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Bulimia nervosa

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yashasvi Aryaputra[2]

Synonyms and keywords: Bulimia, Binge eating and purging

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yashasvi Aryaputra[2]

Overview

Bulimia is an eating disorder in which an individual purges after they eat large quantities of food in a short period of time. Bulimia is linked with many mental disorders, one of the most prominent of which is depression. Those with this disorder fear gaining weight as a result of the binge eating episodes they go on, so they resort to extreme ways to counteract that such as forcing themselves to vomit.[1]

Historical Perspective

Bulimia is a Greek term that translates to “ravenous hunger”. Gerald Russell became the first person to publish a description of bulimia nervosa in 1979.

Pathophysiology

Bulimia is related to deep psychological issues and feelings of lack of control. They may feel a loss of control during a binge, and consume great quantities of food (over 20,000 calories). There are higher rates of eating disorders in groups involved in activities that emphasize thinness and body type, such as gymnastics, dance and cheerleading, figure skating.

Classification

Bulimia nervosa may be classified in to two types on the basis of purging behavior into purging and non-purging types.

Causes

Screening

Differential Diagnosis

Epidemiology and Demographics

Very few studies regarding bulimia nervosa have been conducted on the general population, and thus, very little data is available. Bulimia nervosa is more prominent in females than in males. 0.1% to 1.4% of males are affected whereas 0.3% to 9.4% of females are affected.

Risk Factors

The risk for Bulimia nervosa may be increased due to possible genetic predisposition, hormonal imbalances, and poor body image and self esteem.

Natural History, Complications and Prognosis

Bulimia typically tends to start in late teens or early 20s. Bulimics go through cycles of over-eating and purging, that may be severe and devastating to the body. This cycle may be repeated several times a week or, in serious cases, several times a day. Bulimics may appear underweight, normal weight or overweight. Bulimia may cause several complications including malnutrition, dehydration, electrolyte imbalance, and vitamin and mineral deficiencies. The Eating Disorders Association of UK estimates it at 10%. An 18% mortality rate has been suggested for anorexia.

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Primary Prevention

Secondary Prevention

Cost-effectiveness of Therapy

Future or Investigational Therapies

References

  1. Hay PJ, Claudino AM (2010). “Bulimia nervosa”. BMJ Clin Evid. 2010. PMC 3275326. PMID 21418667.
Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yashasvi Aryaputra[2]

Overview

Bulimia is a Greek term that translates to “ravenous hunger”. Gerald Russell became the first person to publish a description of bulimia nervosa in 1979.

Historical Perspective

  • Bulimia is a Greek term that translates to “ravenous hunger”.[1][2]
  • While Bulimia is considered an issue in modern day society, it was popular among the ancient Romans and Egyptians to either make more room to eat or because it was viewed as having health benefits.
  • Gerald Russell became the first person to publish a description of bulimia nervosa in 1979. Bulimia nervosa then went on to make an appearance in the DSM-III a year later in 1980.

References

  1. Russell G (1979). “Bulimia nervosa: an ominous variant of anorexia nervosa”. Psychol Med. 9 (3): 429–48. PMID 482466.
  2. Kendler KS, MacLean C, Neale M, Kessler R, Heath A, Eaves L (1991). “The genetic epidemiology of bulimia nervosa”. Am J Psychiatry. 148 (12): 1627–37. doi:10.1176/ajp.148.12.1627. PMID 1842216.
Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yashasvi Aryaputra[2]

Overview

Bulimia is related to deep psychological issues and feelings of lack of control. They may feel a loss of control during a binge, and consume great quantities of food (over 20,000 calories). There are higher rates of eating disorders in groups involved in activities that emphasize thinness and body type, such as gymnastics, dance and cheerleading, figure skating.

Pathophysiology

  • Bulimia is related to deep psychological issues and feelings of lack of control.
  • Sufferers often use the destructive eating pattern to feel in control over their lives.[1]
  • They may hide or hoard food and overeat when stressed or upset.
  • They may feel a loss of control during a binge, and consume great quantities of food (over 20,000 calories).[2]
  • There are higher rates of eating disorders in groups involved in activities that emphasize thinness and body type, such as gymnastics, dance and cheerleading, figure skating.[3]
  • Bulimia is more prevalent among Caucasians, but is increasing among African Americans and Hispanics.

References

Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yashasvi Aryaputra[2]

Overview

Bulimia nervosa may be classified in to two types on the basis of purging behavior into purging and non-purging types.

Classification

Two subtypes of bulimia are distinguished by the way the bulimic relieves themselves of the binge.

