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Postprandial Somnolence: Why a “Food Coma” Happens

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Have you ever eaten a meal, and 30 minutes to an hour later, felt a wave of somnolence sweep over your body? While it’s normal to feel sleepy after eating a large meal, such as Thanksgiving dinner, it’s not normal to frequently experience fatigue, brain fog, or other symptoms after normal-sized meals

postprandial somnolence food coma

Postprandial fatigue, colloquially referred to as a “food coma,” is defined as a substantial decrease in energy levels after meals. Read on to learn about what postprandial fatigue is, the underlying causes of this condition, and how to resolve it with diet and lifestyle changes. 

No, It’s Not Normal to Feel Tired After Meals

Postprandial fatigue is a state of drowsiness that occurs after a meal. Typically, post-meal sleepiness hits 30 minutes to an hour after eating and can endure for several hours. However, the fatigue may also occur with a host of other symptoms, including:

  • Brain fog and cognitive impairment 
  • Nausea
  • Bloating
  • Loss of motivation
  • Dizziness
  • Mood changes, including irritability
  • Sweating
  • Shaking
  • Flushing 

While it’s normal to feel tired after eating a larger meal, it’s not normal to feel tired after eating standard-sized meals daily. You shouldn’t feel sick, cognitively fuzzy, or like you need to take a nap after eating. Rather, these symptoms signify that something is not quite right inside your body and warrants attention. 

Causes of Postprandial Somnolence

There are seven potential causes of postprandial fatigue. While each cause is distinct, postprandial fatigue can be triggered by any combination of these factors. The seven causes of postprandial fatigue include:

  1. Changes in blood flow to the brain and activation of parasympathetic nervous system activity 
  2. Reactive hypoglycemia
  3. Insulin resistance
  4. Meal-induced oxidative stress
  5. High fat intake
  6. Metabolic endotoxemia
  7. Chronic inflammation 

Changes in Blood Flow to the Brain and Parasympathetic Nervous System Activity 

After a meal, copious quantities of blood are routed to the gastrointestinal tract to facilitate digestion and the shuttling of absorbed nutrients to target cells and tissues. This process reroutes blood away from the brain. Some scientists argue that the rerouting of blood away from the brain to the digestive organs precipitates hypoarousal and sleepiness. Eating smaller meals may place less demand for blood flow to the digestive organs, resulting in a concordant decrease in the amount of blood shunted away from the brain. One study supporting this finding found that the consumption of larger meals led to more significant sleepiness during a long, monotonous driving task. (1)

The act of digestion also shifts the body out of the “fight, flight, or freeze” sympathetic nervous system state and into the “rest and digest” parasympathetic nervous system state. (2) This shift may, in part, be responsible for the meal-induced sleepiness. We don’t want to prevent our bodies from shifting into the parasympathetic state while eating since this nervous system state facilitates gastric acid and digestive enzyme production for adequate food digestion. However, eating small meals may mitigate the magnitude of parasympathetic activation. 

Reactive Hypoglycemia

Reactive hypoglycemia is low blood sugar that occurs after a meal, usually within four hours of eating. (3) It occurs when glucose drops to 70 mg/dL or lower in the postprandial period, accompanied by symptoms that resolve upon normalization of glucose levels. The causes of reactive hypoglycemia are not well understood; however, two confirmed reasons include bariatric surgery, which reduces the stomach’s size and causes food to rapidly enter the small intestine, precipitating a sudden rise and fall in blood glucose, and insulin overdose by people with type 2 diabetes. (4) Subclinical hypothyroidism may play a role in the condition, as well. (5) 

Reactive hypoglycemia symptoms include shaking, rapid heart rate, weakness, and hunger, thus overlapping with several classic signs of postprandial fatigue. 

Both Increased and Decreased Insulin Sensitivity May Trigger Reactive Hypoglycemia 

What causes reactive hypoglycemia? Consuming meals high in refined carbohydrate can trigger reactive hypoglycemia; the high glucose load of the meal triggers a release of insulin that “overshoots” the amount of insulin required to shuttle glucose into cells; this exaggerated insulin response causes a sudden uptake of blood sugar into cells and thus a sudden drop in circulating glucose, causing symptoms. Reactive hypoglycemia may also be triggered by increased activity of incretins, which are metabolic hormones that stimulate a decrease in blood glucose after eating, augmenting insulin’s effects. On the flip side, insulin resistance (more on this shortly) may also trigger reactive hypoglycemia by delaying insulin secretion after a meal; when insulin is finally released, it is released en masse and overshoots the amount of glucose remaining in the blood. (6) Blood glucose thus drops rapidly, leading to symptoms of reactive hypoglycemia. In both cases, the goal of treatment is to implement diet and lifestyle changes that reduce insulin levels. 

