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Accelerometer-derived sleep timing and CVD — UK Biobank cohort study

There is a possible relationship between sleep onset timing and the risk of developing cardiovascular disease (CVD), particularly for women, found a UK Biobank cohort study.

Cardiovascular disease (CVD) continues to be the most significant cause of mortality worldwide, with an estimated 18.6 million deaths each year. Primary prevention of it has become a mainstay of addressing this considerable global challenge. Most clinical efforts are directed towards minimising modifiable risk factors through lifestyle changes and medical intervention.

Traditional modifiable risk factors are well-defined, including hypertension, obesity, diabetes, smoking, and hypercholesterolaemia. The impact of these factors has been shown to be reduced through lifestyle changes. However, poor population-level adherence to lifestyle advice is a considerable challenge to preventive efforts.

Sleep health is an important contributor to a personʼs general health and well-being. While much focus is devoted to disorders of sleep, assessing good sleep is also important. Sleep health can be considered as a multidimensional construct including sleep duration (time in 24 h spent asleep), sleep continuity or efficiency (ease of falling asleep and returning to sleep), sleep timing (when sleep occurs), alertness (ability to maintain attentive wakefulness), and sleep quality (subjective rating of good/poor sleep).

These domains can be measured, and different techniques are appropriate for different domains. Sleep quality is generally thought to represent the subjective assessment of ‘goodʼ or ‘poorʼ sleep, and as such, is best measured through subjective self-report, whereas sleep timing, duration, and continuity can be successfully measured through actigraphy, including by wrist-worn accelerometers.

Evidence suggests circadian rhythm disruption could be an understudied risk factor for CVD, and that prolonged misalignment of circadian rhythms is associated with elevated blood pressure, reduced sleep quality, increased risk for cardiovascular disorders, and may also stimulate atherosclerosis, providing a possible biological mechanism for increased cardiovascular risk.

These changes may promote CVD in a sexually dimorphic manner. Circadian rhythm disruption is likely strongly related to disrupted sleep timing. Similarly, shift work will also disrupt sleep timing, and has also been associated with increased cardiovascular risk. There is, therefore, evidence suggesting that disrupted sleep timing could be a useful risk factor for the prediction of CVD risk.

A team of researchers has published its extensive study in European Heart Journal Digital Health.

They said that to the best of their knowledge, this was one of the most extensive studies to date to investigate the relationship between objectively assessed sleep parameters and CVD risk, and that they had demonstrated a clear association between timing of sleep and CVD risk, particularly for women.

Study details

Accelerometer-derived sleep onset timing and cardiovascular disease incidence: a UK Biobank cohort study
Shahram Nikbakhtian, Angus B Reed, Bernard Dillon Obika, Davide Morelli, Adam C Cunningham, Mert Aral, David Plans.

Published in European Heart Journal Digital Health on 9 November 2021

Abstract

Aims
Growing evidence suggests poor sleep health is associated with cardiovascular risk. However, research 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 seven 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 3,172 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 10pm–10.59pm 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 <10pm, 11pm–11.59pm, and ≥12am, respectively, compared to 10pm–10.59pm. Importantly, sensitivity analyses revealed this association with increased CVD risk was stronger in females, with only sleep onset <10pm 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.

 

European Heart Journal article – Accelerometer-derived sleep onset timing and cardiovascular disease incidence: a UK Biobank cohort study (Open access)

 

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