Racial discrimination is associated with a measure of red blood cell oxidative stress: a potential pathway for racial health disparities.

Racial discrimination is associated with a measure of red blood cell oxidative stress: a potential pathway for racial health disparities.
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DOI:
10.1007/s12529-011-9188-z
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发表时间:
2012-12
影响因子:
2.7
通讯作者:
Evans MK
Evans MK
中科院分区:
心理学4区
文献类型:
--
作者:
Szanton SL;Rifkind JM;Mohanty JG;Miller ER 3rd;Thorpe RJ;Nagababu E;Epel ES;Zonderman AB;Evans MK

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在许多被假设为氧化应激前兆的情况下,存在种族健康差异。这些疾病包括心血管疾病、糖尿病和早衰。小型临床研究表明,心理压力可能会增加氧化应激。然而,流行病学研究证实这种关联受到同质人群和未测量的潜在混杂因素的限制。我们测试了自我报告的种族歧视和红细胞(RBC)氧化应激之间的横断面关联,在一个双种族、社会经济异质性的人群中,有良好的测量混杂因素。我们对629名连续参加“跨生命周期多样性社区健康老龄化”(HANDLS)研究的参与者进行了横断面分析。HANDLS是一项前瞻性流行病学研究,由美国国家老龄研究所开展,研究对象为3721名年龄在30-64岁之间的不同社会经济背景的白人和非裔美国人。种族歧视是基于自我报告。用荧光血红素降解产物测定红细胞氧化应激。潜在的混杂因素包括年龄、吸烟状况、肥胖和c反应蛋白。参与者的平均年龄为49岁(SD = 9.27)。在多变量线性回归模型中,调整年龄、吸烟、c反应蛋白水平和肥胖后,种族歧视与RBC氧化应激显著相关(Beta=0.55 P<0.05)。当按种族分层时,白人的歧视与RBC氧化应激无关,但非裔美国人的歧视与RBC氧化应激显著相关(Beta值=0.36,P<0.05)。这些发现表明,种族歧视可能通过可识别的细胞途径放大心血管和其他与年龄相关的疾病风险。
There are racial health disparities in many conditions for which oxidative stress is hypothesized to be a precursor. These include cardiovascular disease, diabetes, and premature aging. Small clinical studies suggest that psychological stress may increase oxidative stress. However, confirmation of this association in epidemiological studies has been limited by homogenous populations and unmeasured potential confounders. We tested the cross-sectional association between self-reported racial discrimination and red blood cell (RBC) oxidative stress in a biracial, socioeconomically heterogeneous population with well-measured confounders. We performed a cross-sectional analysis of a consecutive series of 629 participants enrolled in the Healthy Aging in Neighborhoods of Diversity across the Life Span (HANDLS) study. Conducted by the National Institute on Aging Intramural Research Program, HANDLS is a prospective epidemiological study of a socioeconomically diverse cohort of 3721 whites and African Americans aged 30–64 years. Racial discrimination was based on self-report. RBC oxidative stress was measured by fluorescent heme degradation products. Potential confounders were age, smoking status, obesity, and C-reactive protein. Participants had a mean age of 49 years (SD = 9.27). In multivariable linear regression models, racial discrimination was significantly associated with RBC oxidative stress (Beta=0.55 P<0.05) after adjustment for age, smoking, C-reactive protein level, and obesity. When stratified by race, discrimination was not associated with RBC oxidative stress in Whites but was associated significantly for African-Americans (Beta=0.36, P<0.05). These findings suggest that there may be identifiable cellular pathways by which racial discrimination amplifies cardiovascular and other age-related disease risks.
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