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This chapter provides an overview of idiopathic hypersomnia together with a discussion on the nosological limits of the condition. It presents the history, clinical features, diagnostic procedures, treatment and differential diagnosis of idiopathic hypersomnia. All efforts to clarify demographics, pathophysiology and treatment have been hampered by the nosological uncertainty on the borders of idiopathic hypersomnia. The latest International Classification of Sleep Disorders confirmed the distinction of two forms of idiopathic hypersomnia and used a new wording of idiopathic hypersomnia with long sleep time and idiopathic hypersomnia without long sleep time. The diagnosis of idiopathic hypersomnia with long sleep time is mainly based on clinical features and on the absence of associated symptoms such as snoring or cataplexy. However, polysomnography and the multiple sleep latency test (MSLT) are indispensable to rule out other conditions. Further research is necessary to specify the limits of idiopathic hypersomnia with and without long sleep time.
The present review investigates the role of sleep and its alteration in triggering metabolic disorders. The reduction of the amount of time sleeping has become an endemic condition in modern society and the current literature has found important associations between sleep loss and alterations in nutritional and metabolic aspects. Studies suggest that individuals who sleep less have a higher probability of becoming obese. It can be related to the increase of ghrelin and decrease of leptin levels, generating an increase of appetite and hunger. Sleep loss has been closely associated with problems in glucose metabolism and a higher risk for the development of insulin resistance and diabetes, and this disturbance may reflect decreased efficacy of the negative-feedback regulation of the hypothalamic–pituitary–adrenal axis. The period of sleep is also associated with an increase of blood lipid concentrations, which can be intensified under conditions of reduced sleep time, leading to disorders in fat metabolism. Based on a review of the literature, we conclude that sleep loss represents an important risk factor for weight gain, insulin resistance, type 2 diabetes and dyslipidaemia. Therefore, an adequate sleep pattern is fundamental for the nutritional balance of the body and should be encouraged by professionals in the area.
Although homeostatic mechanisms remain of utmost importance, rhythmic changes are present also. The main ones have a period of 24 h (circadian) or about 2–3 h (ultradian). Circadian rhythms are derived from a body clock, found in the base of the brain, and from the pattern of our sleep wake cycle, including activity and meal times. These rhythms promote the regular changes between an active wake period and a recuperative sleep period. Ultradian rhythms are also widespread and reflect external (lifestyle) and internal factors. The internal factors include biochemical need and some sort of oscillator; but details of how many oscillators, and exactly where they are, remain to be established. Food intake, appetite, digestion and metabolism have been shown to illustrate these principles. Moreover, these principles become important when special circumstances exist as far as meal times are concerned; the particular diffculties of night workers is a good example.
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