Purging Type

Purging type is the more common type of bulimia, and involves any of self-induced vomiting, laxatives, diuretics, tapeworms, enemas, or ipecac, to rapidly extricate the contents from their body.[1]

Non-Purging Type

Non-purging type occurs in only approximately 6%-8% of bulimia cases, as it is a less effective means of ridding the body of such a large number of calories. It involves doing excessive exercise or fasting after a binge, to counteract the large amount of calories previously ingested. This often occurs in purging-type bulimics but is a secondary form of weight control.[2]

References

  1. Durand, Mark, Barlow, David. “Essentials of Abnormal Psychology Fourth Ed.” Thomson Wadsworth, CA 2006, ISBN 0-534-60575-3
  2. Durand, Mark, Barlow, David. “Essentials of Abnormal Psychology Fourth Ed.” Thomson Wadsworth, CA 2006, ISBN 0-534-60575-3
Causes
Differentiating Bulimia nervosa from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Overview

Differential Diagnosis

Differences from Anorexia Nervosa

The main criteria differences involve weight: an anorexic must have a body mass index of less than 17.5. Typically an anorexic is defined by the refusal to maintain a normal weight by self-starvation.

Another criterion which must usually be met is amenorrhea, the loss of a female’s menstrual cycle not caused by the normal cessation of menstruation during menopause for a period of three months. Generally the anorexic does not engage in regular binging and purging sessions. If binging and purging occurs but rarely, and the patient also fails to maintain a minimum weight, they are classified as a purging anorexic, due to the underweight criterion being met and cessation of menstruation. [2]

Characteristically, bulimics feel more shame and out of control with their behaviors, as the anorexic meticulously controls their intake, a symptom that calms their anxiety around food as s/he feels s/he has control of it, naïve to the notion that it, in fact, controls him/her. For this reason, the bulimic is more likely to admit to having a problem, as they do not feel they are in control of their behavior. The anorexic is more likely to believe they are in control of their eating and much less likely to admit that a problem exists.

Anorexics and bulimics have an overpowering sense of self determined by their body and their perceptions of it. They trace all their achievements and successes to it, and so are often depressed as they feel they are consistently failing to achieve the perfect body. Bulimics feel that they are a failure because s/he cannot achieve a low weight, and this outlook infiltrates into all aspects of their lives. Anorexics cannot see that they are underweight and constantly work towards a goal that they cannot meet. They too allow this failure to define their self worth. As both the anorexic and bulimic never feel satisfaction in the more important part of their lives, depression often accompanies these disorders.[3]

Other Differentials

Bulimia nervosa should also be differentiated from other diseases that cause chronic nausea and vomiting. The differentials include the following:[4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35]

Disorder Clinical features Laboratory findings
Chronic nausea Vomiting Diarrhea Retching Lethargy Social withdrawal Photophobia Epigastric pain/burning Lanugo hair Hypogonadism Russel’s sign Body mass index (normal range: 18.5 to 24.9) Complete blood count (CBC) Electrolyte imabalance Lipase and amylase levels Gastric scintigraphy Ambulatory esophageal pH and impedance testing
Gastroparesis ✔ (within 1 hour of eating)
  • Normal (maybe elevated if chronic renal failure is the cause of gastroparesis- usually less than threefold)
  • Periodic measurement of radiolabeled solid meal:  
    • Grade 1 (mild), 11%-20% retention at 4 h
    • Grade 2 (moderate), 21%-35% retention at 4 h
    • Grade 3 (severe), 36%-50% retention at 4 h
    • Grade 4 (very severe), > 50% retention at 4 h
  • Impedance testing (antroduodenal manometery): Loss of normal fasting migratory motor complexes (MMCs) and reduced postprandial antral contractions and, in some cases pylorospasm
Anorexia nervosa
  • Increased
Bulimia nervosa Normal
  • Increased
Rumination syndrome ✔ (Regurgitation more common- within minutes of meal intake)
  • Normal
  • Normal
  • Esophageal pH: Fall in esophageal pH immediately after reguritation (occurs while patient is awake and erect; this is in contrast to GERD, where reflux occurs diurnally and supine position)
Functional dyspepsia Normal
  • Normal
  • Esophageal pH: May be decreased if patient develops reflux
Cyclic vomiting syndrome
  • Rapid or normal
  • Esophageal pH: Decreased
Pancreatitis Normal
  • Increased
  • Not indicated
  • Esophageal pH: Normal
Gastric outlet obstruction ✔ (within 1 hour of eating)
  • Esophageal pH: Increased
  • Esophageal manometery:   High manoraetric score

