Department of Psychology, Northwestern University, Swift Hall, 2029 Sheridan Road, Evanston, IL, 60208, United States.
Department of Psychology, Georgetown University, 306N White-Gravenor Hall, 37(th) and O Streets, NW, Washington DC, 20057, United States.
Psychoneuroendocrinology. 2021 Jan;123:104917. doi: 10.1016/j.psyneuen.2020.104917. Epub 2020 Oct 17.
Cardiovascular diseases are patterned by race and socioeconomic status, and chronic low-grade inflammation is proposed as a key underlying mechanism. Theories for how racial and socioeconomic disadvantages foster inflammation emphasize a lifecourse approach: social disadvantages enable chronic or repeated exposure to stressors, unhealthy behaviors, and environmental risks that accumulate across the lifecourse to increase low-grade inflammation. However, single samples rarely include multiple racial and socioeconomic groups that each span a wide age range, precluding examination of this proposition. To address this issue, the current study combined seven studies that measured C-reactive protein and interleukin-6, producing a pooled sample of 1650 individuals aged 11-60 years. We examined (a) whether race and socioeconomic disparities in inflammatory biomarkers vary across the lifecourse, (b) whether adiposity operates as a pathway leading to these disparities, and (c) whether any indirect pathways through adiposity also vary across the lifecourse. Relative to White individuals, Black individuals exhibited higher, whereas Asian individuals exhibited lower, levels of inflammatory biomarkers, and adiposity accounted for these racial differences. Similarly, lower socioeconomic status was associated with higher inflammatory biomarkers via elevated adiposity. Importantly, both racial and socioeconomic disparities, as well as their pathways via adiposity, widened across the lifecourse. This pattern suggests that the impact of social disadvantages compound with age, leading to progressively larger disparities in low-grade inflammation. More broadly, these findings highlight the importance of considering age when examining health disparities and formulating conceptual models that specify how and why disparities may vary across the lifecourse.
心血管疾病存在种族和社会经济地位差异模式,慢性低度炎症被认为是其关键潜在机制。关于种族和社会经济劣势如何促进炎症的理论强调了一种生命周期方法:社会劣势使人们能够长期或反复暴露于压力源、不健康行为和环境风险中,这些风险会在生命周期中积累,从而增加低度炎症。然而,单一样本很少包括跨越广泛年龄范围的多个种族和社会经济群体,从而无法检验这一假设。为了解决这个问题,本研究结合了七项测量 C 反应蛋白和白细胞介素 6 的研究,得出了一个包含 1650 名年龄在 11-60 岁之间的个体的汇总样本。我们检验了:(a) 炎症生物标志物的种族和社会经济差异是否随生命周期而变化;(b) 肥胖是否是导致这些差异的途径;(c) 通过肥胖的任何间接途径是否也随生命周期而变化。与白人个体相比,黑人个体表现出更高的炎症生物标志物水平,而亚洲个体则表现出较低的水平,而肥胖解释了这些种族差异。同样,较低的社会经济地位通过增加肥胖与较高的炎症生物标志物相关。重要的是,种族和社会经济差异及其通过肥胖的途径,随着生命周期的延长而扩大。这种模式表明,社会劣势的影响会随着年龄的增长而累积,导致低度炎症的差异越来越大。更广泛地说,这些发现强调了在检查健康差异和制定概念模型时考虑年龄的重要性,这些模型具体说明了差异可能如何以及为何随生命周期而变化。