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: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: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
Project description:Background Nocturnal hypertension, defined by a mean asleep systolic blood pressure (SBP)/diastolic blood pressure (BP) ?120/70 mm Hg, and nondipping SBP, defined by an awake-to-asleep decline in SBP <10%, are each associated with increased risk for cardiovascular disease. Methods and Results We developed predictive equations to identify adults with a high probability of having nocturnal hypertension or nondipping SBP using data from the CARDIA (Coronary Artery Risk Development in Young Adults) study (n=787), JHS (Jackson Heart Study) (n=1063), IDH (Improving the Detection of Hypertension) study (n=395), and MHT (Masked Hypertension) study (n=772) who underwent 24-hour ambulatory BP monitoring. Participants were randomized to derivation (n=2511) or validation (n=506) data sets. The prevalence rates of nocturnal hypertension and nondipping SBP were 39.7% and 44.9% in the derivation data set, respectively, and 36.6% and 44.5% in the validation data set, respectively. The predictive equation for nocturnal hypertension included age, race/ethnicity, smoking status, neck circumference, height, high-density lipoprotein cholesterol, albumin/creatinine ratio, and clinic SBP and diastolic BP. The predictive equation for nondipping SBP included age, sex, race/ethnicity, waist circumference, height, alcohol use, high-density lipoprotein cholesterol, and albumin/creatinine ratio. Concordance statistics (95% CI) for nocturnal hypertension and nondipping SBP predictive equations in the validation data set were 0.84 (0.80-0.87) and 0.73 (0.69-0.78), respectively. Compared with reference models including antihypertensive medication use and clinic SBP and diastolic BP as predictors, the continuous net reclassification improvement (95% CI) values for the nocturnal hypertension and nondipping SBP predictive equations were 0.52 (0.35-0.69) and 0.51 (0.34-0.69), respectively. Conclusions These predictive equations can direct ambulatory BP monitoring toward adults with high probability of having nocturnal hypertension and nondipping SBP.
| S-EPMC7033845 | biostudies-literature
Project description:Obesity and a nondipping circadian blood pressure (BP) pattern are associated with diastolic dysfunction. Ectopic lipid accumulation is increasingly recognized as an important metabolic abnormality contributing to diastolic dysfunction. However, little is known about the contribution of different lipids and the composition of lipid analytes to diastolic dysfunction. We have performed functional and structural studies and analyzed cardiac lipid profile at two time points during progression to diastolic dysfunction in a genetic model of obesity. Serial cardiac magnetic resonance imaging and telemetric measures of BP between 12 and 15 wk of age in obese male db/db mice indicated a nondipping circadian BP pattern and normal diastolic function at 12 wk that progressed to a deteriorating nondipping pattern and onset of diastolic dysfunction at 15 wk of age. Lipidomic analysis demonstrated elevated fatty acids and ceramides in db/db at 12 wk, but their levels were decreased at 15 wk, and this was accompanied by persistent mitochondrial ultrastructural abnormalities in concert with evidence of increased fatty acid oxidation and enhanced production of reactive oxygen species. Triacylglyceride and diacylglyceride levels were elevated at both 12 and 15 wk, but their composition changed to consist of more saturated and less unsaturated fatty acyl at 15 wk. An increase in the lipid droplets was apparent at both time points, and this was associated with increases in phosphatidycholine. In conclusion, a distinct pattern of myocardial lipid remodeling, accompanied by oxidative stress, is associated with the onset of diastolic dysfunction in obese, insulin-resistant db/db mice.
| S-EPMC3529378 | biostudies-literature
Project description:There are limited data about the role of gender on the relationship between sleep duration and blood pressure (BP) from rural populations.We conducted a cross-sectional rural population-based study. This report includes 1033 men and 783 women aged 18-65 years from a cohort of twins enrolled in Anhui, China, between 2005 and 2008. Sleep duration was derived from typical bedtime, wake-up time, and sleep latency as reported on a standard sleep questionnaire. Primary outcomes included measured systolic blood pressure (SBP) and diastolic blood pressure (DBP). High blood pressure (HBP) was defined as SBP ?130 mmHg, DBP ?85 mmHg, or physician diagnosed hypertension. Linear and logistic regression models were used to assess gender-specific associations between sleep duration and BP or HBP, respectively, with adjustment for known risk factors including adiposity and sleep-related disorder risk from the questionnaires. Generalized estimating equations were used to account for intra-twin pair correlations.Compared with those sleeping 7 to <9h, women sleeping <7h had a higher risk of HBP (odds ratios [ORs] 3.0, 95% confidence interval [CI], 1.4-6.6); men sleeping ?9h had a higher risk of HBP (ORs=1.5, 95%CI: 1.1-2.2).Among rural Chinese adults, a gender-specific association of sleep duration with BP exists such that HBP is associated with short sleep duration in women and long sleep duration in men. Longitudinal studies are needed to further examine the temporal relationship and biological mechanisms underlying sleep duration and BP in this population. Our findings underscore the potential importance of appropriate sleep duration for optimal blood pressure.
| S-EPMC3755492 | biostudies-literature