Racial Discrimination and Metabolic Syndrome in Young Black Adults.

Importance: Metabolic syndrome (MetS) is a common health condition that predisposes individuals to cardiovascular disease (CVD) and disproportionately affects Black and other racially and ethnically minoritized people. Concurrently, Black individuals also report more exposure to racial discrimination compared with White individuals; however, the role of discrimination in the development of MetS over time and associated mediators in these pathways remain underexplored. Objective: To evaluate the association between racial discrimination and MetS in rural Black individuals transitioning from late adolescence into early adulthood and to identify potential mediating pathways. Design, Setting, and Participants: This longitudinal cohort study included Black adolescents enrolled in the Strong African American Families Healthy Adults (SHAPE) Project between June 2009 and May 2021. Families resided in rural counties of Georgia, where poverty rates are among the highest in the nation. Analyses included 322 of the 500 participants who originally enrolled in SHAPE and who were eligible to participate. Guardians provided information about socioeconomic disadvantage. Analyses were conducted in April 2023. Exposures: Youths reported exposure to racial discrimination annually from ages 19 to 21 years. Main Outcomes and Measures: MetS was the main health outcome and was measured at ages 25 and 31 years. MetS was diagnosed according to the International Diabetes Federation guidelines, which requires central adiposity (ie, waist circumference ≥94 cm for males and ≥80 cm for females) and at least 2 of the 4 additional components: signs of early hypertension (ie, systolic blood pressure ≥130 mm Hg or diastolic blood pressure ≥85 mm Hg); elevated triglyceride levels (ie, >150 mg/dL); elevated fasting glucose level (ie, ≥100 mg/dL); or lowered high-density lipoprotein levels (ie, <40 mg/dL in men and <50 mg/dL in women). At age 25 years, markers of inflammatory activity (ie, soluble urokinase plasminogen activator receptor [suPAR]) and sleep problems were collected to consider as potential mediators. Results: In 322 participants (210 [65.2%] female) ages 19 to 21 years, more frequent exposure to racial discrimination was associated with higher suPAR levels (b = 0.006; 95% CI, 0.001-0.011; P = .01) and more sleep problems at age 25 years (b = 0.062; 95% CI, 0.028-0.097; P < .001) as well as a 9.5% higher risk of MetS diagnosis at age 31 years (odds ratio [OR], 1.10; 95% CI, 1.01-1.20; P = .03). Both suPAR (b = 0.015; 95% CI, 0.002-0.037) and sleep problems (b = 0.020; 95% CI, 0.002-0.047) at age 25 years were significant indirect pathways. No significant interactions between sex and discrimination emerged. Conclusions and Relevance: This study suggests that racial discrimination in late adolescence is associated with MetS among Black young adults through biobehavioral pathways. Thus, health interventions for MetS in Black adults will need to contend with sleep behaviors and inflammatory intermediaries as well as address and reduce exposure to racial discrimination to narrow disparities and promote health equity.

Interpersonal violence exposure and inflammation during adolescence and young adulthood.

Exposure to violence increases young peoples' risk of developing mental and physical health problems. Chronic stress-related upregulation of innate immune system activity and the development of low-grade inflammation may partially underlie this health risk. However, much of the previous research has been limited to cross-sectional studies utilizing between-person analytic designs, susceptible to confounding by unmeasured factors. In this six-wave panel study of N=157 female adolescents and young adults, we tested within-person associations between interpersonal violence exposure and multiple measures of inflammatory activity. Ex vivo culture studies suggested that participants' immune cells were more reactive to microbial stimulation and less sensitive to inhibition by glucocorticoids after violence. Numbers of circulating monocyte cells increased after violence, but serum levels of interleukin-6 and c-reactive protein did not. Findings from this within-person analysis suggest that violence exposure up-regulates innate immune system activity during adolescence and young adulthood in ways that may increase mental and physical health risk.

Peer support as moderator of association between socioeconomic status and low-grade inflammation in adolescents.

