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Postprandial somnolence (colloquially known as a food coma or carb coma) is a normal state of drowsiness or lassitude following a meal. Postprandial somnolence has two components: a general state of low energy related to activation of the parasympathetic nervous system in response to mass in the gastrointestinal tract, and a specific state of sleepiness caused by hormonal and neurochemical changes related to the rate at which glucose enters the bloodstream and its downstream effects on amino acid transport in the central nervous system.
In response to the arrival of food in the stomach and small intestine, the activity of the parasympathetic nervous system increases and the activity of the sympathetic nervous system decreases. This shift in the balance of autonomic tone towards the parasympathetic system results in a subjective state of low energy and a desire to be at rest, the opposite of the fight-or-flight state induced by high sympathetic tone. The larger the meal, the greater the shift in autonomic tone towards the parasympathetic system, regardless of the composition of the meal.
When foods with a high glycemic index are consumed, glucose is absorbed rapidly from the gastrointestinal tract into the bloodstream, and in individuals with normal carbohydrate metabolism, insulin levels rise concordantly to drive glucose into the body's tissues and maintain blood glucose levels in the normal range. Insulin stimulates the uptake of valine, leucine, and isoleucine into skeletal muscle, but not uptake of tryptophan. This lowers the ratio of these branched-chain amino acids in the bloodstream relative to tryptophan (an aromatic amino acid), making tryptophan preferentially available to the large neutral amino acid transporter at the blood–brain barrier. Uptake of tryptophan by the brain thus increases. In the brain, tryptophan is converted to serotonin, which is then converted to melatonin. Increased brain serotonin and melatonin levels result in sleepiness.
Evidence suggests that the small rise in blood glucose that occurs after a meal is sensed by glucose-inhibited neurons in the lateral hypothalamus. These orexin-expressing neurons appear to be hyperpolarised (inhibited) by a glucose-activated potassium channel. This inhibition is hypothesized to then reduce output from orexigenic neurons to amineregic, cholinergic, and glutamatergic arousal pathways of the brain, thus decreasing the activity of those pathways, and therefore brain arousal.
Insulin also can cause postprandial somnolence via another mechanism. Insulin increases the activity of Na/K ATPase, causing increased movement of potassium into cells from the extracellular fluid. The large movement of potassium from the extracellular fluid can lead to a mild hypokalemic state. The effects of hypokalemia can include fatigue, muscle weakness, or paralysis. The severity of the hypokalemic state can be evaluated using Fuller's Criteria. Stage 1 is characterized by no symptoms but mild hypokalemia. Stage 2 is characterized with symptoms and mild hypokalemia. Stage 3 is characterized by only moderate to severe hypokalemia.
Although the passage of food into the gastrointestinal tract results in increased blood flow to the stomach and intestines, this is achieved by diversion of blood primarily from skeletal muscle tissue and by increasing the volume of blood pumped forward by the heart each minute. The flow of oxygen and blood to the brain is extremely tightly regulated by the circulatory system and does not drop after a meal, and is not a cause of post-meal sleepiness.
A common myth holds that turkey is especially high in tryptophan, resulting in sleepiness after it is consumed, as may occur at the traditional meal of the American holiday of Thanksgiving. However, the tryptophan content of turkey is comparable to chicken, beef, and other meats and does not result in higher blood tryptophan levels than other common foods. Certain foods, such as soybeans, sesame and sunflower seeds, and certain cheeses, are high in tryptophan. Although it is possible these may induce sleepiness if consumed in sufficient quantities, this is not well-studied.
When alcohol is consumed with a meal, this may contribute to sleepiness after the meal, but is a nonspecific response to alcohol consumption and can occur independently of eating.
|This section requires expansion. (April 2010)|