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.