학술논문
Sleep duration and napping in relation to colorectal and gastric cancer in the MCC-Spain study.
Document Type
Article
Author
Papantoniou, Kyriaki; Castaño-Vinyals, Gemma; Espinosa, Ana; Turner, Michelle C.; Martín-Sánchez, Vicente; Casabonne, Delphine; Aragonés, Nuria; Gómez-Acebo, Inés; Ardanaz, Eva; Jimenez-Moleon, Jose-Juan; Amiano, Pilar; Molina-Barceló, Ana; Alguacil, Juan; Fernández-Tardón, Guillermo; Huerta, José María; Hernández-Segura, Natalia; Perez-Gomez, Beatriz; Llorca, Javier; Vidán-Alli, Juana; Olmedo-Requena, Rocıo
Source
Subject
*COLORECTAL cancer
*SLEEP
*STOMACH cancer
*ETIOLOGY of cancer
*SOCIODEMOGRAPHIC factors
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Language
ISSN
2045-2322
Abstract
Sleep duration is a novel and potentially modifiable risk factor for cancer. We evaluated the association of self-reported sleep duration and daytime napping with odds of colorectal and gastric cancer. We included 2008 incident colorectal cancer cases, 542 gastric cancer cases and 3622 frequency-matched population controls, recruited in the MCC-Spain case–control study (2008–2013). Sleep information, socio-demographic and lifestyle characteristics were obtained through personal interviews. Multivariable adjusted logistic regression models were used to estimate odds ratios (OR) with 95% confidence intervals (CI) for cancer, across categories of sleep duration (≤ 5, 6, 7, 8, ≥ 9 hours/day), daytime napping frequency (naps/week) and duration (minutes/nap). Compared to 7 hours of sleep, long sleep was associated with increased odds of colorectal (OR≥9 hours: 1.59; 95%CI 1.30–1.94) and gastric cancer (OR≥9 hours: 1.95; 1.37–2.76); short sleep was associated with increased odds of gastric cancer (OR≤5 hours: 1.32; 0.93–1.88). Frequent and long daytime naps increased the odds of colorectal (OR6–7 naps/week, ≥30 min: 1.32; 1.14–1.54) and gastric cancer (OR6–7 naps/week, ≥30 min: 1.56; 1.21–2.02). Effects of short sleep and frequent long naps were stronger among participants with night shift-work history. Sleep and circadian disruption may jointly play a role in the etiology of colorectal and gastric cancer. [ABSTRACT FROM AUTHOR]