiliated with the Weizmann Institute of Science, takes a different approach.
Using large datasets and mathematical modeling, the researchers estimate that around half of variation in human lifespan may be genetic—effectively doubling previous estimates.
If correct, this would suggest a substantial genetic contribution to longevity and could strengthen efforts to:
identify longevity associated variants
refine polygenic risk scores
uncover biological pathways that regulate aging
But the conclusion relies on an assumption that many researchers find controversial.
The study attempts to separate intrinsic mortality from extrinsic mortality.
Intrinsic mortality refers to deaths caused by biological aging and age-related diseases such as cancer or cardiovascular disease.
Extrinsic mortality refers to deaths from external causes like accidents or infectious diseases.
The authors assume that extrinsic causes of death do not reflect intrinsic aging and therefore should not be counted when estimating how much lifespan is genetic.
But in reality, aging strongly influences vulnerability to these risks.
Older adults are far more likely to die from infections, falls, and environmental hazards than younger people. Aging affects immune function, balance, bone density, and recovery from injury.
In other words, aging biology still shapes many deaths that appear “external.”
Because of this, many scientists believe the new estimate may overstate the genetic role in lifespan.
Across decades of aging research, one pattern keeps emerging.
Yes, genes affect lifespan. But they rarely determine it.
Human longevity appears to be shaped by a complex mix of:
genetic differences
environmental factors
lifestyle behaviors
medical care
and simple chance
Rather than a single “longevity gene,” researchers increasingly believe that many genes each contribute small effects, interacting with the environment over time. In addition, efforts to identify strong genetic signatures of longevity have largely failed. A small number of exceptions, including APOE gene status, do exist.
The exact percentage of lifespan that is genetic will likely continue to be debated.
But the practical takeaway is remarkably consistent across studies:
Genes influence longevity. They don’t dictate it.
Factors like sleep, metabolic health, physical activity, and nutrition still play an enormous role in shaping how we age.
Or as many researchers like to put it:
Genetics loads the gun. Lifestyle pulls the trigger.
Which means that regardless of the exact number—7%, 30%, or even higher—people still have tremendous power to influence their own aging trajectory.
Most aging research suggests that 7% to 33% of human lifespan is genetic, meaning the majority of variation in longevity is influenced by lifestyle and environmental factors. A recent Science study suggests the number could be closer to 50%, though many researchers debate the assumptions behind that estimate.
Lifespan heritability refers to how much of the differences in how long people live can be explained by genetic differences between individuals. Scientists estimate this using large datasets, family records, and twin studies.
Yes. Even though genes influence lifespan, research consistently shows that lifestyle factors such as diet, exercise, sleep, and metabolic health play a major role in determining life expectancy and healthy aging.
Shenhar et al. Heritability of intrinsic human life span is about 50% when confounding factors are addressed. Science 2026; https://doi.org/10.1126/science.adz1187
Ruby et al. Estimates of the Heritability of Human Longevity Are Substantially Inflated due to Assortative Mating. Genetics 2018; https://doi.org/10.1534/genetics.118.301613
de Magalhães. The genetics of a long life. Science 2022; https://doi.org/10.1126/science.ade3119
Deelen et al. A meta-analysis of genome-wide association studies identifies multiple longevity genes. Nat Commun 2019; https://doi.org/10.1038/s41467-019-11558-2
Smulders and Deelen. Genetics of human longevity: From variants to genes to pathways. J Intern Med 2024; https://doi.org/10.1111/joim.13740
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