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

Author(s):  
Shahram Nikbakhtian ◽  
Angus B Reed ◽  
Bernard Dillon Obika ◽  
Davide Morelli ◽  
Adam C Cunningham ◽  
...  

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.

2021 ◽  
Author(s):  
Shahram Nikbakhtian ◽  
Angus B Reed ◽  
Bernard Dillon Obika ◽  
Davide Morelli ◽  
Adam C Cunningham ◽  
...  

Aims Growing evidence suggests that sleep quality is associated with cardiovascular risk. However, research in this area often relies upon recollection dependant questionnaires or diaries. Accelerometers provide an alternative tool for deriving sleep parameters measuring sleep patterns objectively. This study examines the associations between 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 seven days. From this, we examined the association between sleep onset timing and CVD incidence using a series of Cox proportional hazards models. 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 10:00pm-10:59pm was associated with the lowest CVD incidence. A fully adjusted model, additionally controlling for sleep duration, sleep irregularity, and established CVD risk factors, was unable to eliminate this association, producing hazard ratios of 1.24 (95% CI, 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 <10:00pm, 11:00pm-11:59pm, and & ≥12:00am, respectively, compared to 10:00pm-10:59pm. Importantly, sensitivity analyses revealed this association was stronger in females, with only sleep onset <10:00pm significant for males. Conclusions Our findings suggest an independent 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.


2021 ◽  
Author(s):  
Shahram Nikbakhtian ◽  
Angus Bruno Reed ◽  
Bernard Dillon Obika ◽  
Davide Morelli ◽  
Adam C. Cunningham ◽  
...  

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A58-A59
Author(s):  
Rebecca Burdayron ◽  
Marie-Helene Pennestri ◽  
Elizabeth Keys ◽  
Lianne Tomfohr-Madsen ◽  
Gerald Giesbrecht

Abstract Introduction Poor sleep quality is common during pregnancy and can increase the risk of adverse obstetric and fetal outcomes. Existing research on the association between prenatal sleep and infant sleep is scarce and has focused on other aspects of prenatal sleep such as sleep duration, chronotype, and insomnia symptoms. To our knowledge, no studies have examined the association between prenatal sleep quality and infant sleep outcomes. Thus, this study aimed to investigate whether maternal sleep quality during pregnancy was prospectively associated with infant sleep dimensions, independent of relevant covariates. Methods Participants were a subset of 272 mother-infant dyads enrolled in an ongoing cohort study. Maternal prenatal sleep quality was assessed with the Pittsburgh Sleep Quality Index (PSQI) in early to mid- (M gestational age = 15.12 ± 3.56 weeks) and late- (M gestational age = 32.44 ± 0.99 weeks) pregnancy. Mothers completed the Brief Infant Sleep Questionnaire (BISQ) at 3, 6, and 12 months postpartum. The following infant sleep parameters were assessed: sleep duration (day, night, 24-hour), number of night awakenings, and wake after sleep onset. Prenatal depressive symptoms were assessed with the Edinburgh Postnatal Depression Scale (EPDS) at both pregnancy time points. Other covariates included maternal age at enrollment, infant age, parity, and co-sleeping status. Results Generalized estimating equations (GEE) models revealed that poorer maternal sleep quality during early-to-mid pregnancy did not significantly predict infant sleep parameters after adjustment for covariates (p &gt; .05). However, in late pregnancy, poorer maternal sleep quality significantly predicted shorter 24-hour sleep duration and longer wake after sleep onset, but not daytime sleep duration, nighttime sleep duration, and number of night awakenings (p &lt; .05). Conclusion Study findings advance our understanding of the prospective link between maternal prenatal sleep quality and infant sleep. Results indicate that maternal sleep quality during late gestation may play a role in the development of infant sleep patterns. These findings have important implications for intervention efforts targeting maternal sleep quality during pregnancy. Future research should use objective measures of sleep, such as actigraphy, to better elucidate the effects of prenatal sleep quality on infant sleep outcomes. Support (if any) The Canadian Institutes of Health Research (CIHR)


2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1508-1508
Author(s):  
Mengjie Yuan ◽  
R Taylor Pickering ◽  
Martha Singer ◽  
Lynn l Moore

