Blood pressure · 2025
Physical Activity, sleep disorders and hypertension: observational and Mendelian randomization analyses.
СтатьяНаблюдательное исследованиеНазвание и аннотация: Перевод в очереди
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Qiu Baizhi, Wang Qin, Ling Zhishan, Wen Shuyang, Yao Qiuru, Xiao Yupeng, Xu Xiaoyi, Li Zifan, Long Siying, Yang Tingting, Liu Wei, Huang Guozhi, Zeng Qing
Аннотация
BACKGROUND: The interrelationships between physical activity (PA), sleep disorders, and hypertension remain incompletely characterised, particularly regarding potential interactions between PA and sleep disorders on hypertension risk. This study aimed to investigate these associations using complementary epidemiological approaches.
METHODS: We conducted a population-based observational analysis of 18,052 adults aged ≥18 years using data from the National Health and Nutrition Examination Survey, a nationally representative cross-sectional survey (2005-2018). Weighted multivariate logistic regression models were used to examine the associations between PA, sleep disorders, and hypertension, as well as the interaction effect of PA and sleep disorders on hypertension. Additionally, we performed a two-sample Mendelian randomisation (MR) analysis was conducted to assess the causal relationship between PA, sleep disorders, and hypertension.
RESULTS: The analysis of observational data shows that sleep disorders are significantly associated with a higher risk of hypertension, with an odds ratio (OR) of 1.61 (95% CI: 1.10-2.35, p = 0.015). Restricted Cubic Spline (RCS) analysis revealed an S-shaped dose-response relationship between PA and hypertension (P-non-linear < 0.001). The MR analysis results were consistent with these findings.
CONCLUSIONS: Convergent evidence from observational and genetic analyses identified sleep disorders as an independent risk factor for hypertension. The non-monotonic S-shaped association between PA and hypertension underscored the importance of personalised activity prescriptions for cardiovascular risk optimisation. Notably, no significant interaction was observed between PA and sleep disorders, suggesting that their effects on hypertension are likely independent.
METHODS: We conducted a population-based observational analysis of 18,052 adults aged ≥18 years using data from the National Health and Nutrition Examination Survey, a nationally representative cross-sectional survey (2005-2018). Weighted multivariate logistic regression models were used to examine the associations between PA, sleep disorders, and hypertension, as well as the interaction effect of PA and sleep disorders on hypertension. Additionally, we performed a two-sample Mendelian randomisation (MR) analysis was conducted to assess the causal relationship between PA, sleep disorders, and hypertension.
RESULTS: The analysis of observational data shows that sleep disorders are significantly associated with a higher risk of hypertension, with an odds ratio (OR) of 1.61 (95% CI: 1.10-2.35, p = 0.015). Restricted Cubic Spline (RCS) analysis revealed an S-shaped dose-response relationship between PA and hypertension (P-non-linear < 0.001). The MR analysis results were consistent with these findings.
CONCLUSIONS: Convergent evidence from observational and genetic analyses identified sleep disorders as an independent risk factor for hypertension. The non-monotonic S-shaped association between PA and hypertension underscored the importance of personalised activity prescriptions for cardiovascular risk optimisation. Notably, no significant interaction was observed between PA and sleep disorders, suggesting that their effects on hypertension are likely independent.