Structural racism in primary schools and changes in epigenetic age acceleration among Black and White youth.

Structural racism generates racial inequities in U.S. primary education, including segregated schools, inequitable funding and resources, racial disparities in discipline and achievement, and hostile racial climates, which are risk factors for adverse youth health and development. Black youth are disproportionately exposed to adverse school contexts that may become biologically embedded via stress-mediated epigenetic pathways. This study examined whether childhood exposure to adverse school contexts is associated with changes in epigenetic aging during adolescent development. DNA methylation-based epigenetic clocks were calculated from saliva samples at ages 9 and 15 among Black (n = 774) and White (n = 287) youth in the Future of Families and Child Wellbeing Study (2009-2015). We performed latent class analyses to identify race-specific primary school contexts using administrative data on segregation, discipline, achievement, resources, economic disadvantage, and racial harassment. We then estimated change in epigenetic age acceleration from childhood to adolescence across school typologies using GrimAge, PhenoAge, and DunedinPACE epigenetic clocks. Three distinct school contexts were identified for Black youth: segregated and highly-disadvantaged (17.0%), segregated and moderately-disadvantaged (52.1%), and integrated and moderately-disadvantaged (30.8%). Two school contexts emerged for White youth: integrated and unequal (46.5%) and predominantly White & advantaged (53.5%). At age 15, Black youth who attended segregated and highly-disadvantaged primary schools experienced increases in their speed of epigenetic aging with GrimAge and DunedinPACE. Slowed epigenetic aging with GrimAge was observed for Black youth who attended integrated and moderately-disadvantaged schools. School contexts were not associated with changes in epigenetic age acceleration for White youth. Our findings suggest that manifestations of structural racism in primary school contexts are associated with early-life epigenetic age acceleration and may forecast future 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.

Do trait psychological characteristics moderate sympathetic arousal to racial discrimination exposure in a natural setting?

Personality and psychological traits are known to influence how individuals react to and cope with stress, and thus, have downstream health and aging consequences. However, research considering psychological health traits as individual-level difference factors moderating the links been racism-related stress and health for racial and ethnic minorities in the United States is rare. Using intensive daily diaries and a wearable sensor that continuously recorded sympathetic nervous system arousal in a sample of racial and ethnic minority college students (80% African American, first-generation Black, or African; 20% Latinx), we linked arousal to racism-related experiences dynamically throughout the day as participants naturally went about their lives. Findings suggest that multiple traits are associated with increased arousal in real time when interpersonal discrimination is perceived, but that only anger and anxiety also predicted increased arousal during moments of rumination and reflection on race-related inequities. Vicarious discrimination exposure moments were also linked to suppressed arousal in general, but particularly for more anxious individuals. We use a stress appraisal and coping framework to elucidate the ways in which individual psychological differences may inform physiological responses to race-related stress. The biopsychosocial pathways by which cognitive appraisal and interpersonal race-related stress contribute to racial health disparities are also discussed.

Race and ethnic variation in college students' allostatic regulation of racism-related stress.

Racism-related stress is thought to contribute to widespread race/ethnic health inequities via negative emotion and allostatic stress process up-regulation. Although prior studies document race-related stress and health correlations, due to methodological and technical limitations, they have been unable to directly test the stress-reactivity hypothesis in situ. Guided by theories of constructed emotion and allostasis, we developed a protocol using wearable sensors and daily surveys that allowed us to operationalize and time-couple self-reported racism-related experiences, negative emotions, and an independent biosignal of emotional arousal. We used data from 100 diverse young adults at a predominantly White college campus to assess racism-related stress reactivity using electrodermal activity (EDA), a biosignal of sympathetic nervous system activity. We find that racism-related experiences predict both increased negative emotion risk and heightened EDA, consistent with the proposed allostatic model of health and disease. Specific patterns varied across race/ethnic groups. For example, discrimination and rumination were associated with negative emotion for African American students, but only interpersonal discrimination predicted increased arousal via EDA. The pattern of results was more general for Latinx students, for whom interpersonal discrimination, vicarious racism exposure, and rumination significantly modulated arousal. As with Latinx students, African students were particularly responsive to vicarious racism while 1.5 generation Black students were generally not responsive to racism-related experiences. Overall, these findings provide support for allostasis-based theories of mental and physical health via a naturalistic assessment of the emotional and sympathetic nervous system responding to real-life social experiences.

