Damage accumulation splits ageing into two regimes
Why do some animals live for a few weeks and others for hundreds of years?
Researchers fitted survival data from dozens of species, from short-lived insects to long-lived mammals, to a mathematical model of damage accumulation and removal. The model, published in Nature Aging, describes ageing as a gradual build-up of damage in cells and tissues. But the analysis reveals that not all animals age in the same way: two fundamentally different regimes exist.
Ballistic versus quasi-steady-state
Short-lived species age in what the researchers call the ‘ballistic regime’. Damage accumulates rapidly and linearly, without reaching equilibrium. Ageing in these animals follows a straight trajectory toward death. Long-lived mammals, including humans, operate in a ‘quasi-steady-state regime’: damage and repair remain in balance for longer. Ageing is slower, and variation in lifespan is greater.
The researchers show that the rate of damage production is the strongest predictor of lifespan, stronger than the rate of damage repair. In other words, slowing or preventing damage accumulation appears to matter more than accelerating repair.
What this means for longevity research
This stochastic model (a model based on probabilistic processes) provides a new framework for comparing ageing across species. It aligns with earlier findings showing that levels of oxidative damage, DNA damage, and protein aggregation correlate with lifespan across the animal kingdom.
From a longevity science perspective, the implication is worth noting: if damage production is more decisive than repair capacity, prioritising damage-prevention strategies over repair therapies could be a rational approach. But the authors emphasise this is a modelling result. Whether and how it translates to clinical applications requires further research.