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OBJECTIVES: Growing evidence suggests that religiosity is an important social determinant of health, including cognitive health. Yet most prior work focused on older adults or was conducted in racially and denominationally homogeneous regional samples. This study investigates the association of religious service attendance in midlife with cognitive function later in midlife. METHODS: Using data from the Coronary Artery Risk Development in Young Adults (CARDIA) study, a racially and geographically diverse prospective cohort study, we explored the association of religious service attendance in midlife with cognitive function 5 years later. Cognitive function was measured using four cognitive tests administered by CARDIA technicians. Multivariable linear regression was used for analyses. Primary analyses controlled for sociodemographics, physical health, depression, and prior religious involvement. Sensitivity analyses additionally controlled for baseline cognition and social support. RESULTS: Our study population included 2,716 participants (57.2% female, 44.9% Black, and mean age 50). In primary analyses, attending services more than weekly (compared to never) in midlife was associated with better global cognition (β = 0.14 standard deviations, 95% [confidence interval] CI = 0.02, 0.26) and verbal memory (β = 0.17 standard deviations, 95% CI = 0.04, 0.30), but not with processing speed (β = 0.04 standard deviations, 95% CI = -0.08, 0.16). A reverse association was observed with executive function (β = -0.16 standard deviations, 95% CI = -0.30, -0.02). Most findings persisted in analyses accounting for loss to follow-up via inverse probability weighting. DISCUSSION: Our findings suggest that frequent involvement in religious services at midlife is associated with better global cognition and verbal memory but worse executive function. There was no association with processing speed.

BackgroundDespite their well-established benefits for the prevention of cardiovascular disease, robust evidence on the effects of statins on cognition is largely inconclusive. We apply various study designs and analytical approaches to mimic randomized controlled trial effects from observational data.MethodsWe used observational data from 5 580 participants enrolled in the Cardiovascular Health Study from 1989/1990 to 1999/2000. We conceptualized the cohort as an overlapping sequence of nonrandomized trials. We compared multiple selection (eligible population, prevalent users, new users) and analytic approaches (multivariable adjustment, inverse-probability treatment weights, propensity score matching) to evaluate the association between statin use and 5-year change in global cognitive function, assessed using the Modified Mini-Mental State Examination (3MSE).ResultsWhen comparing prevalent users to nonusers (N = 2 772), statin use was associated with slower cognitive decline over 5 years (adjusted annual change in 3MSE = 0.34 points/year; 95% CI: 0.05-0.63). Compared to prevalent user design, estimates from new user designs (eg, comparing eligible statin initiators to noninitiators) were attenuated showing either null or negative association, though not significant. For example, in a propensity score-matched sample of statin-eligible individuals (N = 454), the annual 3MS change comparing statin initiators to noninitiators was -0.21 points/year (95% CI: -0.81 to 0.39).ConclusionsThe association of statin use and cognitive decline is attenuated toward the null when using rigorous analytical approaches that more closely mimic randomized controlled trials. Point estimates, even within the same study, may vary depending on the analytical methods used. Further studies that leverage natural or quasi experiments around statin use are needed to replicate our findings.

Racial residential segregation is associated with multiple adverse health outcomes in Black individuals. Yet, the influence of structural racism and racial residential segregation on brain aging is less understood. In this study, we investigated the association between cumulative exposure to racial residential segregation over 25 years (1985-2010) in young adulthood, as measured by the Getis-Ord Gi* statistic, and year 25 measures of brain volume (cerebral, gray matter, white matter, and hippocampal volumes) in midlife. We studied 290 Black participants with available brain imaging data who were enrolled in the Coronary Artery Risk Development in Young Adults (CARDIA) Study, a prospective cohort study. CARDIA investigators originally recruited 2,637 Black participants aged 18-30 years from 4 field centers across the United States. We conducted analyses using marginal structural models, incorporating inverse probability of treatment weighting and inverse probability of censoring weighting. We found that compared with low/medium segregation, greater cumulative exposure to a high level of racial residential segregation throughout young adulthood was associated with smaller brain volumes in general (e.g., for cerebral volume, β = -0.08, 95% confidence interval: -0.15, -0.02) and with a more pronounced reduction in hippocampal volume, though results were not statistically significant. Our findings suggest that exposure to segregated neighborhoods may be associated with worse brain aging.