Abstract Objectives Few studies have estimated the independent effects of butter and margarine on risk of cardiovascular disease (CVD). Our goal was to examine these effects as well as that of other fats and oils on risk of CVD and markers of cardiometabolic risk in subjects in the prospective Framingham Offspring Study. Methods Data from 2038 adults, who were free of CVD and diabetes through exam 5 were included. Intakes of butter, margarine, mayonnaise, oils, and shortening were assessed using 3-day diet records at exams 3 and 5. Concentrations of low-density lipoproteins (LDL), high-density lipoproteins (HDL), and their particle sizes were analyzed cross-sectionally at exam 5. Subjects were followed from exam 5 to 9 for incident CVD and type 2 diabetes (T2DM) (median follow-up, 16.9 years). Cox proportional hazards models were used to estimate risk of CVD and T2DM and generalized linear models were used to evaluate effects on other cardiometabolic outcomes, while adjusting for age, sex, pack-years of smoking, BMI, physical activity, intakes of other fats, hypertension and use of lipid-lowering medication. Intake of each type of dietary fat was categorized as low, moderate, or high using sensitivity analyses. Results Intake of &gt;5 g/day of butter (vs. non-consumers) had no effect on CVD risk but was associated with a non-statistically significant 24% lower risk of T2DM. In men, higher butter intake was linked with larger LDL and HDL particles sizes (P &lt; 0.01 for both) and a lower LDL: HDL ratio (P &lt; 0.01). Consuming &gt;7 g/day (vs. ≤2) of margarine was associated with a 48% (95% CI: 1.03–2.13) increased risk of CVD and a 68% (95% CI: 1.00–2.82) higher risk of T2DM in women. In men, higher margarine intake was associated with much weaker, non-statistically significant increased risks of CVD and T2DM. Finally, total intake of oils (&gt;7 vs. ≤2 g/day) was associated with a strong reduced risk of T2DM (HR: 0.55; 95% CI: 0.36–0.85) in men but not women. There was no effect of margarine or oils on lipid particle sizes in either men or women. Conclusions While butter intake had no adverse effect on risk of CVD in either men or women, it was beneficially associated with lipid profiles in men. In women, higher intakes of margarine but not butter were associated with increased risks of both CVD and T2DM. Finally greater oil consumption led to lower risks of T2DM in men. Funding Sources NHLBI National Dairy Council.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
C Magnussen

Abstract Background Knowledge about the impact of modifiable risk factors for cardiovascular disease (CVD) onset is essential to improve CVD prevention. Purpose We estimated population-attributable fractions (PAFs) of body-mass-index (BMI), systolic blood pressure (SBP), diabetes, blood lipids (non-high-density lipoprotein cholesterol; non-HDL-C) and daily smoking for CVD. Methods Harmonized data from MOnica Risk, Genetics, Archiving and Monograph (MORGAM) and Biomarkers for Cardiovascular Risk Assessment in Europe (BiomaCaRE) consortia were used to calculate hazard ratios (HRs; 95% CI) and PAFs for incident CVD (myocardial infarction or coronary death, unstable angina, cardiac revascularization, ischemic stroke). PAFs for single risk factors or any combination of them were estimated using methods by Laaksonen 2011. Results We included 150,190 participants (77,801 men and 72,389 women) without CVD at baseline. Strongest associations were seen for SBP ≥160 mmHg (HR 1.79, 1.67–1.92 men; HR 1.93, 1.75–2.14 women), diabetes (HR 2.02, 1.86–2.20 men; HR 2.29, 2.06–2.55 women), non-HDL-C ≥220 mg/dL (HR 3.11, 2.49–3.88 men; HR 2.27, 1.68–3.05 women), daily smoking (HR 1.82, 1.73–1,90 men; HR 2.16, 2.0–2.33 women). Table 1 provides PAFs for incident CVD. Overall PAFs for men and women were 73.7% (67.7–79.1) and 73.3% (64.9–80.9). Table 1. PAFs (%) for 5-year incident CVD Risk factor/category PAFs (95% CI), men PAFs (95% CI), women Underweight 0.1 (−0.1, 0.3) 0.2 (−0.1, 0.6) Pre-obesity 6.6 (4.3, 8.9) 4.3 (1.5, 6.9) Obesity 3.9 (2.7, 5.3) 8.0 (5.3, 10.5) SBP 130 to <140 mmHg 2.8 (1.7, 4.0) 2.7 (1.3, 4.0) SBP 140 to <160 mmHg 9.7 (8.1, 11.3) 9.3 (6.7, 11.6) SBP ≥160 mmHg 11.3 (9.7, 12.8) 18.9 (16.2, 21.8) Diabetes 5.2 (4.5, 6.2) 7.8 (6.5, 9.4) non-HDL-C 100 to <145 mg/dL 4.3 (1.8, 6.4) 3.3 (0.5, 6.5) non-HDL-C 145 to <185 mg/dL 13.9 (9.8, 17.5) 11.3 (6.0, 16.2) non-HDL-C 185 to <220 mg/dL 15.8 (12.8, 18.4) 12.8 (8.8, 17.0) non-HDL-C ≥220 mg/dL 16.7 (14.6, 18.5) 17.0 (12.5, 21.1) Daily smoking 16.5 (15.0, 18.3) 12.3 (10.7, 13.7) The N CVD events/N used was 8,302/77,801 for men and 4,071/72,389 for women. Conclusion Uncontrolled risk factors, especially non-HDL-C and SBP in the highest category, daily smoking and diabetes had the highest impact for incident CVD. All risk factors combined accounted for a PAF of 73%. Targeting risk factors would lead to a substantial reduction of CVD onset. Acknowledgement/Funding BiomarCaRE: EU Seventh Framework Programme (FP7/2007-2013), No. HEALTH-F2-2011-278913. MORGAM: EU FP 7 CHANCES (HEALTH-F3-2010-242244).