How can you determine if postprandial hypoglycemia is contributing to your postprandial symptoms? One strategy that is not diagnostic but can still reveal helpful information is to measure your blood glucose at home using a handheld glucometer. Once you get the glucometer, test your glucose for three days, at the following time points:

  1. First thing in the morning, after at least 12 hours of fasting, and before breakfast.
  2. Just before lunch, without consuming any food between breakfast and lunch. 
  3. Forty-five minutes after you finish lunch.
  4. One hour and 45 minutes after you finish lunch.
  5. Two hours and 45 minutes after you finish lunch.
  6. You can check again at approximately the four- and five-hour marks or wait and see if you experience symptoms of reactive hypoglycemia. If and when you feel symptoms, measure your glucose immediately to see if it is low. 

Record what you ate at the meal and your blood glucose at each of the time points listed above. Keep in mind that a glucometer is not a means of diagnosing reactive hypoglycemia, but it can help you get a sense of your glycemic control. 

In a clinical setting, a doctor can diagnose reactive hypoglycemia using a test called a mixed-meal tolerance test. The test involves drinking a beverage that contains protein, carbs, and fats. Blood glucose is subsequently checked multiple times over the next five hours to watch for a significant drop in glucose levels. 

Conventional wisdom recommends treating reactive hypoglycemia with the consumption of “fast-acting carbs,” such as corn syrup, fruit juice, nonfat milk, and candy. While this is a decent short-term solution (especially for those with insulin-dependent diabetes), it does nothing to address the underlying cause of the reactive hypoglycemia and may continue to send the body on a blood sugar roller coaster, perpetuating the problem. It makes a lot more sense to work on stabilizing blood glucose and improving insulin resistance through dietary strategies, such as: 

  • Reducing insulin levels
    • You can reduce insulin levels through the following strategies:
      • Reduce your intake of acellular carbohydrates or foods that contain carbohydrates released from plant cell walls (think: flour-based foods): Acellular carbs trigger a rapid rise and fall in blood glucose. Instead, choose fiber-rich carbohydrate options, such as starchy tubers and whole fruit. The fibrous matrix of these foods slows the absorption of carbohydrates, allowing your pancreas to fine-tune its release of insulin. 
      • Always consume protein with carbohydrates: Protein attenuates postprandial blood glucose fluctuations. 
      • Eat smaller, more frequent meals: This strategy is appropriate for reactive hypoglycemia in the absence of insulin resistance. Less food coming in at a given time reduces the amount of insulin needed to address the glucose load. 
  • Addressing insulin resistance: If insulin resistance contributes to your reactive hypoglycemia, you must address it (more on this below).  

Insulin Resistance 

While reactive hypoglycemia can contribute to postprandial fatigue, insulin resistance is another equally plausible cause. Insulin resistance is a condition in which cells in the skeletal muscle, fat, and liver fail to respond appropriately to the hormone insulin and cannot effectively take up circulating glucose from the blood. One mechanism through which insulin resistance may cause postprandial fatigue is by triggering a delayed postprandial release of insulin that overshoots the amount of insulin needed to take up circulating glucose. This overshoot subsequently causes a drop in circulating glucose along with symptoms such as fatigue, dizziness, and brain fog. (7)

Emerging research indicates that insulin resistance is a continuum that starts with hyperinsulinemia (high levels of insulin) and progresses to impaired glucose disposal at the cellular level. Left unaddressed, this continuum may lead to the excessive accumulation of fat in the liver and even type 2 diabetes. Potential causes of insulin resistance include: 

  • Prolonged consumption of a diet high in refined carbohydrates—aka the Standard American Diet (8)
  • Excess body fat, including those with the “skinny-fat” phenotype (9)
  • Chronic inflammation (10)
  • Lack of physical activity (11)
  • Sleep deprivation (12)
  • Nutrient deficiencies, including low levels of vitamin D, magnesium, and chromium (13, 14, 15) 
  • A lack of non-exercise physical activity (NEPA) 
  • Exposure to environmental toxins

In many cases, a combination of these factors contributes to insulin resistance, so you must address multiple diet and lifestyle factors if you want to improve insulin resistance.

