Divergence in Age Patterns of Mortality Change Drives International Divergence in Lifespan Inequality

In the past six decades, lifespan inequality has varied greatly within and among countries even while life expectancy has continued to increase. How and why does mortality change generate this diversity? We derive a precise link between changes in age-specific mortality and lifespan inequality, measured as the variance of age at death. Key to this relationship is a young–old threshold age, below and above which mortality decline respectively decreases and increases lifespan inequality. First, we show for Sweden that shifts in the threshold’s location have modified the correlation between changes in life expectancy and lifespan inequality over the last two centuries. Second, we analyze the post–World War II (WWII) trajectories of lifespan inequality in a set of developed countries—Japan, Canada, and the United States—where thresholds centered on retirement age. Our method reveals how divergence in the age pattern of mortality change drives international divergence in lifespan inequality. Most strikingly, early in the 1980s, mortality increases in young U.S. males led to a continuation of high lifespan inequality in the United States; in Canada, however, the decline of inequality continued. In general, our wider international comparisons show that mortality change varied most at young working ages after WWII, particularly for males. We conclude that if mortality continues to stagnate at young ages yet declines steadily at old ages, increases in lifespan inequality will become a common feature of future demographic change.     

Lifespan Variation by Occupational Class: Compression or Stagnation Over Time?

Cross-sectional analyses of adult lifespan variation have found an inverse association between socioeconomic position and lifespan variation, but the trends by social class are unknown. We investigated trends in lifespan variation over four decades (1971–2010) by occupational social class (manual, lower nonmanual, upper nonmanual, other) using Finnish register data. We performed age and cause-of-death decompositions of lifespan variation for each sex (a) by occupational class over time and (b) between occupational classes at a shared level of life expectancy. Although life expectancy increased in all classes, lifespan variation was stable among manual workers and decreased only among nonmanual classes. These differences were caused by early-adult mortality: older-age lifespan variation declined for all the classes, but variation in early-adult mortality increased for all classes except the highest. The manual class’s high and stagnant lifespan variation was driven by declines in circulatory diseases that were equally spread over early mortality-compressing and older mortality-expanding ages, as well as by high early-adult mortality from external causes. Results were similar for men and women. The results of this study, which is the first to document trends in lifespan variation by social class, suggest that mortality compression is compatible with increasing life expectancy but currently achieved only by higher occupational classes.     

Trends in Education-Specific Life Expectancy,Data Quality,and Shifting Education Distributions: A Note on Recent Research

Several recent articles have reported conflicting conclusions about educational differences in life expectancy, and this is partly due to the use of unreliable data subject to a numerator-denominator bias previously reported as ranging from 20 % to 40 %. This article presents estimates of life expectancy and lifespan variation by education in the United States using more reliable data from the National Health Interview Survey. Contrary to prior conclusions in the literature, I find that life expectancy increased or stagnated since 1990 among all education-race-sex groups except for non-Hispanic white women with less than a high school education; there has been a robust increase in life expectancy among white high school graduates and a smaller increase among black female high school graduates; lifespan variation did not increase appreciably among high school graduates; and lifespan variation plays a very limited role in explaining educational gradients in mortality. I also discuss the key role that educational expansion may play in driving future changes in mortality gradients. Because of shifting education distributions, within an education-specific synthetic cohort, older age groups are less negatively selected than younger age groups. We could thus expect a greater concentration of mortality at younger ages among people with a high school education or less, which would be reflected in increasing lifespan variability for this group. Future studies of educational gradients in mortality should use more reliable data and should be mindful of the effects of shifting education distributions.     