Race moderates the association of perceived everyday discrimination and hair cortisol concentration.

The influence of discrimination on hypothalamic-pituitary-adrenal (HPA) axis function is considered to be more pronounced for racial minority versus majority groups, although empirical support for this argument is not strong. This study examined whether the association of perceived discrimination was more strongly associated with long-term, retrospective cortisol output (as measured by hair cortisol concentration [HCC]) among African American compared to White adults. Participants included 141 community-dwelling adults (72 White, 69 African American; mean age 45.8 years; 67% females). The Everyday Discrimination Scale assessed perceived discrimination. The first 3 cm of proximal scalp hair was analyzed for HCC using enzyme-linked immunoassay. Associations between race, perceived discrimination and HCC were examined using hierarchical multiple regression. African Americans had higher HCC than Whites, but both groups reported perceived discrimination with similar frequency. Race moderated the association between perceived discrimination and HCC (R2 interaction = 0.03, p = 0.007) such that perceived discrimination was positively associated with HCC among African Americans (ß = 0.28, p = 0.007), but not Whites (ß = -0.11, p = 0.274). Perceived discrimination did not mediate the association between race and HCC (ß for indirect effect = 0.025, 95% CI [-.003, 0.087]). Although perceived discrimination did not differ between races, perceived discrimination was positively associated with retrospective levels of cortisol in scalp hair among African Americans but not Whites. This may suggest that characteristics of discrimination other than frequency are particularly salient to HPA axis function among African Americans (e.g. attribution, severity, historical context).LAY SUMMARYThis study found that greater perceived discrimination frequency was associated with greater long-term cortisol secretion (i.e. hair cortisol concentration) among African American compared to White adults. Both groups reported similar discrimination frequency, so the uniqueness of African Americans' experience with discrimination may be salient to HPA axis upregulation for this population.

Stress-Related Biosocial Mechanisms of Discrimination and African American Health Inequities.

This review describes stress-related biological mechanisms linking interpersonal racism to life course health trajectories among African Americans. Interpersonal racism, a form of social exclusion enacted via discrimination, remains a salient issue in the lives of African Americans, and it triggers a cascade of biological processes originating as perceived social exclusion and registering as social pain. Exposure to discrimination increases sympathetic nervous system activation and upregulates the HPA axis, increasing physiological wear and tear and elevating the risks of cardiometabolic conditions. Consequently, discrimination is associated with morbidities including low birth weight, hypertension, abdominal obesity, and cardiovascular disease. Biological measures can provide important analytic tools to study the interactions between social experiences such as racial discrimination and health outcomes over the life course. We make future recommendations for the study of discrimination and health outcomes, including the integration of neuroscience, genomics, and new health technologies; interdisciplinary engagement; and the diversification of scholars engaged in biosocial inequities research.

Life course SES and cardiovascular risk: Heterogeneity across race/ethnicity and gender.

We examine four life course models as they relate to adolescent SES, adult SES, and cardiovascular risk--the sensitive period, pathways, accumulation, and social mobility models. Accounting for race/ethnic and gender differences in life course processes, we analyzed Waves I and IV of the National Longitudinal Study of Adolescent to Adult Health, a nationally representative sample of individuals enrolled in grades 7-12 when they were first interviewed in 1994/5. We restricted our sample to whites, blacks, and Latinos who were interviewed in Waves I and IV and provided biomarker data (n = 11,397). The cardiovascular risk score at Wave IV combined waist circumference, blood pressure, hemoglobin A1c, and C-reactive protein. We found evidence for each of the four life course models for white women, whereas the sensitive period was indicated for white men. Upward mobility was also associated with higher CVD risk among white men as compared to those who were socio-economically advantaged at both time points. The pathway model was significant for Latino women. No life course models were significant for black men or women or Latino men. Our findings demonstrate the importance of applying an intersectional lens to understanding CVD risk over the life course.

