Short sleep duration is associated with a blood pressure nondipping pattern in type 1 diabetes: the DIAPASOM study.
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ABSTRACT:
SUBMITTER: Borel AL
PROVIDER: S-EPMC2732145 | biostudies-literature | 2009 Sep
REPOSITORIES: biostudies-literature
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Short sleep duration is associated with a blood pressure nondipping pattern in type 1 diabetes: the DIAPASOM study.
Borel Anne-Laure AL Benhamou Pierre-Yves PY Baguet Jean-Philippe JP Debaty Isabelle I Levy Patrick P Pépin Jean-Louis JL Mallion Jean-Michel JM
Diabetes care 20090619 9
<h4>Objective</h4>To assess whether nocturnal blood pressure dipping status in type 1 diabetes is correlated with specific sleep characteristics and differences in nocturnal glycemic profiles.<h4>Research design and methods</h4>Twenty type 1 diabetic adult patients underwent sleep studies with simultaneous 24-h ambulatory blood pressure monitoring and continuous nocturnal glucose monitoring.<h4>Results</h4>Altogether, 55% of patients exhibited blunted blood pressure dipping. They did not differ ...[more]
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Project description:BackgroundShort sleep duration is a contributor to cardiovascular disease (CVD) events and mortality. Short sleep duration is associated with an increased risk of high clinic blood pressure (BP). BP measured outside the clinic using 24-h ambulatory blood pressure monitoring (ABPM) is a better predictor of an individual's CVD risk. We examined the association between objectively-assessed sleep duration and 24-h ambulatory blood pressure (ABP).MethodsA total of 893 working adults underwent sleep and ABPM. Participants were fitted with an ABPM device, and measures were taken at 28-30 min intervals. Objective sleep duration, and times of wakefulness and sleep during the 24-h ABPM period were derived from wrist-worn actigraphy. Linear regression, adjusted for age, sex, race/ethnicity, body mass index, smoking status, and diabetes were conducted on the relationship between sleep duration and the ABP measures.ResultsMean age of participants (final n = 729, 59.5% female, 11.9% Hispanic) was 45.2 ± 10.4 y. Mean actigraphy-derived sleep duration was 6.8 ± 1.2 h. Sleep duration <6 h was associated with a 1.73 mmHg higher 24-h systolic BP (p = 0.031) and 2.17 mmHg higher 24-h diastolic BP (p < 0.001). Shorter sleep duration was not associated with mean awake or asleep systolic BP (p = 0.89 and p = 0.92) or mean awake or asleep diastolic BP (p = 0.30 and p = 0.74).ConclusionsTo our knowledge, this is the largest study conducted which assessed sleep duration objectively while measuring 24-h ABP. Shorter sleep duration is associated with higher 24-h BP and potentially cardiovascular risk.
| S-EPMC7803013 | biostudies-literature
Project description:ObjectiveNocturnal hypertension and nondipping systolic blood pressure (SBP) are associated with increased cardiovascular disease (CVD) risk. Short and long sleep duration (SSD and LSD) are also associated with increased CVD risk and may be risk factors for nocturnal hypertension and nondipping SBP. We examined the association between SSD and LSD with sleep BP, nocturnal hypertension, and nondipping SBP among 647 white and African American Coronary Artery Risk Development in Young Adults (CARDIA) study participants who completed 24-h ambulatory BP monitoring, wrist actigraphy, and sleep diaries in 2015-2016.MethodsThe times when participants were asleep and awake were determined from actigraphy complemented by sleep diaries. Nocturnal hypertension was defined as sleep BP ≥120/70 mmHg and nondipping SBP as mean sleep-to-awake SBP ratio >0.90. Sleep duration was categorized as SSD (<6 h), normal sleep duration (NSD: 6-8.9 h), and LSD (≥9 h).ResultsThe prevalence of SSD and LSD were 13.9 and 21.1%, respectively. Compared to participants with NSD, participants with LSD had higher mean sleep SBP (2.1 mmHg, 95% confidence interval [CI] 0.2, 4.1 mmHg) and diastolic BP (1.7 mmHg, 95% CI 0.5, 3.0 mmHg). Participants with LSD had a higher prevalence of nocturnal hypertension (prevalence ratio [PR]: 1.26, 95% CI 1.03-1.54) and nondipping SBP (PR 1.33, 95% CI 1.03-1.72) compared to participants with NSD. There was no evidence of an association between SSD and sleep SBP or DBP, nocturnal hypertension, or nondipping SBP.ConclusionsThese findings suggest that LSD may be associated with nocturnal hypertension and nondipping SBP.
