Anorexia nervosa is characterized by a relentless pursuit of thinness, a morbid fear of obesity, a distorted body image, and restriction of intake relative to requirements, leading to a significantly low body weight. Diagnosis is clinical. Most treatment is with some form of psychologic therapy. Olanzapine may help with weight gain.
Anorexia nervosa occurs predominantly in girls and young women. Onset is usually during adolescence and rarely after age 40.
The etiology is unknown. Other than being female, few risk factors have been identified. In Western society, obesity is considered unattractive and unhealthy, and the desire to be thin is pervasive, even among children. More than 50% of prepubertal girls diet or take other measures to control their weight. Excessive concern about weight or a history of dieting appears to indicate increased risk, and some genetic predisposition probably exists. Studies of identical twins have shown a concordance of < 50%; concordance is lower in fraternal twins. Family and social factors probably play a role. Many patients belong to middle or upper socioeconomic classes, are meticulous and compulsive, have average intelligence, and have very high standards for achievement and success.
Two types of anorexia nervosa are recognized:
Binges are defined as consumption of a much larger amount of food than most people would eat in a similar time period under similar circumstances with loss of control, ie, perceived inability to resist or stop eating.
Endocrine abnormalities are common; they include low levels of gonadal hormones, mildly reduced levels of thyroxine (T4) and triiodothyronine (T3), and increased cortisol secretion. Menses usually cease, but cessation of menses is no longer a criterion for diagnosis. Bone mass declines. In severely undernourished patients, virtually every major organ system may be affected. Susceptibility to infections is typically not increased.
Dehydration and metabolic alkalosis may occur, and serum K and/or Na may be low; all are aggravated by induced vomiting and laxative or diuretic use.
Cardiac muscle mass, chamber size, and output decrease; mitral valve prolapse is commonly detected. Some patients have prolonged QT intervals (even when corrected for heart rate), which, with the risks imposed by electrolyte disturbances, may predispose to tachyarrhythmias. Sudden death, most likely due to ventricular tachyarrhythmias, may occur.
Symptoms and Signs
Anorexia nervosa may be mild and transient or severe and long-standing.
Most patients are lean but are concerned that they are overweight or that specific body areas (eg, thighs, buttocks) are too fat. They persist in efforts to lose weight despite reassurances and warnings from friends and family members that they are thin or even significantly underweight, and they view any weight gain as an unacceptable failure of self-control. Preoccupation and anxiety about weight increase even as emaciation develops.
Anorexia is a misnomer because appetite often remains until patients become significantly cachectic. Patients are preoccupied with food:
Patients often exaggerate their food intake and conceal behavior, such as induced vomiting. Binge-eating/purging occurs in 30 to 50% of patients. The others simply restrict their food intake.
Many patients with anorexia nervosa also exercise excessively to control weight. Even patients who appear cachectic tend to remain very active (including pursuing vigorous exercise programs).
Reports of bloating, abdominal distress, and constipation are common. Patients usually lose interest in sex. Depression occurs frequently.
Common physical findings include bradycardia, low BP, hypothermia, lanugo hair or slight hirsutism, and edema. Body fat is greatly reduced. Patients who vomit frequently may have eroded dental enamel, painless salivary gland enlargement, and/or an inflamed esophagus.
Not recognizing the seriousness of the low body weight and restrictive eating are prominent features of anorexia nervosa., and patients resist evaluation and treatment. They are usually brought to the physician's attention by family members or by intercurrent illness.
Clinical criteria for diagnosis include the following:
In adults, low body weight is defined using the BMI. BMI of < 17 kg/m2 is considered significantly low; BMI 17 to < 18.5 kg/m2 may be significantly low depending on the patient's starting point. For children and adolescents, the BMI percentile for age is used; the 5th percentile is usually given as the cutoff. However, children above the 5th percentile who have not maintained their projected growth trajectory may also be considered to meet the criteria; BMI percentile for age tables and standard growth charts are available from the CDC (see CDC Growth Charts).
Patients may otherwise appear well. The key to diagnosis is eliciting from them an intense fear of fatness that is not diminished by weight loss.
Another mental disorder, such as schizophrenia or primary depression, may cause weight loss and reluctance to eat, but these disorders are not associated with anorexia nervosa.
Rarely, an unrecognized severe physical disorder may cause substantial weight loss. Disorders to consider include malabsorption syndromes (eg, due to inflammatory bowel disease or celiac disease), new-onset type 1 diabetes, adrenal insufficiency, and cancer. Amphetamine abuse may cause similar symptoms.
Mortality rates are high, approaching 10% per decade among affected people who come to clinical attention; unrecognized mild disease probably rarely leads to death. With treatment, half of patients regain most or all of lost weight, and any endocrine and other complications are reversed. About one fourth have intermediate outcomes and may relapse. The remaining one fourth have a poor outcome, including relapses and persistent physical and mental complications. Children and adolescents treated for anorexia nervosa have better outcomes than adults.
Treatment may require life-saving short-term intervention to restore body weight. When weight loss has been severe or rapid or when weight has fallen below about 75% of recommended weight, prompt restoration of weight becomes critical, and hospitalization should be considered. If any doubt exists, patients should be hospitalized. Outpatient treatments may include varying degrees of support and supervision and commonly involve a team of practitioners.
Nutritional supplementation, which begins by providing about 30 to 40 kcal/kg/day, can produce weight gains of up to 1.5 kg/wk during inpatient care and 0.5 kg/wk during outpatient care. Oral feedings using solid foods are best, but very resistant, undernourished patients occasionally require nasogastric feedings. Elemental Ca 1200 to 1500 mg/day and vitamin D 600 to 800 IU/day are commonly prescribed for bone loss.
Once nutritional, fluid, and electrolyte status has been stabilized, long-term treatment begins. Outpatient psychologic therapy is the cornerstone of treatment. Treatments should emphasize behavioral outcomes such as normalized eating and weight. Treatment should continue for a full year after weight is restored. Results are best in adolescents who have had the disorder < 6 mo. Family therapy, particularly using the Maudsley model, is useful for adolescents. This model has 3 phases:
Treatment is complicated by patients' abhorrence of weight gain and denial of illness. The physician should attempt to provide a calm, concerned, stable relationship while encouraging a reasonable caloric intake.
Although psychologic therapy is primary, drugs are sometimes helpful. Second-generation antipsychotics (eg, olanzapine up to 10 mg po once/day) may help produce weight gain and relieve anxiety.
Last full review/revision May 2014 by Evelyn Attia, MD; B. Timothy Walsh, MD
Content last modified May 2014