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Drawing cohort profiles and cohort forecasts from grids of age-period data is common practice in demography. In this research note, we (1) show how demographic measures artificially fluctuate when calculated from the diagonals of age-period rates because of timing and cohort-size bias, (2) estimate the magnitude of these biases, and (3) illustrate how prediction intervals for cohort indicators of mortality may become implausible when drawn from Lee-Carter methods and age-period grids. These biases are surprisingly large, even when the cohort profiles are created from single-age, single-year period data. The danger is that we overinterpret deviations from expected trends that were induced by our own data manipulation., (Copyright © 2023 The Authors.)

Background: US racial-ethnic mortality disparities are well documented and central to debates on social inequalities in health. Standard measures, such as life expectancy or years of life lost, are based on synthetic populations and do not account for the real underlying populations experiencing the inequalities., Methods: We analyze US mortality disparities comparing Asian Americans, Blacks, Hispanics, and Native Americans/Alaska Natives to Whites using 2019 CDC and NCHS data, using a novel approach that estimates the mortality gap, adjusted for population structure by accounting for real-population exposures. This measure is tailored for analyses where age structures are fundamental, not merely a confounder. We highlight the magnitude of inequalities by comparing the population structure-adjusted mortality gap against standard metrics' estimates of loss of life due to leading causes., Results: Based on the population structure-adjusted mortality gap, Black and Native American mortality disadvantage exceedsmortality from circulatory diseases. The disadvantage is 72% among Blacks (men: 47%, women: 98%) and 65% among Native Americans (men: 45%, women: 92%), larger than life expectancy measured disadvantage. In contrast, estimated advantages for Asian Americans are over three times (men: 176%, women: 283%) and, for Hispanics, two times (men: 123%; women: 190%) larger than those based on life expectancy., Conclusions: Mortality inequalities based on standard metrics' synthetic populations can differ markedly from estimates of the population structure-adjusted mortality gap. We demonstrate that standard metrics underestimate racial-ethnic disparities through disregarding actual population age structures. Exposure-corrected measures of inequality may better inform health policies around allocation of scarce resources., Competing Interests: The authors report no conflicts of interest., (Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc.)

Background: Life course epidemiology suggests that early life circumstances affect adult mortality, but most of the evidence is based on cohorts born in the beginning of the 20th century. It remains unclear whether and how the influences of early life circumstances on mortality have changed in later birth cohorts., Methods: Analyses rely on 10% register-based samples of households drawn from the 1950 and the 1975 Finnish censuses, with consistent follow-up of socioeconomic and housing-related characteristics and early mid-life mortality (at ages 30-55 years). We estimate survival models for the associations between childhood circumstances and all-cause, internal and external mortality for cohorts born in 1936-50 and 1961-75 adjusting for attained social characteristics. We estimate sibling intraclass correlations as summary measures of all early life and familial influences., Results: Adverse childhood social circumstances were typically associated with about 10-30% excess cause-specific mortality. These associations were almost fully attenuated by adjustment for achieved later life social characteristics. Early life influences have grown over time for mortality from external causes, particularly as related to home ownership and family type. Differentials have remained stable for internal causes. The intraclass correlations further confirmed the increasing association of early life circumstances on external-cause mortality., Conclusions: Our analyses show that the associations between childhood characteristics and mid-life mortality are substantial and almost fully mediated by achieved adult social characteristics. The increase in the contribution of childhood circumstances to mid-life mortality is driven by ever stronger associations with external causes of death., (© The Author(s) 2020. Published by Oxford University Press on behalf of the International Epidemiological Association.)

Education is negatively associated with most major causes of death. Prior work ignores the premise that cause-specific hazards are interdependent and that both education and mortality depend on cognitive ability. We analyse Swedish men aged 18-63, focusing on months lost due to specific causes-which solves the interdependence problem-and use a structural model that accounts for confounding due to cognitive ability. In a standard Cox model controlling for Intelligence Quotient, improving education is associated with large decreases in mortality for major causes of death. In the structural model, improving education is associated with a small decrease in months lost for most causes and education levels. Among the least educated, however, improving education strongly reduces the months lost, mainly those lost from external causes, such as accidents and suicide. Results suggest that conventional analysis of education and mortality may be biased, even if accounting for observed cognition.

