Xie Qihang, Qu Haoran, Xie Siyu, Li Wenhao, Ouyang Rui, Zhang Chengxiang, Du Ming
Department of Cardiothoracic Surgery, The First Affiliated Hospital of Chongqing Medical University, 1 Youyi Road, Yuzhong District, Chongqing, China.
Department of Child Development, Graduate School of Child Development, Osaka University, Suita, Osaka, Japan.
Sci Rep. 2025 May 23;15(1):17880. doi: 10.1038/s41598-025-00114-2.
Accelerated biological aging has been suggested to be an important risk factor for age-related diseases, but its role in the development of lung cancer is still unclear. The aim of this study was to analyze the relationship between biological aging and lung cancer and its impact on mortality using the NHANES database. We calculated the chronological age-adjusted biological age of 40,765 participants in the U.S. National Health and Nutrition Examination Survey (NHANES) database from 2001 to 2020 using the phenotypic age (PhenoAge) method. Both cross-sectional and longitudinal analyses were performed to assess the associations of biological aging with lung cancer prevalence and mortality in the cohort. Logistic regression and Cox proportional hazards models were used to examine these associations. Sensitivity analysis was conducted using propensity score matching (PSM). Our results indicated that accelerated biological aging was positively associated with an increased risk of developing lung cancer. Individuals with accelerated aging had a greater risk of developing lung cancer than nonaccelerated aging individuals did, with odds ratios of 2.60 (full adjustment 95% CI 1.59-4.22, p < 0.001). According to the fully adjusted models, participants in the Q4 subgroup had a 334% greater risk of developing lung cancer. In addition, accelerated biological aging was positively associated with all-cause mortality among individuals with lung cancer. Our study demonstrated that the identification of individuals with accelerated biological aging represents a promising strategy for the identification of populations at elevated risk of developing lung cancer and serves as an independent predictor of mortality in this population.
加速生物衰老被认为是与年龄相关疾病的一个重要风险因素，但其在肺癌发生发展中的作用仍不清楚。本研究旨在利用美国国家健康与营养检查调查（NHANES）数据库分析生物衰老与肺癌之间的关系及其对死亡率的影响。我们使用表型年龄（PhenoAge）方法计算了2001年至2020年美国国家健康与营养检查调查（NHANES）数据库中40765名参与者按实足年龄调整后的生物年龄。进行了横断面分析和纵向分析，以评估该队列中生物衰老与肺癌患病率和死亡率之间的关联。使用逻辑回归和Cox比例风险模型来检验这些关联。使用倾向评分匹配（PSM）进行敏感性分析。我们的结果表明，加速生物衰老与患肺癌风险增加呈正相关。加速衰老的个体比未加速衰老的个体患肺癌的风险更高，优势比为2.60（完全调整9
5%置信区间1.59 - 4.22，p < 0.001）。根据完全调整模型，Q4亚组的参与者患肺癌的风险高334%。此外，加速生物衰老与肺癌患者的全因死亡率呈正相关。我们的研究表明，识别加速生物衰老的个体是识别患肺癌风险升高人群的一种有前景的策略，并且可作为该人群死亡率的独立预测指标。
