Objective

This paper reviews trends in mortality and morbidity to evaluate whether there has been a compression of morbidity.

Methods

Review of recent research and analysis of recent data for the United States relating mortality change to the length of life without 1 of 4 major diseases or loss of mobility functioning.

Results

Mortality declines have slowed down in the United States in recent years, especially for women. The prevalence of disease has increased. Age-specific prevalence of a number of risk factors representing physiological status has stayed relatively constant; where risks decline, increased usage of effective drugs is responsible. Mobility functioning has deteriorated. Length of life with disease and mobility functioning loss has increased between 1998 and 2008.

Discussion

Empirical findings do not support recent compression of morbidity when morbidity is defined as major disease and mobility functioning loss.

The past 200 years have enabled remarkable increases in human lifespans through improvements in the living environment that have nearly eliminated infections as a cause of death through improved hygiene, public health, medicine, and nutrition. We argue that the limit to lifespan may be approaching. Since 1997, no one has exceeded Jeanne Calment's record of 122.5 years, despite an exponential increase of centenarians. Moreover, the background mortality may be approaching a lower limit. We calculate from Gompertz coefficients that further increases in longevity to approach a life expectancy of 100 years in 21st century cohorts would require 50% slower mortality rate accelerations, which would be a fundamental change in the rate of human aging. Looking into the 21st century, we see further challenges to health and longevity from the continued burning of fossil fuels that contribute to air pollution as well as global warming. Besides increased heat waves to which elderly are vulnerable, global warming is anticipated to increase ozone levels and facilitate the spread of pathogens. We anticipate continuing socioeconomic disparities in life expectancy.

Racial/ethnic minorities have experienced higher COVID-19 infection rates than whites, but it is unclear how individual-level housing, occupational, behavioral, and socioeconomic conditions contribute to these disparities in a nationally representative sample. In this study, we assess the extent to which social determinants of health contribute to racial/ethnic differences in COVID-19 infection. Data are from the Understanding America Study's Understanding Coronavirus in America survey (UAS COVID-19 waves 7-29). UAS COVID-19 is one of the only nationally representative longitudinal data sources that collects information on household, work, and social behavioral context during the pandemic. We analyze onset of COVID-19 cases, defined as a positive test or a diagnosis of COVID-19 from a healthcare provider since the previous survey wave, over a year of follow-up (June 2020-July 2021). We consider educational attainment, economic resources, work arrangements, household size, and social distancing as key social factors that may be structured by racism. Cox hazard models indicate that Hispanic people have 48% higher risk of experiencing a COVID-19 infection than whites after adjustment for age, sex, local infection rate, and comorbidities, but we do not observe a higher risk of COVID-19 among Black respondents. Controlling for engagement in any large or small social gathering increases the hazard ratio for Hispanics by 9%, suggesting that had Hispanics had the same social engagement patterns as whites, they may have had even higher risk of COVID-19. Other social determinants-lower educational attainment, working away from home, and number of coresidents-all independently predict higher risk of COVID-19, but do not explain why Hispanic Americans have higher COVID-19 infection risk than whites.

To examine change from 1991 to 2001 in disability-free life expectancy in the age range 60-90 by gender, race, and education in the United States. Mortality is estimated over two 10-year follow-up periods for persons in the National Health Interview Surveys of 1986/1987 and 1996/1997. Vital status is ascertained through the National Death Index. Disability prevalence is estimated from the National Health and Nutrition Examination Surveys of 1988-1994 and 1999-2002. Disability is defined as ability to perform four activities of daily living without difficulty. Disability-free life expectancy increased only among white men. Disabled life expectancy increased for all groups-black and white men and women. Racial differences in disability-free life expectancy widened among men; gender differences were reduced among whites. Expansion of socioeconomic differentials in disability-free life at older ages occurred among white men and women and black women. The 1990s was a period where the increased years of life between ages 60 and 90 were concentrated in disabled years for most population groups.

