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• W762533598 abstract "Free AccessSleep DeprivationRelationship between Duration of Sleep and Hypertension in Adults: A Meta-Analysis Yan Wang, MD, Hao Mei, PhD, Yan-Rui Jiang, MD, Wan-Qi Sun, MD, Yuan-Jin Song, MD, Shi-Jian Liu, PhD, Fan Jiang, MD, PhD Yan Wang, MD Department of Developmental and Behavioral Pediatrics, Institute of Pediatric Translational Medicine, Shanghai Children's Medical Center affiliated Shanghai Jiaotong University School of Medicine, Ministry of Education Shanghai Key Laboratory of Children's Environmental Health, Shanghai, China Search for more papers by this author , Hao Mei, PhD Department of Epidemiology, Tulane University, New Orleans, LA Search for more papers by this author , Yan-Rui Jiang, MD Department of Developmental and Behavioral Pediatrics, Institute of Pediatric Translational Medicine, Shanghai Children's Medical Center affiliated Shanghai Jiaotong University School of Medicine, Ministry of Education Shanghai Key Laboratory of Children's Environmental Health, Shanghai, China Search for more papers by this author , Wan-Qi Sun, MD Department of Developmental and Behavioral Pediatrics, Institute of Pediatric Translational Medicine, Shanghai Children's Medical Center affiliated Shanghai Jiaotong University School of Medicine, Ministry of Education Shanghai Key Laboratory of Children's Environmental Health, Shanghai, China Search for more papers by this author , Yuan-Jin Song, MD Department of Developmental and Behavioral Pediatrics, Institute of Pediatric Translational Medicine, Shanghai Children's Medical Center affiliated Shanghai Jiaotong University School of Medicine, Ministry of Education Shanghai Key Laboratory of Children's Environmental Health, Shanghai, China Search for more papers by this author , Shi-Jian Liu, PhD Address correspondence to: Fan Jiang, Department of Developmental and Behavioral Pediatrics, Institute of Pediatric Translational Medicine, Shanghai Children's Medical Center affiliated Shanghai Jiaotong University School of Medicine, Ministry of Education Shanghai Key Laboratory of Children's Environmental Health, Shanghai, China86-21-5875057386-21-58706129 E-mail Address: [email protected] and Shi-jian Liu, Department of Bioinformatics and Clinical Epidemiology, Institute of Pediatric Translational Medicine, Shanghai Children's Medical Center affiliated Shanghai Jiaotong University School of Medicine, Shanghai, China E-mail Address: [email protected] Department of Bioinformatics and Clinical Epidemiology, Institute of Pediatric Translational Medicine, Shanghai Children's Medical Center affiliated Shanghai Jiaotong University School of Medicine, Shanghai, China Search for more papers by this author , Fan Jiang, MD, PhD Address correspondence to: Fan Jiang, Department of Developmental and Behavioral Pediatrics, Institute of Pediatric Translational Medicine, Shanghai Children's Medical Center affiliated Shanghai Jiaotong University School of Medicine, Ministry of Education Shanghai Key Laboratory of Children's Environmental Health, Shanghai, China86-21-5875057386-21-58706129 E-mail Address: [email protected] and Shi-jian Liu, Department of Bioinformatics and Clinical Epidemiology, Institute of Pediatric Translational Medicine, Shanghai Children's Medical Center affiliated Shanghai Jiaotong University School of Medicine, Shanghai, China E-mail Address: [email protected] Department of Developmental and Behavioral Pediatrics, Institute of Pediatric Translational Medicine, Shanghai Children's Medical Center affiliated Shanghai Jiaotong University School of Medicine, Ministry of Education Shanghai Key Laboratory of Children's Environmental Health, Shanghai, China Search for more papers by this author Published Online:September 15, 2015https://doi.org/10.5664/jcsm.5024Cited by:121SectionsAbstractPDFSupplemental Material ShareShare onFacebookTwitterLinkedInRedditEmail ToolsAdd to favoritesDownload CitationsTrack Citations AboutABSTRACTObjectives:Epidemiologic studies have shown that chronic short sleep may be associated with the development of hypertension; however, the results are controversial. This meta-analysis was conducted to determine whether the duration of sleep is associated with hypertension.Methods:Reference databases (PubMed, EmBase, the Cochrane Library, Chinese Biological Medicine database) were searched for studies related to sleep duration and hypertension. Sleep duration categories (≤ 5 h, 6 h, 7 h, 8 h, ≥ 9 h) and prevalence or incidence of hypertension in each sleep category were extracted. A general analysis and subgroup analyses stratified by gender, age, study design, and different definitions of sleep duration were conducted to evaluate the relationship between sleep duration and hypertension.Results:Thirteen articles out of a total of 1,628 articles involving 347,759 participants met the inclusion criteria. A U-shaped change in pooled odds ratios (ORs) for hypertension due to the change