# Timing of mortality during development alters the evolution of aging

**Authors:** Peter Lenart, Sacha Psalmon, Benjamin D. Towbin

PMC · DOI: 10.1186/s12862-025-02464-x · BMC Ecology and Evolution · 2025-11-24

## TL;DR

The timing of when survival benefits occur during development strongly influences how quickly or slowly aging evolves in animals.

## Contribution

A new theoretical framework showing that early-life survival benefits accelerate aging, while late-life benefits slow it down.

## Key findings

- Early-life survival benefits increase reproductive success and accelerate aging.
- Late-acting survival benefits reduce the rate of aging evolution.
- Mortality timing during development shapes evolutionary forces on aging.

## Abstract

For most animals, intrinsic senescence-induced mortality increases with age, while deaths from extrinsic threats, such as predation or accidents, decline during development as individuals grow and mature. Age-dependent modulation of extrinsic mortality is known to influence the evolution of aging. Yet, how the precise timing of changes in mortality shapes evolutionary forces, i.e., when they enhance and when they slow-down aging, remains poorly understood.

To address this, we developed two complementary mathematical models that integrate survival benefits arising during development with the progressive increase in mortality associated with senescence. Agent-based simulations and deterministic analyses revealed a strong and consistent influence of the timing of developmental survival benefits on their evolutionary impact: early-life survival benefits accelerate the rate of ageing, while late-acting benefits slow it down. This difference arises because early-life benefits more strongly enhance individual reproductive success. Early-life benefits thereby increase the overall growth potential of the population more strongly than late-life benefits, thereby diminishing the relative evolutionary advantage of increased longevity.

Our results underscore the importance of mortality timing in the evolution of aging and provide a theoretical framework for connecting developmental trajectories to aging dynamics.

The online version contains supplementary material available at 10.1186/s12862-025-02464-x.

## Full-text entities

- **Diseases:** diabetes (MESH:D003920), CRD (MESH:D012140), CVD (MESH:D002318), Mortality (MESH:D003643), GMM (MESH:D004195), sarcopenia (MESH:D055948), cancer (MESH:D009369), accidents (MESH:D000081084)
- **Chemicals:** DA (-), peroxide (MESH:D010545)
- **Species:** Testudines (anapsid reptiles, order) [taxon 8459], Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12642333/full.md

## References

12 references — full list in the complete paper: https://tomesphere.com/paper/PMC12642333/full.md

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Source: https://tomesphere.com/paper/PMC12642333