Human life expectancy has increased steadily over time since the 1800s, but much of the analysis is focused on life expectancy at birth, where the dominant effects involve improvements in early life survival. More interesting are the measures of remaining life expectancy at some adult age. These measures also increase over time, but more slowly. In recent decades, the increase in life expectancy at age 65 has increased at a pace that is on the order of one year in every ten. Since this happened over a span of time in which little to no meaningful progress was made in deliberately treating aging as a medical condition, it is reasonable to ask how it happened. As is usual in matters of human epidemiology, firm answers are hard to come by. Correlations are easy to generate, but it is challenging to prove causation, or determine the relative importance of different contributions to an observed outcome.
Nonetheless, researchers have generated insight from the statistics of human mortality. For example work from fifteen years ago shows an equal split between (a) reduced premature mortality, compressing mortality to a smaller range of later ages, and (b) a reduction in mortality in those later ages. It is an open question as to whether these are both manifestations of the same underlying mechanisms, resulting from improvements in public health, reduced exposure to severe infection, general advances in medicine, and so forth. If we accumulate less damage along the way, do we also tend to live longer? Reliability theory suggests this is the case, building on what is known of the statistics of the failure of complex arrays of redundant parts.
In one sense a reduced mortality due to intrinsic causes and age-related disease is equivalent to a slower pace of aging, as aging is defined by its effects on mortality. In another sense, whether aging has been slowed depends on how one defines aging - at the level of mechanisms, capacity, and cellular biology rather than at the level of epidemiology and mortality, that is. Today's open access paper is a consideration of whether we can or should say that increased life expectancy means that aging is slowed versus postponed, and that is a distinction that really does force one to engage with how exactly aging is defined. What, mechanistically, is aging, exactly, if the pace of aging does not change, but the age of onset of aging can vary? This is a very different view to that provided by reliability theory.
The rhythm of aging: Stability and drift in the individual rate of senescence
Human aging is marked by a steady rise in the risk of dying with age - a process demographers call senescence. Over the past century, life expectancy has risen dramatically, but is this because we are aging slower, or simply starting it later? This has been framed as a testable hypothesis: the rate at which the risk of dying increases with age for humans may be a basic biological constant that is very similar and perhaps invariant across individuals and over time. From this perspective, gains in life expectancy would reflect delayed aging, not a change in the underlying process of senescence. But if the rate of aging is truly changing, it would suggest that the biological processes underlying senescence are more responsive to environmental, behavioral, or historical conditions than previously assumed.
We focus on actuarial senescence - the age-related rise in mortality risk - which, in most adult populations, shows an exponential increase in mortality with age, well described by the Gompertz law. The Gompertz slope measures how quickly risk accelerates as deterioration accumulates. Though not a direct biological measure, is widely used as a proxy for the rate of aging. Empirical tests of this hypothesis have yielded mixed findings. This may suggest that the variations in could be historically driven. Period events - such as wars, pandemics, and economic crises - strike multiple cohorts at once, just at different ages, and their lasting consequences can subtly distort the mortality patterns within each exposed cohort through cumulative shifts. As a consequence, when we estimate cohort by cohort, we may be tracing not a pure signal of the aging process, but the lasting effects of these shared historical events. As these shocks accumulate over time, they can produce variations that mimic a change in the slope of mortality, even if the underlying biological rate is constant.
We ask whether cohort-to-cohort variation in the Gompertz slope reflects a shift in the pace of aging or the effects of period shocks. We test this idea using a framework that decomposes the pace of senescence into three components: a biological baseline, a long-term trend, and the cumulative impact of period shocks. Applying this to cohort mortality data above age 80 from 12 countries, we find that once period shocks are accounted for, there is no statistical evidence of a long-term trend, consistent with the hypothesis. Analyses using lower starting ages yield the same qualitative conclusion. Rather than indicating a change in the process that drives senescence, these variations are consistent with echoes of shared historical events. Together, these findings indicate no evidence of a persistent directional change in the individual rate of aging.
This stability does not imply that aging is fixed in all aspects. Over the past century, survival has shifted toward older ages and life expectancy has increased substantially. These improvements may primarily reflect declines in baseline and background mortality rather than persistent changes in the rate at which mortality rises with age. In demographic terms, the onset of senescence may be postponed even if its tempo remains stable.
View the full article at FightAging
