The observation that 64% of English adults are overweight or obese despite a rising prevalence in weight-loss attempts suggests our understanding of energy balance is fundamentally flawed. Weight-loss is induced through a negative energy balance; however, we typically view weight change as a static function, in that energy intake and energy expenditure are independent variables, resulting in a fixed rate of weight-loss assuming a constant energy deficit. Such static modelling provides the basis for the clinical assumption that a 14644 kJ (3500 kcal) deficit translates to a 1 lb weight-loss. However, this ‘3500 kcal (14644 kJ) rule’ is consistently shown to significantly overestimate weight-loss. Static modelling disregards obligatory changes in energy expenditure associated with the loss of metabolically active tissue, i.e. skeletal muscle. Additionally, it disregards the presence of adaptive thermogenesis, the underfeeding-associated fall in resting energy expenditure beyond that caused by loss of fat-free mass. This metabolic manipulation of energy expenditure is observed from the onset of energy restriction to maintain weight at a genetically pre-determined set point. As a result, the observed magnitude of weight-loss is disproportionally less, followed by earlier weight plateau, despite strict compliance to a dietary intervention. By simulating dynamic changes in energy expenditure associated with underfeeding, mathematical modelling may provide a more accurate method of weight-loss prediction. However, accuracy at an individual level is limited due to difficulty estimating energy requirements, physical activity and dietary intake in free-living individuals. In the present paper, we aim to outline the contribution of dynamic changes in energy expenditure to weight-loss resistance and weight plateau.

The purpose of the present study was to compare next-morning responses of RMR and appetite to pre-sleep consumption of casein protein (CP) in pre- and postmenopausal women. The study was a randomised, crossover, double-blind, placebo-controlled trial. Seven sedentary premenopausal (age: 19·9 (sd 1·2) years; BMI: 23·1 (sd 2·6) kg/m2) and seven sedentary postmenopausal (age: 56·4 (sd 4·9) years; BMI: 26·3 (sd 3·5) kg/m2) women participated. During visit one, anthropometrics and body composition were measured. Following visit one, subjects consumed either CP (25 g) or placebo (PL) ≥2 h after their last meal and ≤30 min prior to sleep on the night before visits two and three. Visits two and three occurred ≥1 week after visit one and were 48 h apart. During visits two and three, RMR (VO2), RER and appetite were measured via indirect calorimetry and visual analogue scale, respectively. Anthropometrics and body composition were analysed by one-way ANOVA. RMR and measures of appetite were analysed using a 2 × 2 (menopause status × CP/PL) repeated-measures ANOVA. Significance was accepted at P ≤ 0·05. RMR was significantly lower in postmenopausal compared with premenopausal women under both conditions (P = 0·003). When consumed pre-sleep CP did not alter RMR, RER or appetite compared with PL when assessed next morning in pre- and postmenopausal women. These data contribute to growing evidence that pre-sleep consumption of protein is not harmful to next-morning metabolism or appetite. In addition, these data demonstrate that menopause may not alter next-morning RMR, RER or appetite after pre-sleep consumption of CP.

Dietary fatty acid (FA) composition may influence metabolism, possibly affecting weight management. The purpose of this study was to compare the effects of a 5-d diet rich in PUFA v. MUFA. A total of fifteen normal-weight men participated in a randomised cross-over design with two feeding trials (3 d lead-in diet, pre-diet visit, 5-d PUFA- or MUFA-rich diet, post-diet visit). The 5-d diets (50 % fat) were rich in either PUFA (25 % of energy) or MUFA (25 % of energy). At pre- and post-diet visits, subjects consumed breakfast and lunch test meals, rich in the FA for that 5-d diet. Indirect calorimetry was used for 4 h after each meal. There were no treatment differences in fasting metabolism acutely or after the 5-d diet. For acute meal responses before diet, RER was higher for PUFA v. MUFA (0·86 (sem 0·01) v. 0·84 (sem 0·01), P<0·05), whereas diet-induced thermogenesis (DIT) was lower for PUFA v. MUFA (18·91 (SEM 1·46) v. 21·46 (SEM 1·34) kJ, P<0·05). After the 5-d diets, the change in RER was different for PUFA v. MUFA (−0·02 (sem 0·01) v. 0·00 (sem 0·01), P<0·05). Similarly, the change in fat oxidation was greater for PUFA v. MUFA (0·18 (sem 0·07) v. 0·04 (sem 0·06) g, P<0·05). In conclusion, acutely, a MUFA-rich meal results in lower RER and greater DIT. However, after a 5-d high-fat diet, the change in metabolic responses was greater in the PUFA diet, showing the metabolic adaptability of a PUFA-rich diet.

