Appetite sensations and satiety quotient : predictors of energy intake and weight loss

PURPOSE: The aim of this study was to further evaluate the validity and clinical meaningfulness of appetite sensations to predict overall energy intake as well as body weight loss. METHODS: Men (n=176) and women (n=139) involved in six weight loss studies were selected to participate in this study. Visual analogue scales were used to measure appetite sensations before and after a fixed test meal. Fasting appetite sensations, 1 h post-prandial area under the curve (AUC) and the satiety quotient (SQ) were used as predictors of energy intake and body weight loss. Two separate measures of energy intake were used: a buffet style ad libitum test lunch and a three-day self-report dietary record. RESULTS: One-hour post-prandial AUC for all appetite sensations represented the strongest predictors of ad libitum test lunch energy intake (p0.001). These associations were more consistent and pronounced for women than men. Only SQ for fullness was associated with ad libitum test lunch energy intake in women. Similar but weaker relationships were found between appetite sensations and the 3-day self-reported energy intake. Weight loss was associated with changes in appetite sensations (p0.01) and the best predictors of body weight loss were fasting desire to eat; hunger; and PFC (p0.01). CONCLUSIONS: These results demonstrate that appetite sensations are relatively useful predictors of spontaneous energy intake, free-living total energy intake and body weight loss. They also confirm that SQ for fullness predicts energy intake, at least in women.

Is it possible to dissociate ‘liking’ and ‘wanting’ for foods in humans? A novel experimental procedure

Berridge's model (e.g. [Berridge KC. Food reward: Brain substrates of wanting and liking. Neurosci Biobehav Rev 1996;20:1–25.; Berridge KC, Robinson T E. Parsing reward. Trends Neurosci 2003;26:507–513.; Berridge KC. Motivation concepts in behavioral neuroscience. Physiol Behav 2004;81:179–209]) outlines the brain substrates thought to mediate food reward with distinct ‘liking’ (hedonic/affective) and ‘wanting’ (incentive salience/motivation) components. Understanding the dual aspects of food reward could throw light on food choice, appetite control and overconsumption. The present study reports the development of a procedure to measure these processes in humans. A computer-based paradigm was used to assess ‘liking’ (through pleasantness ratings) and ‘wanting’ (through forced-choice photographic procedure) for foods that varied in fat (high or low) and taste (savoury or sweet). 60 participants completed the program when hungry and after an ad libitum meal. Findings indicate a state (hungry–satiated)-dependent, partial dissociation between ‘liking’ and ‘wanting’ for generic food categories. In the hungry state, participants ‘wanted’ high-fat savoury > low-fat savoury with no corresponding difference in ‘liking’, and ‘liked’ high-fat sweet > low-fat sweet but did not differ in ‘wanting’ for these foods. In the satiated state, participants ‘liked’, but did not ‘want’, high-fat savoury > low-fat savoury, and ‘wanted’ but did not ‘like’ low-fat sweet > high-fat sweet. More differences in ‘liking’ and ‘wanting’ were observed when hungry than when satiated. This procedure provides the first step in proof of concept that ‘liking’ and ‘wanting’ can be dissociated in humans and can be further developed for foods varying along different dimensions. Other experimental procedures may also be devised to separate ‘liking’ and ‘wanting’.

Overeating as a clue to weight gain: behavioural and physiological interactions in the control of food intake

It has been estimated that 25-50% of people in most affluent societies are either obese or overweight. These disorders are the result of an imbalance between calorific intake and energy expenditure over a prolonged time period. These types of disorders are among the most common health problems in industrialized societies. Addressing these issues and offering new strategies, this thorough new study draws together contributions from interdisciplinary and international group of specialists, includes recent research on genetic influences, features discussions of epidemiological studies and covers both biological and social aspects of obesity.

Cholecystokinin and leptin: their influence upon the eating behaviour and nutrient intake of dialysis patients

