Social determinants of health and diabetes: using a nationally representative sample to determine which social determinant of health model best predicts diabetes risk.

OBJECTIVES: Social determinants of health (SDOH) research demonstrates poverty, access to healthcare, discrimination, and environmental factors influence health outcomes. Several models are commonly used to assess SDOH, yet there is limited understanding of how these models differ regarding their ability to predict the influence of social determinants on diabetes risk. This study compares the utility of four SDOH models for predicting diabetes disparities. STUDY DESIGN: We utilized The National Longitudinal Study of Adolescent to Adulthood (Add Health) to compare SDOH models and their ability to predict risk of diabetes and obesity. METHODS: Previous literature has identified the World Health Organization (WHO), Healthy People, County Health Rankings, and Kaiser Family Foundation as the conventional SDOH models. We used these models to operationalize SDOH using the Add Health dataset. Add Health data were used to perform logistic regressions for HbA1c and linear regressions for body mass index (BMI). RESULTS: The Kaiser model accounted for the largest proportion of variance (19%) in BMI. Race/ethnicity was a consistent factor predicting BMI across models. Regarding HbA1c, the Kaiser model also accounted for the largest proportion of variance (17%). Race/ethnicity and wealth was a consistent factor predicting HbA1c across models. CONCLUSION: Policy and practice interventions should consider these factors when screening for and addressing the effects of SDOH on diabetes risk. Specific SDOH models can be constructed for diabetes based on which determinants have the largest predictive value.

Cardiorespiratory fitness and physical activity in the lens of social justice - Reporting on the disparities that exist.

Cardiorespiratory fitness (CRF), heavily influenced by physical activity (PA), represents a strong and independent risk factor for a wide range of health conditions, most notably, cardiovascular disease. Substantial disparities in CRF have been identified between white and non-white populations. These disparities may partly account for group differences in susceptibility to poor health outcomes, including non-communicable disease. Race and ethnic differences in CRF may partly be explained by social injustices rooted in persistent structural and systemic racism. These forces contribute to environments that are unsupportive for opportunities to achieve optimal CRF levels. This review aims to examine, through the lens of social justice, the inequities in key social ecological factors, including socioeconomic status, the built environment, and structural racism, that underly the systemic differences in CRF and PA in vulnerable communities. Further, this review highlights current public health initiatives, as well as opportunities in future research, to address inequities and enhance CRF through the promotion of regular PA.

The effects of childhood maltreatment on social support, inflammation, and depressive symptoms in adulthood.

RATIONALE: Social Safety Theory (SST) suggests that social threats increase inflammation, exacerbating health risks, but that social support may decrease inflammatory signaling. One of the key health problems affected by both social forces and inflammation is major depression. OBJECTIVE: The present study sought to test aspects of the SST, to understand how social support and inflammation may mediate the effects of childhood maltreatment on depressive symptoms in adulthood. METHODS: This study utilized data from the national Midlife Development in the United States study (n = 1969; mean age 53; 77.2% White; 53.6% female) to model the effects of childhood maltreatment on depressive symptoms in adulthood and the potential serial mediating effects of social support and inflammation. Analyses were conducted via structural equation modeling, using the four subscales of the Center for Epidemiologic Studies Depression Scale to indicate depressive symptoms, the five subscales of the Childhood Trauma Questionnaire to indicate childhood maltreatment, and the Positive Relations Scale and a network level measure of support as indicators of social support. Inflammation was indexed using C-reactive protein (CRP). The model was estimated via maximum likelihood with robust standard errors and significance of indirect effects were assessed via a Sobel test. RESULTS: Childhood maltreatment was associated with increased depressive symptoms and CRP but decreased social support. Social support was associated with decreased depressive symptoms while CRP was associated with increased depressive symptoms. Assessing indirect effects yielded no serial mediation effect; however, a significant indirect effect from childhood maltreatment to depressive symptoms through social support was identified. CONCLUSIONS: Analyses indicate mixed support for the SST with respect to depressive symptoms. Results highlight the role of social support in mitigating the effects depressive symptoms in adulthood; although, alternative strategies may be needed to decrease the effects of childhood maltreatment on inflammation as indexed by CRP.