Generations of epigenetic clocks and their links to socioeconomic status in the Health and Retirement Study.

Aim: This is a brief description of links between nine epigenetic clocks related to human aging and socioeconomic and behavioral characteristics as well as health outcomes. Materials & methods: We estimate frequently used and novel clocks from one data source, the Health and Retirement Study. Results: While all of these clocks are thought to reflect "aging," they use different CpG sites and do not strongly relate to each other. First and fourth generation clocks are not as linked to socioeconomic status or health outcomes as second and third generation clocks. Conclusion: Epigenetic clocks reflect exciting new tools and their continued evolution is likely to improve our understanding of how exposures get under the skin to accelerate aging.

Biological aging occurs much earlier than mortality and the onset of diseases associated with age that can be clinically diagnosed. In fact, changes in biology that accelerate aging can occur throughout life in response to adverse exposures, behaviors and experiences. One such change is methylation or the attachment of methyl groups to genetic markers to affect their activity. Epigenetic clocks are measures of the amount of methylation that is related to aging. They are called clocks because they are measured in years or ticks of time or in change in years relative to age. We show that not all epigenetic clocks are the same in how they relate to socioeconomic status and health behaviors as well as subsequent mortality and morbidity. There are now four generations of these clocks developed in a little more than 10 years. The second and third generation clocks are more closely associated with lifetime socioeconomic status, health behaviors and health outcomes probably because they have been developed by relating them to health indicators in contrast to epigenetic measures that were developed because of their relation to age. Incorporating epigenetic measures into population studies reflects the beginning of our ability to measure some aspects of aging long before old age; it also provides entry to monitoring, measuring and intervening on biological aging throughout life.

Epigenetic Aging Helps Explain Differential Resilience in Older Adults.

Past research suggests that resilience to health hazards increases with age, potentially because less resilient individuals die at earlier ages, leaving behind their more resilient peers. Using lifetime cigarette smoking as a model health hazard, we examined whether accelerated epigenetic aging (indicating differences in the speed of individuals' underlying aging process) helps explain age-related resilience in a nationally representative sample of 3,783 older U.S. adults from the Health and Retirement Study. Results of mediation moderation analyses indicated that participants aged 86 or older showed a weaker association between lifetime cigarette smoking and mortality relative to participants aged 76-85 and a weaker association between smoking and multimorbidity relative to all younger cohorts. This moderation effect was mediated by a reduced association between smoking pack-years and epigenetic aging. This research helps identify subpopulations of particularly resilient individuals and identifies epigenetic aging as a potential mechanism explaining this process. Interventions in younger adults could utilize epigenetic aging estimates to identify the most vulnerable individuals and intervene before adverse health outcomes, such as chronic disease morbidity or mortality, manifest.

The embodiment of parental death in early life through accelerated epigenetic aging: Implications for understanding how parental death before 18 shapes age-related health risk among older adults.

Parental death in early life has been linked to various adverse health outcomes in older adulthood. This study extends prior research to evaluate how parental death in early life is tied to accelerated epigenetic aging, a potentially important biological mechanism from which social and environmental exposures impact age-related health. We used data from the 2016 Venous Blood Study (VBS), a component of the Health and Retirement Study (HRS), to examine the association between parental death in early life and accelerated epigenetic aging as measured by three widely used epigenetic clocks (PCPhenoAge, PCGrimAge, and DunedinPACE). We also assessed whether some of the association is explained by differences in educational attainment, depressive symptoms, and smoking behavior. Methods included a series of linear regression models and formal mediation analysis. Findings indicated that parental death in early life is associated with accelerated epigenetic aging for PCPhenoAge and DunedinPACE. The inclusion of educational attainment, depressive symptoms, and smoking behavior attenuated this association, with formal mediation analysis providing additional support for these observations. Parental death in early life may be one of the most difficult experiences an individual may face. The elevated biological risk associated with parental death in early life may operate through immediate changes but also through more downstream risk factors. This study highlights how early life adversity can set in motion biological changes that have lifelong consequences.

Immune cells are associated with mortality: the Health and Retirement Study.

