**7. Prostaglandins and sleep**

Prostaglandins (PGs) are synthesized from arachidonic acid by activated cyclo-oxygenase (COX) in response to various stimuli in various types of cells. When synthesized, PGs are immediately released and exert their actions on cells in the vicinity of their synthesis [44]. PGs act in many parts of the body, including the reproductive system, the nervous system, the cardiovascular system, the immune system and gastrointestinal system [45]. Due to their diverse biological activity, there is potential for prostaglandin analogs (prostanoids) to function as effective therapeutic agents.

Sleep, a complex phenomenon, is not merely the result of physical fatigue or decrease in activity; instead it is a complicated behavioural state requiring the integration of several neuronal processes. Prostaglandins (PGs) are ubiquitously distributed in mammalian tissues, exerting a variety of physiological and pathological effects such as disaggregation of blood platelets [46], relaxation of smooth muscle [47] and pain and inflammation [48]. It is generally accepted that PGD2 is one of the major PGs unique to the CNS, when compared to the relatively low concentrations present in peripheral tissue [49]. Studies have revealed a variety of endogenous substances that convincingly induce sleep. Among the multitude of sleeppromoting substances, PGD2 has been described as a somnolence promoting substance in the adult rat by acting on the traditional sleep centres of the VLPO area. PGD2 is produced from PGH2 precursor by enzyme PGDS that is predominately synthesised in the leptomeningeal layers and CP of the brain.

vulnerability of these tissues may contribute to some of the functional effects of sleep depri‐ vation. The relationship between Glutathione (GSH) and sleep has been shown that it defends the cells from destructive agents such as free radicals, chemical toxins, and heavy metals that constantly assault the cells and inhibit their optimum function, causing disease and acceler‐ ating the aging process. Studies have shown that sleep deprived animals have lower gluta‐ thione levels in certain parts of the brain. The two brain areas involved in sleep are the thalamus and hypothalamus. These areas are particularly vulnerable to glutathione depletion and can lead to sleeping problems [60]. It has been reported that GSH is the only antioxidant that does not become a free radical itself after donating a free electron [62]. Further research suggested that high blood GSH concentrations correlates with long lifespan both in animals and humans [63]. Mancuso et al [64] observed that GSH levels were lower in patients with OSAS than in controls and suggests that antioxidant defences are impaired in patients with Obstructive sleep apnea syndrome (OSAS). Recently, Ntalapascha et al (2012) reported that overnight changes (%) in plasma biomarkers were significantly different between OSAS and controls for GSH/

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

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

197

In a recent large survey on more than 4500 people the association of many different nutrients to sleep were studied. [66] The nutrients associated with difficulty falling asleep in order of importance were lack of alpha carotene, lack of selenium, lack of dodecanoic acid, lack of calcium and increased hexadecanoic acid. [66]Difficulty maintaining sleep was associated with increased use of salt, less butanoic acid, less carbohydrates, less dodecanoic acid, less vitamin D, less lycopene, more hexanoic acid and more moisture. Non-restorative sleep was associated with more butaneoic acid less calcium, less vitamin C, less plain water, more moisture and more cholesterol. In the same survey increased daytime sleepiness was associated more moisture, more theobromine (see above for caffeine), less potassium and less plain water. [66]

Management of sleep disturbances combines nonpharmacologic and pharmacologic ap‐ proaches individualized for the patient. According to the International Classification of Sleep Disorders (ICSD-2, 2005) [67] there are around 90 distinct sleep disorders. The cumulative effects of sleep loss and sleep disorders have been associated with a wide range of deleterious health consequences including an increased risk of hypertension, diabetes, obesity, depression, heart attack, stroke and nutritional status of an individual could play a major role on sleep quality. Observational studies have shown a link between sleep [68] and vitamins and minerals, whether taken in combination or individually, are the most frequently consumed dietary supplements among people today. Unlike other dietary supplement ingredients, vitamins and certain minerals are considered essential nutrients for which standards of

GSSG, controls had increased GSH levels overnight whereas OSAS did not.

**9. Dietary nutrients and sleep**

**10. Vitamins and minerals and sleep**

adequacy are needed.

Prostaglandin D2 (PGD2) is a biologically active primary prostaglandin and a common product of arachidonic metabolism in mammals. As a major eicosanoid product of mast cells PGD2 is released in large quantities during allergic and asthmatic anaphylaxis. Several studies have reported a crucial role for the prostaglandin D system in sleep regulation. This PGD2 accumulates in the cerebrospinal fluid (CSF), where it induces physiologic sleep in rats and humans. PGD2 and PGE2 are found in high concentrations in the hypothalamus compared to other regional areas of the brain [50, 51]. In addition, marked elevations of endogenous PGD2 concentrations in CSF occur in patients who suffer African sleeping sickness [52]. Continuous infusion of PGD, into the lateral cerebral ventricle of monkeys during the diurnal period induced a sleep pattern similar to physiological night sleep [53]. It is involved in the regulation of reducing body temperature in sleep [54]. It is also produced in the brain via an alternative pathway involving a soluble, secreted PGD-synthase also known as β-trace [55]. PGD2 acts in the central nervous system in sleep induction and lowering of body temperature [51].Further pharmacological actions include inhibition of platelet aggregation and relaxation of vascular smooth muscle [56].