of sleep duration was observed. The unadjusted OR for hypertension of individuals who slept ≤ 5 h vs 7 h was 1.61, 95% CI = 1.28–2.02; those who slept ≥ 9 h vs 7 h was 1.29, 95% CI = 0.97–1.71. The pooled ORs were still significant after adjusted by age and gender. Women deprived of sleep (sleep time ≤ 5 h vs 7 h, OR = 1.68, 95% CI = 1.39–2.03) had a higher risk of hypertension than men (OR = 1.30, 95% CI = 0.93–1.83).Conclusion:Excessively longer and shorter periods of sleep may both be risk factors for high blood pressure; these associations are stronger in women than men.Citation:Wang Y, Mei H, Jiang YR, Sun WQ, Song YJ, Liu SJ, Jiang F. Relationship between duration of sleep and hypertension in adults: a meta-analysis. J Clin Sleep Med 2015;11(9):1047–1056.INTRODUCTIONSleep is an important physiological process and it takes up approximately one third of our lives. Due to the accelerated pace of modern life, the average duration of nightly sleep has decreased considerably. In Finland, the self-reported duration of sleep has decreased by about 18 min over the last 33 years.1 National surveys in the U.S. have shown a 1.5- to 2-hour decline in self-reported sleep duration over the past 50 years.2 The National Sleep Foundation has reported an increase from 12% to 16% of subjects sleeping less than 6 hours on work-days between 1998 and 2005.3 These data suggest an emerging trend of reduced sleep, which leads to a growing sleep debt among the general population.Sleep deprivation has long been associated with neurocognitive impairment, attenuation of physical strength and skill, and increased impaired judgment.4–7 However, excessively long of sleep may also leads to injury of health. Several studies have reported an association between the duration of sleep and chronic conditions, including type 2 diabetes, obesity, atherosclerosis, and hypertension.8–10 The associations between the duration of sleep and hypertension, in particular, have stimulated debate. One U.S. investigation showed that short periods of sleep led to hypertension in middle-aged adults,11 but a British study on a middle-aged population showed this influence to be real only in females and not statistically significant in males.10 An investigation by Robillard showed that sleep deprivation led to hypertension in the elderly, but there were also other studies that showed no association between the duration of sleep and hypertension in the elderly.12,13 There are also several studies showing that long periods of sleep are also associated with a higher risk for hypertension.14,15 This is in contrast to the conclusion that long periods of sleep may be a protective factor with respect to metabolic syndrome.16 It is difficult to reach a consensus using existing studies because they were performed on individuals of different races and used different sample sizes. For this reason, we conducted a meta-analysis to assess whether the evidence supports the existence of a relationship between the duration of sleep and hypertension.Most recently, we found an article describing a meta-analysis of the association between short sleep duration and hypertension.17 However, they defined short sleep duration as a duration ≤ 5, 4–5, ≤ 6, or < 7 h per night and this discordant definition of short sleep duration might not be able to show any clear association between a specific sleep duration and hypertension. In addition, they only assessed nighttime sleep duration in their study rather than 24-h sleep duration which might be an important parameter for elderly population with regular naps.18 In the present study, we used uniform standards and more meticulous analysis to determine whether the evidence supports the presence of a relationship between duration of sleep and hypertension using data collected from a large population, to determine whether individuals of different ages and genders have different susceptibilities; whether nighttime and 24-h sleep duration have different relationships with hypertension in general population; and to obtain an overall risk estimate.METHODSIdentification of Eligible StudiesThe PubMed (1966 to September 12, 2012), EmBase (1950 to September 12, 2012), Cochrane Library (1993 to September 12, 2012), and Chinese Biological Medicine (1978 to September 12, 2012) databases were searched using “sleep duration,” “sleep deprivation,” and “sleep quality” as keywords or major descriptors. The results were then crossed with the keywords “hypertension” and “high blood pressure.” There were no further restrictions regarding language or age. We tried our best to search more related literature. Grey literatures and reference lists of relevant articles were also carefully retrieved.Included and Excluded CriteriaReliable assessment of sleep duration is a challenging task that is made more difficult by the usage of different methods, instruments, and definitions in the various studies. Subjective measure of sleep duration included self-reports of average