美国成年人中心性肥胖与骨关节炎之间的关系:生物老化加速的中介作用

IF 6.8 4区 医学 Q1 NUTRITION & DIETETICS
Qiang He, Jie Mei, Chengxin Xie, Zhen Wang, Xin Sun, Mengmeng Xu
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引用次数: 0

摘要

研究目的本研究旨在探讨中心性肥胖与骨关节炎风险之间的关系,以及生物年龄和生物衰老进展在这一关系中的中介作用:研究基于 2005-2018 年美国国家健康与营养调查(NHANES)的数据。研究使用 13 个常用的临床特征来计算 Klemera-Doubal 法年龄(KDM-Age)和表型年龄(Pheno-Age),作为衡量生物衰老的两个指标。此外,还计算了 KDM-Age 提前期和 Pheno-Age 提前期,作为衡量生物衰老提前期的两个指标。加权多变量逻辑回归用于分析中心性肥胖与骨关节炎(OA)风险之间的关系。然后应用中介分析来阐明生物衰老和生物衰老进展在这一关系中的作用:本研究共纳入 31,162 名年龄≥20 岁的受试者,其中 3,964 名受试者报告患有 OA(14%)。与非 OA 组相比,OA 组在中心性肥胖、KDM-Age、KDM-Age 提前量、PhenoAge 和 PhenoAge 提前量方面的比例明显更高。与非中心性肥胖组相比,中心性肥胖组的 KDM-年龄、KDM-年龄提前期、PhenoAge、PhenoAge 提前期更高,患 OA 的风险也更高(p p p 结论:中心性肥胖会增加患 OA 的风险:中心性肥胖会增加罹患 OA 的风险,这种关联的部分原因是生物老化和生物老化提前。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Relationship Between Central Obesity and Osteoarthritis in US Adults: The Mediating Role of Biological Aging Acceleration.

Objective: This study aims to investigate the association between central obesity and the risk of osteoarthritis, and the mediating role of biological age and biological aging advance in this relationship.

Methods: The study is based on data from the National Health and Nutrition Examination Survey (NHANES) for the years 2005-2018. Thirteen commonly used clinical traits were used to calculate the Klemera-Doubal method age (KDM-Age) and phenotypic age (Pheno-Age) as two measures of biological aging. Additionally, KDM-Age advance and Pheno-Age advance were calculated as two measures of biological aging advance. Weighted multivariable logistic regression was used to analyze the association between central obesity and the risk of osteoarthritis (OA). Mediation analysis was then applied to elucidate the role of biological aging and biological aging advance in this relationship.

Results: A total of 31,162 subjects aged ≥20 years were included in this study, of which 3,964 subjects reported having OA (14%). Compared to the Non-OA group, the OA group showed significantly higher proportions of central obesity, KDM-Age, KDM-Age advance, PhenoAge, and PhenoAge advance. Compared to the Non-central obesity group, the central obesity group had higher KDM-Age, KDM-Age advance, PhenoAge, PhenoAge advance, and a higher risk of OA (p < 0.05). Additionally, higher KDM-Age, KDM-Age advance, PhenoAge, and PhenoAge advance were positively correlated with the risk of OA (p < 0.05). Mediation analysis revealed that part of the association between central obesity and the risk of OA was mediated by KDM-Age, KDM-Age advance, PhenoAge, and PhenoAge advance (p < 0.05).

Conclusion: Central obesity increases the risk of OA, with part of this association being mediated by biological aging and biological aging advance.

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