The Bath Breakfast Project is a series of randomised controlled trials exploring the effects of extended morning fasting on energy balance and health. These trials were categorically not designed to answer whether or not breakfast is the most important meal of the day. However, this review will philosophise about the meaning of that question and about what questions we should be asking to better understand the effects of breakfast, before summarising how individual components of energy balance and health respond to breakfast v. fasting in lean and obese adults. Current evidence does not support a clear effect of regularly consuming or skipping breakfast on body mass/composition, metabolic rate or diet-induced thermogenesis. Findings regarding energy intake are variable, although the balance of evidence indicates some degree of compensatory feeding later in the day such that overall energy intake is either unaffected or slightly lower when breakfast is omitted from the diet. However, even if net energy intake is reduced, extended morning fasting may not result in expected weight loss due to compensatory adjustments in physical activity thermogenesis. Specifically, we report that both lean and obese adults expended less energy during the morning when remaining in the fasted state than when consuming a prescribed breakfast. Further research is required to examine whether particular health markers may be responsive to breakfast-induced responses of individual components of energy balance irrespective of their net effect on energy balance and therefore body mass.

The Deltatrac™ II Metabolic Monitor (Datex-Ohmeda Inc.) is considered the standard reference machine in indirect calorimetry; however, it is no longer commercially available thus there is a need for new machines. The gas exchange measurement (GEM; GEM Nutrition Ltd) and the ECAL (Health Professional Solutions) are alternative measuring systems. The aim of this study was to compare the ECAL and GEM with Deltatrac for measures of RMR and the GEM to the Deltatrac for measures of diet-induced thermogenesis (DIT). Twenty healthy participants were tested on test day 1 (T1) and test day 2 (T2). RMR was measured in a randomised order for 30 min on the Deltatrac, the GEM and the ECAL. Following this, a 1553 kJ meal was consumed and DIT was measured on the Deltatrac and the GEM in alternating 15 min intervals for 4 h. The GEM reported consistently higher values than the Deltatrac for VO2, VCO2, RMR and fat oxidation (P < 0·005). The ECAL was significantly higher than the Deltatrac for measures of VO2, RMR, carbohydrate oxidation (T2) and respiratory quotient and fat oxidation (T1, T2) (P < 0·05). There were no significant differences within repeated RMR measures on the ECAL, the GEM or the Deltatrac. DIT measures were consistently higher on the GEM (T1) (P < 0·005); however, there were no significant differences between repeated measures. The findings suggest that while the GEM and the ECAL were not accurate alternatives to the Deltatrac, they may be reliable for repeated measures.

Barley β-glucan (BG) has been shown to reduce glycaemic response (GR) in some studies. It is hypothesised that this reduction may be a function of its physical properties that delay gastric emptying (GE). The effect of these changes in GR and GE on diet-induced thermogenesis (DIT) is not known. The aim of the present study was to assess the effect of BG of different molecular weights and purities on GR, GE and DIT in healthy subjects. This was a randomised, single-blind, repeated-measures design where fifteen healthy subjects were tested on three occasions following an overnight fast. Following the baseline measurements, the volunteers were fed a soup containing high-molecular-weight BG (HBG), a soup containing low-molecular-weight BG (LBG) or a control soup with no BG (CHO). Following the consumption of the breakfast, GR was measured using finger-prick blood samples, GE was determined using the 13C-octanoic acid breath test and DIT was measured using indirect calorimetry. There was a difference in GR AUC between the soups after 60 min but not after 120 min. The CHO and LBG meals had a greater GR than the HBG meal. There were differences in all GE time points, with the HBG meal having the slowest GE time. There was a correlation between the GR and the initial GE times. There were differences in total DIT between the three test meals with the HBG meal having the lowest DIT. The present study indicates that HBG has the ability to delay GE due to increased viscosity, resulting in a decreased GR and DIT.

