Science
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30.3.2026

How Heritable Is a Long Life?

A new study comes to a surprising conclusion — and raises an old question anew

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What this article is about

• Genes may explain around half of how long humans live — more than previously thought

• Previous studies had an important mistake: They did not exclude accidental deaths and infectious diseases

• This doesn't change the meaning of lifestyle — but it does change how aging research will work in the future

• What the new number means and doesn't mean

How long someone lives depends on many things: diet, exercise, sleep, social environment, happiness. For decades, scientists were of the opinion that genes played a rather minor role — perhaps 20 to 25 percent. A new study, published in the journal Science, questions this.

Why earlier studies underestimated the role of genes

The previous estimates were based on historical data — from a time when many people died young from infectious diseases, consequences of accidents or in wars. These deaths have little to do with our own biology. However, they have superimposed the genetic influence on aging in the data and thus made it invisible.

Researchers from the Weizmann Institute of Science in Israel have corrected this mistake. They analyzed over 100 years of data from Danish and Swedish twin registers — and developed a mathematical model that distinguishes between external causes of death and those caused by biological aging.

The result: If you only look at biologically related deaths, genes explain around 50 percent of the differences in how old people live to be. This is more than twice as many as previously assumed — and similar to many other physical characteristics.

What that means — and what it doesn't

50 percent sounds like fate. It isn't.

Heredity is not a personal prognosis. It is a statistical statement: It describes how much of the differences between people in a particular population is explained by genetic variation. It says nothing about how an individual person's life works.

A comparison: Body size is around 80 percent hereditary. Nevertheless, people in Europe are significantly taller today than they were 100 years ago — because nutrition and living conditions have improved. The genes were the same; the environment had changed.

The same applies: lifestyle, prevention and medical care remain decisive. The other half — the non-genetic one — can be influenced by behavior and the environment. And because these factors can be changed, they often have more leverage in practice.

Why the study is still important

The finding that genes play a bigger role than expected has consequences for research in particular. So far, there has been little reason to search specifically for gene variants that influence aging — if genes barely play a role anyway, then what's the point?

With a heredity of 50 percent, this picture is changing. It is now more worthwhile to understand the genetic basis of aging — with the long-term goal of developing more targeted therapies and preventive approaches.

A side effect of the study is also interesting: Twins born in later decades — when infectious diseases and accidents were fatal less frequently — showed a clearer genetic connection with their lifespan. This confirms the thesis: The safer the environment, the more visible the genetic influence on aging becomes.

One limitation to keep in mind

The study is based on historical data from Scandinavia. Whether these figures still apply to today's societies is an open question — new chronic influences such as lack of exercise, air pollution or permanent stress could shift the picture again. The heredity of longevity is not a fixed number, but depends on context.

What we know
  • Genes explain around 50% of the differences in the biological lifespan — more than twice as many as previously estimated
  • Previous studies did not differentiate between external and biological causes of death and have therefore systematically underestimated the genetic influence
  • The lower the extrinsic mortality rate in a society, the more clearly the genetic influence on aging becomes visible
  • Heredity and lifestyle influence are not mutually exclusive — both can be strong at the same time

What we don't know
  • Which specific genes or gene variants are responsible for the effect
  • Whether the figures can be transferred to current populations with modern disease profiles
  • How genetic factors interact with specific lifestyle interventions

What is often overinterpreted
  • “50% hereditary” does not mean that the life span is predetermined — heritability is a population statistic, not an individual judgment
  • The study does not devalue lifestyle — the non-genetic half can be influenced by behavior and the environment
  • The results apply to historical cohorts in Scandinavia — a direct transfer to the present is uncertain

References

  1. Shenhar B et al. (2026). Heritability of intrinsic human life span is about 50% when confounding factors are addressed. Science, 391 (6784), 504—510. doi:10.1126/science.adz1187
  2. Bakula D, Scheibye-Knudsen M. (2026). Rethinking the heritability of aging. Science. doi:10.1126/science.aee3844

Experte

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Glossary

What this article is about

• Genes may explain around half of how long humans live — more than previously thought

• Previous studies had an important mistake: They did not exclude accidental deaths and infectious diseases

• This doesn't change the meaning of lifestyle — but it does change how aging research will work in the future

• What the new number means and doesn't mean

How long someone lives depends on many things: diet, exercise, sleep, social environment, happiness. For decades, scientists were of the opinion that genes played a rather minor role — perhaps 20 to 25 percent. A new study, published in the journal Science, questions this.