Life course epidemiology is hampered by the absence of large studies with exposures and outcomes measured at different life stages in the same individuals. We describe when the effect of an exposure (A) on an outcome (Y) in a target population is identifiable in a combined ("synthetic") cohort created by pooling an early-life cohort including measures of A with a late-life cohort including measures of Y. We enumerate causal assumptions needed for unbiased effect estimation in the synthetic cohort and illustrate by simulating target populations under four causal models. From each target population, we randomly sampled early- and late-life cohorts and created a synthetic cohort by matching individuals from the two cohorts based on mediators and confounders. We estimated the effect of A on Y in the synthetic cohort, varying matching variables, the match ratio, and the strength of association between matching variables and A. Finally, we compared bias in the synthetic cohort estimates when matching variables did not d-separate A and Y to the bias expected in the original cohort. When the set of matching variables includes all variables d-connecting exposure and outcome (i.e., variables blocking all backdoor and front-door pathways), the synthetic cohort yields unbiased effect estimates. Even when matching variables did not fully account for confounders, the synthetic cohort estimate was sometimes less biased than comparable estimates in the original cohort. Methods based on merging cohorts may hasten the evaluation of early- and mid-life determinants of late-life health but rely on available measures of both confounders and mediators. [ABSTRACT FROM AUTHOR]

The authors examined the relationship of prepregnancy body mass index (BMI) and gestational weight gain (GWG) with child neurodevelopment. Mother-child dyads were a subgroup (n = 2,084) of the Child Health and Development Studies from the Oakland, California, area enrolled during pregnancy from 1959 to 1966 and followed at child age 9 years. Linear regression was used to examine associations between prepregnancy BMI, GWG, and standardized Peabody Picture Vocabulary Test and Raven Progressive Matrices scores and to evaluate effect modification of GWG by prepregnancy BMI. Before pregnancy, 77% of women were normal weight, 8% were underweight, 11% were overweight, and 3% were obese. Associations between GWG and child outcomes did not vary by prepregnancy BMI, suggesting no evidence for interaction. In multivariable models, compared to normal prepregnancy BMI, prepregnancy overweight and obesity were associated with lower Peabody scores (b: -1.29; 95% CI [-2.6, -0.04] and b: -2.7; 95% CI [-5.0, -0.32], respectively). GWG was not associated with child Peabody score [b: -0.03 (95% CI: -0.13, 0.07)]. Maternal BMI and GWG were not associated with child Raven score (all P >0.05). Maternal prepregnancy overweight and obesity were associated with lower scores for verbal recognition in mid-childhood. These results contribute to evidence linking maternal BMI with child neurodevelopment. Future research should examine the role of higher prepregnancy BMI values and the pattern of pregnancy weight gain in child cognitive outcomes.

Extensive evidence leads us to expect that health disparities by race and socioeconomic status found in one generation might be reproduced in the next. To the extent that this occurs it is important to assess life course processes responsible for the reproduction. Prospective evidence concerning such life course processes is hard to come by as it requires long-term follow-up of individuals from childhood through adult life. We present data from the Child Health and Development Disparities study that provides evidence relevant to this issue with respect to self-rated health. Mothers and offspring recruited in California's Bay Area between 1959 and 1967 were assessed during pregnancy with follow-up exams of offspring along with in-person interviews with mothers (at offspring ages 5, 9-11, 15-17) and offspring (at ages 15-17, ∼50). Available data allow us to assess the importance of three potential life course pathways in the reproduction of inequalities in self-rated health - socioeconomic pathways, cognitive pathways and pathways involving emerging health itself. As expected we found that race and SES disparities in SRH are reproduced across generations. They are evident in mothers, not strong or significant in offspring at 15-17, but present once again in offspring at age ∼50. Concerning potential pathways, we found that indicators of child health were related to adult SRH and played some role in accounting for race but not SES disparities in adult SRH. Cognitive abilities were unrelated to adult SRH with childhood SES controlled. Childhood SES was associated with adult SRH independent of other childhood factors and is reduced to non-significance only when offspring college attainment is controlled. Race and SES disparities in self-reported health in one generation are re-expressed in the next with strongest support for SES pathways in this transmission.