sleep during the day and night over the course of one week. We have followed previous studies that reported sleep duration categories of ≤ 5 h, 6 h, 7 h, 8 h, and ≥ 9 h. Seven hours was treated as a baseline.19,20 Objective methods in large population mainly included polysomnography. Assessment criteria for hypertension were as follows: individuals who had systolic blood pressure readings ≥ 140 mm Hg or diastolic readings ≥ 90 mm Hg or who had been diagnosed with hypertension and used antihypertensive drugs.Studies were excluded if they did not meet the definitions of hypertension or if there were no available sleep duration data or suitable reference sleep times in the article. If the duration and sources of study population recruitment overlapped more than 30% in two or more papers by the same authors, we only included one of the studies.Data ExtractionData were independently extracted by two investigators (Wang Y. and Liu S.) and checked by the other authors of this manuscript. In the case of discrepancies in confirming the study design or effect size calculations, results were carefully discussed until both investigators agreed or the third author participated. Sample characteristics included study design, country or area, study population, number of included patients, sleep duration categories, diagnostic criteria for hypertension, participants' mean age, gender, method of collection of sleep duration and high blood pressure data, and risk-effect odds ratio (OR) or adjusted OR by age, sex, or adjusted OR by age, sex, physical activity, body mass index, smoking, alcohol consumption, coffee consumption, educational level, number of social ties, depression, depressive symptoms, diabetes mellitus, and other risk factors in different model according to available variables in individual study.Study design included cross-sectional, case-control, and prospective techniques. In other studies that did not describe their specific study design type, this was inferred from the study methods. The method of assessment of sleep time included self-reports and polysomnography. The most common question was, “How many hours of sleep do you usually get in a day or at night, on average?” As for the age group, we referenced the original articles. The elderly group was defined as > 60 years, while the middle aged was referenced 45–60 years.If different periods of sleep were measured but no information regarding the association between sleep time and hyper-tension was reported, we contacted the authors and requested the missing information. If there was no response or the authors could not supply the data, then these studies were excluded.Data Synthesis and EffectsThe effects of measures of interest were odds ratios (OR) for case-control studies and relative risks (RR) for cohort studies, using the corresponding 95% confidence intervals. Random and fixed-effects models were computed. The differences between fixed and random effect models were profoundly affected by the way significance testing was conducted. Significance testing in fixed-effects models is based on the total number of participants. This allows great statistical power but limited generalizability. Significance testing in the random-effects models is based on the total number of studies included in the meta-analysis, resulting in lower statistical power but greater generalizability. In view of the higher generalizability, we preferred the random-effects model.We accessed the quality of each subgroup effects using GRADEprofiler 3.6 (GRADE Working Group).21,22 GRADE offers 4 levels of evidence quality: high, moderate, low, and very low. Randomized trials begin as high quality evidence and observational studies as low quality evidence. Quality may be downgraded as a result of limitations in study design or implementation, inconsistency of evidence (heterogeneity), indirectness of evidence, imprecision of estimates (wide confidence intervals), or publication bias. Quality may be upgraded because of a very large magnitude of effect, a dose-response gradient, and if all plausible biases would reduce an apparent treatment effect.Heterogeneity Meta-Regression and Subgroup AnalysisStatistical heterogeneity among studies was estimated using a χ2 test, Q statistics with corresponding p values, and I2 statistics. If the p value was > 0.10 or I2 ≤ 50%, statistical heterogeneity among studies was not considered apparent and a fixed-effects model was applied. When heterogeneity was present, meta-regression analysis was undertaken to determine the association between predictor variables and the effect size. Subgroups were established according to potential confounding variables. A random-effects model was used to determine pooled odds ratios and relative risks. We stratified the sleep participants by age, gender, and study design type, and then calculated the summary risk of sleep time for hypertension. The heterogeneity of each subgroup was also been evaluated.Sensitivity AnalysisWhen