OBJECTIVE: Individuals who grow up in low-socioeconomic status (SES) families are at an increased risk of health problems across the lifespan. Although supportive social relationships are postulated to be a protective factor for the health of these individuals, the role of friend support in adolescence is not well understood. Given that low-grade inflammation is one key biological mechanism proposed to explain links between family SES and health outcomes, we examined whether adolescents' friend support buffers the association between family SES and low-grade inflammation among adolescents. METHOD: 277 dyads of adolescents (63.5% female; 39.4% White, 38.3% Black, and 32.1% Hispanic; Mage = 13.92 years) and one of their parents participated in this longitudinal study (two waves approximately 2 years apart). Parents reported family objective SES (i.e., income, savings, and education) and family subjective SES (i.e., subjective social status). Adolescents reported perceived friend support. Fasting antecubital blood was drawn from adolescents at both visits. Low-grade inflammatory activity was represented by a composite of inflammatory biomarkers and numbers of classical monocytes. RESULTS: Adolescents' friend support moderated the associations of family subjective SES with both the inflammation composite and classical monocyte counts across cross-sectional, longitudinal, and prospective change (only significant for the inflammation composite) analyses. Specifically, lower family subjective SES was associated with higher levels of low-grade inflammation only among adolescents lower, but not higher, in friend support. No moderation was observed for objective SES. CONCLUSION: Supportive peer relationships buffer the link between family subjective, but not objective, SES and low-grade inflammation in adolescence. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Social and psychological adversity are associated with distinct mother and infant gut microbiome variations.

Health disparities are driven by underlying social disadvantage and psychosocial stressors. However, how social disadvantage and psychosocial stressors lead to adverse health outcomes is unclear, particularly when exposure begins prenatally. Variations in the gut microbiome and circulating proinflammatory cytokines offer potential mechanistic pathways. Here, we interrogate the gut microbiome of mother-child dyads to compare high-versus-low prenatal social disadvantage, psychosocial stressors and maternal circulating cytokine cohorts (prospective case-control study design using gut microbiomes from 121 dyads profiled with 16 S rRNA sequencing and 89 dyads with shotgun metagenomic sequencing). Gut microbiome characteristics significantly predictive of social disadvantage and psychosocial stressors in the mothers and children indicate that different discriminatory taxa and related pathways are involved, including many species of Bifidobacterium and related pathways across several comparisons. The lowest inter-individual gut microbiome similarity was observed among high-social disadvantage/high-psychosocial stressors mothers, suggesting distinct environmental exposures driving a diverging gut microbiome assembly compared to low-social disadvantage/low-psychosocial stressors controls (P = 3.5 × 10-5 for social disadvantage, P = 2.7 × 10-15 for psychosocial stressors). Children's gut metagenome profiles at 4 months also significantly predicted high/low maternal prenatal IL-6 (P = 0.029), with many bacterial species overlapping those identified by social disadvantage and psychosocial stressors. These differences, based on maternal social and psychological status during a critical developmental window early in life, offer potentially modifiable targets to mitigate health inequities.

Discrimination and Inflammation in Adolescents of Color.

Background: This study examined how experiences with discrimination relate to inflammation, a key biological pathway in mental and physical illnesses, and whether associations are moderated by gender across two samples of adolescents of color. Methods: Study 1 was a longitudinal study of 419 African American adolescents assessed on discrimination (ages 19-20), with trajectories of biomarkers of low-grade inflammation (C-reactive protein and soluble urokinase plasminogen activator receptor) measured from ages 25 to 29. Study 2 was a cross-sectional study of 201 eighth graders of color assessed on discrimination and mechanistic indicators of a proinflammatory phenotype: 1) in vitro studies of immune cells' inflammatory cytokine responses to stimuli; 2) in vitro studies of cells' sensitivity to anti-inflammatory agents; 3) circulating numbers of classical monocytes, key cellular drivers of low-grade inflammation; and 4) a composite of six biomarkers of low-grade inflammation. Results: Interactions of discrimination by gender were found across both studies. In study 1, African American males experiencing high discrimination showed increasing trajectories of soluble urokinase plasminogen activator receptor over time (p < .001). In study 2, adolescent boys of color experiencing greater discrimination evinced a more proinflammatory phenotype: larger cytokine responses to stimuli (p = .003), lower sensitivity to anti-inflammatory agents (p = .003), higher numbers of classical monocytes (p = .008), and more low-grade inflammation (p = .003). No such associations were found in females. Conclusions: Discrimination is a pressing societal issue that will need to be addressed in efforts to promote health equity. This study suggests that adolescent males of color may be particularly vulnerable to its effects on mental health-relevant inflammatory processes.

