Additive Contributions of Childhood Adversity and Recent Stressors to Inflammation at Midlife: Findings From the MIDUS Study
Additive Contributions of Childhood Adversity and Recent Stressors to Inflammation at Midlife: Findings From the MIDUS Study
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DOI：
10.1037/dev0000049
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发表时间：
2015-11-01
影响因子：
4
通讯作者：
Miller, Gregory E.
中科院分区：
文献类型：
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作者：
Hostinar, Camelia E.;Lachman, Margie E.;Miller, Gregory E.
我们研究了自我报告的不良童年经历（ACE）和最近的生活事件（RLE）对中年炎症的共同贡献，通过测试3个相互竞争的理论模型：压力产生，压力积累和早期生活压力敏感化。我们的目的是确定逆境和炎症之间的潜在介质。参与者是来自美国中年生物标志物项目（MIDUS）的1，180名中年和老年人（M年龄= 57.3岁，SD = 11.5; 56%女性）。炎症的综合指标来自5种生物标志物：C-反应蛋白、白细胞介素-6、纤维蛋白原、E-选择素和ICAM-1的血清水平。参与者提供了关于ACE、RLE、当前生活方式指数（吸烟、饮酒、体育锻炼、腰围）、当前抑郁症状和人口统计学/生物医学特征的自我报告数据。我们还使用了下丘脑-垂体-肾上腺皮质流出（12小时尿皮质醇）和交感神经系统输出（12小时尿去甲肾上腺素和肾上腺素）的指数。分析表明，ACE和RLE独立地与更高水平的炎症相关，控制彼此的影响。它们之间的相互作用不显著。结果与ACE和炎症之间的关联通过较高的尿去甲肾上腺素输出、较大的腰围、吸烟和较低的运动水平介导的假设一致，而较高的腰围和更多的吸烟部分介导了RLE和炎症之间的关联。支持压力累积模型，ACE和RLE在中年时对炎症有独特的和累加的贡献，没有证据表明协同效应。结果还表明，去甲肾上腺素输出和生活方式指数可能有助于解释先前的压力源如何在中年时促进炎症。
We examined the joint contributions of self-reported adverse childhood experiences (ACEs) and recent life events (RLEs) to inflammation at midlife, by testing 3 competing theoretical models: stress generation, stress accumulation, and early life stress sensitization. We aimed to identify potential mediators between adversity and inflammation. Participants were 1,180 middle-aged and older adults from the Midlife in the United States (MIDUS) Biomarker Project (M age = 57.3 years, SD = 11.5; 56% female). A composite measure of inflammation was derived from 5 biomarkers: serum levels of C-reactive protein, interleukin-6, fibrinogen, E-selectin, and ICAM-1. Participants provided self-report data regarding ACEs, RLEs, current lifestyle indices (cigarette smoking, alcohol consumption, physical exercise, waist circumference), current depressive symptoms, and demographic/biomedical characteristics. We also used indices of hypothalamic-pituitary-adrenocortical outflow (12-hr urinary cortisol) and sympathetic nervous system output (12-hr urinary norepinephrine and epinephrine). Analyses indicated that ACEs and RLEs were independently associated with higher levels of inflammation, controlling for each other's effects. Their interaction was not significant. The results were consistent with the hypothesis that associations between ACEs and inflammation were mediated through higher urinary norepinephrine output, greater waist circumference, smoking, and lower levels of exercise, whereas higher waist circumference and more smoking partially mediated the association between RLEs and inflammation. In support of the stress accumulation model, ACEs and RLEs had unique and additive contributions to inflammation at midlife, with no evidence of synergistic effects. Results also suggested that norepinephrine output and lifestyle indices may help explain how prior stressors foster inflammation at midlife.