Hence, there are short-term experimental data that suggest mechanisms by which long-term sleep deprivation may lead to adverse cardiovascular events. In contrast, we have no reason to suspect that increased sleep duration would cause CHD and were somewhat surprised by the observation. In searching for possible explanations for this association, only 2 basic concepts emerged. First, some confounder could lead to CHD and an increased need for sleep.
An example might be obstructive sleep apnea. There are data 11 - 13 to show that sleep apnea is associated with adverse cardiovascular outcomes and that it is known to fragment sleep, potentially increasing the need for sleep. However, to our knowledge, no evidence shows that patients with sleep apnea sleep longer than subjects without sleep apnea.
Thus, this explanation for our findings seems unlikely.
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Second, reverse causality may be a possible explanation. That is, increased sleep duration may be an early symptom of cardiac disease and may predate an official diagnosis of CHD. Third, increased sleep itself could lead to cardiovascular disease. Although this concept is consistent with the results of this study, we know of no plausible explanation for such a cause-and-effect relationship.
Thus, the association of increased sleep duration and CHD remains unexplained. Strengths of the present study include the large sample size and the high rate of follow-up. Also, CHD was assessed prospectively, eliminating possible bias due to retrospective recall that may be present in case-control and cross-sectional analyses. We also acknowledge that there are several limitations in the present study. First, all subjects were women. It is possible that men differ from women in effects of sleep duration on incident CHD.
However, a prior epidemiologic study 4 demonstrated little difference in the RRs of death in men and women from a decreased sleep time, and another 2 showed that the adverse risk in women may actually be lower than in men. Second, information about sleep duration and other potential risk factors was self-reported by female nurses. The reliability of self-reported sleep duration was not validated and its stability over time is not known.
Indeed, given the age range of the participants of the study, changes in lifestyle and sleep pattern in some subjects likely occurred during the year study period. Nevertheless, questions about self-reported sleep duration have been investigated in other studies, 14 , 15 and have been demonstrated to be valid measures when compared with quantitative sleep assessments with actigraphy. Despite this, some misclassification of the sleep duration variable seems likely. However, because outcomes were assessed prospectively, any misclassification of sleep duration would be nondifferential for CHD.
Therefore, this would tend to underestimate, rather than overestimate, the effects of sleep duration. Third, our study was observational in design and, thus, we cannot conclude definitively that decreased sleep duration caused CHD. We cannot rule out the presence of unknown confounders that were not accounted for in the final analysis. Because of the substantial change in the RRs by adding known confounders, it is possible that some residual confounding remains. However, it is doubtful that this residual unexplained confounding would completely eliminate the effect seen.
Finally, the cause of restricted sleep was not ascertained in our study. Subjects may have had a decreased sleep duration from insomnia an inability to fall or stay asleep , work or family responsibilities, or staying up late to watch television. It is possible that the cause of sleep restriction may differentially affect the risk of CHD.
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However, this cannot be determined from our study. Long-term sleep deprivation is common in today's society. The cause of this is multifactorial. Given these results and those of the short-term experimental studies cited previously, adequate daily sleep should not be considered a luxury, but an important component of a healthy lifestyle.
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In conclusion, our data suggest that a short self-reported sleep duration is associated with an increased risk of CHD. This association persists even after adjustment for age, smoking status, obesity, hypertension, diabetes mellitus, and other cardiovascular risk factors. Although cause and effect cannot be proved definitively in this observational study, our results suggest that insufficient duration of sleep may increase CHD risk. Further studies are needed to elucidate better the biological mechanism underlying this association, and to determine whether the cause of the sleep deprivation insomnia vs lifestyle choices affects its cardiovascular consequences.
Finally, the explanation for the increased CHD in patients sleeping 9 hours or longer is unclear and must await data defining why these individuals slept as much as they did. Such information might lead to a logical explanation for the observed increase in CHD. Corresponding author: Najib T. All Rights Reserved.
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