**1. Introduction**

Many people suffer from excessive sleepiness during the afternoon hours. In all human individuals the alertness level decreases after the noon peak. This afternoon dip or "postpran‐ dial dip" is physiological. The alertness level rises again later in the afternoon and early evening, reaching another peak at about 7 to 8 p.m. Obesity is a recognized public health problem. It is a strong risk factor for type 2 diabetes and cardiovascular disease. Obesity is also the strongest risk factor of obstructive sleep apnea. Nutritional factors are important also in many other sleep disorders. Many patients with restless legs syndrome have low blood ferritin levels. [1] Sleepy patients with hypersomnias should avoid rapidly absorbing carbohydrates at daytime to minimize afternoon sleepiness. Adenosine is accumulating in the brain, notably in the basal forebrain, during wake, increasing the sleep pressure. [2] Caffeine, the most commonly used stimulant, is an adenosine receptor antagonist. During deep slow wave sleep glucose is stored in the glial cells. [3, 4] The brain-gut relationship is important also in the sleepwake regulation, although well-done studies on that topic are still scarce.

Sleep disorders are a large and under-recognised problem in many parts of the world. The international classification of sleep disorders (ICSD), the most frequent and often the most severe are obstructive sleep apnoea (OSA), narcolepsy, restless legs syndrome (RLS), periodic limb movement disorder, insomnia, parasomnias, circadian rhythm disorders including jet lag and shift work, and sudden infant death syndrome. However, the major research focuses on OSA, insomnia and RLS since they are among the most highly prevalent sleep disorders and there are established links between them and other health conditions, which is the area where the majority of costs are incurred. The health system costs of sleep disorders comprise the cost of the sleep disorders themselves and the share of health costs from other conditions attributed

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to sleep disorders. The total European cost of brain disorders in 2010 was €798 billion [5], headaches and sleep disorders, meanwhile, only cost 285 and 348 euros respectively [6]. "The human brain is not only the site of our personality, thoughts, feelings and other human characteristics; it is also the seat of many chronic disabling diseases. These diseases have not received the attention that has been devoted to heart disease, cancer or AIDS, but in recent years there has been a growing awareness of their importance" [5]. A growing body of evidence indicates that free radical formation is a mediator of the excessive lipid peroxidation and cell damage seen in neurological disorders [7]. Antioxidant vitamins and trace elements have been shown to have biological activity in acting as scavengers for free radical's delays the onset of defined milestones in the development of a disease. Therefore, micronutrients such as vitamins, minerals or trace elements are supported by evidence that it can delay deterioration of the disease.

should not forget the emotional aspects of eating (smell, taste, and situational factors during

Nutrition, Sleep and Sleep Disorders – Relations of Some Food Constituents and Sleep

http://dx.doi.org/10.5772/58345

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Cholecystokinin is secreted by duodenal and jejunal cells after eating food. CCK acts on vagal neurons projecting to the brainstem, giving a signal of satiety inhibiting further need for eating. Ghrelin is secreted when a person is hungry and it increases appetite. It acts on the hypothal‐

Leptin is manufactured mainly in fat cells in adipose tissue. Leptin counteracts the effects of neuropeptide Y and inhibits secretion of alpha-MSH (alpha melanocyte-stimulating hormone).

Alpha-MSH is in the arcuate nucleus in the brain where it acts to suppress appetite. Alpha-

Serotonin is an important neurotransmitter in the central nervous system (CNS) with impor‐ tant effects on sleep-wake regulation. Serotonin also has an important role in regulation of the gastrointestinal (GI) function through an interaction with the ENS. Up to 60-90 % of the total body amount of serotonin is in the GI tract, and 2-20% of all enteric neurons express serotonin. Stimulatory receptors include β-adrenoceptors, muscarinic and nicotinic Ach receptors and 5- HT3 receptors. Inhibitory receptors include alpha2-adrenceptors, histamine H3, GABA-B, adenosine A2, and 5-HT4 receptors. In the GI tract 5-HT is eliminated mainly by monoamine

Hypocretin (orexin) was originally considered to be important especially in central control of food intake [9, 10] but it is essential also in control of sleep and wakefulness. There are about 70 000 hypocretin neurons in the lateral hypothalamus. Narcolepsy, a central hypersomnia with excessive daytime sleepiness and cataplexy, is characterized by destruction of the hypocretin neurons. [11, 12] Hypocretin is involved also in energy homeostasis, nociception, reward seeking behavior, and drug addiction. [13-19] In addition to brain, hypocretins are also widely present in the gastrointestinal tract12 where they have a role in regulation of peristaltic GI motility, and in gastric, intestinal and pancreatic secretions. The hypothalamic hypocretin cells are intermingled with MCH neurons. Both hypocretin-and MCH-cells are glucosesensing neurons. Decrease of glucose increases activity of hypocretin neurons and decreases activity of the MCH cells, producing wakefulness. Respectively, increase of glucose decreases activity of hypocretin and increases activity of MCH, producing sleepiness. These interactions explain at least partly the alerting effects of fasting and the observations that eating rapidly absorbing carbohydrates, provoking fast increase of blood glucose, increase sleepiness.

Coffee is the world's most common psychoactive drug. Coffee includes caffeine, which is also present in coffee, tea, cola and chocolate. The stimulant and wake-producing properties of caffeine depend on its ability to reduce adenosine transmission in the brain. Caffeine acts as

an antagonist to adenosine A1 and especially to adenosine A2 receptors. [20, 13]

amus stimulating feeding, counteracting the inhibitory effects of leptin.

Leptin decreases appetite and inhibits food intake contrary to ghrelin.

MSH may have also some function in the sleep-wake regulation.

eating).

oxidase metabolism. [8]

**4. Caffeine and sleep**

Different nutritional factors, and eating, can have an effect on the CNS by different mechanisms: direct nervous connections through the vagus nerve and nucleus tractus solitarius, humoral effects, affecting absorption of different molecules, emotional and cognitive processes.
