Food comas result from hormonal and neurochemical changes, not from blood redirected to your stomach.

The medical term for a food coma is postprandial somnolence. For decades, the "blood-shift hypothesis" suggested that blood was diverted from the brain to the digestive tract. However, modern Doppler ultrasound studies have definitively shown that cerebral blood flow is tightly regulated and does not decrease after eating. Instead, the phenomenon is driven by the parasympathetic nervous system and chemical signaling.When you eat a meal—particularly one high in carbohydrates—your pancreas releases insulin to regulate glucose levels. This insulin surge allows the amino acid tryptophan to cross the blood-brain barrier more readily, where it is converted into serotonin and then melatonin. These neurochemicals are primary drivers of relaxation and sleepiness. Additionally, research from the University of Manchester discovered that glucose can suppress the brain cells responsible for maintaining wakefulness and alertness.These cells, called orexin neurons, are located in the hypothalamus and respond sensitively to glucose levels. When glucose rises after eating, it inhibits these neurons, reducing wakefulness. The effect is often most pronounced between 1:00 PM and 3:00 PM because it coincides with the body's natural circadian dip in alertness. This combination of hormonal shifts and cellular inhibition creates the characteristic heavy-lidded feeling that follows a substantial meal.