Disparities In Disease Risk Research Articles

Social and structural barriers and facilitators to HIV healthcare and harm reduction services for people experiencing syndemics in Manitoba: study protocol

IntroductionIn Manitoba, Canada, there has been an increase in the number of people newly diagnosed with HIV and those not returning for regular HIV care. The COVID-19 pandemic resulted in...

Disparities in COVID-19 risk exposure: Evidence from geolocation data

We examine the determinants of COVID-19 risk exposure in the context of the initial wave in New York City. In the first wave of the pandemic, out-of-home activity and household crowding were strongly associated with hospitalization at an individual level. After mass layoffs and shelter in place restrictions, out-of-home mobility decreased in importance for the risk of COVID-19 hospitalization, while the household crowding channel remained important. A larger share of individuals in crowded housing or with high measures of out-of-home mobility were Black, Hispanic, and lower-income—which contributed to disparities in disease risk. We conclude that structural socio-economic inequalities helped determine the cross-section of COVID-19 risk exposure in urban areas.

The role of mitochondria in the pathogenesis of Kawasaki disease.

Kawasaki disease is a systemic vasculitis, especially of the coronary arteries, affecting children. Despite extensive research, much is still unknown about the principal driver behind the amplified inflammatory response. We propose mitochondria may play a critical role. Mitochondria serve as a central hub, influencing energy generation, cell proliferation, and bioenergetics. Regulation of these biological processes, however, comes at a price. Release of mitochondrial DNA into the cytoplasm acts as damage-associated molecular patterns, initiating the development of inflammation. As a source of reactive oxygen species, they facilitate activation of the NLRP3 inflammasome. Kawasaki disease involves many of these inflammatory pathways. Progressive mitochondrial dysfunction alters the activity of immune cells and may play a role in the pathogenesis of Kawasaki disease. Because they contain their own genome, mitochondria are susceptible to mutation which can propagate their dysfunction and immunostimulatory potential. Population-specific variants in mitochondrial DNA have also been linked to racial disparities in disease risk and treatment response. Our objective is to critically examine the current literature of mitochondria’s role in coordinating proinflammatory signaling pathways, focusing on potential mitochondrial dysfunction in Kawasaki disease. No association between impaired mitochondrial function and Kawasaki disease exists, but we suggest a relationship between the two. We hypothesize a framework of mitochondrial determinants that may contribute to ethnic/racial disparities in the progression of Kawasaki disease.

Advancing Health Equity Through Equity-Centered Leadership Development with Interprofessional Healthcare Teams

IntroductionEvents of spring 2020—the COVID19 pandemic and re-birth of a social justice movement—have thrown disparities in disease risk, morbidity, and mortality in sharp relief. In response, healthcare organizations have shifted attentions and resources towards equity, diversity, and inclusion (EDI) issues and initiatives like never before. Focused, proven equity-centered skill and mindset development is needed for healthcare professionals to operationalize these pledges and stated aims.AimThis article highlights program evaluation results for this Clinical Scholars National Leadership Institute (CSNLI) specific to EDI. We will show that CSNLI imparts the valuable and essential skills to health professionals that are needed to realize health equity through organizational and system change.SettingInitial cohort of 29 participants in CSNLI, engaging in the program over 3 years through in-person and distance-based learning offerings and activities.Program DescriptionThe CSNLI is a 3-year, intensive leadership program that centers EDI skill development across personal, interpersonal, organizational, and systems domains through its design, competencies, and curriculum.Program EvaluationA robust evaluation following the Kirkpatrick Model offers analysis of four data collecting activities related to program participants’ EDI learning, behavioral change, and results.DiscussionOver the course of the program, participants made significant gains in competencies related to equity, diversity, and inclusion. Furthermore, participants demonstrated growth in behavior change and leadership activities in the areas of organizational and system change. Results demonstrate the need to center both leader and leadership development on equity, diversity, and inclusion curriculum to make real change in the US Healthcare System.

POSA389 Who Can We See in RWD? Assessing Capture of Demographic Data Across Multiple Countries

Real-world data (RWD) and real-world evidence (RWE) play an increasing role in healthcare decision-making, including regulatory decisions, clinical care, guideline development, and reimbursement/payer decisions. As such, the capture, completeness, and quality of these data underlying these analyses are imperative. Demographic data are critical to the identification of disparities in disease risk and care quality. However, the extent to which these characteristics are collected and recorded in RWD sources is not well known.

Geographic Disparities of Cervical Cancer Survival in California, United States

Background/Aim: Mapping crude and adjusted geographic distributions of disease outcomes is a useful tool for identifying risk factors of public health concern. The crude spatial pattern of disease is often what is observed by public health practitioners, but these patterns may be due to important spatially-varying predictors such as socioeconomic status, race/ethnicity, or environmental exposures. Individual-level spatial analyses can provide insight regarding geographic disparities in disease risk by adjusting for these variables without aggregation bias. Methods: We conducted a spatial analysis of cervical cancer survival among 17,541 cases diagnosed throughout California United States from 1995-2009 using MapGAM, an R package that estimates spatial hazard ratios (HR) and corresponding 95% confidence intervals (CI) in a generalized additive model framework with a non-parametric bivariate smooth term of location. Survival models were adjusted for patient age, tumor characteristics, race, socioeconomic status, care at a high-volume hospital (HVH), non-adherence to treatment guidelines, distance to receive care, and distance to closest HVH. Results were mapped in R also using MapGAM. Results: After controlling for patient and tumor characteristics, we observed significant areas of low HR in the San Francisco Bay area, Ventura and Los Angeles Counties. When distance and quality care variables were included in the model, HR northeast of Sacramento became elevated and significant due to reverse spatial confounding. Living within 30 miles of a HVH was protective [HR:0.86, 95% CI:0.77,0.97]. The fully adjusted spatial analysis reveals geographic disparities not due to quality of care. Conclusions: Quality of care indicators were the most influential on geographic disparities, but areas of poorer cervical cancer survival may be related to spatially-varying social or environmental stressors that warrant further investigation. The use of a bivariate smoother of location within the survival model allows for more advanced spatial analyses for exploring potential predictors of geographic disparities.