Introduction: Age-related immunosenescence is characterized by changes in immune cell subsets and is associated with mortality. However, since immunosenescence is associated with other concurrent age-related changes such as inflammation and multi-organ dysfunction, it is unclear whether the association between age-related immunosenescence and mortality is independent of other concurrent age-related changes. To address these limitations, we evaluated the independent association between immune cell subsets and mortality after adjustment for age-related inflammation and biologic age. Methods: Data for this study was obtained from the 2016 interview of the Health and Retirement Study (N=6802). Cox proportional hazards regression models were used to estimate the association between 25 immune cell subsets (11 T-cell subsets, 4 B-cell subsets, 3 monocyte subsets, 3 natural killer cell subsets, 3 dendritic cell subsets, and neutrophils) and 4-year mortality adjusting for covariates such as the Klemera-Doubal algorithm biological age, chronological age, gender, race/ethnicity, BMI, smoking status, comorbidity index, CMV seropositivity, and inflammatory latent variable comprising C-reactive protein, and 4 cytokines (interleukin-10, interleukin-1 receptor antagonist, interleukin-6, and soluble tumor necrosis factor). Results: Four hundred and seventy-six participants died during the study period with an overall median follow up time of 2.5 years. After controlling for covariates and adjustment for sample-weights, total T cells [HR: 0.86, p=0.004], NK CD56LO cells [HR: 0.88, p=0.005], and neutrophils [HR: 1.22, p=0.004] were significantly associated with mortality. Conclusions: These findings support the idea that an aging immune system is associated with short-term mortality independent of age-related inflammation or other age-related measures of physiological dysfunction. If replicated in other external cohorts, these findings could identify novel targets for both monitoring and intervention to reduce the age-related mortality.

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.

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.

Chronic Stress and Latent Virus Reactivation: Effects on Immune Aging, Chronic Disease Morbidity, and Mortality.

OBJECTIVES: Social stress has been shown to affect immune functioning. Past research has found that chronic social stress and latent viral infections accelerate immune aging, leading to chronic disease morbidity and mortality. Chronic stress may also reactivate latent viral infections, like cytomegalovirus (CMV), accelerating the aging of the immune system. METHOD: Utilizing panel survey data from 8,995 U.S. adults aged 56 or older from the Health and Retirement Study, this study investigates whether chronic stress interacts with CMV positivity to drive aging of the immune system, multimorbidity, and mortality. RESULTS: Results of moderated mediation analysis indicate that the effect of CMV positivity on morbidity and mortality as mediated by immune aging indicators is amplified by chronic stress. DISCUSSION: These findings suggest that immune aging is a biological pathway underlying the stress process and help explain past findings in the literature on stress and health.

ADHD genetic burden associates with older epigenetic age: mediating roles of education, behavioral and sociodemographic factors among older adults.

BACKGROUND: Shortened lifespans are associated with having Attention Deficit Hyperactivity Disorder (ADHD), which is likely mediated by related behavioral and sociodemographic factors that are also associated with accelerated physiological aging. Such factors include exhibiting more depressive symptoms, more cigarette smoking, higher body mass index, lower educational attainment, lower income in adulthood, and more challenges with cognitive processes compared to the general population. A higher polygenic score for ADHD (ADHD-PGS) is associated with having more characteristic features of ADHD. The degree to which (1) the ADHD-PGS associates with an epigenetic biomarker developed to predict accelerated aging and earlier mortality is unknown, as are whether (2) an association would be mediated by behavioral and sociodemographic correlates of ADHD, or (3) an association would be mediated first by educational attainment, then by behavioral and sociodemographic correlates. We evaluated these relationships in a population-based sample from the US Health and Retirement Study, among N = 2311 adults age 50 and older, of European-ancestry, with blood-based epigenetic and genetic data. The ADHD-PGS was calculated from a prior genomewide meta-analysis. Epigenome-wide DNA methylation levels that index biological aging and earlier age of mortality were quantified by a blood-based biomarker called GrimAge. We used a structural equation modeling approach to test associations with single and multi-mediation effects of behavioral and contextual indicators on GrimAge, adjusted for covariates. RESULTS: The ADHD-PGS was significantly and directly associated with GrimAge when adjusting for covariates. In single mediation models, the effect of the ADHD-PGS on GrimAge was partially mediated via smoking, depressive symptoms, and education. In multi-mediation models, the effect of the ADHD-PGS on GrimAge was mediated first through education, then smoking, depressive symptoms, BMI, and income. CONCLUSIONS: Findings have implications for geroscience research in elucidating lifecourse pathways through which ADHD genetic burden and symptoms can alter risks for accelerated aging and shortened lifespans, when indexed by an epigenetic biomarker. More education appears to play a central role in attenuating negative effects on epigenetic aging from behavioral and sociodemographic risk factors related to ADHD. We discuss implications for the potential behavioral and sociodemographic mediators that may attenuate negative biological system effects.

