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Logo of nihpaAbout Author manuscriptsSubmit a manuscriptHHS Public Access; Author Manuscript; Accepted for publication in peer reviewed journal;
Circulation. Author manuscript; available in PMC 2009 December 28.
Published in final edited form as:
PMCID: PMC2798149

Sleep Quality and Elevated Blood Pressure in Adolescents

Sogol Javaheri, MA,1 Amy Storfer-Isser, MS,1,2,4 Carol L Rosen, MD,1,2,3 and Susan Redline, MD MPH1,2,4



We assessed whether insufficient sleep is associated with pre-hypertension in healthy adolescents.

Methods and Results

Cross-sectional analysis of 238 adolescents, all without sleep apnea or severe co-morbidities. Participants underwent multiple day wrist actigraphy at home to provide objective estimates of sleep patterns. In a clinical research facility, overnight polysomnography, anthropometry, and 9 blood pressure (BP) measurements over 2 days were made. Exposures were actigraphy-defined low weekday sleep efficiency, an objective measure of sleep quality (low sleep efficiency ≤85%) and short sleep duration (≤6.5 hrs). The main outcome was pre-hypertension (≥90th%ile for age, sex, and height), with systolic and diastolic BP as continuous measures as secondary outcomes. Pre-hypertension, low sleep efficiency, and short sleep duration occurred in 14%, 26%, and 11% of the sample, respectively. In unadjusted analyses, the odds of pre-hypertension was increased 4.5-fold (95% CI: 2.1, 9.7) in adolescents with low sleep efficiency and 2.8-fold (95% CI: 1.1,7.3) in those with short sleep. In analyses adjusted for gender, BMI percentile and socioeconomic status, the odds of pre-hypertension was increased 3.5-fold (95% CI: 1.5. 8.0) for low sleep efficiency and 2.5 fold (95% CI: 0.9, 6.9) for short sleep. Adjusted analyses showed that adolescents with low sleep efficiency, on average, had a 4.0 ± 1.2 mm Hg higher systolic BP compared to other children(p<0.01).


Poor sleep quality is associated with pre-hypertension in healthy adolescents. Associations are not explained by socioeconomic status, obesity, sleep apnea or known co-morbidities, suggesting that inadequate sleep quality is associated with elevated blood pressure.

Keywords: blood pressure, epidemiology, pediatrics


Hypertension is an increasingly prevalent health problem in adults and adolescents alike. Between 1988 and 1999, pre-hypertension (i.e., a blood pressure {BP} ≥ the 90th percentile for height, age, and gender) and hypertension were estimated to increase in children by 2.3% and 1%, respectively. 1 Childhood hypertension is associated with hypertension in adulthood, a risk factor for cardiovascular disease incidence and mortality. 2-5 It is also associated with end-organ damage in both children and adults, notably left ventricular hypertrophy. 6, 7

Several studies have implicated insufficient sleep as a risk factor for hypertension in adults 8-12. Although the etiology is unclear, experimental studies indicate that shorter sleep results in metabolic and endocrine dysfunction that may contribute to cardiovascular disease. 13-17 Studies in both adult and pediatric populations also have reported associations of shorter sleep duration to obesity and impaired glucose tolerance. 14, 18, 19 These findings have a potentially large public impact given the frequency of sleep curtailment. 20

Few studies have addressed the relationship between sleep and hypertension in children. A higher level of diastolic, but not systolic blood pressure (BP) was reported in children with obstructive sleep apnea compared to primary snorers. 21 The Tucson’s Children’s Assessment of Sleep Apnea Study found that elevations in systolic and diastolic BP were independently associated with sleep efficiency, respiratory disturbance index (a measure of sleep apnea), and obesity in 230 children aged 6 to 11 years.22 To our knowledge no studies have examined the association between insufficient sleep and BP in adolescents free of sleep apnea. In this report, we examine the relationship between pre-hypertension and systolic and diastolic BP levels with objective measures of sleep quality and duration in a community-based cohort of adolescents. First, we hypothesize that adolescents with poor sleep quality or short sleep duration will be at increased odds of pre-hypertension. Second, we posit that adolescents with short sleep duration or poor sleep quality will have higher systolic and diastolic blood pressure readings on average compared to adolescents with better quality sleep. We excluded adolescents with clinically significant levels of sleep apnea to minimize the influence of this exposure on BP and sleep duration measurement.


