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Subjects eat food from a plate that sits on a scale connected to a computer that records the weight loss of the plate during the meal and makes up a curve of food intake, meal duration and rate of eating modeled by a quadratic equation. The purpose of the method is to change eating behavior by providing visual feedback on the computer screen that the subject can adapt to because her/his own rate of eating appears on the screen during the meal. The data generated by the method is automatically analyzed and fitted to the quadratic equation using a custom made algorithm. The method has the advantage of recording eating behavior objectively and offers the possibility of changing eating behavior both in experiments and in clinical practice. A limitation may be that experimental subjects are affected by the method. The same limitation may be an advantage in clinical practice, as eating behavior is more easily stabilized by the method. A treatment that uses this method has normalized body weight and restored the health of several hundred patients with anorexia nervosa and other eating disorders and has reduced the weight and improved the health of severely overweight patients.

Background: Speed of eating, an important aspect of eating behaviour, has recently been related to loss of control of food intake and obesity. Very little time is allocated for lunch at school and thus children may consume food more quickly and food intake may therefore be affected. Study 1 measured the time spent eating lunch in a large group of students eating together for school meals. Study 2 measured the speed of eating and the amount of food eaten in individual school children during normal school lunches and then examined the effect of experimentally increasing or decreasing the speed of eating on total food intake., Methods: The time spent eating lunch was measured with a stop watch in 100 children in secondary school. A more detailed study of eating behaviour was then undertaken in 30 secondary school children (18 girls). The amount of food eaten at lunch was recorded by a hidden scale when the children ate amongst their peers and by a scale connected to a computer when they ate individually. When eating individually, feedback on how quickly to eat was visible on the computer screen. The speed of eating could therefore be increased or decreased experimentally using this visual feedback and the total amount of food eaten measured., Results: In general, the children spent very little time eating their lunch. The 100 children in Study 1 spent on average (SD) just 7 (0.8) minutes eating lunch. The girls in Study 2 consumed their lunch in 5.6 (1.2) minutes and the boys ate theirs in only 6.8 (1.3) minutes. Eating with peers markedly distorted the amount of food eaten for lunch; only two girls and one boy maintained their food intake at the level observed when the children ate individually without external influences (258 (38) g in girls and 289 (73) g in boys). Nine girls ate on average 33% less food and seven girls ate 23% more food whilst the remaining boys ate 26% more food. The average speed of eating during school lunches amongst groups increased to 183 (53)% in the girls and to 166 (47)% in the boys compared to the speed of eating in the unrestricted condition. These apparent changes in food intake during school lunches could be replicated by experimentally increasing the speed of eating when the children were eating individually., Conclusions: If insufficient time is allocated for consuming school lunches, compensatory increased speed of eating puts children at risk of losing control over food intake and in many cases over-eating. Public health initiatives to increase the time available for school meals might prove a relatively easy way to reduce excess food intake at school and enable children to eat more healthily.

While the average frequency of chewing and food intake have been reported before, a detailed description of the pattern of chewing and the cumulative intake of food over the course of a meal have not. In order to achieve this goal, video recording of the maxillary-mandibular region of women eating food from a plate was synchronized with video recording of the plate and computer recording of the weight-loss of the plate. Video recording of chewing correlated strongly with chewing identified by magnetic tracking of jaw displacement in a test with chewing gum at three different frequencies, thus ensuring the validity of video recording of chewing. Weight-loss data were corrected by convolution algorithms, validated against human correction, using sliding window filtering to correct errors with video events as reference points. By use of this method, women ate on average 264 g of food over 114 min, they took an average of 51 mouthfuls during the meal and displayed on average 794 chews with 15 chews per chewing sequence. The number of mouthfuls decreased and the duration of the pauses after each mouthful increased in the middle of the meal and these measures were then restored. The ratio between chewing sequences and subsequent pauses remained stable although the weight of each mouthful decreased by the end of the meal, a measure that is hypothesized to be reflected in a decelerated speed of eating. The method allows this hypothesis to be tested and its implication for clinical intervention to be examined., (Copyright © 2011 Elsevier Inc. All rights reserved.)