Chilli peppers have been shown to enhance diet-induced thermogenesis (DIT) and reduce energy intake (EI) in some studies, but there are few data on other pungent spices. The primary aim of the present study was to test the acute effects of black pepper (pepper), ginger, horseradish and mustard in a meal on 4 h postprandial DIT. The secondary aim was to examine the effects on subjective appetite measures, ad libitum EI and energy balance. In a five-way placebo-controlled, single-blind, cross-over trial, twenty-two young (age 24·9 (sd 4·6) years), normal-weight (BMI 21·8 (sd 2·1) kg/m2) males were randomly assigned to receive a brunch meal with either pepper (1·3 g), ginger (20 g), horseradish (8·3 g), mustard (21 g) or no spices (placebo). The amounts of spices were chosen from pre-testing to make the meal spicy but palatable. No significant treatment effects were observed on DIT, but mustard produced DIT, which tended to be larger than that of placebo (14 %, 59 (se 3) v. 52 (se 2) kJ/h, respectively, P= 0·08). No other spice induced thermogenic effects approaching statistical significance. Subjective measures of appetite (P>0·85), ad libitum EI (P= 0·63) and energy balance (P= 0·67) also did not differ between the treatments. Finally, horseradish decreased heart rate (P= 0·048) and increased diastolic blood pressure (P= 0·049) compared with placebo. In conclusion, no reliable treatment effects on appetite, EI or energy balance were observed, although mustard tended to be thermogenic at this dose. Further studies should explore the possible strength and mechanisms of the potential thermogenic effect of mustard actives, and potential enhancement by, for example, combinations with other food components.

The sympathetic nervous system is involved in the control of energy metabolism and expenditure. Diet-induced thermogenesis is mediated partly by the ß-adrenergic component of this system. The aim of the present study was to investigate the role of genetic variation in the ß2-adrenoceptor in diet-induced thermogenesis. Data from twenty-four subjects (fourteen men and ten women; BMI 26·7(sem 0·8) kg/m2; age 45·2(sem1·4) years) with different polymorphisms of the ß2-adrenoceptor at codon 16 (Gly16Gly, Gly16Arg or Arg16Arg) were recruited for this study. Subjects were given a high-carbohydrate liquid meal, and the energy expenditure, respiratory exchange ratio, and plasma concentrations of NEFA, glycerol, glucose, insulin and catecholamines were measured before and over 4 h after the meal. The AUC of energy expenditure (diet-induced thermogenesis) was not significantly different between polymorphism groups, nor was the response of any of the other measured variables to the meal. In a multiple regression model, the only variable that explained a significant proportion (32 %) of the variation in diet-induced thermogenesis was the increase in plasma adrenaline in response to the meal (P<0·05). The ß2-adrenoceptor codon16 polymorphisms did not contribute significantly. In conclusion, an independent contribution of the codon 16 polymorphism of the ß2-adrenoceptor gene to the variation in thermogenic response to a high-carbohydrate meal could not be demonstrated. The interindividual variation in thermogenic response to the meal was correlated with variations in the plasma adrenaline response to the meal.

Patients with Parkinson's disease (PD) often lose weight, but after subthalamic nucleus deep brain stimulation (STN-DBS), they gain weight. We compared daily energy intake (DEI), resting energy expenditure (REE) and substrate oxidation rates (measured by indirect calorimetry) in nineteen STN-DBS-treated patients (Group S), thirteen others on pharmacologic treatment by levodopa (Group L) and eight control subjects. We also determined the acute effects of STN-DBS and levodopa on REE and substrate oxidation rates. STN-DBS treated patients gained 9·7 (sem 7·1) kg after surgery, whereas patients on pharmacologic treatment lost 3·8 (sem 10·0) kg since diagnosis. In STN-DBS-treated patients, REE (−16·5 %; P<0·001), lipid oxidation (−27 %; P<0·05) and protein oxidation (−46 %; P<0·05) were decreased, whereas glucose oxidation was elevated (+81 %; P<0·05) as compared to patients on pharmacologic treatment. Levodopa acutely reduced REE (−8·3 %; P<0·05) and glucose oxidation (−37 %; P<0·01) with a slight hyperglycaemic effect (after levodopa challenge: 5·6 (sem 0·8) v. before levodopa challenge: 5·3 (sem 0·6) mmol/l; P<0·01). Switching ‘on’ STN-DBS acutely reduced REE (−17·5 %; P<0·01) and lipid oxidation (−24 %; P<0·001) 30 min after starting stimulation. Fasting glycaemia was slightly but significantly reduced (5·4 (sem 1·4) v. 5·5 (sem 1·3) mmol/l; P<0·01). After STN-DBS, the normalization of REE and the reduction in lipid and protein oxidation contribute to the restoration of weight. As levodopa decreases glucose oxidation, the reduction in daily dose of levodopa in STN-DBS-treated patients helps prevent the effect of weight gain on glycaemia.

