Ari Shechter

Sleep restriction increases the neuronal response to unhealthy food in normal-weight individuals.

Context:Sleep restriction alters responses to food. However, the underlying neural mechanisms for this effect are not well understood.Objective:The purpose of this study was to determine whether there is a neural system that is preferentially activated in response to unhealthy compared with healthy foods.Participants:Twenty-five normal-weight individuals, who normally slept 7–9 h per night, completed both phases of this randomized controlled study.Intervention:Each participant was tested after a period of five nights of either 4 or 9 h in bed. Functional magnetic resonance imaging (fMRI) was performed in the fasted state, presenting healthy and unhealthy food stimuli and objects in a block design. Neuronal responses to unhealthy, relative to healthy food stimuli after each sleep period were assessed and compared.Results:After a period of restricted sleep, viewing unhealthy foods led to greater activation in the superior and middle temporal gyri, middle and superior frontal gyri, left inferior parietal lobule, orbitofrontal cortex, and right insula compared with healthy foods. These same stimuli presented after a period of habitual sleep did not produce marked activity patterns specific to unhealthy foods. Further, food intake during restricted sleep increased in association with a relative decrease in brain oxygenation level-dependent (BOLD) activity observed in the right insula.Conclusion:This inverse relationship between insula activity and food intake and enhanced activation in brain reward and food-sensitive centers in response to unhealthy foods provides a model of neuronal mechanisms relating short sleep duration to obesity.

Experimental sleep curtailment causes wake-dependent increases in 24-h energy expenditure as measured by whole-room indirect calorimetry

BACKGROUND Epidemiologic evidence has shown a link between short sleep and obesity. Clinical studies suggest a role of increased energy intake in this relation, whereas the contributions of energy expenditure (EE) and substrate utilization are less clearly defined. OBJECTIVE Our aim was to investigate the effects of sleep curtailment on 24-h EE and respiratory quotient (RQ) by using whole-room indirect calorimetry under fixed-meal conditions. DESIGN Ten females aged 22-43 y with a BMI (in kg/m²) of 23.4-27.5 completed a randomized, crossover study. Participants were studied under short- (4 h/night) and habitual- (8 h/night) sleep conditions for 3 d, with a 4-wk washout period between visits. Standardized weight-maintenance meals were served at 0800, 1200, and 1900 with a snack at 1600. Measures included EE and RQ during the sleep episode on day 2 and continuously over 23 h on day 3. RESULTS Short compared with habitual sleep resulted in significantly higher (± SEM) 24-h EE (1914.0 ± 62.4 compared with 1822.1 ± 43.8 kcal; P = 0.012). EE during the scheduled sleep episode (0100-0500 and 2300-0700 in short- and habitual-sleep conditions, respectively) and across the waking episode (0800-2300) were unaffected by sleep restriction. RQ was unaffected by sleep restriction. CONCLUSIONS Short compared with habitual sleep is associated with an increased 24-h EE of ~92 kcal (~5%)--lower than the increased energy intake observed in prior sleep-curtailment studies. This finding supports the hypothesis that short sleep may predispose to weight gain as a result of an increase in energy intake that is beyond the modest energy costs associated with prolonged nocturnal wakefulness.

Sleep, Hormones, and Circadian Rhythms throughout the Menstrual Cycle in Healthy Women and Women with Premenstrual Dysphoric Disorder

A relationship exists between the sleep-wake cycle and hormone secretion, which, in women, is further modulated by the menstrual cycle. This interaction can influence sleep across the menstrual cycle in healthy women and in women with premenstrual dysphoric disorder (PMDD), who experience specific alterations of circadian rhythms during their symptomatic luteal phase along with sleep disturbances during this time. This review will address the variation of sleep at different menstrual phases in healthy and PMDD women, as well as changes in circadian rhythms, with an emphasis on their relationship with female sex hormones. It will conclude with a brief discussion on nonpharmacological treatments of PMDD which use chronotherapeutic methods to realign circadian rhythms as a means of improving sleep and mood in these women.

Alterations in sleep architecture in response to experimental sleep curtailment are associated with signs of positive energy balance.

