Postprandial somnolence

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An oil painting of a young woman having a siesta, or an afternoon nap, which usually occurs after the mid-day meal. Bridgman, Frederick Arthur - The Siesta (Afternoon in Dreams).png
An oil painting of a young woman having a siesta, or an afternoon nap, which usually occurs after the mid-day meal.

Postprandial somnolence (colloquially known as food coma, after-dinner dip, or "the itis") 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. [1] While there are numerous theories surrounding this behavior, such as decreased blood flow to the brain, neurohormonal modulation of sleep through digestive coupled signaling, or vagal stimulation, very few have been explicitly tested. To date, human studies have loosely examined the behavioral characteristics of postprandial sleep, demonstrating potential shifts in EEG spectra and self-reported sleepiness. [2] To date, the only clear animal models for examining the genetic and neuronal basis for this behavior are the fruit fly, the mouse, and the nematode Caenorhabditis elegans . [3] [4] [5]

Contents

Physiology

The exact cause of postprandial somnolence is unknown but there are some scientific hypotheses:

Adenosine and hypocretin/orexin hypothesis

Increases in glucose concentration excite and induce vasodilation in ventrolateral preoptic nucleus neurons of the hypothalamus via astrocytic release of adenosine that is blocked by A2A receptor antagonists like caffeine. [4] Evidence also suggests that the small rise in blood glucose that occurs after a meal is sensed by glucose-inhibited neurons in the lateral hypothalamus. [6] 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 aminergic, cholinergic, and glutamatergic arousal pathways of the brain, thus decreasing the activity of those pathways. [7]

Parasympathetic activation

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. [8] [9] 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.[ citation needed ]

Insulin, large neutral amino acids, and tryptophan

When foods with a high glycemic index are consumed, the carbohydrates in the food are more easily digested than low glycemic index foods. Hence, more glucose is available for absorption. It should not be misunderstood that glucose is absorbed more rapidly because, once formed, glucose is absorbed at the same rate. It is only available in higher amounts due to the ease of digestion of high glycemic index foods. 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. [10] 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 [11] [12] (an aromatic amino acid), making tryptophan preferentially available to the large neutral amino acid transporter at the blood–brain barrier. [13] [12] Uptake of tryptophan by the brain thus increases. In the brain, tryptophan is converted to serotonin, [14] which is then converted to melatonin. Increased brain serotonin and melatonin levels result in sleepiness. [15] [16]

Insulin-induced hypokalemia

Insulin can also 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. [17] 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. [18] The severity of the hypokalemic state can be evaluated using Fuller's Criteria. [19] 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.

Cytokines

Cytokines are somnogenic and are likely key mediators of sleep responses to infection [20] and food. [21] Some proinflammatory cytokines correlate with daytime sleepiness. [22]

Myths about the causes of post-prandial somnolence

Cerebral blood flow and oxygen delivery

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.[ citation needed ] The flow of oxygen and blood to the brain is extremely tightly regulated by the circulatory system [23] and does not drop after a meal.

Turkey and tryptophan

A common myth holds that turkey is especially high in tryptophan, [24] [25] [26] resulting in sleepiness after it is consumed, as may occur at the traditional meal of the North American holiday of Thanksgiving. However, the tryptophan content of turkey is comparable to chicken, beef, and other meats, [27] 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 also high in tryptophan. Whether it is possible or not that these may induce sleepiness if consumed in sufficient quantities has yet to be studied.[ medical citation needed ]

Counteraction

A 2015 study, reported in the journal Ergonomics, showed that, for twenty healthy subjects, exposure to blue-enriched light during the post-lunch dip period significantly reduced the EEG alpha activity, and increased task performance. [28]

See also

Related Research Articles

<span class="mw-page-title-main">Hypoglycemia</span> Decrease in blood sugar

Hypoglycemia, also spelled hypoglycaemia or hypoglycæmia, sometimes called low blood sugar, is a fall in blood sugar to levels below normal, typically below 70 mg/dL (3.9 mmol/L). Whipple's triad is used to properly identify hypoglycemic episodes. It is defined as blood glucose below 70 mg/dL (3.9 mmol/L), symptoms associated with hypoglycemia, and resolution of symptoms when blood sugar returns to normal. Hypoglycemia may result in headache, tiredness, clumsiness, trouble talking, confusion, fast heart rate, sweating, shakiness, nervousness, hunger, loss of consciousness, seizures, or death. Symptoms typically come on quickly.

<span class="mw-page-title-main">Fructose</span> Simple ketonic monosaccharide found in many plants

Fructose, or fruit sugar, is a ketonic simple sugar found in many plants, where it is often bonded to glucose to form the disaccharide sucrose. It is one of the three dietary monosaccharides, along with glucose and galactose, that are absorbed by the gut directly into the blood of the portal vein during digestion. The liver then converts most fructose and galactose into glucose for distribution in the bloodstream or deposition into glycogen.

Insulin resistance (IR) is a pathological condition in which cells in insulin-sensitive tissues in the body fail to respond normally to the hormone insulin or downregulate insulin receptors in response to hyperinsulinemia.

