July 3rd, 2026
If used sensibly, models of aging can offer some insight into the bounds of the possible with regard to which classes of biological mechanism are more or less important in determining pace of aging, onset of disease, and life span. Researchers here use a specific type of model, the saturating removal model of damage accumulation, and tinker with the parameters to see which of the processes represented by those parameters best predict the observed range of life spans across species. Perhaps the most interesting outcome is that mice and humans end up in different broad buckets in terms of categorizing how mechanisms of aging interact; this is far from the only study to suggest that this is the case.
The saturating removal (SR) model was defined and calibrated based on longitudinal damage measurements in mice (senescent cells) and Escherichia coli (membrane damage). The model is based on the simplifying hypothesis that the damage that causes aging can be summarized by a scalar x and that life cannot persist above a certain level of x. The biochemical nature of x can be different in each species. The SR model describes the dynamics of damage by a stochastic differential equation that includes production, removal, and noise. Production rises linearly with age, whereas removal saturates at high damage. Death occurs when damage exceeds a threshold. The SR model explains many quantitative patterns of aging including Gompertz and Weibull hazard curves, distributions of human frailty index, disease incidence curves, and heritability of lifespan.
