Objective Measurements of Energy Balance Are Associated With Sleep Architecture in Healthy Adults.

Study Objectives: We objectively measured body composition, energy expenditure, caloric intake, and sleep in a large, diverse sample of healthy men and women and determined how energy balance and diet associated with sleep physiology. Methods: Healthy adults (n = 50; 21-50 years) participated in an in-laboratory study involving two baseline sleep nights (BL1-2, 10 hours time-in-bed/night, 2200-0800 hours). Polysomnography was recorded on BL2. Demographic information, body composition, and energy expenditure measurements were collected at study admittance and on BL1. Daily food/drink intake was recorded both before (on BL1) and after (on BL2) the sleep measurement. Partial Pearson's correlations assessed the relationship between energy balance and sleep physiology variables. Results: At baseline, greater fat-free mass associated with lower total sleep time (r = -0.52, p = .030), lower sleep efficiency (r = -0.53, p = .004), and greater wake after sleep onset (r = 0.55, p = .002). Higher body fat percentage (r = 0.39, p = .038) and being overweight (Body Mass Index [BMI] 25-30; p = .026) associated with more rapid eye movement (REM) sleep. Higher protein intake (r's = 0.46-0.52; p's < .001-.002) and lower carbohydrate intake (r's = -0.31 to -0.34; p's = .027-.046) on BL1 and BL2 associated with more REM sleep. Greater fiber consumption on BL1 and BL2 associated with more slow-wave sleep (SWS; r's = 0.33-0.35; p's = .02-.03). More SWS related to increased carbohydrate intake the following day (BL2, r = 0.32, p = .037). Conclusions: Body composition and diet were related to baseline sleep characteristics, including SWS and REM sleep duration and sleep maintenance. Future studies should further evaluate the influence of energy balance measures on sleep physiology, since dietary interventions may be useful in treating insufficient sleep, poor sleep quality, excessive sleepiness or other sleep disorders.

Phenotypic vulnerability of energy balance responses to sleep loss in healthy adults.

Short sleep duration is a risk factor for increased hunger and caloric intake, late-night eating, attenuated fat loss when dieting, and for weight gain and obesity. It is unknown whether altered energy-balance responses to sleep loss are stable (phenotypic) over time, and the extent to which individuals differ in vulnerability to such responses. Healthy adults experienced two laboratory exposures to sleep restriction separated by 60-2132 days. Caloric intake, meal timing and weight were objectively measured. Although there were substantial phenotypic differences among participants in weight gain, increased caloric intake, and late-night eating and fat intake, responses within participants showed stability across sleep restriction exposures. Weight change was consistent in both normal-weight and overweight adults. Weight change and increased caloric intake were more stable in men whereas late-night eating was consistent in both genders. This is the first evidence of phenotypic differential vulnerability and trait-like stability of energy balance responses to repeated sleep restriction, underscoring the need for biomarkers and countermeasures to predict and mitigate this vulnerability.

Altered salience network connectivity predicts macronutrient intake after sleep deprivation.

Although insufficient sleep is a well-recognized risk factor for overeating and weight gain, the neural mechanisms underlying increased caloric (particularly fat) intake after sleep deprivation remain unclear. Here we used resting-state functional magnetic resonance imaging and examined brain connectivity changes associated with macronutrient intake after one night of total sleep deprivation (TSD). Compared to the day following baseline sleep, healthy adults consumed a greater percentage of calories from fat and a lower percentage of calories from carbohydrates during the day following TSD. Subjects also exhibited increased brain connectivity in the salience network from the dorsal anterior cingulate cortex (dACC) to bilateral putamen and bilateral anterior insula (aINS) after TSD. Moreover, dACC-putamen and dACC-aINS connectivity correlated with increased fat and decreased carbohydrate intake during the day following TSD, but not during the day following baseline sleep. These findings provide a potential neural mechanism by which sleep loss leads to increased fat intake.

Cognitive workload and sleep restriction interact to influence sleep homeostatic responses.