<span class="mw-page-title-main">Tryptophan</span> Chemical compound

Tryptophan (symbol Trp or W) is an α-amino acid that is used in the biosynthesis of proteins. Tryptophan contains an α-amino group, an α-carboxylic acid group, and a side chain indole, making it a polar molecule with a non-polar aromatic beta carbon substituent. Tryptophan is also a precursor to the neurotransmitter serotonin, the hormone melatonin, and vitamin B3 (niacin). It is encoded by the codon UGG.

<span class="mw-page-title-main">Hyperglycemia</span> Too much blood sugar, usually because of diabetes

Hyperglycemia or hyperglycaemia is the situation in which blood glucose level is higher than in a healthy subject. A fasting healthy human shows blood glucose level up to 5.6 mmol/L (100 mg/dL). After a meal (postprandial) containing carbohydrates, healthy subjects show postpandrial euglycemic peaks of less than 140 mg/dL (7.8 mmol/L). Therefore, fasting hyperglycemia are values of blood glucose higher than 5.6 mmol/L (100 mg/dL) whereas postprandial hyperglycemia are values higher than 140 mg/dL (7.8 mmol/L). Postprandial hyperglycemic levels as high as 155 mg/dL (8.6 mmol/L) at 1-h are associated with T2DM-related complications, which worsen as the degree of hyperglycemia increases. Patients with diabetes are oriented to avoid exceeding the recommended postprandial threshold of 160 mg/dL (8.89 mmol/L) for optimal glycemic control. Values of blood glucose higher than 160 mg/dL are classified as ‘very high’ hyperglycemia, a condition in which an excessive amount of glucose (glucotoxicity) circulates in the blood plasma. These values are higher than the renal threshold of 180 mg/dL (10 mmol/L) up to which glucose reabsorption is preserved at physiological rates and insulin therapy is not necessary. Blood glucose values higher than the cutoff level of 200 mg/dL (11.1 mmol/L) are used to diagnose T2DM and strongly associated with metabolic disturbances, although symptoms may not start to become noticeable until even higher values such as 13.9–16.7 mmol/L (~250–300 mg/dL). A subject with a consistent fasting blood glucose range between ~5.6 and ~7 mmol/L is considered slightly hyperglycemic, and above 7 mmol/L is generally held to have diabetes. For diabetics, glucose levels that are considered to be too hyperglycemic can vary from person to person, mainly due to the person's renal threshold of glucose and overall glucose tolerance. On average, however, chronic levels above 10–12 mmol/L (180–216 mg/dL) can produce noticeable organ damage over time.

<span class="mw-page-title-main">Glycemic index</span> Number assigned to food

The glycemic (glycaemic) index is a number from 0 to 100 assigned to a food, with pure glucose arbitrarily given the value of 100, which represents the relative rise in the blood glucose level two hours after consuming that food. The GI of a specific food depends primarily on the quantity and type of carbohydrate it contains, but is also affected by the amount of entrapment of the carbohydrate molecules within the food, the fat and protein content of the food, the amount of organic acids in the food, and whether it is cooked and, if so, how it is cooked. GI tables, which list many types of foods and their GIs, are available. A food is considered to have a low GI if it is 55 or less; high GI if 70 or more; and mid-range GI if 56 to 69.

<span class="mw-page-title-main">Glucokinase</span> Enzyme participating to the regulation of carbohydrate metabolism

Glucokinase is an enzyme that facilitates phosphorylation of glucose to glucose-6-phosphate. Glucokinase occurs in cells in the liver and pancreas of humans and most other vertebrates. In each of these organs it plays an important role in the regulation of carbohydrate metabolism by acting as a glucose sensor, triggering shifts in metabolism or cell function in response to rising or falling levels of glucose, such as occur after a meal or when fasting. Mutations of the gene for this enzyme can cause unusual forms of diabetes or hypoglycemia.

The glycemic response to a food or meal is the effect that food or meal has on blood sugar (glucose) levels after consumption. It is normal for blood glucose and insulin levels to rise after eating and then return again to fasting levels over a short period of time. This is particularly so after consumption of meals rich in certain carbohydrates. Glycemic management refers to the selection of foods to manage your blood sugar levels.

The glycemic load (GL) of food is a number that estimates how much the food will raise a person's blood glucose level after it is eaten. One unit of glycemic load approximates the effect of eating one gram of glucose. Glycemic load accounts for how much carbohydrate is in the food and how much each gram of carbohydrate in the food raises blood glucose levels. Glycemic load is based on the glycemic index (GI), and is calculated by multiplying the weight of available carbohydrate in the food (in grams) by the food's glycemic index, and then dividing by 100.

<span class="mw-page-title-main">Tagatose</span> Chemical compound

Tagatose is a hexose monosaccharide. It is found in small quantities in a variety of foods, and has attracted attention as an alternative sweetener. It is often found in dairy products, because it is formed when milk is heated. It is similar in texture and appearance to sucrose :215 and is 92% as sweet,:198 but with only 38% of the calories.:209 Tagatose is generally recognized as safe by the Food and Agriculture Organization and the World Health Organization, and has been since 2001. Since it is metabolized differently from sucrose, tagatose has a minimal effect on blood glucose and insulin levels. Tagatose is also approved as a tooth-friendly ingredient for dental products. Consumption of more than about 30 grams of tagatose in a dose may cause gastric disturbance in some people, as it is mostly processed in the large intestine, similar to soluble fiber.:214

<span class="mw-page-title-main">Reactive hypoglycemia</span> Medical condition

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References

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