Evidence for the Association Between Adverse Childhood Family Environment, Child Abuse, and Caregiver Warmth and Cardiovascular Health Across the Lifespan: The Coronary Artery Risk Development in Young Adults (CARDIA) Study.

BACKGROUND: This study aimed to quantify the association between childhood family environment and longitudinal cardiovascular health (CVH) in adult CARDIA (Coronary Artery Risk Development in Young Adults) Study participants. We further investigated whether the association differs by adult income. METHODS: We applied the CVH framework from the American Heart Association including metrics for smoking, cholesterol, blood pressure, glucose, body mass index, physical activity, and diet. CVH scores (range, 0-14) were calculated at years 0, 7, and 20 of the study. Risky Family environment (range, 7-28) was assessed at year 15 retrospectively, for childhood experiences of abuse, caregiver warmth, and family or household challenges. Complete case ordinal logistic regression and mixed models associated risky family (exposure) with CVH (outcome), adjusting for age, sex, race, and alcohol use. RESULTS: The sample (n=2074) had a mean age of 25.3 (±3.5) years and 56% females at baseline. The median risky family was 10 with ideal CVH (≥12) met by 288 individuals at baseline (28.4%) and 165 (16.3%) at year 20. Longitudinally, for every 1-unit greater risky family, the odds of attaining high CVH (≥10) decreased by 3.6% (OR, 0.9645 [95% CI, 0.94-0.98]). Each unit greater child abuse and caregiver warmth score corresponded to 12.8% lower and 11.7% higher odds of ideal CVH (≥10), respectively (OR, 0.872 [95% CI, 0.77-0.99]; OR, 1.1165 [95% CI, 1.01-1.24]), across all 20 years of follow-up. Stratified analyses by income in adulthood demonstrated associations between risky family environment and CVH remained significant for those of the highest adult income (>$74k), but not the lowest (<$35k). CONCLUSIONS: Although risky family environmental factors in childhood increase the odds of poor longitudinal adult CVH, caregiver warmth may increase the odds of CVH, and socioeconomic attainment in adulthood may contextualize the level of risk. Toward a paradigm of primordial prevention of cardiovascular disease, childhood exposures and economic opportunity may play a crucial role in CVH across the life course.

Cardiovascular variability, sociodemographics, and biomarkers of disease: the MIDUS study.

Introduction: Like heart rate, blood pressure (BP) is not steady but varies over intervals as long as months to as short as consecutive cardiac cycles. This blood pressure variability (BPV) consists of regularly occurring oscillations as well as less well-organized changes and typically is computed as the standard deviation of multiple clinic visit-to-visit (VVV-BP) measures or from 24-h ambulatory BP recordings (ABPV). BP also varies on a beat-to-beat basis, quantified by methods that parse variation into discrete bins, e.g., low frequency (0.04-0.15 Hz, LF). However, beat-to-beat BPV requires continuous recordings that are not easily acquired. As a result, we know little about the relationship between LF-BPV and basic sociodemographic characteristics such as age, sex, and race and clinical conditions. Methods: We computed LF-BPV during an 11-min resting period in 2,118 participants in the Midlife in the US (MIDUS) study. Results: LF-BPV was negatively associated with age, greater in men than women, and unrelated to race or socioeconomic status. It was greater in participants with hypertension but unrelated to hyperlipidemia, hypertriglyceridemia, diabetes, elevated CRP, or obesity. LF-diastolic BPV (DBPV), but not-systolic BPV (SBPV), was negatively correlated with IL-6 and s-ICAM and positively correlated with urinary epinephrine and cortisol. Finally, LF-DBPV was negatively associated with mortality, an effect was rendered nonsignificant by adjustment by age but not other sociodemographic characteristics. Discussion: These findings, the first from a large, national sample, suggest that LF-BPV differs significantly from VVV-BP and ABPV. Confirming its relationship to sociodemographic risk factors and clinical outcomes requires further study with large and representative samples.

Social relationships and epigenetic aging in older adulthood: Results from the Health and Retirement Study.