Using historical data from 1,763 birth cohorts from 1800 to 1935 in 13 developed countries, we show that what is now seen as normal-a large excess of female life expectancy in adulthood-is a demographic phenomenon that emerged among people born in the late 1800s. We show that excess adult male mortality is clearly rooted in specific age groups, 50-70, and that the sex asymmetry emerged in cohorts born after 1880 when male:female mortality ratios increased by as much as 50% from a baseline of about 1.1. Heart disease is the main condition associated with increased excess male mortality for those born after 1900. We further show that smoking-attributable deaths account for about 30% of excess male mortality at ages 50-70 for cohorts born in 1900-1935. However, after accounting for smoking, substantial excess male mortality at ages 50-70 remained, particularly from cardiovascular disease. The greater male vulnerability to cardiovascular conditions emerged with the reduction in infectious mortality and changes in health-related behaviors.

Background

Little is known about the health and functioning of individuals who become centenarians in the years prior to reaching age 100. We examined long-term trajectories of disease, disability, and cognitive function in a sample of U.S. centenarians to determine how their aging experience differs from their nonsurviving cohort counterparts, and if there is heterogeneity in the aging experience of centenarians.

Methods

Data are from the 1993-2010 waves of the nationally representative Health and Retirement Study. Among those who had the potential to become centenarians, we identified 1,045 respondents who died before reaching age 100 and 96 who survived to their 100th birthday. Respondents, or their proxies, reported on diagnosis of six major diseases (hypertension, heart disease, lung disease, stroke, cancer, and diabetes), limitations in activities of daily living, and cognitive function.

Results

As they age to 100, centenarians are generally healthier than nonsurviving members of their cohort, and a number of individuals who become centenarians reach 100 with no self-reported diseases or functional impairments. About 23% of centenarians reached age 100 with no major chronic disease and approximately the same number had no disability (18%). Over half (55%) reached 100 without cognitive impairment. Disease and functioning trajectories of centenarians differ by sex, education, and marital status.

Conclusions

While some centenarians have poor health and functioning upon reaching age 100, others are able to achieve exceptional longevity in relatively good health and without loss of functioning. This study underscores the importance of examining variation in the growing centenarian population.

The success of the current biomedical paradigm based on a "disease model" may be limited in the future because of large number of comorbidities inflicting older people. In recent years, there has been growing empirical evidence, based on animal models, suggesting that the aging process could be delayed and that this process may lead to increases in life expectancy accompanied by improvements in health at older ages. In this review, we explore past, present, and future prospects of healthy life expectancy and examine whether increases in average length of life associated with delayed aging link with additional years lived disability-free at older ages. Trends in healthy life expectancy suggest improvements among older people in the United States, although younger cohorts appear to be reaching old age with increasing levels of frailty and disability. Trends in health risk factors, such as obesity and smoking, show worrisome signs of negative impacts on adult health and mortality in the near future. However, results based on a simulation model of delayed aging in humans indicate that it has the potential to increase not only the length of life but also the fraction and number of years spent disability-free at older ages. Delayed aging would likely come with additional aggregate costs. These costs could be offset if delayed aging is widely applied and people are willing to convert their greater healthiness into more years of work.

Background

A person's rate of aging has important implications for his/her risk of death and disease; thus, quantifying aging using observable characteristics has important applications for clinical, basic, and observational research. Based on routine clinical chemistry biomarkers, we previously developed a novel aging measure, Phenotypic Age, representing the expected age within the population that corresponds to a person's estimated mortality risk. The aim of this study was to assess its applicability for differentiating risk for a variety of health outcomes within diverse subpopulations that include healthy and unhealthy groups, distinct age groups, and persons with various race/ethnic, socioeconomic, and health behavior characteristics.

