The goal of the current study was to estimate the prevalence of sleep bruxism (SB) in the general population using a representative sample of 1,042 individuals who answered questionnaires and underwent polysomnography (PSG) examinations. After PSG, the individuals were classified into 3 groups: absence of SB, low-frequency SB, and high-frequency SB. The results indicated that the prevalence of SB, indicated by questionnaires and confirmed by PSG, was 5.5%. With PSG used exclusively as the criterion for diagnosis, the prevalence was 7.4% regardless of SB self-reported complaints. With questionnaires alone, the prevalence was 12.5%. Of the 5.5% (n = 56) with confirmed SB, 26 were classified as low-frequency SB, and 30 as high-frequency. The episodes of SB were more frequent in stage 2 sleep, and the phasic bruxism events were more frequent than tonic or mixed events in all sleep stages in individuals with SB. A positive association was observed between SB and insomnia, higher degree of schooling, and a normal/overweight body mass index (BMI). These findings demonstrate the prevalence of SB in a population sampled by PSG, the gold standard methodology in the investigation of sleep disorders, combined with validated questionnaires.

Poor sleep quality due to sleep disorders and sleep loss is highly prevalent in the modern society. Underlying mechanisms show that stress is involved in the relationship between sleep and metabolism through hypothalamic–pituitary–adrenal (HPA) axis activation. Sleep deprivation and sleep disorders are associated with maladaptive changes in the HPA axis, leading to neuroendocrine dysregulation. Excess of glucocorticoids increase glucose and insulin and decrease adiponectin levels. Thus, this review provides overall view of the relationship between sleep, stress, and metabolism from basic physiology to pathological conditions, highlighting effective treatments for metabolic disturbances.

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SUMMAR Y Since previous data of our group showed increased concentrations in HPA axis hormones in sleep deprived rats, we hypothesized that this augmentation could produce effects in other hormonal systems, particularly in the sexual system. Considering that little is known about how the hormonal system changes during the recovery period after sleep deprivation (SD), our objective was to examine from what point SD alters sexual and stress-related hormones along with plasma catecholamine concentrations during 4 days. We also sought to verify the time course of their recovery after an equivalent period of recovery sleep. Rats were deprived of sleep by the platform technique for 1-4 days and were allowed to recover for the same period. Plasma catecholamines [dopamine (DA) and noradrenaline (NOR)], testosterone, estrone, progesterone, prolactin, corticosterone and adrenocorticotropic hormone (ACTH) concentrations were measured. Comparisons between groups showed that the SD procedure used in the present study produced marked alterations in almost all studied hormones from 24 h of SD, except for estrone and prolactin (which required 96 h of SD to become altered). Testosterone and estrone decreased, whereas progesterone, prolactin, corticosterone, ACTH, DA and NOR increased. During recovery period, progesterone, prolactin and corticosterone concentrations returned to control levels, whereas testosterone, estrone, NOR and DA did not. In addition, after 48 h of recovery ACTH and NOR decreased below control concentrations, remaining low until 96 h of sleep recovery. Thus, SD showed long lasting, differential effects upon these neurochemicals suggesting that each has its own pattern of responses to SD as well as variable periods of recovery.k e y w o r d s catecholamines, corticosterone, prolactin, rebound, sleep deprivation, testosterone INTRODUCTIONSleep loss is considered a health risk factor that contributes to several disease processes (Miller and Bartus, 1982), reduces longevity (Kripke, 1979) and leads to behavioral (Andersen et al., 2000(Andersen et al., , 2003Tufik et al., 1978), hormonal (Andersen et al., 2004a;Spiegel et al., 1999) and neurochemical (D'Almeida et al., 1998;Farooqui et al., 1996;Martins et al., 2004;Pedrazzoli et al., 2004) alterations.The endocrine system is responsible for physiological integration of multiple organs by different actions of the endocrine axis. However, hormonal effects are not only determined by circulating levels, but also by the time that the organ is exposed to a specific hormone. For example, an acute rise in cortisol concentration is associated with increased attention (Erickson et al., 2003) but raised concentrations, sustained chronically, reduce synaptic and neuronal populations in the hippocampus (Magarin˜os et al., 1998). Because sleep deprivation (SD) induces profound changes in the secretory patterns in distinct endocrine axes in humans, the investigation of hormone secretion could provide some insight Correspondence: Rua Napolea˜o de Barros,

The skin exposome is defined as the totality of environmental exposures over the life course that can induce or modify various skin conditions. Here, we review the impact on the skin of solar exposure, air pollution, hormones, nutrition and psychological factors. Photoageing, photocarcinogenesis and pigmentary changes are well‐established consequences of chronic exposure of the skin to solar radiation. Exposure to traffic‐related air pollution contributes to skin ageing. Particulate matter and nitrogen dioxide cause skin pigmentation/lentigines, while ozone causes wrinkles and has an impact on atopic eczema. Human skin is a major target of hormones, and they exhibit a wide range of biological activities on the skin. Hormones decline with advancing age influencing skin ageing. Nutrition has an impact on numerous biochemical processes, including oxidation, inflammation and glycation, which may result in clinical effects, including modification of the course of skin ageing and photoageing. Stress and lack of sleep are known to contribute to a pro‐inflammatory state, which, in turn, affects the integrity of extracellular matrix proteins, in particular collagen. Hormone dysregulation, malnutrition and stress may contribute to inflammatory skin disorders, such as atopic dermatitis, psoriasis, acne and rosacea.

Sleep deprivation is now recognized as an increasingly common condition inherent to modern society, and one that in many ways, is detrimental to certain physiological systems, namely, immune function. Although sleep is now viewed by a significant body of researchers as being essential for the proper working of a host of defense systems, the consequences of a lack of sleep on immune function remains to be fully comprehended. The aim of the current study was to investigate how paradoxical sleep deprivation (PSD) for 24 and 96 h and sleep restriction (SR) for 21 days by the modified multiple-platform method, and their respective 24-h recovery periods, affect immune activation in rats. To this end, we assessed circulating white blood cell counts, lymphocyte count within immune organs, as well as Ig and complement production. The data revealed that PSD for 96 h increased complement C3 and corticosterone concentration in relation to the control group. In contrast, the spleen weight, total leukocytes, and lymphocytes decreased during SR for 21 days when compared with the control group, although production of a certain class of immunoglobulin, the IgM, did increase. After recovery sleep, lymphocyte count in axillary lymph nodes grew when rats had rebound sleep after PSD for 24 h, neutrophils increased after PSD 96 h and lymphocytes numbers were higher after SR 21 days. Such alterations during sleep deprivation suggest only minor alterations of nonspecific immune parameters during acute PSD, and a significant impairment in cellular response during chronic SR.

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