Daytime Sleeps: Metabolic Disruptor Or Just A Myth?

Sleep is intricately connected to various hormonal and metabolic processes in the body and is important in maintaining metabolic homeostasis. While your baseline metabolic rate will stay the same throughout the day and night, you will burn fewer calories at night, which can have an effect on your weight-loss efforts. Other factors, including sleep and stress, can also affect your metabolism at night.

Sleep deprivation can affect your gut biome – the bacteria in your digestive system that digest food and control metabolism. Poor or disturbed sleep can cause changes in your stomach’s microbial community structure. This affects the way your body digests and metabolises food.

Sleep deprivation may affect your body’s ability to convert food and fat into energy. Research has shown that sleeping less diminishes your ability to break down fat into energy – meaning your body stores it instead of consuming it. This is especially true if you don’t get rest on a consistent basis.

Shortened sleeping times may impair the way your body metabolises glucose, which increases your risk of type 2 diabetes. It also results in weight gain, which can increase your resistance to insulin. Both affect the way your body absorbs and processes glucose.

Sleep deprivation can lead to increased insulin resistance and impaired glucose tolerance, which can cause metabolic dysregulation.

Sleep is essential to regulating the hormones that affect hunger and appetite. A lack of sleep may affect the body’s regulation of the neurotransmitters ghrelin and leptin, which control appetite. The body naturally increases and decreases the levels of these neurotransmitters throughout the day, signalling the need to consume calories.

A lack of sleep may lead to increased appetite and diminished feelings of fullness. Sleep-deprived individuals tend to choose foods that are high in calories and carbohydrates.

Sleep deprivation can cause metabolic dysregulation through myriad pathways involving sympathetic overstimulation, hormonal imbalance, and subclinical inflammation

Sympathetic Overstimulation

Sympathetic nervous system activity is generally decreased during deep sleep, but sleep deprivation is associated with an elevation of sympathovagal balance, with higher sympathetic but lower parasympathetic tone. Most endocrine organs are sensitive to changes in sympathovagal balance. For example, sleep deprivation has been shown to increase sympathetic nervous system activity, which in turn increases levels of circulating free fatty acids because of the stimulation of lipolysis, which promotes insulin resistance.

Hormonal Imbalance

The release of hormones by the pituitary is markedly influenced by sleep. Modulation of pituitary-dependent hormonal release is partly mediated by the modulation of the activity of hypothalamic-releasing and/or hypothalamic-inhibiting factors controlling pituitary function. During sleep, these hypothalamic factors may be activated or inhibited. The other pathway by which sleep affects peripheral endocrine regulation is via the modulation of autonomic nervous system activity.

Sleep loss is associated with an increase in appetite that is excessive in relation to the caloric demands of extended wakefulness. Sleep loss is associated with an increase in appetite that is excessive in relation to the caloric demands of extended wakefulness. The regulation of leptin, a hormone released by the fat cells that signals satiety to the brain and thus suppresses appetite, is markedly dependent on sleep duration. After 6 days of bedtime restriction to 4 hours per night, the plasma concentration of leptin was markedly decreased, particularly during the nighttime. In a later study, the levels of ghrelin, a peptide that is secreted by the stomach and stimulates appetite, were measured with the levels of leptin after 2 days of sleep restriction (4 hours of sleep) or sleep extension (10 hours of bedtime). Sleep restriction was associated with reductions in leptin (the appetite suppressant) and elevations in ghrelin (the appetite stimulant) and increased hunger and appetite, especially an appetite for foods with high-carbohydrate contents.

Subclinical Inflammation

Experimental sleep deprivation has been found to alter immune response and increase proinflammatory markers such as IL-6, TNF- α, and CRP.

Sleep deprivation can lead to increased ghrelin and decreased leptin levels, which can increase appetite and hunger

A study on two days of sleep restriction (4 hours) in healthy subjects revealed a 28% increase in blood ghrelin levels, an 18% decrease in blood leptin levels, and a 23-24% increase in hunger and appetite, especially for high-calorie foods with high carbohydrate content.