Methods and findings

Phenotypic Age was calculated based on a linear combination of chronological age and 9 multi-system clinical chemistry biomarkers in accordance with our previously established method. We also estimated Phenotypic Age Acceleration (PhenoAgeAccel), which represents Phenotypic Age after accounting for chronological age (i.e., whether a person appears older [positive value] or younger [negative value] than expected, physiologically). All analyses were conducted using NHANES IV (1999-2010, an independent sample from that originally used to develop the measure). Our analytic sample consisted of 11,432 adults aged 20-84 years and 185 oldest-old adults top-coded at age 85 years. We observed a total of 1,012 deaths, ascertained over 12.6 years of follow-up (based on National Death Index data through December 31, 2011). Proportional hazard models and receiver operating characteristic curves were used to evaluate all-cause and cause-specific mortality predictions. Overall, participants with more diseases had older Phenotypic Age. For instance, among young adults, those with 1 disease were 0.2 years older phenotypically than disease-free persons, and those with 2 or 3 diseases were about 0.6 years older phenotypically. After adjusting for chronological age and sex, Phenotypic Age was significantly associated with all-cause mortality and cause-specific mortality (with the exception of cerebrovascular disease mortality). Results for all-cause mortality were robust to stratifications by age, race/ethnicity, education, disease count, and health behaviors. Further, Phenotypic Age was associated with mortality among seemingly healthy participants-defined as those who reported being disease-free and who had normal BMI-as well as among oldest-old adults, even after adjustment for disease prevalence. The main limitation of this study was the lack of longitudinal data on Phenotypic Age and disease incidence.

Conclusions

In a nationally representative US adult population, Phenotypic Age was associated with mortality even after adjusting for chronological age. Overall, this association was robust across different stratifications, particularly by age, disease count, health behaviors, and cause of death. We also observed a strong association between Phenotypic Age and the disease count an individual had. These findings suggest that this new aging measure may serve as a useful tool to facilitate identification of at-risk individuals and evaluation of the efficacy of interventions, and may also facilitate investigation into potential biological mechanisms of aging. Nevertheless, further evaluation in other cohorts is needed.

Background

There are large differences in adult mortality across schooling groups in many high-income countries (HICs). An important open question is whether there are similar gradients in adult mortality in middle-income countries (MICs), where schooling and healthcare quality tends to be lower and health-related behaviors are often not strongly patterned by schooling.

Methods

We present one of the first international-comparative studies on schooling differences in adult mortality across MICs using harmonizedlongitudinal data on adults ages 50+ from China, Costa Rica, Indonesia, Mexico, South Africa, and South Korea. We use Cox proportional hazards models to estimate differences in the hazard of mortality across schooling groups overall and separately by sex and broad age groups. We also estimate schooling gradients in smoking and body mass index to determine whether risk factor gradients potentially explain mortality patterns.

Results

Only adults with tertiary schooling have a consistent adult mortality advantage compared to those with no schooling. We do not find evidence that individuals with primary schooling have a lower hazard of mortality compared to individuals with no schooling in five of the six countries. The mortality advantage for individuals with secondary schooling is mixed, with evidence of lower mortality relative to those with no schooling in Mexico, South Africa, and South Korea. Gradients in BMI and smoking are inconsistent across countries and unlikely to explain mortality differences.

Conclusions

We find that adult mortality and risk factor gradients in MICs can be much different than the established patterns seen in modern HICs. Our results highlight that adult mortality gradients are not an inevitability and are not found in all populations. Understanding what factors give rise to inequalities in adult mortality and what can be done to minimize gradients while still ensuring continued mortality improvements in MICs is a crucial focus for research and policy.

While deleterious consequences of smoking on health have been widely publicized, in many developing countries, smoking prevalence is high and increasing. Little is known about the dynamics underlying changes in smoking behavior. This paper examines socio-economic and demographic characteristics associated with smoking initiation and quitting in Mexico between 2002 and 2010. In addition to the influences of age, gender, education, household economic resources and location of residence, changes in marital status, living arrangements and health status are examined. Drawing data from the Mexican Family Life Survey, a rich population-based longitudinal study of individuals, smoking behavior of individuals in 2002 is compared with their behavior in 2010. Logistic models are used to examine socio-demographic and health factors that are associated with initiating and quitting smoking. There are three main findings. First, part of the relationship between education and smoking reflects the role of economic resources. Second, associations of smoking with education and economic resources differ for females and males. Third, there is considerable heterogeneity in the factors linked to smoking behavior in Mexico indicating that the smoking epidemic may be at different stages in different population subgroups. Mexico has recently implemented fiscal policies and public health campaigns aimed at reducing smoking prevalence and discouraging smoking initiation. These programs are likely to be more effective if they target particular socio-economic and demographic sub-groups.