Study Population

The sample was derived from the Cleveland Children’s Sleep and Health Study (CCSHS), a longitudinal cohort study. Data for this analysis are from 238 adolescents free of severe illnesses who participated in an examination performed 2002-2006 aimed at participants aged 13 to 16 years. Details of the study population have been reported elsewhere25,23 and are reviewed in an On Line Supplement.

Study Protocol

Adolescents underwent 5 to 7 day wrist actigraphy and completed a daily sleep log at home during the week prior to a clinical research center exam and when free of acute illness. After this period of in-home monitoring, participants were studied in a dedicated clinical research center where overnight polysomnography, physiological and anthropometric assessments were performed using a standardized protocol .23,24 Examinations at the research center began at approximately 17:00 and ended the following day at 11:00. Informed consent was obtained from the child’s legal guardian and written assent was obtained from the child. The study was approved by the governing institutional review board.



Sleep wake estimation was made using wrist actigraphy (Octagonal Sleep Watch 2.01; AMI, Ambulatory Monitoring Inc., Ardsley, NY) analyzed using the Action-W software and the Time Above Threshold algorithm. 25 Using weekday data (minimal 3 days), mean sleep duration and mean sleep efficiency, an objective measure of sleep continuity and quality, defined as the percentage time in bed estimated to be asleep (i.e., total time estimated to be asleep/total time in bed for the major sleep period) *100) were calculated. Adolescents with a sleep efficiency ≤85% were considered to have low sleep efficiency. Given the lack of data on cutoffs for defining “short sleep duration” in this age, we used the lowest decile of mean sleep duration on weekdays to define short sleep duration, which approximated 6.5 hours.

Blood Pressure

Three BP readings were obtained at each of three times (21:00 [supine] the night of the polysomnography, 08:00 [supine], and 9:30 [sitting] the following morning) following published guidelines. 23 After a 10 minute rest period, BP was obtained using a calibrated sphygmomanometer by trained nurses. The mean systolic BP and diastolic BP values used in primary analyses were based on the average of all nine measurements. Pre-hypertension was identified if the systolic and/or diastolic BP ≥90th percentile for age, gender, and height. 4 Hypertension (HTN) was defined as systolic BP or diastolic BP ≥ 95th percentile. One adolescent using anti-hypertensive medication was classified as having HTN.

Other Measurements

A rigid stadiometer was used to measure height, and a calibrated digital scale to measure weight. Body mass index was calculated by dividing the weight in kilograms by height in meters squared and converted into age and sex adjusted percentiles ( Overweight was defined as a BMI ≥ 95th percentile. Adolescents who were reported to snore loudly at least 1-2 times per week during the past month were categorized as snorers. The apnea hypopnea index was defined as all obstructive apneas and l hypopneas with a ≥ 3% desaturation per sleep hour from the polysomnogram. Socioeconomic status (SES) measures included parent report of educational level and family income. Additionally, the census tract of the child’s residence when initially enrolled in the study was linked to the corresponding 2000 U.S. Census Bureau database, and median income of the census tract was ascertained ( A composite SES z-score was created by averaging the sample z-scores for these three measures. Tanner staging was performed by a physician to determine pubertal status 26, 27 . Preterm status was ascertained from birth records and defined as a gestational age <37 weeks. Attention Deficit Hyperactivity Disorder (ADHD) was defined as parent reported doctor’s diagnosis of ADHD and either condition currently present or medication/stimulant use for ADHD during the past year. Using a standardized questionnaire, adolescents reported the frequency with which they consumed caffeine after 6 PM in the evening during the past month; those reporting “frequently” or “always” consuming caffeine were coded as consuming caffeine in the evening.

