Cecilia Bergh

Treatment of childhood obesity by retraining eating behaviour: randomised controlled trial

Objective To determine whether modifying eating behaviour with use of a feedback device facilitates weight loss in obese adolescents. Design Randomised controlled trial with 12 month intervention. Setting Hospital based obesity clinic. Participants 106 newly referred obese young people aged 9-17. Interventions A computerised device, Mandometer, providing real time feedback to participants during meals to slow down speed of eating and reduce total intake; standard lifestyle modification therapy. Main outcome measures Change in body mass index (BMI) standard deviation score (SDS) over 12 months with assessment 18 months after the start of the intervention. Secondary outcomes were body fat SDS, metabolic status, quality of life evaluation, change in portion size, and eating speed. Results Using the last available data on all participants (n=106), those in the Mandometer group had significantly lower mean BMI SDS at 12 months compared with standard care (baseline adjusted mean difference 0.24, 95% confidence interval 0.11 to 0.36). Similar results were obtained when analyses included only the 91 who attended per protocol (baseline adjusted mean difference 0.27, 0.14 to 0.41; P<0.001), with the difference maintained at 18 months (0.27, 0.11 to 0.43; P=0.001) (n=87). The mean meal size in the Mandometer group fell by 45 g (7 to 84 g). Mean body fat SDS adjusted for baseline levels was significantly lower at 12 months (0.24, 0.10 to 0.39; P=0.001). Those in the Mandometer group also had greater improvement in concentration of high density lipoprotein cholesterol (P=0.043). Conclusions Retraining eating behaviour with a feedback device is a useful adjunct to standard lifestyle modification in treating obesity among adolescents. Trial registration ClinicalTrials.gov NCT00407420.

Randomized controlled trial of a treatment for anorexia and bulimia nervosa

Evidence for the effectiveness of existing treatments of patients with eating disorders is weak. Here we describe and evaluate a method of treatment in a randomized controlled trial. Sixteen patients, randomly selected out of a group composed of 19 patients with anorexia nervosa and 13 with bulimia nervosa, were trained to eat and recognize satiety by using computer support. They rested in a warm room after eating, and their physical activity was restricted. The patients in the control group (n = 16) received no treatment. Remission was defined by normal body weight (anorexia), cessation of binge eating and purging (bulimia), a normal psychiatric profile, normal laboratory test values, normal eating behavior, and resumption of social activities. Fourteen patients went into remission after a median of 14.4 months (range 4.9–26.5) of treatment, but only one patient went into remission while waiting for treatment (P = 0.0057). Relapse is considered a major problem in patients who have been treated to remission. We therefore report results on a total of 168 patients who have entered our treatment program. The estimated rate of remission was 75%, and estimated time to remission was 14.7 months (quartile range 9.6 ≥ 32). Six patients (7%) of 83 who were treated to remission relapsed, but the others (93%) have remained in remission for 12 months (quartile range 6–36). Because the risk of relapse is maximal in the first year after remission, we suggest that most patients treated with this method recover.

Social, psychological and physical consequences of pathological gambling in Sweden.

Social, psychological and physical consequences of pathological gambling reported by 42 pathological gamblers recruited mainly by advertising were compared with data on 63 pathological gamblers identified by case-finding within districts of probation, in- and out-patient psychiatric care and social welfare authorities. The two studies gave similar results. Financial breakdown, impaired relations with family and friends, and psychological problems occurred in about 50% of the pathological gamblers. Physical consequences were perceived to be of minor significance. Gambling became a solitary behavior as illegal behaviors to finance gambling increased. The pathological gamblers frequently abused alcohol. Despite these signs of social decay the pathological gamblers strove not to be a burden in society.

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.

Understanding eating disorders

The outcome in eating disorders remains poor and commonly used methods of treatment have little, if any effect. It is suggested that this situation has emerged because of the failure to realize that the symptoms of eating disorder patients are epiphenomena to starvation and the associated disordered eating. Humans have evolved to cope with the challenge of starvation and the neuroendocrine mechanisms that have been under this evolutionary pressure are anatomically versatile and show synaptic plasticity to allow for flexibility. Many of the neuroendocrine changes in starvation are responses to the externally imposed shortage of food and the associated neuroendocrine secretions facilitate behavioral adaptation as needed rather than make an individual merely eat more or less food. A parsimonious, neurobiologically realistic explanation why eating disorders develop and why they are maintained is offered. It is suggested that the brain mechanisms of reward are activated when food intake is reduced and that disordered eating behavior is subsequently maintained by conditioning to the situations in which the disordered eating behavior developed via the neural system for attention. In a method based on this framework, patients are taught how to eat normally, their physical activity is controlled and they are provided with external heat. The method has been proven effective in a randomized controlled trial.

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.

Normalizing Eating Behavior Reduces Body Weight and Improves Gastrointestinal Hormonal Secretion in Obese Adolescents

HYPOTHESIS Retraining obese adolescents to eat more slowly will lead to beneficial changes in circulating concentrations of gastrointestinal satiety hormones. METHODS Ghrelin and peptide tyrosine-tyrosine were measured during an oral glucose tolerance test, at baseline and at 12 months during a randomized trial assessing the clinical effectiveness of a device (Mandometer) designed to retrain eating behavior. This computerized scale provided real-time feedback during meals in the intervention arm (n = 14) to slow down the speed of eating. The control group (n = 13) received only standard care aimed at improving lifestyle behavior. The Mandometer elicited greater improvements in weight loss than standard care. RESULTS Compared with baseline, only those using the Mandometer exhibited lower mean levels of fasting ghrelin (48.14 ± 18.47 vs. 68.45 ± 17.78 pg/ml; P = 0.002) and mean ghrelin area under the curve (72.08 ± 24.11 vs. 125.50 ± 29.72 pg/ml × min; P < 0.001) at 12 months. Absolute mean suppression in ghrelin at 60 min was enhanced (-40.50 ± 21.06 vs. -12.14 ± 19.74 pg/ml × min; P = 0.001). Peptide tyrosine-tyrosine response at 90 min remained unaltered in the standard care arm, whereas those in the Mandometer arm increased (P < 0.001): the mean 90-min response increased by 72 pg/ml [95% confidence interval (CI) 52-92 pg/ml] between baseline and 12 months. In a partial correlation analysis adjusting for change (Δ) in body mass index sd scores, Δ meal duration correlated negatively with Δ absolute suppression in ghrelin at 60 min (r = -0.58; P = 0.037; 95% CI -0.79 to -0.27) and Δ ghrelin area under the curve (r = -0.62; P = 0.025; 95% CI -0.81 to -0.31). CONCLUSIONS Retraining obese adolescents to eat more slowly has a significant impact on the gastrointestinal hormone response to a carbohydrate load, suggesting that externally modifiable eating behaviors actually regulate the hormonal response to food.

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.