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EDITORIAL COMMENT |
University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0667, Email: DKripke@UCSD.edu
Dew et al. provide the first objective EEG evidence that disturbances of sleep predict a shortened life span (1). Those elderly volunteers with sleep latency >30 minutes (25.5% of the sample) had a relative mortality hazard of 2.14 compared with the others with p < .005, a significance that met Bonferroni criteria. This means that those who needed >30 minutes to fall asleep were more than twice as likely to die over a mean follow-up of 12.8 years, other things being equal. The study was well controlled to exclude any confounding of sleep disturbance with psychiatric disorders. There was also control for age, gender, and medical burden, which is a catch-all metric for controlling for numerous medical comorbidities.
Poor sleep efficiency (a higher percentage of time in bed spent awake) was also a predictor of mortality, but this measure included the effect of sleep latency. Without considering sleep latency, sleep maintenance had only a marginal association with mortality. Surprisingly, the study did not suggest that too little sleep caused increased mortality. Total sleep time was not a significant hazard predictor, even though 40% of the sample slept less than 6.0 hours in bed. A marginally significant effect of either high or low rapid eye movement (REM) sleep percentage was also reported. Because this seems an artificial way of summarizing REM sleep, and other measures of REM sleep were not significant, this effect would need replication. Indeed, as the authors strongly urge, the entire study needs replication. Perhaps there are other research groups who can find sufficient sleep data already collected to replicate the study.
What could be causing this excess mortality? If short sleep and depression are not the cause of the excess mortality, other plausible possibilities mentioned by the authors would be sleep apnea, circadian rhythm disorganization, and impending dementia. Napping might be a cause of circadian rhythm disorganization, but reciprocally, napping might reflect deterioration of the suprachiasmatic nucleus (an important body clock regulating sleep-wake), which seems to undergo early damage in Alzheimer’s disease (2). Although the subjects were asked not to nap, many elders do nap during the day, often involuntarily and sometimes without being aware of it. Napping could cause increased sleep latency, poor sleep efficiency, and even altered REM sleep percentage, all of which could be stigmata of the underlying pathophysiologic processes.
What should be done? Recognized short-term treatments for a long sleep latency include hypnotic drugs and behavioral therapy (3, 4). Continuous positive airway pressure is a recognized treatment for sleep apnea. None of these treatments has been studied on a long-term scale sufficient to evaluate its effect on mortality. As we expand epidemiologic evidence of possible risks of sleep disorders, long-term clinical trials will be necessary both to explore causality and to demonstrate solutions.
REFERENCES
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