IOAKIMIDIS I, M. ZANDIAN, F. ULBL, C. BERGH, M LEON, AND P. SÖDERSTEN. How eating affects mood. PHYSIOL BEHAV 2011 (000) 000-000. We hypothesize that the changes in mood that are associated with eating disorders are caused by a change in eating behavior. When food is in short supply, the rhythm of the neural network for eating, including orbitofrontal cortex and brainstem, slows down and we suggest that this type of neural activity activates a partially overlapping neural network for mood, including dorsal raphe serotonin projections to the orbitofrontal and prefrontal cortex. As a consequence, people who restrict the amount of food that they consume, either by choice or by their limited access to food, become preoccupied with food and food-related behavior. Most eating disorders emerge from a history of dietary restriction and we suggest that disordered eating consequent upon food restriction produces the altered mental state of patients with eating disorders. Based on the present hypothesis, eating disorders are not the result of a primary mental disorder. Rather, this notion suggests that the patients should be treated by learning to eat an appropriate amount of food at an appropriate rate., (Copyright © 2011 Elsevier Inc. All rights reserved.)

It has been suggested that restrained eating is a cognitive strategy that an individual uses for control of food intake. If losing control, the restrained eater enters a state of disinhibition and is therefore thought to be at risk for developing eating disorders and obesity. Restrained eaters eat at a constant rate and can therefore also be referred to as linear eaters. Here, we have tested the hypothesis that restrained eating is a state that can be modified by teaching linear eaters to eat at a decelerated rate. Seventeen female linear eaters scored high on a scale for restrained eating. When challenged to eat at an increased rate, a test of disinhibition, the women overate by 16% on average. The women then practiced eating at a decelerated rate by use of feedback from a training curve displayed on a computer screen during the meals. The training occurred three times each week and lasted eight weeks. When re-tested in the absence of feedback, the women ate at a decelerated rate, they did not overeat in the test of disinhibition and they scored lower on the scale for restrained eating. It is suggested that restrained eating is a state that can be reduced by training.

Women were divided into those eating at a decelerated or linear rate. Eating rate was then experimentally increased or decreased by asking the women to adapt their rate of eating to curves presented on a computer screen and the effect on food intake and satiety was studied. Decelerated eaters were unable to eat at an increased rate, but ate the same amount of food when eating at a decreased rate as during the control condition. Linear eaters ate more food when eating at an increased rate, but less food when eating at a decreased rate. Decelerated eaters estimated their level of satiety lower when eating at an increased rate but similar to the control condition when eating at a decreased rate. Linear eaters estimated their level of satiety similar to the control level despite eating more food at an increased rate and higher despite eating less food at a decreased rate. The cumulative satiety curve was fitted to a sigmoid curve both in decelerated and linear eater under all conditions. Linear eaters rated their desire to eat and estimated their prospective intake lower than decelerated eaters and scored higher on a scale for restrained eating. It is suggested that linear eaters have difficulty maintaining their intake when eating rate is dissociated from its baseline level and that this puts them at risk of developing disordered eating. It is also suggested that feedback on eating rate can be used as an intervention to treat eating disorders.

We present the case of an Australian girl with severe anorexia nervosa who had previously been resistant to treatment, and who was subsequently treated successfully by an innovative programme at the Karolinska Institute in Stockholm. The programme is based on a distinctive concept of causation of eating disorders in which it is postulated that they develop as a consequence of starvation rather than a primary mental disorder. The treatment focuses on relearning how to eat and perceive satiety using a unique feed-back system, together with provision of warmth, limitation of exercise and facilitating social adaptation.

