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生物衰老,吸烟和慢性阻塞性肺病之间的调解者:来自中国医院的队列研究的证据
Dongming Xie1, Ao Lin2, Feng Luo1
1The Key Laboratory of Advanced Interdisciplinary Studies, The First Affiliated Hospital; The Institute for Chemical Carcinogenesis, School of Public Health, Guangzhou Medical University, Guangzhou, Guangdong, China.
通过克莱梅拉 - 杜巴尔方法 - 生物衰老加速 (KDM-BAAc) 测量的加速生物衰老显著增加了中国成年人的慢性阻塞性肺病 (COPD) 风险. 这种衰老过程中介于吸烟对COPD发展的影响的14.3%.
科学领域:
- 老年学是一门学科.
- 肺部病理学 肺部病理学
- 流行病学 流行病学
背景情况:
- 慢性阻塞性肺病 (COPD) 是一个主要的全球健康问题,老龄化和吸烟是主要的风险因素.
- 生物衰老在中介吸烟与COPD之间的联系中的作用在中国人群中尚未得到充分研究.
研究的目的:
- 调查加速生物衰老与COPD风险之间的关联.
- 量化生物衰老加速在吸烟-COPD关系中的调解作用,在中国队列中.
主要方法:
- 一项基于医院的队列研究招募了1,269名没有COPD的中国成年人 (40-84岁).
- 克莱梅拉-杜巴尔方法-生物年龄 (KDM-BA) 用11个生物标志物计算,并推导出KDM-BA加速 (KDM-BAAc).
- 考克斯模型和受限立方线模型评估了KDM-BAAc与COPD风险和剂量反应关系的关联,而反事实调解分析量化了其调解作用.
主要成果:
- 在3.4年的时间里,发现了47例COPD病例 (10.90/1000人年).
- 较高的KDM-BAAc与COPD发病率的增加有关 (RR=2.28) 和每年加速的7%更高的COPD风险 (HR=1.07).
- 观察到一种显著的剂量反应关系,KDM-BAAc调解了吸烟对COPD的影响的14.3%.
结论:
- 加快的生物衰老是中国成年人COPD发展的重要危险因素.
- 生物衰老加速在吸烟和COPD之间确立的关联中发挥着关键的调解作用.
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