State- and Provider-Level Racism and Health Care in the U.S.

INTRODUCTION: This study examines the associations between state-level and provider sources of racism and healthcare access and quality for non-Hispanic Black and White individuals. METHODS: Data from 2 sources were integrated: (1) data from the Association of American Medical Colleges' Consumer Survey of Health Care Access (2014-2019), which included measures of self-reported healthcare access, healthcare quality, and provider racial discrimination and (2) administrative data compiled to index state-level racism. State-level racism composite scores were calculated from federal sources (U.S. Census, Department of Labor, Department of Justice). The data set comprised 21,030 adults (n=2,110 Black, n=18,920 White) who needed care within the past year. Participants were recruited from a national panel, and the survey employed age-insurance quotas. Logistic and linear regressions were conducted in 2020, adjusting for demographic, geographic, and health-related covariates. RESULTS: Among White individuals, more state-level racism was associated with 5% higher odds of being able to get care and 6% higher odds of sufficient time with provider. Among Black individuals, more state-level racism was associated with 8% lower odds of being able to get care. Provider racial discrimination was also associated with 80% lower odds of provider explaining care, 77% lower odds of provider answering questions, and 68% lower odds of sufficient time with provider. CONCLUSIONS: State-level racism may engender benefits to healthcare access and quality for White individuals and may decrease access for Black individuals. Disparities may be driven by both White advantage and Black disadvantage. State-level policies may be the actionable levers of healthcare inequities with implications for preventive medicine.

Integrating Biomarkers in Social Stratification and Health Research.

This article provides an overview of the integration of biomarkers and biological mechanisms in social science models of stratification and health. The goal in reviewing this literature is to highlight research that identifies the social forces that drive inequalities over the life course and across generations. The article is structured in the following way. First, descriptive background information on biomarkers is presented, followed secondly by a review of the general theoretical paradigms that lend themselves to an integrative approach. Third, the biomarkers used to capture several biological systems that are most responsive to social conditions are described. Fourth, research that explicates how social exposures "get under the skin" to affect physiological functioning and downstream health is discussed, using socioeconomic disadvantage as an illustrative social exposure. The review ends with emerging directions in the use of biomarkers in social science research. This article endeavors to encourage sociologists to embrace biosocial approaches in order to elevate the importance of social factors in biomedical processes and to intervene on the social conditions that create inequities.

College completion predicts lower depression but higher metabolic syndrome among disadvantaged minorities in young adulthood.

Individuals with higher educational attainment live healthier and longer lives. However, not everyone benefits equally from higher education. In particular, the black-white gap in life expectancy is greater at higher levels of educational attainment. Furthermore, recent research suggests that disadvantaged African Americans in the rural Southeast who attend college have worse physical health than their similarly disadvantaged peers who do not attend college. The extent to which this pattern generalizes to a nationally representative, mixed-race sample is unknown. Using data from the National Longitudinal Study of Adolescent to Adult Health, we test whether the health benefits associated with college completion vary by level of childhood disadvantage for depression and metabolic syndrome in young adulthood, across race/ethnicity. We find uniform lower depression associated with college completion regardless of childhood disadvantage, and across non-Hispanic white, non-Hispanic black, and Hispanic young adults. College completion is associated with lower metabolic syndrome for whites across all levels of childhood disadvantage. In contrast, college completion is associated with higher metabolic syndrome among black and Hispanic young adults from disadvantaged childhood environments. Our findings suggest that, for minorities from disadvantaged backgrounds, finishing college pays substantial dividends for mental health but simultaneously exacts costs with regard to physical health. This pattern contrasts starkly with whites and minorities from more privileged backgrounds, for whom college completion is associated with benefits to both mental and physical health. These results suggest that racial disparities in health may persist in part because the health of upwardly mobile minorities is compromised in young adulthood.

Young Adult Risk Factors for Cancer: Obesity, Inflammation, and Sociobehavioral Mechanisms.

INTRODUCTION: The paper assesses social disparities in the burdens of metabolic and inflammatory risks for cancer in the U.S. young adult population and examines psychosocial and behavioral mechanisms in such disparities. METHODS: Using data of 7,889 individuals aged 12-32 years from the National Longitudinal Study of Adolescent to Adult Health from 1994 to 2009, generalized linear models were used to assess the sex, race/ethnicity, and SES differences in the risks of obesity and inflammation, measured by C-reactive protein. Further tests examined the extent to which social isolation, smoking, physical inactivity, alcohol abuse, and illicit drug use explain social differentials in each biomarker outcome. RESULTS: Women, blacks, Hispanics, and socioeconomically disadvantaged groups had higher risks of obesity and elevated C-reactive protein, with the SES gradients being more pronounced in female participants. Health-related behaviors showed large variation across sex, race, and SES strata. After adjusting for these behavioral variables, sex, and race disparities in obesity and excess inflammation in blacks diminished, whereas the adolescent SES disparity in obesity remained. The associations of adolescent and young adult SES disadvantage and inflammation were also explained by behavioral mechanisms. Behavioral factors associated with higher risks of obesity and inflammation differed, with the exception of fast food consumption, a risk factor for both. CONCLUSIONS: This study provides new knowledge of social distribution of early life exposures to physiologic precedents to cancer development later in life with implications for prevention and early intervention of modifiable risky behaviors in adolescents and young adults.

