Department of Cardiovascular Surgery, the First Affiliated Hospital of Zhejiang University School of Medicine, Number 79 Qingchun Road, Hangzhou, China.
J Transl Med. 2024 Feb 16;22(1):160. doi: 10.1186/s12967-024-04956-8.
Telomere length has long been recognized as a valuable biomarker of aging and is inversely correlated with chronological age. Various lifestyle factors have been implicated in telomere shortening or preservation; however, the association between lifestyle factors and telomere length remains controversial. To address this issue, we conducted a Mendelian randomization (MR) analysis to investigate the potential causal associations between multiple lifestyle factors and telomere length.
Independent genetic variants strongly associated with lifestyle factors (tobacco smoking, sleep duration, insomnia, and physical activity) were selected as instrumental variables from corresponding genome-wide association studies (GWASs). Summary-level data for telomere length was obtained from a GWAS comprising 472,174 European ancestries. Univariable and multivariable MR analyses were performed to assess the relationships.
The genetic liability to lifetime smoking was robustly associated with shorter telomere length (odd ratio [OR]: 0.882; 95% confidence interval [CI]: 0.847-0.918). Genetically predicted insomnia was also linked to shorter telomere length (OR: 0.972; 95% CI: 0.959-0.985), while no significant association was observed between sleep duration and telomere length. Furthermore, a suggestive association was found between moderate-to-vigorous physical activity and longer telomere length (OR: 1.680; 95% CI: 1.115-2.531). In multivariable MR analyses, adjusting for potential mediators such as body mass index, type 2 diabetes, alcohol consumption, and alcohol use disorder, the associations of lifetime smoking and insomnia with telomere length remained robust.
Our findings suggest that smoking and insomnia may contribute to telomere shortening, while physical activity may play a role in telomere length maintenance. These findings underscore the importance of managing positive risk factors and adopting a healthy lifestyle to promote telomere health.
端粒长度长期以来一直被认为是衰老的有价值的生物标志物,与实际年龄呈负相关。各种生活方式因素与端粒缩短或保存有关;然而,生活方式因素与端粒长度之间的关系仍然存在争议。为了解决这个问题,我们进行了孟德尔随机化(MR)分析,以研究多种生活方式因素与端粒长度之间的潜在因果关系。
从相应的全基因组关联研究(GWAS)中选择与生活方式因素(吸烟、睡眠时间、失眠和体力活动)强烈相关的独立遗传变异作为工具变量。端粒长度的汇总水平数据来自一项包含 472,174 个欧洲血统的 GWAS。进行单变量和多变量 MR 分析以评估关系。
终生吸烟的遗传易感性与较短的端粒长度密切相关(比值比 [OR]:0.882;95%置信区间 [CI]:0.847-0.918)。遗传预测的失眠也与较短的端粒长度有关(OR:0.972;95% CI:0.959-0.985),而睡眠时间与端粒长度之间没有显著关联。此外,中度至剧烈体力活动与较长的端粒长度之间存在提示性关联(OR:1.680;95% CI:1.115-2.531)。在多变量 MR 分析中,调整潜在中介因素,如体重指数、2 型糖尿病、饮酒和酒精使用障碍,终生吸烟和失眠与端粒长度的关联仍然稳健。
我们的研究结果表明,吸烟和失眠可能导致端粒缩短,而体力活动可能在端粒长度维持中发挥作用。这些发现强调了管理积极风险因素和采取健康生活方式以促进端粒健康的重要性。