Metabolic state, neurohormones, and vagal stimulation, not increased serotonin, orchestrate postprandial drowsiness

Several theories have arisen to explain postprandial sleepiness. Of these, the most prevalent theory assumes that blood flow is redistributed after a meal. This premise fails, however, because cardiac regulation strictly controls cerebral blood flow (CBF) and brain oxygenation. Another theory proposes that an elevated ratio of free l-tryptophan to large neutral amino acids (LNAA) in the blood increases cerebral serotonin (5HT) levels, which in turn induces drowsiness. But this theory does not explain why fatty meals, which reduce extracellular 5HT, induce more intense sleepiness than meals of carbohydrates, or why protein-rich meals, which actually lower cerebral 5HT, do not differ significantly from carbohydrate meals in promoting sleep. Some studies fail to confirm the presumptive role of 5HT in mood or drowsiness. Reviewing the history of theory and experimentation in this field, we conclude that 5HT is not the principal determinant in postprandial sleepiness. We propose instead that the arcuate nucleus (ARC) modulates satiety in response to metabolic indicators of energy state, postprandial neuropeptide secretion from the gut, and vagus nerve stimulation. The ARC integrates these satiety signals and forwards them to the ventromedial hypothalamus (VMH), which indirectly stimulates the sleep centers (i.e., the ventrolateral preoptic nucleus (VLPO) and median preoptic nucleus (MnPO)) by inhibiting the lateral hypothalamic area (LHA), which coordinates arousal centers. Neuropeptides or satiety signals may activate sleep centers directly to provoke postprandial somnolence. This model may resolve contradictions and inconsistencies in data that previous theories could not explain.