2020 ◽  
Author(s):  
Melker Staffan Johansson ◽  
Karen Søgaard ◽  
Eva Prescott ◽  
Jacob Louis Marott ◽  
Peter Schnohr ◽  
...  

Abstract Background: It is unclear whether walking can decrease cardiovascular disease (CVD) risk or if high intensity physical activity (HIPA) is needed, and whether the association is modified by age. We investigated how sedentary behaviour, walking, and HIPA, were associated with systolic blood pressure (SBP), waist circumference (WC), and low-density lipoprotein cholesterol (LDL-C) among adults and older adults in a general population sample using compositional data analysis. Specifically, the measure of association was quantified by reallocating time between sedentary behaviour and 1) walking, and 2) HIPA. Methods: Cross-sectional data from the fifth examination of the Copenhagen City Heart Study was used. Using the software Acti4, we estimated daily time spent in physical behaviours from accelerometer data worn 24 h/day for 7 days (i.e., right frontal thigh and iliac crest; median wear time: 6 days, 23.8 h/day). SBP, WC, and LDL-C were measured during a physical examination. Inclusion criteria were ≥5 days with ≥16 h of accelerometer recordings per day, and no use of antihypertensives, diuretics or cholesterol lowering medicine. The 24-hour physical behaviour composition consisted of sedentary behaviour, standing, moving, walking, HIPA (i.e., sum of climbing stairs, running, cycling and rowing), and time in bed. We used fitted values from linear regression models to predict the difference in outcome given the investigated time reallocations relative to the group-specific mean composition. Results: Among 1053 eligible participants, we found an interaction between the physical behaviour composition and age. Age-stratified analyses (i.e., </≥65 years; 773 adults, 280 older adults) indicated that less sedentary behaviour and more walking was associated with lower SBP among older adults only. For less sedentary behaviour and more HIPA, the results i) indicated an association with lower SBP irrespective of age, ii) showed an association with a smaller WC among adults, and iii) showed an association with a lower LDL-C in both age groups. Conclusions: Less sedentary behaviour and more walking seems to be associated with lower CVD risk among older adults, while HIPA types are associated with lower risk among adults. Therefore, to reduce CVD risk, the modifying effect of age should be considered in future physical activity-promoting initiatives.


2021 ◽  
Vol 10 (4) ◽  
Author(s):  
Xiang Gao ◽  
Djibril M. Ba ◽  
Kanika Bagai ◽  
Guodong Liu ◽  
Chaoran Ma ◽  
...  