Background We have used serial visual analogue scores to demonstrate disturbances of the appetite profile in dialysis patients. This is potentially important as dialysis patients are prone to malnutrition yet have a lower nutrient intake than controls. Appetite disturbance may be influenced by accumulation of appetite inhibitors such as leptin and cholecystokinin (CCK) in dialysis patients. Methods Fasting blood samples were drawn from 43 controls, 50 haemodialysis (HD) and 39 peritoneal dialysis (PD) patients to measure leptin and CCK. Hunger and fullness scores were derived from profiles compiled using hourly visual analogue scores. Nutrient intake was derived from 3 day dietary records. Results Fasting CCK was elevated for PD (6.73 ± 4.42 ng/l vs control 4.99 ± 2.23 ng/l, P < 0.05; vs HD 4.43 ± 2.15 ng/l, P < 0.01). Fasting CCK correlated with the variability of the hunger (r = 0.426, P = 0.01) and fullness (r = 0.52, P = 0.002) scores for PD. There was a notable relationship with the increase in fullness after lunch for PD (r = 0.455, P = 0.006). When well nourished PD patients were compared with their malnourished counterparts, CCK was higher in the malnourished group (P = 0.004). Leptin levels were higher for the dialysis patients than controls (HD and PD, P < 0.001) with pronounced hyperleptinaemia evident in some PD patients. Control leptin levels demonstrated correlation with fullness scores (e.g. peak fullness, r = 0.45, P = 0.007) but the dialysis patients did not. PD nutrient intake (energy and protein intake, r = -0.56, P < 0.0001) demonstrated significant negative correlation with leptin. Conclusion Increased CCK levels appear to influence fullness and hunger perception in PD patients and thus may contribute to malnutrition. Leptin does not appear to affect perceived appetite in dialysis patients but it may influence nutrient intake in PD patients via central feeding centres.

Prandial subcutaneous injections of glucagon-like peptide-1 cause weight loss in obese human subjects

Recombinant glucagon-like peptide-1 (7–36)amide (rGLP-1) was recently shown to cause significant weight loss in type 2 diabetics when administered for 6 weeks as a continuous subcutaneous infusion. The mechanisms responsible for the weight loss are not clarified. In the present study, rGLP-1 was given for 5d by prandial subcutaneous injections (PSI) (76nmol 30min before meals, four times daily; a total of 302·4nmol/24h) or by continuous subcutaneous infusion (CSI) (12·7nmol/h; a total of 304·8nmol/24h). This was performed in nineteen healthy obese subjects (mean age 44·2 (sem 2·5) years; BMI 39·0 (sem 1·2)kg/m2) in a prospective randomised, double-blind, placebo-controlled, cross-over study. Compared with the placebo, rGLP-1 administered as PSI and by CSI generated a 15% reduction in mean food intake per meal (P=0·02) after 5d treatment. A weight loss of 0·55 (sem 0·2) kg (P<0·05) was registered after 5d with PSI of rGLP-1. Gastric emptying rate was reduced during both PSI (P<0·001) and CSI (P<0·05) treatment, but more rapidly and to a greater extent with PSI of rGLP-1. To conclude, a 5d treatment of rGLP-1 at high doses by PSI, but not CSI, promptly slowed gastric emptying as a probable mechanism of action of increased satiety, decreased hunger and, hence, reduced food intake with an ensuing weight loss.

Disturbed appetite and nutrient intake in peritoneal dialysis patients

OBJECTIVE Malnutrition is common among peritoneal dialysis (PD) patients. Reduced nutrient intake contributes to this. It has long been assumed that this reflects disturbed appetite. We set out to define the appetite profiles of a group of PD patients using a novel technique. DESIGN Prospective, cross-sectional comparison of PD patients versus controls. SETTING Teaching hospital dialysis unit. PATIENTS 39 PD patients and 42 healthy controls. INTERVENTION Visual analog ratings were recorded at hourly intervals to generate daily profiles for hunger and fullness. Summary statistics were generated to compare the groups. Food intake was measured using 3-day dietary records. MAIN OUTCOME MEASURES Hunger and fullness profiles. Derived hunger and fullness scores. RESULTS Controls demonstrated peaks of hunger before mealtimes, with fullness scores peaking after meals. The PD profiles had much reduced premeal hunger peaks. A postmeal reduction in hunger was evident, but the rest of the trace was flat. The PD fullness profile was also flatter than in the controls. Mean scores were similar despite the marked discrepancy in the profiles. The PD group had lower peak hunger and less diurnal variability in their hunger scores. They also demonstrated much less change in fullness rating around mealtimes, while the mean and peak fullness scores were little different. The reported nutrient intake was significantly lower for PD. CONCLUSION The data suggest that PD patients normalize their mean appetite perception at a lower level of nutrient intake than controls, suggesting that patient-reported appetite may be misleading in clinical practice. There is a loss of the usual daily variation for the PD group, which may contribute to their reduced food intake. The technique described here could be used to assess the impact of interventions upon the abnormal PD appetite profile.

