How many hours of sleep are needed to stay in good health?
This frequent and still partly unresolved question has become an important social issue. This is because modern lifestyle contributes to a growing trend of reduced sleep duration, especially on weekdays, leading to chronic sleep deprivation .
Sleep requirements constitute a continuum and are normally distributed in the general population. The amount of sleep we need depends on various factors. Age and sex are important determinants, but we should not forget specific conditions such as pregnancy and previous sleep deprivation. Also, quality of sleep is significantly related to the number of sleep hours required for an effective nocturnal rest. However, the length of sleep needed in a given person is also an individual feature, probably with a genetic background. In fact, the individual sleep pattern is already evident in childhood and tends to persist throughout a person's life [2–4]. Whereas most normal adults typically require 7–8 h of sleep every 24 h for well being, some individuals may need more or less sleep time to avoid experiencing daytime somnolence and/or impairment in daytime performance.
Another reason for which the optimal sleep duration is not a universal number is the fact that it is determined by two different factors: a person's basal sleep need (i.e. the amount of sleep one needs on a regular basis for optimal daytime performance), and person's sleep debt (i.e. the accumulated deficit of sleep time due to poor sleep habits in previous days, related to a number of pathologic conditions, shift work and need of afterhours work or awakenings due to environmental interferences). Given these complex mechanisms, the impact of sleep on health-related outcomes is, thus, determined by the individual interaction between basal sleep need and sleep debt, more than by just the absolute sleep duration.
In recent years, the evaluation of individual sleep patterns has gained considerable interest due to the growing evidence of the relevance of sleep features in the context of cardiovascular and metabolic alterations. More specifically, a number of studies have suggested that short (<7 h) sleep duration is associated with an increased prevalence of arterial hypertension [5–8], particularly when combined with subjective insomnia . These cross-sectional observations were extended by the finding of increased risk of developing hypertension in middle-aged short sleepers in longitudinal studies [8,10,11]. Moreover, as recently summarized by Cappuccio et al. in two meta-analyses, sleep duration appears to directly and indirectly predict cardiovascular outcomes and all-cause mortality. Interestingly, in these meta-analyses the observed relationship between sleep duration and outcome was U-shaped, both too long and too short sleep duration being associated with worse prognosis [12,13].
The article by Faraut et al. published in the current issue of Journal of Hypertension provides further evidence in this field by addressing the association between hypertension and sleep duration in patients referring to primary care physicians in the frame of a cross-sectional survey, which included about 1000 participants. The principal finding of this study is that sleeping 5 h or less was independently associated with higher prevalence of hypertension, the point estimate of odds ratio being 1.8 compared with a reference group sleeping 7 h. This finding largely confirms the results obtained in previous studies. Moreover, the study by Faraut et al. has the obvious limitation of any cross-sectional analysis, that is the inherent inability to demonstrate the causal nature of such relationship. Another limitation of this study is that sleep duration was self-assessed, with no information on the time window over which sleep patterns were explored. Although self-assessment of sleep was used in previous studies, this approach certainly does not guarantee a precise assessment of mechanisms linking short sleep with hypertension . In fact, insomnia or sleep deprivation is variably assessed by history of symptoms in the preceding weeks, months or years, thus including in the analysis the duration of sleep characterizing both occasional as well as chronic insomnia patients. Finally, definition of hypertension was based on conventional blood pressure (BP) measurements only, without any assessment of out-of-office BP levels and particularly of nocturnal BP . Notwithstanding the above limitations, some features of this study make it somewhat different compared with previous reports. The study was performed in a primary care setting, so that its results apply to the real life situation in which a large proportion of hypertensive patients are handled. This has allowed the authors to collect information on a large number of variables, including a number of clinical, lifestyle and psychosocial factors, which might be involved in mediating the observed relationship. This clearly reinforces the validity of the main findings of the study. Particularly, such an approach has allowed the authors to assess the possible role of depression and anxiety in this context . In fact, their data indicate that the association of these psychological traits with hypertension might be mediated by the fact that sleep duration (and possibly also sleep quality) is altered in persons with anxiety and depression in line with what reported previously .
Although this article adds to the available literature emphasizing the impact of short sleep duration on cardiovascular risk, many aspects of this complex relation still need to be clarified, also because of a number of limitations of the available studies on this issue (Table 1). On one hand, the mechanisms linking the two phenomena remain largely unexplored. Among the responsible factors for the adverse consequences of short sleep, an increased sympathetic activity might play a pivotal role, also through its well known effects on BP and heart rate variability, including the enhancement of short lasting BP fluctuations and the blunting of day–night BP fall. This autonomic derangement might be both a fundamental determinant of the cardiovascular complications of short sleep, but at the same time, being associated with a hyperarousal state, it might also be one of the reasons for sleep alterations in the frame of a closed loop interaction . Exploring the mechanisms behind the link between short sleep duration and hypertension is not just of academic interest, however, because the identification of underlying pathophysiological processes may allow the development and implementation of strategies aimed at reducing the risks of too short (or too long) sleep. On the other hand, more information is needed on specific features characterizing sleep quality and effectiveness, which may be more directly related to cardiovascular outcomes than sleep duration by itself.
Conflicts of interest
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