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Associations among caffeinated energy drink use, anxiety, and sleep quality were examined in a young adult sample (N = 107). A 7-day retrospective survey methodology was used to assess consumption [...]

Several pieces of evidence support that sleep duration plays a role in body weight control. Nevertheless, it has been assumed that. after the identification of orexins (hypocretins), the molecular basis of the interaction between sleep and energy homeostasis has been provided. However, no study has verified the relationship between neuropeptide Y (NPY) and orexin changes during hyperphagia induced by sleep deprivation. In the current study we aimed to establish the time course of changes in metabolite, endocrine, and hypothalamic neuropeptide expression of Wistar rats sleep deprived by the platform method for a distinct period (from 24 to 96 h) or sleep restricted for 21 days (SR-21d). Despite changes in the stress hormones, we found no changes in food intake and body weight in the SR-21d group. However, sleep-deprived rats had a 25-35% increase in their food intake from 72 h accompanied by slight weight loss. Such changes were associated with increased hypothalamus mRNA levels of prepro-orexin (PPO) at 24 h followed by NPY at 48 h of sleep deprivation. Conversely, sleep recovery reduced the expression of both PPO and NPY, which rapidly brought the animals to a hypophagic condition. Our data also support that sleep deprivation rapidly increases energy expenditure and therefore leads to a negative energy balance and a reduction in liver glycogen and serum triacylglycerol levels despite the hyperphagia. Interestingly, such changes were associated with increased serum levels of glucagon, corticosterone, and norepinephrine, but no effects on leptin, insulin, or ghrelin were observed. In conclusion, orexin activation accounts for the myriad changes induced by sleep deprivation, especially the hyperphagia induced under stress and a negative energy balance. neuropeptide Y; leptin; glucagon; insulin; liver glycogen; triacylglycerol doi:10.1152/ajpendo.00660.2009.

Chronic restriction of a basic biological need induces adaptations to help meet requisites for survival. The adaptations to chronic restriction of sleep are unknown. A single episode of 10 days of partial sleep loss in rats previously was shown to be tolerated and to result in increased food intake and loss of body weight as principal signs. The purpose of the present experiment was to investigate the extent to which adaptation to chronic sleep restriction would ameliorate short-term effects and result in a changed internal phenotype. Rats were studied during 10 wk of multiple periods of restricted and unrestricted sleep to allow adaptive changes to develop. Control rats received the same ambulatory requirements only consolidated into periods that lessened interruptions of their sleep. The results indicate a latent period of relatively stable food and water intake without weight gain, followed by a dynamic phase marked by enormous increases in food and water intake and progressive loss of body weight, without malabsorption of calories. Severe consequences ensued, marked especially by changes to the connective tissues, and became fatal for two individuals. The most striking changes to internal organs in sleep-restricted rats included lengthening of the small intestine, decreased size of adipocytes, and increased incidence of multilocular adipocytes. Major organs accounted for an increased proportion of total body mass. These changes to internal tissues appear adaptive in response to high energy production, decomposition of lipids, and increased need to absorb nutrients, but ultimately insufficient to compensate for inadequate sleep. sleep rebound; adaptation; metabolism; adiposity; connective tissues; visceral organs doi: 10.1152/ajpregu.00230.2009.

Background/Objectives: This study investigates determinants of sleep duration and its impact on nutritional status, resting energy expenditure (REE), cardiometabolic risk factors and hormones in children/adolescents. Subjects/Methods: In 207 girls and 207 boys (13.0 [+ or -] 3.4 (6.1-19.9) years) body mass index standard deviation score (BMI SIDS), waist circumference (WC) z-score, body composition (air-displacement plethysmography), REE (ventilated hood system; n = 312) and cardiometabolic risk factors/hormones (n = 250) were assessed. Greater than 90th percentile of BMI/WC references was defined as overweight/overwaist. Sleep duration, media consumption (TV watching/computer use), physical activity, dietary habits, parental BMI, socio-economic status and early infancy were assessed by questionnaire. Short sleep was defined as < 10 h per day for children < 10 years and otherwise < 9 h per day. Results: Total 15.9% participants were overweight, mean sleep duration was 8.9 [+ or -] 1.3 h per day. Age explained most variance in sleep (girls: 57.0%; boys: 41.2%) besides a high nutrition quality score (girls: 0.9%) and a low media consumption (boys: 1.3%). Sleep was inversely associated with BMI SDS/WC z-score (girls: r = -0.17/-0.19, P Conclusions: Age mostly determined sleep. Short sleep was related to a higher BMI SDS/WC z-score (girls/boys), a lower REE (boys), higher leptin (girls) and lower adiponectin levels (boys). doi:10.1038/ejcn.2008.41; published online 30 July 2008 Keywords: sleep duration; overweight; REE; cardiometabolic risk factors; hormones, Introduction Childhood overweight is a major public health concern of complex aetiology and short sleep duration was considered as a determinant. Already Locard et al. (1992) showed that short sleep [...]

