Bulimia nervosa

Bulimia nervosa
Classification and external resources
ICD-10 F50.2
ICD-9 307.51
DiseasesDB 1770
eMedicine emerg/810 med/255
MeSH D052018

Bulimia nervosa is an eating disorder characterized by recurrent binge eating, followed by compensatory behaviors.[1] The most common form is defensive vomiting, sometimes called purging; fasting, the use of laxatives, enemas, diuretics, and over exercising are also common.[2]

The word bulimia derives from the Latin (būlīmia), which originally comes from the Greek βουλιμία (boulīmia; ravenous hunger), a compound of βους (bous), ox + λιμός (līmos), hunger.[3] Bulimia nervosa was named and first described by the British psychiatrist Gerald Russell in 1979.[4][5]

Contents

Signs and symptoms

These cycles often involve rapid and out-of-control eating, which may stop when the bulimic is interrupted by another person or the stomach hurts from overextension, followed by self-induced vomiting or other forms of purging. This cycle may be repeated several times a week or, in more serious cases, several times a day,[6] and may directly cause:

The frequent contact between teeth and gastric acid, in particular, may cause:

Related disorders

Bulimics are much more likely than non-bulimics to have an affective disorder, such as depression or general anxiety disorder: A 1985 Columbia University study on female bulimics at New York State Psychiatric Institute found 70% had suffered depression some time in their lives (as opposed to 25.8% for adult females in a control sample from the general population), rising to 88% for all affective disorders combined.[11] Another study by the Royal Children's Hospital in Melbourne on a cohort of 2000 adolescents similarly found that those meeting at least two of the DSM-IV criteria for bulimia nervosa or anorexia nervosa had a sixfold increase in risk of anxiety and a doubling of risk for substance dependency.[12] Bulimia also has negative effects on the sufferer's dental health due to the acid passed through the mouth from frequent vomiting causing acid erosion, mainly on the posterior dental surface.

Diagnosis

The onset of bulimia nervosa is often during adolescence, between 13 and 20 years of age, and many cases have previously suffered obesity, with many sufferers relapsing in adulthood into episodic binging and purging even after initially successful treatment and remission.[13]

Bulimia nervosa can be difficult to detect, compared to anorexia nervosa, because bulimics tend to be of average or slightly above or below average weight. Many bulimics may also engage in significantly disordered eating and exercising patterns without meeting the full diagnostic criteria for bulimia nervosa.[14] The diagnostic criteria utilized by the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV TR) published by the American Psychiatric Association includes repetitive episodes of binge eating (a discrete episode of overeating during which the individual feels out of control of consumption) compensated for by excessive or inappropriate measures taken to avoid gaining weight.[15] The diagnosis is made only when the behavior is not a part of the symptom complex of Anorexia Nervosa and when the behavior reflects an overemphasis on physical mass or appearance.

There are two sub-types of bulimia nervosa:

Management

Pharmacological

Some researchers have hypothesized a relationship to mood disorders and clinical trials have been conducted with tricyclic antidepressants,[17] MAO inhibitors, mianserin, fluoxetine,[18] lithium carbonate, nomifensine, trazodone, and bupropion. Research groups who have seen a relationship to seizure disorders have attempted treatment with phenytoin, carbamazepine, and valproic acid. Opiate antagonists naloxone and naltrexone, which block cravings for gambling, have also been used.[19]

There has also been some research characterizing bulimia nervosa as an addiction disorder, and limited clinical use of topiramate, which blocks cravings for opiates, cocaine, alcohol and food.[20] Researchers have also report positive outcomes when bulimics are treated in an addiction-disorders inpatient unit.[21]

Psychotherapy

There are several empirically-supported psychosocial treatments for bulimia nervosa. Cognitive behavioral therapy (CBT), which involves teaching clients to challenge automatic thoughts and engage in behavioral experiments (e.g., in session eating of "forbidden foods") has demonstrated efficacy both with and without concurrent antidepressant medication.[22][23] Researchers have also reported some positive outcomes for interpersonal psychotherapy and dialectical behavior therapy.[24][25]