Statistical Analysis

Between-group differences for the binary outcome, pre-hypertension, were assessed using the Pearson chi-square test for categorical variables, the two-sample t-test for normally distributed variables, and the Wilcoxon Rank-Sum test for non-normally distributed measures. To assess confounding, associations between the primary exposures, low sleep efficiency (≤85%) and short sleep duration (≤6.5 hrs), and sociodemographic characteristics were also examined. Spearman and Pearson correlations assessed the strength of the linear relationship between sleep characteristics obtained from polysomnography and actigraphy. Logistic regression analyses were used examine whether adolescents with short sleep duration or low sleep efficiency were at increased odds of pre-hypertension. Given the relatively small number of adolescents with pre-hypertension, covariate adjustment was limited to the SES z-score and the 2 variables most strongly associated with pre-hypertension: gender and BMI percentile. Multiple linear regression, adjusting for age, gender, race, preterm status, BMI percentile, and SES z-score, was used to examine the linear associations between sleep duration or sleep efficiency with continuously measured systolic and diastolic blood pressure levels. Additional analyses included low sleep efficiency from the polysomnography as the exposure. Residual confounding by snoring or the apnea hypopnea index also was assessed by including these measures as covariates in the adjusted analyses.

Statement of Responsibility

The authors had full access to and take full responsibility for the integrity of the data. All authors have read and agree to the manuscript as written.


Characteristics of the analytic sample are shown in Table 1. The average participant was age 13.7 ± 0.7 years. As designed, the sample had an approximately 50% representation of boys, African Americans and children born prematurely. One fifth of the sample was overweight. Approximately one-fourth reported their household income as less than $20,000 per year. Sixty-one adolescents (26%) had low sleep efficiency. Average weekday sleep duration was 7.71 hours and 11% of the sample slept ≤ 6.5 hrs.

Table 1
Sample Characteristics

Sample characteristics stratified by pre-hypertension are also shown in Table 1. Overall, 33 children (14%) met the criteria for pre-hypertension, including 19 who had pre-hypertension and 14 who were hypertensive. Compared to normotensive adolescents, those with pre-hypertension tended to have a higher proportion of males, higher BMI and were more frequently from neighborhoods with a low median income (p-values between 0.05 - 0.10). Both low sleep efficiency (p<.0001) and short sleep duration (p = 0.06) were more than two-fold more prevalent in those with pre-hypertension compared to normotensive adolescents.

The distribution of various BP measures is further detailed in Table 2. Using the mean of nine BP readings, approximately 11% of the sample was classified with elevated systolic BP and 5% with elevated diastolic BP. All measures of systolic BP were significantly higher among the adolescents with low sleep efficiency compared to those with higher sleep efficiency. Adolescents with low sleep efficiency also had a higher prevalence of elevated diastolic BP and had higher 08:00 diastolic BP values. Adolescents with short sleep duration did not differ from those with longer sleep duration in regards to systolic BP, but had a higher average diastolic BP and higher prevalence of elevated diastolic BP (24.0% vs 2.4%; p<0.001).

Table 2
Blood Pressure In Subgroups Defined by Sleep Quality

To assess confounding, associations among the sleep exposures and sociodemographic characteristics were examined (see on-line supplement). Adolescents with low sleep efficiency had a higher BMI, were more often male, and were from households with lower incomes and lower levels of caregiver education. These characteristics were not significantly associated with short sleep duration. Approximately two-thirds (68.0%) of adolescents with short sleep duration also had low sleep efficiency, while 27.9% of adolescents with low sleep efficiency also had short sleep duration. The correlation between mean weekday sleep efficiency and sleep efficiency from the night of the polysomnography was low (r= 0.13, p=0.04), as was the correlation between mean weekday sleep duration and sleep duration from the night of the polysomnography (r=-0.06, p=0.37). Approximately one-third (32.8%) of adolescents with low sleep efficiency based on actigraphy also had low sleep efficiency from the polysomnography.

