睡眠剥夺作为多系统生理应激源：共享机制与临床意义的综述。

文献信息

中文摘要

目的： 睡眠不足和睡眠紊乱日益被视为全身性而非仅限于神经系统的应激源。本叙述性综述综合了关于睡眠不足对认知、免疫、代谢、心血管、生殖和基因组影响的证据，并检验这些看似多样的生理后果是否反映数量有限的共同上游机制。在此，睡眠不足是一个总括性术语，指睡眠时长不足，涵盖睡眠限制和剥夺；睡眠碎片化、睡眠质量差、失眠障碍、阻塞性睡眠呼吸暂停和昼夜节律失调被视为不同但相互重叠的紊乱形式。
方法： 对PubMed、Google Scholar和ScienceDirect的结构化检索（2026年1月至8月）为遵循SANRA的叙述性综合提供了依据。优先纳入系统综述、荟萃分析、指南和大型观察性研究；实验性人体和临床前动物研究用于说明机制。每项原始来源的设计均使用五个预先设定的证据类别加以命名。未进行定量合并或偏倚风险评估。
结果： 三种机制反复出现：交感神经和下丘脑-垂体-肾上腺轴过度激活、低度全身性炎症以及昼夜节律和激素失同步。证据强度因系统而异。前瞻性队列的荟萃分析支持睡眠时长与2型糖尿病、心脑血管疾病和全因死亡率之间的U型关联，且睡眠规律性优于睡眠时长。对照人体实验支持海马编码受损、疫苗反应减弱以及食欲激素和能量平衡的不良变化。生殖和基因组证据较弱，主要依赖啮齿动物模型和小型横断面人体样本。仅睡眠时长与癌症发病率无一致关联，而睡眠质量差和昼夜节律紊乱与癌症进展和死亡率的关联更为一致。
结论： 睡眠时长、规律性、质量、连续性和昼夜节律一致性产生可区分的影响，最好被视为独立的临床干预目标。此处描述的机制汇聚具有产生假设的性质，而非已证实的因果通路：大多数人体证据为观察性，不能排除双向因果。在这些局限内，该框架可为咨询、干预设计和公共卫生信息传播提供依据。

英文摘要

PURPOSE: Insufficient and disrupted sleep are increasingly recognized as systemic, not narrowly neurological, stressors. This narrative review synthesizes evidence on the cognitive, immune, metabolic, cardiovascular, reproductive, and genomic consequences of insufficient sleep and examines whether these seemingly diverse physiological consequences reflect a limited number of shared upstream mechanisms. Here, insufficient sleep is an overarching term for inadequate sleep duration, encompassing restriction and deprivation; fragmentation, poor sleep quality, insomnia disorder, obstructive sleep apnea, and circadian misalignment are treated as distinct but overlapping forms of disruption.
METHODS: Structured searches of PubMed, Google Scholar, and ScienceDirect (January-August 2026) informed a SANRA-guided narrative synthesis. Systematic reviews, meta-analyses, guidelines, and large observational studies were prioritized; experimental human and preclinical animal studies illustrate mechanism. The design of each primary source is named using five prespecified evidence categories. No quantitative pooling or risk-of-bias assessment was performed.
RESULTS: Three mechanisms recur: sympathetic and hypothalamic-pituitary-adrenal axis hyperactivation, low-grade systemic inflammation, and circadian and hormonal desynchronization. Evidence strength varies by system. Meta-analyses of prospective cohorts support U-shaped associations of sleep duration with type 2 diabetes, cardio-cerebrovascular disease, and all-cause mortality, with sleep regularity outperforming duration. Controlled human experiments support impaired hippocampal encoding, attenuated vaccine responses, and adverse shifts in appetite hormones and energy balance. Reproductive and genomic evidence is weaker, resting largely on rodent models and small cross-sectional human samples. Sleep duration alone shows no consistent association with cancer incidence, whereas poor sleep quality and circadian disruption are linked more consistently to cancer progression and mortality.
CONCLUSIONS: Sleep duration, regularity, quality, continuity, and circadian alignment exert distinguishable influences and are best treated as separate clinical targets. The mechanistic convergence described here is hypothesis-generating rather than a demonstrated causal pathway: most human evidence is observational and bidirectional causation cannot be excluded. Within these limits, the framework informs counseling, intervention design, and public health messaging.