Eating disorder: Bulimia nervosa (binge eating disorder)

• What is Bulimia Nervosa
• Statistics on Bulimia Nervosa
• Risk Factors for Bulimia Nervosa
• Progression of Bulimia Nervosa
• Symptoms of Bulimia Nervosa
• Clinical Examination of Bulimia Nervosa
• How is Bulimia Nervosa Diagnosed?
• Prognosis of Bulimia Nervosa
• How is Bulimia Nervosa Treated?
• Bulimia Nervosa References

What is Bulimia Nervosa

Bulimia nervosa is a psychological disease. Bulimia nervosa is characterised by the episodic, uncontrolled and impulsive binge eating followed by self-induced vomiting or consumption of laxatives or purgatives to avoid the weight gain associated with such behaviour.

Statistics on Bulimia Nervosa

Bulimia nervosa is more common in women than in men. Bulimia generally starts at about 16 to 18 years of age. Any given woman has a 1-4% chance of developing this condition throughout her lifetime.

Bulimia is often found in association with other eating disorders such as anorexia nervosa.

Risk Factors for Bulimia Nervosa

There are few predisposing factors for the development of this eating disorder. The main risk factor of bulimia is a family history of psychiatric illness or a co-existing psychiatric problem. If another close family member has suffered from depression or eating disorder in the past, the risk of developing bulimia is increased.

If the patient has suffered or is suffering from depression, they are also more likely to develop an eating disorder. Whether this trend represents a genetic or environmental link is not entirely known.

Progression of Bulimia Nervosa

Excessive dieting by bulimia patients commonly have a history which progresses to bulimia-type behaviour (induced vomiting) with repeating diet failure. The patient will regularly engage in eating binges followed by the bulimia behaviours of vomiting and use of purgatives/laxatives to avoid the calorie content of the food.

Excessive vomiting and laxative induced diarrhoea may result in an electrolyte imbalance which could be potentially life-threatening if left untreated. Binge eating disorder is bulimia without the vomiting and other weight-reducing strategies.

How is Bulimia Nervosa Diagnosed?

Without the occurrence of complications, investigations such as blood tests are not warranted for this bulimia.

Unless sufferers come forward with their condition it can be hard for even the closest of friends and family to see any signs completely out of the ordinary.

Prognosis of Bulimia Nervosa

Prognosis for bulimia nervosa is better than for anorexia nervosa. With treatment for bulimia, approximately 60% of patients will recover.

How is Bulimia Nervosa Treated?

There is usually no requirement for hospital admission for bulimia illness sufferers, unless the patient is suffering from an electrolyte disturbance that can be induced by long-term vomiting and diarrhoea. It must be stressed that the electrolyte complications of bulimia can be life-threatening.

Bulimia treatment tends to focus on breaking the binge-purge cycles.

Patients will benefit most from psychotherapy in a number of settings. Individual and group psychotherapy have been proven to imporve the outcome of patients with bulimia nervosa. The use of anti-depressants such as fluoxetine, in combination with psychotherapy increases the overall outcome of this eating disorder.

More information

For more information on nutrition, including information on types and composition of food, nutrition and people, conditions related to nutrition, and diets and recipes, as well as some useful videos and tools, see Nutrition.

For more information on psychology and psychotherapy, including different types of therapy, see Psychology and Psychotherapy.

Bulimia Nervosa References

1. American Psychiatric Association: Diagnostic and statistical manual of mental disorders, 4th ed. American Psychiatric Press, Inc; 1994.
2. eMedicine
3. Kumar P, Clark M. Clinical Medicine. Fourth Ed. WB Saunders, 2002.
4. Sadock BJ., Sadock VA. Kaplan and Sadock’s Pocket Handbook of Clinical Psychiatry 3rd Edition. Lippincott Williams and Wilkins 1996.