Williams Jacob Corum, Hum Ryan Malcolm, Alam Uazman, Zhao Sizheng Steven
NIHR/Wellcome Trust Clinical Research Facility, Manchester University NHS Foundation Trust, Grafton St, Manchester, M13 9WL, UK.
Versus Arthritis Centre for Genetics and Genomics, Centre for Musculoskeletal Research, The University of Manchester, Manchester, UK.
Rheumatol Int. 2024 Dec;44(12):2961-2966. doi: 10.1007/s00296-024-05636-y. Epub 2024 Jun 25.
Sleep disturbance has been associated with chronic widespread pain (CWP), but their causal relationship remains unclear. We aimed to examine the causal relationship and direction between CWP and sleep traits, namely insomnia, sleep duration and chronotype, using Mendelian Randomization.
We used genetic association data from ~0.5 million individuals and up to 1.8 million controls from the UK Biobank (UKB). All traits were defined predominantly by self-report. Short sleep duration was defined as average ≤6 hours per 24 hours. Chronotype refers to the inclination to sleep at certain times where some wake and go to bed early ('morning' person), and others wake and go to sleep later ('evening' person). To permit use of the largest available genetic association data, we used the Causal Analysis Using Summary Effect estimates (CAUSE) method, which allows for sample overlap.
Insomnia (OR 1.009, 95% credible interval 1.005, 1.014; p = 0.018 that the causal model is a better fit than non-causal model) and short sleep duration (OR 1.060, 95%CrI 1.038, 1.083; p = 0.040) were causally associated with increased risk of CWP, with limited evidence for reverse causation. There was no evidence in support of long sleep duration or chronotype being associated with CWP.
This study suggest that insomnia and short sleep duration (≤6 hours) are associated with an increased risk of CWP. Improving short sleep duration and insomnia, rather than chronotype, may be effective in reducing the risk of CWP, although these results should be replicated in epidemiological and interventional studies.
睡眠障碍与慢性广泛性疼痛（CWP）有关，但其因果关系仍不明确。我们旨在使用孟德尔随机化方法研究CWP与睡眠特征（即失眠、睡眠时间和昼夜节律类型）之间的因果关系及方向。
我们使用了来自英国生物银行（UKB）约50万个体和多达180万对照的基因关联数据。所有特征主要通过自我报告定义。短睡眠时间定义为每24小时平均≤6小时。昼夜节律类型是指在某些时间入睡的倾向，有些人醒得早且睡得早（“早晨型”的人），而另一些人醒得晚且睡得晚（“晚上型”的人）。为了能够使用最大可用的基因关联数据，我们使用了基于汇总效应估计的因果分析（CAUSE）方法，该方法允许样本重叠。
失眠（比值比1.009，95%可信区间1.005，1.014；因果模型比非因果模型拟合更好的p = 0.018）和短睡眠时间（比值比1.060，95%可信区间1.038，1.083；p = 0.040）与CWP风险增加存在因果关联，反向因果关系的证据有限。没有证据支持长睡眠时间或昼夜节律类型与CWP有关。
本研究表明，失眠和短睡眠时间（≤6小时）与CWP风险增加有关。改善短睡眠时间和失眠，而非昼夜节律类型，可能对降低CWP风险有效，尽管这些结果应在流行病学和干预性研究中得到重复验证。
