Human life expectancy is more hereditary than previously thought, according to a study

A key caveat is that the flagship estimate of 55% heritability depends on modeling choices and on conditioning the analysis on survival to specific “cutoff” ages (in one dataset, both twins must survive to older ages), which can affect correlations in nontrivial ways. I would therefore treat the 55% figure as a model-based estimate tied to a particular definition of “intrinsic” lifespan, not as a single settled fact. In this study, “extrinsic mortality” is defined as an age-independent background risk rather than external causes of death, which is important for interpreting the headline results. As a demographer, I usually think of extrinsic mortality as deaths from external or behavioral causes that are strongly patterned by age and by social conditions, which is quite a different concept.

Even if this work motivates the search for genetic predictors of longevity, and even if such efforts are successful, practical benefits from personalized interventions are likely to arrive unevenly and may reinforce existing socioeconomic inequalities in lifespan. By contrast, the largest and most durable gains in longevity have historically come from population-level improvements in living conditions, education, public health, and social protection, and from medical innovations only insofar as they diffuse widely across social groups. These “unexciting” interventions raise standards of living broadly, leading not only to longer lives but to healthier and more enjoyable lives, while also reducing inequalities in survival across social groups.

How much of our life expectancy is written in our genes? A new study using data from twins suggests that the answer may be: more than we thought, although with important nuances. By analysing records of twins from Denmark, Sweden and the United States, researchers estimate that approximately 55% of the variation in human lifespan is genetically heritable.

A key contribution of the study is the distinction between intrinsic mortality—deaths resulting from internal biological processes—and extrinsic mortality, which comes from external causes such as accidents, violence, infections, or environmental risks. Using mathematical models applied to twin birth cohorts, the authors show that extrinsic mortality can systematically mask the genetic contribution to longevity. When external causes of death are taken into account, the genetic signal becomes clearer.

These findings reinforce the link between genetics and longevity. However, they should be interpreted with caution.

As the authors emphasise, heritability is a population statistic: it applies to a specific population, in a specific environment and at a specific point in time. It does not imply that lifespan is fixed for an individual. Life is inherently stochastic, and heritability should not be understood as a deterministic measure.

Furthermore, intrinsic mortality and heritability are not directly observed but inferred from statistical models based on assumptions about the evolution of mortality in cohorts. These models do not identify specific genes or incorporate detailed data on causes of death or genomic information; they focus on modelling the mathematical correlations of longevity between twins.

The study leaves fundamental questions open. If longevity is partly heritable, which genes are involved? Research in organisms such as C. elegans and mice has sought specific “longevity genes”. More recent whole-genome association studies have identified variants related to lifespan, but each explains only a small fraction of the total variation. The interaction between genes, environment and ageing remains one of the greatest challenges in biology.

At the mechanistic level, the complexity is even greater. Health and longevity result from the continuous interaction between environmental factors and biological responses, modulated by gene expression and epigenetic regulation. Although some diseases, such as Huntington's, clearly show the direct impact of genetic mutations, most deaths are the result of a complex interaction between genetic susceptibility, environmental exposure and physiological adaptation.

Ultimately, the central question remains: how long can humans live? If part of longevity is inherited, what will happen as societies continue to reduce external mortality through medical advances? Will future interventions—medical, environmental, or even genomic—be able to redefine the limits of human life? Genetics matters, no doubt. But it is only one piece of a deeply interconnected system in which biology, environment and chance are inseparable.