Socioeconomic status and immune aging in older US adults in the health and retirement study.

Socioeconomic and demographic factors including educational attainment, race and ethnicity, and childhood socioeconomic status (SES) are powerful predictors of inequalities in aging, morbidity, and mortality. Immune aging, including accumulation of late-differentiated, senescent-like lymphocytes and lower levels of naïve lymphocytes, may play a role in the development of the age-related health inequalities. This study used nationally representative data from more than 9,000 US adults from the Health and Retirement Study to investigate associations between educational attainment, race and ethnicity, and childhood SES and lymphocyte percentages. Respondents with lower educational attainment, Hispanic adults, and those who had a parent with less than a high school education had lymphocyte percentages consistent with more immune aging compared to those with greater educational attainment, non-Hispanic White adults, and respondents who had parents with a high school education, respectively. Associations between education, Hispanic ethnicity, and parents' education and late differentiated senescent-like T lymphocytes (TemRA) and B cells were largely driven by cytomegalovirus (CMV), suggesting it is a factor in observed SES inequalities in immunosenescence. Naïve T lymphocytes may be particularly affected by socioeconomic position and may therefore be of particular interest to research interested in inequalities in health and aging.

School Disengagement Predicts Accelerated Aging among Black American Youth: Mediation by Psychological Maladjustment and Moderation by Supportive Parenting.

Early experiences of school disengagement may serve as a warning sign for later young adult adjustment difficulties and eventually contribute to accelerated aging among Black American youth. At the same time, supportive parenting may play a protective role. Using longitudinal data from the Family and Community Health Study (FACHS), we examined psychological maladjustment (comprising depression, lack of self-regulation, and low self-esteem) as a mediator of the relationship between school disengagement and accelerated aging. We also examined the effect of supportive parenting in buffering the impact of school disengagement on adulthood outcomes by controlling for covariates. Hypotheses were examined in a sample of 386 (Mean age = 28.68; Females = 62.7%; Males = 37.3%) Black American youth who were followed into young adulthood. Path modeling was used to test hypothesized relationships. We found school disengagement, i.e., problems with school attendance, performance, and engagement, reported across ages 10-18, predicted psychological maladjustment, which, in turn, predicted accelerated aging at age 29. We also found a buffering effect for supportive parenting. No significant gender difference in the indirect effect or buffering effect was found. This study highlights the potential importance of greater attention to school disengagement to identify and potentially influence long-term health trajectories and adult outcomes for Black American youth.

Do Loneliness and Per Capita Income Combine to Increase the Pace of Biological Aging for Black Adults across Late Middle Age?

In a sample of 685 late middle-aged Black adults (M age at 2019 = 57.17 years), we examined the effects of loneliness and per capita income on accelerated aging using a newly developed DNA-methylation based index: the DunedinPACE. First, using linear, mixed effects regression in a growth curve framework, we found that change in DunedinPACE was dependent on age, with a linear model best fitting the data (b = 0.004, p < 0.001), indicating that average pace of change increased among older participants. A quadratic effect was also tested, but was non-significant. Beyond the effect of age, both change in loneliness (b = 0.009, p < 0.05) and change in per capita income (b = -0.016, p < 0.001) were significantly associated with change in DunedinPACE across an 11-year period, accounting for significant between person variability observed in the unconditional model. Including non-self-report indices of smoking and alcohol use did not reduce the association of loneliness or per capita income with DunedinPACE. However, change in smoking was strongly associated with change in DunedinPACE such that those reducing their smoking aged less rapidly than those continuing to smoke. In addition, both loneliness and per capita income were associated with DunedinPACE after controlling for variation in cell-types.

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.

Patterns of Co-occurring Developmental Failures in Adolescence: Socioeconomic and Genetic Antecedents and Health Outcomes in Adulthood.

