Circulating leptin moderates the effect of stress on snack intake independent of body mass

Prior studies have demonstrated influences of leptin on hunger and satiety, the processing of food reward, and taste and palatability perception. This pilot study tested whether leptin accounts for variability in stress-induced changes in snack intake, and explored potential mechanisms underlying this effect. Thirty-four normal weight and class I obese women were exposed to a 30-minute mental stressor and a non-stressful control task in counterbalanced order on consecutive days. Higher serum leptin concentrations predicted decreases in snack intake following the stressor relative to the control condition. Leptin was not a significant predictor of overall hunger or stress-induced changes in hunger, but was associated with greater perceived palatability of one of the four snacks. Overall, findings suggest that leptin may moderate the effect of stress on energy intake through non-homeostatic mechanisms.     

Impact of ketosis on appetite regulation—a review

To reduce the health burden of obesity, it is important to identify safe and practical treatments that are effective for weight loss while concurrently preventing weight regain. Diet-induced weight loss is usually followed by a concomitant increase in ghrelin secretion and feelings of hunger, which may compromise weight loss goals and increase the risk of weight regain. The aim of this review is to describe the status of knowledge regarding the impact of ketosis, induced by diet or exogenous ketones (ketone esters), on appetite and the potential mechanisms involved. Ketogenic diets (KDs) have been shown to prevent an increase in ghrelin secretion, otherwise seen with weight loss, as well as to reduce hunger and/or prevent hunger. However, the exact threshold of ketosis needed to induce appetite suppression, as well as the exact mechanisms that mediate such an effect, has yet to be elucidated. Use of exogenous ketones may provide an alternative to KDs, which have poor long-term adherence due to their restrictive nature. Ketone esters have been shown to have concentration-dependent effects on food intake and body weight in rodent models, with effects becoming apparent when 30% of total dietary energy comes from ketone esters (threshold effect). In humans, acute consumption of a ketone ester drink reduced feelings of hunger and increased satiety compared to a dextrose drink. With the emerging widespread acceptance of KDs and exogenous ketones in mainstream media and the diet culture, it is important to fully understand their role on appetite control and weight management and the potential mechanisms mediating this role.     

Gastric pacing for morbid obesity: plasma levels of gastrointestinal peptides and leptin

OBJECTIVE: A gastric pacemaker has been developed to treat morbid obesity. Patients experience increased satiety, the ability to reduce food intake, and a resultant weight loss. However, the mechanism behind the changed eating behavior in paced patients is still under investigation. RESEARCH METHODS AND PROCEDURES: This study was performed on 11 morbidly obese patients (mean BMI, 46.0 kg/m2) treated with gastric pacing. The peripheral blood levels of satiety signals of cholecystokinin (CCK), somatostatin, glucagon-like peptide-1 (GLP-1), and leptin were studied 1 month before gastric pacer implantation, 1 month after implantation, and 6 months after activation of electrical stimulation. Blood samples were drawn 12 hours after fasting and in response to a hypocaloric meal (270 kcal). Patients were followed monthly for vital signs and weight level. RESULTS: Gastric pacing resulted in a significant weight loss of a mean of 10.4 kg (4.4 BMI units). No negative side effects or complications were observed during the treatment. After activation of the pacemaker, meal-related response of CCK and somatostatin and basal levels of GLP-1 and leptin were significantly reduced (p < 0.05) compared with the tests before gastric pacing. The weight loss correlated significantly with a decrease of leptin levels (R = 0.79, p < 0.01). DISCUSSION: Gastric pacing is a novel and promising therapy for morbid obesity. Activation of the gastric pacer was associated with a decrease in plasma levels of CCK, somatostatin, GLP-1, and leptin. More studies are necessary to elucidate the correlations between satiety, weight loss, and digestive neuro-hormone changes.     

