More than half of your lifespan is shaped by genetics
Briefly

More than half of your lifespan is shaped by genetics
"According to the study, led by molecular biologist Uri Alon from the Weizmann Institute of Science in Israel, up to 55% of the variation in human lifespan is determined by genetic factors, after accounting for the effects of external causes of death, such as accidents or infections. This rate is more than double previous estimates, which placed the heritability of human lifespan between 6% and 33%."
"A genetic contribution of 55% aligns far more closely with what has been observed in laboratory mice and other animals, as well as with the known influence of other human physiological traits. A key element of the study is the idea that not all deaths reflect the same underlying biology of aging. The researchers distinguish between extrinsic mortality deaths caused by external factors such as accidents, violence, infections or environmental toxins and intrinsic mortality, which stems from internal biological deterioration and the aging process itself."
"The authors of the study note that much of the earlier research on this topic relied on cohorts of people who lived and died in the 19th century or the first half of the 20th. Those studies often failed to specify causes of death. They also reflect a period in which deaths from infections and other external factors were far more common than today a distortion that, according to the new paper, has not been adequately corrected in subsequent analyses."
Mathematical models reassessed large twin datasets, distinguishing intrinsic mortality (internal biological aging) from extrinsic mortality (accidents, infections, violence, environmental toxins). After accounting for external causes of death, genetic factors explain up to 55% of variation in human lifespan, more than double prior estimates of 6–33%. This higher heritability matches findings from laboratory mice and other animals and aligns with genetic influence on other physiological traits. Earlier analyses that used cohorts with high rates of infection and unspecified causes of death underestimated genetic contributions because extrinsic mortality masked intrinsic aging-related patterns. Modeling twin data including identical and fraternal pairs improved separation of inherited effects from environmental and accidental influences.
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