Programmed Aging

What it proposes

Aging is the outcome of an evolved genetic program, with active regulation that produces predictable, sometimes timed, decline. In strong form: aging serves a population-level fitness purpose (turnover of generations enables adaptation).

The traditional objection

Standard evolutionary theory (Williams 1957) held that selection cannot favour a program that harms the individual, because individuals carrying “non-aging” mutations would out-reproduce others. Programmed aging was therefore considered impossible without group-level selection mechanisms, which are usually weak.

Renewed interest

Modern evidence consistent with at least some programmed element:

• Epigenetic clocks tick at a remarkably steady rate within species, suggesting a regulated process.
• Yamanaka reprogramming can rewind epigenetic age in cells — evidence that age is encoded in a program of marks, not just damage.
• Lifespan-determining genes (daf-2, sirtuins, mTOR) tightly regulate aging in many species.
• Pan-mammalian lifespan ranges spanning four orders of magnitude with related anatomies are hard to explain by damage alone.

How to think about it

The current synthesis: aging is part programmed (the regulated component) and part stochastic damage (the accumulated component). Where they meet differs by tissue and species.

More on this topic

• Disposable Soma Theory — Theory.
• Born to Run — Christopher McDougall (2009) — Book.
• The Telomere Effect — Elizabeth Blackburn & Elissa Epel (2017) — Book.
• Telomere Attrition — Hallmark.
• Telomerase (TERT / TERC) — Pathway.

Related entries

Antagonistic pleiotropy, Information theory of aging, Epigenetic alterations.