Growing evidence suggests that social relationship quality can influence age-related health outcomes, although how the quality of one's relationships directly relates to the underlying aging process is less clear. We hypothesized that the absence of close relationships as well as lower support and higher strain within existing relationships would be associated with an accelerated epigenetic aging profile among older adults in the Health and Retirement Study. Adults (N = 3,647) aged 50-100 years completed ratings of support and strain in relationships with their spouse, children, other family members, and friends. They also provided a blood sample that was used for DNA methylation profiling to calculate a priori-specified epigenetic aging measures: Horvath, Hannum, PhenoAge, GrimAge, and Dunedin Pace of Aging methylation (DunedinPoAm38). Generalized linear models that adjusted for chronological age, sex, and race/ethnicity and applied a false discovery rate correction revealed that the absence of marital and friend relationships related to an older GrimAge and faster DunedinPoAm38. Among those with existing relationships, lower support from a spouse, child, other family, and friends and higher strain with friends related to an older PhenoAge and GrimAge and faster DunedinPoAm38. In secondary analyses that further adjusted for socioeconomic and lifestyle factors, lower support from other family members and friends was associated with greater epigenetic aging. Findings suggest that the absence of close relationships and lower support within existing relationships-particularly with family members and friends-relate to accelerated epigenetic aging in older adulthood, offering one mechanism through which social relationships might influence risk for age-related declines and disease.

The effect of poverty on the relationship between household education levels and obesity in U.S. children and adolescents: an observational study.

Background: Although ample evidence has shown the link between childhood obesity and socioeconomic status including family income and household education levels, the mediating role of poverty in the association between household education levels and childhood obesity is unclear. This study aimed to quantify the extent to which family poverty levels contribute to the association between household education levels and obesity among US children and adolescents. Methods: This cohort study used the nationally representative data of 21,754 US children and adolescents aged 6-17 years (National Health and Nutrition Examination Survey 1999-2018). We applied mediation analysis of the association between household education levels (less than high school, high school, and college or above) and obesity mediated through poverty (≤138% vs. >138% federal poverty level), adjusting for demographic characteristics of household head and their offspring. Obesity was defined as age- and sex-specific body mass index in the 95th percentile or greater using the 2000 Centers for Disease Control and Prevention growth charts. Findings: Among 21,754 children and adolescents (weighted N = 43,544,684; mean age, 11.6 years; female, 49%), 9720 (weighted percentage, 33.0%) were classified as living in poverty and 4671 (weighted percentage, 19.1%) met the criteria for obesity. Low household education level (less than high school) showed increased risks of poverty (adjusted relative risk [95% CI], 5.82 [4.90-6.91]) and obesity (adjusted relative risk [95% CI], 1.94 [1.68-2.25]) compared to high household education level (college or above). We also quantified that poverty mediated 18.9% of the association between household education levels and obesity among children and adolescents. The mediation effect was consistently observed across age, gender, and race/ethnicity. Interpretation: Poverty mediated the association between the low educational status of household heads and their offspring's obesity. Our findings highlight the importance of reducing obesity risk among the low-income population to minimize the burden of intergenerational health disparities due to socioeconomic status. Funding: Japan Society for the Promotion of Sciences (22K17392).

Short sleep and insomnia are associated with accelerated epigenetic age.