STUDY OBJECTIVES: Determine the effects of high versus moderate workload on sleep physiology and neurobehavioral measures, during sleep restriction (SR) and no sleep restriction (NSR) conditions. DESIGN: Ten-night experiment involving cognitive workload and SR manipulations. SETTING: Controlled laboratory environment. PARTICIPANTS: Sixty-three healthy adults (mean ± standard deviation: 33.2 ± 8.7 y; 29 females), age 22-50 y. INTERVENTIONS: Following three baseline 8 h time in bed (TIB) nights, subjects were randomized to one of four conditions: high cognitive workload (HW) + SR; moderate cognitive workload (MW) + SR; HW + NSR; or MW + NSR. SR entailed 5 consecutive nights at 4 h TIB; NSR entailed 5 consecutive nights at 8 h TIB. Subjects received three workload test sessions/day consisting of 15-min preworkload assessments, followed by a 60-min (MW) or 120-min (HW) workload manipulation comprised of visually based cognitive tasks, and concluding with 15-min of postworkload assessments. Experimental nights were followed by two 8-h TIB recovery sleep nights. Polysomnography was collected on baseline night 3, experimental nights 1, 4, and 5, and recovery night 1 using three channels (central, frontal, occipital [C3, Fz, O2]). MEASUREMENTS AND RESULTS: High workload, regardless of sleep duration, increased subjective fatigue and sleepiness (all P < 0.05). In contrast, sleep restriction produced cumulative increases in Psychomotor Vigilance Test (PVT) lapses, fatigue, and sleepiness and decreases in PVT response speed and Maintenance of Wakefulness Test (MWT) sleep onset latencies (all P < 0.05). High workload produced longer sleep onset latencies (P < 0.05, d = 0.63) and less wake after sleep onset (P < 0.05, d = 0.64) than moderate workload. Slow-wave energy-the putative marker of sleep homeostasis-was higher at O2 than C3 only in the HW + SR condition (P < 0.05). CONCLUSIONS: High cognitive workload delayed sleep onset, but it also promoted sleep homeostatic responses by increasing subjective fatigue and sleepiness, and producing a global sleep homeostatic response by reducing wake after sleep onset. When combined with sleep restriction, high workload increased local (occipital) sleep homeostasis, suggesting a use-dependent sleep response to visual work. We conclude that sleep restriction and cognitive workload interact to influence sleep homeostasis.

Sex and race differences in caloric intake during sleep restriction in healthy adults.

BACKGROUND: Evidence indicates that men and African Americans may be more susceptible to weight gain resulting from sleep loss than women and whites, respectively. Increased daily caloric intake is a major behavioral mechanism that underlies the relation between sleep loss and weight gain. OBJECTIVE: We sought to assess sex and race differences in caloric intake, macronutrient intake, and meal timing during sleep restriction. DESIGN: Forty-four healthy adults aged 21-50 y (mean ± SD: 32.7 ± 8.7 y; n = 21 women, n = 16 whites) completed an in-laboratory protocol that included 2 consecutive baseline nights [10 or 12 h time in bed (TIB)/night; 2200-0800 or 2200-1000] followed by 5 consecutive sleep-restriction nights (4 h TIB/night; 0400-0800). Caloric intake and meal-timing data were collected during the 2 d after baseline sleep and the first 3 d after sleep restriction. RESULTS: During sleep restriction, subjects increased daily caloric intake (P < 0.001) and fat intake (P = 0.024), including obtaining more calories from condiments, desserts, and salty snacks (Ps < 0.05) and consumed 532.6 ± 295.6 cal during late-night hours (2200-0359). Relative to women, men consumed more daily calories during baseline and sleep restriction, exhibited a greater increase in caloric intake during sleep restriction (d = 0.62), and consumed a higher percentage of daily calories during late-night hours (d = 0.78, Ps < 0.05). African Americans and whites did not significantly differ in daily caloric intake, increased caloric intake during sleep restriction, or meal timing. However, African Americans consumed more carbohydrates, less protein, and more caffeine-free soda and juice than whites did during the study (Ps < 0.05). CONCLUSIONS: Men may be more susceptible to weight gain during sleep loss than women due to a larger increase in daily caloric intake, particularly during late-night hours. These findings are relevant to the promotion of public health awareness by highlighting nutritional risk factors and modifiable behaviors for weight gain related to sleep-wake timing.

