This article needs additional citations for verification. (October 2015) (Learn how and when to remove this template message)
Postprandial somnolence (colloquially known as the itis, food coma, after dinner dip, or postprandial sleep,) 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. 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. To date, the only clear animal models for examining the genetic and neuronal basis for this behavior are the fruit fly and the mouse.
Adenosine and hypocretin/orexin hypothesisEdit
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. 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. 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.
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.
Insulin, large neutral amino acids, and tryptophanEdit
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. 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.
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.
Myths about the causes of post-prandial somnolenceEdit
Cerebral blood flow and oxygen deliveryEdit
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.
Turkey and tryptophanEdit
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 North 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.
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.
- Keys, Jazz (29 March 2017). "Slave Food: The Impact of Unhealthy Eating Habits on the Black Community". Ebony Magazine. Retrieved 5 August 2018.
- Murphy KR, Deshpande SA, Yurgel ME, Quinn JP, Weissbach JL, Keene AC, Dawson-Scully K, Huber R, Tomchik SM, Ja WW (November 2016). "Drosophila". eLife. 5. doi:10.7554/eLife.19334. PMC . PMID 27873574.
- Donlea JM, Alam MN, Szymusiak R (June 2017). "Neuronal substrates of sleep homeostasis; lessons from flies, rats and mice". Current Opinion in Neurobiology. 44: 228–235. doi:10.1016/j.conb.2017.05.003. PMID 28628804.
- Burdakov D, Jensen LT, Alexopoulos H, Williams RH, Fearon IM, O'Kelly I, Gerasimenko O, Fugger L, Verkhratsky A (June 2006). "Tandem-pore K+ channels mediate inhibition of orexin neurons by glucose". Neuron. 50 (5): 711–22. doi:10.1016/j.neuron.2006.04.032. PMID 16731510.
- Kosse C, Gonzalez A, Burdakov D (January 2015). "Predictive models of glucose control: roles for glucose-sensing neurones". Acta Physiologica. 213 (1): 7–18. doi:10.1111/apha.12360. PMC . PMID 25131833.
- "The Autonomic Nervous System". Archived from the original on 11 June 2008. Retrieved 12 June 2008.
- Streeten, DVH. "The Parasympathetic Nervous System". National Dysautonomia Research Foundation. Retrieved 18 July 2010.
- Jenkins DJ, Wolever TM, Taylor RH, Barker H, Fielden H, Baldwin JM, Bowling AC, Newman HC, Jenkins AL, Goff DV (March 1981). "Glycemic index of foods: a physiological basis for carbohydrate exchange". The American Journal of Clinical Nutrition. 34 (3): 362–6. doi:10.1093/ajcn/34.3.362. PMID 6259925.
- Wurtman RJ, Wurtman JJ, Regan MM, McDermott JM, Tsay RH, Breu JJ (January 2003). "Effects of normal meals rich in carbohydrates or proteins on plasma tryptophan and tyrosine ratios". The American Journal of Clinical Nutrition. 77 (1): 128–32. doi:10.1093/ajcn/77.1.128. PMID 12499331.
- Banks WA, Owen JB, Erickson MA (October 2012). "Insulin in the brain: there and back again". Pharmacology & Therapeutics. 136 (1): 82–93. doi:10.1016/j.pharmthera.2012.07.006. PMC . PMID 22820012.
- Boado RJ, Li JY, Nagaya M, Zhang C, Pardridge WM (October 1999). "Selective expression of the large neutral amino acid transporter at the blood-brain barrier". Proceedings of the National Academy of Sciences of the United States of America. 96 (21): 12079–84. PMID 10518579.
- Fernstrom JD, Wurtman RJ (December 1971). "Brain serotonin content: increase following ingestion of carbohydrate diet". Science. 174 (4013): 1023–5. doi:10.1126/science.174.4013.1023. PMID 5120086.
- Afaghi A, O'Connor H, Chow CM (February 2007). "High-glycemic-index carbohydrate meals shorten sleep onset". The American Journal of Clinical Nutrition. 85 (2): 426–30. doi:10.1093/ajcn/85.2.426. PMID 17284739.
- "The Glycemic Index Concept | Official web site of the Montignac Method". www.montignac.com. Retrieved 17 March 2018.
- "Sodium Pumps". Vivo.colostate.edu. 29 April 2006. Retrieved 6 February 2013.
- "Hypokalemia - PubMed Health". Ncbi.nlm.nih.gov. Retrieved 6 February 2013.
- "Evaluation of hypokalemia Diagnostic Approach - Epocrates Online". Online.epocrates.com. doi:10.1136/bcr.07.2008.0577. Retrieved 6 February 2013.
- "Anesthetist: Vascular Autoregulation". Anaesthetist.com. Retrieved 12 June 2008.
- Bazar KA, Yun AJ, Lee PY (2004). "Debunking a myth: neurohormonal and vagal modulation of sleep centers, not redistribution of blood flow, may account for postprandial somnolence". Medical Hypotheses. 63 (5): 778–82. doi:10.1016/j.mehy.2004.04.015. PMID 15488646.
- Helmenstine, Anne Marie. "Does Eating Turkey Make You Sleepy?". About.com. Retrieved 13 November 2013.
- "Is there something in turkey that makes you sleepy?". HowStuffWorks. Retrieved 13 November 2013.
- McCue, Kevin. "Thanksgiving, Turkey, and Tryptophan". Chemistry.org. Archived from the original on 4 April 2007. Retrieved 17 August 2007.
- Holden, Joanne. "USDA National Nutrient Database for Standard Reference, Release 20". Nutrient Data Laboratory, Agricultural Research Service, United States Department of Agriculture. Retrieved 2 October 2007.
- Baek H, Min BK (2015). "Blue light aids in coping with the post-lunch dip: an EEG study". Ergonomics. 58 (5): 803–10. doi:10.1080/00140139.2014.983300. PMID 25559376.