Lin Shujuan, Gu Simeng, Li Junpeng, Gong Qinghai, Zhang Yan, Tong Feng, Xu Yanchang, Jiang Danjie
Key Laboratory of Translational Tumor Medicine in Fujian Province, School of Basic Medicine Science, Putian University, Putian, China.
Zhejiang Provincial Center for Disease Control and Prevention, Hangzhou, China.
Sleep Breath. 2025 Sep 18;29(5):288. doi: 10.1007/s11325-025-03452-7.
The impact of sleep patterns on gastrointestinal cancer mortality has not been comprehensively explored. Moreover, the interaction between sleep patterns and genetic susceptibility with gastrointestinal cancer mortality remains uncertain.
The study included a total of 379 845 participants from the UK Biobank. A poor sleep pattern was defined by short sleep (< 7 h/day) or long sleep (> 9 h/day), late chronotype, frequent insomnia, snoring, and frequent daytime dozing. The outcomes were mortality of any gastrointestinal cancers and six site-specific gastrointestinal cancers. Polygenic risk score was generated to characterize genetic risk. Multivariable cox proportional hazards regression models were use to analyze the associations of sleep patterns and genetic susceptibility with gastrointestinal cancer mortality.
A poor sleep pattern was associated with the increased risk of mortality from overall gastrointestinal cancer (HR 1.32, 95% CI 1.16-1.49), esophagus cancer (HR 1.37, 95% CI 1.02-1.85) and liver cancer (HR 2.01, 95% CI 1.48-2.74). Participants with a poor sleep pattern and high genetic risk combination had the highest mortality risks for esophagus, stomach, colorectal, and liver cancer. Significant multiplicative interactions (HR 1.51, 95% CI 1.05-2.18) and additive interactions (RERI 0.54, 95% CI 0.13-0.95; AP 0.34, 95% CI 0.10-0.58) of an intermediate sleep pattern and high genetic risk were observed on esophagus cancer mortality.
A poor sleep pattern is associated with increased risks of gastrointestinal cancer mortality independent of the conventional risk factors, and the association is modified by genetic susceptibility.
睡眠模式对胃肠道癌死亡率的影响尚未得到全面探究。此外，睡眠模式与遗传易感性在胃肠道癌死亡率方面的相互作用仍不明确。
该研究纳入了英国生物银行的379845名参与者。不良睡眠模式定义为睡眠短（<7小时/天）或睡眠长（>9小时/天）、晚睡型、频繁失眠、打鼾以及频繁日间打盹。结局指标为任何胃肠道癌和六种特定部位胃肠道癌的死亡率。生成多基因风险评分以表征遗传风险。使用多变量考克斯比例风险回归模型分析睡眠模式和遗传易感性与胃肠道癌死亡率的关联。
不良睡眠模式与总体胃肠道癌（风险比1.32，95%置信区间1.16 - 1.49）、食管癌（风险比1.37，95%置信区间1.02 - 1.85）和肝癌（风险比2.01，95%置信区间1.48 - 2.74）死亡风险增加相关。睡眠模式不良且遗传风险高的参与者在食管癌、胃癌、结直肠癌和肝癌方面具有最高的死亡风险。在食管癌死亡率方面，观察到中等睡眠模式和高遗传风险之间存在显著的相乘交互作用（风险比1.51，95%置信区间1.05 - 2.18）和相加交互作用（相对超额危险度增量0.54，95%置信区间0.13 - 0.95；归因比例0.34，95%置信区间0.10 - 0.58）。
不良睡眠模式与胃肠道癌死亡率增加相关，独立于传统风险因素，且该关联受到遗传易感性的影响。
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