Intro
When people argue about whether longevity is “genetic” or “lifestyle,” they often talk past each other. A crucial missing concept is the difference between extrinsic mortality (deaths caused by external forces) and intrinsic mortality (deaths driven by biological aging).
This distinction matters because it changes how we interpret lifespan data — especially heritability estimates.
Key Points
- Extrinsic mortality (accidents, infections, violence) can mask genetic signal in lifespan studies.
- Intrinsic mortality reflects the biology of aging and age-related disease.
- Mixing both together can make lifespan heritability look artificially low.
- Modern populations have lower extrinsic mortality, so intrinsic biology becomes more visible in the data.
Extrinsic Mortality
Extrinsic mortality refers to deaths caused by factors originating outside the body, such as:
- Accidents (transport, falls, occupational injury)
- Infections (especially historically, before antibiotics and vaccines)
- Violence and warfare
- Environmental hazards
Extrinsic mortality tends to be more prominent earlier in adulthood and varies strongly across time, geography, and social conditions.
Intrinsic Mortality
Intrinsic mortality refers to deaths caused by processes originating within the body — the core machinery of aging and age-related disease — such as:
- Cancer
- Cardiovascular disease
- Neurodegenerative disease (including dementia-related pathways)
- Progressive loss of physiological function with age
Intrinsic mortality typically rises steeply with age and is often modeled as an exponential increase in later life.
Why This Changes Longevity Research
Heritability is estimated from patterns of similarity among relatives (for example, identical vs non-identical twins). When a large share of deaths are extrinsic, those deaths can “break” lifespan similarity even in genetically identical people.
That doesn’t prove genetics are unimportant. It often means the outcome being measured includes many deaths that are not driven by aging biology.
In practice, separating extrinsic from intrinsic mortality helps:
- Interpret heritability estimates more accurately
- Compare cohorts across time periods fairly
- Frame longevity research around aging mechanisms rather than historical hazards
FAQ
Q: What’s the simplest way to remember the difference?
A: Extrinsic = outside causes (accidents, infections). Intrinsic = inside causes (aging biology, age-related disease).
Q: Does this mean modern lifespan is “more genetic” than historical lifespan?
A: Often, yes — because modern societies have reduced many extrinsic deaths, genetic differences in intrinsic aging become easier to detect.
Q: If intrinsic lifespan is highly heritable, should people stop focusing on lifestyle?
A: No. Heritability isn’t destiny. Lifestyle can change risk, compress morbidity, and interact with genetic predispositions.
Q: Why do studies use cutoff ages (e.g., only include people who survive past a certain age)?
A: To reduce bias from early deaths. But cutoff choice can also discard informative deaths; best practice depends on the cohort and the amount of extrinsic mortality.
Q: What’s the practical takeaway for readers?
A: Separate “avoidable external hazards” from “aging biology.” Both matter — but they answer different questions.
Further Reading
- Science paper: https://www.science.org/doi/10.1126/science.adz1187
- Related post: Longevity Genetics Just Got Rehabilitated