heterogeneity was observed, we conducted a sensitivity analysis in which one study was removed and the effects of the remaining studies were pooled to determine whether the results were affected in any statistically significant way. The effects of pooled individual studies were evaluated through both fixed and random-effects models.Publication BiasPublication bias was evaluated using funnel plots and Egger test. p values < 0.10 were considered to be statistically significant. The Duval and Tweedie Trim and Fill test was used because it estimates the number of theoretically missing studies and computes the combined effect estimate. If the meta-analysis captured all relevant studies, then these studies were also included in the analysis. The meta-analyses and subgroup analyses were performed using Review Manager Version 5.1.7 (Nordic Cochrane Centre, Cochrane Collaboration, Copenhagen, Denmark). Adjusted odds radios of sleep time for hypertension, meta-regression analysis, sensitivity analysis, and publication bias were performed using Stata software version 12.0 (Stata Corp, College Station, TX, U.S.). All statistical tests were two-tailed.RESULTSSearch ResultsWe identified 1,628 potentially relevant articles from our search of the published literature (Figure 1). We excluded 1,615 articles, including 102 duplicated articles: 1,375 articles were excluded after title review. Another 93 articles were excluded after abstract review; then 58 full-text articles were retrieved and carefully evaluated, and 35 of these studies were excluded because of a lack of available data regarding the duration of sleep and hypertension, including 7 articles related to pediatric hypertension because of various diagnostic criteria.23–29 The remaining 23 studies were carefully analyzed, and 4 studies were excluded because of a lack of suitable sleep time categorization.30–33 Three studies were excluded because the diagnostic criteria for hypertension did not meet the WHO guideline criteria.6,34,35 Two studies were excluded because of a lack of suitable hypertension population data.36,37 One study was excluded as an approximate duplicate (the same author published 2 related papers on the same population).38 Thus 10 studies were excluded (Table S1, supplemental material), and 13 articles were ultimately included in the meta-analysis.Figure 1: Flow chart of study selection.Download FigureStudy CharacteristicsSummary characteristics of the 13 included studies are given (Table 1). Of the 13 included studies, 4 were from the United States and one each from Australia, Brazil, France, Germany, South Korea, Mainland China, Spain, Taiwan, and the United Kingdom.10,11,13–15,39–46 These studies included 347,759 participants, of whom 115,007 had hypertension. The cases and total participants for each sleep duration category were as follows: 7,452 of 19,695 had ≤ 5 h of sleep; 17,524 of 53,603 had 6 h; 26,648 of 92,895 had 7 h; 41,073 of 126,544 had 8 h; and 22,310 of 54,534 had ≥ 9 h. All participants were > 18 years old. There were 6 cross-sectional studies and 7 prospective cohort studies. Two studies included both cross-sectional surveys and prospective cohort investigation.10,13Table 1 Summary of the 13 studies included in the meta-analysis.Table 1 Summary of the 13 studies included in the meta-analysis.Relationship of Sleep Duration and HypertensionWe evaluated the quality of included literature: the quality of all studies was low because study design type of included literature was observational study (Figure S3A–S3D, supplemental material). Some pooled effects was downgraded because of heterogeneity leading to serious inconsistency.The unadjusted summary risk estimates of every sleep duration group for hypertension are shown (Figures 2A–2D). Overall, we observed statistically significant associations between pooled ORs of sleep duration and hypertension. In groups of individuals who slept ≤ 5 h vs those who slept 7 h, the combined OR was 1.61, 95% CI = 1.28–2.02; those who slept 6 h vs those who slept 7 h the combined OR was 1.24, 95% CI = 1.20–1.28; those who slept 8 h vs those who slept 7 h, the combined OR was 1.12, 95% CI = 1.10–1.14 and those who slept > 9 h vs those who slept 7 h, the combined OR was 1.29, 95% CI = 0.97–1.71. We applied the random-effects model to all groups because of heterogeneity (p < 0.10, I2 > 50%).Figure 2: Forest plot of association between sleep duration and hypertension.Odds ratios (ORs) in the individual study are presented as squares with 95% confidence intervals (CIs) presented as extended lines. The pooled OR with its 95% CI is shown as a diamond. (A) Those who slept ≤ 5 h versus those who slept 7 h. (B) Those who slept 6 h versus those who slept 7 h. (C) Those who slept 8 h versus those who slept 7 h. (D) Those who slept ≥ 9 h versus those who slept 7 h.Download FigureMeta-regressionWe conducted meta-regression analysis in order to determine the source of this heterogeneity. Risk factors included