In addition, several studies have indicated that sleep deprivation affects food preferences. Sleep-deprived individuals tend to choose foods that are high in calories and carbohydrates.

Sleep deprivation can cause a reduction in muscle tone and an anti-insulin-like effect, leading to a relative state of insulin resistance

Sleep deprivation can affect the body's regulation of the neurotransmitters ghrelin and leptin, which are thought to be central to appetite. Ghrelin promotes hunger, and leptin contributes to feeling full. The body naturally increases and decreases the levels of these neurotransmitters throughout the day, signalling the need to consume calories. A lack of sleep may affect the body's regulation of these neurotransmitters. In one study, men who got 4 hours of sleep had increased ghrelin and decreased leptin compared to those who got 10 hours of sleep. This dysregulation of ghrelin and leptin may lead to increased appetite and diminished feelings of fullness in people who are sleep-deprived.

Sleep deprivation may also affect the body's ability to convert food and fat into energy. Research has shown that sleeping less diminishes the body's ability to break down fat into energy, meaning the body stores it instead of consuming it. This is especially true if a person doesn't get rest on a consistent basis.

In addition, sleep deprivation commonly leads to metabolic dysregulation. Poor sleep is associated with increased oxidative stress, glucose (blood sugar) intolerance (a precursor to diabetes), and insulin resistance. Extra time spent awake may increase the opportunities to eat, and sleeping less may disrupt circadian rhythms, leading to weight gain.

Furthermore, sleep deprivation can lead to increased levels of ghrelin, which increases appetite, and leptin, which suppresses satiety hormones, making a person feel hungrier even when eating the same amount of food. Interrupted sleep is linked to an increased risk of obesity and diabetes as a result of changes to how the body regulates glucose, insulin resistance, and the hormones that control food intake and hunger.

Sleep deprivation can affect the gut biome, the bacteria in the digestive system that control metabolism

Sleep deprivation has been found to cause a reduction in Bacteroidetes and an increase in Firmicutes, with the ratio of Firmicutes to Bacteroidetes rising. This dysbiosis of gut microbiota has been linked to a decrease in beneficial bacteria, such as Akkermansia, Bacteroides, and Faecalibacterium, and an increase in pathogenic bacteria, such as g_Aeromonas.

The gut-brain axis plays a critical role in sleep deprivation-induced neurological disorders. The bidirectional communication between the gut microbiota and the brain is termed the microbiota-gut-brain axis. Sleep deprivation has been found to increase the permeability of the blood-brain barrier, allowing harmful metabolites to enter the brain and impair neuronal functions.

Additionally, sleep deprivation may affect the body's ability to convert food and fat into energy. Sleep loss has been shown to diminish the body's ability to break down fat into energy, leading to fat storage instead. This is especially true if an individual does not get consistent rest.

Furthermore, shortened sleeping times may impair the way the body metabolises glucose, increasing the risk of type 2 diabetes and weight gain, which can further increase resistance to insulin.

Sleep deprivation can affect the body's ability to convert food and fat into energy

Additionally, sleep deprivation can affect the production of hormones that regulate appetite and energy use. For example, sleep debt is associated with increased levels of ghrelin, which stimulates hunger, and decreased levels of leptin, which signals fullness. Sleep deprivation can also affect the gut biome, the bacteria in the digestive system that control metabolism, leading to changes in the stomach's microbial community structure and the way the body digests and metabolises food.

Furthermore, sleep deprivation can reduce energy levels, leading to decreased physical activity and a slower metabolism. It can also affect the endocannabinoid system, which plays a key role in the brain's regulation of appetite, leading to increased hunger and reduced ability to resist food. Finally, shortened sleeping times may impair the way the body metabolises glucose, increasing the risk of type 2 diabetes and weight gain, which can further increase resistance to insulin.

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