Birth weight, early life course BMI, and body size change: Chains of risk to adult inflammation?

This paper examines how body size changes over the early life course to predict high sensitivity C-reactive protein in a U.S. based sample. Using three waves of the National Longitudinal Study of Adolescent Health (Add Health), we test the chronic disease epidemiological models of fetal origins, sensitive periods, and chains of risk from birth into adulthood. Few studies link birth weight and changes in obesity status over adolescence and early adulthood to adult obesity and inflammation. Consistent with fetal origins and sensitive periods hypotheses, body size and obesity status at each developmental period, along with increasing body size between periods, are highly correlated with adult CRP. However, the predictive power of earlier life course periods is mediated by body size and body size change at later periods in a pattern consistent with the chains of risk model. Adult increases in obesity had effect sizes of nearly 0.3 sd, and effect sizes from overweight to the largest obesity categories were between 0.3 and 1 sd. There was also evidence that risk can be offset by weight loss, which suggests that interventions can reduce inflammation and cardiovascular risk, that females are more sensitive to body size changes, and that body size trajectories over the early life course account for African American- and Hispanic-white disparities in adult inflammation.

Hard Times and Heart Break: Linking Economic Hardship and Relationship Distress.

We used the Fragile Families and Child Well-Being Study to examine an integrated mediational model linking economic hardship to relationship distress. Depressive symptoms, partner's discord, parenting stress, and coparenting are combined into a joint model linking economic hardship to relationship distress among mothers and fathers in intimate relationships. Although economic hardship is significantly associated with each mediating factor, only discord is associated with both relationship distress and dissolution in the full model. Moreover, comparisons using multigroup structural equation modeling indicate that while economic hardship is associated with higher discord among both mothers and fathers, the influence is substantially larger among fathers. We suggest that the link between hardship and relationship distress is largely contingent on interactional processes (i.e., discord) and how mothers perceive their child's father in the midst of economic hard times.

The differential contributions of teen drinking homophily to new and existing friendships: An empirical assessment of assortative and proximity selection mechanisms.

Alcohol use is pervasive in adolescence. Though most research is concerned with how friends influence drinking, alcohol is also important for connecting teens to one another. Prior studies have not distinguished between new friendship creation, and existing friendship durability, however. We argue that accounting for distinctions in creation-durability processes is critical for understanding the selection mechanisms drawing drinkers into homophilous friendships, and the social integration that results. In order to address these issues, we appliedstochastic actor based models of network dynamics to National Longitudinal Study of Adolescent Health data. Adolescents only modestly prefer new friendships with others who drinker similarly, but greatly prefer friends who indirectly connect them to homophilous drinkers. These indirect homophilous drinker relationships are shorter lived, however, and suggest that drinking is a social focus that connects adolescents via proximity, rather than assortativity. These findings suggest that drinking leads to more situational and superficial social integration.

Transgenerational Consequences of Racial Discrimination for African American Health.

Disparities in African American health remain pervasive and persist transgenerationally. There is a growing consensus that both structural and interpersonal racial discrimination are key mechanisms affecting African American health. The Biopsychosocial Model of Racism as a Stressor posits that the persistent stress of experiencing discrimination take a physical toll on the health of African Americans and is ultimately manifested in the onset of illness. However, the degree to which the health consequences of racism and discrimination can be passed down from one generation to the next is an important avenue of exploration. In this review, we discuss and link literature across disciplines demonstrating the harmful impact of racism on African American physical health and the health of their offspring.

School racial composition and race/ethnic differences in early adulthood health.

We investigate whether school racial composition is associated with racial and ethnic differences in early adult health. We then examine whether perceived discrimination, social connectedness, and parent support attenuates this relationship. Using U.S. data from Waves I and IV of the National Longitudinal Survey of Adolescent Health, we found that black adolescents attending predominantly white schools reported poorer adult health while Asians reported better health. Further research is warranted to understand whether there are qualitative differences in the treatment of racial and ethnic minorities within certain school contexts and how that differential treatment is related to adult health outcomes.