study design (cross-sectional, case-control, or cohort design), sleep duration (≤ 5 h, 6 h, 7 h, 8 h, ≥ 9 h), different definitions of sleep duration (night sleep time only or 24-h total), age (middle aged or elderly), and country or area. The result of meta-regression demonstrated study design in sleep 5 h vs 7 h (p = 0.02) and sleep duration in 9 h vs 7 h (p = 0.01) contributed to the heterogeneity. Statistical comparisons with regard to specific sleep indices follow (Table 2). The heterogeneity of each subgroup was shown in (Table S2, supplemental material).Table 2 Meta-regression analysis.Table 2 Meta-regression analysis.Stratified AnalysisWe then conducted subgroup analyses and stratified the pooled risk estimate by gender, age, study design, and different definitions of sleep duration, and compared the different subgroup summary risk estimates and trends (Figure 3). In the sex subgroup analyses, women deprived of sleep (sleep time ≤ 5 h, OR = 1.68, 95% CI = 1.39–2.03, random-effects model) had a higher risk of hypertension than men (OR = 1.30, 95%CI = 0.93–1.83, random-effects model), and either men or women who slept longer (sleep time ≥ 8 h versus 7 h) had an increased risk of hypertension. With respect to study design, the risk estimate and confidence interval of the prospective cohort study were found to be smaller than those of the cross-sectional studies among individuals who slept for different periods. Relative risk of sleep time ≤ 5 h in prospective cohort studies was found to be 1.31 (95% CI = 1.15–1.49, random-effects model); and the OR was 1.81 (95% CI = 1.56–2.10, random-effects model) in cross-sectional studies. In the age subgroup analyses, the pooled OR (OR = 1.61, 95% CI = 1.27–2.04, random-effects model) for short sleep duration (sleep time ≤ 5 h) for hypertension in middle-aged people was higher than in older people (OR = 1.25, 95% CI = 0.94–1.68, random-effects model); conversely, long periods of sleep (sleep time ≥ 9 h, OR = 1.30, 95% CI = 1.04–1.63, random-effects model) in older people were associated with a greater risk of hypertension than in middle-aged people (OR = 1.16, 95% CI = 0.73–1.85, random-effects model). In the different sleep duration definition subgroups, only sleep duration ≤ 5 h was accompanied with high risk of hypertension in nighttime sleep analysis, while in 24-h sleep duration analysis, all short and long sleep durations groups were related to hypertension compared with 7-h reference group.Figure 3: Subgroup analysis of association between the duration of sleep and hypertension.Pooled odds ratios (ORs) in each group are presented as squares with 95% confidence intervals (CIs) are represented by extended lines. The horizontal reference line represents an OR value of “one.” The dashed line represents the effects of different sleep durations on hypertension. (A) The male subgroup. (B) The female subgroup. (C) The cross-sectional study subgroup. (D) The cohort study subgroup. (E) The middle-aged subgroup. (F) The older-aged subgroup. (G) The night sleep duration subgroup. (H) The 24 h sleep duration subgroup.Download FigureSensitivity AnalysisWe also conducted a sensitivity analysis to evaluate whether removal of a study from this analysis significantly affected remaining pooled results. Two studies performed on individuals who slept ≤ 5 h vs 7 h (those by Fang et al. and Magee et al.) were omitted, and the remaining pooled effects were statistically significant. When one study of those individuals who slept 8 h vs 7 h and ≥ 9 h vs 7 h (Magee et al.), was omitted, the remaining pooled effects were statistically significant (Figures S1A–S1C, supplemental material).We extracted adjusted odds ratios from 4 included studies.13,40,41,43 The summary odds ratio simultaneously adjusted by age and gender for ≤ 5 h vs 7 h was 1.23, 95% CI = 1.01–1.49; for 6 h vs 7 h was 1.13, 95% CI = 1.02–1.25; for 8 h vs 7 h was 1.06, 95% CI = 0.96–1.17; and for ≥ 9 h vs 7 h was 1.18, 95% CI = 1.03–1.36. The first, second, and fourth comparisons above were statistically significant.Publication BiasWe then evaluated publication bias using a funnel plot (Figure S2A–S2D, supplemental material) and Egger's test. No groups showed publication bias (for those who slept ≤ 5 h vs 7 h, t = 0.68, p = 0.509, 95% CI = −2.18–4.14; for those who slept 6 h vs 7 h, t = 0.43, p = 0.68, 95% CI = −2.33–3.46; for those who slept 8 h vs 7 h, t = 0.35, p = 0.73, 95% CI = −1.45–2.00; and for those who slept 9 h vs 7 h t = −0.84, p = 0.42, 95% CI = −3.21–1.47).DISCUSSIONOur extensive analysis showed that relative to the group of the people with 7 h daily sleep, all other sleep durations groups (≤ 5 h, 6 h, 8h, and ≥ 9 h groups) were accompanied by some higher risk of hypertension. The pooled odds ratio (OR) was still significant, even after adjusted by age and gender. This indicates that excessively longer or shorter periods of sleep may both be risk factors for high blood pressure, especially in female. Further