Biology:Postprandial somnolence

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Short description: State of drowsiness or lassitude following a meal
Frederick Arthur Bridgman – The Siesta (1878)
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]

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.

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

References

  1. ↑ Drayer, Lisa. "Are 'food comas' real or a figment of your digestion?". CNN. https://www.cnn.com/2017/02/03/health/food-comas-drayer/index.html. 
  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. https://www.sciencedirect.com/science/article/abs/pii/S0031938411005555. 
  3. ↑ Murphy, Keith R.; Deshpande, Sonali A.; Yurgel, Maria E.; Quinn, James P.; Weissbach, Jennifer L.; Keene, Alex C.; Dawson-Scully, Ken; Huber, Robert et al. (November 2016). "Postprandial sleep mechanics in Drosophila". eLife 5. doi:10.7554/eLife.19334. PMID 27873574. 
  4. ↑ 4.0 4.1 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. https://linkinghub.elsevier.com/retrieve/pii/S0959438816302458. 
  5. ↑ Juozaityte, Vaida; Pladevall-Morera, David; Podolska, Agnieszka; Nørgaard, Steffen; Neumann, Brent; Pocock, Roger (2017-02-13). "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. PMID 28193866. 
  6. ↑ Burdakov, Denis; Jensen, Lise Torp; Alexopoulos, Haris; Williams, Rhiannan Hope; Fearon, Ian M.; O'Kelly, Ita; Gerasimenko, Oleg; Fugger, Lars et al. (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. 
  7. ↑ "Predictive models of glucose control: roles for glucose-sensing neurones". Acta Physiologica 213 (1): 7–18. January 2015. doi:10.1111/apha.12360. PMID 25131833. 
  8. ↑ "The Autonomic Nervous System". http://microvet.arizona.edu/Courses/VSC401/autonomicNervous.html. 
  9. ↑ Streeten, DVH. "The Parasympathetic Nervous System". http://www.ndrf.org/ans.html#The%20Parasympathetic%20System. 
  10. ↑ "Glycemic index of foods: a physiological basis for carbohydrate exchange". The American Journal of Clinical Nutrition 34 (3): 362–6. March 1981. doi:10.1093/ajcn/34.3.362. PMID 6259925. 
  11. ↑ "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. January 2003. doi:10.1093/ajcn/77.1.128. PMID 12499331. http://www.ajcn.org/cgi/content/abstract/77/1/128. 
  12. ↑ 12.0 12.1 "Insulin in the brain: there and back again". Pharmacology & Therapeutics 136 (1): 82–93. October 2012. doi:10.1016/j.pharmthera.2012.07.006. PMID 22820012. 
  13. ↑ "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. October 1999. doi:10.1073/pnas.96.21.12079. PMID 10518579. Bibcode: 1999PNAS...9612079B. 
  14. ↑ "Brain serotonin content: increase following ingestion of carbohydrate diet". Science 174 (4013): 1023–5. December 1971. doi:10.1126/science.174.4013.1023. PMID 5120086. Bibcode: 1971Sci...174.1023F. 
  15. ↑ "High-glycemic-index carbohydrate meals shorten sleep onset". The American Journal of Clinical Nutrition 85 (2): 426–30. February 2007. doi:10.1093/ajcn/85.2.426. PMID 17284739. 
  16. ↑ "The Glycemic Index Concept | Official web site of the Montignac Method" (in en). http://www.montignac.com/en/the-glycemic-index-concept/. 
  17. ↑ "Sodium Pumps". Vivo.colostate.edu. 29 April 2006. http://www.vivo.colostate.edu/hbooks/molecules/sodium_pump.html. 
  18. ↑ "Hypokalemia - PubMed Health". Ncbi.nlm.nih.gov. https://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001510/. 
  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. PMID 21686739. PMC 3027774. https://online.epocrates.com/u/292159/Evaluation+of+hypokalemia/Diagnosis/Approach. 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. 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". http://www.anaesthetist.com/physiol/basics/autoreg/Findex.htm#index.htm. 
  24. ↑ Helmenstine, Anne Marie. "Does Eating Turkey Make You Sleepy?". About.com. http://chemistry.about.com/od/holidaysseasons/a/tiredturkey.htm. 
  25. ↑ "Is there something in turkey that makes you sleepy?". HowStuffWorks. 7 November 2007. http://home.howstuffworks.com/question519.htm. 
  26. ↑ McCue, Kevin. "Thanksgiving, Turkey, and Tryptophan". Chemistry.org. http://www.chemistry.org/portal/a/c/s/1/feature_ent.html?DOC=enthusiasts%5Cent_tryptophan.html. 
  27. ↑ Holden, Joanne. "USDA National Nutrient Database for Standard Reference, Release 20". Nutrient Data Laboratory, Agricultural Research Service, United States Department of Agriculture. http://www.ars.usda.gov/nutrientdata. 
  28. ↑ "Blue light aids in coping with the post-lunch dip: an EEG study". Ergonomics 58 (5): 803–10. 2015. doi:10.1080/00140139.2014.983300. PMID 25559376. 



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