A wealth of data supports the idea that the stomach and cholecystokinin octapeptide (CCK-8) normally play important roles in meal size and satiety. We studied long-term gastrectomized humans to further evaluate this possibility. Ten humans, who were gastrectomized 8 (3-12) years earlier, and eight controls ate a meal from a plate placed on a scale connected to a computer and estimated their satiety every minute using a computerized rating scale. Blood levels of CCK-8 were measured before and after the meal. There was no difference between the groups in the amount of food consumed or in the perception of satiety during the meal. Gastrectomized humans had higher blood levels of CCK-8 than controls before the meal; the levels increased after the meal in the controls but not in the gastrectomized subjects. It is suggested that although the stomach and CCK-8 normally are involved in the control of meal size and satiety, their roles are dispensable.

I.p. injections of DSP-4 in male rats decreased norepinephrine (NE) levels to varying degrees throughout the brain with 66.7% reductions in the hypothalamic paraventricular nucleus. Intake of intraorally infused sucrose was reduced for 14 days but daily pellet intake recovered within 5 days post-injection. Intraventricular NE restored intraoral sucrose intake in DSP-4-lesioned rats without affecting controls. Intraventricular infusion of neuropeptide Y (NPY) reduced intraoral intake in controls but had no effect in DSP-4-lesioned rats. NPY markedly inhibited intraoral intake in DSP-4-treated rats that also received NE. These data confirm studies showing that NPY decreases consummatory ingestive behavior and suggest that this inhibition involves ascending noradrenergic projections from locus coeruleus.

We investigated if the taste of a sucrose solution becomes progressively more aversive during intraoral infusion and if this contributes to the termination of the intake in male rats. The display of aversive behavior, such as gapes and chin rubs, but not headshakes, forelimb flails or orofacial grooming, varied with the concentration of an intraorally infused solution of quinine hydrochloride (QHCl) and increased by the time the rat rejected an intraorally infused 2 M solution of sucrose. Activation of gapes and chin rubs by brief intraoral infusion of QHCl advanced the rejection of the sucrose solution if given late during intraoral infusion, but blockade of gaping by anaesthesization of the oral cavity with Xylocain did not prolong the intake of the sucrose solution. Headshakes and forelimb flails could be elicited by stimulating the head and limbs with sucrose, and gapes and chin rubs were activated by infusion of a 2 M solution of sucrose into the stomach or duodenum but not by infusion of glucose into the jugular or hepatic portal vein. Preventing filling of the gastrointestinal tract during intraoral infusion of sucrose (sham feeding) eliminated the display of gapes and chin rubs. It is suggested that an increase in the aversiveness of the taste of a sucrose solution contributes to the rejection of that solution during intraoral infusion. However, rats can reject a sucrose solution in the absence of any behavioral sign of aversion and none of the so-called "taste-related" aversive behaviors is exclusively dependent upon stimulation of the taste receptors in the oral cavity.

Anorexia, nausea, and vomiting are common symptoms of uremic intoxication. Fractions in the middle molecule weight range, isolated from normal urine and uremic plasma ultrafiltrate, inhibit ingestive behavior in the rat. To investigate their site of action and specificity, male rats were injected intraperitoneally, intravenously, or intracerebroventricularly with concentrated fractions of uremic plasma ultrafiltrate or normal urine (molecular weight range: 1.0 to 5.0 kD) and tested for ingestive and sexual behavior. An intraperitoneal injection of 0.5 ml of urine fraction (10:1) or 2.0 ml of uremic plasma ultrafiltrate fraction (25:1) inhibited carbohydrate intake by 76.3 and 45.9%, respectively, but an intravenous injection had no effect. However, intravenous injection of higher doses inhibited carbohydrate ingestion. An intracerebroventricular injection of 5 or 10 microl of urine (20:1) middle molecule fraction inhibited carbohydrate intake by 13.4 and 41.6%, respectively. An injection of 5 or 10 microl of uremic plasma ultrafiltrate (125:1) middle molecule fraction inhibited carbohydrate intake by 22.6 and 49.5%, respectively. Injections of the corresponding fraction from normal plasma ultrafiltrate had no effect. Injection of urine or uremic plasma ultrafiltrate middle molecule fractions did not affect the display of sexual behavior. These results suggest that middle molecule fractions from uremic plasma ultrafiltrate or normal urine act in the splanchnic region and/or brain to inhibit food intake and that the effect is specific for ingestive behavior.

