Remaining life expectancy at 65 has increased by a year with every passing decade since at least the middle of the 20th century, an improvement that has occurred without deliberate targeting of the mechanisms of aging. To what degree is this observed trend in human life expectancy due to (a) a general slowing of aging that will carry on throughout the entire life span, and thus lengthen maximum observed life span, or (b) a more selective slowing of processes of aging that does not meaningfully impact lifespan-limiting mechanisms that operate in late life, and thus does not lengthen maximum life span?
For example, we know that supercentenarians (the tiny fraction of people who live to be age 110 and older) exhibit significant degrees of transthyretin amyloidosis, and this may be the majority cause of death in that age category. Much earlier in old age, this form of amyloidosis is present but probably not a major killer in comparison to other mechanisms of aging. It is entirely plausible that positive effects on life span resulting from past improvements in medical technology and changing lifestyle choices could have limited effects on this one specific issue, and thus would have a limited effect on maximum human lifespan.
Whether or not this is the case or is an open question, however. This is an interesting area of scientific inquiry, and today's open access paper is a worthy and novel addition to the literature regarding historical trends in life expectancy, but this work is of limited relevance to efforts to extend human life. We have a list of causative mechanisms of aging to target for repair, and a biotechnology community advanced enough to undertake that work. The best approach to the treatment of aging as a medical condition is to start fixing issues and see how it goes: clearance of senescent cells, for example, is performing exceptionally well in animal models, and will hopefully see greater progress into human use in the years ahead.
A key but unresolved issue in the study of human mortality at older ages is whether mortality is being compressed (which implies that we may be approaching a maximum limit to the length of life) or postponed (which would imply that we are not). We summarize historical mortality data in 19 currently-industrialized countries by birth cohort using a variant of the Gompertz mortality law, and find that it fits cohort mortality data extremely well. Using this law, we identify the youngest age at which individuals in each cohort reach an assumed mortality plateau, which we call the Gompertzian Maximum Age (GMA). We find that over much of the period covered by our data, there was no increase in the GMA. Historical improvements in life expectancy were therefore largely the result of mortality compression. We demonstrate, however, that there have been episodes where the GMA increased. The presence of these episodes of mortality postponement suggests that the maximum length of a human life is not, in fact, fixed.
The first episode of mortality postponement that we identify occurred for cohorts born in the early part of the second half of the 19th century, and was more pronounced for females than for males. Over this period, the GMA increased by around 5 years. We can only speculate as to the causes of this increase, but as the first of these cohorts reached age 50 just after 1900 and the last reached age 100 in 1980, this may be related to a first wave of improvements in public health and medical technology. We identify a second, and much more significant, episode of mortality postponement, which is affecting cohorts born between 1910 and 1950 (so those currently aged between 70 and 110). We estimate that the GMA for these cohorts may increase by as much as 10 years, and remaining life expectancy at age 50 by as much as 8 years, depending on the country.
The timing of these episodes of mortality postponement explain why longevity records have been so slow to increase in recent years - cohorts old enough to have broken longevity records were too old to experience the current bout of postponement - and identifies significant potential for longevity records to rise by the year 2060 as younger cohorts, who did experience it, reach advanced old age. Our results on the division of changes in remaining life expectancy at age 50 across cohorts between compression and postponement are robust to our modelling choices. Likewise, our conclusion that longevity records will likely be broken in the coming decades is also robust to a wide range of possible assumptions. But our predictions of precisely by how much these records will rise, and when, depend on our modelling assumptions, in particular on the maximum mortality rate we assume.
We emphasise further that cohorts born before 1950 will only have the potential to break existing longevity records if policy choices continue to support the health and welfare of the elderly, and the political, environmental and economic environment remains stable. The emergence of Covid-19 and its outsize effect on the mortality of the elderly provides a salutary warning that none of this is certain. If, however, the GMA does increase as the current mortality experience of incomplete cohorts suggests is likely, the implications for human societies, national economies, and individual lives will be profound.