Does lack of sleep cause diabetes?

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ABSTRACTSeveral lines of evidence indicate that chronic lack of sleep may contribute to the risk of type 2 diabetes mellitus. Adequate sleep and good sleep hygiene should be included among the goals of a healthy lifestyle, especially for patients with diabetes. We urge clinicians to recommend at least 7 hours of uninterrupted sleep per night as part of a healthy lifestyle.


  • Sleep loss and sleep disturbances have become very common in our society, and so have obesity and type 2 diabetes.
  • In epidemiologic studies, people who reported sleeping less were at higher risk of diabetes or disordered glucose metabolism.
  • In laboratory studies, short-term sleep deprivation caused measurable changes in glucose metabolism, hormone levels, autonomic nervous system activity, and other variables, which are plausible mechanisms by which loss of sleep could contribute to diabetes.
  • Obstructive sleep apnea is very common in people with diabetes and may be directly linked to diabetes risk and worse diabetes control. Diabetic patients should be systematically assessed for obstructive sleep apnea, and patients with known obstructive sleep apnea should be screened for diabetes.



Adults are sleeping less and less in our society. Yet sleep is no longer thought of as strictly a restorative process for the body. The importance of sleep for metabolic function and specifically glucose homeostasis is now widely accepted, as many studies have shown a correlation between sleep deprivation or poor sleep quality and an increased risk of diabetes.

Obesity and aging are both associated with worse sleep. As the prevalence of obesity and diabetes increases, and as the number of elderly people increases, it is imperative to target sleep in the overall treatment of our patients.

In the pages that follow, we examine the evidence of a link between sleep loss (both short sleep duration and poor-quality sleep) and the risk of diabetes. (For evidence linking short sleep duration and the related problem of obesity, we invite the reader to refer to previous publications on the topic.1,2)


The prevalence of obesity and, consequently, of type 2 diabetes mellitus has increased alarmingly worldwide and particularly in the United States in the past few decades. Such a rapid increase cannot be explained simply by an alteration in the genetic pool; it is more likely due to environmental, socioeconomic, behavioral, and demographic factors and the interaction between genetics and these factors. Besides traditional lifestyle factors such as high-calorie diets and sedentary habits, other, nontraditional behavioral and environmental factors could be contributing to the epidemic of obesity and diabetes.

At the same time, people are sleeping less, and sleep disorders are on the rise. According to recent polls from the US Centers for Disease Control and Prevention, approximately 29% of US adults report sleeping less than 7 hours per night, and 50 to 70 million have chronic sleep and wakefulness disorders.3

The sleep curtailment of our times probably is partly self-imposed, as the pace and the opportunities of modern society place more demands on time for work and leisure activities and leave less time for sleep.

The quality of sleep has also declined as the population has aged and as the prevalence of obesity and its related sleep disorders has increased. Furthermore, patients with type 2 diabetes tend to sleep less, and to sleep poorly.4,5 Poor sleep quality generally results in overall sleep loss.


The human body regulates blood levels of glucose within a narrow range.

Glucose tolerance refers to the ability to maintain euglycemia by disposing of exogenous glucose via insulin-mediated and non–insulin-mediated mechanisms. Normal glucose tolerance depends on the ability of the pancreatic beta cells to produce insulin. As insulin sensitivity declines, insulin secretion increases to maintain normal glucose levels. Diabetes becomes manifest when the pancreatic beta cells fail to compensate for the decreased insulin sensitivity.

Glucose tolerance varies in a circadian rhythm, including during the different stages of sleep.


Sleep has often been thought of as a “restorative” process for the mind and the body; however, many studies have shown that it also directly affects many metabolic and hormonal processes.6

Sleep has five stages: rapid eye movement (REM) sleep and stages 1, 2, 3, and 4 of non-REM sleep. The deeper stages of non-REM sleep, ie, stages 3 and 4, are also known as slow-wave sleep and are thought to be the most restorative.

Additionally, the onset of slow-wave sleep is temporally associated with transient metabolic, hormonal, and neurophysiologic changes, all of which can affect glucose homeostasis. The brain uses less glucose,7 the pituitary gland releases more growth hormone and less corticotropin,8 the sympathetic nervous system is less active, and conversely, vagal tone is increased.9

As a result, in the first part of the night, when slow-wave sleep predominates, glucose metabolism is slower. These effects are reversed in the second part of the night, when REM sleep, stage 1, and awakening are more likely.

In view of these important changes in glucose metabolism during sleep, it is not surprising that getting less sleep or poorer sleep on a regular basis could affect overall glucose homeostasis.


Laboratory and epidemiologic evidence supports an association between short sleep duration (< 7 hours per night) and the risk of diabetes, and also between poor sleep quality and the risk of diabetes. We will explore putative mechanisms for these relationships.

Laboratory studies of short sleep duration and glucose metabolism

Studies in small numbers of healthy volunteers who underwent experimental sleep restriction or disruption have revealed mechanisms by which sleep loss might increase the risk of diabetes.

Kuhn et al10 performed the very first laboratory study of the effect of sleep deprivation on metabolism. Published in 1969, it showed that total sleep deprivation led to a marked increase in glucose levels.

A caution in extrapolating such results to real-life conditions is that total sleep deprivation is uncommon in humans and is inevitably followed by sleep recovery, with normalization of glucose metabolism. However, people in modern society are experiencing recurrent partial sleep deprivation, and its effect on glucose metabolism may be different.

Spiegel et al,11 in landmark laboratory studies of partial sleep deprivation in healthy, lean adults, found that restricting sleep to 4 hours per night for 6 nights resulted in a 40% decrease in glucose tolerance, to levels similar to those seen in older adults with impaired glucose tolerance. This metabolic change was paralleled by an increase in the activity of the sympathetic nervous system, and both of these effects reversed with sleep recovery.

A criticism of these initial studies is that they restricted sleep to 4 hours, a restriction more severe than that seen in real life.

Nedeltcheva et al12 more recently examined the effects of less-severe sleep curtailment (5.5 hours per night for 14 nights) in sedentary middle-aged men and women. This degree of bedtime restriction led to a decrease in glucose tolerance due to decreased insulin sensitivity in the absence of adequate beta cell compensation.

Such recurrent bedtime restriction is closer to the short sleep duration experienced by many people in everyday life, and in people at risk it may facilitate the development of insulin resistance, reduced glucose tolerance, and ultimately diabetes. Indeed, epidemiologic studies suggest that people who sleep less than 6 hours per night are at higher risk of type 2 diabetes.


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