Background Restless legs syndrome (RLS) is associated with higher cardiovascular disease (CVD) risk. However, it remains unknown whether treatment of RLS lowers the cardiovascular risk associated with RLS. Methods and Results All data were collected retrospectively, but subjects were prospectively followed forward in time to determine outcomes of interest. We used the Truven Health MarketScan Commercial Claims and Encounters database from January 1, 2006, through December 31, 2014. Participants were 169 393 individuals, which included 24 199 nonpregnant participants with an RLS diagnosis (16 694 receiving treatments for RLS and 7505 without treatment) during 2006 to 2008 and 145 194 age‐ and sex‐matched participants without RLS. All participants were free of CVD before January 1, 2009 (analysis baseline). Incident CVD cases (myocardial infarction, angina, stroke, atrial fibrillation, and heart failure) were identified. We adjusted for potential confounders, such as presence of chronic conditions and medication use. We identified 16 574 incident CVD cases during 2009 to 2014. Relative to the non‐RLS group, the adjusted hazard ratio (HR) for future CVD was 1.26 (95% CI, 1.20–1.32) ( P <0.001) for the RLS with treatment group, and 1.53 (95% CI, 1.42–1.65) ( P <0.001) for the RLS without treatment group. Significant lower CVD risk was observed for all different RLS treatments, including dopaminergics, anticonvulsants, benzodiazepines, and opiates (adjusted HRs range, 0.71‐0.84; P <0.001 for all), except for ergot‐dopamine use. Conclusions RLS was associated with higher future CVD risk. However, RLS was associated with statistically significantly less future cardiovascular risk in RLS patients with treatment than in those without treatment.


2020 ◽  
Author(s):  
Alice R Carter ◽  
Dipender Gill ◽  
Richard Morris ◽  
George Davey Smith ◽  
Amy E Taylor ◽  
...  

AbstractImportanceThe most socioeconomically deprived individuals remain at the greatest risk of cardiovascular disease. Differences in risk adjusted use of statins between educational groups may contribute to these inequalities.ObjectiveTo identify whether people with lower levels of educational attainment are less likely to take statins for a given level of cardiovascular risk.DesignCross-sectional analysis of a population-based cohort study and linked longitudinal primary care records.SettingUK Biobank data from baseline assessment centres, linked primary care data and hospital episode statisticsParticipantsUK Biobank participants (N = 489 679, mean age = 56, 54% female) with complete data on educational attainment and self-reported medication use. Secondary analyses were carried out on a subsample of participants with linked primary care data (N = 217 675).Main outcome measuresStatin use self-reported to clinic nurses at baseline assessment centres, validated with linked prescription data in a subsample of participants in secondary analyses.ResultsGreater education was associated with lower statin use, whilst higher cardiovascular risk (assessed by QRISK3 score) was associated with higher statin use in both females and males. There was evidence of an interaction between QRISK3 and education, such that for the same QRISK3 score, people with more education were more likely to report taking statins. For example, in women with 7 years of schooling, equivalent to leaving school with no formal qualifications, a one unit increase in QRISK3 score was associated with a 6% higher odds of statin use (odds ratio (OR) 1.06, 95% CI 1.05, 1.06). In contrast, in women with 20 years of schooling, equivalent to obtaining a degree, a one unit increase in QRISK3 score was associated with an 11% higher odds of statin use (OR 1.11, 95% CI 1.10, 1.11). Comparable ORs in men were 1.04 (95% CI 1.04, 1.05) for men with 7 years of schooling and (95% CI 1.07, 1.07) for men with 20 years of schooling.ConclusionsFor the same level of cardiovascular risk, individuals with lower educational attainment are less likely to receive statins, likely contributing to health inequalities.SummaryWhat is already known on this topic?Despite reductions in the rates of cardiovascular disease in high income countries, individuals who are the most socioeconomically deprived remain at the highest risk.Although intermediate lifestyle and behavioural risk factors explain some of this, much of the effect remains unexplained.What does this study add?For the same increase in QRISK3 score, the likelihood of statin use increased more in individuals with high educational attainment compared with individuals with lower educational attainment.These results were similar when using UK Biobank to derive QRISK3 scores and when using QRISK scores recorded in primary care records, and when using self-reported statin prescription data or prescription data from linked primary care records.The mechanisms leading to these differences are unknown, but both health seeking behaviours and clinical factors may contribute.


2020 ◽  
Vol 75 (9) ◽  
pp. e95-e102 ◽  
Author(s):  
Alfonso J Alfini ◽  
Jennifer A Schrack ◽  
Jacek K Urbanek ◽  
Amal A Wanigatunga ◽  
Sarah K Wanigatunga ◽  
...  

