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身体活动与炎症在老年墨西哥裔美国人死亡率、认知功能和抑郁症状中的作用。

The Roles of Physical Activity and Inflammation in Mortality, Cognition, and Depressive Symptoms Among Older Mexican Americans.

机构信息

Department of Epidemiology, Fielding School of Public Health, University of California, Los Angeles, Los Angeles, California.

Department of Epidemiology and Biostatistics, School of Medicine, University of California, San Francisco, San Francisco, California.

出版信息

Am J Epidemiol. 2019 Nov 1;188(11):1944-1952. doi: 10.1093/aje/kwz180.

Abstract

A higher level of physical activity (PA) is associated with decreased risk of mortality, dementia, and depression, yet the mechanisms involved are not well understood, and little evidence exists for Mexican Americans. With data from the Sacramento Area Latino Study on Aging (1998-2007), we used Cox proportional hazards regression to separately evaluate associations of baseline PA level with mortality, dementia/cognitive impairment without dementia (CIND), and depressive symptoms, and we estimated the mediating effects of inflammatory markers in additive hazard models. A low level of PA (<35 metabolic equivalent of task-hours/week) was associated with increased mortality (hazard ratio (HR) = 1.50, 95% confidence interval (CI): 1.20, 1.88), dementia/CIND (HR = 1.37, 95% CI: 0.96, 1.96), and depressive symptoms (HR = 1.23, 95% CI: 1.00, 1.52). A low PA level added 512 (95% CI: -34, 1,058) cases of dementia/CIND per 100,000 person-years at risk (direct effect), while, through a mediating path, interleukin 6 (IL-6) added another 49 (95% CI: 5, 94) cases, or 9% of the total effect. For mortality, 8%-10% of the PA total effect was mediated through IL-6, tumor necrosis factor α (TNF-α), or TNF-α receptors. None of the inflammatory markers mediated the association between PA and depressive symptoms. Our results suggest that antiinflammation (especially as assessed by IL-6 and TNF-α levels) may partly explain how PA protects against dementia/CIND and mortality.

摘要

更高水平的身体活动(PA)与降低死亡率、痴呆和抑郁的风险相关,但涉及的机制尚不清楚,并且针对墨西哥裔美国人的证据很少。利用来自萨克拉门托拉丁裔老龄化研究(1998-2007 年)的数据,我们使用 Cox 比例风险回归分别评估基线 PA 水平与死亡率、痴呆/无痴呆认知障碍(CIND)和抑郁症状的关联,并在附加危险模型中估计炎症标志物的中介效应。低水平的 PA(<35 代谢当量任务小时/周)与死亡率增加相关(风险比(HR)=1.50,95%置信区间(CI):1.20,1.88),痴呆/CIND(HR=1.37,95%CI:0.96,1.96)和抑郁症状(HR=1.23,95%CI:1.00,1.52)。低 PA 水平每增加 100,000 人年风险 512 例(95%CI:-34,1,058)痴呆/CIND(直接效应),而通过中介途径,白细胞介素 6(IL-6)又增加了 49 例(95%CI:5,94),即总效应的 9%。对于死亡率,PA 总效应的 8%-10%通过 IL-6、肿瘤坏死因子-α(TNF-α)或 TNF-α 受体介导。炎症标志物均未介导 PA 与抑郁症状之间的关联。我们的结果表明,抗炎(尤其是通过 IL-6 和 TNF-α 水平评估)可能部分解释了 PA 如何预防痴呆/CIND 和死亡率。

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