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

Author:

Nikbakhtian Shahram1,Reed Angus B1ORCID,Obika Bernard Dillon12ORCID,Morelli Davide13ORCID,Cunningham Adam C1ORCID,Aral Mert1ORCID,Plans David145ORCID

Affiliation:

1. Huma Therapeutics, 13-14th Floor, Millbank Tower, 21-24 Millbank, London SW1P 4QP, UK

2. Barking, Haveridge and Redbridge University Hospitals NHS Trust, London, UK

3. Department of Engineering Science, Institute of Biomedical Engineering, University of Oxford, Parks Road, Oxford, OX1 3PJ, UK

4. Department of Science, Innovation, Technology and Entrepreneurship, University of Exeter, Rennes Drive, Exeter EX4 4PU, UK

5. Department of Experimental Psychology, University of Oxford, Anna Watts Building, Woodstock Rd, Oxford OX2 6GG, UK

Abstract

Abstract Aims Growing evidence suggests that poor sleep health is associated with cardiovascular risk. However, research in this area often relies upon recollection dependent questionnaires or diaries. Accelerometers provide an alternative tool for measuring sleep parameters objectively. This study examines the association between wrist-worn accelerometer-derived sleep onset timing and cardiovascular disease (CVD). Methods and results We derived sleep onset and waking up time from accelerometer data collected from 103 712 UK Biobank participants over a period of 7 days. From this, we examined the association between sleep onset timing and CVD incidence using a series of Cox proportional hazards models. A total of 3172 cases of CVD were reported during a mean follow-up period of 5.7 (±0.49) years. An age- and sex-controlled base analysis found that sleep onset time of 10:00 p.m.–10:59 p.m. was associated with the lowest CVD incidence. An additional model, controlling for sleep duration, sleep irregularity, and established CVD risk factors, did not attenuate this association, producing hazard ratios of 1.24 (95% confidence interval, 1.10–1.39; P < 0.005), 1.12 (1.01–1.25; P = 0.04), and 1.25 (1.02–1.52; P = 0.03) for sleep onset <10:00 p.m., 11:00 p.m.–11:59 p.m., and ≥12:00 a.m., respectively, compared to 10:00 p.m.–10:59 p.m. Importantly, sensitivity analyses revealed this association with increased CVD risk was stronger in females, with only sleep onset <10:00 p.m. significant for males. Conclusions Our findings suggest the possibility of a relationship between sleep onset timing and risk of developing CVD, particularly for women. We also demonstrate the potential utility of collecting information about sleep parameters via accelerometry-capable wearable devices, which may serve as novel cardiovascular risk indicators.

Funder

Huma Therapeutics Ltd

Publisher

Oxford University Press (OUP)

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