A multilevel framework to investigate cardiovascular health disparities among South Asian immigrants in the United States.

PURPOSE: Prior studies of cardiovascular health (CVH) disparities among immigrants of South Asian origin in the United States have examined South Asians as one homogenous group, focused primarily on Indian-origin immigrants, and examined risk at the individual level. METHODS: We present current knowledge and evidence gaps about CVH in the three largest South Asian-origin populations in the United States-Bangladeshi, Indian, and Pakistani-and draw on socioecological and lifecourse frameworks to propose a conceptual framework for investigating multilevel risk and protective factors of CVH across these groups. RESULTS: The central hypothesis is that CVH disparities among South Asian populations exist due to differences in structural and social determinants, including lived experiences like discrimination, and that acculturation strategies and resilience resources (e.g., neighborhood environment, education, religiosity, social support) ameliorate stressors to act as health protective factors. RESULTS: Conclusions: Our framework advances conceptualization of the heterogeneity and drivers of cardiovascular disparities in diverse South Asian-origin populations. We present specific recommendations to inform the design of future epidemiologic studies on South Asian immigrant health and the development of multilevel interventions to reduce CVH disparities and promote well-being.

Socioeconomic disadvantage, chronic stress, and proinflammatory phenotype: an integrative data analysis across the lifecourse.

Socioeconomic disadvantage confers risk for many chronic illnesses, and theories have highlighted chronic psychological stress and alterations to inflammatory processes as key pathways. Specifically, disadvantage can heighten chronic stress, which may promote a proinflammatory phenotype characterized by immune cells mounting exaggerated cytokine responses to challenge and being less sensitive to inhibitory signals. Importantly, lifecourse perspectives emphasize that such immune alterations should be more potent earlier in life during a sensitive period when bodily tissues are highly plastic to environmental inputs. However, examining these propositions is resource intensive, as they require cell-culturing approaches to model functional inflammatory activities, a wide age range, and longitudinal data. Here, we integrated data from five independent studies to create a diverse sample of 1,607 individuals (960 with longitudinal data; 8 to 64 years old; 359 Asian, 205 Black, and 151 Latino/a). Leveraging the resulting lifecourse data, rich interview assessments of disadvantage and stress, and ex vivo assessments of inflammation, we examined two questions: (1) Does chronic stress account for the link between disadvantage and proinflammatory phenotype? (2) Is there a developmental period during which inflammatory responses are more sensitive to disadvantage and chronic stress? Disadvantage was associated with higher chronic stress, which was linked with a proinflammatory phenotype cross-sectionally, longitudinally, and in terms of prospective change across 1.5 to 2 years. Consistent with the sensitive period hypothesis, the magnitude of these indirect associations was strongest in earlier decades and declined across the lifecourse. These findings highlight the importance of taking a lifecourse perspective in examining health disparities.

What Are the Health Consequences of Upward Mobility?

Health disparities by socioeconomic status (SES) have been extensively documented, but less is known about the physical health implications of achieving upward mobility. This article critically reviews the evolving literature in this area, concluding that upward mobility is associated with a trade-off, whereby economic success and positive mental health in adulthood can come at the expense of physical health, a pattern termed skin-deep resilience. We consider explanations for this phenomenon, including prolonged high striving, competing demands between the environments upwardly mobile individuals seek to enter and their environments of origin, cultural mismatches between adaptive strategies from their childhood environments and those that are valued in higher-SES environments, and the sense of alienation, lack of belonging, and discrimination that upwardly mobile individuals face as they move into spaces set up by and for high-SES groups. These stressors are hypothesized to lead to unhealthy behaviors and a dysregulation of biological systems, with implications for cardiometabolic health.

Recommendations for Assessment of Environmental Exposures in Longitudinal Life Course Studies Such as the National Children's Study.