Why earlier studies underestimated the role of genes

The previous estimates were based on historical data — from a time when many people died young from infectious diseases, consequences of accidents or in wars. These deaths have little to do with our own biology. However, they have superimposed the genetic influence on aging in the data and thus made it invisible.

Researchers from the Weizmann Institute of Science in Israel have corrected this mistake. They analyzed over 100 years of data from Danish and Swedish twin registers — and developed a mathematical model that distinguishes between external causes of death and those caused by biological aging.

The result: If you only look at biologically related deaths, genes explain around 50 percent of the differences in how old people live to be. This is more than twice as many as previously assumed — and similar to many other physical characteristics.

What that means — and what it doesn't

50 percent sounds like fate. It isn't.

Heredity is not a personal prognosis. It is a statistical statement: It describes how much of the differences between people in a particular population is explained by genetic variation. It says nothing about how an individual person's life works.

A comparison: Body size is around 80 percent hereditary. Nevertheless, people in Europe are significantly taller today than they were 100 years ago — because nutrition and living conditions have improved. The genes were the same; the environment had changed.

The same applies: lifestyle, prevention and medical care remain decisive. The other half — the non-genetic one — can be influenced by behavior and the environment. And because these factors can be changed, they often have more leverage in practice.

Why the study is still important

The finding that genes play a bigger role than expected has consequences for research in particular. So far, there has been little reason to search specifically for gene variants that influence aging — if genes barely play a role anyway, then what's the point?

With a heredity of 50 percent, this picture is changing. It is now more worthwhile to understand the genetic basis of aging — with the long-term goal of developing more targeted therapies and preventive approaches.

A side effect of the study is also interesting: Twins born in later decades — when infectious diseases and accidents were fatal less frequently — showed a clearer genetic connection with their lifespan. This confirms the thesis: The safer the environment, the more visible the genetic influence on aging becomes.

One limitation to keep in mind

The study is based on historical data from Scandinavia. Whether these figures still apply to today's societies is an open question — new chronic influences such as lack of exercise, air pollution or permanent stress could shift the picture again. The heredity of longevity is not a fixed number, but depends on context.

What we know
  • Genes explain around 50% of the differences in the biological lifespan — more than twice as many as previously estimated
  • Previous studies did not differentiate between external and biological causes of death and have therefore systematically underestimated the genetic influence
  • The lower the extrinsic mortality rate in a society, the more clearly the genetic influence on aging becomes visible
  • Heredity and lifestyle influence are not mutually exclusive — both can be strong at the same time

What we don't know
  • Which specific genes or gene variants are responsible for the effect
  • Whether the figures can be transferred to current populations with modern disease profiles
  • How genetic factors interact with specific lifestyle interventions

What is often overinterpreted
  • “50% hereditary” does not mean that the life span is predetermined — heritability is a population statistic, not an individual judgment
  • The study does not devalue lifestyle — the non-genetic half can be influenced by behavior and the environment
  • The results apply to historical cohorts in Scandinavia — a direct transfer to the present is uncertain

Experte

Basel

Dr. Manuel Puntschuh

Referenzen

  1. Shenhar B et al. (2026). Heritability of intrinsic human life span is about 50% when confounding factors are addressed. Science, 391 (6784), 504—510. doi:10.1126/science.adz1187
  2. Bakula D, Scheibye-Knudsen M. (2026). Rethinking the heritability of aging. Science. doi:10.1126/science.aee3844

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