Zhao Huanqiang, Wen Ping, Xiong Yu, Xu Qixin, Zi Yang, Zheng Xiujie, Chen Shiguo, Qin Yueyuan, Shao Shuyi, Tu Xinzhi, Zheng Zheng, Li Xiaotian
Shenzhen Maternity and Child Healthcare Hospital, Shenzhen, Guangdong.
Obstetrics and Gynecology Hospital, Fudan University.
J Hypertens. 2024 Sep 1;42(9):1606-1614. doi: 10.1097/HJH.0000000000003771. Epub 2024 May 23.
Unhealthy sleep patterns are common during pregnancy and have been associated with an increased risk of developing hypertensive disorders of pregnancy (HDPs) in observational studies. However, the causality underlying these associations remains uncertain. This study aimed to evaluate the potential causal association between seven sleep traits and the risk of HDPs using a two-sample Mendelian randomization study.
Genome-wide association study (GWAS) summary statistics were obtained from the FinnGen consortium, UK Biobank, and other prominent consortia, with a focus on individuals of European ancestry. The primary analysis utilized an inverse-variance-weighted MR approach supplemented by sensitivity analyses to mitigate potential biases introduced by pleiotropy. Furthermore, a two-step MR framework was employed for mediation analyses.
The data analyzed included 200 000-500 000 individuals for each sleep trait, along with approximately 15 000 cases of HDPs. Genetically predicted excessive daytime sleepiness (EDS) exhibited a significant association with an increased risk of HDPs [odds ratio (OR) 2.96, 95% confidence interval (95% CI) 1.40-6.26], and the specific subtype of preeclampsia/eclampsia (OR 2.97, 95% CI 1.06-8.3). Similarly, genetically predicted obstructive sleep apnea (OSA) was associated with a higher risk of HDPs (OR 1.27, 95% CI 1.09-1.47). Sensitivity analysis validated the robustness of these associations. Mediation analysis showed that BMI mediated approximately 25% of the association between EDS and HDPs, while mediating up to approximately 60% of the association between OSA and the outcomes. No statistically significant associations were observed between other genetically predicted sleep traits, such as chronotype, daytime napping, sleep duration, insomnia, snoring, and the risk of HDPs.
Our findings suggest a causal association between two sleep disorders, EDS and OSA, and the risk of HDPs, with BMI acting as a crucial mediator. EDS and OSA demonstrate promise as potentially preventable risk factors for HDPs, and targeting BMI may represent an alternative treatment strategy to mitigate the adverse impact of sleep disorders.
孕期不健康的睡眠模式很常见,在观察性研究中,其与妊娠高血压疾病(HDPs)发生风险增加有关。然而,这些关联背后的因果关系仍不确定。本研究旨在使用两样本孟德尔随机化研究评估七种睡眠特征与HDPs风险之间的潜在因果关联。
全基因组关联研究(GWAS)汇总统计数据来自芬兰基因联盟、英国生物银行和其他知名联盟,重点关注欧洲血统个体。主要分析采用逆方差加权MR方法,并辅以敏感性分析以减轻多效性引入的潜在偏差。此外,采用两步MR框架进行中介分析。
分析的数据包括每种睡眠特征的200000 - 500000名个体,以及约15000例HDPs病例。基因预测的白天过度嗜睡(EDS)与HDPs风险增加显著相关[优势比(OR)2.96,95%置信区间(95%CI)1.40 - 6.26],以及子痫前期/子痫的特定亚型(OR 2.97,95%CI 1.06 - 8.3)。同样,基因预测的阻塞性睡眠呼吸暂停(OSA)与HDPs风险较高相关(OR 1.27,95%CI 1.09 - 1.47)。敏感性分析验证了这些关联的稳健性。中介分析表明,BMI介导了EDS与HDPs之间约25%的关联,同时介导了OSA与结局之间高达约60%的关联。在其他基因预测的睡眠特征,如昼夜节律类型、白天小睡、睡眠时间、失眠、打鼾与HDPs风险之间未观察到统计学显著关联。
我们的研究结果表明,两种睡眠障碍,即EDS和OSA,与HDPs风险之间存在因果关联,并以BMI作为关键中介因素。EDS和OSA有望成为HDPs潜在的可预防风险因素,针对BMI可能代表一种减轻睡眠障碍不良影响的替代治疗策略。