Jim Oeppen

The new trends in survival improvement require a revision of traditional gerontological concepts

In 1960, Strehler and Mildvan (SM) theoretically predicted that the parameters of the Gompertz approximation to a mortality curve are negatively correlated. This means that the changes in the human mortality rate resulting from improvement in living standards, progress in health care or the influence of other factors must follow certain regularities prescribed by dependence between the Gompertz parameters. Such dependence, called SM correlation, was then confirmed in a number of empirical studies using period data on human mortality. Since the SM theory was based on the cohort model of mortality, it was tacitly assumed that period and cohort SM correlation patterns are similar. The remarkable stability of the SM correlation pattern revealed in these studies was often regarded as manifestation of a universal demographic law regulating changes in the age pattern of mortality rates. In this paper, we investigated trends in mortality decline in France, Japan, Sweden and the United States. In contrast with traditional expectations, we found that the SM correlation pattern was relatively stable only in certain periods of a populations survival history. Recently, several new correlation patterns emerged and, despite some differences in the timing of the changes, the new patterns are remarkably similar in all four countries. Contrary to traditional expectations, the patterns are not the same for cohort and period mortality data when SM correlations are calculated for France, Sweden and the United States. We show that some changes in the patterns of SM correlation admit interpretation in terms of a biological mechanism of individual adaptation (survival trade off). Some other patterns, however, contradict basic postulates of the SM theory. This indicates the need for revision of traditional concepts establishing the relationship between physiological and demographic patterns of aging.

New age patterns of survival improvement in Sweden: do they characterize changes in individual aging?

The parameters of the Gompertz approximation to the mortality curve are negatively correlated. Strehler and Mildvan [Science 132 (1960) 14] predicted this property of the mortality curve using a mathematical model of mortality and aging and then confirmed it in empirical studies. Despite the fact that their theory was based on the cohort model of mortality the SM correlation was also revealed in the analysis of period mortality data. In fact, most applications of the SM model to human data use Gompertzs approximation to the period mortality rate. Many researchers studying SM correlation consider it a universal demographic law. Such correlation prescribes a certain regularity in mortality changes. All mortality curves must intersect at one point. Mortality decline must produce the rectangularization of survival curves. In this paper we investigated the changes in the patterns of mortality decline in Sweden between 1861 and 1999. We found a difference in patterns of SM correlation for cohort and period mortality data. We investigated trends in survival improvement and found that the tendency to rectangularization of the survival curve existed for only a limited period of time. Then it was gradually replaced by near parallel shift of the survival curve to the right. We found that the pattern of SM correlation was relatively stable only at certain phases of the survival history of male and female populations. We analyzed past and recent patterns of survival changes and discussed possible causes for instability of SM correlation both in cohort and in period mortality data.

Losses of expected lifetime in the United States and other developed countries: methods and empirical analyses.

Patterns of diversity in age at death are examined using e†, a dispersion measure that equals the average expected lifetime lost at death. We apply two methods for decomposing differences in e†. The first method estimates the contributions of average levels of mortality and mortality age structures. The second (and newly developed) method returns components produced by differences between age- and cause-specific mortality rates. The United States is close to England and Wales in mean life expectancy but has higher life expectancy losses and lacks mortality compression. The difference is determined by mortality age structures, whereas the role of mortality levels is minor. This is related to excess mortality at ages under 65 from various causes in the United States. Regression on 17 country-series suggests that e† correlates with income inequality across countries but not across time. This result can be attributed to dissimilarity between the age- and cause-of-death structures of temporal mortality reduction and intercountry mortality variation. It also suggests that factors affecting overall mortality decrease differ from those responsible for excess lifetime losses in the United States compared with other countries. The latter can be related to weaknesses of health system and other factors resulting in premature death from heart diseases, amenable causes, accidents and violence.

What are the effects of maternal and pre-adult environments on ageing in humans, and are there lessons from animal models?

An open issue in research on ageing is the extent to which responses to the environment during development can influence variability in life span in animals, and the health profile of the elderly in human populations. Both affluence and adversity in human societies have profound impacts on survivorship curves, and some of this effect may be traceable to effects in utero or in infancy. The Barker Hypothesis that links caloric restriction in very early life to disruptions of glucose-insulin metabolism in later life has attracted much attention, as well as some controversy, in medical circles. It is only rarely considered by evolutionary biologists working on phenotypic plasticity, or by biogerontologists studying model organisms such as C. elegans or Drosophila. One crucial mechanism by which animals can respond in an adaptive manner to adverse conditions, for example in nutrition or infection, during development is phenotypic plasticity. Here we begin with a discussion of adaptive plasticity in animals before asking what such phenomena may reveal of relevance to rates of ageing in animals, and in humans. We survey the evidence for effects on adult ageing of environmental conditions during development across mammalian and invertebrate model organisms, and ask whether evolutionary conserved mechanisms might be involved. We conclude that the Barker Hypothesis is poorly supported and argue that more work in human populations should be integrated with multi-disciplinary studies of ageing-related phenomena in experimental populations of different model species that are subjected to nutritional challenges or infections during pre-adult development.

Comparing the Results from Generalised Inverse Projection and Stochastic Inverse Projection

Since the introduction of Lee’s Inverse Projection (IP — [7]), several modifications have been made to overcome some of its methodological limitations and make the procedure suitable for the existing sources, which may be very different from country to country. In this field, two procedures in particular instigated a lively discussion among demographers in the 1990s, due to their completely different approaches: Generalised Inverse Projection (GIP — [11, 12]) and Stochastic Inverse Projection (SIP — [2, 3]).