Staggered meal consumption facilitates appetite control without affecting postprandial energy intake

Meal pattern may influence hormone and appetite dynamics and food intake. The objective of the study was to determine the effects of staggered compared with nonstaggered meal consumption on hormone and appetite dynamics, food reward (i.e. "liking," "wanting"), and subsequent energy intake. The study was conducted in a randomized cross-over design. Participants (n = 38, age = 24 ± 6 y, BMI = 25.0 ± 3.1 kg/m(2)) came to the university twice for consumption of a 4-course lunch (40% of the daily energy requirements) in 0.5 h (nonstaggered) or in 2 h with 3 within-meal pauses (staggered) followed by ad libitum food intake. Throughout the test sessions, glucagon-like peptide (GLP)-1, peptide tyrosine-tyrosine (PYY(3-36)), ghrelin, appetite, and food reward were measured. In the staggered compared with nonstaggered meal condition, peak values of GLP-1, PYY(3-36), and satiety were lower and time to peak values were higher (P < 0.02); the nadir value of hunger was higher, and time to nadir values of ghrelin and hunger were higher (P < 0.0001). Prior to ad libitum food intake, GLP-1 concentrations and satiety ratings were greater, ghrelin concentrations and hunger ratings were smaller, and food "wanting" was less in the staggered compared with nonstaggered meal condition (P < 0.05). However, this did not affect ad libitum energy intake (1.7 ± 0.3 vs. 1.9 ± 0.2 MJ). In conclusion, staggered compared with nonstaggered meal consumption induces less pronounced hormone and appetite dynamics. Moreover, it results in higher final GLP-1 concentrations and satiety ratings, lower ghrelin concentrations and hunger ratings, and lower food "wanting" prior to ad libitum food intake. However, this was not translated into lower energy intake.     

Gastrointestinal hormones: the regulation of appetite and the anorexia of ageing

Loss of appetite is frequently observed during ageing, termed the ‘anorexia of ageing’. Ageing is associated with the inability to appropriately increase food intake after under‐eating in the short‐ and long‐term. Older people also report lower feelings of hunger and increased feelings of satiety and fullness. Gastrointestinal peptide hormones are a major part of the appetite regulatory system and are released in response to nutritional stimuli. They can be classified as: anorexigenic (satiety) [e.g. peptide tyrosine tyrosine (PYY), glucagon‐like peptide‐1, pancreatic polypeptide, oxyntomodulin and cholecystokinin (CCK)] or orexigenic (hunger) (e.g. ghrelin). Although the control of appetite is not fully understood, it is clear that these hormones play an important role, and may influence the development and treatment of obesity and under‐nutrition. The literature shows a consistent finding that there is a loss of appetite in those aged over 65 years, although how this loss is mediated is not yet clear. Some evidence suggests that with advancing age there is an increase in satiety hormones, such as CCK and PYY, and a decrease in the hunger hormone, ghrelin. However, not all studies agree, emphasising the need for more in‐depth research to clarify age‐related changes. This knowledge will enable us to develop therapies to help prevent under‐nutrition during ageing. This review explores how age influences gastrointestinal appetite hormones in humans, as well as how this may contribute to the development of age‐related malnutrition.     

Lack of association between plasma leptin levels and appetite in children with iron deficiency.

A negative correlation between leptin and appetite or food intake has been shown in healthy individuals. However, the role of leptin in clinical conditions characterized by anorexia has not been established. One of the well-known clinical features of iron-deficiency anemia is poor appetite. We examined the changes in plasma leptin levels in relation to expected improvement in appetite with iron treatment in children with iron deficiency. In 24 infants and small children (mean age +/- standard deviation = 19.6 +/- 7.7 months) with iron deficiency, we studied plasma leptin levels before and after iron therapy. After 15.0 +/- 2.4 wk of iron treatment, serum ferritin levels improved significantly, with accompanying increases in their subjective appetite scores and food intakes. However, as their mean age and plasma leptin levels adjusted their body mass indexes were unchanged. Serum ferritin correlated significantly with appetite score (r = 0.680, P < 0.001) and food intake (r = 0.480, P < 0.01). Leptin correlated only with body mass index (r = 0.405, P < 0.01). Lack of association between plasma leptin levels and degree of appetite in iron-deficient children treated with iron suggests a leptin-independent mechanism for the observed increase in appetite.     