| S-EPMC8571489 | biostudies-literature
Project description:Background Sleep characteristics and disorders are associated with higher blood pressure (BP) when measured in the clinic setting. Methods and Results We tested whether self-reported sleep characteristics and likelihood of obstructive sleep apnea (OSA) were associated with nocturnal hypertension and nondipping systolic BP (SBP) among participants in the CARDIA (Coronary Artery Risk Development in Young Adults) study who completed 24-hour ambulatory BP monitoring during the year 30 examination. Likelihood of OSA was determined using the STOP-Bang questionnaire. Global sleep quality, habitual sleep duration, sleep efficiency, and midsleep time were obtained from the Pittsburgh Sleep Quality Index. Nocturnal hypertension was defined as mean asleep SBP ≥120 mm Hg or diastolic BP ≥70 mm Hg. Nondipping SBP was defined as a decline in awake-to-asleep SBP <10%. Among 702 participants, the prevalence of nocturnal hypertension and nondipping SBP was 41.3% and 32.5%, respectively. After multivariable adjustment including cardiovascular risk factors, the prevalence ratios (PRs) for nocturnal hypertension and nondipping SBP associated with high versus low likelihood of OSA were 1.32 (95% CI, 1.00-1.75) and 1.31 (95% CI, 1.02-1.68), respectively. The association between likelihood of OSA and nocturnal hypertension was stronger for white participants (PR: 2.09; 95% CI, 1.23-3.48) compared with black participants (PR: 1.11; 95% CI, 0.79-1.56). The PR for nondipping SBP associated with a 1-hour later midsleep time was 0.92 (95% CI, 0.85-0.99). Global sleep quality, habitual sleep duration, and sleep efficiency were not associated with either nocturnal hypertension or nondipping SBP. Conclusions These findings suggest that addressing OSA risk and sleep timing in a clinical trial may improve BP during sleep.
| S-EPMC7428601 | biostudies-literature
Project description:OBJECTIVE: Sleep restriction has been associated with deteriorated insulin sensitivity. The effects of short sleep duration have been explored little in patients with type 1 diabetes. This study addresses the question of whether sleep curtailment affects HbA1c levels in patients with type 1 diabetes. RESEARCH DESIGN AND METHODS: Seventy-nine adult patients with type 1 diabetes (median age 40 years [IQR 23-49]; 47% men) were recruited to wear a wrist actimetry sensor during 3 consecutive days to assess mean sleep duration during normal daily life. A subsample of 37 patients also performed 24-h ambulatory blood pressure monitoring (ABPM). Medical history, sleep questionnaires, and diabetes-related quality of life (DQOL) were assessed. RESULTS: Patients having shorter sleep duration--less than 6.5 h (n=21)--had higher levels of HbA1c (P=0.01) than patients with longer sleep duration, above 6.5 h (n=58). In a multivariable regression model including shorter versus longer sleep duration, diabetes duration, DQOL score, and daily activity, sleep duration was the only variable independently associated with HbA1c (R2=10%). In patients who performed 24-h ABPM, patients with a nondipping pattern of blood pressure exhibited shorter sleep duration than patients with a dipping pattern of blood pressure. CONCLUSIONS: Shorter sleep duration is associated with higher HbA1c levels in patients with type 1 diabetes, as well as with a nondipping pattern of blood pressure, anticipating a long-term deleterious impact on the risk of microvascular complications. Further studies should test whether extending the duration of sleep may improve both HbA1c and blood pressure in type 1 diabetes.