Male rats were injected with 6-hydroxydopamine in the lateral hypothalamus and tested for ingestive behavior starting on the day after the injection. The rats did not eat food pellets but readily ingested an intraorally infused nutritive solution. If given three daily intraoral infusions, 6-hydroxydopamine-treated rats defended their body weight and were as sensitive to the inhibitory effect of cholecystokinin octapeptide on intake as controls. Dopamine was reduced by 94% in the dorsal striatum five days after the 6-hydroxydopamine injection. Noradrenaline and serotonin were less markedly affected. Thus, while appetitive ingestive behavior is disrupted, consummatory ingestive behavior and body weight regulatory competence are only marginally affected by massive damage to forebrain dopamine neural networks.

A dopamine D1 (SKF-38393, 1 mg)- or D2 (LY-171555, 0.1 mg)-receptor agonist inhibited intake of an intraorally infused solution of sucrose by male rats, a test of consummatory ingestive behavior. Treatment with a D1 (SCH-39166, 0.1 mg) or D2 (raclopride, 0.6 mg) antagonist reversed inhibition by the respective agonist but enhanced the inhibitory effect of cholecystokinin octapeptide (CCK-8; 1.8 micrograms). It was not possible to demonstrate specific effects of D1 and D2 agonists on intake of pellets, a test that does not discriminate consummatory ingestive behavior from appetitive ingestive behavior, i.e., behavior used to obtain food. The results demonstrate specific involvement of dopamine D1 and D2 receptors in inhibition of consummatory ingestive behavior.

Ingestive behavior was activated in male rats by intraoral infusion of a 1-M solution of sucrose. Injection of cholecystokinin octapeptide (CCK-8; 1.6 or 5.0 micrograms) inhibited ingestion of the sucrose solution and increased the concentration of 5-hydroxytryptamine (5-HT) in the paraventricular hypothalamic nuclei. The inhibitory effect of the low, but not the high, dose of CCK-8 was attenuated by depleting 5-HT in the brain with p-chlorophenylalanine (PCPA; 100 mg/kg for 3 days). Treatment with 5-hydroxytryptophan (20 mg/kg) increased the concentration of 5-HT in the brain of rats pretreated with either NaCl or PCPA and enhanced the inhibitory effect of CCK-8 on ingestive behavior in the PCPA-, but not NaCl-, treated rats. 5-HT may play a role in the mechanism of action of CCK-8 but additional factors must be involved.

In food-deprived male rats IP injection of cholecystokinin octapeptide (CCK-8, 5 micrograms), ingestion of food or ejaculation caused a comparable increase in plasma concentrations of CCK-8 and inhibited food intake. IV injection of 0.1 microgram CCK-8 interrupted ongoing feeding and greatly increased plasma CCK-8 levels. Osmotic minipumps delivering 0.5 micrograms CCK-8/h implanted IP reduced meal size and caused a modest increase in plasma CCK-8 levels. Injection of 5 micrograms CCK-8 IP produced an abrupt but transient increase in plasma CCK-8 concentrations whereas plasma concentrations of CCK-8 increased gradually with feeding. Injection of 5 micrograms CCK-8 IP, but not feeding, caused a marked increase in plasma oxytocin levels. The suppression of feeding, but not the increase in oxytocin, induced by IP CCK-8 was reversed by ICV injection of the CCK antagonist proglumide in a dose (100 micrograms) which failed to affect food intake if injected IP. Deprivation of food decreased and feeding increased the concentration of CCK-like immunoreactivity in the CSF. It is suggested that CCK-8 inhibits feeding in physiological doses by a specific mechanism in which peripheral as well as central neural CCK is involved.

