In a recent NBC News article, freelance health journalist David Cox reports on a major new study published in Science suggesting that a person’s genes shape lifespan far more than earlier estimates allowed. The study led by Ben Shenhar of the Weizmann Institute of Science in Israel, drawing on twin study data, has concluded that the genetic contribution to lifespan can be as high as 55 percent. Earlier research had estimated this figure to be between 6 and 33 percent.
Below are the key highlights, primarily based on David Cox’s NBC News article:
- A new way of slicing the data. Cox explains that the researchers distinguished between extrinsic mortality, which includes deaths caused by accidents, homicides, environmental hazards, and infections, and intrinsic mortality, which encompasses deaths resulting from age-related diseases, genetic mutations, and the natural decline of the body. By analyzing these two categories separately, they claim to have obtained a clearer understanding of the relationship between genes and lifespan.
- The 50 percent figure is consistent. Shenhar informed Cox that twin studies conducted on most human traits, including the age at which menopause begins, consistently reveal a heritability rate of approximately 50 percent. Additionally, height, body fat distribution, and muscle build exhibit comparable levels of heritability.
- Other species hint at the same story. Morten Scheibye-Knudsen of the University of Copenhagen, who wrote the editorial that ran alongside the study, told Cox that humans top out around 120 years, yeast cells live 13 days, and bowhead whales reach 200, so genes clearly set lifespan limits.
- Not everyone is fully convinced. Eric Verdin, head of the Buck Institute for Research on Aging, told Cox the line between intrinsic and extrinsic mortality is fuzzier than it looks, since vulnerability to infections like Covid or flu has a genetic component. Shenhar added that the team re-ran the analysis to account for this and still landed near 50 percent.
- The hunt for longevity genes continues. Centenarians appear to carry a lower risk of chronic disease, and a few protective gene variants have been identified, such as FOXO3, APOE, and SIRT6. Verdin suspects long life depends on combinations of genes rather than any single one.
Cox concludes by emphasizing that the findings should not be interpreted as fatalistic. Verdin expresses concern that the study might discourage individuals from maintaining healthy habits. However, Shenhar stresses that lifestyle factors still account for the remaining 45 percent of the variance, and diet and exercise can still influence an individual’s position within their genetic range.
Acknowledgement: This summary was generated using AI writing tools as part of my AI Explorations process. For more information, please refer to the original article listed below.