There is evidence that food consistency may influence postprandial physiological responses. Recently we found that homogenization of a vegetable-rich meal significantly delayed the gastric emptying rate and was more satiating than the same meal in solid–liquid form. In this present study we investigated whether homogenization also influences endocrine and metabolic responses to the meal. Eight healthy men, aged 21–28 (mean 24·5) years, were given the meal (cooked vegetables 250 g, cheese 35 g, croutons 50 g and olive oil 25 g, with water 300 ml; total energy 2·6 MJ) in both solid–liquid (SM) and homogenized (HM) form, in random order, at 1-week intervals. Variables assayed were plasma glucose, insulin and glucose-dependent insulinotropic peptide (GIP) levels for 2 h and diet-induced thermogenesis (DIT) for 5 h. Plasma glucose pattern was similar after both meals. However, HM induced significantly greater insulin, GIP and DIT responses than SM. Mean integrated areas under the curves (AUC) were 1·7 (SEM 0·38) V. 1·2 (sem 0·33) U/l per 120 min (P = 0·005) for insulin, 19·9 (sem 2·44) v. 16 (sem 1·92) nmol/l per 120 min (P = 0·042) for GIP, and 237·7 (sem 16·32) v. 126·4 (sem 23·48) kJ/300 min (P = 0·0029) for DIT respectively. Differences between GIP-AUC after HM and SM correlated significantly with differences between insulin-AUC after HM and SM (r2 0·62, P = 0·021). These findings demonstrate that homogenization of a meal results in a coordinated series of changes of physiological gastroentero–pancreatic functions and confirm that the physical state of the meal plays an important role in modulating endocrine and metabolic responses to food.

The effects of dietary red pepper added to high-fat (HF) and high-carbohydrate (HC) meals on energy metabolism were examined in thirteen Japanese female subjects. After ingesting a standardized dinner on the previous evening, the subjects took an experimental breakfast (1883 kJ) under the following four conditions: HF meal, HF and red-pepper (10 g) meal, HC meal, or HC and red-pepper meal. Palatability of the experimental meals was measured immediately after the meals. Expired air was collected before and for 210 min after the meal to determine energy expenditure and macronutrient oxidation. Diet-induced thermogenesis was significantly higher after the HC meals than after the HF meals. Lipid oxidation was significantly lower and carbohydrate oxidation was significantly higher after the HC meals than after the HF meals. Addition of red pepper to the experimental meals significantly increased diet-induced thermogenesis and lipid oxidation, particularly after the HF meal. On the other hand, carbohydrate oxidation was significantly decreased by the addition of red pepper to the experimental meals. Addition of red pepper to the HC meal increased the perceived oiliness of the meal to the same level as that of the HF meals. These results indicate that red pepper increases diet-induced thermogenesis and lipid oxidation. This increase in lipid oxidation is mainly observed when foods have a HF content whereas the increase in the perceived oiliness of the meal was found under the HC meal conditions.

The possible involvement of thyroid hormones in avian diet-induced thermogenesis (DIT) was investigated in two lines of cockerels divergently selected for high (R-) or low (R+) food efficiency. For a given body weight, R+ cockerels exhibited a higher food intake than R- cockerels (+49 to +76%) and increased DIT (+25%). Plasma thyroxine (T4) levels did not differ between lines whatever the feeding status of the birds. Plasma 3,5,3'-triiodothyronine (T3) level was lower in fasted R+ than in fasted R- cockerels while the opposite was observed after a meal. Iopanic acid injections reduced both plasma T3 concentrations and heat production to the same levels in both lines. Hepatic 5'-deiodinase activity measured with an exogenous sulfhydryl group (dithiothreitol) did not differ between lines, but when the sulfhydryl group was omitted, the activity was higher in R+ than in R- birds (90 ν. 42 pmol T3/min per liver). T3-binding capacity of isolated hepatic nuclei was higher (+76%) in R+ than in R- birds. Long-term or acute pair-feeding of R+ cockerels to the level of R- controls did not alter these results. The present results suggest that T3, mainly originating from peripheral conversion of T4 to T3, is involved in DIT in the R+ line. Availability of endogenous sulfhydryl groups appears to play an important part in the modulation of hepatic deiodinase activity. The higher concentration of nuclear T3 receptors may further increase the effects of the hormone, suggesting a major role of thyroid hormones associated with catecholamines in the stimulation of avian DIT. The underlying thermogenic mechanisms remain to be elucidated.

