A meta-analysis of the associations between insufficient sleep duration and antibody response to vaccination.

Vaccination is a major strategy to control a viral pandemic. Simple behavioral interventions that might boost vaccine responses have yet to be identified. We conducted meta-analyses to summarize the evidence linking the amount of sleep obtained in the days surrounding vaccination to antibody response in healthy adults.

Transportation noise impairs cardiovascular function without altering sleep: The importance of autonomic arousals.

Aims: Chronic exposure to nocturnal transportation noise has been linked to cardiovascular disorders with sleep impairment as the main mediator. Here we examined whether nocturnal transportation noise affects the main stress pathways, and whether it relates to changes in the macro and micro structure of sleep.

Methods And Results: Twenty-six young healthy participants (12 women, 24.

Adverse impact of nocturnal transportation noise on glucose regulation in healthy young adults: Effect of different noise scenarios.

Background: Epidemiological evidence indicates an association between transportation noise exposure and a higher risk of developing type 2 diabetes. Sleep disturbances are thought to be one of the mechanisms as it is well established that a few nights of short or poor sleep impair glucose tolerance and insulin sensitivity in healthy good sleepers.

Objectives: The present study aimed to determine the extent to which exposure to nocturnal transportation noise affects glucose metabolism, and whether it is related to noise-induced sleep alterations.

Effects of Insufficient Sleep on Pituitary-Adrenocortical Response to CRH Stimulation in Healthy Men.

Study Objectives: Severe sleep restriction results in elevated evening cortisol levels. We examined whether this relative hypercortisolism is associated with alterations in the pituitary-adrenocortical response to evening corticotropin-releasing hormone (CRH) stimulation.

Methods: Eleven subjects participated in 2 sessions (2 nights of 10 hours vs.

The important role of sleep in metabolism.

Both reduction in total sleep duration with slow-wave sleep (SWS) largely preserved and alterations of sleep quality (especially marked reduction of SWS) with preservation of total sleep duration are associated with insulin resistance without compensatory increase in insulin secretion, resulting in impaired glucose tolerance and increased risk of type 2 diabetes. When performed under rigorously controlled conditions of energy intake and physical activity, sleep restriction is also associated with a decrease in circulating levels of leptin (an anorexigenic hormone) and an increase in circulating levels of ghrelin (an orexigenic hormone), hunger and appetite. Furthermore, sleep restriction is also associated with a stimulation of brain regions sensitive to food stimuli, indicating that sleep loss may lead to obesity through the selection of high-calorie food.

Impact of obesity in children with narcolepsy.

Aims: To evaluate the impact of obesity on clinical and sleep characteristics in a population of narcoleptic children.

Methods: Data from the children diagnosed with idiopathic narcolepsy in the National Reference Centers for Narcolepsy were collected between 2008 and 2011. Clinical and electrophysiological characteristics were compared between obese (body mass index [BMI] greater than P97) and nonobese children.

A phenomenological model for circadian and sleep allostatic modulation of plasma cortisol concentration.

Both circadian rhythmicity and sleep play significant roles in the regulation of plasma cortisol concentration by the hypothalamo-pituitary-adrenal (HPA) axis. Numerous studies have found links between sleep and changes in cortisol concentration, but the implications of these results have remained largely qualitative. In this article, we present a quantitative phenomenological model to describe the effects of different sleep durations on cortisol concentration.

Sleep and metabolic function.

Evidence for the role of sleep on metabolic and endocrine function has been reported more than four decades ago. In the past 30 years, the prevalence of obesity and diabetes has greatly increased in industrialized countries, and self-imposed sleep curtailment, now very common, is starting to be recognized as a contributing factor, alongside with increased caloric intake and decreased physical activity. Furthermore, obstructive sleep apnea, a chronic condition characterized by recurrent upper airway obstruction leading to intermittent hypoxemia and sleep fragmentation, has also become highly prevalent as a consequence of the epidemic of obesity and has been shown to contribute, in a vicious circle, to the metabolic disturbances observed in obese patients.

Role of sleep duration in the regulation of glucose metabolism and appetite.

Sleep curtailment has become a common behavior in modern society. This review summarizes the current laboratory evidence indicating that sleep loss may contribute to the pathophysiology of diabetes mellitus and obesity. Experimentally induced sleep loss in healthy volunteers decreases insulin sensitivity without adequate compensation in beta-cell function, resulting in impaired glucose tolerance and increased diabetes risk.

