We defend the hypothesis that life-spanning population survivorship curves, as described by Gompertz' law and composed from cross-sectional data (here mortality), reflect an intrinsic aging principle active in each subject of that population. In other words Gompertz' law reflects aging of a prototypical subject, provided minimal (or no) external causes of death (i.e. fatal infections, starvation, accidents). Our approach deviates from the traditional (exponential) Gompertz' hazard function. For instance, the here formulated Gompertz' law accurately describes old-age deceleration of both all-cause mortality and the incidence of some ageing-associated cancers, as illustrated for the Dutch population. We consider the possibility that the old-age expression and progression of cancer and other pathologies becomes suppressed, because of random (and exponential) accumulation of damage during life. Gompertz' law may trigger new concepts and models describing life-spanning physiological and pathological processes of aging. We discuss (and reject) various aging models (e.g. a predominant role of individual variations at birth; reliability theory) and point to the explanatory potential of network models and systemic regulatory models.
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