eMedicine Specialties > Pediatrics: Developmental and Behavioral > Medical Topics

Eating Disorder: Bulimia

Author: Megan A Moreno, MD, MSEd, Department of Pediatrics, Adolescent Medicine and STD/HIV Fellow, Children's Hospital and Regional Medical Center
Coauthor(s): Robert Judd, MD, Associate Professor, Department of Pediatrics, Division of Pediatric Gastroenterology, University of Wisconsin at Madison
Contributor Information and Disclosures

Updated: Feb 25, 2008

Introduction

Background

For thousands of years, humans have engaged in occasional eating binges when adequate food supplies are available. The practice of vomiting after overeating also dates back thousands of years. The examination and definition of abnormal eating patterns as eating disorders did not occur until roughly 20 years ago. Bulimia nervosa (BN) was first described in 1979 as a disorder that involves binge eating followed by inappropriate behavior to avoid weight gain. Criteria for the diagnosis of BN did not emerge until provided by the American Psychiatric Association in 1980.

Criteria for the diagnosis of bulimia include preoccupation with eating and overeating large amounts of food in short periods, also described as binge eating. This behavior is then followed by inappropriate behavior to avoid weight gain, most notably, self-induced vomiting. Other methods of avoiding weight gain include laxative and diuretic abuse and excessive exercise. BN is a disease with a highly focused patient population; it is predominantly found in women and is virtually nonexistent in nonindustrialized countries.

Pathophysiology

BN is a disease that most likely emerges from a complex integration of many factors. These factors may be psychological, cultural, environmental, and societal. Many proposed associated factors are involved in the development of bulimia. These factors can include chemical imbalances in neurotransmitters, such as serotonin or pancreatic polypeptides (eg, pancreatic peptide YY [PYY]). Psychological and psychiatric problems are also thought to contribute to the development of bulimia. Another contributing factor is family problems. Participation in extracurricular activities that emphasize body shape and image has also been linked to the development of bulimia.

The binge and purge cycle characteristic of bulimia affects multiple organ systems. The GI system can be affected by the overeating associated with binge episodes. This overeating can stretch the stomach or delay gastric emptying. Purging can induce esophagitis or esophageal rupture due to vomiting. Pancreatitis can also occur. Electrolyte abnormalities can include hypokalemia and hypochloremia. Cardiovascular abnormalities can lead to arrhythmias, arrest, cardiac rupture, or pneumomediastinum. The pulmonary system can be damaged by aspiration of gastric contents upon vomiting. Renal function impairment is also possible.

Frequency

United States

Lifetime prevalence among women is 1-3%, and a comparable percentage of women have less severe variants of the disorder. Lifetime prevalence among men is 0.1%.

International

Although no concrete data are available, bulimia is a disease that is highly culturally dependent. It is found solely in societies in which a high cultural value is placed on slimness and is virtually nonexistent in nonindustrialized countries.

Mortality/Morbidity

  • Death is a relatively uncommon outcome for bulimia. Approximately 0-3% of women with the disease eventually die from complications of the disease; however, these numbers may be underestimated due to low ascertainment rates and short follow-up periods.
  • The leading cause of death among patients with eating disorders is suicide, which is more common in patients with BN than in those with anorexia nervosa (AN). Factors most strongly associated with suicide attempt or suicidal ideation in patients with eating disorders include concurrent drug use, alcohol use, and tobacco use.1 Suicide risk should be carefully monitored in patients with eating disorders who also have these risk factors.
  • One third of patients who present for treatment of BN have past histories of AN.
  • Bulimia has many complications (see Complications).

Race

Bulimia has traditionally been thought of as a disease that predominantly affects whites. The low incidence of eating disorders among nonwhites has been attributed to differences among ethnic groups in ideal body image. Studies have shown that black women are less likely to develop eating disorders and tend to express more satisfaction with their bodies than white women of similar weight; however, other studies suggest that the incidence of bulimia among minority groups is higher than previously thought. Studies suggest that patients from higher socioeconomic groups are more likely to seek treatment, making the incidence within these groups appear to be higher.

