Going to sleep between 10 and 11 p.m. associated with lowest risk of developing CVD

Accelerometer-derived sleep onset timing and cardiovascular disease incidence: a UK Biobank cohort study

Literature - Nikbakhtian S, Reed AB, Obika BD et al. - EHJ - Digital Health, 2021, ztab088, https://doi.org/10.1093/ehjdh/ztab088

Introduction and methods

Aim of the study

Good sleep is of great importance for a person’s health and wellbeing. Studies have suggested that circadian rhythm disruption may be associated with increased risk for CVD [1-3]. Previous studies on the relationship between sleep and risk of developing CVD often used self-reported sleep measures and a small number of participants [4-5]. This study assessed the association between sleep timing and risk for CVD using objectively measured sleep parameters using wrist-worn accelerometers in a large UK Biobank cohort.

Study design

A total of 88026 participants with accelerometer data (57.9% women, mean age 61.43 ± 7.8 years) who were enrolled in the UK Biobank were included in the analyses of this study. Participants wore the accelerometer on their wrist for 7 days and continued with their normal activities. Participants were categorized according to sleep onset time (SOT): SOT <10:00 p.m., 10:00 p.m. to 10:59 p.m., 11:00 p.m. to 11:59 p.m., ≥12:00 a.m. Mean follow-up was 5.7 ± 0.49 years.


CVD incidence was defined as the first occurrence of a CVD event (MI, HF, chronic IHD, stroke, or TIA). Fatal CVD outcomes were not included in the analysis.

Main results

  • A U-shaped relationship was found between SOT and CVD incidence. SOTs between 10:00 p.m. and 10:59 p.m. had the lowest incidence rate of CVD and the incidence rate increased at earlier and later SOTs.
  • With SOTs between 10:00 p.m. and 10:59 p.m. as the reference group, HR for CVD incidence in the SOT categories <10 p.m., 11:00 p.m. to 11:59 p.m., and ≥12 a.m. were 1.24 (95% CI 1.10-1.39, P<0.005), 1.12 (95% CI 1.01-1.25, P= 0.04), and 1.25 (95% CI 1.02-1.52, P=0.03), respectively, after adjustment for sleep duration, sleep irregularity and established CVD risk factors.
  • The association between SOT and CVD incidence was more pronounced in women than in men. SOT <10:00 p.m. and ≥12:00 a.m. were associated with increased incidence rates of CVD in women (HR 1.34, 95% CI 1.11-1.61, P<0.005 and HR 1.63, 95% CI 1.20-2.21, P<0.005, respectively). In contrast, only SOTs<10:00 pm were associated with increased CVD incidence in men (HR = 1.17, 95% CI, 1.01-1.35, P=0.03).


Sleep onset between 10:00pm and 10:59pm was associated with the lowest risk of developing CVD, even after adjustment for sleep duration, sleep irregularity and established CVD risk factors. The observed relationship between SOT and CVD incidence was U-shaped with higher CVD risk at earlier and later sleep onset, particularly in women.


1. Scheer FA, Hilton MF, Mantzoros CS, Shea SA. Adverse metabolic and cardiovascular consequences of circadian misalignment. Proc Natl Acad Sci USA 2009;106:4453–4458.

2. Portaluppi F, Tiseo R, Smolensky MH, Hermida RC, Ayala DE, Fabbian F. Circadian rhythms and cardiovascular health. Sleep Med Rev 2012;16:151–166.

3. Morris CJ, Yang JN, Garcia JI, et al. Endogenous circadian system and circadian misalignment impact glucose tolerance via separate mechanisms in humans. Proc Natl Acad Sci USA 2015;112:E2225–E2234.

4. Huang T, Mariani S, Redline S. Sleep irregularity and risk of cardiovascular events: the multi-ethnic study of atherosclerosis. J Am Coll Cardiol 2020;75:991–999.

5. Yan B, Li R, Li J, et al. Sleep timing may predict congestive heart failure: a community-based cohort study. J Am Heart Assoc 2021;10:e018385.

Find this article online at EHJ - Digital Health.

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