Lifespan Disparity as an Additional Indicator for Evaluating Mortality Forecasts

Evaluating the predictive ability of mortality forecasts is important yet difficult. Death rates and mean lifespan are basic life table functions typically used to analyze to what extent the forecasts deviate from their realized values. Although these parameters are useful for specifying precisely how mortality has been forecasted, they cannot be used to assess whether the underlying mortality developments are plausible. We therefore propose that in addition to looking at average lifespan, we should examine whether the forecasted variability of the age at death is a plausible continuation of past trends. The validation of mortality forecasts for Italy, Japan, and Denmark demonstrates that their predictive performance can be evaluated more comprehensively by analyzing both the average lifespan and lifespan disparity—that is, by jointly analyzing the mean and the dispersion of mortality. Approaches that account for dynamic age shifts in survival improvements appear to perform better than others that enforce relatively invariant patterns. However, because forecasting approaches are designed to capture trends in average mortality, we argue that studying lifespan disparity may also help to improve the methodology and thus the predictive ability of mortality forecasts.     

Lifespan Dispersion in Times of Life Expectancy Fluctuation: The Case of Central and Eastern Europe

Central and Eastern Europe (CEE) have experienced considerable instability in mortality since the 1960s. Long periods of stagnating life expectancy were followed by rapid increases in life expectancy and, in some cases, even more rapid declines, before more recent periods of improvement. These trends have been well documented, but to date, no study has comprehensively explored trends in lifespan variation. We improved such analyses by incorporating life disparity as a health indicator alongside life expectancy, examining trends since the 1960s for 12 countries from the region. Generally, life disparity was high and fluctuated strongly over the period. For nearly 30 of these years, life expectancy and life disparity varied independently of each other, largely because mortality trends ran in opposite directions over different ages. Furthermore, we quantified the impact of large classes of diseases on life disparity trends since 1994 using a newly harmonized cause-of-death time series for eight countries in the region. Mortality patterns in CEE countries were heterogeneous and ran counter to the common patterns observed in most developed countries. They contribute to the discussion about life expectancy disparity by showing that expansion/compression levels do not necessarily mean lower/higher life expectancy or mortality deterioration/improvements.     

The Biodemography of Variation in Human Frailty

A population is composed of individuals who are heterogeneous in their susceptibility to death and disease. This heterogeneity is reflected in the age-specific incidence or mortality (hazard) function. This variation has typically been hidden--that is, not measured directly--and has generally been modeled in a purely empirical statistical way, because there is no theory in demography for the distribution of frailty. A substantial fraction of variation in frailty, however, has an underlying genetic basis, for which there is a formal theory. This theory, based on evolutionary biology and on the nature of mendelian transmission, provides prior constraints on the distribution of variation in the population as well as providing methods for identifying genes involved in many important diseases. The accumulating effects of environmental exposures with age are another major component of variation in frailty. In some important instances, this variation and its effect on the age-specific hazard function can also be understood in terms of cause-specific biological processes. These biological considerations may enable demographers to model frailty, and thus mortality, in a better way.     

A Quiescent Phase in Human Mortality? Exploring the Ages of Least Vulnerability

Demographic studies of mortality often emphasize the two ends of the lifespan, focusing on the declining hazard after birth or the increasing risk of death at older ages. We call attention to the intervening phase, when humans are least vulnerable to the force of mortality, and consider its features in both evolutionary and historical perspectives. We define this quiescent phase (Q-phase) formally, estimate its bounds using life tables for Swedish cohorts born between 1800 and 1920, and describe changes in the morphology of the Q-phase. We show that for cohorts aging during Sweden’s demographic and epidemiological transitions, the Q-phase became longer and more pronounced, reflecting the retreat of infections and maternal mortality as key causes of death. These changes revealed an underlying hazard trajectory that remains relatively low and constant during the prime ages for reproduction and investment in both personal capital and relationships with others. Our characterization of the Q-phase highlights it as a unique, dynamic, and historically contingent cohort feature, whose increased visibility was made possible by the rapid pace of survival improvements in the nineteenth and twentieth centuries. This visibility may be reduced or sustained under subsequent demographic regimes.     