Intraperitoneal injection of 5 micrograms cholecystokinin octapeptide (CCK-8) into male rats deprived of food for 48 h produced a transient (less than 15 min) increase in plasma levels of CCK-8 but suppressed food intake for an extended period (45 min). Plasma concentrations of CCK-8 after i.p. injection of CCK-8 were raised to levels which were fairly comparable to those after feeding. Intracerebroventricular (i.c.v.) injection of the CCK antagonist proglumide (100 micrograms) reversed the effect of CCK-8 on food intake, while i.p. injection of proglumide (100 micrograms) did not have this effect. Feeding increased the plasma concentrations of somatostatin and gastrin but not of oxytocin, and somatostatin and oxytocin but not gastrin were released in response to i.p. injection of CCK-8. However, neither somatostatin nor oxytocin affected food intake, and their release in response to CCK-8 was unaffected by i.c.v. injection of proglumide. These results support the suggestion that CCK-8 is a physiological 'satiety' peptide, which can affect food intake in rats by mechanisms involving both peripheral and central CCK receptors.

On the standard perspective, anorexia nervosa and other eating disorders are caused by genetically determined, neurochemically mediated mental illnesses. Standard treatment, cognitive behavioral therapy (CBT), targets cognitive processes thought to maintain the disorders. Effective neurochemically based treatments are not available and the rate of remission is ≤25% 1 year after CBT, with unknown outcomes in the long-term. With starvation as the major threat in biological history, the evolutionary perspective focuses on foraging for food and eating behavior. A neural network, including hypothalamic arcuate peptide-neurons, brainstem serotonin- and dopamine-neurons and their prefrontal cortical projections, mediates (rather than controls) the behavioral adaptations to variations in food availability; activation of the network is associated with opposing behavioral outcomes depending upon external variations. In the clinic, the control of eating behavior is therefore outsourced to a machine that provides feedback on how to eat. Hundreds of eating disorders patients have recovered by practicing eating; the rate of remission is 75% in on average 1 year of treatment, the rate of relapse is 10% over 5 years of follow-up and no patient has died. A two-parameter asymptotic exponential growth curve modeled the eating behavior of 17 healthy women but not that of 17 women with anorexia nervosa. When in remission, the eating behavior of the anorexic women approached that of the healthy women. It is suggested that the treatment of eating disorders should focus on eating behavior. [ABSTRACT FROM AUTHOR]

Abstract: Outcome in anorexia nervosa remains poor and a new way of looking at this condition is therefore needed. To this aim, we review the effects of food restriction and starvation in humans. It is suggested that body weight remains stable and relatively low when the access to food requires a considerable amount of physical activity. In this condition, the human homeostatic phenotype, body fat content is also low and as a consequence, the synthesis and release of brain neurotransmitters are modified. As an example, the role of neuropeptide Y is analyzed in rat models of this state. It is suggested that the normal behavioral role of neuropeptide Y is to facilitate the search for food and switch attention from sexual stimuli to food. Descriptive neuroendocrine studies on patients with anorexia nervosa have not contributed to the management of the patients and the few studies in which hormones have been administered have, at best, reversed an endocrine consequence secondary to starvation. In a modified framework for understanding the etiology and treatment of anorexia nervosa it is suggested that the condition emerges because neural mechanisms of reward and attention are engaged. The neural neuropeptide Y receptor system may be involved in the maintenance of the behavior of eating disorder patients because the localization of these receptors overlaps with the neural systems engaged in cue-conditioned eating in limbic and cortical areas. The eating behavior of patients with anorexia nervosa, and other eating disorders as well, is viewed as a cause of the psychological changes of the patients. Patients are trained to re-learn normal eating habits using external support and as they do, their symptoms, including the psychological symptoms, dissolve. [Copyright &y& Elsevier]