Modjtaba Zandian

Decelerated and linear eaters: effect of eating rate on food intake and satiety.

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.

A method for the control of eating rate: a potential intervention in eating disorders.

A method for the control of eating rate gave subjects feedback from a computer screen on how much and at what rate to eat during a meal. The method also allowed us to record the development of satiety during the meal. Linear eaters—that is, women selected for eating at an approximately constant rate—underate when challenged to eat at a lower rate and overate when challenged to eat at a higher rate, thereby modeling the eating behavior of patients with anorexia nervosa and binge eating disorder, respectively. In both cases, the women’s postmeal perception of satiety mimicked that of the respective patient group. The results provide support for the notion that linear eaters have the capacity to exhibit disordered eating.

Cause and treatment of anorexia nervosa

The hypothesis that eating disorders are caused by an antecedent mental disorder, presently believed to be an obsessive compulsive disorder, has been clinically implemented during many years but has not improved treatment outcome. Alternatively, eating disorders are eating disorders and the symptoms of anorexic patients and probably bulimic patients as well, are epiphenomena which emerge as a consequence of starvation. This hypothesis is supported by the observations of the effects of a 6 month long period of semi-starvation on healthy human volunteers, which demonstrated not only the emergence of psychiatric symptoms but also the reduction in eating rate which is typical of anorexia nervosa patients. On this framework training anorexic patients how to eat may be a useful intervention. We report that anorexic patients, either with a body mass index<14 or >15.5 display the same pattern of eating behavior, with a low level of intake, a slow eating rate and a high level of satiety. They also have the same, high level of psychiatric symptoms, including obsessive compulsive symptoms. Training patients to eat more food at a progressively higher rate reverses these symptoms and patients remain free of symptoms during an extended period of follow-up. It is suggested that the pattern of eating behavior mediates between the starved condition and the psychopathology of anorexia nervosa.

Obesity and the brain

The world-wide increase in obesity has markedly stimulated research on the possibility that its cause can be found the brain. However, this research has produced little that can be used to treat obesity. The reason for the limited success of this approach may be that it relies on the hypothesis that the brain controls behavior. We suggest that this hypothesis is an artefact of the powerful tools used in behavioral neuroscience and that the brain has a permissive rather than causal role in eating behavior. Drugs affecting brain function are largely ineffective in treating obesity and may remain ineffective. Instead, we hypothesize that humans need external support to control body weight because they have evolved to pay a high physical price for food and are able to eat large amounts of food without constraints when that price is minimal. Two randomized controlled trials verify the hypothesis that support on how to eat normally and how to feel a normal level of fullness by use of on-line, real time feedback on a computer screen enables under- as well as overweight patients to adjust their eating behavior and improve their health.

Meal size, satiety and cholecystokinin in gastrectomized humans.

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.

Effective Treatment of Eating Disorders: Results at Multiple Sites

We report the results of a study based on 1,428 patients with eating disorders treated at 6 clinics. These patients were consecutively referred over 18 years and used inpatient and outpatient treatment. The subjects were diagnosed with anorexia nervosa, bulimia nervosa, or an eating disorder not otherwise specified. Patients practiced a normal eating pattern with computerized feedback technology, they were supplied with external heat, their physical activity was reduced, and their social habits restored to allow them to return to their normal life. The estimated rate of remission for this therapy was 75% after a median of 12.5 months of treatment. A competing event such as the termination of insurance coverage, or failure of the treatment, interfered with outcomes in 16% of the patients, and the other patients remained in treatment. Of those who went in remission, the estimated rate of relapse was 10% over 5 years of follow-up and there was no mortality. These data replicate the outcomes reported in our previous studies and they compare favorably with the poor long-term remission rates, the high rate of relapse, and the high mortality rate reported with standard treatments for eating disorders.

Linear eaters turned decelerated: Reduction of a risk for disordered eating?

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.

How eating affects mood

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.

Psychoneuroendocrinology of anorexia nervosa

It is suggested that the symptoms of anorexia nervosa are physiological responses to starvation. There is no evidence of a neural or non-neural dysfunction that predisposes women for anorexia nervosa and the endocrine and psychological consequences of starvation are reversed once patients have re-learnt how to eat and regained a normal body weight. Because variability in the supply of food may be a common evolutionary condition, it is more likely that body weight is variable than constant in normal circumstances. The role of the neuroendocrine system in times of feast and famine is to allow the individual to adopt behavioral strategies as needed rather than maintaining body weight homeostasis. Treatment of anorexic patients should aim at reducing their high level of physical activity in order to facilitate eating.

Description of chewing and food intake over the course of a meal

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.