Decomposing change in life expectancy: A bouquet of formulas in honor of Nathan Keyfitz’s 90th birthday

We extend Nathan Keyfitz's research on continuous change in life expectancy over time by presenting and proving a new formula for decomposing such change. The formula separates change in life expectancy over time into two terms. The first term captures the general effect of reduction in death rates at all ages, and the second term captures the effect of heterogeneity in the pace of improvement in mortality at different ages. We extend the formula to decompose change in life expectancy into age-specific and cause-specific components, and apply the methods to analyze changes in life expectancy in Sweden and Japan.     

Being Born Under Adverse Economic Conditions Leads to a Higher Cardiovascular Mortality Rate Later in Life: Evidence Based on Individuals Born at Different Stages of the Business Cycle

We connect the recent medical and economic literatures on the long-run effects of early-life conditions by analyzing the effects of economic conditions on the individual cardiovascular (CV) mortality rate later in life, using individual data records from the Danish Twin Registry covering births since the 1870s and including the cause of death. To capture exogenous variation of conditions early in life, we use the state of the business cycle around birth. We find significant negative effects of economic conditions around birth on the individual CV mortality rate at higher ages. There is no effect on the cancer-specific mortality rate. From variation within and between monozygotic and dizygotic twin pairs born under different conditions, we conclude that the fate of an individual is more strongly determined by genetic and household-environmental factors if early-life conditions are poor. Individual-specific qualities come more to fruition if the starting position in life is better.     

Changes in the age dependence of mortality and disability: Cohort and other determinants

Though the general trend in the United States has been toward increasing life expectancy both at birth and at age 65, the temporal rate of change in life expectancy since 1900 has been variable and often restricted to specific population groups. There have been periods during which the age- and gender-specific risks of particular causes of death have either increased or decreased. These periods partly reflect the persistent effects of population health factors on specific birth cohorts. It is important to understand the ebbs and flows of cause-specific mortality rates because general life expectancy trends are the product of interactions of multiple dynamic period and cohort factors. Consequently, we first review factors potentially affecting cohort health back to 1880 and explore how that history might affect the current and future cohort mortality risks of major chronic diseases. We then examine how those factors affect the age-specific linkage of disability and mortality in three sets of birth cohorts assessed using the 1982, 1984, and 1989 National Long Term Care Surveys and Medicare mortality data collected from 1982 to 1991. We find large changes in both mortality and disability in those cohorts. providing insights into what changes might have occurred and into what future changes might be expected.     

How Change in Age-specific Mortality Affects Life Expectancy

At current mortality rates, life expectancy is most responsive to change in mortality rates at older ages. Mathematical formulae that describe the linkage between change in age-specific mortality rates and change in life expectancy reveal why. These formulae also shed light on how past progress against mortality has been translated into increases in life expectancy – and on the impact that future progress may have. Furthermore, the mathematics can be adapted to study the effect of mortality change in heterogeneous populations in which those who did at some age would, if saved, enjoy a different life expectancy than those who live.     

Variation in life expectancy during the twentieth century in The United States

The National Center for Health Statistics (NCHS) reports life expectancy at birth (LE) for each year in the United States. Censal year estimates of LE use complete life tables. From 1900 through 1947, LEs for intercensal years were interpolated from decennial life tables and annual crude death rates. Since 1948, estimates have been computed from annual life tables. A substantial drop in variation in LE occurred in the 1940s. To evaluate these methods and examine variation without artifacts of different methods, we estimated a consistent series of both annual abridged life tables and LEs from official NCHS age-specific death rates and also LEs using the interpolation method for 1900-1998. Interpolated LEs are several times as variable as life table estimates, about 2 times as variable before 1940 and about 6.5 times as variable after 1950. Estimates of LE from annual life tables are better measures than those based on the mixed methods detailed in NCHS reports. Estimates from life tables show that the impact of the 1918 influenza pandemic on LE was much smaller than indicated by official statistics. We conclude that NCHS should report official estimates of intercensal LE for 1900-1948 computed from life tables in place of the existing LEs that were computed by interpolation.     

