工作压力相关 CRP 是由闲暇时间体力活动介导的：MONICA/KORA 研究的结果。
Job strain associated CRP is mediated by leisure time physical activity: results from the MONICA/KORA study.
机构信息
Institute of Epidemiology II, Helmholtz Zentrum Muenchen, German Research Center for Environmental Health, 85764 Neuherberg, Germany.
出版信息
Brain Behav Immun. 2012 Oct;26(7):1077-84. doi: 10.1016/j.bbi.2012.07.004. Epub 2012 Jul 17.
BACKGROUND
Psychological stress at work is considered a cardiac risk factor, yet whether it acts directly through neuroimmune processes, or indirectly by increasing behavioral risk factors, is uncertain. Cross-sectional associations between job strain and serum biomarkers of inflammation and endothelial dysfunction were investigated. Secondary analyses explored the role of psychosocial/cardiometabolic risk factors as mediators of job stress associated inflammation in healthy workers.
METHODS
Information on risk factors was obtained in standardized personal interviews of a subcohort of working participants in the MONICA/KORA population (n = 951). Work stress was measured by the Karasek job strain index. Biomarkers were measured from non-fasting venous blood. Multivariate regression analyses were used to examine the association of job strain with inflammatory biomarkers. Mediation analysis (Sobel test) was used to determine the effect of psychosocial risk factors on the association between job strain and C-reactive protein (CRP).
RESULTS
High job strain was reported by half (n = 482, 50.7%) of the study participants. While workers with high job strain were more likely to have adverse workplace conditions (competition with coworkers, job dissatisfaction and insecurity), sleeping problems, depressive symptoms, a Type A personality, and be physically inactive, no differences in cardiometabolic risk factors were detected. A strong and robust association between job strain and CRP was observed in age and sex adjusted models, as well as models adjusted for classic coronary heart disease risk factors (β = 0.39, p = 0.006 and β = 0.27, p = 0.03, respectively). Adjustment for physical activity abrogated this effect (β = 0.23, p = 0.07), and a mediating effect of physical activity on stress-associated inflammation was demonstrated (p = 0.04).
CONCLUSIONS
The analyses provide evidence for both a direct and an indirect effect of job strain on inflammation.
背景
工作中的心理压力被认为是心脏危险因素，但它是通过神经免疫过程直接作用，还是通过增加行为危险因素间接作用，尚不确定。本研究旨在调查工作压力与炎症和血管内皮功能障碍的血清生物标志物之间的横断面关系。进一步的分析探讨了心理社会/心血管代谢危险因素作为工作压力相关炎症的中介因素在健康工作者中的作用。
方法
在 MONICA/KORA 人群的工作参与者亚队列的标准化个人访谈中获取了风险因素信息（n = 951）。工作压力通过 Karasek 工作压力指数进行测量。从非禁食静脉血中测量生物标志物。使用多元回归分析检查工作压力与炎症生物标志物之间的关联。使用中介分析（Sobel 检验）确定心理社会风险因素对工作压力与 C 反应蛋白（CRP）之间关联的影响。
结果
研究参与者中有一半（n = 482，50.7%）报告了高工作压力。尽管高工作压力的工人更有可能处于不利的工作环境（与同事竞争、工作不满和不安定）、睡眠问题、抑郁症状、A型人格和缺乏身体活动，但未发现心血管代谢危险因素存在差异。在年龄和性别调整模型以及调整经典冠心病危险因素模型中，均观察到工作压力与 CRP 之间存在强而稳健的关联（β = 0.39，p = 0.006 和β = 0.27，p = 0.03）。调整身体活动后，该效应减弱（β = 0.23，p = 0.07），并证明了身体活动对与压力相关的炎症的中介作用（p = 0.04）。
结论
这些分析为工作压力对炎症的直接和间接作用提供了证据。
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