During the month of Ramadan intermittent fasting, Muslims eat exclusively between sunset and sunrise, which may affect nocturnal sleep. The effects of Ramadan on sleep and rectal temperature (Tre) were examined in eight healthy young male subjects who reported at the laboratory on four occasions: (i) baseline 15 days before Ramadan (BL); (ii) on the eleventh day of Ramadan (beginning of Ramadan, BR); (iii) on the twenty‐fifth day of Ramadan (end of Ramadan, ER); and (iv) 2 weeks after Ramadan (AR). Although each session was preceded by an adaptation night, data from the first night were discarded. Polysomnography was taken on ambulatory 8‐channel Oxford Medilog MR‐9000 II® recorders. Standard electroencephalogram (EEG), electro‐oculogram (EOG) and electromyogram (EMG) recordings were scored visually with the PhiTools ERA© software. The main finding of the study was that during Ramadan sleep latency is increased and sleep architecture modified. Sleep period time and total sleep time decreased in BR and ER. The proportion of non‐rapid eye movement (NREM) sleep increased during Ramadan and its structure changed, with an increase in stage 2 proportion and a decrease in slow wave sleep (SWS) duration. Rapid eye movement (REM) sleep duration and proportion decreased during Ramadan. These changes in sleep parameters were associated with a delay in the occurrence of the acrophase of Tre and an increase in nocturnal Tre during Ramadan. However, the 24‐h mean value (mesor) of Tre did not vary. The nocturnal elevation of Tre was related to a 2–3‐h delay in the acrophase of the circadian rhythm. The amplitude of the circadian rhythm of Tre was decreased during Ramadan. The effects of Ramadan fasting on nocturnal sleep, with an increase in sleep latency and a decrease in SWS and REM sleep, and changes in Tre, were attributed to the inversion of drinking and meal schedule, rather than to an altered energy intake which was preserved in this study.

Aims/hypothesis Sleep loss is associated with insulin resistance and an increased risk for type 2 diabetes, yet underlying mechanisms are not understood. Elevation of circulating non-esterified (i.e. free) fatty acid (NEFA) concentrations can lead to insulin resistance and plays a central role in the development of metabolic diseases. Circulating NEFA in healthy individuals shows a marked diurnal variation with maximum levels occurring at night, yet the impact of sleep loss on NEFA levels across the 24 h cycle remains unknown. We hypothesised that sleep restriction would alter hormones that are known to stimulate lipolysis and lead to an increase in NEFA levels. Methods We studied 19 healthy young men under controlled laboratory conditions with four consecutive nights of 8.5 h in bed (normal sleep) and 4.5 h in bed (sleep restriction) in randomised order. The 24 h blood profiles of NEFA, growth hormone (GH), noradrenaline (norepinephrine), cortisol, glucose and insulin were simultaneously assessed. Insulin sensitivity was estimated by a frequently sampled intravenous glucose tolerance test. Results Sleep restriction relative to normal sleep resulted in increased NEFA levels during the nocturnal and early-morning hours. The elevation in NEFA was related to prolonged nocturnal GH secretion and higher early-morning noradrenaline levels. Insulin sensitivity was decreased after sleep restriction and the reduction in insulin sensitivity was correlated with the increase in nocturnal NEFA levels. Conclusions/interpretation Sleep restriction in healthy men results in increased nocturnal and early-morning NEFA levels, which may partly contribute to insulin resistance and the elevated diabetes risk associated with sleep loss.

The circadian rhythms and PSG of patients receiving mechanical ventilation and intravenous sedation exhibit pronounced temporal disorganization. The finding that most subjects exhibited preserved, but phase delayed, excretion of aMT6s suggests that the circadian pacemaker of such patients may be free-running.

Introduction Sleep curtailment is an endemic behavior in modern society. Well-controlled laboratory studies have shown that sleep loss in young adults is associated with increased desire for high-calorie food and obesity risk. However, the relevance of these laboratory findings to real life is uncertain. We conducted a 3 week, within-participant, intervention study to assess the effects of extended bedtimes on sleep duration and food desire under real life conditions in individuals who are at risk for obesity. Methods Ten overweight young adults reporting average habitual sleep duration of less than 6.5 hours were studied in the home environment. Habitual bedtimes for 1-week (baseline) were followed by bedtimes extended to 8.5 hours for 2-weeks (intervention). Participants were unaware of the intervention until after the baseline period. Participants received individualized behavioural counselling on sleep hygiene on the first day of the intervention period. Sleep duration was recorded by wrist actigraphy throughout the study. Participants rated their sleepiness, vigor and desire for various foods using visual analog scales at the end of baseline and intervention periods. Results On average, participants obtained 1.6 hours more sleep with extended bedtimes (5.6 vs. 7.1; p<0.001) and reported being less sleepy (p=0.004) and more vigorous (p=0.034). Additional sleep was associated with a 14% decrease in overall appetite (p=0.030) and a 62% decrease in desire for sweet and salty foods (p=0.017). Desire for fruits, vegetables and protein-rich nutrients was not affected by added sleep. Conclusions Sleep duration can be successfully increased in real life settings and obtaining adequate sleep is associated with less desire for high calorie foods in overweight young adults who habitually curtail their sleep.

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