An analysis of twin cohort data suggests that human life span is far more heritable than previously believed. The findings of the analysis show that once deaths from external factors, such as accidents or infectious disease, are accounted for, genetics may explain ~50% of how long we live. "[T]he study … has important consequences for aging research," write Daniela Bakula and Morten Scheibye-Knudsen in a related Perspective. "A substantial genetic contribution strengthens the rationale for large-scale efforts to identify longevity-associated variants, refine polygenic risk scores, and link genetic differences to specific biological pathways that regulate aging." Understanding the heritability of human life span is a central question in aging research, yet measuring the genetic influence on longevity remains challenging. Although some genes linked to life span have been identified, external environmental forces, such as disease or living conditions, exert a powerful influence on how long someone lives and often obscure or confound potential genetic effects. Moreover, previous studies have produced widely varying estimates of human life-span heritability, fueling skepticism about the role of genetics in aging. These conclusions are striking, given that life span is far more heritable in laboratory mice and that most human physiological traits show much more genetic determination. According to Ben Shenhar and colleagues, this discrepancy may arise from overlooked confounders in previous research, particularly the heavy burden of "extrinsic" mortality – deaths due to external causes – in the historical populations that underpin these studies. These external causes of death likely dilute the measurable impact of genetics, which primarily shapes "intrinsic" mortality driven by aging and internal biological decline.
Shenhar et al. used mathematical models, simulations of human mortality, and multiple large-scale twin cohort datasets to disentangle intrinsic and extrinsic sources of death. According to the findings, extrinsic mortality systematically depresses estimates of life-span heritability. Once deaths from external causes are properly accounted for, the authors show that the genetic contribution to human life span rises dramatically to roughly 55% – more than double previous estimates – suggesting that genetics is a central force in human aging. These revised estimates align human life span with the heritability of most other complex physiological traits and with the life-span heritability observed in other species.