Since insulin resistance occurs across a spectrum, fasting glucose, insulin, and hemoglobin A1c have limited utility in identifying the early stages of insulin resistance. An oral glucose tolerance test is a clinically available, preferred method for assessing insulin resistance and can identify insulin resistance in its early stages before fasting blood glucose levels are impaired. (16)  

Meal-Induced Oxidative Stress  

Certain types of meals induce oxidative stress, which is an imbalance between free radicals and antioxidant levels in the body. Research indicates that certain meals, namely meals that are simultaneously high in carbohydrates and fat, induce oxidative stress. Oxidative stress, in turn, may contribute to postprandial fatigue and other postprandial symptoms by generating an inflammatory response. 

The two meal components most likely to trigger oxidative stress include acellular carbohydrates and industrial seed oils. I touched on the concept of acellular carbohydrates earlier in this article, so please refer back to the section on reactive hypoglycemia for details. Industrial seed oils trigger oxidative stress because they contain rancid lipid byproducts with a penchant for “stealing” electrons from your proteins and DNA. (17)

A single high-fat, high-carbohydrate meal induces postprandial inflammation even in healthy people. (18) This inflammatory response is even more pronounced in unhealthy individuals with underlying metabolic dysfunction. 

The solution to avoiding meal-induced oxidative stress is to minimize your intake of processed foods and focus on eating a minimally processed, whole-foods diet rich in antioxidant nutrients, including vitamin C, vitamin E, and phytonutrients. 

High Dietary Fat Intake 

High-fat ketogenic diets are currently all the rage and work well for many people. However, some people report feeling sleepy, foggy, and generally unwell after eating a high-fat meal. There are a few potential reasons for this. 

For one, consuming a high-fat meal may promote sleepiness through the release of cholecystokinin (CCK), a hormone secreted by cells of the duodenum (the first portion of the small intestine) that stimulates the release of bile and digestive enzymes in the intestine. (19) The magnitude of CCK release may vary from one person to the next, impacting how sleepy (or not) an individual feels after eating a high-fat meal. 

However, a high dietary fat intake may also contribute to postprandial fatigue if most of your dietary fats come from saturated fat and the gut is in a state of disrepair. (20) Combining these two factors increases the translocation of lipopolysaccharide (LPS) (more on this below under “Metabolic Endotoxemia”) from the gut into the systemic circulation, precipitating a chronic inflammatory response that causes fatigue. In this case, addressing gut imbalances and shifting your fat intake away from saturated fats and more toward monounsaturated fats and omega-3 from fatty cold-water fish may attenuate postprandial fatigue. 

Metabolic Endotoxemia

Metabolic endotoxemia may sound like a scary emergency room scenario, but it is actually quite common. It’s also an important factor in the development of many chronic health conditions, including obesity, diabetes, and non-alcoholic fatty liver disease. (21) Metabolic endotoxemia occurs when LPS, a pro-inflammatory compound found in the outer cell wall of Gram-negative bacteria, leaks from the inside of your intestine (referred to as the “lumen”) into your systemic blood circulation. A permeable intestine, or “leaky gut,” permits the leakage of LPS from the gut into the blood circulation. 

Once in the bloodstream, LPS triggers the release of cytokines by the immune system, contributing to chronic, low-grade inflammation. This inflammatory response may contribute to fatigue, brain fog, and generalized cognitive impairment after a meal. (22)

In some individuals, postprandial fatigue is accompanied by lethargy and a complete lack of motivation to do just about anything. This decline in motivation that some people experience after eating may be attributable to increased circulating levels of LPS. In preclinical research, LPS has been found to reduce animals’ willingness to exert effort for a particular reward, including candy; the decline in motivation experienced by LPS-exposed animals suggests that LPS reduces motivation by impacting the neurobehavioral system. (23)

Diet and Dysbiosis Influence Metabolic Endotoxemia 

Diet has a significant influence on intestinal barrier integrity and plays a critical role in the pathogenesis of metabolic endotoxemia. Consuming an anti-inflammatory, nutrient-dense, whole-foods diet is a crucial first step toward improving the health of the gut barrier and microbiota. 

