Does lack of sleep cause diabetes?

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Putative mechanisms linking short sleep duration and the risk of diabetes

The effects of sleep loss on glucose metabolism are likely multifactorial, involving several interacting pathways.

Decreased brain glucose utilization has been shown on positron emission tomography in sleep-deprived subjects.25

Hormonal dysregulation. Sleep deprivation is associated with disturbances in the secretion of the counterregulatory hormones growth hormone26 and cortisol.11

Young, healthy volunteers who were allowed to sleep only 4 hours per night for 6 nights showed a change in their patterns of growth hormone release, from a normal single pulse to a biphasic pattern.26 They were exposed to a higher overall amount of growth hormone in the sleep-deprived condition, which could contribute to higher glucose levels.

Also, evening cortisol levels were significantly higher in young, healthy men who were allowed to sleep only 4 hours per night for 6 nights,11 as well as in young, healthy women who were allowed to sleep only 3 hours for 1 night.27 A cross-sectional analysis that included 2,751 men and women also demonstrated that short sleep duration and sleep disturbances are independently associated with more cortisol secretion in the evening.28 Elevated evening cortisol levels can lead to morning insulin resistance.29

Inflammation. Levels of inflammatory cytokines, inflammation, or both increase as sleep duration decreases, which in turn can also increase insulin resistance.30,31

Sympathetic nervous system activity. Patients who have been sleep-deprived have been shown to have higher sympathetic nervous system activity, lower parasympathetic activity, or both.11,32 The sympathetic nervous system inhibits insulin release while the parasympathetic system stimulates it, so these changes both increase glucose levels.33 Moreover, overactivity of the sympathetic nervous system results in insulin resistance.34

Excess weight is a well-established risk factor for type 2 diabetes mellitus, and several epidemiologic studies have suggested that sleep loss may increase the risk of becoming overweight or obese,1,35 which would ultimately increase the risk of type 2 diabetes.

A primary mechanism linking sleep deprivation and weight gain is likely to be hyperactivity of the orexin system. Orexigenic neurons play a central role in wakefulness, but, as suggested by the name, they also promote feeding.36 Studies in animals have indicated that the orexin system is overactive during sleep deprivation,37–39 and this could be in part mediated by the increase in sympathetic activity.

Increased sympathetic activity also affects the levels of peripheral appetite hormones, inhibiting leptin release40 and stimulating ghrelin release.41 Lower leptin levels and higher ghrelin levels act in concert to further activate orexin neurons,42,43 resulting in increased food intake.

One could also argue that less time sleeping also allows more opportunity to eat.44

Reduced energy expenditure. Sleep loss and its associated sleepiness and fatigue may result in reduced energy expenditure, partly due to less exercise but also due to less nonexercise activity thermogenesis. To date, reduced energy expenditure is an unexplored pathway that could link short sleep, the risk of obesity, and ultimately diabetes. In many overweight and obese people, this cascade of negative events is likely to be accelerated by sleep-disordered breathing, a reported independent risk factor for insulin resistance.45,46


Slow-wave sleep and diabetes

Slow-wave sleep, the most restorative sleep, is associated with metabolic, hormonal, and neurophysiologic changes that affect glucose homeostasis. Its disturbance may have deleterious effects on glucose tolerance.

Shallow slow-wave sleep occurs in elderly people47 and in obese people, even in the absence of obstructive sleep apnea.48,49 Both groups are also at higher risk of diabetes.50 One wonders if the decreased slow-wave sleep could in part contribute to the risk of diabetes in these groups.

A few studies specifically tested the effect of experimental suppression of slow-wave sleep on glucose homeostasis.

Tasali et al51 evaluated nine young, lean, nondiabetic men and women after 2 consecutive nights of undisturbed sleep and after 3 consecutive nights of suppressed slow-wave sleep without a change in total sleep duration or in REM sleep duration. Slow-wave sleep was disturbed by “delivering acoustic stimuli of various frequencies and intensities” whenever the subjects started to go into stage 3 or stage 4 sleep. This decreased the amount of slow-wave sleep by nearly 90%, which is comparable to the degree of sleep fragmentation seen in moderate to severe obstructive sleep apnea. After 3 nights of slow-wave sleep suppression, insulin sensitivity decreased by 25%, without a compensatory increase in insulin release, which resulted in a reduction in glucose tolerance of 23%, a value seen in older adults with impaired glucose tolerance.52

Stamatakis et al53 confirmed these findings in a similar study of 11 healthy, normal volunteers whose sleep was fragmented for 2 nights across all stages of sleep using auditory and mechanical stimuli. Insulin sensitivity significantly decreased, as did glucose effectiveness (ability of glucose to dispose itself independently of an insulin response) after the 2 nights of disturbed sleep quality.

These results support the hypothesis that poor sleep quality with short durations of slow-wave sleep, as seen with aging and obesity, could contribute to the higher risk of type 2 diabetes in these populations. These data also suggest that more studies are needed to look at the relationship between amount and quality of slow-wave sleep and diabetes risk.

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