Religious Pathways from Adolescence to Adulthood.

Prior research suggests the significance of religion for development and wellbeing in adolescence and beyond. Further, new developments and applications of statistical methods have led to ways of better accounting for the multidimensional nature of religiosity (e.g. latent class analysis), as well as the dynamic aspects of religiosity (e.g. latent growth curve models). Yet, rarely if ever are both features of religiosity incorporated and examined together. Therefore, we propose and conduct a latent class analysis using data from the National Longitudinal Study of Adolescent to Adult Health (Add Health) to identify seven distinct pathways of religiosity that involve independently changing levels of religious affiliation, religious service attendance, personal importance of religion, and prayer from adolescence to adulthood. We also show how individuals' religious pathways are related to gender, race, parents' education, their own education, and family formation experiences in the transition to adulthood. Our findings inform the study of how multiple dimensions of religiosity take shape across adolescence and the transition to adulthood, and suggest a new way for measuring the dynamics of religiosity in studies of the impact of religion across the life course.

Developmental timing of suicide attempts and cardiovascular risk during young adulthood.

OBJECTIVE: Self-control/self-regulation has received increased attention in health research. Suicide attempts index severe dysregulation in emotional, behavioral, and/or physiological domains. The current study tested whether own and/or others' suicide attempts during the early life course predicted cardiovascular risk by young adulthood and whether developmental timing of suicide attempts, sex of the person, and source of suicide attempts exposure modified these associations. METHOD: Data came from the National Longitudinal Study of Adolescent to Adult Health (Add Health). At each assessment during Waves I-IV (covering approximately ages 12-32 years), participants reported whether they and/or a friend/family member had attempted suicide. At Wave IV, trained interviewers assessed participants' obesity and hypertension and collected bloodspots from which high-sensitivity C-reactive protein (hs-CRP) was assayed. Sample sizes in the present analyses ranged from n = 7,884 to n = 8,474. RESULTS: Exposure to own and others' suicide attempts during adolescence was relatively common. In males, suicide attempts during adolescence (∼age 15 years) were associated with hypertension and elevated inflammation more than 1 decade later. Associations among suicide attempts by others and cardiovascular risk also emerged. CONCLUSIONS: Exposure to one's own or others' severe dysregulation in the form of suicide attempts during the early life course signals risk for cardiovascular health problems by the late twenties. Adolescent males who attempted suicide and individuals exposed to suicide attempts in their social network may benefit from a dual focus on mental and physical health in care. (PsycINFO Database Record

Effects of acute and repeated administration of Staphylococcal enterotoxin A on Morris water maze learning, corticosterone and hippocampal IL-1ß and TNFα.

Staphylococcal enterotoxin A (SEA) is a bacterial superantigen that induces pronounced T cell expansion and cytokine production. In addition, SEA activates the HPA axis and forebrain regions relevant to cognitive functions. Since learning-related cognitive changes have not been assessed in response to SEA, spatial learning in the Morris water maze (MWM) was determined in male C57BL/6J mice subjected to acute or repeated injections of 5µg SEA or Saline. Injections were given 2h prior to 4-5days of hidden platform sessions. Animals were then rested for 1month and given retraining without further injections. In addition, splenic IL-1ß, IL-2 and TNFα, plasma corticosterone, and hippocampal IL-1ß and TNFα were measured after the regimen of treatment used in the behavioral experiments. The results showed no learning impairment following acute or repeated SEA challenge. Moreover, when retested 1month later, and without further injections, the SEA group showed more rapid relearning of the MWM. This suggested that coincidental superantigenic T cell activation and training served to promote long-term improvement in recovery of learning. Furthermore, repeated SEA challenge continued to drive increases in plasma corticosterone, but with a compensatory reduction in hippocampal IL-1ß. However, while hippocampal TNFα was reduced after acute and repeated SEA treatment, this was not statistically significant. In view of the importance of modest glucocorticoid elevations and hippocampal IL-1ß in promoting contextual learning, the data point to the hypothesis that SEA promotes long-term plasticity by restraining disruptive increases in hippocampal IL-1ß, and possibly TNFα, during learning.