Gut dysbiosis increases the absorption and systemic circulation of LPS, so it is also essential to address gut imbalances alongside dietary treatment. (24) 

Chronic Inflammation

Inflammation is a common thread linking many of the chronic diseases we face in our society today, ranging from type 2 diabetes to cardiovascular disease. Chronic inflammation compromises gut barrier integrity, allowing substances to “leak” from the intestinal lumen into the systemic circulation. It may also contribute to fatigue by reducing cellular energy availability or the adenosine triphosphate (ATP) available to fuel cellular processes. (25) Gut imbalances and chronic infections, such as Lyme disease, can also contribute to chronic inflammation, resulting in uncomfortable (and sometimes debilitating) postprandial symptoms. 

Interleukin-1, a pro-inflammatory cytokine, contributes to postprandial fatigue in both lean and obese individuals. (26) This pro-inflammatory cytokine is often upregulated in chronic infections, suggesting a link between chronic infectious processes and postprandial fatigue. 

Mitochondrial Dysfunction

While there is currently no research on postprandial fatigue and mitochondrial dysfunction (that I am aware of), a robust body of research indicates that mitochondrial dysfunction plays an essential role in chronic fatigue syndrome, a disorder characterized by extreme fatigue that is disproportional to exertion and doesn’t improve with rest. In theory, mitochondrial dysfunction could also play a role in postprandial fatigue by disrupting the mitochondria’s ability to transform food-based energy into cellular energy, or ATP. Several diet and lifestyle strategies can improve mitochondrial function, including intermittent fasting, eating a nutrient-dense diet rich in B vitamins and other nutritional cofactors essential for mitochondrial energy production, and engaging in aerobic exercise and resistance training. (27, 28, 29)  

How to Resolve Postprandial Fatigue 

To resolve postprandial fatigue and other uncomfortable, abnormal postprandial symptoms, you’ll need to identify and address the root causes of the issue. The following steps will help you address underlying causes ranging from gut dysfunction to chronic inflammation, allowing you to eat and feel well. 

1. Address Gut Imbalances 

Gut imbalances, including small intestinal bacterial overgrowth (SIBO), leaky gut, and gut infections, influence multiple aspects of postprandial fatigue, including blood sugar dysregulation, metabolic endotoxemia, and chronic inflammation. Addressing gut imbalances is thus crucial for resolving postprandial fatigue and other uncomfortable postprandial symptoms. 

When it comes to addressing gut imbalances, it is best to test rather than guess. Functional labs such as the trio-smart breath test and Genova GI Effects stool test can identify SIBO and imbalances in the gut microbiota, digestion, and intestinal barrier function. Treatment of gut imbalances may involve pharmaceuticals, such as antibiotics or antimicrobial herbs, and support for the gut barrier and digestion. 

2. Optimize Your Diet 

Find the types of fats that work for you. If you’ve been routinely eating a diet high in saturated fat, such as fatty cuts of red meat, butter, and full-fat dairy products, try shifting toward eating more monounsaturated fat-rich foods, such as extra-virgin olive oil, avocado oil and avocados, and macadamia nuts. 

Adjust your carb and protein intake to levels that keep your blood sugar stable. Reducing your intake of acellular carbs and focusing primarily on eating cellular carbs (starchy tubers, whole fruits, and whole grains and legumes, if tolerated) is a crucial first step. Tracking your food intake in Cronometer for a few days can help you identify patterns in your food intake and postprandial symptoms. Continuous glucose monitoring can also help ascertain your postprandial glycemic response to foods, providing you with real-time feedback that you can use to modify your diet and improve your symptoms.  

Eat the rainbow. Dietary phytochemicals impart foods with vibrant colors and can attenuate metabolic endotoxemia, oxidative stress, and chronic inflammation while also acting as fuel for beneficial gut bacteria. Certain foods and nutrients can help with metabolic endotoxemia, including sulforaphane (found in cruciferous vegetables), anthocyanins (found in blue, purple, red, and black foods), and epicatechin (found in dark chocolate and tea). (30, 31, 32) 

Avoid industrial seed oils, including canola, corn, cottonseed, soybean, and safflower oils, as these are a significant source of pro-inflammatory oxidized lipid byproducts. Instead, cook with butter, ghee, and other animal fats such as tallow and lard (unless you are sensitive to saturated fat), or try olive oil and avocado oil instead. Also, be sure to include plenty of fatty cold-water fish in your diet for the anti-inflammatory omega-3 fatty acids EPA and DHA. 