stratified analysis showed that cross-sectional studies depicted an obvious U-shaped change in pooled ORs for hypertension due to the change in the duration of sleep. The existence of this association was also supported in the prospective cohort studies, although it became attenuated to some extent.In our general analysis of sleep duration and hypertension, all suitable studies showed extreme sleep periods to be associated with a higher risk for hypertension. Sleep duration 5 h or less was found to have the largest OR relative to 7 hours. Although it appears that sleep deprivation causes hypertension, the mechanism(s) underlying this association is not well understood. There are some relevant theories, and nocturnal sympathetic activation is likely to be the key.47 Under normal sleep conditions, the vagal system is activated and catecholamine biosynthesis is decreased.48,49 Sleep deprivation, however, seems to act as a stressor on the body and activates the sympathetic system,50 based on evaluations of serum stress hormones after sleep deprivation. As a result, the rennin-angiotensin-aldosterone system is stimulated, and the synthesis of central catecholamines is increased.51–53 This leads to blood vessel constriction, which increases blood pressure, potentially leading to hypertension.54 Another study has shown that after a period of chronic sleep deprivation, flow-mediated dilation of artery and intracellular magnesium concentrations both decreased.55 Magnesium is considered a physiologic calcium antagonist capable of decreasing vascular tone.56–58 Magnesium deficiency leads to arterial constriction thus affecting vessel dilation. In this way, conditions of long-term vascular tension after sleep restriction may play a role in the development of hypertension. Maintaining a healthy lifestyle is important to the establishment of normal biological rhythms. The central biological clock or suprachiasmatic nucleus (SCN) requires repeated metabolic cues from light exposure, sleep, activity, and feeding to generate and organize autonomic rhythms.59,60 Dramatic alterations in these parameters due to prolonged wakefulness lead to a disturbance in circadian rhythmicity of blood pressure, and finally results in hypertension.61Excessively long periods of sleep are also associated with increased risk of hypertension. The underlying biologic mechanisms are not well understood, but other risk factors might impact the association, including physical activity. In one study, long periods of sleep were often accompanied by less physical activity, and inactivity was related to increased risk of hypertension.9 A study from the Netherlands showed that long periods of sleep were related to high total cholesterol concentrations and a high total/HDL cholesterol ratio.62 There are also studies showing that long periods of sleep are associated with diabetes, obesity, and chronic heart disease.14,62,63 These diseases are often accompanied by hypertension. Long periods of sleep may be related to sleep-disordered breathing or poor sleep quality.64–66 These phenomena indicate that long periods of sleep may constitute another marker of poor health.In our further stratified analysis, we found that the associations between short sleep duration and hypertension are stronger in women than men. The results from a recent published study might partially explain the mechanisms underlying these sex differences.67 In their experimental sleep deprivation study, they found sleep deprivation increased blood pressure in both men and women, but the sympathetic baroreflex operating point was shifted rightward and downward only in men, not in women. The baroreflex detected increased in arterial pressure and consequently reduced muscle sympathetic nerve activity (MSNA), which in turn had a protective function on blood pressure. Women, on the other hand, demonstrated a significant increase in arterial blood pressure similar to the men, but the acute hypertensive response was not accompanied by a concurrent decrease of MSNA. In addition, sleep deprivation has also repeatedly been shown to significantly decrease testosterone levels which were correlated to reductions of MSNA in men.68–70 The self-reported sleep habits between men and women also tends to be different; women were more likely to report feeling unrested, but less likely to have an high Epworth Sleepiness Scale score.71 This error may be almost impossible to eliminate.In our analysis stratified by age, extremely short sleep duration (≤ 5 h) is associated with hypertension only in the middle-aged population but not in the elderly group. It is important to pay attention to the phenomenon that the elderly are often retired and therefore have more opportunity to nap. In addition, the prevalence of excessive daytime sleepiness (EDS) increases in older populations.18 So for the elderly group, it is worth investigating the association between nighttime or 24-h sleep duration with hypertension separ" @default.
