Sleep is a naturally recurring state of mind and body occurring periodically, resulting in reduced consciousness, increased muscle relaxation and altered response to stimuli.
Based on the brain pattern of electric activity, eye movement and skeletal muscle tone, human sleep is split into two stages.
The first stage is non-rapid eye movement (NREM) and is further divided into different sleep groups (stage 1, stage 2 and stage 3, more commonly referred to as Slow-wave sleep (SWS) or deep sleep), along with rapid eye movement (REM) which occurs 60-90 minutes at the start of sleep and is characterised by the random rapid movement of the eyes.
The second stage of sleep is called Rapid Eye Movement (REM) or desynchronised sleep because it resembles the state of walking, including fast and low voltage brain waves.
Inadequate sleep duration and misaligned or irregular sleep (for example, because of shift work) have been shown to impair cognitive performance and is also linked to increased mortality. Both epidemiological and experimental studies have shown that sleep quality is essential in regulating metabolism.
What is the evidence that sleeps affects glucose metabolism?
Large-scale epidemiological, mainly cross-sectional studies across populations including teenagers, middle-aged and elderly people, people with high blood pressure and pregnant women have shown that insufficient, poor or short sleep is associated with pre-diabetic features such as high fasting blood sugar levels, elevated glucose after meals and high insulin levels or indicators of whole-body insulin resistance.
In people who already have diabetes, inadequate sleep is detrimental because it negatively impacts glycaemic control. It is worth keeping in mind that the results were obtained from cross-sectional studies, which are subject to some bias due to the uncertainty of causality.
Prospective studies are more robust way to understand how sleep controls blood sugar levels. Participants without diabetes who have variable sleep habits and sleep duration are monitored for an extended period including recording any newly diagnosed cases of type 2 diabetes.
These prospective studies show that people who sleep for less time have a higher relative risk of developing type 2 diabetes compared to those with normal sleep time, after adjustments for known risk factors. The study surveyed 661 to 70,026 adults over 4 to 32 years plus meta-analyses, supports cross-sectional studies.
Experimental studies have shown that healthy human volunteers exposed to a strict pattern of total sleep deprivation, lasting from one to five days, can develop insulin resistance and β-cell dysfunction. Sleep deprivation increased insulin resistance combined with defects in insulin secretion, fasting and glucose levels after eating.
Total sleep deprivation, though, is not realistic. In real-life scenarios, partial sleep deprivation, of only four to fiver hours sleep, is a better representation. These studies show that participants who have partial sleep deprivation have impairments in many parameters of glucose tolerance and insulin sensitivity.
Metabolic impact of shift work
Numerous studies have identified that shift work and disrupted sleep patterns impairs metabolic function and glucose homeostasis through increased glucose intolerance, insulin resistance and metabolic syndrome.
A meta-analysis of observational studies identified that men who were subject to shift work had a higher risk of developing Type 2 diabetes
How does sleep affect glucose metabolism?
Currently, the molecular mechanism of how sleep affects glucose homeostasis is still not fully understood.
The main suggested mechanism is that sleep disruptions can affect the hypothalamo-pituitary-adrenal (HPA) axis. Studies have shown that sleep disruption leads to increased circulation of the hormones cortisol catecholamines and increased sympathetic activation, seen both after total and partial sleep deprivation
Sleep deprivation has been suggested to result in increased levels of pro-inflammatory cytokines decreased thyroid-stimulating hormone levels, impaired growth hormone secretion, and changes in the secretion of molecules called adipokines from body fat.
How does sleep affect appetite?
Appetite is regulated by two hormones that have contrasting functions; leptin and ghrelin.
Leptin is produced by body fat after a meal and promotes feeling full after eating.
Ghrelin is an appetite-stimulating molecule primarily made in the stomach.
Both hormones have circadian rhythms, meaning they follow a 24 hour cycle. Leptin has been shown to peak in the early part of the sleep period, whilst ghrelin tends to peak later in the night.
Experimental evidence has shown that participants who have undergone sleep restrictions prefer fat and carbohydrate-rich foods and have a 20% increase in daily caloric intake. The underlying mechanism is that sleep restrictions resulted in decreased leptin production and increased ghrelin.
Two studies identified that extended total sleep deprivation was associated with a decrease in leptin concentrations. Partial sleep deprivation where participants spent six nights of four hour asleep compared to six nights of 12 hour sleep, resulted in a 19% reduction in leptin levels. Other studies have identified that the highest leptin concentration was reduced between sleep restricted compared to regular sleep periods.
However, opposite or conflicting results have also been suggesting that other factors, such as decreased levels of a molecule anorexigenic peptide YY, may also play a role in how sleep affects appetite.
How does the research at the Quadram Institute impact glucose and sleep?
The Dietary BIoactives and Microbiome DivErsity (DIME) is a randomised human pilot study carried out at the Quadram Institute.
The DIME study aims to assess the effect of diets rich in plant bioactives, also known as phytochemicals, on gut microbiome diversity and markers of metabolic health in healthy people.
The phytochemicals are polyphenols found in foods such as berries, grapes, dark chocolate/cacao and red wine.and sulphur-containing compounds derived from allium and cruciferous vegetables such as onions, garlic, broccoli, cabbage, cauliflower and brussels sprouts, and carotenoids.
Food rich in carotenoids include carrots, sweet potatoes, apricots, melons and mangoes.
One of the aims of the DIME study is to assess how a diet rich in plant bioactives can affect blood sugar levels and see how that, in turn, impacts sleep quality.
Written by Federico Bernuzzi, PhD, Research Scientist in the Food Databanks National Capability based at the Quadram Institute.
Acknowledgements: The Food Nutrition Security Cloud (FNS-Cloud) has received funding from the European Union’s Horizon 2020 Research and Innovation programme (H2020-EU.184.108.40.206. – A sustainable and competitive agri-food industry) under Grant Agreement No. 863059