An important step toward understanding the relationship between the environment and child health and development is the comprehensive cataloging of external environmental factors that may modify health and development over the life course. Our understanding of the environmental influences on health is growing increasingly complex. Significant key questions exist as to what genes, environment, and life stage mean to defining normal variations and altered developmental trajectories throughout the life course and also across generations. With the rapid advances in genetic technology came large-scale genomic studies to search for the genetic etiology of complex diseases. While genome-wide association studies (GWAS) have revealed genetic factors and networks that advance our understanding to some extent, it is increasingly recognized that disease causation is largely non-genetic and reflects interactions between an individual's genetic susceptibility and his or her environment. Thus, the full promise of the human genome project to prevent or treat disease and promote good health arguably depends on a commitment to understanding the interactions between our environment and our genetic makeup and requires a design with prospective environmental data collection that considers critical windows of susceptibility that likely correspond to the expression of specific genes and gene pathways. Unlike the genome, which is static, relevant exposures as well as our response to exposures, change over time. This has fostered the complementary concept of the exposome ideally defined as the measure of all exposures of an individual over a lifetime and how those exposures relate to health. The exposome framework considers multiple external exposures (e.g., chemical, social) and behaviors that may modify exposures (e.g., diet), as well as consequences of environmental exposures indexed via biomarkers of physiological response or measures of behavioral response throughout the lifespan. The exposome concept can be applied in prospective developmental studies such as the National Children's Study (NCS) with the practical understanding that even a partial characterization will bring major advances to health. Lessons learned from the NCS provide an important opportunity to inform future studies that can leverage these evolving paradigms in elucidating the role of environment on health across the life course.

The Relationship Between Disproportionate Social Support and Metabolic and Inflammatory Markers: Moderating Role of Socioeconomic Context.

OBJECTIVE: The present study examines the association of disproportionate social support (the relative balance of support given versus received) on metabolic and inflammatory outcomes and whether effects vary by socioeconomic context. METHODS: We enrolled a sample of 307 parental caregivers living with a child with a chronic illness. Parents were assessed on four dimensions of social support: emotional support received, instrumental support received, emotional support given, and instrumental support given. Disproportionate social support was calculated as the difference between support received and support given. Participants provided sociodemographic information, were interviewed about financial stress, and were assessed on metabolic (systolic blood pressure, diastolic blood pressure, total cholesterol, body fat percent, and body mass index) and inflammatory (interleukin 6 and C-reactive protein) outcomes. RESULTS: More disproportionate instrumental and emotional support was associated with higher inflammation (b = 0.10, SE = 0.04, p = .014; b = 0.0.09, SE = 0.05, p = .042, respectively). We observed significant interactions between disproportionate social support and income (b = -0.04, SE = 0.02, p = .021). Parents from lower-income households who gave more emotional support than they received had higher inflammation compared with those from higher-income households. We also observed a significant interaction between disproportionate instrumental support and income (b = 0.04, SE = 0.02, p = .006). Parents from lower-income households who received more instrumental support than they gave had worse metabolic outcomes compared with parents from higher-income households. Parallel interaction patterns were observed using an interview-based measure of financial stress. CONCLUSIONS: These findings show that disproportionate social support has implications for physical health, particularly for caregivers from socioeconomically disadvantaged households.

Association of Wealth With Longevity in US Adults at Midlife.

