Physiological senescence is characterized by the increasing limitation of capabilities of an organism resulting from the progressive accumulation of molecular damage, which at group (cohort) level translates into, among other things, an increase in mortality risks with age. Physiological senescence is generally thought to begin at birth, if not earlier, but models of demographic aging (i.e., an increase in mortality risks) normally start at considerably later ages. This apparent inconsistency can be solved by assuming the existence of two mortality regimes: "latent" and "manifest" aging. Up to a certain age, there is only latent aging: physiological senescence occurs, but its low level does not trigger any measurable increase in mortality. Past a certain level (and age), molecular damage is such that mortality risks start to increase. We first discuss why this transition from latent to manifest aging should exist at all, and then we turn to the empirical estimation of the corresponding threshold age by applying Bai's approach to the estimation of breakpoints in time series. Our analysis, which covers several cohorts born between 1850 and 1938 in 14 of the countries included in the Human Mortality Database, indicates that an age at the onset of manifest aging can be identified. However, it has not remained constant: it has declined from about 43 and 47 years, respectively, for males and females at the beginning of the period (cohorts born in 1850-1869) to about 31 for both males and females toward its end (cohorts born in 1920-1938). A discussion of why this may have happened ensues.

Aux âges adultes, la force de mortalité s’accroît de façon plus ou moins exponentielle avec l’âge, et le paramètre associé à l’âge, ? , permet d’évaluer le taux de sénescence (vieillissement) d’une génération. L’hypothèse a été récemment avancée que le taux de sénescence au niveau individuel serait une constante biologique, proche de 0,1. Cet article contribue au débat de deux façons : il propose d’abord une méthode simple fondée sur une analyse classique des données de panel longitudinal, afin de comparer le taux de sénescence ? entre différentes cohortes et différents groupes où jouent des effets de fragilité et de période, et il présente ensuite quelques estimations empiriques de ? , par sexe, pour diverses cohortes, dans différents pays. La méthodologie proposée est appliquée aux données de la Human Mortality Database pour les générations nées entre 1878 et 1912 (Danemark, Finlande, Norvège, Suède et Suisse), observées entre 65 et 98 ans de 1943 à 2010. Le taux de sénescence ? apparaît effectivement proche de 0,1 : la plupart des écarts qui ressortent de l’analyse (par pays, sexe, génération et âge) sont très faibles en termes absolus, en particulier pour les femmes, même s’ils sont statistiquement significatifs.

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Some European countries, such as Greece and Spain, were severely hit by the 2008 economic crisis whereas others, such as Germany, were practically spared by it. This divergence allowed us to implement a difference in differences research design which offered the possibility to observe the long-lasting effects produced by the crisis on European life expectancy. Our analysis—based on Eurostat data from 2001 to 2019—shows that life expectancy increased faster, after the onset of the crisis, in those countries where the rise in unemployment was more intense. Furthermore, our results show that this gain in life expectancy persisted, and sometimes further increased, until 2019 when most macro-economic variables had returned to their pre-crisis values. Previous research has identified that mortality behaves procyclically in developed countries: when the economy slows down mortality decreases and vice versa. Our findings show, by contrast, that life expectancy behaves asymmetrically: it responded to an increase but not to a decrease in unemployment. This calls for a reconsideration of the causal mechanisms linking together the economic cycle and mortality in developed countries.