References

  1. Diagnostic and statistical manual of mental disorders : DSM-5. Washington, D.C: American Psychiatric Association. 2013. ISBN 0890425558.
  2. Diagnostic Statistics Manual IV
  3. Durand, Mark, Barlow, David. “Essentials of Abnormal Psychology Fourth Ed.” Thomson Wadsworth, CA 2006, ISBN 0-534-60575-3
  4. Parkman HP (2015). “Idiopathic gastroparesis”. Gastroenterol. Clin. North Am. 44 (1): 59–68. doi:10.1016/j.gtc.2014.11.015. PMC 4324534. PMID 25667023.
  5. Werlin SL, Fish DL (2006). “The spectrum of valproic acid-associated pancreatitis”. Pediatrics. 118 (4): 1660–3. doi:10.1542/peds.2006-1182. PMID 17015559.
  6. Noddin L, Callahan M, Lacy BE (2005). “Irritable bowel syndrome and functional dyspepsia: different diseases or a single disorder with different manifestations?”. MedGenMed. 7 (3): 17. PMC 1681633. PMID 16369243.
  7. Gupta R, Kalla M, Gupta JB (2012). “Adult rumination syndrome: Differentiation from psychogenic intractable vomiting”. Indian J Psychiatry. 54 (3): 283–5. doi:10.4103/0019-5545.102434. PMC 3512372. PMID 23226859.
  8. Sağlam F, Sivrikoz E, Alemdar A, Kamalı S, Arslan U, Güven H (2015). “Bouveret syndrome: A fatal diagnostic dilemma of gastric outlet obstruction”. Ulus Travma Acil Cerrahi Derg. 21 (2): 157–9. PMID 25904280.
  9. Talley NJ (2011). “Rumination syndrome”. Gastroenterol Hepatol (N Y). 7 (2): 117–8. PMC 3061016. PMID 21475419.
  10. Tutuian R, Castell DO (2004). “Rumination documented by using combined multichannel intraluminal impedance and manometry”. Clin. Gastroenterol. Hepatol. 2 (4): 340–3. PMID 15067630.
  11. Kessing BF, Smout AJ, Bredenoord AJ (2014). “Current diagnosis and management of the rumination syndrome”. J. Clin. Gastroenterol. 48 (6): 478–83. doi:10.1097/MCG.0000000000000142. PMID 24921208.
  12. Parkman HP (2009). “Assessment of gastric emptying and small-bowel motility: scintigraphy, breath tests, manometry, and SmartPill”. Gastrointest. Endosc. Clin. N. Am. 19 (1): 49–55, vi. doi:10.1016/j.giec.2008.12.003. PMID 19232280.
  13. Waseem S, Moshiree B, Draganov PV (2009). “Gastroparesis: current diagnostic challenges and management considerations”. World J. Gastroenterol. 15 (1): 25–37. PMC 2653292. PMID 19115465.
  14. Mearin F, Camilleri M, Malagelada JR (1986). “Pyloric dysfunction in diabetics with recurrent nausea and vomiting”. Gastroenterology. 90 (6): 1919–25. PMID 3699409.
  15. Abell TL, Camilleri M, Donohoe K, Hasler WL, Lin HC, Maurer AH, McCallum RW, Nowak T, Nusynowitz ML, Parkman HP, Shreve P, Szarka LA, Snape WJ, Ziessman HA (2008). “Consensus recommendations for gastric emptying scintigraphy: a joint report of the American Neurogastroenterology and Motility Society and the Society of Nuclear Medicine”. Am. J. Gastroenterol. 103 (3): 753–63. doi:10.1111/j.1572-0241.2007.01636.x. PMID 18028513.
  16. Jiang CF, Ng KW, Tan SW, Wu CS, Chen HC, Liang CT, Chen YH (2002). “Serum level of amylase and lipase in various stages of chronic renal insufficiency”. Zhonghua Yi Xue Za Zhi (Taipei). 65 (2): 49–54. PMID 12014357.
  17. Szmukler, G. I.; Young, G. P.; Lichtenstein, M.; Andrews, J. T. (1990). “A serial study of gastric emptying in anorexia nervosa and bulimia”. Australian and New Zealand Journal of Medicine. 20 (3): 220–225. doi:10.1111/j.1445-5994.1990.tb01023.x. ISSN 0004-8291.
  18. Diamanti A, Bracci F, Gambarara M, Ciofetta GC, Sabbi T, Ponticelli A, Montecchi F, Marinucci S, Bianco G, Castro M (2003). “Gastric electric activity assessed by electrogastrography and gastric emptying scintigraphy in adolescents with eating disorders”. J. Pediatr. Gastroenterol. Nutr. 37 (1): 35–41. PMID 12827003.
