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The heritability of human lifespan is roughly 50%, once external mortality is addressed
Science
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.
Expert Reaction
These comments have been collated by the Science Media Centre to provide a variety of expert perspectives on this issue. Feel free to use these quotes in your stories. Views expressed are the personal opinions of the experts named. They do not represent the views of the SMC or any other organisation unless specifically stated.
Dr. Jack da Silva
"This is an impressively thorough study. We’ve known for quite some time that there is a lot of genetic variation for lifespan in populations of organisms such as fruit flies studied in the laboratory, and that single genes can have a very large effect on lifespan in these organisms.
The present study usefully shows that the same is true for humans. The study is also valuable in teasing out the effects of things that can kill us that aren’t age-related, such as accidents and infections, which has been a difficult task in the past."
Professor Tony Blakely is a Professorial Fellow in Epidemiology from the University of Melbourne
"This study finds that over half of how long we live is inherited. The authors also state: 'Heritability is a statistic that applies to a particular population in a particular environment at a particular time —it is not a fixed quantity like the gravitational constant.' Elaborating on this caveat from the authors, their study is among homogenous populations (i.e. where individuals are quite similar), namely twins in Denmark and Sweden. In more heterogeneous populations, the hereditary component will decrease. For example, across all Australians of all countries of birth and socioeconomic position, and even removing injury and infectious disease deaths, non-hereditary variation in longevity will be larger.
Second, the major drivers of increasing longevity in the last 200 years are lifestyle factors and sanitation; our genes have not changed much in the last 200 years!
That all said, what this study usefully demonstrates is that for people living in a certain context (time, place, person), and putting injury and infectious disease deaths aside, there is – unsurprisingly – a large amount of heritability of how long we might expect to live. Which reveals that our chances of developing fatal diseases (e.g. a type of cancer) is in moderate to large part, inheritable.
Whether there are genes that have some overall regulation of ageing that can be targeted to develop treatments to increase our lifespan is moot. It may be that this study is just a manifestation of the many genetic influences on many diseases, summed up to longevity. "
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