Patterns and Life Course Determinants of Black-White Disparities in Biological Age Acceleration: A Decomposition Analysis.

Despite the prominence of the weathering hypothesis as a mechanism underlying racialized inequities in morbidity and mortality, the life course social and economic determinants of Black-White disparities in biological aging remain inadequately understood. This study uses data from the Health and Retirement Study (n = 6,782), multivariable regression, and Kitagawa-Blinder-Oaxaca decomposition to assess Black-White disparities across three measures of biological aging: PhenoAge, Klemera-Doubal biological age, and homeostatic dysregulation. It also examines the contributions of racial differences in life course socioeconomic and stress exposures and vulnerability to those exposures to Black-White disparities in biological aging. Across the outcomes, Black individuals exhibited accelerated biological aging relative to White individuals. Decomposition analyses showed that racial differences in life course socioeconomic exposures accounted for roughly 27% to 55% of the racial disparities across the biological aging measures, and racial disparities in psychosocial stress exposure explained 7% to 11%. We found less evidence that heterogeneity in the associations between social exposures and biological aging by race contributed substantially to Black-White disparities in biological aging. Our findings offer new evidence of the role of life course social exposures in generating disparities in biological aging, with implications for understanding age patterns of morbidity and mortality risks.

Lifecourse Traumatic Events and Cognitive Aging in the Health and Retirement Study.

INTRODUCTION: Much of the heterogeneity in the rate of cognitive decline and the age of dementia onset remains unexplained, and there is compelling data supporting psychosocial stressors as important risk factors. However, the literature has yet to come to a consensus on whether there is a causal relationship and, if there is, its direction and strength. This study estimates the relationship between lifecourse traumatic events and cognitive trajectories and predicted dementia incidence. METHODS: Using data on 7,785 participants aged ≥65 years from the Health and Retirement Study, this study estimated the association between lifecourse experience of 10 traumatic events (e.g., losing a child) and trajectories of Telephone Interview for Cognitive Status from 2006 to 2016 using linear mixed-effects models and predicted incident dementia from 2006 to 2014 using cumulative incidence functions (data analysis was in 2020-2022). Inverse probability weights accounted for loss to follow-up and confounding by sex, education, race/ethnicity, and age. RESULTS: Experiencing 1 or more traumatic events over the lifecourse was associated with accelerated decline compared with experiencing no events (e.g., ß= -0.05 [95% CI= -0.07, -0.02] Health and Retirement Study-Telephone Interview for Cognitive Status units/year; 1 vs 0 events). In contrast, experiencing traumatic events was associated with better cognitive function cross-sectionally. Furthermore, the impact of trauma on cognitive decline was of greater magnitude when it occurred after the age of 64 years. However, the magnitude and direction of association varied by the specific traumatic event. There were no associations with predicted incident dementia. CONCLUSIONS: These results suggest that researchers and clinicians should not aggregate traumatic events for understanding the risk of accelerated cognitive decline.

Immune function, cortisol, and cognitive decline & dementia in an aging latino population.

BACKGROUND: The etiology of dementias and cognitive decline remain largely unknown. It is widely accepted that inflammation in the central nervous system plays a critical role in the pathogenesis of dementia. However, less is known about the role of the peripheral immune system and interactions with cortisol, though evidence suggests that these, too, may play a role. METHODS: Using data from 1337 participants aged 60+ years from the Sacramento Area Latino Study of Aging (observational cohort) we investigated variation in trajectories of cognitive decline by pathogen IgG and cytokine levels. Linear mixed effects models were used to examine the association between baseline Interleukin (IL)-6, C-reactive protein, tumor necrosis factor (TNF)-α, and five persistent pathogens' IgG response and trajectories of cognition over 10 years, and to examine interactions between immune biomarkers and cortisol. Stratified cumulative incidence functions were used to assess the relation between biomarkers and incident dementia. Inverse probability weights accounted for loss-to-follow-up and confounding. RESULTS: IL-6, TNF-α, and CMV IgG were statistically significantly associated with a higher log of Modified Mini-Mental State Examination errors (IL-6, ß=0.0935 (95%CI: 0.055, 0.13), TNF-alpha ß= 0.0944 (95%CI: 0.032, 0.157), and CMV, ß= 0.0409 (95%CI: 0.013, 0.069)). Furthermore, cortisol interacted with HSV-1 and IL-6, and CRP for both cross-sectional cognitive function and rate of decline. No statistically significant relationship was detected between biomarkers and incidence of dementia. CONCLUSIONS: These findings support the theory that the peripheral immune system may play a role in cognitive decline but not incident dementia. Furthermore, they identify specific markers amenable for intervention for slowing decline.