This study investigates (1) conjoint latent classes of adolescent co-occurring developmental problems (obesity, depressive symptoms, and low educational attainment), (2) socioeconomic and genetic influences on these classes of adolescents' problem trajectories, and (3) physical health consequences of those latent classes. Data from the National Longitudinal Study of Adolescent to Adult Health (Add Health; N = 9,107; mean age = 15.5 years; Female = 52.9 per cent) were used to identify classes of early socioeconomic adversity and conjoint trajectory groups of co-occurring developmental problems. Profiles of social antecedents, genetic endowments (polygenic scores), and physical health outcomes in young adulthood were compared across identified four conjoint trajectory risk groups (overall high-risk, overall low-risk, BMI-risk or obesity, low education-risk). The results showed that youth with overall high-risk and BMI/education-specific risk trajectory groups were more likely to be Black or Hispanic, reported more adverse socioeconomic characteristics and genetic endowment, and averaged significantly poorer physical health in young adulthood compared with youth in the overall low-risk problem trajectory group. Less pronounced differences emerged between the high-risk and problem-specific-risk groups. The findings highlight heterogeneity in adolescent co-occurring developmental problems. Adolescent heterogeneous problem co-development is associated with background socioeconomic and genetic characteristics and physical health in young adulthood.

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.

Midlife financial strain and later-life health and wellbeing of husbands and wives: Linking and moderating roles of couple intimacy trajectories.

This study investigates (a) heterogeneous trajectories of couple intimacy over the mid-later years (average ages of 40-65) and (b) how these intimacy classes are differentially associated with spouses' midlife financial strain as well as their later-life health and wellbeing outcomes. The sample was comprised of white couples in long-term marriages from the rural Mid-west who experienced the economic downturn of the farm crisis in late 1980s. Couple-level measures of emotional intimacy and sexual intimacy were created by summing husbands' and wives' reports. Using growth mixture modeling with a sample of 304 couples, conjoint intimacy classes were identified from trajectories of couple emotional intimacy and sexual intimacy. Three qualitatively different latent intimacy classes of couples were identified: Consistently High, Moderate and Increasing, and Chronically Low. Intimacy classes were differentially associated with midlife financial strain and later-life health and wellbeing. Spouses with consistently high and moderate and increasing intimacy in their mid-later years averaged lower financial strain in early midlife and better health and wellbeing outcomes in later years (>67 years) compared to those with consistently low intimacy after controlling for lagged health measures. The identification of couple intimacy trajectory groups provides a potentially useful prognostic tool for counseling efforts that can promote and develop resiliency factors to aid in the redirection of adverse couple intimacy trajectories.

En el presente estudio se investigan las a) trayectorias heterogéneas de la intimidad de la pareja durante los años de la mediana edad y la vejez (edades promedio de 40 a 65 años) y b) cómo estas clases de intimidad se asocian diferencialmente con la presión económica de la mediana edad de los cónyuges, así como con los resultados en la salud y el bienestar en la vejez. La muestra estuvo compuesta de parejas blancas en matrimonios duraderos de zonas rurales del centro de los Estados Unidos que sufrieron la recesión económica de la crisis agrícola a fines de la década de los ochenta. Las medidas a nivel de la pareja de la intimidad emocional y la intimidad sexual se crearon sumando los informes de los esposos y las esposas. Utilizando un modelo de combinación de crecimiento con una muestra de 304 parejas, se identificaron clases de intimidad conjunta a partir de las trayectorias de la intimidad emocional y la intimidad sexual de la pareja. Se identificaron tres clases de parejas cualitativamente diferentes según su intimidad latente: constantemente alta, moderada y en aumento, y crónicamente baja. Las clases de intimidad estuvieron asociadas diferencialmente con la presión económica en la mediana edad y la salud y el bienestar en la vejez. Los cónyuges con intimidad constantemente alta, y moderada y en aumento entre la mediana edad y la vejez promediaron una menor presión económica a principios de la mediana edad y mejores resultados en la salud y el bienestar durante la vejez (más de 67 años) en comparación con aquellos que tenían una intimidad constantemente baja después de tener en cuenta las medidas de salud retardadas. La identificación de los grupos de trayectorias de la intimidad de la pareja ofrece una herramienta de pronóstico que puede ser útil para el trabajo de terapia orientado a personas y a parejas, ya que puede promover y desarrollar factores de resiliencia que ayuden a redirigir las trayectorias desfavorables de la intimidad de la pareja.

Trajectories of adolescent stressful life events and young adults' socioeconomic and relational outcomes: Weight and depressive symptoms as mediators.