Byline: Milagros I. Figueroa-Ramos (1,2), Carmen Mabel Arroyo-Novoa (1,2), Kathryn A. Lee (2), Geraldine Padilla (2), Kathleen A. Puntillo (2) Keywords: Sleep; Sleep deprivation; Delirium; Intensive care unit; Mechanisms Abstract: Sleep deprivation and delirium are conditions commonly encountered in intensive care unit patients. Sleep in these patients is characterized by sleep fragmentation, an increase in light sleep, and a decrease of both slow wave sleep and rapid eye movement sleep. The most common types of delirium in this population are hypoactive and mixed-type. Knowledge about the mechanisms of sleep and delirium has evolved over time, but these phenomena are not yet well understood. What is known, however, is that different areas in the brainstem transmit information to the thalamus and cortex necessary for sleep--wake regulation. Delirium is related to an imbalance in the synthesis, release, and inactivation of some neurotransmitters, particularly acetylcholine and dopamine. The relationship between sleep deprivation and delirium has been studied for many years and has been viewed as reciprocal. The link between them may be ascribed to shared mechanisms. An imbalance in neurotransmitters as well as alteration of melatonin production may contribute to the pathogenesis of both phenomena. A better understanding of the mechanisms and factors that contribute to sleep deprivation and delirium can guide the development of new methods and models for prevention and treatment of these problems and consequently improve patient outcomes. Author Affiliation: (1) School of Nursing, University of Puerto Rico, Medical Sciences Campus, PO Box 365067, San Juan, Puerto Rico, 00936-5067 (2) School of Nursing, University of California, San Francisco, 2 Koret Way, N 631, San Francisco, CA, 94143-0610, USA Article History: Registration Date: 09/01/2009 Received Date: 06/07/2008 Accepted Date: 12/11/2008 Online Date: 23/01/2009

Sleep is understood to possess recuperative properties and, conversely, sleep loss is associated with disease and shortened life span. Despite these critical attributes, the mechanisms and functions by which sleep and sleep loss impact health still are speculative. One of the most consistent, if largely overlooked, signs of sleep loss in both humans and laboratory rats is a progressive increase in circulating phagocytic cells, mainly neutrophils. The destination, if any, of the increased circulating populations has been unknown and, therefore, its medical significance has been uncertain. The purpose of the present experiment was to determine the content and location of neutrophils in liver and lung tissue of sleep-deprived rats. These are two principal sites affected by neutrophil migration during systemic inflammatory illness. The content of neutrophils in the intestine also was determined. Sleep deprivation in rats was produced for 5 and 10 days by the Bergmann-Rechtschaffen disk method, which has been validated for its high selectivity under freely moving conditions and which was tolerated and accompanied by a deep negative energy balance. Comparison groups included basal conditions and 48 h of sleep recovery after 10 days of sleep loss. Myeloperoxidase (MPO), an enzyme constituent of neutrophils, was extracted from liver, lung, and intestinal tissues, and its activity was determined by spectrophotometry. Leukocytes were located in vasculature and interstitial spaces in the liver and the lung by immunohistochemistry. Heine oxygenase-1, also known as heat shock protein-32 and a marker of cellular stress, and corticosterone also were measured. The results indicate neutrophil migration into extravascular liver and lung tissue concurrent with cell stress and consistent with tissue injury or infection induced by sleep loss. Plasma corticosterone was unchanged. Recovery sleep was marked by increased lung heme oxygenase-1, increased intestinal MPO activity, and abnormally low corticosterone, suggesting ongoing reactive processes as a result of prior sleep deprivation. sleep deprivation; sleep rebound; granulocytes; myeloperoxidase; heine oxygenase-1; leukocytosis