Decrease in Incidence of Colorectal Cancer Among Individuals 50 Years or Older After Recommendations for Population-based Screening.

BACKGROUND & AIMS: The incidence of colorectal cancer (CRC) in the United States is increasing among adults younger than 50 years, but incidence has decreased among older populations after population-based screening was recommended in the late 1980s. Blacks have higher incidence than whites. These patterns have prompted suggestions to lower the screening age for average-risk populations or in blacks. At the same time, there has been controversy over whether reductions in CRC incidence can be attributed to screening. We examined age-related and race-related differences in CRC incidence during a 40-year time period. METHODS: We determined the age-standardized incidence of CRC from 1975 through 2013 by using the population-based Surveillance, Epidemiology, and End Results (SEER) program of cancer registries. We calculated incidence for 5-year age categories (20-24 years through 80-84 years and 85 years or older) for different time periods (1975-1979, 1980-1984, 1985-1989, 1990-1994, 1995-1999, 2000-2004, 2005-2009, and 2010-2013), tumor subsite (proximal colon, descending colon, and rectum), and stages at diagnosis (localized, regional, and distant). Analyses were stratified by race (white vs black). RESULTS: There were 450,682 incident cases of CRC reported to the SEER registries during the entire period (1975-2013). Overall incidence was 75.5/100,000 white persons and 83.6/100,000 black persons. CRC incidence peaked during 1980 through 1989 and began to decrease in 1990. In whites and blacks, the decreases in incidence between the time periods of 1980-1984 and 2010-2013 were limited to the screening-age population (ages 50 years or older). Between these time periods, there was 40% decrease in incidence among whites compared with 26% decrease in incidence among blacks. Decreases in incidence were greater for cancers of the distal colon and rectum, and reductions in these cancers were greater among whites than blacks. CRC incidence among persons younger than 50 years decreased slightly between 1975-1979 and 1990. However, among persons 20-49 years old, CRC incidence increased from 8.3/100,000 persons in 1990-1994 to 11.4/100,000 persons in 2010-2013; incidence rates in younger adults were similar for whites and blacks. CONCLUSIONS: On the basis of an analysis of the SEER cancer registries from 1975 through 2013, CRC incidence decreased only among individuals 50 years or older between the time periods of 1980-1984 and 2010-2013. Incidence increased modestly among individuals 20-49 years old between the time periods of 1990-1994 and 2010-2013. The decision of whether to recommend screening for younger populations requires a formal analysis of risks and benefits. Our observed trends provide compelling evidence that screening has had an important role in reducing CRC incidence.

An age-period-cohort analysis of obesity and incident esophageal adenocarcinoma among white males.

The incidence of esophageal adenocarcinoma (EAC) has increased in recent decades. Increases in incidence have been attributed to changes in the prevalence of risk factors for EAC; however, the extent to which these changes explain increases in EAC incidence has not been studied in detail. We used age-period-cohort analysis to estimate changes in the incidence of EAC among white males by age, time period, and birth cohort. Incidence rates per 100,000 individuals were analyzed from 1973 to 2012. Hierarchical Poisson models were used to estimate age, period, and cohort effects, whereby age-specific incidence rates were nested within periods and cohorts. The prevalence of obesity for each time period and birth cohort was included in the model as a fixed-effect. Incidence increased with advancing age (ß = 0.12, P < 0.01). There were significant period and birth cohort effects, although the period effect was much larger than the cohort effect. The period effect decreased dramatically when obesity was included as a fixed effect, while the small cohort effect remained unchanged. Results suggest much of the increase in the incidence of EAC can be attributed to a period effect, which may be due to changes in the prevalence of obesity over time.

The physiological impacts of wealth shocks in late life: Evidence from the Great Recession.