| S-EPMC3781526 | biostudies-literature
Project description:BackgroundPatients with peripheral vascular disease (PVD) are often underdiagnosed and undertreated. Nocturnal nondipping blood pressure (BP) pattern, as diagnosed by ambulatory BP monitoring (ABPM), is associated with increased cardiovascular risk, but has not been studied in patients with PVD. We aimed to investigate if a nondipping BP pattern predicts cardiovascular events or all-cause death in outpatients with PVD.MethodsConsecutive outpatients with carotid or lower-extremity PVD were examined with 24-hour ABPM (n = 396). Nondipping was defined as a < 10% fall in systolic BP level during night-time. We used Cox regression models adjusting for potential confounders. We also evaluated the incremental prognostic value of dipping status in the COPART risk score. Our primary composite outcome was cardiovascular events or all-cause death.ResultsIn the cohort (mean age 70; 40% women), 137 events occurred during a 5.1-year median follow-up; incident rate of 7.35 events per 100 person-years. Nondipping was significantly associated with outcome (hazard ratio 1.55, 95% CI 1.07-2.26, p = 0.021) in a fully adjusted model. When adding nondipping to the risk markers in the COPART risk score, the model fit significantly improved (χ2 7.91, p < 0.005) and the C-statistic increased from 0.65 to 0.67.ConclusionIn a cohort of outpatients with PVD, nondipping was an independent risk factor for future cardiovascular events or mortality and seemed to be a strong predictor in patients with carotid artery disease but not in lower-extremity PVD. Additional studies are needed to evaluate the clinical utility of ABPM for improved prevention in these high-risk patients. (ClinicalTrials.gov Identifier: NCT01452165).
| S-EPMC10408241 | biostudies-literature
Project description:ImportanceUnderstanding the interplay between sleep duration, dietary habits, and the risk of developing type 2 diabetes (T2D) is crucial for public health and diabetes prevention strategies.ObjectiveTo investigate the associations of type of diet and duration of sleep with the development of T2D.Design, setting, and participantsData derived from the UK Biobank baseline investigation (2006-2010) were analyzed for this cohort study between May 1 and September 30, 2023. The association between sleep duration and healthy dietary patterns with the risk of T2D was investigated during a median (IQR) follow-up of 12.5 (11.8-13.2) years (end of follow-up, September 30, 2021).ExposureFor the analysis, 247 867 participants were categorized into 4 sleep duration groups: normal (7-8 hours per day), mild short (6 hours per day), moderate short (5 hours per day), and extreme short (3-4 hours per day). Their dietary habits were evaluated based on population-specific consumption of red meat, processed meat, fruits, vegetables, and fish, resulting in a healthy diet score ranging from 0 (unhealthiest) to 5 (healthiest).Main outcomes and measuresCox proportional hazards regression analysis was used to calculate hazard ratios (HRs) and 95% CIs for the development of T2D across various sleep duration groups and healthy diet scores.ResultsThe cohort comprised 247 867 participants with a mean [SD] age of 55.9 [8.1] years, of whom 52.3% were female. During the follow-up, 3.2% of participants were diagnosed with T2D based on hospital registry data. Cox regression analysis, adjusted for confounding variables, indicated a significant increase in the risk of T2D among participants with 5 hours or less of daily sleep. Individuals sleeping 5 hours per day exhibited a 1.16 adjusted HR (95% CI, 1.05-1.28), and individuals sleeping 3 to 4 hours per day exhibited a 1.41 adjusted HR (95% CI, 1.19-1.68) compared with individuals with normal sleep duration. Furthermore, individuals with the healthiest dietary patterns had a reduced risk of T2D (HR, 0.75 [95% CI, 0.63-0.88]). The association between short sleep duration and increased risk of T2D persisted even for individuals following a healthy diet, but there was no multiplicative interaction between sleep duration and healthy diet score.Conclusions and relevanceIn this cohort study involving UK residents, habitual short sleep duration was associated with increased risk of developing T2D. This association persisted even among participants who maintained a healthy diet. To validate these findings, further longitudinal studies are needed, incorporating repeated measures of sleep (including objective assessments) and dietary habits.
