Imagine you’ve just finished enjoying a large meal such as a traditional holiday meal, say at Christmas, Thanksgiving or Easter. You get up from the table and then quickly find yourself a comfortable place to relax…because all you want to do is rest and maybe even take a good nap. This is the state of food coma or, as it is known in medical circles, postprandial somnolence. It is a real phenomenon though it doesn’t come close to an actual coma. Postprandial somnolence is simply the state of extreme lethargy and sleepiness along with a feeling of bloating induced by the consumption of a large amount of food.
There have been several theories regarding the cause of postprandial somnolence presented in the past. One of them is that blood flow is shunted from the brain to the GI tract to aid in after-meal digestion. This however is untrue. Blood flow to the brain is tightly regulated by the circulatory system and is kept in a steady, unchanging state throughout a wide range of physiological states (1,2). For instance, during exercise, when blood flow to the muscles increases, there is no change in blood flow in the brain. The same is true following eating. This is confirmed by the observed lack of change in blood flow to the brain through the carotid artery after eating. The small increase in blood flow to the digestive tract after meals comes from the skeletal muscle tissue (3).
Another theory proposed that elevated levels of l-tryptophan from meat, especially poultry, increases serotonin levels which in turn increases drowsiness. L-tryptophan is an essential amino acid that cannot be produced by the human body and so must be obtained in food. It is used in the production of B vitamins and serotonin, a brain chemical that influences mood and promotes relaxation. From serotonin, melatonin is produced which is involved in sleep/wake cycles and promotes sleep. It is a myth however that it is the l-tryptophan in poultry that causes sleepiness after a large meal. For one thing, many commonly consumed foods are rich sources of l-tryptophan. Examples are all types of poultry and other meats, cheese, milk, fish, eggs, oats, soybeans, sesame and sunflower seeds. And even if blood levels of l-tryptophan are increased by eating foods high in l-tryptophan, brain levels are more likely to decrease rather than increase. This is because l-tryptophan ingested as part of a protein-containing meal forces it to compete with other amino acids for absorption into the brain across the blood-brain barrier. Other amino acids are much more plentiful than tryptophan and so the amount of tryptophan actually entering the brain blood circulation is low (4).
CAUSES OF POSTPRANDIAL SOMNOLENCE
So what is the cause of the extreme fatigue induced by the consumption of an extra-large meal? It appears that a variety of body processes may come into play (3).
Macronutrient constituents of a meal
Interestingly it was a 2016 study on fruit flies (Drosophila melanogaster) that provided our most recent insight on the relationship between eating and drowsiness (5). The humble fruit fly proved to be an excellent research subject for this investigation. It is difficult to study sleep in people who know they are being watched. They simply do not sleep “normally”. But fruit flies are not affected in this way and they, like us, sleep more after a large meal.
Flies and other insects do indeed go into a sleep-like state with periods of immobility, difficulty in arousal and increased need for extra sleep after sleep deprivation. Insects have a nervous system and their neurobiological processes, although not the same, do have similarities to our own in this regard (6).
Fruit flies have shown a well-documented interaction between sleep and metabolism. When starving they suppress sleep and increase their activity. They sleep after eating but, after certain meals, they sleep for significantly longer periods of time. This study discovered some foods that were much better at putting the fruit flies to sleep than others and it was the ingestion of protein and salt that promoted the deepest sleep in the flies. Carbohydrates do not have the same effect. Scientists theorize that carbohydrate is easy to come by but protein and salt call for more dedicated digestion.
The little Drosophila has expanded our understanding of the neurobiological connection between eating and sleep including postprandial somnolence. Researchers now plan to continue their research by looking more deeply at brain structures that induce this deeper sleep (5).
Other studies have found that high-fat meals are associated with more intense sleepiness than meals higher in carbohydrate or protein in spite of the fact that high-fat meals result in reduced serotonin blood levels (2).
Postprandial Lipemia (sometimes known as “Blood Sludge”)
Postprandial lipemia occurs after the ingestion of a high-fat meal. In this state, the fat content of the blood is increased and the blood itself appears to be more “milky” (lactescent). Red blood cells become stickier and are more apt to clump together (7,8). Triglyceride-rich lipoprotein levels increase and they are carried in the blood within small lipoproteins called “chylomicrons”. The chylomicrons are what show up as the “milkiness” in the blood. Along with these changes there is increased formation of LDL (Low Density Lipoprotein) and VLDL (Very Low Density Lipoprotein). The cumulative result of all these changes is a decrease in blood flow of about 20% along with a corresponding decrease in oxygen level in the blood which together bring on feelings of lassitude and drowsiness (9,10,11,7). Oxidative stress and damaging effects on the endothelial lining of the blood vessels follow, leading to stiffened blood vessels, increased blood clotting and accelerated development of atherosclerotic plaques within the blood vessels (12,13,10,14,15).