OBJECTIVE: Short sleep and insomnia are each associated with greater risk for age-related disease, which suggests that insufficient sleep may accelerate biological aging. We examine whether short sleep and insomnia alone or together relate to epigenetic age among older adults. METHODS: A total of 3,795 men (46.3%) and women aged 56-100 years from the Health and Retirement Study were included. Insomnia was defined as reporting at least one insomnia symptom (difficulty falling asleep, waking up at night, or waking up too early in the morning) and feeling unrested when waking up most of the time. Those reporting <6 hours of bedtime were categorized as short sleepers. Three second- or third-generation epigenetic age acceleration clocks were derived from the 2016 HRS Venous Blood Study. The linear regression analysis was adjusted for age, sex, race/ethnicity, education, and obesity status. RESULTS: Insomnia and short sleep were associated with an 0.49 (95%CI:0.03-0.94; P:0.04) and 1.29 (95%CI:0.52-2.07; P:0.002) years acceleration of GrimAge, respectively, as well as a faster pace of aging (DunedinPACE; 0.018 (95%CI:0.004-0.033; P:0.02); 0.022(95%CI:-0.004-0.048; P:0.11)). Compared to healthy sleepers, individuals with the combination of short sleep and insomnia had an accelerated GrimAge (0.97 years; 95%CI:0.07-1.87; P:0.04) and a greater DunedinPACE (0.032; 95%CI:0.003-0.060; P:0.04). CONCLUSION: Our findings indicate short sleep, insomnia, and the combination of the two, are linked to epigenetic age acceleration, suggesting that these individuals have an older biological age that may contribute to risk for comorbidity and mortality.

Social genomics, cognition, and well-being during the COVID-19 pandemic.

INTRODUCTION: Adverse psychosocial exposure is associated with increased proinflammatory gene expression and reduced type-1 interferon gene expression, a profile known as the conserved transcriptional response to adversity (CTRA). Little is known about CTRA activity in the context of cognitive impairment, although chronic inflammatory activation has been posited as one mechanism contributing to late-life cognitive decline. METHODS: We studied 171 community-dwelling older adults from the Wake Forest Alzheimer's Disease Research Center who answered questions via a telephone questionnaire battery about their perceived stress, loneliness, well-being, and impact of COVID-19 on their life, and who provided a self-collected dried blood spot sample. Of those, 148 had adequate samples for mRNA analysis, and 143 were included in the final analysis, which including participants adjudicated as having normal cognition (NC, n = 91) or mild cognitive impairment (MCI, n = 52) were included in the analysis. Mixed effect linear models were used to quantify associations between psychosocial variables and CTRA gene expression. RESULTS: In both NC and MCI groups, eudaimonic well-being (typically associated with a sense of purpose) was inversely associated with CTRA gene expression whereas hedonic well-being (typically associated with pleasure seeking) was positively associated. In participants with NC, coping through social support was associated with lower CTRA gene expression, whereas coping by distraction and reframing was associated with higher CTRA gene expression. CTRA gene expression was not related to coping strategies for participants with MCI, or to either loneliness or perceived stress in either group. DISCUSSION: Eudaimonic and hedonic well-being remain important correlates of molecular markers of stress, even in people with MCI. However, prodromal cognitive decline appears to moderate the significance of coping strategies as a correlate of CTRA gene expression. These results suggest that MCI can selectively alter biobehavioral interactions in ways that could potentially affect the rate of future cognitive decline and may serve as targets for future intervention efforts.

Childhood environment early life stress, caregiver warmth, and associations with the cortisol diurnal curve in adulthood: The coronary artery risk development in young adults (CARDIA) study.

BACKGROUND: Early life stress (ELS) is associated with increased morbidity and mortality across the lifecourse. Studies observing a relationship between ELS and stress physiology (cortisol), may help explain the connection to poor health outcomes, but have been limited by cortisol measures used. PURPOSE: We examined the association between ELS measured by a Risky Family (RF) environment questionnaire, and adult diurnal cortisol profile inclusive of multiple cortisol measures. METHODS: RF and cortisol were collected from Coronary Artery Risk Development in Young Adults Study participants at follow-up (Year 15). Complete case (n = 672) data were included in multi-variable regression analyses with log transformed cortisol measures (outcomes) including wake-up cortisol, cortisol awakening response [CAR], AUC and five other cortisol diurnal curve measures. RESULTS: Participants were age 39.9 + /- 3.7 years and 51.6% Black. For every 1 unit increase in RF, there was a 1.4% greater wake-up cortisol and flatter CAR after adjustment for age, sex, income, and smoking (B=0.014, p = 0.023; B=-0.014, p = 0.028, respectively). Each unit increase in caregiver warmth/affection was associated with a 6.9% higher (steeper) CAR (B=0.069, p = 0.03). Results remained significant after adjusting for other covariates except social support in adulthood. An interaction between child abuse and caregiver warmth was nearly significant (p = 0.068), such that for those with exposure to the greatest caregiver warmth and lowest child abuse, CAR was steepest CONCLUSIONS: We demonstrate that ELS is associated with altered cortisol regulation in adulthood. However, further research is needed to assess how healthy relationships throughout the life course may modulate cortisol regulation in adulthood.