| S-EPMC10915681 | biostudies-literature
Project description:Whether sex influences the association of obstructive sleep apnea (OSA) with markers of cardiovascular risk in patients with hypertension is unknown. In this study, 95 hypertensive participants underwent carotid-femoral pulse wave velocity, 24-hour ambulatory blood pressure monitoring, echocardiogram, and polysomnography after a 30-day standardized treatment with hydrochlorothiazide plus enalapril or losartan. OSA was present in 52 patients. Compared with non-OSA patients, pulse wave velocity values were higher in the OSA group (men: 11.1±2.2 vs 12.7±2.4 m/s, P=.04; women: 11.8±2.4 vs 13.2±2.2 m/s, P=.03). The proportion of diastolic dysfunction was significant in men and women with OSA. Compared with non-OSA patients, nondipping systolic blood pressure in OSA was higher in men (14.3% vs 46.4%) and in women (41.4% vs 65.2%). OSA was independently associated with pulse wave velocity (β=1.050; P=.025) and nondipping systolic blood pressure (odds ratio, 3.03; 95% confidence interval, 1.08-8.55; P=.035) in the regression analysis. In conclusion, OSA is independently associated with arterial stiffness and nondipping blood pressure in patients with hypertension regardless of sex.
| S-EPMC8030757 | biostudies-literature
Project description:Few studies have considered psychosocial characteristics when investigating the associations between sleep duration and blood pressure (BP). In this study, we took propensity score matching (PSM) to adjust for psychosocial characteristics when comparing BP between individuals with short sleep duration and those with normal sleep duration. A total of 429 participants were included. 72 participants with sleep duration ≤6 h and 65 participants with sleep duration >6 h were matched after PSM. We compared office BP, 24-hour BP, and prevalence of hypertension in the populations before and after PSM, respectively. In the unmatched population, participants with sleep duration ≤6 h were observed with higher office diastolic BP (DBP) and 24-h systolic BP (SBP)/DBP (all P < 0.05). In the matched populations, the differences between the two groups (sleep duration ≤6 h vs. sleep duration >6 h) in office DBP (88.4 ± 10.9 vs. 82.5 ± 11.1 mm Hg; P=0.002), 24-h SBP (134.7 ± 12.0 vs. 129.3 ± 11.6 mm Hg; P=0.009), and 24-h DBP (83.4 ± 9.9 vs. 78.1 ± 10.1 mm Hg; P=0.002) become more significant. Participants with sleep duration ≤6 h only show higher prevalence of hypertension based on 24-h BP data, while analysis after PSM further revealed that these with sleep duration ≤6 h presented about 20% higher prevalence of elevated BP up to office diagnosed hypertension threshold. Therefore, psychosocial characteristics accompanied with short sleep duration should be fully valued in individuals at risks for elevated BP. This trial is registered with NCT03866226.