Importance: Wealthy adults tend to live longer than those with less wealth. However, a challenge in this area of research has been the reduction of potential confounding by factors associated with the early environment and heritable traits, which could simultaneously affect socioeconomic circumstances in adulthood and health across the life course. Objective: To identify the association between net worth at midlife and subsequent all-cause mortality in individuals as well as within siblings and twin pairs. Design Setting and Participants: This cohort study conducted a series of analyses using data from the Midlife in the United States (MIDUS) study, an ongoing national study of health and aging. The sample included adults (unrelated individuals, full siblings, and dizygotic and monozygotic twins) aged 20 to 75 years, who participated in wave 1 of the MIDUS study, which occurred from 1994 to 1996. The analyses were conducted between November 16, 2019, and May 18, 2021. Exposures: Self-reported net worth (total financial assets minus liabilities) at midlife (the middle years of life). Main Outcomes and Measures: All-cause mortality was tracked over nearly 24 years of follow-up, with a censor date of October 31, 2018. Survival models tested the association between net worth and all-cause mortality. Discordant sibling and twin analyses compared longevity within siblings and twin pairs who, given their shared early experiences and genetic backgrounds, were matched on these factors. Results: The full sample comprised 5414 participants, who had a mean (SD) age of 46.7 (12.7) years and included 2766 women (51.1%). Higher net worth was associated with lower mortality risk (hazard ratio [HR], 0.95; 95% CI, 0.94-0.97; P < .001). Among siblings and twin pairs specifically (n = 2490), a similar within-family association was observed between higher net worth and lower mortality (HR, 0.94; 95% CI, 0.91-0.97; P = .001), suggesting that the sibling or twin with more wealth tended to live longer than their co-sibling or co-twin with less wealth. When separate estimates were performed for the subsamples of siblings (HR, 0.94; 95% CI, 0.90-0.97; P = .002), dizygotic twins (HR, 0.94; 95% CI, 0.86-1.02; P = .19), and monozygotic twins (HR, 0.95; 95% CI, 0.87-1.04; P = .34), the within-family estimates of the net worth-mortality association were similar, although the precision of estimates was reduced among twins. Conclusions and Relevance: This cohort study found that wealth accumulation at midlife was associated with longevity in US adults. Discordant sibling analyses suggested that this association is unlikely to be simply an artifact of early experiences or heritable characteristics shared by families.

Race, socioeconomic status, and low-grade inflammatory biomarkers across the lifecourse: A pooled analysis of seven studies.

Cardiovascular diseases are patterned by race and socioeconomic status, and chronic low-grade inflammation is proposed as a key underlying mechanism. Theories for how racial and socioeconomic disadvantages foster inflammation emphasize a lifecourse approach: social disadvantages enable chronic or repeated exposure to stressors, unhealthy behaviors, and environmental risks that accumulate across the lifecourse to increase low-grade inflammation. However, single samples rarely include multiple racial and socioeconomic groups that each span a wide age range, precluding examination of this proposition. To address this issue, the current study combined seven studies that measured C-reactive protein and interleukin-6, producing a pooled sample of 1650 individuals aged 11-60 years. We examined (a) whether race and socioeconomic disparities in inflammatory biomarkers vary across the lifecourse, (b) whether adiposity operates as a pathway leading to these disparities, and (c) whether any indirect pathways through adiposity also vary across the lifecourse. Relative to White individuals, Black individuals exhibited higher, whereas Asian individuals exhibited lower, levels of inflammatory biomarkers, and adiposity accounted for these racial differences. Similarly, lower socioeconomic status was associated with higher inflammatory biomarkers via elevated adiposity. Importantly, both racial and socioeconomic disparities, as well as their pathways via adiposity, widened across the lifecourse. This pattern suggests that the impact of social disadvantages compound with age, leading to progressively larger disparities in low-grade inflammation. More broadly, these findings highlight the importance of considering age when examining health disparities and formulating conceptual models that specify how and why disparities may vary across the lifecourse.

Youth Who Achieve Upward Socioeconomic Mobility Display Lower Psychological Distress But Higher Metabolic Syndrome Rates as Adults: Prospective Evidence From Add Health and MIDUS.

Background People with higher socioeconomic status generally enjoy better cardiovascular health across the life course than those with lower status. However, recent studies of upward mobility, where a child goes on to achieve higher socioeconomic status than his or her parents, suggest that it entails a tradeoff between better psychological well-being and worse cardiometabolic health. In this study, we consider further evidence of this tradeoff in 2 multidecade studies, asking how upward income mobility relates to subsequent perceived stress, depressive symptoms, and metabolic syndrome. We ask parallel questions about downward mobility. Finally, given shifting patterns of mobility in recent generations, we also consider whether mobility's association with health outcomes differs for individuals born in the middle and later parts of the 20th century. Methods and Results We analyzed prospective data from Add Health (National Longitudinal Study of Adolescent Health; N=7542) and MIDUS (Midlife in the United States Study; N=1877). In both studies, evidence of the tradeoff was observed. Upward mobility presaged lower perceived stress and fewer depressive symptoms, in combination with higher metabolic syndrome rates. In contrast, downward mobility presaged worse outcomes on all health indicators. The magnitude of the mobility-health associations was similar across cohorts. Conclusions These findings provide evidence that upward income mobility is associated with a tradeoff between well-being and cardiometabolic health. The similarity of the findings across cohorts suggests that this tradeoff is a generalized consequence of ascending the socioeconomic hierarchy, at least for Americans born in the middle and later parts of the 20th century.