Effects of a healthy meal course on spontaneous energy intake, satiety and palatability

Many food components can influence satiety or energy intake. Combined together, these food components could represent an interesting dietary strategy in the prevention and treatment of obesity. The aims of this study were: 1) to determine the effect of a functional food in the form of a healthy meal course on subsequent energy intake and satiety; 2) to verify if it is possible to maintain palatability while preserving the satiating effects of the test meal. Thirteen subjects were invited to eat two lunch sessions: healthy and control meal courses (2090 kJ/meal). Anthropometric and ad libitum food intake measurements, and visual analogue scales (VAS) were performed during the two lunch sessions. The healthy main course acutely decreased energy intake during the rest of the meal (-744 kJ, P相似文献   

Brain somatic cross-talk: ghrelin, leptin and ultimate challengers of obesity

Energy balance is largely regulated by the central nervous system (CNS), which senses metabolic status from a wide range of humoral and neural signals, and controls energy intake. Accumulating evidence supports the model that stimulation of leptin- and ghrelin-responsive pathways, including the central melanocortin system, in the hypothalamus, contributes to the maintenance of body weight. Ghrelin is the brain-gut peptide with growth hormone-releasing and appetite-inducing activities. It is mainly secreted from the stomach and acts as an afferent signal to the hypothalamus and hindbrain. Leptin, the adipocyte hormone, is believed to tonically act as an afferent signal from adipose tissue to the brain, in particular hypothalamus, as a part of negative feedback loop regulating the size of energy stores and energy balance. Dysregulation of these pathways is a marker of changes in energy balance. Ghrelin is negatively correlated with weight and obese subjects have lower ghrelin levels than lean subjects, consistent with a compensatory rather than causal role for ghrelin in obesity. On the contrary, circulating leptin levels correlate in proportion to adiposity being high in obesity suggesting that human obesity is associated with insensitivity to leptin. The leptin resistance in diet-induced obesity emphasizes that environmental factors can modulate leptin sensitivity. It is speculated that through hypothalamic/pituitary axis ghrelin and leptin operate as a metabolic switch. Ghrelin actually transfers information from the stomach to the hypothalamus in cooperation with leptin and provides calories that growth hormone (GH) needs for growth and repair. Pharmacological manipulations of circulating hormone levels may work well in "cheating" the brain regarding information from the periphery. It might also be necessary to combine two or three agents to fight obesity. A combination of drugs that decrease preprandial appetite (ghrelin antagonist) and increase post-prandial satiety (gut hormone fragment peptide YY 3-36) might have a chance of achieving sustained weight loss. The administration of exogenous satiety hormone peptide YY 3-36 (PYY) may prevent the action of appetite-stimulating hypothalamic circuits on the anorexigenic melanocortin pathways.     

Relation between appetite ratings before and after a standard meal and estimates of daily energy intake in obese and reduced obese individuals

The aim of the present study was to relate appetite ratings before and after a standard breakfast to estimates of daily energy intake, before and after weight loss obese men and women. Nineteen obese subjects (9 men and 10 women) took part in a 15-week drug-based weight-loss program coupled to energy intake restriction. Body weight and body composition were significantly decreased in men and women. Both before and after the weight loss program, desire to eat, hunger, fullness and prospective food consumption (PFC) were measured after an overnight fast and at 10-min intervals in the hour following the ingestion of a standardized breakfast. Energy intakes were also measured and reported before and after weight loss.Fasting desire to eat and postprandial area under the curve (AUC) for hunger were significantly increased (p<0.05) after the intervention. No association was observed between measured or reported energy intakes and appetite ratings before weight loss in either men or women. Reported energy intake was not associated with appetite sensations after weight loss either. In contrast, measured energy intake was significantly associated with postprandial AUC for fullness (r=-0.90, p<0.01) and PFC (r=0.80, p<0.01) in men at the end of the program. In stepwise multiple regression analysis, only postprandial AUC for PFC contributed independently to the variance of measured energy intake after weight loss (r(2)=0.60, p=0.01).This study did not show consistent associations between averaged appetite ratings after a meal and daily energy intake, either before or after weight loss.     