Heterogeneity in the Association Between the Presence of Coronary Artery Calcium and Cardiovascular Events: A Machine-Learning Approach in the MESA Study.

BACKGROUND: Coronary artery calcium (CAC) has been widely recognized as an important predictor of cardiovascular disease (CVD). Given the finite resources, it is important to identify individuals who would receive the most benefit from detecting positive CAC by screening. However, the evidence is limited as to whether the burden of positive CAC on CVD differs by multidimensional individual characteristics. We sought to investigate the heterogeneity in the association between positive CAC and incident CVD. METHODS: This cohort study included adults from MESA (Multi-Ethnic Study of Atherosclerosis) ages ≥45 years and free of cardiovascular disease. After propensity score matching in a 1:1 ratio, we applied a machine learning causal forest model to (1) evaluate the heterogeneity in the association between positive CAC and incident CVD, and (2) predict the increase in CVD risk at 10-years when CAC>0 (versus CAC=0) at the individual level. We then compared the estimated increase in CVD risk when CAC>0 to the absolute 10-year atherosclerotic CVD (ASCVD) risk calculated by the 2013 American College of Cardiology/American Heart Association pooled cohort equations. RESULTS: Across 3328 adults in our propensity score-matched analysis, our causal forest model showed the heterogeneity in the association between CAC>0 and incident CVD. We found a dose-response relationship of the estimated increase in CVD risk when CAC>0 with higher 10-year ASCVD risk. Almost all individuals (2293 of 2428 [94.4%]) with borderline risk of ASCVD or higher showed ≥2.5% increase in CVD risk when CAC>0. Even among 900 adults with low ASCVD risk, 689 (69.2%) showed ≥2.5% increase in CVD risk when CAC>0; these individuals were more likely to be male, Hispanic, and have unfavorable CVD risk factors than others. CONCLUSIONS: The expected increases in CVD risk when CAC>0 were heterogeneous across individuals. Moreover, nearly 70% of people with low ASCVD risk showed a large increase in CVD risk when CAC>0, highlighting the need for CAC screening among such low-risk individuals. Future studies are needed to assess whether targeting individuals for CAC measurements based on not only the absolute ASCVD risk but also the expected increase in CVD risk when CAC>0 improves cardiovascular outcomes.

Association of Attending a High-Performing High School With Substance Use Disorder Rate and Health Outcomes in Young Adults.