The results of the logistic regression models of the association between each sleep measure and the odds of pre-hypertension are shown in Tables Tables3a3a and and3b.3b. After adjusting for gender, BMI percentile and SES z-score, those with low sleep efficiency had 3.5 times the odds of pre-hypertension compared to those without low sleep efficiency (95% CI: 1.54, 7.96). Short sleep duration was associated with a 2.8-fold increased odds of pre-hypertension in unadjusted analyses (95% CI: 1.07, 7.34), but this association was modestly attenuated after adjusting for gender, BMI percentile and SES z-score (OR: 2.54; 95% CI: 0.93, 6.90).

Table 3a
Association Between Low Sleep Efficiency And Odds of Pre-Hypertension
Table 3b
Association Between Short Sleep And Odds of Pre-Hypertension

The unadjusted and adjusted associations between continuously measured systolic and diastolic BP levels with sleep efficiency are shown in Table 4. After adjusting for age, gender, race, term status, BMI percentile and SES z-score, the model predicts that each 5 percentage increase in sleep efficiency was associated with a 1.5 ± .40 mmHg decrease in systolic BP (p<.001). Weaker associations were observed between sleep efficiency and diastolic BP; i.e., each 5 percentage increase in sleep efficiency was associated with a 0.65 ± .35 decrease in diastolic BP (p=.05). When modeling low sleep efficiency as a dichotomous exposure, the adjusted model estimates that adolescents with low sleep efficiency had a mean systolic BP that was on average, 3.99 ± 1.24 mm Hg higher compared to those with higher sleep efficiency (p=0.002). Including sleep duration as a continuously measured covariate did not alter the primary associations of sleep efficiency and BP (data not shown).

Table 4
Association Between Actigraphy Sleep Efficiency (per 1% increase) & Continuously Measured BP

Similar to the models of pre-hypertension, sleep duration was more weakly associated with continuously measured systolic and diastolic blood pressure compared to sleep efficiency (Table 5).

Table 5
Association Between Actigraphy Sleep Duration (per 1 hour increase) & Continuously Measured BP

Additional Analyses

The primary analyses also were repeated with low sleep efficiency ascertained via polysomnography as the exposure. Consistent with the results of the primary analysis, after adjusting for gender, BMI-percentile and SES z-score, those with polysomnography sleep efficiency ≤85% had nearly 3 times the odds of pre-hypertension as those with better sleep (OR=2.83, 95% CI: 1.28, 6.24). Also consistent with the results of the actigraphy-defined sleep exposures, in adjusted analyses, each one percentage increase in sleep efficiency was associated with a 0.20 ± .06 decrease in systolic BP (p<.001). Similarly, those with low polysomnography sleep efficiency had systolic BP that was 3.26 ± 1.25 mm HG higher on average compared to those with better sleep (p=0.01).

Although analyses were restricted to children without clinically significant sleep apnea, additional analyses assessed potential residual confounding by snoring or the apnea hypopnea index (i.e., in an apnea hypopnea index range of 0 - 4.9). The results show that loud snoring was not significantly associated with pre-hypertension, systolic BP or diastolic BP. In contrast, while the apnea hypopnea index does not confound the association between the outcomes and the sleep exposures, it was associated with increased odds of pre-hypertension after adjusting for low sleep efficiency, gender and BMI percentile; i.e., for each one-unit increase in the apnea hypopnea index, the odds of pre-hypertension increased by 47% (OR=1.47, 95% CI: 1.00, 2.17). Similarly, the apnea hypopnea index was significantly associated with systolic BP in adjusted models; after adjusting for subject characteristics and low sleep efficiency, for each one-unit increase in apnea hypopnea index, mean systolic BP increases by 1.65 mm Hg on average (p=0.009).


To our knowledge, this is the first reported association between low sleep efficiency and short sleep duration objectively measured in the child’s usual sleep environment with elevated BP (pre-hypertension or hypertension) in adolescents without clinically significant levels of sleep apnea. Specifically, adolescents with poor sleep quality, as measured by a sleep efficiency of ≤ 85%, were at 3.5-fold increased odds of being pre-hypertensive or hypertensive. Similar findings were observed when single night polysomnography was used to quantify sleep efficiency. The association between low sleep efficiency and pre-hypertension persisted even after adjusting for gender, SES and adiposity. The results did not appreciably change after adjusting for snoring or the apnea hypopnea index. Short sleep duration was also associated with a 2.5-fold increase in odds of pre-hypertension or hypertension. However, it was not clear if this association was attributable to the low sleep efficiency found in a majority of the adolescents with short sleep duration.