The present study describes the effect of replacement of digestible starch by resistant starch (RS) on diet-induced thermogenesis (DIT), postprandial glucose and insulin responses, and colonic fermentation. Ten healthy males consumed three test meals, consisting of diluted, artificially-sweetened fruit syrup and either 50 g raw potato starch (550 g RS/kg), or 50 g pregelatinized potato starch (0 g RS/kg) or 30 g pregelatinized potato starch plus 20 g lactulose (670 g indigestible disaccharide/kg). The meals were served in the morning after an overnight fast. Each volunteer consumed each meal twice on six separate days in random order. Metabolic rate was measured by indirect calorimetry in the fasting state for 15 min and postprandially for 5 h. Shortly before and hourly up to 7 h after consumption of the test meal, end-expiratory breath samples were obtained for H2 and CH4 analysis. Shortly before the meal and 30, 60, 180, and 300 min postprandiaily, blood samples were taken for glucose and insulin analyses. Postprandial increases in glucose and insulin levels were proportional to the amount of digestible carbohydrate in the meal. Breath H2 and CH4 concentrations indicated that the pregelatinized starch was not fermented and that lactulose was fermented rapidly. Fermentation of the raw starch started only 6 to 7 h after consumption, resulting in a rise in breath H2 but not in CH4. The replacement of 27 g digestible starch by RS in a single meal lowered DIT by on average 90 kJ/5 h, as could also be calculated by assuming that RS does not contribute to DIT. The ingestion of lactulose resulted in a substantial rise in DIT which was most probably caused by its fermentation.

The pattern of food intake can affect the regulation of body weight and lipogenesis. We studied the effect of meal frequency on human energy expenditure (EE) and its components. During 1 week ten male adults (age 25–61 years, body mass index 20·7–30·4 kg/m2) were fed to energy balance at two meals/d (gorging pattern) and during another week at seven meals/d (nibbling pattern). For the first 6 d of each week the food was provided at home, followed by a 36 h stay in a respiration chamber. O2 consumption and CO2 production (and hence EE) were calculated over 24 h. EE in free-living conditions was measured over the 2 weeks with doubly-labelled water (average daily metabolic rate, ADMR). The three major components of ADMR are basal metabolic rate (BMR), diet-induced thermogenesis (DIT) and EE for physical activity (ACT). There was no significant effect of meal frequency on 24 h EE or ADMR. Furthermore, BMR and ACT did not differ between the two patterns. DIT was significantly elevated in the gorging pattern, but this effect was neutralized by correction for the relevant time interval. With the method used for determination of DIT no significant effect of meal frequency on the contribution of DIT to ADMR could be demonstrated.

The impact of alcohol (ethanol) on resting energy expenditure of male non-obese volunteers was determined in two studies. In the first study the thermic effect of alcohol on resting metabolic rate (RMR) was assessed in ten male non-obese volunteers. In the second study the impact of alcohol on diet-induced thermogenesis (DIT) was determined in twelve male non-obese volunteers. Energy expenditure was measured with a ventilated-hood system. RMR was measured for 60 min with the subjects in a fasting state. In the first study subjects received in random order 20 g alcohol in concentrations of 75, 180 and 300 ml/I water respectively. After measurement of the RMR the thermic effect of alcohol was measured for 90 min. In the second study volunteers received in random order and in duplicate either a meal of food (2 MJ) plus an alcoholic aperitif (20 g alcohol in a 180 ml/1 solution) or an isoenergetic meal of food alone (2.55 MJ) plus a placebo aperitif containing no alcohol. DIT was measured for 240 min. Alcohol induced a significant thermic effect, which varied between 0.22 and 0.30 kJ/min. No systematic difference in DIT was observed among the different concentrations. DIT was not significantly affected by the ingestion of alcohol. Total DIT was 219 (SE 14) kJ for the alcohol treatment and 185 (SE 20) kJ for the control treatment. The results do not support the suggestion that alcohol is less efficiently used as an energy source in comparison with, for example, fats and carbohydrates.