Importance: Interventions directly targeting social factors, such as education, may have the potential to greatly improve health. Objective: To examine the association of attending a high-performing public charter high school with rates of substance use disorder and physical and mental health. Design, Setting, and Participants: This cohort study used the random school admissions lottery system of high-performing public charter high schools in low-income neighborhoods of Los Angeles, California, to examine the health outcomes of students who applied to at least 1 of 5 of these high schools. Participants attended 147 different high schools and were randomly selected from those who won the admissions lottery (intervention group) and those who were placed on a waiting list (control group). Participants were surveyed at the end of grade 8 through transition into grade 9 and then from grade 10 through 3 years after high school completion (at age 21 years). Surveys were conducted from March 2013 through November 2021. Intervention: Attendance at a high-performing public charter high school. Main Outcomes and Measures: Self-reported alcohol use disorder and cannabis misuse, delinquent behaviors, physical and mental health, and body mass index. Results: Of the 1270 participants at baseline (mean [SD] age, 14.2 [0.47] years; 668 female individuals [52.6%]). The control group included 576 individuals (45.4%), and 694 individuals (54.6%) were in the intervention group. Both groups were similar in almost all characteristics at baseline, and the median (IQR) follow-up was 6.4 (6.0-6.7) years. Participants attending a high-performing public charter high school had a 53.33% lower rate of hazardous or dependent alcohol use disorder compared with those in the control group (5.43% vs 11.64%; difference, -6.21% [95% CI, -11.87% to -0.55%]; P = .03). Among male participants, the intervention group had a 42.05% lower rate of self-reported fair or poor physical health (13.33% vs 23.01%; difference, -9.67% [95% CI, -18.30% to -1.05%]; P = .03) and a 32.94% lower rate of obesity or overweight (29.28% vs 43.67%; difference, -14.38% [95% CI, -25.74% to -3.02%]; P = .02) compared with the control group. Among female participants, attending a high-performing public charter high school was associated with worse physical health outcomes (30.29% vs 13.47% reporting fair or poor health; difference, 16.82% [95% CI, 0.36% to 33.28%]; P = .045) and higher rates of overweight or obesity (52.20% vs 32.91%; difference, 19.30% [95% CI, 3.37% to 35.22%]; P = .02) at age 21 years. Few differences in mental health outcomes were observed. Adjusting for educational outcomes did not significantly change these findings. Conclusions and Relevance: Results of this study suggest that attending a high-performing public charter high school was associated with lower rates of substance use disorder independent of academic achievement. Physical health and obesity outcomes were also better but only for young men; the intervention group had worse physical health outcomes among young women for unclear reasons. Schools are a potent social determinant of health and an important target for future health interventions.

Lifetime exposure to smoking, epigenetic aging, and morbidity and mortality in older adults.

BACKGROUND: Cigarette smoke is a major public health concern. Epigenetic aging may be an important pathway by which exposure to cigarette smoke affects health. However, little is known about how exposure to smoke at different life stages affects epigenetic aging, especially in older adults. This study examines how three epigenetic aging measures (GrimAge, PhenoAge, and DunedinPoAm38) are associated with parental smoking, smoking in youth, and smoking in adulthood, and whether these epigenetic aging measures mediate the link between smoke exposure and morbidity and mortality. This study utilizes data from the Health and Retirement Study (HRS) Venous Blood Study (VBS), a nationally representative sample of US adults over 50 years old collected in 2016. 2978 participants with data on exposure to smoking, morbidity, and mortality were included. RESULTS: GrimAge is significantly increased by having two smoking parents, smoking in youth, and cigarette pack years in adulthood. PhenoAge and DunedinPoAm38 are associated with pack years. All three mediate some of the effect of pack years on cancer, high blood pressure, heart disease, and mortality and GrimAge and DunedinPoAm38 mediate this association on lung disease. CONCLUSIONS: Results suggest epigenetic aging is one biological mechanism linking lifetime exposure to smoking with development of disease and earlier death in later life. Interventions aimed at reducing smoking in adulthood may be effective at weakening this association.

Social stressors associated with age-related T lymphocyte percentages in older US adults: Evidence from the US Health and Retirement Study.

Exposure to stress is a risk factor for poor health and accelerated aging. Immune aging, including declines in naïve and increases in terminally differentiated T cells, plays a role in immune health and tissue specific aging, and may contribute to elevated risk for poor health among those who experience high psychosocial stress. Past data have been limited in estimating the contribution of life stress to the development of accelerated immune aging and investigating mediators such as lifestyle and cytomegalovirus (CMV) infection. This study utilizes a national sample of 5,744 US adults over age 50 to assess the relationship of social stress (viz., everyday discrimination, stressful life events, lifetime discrimination, life trauma, and chronic stress) with flow cytometric estimates of immune aging, including naïve and terminally differentiated T cell percentages and the ratio of CD4+ to CD8+ cells. Experiencing life trauma and chronic stress was related to a lower percentage of CD4+ naïve cells. Discrimination and chronic stress were each associated with a greater percentage of terminally differentiated CD4+ cells. Stressful life events, high lifetime discrimination, and life trauma were related to a lower percentage of CD8+ naïve cells. Stressful life events, high lifetime discrimination, and chronic stress were associated with a higher percentage of terminally differentiated CD8+ cells. High lifetime discrimination and chronic stress were related to a lower CD4+:CD8+ ratio. Lifestyle factors and CMV seropositivity partially reduced these effects. Results identify psychosocial stress as a contributor to accelerating immune aging by decreasing naïve and increasing terminally differentiated T cells.

