Background: Disparities in insulin resistance between Black and White adults in the United States are well documented, yet relatively little is known about the psychosocial or biological antecedents of these inequities. The current study examined childhood adversity and contemporaneous psychosocial stressors in adulthood as possible mediators of the racial disparity in insulin resistance. Inflammatory and hypothalamic-pituitary adrenal (HPA) axis mechanisms implicated in associations between lifespan stress exposure and insulin resistance were also considered.
Methods: Data were derived from the biomarker component of the Midlife in the United States Study (N = 1170, 20% Black, 56% female, Mean age = 54.7 years, SD = 11.6). A homeostatic model assessment of insulin resistance (HOMA-IR) was calculated from fasting glucose and insulin concentrations. Twelve risk factors relating to household dysfunction, socioeconomic disadvantage, and maltreatment were sum scored to index childhood adversity. Measures of adult stress included socioeconomic adversity, major stressful events, everyday discrimination, and lifetime discrimination.
Results: Levels of insulin resistance were higher among Black than White adults. Childhood adversity was positively associated with HOMA-IR, and attenuated 18% of the race difference. Measures of adult stress mediated 33% of the association between childhood adversity and HOMA-IR, and accounted for an additional 47% of the race difference. Higher inflammation and lower nocturnal cortisol both played an important role in mediating the association between stress exposure and HOMA-IR.
Conclusions: Findings are consistent with prior research showing that childhood adversity and adult stress are salient predictors of glucose metabolism, and extend this work by showing that lifespan stress exposures attenuate a significant portion of the Black-White disparity in HOMA-IR. Results also suggest stress effects on insulin resistance through inflammatory and HPA-axis pathways.
Keywords: Adult psychosocial stress; Adverse childhood experiences; Cortisol; Health inequalities; Inflammation; Insulin resistance.
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