Background: Individuals of Mexican ancestry in the United States experience substantial socioeconomic disadvantages compared with non-Hispanic white individuals; however, some studies show these groups have similar dementia risk. Evaluating whether migration selection factors (e.g., education) associated with risk of Alzheimer disease and related dementia (ADRD) explain this paradoxical finding presents statistical challenges. Intercorrelation of risk factors, common with social determinants, could make certain covariate patterns very likely or unlikely to occur for particular groups, which complicates their comparison. Propensity score (PS) methods could be leveraged here to diagnose nonoverlap and help balance exposure groups. Methods: We compare conventional and PS-based methods to examine differences in cognitive trajectories between foreign-born Mexican American, US-born Mexican American, and US-born non-Hispanic white individuals in the Health and Retirement Study (1994-2018). We examined cognition using a global measure. We estimated trajectories of cognitive decline from linear mixed models adjusted for migration selection factors also associated with ADRD risk conventionally or with inverse probability weighting. We also employed PS trimming and match weighting. Results: In the full sample, where PS overlap was poor, unadjusted analyses showed both Mexican ancestry groups had worse baseline cognitive scores but similar or slower rates of decline compared with non-Hispanic white adults; adjusted findings were similar, regardless of method. Focusing analyses on populations where PS overlap was improved (PS trimming and match weighting) did not alter conclusions. Conclusions: Attempting to equalize groups on migration selection and ADRD risk factors did not explain paradoxical findings for Mexican ancestry groups in our study. [ABSTRACT FROM AUTHOR]

Racial residential segregation is associated with multiple adverse health outcomes in Black individuals. Yet, the influence of structural racism and racial residential segregation on brain aging is less understood. In this study, we investigated the association between cumulative exposure to racial residential segregation over 25 years (1985–2010) in young adulthood, as measured by the Getis-Ord Gi* statistic, and year 25 measures of brain volume (cerebral, gray matter, white matter, and hippocampal volumes) in midlife. We studied 290 Black participants with available brain imaging data who were enrolled in the Coronary Artery Risk Development in Young Adults (CARDIA) Study, a prospective cohort study. CARDIA investigators originally recruited 2,637 Black participants aged 18–30 years from 4 field centers across the United States. We conducted analyses using marginal structural models, incorporating inverse probability of treatment weighting and inverse probability of censoring weighting. We found that compared with low/medium segregation, greater cumulative exposure to a high level of racial residential segregation throughout young adulthood was associated with smaller brain volumes in general (e.g. for cerebral volume, β = –0.08, 95% confidence interval: −0.15, −0.02) and with a more pronounced reduction in hippocampal volume, though results were not statistically significant. Our findings suggest that exposure to segregated neighborhoods may be associated with worse brain aging. [ABSTRACT FROM AUTHOR]

Abstract Background Polychlorinated biphenyls (PCBs), known endocrine disruptors, were banned in 1979 but persist in the environment. Previous studies are inconsistent regarding prenatal exposure to PCBs and pregnancy outcomes. We investigated associations between prenatal exposure to PCBs and gestational length and birth weight. Methods In a sample of 600 infants (born between 1960 and 1963) randomly selected from Child Health and Development Studies participants followed through adolescence we measured 11 PCB congeners in maternal post partum sera (within three days of delivery). Length of gestation was computed from the reported first day of the last menstrual period (LMP) and delivery date. Linear regression was used to estimate associations between PCB exposure and gestational age and birth weight, adjusting for potential confounders. PCBs were grouped according to hypothesized biological action (1b (sum of weak phenobarbital inducers), 2b (sum of limited dioxin activity), and 3 (sum of CYP1A and CYP2b inducers)) or degree of ortho- substitution (mono, di, tri). Secondary analyses examined associations between total PCB exposure and exposure to individual congeners. Results Each unit increase in mono-ortho substituted PCBs was associated with a 0.30 week decrease (95% confidence interval (CI) -0.59, -0.016), corresponding to a 2.1 (95% CI −4.13, -0.11) day decrease in length of gestation. Similar associations were estimated for di-ortho substituted PCBs, (1.4 day decrease; (95% CI −2.9, 0.1)) and group 3 PCBs (0.84 day decrease; (95% CI −1.8, 0.11). We found similar associations in congener specific analyses and for the sum of congeners. Conclusions Our study provides new evidence that PCB exposure shortens length of gestation in humans. This may have public health implications for population exposures.