Unbalanced serum leptin and ghrelin dynamics prolong postprandial satiety and inhibit hunger in healthy elderly: another reason for the "anorexia of aging"

BACKGROUND: In healthy elderly, a reduction from the appetite and food intake of younger years has been defined as the "anorexia of aging," which may cause malnutrition. Leptin and ghrelin may alter the control of hunger and satiety and thus lead to anorexia. OBJECTIVE: The aim of this study was to investigate how aging affects serum leptin and ghrelin concentrations in response to a meal and the relation of those hormones to hunger and satiety sensations. DESIGN: We studied 8 community-dwelling elderly (x +/- SD age: 78 +/- 1 y) subjects and 8 younger (29.5 +/- 1 y) control subjects. Under fasting conditions and for 4 h after an 800-kcal mixed meal, satiety and hunger were evaluated at intervals, by using a visual analogic scale. Blood samples for leptin, ghrelin, and insulin measurements were collected at the following times: 30 min before and immediately and 30, 60, 120, and 240 min after the meal. RESULTS: Postprandial satiety lasted significantly longer in the elderly than in the control subjects, and hunger was suppressed in the elderly throughout the observation. Fasting leptin was higher in the elderly than in the young (x +/- SE: 4.3 +/- 1.9 and 1.3 +/- 0.4 ng/mL, respectively; P < 0.05), and postprandial fluctuation was not significant. Fasting insulin also was significantly higher in the elderly than in the young (6.8 +/- 1.3 and 3.5 +/- 0.6 mU/L, respectively; P < 0.05), and the postprandial insulin rise was greater in the elderly. Fasting and postprandial ghrelin values did not differ significantly between the 2 groups. Insulin was inversely correlated with hunger and directly correlated with satiety scores. CONCLUSIONS: In healthy elderly, anorexigenic signals prevail over orexigenic signals, and they contribute to prolonged satiety and inhibition of hunger. This condition may lead to a calorie deficit and finally to malnutrition in the elderly.     

Biomarkers of satiation and satiety

This review's objective is to give a critical summary of studies that focused on physiologic measures relating to subjectively rated appetite, actual food intake, or both. Biomarkers of satiation and satiety may be used as a tool for assessing the satiating efficiency of foods and for understanding the regulation of food intake and energy balance. We made a distinction between biomarkers of satiation or meal termination and those of meal initiation related to satiety and between markers in the brain [central nervous system (CNS)] and those related to signals from the periphery to the CNS. Various studies showed that physicochemical measures related to stomach distension and blood concentrations of cholecystokinin and glucagon-like peptide 1 are peripheral biomarkers associated with meal termination. CNS biomarkers related to meal termination identified by functional magnetic resonance imaging and positron emission tomography are indicators of neural activity related to sensory-specific satiety. These measures cannot yet serve as a tool for assessing the satiating effect of foods, because they are not yet feasible. CNS biomarkers related to satiety are not yet specific enough to serve as biomarkers, although they can distinguish between extreme hunger and fullness. Three currently available biomarkers for satiety are decreases in blood glucose in the short term (<5 min), which have been shown to be involved in meal initiation; leptin changes during longer-term (>2-4 d) negative energy balance; and ghrelin concentrations, which have been implicated in both short-term and long-term energy balance. The next challenge in this research area is to identify food ingredients that have an effect on biomarkers of satiation, satiety, or both. These ingredients may help consumers to maintain their energy intake at a level consistent with a healthy body weight.     

