What does it mean that intrinsic lifespan is ~50% heritable?

It means that, in a given population and environment, around half of the variation in lifespan attributed to intrinsic (aging-related) mortality can be explained by genetic differences. It does not mean genes determine any one person’s lifespan.

Why were older estimates of lifespan heritability lower?

Older studies were confounded by extrinsic mortality (accidents, infections, violence), especially in historical cohorts. Those deaths add noise that weakens lifespan similarity even among genetically identical people, lowering estimated heritability.

Does this mean lifestyle doesn’t matter?

No. Heritability is a population statistic, not fate. Lifestyle and environment still influence disease risk, functional decline, and whether genetic predispositions are expressed.

What is the practical takeaway for longevity research?

Separating intrinsic from extrinsic mortality can clarify genetic signal, improve study design, and strengthen the case for identifying longevity-associated variants and mechanisms of aging.

Longevity Genetics Just Got Rehabilitated

Hook

For years, the safe answer has been:

Longevity is mostly lifestyle. Genetics barely matter.

A new paper in Science just made that position very uncomfortable.

Not because the data changed —
but because we finally stopped counting the wrong deaths.

Context: Why Longevity Genetics Fell Out of Favor

Most human longevity datasets come from people born in the late 1800s and early 1900s.

Those cohorts died in large numbers from hazards that had little to do with aging biology:

infections that are now treatable
accidents and workplace injuries
violence and war

If you treat those deaths as “aging,” you blur the signal you’re trying to measure.

The Missing Distinction

The paper separates mortality into two categories:

Extrinsic mortality

Deaths caused by external forces: accidents, infections, violence, environment.

Intrinsic mortality

Deaths caused by biological aging: cancer, cardiovascular disease, neurodegeneration.

Only intrinsic mortality reflects how fast a body actually ages.

🧠 Why Heritability Was Underestimated

Heritability depends on correlation.

Identical twins should die at similar ages if genetics matter.

But extrinsic deaths can “break” that correlation:

one twin dies young from infection or accident
the other lives decades longer

Same genes. Different lifespans.

That doesn’t prove genetics are weak — it proves the outcome included many deaths unrelated to aging.

The Result That Changes the Conversation

Once extrinsic deaths are accounted for:

Intrinsic human lifespan appears ~50–55% heritable.

That’s:

more than double many classic estimates
in the same range as many complex human traits

Why This Holds Up

The authors check the prediction in multiple ways (including twin data with different levels of extrinsic mortality), and the pattern behaves like a real effect: as extrinsic mortality falls, estimated heritability rises.

What This Does Not Mean

genetics ≠ destiny
heritability ≠ “genes decide your lifespan”
environment, healthcare, and random biological variation still matter

But it does mean aging biology is not marginal.

FAQ

Q: What does “~50% heritable” actually mean?
A: It’s a population-level statistic: roughly half of the variation in intrinsic (aging-related) lifespan is associated with genetic variation in that population and context.

Q: Why does removing extrinsic mortality change the estimate so much?
A: Extrinsic deaths add noise that isn’t tightly coupled to aging mechanisms, reducing twin correlations and pushing heritability estimates down.

Q: Does this invalidate lifestyle advice?
A: No. Lifestyle can still shift disease risk and functional decline, often by interacting with inherited biology.

Q: What’s the cleanest next step for readers?
A: Understand the distinction and don’t confuse “avoidable hazards” (extrinsic) with “aging mechanisms” (intrinsic). See: Intrinsic vs Extrinsic Mortality.