These blood effects are most pronounced after a meal containing saturated fatty acids (SFAs), such as those found in high amounts in animal fat. However, monounsaturated fatty acids (MUFA – the main fatty acids in olive oil) and polyunsaturated fatty acids (PUFA), found in vegetables and fish, cause a similar although sometimes lesser effect (16,17).
After ingestion of refined sugar the glucose levels in the blood quickly spike upwards and then, with the subsequent release of insulin from the pancreas, fall quickly, sometimes to below their starting level. The result is fatigue and drowsiness. However, all carbohydrates are not equal and, when consuming whole carbohydrates such as fruit, the increase in blood sugar is much lower when compared to the effects from eating refined sugar and the fall into hypoglycemia does not occur. (18)
High blood levels of CCK is associated with after-meal sleepiness. CCK is a hunger-suppressing hormone that is released by the gut during and after eating. It aids digestion and reduces appetite. Results of scientific studies reveal that significantly greater feelings of fatigue occur three hours after eating a high-fat low-carbohydrate meal than after ingesting a low-fat high-carbohydrate meal. Cholecystokinin (CCK) levels are observed to be higher after the high-fat meal than after the low-fat meal (19).
Orexin (aka hypocretin) is a protein released from neurons in the hypothalamus of the brain that regulates appetite and wakefulness. Its release in stimulated by low blood sugar levels and reduced by high blood sugar (20). Orexin is an integral part of the body’s sleep/wake regulation system and low amounts can cause fatigue and sleepiness (21).
ADDING UP THESE CAUSES OF POSTPRANDIAL SOMNOLENCE
After reviewing all the physiological processes affected by eating a large meal, it is no surprise that fatigue and drowsiness are its after-effects. High amounts of protein and/or salt seem to induce deeper sleep as evidenced by fruit fly studies. High-fat meals result in reduced oxygen in the blood as well as low serotonin and high cholecystokinin levels, both of which are associated with drowsiness. Sugary sauces and desserts cause large increases in blood sugar followed by very low levels that contribute to sleepiness. As well, high blood sugar can decrease orexin levels with accompanying sleepiness.
HOW TO AVOID POSTPRANDIAL SOMNOLENCE
Now that you are aware of the cause of food coma it should not be too difficult to prevent it if you so desire. Here are some tips;
Avoid refined carbohydrates such as sugary drinks, sauces and desserts.
Eat a smaller meal. Make sure you don’t dig into the meal on a completely empty stomach. Have a snack consisting of whole carbohydrates such as fruit, cut vegetables or nuts beforehand so that you are not ravenous and prone to overeating.
Balance the macronutrient content of the meal. Try to eat moderate amounts of protein.
Limit fatty foods including those containing high amounts of saturated fat, cholesterol and vegetable oils. A study of dietary patterns in truck drivers found that prudent eating patterns, those that included more nutrient-dense lower-fat foods in smaller-sized meals, resulted in less sleepiness when driving after the meal (22).
Micronutrients are important too as they offer protection from postprandial lipemia (23). Fill your plate with more vegetables and fewer animal-sourced foods.
Get enough sleep before the meal, especially if you plan to drive a long distance afterwards. A study of drivers found they were much sleepier after eating a larger meal than a smaller one, especially if they were already tired.
Exercise before your meal. Many studies have shown that such exercise can decrease the incidence of postprandial lipemia (23).
Get up and move after your meal too. Exercising for a short amount of time appears to be equally as beneficial as longer exercise bouts to decrease postprandial lipemia (23). Body movement will increase blood circulation, clear extra fatty particles from the bloodstream and stimulate muscles.
2 Kim, S.W., Lee, B.I. Metabolic state, neurohormones, and vagal stimulation, not increased serotonin, orchestrate postprandial drowsiness. Bioscience Hypotheses. 2009; 2(6): 422-427.
3 Bazar, K.A., Yun, A.J., Lee, P.Y. Debunking a myth – neurohormonal and vagal modulation of sleep centers, not redistribution of blood flow, may account for postprandial somnolence. Medical Hypotheses. 2004; 763: 778-782.
