Obesity is a serious health problem because of its co-morbidities. The solution, implying weight loss and long-term weight maintenance, is conditional on: (i) sustained satiety despite negative energy balance, (ii) sustained basal energy expenditure despite BW loss due to (iii) a sparing of fat-free mass (FFM), being the main determinant of basal energy expenditure. Dietary protein has been shown to assist with meeting these conditions, since amino acids act on the relevant metabolic targets. This review deals with the effects of different protein diets during BW loss and BW maintenance thereafter. Potential risks of a high protein diet are dealt with. The required daily intake is 0·8-1·2 g/kg BW, implying sustaining the original absolute protein intake and carbohydrate and fat restriction during an energy-restricted diet. The intake of 1·2 g/kg BW is beneficial to body composition and improves blood pressure. A too low absolute protein content of the diet contributes to the risk of BW regain. The success of the so-called 'low carb' diet that is usually high in protein can be attributed to the relatively high-protein content per se and not to the relatively lower carbohydrate content. Metabolic syndrome parameters restore, mainly due to BW loss. With the indicated dosage, no kidney problems have been shown in healthy individuals. In conclusion, dietary protein contributes to the treatment of obesity and the metabolic syndrome, by acting on the relevant metabolic targets of satiety and energy expenditure in negative energy balance, thereby preventing a weight cycling effect.

Social jetlag represents the discrepancy between circadian and social clocks, which is measured as the difference in hours in midpoint of sleep between work days and free days. Previous studies have shown social jetlag to be associated with body mass index (BMI), glycated hemoglobin levels, heart rate, depressive symptoms, smoking, mental distress and alcohol use. The objective of our current study was to investigate, in a group of 145 apparently healthy participants (67 men and 78 women, aged 18-55 years, BMI 18-35 kg/m(2)), the prevalence of social jetlag and its association with adverse endocrine, behavioral and cardiovascular risk profiles as measured in vivo. participants with ≥2 h social jetlag had higher 5-h cortisol levels, slept less during the week, were more often physically inactive and had an increased resting heart rate, compared with participants who had ≤1 h social jetlag. We therefore concluded that social jetlag is associated with an adverse endocrine, behavioral and cardiovascular risk profile in apparently healthy participants. These adverse profiles put healthy participants at risk for development of metabolic diseases and mental disorders, including diabetes and depression, in the near future.

IntroductIonThe prevalence of overweight and obesity has increased worldwide to epidemic proportions (1). Obesity results from a chronic deregulation of energy balance, with energy intake exceeding energy expenditure, leading to the storage of the excessive energy as fat (2). This chronic deregulation of energy balance may be caused, in part, by stress, because in Western society high levels of ambient stress are abundantly present (3).Several human studies in laboratory settings indicate that, in adults, acute stress may influence energy intake (3-7). Acute stress alters food preference, eating frequency, and amount of energy intake (3,5). During stress, food preference is altered toward intake of sweet foods and foods with saturated fats, next to an increase in the intake frequency and amount of food intake (4,6,7). However, not all studies that investigated the relationship between energy intake and stress have yielded conclusive results (8,9). Stress may also result in a decrease in energy intake (8,9). These individual differences in response to stress may relate to eating behavior characteristics (4-7), as are determined using the Three Factor Eating Questionnaire (TFEQ). The TFEQ assesses three factors involved in eating behavior: dietary restraint, disinhibition, and hunger (10).An increase in energy intake during stress has been found in individuals with high scores on dietary restraint and/or disinhibition (4-7).A possible technique to study the effect of stress on food intake is the "eating in the absence of hunger" paradigm (11). Eating in the absence of hunger is the behavioral phenotype in which individuals eat when exposed to large portions of palatable foods in the absence of hunger. The paradigm has primarily been used in children (11) and was thought to resemble disinhibited eating patterns observed in adults (11). Therefore, the objective of our study was to investigate the effect of acute psychological stress on food intake, using the eating in the absence of hunger paradigm, in normal and overweight men and women, while taking dietary restraint and disinhibition into account. Methods and Procedures subjectsThe study was approved by the Medical Ethical Committee of the University Maastricht, and informed, written consent was obtained from all subjects. Healthy, medication-free, nonsmoking men (n = 65) and women (n = 65), 18-45 years and with a BMI of 20-35 kg/m 2 were recruited to complete all phases of this study. A medical history

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 ¼ 21.5 ± 2.2 kg/m 2 , age ¼ 24.3 ± 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±5 mm VAS). Breakfast energy intake (3±1 MJ) and liking were similar in all conditions. Wanting was lower postprandially (D ¼ À0.3 items/category, Po0.01). Breakfast decreased hunger (À42 mm VAS, Po0.01). Postprandially, energy intake (À1.1 MJ), protein intake (À14.7 g) and carbohydrate intake (À32.7 g all Po0.05) were lower. Fat intake was not different (À7.3, P ¼ 0.4). Putamen activity was not lower postprandially. Cortisol levels were increased in the stress condition (Area under the curve of cortisol: DAUC ¼ þ 2.2 Â 10 4 nmol min À1 l À1 , Po0.05). Satiety was lower after breakfast (À8 mm VAS, Po0.01). 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 (Po0.05). Brain activation was reduced in reward areas: amygdala, hippocampus and cingulate cortex (AUC ¼ À13.33, À1.34, À2.56% blood oxygen level dependent (BOLD) s for choosing breakfast and AUC ¼ À9.31, À1.25, À2.34%BOLD so0.05 for choosing the second meal). Putamen activation was decreased postprandially (AUC ¼ À1.2%BOLD s, Po0.05). 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.