Effects of Experimental Sleep Restriction on Weight Gain, Caloric Intake, and Meal Timing in Healthy Adults.

STUDY OBJECTIVES: Examine sleep restriction's effects on weight gain, daily caloric intake, and meal timing. DESIGN: Repeated-measures experiments assessing body weight at admittance and discharge in all subjects (N = 225) and caloric intake and meal timing across days following 2 baseline nights, 5 sleep restriction nights and 2 recovery nights or across days following control condition nights in a subset of subjects (n = 37). SETTING: Controlled laboratory environment. PARTICIPANTS: Two hundred twenty-five healthy adults aged 22-50 y (n = 198 sleep-restricted subjects; n = 31 with caloric intake data; n = 27 control subjects; n = 6 with caloric intake data). INTERVENTIONS: Approximately 8-to-1 randomization to an experimental condition (including five consecutive nights of 4 h time in bed [TIB]/night, 04:00-08:00) or to a control condition (all nights 10 h TIB/night, 22:00-08:00). MEASUREMENTS AND RESULTS: Sleep-restricted subjects gained more weight (0.97 ± 1.4 kg) than control subjects (0.11 ± 1.9 kg; d = 0.51, P = 0.007). Among sleep-restricted subjects, African Americans gained more weight than Caucasians (d = 0.37, P = 0.003) and males gained more weight than females (d = 0.38, P = 0.004). Sleep-restricted subjects consumed extra calories (130.0 ± 43.0% of daily caloric requirement) during days with a delayed bedtime (04:00) compared with control subjects who did not consume extra calories (100.6 ± 11.4%; d = 0.94, P = 0.003) during corresponding days. In sleep-restricted subjects, increased daily caloric intake was due to more meals and the consumption of 552.9 ± 265.8 additional calories between 22:00-03:59. The percentage of calories derived from fat was greater during late-night hours (22:00-03:59, 33.0 ± 0.08%) compared to daytime (08:00-14:59, 28.2 ± 0.05%) and evening hours (15:00-21:59, 29.4 ± 0.06%; Ps < 0.05). CONCLUSIONS: In the largest, most diverse healthy sample studied to date under controlled laboratory conditions, sleep restriction promoted weight gain. Chronically sleep-restricted adults with late bedtimes may be more susceptible to weight gain due to greater daily caloric intake and the consumption of calories during late-night hours. CITATION: Spaeth AM; Dinges DF; Goel N. Effects of experimental sleep restriction on weight gain, caloric intake, and meal timing in healthy adults. SLEEP 2013;36(7):981-990.

Hallazgos neuroendocrinos en el síndrome de ingesta nocturna / Neuroendocrine levels, circadian profiles, and sleep in night eating syndrome: integration of findings

El síndrome de ingesta nocturna (SIN) se caracteriza porhiperfagia vespertina y despertares acompañados deingesta nocturna de alimentos. Dilucidar el trastorno enla fisiología del sueño y la fisiología neuroendocrina subyacenteal síndrome clínico es fundamental y ayudará acentrar los tratamientos. Llevamos a cabo un estudio con15 mujeres internadas con sobrepeso y SIN y 14 participantescontroles similares para comparar las concentracionesen 25 horas y los patrones circadianos de los perfilesneuroendocrinos y de ingesta calórica y las característicaspolisomnográficas...

Night eating syndrome (NES) is characterized by eveninghyperphagia and awakenings with nocturnal foodingestions. Elucidation of the disturbance in sleep and neuroendocrine physiology that underlies the clinical syndrome is crucial and helps to target treatments. We conducted an inpatient study of 15 overweight women with NES and 14 similar control participants to compare the 25 h levels and circadian patterns of neuroendocrine and caloric intake profiles and polysomnographic features...