Maudsley Family Therapy or "Family Based Treatment" (FBT), developed at the Maudsley Hospital in London for the treatment of anorexia nervosa (AN) has been shown to have positive results for the treatment of bulimia nervosa. FBT has been shown through empirical research to be the most efficacious treatment of AN for patients under the age of eighteen and within three years of onset of illness. The studies to date using FBT to treat BN have been promising.[26]

Some researchers have also claimed positive outcomes in hypnotherapy treatment.[27][28][29]

Other

Brain-derived neurotrophic factor (BDNF) is under investigation as a possible cause.[30][31]

Epidemiology

There are little data on the prevalence of bulimia nervosa in-the-large, on general populations. Most studies conducted thus far have been on convenience samples from hospital patients, high school or university students. These have yielded a wide range of results: between 0.1% and 1.4% of males, and between 0.3% and 9.4% of females.[32] Studies on time trends in the prevalence of bulimia nervosa have also yielded inconsistent results.[33]

Country Year Sample size and type Incidence
Australia 2008 1,943 adolescents (ages 15–17) 1.0% male 6.4% female[12]
Portugal 2006 2,028 high school students 0.3% female[34]
Brazil 2004 1,807 students (ages 7–19) 0.8% male 1.3% female[35]
Spain 2004 2,509 female adolescents (ages 13–22) 1.4% female[36]
Hungary 2003 580 Budapest residents 0.4% male 3.6% female[37]
Australia 1998 4,200 high school students 0.3% combined[38]
USA 1996 1,152 college students 0.2% male 1.3% female[39]
Norway 1995 19,067 psychiatric patients 0.7% male 7.3% female[40]
Canada 1995 8,116 (random sample) 0.1% male 1.1% female[41]
Japan 1995 2,597 high school students 0.7% male 1.9% female[42]
USA 1992 799 college students 0.4% male 5.1% female[43]

There are higher rates of eating disorders in groups involved in activities which idealize a slim physique, such as dance,[37] gymnastics, modeling, cheerleading, running, acting, rowing and figure skating. Bulimia is more prevalent among Caucasians.[44] Exposure to mass media also appears to have an effect: a survey of 15–18 year-old high schoolgirls in Nadroga, Fiji found the self-reported incidence of purging rose from 0% in 1995 (a few weeks after the introduction of television in the province) to 11.3% in 1998.[45]