Twenty-four-hour profiles of acylated and total ghrelin: relationship with glucose levels and impact of time of day and sleep.

Context: The acylation of ghrelin is essential for its stimulatory effects on GH release and appetite. Most of the physiology of ghrelin has been defined based on the assay of total ghrelin (TG), which mainly reflects levels of unacylated ghrelin. Whether levels of acylated ghrelin (AG) are influenced by circadian time and sleep and impact glucose regulation under physiologic conditions is not known.

Effects of poor and short sleep on glucose metabolism and obesity risk.

The importance of sleep to hormones and glucose metabolism was first documented more than four decades ago. Since then, sleep curtailment has become an endemic behavior in modern society. In addition, the prevalence of sleep disorders, particularly obstructive sleep apnea (OSA), has increased.

Metabolic consequences of sleep and sleep loss.

Reduced sleep duration and quality appear to be endemic in modern society. Curtailment of the bedtime period to minimum tolerability is thought to be efficient and harmless by many. It has been known for several decades that sleep is a major modulator of hormonal release, glucose regulation and cardiovascular function.

The metabolic consequences of sleep deprivation.

The prevalence of diabetes and obesity is increasing at an alarming rate worldwide, and the causes of this pandemic are not fully understood. Chronic sleep curtailment is a behavior that has developed over the past 2-3 decades. Laboratory and epidemiological studies suggest that sleep loss may play a role in the increased prevalence of diabetes and/or obesity.

Impact of sleep and sleep loss on neuroendocrine and metabolic function.

Background: Sleep exerts important modulatory effects on neuroendocrine function and glucose regulation. During the past few decades, sleep curtailment has become a very common behavior in industrialized countries. This trend toward shorter sleep times has occurred over the same time period as the dramatic increases in the prevalence of obesity and diabetes.

Sleep loss: a novel risk factor for insulin resistance and Type 2 diabetes.

Chronic sleep loss as a consequence of voluntary bedtime restriction is an endemic condition in modern society. Although sleep exerts marked modulatory effects on glucose metabolism, and molecular mechanisms for the interaction between sleeping and feeding have been documented, the potential impact of recurrent sleep curtailment on the risk for diabetes and obesity has only recently been investigated. In laboratory studies of healthy young adults submitted to recurrent partial sleep restriction, marked alterations in glucose metabolism including decreased glucose tolerance and insulin sensitivity have been demonstrated.

Impact of carbohydrate-rich meals on plasma epinephrine levels: dysregulation with aging.

Context: Plasma norepinephrine (NE) and epinephrine (E) levels are indicators of peripheral sympathetic and adrenomedullary activities, respectively. The sympathoadrenomedullary system is involved in the metabolic response to carbohydrate intake and is affected by aging; however, the relationship between glucose metabolism and adrenomedullary activity in older adults remains poorly defined.

Objective: The objective of this study was to examine the changes in the impact of carbohydrate-rich meals on circulating catecholamines with aging.

Brief communication: Sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite.

Background: Total sleep deprivation in rodents and in humans has been associated with hyperphagia. Over the past 40 years, self-reported sleep duration in the United States has decreased by almost 2 hours.

Objective: To determine whether partial sleep curtailment, an increasingly prevalent behavior, alters appetite regulation.

Leptin levels are dependent on sleep duration: relationships with sympathovagal balance, carbohydrate regulation, cortisol, and thyrotropin.

Sleep plays an important role in energy homeostasis. The present study tests the hypothesis that circulating levels of leptin, a hormone that signals energy balance to the brain, are influenced by sleep duration. We also analyzed associations between leptin and sympathovagal balance, cortisol, TSH, glucose, and insulin under different bedtime conditions.

Reciprocal interactions between the GH axis and sleep.

For more than 30 years, growth hormone (GH) has been observed to be preferentially secreted during deep, slow-wave sleep (SWS). However, the mechanisms that underlie this robust relationship that links anabolic processes in the body with behavioral rest and decreased cerebral metabolism remain to be elucidated. Current evidence indicates that GH secretion during the beginning of sleep appears to be primarily regulated by GH-releasing hormone (GHRH) stimulation occurring during a period of relative somatostatin withdrawal, which also is associated with elevated levels of circulating ghrelin.