The Effect of the Great Recession on Italian Life Expectancy.

The 2008 economic crisis, also called the Great Recession, produced only a moderate rise in unemployment in Italy, but the consequences for public debt management were far more serious. Italy makes for a good case study for evaluating the effect on life expectancy at birth of the cost containment program in the health care system, implemented after the crisis began. To this end we employed the Artificial Control method using the data from the Human Mortality Database to assess the causal effect of the 2008 economic crisis on the subsequent evolution of life expectancy at birth (until 2019, before the onset of the COVID-19 pandemic). Our analysis identifies a significant deceleration in the progression of Italian life expectancy. Ten years after the onset of the crisis, Italy appears to have lost almost 1 year of life expectancy with respect to what would have been expected had the crisis never happened.

The long-term effect of the Great Recession on European mortality.

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.

The effect of disease burden on the speed of aging: an analysis of the Sardinian mortality transition.

According to the constant senescence hypothesis, senescence cannot be accelerated or decelerated by exogenous factors. Two contrasting theories have been proposed in the literature. According to the inflammaging theory, those individuals who have experienced a higher antigenic load will experience more rapid senescence. Instead, the calorie restriction theory stresses that excessive daily calorie intake can produce an acceleration in senescence. To test these theories, this paper analyzes the evolution of the rate of aging in Sardinia (Italy). In this population, the epidemiological transition started without any substantial modification in nutritional levels. This allows us to test the constant senescence hypothesis against the inflammaging theory, without the possible confounding effect produced by the nutrition transition. To accomplish this aim, the longitudinal life tables from 80 years onwards for Sardinian cohorts born between 1866 and 1908 were reconstituted. They were then used to estimate the rate of aging by means of the Gamma-Gompertz model. Coherently with the inflammaging theory, the results show that the Sardinian population experienced a dramatic decrease in the rate of aging that coincided with the onset of the epidemiological transition.

Rethinking mortality deceleration.

The evolution of mortality shows a marked deceleration at older ages. This phenomenon is generally thought to be an effect of selection: mortality decelerates because it progressively selects the most robust individuals in the cohort. Other processes, however, may contribute to mortality deceleration as well. People may not be passive in the face of ageing and may try to counter it by modifying their behaviours and lifestyles. In this paper, I propose a method to test whether selection is to be considered the unique mechanism responsible for mortality deceleration. I applied this method to the life tables of selected female cohorts drawn from the Human Mortality Database. The results indicate mortality decelerates more rapidly than predicted by the selection theory.

On the beginning of mortality acceleration.

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.