Sleep reduction is associated with increased energy intake and weight gain, though few studies have explored the relationship between sleep architecture and energy balance measures in the context of experimental sleep restriction. Fourteen males and 13 females (body mass index: 22-26 kg/m(2)) participated in a crossover sleep curtailment study. Participants were studied under two sleep conditions: short (4 h/night; 0100-0500 h) and habitual (9 h/night; 2200-0700 h), for 5 nights each. Sleep was polysomnographically recorded nightly. Outcome measures included resting metabolic rate (RMR), feelings of appetite-satiety, and ad libitum food intake. Short sleep resulted in reductions in stage 2 sleep and rapid eye movement (REM) sleep duration (P < 0.001), as well as decreased percentage of stage 2 sleep and REM sleep and increased slow wave sleep (SWS) percentage (P < 0.05). Linear mixed model analysis demonstrated a positive association between stage 2 sleep duration and RMR (P = 0.051). Inverse associations were observed between REM sleep duration and hunger (P = 0.031) and between stage 2 sleep duration and appetite for sweet (P = 0.015) and salty (P = 0.046) foods. Stage 2 sleep percentage was inversely related to energy consumed (P = 0.024). Stage 2 sleep (P = 0.005), SWS (P = 0.008), and REM sleep (P = 0.048) percentages were inversely related to fat intake, and SWS (P = 0.040) and REM sleep (P = 0.050) were inversely related to carbohydrate intake. This study demonstrates that changes in sleep architecture are associated with markers of positive energy balance and indicate a means by which exposure to short sleep duration and/or an altered sleep architecture profile may lead to excess weight gain over time.

Sleep disturbances, body fat distribution, food intake and/or energy expenditure: pathophysiological aspects

Abstract Data from cross-sectional and longitudinal studies have illustrated a relationship between short sleep duration (SSD) and weight gain. Individuals with SSD are heavier and gain more weight over time than normal-duration sleepers. This sleep-obesity relationship may have consequences for obesity treatments, as it appears that short sleepers have reduced ability to lose weight. Laboratory-based clinical studies found that experimental sleep restriction affects energy expenditure and intake, possibly providing a mechanistic explanation for the weight gain observed in chronic short sleepers. Specifically, compared to normal sleep duration, sleep restriction increases food intake beyond the energetic costs of increased time spent awake. Reasons for this increased energy intake after sleep restriction are unclear but may include disrupted appetite-regulating hormones, altered brain mechanisms involved in the hedonic aspects of appetite, and/or changes in sleep quality and architecture. Obstructive sleep apnea (OSA) is a disorder at the intersection of sleep and obesity, and the characteristics of the disorder illustrate many of the effects of sleep disturbances on body weight and vice versa. Specifically, while obesity is among the main risk factors for OSA, the disorder itself and its associated disturbances in sleep quality and architecture seem to alter energy balance parameters and may induce further weight gain. Several intervention trials have shown that weight loss is associated with reduced OSA severity. Thus, weight loss may improve sleep, and these improvements may promote further weight loss. Future studies should establish whether increasing sleep duration/improving sleep quality can induce weight loss.

Fiber and Saturated Fat Are Associated with Sleep Arousals and Slow Wave Sleep.

STUDY OBJECTIVES Sleep restriction alters food intake, but less is known about how dietary patterns affect sleep. Current goals were to determine whether: (1) sleep is different after consumption of a controlled diet vs. an ad libitum diet, and (2) dietary intake during ad libitum feeding is related to nocturnal sleep. METHODS Twenty-six normal weight adults (30-45 y), habitually sleeping 7-9 h/night, participated in a randomized-crossover inpatient study with 2 phases of 5 nights: short (4 h in bed) or habitual (9 h in bed) sleep. Only data from the habitual sleep phase were used for the present analyses. During the first 4 days, participants consumed a controlled diet; on day 5, food intake was self-selected. Linear regression was used to determine relations between daytime food intake and nighttime sleep on day 5. RESULTS Sleep duration did not differ after 3 days of controlled feeding vs. a day of ad libitum intake. However, sleep after ad libitum eating had less slow wave sleep (SWS, P = 0.0430) and longer onset latency (P = 0.0085). Greater fiber intake predicted less stage 1 (P = 0.0198) and more SWS (P = 0.0286). Percent of energy from saturated fat predicted less SWS (P = 0.0422). Higher percent of energy from sugar and other carbohydrates not considered sugar or fiber was associated with arousals (P = 0.0320 and 0.0481, respectively). CONCLUSIONS Low fiber and high saturated fat and sugar intake is associated with lighter, less restorative sleep with more arousals. Diet could be useful in the management of sleep disorders but this needs to be tested. CLINICAL TRIAL REGISTRATION http://www.clinicaltrials.gov, #NCT00935402.

Fasting plasma adropin concentrations correlate with fat consumption in human females

This study investigated whether plasma adropin concentrations are influenced by sleep restriction and correlate with dietary preferences.

