Depner Christopher M
Department of Health and Kinesiology, University of Utah, Salt Lake City, UT, United States.
Front Sleep. 2023;2. doi: 10.3389/frsle.2023.1293941. Epub 2023 Dec 4.
Approximately one in three adults in the United States sleeps less than the recommended 7 h per night. Decades of epidemiological data and data from experimental sleep restriction studies demonstrate short sleep duration is associated with adverse cardiometabolic risk, including risk of type 2 diabetes and cardiovascular disease. However, the precise mechanisms underlying this risk are not fully elucidated and there is a lack of sleep-based interventions designed to mitigate such risk. One strategy to overcome these limitations is to develop biomarkers that link habitual short sleep duration with adverse cardiometabolic risk. Such biomarkers could inform biochemical mechanisms, identify new targets for interventions, support precision medicine by identifying individuals most likely to benefit from sleep-based interventions, and ultimately lead to improved cardiometabolic health in people with habitual short sleep durations. Early progress demonstrates proof-of-principle that omics-based technologies are a viable approach to create biochemical signatures (biomarkers) of short sleep duration, primarily derived from acute studies of experimental sleep restriction. Yet, much work remains. Notably, studies that translate early findings from experimental sleep restriction to free-living adults with habitual short sleep duration have high potential to advance the field. Such studies also create an exciting opportunity for larger randomized controlled trials that simultaneously identify biomarkers of habitual short sleep duration and evaluate the efficacy of sleep-based interventions. Ultimately, early progress in developing molecular biomarkers of short sleep duration combined with the prior decades of progress in the sleep and metabolism fields provide the foundation for exciting progress in the biomarker development space.
在美国,约三分之一的成年人每晚睡眠时间少于建议的7小时。数十年的流行病学数据以及实验性睡眠限制研究的数据表明,短睡眠时间与不良心脏代谢风险相关,包括2型糖尿病和心血管疾病风险。然而,这种风险背后的确切机制尚未完全阐明,且缺乏旨在减轻此类风险的基于睡眠的干预措施。克服这些局限性的一种策略是开发将习惯性短睡眠时间与不良心脏代谢风险联系起来的生物标志物。此类生物标志物可以揭示生化机制,确定新的干预靶点,通过识别最有可能从基于睡眠的干预措施中获益的个体来支持精准医学,并最终改善习惯性短睡眠时间人群的心脏代谢健康状况。早期进展证明了基于组学技术是创建短睡眠时间生化特征(生物标志物)的可行方法,主要来自实验性睡眠限制的急性研究。然而,仍有许多工作要做。值得注意的是,将实验性睡眠限制的早期发现转化为习惯性短睡眠时间的自由生活成年人的研究有很大潜力推动该领域的发展。此类研究还为更大规模的随机对照试验创造了一个令人兴奋的机会,这些试验可以同时识别习惯性短睡眠时间的生物标志物并评估基于睡眠的干预措施的疗效。最终,短睡眠时间分子生物标志物开发的早期进展,结合睡眠和代谢领域此前数十年的进展,为生物标志物开发领域取得令人兴奋的进展奠定了基础。