Wu Shuai, Peng MaoHuan, Zuo YuHua, Wang MengMeng, Feng ZhaoYan, Wang HuanHuan, Sun MingZe, Gu JiaHui, Wang XinRu, Han Fang, Dong XiaoSong
Division of Sleep Medicine, Peking University People's Hospital, Beijing, China.
Division of Sleep Medicine, Peking University People's Hospital, Beijing, China; School of Nursing, Peking University, Beijing, China.
Sleep Med. 2025 Oct;134:106722. doi: 10.1016/j.sleep.2025.106722. Epub 2025 Aug 14.
Social jetlag, representing the misalignment between endogenous circadian rhythms and socially imposed sleep schedules, has been associated with various adverse health outcomes. However, its potential relationship with obstructive sleep apnea (OSA) severity, as quantified by the apnea-hypopnea index (AHI), remains unclear.
This retrospective study analyzed data from participants with OSA (AHI ≥5 events/hour) who completed sleep questionnaires and underwent polysomnography at our sleep center. Exclusions included non-OSA, prior OSA treatment, shift work, sleep-affecting medication use, or incomplete data. Social jetlag was defined as the actual difference between mid-sleep on work days and free days, and categorized as minimal (<1 h), moderate (1 to <2 h), and severe (≥2 h). Multiple linear regression assessed the association between social jetlag and AHI, adjusting for age, gender, body mass index (BMI), history of smoking and alcohol, hypertension, hyperlipidemia, and diabetes. Mediation analysis evaluated the Epworth Sleepiness Scale (ESS) as a mediator, with subgroup analyses and generalized additive models (GAM) exploring effect modification and non-linearity.
Among 2383 analyzed participants, severe social jetlag was independently associated with higher AHI (β = 6.90; 95 % CI: 2.18 to 11.61; p = 0.004; p-trend = 0.014), unlike the moderate group (p = 0.389). ESS mediated 19.4 % of this effect (indirect effect β = 0.46; 95 % CI: 0.22 to 0.72; p < 0.001). In a matched cohort analysis stratified by social jetlag severity (n = 637), AHI and ESS rose with social jetlag severity (AHI: 34.9 vs. 39.4 vs. 45.5 events/hour, p < 0.001; ESS: 10.1 vs. 11.2 vs. 11.8, p = 0.015), while habitual sleep duration decreased (7.0 vs. 6.8 vs. 6.6 h; p = 0.013). Stronger associations were observed in males (β = 2.94; 95 % CI: 1.34 to 4.54; p < 0.001; p-interaction <0.001) and smokers (β = 3.31; 95 % CI: 0.90 to 5.71; p = 0.007; p-interaction = 0.003), with significant effects in BMI 24-28 kg/m, non-hypertensive, and non-diabetic subgroups (all p < 0.05). GAM analysis revealed a gradual, non-linear AHI increase with social jetlag below 2 h, accelerating beyond 2 h.
Severe Social jetlag independently increases AHI in individuals with OSA, partially mediated by daytime sleepiness, with pronounced effects in males and smokers. These findings suggest circadian misalignment as a potentially modifiable factor influencing OSA severity.
社会时差反映了内源性昼夜节律与社会强加的睡眠时间表之间的失调，与多种不良健康后果相关。然而，其与阻塞性睡眠呼吸暂停（OSA）严重程度（通过呼吸暂停低通气指数（AHI）量化）之间的潜在关系仍不清楚。
这项回顾性研究分析了在我们睡眠中心完成睡眠问卷并接受多导睡眠监测的阻塞性睡眠呼吸暂停患者（AHI≥5次/小时）的数据。排除标准包括非阻塞性睡眠呼吸暂停、既往阻塞性睡眠呼吸暂停治疗史、轮班工作、使用影响睡眠的药物或数据不完整。社会时差定义为工作日和休息日中间睡眠时间的实际差异，并分为最小（<1小时）、中度（1至<2小时）和重度（≥2小时）。多元线性回归评估社会时差与AHI之间的关联，并对年龄、性别、体重指数（BMI）、吸烟和饮酒史、高血压、高脂血症和糖尿病进行校正。中介分析评估爱泼华嗜睡量表（ESS）作为中介因素，亚组分析和广义相加模型（GAM）探索效应修正和非线性关系。
在2383名分析参与者中，与中度组（p = 0.389）不同，重度社会时差与较高的AHI独立相关（β = 6.90；95%CI：2.18至11.61；p = 0.004；p趋势 = 0.014）。ESS介导了这种效应的19.4%（间接效应β = 0.46；95%CI：0.22至0.72；p < 未找到相关内容0.001）。在按社会时差严重程度分层的匹配队列分析中（n = 637），AHI和ESS随着社会时差严重程度的增加而升高（AHI：3与阻塞性睡眠呼吸暂停严重程度相关的因素4.9次/小时 vs. 39.4次/小时 vs. 45.5次/小时，p < 0.001；ESS：10.1 vs. 11.2 vs. 11.8，p =未找到相关内容0.015），而习惯性睡眠时间减少（7.0小时 vs. 6.8小时 vs. 6.6小时；p = 0.013）。在男性（β = 2.94；95%CI：1.34至4.54；p < 0.001；p交互作用 < 0.001）和吸烟者（β = 3.31；95%CI：0.90至5.71；p = 0.007；p交互作用 = 0.003）中观察到更强的关联，在BMI为24 - 28 kg/m²、非高血压和非糖尿病亚组中具有显著影响（均p < 0.05）。GAM分析显示，社会时差低于2小时时，AHI呈逐渐非线性增加，超过2小时后加速增加。
严重社会时差独立增加阻塞性睡眠呼吸暂停患者的AHI，部分由白天嗜睡介导，在男性和吸烟者中影响显著。这些发现表明昼夜节律失调是影响阻塞性睡眠呼吸暂停严重程度的一个潜在可改变因素。