The effect of eating frequency on appetite control and food intake: brief synopsis of controlled feeding studies

Increased eating frequency is postulated to increase metabolism, reduce hunger, improve glucose and insulin control, and reduce body weight, making it an enticing dietary strategy for weight loss and/or the maintenance of a healthy body weight. Because past research has primarily focused on the effects of eating frequency on changes in energy expenditure and body weight, limited data exist surrounding the impact of eating frequency on appetite control and energy intake. We provide a brief review of the controlled-feeding studies that primarily targeted the appetitive, hormonal, and food intake responses potentially altered with eating frequency. The 3 meal/d pattern served as the reference for defining increased or reduced eating frequency. In general, increased eating frequency led to lower peaks (P < 0.05) in perceived appetite, satiety, glucose, insulin, ghrelin, and PYY responses compared with reduced eating frequency. However, when examining these responses over the course of the day (i.e. using area under the curve assessments), no differences in any of these outcomes were observed. The rate of gastric emptying also appears to be unaltered with increased eating frequency. Subsequent food intake was examined in several studies with conflicting results. Regarding the effect of reduced eating frequency, several studies indicate significant increases in perceived appetite and reductions in perceived satiety when 1 or 2 meals were eliminated from the daily diet. Taken together, these findings suggest that increased eating frequency (>3 eating occasions/d) has minimal, if any, impact on appetite control and food intake, whereas reduced eating frequency(<3 eating occasions/d) negatively effects appetite control.     

Neuropeptide Y, alpha-melanocyte-stimulating hormone, and monoamines in food intake regulation

Obesity is increasing in severity and prevalence in the United States and represents a major public health issue. No effective pharmacologic treatment leading to sustained weight loss currently exists. The growing interest in the regulation of food intake stems from the current drug treatments for obesity, almost all of which interfere with the monoamine system. Our knowledge of potential interactions between the orexigenic and anorexigenic pathways is limited and fragmented, making the development of targeted drug therapy for obesity difficult. The present review of the interaction of neuropeptides and monoamines emphasizes the complexity of the central mechanisms that regulate feeding behavior. Two main systems are implicated in food intake regulation: neuropeptide Y (NPY) and pro-opiomelanocortin. alpha-Melanocyte-stimulating hormone is a tridecapeptide cleaved from pro-opiomelanocortin that acts to inhibit food intake. The predominant NPY orexigenic receptors are NPY-Y1 and NPY-Y5, and the two anorexigenic melanocortin receptors involved in hypothalamic food intake control are MC3-R and MC4-R. Both neuropeptides interact with monoamines in the hypothalamus to control physiologic states such as hunger, satiation, and satiety. Serotonin suppresses food intake and body weight, acting mainly through the serotonin 1B receptor. Dopamine regulates hunger and satiety by acting in specific hypothalamic areas, through the D1 and D2 receptors. Noradrenaline activation of alpha1- and beta2-adrenoceptors decreases food intake, and stimulation of the alpha2-adrenoceptor increases food intake. A better understanding of the detailed mechanisms underlying the pathogenesis of hyperphagia and hypophagia is needed to develop new therapeutic approaches to obesity.     

