The Life Course Origins of the Race Disparity in Cognitive Functioning in Brazil

Background Cognitive health is a major concern for understanding population health in Brazil. Race inequalities have been found for several health outcomes but less is known about older adult cognitive health. Health inequalities have been tied to several life course factors, but less is known about how the racial stratification in Brazil may contribute to race disparities in cognitive health. Method: Data come from the Brazilian Longitudinal Study of Aging. We used nested regression models to examine the life course origins of the race differences in cognitive functioning. Results Whites had better cognitive functioning than non-Whites. Education reduced these differences by about half. Health behaviors and cardiometabolic conditions had little to no impact. Discussion Race differences in cognitive functioning in Brazil are in large part attributable to educational opportunities. These finding point to the importance of cognitive development in childhood to understand racial disparities in later life cognitive health.

Police Use of Force as an Extension of Arrests: Examining Disparities across Civilian and Officer Race

The United States is embroiled in an important debate about police use of force tactics. I find that black civilians are disproportionately likely to be involved in a use of force incident during an arrest, examining data from Dallas, Texas. However, this race disparity stems from differences in the initial likelihood of arrest. Further, I fail to find evidence of taste-based racial bias in use of force conditional on arrest, leveraging variation across officer and civilian race. The results suggest that reforms that narrowly focus on force-related protocols may be unlikely to reduce racial disparities in use of force.

Breast cancer molecular subtypes association with clinical outcomes and race.

e12575 Background: Breast Cancer (BC) has been classified into four subtypes: Luminal A (LABC), Luminal B (LBBC), Triple negative (TNBC) and HER2-enriched (HER2e). BC mortality in Black women is significantly higher than in Whites and Asians. BC in Blacks has been characterized by higher grade and later stage. Causes of the Black-White BC survival disparity have been investigated, including differences in: diagnostic stage, socioeconomics, and comorbidities. These have led researchers to investigate the differences in tumor molecular subtype and their association with clinical outcomes and races. Methods: This study used the Surveillance, Epidemiology, and End Results – 18 (SEER-18) Registries research data between 2010 and 2013 that included over 212,000 patients. Descriptive statistics, Odds ratios (OR) and 95%Confidence intervals (CI) were used to study the association between BC stage, grade, and mortality and BC molecular subtypes across different races. We employed Cox regression models to explore the race disparity in BC mortality before and after controlling for BC molecular subtype and other clinical and social factors. Results: TNBC had more high grade cancer compared to HER2e subtype (OR, 1.5; CI, 1.3 - 1.8), LBBC (OR, 4.5; CI, 4.0 - 5.0) and LABC (OR, 12.2; CI, 11.2 – 13.3) for Black. BC mortality was higher in TNBC subtype compared to HER2e subtype (OR, 1.3; CI, 1.1 - 1.6), LBBC (OR, 2.4; CI, 2.0 - 2.9), and LABC (OR, 2.8; CI, 2.4 – 3.2) for Blacks. Results are consistent for all races. HER2e subtype had more late cancer stage compare to LBBC (OR, 1.2; CI, 1.0 - 1.4), TNBC (OR, 1.4; CI, 1.2 - 1.6) and LABC (OR, 2.1; CI, 1.8 - 2.4) in Blacks with similar results in all races. BC mortality in Blacks was higher compare with Whites (HR, 1.9; CI, 1.8 - 2.0) and Asian (HR, 2.7; CI, 2.5 - 3.0). After controlling for cancer subtype and other factors in the Cox regression model, the corresponding HRs ware significantly decreased to 1.2 (CI, 1.1 -1.3) and 1.6 (9CI, 1.5 -1.8). Blacks have heighst percent in stage IV and grade higer grade of disease. Conclusions: Molecular subtypes of BC contribute differently to risks of late cancer stage, high cancer grade and BC specific mortality. These differences are consistent in all races. The molecular subtypes and other social and clinical factors may explain part of the BC mortality race disparity.

Abstract MP020: Sleep as a Mediator of Racial Disparities in Cardiometabolic Disease Risk: The Coronary Artery Risk Development in Young Adults (CARDIA) Study

Introduction: Approximately half of the disparity in premature mortality between African American (AA) and European American (EA) adults is due to greater hypertension, diabetes, and stroke risk. The current study tests sleep as a mediator of racial disparities in cardiometabolic (CMB) disease risk in adulthood. Methods: A total of 618 CARDIA Study members took part in a sleep sub-study (2003-2005) and had measured CMB risk (2000-2011; mean age at baseline=40.1; 43.5% AA; 56.5% EA; 42.1% male). Sleep efficiency (% of time in bed asleep) and total sleep time were assessed via actigraphy for six total nights in years 17 and 18 of the CARDIA Study. CMB risk was assessed in years 15 and 25 from borderline high (coded as 1) and high (coded as 2) levels in seven markers using recommended cutpoints from NCEP ATP III and AHA: blood pressure, glucose, insulin resistance, waist circumference, triglycerides, HDL-C, and C-reactive protein. Scores were averaged across markers, ranging from 0 to 2 (a score of 1 indicates a borderline high average in the seven markers). Using linear path models, sleep variables were tested as mediators of racial disparities in ten-year changes in CMB risk. Results: AAs obtained less efficient sleep and less total sleep than EAs (76.5% vs 84.3%; 5.63 hrs vs. 6.43 hrs), and AAs had higher CMB risk at both periods (Mean at Y15: .75 vs. .55; Y25: .94 vs. .67) ( p ’s < .001). Mediation tests are shown in the Table. Race was indirectly associated with increasing CMB risk over the ten-year period via sleep efficiency, explaining 25% of the racial disparity. Racial disparities in CMB risk were attenuated by 24.5% when adjusting for sleep time, although the mediation test was not significant. After adjusting for education and household income, 18.1% of the race disparity in diverging CMB risk was explained by sleep efficiency and 20.8% by sleep time. Conclusions: Differences in sleep likely contribute to greater CMB risk among AAs as compared to EAs in adulthood. Sleep may be an important intervention point to reduce racial health disparities.