Diabetes – the cost of counting sheep?

20. February 2015
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Does poor sleep increase the risk of diabetes? A relationship between sleep and metabolic balance has been suggested by a number of studies so far. As global incidence rates of diabetes are on the rise, establishing the mechanisms behind this is crucial.

Diabetes and obesity are among the leading causes of long-term morbidity and mortality worldwide. In the UK alone, the number of people diagnosed with diabetes has increased from 1.4 million in 1996, to 2.6 million in 2010. As this number is expected to rise, the need to identify the underlying causes is self-evident.

Several studies have suggested a link between sleep duration, quality, Circadian rhythm disruptions and risk of developing Type 2 Diabetes (T2D). But what is the nature of this relationship? Does poor sleep predispose towards T2D, or is it simply a symptom of some other underlying morbidity?

To answer these questions, researchers turned to healthy participants, submitting them to different sleep patterns and studying the ensuing metabolic effects. One such study was carried out by the group headed by Karine Spiegel in the late 1990s. Under strict laboratory conditions, they submitted healthy male participants to several different sleep conditions, including restricting sleep to just four hours on six consecutive nights. Although both calorific and nutrient intake were the same as for normal sleep durations, they found that restricting sleep led to impaired glucose metabolism and insulin insensitivity.

These findings were corroborated by a number of studies using healthy volunteers, who were subjected to short-term sleep curtailment (5-14 consecutive nights). Glucose tolerance tests showed that insulin sensitivity was reduced by 18-24 %, without a compensatory increase in insulin levels.

So should we simply spend all day in bed to preserve metabolic health? Not necessarily. Interestingly, an analysis of several studies investigating links between diabetes and sleep duration showed that both long (>6 hours/night) and short sleep duration was linked to a higher risk of developing T2D. Clearly, total sleep duration is not the only factor in this equation.

Quantity and Quality

Perhaps not surprisingly, sleep duration in itself is not necessarily the pivotal factor. Patients suffering from Obstructive Sleep Apnea Syndrome (OSAS) – a medical condition in which breathing is periodically disrupted for 20-40 seconds at a time due to obstruction of the upper airways – often report sleeping longer overall, but their sleep is fragmented due to repeated hypoxia. Even in healthy people, self-reported sleep duration is not reliable, since it is often interpreted as ‘time in bed’ rather than the actual amount of sleep per se. Thus, it is necessary to examine the quality of sleep – in other words, different phases within the sleep cycle.

The disruption of so-called Slow Wave Sleep (SWS) has emerged as a potentially crucial factor in this context. SWS, also known as ‘deep sleep’, is the sleep state during which the brain’s glucose utilization is minimal. Studies using intravenous glucose infusion during all stages of sleep showed that glucose tolerance was lowest during SWS. One clue as to the importance of this sleep phase is that it is often compromised in OSAS patients, due to frequent sleep disruptions. Typically, both obesity and T2D incidence rates are higher in such patient groups, perhaps suggesting a link between SWS disruption and impaired glucose metabolism.

Early Birds vs. Night Owls

However, sleep duration and quality are not the only factors which have a bearing on metabolic balance. So-called Clock-Genes are expressed in nearly all mammalian cells – they act as a sort of biological clock regulated by the light/dark cycle, governing phases of activity and inactivity. As such, Circadian cycles are intricately linked with metabolic regulation, as they govern energy expenditure and storage. Glucose tolerance, insulin sensitivity, and glucose and insulin plasma levels exhibit characteristic variations throughout the day, and are connected with the Circadian rhythm. However, this rhythm can be disrupted – either through impairments of the underlying biological clock, or through misalignment of activity cycles and environmental conditions. Changing lifestyles often cause a shift in these patterns, leading to Circadian misalignment.

Recent evidence suggests Circadian misalignment has a considerable impact on metabolic homeostasis and may predispose towards T2D. Shift workers often exhibit changes in glucose and lipid metabolism and have a higher risk of developing metabolic syndrome, T2D, and obesity. Additionally, impaired sleep and changes in Circadian rhythm are often found in obese and diabetic patients. Some of the strongest evidence suggesting a link between glucose metabolism, T2D and Circadian rhythm comes from the animal literature. A study carried out on mice presenting with Clock-Gene mutations showed that this not only led to a significant change in Circadian behaviour, but also to impairments in glucose and lipid metabolism.

Our bodies on sleep

So how do alterations in sleep cycles lead to metabolic changes? The answer to this question seems to be a mixture of different factors. Disrupted sleep leads to an overall increase in Central Nervous System activity. This has been linked with an increase in plasma free fatty acids, causing ectopic fat depots in liver and muscles and inhibiting insulin secretion. Furthermore, our internal biological clocks are designed to optimize energy expenditure and storage for our daily activity cycles. As such, levels of hormones responsible for regulating food intake are closely linked with Circadian cycles. The problem is that as our lifestyles shift from being tied to natural light/dark cycles to late night work and social commitments, this wreaks havoc on our biological clocks. In addition, sleep restriction in itself has been shown to cause an increase in levels of ghrelin – a hormone which makes us feel hungry – while at the same time, levels of leptin – a hormone which curbs our appetite – are reduced. In other words, if we sleep less, we end up feeling hungrier. However, lack of sleep does not necessarily induce higher levels of physical activity – quite the opposite, in fact. This may result in a vicious cycle of increased energy intake combined with reduced activity, resulting in weight gain, higher BMI and even obesity, which in turn are linked with a higher risk of developing T2D.

Although we may not know exactly how our changing sleep and activity patterns affect metabolic health, the evidence presented so far is strong enough to highlight the importance of tackling insomnia and poor sleep to prevent damage to our health. Given the high prevalence of sleep disorders, obesity and diabetes worldwide, we need to do everything we can to tackle the toll this is taking – both in terms of public health services, as well as patient suffering.

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