How much of your future lifespan is already decided before you are born? A new analysis of more than a century of twin records suggests that genes may account for about half of how long people live once deaths from accidents, infections and violence are stripped out. <\/p>\n\n\n\n
The work, carried out at the Weizmann Institute of Science in Israel<\/a> and published in the journal Science<\/em> in January 2026, roughly doubles earlier estimates of the genetic share of longevity.<\/p>\n\n\n\n Some news outlets have already summed it up in a blunt way, saying that roughly 50 percent of human lifespan is set in the womb. <\/p>\n\n\n\n The researchers themselves describe a more nuanced picture in which genes and everything else each supply about half of the variation in how long people live, with a heavy dose of randomness still in the mix. So is your lifespan written in stone or is there still room to move the needle?<\/p>\n\n\n\n The study led by doctoral student Ben Shenhar dug into large twin registries from Sweden and Denmark that track identical and fraternal twins. Because identical twins share almost all their DNA while fraternal twins share about half, comparing their lifespans can reveal how much genes matter compared with the environment. <\/p>\n\n\n\n These kinds of twin studies have been a classic tool in genetics for decades.<\/p>\n\n\n\n The team worked under the guidance of systems biologist Uri Alon at the Weizmann Institute and used mathematical models to reanalyze the old records. They also drew on newer datasets that, for the first time in this context, included twins raised apart, which helps separate genetic effects from the way families and neighborhoods shape health. <\/p>\n\n\n\n To sharpen the picture, the researchers even simulated virtual twins in a computer to test how different patterns of death would affect the apparent role of heredity.<\/p>\n\n\n\n Older twin studies treated all deaths the same, whether someone died quietly in their nineties or from cholera in their thirties. The new work focuses on extrinsic mortality<\/a>, a term that covers deaths from outside the body, including infectious disease, accidents and violence. <\/p>\n\n\n\n In the time before antibiotics and modern sanitation, these external dangers were roughly ten times more common than they are today, especially in the Scandinavian cohorts the team analyzed.<\/p>\n\n\n\n That matters because when the cause of death is missing in the historical records, an early death from an infection can easily hide the fact that the twin pair shared a strong underlying biology for long life. <\/p>\n\n\n\n If one twin reached 90 through natural aging while the other died at 30 from an epidemic, a simple comparison would say genes did not matter very much. By building a model that estimates and filters out these extrinsic deaths, the researchers showed that earlier work had systematically underestimated the genetic contribution to lifespan.<\/p>\n\n\n\n Once those external causes are accounted for, the Weizmann team concludes that intrinsic human lifespan, the part driven by aging processes and inherited risk, is a bit more than 50 percent heritable. <\/p>\n\n\n\n For many years, human lifespan was thought to be shaped almost entirely by non-genetic factors, \u201cfueling skepticism about genetic determinants of longevity,\u201d Shenhar said in a Weizmann news release. <\/p>\n\n\n\n That figure is similar to the heritability of many other complex traits and lines up with studies of lifespan<\/a> in mice and other animals.<\/p>\n\n\n\n Earlier twin work had suggested that only 20 to 25 percent of variation in lifespan was genetic, and some large family tree studies put the number closer to 6 percent. <\/p>\n\n\n\n A 2019 meta analysis of genome wide association studies in Nature Communications did identify several longevity-related genetic variants<\/a>, but their effects looked modest against those lower heritability estimates. With the new numbers, researchers say there is a stronger incentive to keep hunting for protective gene variants that slow aging or delay disease.<\/p>\n\n\n\n For people reading about this study between work emails and dinner plans, the obvious question is what it means for everyday choices. <\/p>\n\n\n\n A genetic contribution of about 50 percent does not erase the impact of diet, smoking, exercise<\/a>, pollution or access to health care, which still make up the other half of the picture. Researchers and doctors stress that lifestyle can either soften or amplify the risks written into your DNA.<\/p>\n\n\n\n The new work also fits with studies of specific genes that appear to protect some people well into old age<\/a>, such as those highlighted in the Nature Communications<\/em> meta analysis of genome wide association studies that spotlighted variants in the APOE region and other pathways. <\/p>\n\n\n\n Lead author Ben Shenhar has pointed to people who reach 100 without major disease as examples of individuals who may carry clusters of such protective variants, although most of us will never be so lucky. It is an idea that captures the sense that part of your lifespan may already be shaped before you are born, even though it is far from fixed.<\/p>\n\n\n\n A perspective article in Science<\/em> argues that the new estimates should prompt scientists to rethink long-held assumptions about the biology of aging and to invest more in genetic studies of longevity. <\/p>\n\n\n\n At the same time, the Weizmann team notes that their data come mostly from Scandinavian and European populations, so future work will need to test how well the results hold in other groups and the practical message for now is that while genes matter a lot, lifestyle and environment still control the rest of the story.\u00a0<\/p>\n\n\n\n The main study has been published in the journal Science<\/em><\/a>.<\/p>\n","protected":false},"excerpt":{"rendered":" How much of your future lifespan is already decided before you are born? A new analysis of more than a … <\/p>\nWhat the researchers actually measured<\/h2>\n\n\n\n
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