Peripheral and central signals in the control of eating in normal, obese and binge-eating human subjects

The worldwide increase in the incidence of obesity is a consequence of a positive energy balance, with energy intake exceeding expenditure. The signalling systems that underlie appetite control are complex, and the present review highlights our current understanding of key components of these systems. The pattern of eating in obesity ranges from over-eating associated with binge-eating disorder to the absence of binge-eating. The present review also examines evidence of defects in signalling that differentiate these sub-types. The signalling network underlying hunger, satiety and metabolic status includes the hormonal signals leptin and insulin from energy stores, and cholecystokinin, glucagon-like peptide-1, ghrelin and peptide YY3-36 from the gastrointestinal tract, as well as neuronal influences via the vagus nerve from the digestive tract. This information is routed to specific nuclei of the hypothalamus and brain stem, such as the arcuate nucleus and the solitary tract nucleus respectively, which in turn activate distinct neuronal networks. Of the numerous neuropeptides in the brain, neuropeptide Y, agouti gene-related peptide and orexin stimulate appetite, while melanocortins and alpha-melanocortin-stimulating hormone are involved in satiety. Of the many gastrointestinal peptides, ghrelin is the only appetite-stimulating hormone, whereas cholecystokinin, glucagon-like peptide-1 and peptide YY3-36 promote satiety. Adipose tissue provides signals about energy storage levels to the brain through leptin, adiponectin and resistin. Binge-eating has been related to a dysfunction in the ghrelin signalling system. Moreover, changes in gastric capacity are observed, and as gastric capacity is increased, so satiety signals arising from gastric and post-gastric cues are reduced. Understanding the host of neuropeptides and peptide hormones through which hunger and satiety operate should lead to novel therapeutic approaches for obesity; potential therapeutic strategies are highlighted.     

Effects of weekly administration of pegylated recombinant human OB protein on appetite profile and energy metabolism in obese men

BACKGROUND: Results of leptin administration in mice, rats, and humans provide a rationale for therapeutic augmentation of circulating leptin (OB protein) concentrations in obese humans; this may reduce food intake, increase metabolic rate, and lower body mass. OBJECTIVE: We assessed the effects of weekly subcutaneous pegylated polyethylene glycol (PEG)-OB protein administration on appetite and energy metabolism in obese men. DESIGN: We performed a randomized, double-blind, placebo-controlled trial in 30 obese men [body mass index (in kg/m(2)): 34.2 +/- 3.6; age: 44.7 +/- 7 y]. Subjects received 20 mg PEG-OB protein/wk for 12 wk while limiting their energy intake to 2.1 MJ/d. RESULTS: During treatment, appetite and hunger before breakfast decreased and remained lower in the PEG-OB-protein group, whereas they increased and remained higher in the placebo group (P < 0.0001). During treatment, hunger decreased in the PEG-OB-protein group (P < 0.05) and cognitive restraint increased in the placebo group (P < 0.0001). Neither appetite nor food intake changed significantly during the ad libitum evening meal. Under energy balance conditions in the respiration chamber, appetite at the end of treatment was not significantly different from baseline despite similar, significant reductions in 24-h energy intake, energy expenditure, sleeping metabolic rate, body mass, fat mass, and fat-free mass (P < 0.01 for all) in both groups. CONCLUSION: Treatment with PEG-OB protein modified subjective appetite at a dosage that produced no changes in body composition, energy expenditure, or body mass loss relative to placebo treatment, suggesting that PEG-OB protein has central rather than peripheral biological activity in obese men.     

A critical interaction: leptin and ghrelin

Continuing research has increased our understanding of regulatory factors involving appetite, food intake, and energy metabolism. There appears to be a complex interaction among insulin, leptin, and ghrelin. A new study explored these interactions and indicates that leptin may regulate ghrelin levels and affect body weight changes.     

Variety,Palatability, and Obesity

Among the key characteristics of the Western obesogenic food environment is a highly palatable and varied food supply. Laboratory investigations of eating behavior in both humans and animals established key roles for palatability and variety in stimulating appetite, delaying satiety, and promoting excessive energy intake. There is a robust effect of food palatability and variety on short-term food intake, and increased variety and palatability also cause weight gain in animal models. However, laboratory paradigms do not replicate the complexities of eating in a natural setting, and there is a shortage of evidence to estimate the magnitude of effects on weight in humans. There are substantial individual differences in susceptibility to the palatability effect and this may be a key determinant in individual vulnerability to weight gain. The understanding of pathways through which palatability and variety can affect eating is advancing, and epidemiologic and intervention studies are needed to translate laboratory findings into applications in public health or clinical domains, and to establish whether there is a role for greater regulation of the food environment in tackling increases in obesity.     

