Postprandial somnolence

Postprandial somnolence (colloquially known as a food coma, carb coma, 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. The increased sleepiness is thought to be caused by hormonal and neurochemical changes related to the rate at which glucose enters the bloodstream and its downstream effects on amino acid transport in the central nervous system, though there is a lack of evidence to support this.

Physiology

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.[1][2] 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 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.[3] 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[4] (an aromatic amino acid), making tryptophan preferentially available to the large neutral amino acid transporter at the blood–brain barrier.[5] Uptake of tryptophan by the brain thus increases. In the brain, tryptophan is converted to serotonin,[6] which is then converted to melatonin. Increased brain serotonin and melatonin levels result in sleepiness.[7] [8]

Hypocretin/orexin hypothesis

Evidence suggests that the small rise in blood glucose that occurs after a meal is sensed by glucose-inhibited neurons in the lateral hypothalamus.[9] 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 amineregic, cholinergic, and glutamatergic arousal pathways of the brain, thus decreasing the activity of those pathways, and therefore brain arousal.

Insulin-induced hypokalemia

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.[10] 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.[11] The severity of the hypokalemic state can be evaluated using Fuller's Criteria.[12] 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 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. The flow of oxygen and blood to the brain is extremely tightly regulated by the circulatory system and does not drop after a meal,[13] and is not a cause of post-meal sleepiness.[14]

Turkey and tryptophan

A common myth holds that turkey is especially high in tryptophan,[15][16][17] 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[18] 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.

Counteraction

In 2015 a 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.[19]

See also

References

  1. ↑ "The Autonomic Nervous System". Retrieved 2008-06-12.
  2. ↑ Parasympathetic System "The Parasympathetic Nervous System" Check |url= value (help). Retrieved 2010-07-18.
  3. ↑ DJ Jenkins; et al. (1981), Glycemic index of foods: a physiological basis for carbohydrate exchange., Am J Clin Nutr 34; 362-366
  4. ↑ Wurtman RJ, Wurtman JJ, Regan MM, McDermott JM, Tsay RH, Breu JJ (2003). "Effects of normal meals rich in carbohydrates or proteins on plasma tryptophan and tyrosine ratios". Am. J. Clin. Nutr. 77 (1): 128–32. PMID 12499331.
  5. ↑ "Proceedings of the National Academy of Sciences: The LNAA Transport at the Blood Brain Barrier". Retrieved 2008-06-12.
  6. ↑ Fernstrom JD, Wurtman RJ (1971). "Brain serotonin content: increase following ingestion of carbohydrate diet". Science 174 (4013): 1023–5. doi:10.1126/science.174.4013.1023. PMID 5120086.
  7. ↑ Afaghi A, O'Connor H, Chow CM (2007). "High-glycemic-index carbohydrate meals shorten sleep onset". Am. J. Clin. Nutr. 85 (2): 426–30. PMID 17284739.
  8. ↑ http://www.montignac.com/en/the-glycemic-index-concept/
  9. ↑ Burdakov D, Jensen LT, Alexopoulos H, 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.
  10. ↑ "Sodium Pumps". Vivo.colostate.edu. 2006-04-29. Retrieved 2013-02-06.
  11. ↑ "Hypokalemia - PubMed Health". Ncbi.nlm.nih.gov. Retrieved 2013-02-06.
  12. ↑ "Evaluation of hypokalemia Diagnostic Approach - Epocrates Online". Online.epocrates.com. doi:10.1136/bcr.07.2008.0577. Retrieved 2013-02-06.
  13. ↑ "Anesthetist: Vascular Autoregulation". Retrieved 2008-06-12.
  14. ↑ 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.". Med Hypotheses. 63 (5): 778–82. doi:10.1016/j.mehy.2004.04.015. PMID 15488646.
  15. ↑ Helmenstine, Anne Marie. "Does Eating Turkey Make You Sleepy?". About.com. Retrieved 2013-11-13.
  16. ↑ "Is there something in turkey that makes you sleepy?". HowStuffWorks. Retrieved 2013-11-13.
  17. ↑ McCue, Kevin. "Thanksgiving, Turkey, and Tryptophan". Chemistry.org. Archived from the original on 2007-04-04. Retrieved 2007-08-17.
  18. ↑ Joanne Holden, Nutrient Data Laboratory, Agricultural Research Service. "USDA National Nutrient Database for Standard Reference, Release 20". United States Department of Agriculture. Retrieved 2007-10-02.
  19. ↑ Baek, Hongchae; Byoung-Kyong Min (2015). "Blue light aids in coping with the post-lunch dip: an EEG study". Ergonomics 58 (5): 803–810. doi:10.1080/00140139.2014.983300.
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