Some population studies suggest an equal incidence of bulimia in blacks and whites. Overall, strong circumstantial evidence suggests that cultural factors play large roles in eating disorder development. Most cases of BN originate in industrialized countries. In general, industrialized countries are places where food is plentiful and a preoccupation with thinness in women is present.

Sex

Bulimia primarily occurs in young women. Males comprise only 2-8% of all bulimia cases.

Age

Bulimia is most common in adolescents and young adults. Median age of onset is 18 years.

Clinical

History

Obtaining a thorough history is essential in any patient in whom bulimia is suggested.

  • Patients often deny the problem; however, thorough and careful questioning may reveal clues that the patient has bulimia.
  • Often, patients have a history of dieting attempts and may admit to feeling fat even when they appear thin.
  • Patients often state that their self-esteem is linked closely to their body weight or shape.
  • The patient may have a history of using diet pills, laxatives, ipecac, or thyroid medication to lose weight.
  • Patients may become vegetarians.
  • Diabetic patients may withhold insulin.
  • Patients who admit to purging behavior often describe a history of uncontrolled eating binges at least twice weekly. 
    • During these binges, large amounts of food are consumed in private. Some patients plan ahead for binges by secretly hoarding food.
    • Patients may describe feeling a loss of control when the binge begins, then a period of frenzied and rapid eating.
    • The binge is followed by inappropriate compensatory behavior, usually self-induced vomiting.

Physical

The diagnosis of bulimia is not conditional on physical findings. Physical findings may not be present in all patients. Patients may have some findings, all findings, or none at all. The following physical findings are associated with bulimia:

  • General  
    • Normal body weight, but may be increased or decreased
    • Often frequent fluctuations in weight
    • Loss of subcutaneous fat
  • Vital signs 
    • Temperature - Hypothermia
    • Blood pressure - Hypotension
  • Head, ears, eyes, nose, and throat
    • Dental erosion - Decalcification of dental surfaces exposed to vomitus (Amalgams and fillings are relatively resistant to acid and often project above the surface of the teeth.)
    • Palatal trauma
    • Painless enlargement of parotid glands
  • Cardiovascular - Bradycardia
  • Abdomen - Frequent complaints of diffuse pain upon palpation
  • Extremities 
    • Metacarpal phalangeal bruises, calluses, scarring, abrasions (Russell sign)
    • Edema possible if patient abuses laxatives or diuretics
    • Proximal muscle weakness if patient abuses ipecac
    • Waddling gait if patient abuses ipecac

Causes

Bulimia nervosa (BN) is a complex disease that most likely emerges from an integration of physiological, psychological, and environmental factors. Currently, no defined single cause of BN is recognized. Several factors are believed to play a strong role in the development of bulimia.