Given documented links between individual socioeconomic status (SES) and health, it is likely that-in addition to its impacts on individuals' wallets and bank accounts-the Great Recession also took a toll on individuals' disease and mortality risk. Exploiting a quasi-natural experiment design, this study utilizes nationally representative, longitudinal data from the National Social Life, Health, and Aging Project (NSHAP) (2005-2011) (N = 930) and individual fixed effects models to examine how household-level wealth shocks experienced during the Great Recession relate to changes in biophysiological functioning in older adults. Results indicate that wealth shocks significantly predicted changes in physiological functioning, such that losses in net worth from the pre-to the post-Recession period were associated with increases in systolic blood pressure and C-reactive protein over the six year period. Further, while the association between wealth shocks and changes in blood pressure was unattenuated with the inclusion of other indicators of SES, psychosocial well-being, and health behaviors in analytic models, we document some evidence of mediation in the association between changes in wealth and changes in C-reactive protein, which suggests specificity in the social and biophysiological mechanisms relating wealth shocks and health at older ages. Linking macro-level conditions, meso-level household environments, and micro-level biological processes, this study provides new insights into the mechanisms through which economic inequality contributes to disease and mortality risk in late life.

Age-Specific Variation in Adult Mortality Rates in Developed Countries.

This paper investigates historical changes in both single-year-of-age adult mortality rates and variation of the single-year mortality rates around expected values within age intervals over the past two centuries in 15 developed countries. We apply an integrated Hierarchical Age-Period-Cohort-Variance Function Regression Model to data from the Human Mortality Database. We find increasing variation of the single-year rates within broader age intervals over the life course for all countries, but the increasing variation slows down at age 90 and then increases again after age 100 for some countries; the variation significantly declined across cohorts born after the early 20th century; and the variation continuously declined over much of the last two centuries but has substantially increased since 1980. Our further analysis finds the recent increases in mortality variation are not due to increasing proportions of older adults in the population, trends in mortality rates, or disproportionate delays in deaths from degenerative and man-made diseases, but rather due to increasing variations in young and middle-age adults.

Clarifying hierarchical age-period-cohort models: A rejoinder to Bell and Jones.

Previously, Reither et al. (2015) demonstrated that hierarchical age-period-cohort (HAPC) models perform well when basic assumptions are satisfied. To contest this finding, Bell and Jones (2015) invent a data generating process (DGP) that borrows age, period and cohort effects from different equations in Reither et al. (2015). When HAPC models applied to data simulated from this DGP fail to recover the patterning of APC effects, B&J reiterate their view that these models provide "misleading evidence dressed up as science." Despite such strong words, B&J show no curiosity about their own simulated data--and therefore once again misapply HAPC models to data that violate important assumptions. In this response, we illustrate how a careful analyst could have used simple descriptive plots and model selection statistics to verify that (a) period effects are not present in these data, and (b) age and cohort effects are conflated. By accounting for the characteristics of B&J's artificial data structure, we successfully recover the "true" DGP through an appropriately specified model. We conclude that B&Js main contribution to science is to remind analysts that APC models will fail in the presence of exact algebraic effects (i.e., effects with no random/stochastic components), and when collinear temporal dimensions are included without taking special care in the modeling process. The expanded list of coauthors on this commentary represents an emerging consensus among APC scholars that B&J's essential strategy--testing HAPC models with data simulated from contrived DGPs that violate important assumptions--is not a productive way to advance the discussion about innovative APC methods in epidemiology and the social sciences.

The impact of obesity on US mortality levels: the importance of age and cohort factors in population estimates.

OBJECTIVES: To estimate the percentage of excess death for US Black and White men and women associated with high body mass, we examined the combined effects of age variation in the obesity-mortality relationship and cohort variation in age-specific obesity prevalence. METHODS: We examined 19 National Health Interview Survey waves linked to individual National Death Index mortality records, 1986-2006, for age and cohort patterns in the population-level association between obesity and US adult mortality. RESULTS: The estimated percentage of adult deaths between 1986 and 2006 associated with overweight and obesity was 5.0% and 15.6% for Black and White men, and 26.8% and 21.7% for Black and White women, respectively. We found a substantially stronger association than previous research between obesity and mortality risk at older ages, and an increasing percentage of mortality attributable to obesity across birth cohorts. CONCLUSIONS: Previous research has likely underestimated obesity's impact on US mortality. Methods attentive to cohort variation in obesity prevalence and age variation in obesity's effect on mortality risk suggest that obesity significantly shapes US mortality levels, placing it at the forefront of concern for public health action.