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• W762533598 title "Relationship between Duration of Sleep and Hypertension in Adults: A Meta-Analysis" @default.
• W762533598 cites W124262366 @default.
• W762533598 cites W140877541 @default.
• W762533598 cites W146265137 @default.
• W762533598 cites W1488974332 @default.
• W762533598 cites W1509765910 @default.
• W762533598 cites W1522008731 @default.
• W762533598 cites W1550940849 @default.
• W762533598 cites W1586093278 @default.
• W762533598 cites W1680594450 @default.
• W762533598 cites W1717754754 @default.
• W762533598 cites W1770765878 @default.
• W762533598 cites W1969838275 @default.
• W762533598 cites W1972370821 @default.
• W762533598 cites W1975848769 @default.
• W762533598 cites W1976234290 @default.
• W762533598 cites W1978378127 @default.
• W762533598 cites W1980032301 @default.
• W762533598 cites W1982491358 @default.
• W762533598 cites W1983398247 @default.
• W762533598 cites W1984000608 @default.
• W762533598 cites W1986323681 @default.
• W762533598 cites W1990399549 @default.
• W762533598 cites W1990672256 @default.
• W762533598 cites W1992914313 @default.
• W762533598 cites W1993548744 @default.
• W762533598 cites W1996391039 @default.
• W762533598 cites W1997151200 @default.
• W762533598 cites W2003011166 @default.
• W762533598 cites W2017874928 @default.
• W762533598 cites W2019206907 @default.
• W762533598 cites W2025303888 @default.
• W762533598 cites W2045209949 @default.
• W762533598 cites W2053210485 @default.
• W762533598 cites W2055788068 @default.
• W762533598 cites W2059820978 @default.
• W762533598 cites W2062472162 @default.
• W762533598 cites W2063947251 @default.
• W762533598 cites W2066146594 @default.
• W762533598 cites W2066978998 @default.
• W762533598 cites W2070052340 @default.
• W762533598 cites W2076877526 @default.
• W762533598 cites W2083542549 @default.
• W762533598 cites W2086258247 @default.
• W762533598 cites W2097837926 @default.
• W762533598 cites W2102619340 @default.
• W762533598 cites W2102934552 @default.
• W762533598 cites W2102972026 @default.
• W762533598 cites W2103971752 @default.
• W762533598 cites W2104811064 @default.
• W762533598 cites W2107471829 @default.
• W762533598 cites W2109376534 @default.
• W762533598 cites W2116063184 @default.
• W762533598 cites W2118591666 @default.
• W762533598 cites W2122288088 @default.
• W762533598 cites W2126811840 @default.
• W762533598 cites W2127097910 @default.
• W762533598 cites W2127331384 @default.
• W762533598 cites W2130507759 @default.
• W762533598 cites W2134236426 @default.
• W762533598 cites W2135251100 @default.
• W762533598 cites W2136189569 @default.
• W762533598 cites W2139826323 @default.
• W762533598 cites W2150819010 @default.
• W762533598 cites W2157422098 @default.
• W762533598 cites W2165010366 @default.
• W762533598 cites W2171647161 @default.
• W762533598 cites W2189437039 @default.
• W762533598 cites W2190946050 @default.
• W762533598 cites W2316139099 @default.
• W762533598 cites W2317083615 @default.
• W762533598 cites W2327636182 @default.
• W762533598 cites W2330623531 @default.
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