A negative educational gradient has been found for many causes of death. This association may be partly explained by confounding factors that affect both educational attainment and mortality. We correct the cause-specific educational gradient for observed individual background and unobserved family factors using an innovative method based on months lost due to a specific cause of death re-weighted by the probability of attaining a higher educational level. We use data on men with brothers from the Swedish Military Conscription Registry (1951-1983), linked to administrative registers. This dataset of some 700,000 men allows us to distinguish between five education levels and many causes of death. The empirical results reveal that raising the educational level from primary to tertiary would result in an additional 20 months of survival between ages 18 and 63. This improvement in mortality is mainly attributable to fewer deaths from external causes. The highly educated gain more than nine months due to the reduction in deaths from external causes, but gain only two months due to the reduction in cancer mortality and four months due to the reduction in cardiovascular mortality. Ignoring confounding would lead to an underestimation of the gains by educational attainment, especially for the less educated. Our results imply that if the education distribution of 50,000 Swedish men from the 1951 cohort were replaced with that of the corresponding 1983 cohort, 22% of the person-years that were lost to death between ages 18 and 63 would have been saved for this cohort., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Before the fall of the Berlin Wall, mortality was considerably higher in the former East Germany than in West Germany. The gap narrowed rapidly after German reunification. The convergence was particularly strong for women, to the point that Eastern women aged 50-69 now have lower mortality despite lower incomes and worse overall living conditions. Prior research has shown that lower smoking rates among East German female cohorts born in the 1940s and 1950s were a major contributor to this crossover. However, after 1990, smoking behavior changed dramatically, with higher smoking intensity observed among women in the eastern part of Germany. We forecast the impact of this changing smoking behavior on East-West mortality differences and find that the higher smoking rates among younger East German cohorts will reverse their contemporary mortality advantage. Mortality forecasting methods that do not account for smoking would, perhaps misleadingly, forecast a growing mortality advantage for East German women. Experience from other countries shows that smoking can be effectively reduced by strict anti-smoking policies. Instead, East Germany is becoming an example warning of the consequences of weakening anti-smoking policies and changing behavioral norms.

A growing body of evidence suggests that reproductive history influences post-reproductive mortality. A potential explanation for this association is confounding by socioeconomic status in the family of origin, as socioeconomic status is related to both fertility behaviours and to long-term health. We examine the relationship between age at first birth, completed parity, and post-reproductive mortality and address the potential confounding role of family of origin. We use Swedish population register data for men and women born 1932-1960, and examine both all-cause and cause-specific mortality. The contributions of our study are the use of a sibling comparison design that minimizes residual confounding from shared family background characteristics and assessment of cause-specific mortality that can shed light on the mechanisms linking reproductive history to mortality. Our results were entirely consistent with previous research on this topic, with teenage first time parents having higher mortality, and the relationship between parity and mortality following a U-shaped pattern where childless men and women and those with five or more children had the highest mortality. These results indicate that selection into specific fertility behaviours based upon socioeconomic status and experiences within the family of origin does not explain the relationship between reproductive history and post-reproductive mortality. Additional analyses where we adjust for other lifecourse factors such as educational attainment, attained socioeconomic status, and post-reproductive marital history do not change the results. Our results add an important new level of robustness to the findings on reproductive history and mortality by showing that the association is robust to confounding by factors shared by siblings. However it is still uncertain whether reproductive history causally influences health, or whether other confounding factors such as childhood health or risk-taking propensity could explain the association., (Copyright © 2016 The Authors. Published by Elsevier Ltd.. All rights reserved.)

The association between advanced maternal and paternal ages at birth and increased mortality among adult offspring is often attributed to parental reproductive aging, e.g., declining oocyte or sperm quality. Less attention has been paid to alternative mechanisms, including parental socio-demographic characteristics or the timing of parental death. Moreover, it is not known if the parental age-adult mortality association is mediated by socioeconomic attainment of the children, or if it varies over the lifecourse of the adult children. We used register-based data drawn from the Finnish 1950 census (sample size 89,737; mortality follow-up 1971-2008) and discrete-time survival regression with logit link to analyze these alternative mechanisms in the parental age-offspring mortality association when the children were aged 35-49 and 50-72. Consistent with prior literature, we found that adult children of older parents had increased mortality relative to adults whose parents were aged 25-29 at the time of birth. For example, maternal and paternal ages 40-49 were associated with mortality odds ratios (ORs) of 1.31 (p<.001) and 1.22 (p<.01), respectively, for offspring mortality at ages 35-49. At ages 50-72 advanced parental age also predicted higher mortality, though not as strongly. Adjustment for parental socio-demographic characteristics (education, occupation, family size, household crowding, language) weakened the associations only slightly. Adjustment for parental survival, measured by whether the parents were alive when the child reached age 35, reduced the advanced parental age coefficients substantially and to statistically insignificant levels. These results indicate that the mechanism behind the advanced parental age-adult offspring mortality association is mainly social, reflecting early parental loss and parental characteristics, rather than physiological mechanisms reflecting reproductive aging., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