Background: Little research has investigated the long‐term relationship between low wages and memory decline, despite the growing share of low‐wage workers in the US labor market. We examined whether cumulative exposure to low wages over 12 years in midlife is associated with memory decline in later life. Method: We used 1992‐2016 data from the Health and Retirement Study, a biennial longitudinal survey of nationally representative samples of Americans aged 50+. We analyzed data from 3,803 individuals born 1936‐1941 using confounder‐adjusted linear mixed‐effects models. Low‐wage was defined as hourly wage lower than two‐thirds of the federal median wage for the corresponding year. Low‐wage exposure history was categorized into 'never', 'intermittent', and 'sustained' based on wages earned from 1992 to 2004. Memory function was measured at each visit from 2004 to 2016 by a memory composite score; on average, participants completed 4.8 memory assessments from 2004‐2016. Estimates were obtained in the total sample and within strata of sex (Nmales = 1,913, Nfemales = 1,890). Result: At the beginning of cognitive follow‐up (2004) our sample was on average 65 years old with a mean memory score of 1.15 standard units. The confounder‐adjusted annual rate of memory decline among workers who never earned low wages was ‐0.12 standard units, 95% CI: [‐0.14, ‐0.10]. Compared with this, memory decline among workers with sustained earning of low midlife wages was significantly faster (βtime*sustained:‐0.012, 95% CI: [‐0.02, ‐0.01]), corresponding to an annual rate of ‐0.13 standard units for this group. Put into terms of "excess cognitive aging", the cognitive aging experienced by workers with sustained exposure to low midlife wages over a 10‐year period is what workers never earning low‐wages would experience in 11 years. Similar associations were found among males and females. No significant association between intermittent earning of low wages and memory decline was observed. Conclusion: Sustained earning of low wages in midlife was significantly associated with a downward trajectory of memory performance in older age. Enhancing social policies to protect low‐wage workers (e.g., increasing minimum wage) may be especially beneficial for the cognitive health of individuals with sustained low‐wage employment in midlife. [ABSTRACT FROM AUTHOR]

Background: Studies on the health effect of Supplemental Nutrition Assistance Program (SNAP) on the cognitive health of older adults are scarce. In this study, we examined the associations of SNAP use and memory function trajectories among US older adults. Method: Our sample included 3,555 SNAP‐eligible participants (aged 50+) from the 1996 Health and Retirement Study survey, among whom 559 were SNAP users and 2,996 were non‐users. SNAP eligibility was constructed based on household income and assets compared to the federal criterion. Memory function was assessed biennially from 1996 through 2016. To account for pre‐existing differences in characteristics and variations in survey attrition between SNAP users and non‐users, we modeled the probability of SNAP use and of attrition using pre‐SNAP exposure (i.e., 1994) demographic and health covariates. We then modeled trajectories of memory function across SNAP use using linear mixed effect models weighted by the inverse probability of treatment (i.e. SNAP use) and of attrition. We also cross‐examined the results in a propensity score (PS) matched sample (N = 1,050). Result: SNAP users in 1996 had lower socioeconomic status and worse health at baseline than SNAP non‐users, and were more likely to be lost to follow‐up. Results using IP‐weights suggested SNAP users had worse memory scores at baseline but slower memory decline compared with non‐users (annual decline rate is ‐0.038 standard units [95%CI = ‐0.044, ‐0.033] for non‐users and ‐0.043 [95%CI = ‐0.046, ‐0.040] for users). Results from the PS‐matched sample also showed SNAP users had slower memory declines compared with non‐users (annual decline rate was ‐0.052 units [95%CI = ‐0.055, ‐0.050] for non‐users and ‐0.048 units [95%CI = ‐0.051, ‐0.046] for users). Conclusion: After accounting for pre‐existing differences between eligible SNAP users and non‐users as well as differential loss to follow‐up, our findings suggested that SNAP participation is associated with slower memory decline among eligible older adults. [ABSTRACT FROM AUTHOR]