| S-EPMC8651353 | biostudies-literature
Project description:Associations between sleep duration and type 2 diabetes (T2D) risk markers in childhood have been little studied. We examined associations between self-reported sleep duration and T2D risk markers in children. Cross-sectional study of 4525 multiethnic UK children aged 9 to 10 years. Sleep time was calculated from self-reported usual time of going to bed and getting up on a school day, validated in a subset using accelerometers. Fasting blood samples provided levels of serum lipids and insulin, plasma glucose, and HbA1c. Physical measures included height, weight, bioimpedance, and blood pressure. Multilevel linear regression models of anthropometric, T2D, and cardiovascular risk markers with sleep duration were adjusted for sex, age, month, ethnicity, socioeconomic position, observer (physical measures only), and random effect of school. On average, children slept 10.5 hours per night (95% range 8.0-12.0 hours). There were strong inverse graded relationships between sleep duration, adiposity, and diabetes risk markers. In adjusted models, a 1-hour-longer sleep duration was associated with 0.19 lower BMI (95% confidence interval [CI] 0.09 to 0.28), 0.03 kg/m5 lower fat mass index (95% CI 0.00 to 0.05 kg/m5), 2.9% lower homeostasis model assessment insulin resistance (95% CI 1.2% to 4.4%), and 0.24% lower fasting glucose (95% CI 0.03% to 0.44%); there was no association with HbA1c or cardiovascular risk. Associations with insulin and glucose remained after an additional adjustment for adiposity markers. The finding of an inverse association between sleep duration and T2D risk markers in childhood is novel. Intervention studies are needed to establish the causality of these associations, which could provide a simple strategy for early T2D prevention.
| S-EPMC7612309 | biostudies-literature
Project description:BACKGROUND:Experimental and epidemiologic data suggest that among nonpregnant adults, sleep duration may be an important risk factor for chronic disease. Although pregnant women commonly report poor sleep, few studies objectively evaluated the quality of sleep in pregnancy or explored the relationship between sleep disturbances and maternal and perinatal outcomes. OBJECTIVE:Our objective was to examine the relationship between objectively assessed sleep duration, timing, and continuity (measured via wrist actigraphy) and maternal cardiovascular and metabolic morbidity specific to pregnancy. STUDY DESIGN:This was a prospective cohort study of nulliparous women. Women were recruited between 16 0/7 and 21 6/7 weeks' gestation. They were asked to wear a wrist actigraphy monitor and complete a daily sleep log for a period of 7 consecutive days. The primary sleep exposure variables were the averages of the following over the total valid nights (minimum 5, maximum 7 nights): short sleep duration during the primary sleep period (<7 h/night), late sleep midpoint (midpoint between sleep onset and sleep offset >5 am), and top quartile of minutes of wake time after sleep onset and sleep fragmentation index. The primary outcomes of interest were a composite of hypertensive disorders of pregnancy (mild, severe, or superimposed preeclampsia; eclampsia; or antepartum gestational hypertension) and gestational diabetes mellitus. We used ?2 tests to assess associations between sleep variables and categorical baseline characteristics. Crude odds ratios and 95% confidence intervals were estimated from univariate logistic regression models to characterize the magnitude of the relationship between sleep characteristics and hypertensive disorders of pregnancy and gestational diabetes. For associations significant in univariate analysis, multiple logistic regression was used to explore further the association of sleep characteristics with pregnancy outcomes. RESULTS:In all, 901 eligible women consented to participate; 782 submitted valid actigraphy studies. Short sleep duration and a later sleep midpoint were associated with an increased risk of gestational diabetes (odds ratio, 2.24; 95% confidence interval, 1.11-4.53; and odds ratio, 2.58; 95% confidence interval, 1.24-5.36, respectively) but not of hypertensive disorders. A model with both sleep duration and sleep midpoint as well as their interaction term revealed that while there was no significant interaction between these exposures, the main effects of both short sleep duration and later sleep midpoint with gestational diabetes remained significant (adjusted odds ratio, 2.06; 95% confidence interval, 1.01-4.19; and adjusted odds ratio, 2.37; 95% confidence interval, 1.13-4.97, respectively). Additionally, after adjusting separately for age, body mass index, and race/ethnicity, both short sleep duration and later sleep midpoint remained associated with gestational diabetes. No associations were demonstrated between the sleep quality measures (wake after sleep onset, sleep fragmentation) and hypertensive disorders or gestational diabetes. CONCLUSION:Our results demonstrate a relationship between short sleep duration and later sleep midpoint with gestational diabetes. Our data suggest independent contributions of these 2 sleep characteristics to the risk for gestational diabetes in nulliparous women.
| S-EPMC5783638 | biostudies-literature