Recent research has shown that dissociative symptoms are related to self-reports of deviant sleep experiences. The present study is the 1st to explore whether sleep loss can fuel dissociative symptoms. Twenty-five healthy volunteers were deprived of sleep for 1 night. Sleepiness and dissociative symptoms were assessed every 6 hr. The authors measured both spontaneous dissociative symptoms and dissociative symptoms induced by dot-staring during sensory deprivation. Sleepiness as well as spontaneous and induced dissociative symptoms were stable throughout the day but increased during the night. These findings provide further evidence for a robust relationship between disruptions in sleep patterns and dissociative symptoms. Keywords: dissociation, sleep deprivation, sleepiness, dissociative disorders

Recent studies indicate that chronic sleep restriction can have negative consequences for brain function and peripheral physiology and can contribute to the allostatic load throughout the body. Interestingly, few studies have examined how the sleep-wake system itself responds to repeated sleep restriction. In this study, rats were subjected to a sleep-restriction protocol consisting of 20 h of sleep deprivation (SD) followed by a 4-h sleep opportunity each day for 5 consecutive days. In response to the first 20-h SD block on day 1, animals responded during the 4-h sleep opportunity with enhanced sleep intensity [i.e., nonrapid eye movement (NREM) delta power] and increased rapid eye movement sleep time compared with baseline. This sleep pattern is indicative of a homeostatic response to acute sleep loss. Remarkably, after the 20-h SD blocks on days 2-5, animals failed to exhibit a compensatory NREM delta power response during the 4-h sleep opportunities and failed to increase NREM and rapid eye movement sleep times, despite accumulating a sleep debt each consecutive day. After losing [approximately equal to] 35 h of sleep over 5 days of sleep restriction, animals regained virtually none of their lost sleep, even during a full 3-day recovery period. These data demonstrate that the compensatory/ homeostatic sleep response to acute SD does not generalize to conditions of chronic partial sleep loss. We propose that the change in sleep-wake regulation in the context of repeated sleep restriction reflects an allostatic process, and that the allostatic load produced by SD has direct effects on the sleep-wake regulatory system. allostasis | homeostasis | sleep deprivation | stress | rodents

Compliance with the Accreditation Council for Graduate Medical Education (ACGME) duty-hour standards is estimated among interns. It is concluded that the interns commonly reported working hours that were noncompliant with the ACGME duty-hour standards in the first year following their implementation.

Objective. Sleep deprivation is commonly used to enhance the effectiveness of pediatric sedation and to decrease sedation failures. We reviewed our sedation database to evaluate the efficacy of sleep deprivation. Methods. The entire pediatric sedation unit database (n = 5640) was reviewed retrospectively. Patients without complete data sets were excluded. The remaining patients were separated into 2 groups: 3272 patients who underwent noninvasive procedures and 1210 who underwent invasive procedures. A subgroup of noninvasive procedure patients Results. In the noninvasive procedure group, the sedation failure rate was 5.7% for the sleep-deprived patients and 5.6% for the non-sleep-deprived patients, whereas the sedation failure rate for children Conclusions. Sleep deprivation had no effect in reducing the pediatric sedation failure rate. The patients having noninvasive procedures who were sleep deprived required significantly more nursing care hours than their non-sleep-deprived counterparts. Routine use of sleep deprivation for pediatric sedation should be critically reevaluated. Pediatrics 2004;113:1204-1208; sleep deprivation, pediatric sedation, sedation failure. ABBREVIATIONS. EEG, electroencephalography; MRI, magnetic resonance imaging; CT, computed tomography., Sedation is frequently required to facilitate diagnostic and therapeutic procedures in children. When sedation is performed, the focus is twofold: safety and efficacy. The American Academy of Pediatrics, the American [...]