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Sleep affects the body’s rate of energy use and release of hormones. There is ample scientific evidence for this going back decades. It was once thought that staying up all night affected one’s appetite and caused a slight weight gain, but that the effect would go away when normal sleep habits were resumed and the sleep debt was repaid.
Now it is known that chronic short sleep of the type experienced by many overscheduled Americans causes increased appetite and is likely linked to putting on body fat.
Roughly, the control mechanism for eating and feeling full consists of two hormones. Leptin is secreted by fat cells and tells the brain that the amount of fat being stored is sufficient or has increased. Leptin says the body has plenty of energy in reserves and the brain should produce the feeling of fullness. ghrelin is a hormone secreted by the digestive system when there is little food in the stomach. It tells the brain to make the person hungry. Leptin and ghrelin are part of the body’s weight homeostasis mechanism.
When we run short of sleep, blood levels of leptin drop. Sleep deprivation also increases levels of the hormone ghrelin, which is known to stimulate the appetite. Sleep homeostasis and weight homeostasis thus interact.
Ghrelin and leptin regulate the body’s energy balance, making the brain feel hungry or full. Chronic insomnia affects the level of ghrelin, but not the level of leptin. There is evidence that reduced sleep adversely effects glucose metabolism.
Which would tend to suggest insomnia should promote weight loss, not weight gain. The explanation for this apparent counter-evidence is that ghrelin levels may be lower during the sleep period for insomniac, they are higher during the day.
People suffering from sleep loss or excessive daytime sleepiness tend to be less physically active and use fewer calories, but surprisingly, scientists have concluded this is not a major factor in weight gain. The physiological mechanisms that cause short sleepers to gain weight appear to be two-fold:
Functional MRI investigation has shown that even after one night of short sleep the area of the brain that senses appetite is more activated than usual. The neurotransmitter orexin, discovered in recent decades and still not totally understood, appears to play a part in both keeping us awake and alert and in the food gathering and hunting instinct. Although you might think we would tend to get sleepy when we are tired and hungry, humans often find new mental energy in these situations – evolution gave us the tenacity to continue to look for food. This is at least partly due to the orexin system which becomes more activated in times of sleep deprivation. People with narcolepsy have a deficiency in the orexin-producing part of the brain. When narcoleptic dogs are exposed to food, they often have a cataplectic attack, suggesting something is being triggered in the orexin circuit. The system may be involved in overall feeding behavior.
Recent research has found a difference between men and women and how the sexes respond to inadequate sleep. After periods of short sleep, the levels of ghrelin were higher in men; levels of appetite-suppressing GLP-1 hormone were lower in women but unchanged in men. The researchers concluded short sleep produces enhanced appetite in men but in feeling less full in women.
The nervous system can be functionally divided into the sympathetic nervous system, the parasympathetic nervous system, and the enteric nervous system.
The parasympathetic system operates outside of conscious thought and controls many background bodily functions. The sympathetic nervous system keeps the body vigilant. It feels to the subject that stress is occurring.
Physiologists have the concept of “sympathovagal balance” to partially describe the body’s state from the interactions of the two systems. In slow-wave sleep the sympathetic system is much less active than in waking (or REM) while parasympathetic system activity goes up as part of the “housekeeping” function of sleep.
During periods of sleep loss, the sympathovagal balance goes up – higher sympathetic and lower parasympathetic activity. This shift affects the release of insulin by the pancreas and the release of leptin by adipose (fat) tissue.
Leptin release by the fat cells is inhibited by activity in the sympathetic system. parasympathetic activity slows release of ghrelin. This would provide a causal explanation. An increase in the sympathovagal balance leads to lower levels of leptin and higher levels of ghrelin.
It’s not just humans, either. Animals with a reduced supply of food sleep less. Animals deprived of sleep develop voracious appetites.
As a society we sleep less than we did a century ago. The rate of Type 2 diabetes is also substantially higher. Is there a connection?
The more obvious risk factors for diabetes are obesity, sugar consumption, and age, all of which have increased over the decades. In the case of diet and weight the cause and effect is easy to see, but sleep duration is not obviously a factor in glucose levels. However, science has found a connection.
The brain is a major user of glucose and when the brain is tired after sleep deprivation, glucose consumption is down. This is not just a hypothesis; it has been shown in PET scans.
Short sleep also increases cytokine levels in the bloodstream, and that can sometimes lead to insulin resistance.
Levels of the stress hormone cortisol are also affected by sleep loss. Cortisol levels decrease in the evening before bedtime. In people with chronic sleep loss, the levels do not decrease as much, possibly leading to increased insulin resistance, which in turn can lead to diabetes and obesity. Levels of thyroid-stimulating hormone decrease in periods of short sleep. Growth hormone release by the brain can be split in people with chronic sleep loss. Researchers have found that rather than a single big dose in the first slow-wave stage of sleep, growth hormone is released twice – once before sleep and once after. This results in greater exposure to growth hormone throughout the body, and that can increase insulin resistance, too.