  • Chemical: A few hypotheses suggest specific chemical abnormalities in the body are associated with bulimia.
    • Serotonin is a neurotransmitter with broad functions within the body. Among these functions, serotonin is involved in the development of satiety. Increased levels of serotonin are associated with decreased food intake. Serotonin is believed to increase postprandial satiety rather than directly decrease appetite.
      • One hypothesis of the development of bulimia involves abnormalities in serotonergic function. Some patients with bulimia have been found to have low serotonin levels. Because serotonin is involved in the development of satiety, these disturbances may contribute to the persistence of binge eating. 
      • A potential hypothesis is that an impaired serotonergic response may contribute to the blunted satiety and prolonged periods of rapid food ingestion present in BN. Dieting has also been associated with altered serotonin function, more markedly in women than in men. Dieting is often a precursor to the development of bulimia; however, not all women who diet develop bulimia. This hypothesis is not thought to provide a sufficient sole explanation for the development of bulimia.
    • Another suggested pathophysiology involves increased levels of peptides involved in mediating appetite. Increased levels of a pancreatic polypeptide PYY, a peptide known to increase appetite, have been found in some patients with bulimia after a period of eating stability. This would suggest that these patients have a higher level of appetite, even when given a normal diet.
  • Psychiatric
    • Premorbid psychiatric disorders are often associated with development of bulimia. These can include affective disorders, anxiety disorders, and substance abuse.
    • Many patients with bulimia have concomitant depression.
  • Psychological and environmental
    • The strongest risk factor in the development of bulimia is history of dieting. Many patients report that their eating binges began in the context of or immediately following a diet. Many patients continue to restrict their caloric intake even when not binge eating.
    • Strong circumstantial evidence suggests that cultural factors play a large role in eating disorder development. Most cases of BN originate in industrialized countries where food is plentiful and a preoccupation with thinness in women is present.
    • Obesity is another risk factor for bulimia.
  • Family
    • Family problems are also associated with the development of bulimia.
    • A history of sexual abuse has been associated in some literature as a risk factor for development of bulimia.
    • A family history of eating disorder increases a child's risk of developing an eating disorder to 2-20 times that of the general population.
  • Interests and activities
    • Certain athletes and groups are thought to be more prone to development of bulimia. Specifically, these include ballet dancers, models, cheerleaders, runners, gymnasts, weight lifters, body builders, jockeys, divers, wrestlers, figure skaters, and field hockey players. Persons in these particular sports and activities often place a high value upon thinness or maintaining a particular weight.
    • The bodies of participants in these activities are often on display in front of crowds or judged in terms of body shape and weight. These high-pressure situations and preoccupation with weight can place teens at risk for eating disorders.

More on Eating Disorder: Bulimia

Overview: Eating Disorder: Bulimia
Differential Diagnoses & Workup: Eating Disorder: Bulimia
Treatment & Medication: Eating Disorder: Bulimia
Follow-up: Eating Disorder: Bulimia
References

References

  1. Fedorowicz VJ, Falissard B, Foulon C, Dardennes R, Divac SM, Guelfi JD, et al. Factors associated with suicidal behaviors in a large French sample of inpatients with eating disorders. Int J Eat Disord. Nov 2007;40(7):589-95. [Medline][Full Text].

  2. Bacaltchuk J, Hay P. Antidepressants versus placebo for people with bulimia nervosa.[update of Cochrane Database Syst Rev. 2001]. Cochrane Database of Systematic Reviews. 2003;4:[Full Text].

  3. Simon GE, Savarino J, Operskalski B, Wang PS. Suicide risk during antidepressant treatment. Am J Psychiatry. Jan 2006;163(1):41-7. [Medline][Full Text].

  4. Keel PK, Mitchell JE. Outcome in bulimia nervosa. Am J Psychiatry. Mar 1997;154(3):313-21. [Medline][Full Text].

  5. Eddy KT, Dorer DJ, Franko DL, Tahilani K, Thompson-Brenner H, Herzog DB. Should bulimia nervosa be subtyped by history of anorexia nervosa? A longitudinal validation. Int J Eat Disord. Nov 2007;40 Suppl:S67-71. [Medline][Full Text].

  6. Morgan JF, Reid F, Lacey JH. The SCOFF questionnaire: assessment of a new screening tool for eating disorders. BMJ. Dec 4 1999;319(7223):1467-8. [Medline][Full Text].

  7. Behrman RE, Kliegman R, Jenson HB. Nelson's Textbook of Pediatrics. 16th ed. Philadelphia, Pa: WB Saunders and Co; 2000.

  8. Carney CP, Andersen AE. Eating disorders. Guide to medical evaluation and complications. Psychiatr Clin North Am. Dec 1996;19(4):657-79. [Medline].

  9. Cotran RS, Kumar V, Collins T. Robbins Pathologic Basis of Disease. 6th ed. Philadelphia, Pa: WB Saunders and Co; 1999.

  10. Dambro MR, Griffith JA, Griffith HG. Griffith's Five Minute Clinical Consult. 5th ed. Baltimore, Md: Williams & Wilkins; 1999.

  11. Ellenhorn MJ. Ellenhorn's Medical Toxicology. 2nd ed. Baltimore, Md: Williams & Wilkins; 1997.

  12. Halmi KA. Models to conceptualize risk factors for bulimia nervosa. Arch Gen Psychiatry. Jun 1997;54(6):507-8. [Medline].

