Slowed Gompertzian ageing in long-lived C. elegans results from expansion of decrepitude, not decelerated ageing

In populations of many animal species, including humans, mortality rates increase exponentially with advancing age. The scale and rate of increase can be set by two parameters, α and β, respectively, of the Gompertz equation. Interventions that extend lifespan can reduce either or both parameters. A long-standing supposition is that β corresponds to biological ageing rate, and α to ageing-independent causes of mortality. Here, we investigate the biological basis of α and β using the nematode Caenorhabditis elegans, through the combined study in populations and individuals of effects of life-extending interventions on mortality and age-changes in health. We demonstrate that reductions in β arise not from slowed biological ageing, but rather from expansion of decrepitude (gerospan) in longer-lived population members. In contrast, reductions in α better reflect healthspan expansion, an indicator of slowed biological ageing. Thus, our investigation presents a new, empirical understanding of the Gompertz parameters that inverts their traditional interpretations.

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Journal
Nature Communications
Published
2026-04-13
DOI
https://doi.org/10.1038/s41467-026-71780-7
Citations
1
Primary Topic
Genetics, Aging, and Longevity in Model Organisms
Type
article
Field-Weighted Citation Impact
9.63

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article

Slowed Gompertzian ageing in long-lived C. elegans results from expansion of decrepitude, not decelerated ageing

Bruce Zhang, David Gems
1 citations
Nature Communications
Genetics, Aging, and Longevity in Model Organisms
9.63
article

Slowed Gompertzian ageing in long-lived C. elegans results from expansion of decrepitude, not decelerated ageing

Bruce Zhang, David Gems
article en
1 citations

Abstract

In populations of many animal species, including humans, mortality rates increase exponentially with advancing age. The scale and rate of increase can be set by two parameters, α and β, respectively, of the Gompertz equation. Interventions that extend lifespan can reduce either or both parameters. A long-standing supposition is that β corresponds to biological ageing rate, and α to ageing-independent causes of mortality. Here, we investigate the biological basis of α and β using the nematode Caenorhabditis elegans, through the combined study in populations and individuals of effects of life-extending interventions on mortality and age-changes in health. We demonstrate that reductions in β arise not from slowed biological ageing, but rather from expansion of decrepitude (gerospan) in longer-lived population members. In contrast, reductions in α better reflect healthspan expansion, an indicator of slowed biological ageing. Thus, our investigation presents a new, empirical understanding of the Gompertz parameters that inverts their traditional interpretations.

Nature Communications
MRC Unit for Lifelong Health and Ageing (GB), University College London (GB)
Wellcome, Wellcome Trust, National Institutes of Health
Openalex Percentile: Top 1%
Genetics, Aging, and Longevity in Model Organisms
9.63
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