Department of Orthopedics, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.
The First Clinical Medical College, Lanzhou University, Lanzhou 730000, China.
Bone. 2024 Dec;189:117255. doi: 10.1016/j.bone.2024.117255. Epub 2024 Sep 14.
This study aimed to investigate the association between biological age acceleration and osteoporosis (OP) risk in middle-aged and older adults using data from the National Health and Nutrition Examination Survey (NHANES). The research focused on analyzing the relationship between two biological aging metrics, Klemera-Doubal Method Age (KDMAge) and Phenotypic Age (PhenoAge), and OP risk.
The study analyzed data from NHANES, which included 6550 participants aged 50 and above from survey cycles 2005-2010 and 2017-2018. Linear and logistic regression were used to investigate the relationship between biological age acceleration (KDMAgeAccel and PhenoAgeAccel) and OP. Subgroup analysis was performed by age, gender and other factors. Multivariable Cox regression analysis yielded Hazard Ratios (HRs) relating biological age acceleration to mortality were evaluated. The study also considered the mediating roles of body mass index (BMI).
KDMAgeAccel (odds ratio [OR] = 2.34, 95 % CI, 1.72-3.18) and PhenoAgeAccel (OR = 2.03, 95 % CI, 1.48-2.78) were significantly associated with increased OP risk and reduced bone mineral density (BMD). Specifically, higher KDMAgeAccel and PhenoAgeAccel were linked to higher OP prevalence and lower BMD at multiple sites. Subgroup analyses indicated that the association between accelerated biological age acceleration and OP risk was consistent across different demographics. Mediation analysis revealed that BMI partially mediated the relationship between accelerated biological age and OP, although other mechanisms are likely involved. Statistical analysis indicated that individuals with higher biological age metrics had increased mortality risk related to OP.
The findings suggest that accelerated biological age is a robust predictor of OP risk and related mortality. KDMAgeAccel and PhenoAgeAccel could serve as valuable biomarkers for identifying individuals at high risk for OP, guiding preventive strategies.
本研究旨在利用国家健康与营养调查(NHANES)的数据,探讨中老年人群生物年龄加速与骨质疏松症(OP)风险之间的关系。研究集中分析了两种生物老化指标——Klemera-Doubal 方法年龄(KDMAge)和表型年龄(PhenoAge)与 OP 风险之间的关系。
本研究分析了 NHANES 的数据,其中包括 2005-2010 年和 2017-2018 年调查周期中 6550 名年龄在 50 岁及以上的参与者。线性和逻辑回归用于研究生物年龄加速(KDMAgeAccel 和 PhenoAgeAccel)与 OP 之间的关系。通过年龄、性别和其他因素进行亚组分析。多变量 Cox 回归分析评估了生物年龄加速与死亡率之间的关系。该研究还考虑了体重指数(BMI)的中介作用。
KDMAgeAccel(比值比[OR] = 2.34,95%置信区间,1.72-3.18)和 PhenoAgeAccel(OR = 2.03,95%置信区间,1.48-2.78)与 OP 风险增加和骨密度(BMD)降低显著相关。具体而言,较高的 KDMAgeAccel 和 PhenoAgeAccel 与更高的 OP 患病率和多个部位较低的 BMD 相关。亚组分析表明,加速的生物年龄与 OP 风险之间的关联在不同人群中是一致的。中介分析表明,BMI 部分介导了加速的生物年龄与 OP 之间的关系,尽管可能涉及其他机制。统计分析表明,生物年龄指标较高的个体与 OP 相关的死亡率风险增加。
研究结果表明,加速的生物年龄是 OP 风险和相关死亡率的有力预测指标。KDMAgeAccel 和 PhenoAgeAccel 可作为识别 OP 风险较高个体的有价值的生物标志物,指导预防策略。