Spice up your food with spices and culinary herbs. When inflammation contributes to postprandial fatigue, the addition of anti-inflammatory spices and herbs to your diet may be helpful. One study found that a spice blend containing basil, bay leaf, black pepper, cinnamon, coriander, cumin, ginger, oregano, parsley, red pepper, rosemary, thyme, and turmeric reduced postprandial inflammation in overweight and obese men. (33)  

Ensure optimal intake of vitamin A, zinc, probiotic foods, and bone broth to support healthy gut function. A healthy gut barrier, in turn, reduces LPS translocation from the gut into the systemic circulation, inhibiting metabolic endotoxemia. 

3. Try Intermittent Fasting

Intermittent fasting is an umbrella term used to describe various meal patterns in which you alternate between periods of voluntary fasting and eating over 24 hours. Intermittent fasting mimics evolutionary eating patterns, as our hunter–gatherer ancestors routinely experienced periods of fasting when food was scarce.

Research indicates that intermittent fasting offers numerous health benefits, several of which have implications for those with postprandial symptoms. For one, intermittent fasting promotes metabolic flexibility or the ability of your “metabolic machinery” to alternate between using glucose and fatty acids (and ketones) for fuel. (34) Greater metabolic flexibility coincides with improved blood glucose control and insulin sensitivity, addressing two critical facets of postprandial fatigue.  

Intermittent fasting reduces inflammation, improves gut health, and supports healthy mitochondrial function, thereby addressing three more underlying causes of postprandial fatigue. (35, 36, 37) 

4. Optimize Your Sleep

The human body naturally experiences a circadian dip in energy in the afternoon. Unfortunately, most of us have schedules that don’t allow us to indulge in a daily afternoon nap to satisfy this natural urge for sleep. However, optimizing your sleep quality the night before may make you feel less of a need for an afternoon nap by dampening this circadian energy dip. (38) In other words, get seven to nine hours of uninterrupted sleep every night in a cool, dark room, and you may feel less postprandial fatigue the following day. 

5. Address Your Stress

Living in chronic stress promotes leaky gut and gut dysbiosis and may thus perpetuate postprandial fatigue problems. (39) Meditation and other mindfulness exercises may improve gut health by facilitating a healthy intestinal microbial balance and inhibiting intestinal inflammation. (40) 

6. Get Moving

Engaging in gentle physical activity after meals is good not only for preventing postprandial fatigue but also for controlling your blood sugar. Taking a post-meal walk, for example, increases blood circulation and stimulates your skeletal muscles to take up circulating glucose, dampening the postprandial blood glucose fluctuation and invigorating your body. (41) 

Engaging in high-intensity exercise in the postprandial period alleviates inflammation induced by a high-fat, high-carbohydrate meal. (42) However, it’s best to wait until your meal has digested a bit before diving into a high-intensity interval training workout.

Exercise also supports mitochondrial function, helping your mitochondria become more efficient at their job of converting food energy into cellular energy, ATP. Aim for a balance of aerobic activity, resistance training, mobility exercises, and NEPA—such as working at a standing desk and taking “movement breaks” throughout the workday—to keep your mitochondria happy. (43) 

To summarize, a little bit of sleepiness after meals is normal. But excessive fatigue, including when it’s accompanied by other symptoms such as dizziness, nausea, and brain fog, is not normal. If you’re feeling uncomfortable symptoms after eating, there’s a good chance that some things are occurring “beneath the hood” of your body that need your attention. There are many strategies you can try on your own to address postprandial symptoms, like those provided in this article, but partnering with a Functional Medicine provider or health coach may also help.

A Functional Medicine practitioner can do the testing required to figure out what’s going on in your body, and a health coach can help you come up with a plan to address your stress levels, exercise goals, diet changes, and more. Health coaches help you follow through with and stick to your goals, while a Functional Medicine practitioner can determine what needs to be worked on in the first place after the required testing. Together—with a Functional Medicine practitioner and a health coach on your team—you’ve got a match made in Functional Medicine heaven.