  19. Ferholt J, Provence S (1976). “Diagnosis and treatment of an infant with psychophysiological vomiting”. Psychoanal Study Child. 31: 439–59. PMID 981449.
  20. Lee H, Rhee PL, Park EH, Kim JH, Son HJ, Kim JJ, Rhee JC (2007). “Clinical outcome of rumination syndrome in adults without psychiatric illness: a prospective study”. J. Gastroenterol. Hepatol. 22 (11): 1741–7. doi:10.1111/j.1440-1746.2006.04617.x. PMID 17914944.
  21. Koskenpato J, Kairemo K, Korppi-Tommola T, Färkkilä M (1998). “Role of gastric emptying in functional dyspepsia: a scintigraphic study of 94 subjects”. Dig. Dis. Sci. 43 (6): 1154–8. PMID 9635600.
  22. Urbain JL, Vekemans MC, Parkman H, Van Cauteren J, Mayeur SM, Van den Maegdenbergh V, Charkes ND, Fisher RS, Malmud LS, De Roo M (1995). “Dynamic antral scintigraphy to characterize gastric antral motility in functional dyspepsia”. J. Nucl. Med. 36 (9): 1579–86. PMID 7658213.
  23. Hejazi RA, Lavenbarg TH, McCallum RW (2010). “Spectrum of gastric emptying patterns in adult patients with cyclic vomiting syndrome”. Neurogastroenterol. Motil. 22 (12): 1298–302, e338. doi:10.1111/j.1365-2982.2010.01584.x. PMID 20723071.
  24. “Gastric outlet obstruction – an overview | ScienceDirect Topics”.
  25. Minami H, McCallum RW (1984). “The physiology and pathophysiology of gastric emptying in humans”. Gastroenterology. 86 (6): 1592–610. PMID 6370777.
  26. Humphries LL, Adams LJ, Eckfeldt JH, Levitt MD, McClain CJ (1987). “Hyperamylasemia in patients with eating disorders”. Ann. Intern. Med. 106 (1): 50–2. PMID 2431640.
  27. Hempen I, Lehnert P, Fichter M, Teufel J (1989). “[Hyperamylasemia in anorexia nervosa and bulimia nervosa. Indication of a pancreatic disease?]”. Dtsch. Med. Wochenschr. (in German). 114 (49): 1913–6. doi:10.1055/s-2008-1066848. PMID 2480214.
  28. Okada R, Okada A, Okada T, Okada T, Hamajima N (2009). “Elevated serum lipase levels in patients with dyspepsia of unknown cause in general practice”. Med Princ Pract. 18 (2): 130–6. doi:10.1159/000189811. PMID 19204432.
  29. Sansone RA, Sansone LA (2012). “Hoarseness: a sign of self-induced vomiting?”. Innov Clin Neurosci. 9 (10): 37–41. PMC 3508961. PMID 23198276.
  30. Tack J, Caenepeel P, Arts J, Lee KJ, Sifrim D, Janssens J (2005). “Prevalence of acid reflux in functional dyspepsia and its association with symptom profile”. Gut. 54 (10): 1370–6. doi:10.1136/gut.2004.053355. PMC 1774686. PMID 15972301.
  31. “gut.bmj.com” (PDF).
  32. Boles RG, Williams JC (1999). “Mitochondrial disease and cyclic vomiting syndrome”. Dig. Dis. Sci. 44 (8 Suppl): 103S–107S. PMID 10490048.
  33. Ranasinghe WK, Smith M (2013). “Gastric outlet obstruction with an elevated serum pancreatic lipase secondary to an infraumbilical hernia”. Ann R Coll Surg Engl. 95 (7): 122–4. doi:10.1308/003588413X13629960047795. PMID 24112485.
  34. Ui, Takashi; Shibusawa, Hiroyuki; Tsukui, Hidenori; Sakuma, Kazuya; Takahashi, Shuhei; Lefor, Alan K.; Hosoya, Yoshinori; Sata, Naohiro; Yasuda, Yoshikazu (2015). “Pretreatment of gastric outlet obstruction with pancrelipase: Report of a case”. International Journal of Surgery Case Reports. 12: 87–89. doi:10.1016/j.ijscr.2015.05.023. ISSN 2210-2612.
Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yashasvi Aryaputra[2]

Overview

Very few studies regarding bulimia nervosa have been conducted on the general population, and thus, very little data is available. Bulimia nervosa is more prominent in females than in males. 0.1% to 1.4% of males are affected whereas 0.3% to 9.4% of females are affected.