Notes

  1. Diagnostic and statistical manual of mental disorders: DSM-IV. Washington, DC: American Psychiatric Association. 1994. ISBN 0-89042-062-9. 
  2. Fairburn, Christopher G. (1995). Overcoming binge eating. New York: Guilford Press. ISBN 0-89862-179-8. 
  3. Douglas Harper (November 2001). "Online Etymology Dictionary: bulimia". Online Etymology Dictionary. http://www.etymonline.com/index.php?search=bulimia&searchmode=none. Retrieved 2008-04-06. 
  4. Russell G (August 1979). "Bulimia nervosa: an ominous variant of anorexia nervosa". Psychological Medicine 9 (3): 429–48. doi:10.1017/S0033291700031974. PMID 482466. 
  5. Palmer R (December 2004). "Bulimia nervosa: 25 years on". The British Journal of Psychiatry : the Journal of Mental Science 185: 447–8. doi:10.1192/bjp.185.6.447. PMID 15572732. 
  6. Eating Disorders. Let's Talk About. American Psychiatric Association. 2005. ISBN 0-89042-352-0. http://www.healthyminds.org/Document-Library/Brochure-Library/Eating-Disorders.aspx. 
  7. Joseph AB, Herr B (May 1985). "Finger calluses in bulimia". The American Journal of Psychiatry 142 (5): 655. PMID 3857013. 
  8. Wynn DR, Martin MJ (October 1984). "A physical sign of bulimia". Mayo Clinic Proceedings. Mayo Clinic 59 (10): 722. PMID 6592415. 
  9. 9.0 9.1 "Eating Disorders". Oral Health Topics A–Z. American Dental Association. http://www.ada.org/public/topics/eating_disorders.asp. 
  10. Mcgilley BM, Pryor TL (June 1998). "Assessment and treatment of bulimia nervosa". American Family Physician 57 (11): 2743–50. PMID 9636337. 
  11. Walsh BT, Roose SP, Glassman AH, Gladis M, Sadik C (1985). "Bulimia and depression". Psychosomatic Medicine 47 (2): 123–31. PMID 3863157. http://www.psychosomaticmedicine.org/cgi/pmidlookup?view=long&pmid=3863157. 
  12. 12.0 12.1 Patton GC, Coffey C, Carlin JB, Sanci L, Sawyer S (April 2008). "Prognosis of adolescent partial syndromes of eating disorder". The British Journal of Psychiatry 192 (4): 294–9. doi:10.1192/bjp.bp.106.031112. PMID 18378993. 
  13. Shader, Richard I. (2004). Manual of Psychiatric Therapeutics. Hagerstwon, MD: Lippincott Williams & Wilkins. ISBN 0-7817-4459-8. 
  14. Walsh JM, Wheat ME, Freund K (August 2000). "Detection, evaluation, and treatment of eating disorders the role of the primary care physician". Journal of General Internal Medicine 15 (8): 577–90. doi:10.1046/j.1525-1497.2000.02439.x. PMID 10940151. 
  15. American Psychiatric Association (2000). "Diagnostic criteria for 307.51 Bulimia Nervosa". Diagnostic and Statistical Manual of Mental Disorders (4th, text revision (DSM-IV-TR) ed.). ISBN 0-89042-025-4. http://behavenet.com/capsules/. Retrieved 2010-03-14. 
  16. Barlow, David H.; Durand, Vincent Mark (2002). Abnormal psychology: an integrative approach. Belmont, CA: Wadsworth/Thomson Learning. ISBN 0-534-63362-5. 
  17. Mitchell JE, Raymond N, Specker S (November 1993). "A review of the controlled trials of pharmacotherapy and psychotherapy in the treatment of bulimia nervosa". The International Journal of Eating Disorders 14 (3): 229–47. doi:10.1002/1098-108X(199311)14:3<229::AID-EAT2260140302>3.0.CO;2-X. PMID 8275060. 
  18. Walsh, B T (1995). "Pharmacotherapy of eating disorders". In Brownell. Eating Disorders and Obesity: A Comprehensive Handbook. New York: Guilford. pp. 329–40. ISBN 978-0-89862-850-0. 
  19. Mitchell JE, Christenson G, Jennings J, et al. (April 1989). "A placebo-controlled, double-blind crossover study of naltrexone hydrochloride in outpatients with normal weight bulimia". Journal of Clinical Psychopharmacology 9 (2): 94–7. doi:10.1097/00004714-198904000-00004. PMID 2656781. 
  20. Slaby, Andrew Edmund (1993). The eating disorders. Berlin: Springer-Verlag. ISBN 0-387-94002-2. 
  21. Wilfley DE, Welch RR, Stein RI, et al. (August 2002). "A randomized comparison of group cognitive-behavioral therapy and group interpersonal psychotherapy for the treatment of overweight individuals with binge-eating disorder". Archives of General Psychiatry 59 (8): 713–21. doi:10.1001/archpsyc.59.8.713. PMID 12150647. http://courses.csusm.edu/psyc340sr/articles/IBT_vs_CBT_Wilfley.pdf. 
  22. Agras WS, Crow SJ, Halmi KA, Mitchell JE, Wilson GT, Kraemer HC (August 2000). "Outcome predictors for the cognitive behavior treatment of bulimia nervosa: data from a multisite study". The American Journal of Psychiatry 157 (8): 1302–8. doi:10.1176/appi.ajp.157.8.1302. PMID 10910795. 
  23. Wilson GT, Loeb KL, Walsh BT, et al. (August 1999). "Psychological versus pharmacological treatments of bulimia nervosa: predictors and processes of change". Journal of Consulting and Clinical Psychology 67 (4): 451–9. doi:10.1037/0022-006X.67.4.451. PMID 10450615. 
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  25. Safer DL, Telch CF, Agras WS (April 2001). "Dialectical behavior therapy for bulimia nervosa". The American Journal of Psychiatry 158 (4): 632–4. doi:10.1176/appi.ajp.158.4.632. PMID 11282700. 
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  30. doi:10.1093/hmg/ddh137
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