  13. Haly PJ, Bacltchuck J. Bulimia Nervosa. American Family Physician. June 2007;75:1699-702.

  14. Hartman BK, Faris PL, Kim SW, Raymond NC, Goodale RL, Meller WH, et al. Treatment of bulimia nervosa with ondansetron. Arch Gen Psychiatry. Oct 1997;54(10):969-70. [Medline].

  15. Hay PJ, Bacaltchuk J, Stefano S. Psychotherapy for bulimia nervosa and binging. Cochrane Database Syst Rev. 2004;(3):CD000562. [Medline][Full Text].

  16. Lilly RZ. Bulimia nervosa. BMJ. Aug 16 2003;327(7411):380-1. [Medline][Full Text].

  17. Muise AM, Stein DG, Arbess G. Eating disorders in adolescent boys: a review of the adolescent and young adult literature. J Adolesc Health. Dec 2003;33(6):427-35. [Medline].

  18. Nicholls D, Viner R. Eating disorders and weight problems. BMJ. Apr 23 2005;330(7497):950-3. [Medline][Full Text].

  19. Siberry GK, Iannone R. The Harriet Lane Handbook: A Manual for Pediatric House Officers. 15th ed. Mosby-Year Book; 2000.

  20. Spindler A, Milos G. Links between eating disorder symptom severity and psychiatric comorbidity. Eat Behav. Aug 2007;8(3):364-73. [Medline].

  21. Taketomo CK, Hodding JH, Kraus DM. Pediatric Dosage Handbook. 6th ed. 1999.

  22. Walsh BT, Devlin MJ. Eating disorders: progress and problems. Science. May 29 1998;280(5368):1387-90. [Medline].

Further Reading

Keywords

BN, bulimia nervosa, bulimia, boulimia, hyperorexia, binge eating, eating disorder, binging and purging, anorexia, anorexia nervosa, AN, self-induced vomiting, laxative abuse, diuretic abuse, overeating, vomiting after overeating, binge and purge cycle, weight problems, abnormal eating patterns, dieting, avoiding weight gain, delayed gastric emptying, esophagitis, esophageal rupture, pancreatitis, hypokalemia, hypochloremia, pneumomediastinum, anorexia nervosa, ipecac abuse, hypothermia, hypotension, affective disorders, anxiety disorders, substance abuse, sexual abuse

Contributor Information and Disclosures

Author

Megan A Moreno, MD, MSEd, Department of Pediatrics, Adolescent Medicine and STD/HIV Fellow, Children's Hospital and Regional Medical Center
Megan A Moreno, MD, MSEd is a member of the following medical societies: Society for Adolescent Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Robert Judd, MD, Associate Professor, Department of Pediatrics, Division of Pediatric Gastroenterology, University of Wisconsin at Madison
Robert Judd, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Medical Editor

Angelo P Giardino, MD, PhD, Clinical Associate Professor, Department of Pediatrics, Baylor College of Medicine; Medical Director, Texas Children's Health Plan, Inc
Angelo P Giardino, MD, PhD is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and American Professional Society on the Abuse of Children
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

CME Editor

Carrie Sylvester, MD, MPH, Director of Education in Child and Adolescent Psychiatry, Professor, Departments of Psychiatry and Pediatrics, Northwestern University Medical School
Carrie Sylvester, MD, MPH is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, American Academy of Pediatrics, American Medical Women's Association, American Psychiatric Association, and American Society for Adolescent Psychiatry
Disclosure: Nothing to disclose.

Chief Editor

Caroly Pataki, MD, Professor of Clinical Psychiatry, Department of Psychiatry and Biobehavioral Sciences, Division Chair of Child and Adolescent Psychiatry, Director of Training, Child and Adolescent Psychiatry Residency Program, University of Southern California Keck School of Medicine
Caroly Pataki, MD is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, New York Academy of Sciences, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

RELATED MEDSCAPE ARTICLES
Resource Centers
 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.