Postprandial thermogenesis and substrate oxidation are unaffected by sleep restriction

Background/objectives:The extent to which alterations in energy expenditure (EE) in response to sleep restriction contribute to the short sleep–obesity relationship is not clearly defined. Short sleep may induce changes in resting metabolic rate (RMR), thermic effect of food (TEF) and postprandial substrate oxidation.Subjects/methods:Ten females (age and body mass index: 22–43 years and 23.4–28 kg m−2) completed a randomized, crossover study assessing the effects of short (4 h per night) and habitual (8 h per night) sleep duration on fasting and postprandial RMR and respiratory quotient (RQ). Measurements were taken after three nights using whole-room indirect calorimetry. The TEF was assessed over a 6-h period following consumption of a high-fat liquid meal.Results:Short versus habitual sleep did not affect RMR (1.01±0.05 and 0.97±0.04 kcal min−1; P=0.23). Fasting RQ was significantly lower after short versus habitual sleep (0.84±0.01 and 0.88±0.01; P=0.028). Postprandial EE (short: 1.13±0.04 and habitual: 1.10±0.04, P=0.09) and RQ (short: 0.88±0.01 and habitual: 0.88±0.01, P=0.50) after the high-fat meal were not different between conditions. TEF was similar between conditions (0.24±0.02 kcal min−1 in both; P=0.98), as was the ∼6-h incremental area under the curve (1.16±0.10 and 1.17±0.09 kcal min−1 × 356 min after short and habitual sleep, respectively; P=0.92).Conclusions:Current findings observed in non-obese healthy premenopausal women do not support the hypothesis that alterations in TEF and postprandial substrate oxidation are major contributors to the higher rate of obesity observed in short sleepers. In exploring a role of sleep duration on EE, research should focus on potential alterations in physical activity to explain the increased obesity risk in short sleepers.

Delayed sleep timing is associated with low levels of free-living physical activity in normal sleeping adults.

OBJECTIVE AND BACKGROUND We and others have reported that experimentally induced short sleep does not affect resting metabolic rate and leads to increased laboratory-measured 24-h energy expenditure. Here, we aimed to determine if sleep timing and/or quality are related to physical activity (PA) levels. METHODS Measures of PA via waist actigraphy, sleep diary, and sleep quality questionnaires were collected over a 7-18-day period in 22 adults (mean age ± standard deviation (SD): 35.8 ± 4.6 years, and mean body mass index ± SD: 23.8 ± 1.1 kg/m(2)) who were on their habitual sleep-wake and activity schedules. RESULTS During the recording period, mean (±SD) bedtime and wake times were 00:17 ± 1:07 h (range: 22:02-02:07 h) and 08:20 ± 1:14 h (range: 06:30-10:11 h), respectively. After controlling for sleep duration, later bedtime, wake time, and midpoint of sleep were associated with less time spent in moderate-to-vigorous PA (p = 0.013, p = 0.005, and p = 0.007, respectively), and increased time in sedentary PA (p = 0.016, p = 0.013, and p = 0.013, respectively). CONCLUSIONS Current results suggest that even relatively small alterations in sleep timing may influence PA. However, causality cannot be inferred from this cross-sectional study. Clinical intervention studies should be conducted to assess the relationship between sleep timing and energy balance.

Diurnal and circadian variation of sleep and alertness in men vs. naturally cycling women

Significance This study quantifies sex differences in the diurnal and circadian variation of sleep and waking while carefully controlling for menstrual cycle phase and hormonal contraceptive use. Compared to men, rhythms of core body temperature, sleep, and subjective alertness are advanced in women during both the midfollicular and midluteal phases. Our study also reveals lower alertness levels at night in women. These sex differences are important for understanding the increased female susceptibility to sleep and wake disturbances. This study quantifies sex differences in the diurnal and circadian variation of sleep and waking while controlling for menstrual cycle phase and hormonal contraceptive use. We compared the diurnal and circadian variation of sleep and alertness of 8 women studied during two phases of the menstrual cycle and 3 women studied during their midfollicular phase with that of 15 men. Participants underwent an ultradian sleep–wake cycle (USW) procedure consisting of 36 cycles of 60-min wake episodes alternating with 60-min nap opportunities. Core body temperature (CBT), salivary melatonin, subjective alertness, and polysomnographically recorded sleep were measured throughout this procedure. All analyzed measures showed a significant diurnal and circadian variation throughout the USW procedure. Compared with men, women demonstrated a significant phase advance of the CBT but not melatonin rhythms, as well as an advance in the diurnal and circadian variation of sleep measures and subjective alertness. Furthermore, women experienced an increased amplitude of the diurnal and circadian variation of alertness, mainly due to a larger decline in the nocturnal nadir. Our results indicate that women are likely initiating sleep at a later circadian phase than men, which may be one factor contributing to the increased susceptibility to sleep disturbances reported in women. Lower nighttime alertness is also observed, suggesting a physiological basis for a greater susceptibility to maladaptation to night shift work in women.