Diurnal dynamic range as index of dysregulation of system dynamics. A cortisol examplar using data from the Study of Midlife in the United States.

We discuss the importance of including measures of dysregulated system dynamics in the operationalization of allostatic load. The concept of allostatic load, as originally proposed by McEwen and Stellar, included dysregulation not only in the resting state of physiological systems, but also in system dynamics. We describe previous work on cortisol diurnal dynamic range (peak to nadir spread) as an index of the health of the hypothalamic-pituitary-adrenal axis, with compression of dynamic range being a marker of dysregulation. In particular, we review the evidence for a) diurnal dynamic range compression in people from disadvantaged backgrounds, b) cross-sectional association of cortisol diurnal dynamic range compression with dysregulation in other systems' resting states, and c) cross-sectional association of cortisol diurnal dynamic range compression with lower scores on cognitive testing. Then, we present new data from the Study of Midlife in the United States (MIDUS) on longitudinal associations of cortisol dynamic range compression with subsequent cognitive decline and all-cause mortality. Briefly, each standard deviation decrement in cortisol diurnal dynamic range is associated with adjusted mortality hazard ratio of 1.35 (95% confidence interval: 1.19, 1.54). Among those who scored at median or lower in executive functioning at baseline and survive, each standard deviation decrement in cortisol dynamic range is associated with 1% greater decline in executive functioning over a decade (95% confidence interval: 0.4%, 2.0%). We conclude that including measures of system dynamics like diurnal dynamic range in the next generation of allostatic load measurement will likely advance understanding of the cumulative physiological burden of chronic stress and life experiences, and improve the prediction of future health consequences.

Turning Vicious Cycles Into Virtuous Ones: the Potential for Schools to Improve the Life Course.

Adolescence is a critical transition period that sets the stage for adulthood and future health outcomes. Marked by key developmental milestones in brain maturation, increasing independence from parents, and greater connections to peers, adolescence is also a time of heightened risk for behavioral health problems, including substance use, violence, delinquency, and mental health issues. High school completion is a significant life course event and a powerful social determinant of health and health disparities. Jessor's Theory of Problem Behavior suggests that adolescent health behaviors and mental health problems are closely tied to poor educational outcomes and peer network formation in a reinforcing feedback loop, or vicious cycle, often leading to school failure, school disengagement, and drop-out. Schools are a novel platform through which vicious cycles can be disrupted and replaced with virtuous ones, simultaneously improving education and health. This article describes the potential for schools to transform health trajectories through interventions creating positive and supportive school climates. In addition, new models such as the Whole School Whole Community Whole Child Model promote whole child well-being, including cognitive, social, emotional, psychological, and physical development. Full-service community schools can serve as a hub coordinating and integrating all available resources to better respond to the needs of children and families. Present in every neighborhood, schools are a way to reach every school-age child and improve their health trajectories, providing an important platform for life course intervention research.

Accelerated epigenetic aging mediates link between adverse childhood experiences and depressive symptoms in older adults: Results from the Health and Retirement Study.

