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

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Hypoglycemia, also 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 both fructose and galactose into glucose, so that dissolved glucose, known as blood sugar, is the only monosaccharide present in circulating blood.

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<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. It is encoded by the codon UGG.

<span class="mw-page-title-main">Glycogen</span> Glucose polymer used as energy store in animals

Glycogen is a multibranched polysaccharide of glucose that serves as a form of energy storage in animals, fungi, and bacteria. It is the main storage form of glucose in the human body.

<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.

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References

  1. ↑ Drayer, Lisa. "Are 'food comas' real or a figment of your digestion?". CNN. Retrieved 11 July 2019.
  2. ↑ Reyner, Louise A.; Wells, SJ; Mortlock, V; Horne, James A. (28 February 2012). "'Post-lunch' sleepiness during prolonged, monotonous driving - effects of meal size". Physiology & Behavior. 105 (4): 1088–91. doi:10.1016/j.physbeh.2011.11.025. ISSN   1873-507X. OCLC   776470639. PMID   22155490. S2CID   26531287.
  3. ↑ Murphy, Keith R.; Deshpande, Sonali A.; Yurgel, Maria E.; Quinn, James P.; Weissbach, Jennifer L.; Keene, Alex C.; Dawson-Scully, Ken; Huber, Robert; Tomchik, Seth M.; Ja, William W. (November 2016). "Postprandial sleep mechanics in Drosophila". eLife. 5. doi: 10.7554/eLife.19334 . PMC   5119887 . PMID   27873574.
  4. 1 2 Donlea, Jeffrey Michael; Alam, Muhammad Noor; Szymusiak, Ronald (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. S2CID   3628811.
  5. ↑ Juozaityte, Vaida; Pladevall-Morera, David; Podolska, Agnieszka; Nørgaard, Steffen; Neumann, Brent; Pocock, Roger (13 February 2017). "The ETS-5 transcription factor regulates activity states in Caenorhabditis elegans by controlling satiety". Proceedings of the National Academy of Sciences . 114 (9): E1651–E1658. doi: 10.1073/pnas.1610673114 . ISSN   0027-8424. PMC   5338484 . PMID   28193866.
  6. ↑ Burdakov, Denis; Jensen, Lise Torp; Alexopoulos, Haris; Williams, Rhiannan Hope; Fearon, Ian M.; O'Kelly, Ita; Gerasimenko, Oleg; Fugger, Lars; Verkhratsky, Alexei (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. S2CID   15036932.
  7. ↑ 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   5767106 . PMID   25131833.
  8. ↑ "The Autonomic Nervous System". Archived from the original on 11 June 2008. Retrieved 12 June 2008.
  9. ↑ Streeten, DVH. "The Parasympathetic Nervous System". National Dysautonomia Research Foundation. Retrieved 18 July 2010.
  10. ↑ 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.
  11. ↑ 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.
  12. 1 2 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   4134675 . PMID   22820012.
  13. ↑ 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. Bibcode:1999PNAS...9612079B. doi: 10.1073/pnas.96.21.12079 . PMC   18415 . PMID   10518579.
  14. ↑ Fernstrom JD, Wurtman RJ (December 1971). "Brain serotonin content: increase following ingestion of carbohydrate diet". Science. 174 (4013): 1023–5. Bibcode:1971Sci...174.1023F. doi:10.1126/science.174.4013.1023. PMID   5120086. S2CID   14345137.
  15. ↑ 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.
  16. ↑ "The Glycemic Index Concept | Official web site of the Montignac Method". www.montignac.com. Retrieved 17 March 2018.
  17. ↑ "Sodium Pumps". Vivo.colostate.edu. 29 April 2006. Archived from the original on 29 July 2012. Retrieved 6 February 2013.
  18. ↑ "Hypokalemia - PubMed Health". Ncbi.nlm.nih.gov. Retrieved 6 February 2013.
  19. ↑ Lin, H. W.; Chau, T.; Lin, C. S.; Lin, S. H. (2009). "Evaluation of hypokalemia Diagnostic Approach - Epocrates Online". BMJ Case Reports. Online.epocrates.com. 2009. doi:10.1136/bcr.07.2008.0577. PMC   3027774 . PMID   21686739 . Retrieved 6 February 2013.
  20. ↑ Krueger, James M.; Majde, Jeannine A. (2017). "Microbial Products and Cytokines in Sleep and Fever Regulation". Critical Reviews in Immunology. 37 (2–6): 291–315. doi:10.1615/CritRevImmunol.v37.i2-6.70.
  21. ↑ Lehrskov, Louise L.; Dorph, Emma; Widmer, Andrea M.; Hepprich, Matthias; Siegenthaler, Judith; Timper, Katharina; Donath, Marc Y. (June 2018). "The role of IL-1 in postprandial fatigue". Molecular Metabolism. 12: 107–112. doi: 10.1016/j.molmet.2018.04.001 . PMC   6001918 . PMID   29705519.
  22. ↑ van de Loo, Aj; Mackus, M; Knipping, K; Kraneveld, Ad; Garssen, J; Roth, T; Verster, Jc (28 April 2017). "0785 Cytokines, Sleep, and Daytime Sleepiness". Sleep. 40 (suppl_1): A291. doi: 10.1093/sleepj/zsx050.784 .
  23. ↑ "Anesthetist: Vascular Autoregulation". Anaesthetist.com. Retrieved 12 June 2008.
  24. ↑ Helmenstine, Anne Marie. "Does Eating Turkey Make You Sleepy?". About.com. Archived from the original on 7 August 2011. Retrieved 13 November 2013.
  25. ↑ "Is there something in turkey that makes you sleepy?". HowStuffWorks. 7 November 2007. Retrieved 13 November 2013.
  26. ↑ McCue, Kevin. "Thanksgiving, Turkey, and Tryptophan". Chemistry.org. Archived from the original on 4 April 2007. Retrieved 17 August 2007.
  27. ↑ 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.
  28. ↑ 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. S2CID   5388522.
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