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炎症作为心理社会压力与肥胖之间关联的中间途径。

Inflammation as an intermediate pathway in the association between psychosocial stress and obesity.

作者信息

Hamer Mark, Stamatakis Emmanual

机构信息

Department of Epidemiology and Public Health, University College London, 1-19 Torrington Place, London WC1E 6BT, UK.

出版信息

Physiol Behav. 2008 Jul 5;94(4):536-9. doi: 10.1016/j.physbeh.2008.03.010. Epub 2008 Mar 30.

DOI:10.1016/j.physbeh.2008.03.010
PMID:18474384
Abstract

Psychosocial stress is associated with risk of obesity although little is known about stress-induced biological mechanisms of obesity. We examined the potential mediating role of inflammatory processes. Data were collected from a nationally representative sample of 7540 individuals (54% women, mean age 46.8+/-15.4 years), from the Scottish Health Surveys. We calculated risk estimates of obesity for increasing numbers of psychosocial stressors (based on social position, education, psychological distress and marital/partner discord) using logistic regression analyses. Obesity was assessed using body mass index and central obesity using waist circumference. Potential mediators included inflammatory markers (C-reactive protein and fibrinogen) and health behaviours (physical activity, smoking, alcohol, and dietary intake). The unadjusted odds ratio of obesity for three or more psychosocial stressors was 1.81 (95% CI, 1.39-2.36, p<0.001). In multivariate analyses that adjusted for age, gender, health behaviours and inflammatory markers the association between psychosocial stress and obesity was attenuated but remained significant (1.49, 1.11-2.00, p<0.001). Inflammatory markers independently accounted for approximately 25% of the association between stress and obesity. We found similar associations in separate analyses of psychosocial stress and central obesity, although results were confounded by overall obesity. In summary, inflammatory processes appear to be an important intermediate pathway in the association between psychosocial stress and obesity.

摘要

心理社会压力与肥胖风险相关,尽管人们对压力诱发肥胖的生物学机制知之甚少。我们研究了炎症过程的潜在中介作用。数据来自苏格兰健康调查中具有全国代表性的7540名个体样本(54%为女性,平均年龄46.8±15.4岁)。我们使用逻辑回归分析计算了心理社会压力源数量增加时(基于社会地位、教育程度、心理困扰和婚姻/伴侣不和)肥胖的风险估计值。肥胖通过体重指数评估,中心性肥胖通过腰围评估。潜在中介因素包括炎症标志物(C反应蛋白和纤维蛋白原)和健康行为(身体活动、吸烟、饮酒和饮食摄入)。三个或更多心理社会压力源导致肥胖的未调整优势比为1.81(95%置信区间,1.39 - 2.36,p<0.001)。在对年龄、性别、健康行为和炎症标志物进行调整的多变量分析中,心理社会压力与肥胖之间的关联减弱但仍显著(1.49,1.11 - 2.00,p<0.001)。炎症标志物独立解释了压力与肥胖之间约25%的关联。在心理社会压力与中心性肥胖的单独分析中我们发现了类似的关联,尽管结果因总体肥胖而混淆。总之,炎症过程似乎是心理社会压力与肥胖之间关联的重要中间途径。

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