Little is known about how biological and psychological consequences of adolescent stressful life events (SLEs) are jointly associated with socioeconomic and relational outcomes in adulthood. To address this gap, the present study involved testing a model based on the life course perspective that posits adolescent SLE trajectories produce parallel trajectories of depressive symptoms and weight status, which are jointly associated with socioeconomic status and intimate relationship quality in adulthood. Prospective data over 13 years from a nationally representative sample of 11,677 US adolescents was utilized. The results demonstrated that trajectories of BMI and depressive symptoms, which showed contemporaneous and longitudinal comorbidities over the early life course, were influenced by adolescent SLEs. Both BMI and depressive symptoms trajectories are additively and jointly associated with socioeconomic status and intimate relationship quality in adulthood. Additionally, adolescent SLE trajectories are directly associated with these adult outcomes. These observed associations persisted even after controlling for early family socioeconomic adversity and race/ethnicity. The theoretical and practical implications of these findings are discussed.

Higher-order trajectories of pain and depressive symptoms link midlife financial stress to women's well-being in later life.

Objectives: Consistent with biopsychosocial models, shared pathophysiological conditions underlying both physical pain and depressive symptoms can result in the clustering of pain and depressive symptoms. However, previous studies have not investigated a higher-order construct capturing both pain and depressive symptoms over time. Furthermore, research has not identified trajectory antecedents (e.g. perceived family financial stress) and their consequences for later-life health and well-being. The present study sought to address these gaps in the research.Method: Using prospective data over 23 years from 244 long-term married women, the present study estimated latent growth curves in a structural equation model (more specifically a parallel trajectory model was estimated).Results: Family financial strain in midlife was, on average, associated with a higher initial level (ß = .37, p < .001) and rate of change (ß = .20, p = .045) of pain-depressive symptoms trajectories, which, in turn, contributed to health and well-being challenges, including the level and rate of change in physical limitations (ß = .50, p < .001 and 0.43, p < .001, respectively), memory impairment (ß = .47 and .47, p < .001, respectively), and loneliness (ß = .63, p = < .001 and .28, p = .022, respectively) in later years. The adverse influence of family financial strain on pain-depressive symptoms trajectories weakened under high levels of marital closeness (ß = -.10, p = .032). Conclusion: These findings emphasize the necessity of policies and interventions that focus on reducing adults' stressful life circumstances and further developing protective factors that can aid in the redirection of adverse pain-depressive symptoms trajectories.Supplemental data for this article are available online at https://doi.org/10.1080/13607863.2021.1993129.

Life course trajectories of chronic financial strain and acute stress reactivity: Steeling in response to recovery from strain.

The steeling hypothesis suggests experiencing moderate strain may improve an individual's ability to cope with future strain, whereas crisis theory suggests that experiencing temporary strain will reduce the effect of future strain. The current study improves on past research by utilizing data from two independent prospective panel studies (one of 553 white rural Midwesterner women and 451 men and one of 624 African American women) spanning 26 and 22 years, respectively. We utilize growth mixture modeling to identify latent groups based on trajectories of financial strain and test interactions between class membership and later acute stressful events on chronic illness and physical health using three subscales from the RAND SF-12. We find being a group that experienced a period of temporary strain weakened the effect of later acute stressors on physical health for both samples and chronic illness for the African American sample. Results support crisis theory and highlight the importance of considering chronic strain as a life course process.

Midlife family financial strain, sense of control and pain in later years: An investigation of rural husbands and wives.

Research focussing on individual biopsychosocial processes leading to physical pain as a health condition is rare. The present study investigated sense of control as a mechanism linking early midlife stress to later-life physical pain for husbands and wives in long-term marriages. Using data from 508 rural husbands and wives over 27 years (1991-2017) with respondents in their early middle years (<42 years on average) in 1991 and in their later years (>67 years on average) in 2017, this study utilized a comprehensive analytical model in an structural equation modelling framework. Family financial stress (FFS) trajectories in early middle years were associated with depleted sense of control, which was related to increased physical pain in later years after controlling for concurrent physical illness, family income and age. In cross-lagged analyses FFS influenced physical pain over mid-later years. Physical pain also influenced FFS, suggesting a bi-directional association between FFS and physical pain. Findings elucidate how early midlife FFS influences the progression of physical pain over mid-later years through sense of control. Findings suggest effective intervention and prevention programs should focus on FFS in early years of adulthood as well as the maintenance and development of adults' sense of control.