Adverse childhood experiences (ACEs) increase risk for depression at subsequent ages and have been linked to accelerated biological aging. We hypothesize that accelerated epigenetic aging may partially mediate the link between ACEs and depression. This study examines 3 three second-generation epigenetic aging measures (viz., GrimAge, PhenoAge, and DunedinPoAm38) as mediators of the link between ACEs and depressive symptoms in older adulthood. We utilize structural equation modeling to assess mediation in the Health and Retirement Study (N = 2672). Experiencing ACEs is significantly associated with an older GrimAge and a faster pace of aging via the DunedinPoAm38. Having an older GrimAge and faster DunedinPoAm38 pace of aging were also significantly associated with more depressive symptoms. PhenoAge was not significantly associated with depressive symptoms and was only associated with experiencing three ACEs. These associations were reduced by socioeconomic and lifestyle factors, including obesity and substance use. GrimAge explained between 9 and 14% of the association between ACEs and adult depressive symptoms, and DunedinPoAm38 explained between 2 and 7% of the association between ACEs and adult depressive symptoms. Findings indicate accelerated aging, as measured by GrimAge and DunedinPoAm38, is associated with ACEs and with depressive symptoms in older Americans. Findings also show these epigenetic aging measures mediate a portion of the association between ACEs and adult depressive symptoms. Epigenetic aging may represent a physiological mechanism underlying the link between early life adversity and adult depression. Weight maintenance and substance use are potentially important areas for intervention.

Allostatic load in the context of disasters.

Environmental disasters, pandemics, and other major traumatic events such as the Covid-19 pandemic or war contribute to psychosocial stress which manifests in a wide range of mental and physical consequences. The increasing frequency and severity of such events suggest that the adverse effects of toxic stress are likely to become more widespread and pervasive in the future. The allostatic load (AL) model has important elements that lend themselves well for identifying adverse health effects of disasters. Here we examine several articulations of AL from the standpoint of using AL to gauge short- and long-term health effects of disasters and to provide predictive capacity that would enable mitigation or prevention of some disaster-related health consequences. We developed a transdisciplinary framework combining indices of psychosocial AL and physiological AL to produce a robust estimate of overall AL in people affected by disasters and other traumatic events. In conclusion, we urge researchers to consider the potential of using AL as a component in a proposed disaster-oriented human health observing system.

Longitudinal Associations Between Discrimination, Neighborhood Social Cohesion, and Telomere Length: The Multi-Ethnic Study of Atherosclerosis.

BACKGROUND: We aimed to examine if neighborhood social cohesion moderated longitudinal associations between baseline reports of discrimination and 10-year changes in leukocyte telomere length (LTL). METHODS: Data are from the Multi-Ethnic Study of Atherosclerosis (N = 1064; age range 45-84 years). Baseline discrimination was measured using the Major Experiences of Discrimination Scale (MDS; none, 1 domain, ≥2 domains) and the Experiences of Discrimination Scale (EDS; none, moderate, high). Neighborhood social cohesion at baseline was assessed via a community survey within census tract-defined neighborhoods. 10-year change in LTL was defined as regression to the mean-corrected 10-year difference in the ratio of telomeric DNA to a single-copy gene (T/S). RESULTS: In linear mixed-effects models, we found that neighborhood social cohesion modified the effect of baseline reports of MDS on 10-year changes in LTL, independent of sociodemographic characteristics, health behaviors, and health conditions (p(χ 2) = .01). Among those residing in neighborhoods with low social cohesion, experiencing major discrimination in ≥2 domains was associated with faster LTL attrition over 10 years, compared to reporting no discrimination (ß = -0.03; 95% confidence interval: -0.06, -0.003). We found no main associations for either discrimination measure and no interaction between EDS and neighborhood social cohesion. CONCLUSIONS: Results indicate that neighborhood social cohesion is an important dimension of the neighborhood context that may moderate the impact of major experiences of discrimination on telomere length attrition. These findings help advance our understanding of the integral role that neighborhood environments play in attenuating the effect of discrimination on accelerated cell aging.

Depression-, Anxiety-, and Anger and Cognitive Functions: Findings From a Longitudinal Prospective Study.

