Debunking a myth: neurohormonal and vagal modulation of sleep centers, not redistribution of blood flow, may account for postprandial somnolence.

It is widely believed that postprandial somnolence is caused by redistribution of blood flow from cerebral to mesenteric vessels after a meal. This belief persists despite its apparent contradiction with a well-known neurophysiologic principle that cerebral perfusion is preferentially maintained under a wide range of physiologic states. For instance, during exercise when a large amount of perfusion is diverted to muscles, blood flow to the brain is maintained. Furthermore, recent evidence suggests that there is no measurable change of blood flow in the common carotid artery during postprandial states. We propose an alternative hypothesis that postprandial release of gut-brain hormones and activation of vagal afferents may play a role in postprandial somnolence through modulation of sleep centers such as the hypothalamus. Feeding alters the milieu of hormones such as melatonin and orexins and also promotes central vagal activation. Emerging evidence suggest that these pathways are also modulators of neural sleep centers. Potential adaptive explanations of postprandial somnolence are explored from a Darwinian perspective.