Epidemiology and Demographics

Age

Bulimia nervosa can occur in people of all ages, although it is more prevalent in younger populations.[1][2]

Gender

Bulimia nervosa is more prominent in females than in males. 0.1% to 1.4% of males are affected whereas 0.3% to 9.4% of females are affected.[1][2]

Race

A recent study shows that African-American teenage girls are 50% more likely to deal with bulimia than Caucasian girls.[1][2]

Developed Countries

Bulimia nervosa is more common in developed countries as opposed to developing countries.[1][2]

Developing Countries

Bulimia nervosa is less common in developing countries as opposed to developed countries.[1][2]

References

  1. 1.0 1.1 1.2 1.3 1.4 Makino M, Tsuboi K, Dennerstein L (2004). “Prevalence of eating disorders: a comparison of Western and non-Western countries”. MedGenMed. 6 (3): 49. PMC 1435625. PMID 15520673.
  2. 2.0 2.1 2.2 2.3 2.4 Hay PJ, Mond J, Buttner P, Darby A (2008). “Eating disorder behaviors are increasing: findings from two sequential community surveys in South Australia”. PLoS One. 3 (2): e1541. doi:10.1371/journal.pone.0001541. PMC 2212110. PMID 18253489.
Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yashasvi Aryaputra[2]

Overview

The risk for Bulimia nervosa may be increased due to possible genetic predisposition, hormonal imbalances, and poor body image and self esteem.

Risk Factors

The following conditions increases the risk of bulimia nervosa:

References

  1. 1.0 1.1 Ribasés M, Gratacòs M, Fernández-Aranda F, Bellodi L, Boni C, Anderluh M; et al. (2004). “Association of BDNF with anorexia, bulimia and age of onset of weight loss in six European populations”. Hum Mol Genet. 13 (12): 1205–12. doi:10.1093/hmg/ddh137. PMID 15115760.
  2. Hirschberg AL (2012). “Sex hormones, appetite and eating behaviour in women”. Maturitas. 71 (3): 248–56. doi:10.1016/j.maturitas.2011.12.016. PMID 22281161.
  3. Papies EK, Nicolaije KA (2012). “Inspiration or deflation? Feeling similar or dissimilar to slim and plus-size models affects self-evaluation of restrained eaters”. Body Image. 9 (1): 76–85. doi:10.1016/j.bodyim.2011.08.004. PMID 21962524.
Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yashasvi Aryaputra[2]

Overview

Bulimia typically tends to start in late teens or early 20s. Bulimics go through cycles of over-eating and purging, that may be severe and devastating to the body. This cycle may be repeated several times a week or, in serious cases, several times a day. Bulimics may appear underweight, normal weight or overweight. Bulimia may cause several complications including malnutrition, dehydration, electrolyte imbalance, and vitamin and mineral deficiencies. The Eating Disorders Association of UK estimates it at 10%. An 18% mortality rate has been suggested for anorexia.

Natural History

  • Bulimia typically tends to start in late teens or early 20s.
  • Bulimics go through cycles of over-eating and purging, that may be severe and devastating to the body.
  • They sometimes involve rapid and out-of-control feeding that stops when the bulimic is interrupted by another person or when his/her stomach hurts from over-extension.
  • This cycle may be repeated several times a week or, in serious cases, several times a day.[1]
  • Some bulimics eat secretly, others eat socially but are bulimic in private.
  • They also differ in “how much” they purge. Some can vomit without gagging themselves after eating.
  • Often when the urge hits, they go to great lengths to purge, as if an uncontrollable urge is making them do so.
  • Medical evidence shows that the chemicals released when purging may make a person feel “high”. This can also lead to extreme dehydration and electrolyte imbalances.
  • Some bulimics do not regard their cycles as a problem, while others despise and fear the vicious and uncontrollable cycle.[2]
  • Bulimics may appear underweight, normal weight or overweight.

Complications

Bulimia can cause following health problems:[1]

Prognosis

  • Eating disorders have one of the highest death rates of all mental illnesses.
  • The Eating Disorders Association of UK estimates it at 10%. An 18% mortality rate has been suggested for anorexia.[3]
  • These death rates are higher than those of some forms of cancer.

References

Diagnosis

Diagnosis

Diagnostic Criteria | History and Symptoms | Physical Examination | Laboratory Findings | Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case Studies

Case #1

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