This condition is not very common in the general population. There are special populations where the disease is more common such as ballet dancers and models . More common in females possibly 90% females and the peak age of onset is about 18 years . It is more common in higher socioeconomic states.
it is clear that since the 1960s there has been a significant increase in eating disorders, of which the two clearest syndromes are anorexia nervosa and bulimia nervosa.
The etiology is multifactorial which is a combination of genetic environmental and sociocultural factors.
Sociocultural causes : The social pressures which lead to dietary restraint include the publication of books and magazines advising weight-reducing diets, the fashion industry which caters mainly for the slimmer figure, television attaching sexual allure and professional success to the possession of a svelte figure, and the emphasis on physical fitness and athleticism .
The main features include anorexia, weight loss, overexercizing, behaviours to loose weight and amenorrhea. There is distorted body image. They have depression with guilt feeling after eating. They have specific eating rituals as selective food with low calories.
3. A characteristic set of attitudes to shape and weight, at the heart of which is the judging of self-worth in terms of shape and weight. These attitudes are expressed as an intense dissatisfaction with shape and weight, a fear of weight gain and fatness, and, in many cases, a pursuit of weight loss and thinness.
The patient must not meet the diagnostic criteria for anorexia nervosa.
obesity results from an elevation of the set-point about which body weight is regulated, and that the aetiology of obesity is to be found in the sources of this elevated set-point. Three such sources are genetic, environmental, and regulatory.
Genetic influences appear to play at least as important a role in the distribution of body fat as in the determination of total body fat or weight. Twin and adoption studies supports the importance of genetics.
Such as sedentary life style and low socioeconomic status.
Adipose tissue is the organ primarily affected in obesity. Adults of average weight have approximately 25 billion fat cells whereas severely obese people may have as many as 150 billion fat cells, as well as an increase in the size of the cells. Genetic influences play a role in excessive proliferation of fat cells, which occurs particularly in people who have been obese since childhood. When weight is lost, it is solely by a decrease in fat cell size; fat cell number appears to be irreversible . As a result, when fat cell size is reduced to normal levels by dieting, people with excessive numbers of fat cells remain significantly obese.
many patients routinely treated for obesity may develop anxiety or depression. A high incidence of emotional disturbances has been reported among obese persons undergoing long-term, in-hospital treatment by fasting or severe calorie restriction
In general, the best method of weight loss is a balanced diet of 1,100 to 1,200 calories. Such a diet can be followed for long periods but should be supplemented with vitamins, particularly iron, folic acid, zinc, and vitamin B6.
Drug treatment is effective because it suppresses appetite, but tolerance to this effect may develop after several weeks of use.
Rimonabant has not been studied in patients with psychiatric disorders. It should thus be used with caution in that population since the most frequent adverse events resulting in discontinuation of the drug in clinical trials were nausea, depression, and anxiety. However, since weight gain is such a common side effect of many psychiatric drugs, and the use of rimonabant to mitigate drug-induced metabolic disturbances may be justified in some patients.
CONCLUSIONS: These results suggest that while menstrual irregularities are common, bulimia nervosa appears to have little impact on later ability to achieve pregnancy. Eating Disorders Am J Psychiatry 159:1048-1050, June 2002
Eating Disorders: WPA Series Evidence and Experience in Psychiatry, vol. 6
Edited by Mario Maj, Katherine Halmi, Juan José Lòpez-Ibor, and Norman Sartorius. New York, John Wiley & Sons, 2003, 435 pp., $135.00.
LAURA L. POST, M.D., Ph.D. Saipan, MP (USA) There is, perhaps, no other subspecialty in the area of mental health that has developed as quickly or spread as broadly as that of eating disorders . This is so because non-Western countries are clinically experiencing morbidity and mortality from eating disorders in their societies and are doing their own research and reporting. Moreover, general medicine has recognized that eating disorders substantially overlap into their realm and are similarly contributing to knowledge in the field. Finally, because eating disorders are complex mixes of psychology and physiology and incorporate multiple distinct syndromes, nonpsychiatric mental health professionals have accumulated their respective expertise in recognition and treatment.
There is one approach that improves the physical and mental health of obese people as well as people of smaller sizes: the health at every size approach. I have used this approach for many years in my practice (6) . The success of the health at every size approach has been documented in an experiment (7) comparing it with the classic eat-less/exercise-more approach (which Drs. Volkow and O’Brien accurately acknowledged as incredibly difficult to sustain). Nondieters who gave up restrained eating , accepted their size, and tuned in to body signals of hunger and satiety improved their physical and mental health, independent of weight change and in contrast to dieters.
If we are truly interested in helping people who are out of control around food, we should stop cr eating more of them by continuing to push dieting. We should advocate for people taking good care of themselves via such avenues as self- and size-acceptance, enjoyable movement, and nourishment of one’s body, soul, and relationships. Moreover, we should stop considering adding to the tremendous amount of prejudice and stigma against individuals with unpopular body size by presuming that they possess a psychiatric disturbance.
Am J Psychiatry 165:424, April 2008 doi: 10.1176/appi.ajp.2007.07081351
Issues for DSM-V: Night Eating Syndrome
Albert Stunkard, M.D., Kelly Allison, Ph.D., and Jennifer Lundgren, Ph.D.
Recent demonstration of an effective treatment for night eating syndrome (1) argues for wider recognition of the disorder to benefit the many persons who suffer from it. These include 1.1%–1.5% of the general population, 6%–16% of patients in weight reduction programs, and 8%–42% of candidates for bariatric surgery. Viewed as a delay in the circadian rhythm of food intake, night eating syndrome is defined by two core criteria: evening hyperphagia (ingestion of at least 25% of daily calories after supper) and/or awakenings with ingestions at least three times a week. These criteria have identified persons whose behavior manifests a coherent biobehavioral model of night eating syndrome, supporting its construct validity. Single photon emission computed tomography has shown significant elevation of serotonin transporters in the midbrain of night eaters (2) . This elevation may result from a genetic vulnerability transmitted as part of the established heritability of night eating syndrome (3) , which is triggered by the stress that night eaters report. Elevations in serotonin transporter levels lead to decreased postsynaptic serotonin transmission and should impair circadian rhythms and satiety. These deficits suggest that improvement in serotonin function should alleviate night eating syndrome, and the selective serotonin reuptake inhibitors do precisely that. Reports of response to paroxetine and fluvoxamine have been accompanied by two larger open-label trials with a strong response to sertraline. Finally, a placebo-controlled, double-blind study of sertraline showed significant improvements in both of the criteria for night eating syndrome (1) .
Night eating may be a pathway to obesity; it preceded the onset of obesity in three studies and predicted major weight gain among female night eaters who were already obese (4) . Five animal models, each of a different etiology, have also shown a circadian dysrhythmia with hyperphagia and obesity. In addition to its contribution to weight gain, night eating syndrome is a source of distress, making it worthy of treatment for its own sake.