Considering the Role of Stress in Populations of High-Risk, Underserved Community Networks Program Centers.

Cancer disparities are associated with a broad range of sociocultural determinants of health that operate in community contexts. High-risk populations may be more vulnerable to social and environmental factors that lead to chronic stress. Theoretical and empirical research indicates that exposure to contextual and sociocultural stress alters biological systems, thereby influencing cancer risk, progression, and, ultimately, mortality. We sought to describe contextual pathways through which stress likely increases cancer risk in high-risk, underserved populations. This review presents a description of the link between contextual stressors and disease risk disparities within underserved communities, with a focus on 1) stress as a proximal link between biological processes, such as cytokine responses, inflammation, and cancer and 2) stress as a distal link to cancer through biobehavioral risk factors such as poor diet, physical inactivity, circadian rhythm or sleep disruption, and substance abuse. These concepts are illustrated through application to populations served by three National Cancer Institute-funded Community Networks Program Centers (CNPCs): African Americans in the Deep South (the South Carolina Cancer Disparities Community Network [SCCDCN]), Native Hawaiians ('Imi Hale-Native Hawaiian Cancer Network), and Latinos in the Lower Yakima Valley of Washington State (The Center for Hispanic Health Promotion: Reducing Cancer Disparities). Stress experienced by the underserved communities represented in the CNPCs is marked by social, biological, and behavioral pathways that increase cancer risk. A case is presented to increase research on sociocultural determinants of health, stress, and cancer risk among racial/ethnic minorities in underserved communities.

Cytokine SNPs: Comparison of allele frequencies by race and implications for future studies

The role of inflammation is being considered in chronic diseases. Previous studies have examined SNPs in a few key inflammatory genes and have included small numbers of African American participants. Variation in the frequencies of inflammatory pathway SNPs may help to explain racial disparities in disease risk. Through a population-based study of 103 African American and 380 Caucasian unrelated, healthy women, we examined the relationships between race and allele frequencies of 70 cytokine and cytokine receptor SNPs. The associations between genotypic and haplotype frequencies and race were also analyzed. Allelic frequencies for 52 out of the 70 SNPs meeting criteria for analysis differed significantly by race. Of the 32 pro-inflammatory and 20 anti-inflammatory SNPs for which the allele frequencies varied significantly by race, variant allele frequency differences between Caucasians and African Americans ranged between 6–37% and 7–53% for pro-inflammatory SNPs and anti-inflammatory SNPs, respectively. Our findings suggest that while allele frequencies do vary by race, racial groups are not simplistically represented by a pro-inflammatory or anti-inflammatory genetic profile. Given the racial variability in allele frequencies in inflammatory gene SNPs, studies examining the association between these SNPs and disease should at least incorporate self-reported race in their analyses.

Longitudinal Analysis of the Insulin-Like Growth Factor System in African-American and European American Children and Adolescents

IGF-I and its binding proteins influence growth, development, and disease risk. Studies have revealed ethnic variations in the IGF system. This longitudinal study was undertaken to test the hypothesis that the ethnic differences in the IGF system exist throughout the pubertal transition, and these differences are mediated at least in part by inherent differences in insulin dynamics. This was a longitudinal study. Annual evaluations were conducted for pubertal maturation, body composition, acute insulin response to glucose (AIRg), and reproductive-endocrine profile. Hormones and binding proteins were determined using standard assays, the AIRg during a frequently sampled iv glucose tolerance test, and body composition by dual-energy x-ray absorptiometry. Mixed model analyses were used to identify and characterize ethnic differences in the IGF system across the pubertal transition after adjusting for ethnicity, sex, age, maturation status, body composition, and reproductive hormones, and to identify the contribution of insulin to IGF binding protein (IGFBP)-1. Subjects included African-American (AA) and European American children (n = 162 at baseline) aged 7-16 yr, evaluated across the pubertal transition. Annual data on IGF-I, IGFBP-1, and IGFBP-3 were examined. IGF-I was higher in AA children at pubertal stage 1 only (P < 0.001). However, IGFBP-3 and IGFBP-1 concentrations were lower in AAs through much of puberty (P < 0.05). The lower IGFBP-1 of AAs was in part explained by greater AIRg. Our data suggest that the higher IGF-I and lower IGFBP-1 and IGFBP-3 levels in AAs as compared with European Americans during puberty suggest potential ethnic differences in circulating bioavailable IGF-I. In addition, higher AIRg in AAs may lead to greater bioavailable IGF-I. Whether these differences in the IGF system account for disparities in disease risk warrants further investigation.