Science Focus (issue 022)

Figure 1 The interactions between the four brain centers before and after ameal. 圖一 與餐後嗜睡相關的四個大腦中樞在進食前後的相互作用 7 Post-Meal Hormonal Change and Food Coma So, what could be the possible reasons behind food coma? With the postprandial increase in insulin level as an example, feeding can promote or inhibit the secret ion of a lot of hormones to maintain homeostasis. Such hormonal changes can al so reduce the desire for food intake by introducing a feeling of satiety. It has been suggested that the hormones involved may simultaneously affect the sleeping centers in the brain and contr ibute to food coma (footnote 1) [1, 2]. We will examine two (of the many) examples – melatonin and orexin. In addition to its role in regulating gastrointestinal motility [3], melatonin is commonly known as a hormone that regulates sleep-wake cycle – high levels of melatonin induce sleep. This has been shown by administrating melatonin to animals and humans in previous studies [2]. In fact, the gut increases the synthesis of melatonin considerably after meal consumption, so such increase is considered to be a contributing factor to food coma [2]. For orexin, it is known to be a hormone which promotes hunger, along with wakefulness, presumably through increasing the fi r ing rate of neurons in an arousal center in the hypothalamus [2], which was hypothesized to work by inhibiting the sleep centers [1]. Therefore, the reduction of orexin after a meal may contribute to the sleep-inducing effect by leaving off the inhibition of the sleep centers [2]. Consider the Bigger Picture: Interactions Between Brain Centers While some scientists incline to attribute the cause of food coma to the action of certain hormones, some take a further step back [1]. On top of the idea that the hunger-satiety axis modulates the sleep-wake axis, this view emphasizes the interaction between brain centers in the hypothalamus, and hormones are considered as just messengers that faci l itate communication between organs. As illustrated by the example of orexin above, there are four major centers in the hypothalamus that affect satiety and drowsiness. They can be simplified as the hunger, satiety, arousal and sleep centers. Hunger often comes with wakefulness; the hunger center is hypothesized to stimulate the arousal center and inhibit the sleep center. The arousal center itself works by inhibiting the sleep center, too. However, in the state of satiety, the satiety center inhibits the hunger center so everything in the pathway becomes the opposite and drowsiness occurs. The interactions are summarized in Figure 1. So, it is useful to understand what would lead to the feel ing of satiety, which intertwines with the occurrence of post-meal sleepiness. In fact, our body judges whether we should feel full by our energy level and by the physical conditions of the stomach [1]. To know whether we are replenished with energy after a meal, arcuate nucleus (ARC; footnote 2) in the hypothalamus detects the increase in the level of a blood-borne metabol ite, malonyl-CoA, whose level correlates with that of ATP (“energy”). Having combined other metabolic signals, ARC can stimulate the sat iety center and inhibit the hunger center through hormonal regulation. This contributes to the feelings of satiety and drowsiness. Meanwhile, our stomach should be stuffed with food for quite a whi le after eat ing. Vagus ner ve branches can sense the gast r ic di stens ion and delayed gastric emptying, which in turn lead to the release of some other gut hormones that stimulate the satiety center by their own actions and through vagal stimulation. This eventually yields the same feelings of being full and sleepy. Furthermore, this can account for the reason why solid food could induce greater drowsiness than liquid food, which is because solid food can cause greater gastric distension and further delay gastric emptying. Food Coma in the Light of Evolution So now, you may all be wondering – is it necessary for the satiety response to link to drowsiness? All it does it gets us into trouble for dozing off during class, right? True, but evolutionary biology suggests that there might be a reason behind post-meal sleepiness. To understand, we need to view this phenomenon in the Darwinian context – any subopt imal ef for t allocation can result in a selection disadvantage [4]. For a species to survive in natural selection, they must spend their limited energy and effort wisely. Speaking of these, some researchers speculated that digestion is a demanding metabolic process that requires focused effort and energy expenditure [2]. In response to that, our body may choose to temporarily lower its sensitivity to external stimuli to let our body