Pathophysiology of Eating Disorders Paper

Pathophysiology of Eating Disorders Paper

Eating disorders are conditions portrayed by severe disturbances in ones eating behavior together with extreme anxiety over body weight.  They present themselves in varied manner though in most cases they appear with harsh medical comorbidity. There are two major classifications of eating disorders including anorexia nervosa and bulimia nervosa with many patients indicating a combination of both. In pathophysiology of the disorders, both psychosocial and biologic factors are implicated (Patricia, 1994)Pathophysiology of Eating Disorders Paper

Psychosocial factors

Michelle et al (2001) state that in families of children with eating disorders, soaring levels of chaos, hostilities, isolation, empathy and low level of nurturance are reported. Anorexia is postulated as a reactin to demands on adolescents to independently behave or as a response to societal pressure to be lean. Patients with anorexia nervosa normally, are high achievers. It is estimated that two thirds of them live with their parents. It is also viewed by many that their bodies are under their parent’s control although solely, family dynamics do not cause anorexia nervosa. Those with bulimia nervosa are depicted to have impulse regulation difficulties.Pathophysiology of Eating Disorders Paper

Biologic factors

Denial of hunger in patients with anorexia nervosa might be as a result of endogenous opioids. Dieting is thought to increase eating disorders developing risk. After purging, patients with bulimia nervosa have been described with increased levels of endorphin which is likely to induce well being feelings. Reduced norepinephrine turnover and activity are implied by low 3-methoxy-4-hydroxyphenylglco levels in the anorexia nervosa patient’s cerebrospinal fluid and urine. Bulimia nervosa patients often gain from antidepressants as they sustain a pathophysiologic role for norepinephrine and serotonin.


Starvation leads to several biochemical changes like thyroid function’s suppression, amenorrhea, hypercortisolemia and non suppression of dexamethasone. Additionally, anorexia risk may rise with a polymorphism of the promoter region of serotonin 2a receptor. Polymorphisms in some genes also play a role at the melancortin. Excessive secretion of ghrelin is experienced in bulimia nervosa. Ghrelin receptor gene polymorphism has been linked with both Prader-Willi syndrome and hyperphagia of bulimia.Pathophysiology of Eating Disorders Paper