The effect of graded levels of exercise on energy intake and balance in free-living men, consuming their normal diet

Objective: To assess the effect of graded increases in exercised-induced energy expenditure (EE) on appetite, energy intake (EI), total daily EE and body weight in men living in their normal environment and consuming their usual diets. Design: Within-subject, repeated measures design. Six men (mean (s.d.) age 31.0 (5.0) y; weight 75.1 (15.96) kg; height 1.79 (0.10) m; body mass index (BMI) 23.3(2.4) kg/m2), were each studied three times during a 9 day protocol, corresponding to prescriptions of no exercise, (control) (Nex; 0 MJ/day), medium exercise level (Mex; ~1.6 MJ/day) and high exercise level (Hex; ~3.2 MJ/day). On days 1-2 subjects were given a medium fat (MF) maintenance diet (1.6 ´ resting metabolic rate (RMR)). Measurements: On days 3-9 subjects self-recorded dietary intake using a food diary and self-weighed intake. EE was assessed by continual heart rate monitoring, using the modified FLEX method. Subjects' HR (heart rate) was individually calibrated against submaximal VO2 during incremental exercise tests at the beginning and end of each 9 day study period. Respiratory exchange was measured by indirect calorimetry. Subjects completed hourly hunger ratings during waking hours to record subjective sensations of hunger and appetite. Body weight was measured daily. Results: EE amounted to 11.7, 12.9 and 16.8 MJ/day (F(2,10)=48.26; P<0.001 (s.e.d=0.55)) on the Nex, Mex and Hex treatments, respectively. The corresponding values for EI were 11.6, 11.8 and 11.8 MJ/day (F(2,10)=0.10; P=0.910 (s.e.d.=0.10)), respectively. There were no treatment effects on hunger, appetite or body weight, but there was evidence of weight loss on the Hex treatment. Conclusion: Increasing EE did not lead to compensation of EI over 7 days. However, total daily EE tended to decrease over time on the two exercise treatments. Lean men appear able to tolerate a considerable negative energy balance, induced by exercise, over 7 days without invoking compensatory increases in EI.

Cross talk between physical activity and appetite control: does physical activity stimulate appetite?

Physical activity has the potential to modulate appetite control by improving the sensitivity of the physiological satiety signalling system, by adjusting macronutrient preferences or food choices and by altering the hedonic response to food. There is evidence for all these actions. Concerning the impact of physical activity on energy balance, there exists a belief that physical activity drives up hunger and increases food intake, thereby rendering it futile as a method of weight control.

Differences in post-prandial responses to fat and carbohydrate loads in habitual high and low fat consumers (phenotypes).

The present study investigated metabolic responses to fat and carbohydrate ingestion in lean male individuals consuming an habitual diet high or low in fat. Twelve high-fat phenotypes (HF) and twelve low-fat phenotypes (LF) participated in the study. Energy intake and macronutrient intake variables were assessed using a food frequency questionnaire. Resting (RMR) and postprandial metabolic rate and substrate oxidation (respiratory quotient; RQ) were measured by indirect calorimetry. HF had a significantly higher RMR and higher resting heart rate than LF. These variables remained higher in HF following the macronutrient challenge. In all subjects the carbohydrate load increased metabolic rate and heart rate significantly more than the fat load. Fat oxidation (indicated by a low RQ) was significantly higher in HF than in LF following the fat load; the ability to oxidise a high carbohydrate load did not differ between the groups. Lean male subjects consuming a diet high in fat were associated with increased energy expenditure at rest and a relatively higher fat oxidation in response to a high fat load; these observations may be partly responsible for maintaining energy balance on a high-fat (high-energy) diet. In contrast, a low consumer of fat is associated with relatively lower energy expenditure at rest and lower fat oxidation, which has implications for weight gain if high-fat foods or meals are periodically introduced to the diet.

Exercise, appetite control, and energy balance

Given the present worldwide epidemic of obesity, it is pertinent to ask how effective exercise could be in helping people to lose weight or to prevent weight gain. There is a widely held belief that exercise is futile for weight reduction because any energy expended in exercise is automatically compensated for by a corresponding increase in energy intake (EI). In other words, exercise elevates the intensity of hunger and drives food consumption. This “commonsense” view appears to originate in an energy-balance model of appetite control, which stipulates that energy expended will drive EI as a consequence of the regulation of energy balance. However, it is very clear that EI (food consumption or eating) is not just a biological matter. Eating does not occur solely to rectify some internal need state. Indeed, an examination of the relation between exercise and appetite control has shown a very weak coupling; most studies have demonstrated that food intake does not immediately rise after exercise, even after very high energy expenditure (EE).[1] The processes of exercise-induced EE and food consumption do not appear to be tightly linked. After exercise, there is only slow and partial compensation for the energy expended. Therefore, exercise can be very useful in helping to bring about weight loss and is even more important in preventing weight gain or weight regain. This editorial explores this issue.