Students of color show health advantages when they attend schools that emphasize the value of diversity.

As the United States becomes more diverse, the ways in which mainstream institutions recognize and address race and ethnicity will be increasingly important. Here, we show that one novel and salient characteristic of an institutional environment, that is, whether a school emphasizes the value of racial and ethnic diversity, predicts better cardiometabolic health among adolescents of color. Using a diverse sample of adolescents who attend more than 100 different schools in predominantly urban locations, we find that when schools emphasize the value of diversity (operationalized as mentioning diversity in their mission statements), students of color, but not white students, have lower values on a composite of five biomarkers of inflammation, have less insulin resistance and compensatory ß-cell activity, and have fewer metabolic syndrome signs and score lower on a continuous metabolic syndrome composite. These results suggest that institutions that emphasize diversity may play an unacknowledged role in protecting the health of people of color and, thus, may be a site for future interventions to reduce health disparities.

Academic disparities and health: How gender-based disparities in schools relate to boys' and girls' health.

RATIONALE: Recent research reveals that, although girls encounter some barriers in school (e.g., in science and math), on balance, boys perform worse academically. Moreover, other research has identified a correlation between exposure to a context characterized by large disparities in performance or resources and a range of negative outcomes, including negative health and well-being, among members of lower status groups. OBJECTIVE: Building on these literatures, the present research tests the relationship between gender disparities in academic performance within a school and students' health outcomes. Specifically, we investigated whether boys had worse health when they attended schools where there was a greater disparity between boys' and girls' academic performance. METHOD: We tested this hypothesis in two different samples with different health outcomes. In a sample of healthy eighth graders (Study 1; 159 girls and 81 boys), we assessed two indices of metabolic syndrome, and in a sample of children with asthma (Study 2; 122 girls and 153 boys), we assessed immune function (Th1 and Th2 cytokine production) and self-reported symptoms. Participants in both samples also reported the name of the school that they attended so that we could access publicly available information about the percentage of girls and the percentage of boys in each school who met expectations for their grade level on standardized tests. RESULTS: In both samples, the greater the gap in a school between the percentage of girls and the percentage of boys who met expectations for their grade level on standardized tests, the worse boys' health. This pattern did not emerge among girls. CONCLUSION: Results thus highlight the negative health correlates of academic disparities among members of lower-performing groups.

The costs of high self-control in Black and Latino youth with asthma: Divergence of mental health and inflammatory profiles.

Emerging evidence in psychology suggests a paradox whereby high levels of self-control when striving for academic success among minority youth can have physical health costs. This study tested the skin-deep resilience hypothesis in asthma- whether minority youth who are striving hard to succeed academically experience good psychological outcomes but poor asthma outcomes. Youth physician-diagnosed with asthma (N = 276, M age = 12.99; 155 = White, 121 = Black/Latino) completed interviews about school stress and a self-control questionnaire. Outcomes included mental health (anxiety/depression) and ex-vivo immunologic processes relevant to asthma (lymphocyte Th-1 and Th-2 cytokine production, and sensitivity to glucocorticoid inhibition). Physician contacts were tracked over a one-year follow-up. For minority youth experiencing high levels of school stress, greater self-control was associated with fewer mental health symptoms (beta = -0.20, p < .05), but worse asthma inflammatory profiles (larger Th-1 and Th-2 cytokine responses, lower sensitivity to glucocorticoid inhibition), and more frequent physician contacts during the one-year follow-up (beta's ranging from 0.22 to 0.43, p's < .05). These patterns were not evident in White youth. In minority youth struggling with school, high levels of self-control are detrimental to asthma inflammatory profiles and clinical outcomes. This suggests the need for health monitoring to be incorporated into academic programs to ensure that 'overcoming the odds' does not lead to heightened health risks in minority youth.

Family obligations and asthma in youth: The moderating role of socioeconomic status.