A Model of Age-specific Fecundability

A new model of the behavioural and physiological causes of age-specific variation in marital fecundability is presented. Total fecundability is decomposed into a series of susceptibility factors (the length of ovarian cycles, the length of the fertile period within each cycle, the probability that a cycle is ovulatory, and the likelihood that an act of unprotected intercourse within the fertile period results in conception) and an exposure factor reflecting the effect of duration of marriage on coital frequency. The impact of intra-uterine mortality on effective fecundability is also modelled. Data on western women, from which standard age curves of fecundability are estimated, suggest that any decline in fecundity between ages 30 and 40 is attributable to changes, not in the ability to conceive, but in the capacity to carry a pregnancy to term. Sensitivity tests suggest that the most important potential sources of inter-population variation in fecundability are intra-uterine death and the incidence of anovulatory cycles.     

A census-based method for estimating adult mortality

Abstract A simple method is presented for converting an age distribution in any closed population into the stationary population corresponding to its current mortality conditions. The conversion only requires a set of age-specific growth rates, which will normally be available from successive censuses. From the stationary population, any life table mortality measure of interest can be computed. The index most robust to normal data errors in developing countries is life expectancy, and the paper focuses on its calculation. The sensitivity of results to various forms of data error is considered, and procedures are proposed for removing errors resulting from differential census coverage completeness and from age misstatement at older ages. Applications of the procedures are made to data from Sweden, India and South Korea. Because of the absence of a radix, estimation of life expectancy usually will begin at the fifth birthday.     

A Cross-National Analysis of Lifespan Inequality, 1950–2015: Examining the Distribution of Mortality Within Countries

Cross-national health research devotes considerable attention to lifespan and survival rate disparities that are found between countries. However, the distribution of mortality across the world is shaped mostly by what happens within countries. We address this striking gap in the literature by modeling length-of-life inequality for individual nation-states. We use life tables from the United Nation’s (2015) World Population Prospects to estimate inequality levels for 200 countries across 13 waves between 1950 and 2015. We find that lifespan inequality is steadily declining across the world, but that each country’s level of inequality, and the rate at which it declines, vary considerably. Our models account for more than 90% of the longitudinal and cross-sectional variation in country-level lifespan inequality during the 1990–2015 period. Maternal mortality is the strongest predictor in our model, while disease prevalence, access to safe water, and health interventions figure prominently, as well. Gross domestic product per capita shows the expected curvilinear association with lifespan inequality, while primary education (both overall enrollment and gender equity in enrollment), external debt, and migration also play critical roles in shaping health outcomes. By contrast, the distribution of political and economic resources (i.e., democracy and income inequality) is less important.

     

