The transition to ageing

Giambattista Salinari, Università degli Studi di Sassari
Gustavo De Santis, Università di Firenze

Ageing may be broadly defined as an increasing limitation of capabilities due to the progressive accumulation of cellular damage; or, more strictly, as we do in this paper, as the increase of mortality risks with age. Several models that refer to vital functions, including Gompertz’s exponential formula on the force of mortality, assume that ageing begins at a certain, if unspecified age. But this (often implicit) assertion is not so obvious as it may appear at first sight. There are two main questions. The former is theoretical: why should a “triggering” age for senescence exist at all? Why do mortality risks start to increase from a given age, and not before or, conversely, why do they not remain constant? In this paper, the conjecture is advanced that somatic damage, which accumulates probably since birth, starts to affect mortality risks only past a certain threshold age: only at that point does “latent” senescence become “observable” senescence. The second question is, instead, empirical: how can one determine this threshold age? To this end, Bai’s approach to the study of breakpoints in time series is applied to a set of female cohorts (on data drawn from the Human Mortality Database), from 14 countries, over several years of birth (1850 to 1937). Results consistently suggest that an age at the onset of observable senescence can be identified. However, it is not stable: it has declined over time from about 48 years at the beginning of the period (cohorts born in 1850-1869) to about 32 at its end (cohorts born in 1920-1937).