4 Fernstrom, J.D., Faller, D.V. Neutral Amino Acids in the Brain: Changes in Response to Food Ingestion. Journal of Neurochemistry June 1978; 30(6): 1531-1538.
5 Bowling Green State University. Neuroscientist probes tiny world of the fruit fly to discover sleep/eating/activity connection. ScienceDaily. ScienceDaily, 9 January 2017. <www.sciencedaily.com/releases/2017/01/170109143607.htm>.
6 Hendricks, J.C., Finn, S.M., Panckeri, K.A., Chavkin, J., Williams, J.A. et al. Rest in Drosophila is a Sleep-like State. Neuron. January 2000; 25: 129–138.
7 Postprandial Microvascular Dysfunction. Circ J. 2009; 73: 1399-1400.
8 Fukuzaki, H., Okamoto, R., Matsuo, T. Studies on Pathophysiological Effects of Postalimentary Lipemia in Patients with Ischemic Heart Disease. Japanese Circulation Journal. April 2975; 39(3):317-324.
9 Regan, T.J., Binak, K., Gordon, S., Defazio, V., Hellems, H.K. Myocardial Blood Flow and Oxygen Consumption during Postprandial Lipemia and Heparin-Induced Lipolysis. Circulation. 1961;23(1) :55–63.
10 Hyson, D., Rutledge, J.C., Berglund, L. Postprandial Lipemia and Cardiovascular Disease. Current Atherosclerosis Reports. November 2003; 5(6): 437-444.
12 Lefèbvre, P.J., Scheen, A.J. The Postprandial State and Risk of Cardiovascular Disease. Diabet Med. 1998;15 Suppl 4:S63-8.
13 Rajendran, P., Rengarajan, T., Thangavel, J., Nishigaki, Y., Sakthisekaran, D., Sethi, G., Nishigaki, I. The vascular endothelium and human diseases. Int J Biol Sci. 2013 Nov 9;9(10):1057-1069.
14 Teeman, C.S., Kurti, S.P., Cull, B.J., Emerson, S.R., Haub, M.D., Rosenkranz, S.K. Postprandial lipemic and inflammatory responses to high-fat meals: a review of the roles of acute and chronic exercise. Nutr Metab (Lond). 2016; 13: 80.
15 Zsotér, T., Fam, W.M., McGregor, M. The Effect of Lipemia on Peripheral Blood Flow. Can Med Assoc J. May 1964; 90(21): 1203–1205.
16 Klop, B., Proctor, S.D., Mamo, J.C., Botham, K.M., Cabezas, M.C. Understanding Postprandial Inflammation and Its Relationship to Lifestyle Behaviour and Metabolic Diseases. Int J Vasc Med. 2012; 2012: 947417.
17 Sciarrillo, C.M., Koemel, N.A., Tomko, P.M., Bode, K.B., Emerson, S.R. Postprandial Lipemic Responses to Various Sources of Saturated and Monounsaturated Fat in Adults. Nutrients 2019; 11(5): 1089.
18 Törrönen, R., Kolehmainen, M., Sarkkinen, E. et al. Postprandial glucose, insulin, and free fatty acid responses to sucrose consumption with blackcurrants and lingonberries in healthy women. Am J Clin Nutr. Sept 2012; 96(3): 527–533.
19 Wells, A.S., Read, N.W., Uvnas-Moberg, P.A. Influences of Fat and Carbohydrate on Postprandial Sleepiness, Mood, and Hormones. Physiology & Behavior. May 1997; 61(5): 679-686.
20 Ouedraogo, R., Näslund, E., Kirchgessner, A.L. Glucose regulates the release of orexin-a from the endocrine pancreas. Diabetes. 2003 Jan;52(1):111-7.
21 Cao, M., Guilleminault, C. Hypocretin and its emerging role as a target for treatment of sleep disorders. Curr Neurol Neurosci Rep. 2011 Apr;11(2):227-234.
22 Martins, A.J., Martini, L.A., Moreno, C.R.C. Prudent diet is associated with low sleepiness among short-haul truck drivers. Nutrition. 2019; 63-64: 61-68.
23 Gill, J.M.R., Hardman, A.E. Postprandial lipemia: effects of exercise and restriction of energy intake compared. Am J Clin Nutr. February 2000; 71(2): 465–471.