References : Eating Disorders in Children and Adolescents

The incidence and prevalence of eating disorders in children and adolescents has increased significantly in recent decades, making it essential for pediatricians to consider these disorders in appropriate clinical settings, to evaluate patients suspected of having these disorders, and to manage (or refer) patients in whom eating disorders are diagnosed. This clinical report includes a discussion of diagnostic criteria and outlines the initial evaluation of the patient with disordered eating. Medical complications of eating disorders may affect any organ system, and careful monitoring for these complications is required. The range of treatment options, including pharmacotherapy, is described in this report. Pediatricians are encouraged to advocate for legislation and policies that ensure appropriate services for patients with eating disorders, including medical care, nutritional intervention, mental health treatment, and care coordination.

Binge-eating disorder, bulimia nervosa, and anorexia nervosa are potentially life-threatening disorders that involve complex psychosocial issues. A strong therapeutic relationship between the physician and patient is necessary for assessing the psychosocial and medical factors used to determine the appropriate level of care. Most patients can be effectively treated in the outpatient setting by a health care team that includes a physician, a registered dietitian, and a therapist. Psychiatric consultation may be beneficial. Patients may require inpatient care if they are suicidal or have life-threatening medical complications, such as marked bradycardia, hypotension, hypothermia, severe electrolyte disturbances, end-organ compromise, or weight below 85 percent of their healthy body weight. For the treatment of binge-eating disorder and bulimia nervosa, good evidence supports the use of interpersonal and cognitive behavior therapies, as well as antidepressants. Limited evidence supports the use of guided self-help programs as a first step in a stepped-care approach to these disorders. For patients with anorexia nervosa, the effectiveness of behavioral or pharmacologic treatments remains unclear

ncreases in the incidence and prevalence of anorexia nervosa (AN), bulimia nervosa (BN), and other eating disorders in children and adolescents make it critically important that pediatricians be familiar with early detection and appropriate management of these disorders. Results of epidemiologic studies have indicated that the numbers of children and adolescents with eating disorders increased steadily from the 1950s onward. During the past decade, the prevalence of obesity in children and adolescents has also increased dramatically, accompanied by further emphasis on dieting and weight loss among children and adolescents.

The epidemiology of eating disorders has gradually changed; there is an increasing prevalence of eating disorders in males and minority populations in the United States20 as well as in countries in which eating disorders had not been commonly seen. Of particular concern is the increasing prevalence of eating disorders at progressively younger ages.  A recent analysis by the Agency for Healthcare Research and Quality revealed that from 1999 to 2006, hospitalizations for eating disorders increased most sharply—119%—for children younger than 12 years.19

It is estimated that approximately 0.5% of adolescent girls in the United States have AN, that approximately 1% to 2% meet diagnostic criteria for BN, and that up to 5% to 10% of all cases of eating disorders occur in males. A large number of people with eating disorders do not meet the strict criteria set forth in the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR) for AN or BN and are labeled as having “partial syndromes” or “eating disorder not otherwise specified” (ED NOS). There are many more patients with ED NOS than there are patients with AN or BN; the prevalence is estimated to be between 0.8% and 14%, depending on the definition used. These patients often experience the same physical and psychological consequences as do those who reach the threshold for diagnosis of AN or BN. Athletes and performers, particularly those who participate in sports and activities that reward a lean body habitus (eg, gymnastics, running, wrestling, dance, modeling) may be at particular risk of developing partial-syndrome eating disorders.

The etiology of eating disorders is multifactorial, and there is increasing evidence from both family and twin studies for a strong genetic component that is shared between AN and BN. The mechanism(s) by which genetic factors influence risk have not been elucidated, but various hypotheses have been proposed. Genetic predisposition to various trait disturbances such as behavioral rigidity, perfectionism, or harm avoidance may be more salient than genetic influences on eating, hunger, or satiety.39,–,41 Genetic effects seem to be “activated” by puberty, and there is strong evidence for genetic-environment interactions.

Dieting has also been implicated as a potent proximal risk factor in the development of disordered eating and eating disorders.  In 1 community-based study, dieters at 5-year follow-up were at significantly higher risk of disordered eating behaviors (eg, vomiting or using diet pills or laxatives) than nondieters and were also at increased risk of obesity. In another large community cohort, dieters were 5 times more likely to develop an eating disorder and severe dieters were 18 times more likely to develop an eating disorder than nondieters.

Neuroendocrine abnormalities have been implicated in the etiology of eating disorders. Leptin is a circulating hormone produced in adipose tissue and seems to have a significant role in mediating the neuroendocrine effects of AN. Leptin concentrations are sensitive to the acute metabolic effects of decreased intake and energy deficits, and decreased circulating leptin concentrations reflect depleted stores of body fat.49,–,51 Physical hyperactivity is a common feature of AN and sometimes manifests as restlessness, athleticism, or compulsive exercise. This hyperactivity also seems to be mediated by leptin.

Physical hyperactivity associated with weight loss seems to occur in animals as well, apparently mediated by hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis. Syndromes that resemble AN, characterized by food refusal, physical overactivity, and extreme weight loss, occur in pigs, sheep, and goats bred for leanness. Caloric restriction coupled with environmental stress produces animal models for binge-eating. These animals overeat dramatically despite nutritional satiety and normal energy status, which strongly suggests that reward circuits are being activated rather than metabolic needs being satisfied.

In community-based studies of adolescents, disturbances of body image and overconcern about body shape are common, although the prevalence of eating disorders remains low. These results reinforce the likelihood of epigenetic effects in which the development of eating disorders reflects the intersection between genetic predisposition, environmental triggers, and personal experience.

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Pediatric Articles Dr Widodo Judarwanto (pediatrician)

100 Favorites Articles for Professional



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