Background: Determinants of changes in cognitive function during aging are not well-understood. We aimed to estimate the effects of depression-, anxiety- and anger symptoms on cognition and on cognition changes, especially on changes in episodic memory (EM) and executive functioning (EF). Methods: We analyze data from the Mid-Life in the Midlife in the United States Biomarker study at two time points including n = 710 women, and n = 542 men (1996/1997) at the first assessment and n = 669 women, and n = 514 men at the second assessment (2013/2014). To assess cognition we used the Brief Test of Adult Cognition (BTACT). To measure depression-, anxiety- and anger symptoms we used the Mood and Anxiety Symptom Questionnaire (MASQ), the Center for Epidemiologic Studies Depression Scale (CES-D) and the State-Trait Anger Expression Inventory (STAXI). We used repeated models analyses to explore changes in cognition, and repeated measures linear mixed-effects models to investigate depression, anxiety and anger effects on cognition. All analyses were adjusted for potential confounders (cognition at baseline, age, education, income). Results: At the first assessment, women had significantly better episodic memory functioning than men; men in the oldest age group had significant better executive functioning. At the second assessment, more education, and white ethnicity were associated with less negative changes on episodic memory and executive functioning. Depression- and anger symptoms were associated with declines in episodic memory among women; anxiety symptoms were associated with declines in episodic memory and executive functioning in both gender in men (EF: ß: -0.02, (95% CI: -0.03, -0.01; EM: ß -0.02 (-0.02, 95% CI: -0.03, -0.01) and in women (EF: ß -0.01, 95% CI: -0.02, -0.0004; EM: ß -0.013, 95% CI: -0.03, -0.001). Conclusions: Depression-, anxiety- and anger symptoms were associated with changes in episodic memory and executive functioning. Further longitudinal studies are critical in populations in more countries to better understand the impact of depression, anxiety and anger symptoms on cognition changes.

Longitudinal Associations between Discrimination, Neighborhood Social Cohesion, and Telomere Length: The Multi-Ethnic Study of Atherosclerosis (MESA).

BACKGROUND: We aimed to examine if neighborhood social cohesion moderated longitudinal associations between baseline reports of discrimination and 10-year changes in Leukocyte Telomere Length (LTL). METHODS: Data are from the Multi-Ethnic Study of Atherosclerosis (MESA; N=1,064; age range 45-84 years). Baseline discrimination was measured using the Major Experiences of Discrimination Scale (MDS; none, 1 domain, ≥2 domains) and the Experiences of Discrimination Scale (EDS; none, moderate, high). Neighborhood social cohesion at baseline was assessed via a community survey within census tract defined neighborhoods. 10-year change in LTL was defined as Regression to the Mean corrected 10-year difference in the ratio of telomeric DNA to a single copy gene (T/S). RESULTS: In linear mixed effects models, we found that neighborhood social cohesion modified the effect of baseline reports of MDS on 10-year changes in LTL, independent of sociodemographic characteristics, health behaviors, and health conditions (p(χ 2)=0.01). Among those residing in neighborhoods with low social cohesion, experiencing major discrimination in ≥2 domains was associated with faster LTL attrition over 10-years, compared to reporting no discrimination (ß=-0.03; 95% CI: -0.06, -0.003). We found no main associations for either discrimination measure and no interaction between EDS and neighborhood social cohesion. CONCLUSIONS: Results indicate that neighborhood social cohesion is an important dimension of the neighborhood context that may moderate the impact of major experiences of discrimination on telomere length attrition. These findings help advance our understanding of the integral role that neighborhood environments play in attenuating the effect of discrimination on accelerated cell aging.

Generativity and Social Well-Being in Older Women: Expectations Regarding Aging Matter.

OBJECTIVES: Beliefs about aging can contribute to health and well-being in older adults. Feeling generative, or that one is caring for and contributing to the well-being of others, can also impact health and well-being. In this study, we hypothesized that those with more positive expectations regarding aging (ERA) in the mental health domain would report greater levels of perceived social support (PSS) and lower levels of loneliness in response to a generativity intervention (vs control condition). METHOD: Participants in this study (n = 73, 100% female) were randomly assigned to a 6-week generativity condition, which involved writing about life experiences and sharing advice with others, or to a control condition, which involved writing about neutral topics. Pre- and postintervention, PSS, and feelings of loneliness were measured. RESULTS: Those in the generativity condition with more positive ERA in the mental health domain reported greater PSS and lower loneliness postintervention. DISCUSSION: These results highlight the importance of psychological factors, such as ERA, in moderating the efficacy of interventions to promote social well-being in older adults.