Structure and change in causes of death: An international summary

Abstract Model patterns of the cause structure of mortality at different levels were established for males and females, based on data for 165 national populations. These patterns suggest that the cause of death most responsible for mortality variation is influenza/bronchitis, followed by 'other infectious and parasitic diseases', respiratory tuberculosis, and diarrhoeal disease. Together, these causes typically account for about 60 per cent of the change in level of mortality from all causes combined. Their respective contributions have not depended in an important way on the initial level of mortality. These results - especially tbe importance of the respiratory and diarrhoeal diseases - imply that past accounts may have over-emphasized the role in mortality decline of specific and well-defined infectious diseases and their corresponding methods of control. There is strong statistical support for the suggestion that most of the remainder of mortality variation should be ascribed to changes in cardio-vascular diseases, but that methods of cause-of-death assignment in high-mortality populations have often obscured the importance of these diseases. When death rates from 'other and unknown' causes are held constant, changes in cardio-vascular disease account for about one-quarter of the decline in mortality from 'all causes'.Although the causal factors are poorly established, corroborative results have been demonstrated cross-sectionally in the United States. The composition of the group of populations most deviant from the structural norms is apparently dominated by differentials in the mode of assigning deaths to cardio-vascular disease. However, when broad groups of regions or periods are distinguished, more subtle differences emerge. Controlling mortality level for all causes combined, diarrhoeal diseases are significantly higher in non-Western populations and southern/eastern Europe than in overseas Europe or northern/western Europe. These differences are probably related to standards of nutrition and personal hygiene, but may also reflect climatic factors. Much higher cardio-vascular mortality in overseas European populations than in non-Western populations at similar overall levels probably reflects variation in habits of life. Regional differences in death rates from violence, maternal mortality, respiratory tuberculosis and influenza/pneumonia/bronchitis are briefly noted and commented upon. Cause-of-death structures at a particular level of mortality display some important changes over time. Respiratory tuberculosis and 'other infectious and parasitic diseases' have tended to contribute less and less to a certain level of mortality. They have in part been 'replaced' by diarrhoeal disease, specifically in non-Western populations. These developments reflect an accelerating rate of medical and public health progress against the specific infectious diseases, and a disappointing rate of progress against diarrhoeal disease. Western and non-western populations have shared to approximately the same extent in the accelerating progress against infectious diseases, and developments during the post-war period are more appropriately viewed as an extension of prior trends rather than as radical departures therefrom. For males, cardio-vascular disease and cancer have significantly increased their contribution to a particular level of mortality, while no such tendency is apparent for females. These developments may be related to changes in personal behaviour and in environmental influences whose differential impact on the sexes has been demonstrated in epidemiological studies. Although we have avoided an explicit treatment of age by having recourse at the outset to standardization, certain of the results are apparently reflected in studies of age patterns of mortality. The joint occurrence in non-Western populations and Southern/Eastern populations of exceptionally high death rates from diarrhoeal disease may explain why the 'South' age-pattern, with it high death rates between ages one and five, is often the most accurate referent for use in Latin America and Asia. The fact that the list of populations with the least deviation cause structure is almost exclusively confined to members of the 'West' group of Coale and Demeny may account for the lack of persistent deviation in this group's age patterns. Finally, tbe increasing importance of cardio-vascular disease and neoplasms in cause-of-death structures for males but not females is probably associated with the changing age patterns of male mortality noted by Coale and Demeny.     

Mortality estimation from registered deaths in less developed countries

Age-specific population growth rates were introduced to demographic analysis in earlier work by Bennett and Horiuchi (1981) and Preston and Coale (1982). In this paper, we derive a method which uses these growth rates to transform what may be a set of incompletely recorded deaths by age into a life table that accurately reflects the true mortality experience of the population under study. The method does not rely on the assumption of stability and, for example, in contrast to intercensal cohort survival techniques, is simple to implement when presented with nontraditional intercensal interval lengths. Thus we can obtain mortality estimates for less developed countries with defective data, despite departures from stability. Further, we assess the sensitivity of the method to violations in various assumptions underlying the procedure: error in estimated growth rates, existence of non-zero net intercensal migration, age dependence in the completeness of death registration, and misreporting of age at death and age in the population. We demonstrate the use of the method in an application to data referring to Argentine females during the period 1960 to 1970.     

[Estimate of indicators of life tables in 1953-1964 and 1964-1982].]

The variable-r method is applied to data from the 1953, 1964, and 1982 censuses of China to produce life tables for 1953-1964 and 1964-1982. The tables are used to discuss a selection of mortality indicators, including infant mortality, age-specific mortality, and life expectancy by sex.     

The response of violent mortality to economic crisis in Russia

From 1992 to 1994 life expectancy for Russian males dropped from 62.0 to 57.6 years. Female life expectancy dropped from 73.8 years to 71.2 years. This drop in life expectancy coincided in time with the introduction of painful economic reforms in Russia, leading to a rapid decrease in real wages and pensions, nearly complete loss of personal savings, and a tremendous increase in the poverty rate. This article examines the temporary changes in mortality for violent causes of death during the crisis period with a special emphasis on age-specific and gender-specific differences in the response to economic crisis.