OBJECTIVE: Fulfilling family obligations-providing instrumental help to and spending time with family-is a common aspect of family relationships. However, whether fulfilling these obligations links with physical health remains unclear. In this study, we investigated whether fulfilling family obligations was associated with asthma outcomes among youth, and whether these associations differed depending on family socioeconomic status (SES). METHOD: Participants were 172 youth, 8 to 17 years of age (Mage = 12.1; 54% boys) who had been physician-diagnosed with asthma and reported on family-obligation frequency; completed the Asthma Control Test (ACT; Nathan et al., 2004), a clinical measure of asthma control; and completed a measure of airway inflammation (i.e., fractional exhaled nitric oxide). Parents also completed the ACT in reference to their asthmatic children and reported on family income. RESULTS: Fulfilling family obligations was not associated with asthma outcomes (ßs < .14, ps > .075). However, SES (family income) interacted with family obligations, such that fulfilling family obligations was associated with greater airway inflammation (interaction term ß = -.17, p = .023) and poorer parent-reported asthma control (interaction term ß = .15, p = .039), only among youth from lower SES backgrounds. Exploratory analyses suggest that these interactions were robust against covariates and were largely consistent across age and the two dimensions of family-obligation behaviors. CONCLUSION: Findings from this study suggest that among youth from lower SES backgrounds, engaging in more frequent family-obligation behaviors may have negative repercussions in terms of their asthma. (PsycINFO Database Record

One size does not fit all: Links between shift-and-persist and asthma in youth are moderated by perceived social status and experience of unfair treatment.

The links between low socioeconomic status and poor health are well established, yet despite adversity, some individuals with low socioeconomic status appear to avoid these negative consequences through adaptive coping. Previous research found a set of strategies, called shift-and-persist (shifting the self to stressors while persisting by finding meaning), to be particularly adaptive for individuals with low socioeconomic status, who typically face more uncontrollable stressors. This study tested (a) whether perceived social status, similar to objective socioeconomic status, would moderate the link between shift-and-persist and health, and (b) whether a specific uncontrollable stressor, unfair treatment, would similarly moderate the health correlates of shift-and-persist. A sample of 308 youth (Meanage = 13.0, range 8-17), physician diagnosed with asthma, completed measures of shift-and-persist, unfair treatment, asthma control, and quality of life in the lab, and 2 weeks of daily diaries about their asthma symptoms. Parents reported on perceived family social status. Results indicated that shift-and-persist was associated with better asthma profiles, only among youth from families with lower (vs. higher) parent-reported perceived social status. Shift-and-persist was also associated with better asthma profiles, only among youth who experienced more (vs. less) unfair treatment. These findings suggest that the adaptive values of coping strategies for youth with asthma depend on the family's perceived social status and on the stressor experienced.

Early-life socioeconomic disadvantage, not current, predicts accelerated epigenetic aging of monocytes.

Low socioeconomic status (SES) in early-life and adulthood independently contribute to increased risk for aging-related chronic diseases. One mechanistic hypothesis for these associations involves faster cellular aging of immune cells, which could plausibly contribute to chronic disease pathogenesis by compromising host resistance and/or up-regulating inflammation. However, little is known about the association between life-course SES and cellular aging. The present study examines the association of early-life and current SES with a novel biomarker of cellular aging termed the "epigenetic clock," in monocytes. Additionally, we examine health behaviors and depressive symptoms as potential explanatory pathways. The study involved 335 participants between the ages of 15 and 55 from Vancouver, Canada and surrounding areas. Enrolled participants had to fit into four life-course SES trajectories, corresponding to low-low, low-high, high-low and high-high combinations of early-life (ages 0 to 5) and current SES respectively. Cellular aging of monocytes was measured using Horvath's DNA methylation derived measure of epigenetic age acceleration. Results indicated that socioeconomic disadvantage during early-life, but not later in life, was associated with accelerated epigenetic aging of monocytes. No early-life SES by current SES interaction was detected, suggesting that socioeconomic mobility is unrelated to epigenetic age acceleration. In path analyses, neither current health behaviors nor current depressive symptoms emerged as mediators of the early-life SES effect. These findings suggest socioeconomic disadvantage in early-life is independently predictive of cellular aging of immune cells, with potential implications for aging-related diseases later in life.