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Postprandial somnolence

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A man taking a siesta, or an afternoon nap, which usually occurs after the mid-day meal

Postprandial somnolence (colloquially known as food coma, after-dinner dip, and postprandial sleep, or by the African-American Vernacular English term the itis[1]) 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.[2] 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.[3] 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.[4][5][6]

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.[5] 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.[7] 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.[8]

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.[9][10] 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.[11] 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[12][13] (an aromatic amino acid), making tryptophan preferentially available to the large neutral amino acid transporter at the blood–brain barrier.[14][13] Uptake of tryptophan by the brain thus increases. In the brain, tryptophan is converted to serotonin,[15] which is then converted to melatonin. Increased brain serotonin and melatonin levels result in sleepiness.[16][17]

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.[18] 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.[19] The severity of the hypokalemic state can be evaluated using Fuller's Criteria.[20] 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[21] and food.[22] Some proinflammatory cytokines correlate with daytime sleepines.[23]

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[24] and does not drop after a meal.

Turkey and tryptophan

A common myth holds that turkey is especially high in tryptophan,[25][26][27] 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,[28] 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. 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.[29]

See also

References

  1. ^ Keys, Jazz (29 March 2017). "Slave Food: The Impact of Unhealthy Eating Habits on the Black Community". Ebony Magazine. Retrieved 5 August 2018.
  2. ^ Drayer, Lisa. "Are 'food comas' real or a figment of your digestion?". CNN. Retrieved 11 July 2019.
  3. ^ Reyner, LA; Wells, SJ; Mortlock, V; Horne, JA (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. PMID 22155490. S2CID 26531287.
  4. ^ 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 5119887. PMID 27873574.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  5. ^ a b 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. S2CID 3628811.
  6. ^ 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.
  7. ^ 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. S2CID 15036932.
  8. ^ 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.
  9. ^ "The Autonomic Nervous System". Archived from the original on 11 June 2008. Retrieved 12 June 2008.
  10. ^ Streeten, DVH. "The Parasympathetic Nervous System". National Dysautonomia Research Foundation. Retrieved 18 July 2010.
  11. ^ 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.
  12. ^ 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.
  13. ^ a b 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.
  14. ^ 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.
  15. ^ 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.
  16. ^ 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.
  17. ^ "The Glycemic Index Concept | Official web site of the Montignac Method". www.montignac.com. Retrieved 17 March 2018.
  18. ^ "Sodium Pumps". Vivo.colostate.edu. 29 April 2006. Archived from the original on 29 July 2012. Retrieved 6 February 2013.
  19. ^ "Hypokalemia - PubMed Health". Ncbi.nlm.nih.gov. Retrieved 6 February 2013.
  20. ^ Lin, H. W.; Chau, T.; Lin, C. S.; Lin, S. H. (2009). "Evaluation of hypokalemia Diagnostic Approach - Epocrates Online". BMJ Case Reports. 2009. Online.epocrates.com. doi:10.1136/bcr.07.2008.0577. PMC 3027774. PMID 21686739. Retrieved 6 February 2013.
  21. ^ 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.
  22. ^ 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.
  23. ^ 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–A291. doi:10.1093/sleepj/zsx050.784.
  24. ^ "Anesthetist: Vascular Autoregulation". Anaesthetist.com. Retrieved 12 June 2008.
  25. ^ Helmenstine, Anne Marie. "Does Eating Turkey Make You Sleepy?". About.com. Retrieved 13 November 2013.
  26. ^ "Is there something in turkey that makes you sleepy?". HowStuffWorks. 7 November 2007. Retrieved 13 November 2013.
  27. ^ McCue, Kevin. "Thanksgiving, Turkey, and Tryptophan". Chemistry.org. Archived from the original on 4 April 2007. Retrieved 17 August 2007.
  28. ^ 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.
  29. ^ 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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