Etiology and Immunopathogenesis of Eating Disorders

Eating disorders in children and adolescents can be of long duration, potentially life-threatening depending on severity of illness, and with likely relapse if adequate alternative coping skills are not developed. A planned and skillful approach to treatment is necessary to obtain a cost-effective, healthy outcome. Patients require ongoing monitoring and treatment with a biopsychosocial perspective using a varied number of professionals, including a primary care clinician, therapist, dietitian, family therapist, and other team members as needed. Outcomes-based research in the field can further clarify ways to deliver cost-effective care in a variety of settings. Clinicians and families need to advocate for adequate coverage of both medical and mental health services for children and adolescents with eating disorders, especially because pathogenesis, medical effects, and necessary treatments all demonstrate the interrelatedness of the medical and psychological in this disease process. Specialized settings such as partial hospitalization programs, therapeutic use of community in a boarding school, and other innovations such as clinical pathways can help address the medical, nutritional, and mental health needs of these patients. Ultimately, the goals include primary prevention plus early recognition and treatment to prevent long-term sequelae

PATHOGENESIS AND ETIOLOGY OF EATING DISORDERS

Despite increasing awareness of the major eating disorders, a specific etiology for the pathogenesis of anorexia nervosa (AN) and bulimia nervosa (BN) remains unclear. Rather than single factor causal theories, eating disorders are now viewed as multifactorial disorders with the symptom pattern representing a final common pathway.2 Interest has focused variously on the contribution of environmental and social factors, psychological predisposition, and biological vulnerability, with recent familial aggregation studies renewing interest in the contribution of genetic predisposition.

Dieting continues to be a common entry point in both syndromes, with the greatest risk being the group of severe dieters. Not surprisingly, therefore, sociocultural and environmental factors as they relate to ideal body shape are thought to play an important role in the development of eating disorders. Reports of AN and BN are more common in industrialized nations where food is plentiful and where thinness for women is correlated with attractiveness. For example, the prevalence of AN in Greek girls living in Germany was double the rate for those girls living in Greece and Turkey where they remained less exposed to Western values equating thinness with beauty.

The prominent physiologic disturbances in AN have led to speculation that the abnormal behaviors are caused by a primary biological abnormality. Disruptions of the pituitary, hypothalamus, and various neurotransmitters have been postulated to be causal factors in the development of AN. However, most of these physiologic disturbances, and more recently, functional imaging studies, resolve with normalization of body weight, an argument against a primarily causal role.

However, recent studies of serotonin in particular have brought renewed interest in this area. The neurotransmitter serotonin is known to affect appetite control, sexual and social behavior, stress responses, and mood. Serotonin modulates feeding by producing the sensation of fullness or satiety. Serotonin antagonists that decrease serotonergic neurotransmission or block receptor activation increase food consumption and promote weight gain. Decreases in brain serotonin function are associated with depression, impulsivity, and aggressive behavior. The major serotonin metabolite, 5-hydroxyindoleacetic acid, is low in people who are underweight with AN, but then rises to above normal levels in those who have made long-standing recoveries. One study7 showed that patients with more severe binge eating have lower cerebrospinal fluid 5-hydroxyindoleacetic acid than do controls. It has been speculated that a premorbid disturbance in serotonergic function might be a risk factor for the development of both AN and BN. A putative allelic association between the B1438 A/G promoter polymorphism of the 5-HT2A gene and AN has been reported, but not consistently so.

Leptin, a hormone secreted by fat cells, seems less likely to play an important role in AN, despite its role in regulating body fat. People with AN or low weight have low serum leptin, consistent with their reduced mass of fat tissue, which increases with weight gain. Interestingly, however, normalization of leptin levels seems to precede normalization of body weight, which may contribute to the difficulties experienced with attaining and maintaining normal weight in AN.

Neuroimaging studies using magnetic resonance imaging scans and more recently, PET scans, demonstrate subtle alterations of function as well as structure of the brains of those girls with AN but have not yet yielded any etiologic understandings.

Clinical and population studies of women have consistently demonstrated an increased association between major depression and AN, with depression a risk factor for development of incident eating disorders in adolescence. First-degree relatives of women with AN have elevated rates of major depression. Although it has been suggested that AN and major depression share a common etiology, it has also been suggested that the risk for AN is distinct from that of other affective disorders. However, many of the clinical features of depression can also result secondarily from starvation and improve with weight restoration.

Familial transmission of risk has emerged as an increasing focus of research attention. There are now multiple case-control studies designed to investigate the familiality of eating disorders, which demonstrate a higher rate of AN in relatives of probands with AN. The frequency of BN is also greater in the relatives of AN probands.

The increased incidence of AN and BN in families is consistent with a range of observations, including

  • the coexistence of binge eating with AN,
  • development of both AN and BN that has been demonstrated in longitudinal studies,
  • the overwhelming predominance of common patterns of gender and personality traits, and
  • comorbidity with mood and anxiety disorders.

source : Ellen S. Rome, Seth Ammerman, David S. Rosen, Richard J. Keller, James Lock, Kathleen A. Mammel, Julie O’Toole, Jane Mitchell Rees, Mary J. Sanders, Susan M. Sawyer, Marcie Schneider, Eric Sigel, and Tomas Jose Silber. Children and Adolescents With Eating Disorders: The State of the Art.  Pediatrics 2003; 111:1 e98-e108; doi:10.1542/peds.111.1.e98

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Curriculum Vitae Dr Widodo judarwanto, Pediatrician

We are guilty of many errors and many faults. But our worst crime is abandoning the children, neglecting the fountain of life.
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