No energy compensation at the meal following exercise indietary restrained and unrestrained women

The objective of this investigation was to compare the acute effects of exercise and diet manipulations on energy intake, between dietary restrained and unrestrained females. Comparisons of two studies using an identical 2 x 2 repeated-measures design (level of activity (rest or exercise) and lunch type (high-fat or low-fat)) including thirteen dietary unrestrained and twelve restrained females were performed. Energy expenditure during the rest session was estimated and the energy cost of exercise was measured by indirect calorimetry. Relative energy intake was calculated by subtracting the energy expenditure of the exercise session from the energy intake of the test meal. Post-meal hedonic ratings were completed after lunch. Energy intake and relative energy intake increased during high-fat conditions compared with the low-fat, independently of exercise (P < 0.001). There was a positive relationship between dietary restraint scores and energy intake or relative energy intake in the rest conditions only (r 0.54, P < 0.01). The decrease of relative energy intake between the rest and exercise conditions was higher in restrained than in unrestrained eaters (P < 0.01). These results confirm that a high-fat diet reversed the energy deficit due to exercise. There was no energy compensation in response to an acute bout of exercise during the following meal. In restrained eaters, exercise was more effective in creating an energy deficit than in unrestrained eaters. Exercise may help restrained eaters to maintain control over appetite.

Selective effects of acute exercise and breakfast interventions on mood and motivation to eat

The effects of exercise and breakfast manipulations on mood and motivation to eat were assessed in 11 healthy females who were regular exercisers and habitual breakfast eaters. The study involved a two by two repeated-measures design, with exercise (or no exercise) and a high-energy breakfast (or low-energy breakfast) as the repeated measures. The exercise or no-exercise session (0800 h) was followed by consumption of the low- or high-energy breakfast (0900 h). An ad libitum lunch test meal was provided 4 hours after the beginning of the exercise session (1200 h). Mood and motivation to eat were continuously tracked from 0800 until 1700 h by an electronic appetite ratings system (EARS). In general, morning subjective mood states (e.g., contentment) were significantly lower in the low-energy breakfast condition, but exercise reversed this effect. Exercise also significantly decreased feelings of lethargy, independent of the breakfast condition. Desire-to-eat and fullness ratings were significantly increased in the low-energy breakfast and high-energy breakfast conditions, respectively. Impairments of mood disappeared in the afternoon after consumption of an ad libitum lunch. In these healthy young adults, the condition inducing the largest energy deficit (exercise and low-energy breakfast) was not associated with the lowest mental states.

Children, Obesity and Exercise: Prevention, Treatment and Management of Childhood and Adolescent Obesity

Throughout the developed world there is an increasing prevalence of childhood obesity. Because of this increase, and awareness of the risks to long term health that childhood obesity presents, the phenomena is now described by many as a global epidemic. Children, Obesity and Exercise provides sport, exercise and medicine students and professionals with an accessible and practical guide to understanding and managing childhood and adolescent obesity. It covers: overweight, obesity and body composition; physical activity, growth and development; psycho-social aspects of childhood obesity; physical activity behaviours; eating behaviours; measuring childrens behaviour; interventions for prevention and management of childhood obesity. Children, Obesity and Exercise addresses the need for authoritative advice and innovative approaches to the prevention and management of this chronic problem.

Physical activity and regulation of food intake: current evidence

Objective: The evidence was reviewed on how physical activity could influence the regulation of food intake by either adjusting the sensitivity of appetite control mechanisms or by generating an energy deficit that could adjust the drive to eat. Design: Interventionist and correlational studies that had a significant influence on the relationship between physical activity and food intake were reviewed. Interventionist studies involve a deliberate imposition of physical activity with subsequent monitoring of the eating response. Correlational studies make use of naturally occurring differences in the levels of physical activity (between and within subjects) with simultaneous assessment of energy expenditure and intake. Subjects: Studies using lean, overweight, and obese men and women were included. Results: Only 19% of interventionist studies report an increase in energy intake after exercise; 65% show no change and 16% show a decrease in appetite. Of the correlational studies, approximately half show no relationship between energy expenditure and intake. These data indicate a rather loose coupling between energy expenditure and intake. A common sense view is that exercise is futile as a form of weight control because the energy deficit drives a compensatory increase in food intake. However, evidence shows that this is not generally true. One positive aspect of this is that raising energy expenditure through physical activity (or maintaining an active life style) can cause weight loss or prevent weight gain. A negative feature is that when people become sedentary after a period of high activity, food intake is not “down-regulated” to balance a reduced energy expenditure. Conclusion: Evidence suggests that a high level of physical activity can aid weight control either by improving the matching of food intake to energy expenditure (regulation) or by raising expenditure so that it is difficult for people to eat themselves into a positive energy balance.