Distinct associations between energy balance and the sleep characteristics slow wave sleep and rapid eye movement sleep.

CONTEXT: Epidemiologically, an inverse relationship between body mass index (BMI) and sleep duration is observed. Intra-individual variance in the amount of slow wave sleep (SWS) or rapid eye movement (REM) sleep has been related to variance of metabolic and endocrine parameters, which are risk factors for the disturbance of energy balance (EB). OBJECTIVE: To investigate inter-individual relationships between EB (EB= energy intake-energy expenditure∣, MJ/24 h), SWS or REM sleep, and relevant parameters in normal-weight men during two 48 h stays in the controlled environment of a respiration chamber. SUBJECTS AND METHODS: A total of 16 men (age 23±3.7 years, BMI 23.9±1.9 kg m(-2)) stayed in the respiration chamber twice for 48 h to assure EB. Electroencephalography was used to monitor sleep (2330-0730 hrs). Hunger and fullness were scored by visual analog scales; mood was determined by State Trait Anxiety Index-state and food reward by liking and wanting. Baseline blood and salivary samples were collected before breakfast. Subjects were fed in EB, except for the last dinner, when energy intake was ad libitum. RESULTS: The subjects slept on average 441.8±49 min per night, and showed high within-subject reliability for the amount of SWS and REM sleep. Linear regression analyses showed that EB was inversely related to the amount of SWS (r=-0.43, P<0.03), and positively related to the amount of REM sleep (r=0.40, P<0.05). Relevant parameters such as hunger, reward, stress and orexigenic hormone concentrations were related to overeating, as well as to the amount of SWS and REM sleep, however, after inclusion of these parameters in a multiple regression, the amount of SWS and REM sleep did not add to the explained variance of EB, which suggests that due to their individual associations, these EB parameters are mediator variables. CONCLUSION: A positive EB due to overeating, was explained by a smaller amount of SWS and higher amount of REM sleep, mediated by hunger, fullness, State Trait Anxiety Index-state scores, glucose/insulin ratio, and ghrelin and cortisol concentrations.

Acute stress and food-related reward activation in the brain during food choice during eating in the absence of hunger.

BACKGROUND: Stress results in eating in the absence of hunger, possibly related to food reward perception. HYPOTHESIS: Stress decreases food reward perception. AIM: Determine the effect of acute stress on food choice and food choice reward-related brain activity. SUBJECTS: Nine females (BMI = 21.5 + or - 2.2 kg/m(2), age = 24.3 + or - 3.5 years). PROCEDURE: Fasted subjects came twice to randomly complete either a rest or stress condition. Per session, two functional MRI scans were made, wherein the subjects chose the subsequent meal (food images). The rewarding value of the food was measured as liking and wanting. Food characteristics (for example, crispiness, fullness of taste and so on), energy intake, amount of each macronutrient chosen, plasma cortisol and Visual Analog Scale (VAS) hunger and satiety were measured. RESULTS: Fasted state was confirmed by high hunger (80 + or - 5 mm VAS). Breakfast energy intake (3 + or - 1 MJ) and liking were similar in all conditions. Wanting was lower postprandially (Delta = -0.3 items/category, P<0.01). Breakfast decreased hunger (-42 mm VAS, P<0.01). Postprandially, energy intake (-1.1 MJ), protein intake (-14.7 g) and carbohydrate intake (-32.7 g all P<0.05) were lower. Fat intake was not different (-7.3, P = 0.4). Putamen activity was not lower postprandially. Cortisol levels were increased in the stress condition (Area under the curve of cortisol: DeltaAUC = +2.2 x 10(4) nmol min(-1) l(-1), P<0.05). Satiety was lower after breakfast (-8 mm VAS, P<0.01). Postprandial energy intake, protein intake and carbohydrate intake were relatively higher compared with the rest condition, resulting from more choice for crispiness and fullness of taste (P<0.05). Brain activation was reduced in reward areas: amygdala, hippocampus and cingulate cortex (AUC = -13.33, -1.34, -2.56% blood oxygen level dependent (BOLD) s for choosing breakfast and AUC = -9.31, -1.25, -2.34%BOLD s<0.05 for choosing the second meal). Putamen activation was decreased postprandially (AUC = -1.2%BOLD s, P<0.05). CONCLUSION: Reward signaling and reward sensitivity were significantly lower under stress, coinciding with increased energy intake from food choice for more crispiness and fullness of taste. The changes in putamen activation may reflect specifically decreased reward prediction sensitivity.

The relationship between leptin, gonadotropic hormones, and body composition during puberty in a Dutch children cohort.

OBJECTIVE: To investigate the relationship between leptin concentrations, gonadotropic hormone concentrations, and body composition during puberty in a Dutch children cohort. DESIGN: In a cohort of 98 children, we determined anthropometric measurements, body composition, and concentrations of leptin, FSH, and LH. RESULTS: Sex differences were observed from Tanner stage 1 onwards in weight, body fat percentage, and leptin/fat mass ratio. In boys and girls, the relationship between leptin concentrations and FM was weaker at Tanner stage 2 (R(2)=0.33 and R(2)=0.39; P<0.001), 3 (R(2)=0.27 and R(2)=0.36; P<0.002), and 4 (R(2)=0.21 and R(2)=0.28; P<0.03) than at Tanner stage 1 (R(2)=0.51 and R(2)=0.67; P<0.001) and 5 (R(2)=0.46 and R(2)=0.78; P<0.01). In girls, a peak in leptin concentrations (8.5+/-6.0 ng/ml) preceded a peak in LH and FSH concentrations (15.1+/-3.5 and 5.0+/-4.5 IU/l). A lead/lag relationship was observed of leptin at Tanner stage 1 to LH and FSH at Tanner stage 2 (R(2)=0.12, P<0.05 and R(2)=0.18, P<0.05). In boys, there was no peak in leptin, LH, and FSH; additionally, leptin at Tanner stage 3 was related FSH at Tanner stage 4 (R(2)=0.17, P<0.04). CONCLUSION: In boys and girls during puberty, factors independent of fat mass become (transiently) more important in the regulation of plasma leptin concentrations. Moreover, in girls, leptin is suggested to act as a permissive factor for the onset of puberty, while, in boys, leptin has a different timing and possibly different function.