Abstract: Sleep duration has been constantly decreasing over the past 50 years. Short sleep duration, sleep quality and, recently, long sleep duration have all been linked to poor health outcomes, increasing the risk of developing metabolic diseases and cardiovascular events. Beyond the duration of sleep, the timing of sleep may also have consequences. Having a tendency to go early to bed (early chronotype) compared with the habit of going to bed later (late chronotype) can interfere considerably with social schedules (school, work). Eventually, a misalignment arises in sleep timing between work days and free days that has been described as ‘social jet lag’. The present review looks at how different sleep habits can interfere with diabetes, excluding sleep breathing disorders, and successively looks at the effects of sleep duration, chronotype and social jet lag on the risk of developing diabetes as well as on the metabolic control of both type 1 and type 2 diabetes. Finally, this review addresses the current state of knowledge of physiological mechanisms that could be linking sleep habits and metabolic health.
Alex’s Notes: The number of Americans getting less than six hours of sleep per night has slowly increased over the past two decades, with 27% reporting their sleep quality as fair or poor. In fact, a recent meta-analysis found that the prevalence of short sleepers (those getting <6 hours/night) increased from 7.6% in 1975 to 9.3% in 2006, and that the odds of not getting enough sleep were greater in full-time workers, men, and the college educated.
Simultaneous to this sleep deficit, diabetes has been steadily increasing. Studies have indeed found short sleep duration to be associated with increased prevalence of type-2 diabetes in European Americans, African Americans, Iranians, Chinese, Japanese, Taiwanese, and Jamaican. Of course causality cannot be determined from these cross-sectional studies, and it may very well be that type-2 diabetes has a negative impact on sleep. Nonetheless, they show there is indeed an association across a wide range of populations and geographic locations.
Further meta-analyses support the associations. One such analysis of ten prospective studies totaling over 107,000 men and women found that getting 5-6 hours of sleep per night or less increased the risk of type-2 diabetes by 28%. Sleeping more than nine hours per night had an even greater risk (48%). A second meta-analysis of primarily European cohorts found short sleep to increase diabetes risk by 33%. Even in type-1 diabetics, short sleep duration (<6.5 hours) is associated with worse glycemic control as represented by HbA1c.
Yet, beyond the duration of sleep, the timing of sleep has a significant impact on health as well. This is characterized by a person’s chronotype, which refers to basic sleep/wake schedules. Some people are morning persons, going to bed and rising early, while others are night owls that stay up late and sleep in. Some studies show that the number of night owls has increased over the past two decades, and that these persons have a 1.3-fold increased risk of all-cause mortality compared to morning larks. Other data suggests that evening types had a 2.5-fold increased risk for type-2 diabetes as compared with morning types, independent of sleep duration and sleep sufficiency. Worse glycemic control has also been documented in later chronotypes.
Why the association and risk?
Our bodies are giant clocks, believe it or not. These clocks are organized in a hierarchy, with the chief being the central clock within the hypothalamus. Other lesser clocks exist in other brain regions and organs such as the muscles, liver, pancreas, and fat cells. Environmental light-dark cycles reset the central clock through light (or a lack of) that enters through the retina. The central clock, in turn, synchronizes the peripheral clocks. At the same, however, we have social information, nutritional intake, and exercise all acting to influence the big boss and his little workers. The problem here is that some estimate the circadian clock to control 10-20% of gene expression.
I’m sure you can see where this is going; the central clock activity dictates both behavioral and metabolic adaptations, leading to regulation of food intake that consequently regulates the peripheral and central clocks in a nice giant feedback circle. When this beautiful system gets thrown in the ring with an unnatural social environment that robs us of our evolutionary light-dark cycles, the whole thing gets readjusted and possibly confused and disorganized.
A great example of this is melatonin, a hormone released by the pineal gland of the brain in response to darkness that is suppressed by light. Coming back to the topic of diabetes, some studies show that melatonin may be one of the hormonal mediators of insulin sensitivity, as melatonin receptors are present on pancreatic β-cells where melatonin acts to inhibit insulin secretion, and insulin receptors are located on the pineal gland. Sure enough, removal of the pancreatic melatonin receptors induces insulin resistance while administration of melatonin restores glucose tolerance. In humans, certain genetic variants of the genes encoding for the melatonin receptors have been associated with increased fasting blood glucose levels and increased risk of type-2 diabetes.
Bringing it together with human trials
Several trials have demonstrated sleep restriction to have a harmful impact on carbohydrate metabolism and endocrine function, insulin sensitivity, and increased risk of type-2 diabetes. More importantly, low levels of sleep have been implicated in one of the fundamental causes of all these problems and more, chronic low-grade inflammation. Unfortunately, both type-2 and type-1 diabetics have worse sleep quality, suggesting that the symptoms of these conditions can influence sleep, which in turn influences glycemic control, creating a cycle whereby diabetes and sleep disturbances fuel one another.
So while the focus of this review has been on diabetes, the takeaway is really to not underappreciate the night and to go to bed.