The ability of habitual exercise to influence appetite and food intake in response to high- and low-energy preloads in man

The present study tested the hypothesis that habitual exercisers demonstrate an increased accuracy of regulation of food intake in compensation for previous dietary energy intake. Twenty-three lean healthy male subjects were divided into two groups on the basis of their habitual exercise levels: non-exercisers (no exercise sessions/week, n 9), and exercisers (>two exercise sessions of 40 min or more/week, n 14). The appetite response to covert liquid preloads of high (2513 kJ) energy (HE) and low (1008 kJ) energy (LE) was investigated Sixty minutes after the preload subjects were offered an ab libitum buffet-style meal and energy intake (EI) was calculated. Subjective hunger and satiety were assessed throughout using self-rated visual-analogue scales. Buffet EI in non-exercisers was not significantly different following the LE or HE preloads (mean compensation 7 %), but the exercise group significantly reduced their energy intake following the HE, compared with the LE, preload (mean compensation 90 %; P=0.0035). A broadly similar pattern of response was observed for both moderate (two to three sessions/week, n 7) and high exercisers (>four sessions/week, n 7). There were no significant differences between hunger or satiety ratings following HE or LE preloads for either group. However non-exercisers scored significantly higher on their self-ratings of hunger at the start of the study, before preload consumption, compared with the exercisers (P<0.01). These findings demonstrate that habitual exercisers have an increased accuracy of short-term regulation of food intake in compensation for preload manipulation, and provide additional support for advocating regular exercise in the prevention of overweight and obesity.     

A new dental approach for reducing food intake

OBJECTIVE: A behavioral recommendation for weight loss is reduction of size of bites of food. This "proof of concept" study tested the efficacy of a new, patented, dental approach, the DDS System, for reducing food intake. This removable tool is inserted into the upper palate of the mouth, reducing the size of the oral cavity, thereby potentially reducing bite size. RESEARCH METHODS AND PROCEDURES: Thirty-two adults (18 to 65 years) with BMI between 27 and 40 were randomly assigned to the control or experimental conditions. Participants ate all meals and stayed between meals at a research center. Day 1 served as baseline for both groups. On Day 2, experimental participants utilized the tool during meals. Changes in subjective ratings of hunger and satiety were measured using visual analog scales before and after each meal. RESULTS: Food intake difference scores were calculated for each participant (Day 2 - Day 1). Analysis of covariance on difference scores, using baseline as a covariate, showed that the experimental group ate significantly less (p < 0.05) on the second day (M = -659.2 kcal/d) compared with the control group (M = -125.9 kcal/d). Analysis of covariance, with ratings on Day 1 as a covariate, revealed that the experimental and control group did not differ on visual analog scale difference scores (premeal - postmeal) from Day 1 to Day 2. DISCUSSION: These findings suggest that use of this tool during meals significantly reduced food intake. This reduction of food intake was not associated with changes in ratings of hunger or satiety.     

Social and cultural perspectives on hunger, appetite and satiety

The aim of this review is to show how hunger, satiety and appetite can be seen as a central research subject for the social sciences, both as the locus where food consumption is bodily regulated and as the nexus where biology, social praxis and cultural meanings meet and are negotiated by the individual. The number of people developing overweight and obesity is increasing, as is the prevalence of eating disorders and weight preoccupation. These tendencies can be considered as expressions of a polarization of eating habits in modern societies, where lack of control or exaggerated control over eating are still more common phenomena. At the same time the tendencies may be seen as the result of a more general ambivalence in relation to food, which influences the experiences of hunger, satiety and appetite and their regulating effect on food consumption.