Abstract Background Poor sleep may increase the likelihood of fatigue, and both are common in later life. However, prior studies of the sleep–fatigue relationship used subjective measures or were conducted in clinical populations; thus, the nature of this association in healthier community-dwelling older adults remains unclear. We studied the association of actigraphic sleep parameters with perceived fatigability—fatigue in response to a standardized task—and with conventional fatigue symptoms of low energy or tiredness. Methods We studied 382 cognitively normal participants in the Baltimore Longitudinal Study of Aging (aged 73.1 ± 10.3 years, 53.1% women) who completed 6.7 ± 0.9 days of wrist actigraphy and a perceived fatigability assessment, including rating of perceived exertion (RPE) after a 5-minute treadmill walk or the Pittsburgh Fatigability Scale (PFS). Participants also reported non-standardized symptoms of fatigue. Results After adjustment for age, sex, race, height, weight, comorbidity index, and depressive symptoms, shorter total sleep time (TST; &lt;6.3 hours vs intermediate TST ≥6.3 to 7.2 hours) was associated with high RPE fatigability (odds ratio [OR] = 2.56, 95% confidence interval [CI] = 1.29, 5.06, p = .007), high PFS physical (OR = 1.88, 95% CI = 1.04, 3.38, p = .035), and high mental fatigability (OR = 2.15, 95% CI = 1.02, 4.50, p = .044), whereas longer TST was also associated with high mental fatigability (OR = 2.19, 95% CI = 1.02, 4.71, p = .043). Additionally, longer wake bout length was associated with high RPE fatigability (OR = 1.53, 95% CI = 1.14, 2.07, p = .005), and greater wake after sleep onset was associated with high mental fatigability (OR = 1.14, 95% CI = 1.01, 1.28, p = .036). Conclusion Among well-functioning older adults, abnormal sleep duration and sleep fragmentation are associated with greater perceived fatigability.


2021 ◽  
Vol 23 (Supplement_2) ◽  
pp. ii29-ii29
Author(s):  
M George ◽  
S Dadhania ◽  
M Williams

Abstract BACKGROUND Sleep disturbance is a common symptom in patients with high grade glioma (HGG). Existing self-reported and uni-dimensional data from questionnaires are of limited value. The observational phase 2 trial, BrainWear (ISRCTN 34351424) provides the first objective analysis of sleep in HGG patients. MATERIAL AND METHODS Patients with HGG were asked to wear an AX3 Axivity tri-axial accelerometer throughout treatment. The study employed a wear-as-long-as-possible approach to accelerometry data collection, and we used age-sex matched controls from the UK Biobank as comparators. Baseline was established as a 7 day period of wear prior to surgery or at least 7 days post-surgery. The dataset for this analysis consists of 21 patients with data at baseline and 15 patients during chemo-radiation. Only 16 of the 21 HGG patients at baseline were included for initial comparisons with healthy controls due to age limitations of the UK Biobank cohort for matching. Raw accelerometer data was processed using the GGIR package, with non-imputation of missing data, exclusion of days with &lt;16 hours of wear time and removal of algorithm-identified problematic data. Mann-Whitney U-tests and unpaired T-tests were used to compare 7 sleep-related features between HGG patients and healthy controls at baseline, with choice of statistical test based on shapiro-wilk derived normality. Secondly, to assess changes in sleep in HGG patients across treatment period, K-means clustering of 5 sleep parameters, available longitudinally, was conducted to explore sleep behaviours at baseline (n = 21) and during chemo-radiation. RESULTS HGG patients (n = 16) exhibited greater daytime inactivity than healthy controls (n = 32) (p &lt; 0.0001, 2.2 vs 0.5 hrs) and more variation in their 24 hour activity rhythm from day to day (p &lt; 0.0001, 0.12 vs 0.18). We identified 5 sleep features which allowed us to cluster patients’ sleep behaviour, and most (62.5%) of HGG patients have a poor sleep profile. This sleep profile was characterised by an average of 5.4 hours of night-time sleep, 2.1 hours of daytime inactivity and disturbed sleep quality. However, evaluation of HGG patient sleep cluster designation at baseline and during chemoradiation, showed HGG patients with data at both timepoints (n = 9) demonstrate stability or improvement in sleep profile. CONCLUSION Patients with HGG have objective evidence of poor sleep compared to healthy matched controls. Further work will explore changes in sleep over time.


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