In adults, poor sleep quality identified by questionnaires has been reported in association with an increased prevalence of hypertension 12 and an increased rate of “non-dipper hypertension.” 28 However, poor sleep quality in adults often occurs in the presence of primary sleep disorders, such as sleep apnea or insomnia, or secondary to numerous co-morbidities. Therefore, adult studies reporting associations with disturbed or reduced sleep and hypertension have been cautiously interpreted due to concerns over residual confounding. 10 One large prospective study reported associations of short sleep duration in women but not men 8, while another study showed no association of hypertension and sleep duration in the elderly, a group with a high prevalence of morbidities. 29 Since adolescents with major co-morbidities, including those with clinically significant levels of sleep apnea, were excluded from our analyses (to minimize confounding and reduce measurement error), it is unlikely that major confounding due to medical illnesses, medications, or sleep-related hypoxemia explains the strong association between low sleep efficiency and elevated BP. Given that the association between BP and low sleep efficiency persisted even after adjusting for average sleep duration, our findings also suggest that recurrent arousals or awakenings from sleep (which reduce sleep efficiency) are associated with elevated blood pressure. Our findings are consistent with a report from a sample of pre-adolescent children studied with single night polysomnography which demonstrated an association between low sleep efficiency and elevated BP after adjusting for the apnea hyponea index. 22

The 3.5-fold odds of pre-hypertension or hypertension in children with low sleep efficiency, if causal, suggests associations with a potential large public health impact. Although the overall prevalence of low sleep efficiency in general pediatric samples is unknown, our prevalence of 26% is likely an under-estimate given the exclusion of children with sleep disorders and significant co-morbidities. Our finding of an increased prevalence of low sleep efficiency among vulnerable population subgroups, such as poorer children and those of minority ethnicity, may be of special concern since these groups are known to be at risk for hypertension and other adverse health outcomes.

Low sleep efficiency was associated with an average adjusted increase in systolic BP of 4 mm Hg. Although limited data are available in children to interpret the clinical significance of this absolute elevation, large cohort studies suggest a log-linear increase in morbidity in association with incremental changes in systolic blood pressure. 30

Short sleep duration was associated with a 2.5-fold increased odds of pre-hypertension, an association partly attributable to low sleep efficiency. Short sleep duration has been increasing in all ages31 and is also associated with an increased risk for obesity. 13, 16-18 Efforts to optimize sleep in childhood, thus, may improve the BP profile of children through obesity dependent and independent pathways. Further work is needed to dissect the relative influences of sleep curtailment from sleep disruption on health outcomes, which will be important in directing whether future interventions would be best directed at improving sleep time, sleep consolidation, or both.

The etiology of low sleep efficiency in healthy adolescents is unclear. Sensitivity analyses did not indicate an association between low sleep efficiency with common childhood disorders such as asthma or attention deficit hyperactivity disorder or with caffeine or tobacco use, nor were these variables confounders in the association between sleep efficiency and BP (data not shown). It is possible that unknown psychological disorders may have confounded our results, but this seems unlikely given the strong associations and community sampling design.

Although children with significant sleep apnea were excluded from our analyses, the apnea hypopnea index (in a range of 0 to 4.9) was significantly associated with pre-hypertension and systolic blood pressure after adjusting for sleep efficiency. The latter suggests that even mild sleep disordered breathing may contribute to abnormal blood pressure levels, a result consistent with reports of more severely affected children from sleep clinic samples. 21

Strengths of this report are the inclusion of a community-based sample of children, minimizing referral biases, and the use of objective measures of sleep duration and multiple measures of BP, minimizing measurement error and reporting biases. By characterizing numerous risk factors and co-morbidities, we were able to restrict the analytical sample to children without disorders likely to confound associations with sleep quality. Although former pre-term children were over-represented by design, there was no evidence of any differences in the exposures, responses, or associations between preterm and full term children, suggesting our results should be generalizable to other pediatric samples.

