The influence of coping with perceived racism and stress on lipid levels in African Americans

应对感知到的种族主义和压力对非裔美国人血脂水平的影响

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Abstract

BACKGROUND: Lipid dysregulation is a major contributor to cardiovascular disease (CVD) risk and is attributed to numerous biological, psychosocial, and behavioral risk factors. Psychological stress has been examined as a predictor of lipid dysregulation; however, the role of coping with perceived racism, a stressor unique to the African American experience, has not been addressed. The current study sought to determine the impact of behavioral coping responses to perceived racism and perceived daily stress on lipid levels in African Americans. METHODS: The sample consisted of 122 African American participants who resided in the Washington, DC, metropolitan area. Data were collected as part of an ongoing study entitled Stress and Psychoneuroimmunological Factors in Renal Health and Disease at Howard University Hospital. RESULTS: Through canonical analysis, distinct profiles of African American lipid function emerged with body mass index, age, and behavioral coping responses to perceived racism being associated with high-density lipoprotein cholesterol (HDL-C), triglycerides, and low-density lipoprotein cholesterol (LDL-C), respectively. Results from linear regression analyses showed that greater endorsement of behavioral coping responses to perceived racism items predicted higher levels of LDL (B = .24, p < .05). This relationship was not mediated by pathophysiological mechanisms associated with the stress response system such as cortisol, norepinephrine, epinephrine, and IL-6. CONCLUSION: The relationship between elevated levels of LDL and behavioral coping responses to perceived racism suggests that African Americans may be at increased risk for CVD due to the unique stress encountered by racism in our culture. Behavioral pathways used to counteract the negative effects of perceived discrimination may better explain this relationship. Further research is necessary to determine other biobehavioral and pathophysiological mechanisms that explain this relationship.

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