Objectives: We sought to analyze how early exposure to the 1918 influenza pandemic is associated with old-age mortality by cause of death., Methods: We analyzed the National Health Interview Survey (n = 81,571; follow-up 1989-2006; 43,808 deaths) and used year and quarter of birth to assess timing of pandemic exposure. We used Cox proportional and Fine-Gray competing hazard models for all-cause and cause-specific mortality, respectively., Results: Cohorts born during pandemic peaks had excess all-cause mortality attributed to increased noncancer mortality. We found evidence for a trade-off between noncancer and cancer causes: cohorts with high noncancer mortality had low cancer mortality, and vice versa., Conclusions: Early disease exposure increases old-age mortality through noncancer causes, which include respiratory and cardiovascular diseases, and may trigger a trade-off in the risk of cancer and noncancer causes. Potential mechanisms include inflammation or apoptosis. The findings contribute to our understanding of the causes of death behind the early disease exposure-later mortality association. The cancer-noncancer trade-off is potentially important for understanding the mechanisms behind these associations.

Background: The German East-West mortality difference narrowed rapidly after the 1990 unification, particularly for women. We analyse recent trends for women aged 50-89 years and document for the first time lower mortality in the East. We study how smoking contributes to this cross-over., Methods: We analyse mortality by cause for women aged 50-89 over the years 1992-2009 for the East and West Germany, excluding Berlin. We compare the East-West mortality rate ratio (MRR) for total mortality and after removing smoking-attributable mortality using the indirect Preston-Glei-Wilmoth method., Results: In the early 1990s mortality was higher in the East. By 2000 mortality for ages 50-64 had declined below that of the West and remained lower thereafter. For example, from 1992-94 to 2005-09 the MRR for ages 55-59 declined from 1.27 to 0.87. Smoking explains a third of the MRR change for ages 50-64, and when smoking-attributable deaths are removed the mortality cross-over vanishes. For example, non-smoking-attributable MRR for ages 55-59 is 1.03 in 2005-09. For ages 65-89 smoking matters less, and mortality remains higher in the East., Conclusions: We show for the first time that mortality for middle-aged women is lower in the former East Germany than in the West. Prior studies have documented convergence and suggested improving living standards and medical care as mechanisms. We show that much of the convergence, and the cross-over, are attributable to smoking. The seeds for the female East-West mortality cross-over were planted before the unification, when the women now aged 50-64 adopted their smoking behaviours.

The relative importance of cohorts' early-life conditions, compared to later period conditions, on adult and old-age mortality is not known. This article studies how cohort-level mortality depends on shocks in cohorts' early- and later-life (period) conditions. I use cohorts' own mortality as a proxy for the early-life conditions, and define shocks as deviations from trend. Using historical data for five European Countries i find that shocks in early-life conditions are only weakly associated with cohorts' later mortality. This may be because individual-level health is robust to early-life conditions, or because at the cohort level scarring, selection, and immunity cancel each other. Shocks in period conditions, measured as deviations from trend in period child mortality, are strongly and positively correlated with mortality at all older ages. The results suggest that at the cohort level changing period conditions drive mortality variation and change.

Background: It is not known how the relationship between weight change and mortality is influenced by initial body mass index (BMI) or the magnitude of weight change., Methods: We use the nationally representative Health and Retirement Study (n = 13,104; follow-up 1992-2006) and Cox regression analysis to estimate relative mortality risks for 2-year weight change by initial BMI among 50- to-70-year-old Americans. We defined small weight loss or gain as a change of 1-2.9 BMI units and large weight loss or gain as a change of 3-5 BMI units., Results: Large and small weight losses were associated with excess mortality for all initial BMI levels below 32 kg/m (eg, hazard ratio [HR] for large weight loss from BMI of 30 = 1.61 [95% confidence interval = 1.31-1.98]; HR for small weight loss from BMI of 30 = 1.19 [1.06-1.28]). Large weight gains were associated with excess mortality only at high BMIs (eg, HR for large weight gain from BMI of 35 = 1.33 [1.00-1.77]). Small weight gains were not associated with excess mortality for any initial BMI level. The weight loss-mortality association was robust to adjustments for health status and to sensitivity analyses considering unobserved confounders., Conclusions: Weight loss is associated with excess mortality among normal, overweight, and mildly obese middle- and older-aged adults. The excess risk increases for larger losses and lower initial BMI. These results suggest that the potential benefits of a lower BMI may be offset by the negative effects associated with weight loss. Weight gain may be associated with excess mortality only among obese people with an initial BMI over 35.