There are no established cutoffs to define thresholds of sleep duration or sleep efficiency that increase morbidity in adolescents. In adults, sleep durations of < 6 hrs have been associated with a variety of adverse health outcomes 15, 19, 32, 33 and sleep efficiencies of < 85% are considered low. Our choice for defining short sleep duration as less than 6.5 hrs was to approximate the cutoff associated with hypertension risk in adults, 10 which, in our sample, represented the lowest decile. However, examination of a larger sample may permit a more comprehensive assessment of dose-response and threshold levels for each sleep exposure.

A limitation of this cross-sectional study is that BP status was determined from measurements made on two consecutive days. Since BP may vary from day to day, repeated measurements over time are needed to identify children with persistent elevations in BP. Another limitation is that the reported associations do not provide proof of causality. We also cannot exclude the possibility that elevated BP operates as a risk factor for poor sleep. It is important, however, to interpret our findings in light of the biological plausibility of the observed associations and experimental data that show acute effects of sleep disruption on BP. Mechanisms linking poor sleep efficiency or sleep deprivation with hypertension may be through disruptions in cortisol secretion 19, 34, 35 and stimulation of the renin-angiotensin system and sympathetic nervous system, as measured by increased secretion of catecholamines 36 and abnormalities in sympathovagal balance, 37 and through abnormal secretion of vasoactive hormones, including endothelin, vasopressin, and aldosterone. 38 Experimental sleep disruption has been associated with elevated BP in sleep in normal subjects. 39 While some experimental models suggest that sustained elevations in BP require sleep fragmentation to occur in a background of intermittent hypoxemia 40 (as occurs with sleep apnea), sleep fragmentation may be associated with elevated BP even in adults with a low apnea hypopnea index 41 or with simple snoring 11. Prospective and interventional studies are needed to provide further evidence of causality and also to address whether improving sleep quality and duration reduce BP and risk of hypertension.

In summary, extensive analyses using objective measures of sleep quality and duration and multiple measures of BP provide evidence for a strong association of low sleep efficiency with increased risk of pre-hypertension and hypertension in a healthy sample of adolescents. Our data suggest that low sleep efficiency may more consistently be associated with pre-hypertension than short sleep duration. Future research is needed to address whether prevention of hypertension in children should not only include weight management and exercise, but also include optimization of sleep. Our data underscore the need to monitor quantity and quality of sleep as part of health supervision in children.

Supplementary Material


Funding: Supported by grants: NIH HL07567, HL60957, RO1 NR02707, M01 RR00080 and 1U54CA116867.


Disclosures: Carol Rosen has received a Subcontract from Advanced Brain Monitoring, Inc to provide clinical research services funded through a NIH SBIR. Susan Redline has received a Subcontract from Cleveland Medical Devices Inv to provide clinical research services as part of a NIH SBIR. S Javaheri and Amy Storfer Isser do not have any disclosures.

Clinical Implications:

Childhood hypertension is a risk factor for adult hypertension and for target-organ damage. Early recognition and intervention of childhood hypertension are believed to be important in reducing risk of cardiovascular morbidity in adulthood. Traditional approaches for intervention focus on the role of overweight as a contributing cause of hypertension, and include weight reduction, increased physical activity and nutritional changes. The current report identifies a significant association between increased blood pressure and poor sleep quality (i.e., increased wake time during the sleep period), found in 26% of a community sample of adolescents. Independent of obesity, gender and socioeconomic status, and unrelated to sleep apnea, adolescents with poor sleep had a 3.5 fold increased risk of pre-hypertension or hypertension. This finding suggests that approaches for optimizing sleep quality and duration in children may complement other behavioral approaches for preventing or treating pediatric hypertension. Monitoring sleep quality and duration in children as part of their health supervision may help identify children who are at risk for both sleep problems and hypertension, and who would benefit from behavioral interventions aimed at improving sleep.


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