Since 2010, US life expectancy growth has stagnated. Much research on US mortality has focused on working-age adults given adverse trends in drug overdose deaths, other external causes of death, and cardiometabolic deaths in midlife. We show that the adverse mortality trend at retirement ages (65+ y) has in fact been more consequential to the US life expectancy stagnation since 2010, as well as excess deaths and years of life lost in 2019, than adverse mortality trends at working ages. These results reveal that the United States is experiencing a "double jeopardy" that is driven by both mid-life and older-age mortality trends, but more so by older-age mortality. Understanding and addressing the causes behind the worsening mortality trend in older ages will be essential to returning to the pace of life expectancy improvements that the United States had experienced for decades. [ABSTRACT FROM AUTHOR]

An introduction is presented in which the editor discusses various topics within the issue, including life expectancy in the U.S. based on socioeconomic status (SES), cardiometabolic health in the U.S. and England, and the role of income in patterning health.

Objectives Reductions in U.S. cardiovascular disease (CVD) mortality have stagnated. While other high life expectancy countries (HLCs) have also recently experienced a stall, the stagnation in CVD mortality in the United States appeared earlier and has been more pronounced. The reasons for the stall are unknown. We analyze cross-national variations in mortality trends to quantify the U.S. exceptionality and provide insight into its underlying causes. Methods Data are from the World Health Organization (2000–2016). We quantified differences in levels and trends of CVD mortality between the United States and 17 other HLCs. We decomposed differences to identify the individual contributions of major CVD subclassifications (ischemic heart disease [IHD], stroke, other heart diseases). To identify potential behavioral explanations, we compared trends in CVD mortality with trends in other causes of death related to obesity, smoking, alcohol, and drugs. Results Our study has four central findings: (a) U.S. CVD mortality is consistently higher than the average of other HLCs; (b) the U.S.–HLC gap declined until around 2008 and increased thereafter; (c) the shift from convergence to divergence was mainly driven by slowing IHD and stroke mortality reductions and increasing mortality from other CVD causes; (d) among the potential risk factors, only obesity- and alcohol-related mortality showed age-specific temporal changes that are similar to those observed for cardiovascular mortality. Discussion The exceptional changes in U.S. CVD mortality are driven by a distinct pattern of slowing reductions in IHD and stroke mortality and deteriorating mortality from other CVD causes. Obesity and alcohol abuse appear to be interrelated factors. [ABSTRACT FROM AUTHOR]

A key concern about population aging is the decline in the size of the economically active population. Working longer is a potential remedy. However, little is known about the length of working life and how it relates to macroeconomic conditions. We use the U.S. Health and Retirement Study for 1992-2011 and multistate life tables to analyze working life expectancy at age 50 and study the impact of the Great Recession in 2007-2009. Despite declines of one to two years following the recession, in 2008-2011, American men aged 50 still spent 13 years, or two-fifths of their remaining life, working; American women of the same age spent 11 years, or one-third of their remaining life, in employment. Although educational differences in working life expectancy have been stable since the mid-1990s, racial differences started changing after the onset of the Great Recession. Our results show that although Americans generally work longer than people in other countries, considerable subpopulation heterogeneity exists. We also find that the time trends are fluctuating, which may prove troublesome as the population ages. Policies targeting the weakest performing groups may be needed to increase the total population trends. [ABSTRACT FROM AUTHOR]

After decades of robust growth, the rise in US life expectancy stalled after 2010. Explanations for the stall have focused on rising drug-related deaths. Here we show that a stagnating decline in cardiovascular disease (CVD) mortality was the main culprit, outpacing and overshadowing the effects of all other causes of death. The CVD stagnation held back the increase of US life expectancy at age 25 y by 1.14 y in women and men, between 2010 and 2017. Rising drug-related deaths had a much smaller effect: 0.1 y in women and 0.4 y in men. Comparisons with other high-income countries reveal that the US CVD stagnation is unusually strong, contributing to a stark mortality divergence between the US and peer nations. Without the aid of CVD mortality declines, future US life expectancy gains must come from other causes--a monumental task given the enormity of earlier declines in CVD death rates. Reversal of the drug overdose epidemic will be beneficial, but insufficient for achieving pre-2010 pace of life expectancy growth. [ABSTRACT FROM AUTHOR]

As parental ages at birth continue to rise, concerns about the effects of fertility postponement on offspring are increasing. Due to reproductive ageing, advanced parental ages have been associated with negative health outcomes for offspring, including decreased longevity. The literature, however, has neglected to examine the potential benefits of being born at a later date. Secular declines in mortality mean that later birth cohorts are living longer. We analyse mortality over ages 30-74 among 1.9 million Swedish men and women born 1938-60, and use a sibling comparison design that accounts for all time-invariant factors shared by the siblings. When incorporating cohort improvements in mortality, we find that those born to older mothers do not suffer any significant mortality disadvantage, and that those born to older fathers have lower mortality. These findings are likely to be explained by secular declines in mortality counterbalancing the negative effects of reproductive ageing. [ABSTRACT FROM AUTHOR]

Background: The first few weeks' post-imprisonment are associated with high mortality, particularly among individuals with a history of substance use. Excess risk may vary by societal context due to a range of penal systems and substance use patterns. Using data on Finnish individuals who had sought treatment for substance use, we studied the association between criminal sanctions with cause-specific mortality.Methods: The database contained 10887 individuals who had sought treatment between 1990 and 2009. Their treatment data were combined with register data on imprisonments and community sanctions and weekly mortality between 1992 and 2015. Mortality was analysed using discrete-time survival models. We controlled for age and sociodemographic factors, and analysed whether education, type of substance used and the type of latest sentence modified the associations.Findings: Mortality was high in the first two weeks after sanctions (all-cause odds ratio [OR] 2.61, 95% confidence interval [CI] 1.67-4.07; drug-related deaths OR 8.52, 95% CI 4.64-15.7). Excess risk declined over time (OR after 12 weeks: 1.19, 95% CI 1.07-1.31). Most of the excess risk was attributable to external causes. Mortality was low during imprisonment, but not during community sanctions. The patterns were similar by level of education, substance use and the type of latest sentence.Conclusions: Community sanctions were not associated with mortality among people with substance use disorders. Mortality was low during imprisonment, but high post-release. Criminal sanctions should be better utilised as intervention touchpoints and follow-up resources should target prisoners with substance use treatment history to reduce post-release mortality. [ABSTRACT FROM AUTHOR]

We used high quality register based data to study the relationship between childhood and adult socio-demographic characteristics and all-cause and cause-specific mortality at ages 35–72 in Finland among cohorts born in 1936–1950. The analyses were based on a 10% sample of households drawn from the 1950 Finnish Census of Population with the follow-up of household members in subsequent censuses and death records beginning from the end of 1970 through the end of 2007. The strengths of these data come from the fact that neither childhood nor adult characteristics are self reported and thus are not subject to recall bias, misreporting and no loss to follow-up after age 35. In addition, the study population includes several families with at least two children enabling us to control for unobserved family characteristics. We documented significant associations between early life social and family conditions on all-cause mortality and cause-specific mortality, with protective effects of higher childhood socio-demographic characteristics varying between 10% and 30%. These associations were mostly mediated through adult educational attainment and occupation, suggesting that the indirect effects of childhood conditions were more important than their direct effects. We further found that adult socioeconomic status was a significant predictor of mortality. The associations between adult characteristics and mortality were robust to controls for observed and unobserved childhood characteristics. The results imply that long-term adverse health consequences of disadvantaged early life social circumstances may be mitigated by investments in educational and employment opportunities in early adulthood. [ABSTRACT FROM AUTHOR]

Purpose: To identify life-long body mass index (BMI) trajectories across two related generations and estimate their associated mortality risks and population attributable deaths.Methods: We use prospective cohort data from the Framingham Heart Study (1948-2011) original (4576 individuals, 3913 deaths) and offspring (3753 individuals, 967 deaths) cohorts and latent trajectory models to model BMI trajectories from age 31 to 80 years. Survival models are used to estimate trajectory-specific mortality risk.Results: We define seven BMI trajectories among original cohort and six among offspring cohort. Among original cohort, people who are normal weight at age 31 years and gradually move to overweight status in middle or later adulthood have the lowest mortality risk even compared to those who maintain normal weight throughout adulthood, followed by overweight stable, lower level of normal weight, overweight downward, class I obese upward, and class II/III upward trajectories. Mortality risks associated with obesity trajectories have declined across cohorts, while the prevalence of high-risk trajectories has increased.Conclusions: The mortality impact of weight gain depends on an individual's BMI trajectory. Population attributable deaths associated with unhealthy weight trajectories have grown over generations because the prevalence has increased, offsetting the decline in trajectory-specific mortality risks. [ABSTRACT FROM AUTHOR]