eMedicine Specialties > Emergency Medicine > Psychosocial

Bulimia

Author: Rebeka Barth, MD, Staff Physician, Stanford-Kaiser Emergency Medicine Residency, Stanford University School of Medicine
Coauthor(s): Rebecca Smith-Coggins, MD, FACEP, Associate Professor, Department of Surgery/Emergency Medicine, Student Life Advisor, Stanford School of Medicine, Stanford University
Contributor Information and Disclosures

Updated: Sep 19, 2008

Introduction

Background

Bulimia nervosa (BN) is an eating disorder characterized by eating binges typically followed by efforts to purge calories through self-induced vomiting, laxative and/or diuretic abuse, prolonged fasting, or excessive exercise. Fear of weight gain leads to the characteristic purging behavior, but bulimia nervosa is centered around the practice of binge eating. Most patients with bulimia are of normal weight or are overweight. Although some patients with anorexia nervosa also manifest purging behavior, anorexia is characterized by the practice of starvation due to intense fear of becoming fat, even though the person is significantly underweight.

The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), describes diagnostic criteria for bulimia nervosa and includes the following1 :

  • Recurrent episodes of binge eating, characterized by the following: 
    • Eating an amount of food, in a discrete period of time, that is larger than most people would eat during a similar period of time under similar circumstances
    • A perceived lack of control over eating during the episode of binge eating
  • Recurrent inappropriate compensatory behavior used to prevent weight gain
  • Occurrence of binge eating and inappropriate compensatory behaviors, on average, at least twice a week for 3 months
  • Self-evaluation unduly influenced by body shape and weight
  • Does not occur exclusively during episodes of anorexia nervosa
Bulimia nervosa may be categorized as the purging type if, during the current episode, the person has regularly engaged in self-induced vomiting or in the misuse of laxatives, diuretics, or enemas. Bulimia nervosa may be categorized as the nonpurging type if other inappropriate compensatory behaviors, such as fasting or excessive exercise, have been used without self-induced vomiting or misuse of laxatives, diuretics, or enemas.

Individuals who binge eat without regularly engaging in the characteristic inappropriate compensatory behaviors of bulimia nervosa are currently included in the category of eating disorders not otherwise specified (NOS) in the DSM-IV. Some researchers believe binge eating disorder (BED) is a milder form, or subset of bulimia nervosa, while others argue that it is its own distinct disorder. In contrast with bulimia nervosa, patients are typically overweight or obese and do not engage in compensatory behaviors.

Pathophysiology

Bulimia is a complex disorder of multifactorial etiology characterized by recurrent binge eating, compensatory behaviors to avoid weight gain, and related behavioral and physiologic symptoms. Cultural attitudes toward standards of physical attractiveness are believed to contribute to bulimic behaviors, but mounting evidence shows that genetic factors play a role.

Bulimia and other eating disorders may be related to abnormal neurotransmitter systems. The serotonin system, which is involved in the regulation of food intake, has been specifically implicated.

Impaired satiety, decreased resting metabolic rate, and abnormal neuroendocrine regulation have been noted in studies of patients with bulimia. Abnormal levels of leptin, ghrelin, the "satiety peptide" cholecystokinin (CCK), and androgens have all been implicated as playing a role in satiety signaling and binge-eating behavior. Leptin, the protein product of the OB gene, is thought to influence weight regulation by acting in the central nervous system to decrease food intake. In rodents, leptin administration decreases meal size, suggesting that decreased leptin function could contribute to diminished satiety responses and large binge meals noted in bulimia nervosa. However, one small study shows decreased levels of leptin in anorexia nervosa but no evidence of decreased leptin levels in bulimia nervosa. Food deprivation (dieting) may play a role in inducing bingeing. Ghrelin, a hormone produced primarily by the stomach, increases food intake and is thought to play a role in long-term regulation of body weight. Ghrelin may blunt the appetite-reducing effect of leptin. Some studies suggest increased androgen sensitivity and association with polycystic ovarian syndrome (PCOS) in bulimia nervosa.2 Androgens have appetite-stimulating effects and could impair impulse control.

Sociocultural environment certainly contributes to the pathology of bulimia, and bulimia is more prevalent in cultures in which thinness is idealized. Binges may occur habitually or may be triggered by feelings of anger, anxiety, or depression. Guilt and dysphoria are common feelings after binges; however, some patients feel the binges to be soothing.

Binges are typically followed by efforts to prevent weight gain. Self-induced vomiting via manual stimulation of the gag reflex is most common, but ingestion of syrup of ipecac, laxative or diuretic misuse, extreme caloric restriction, or intense exercise may complete the cycle. Although the act of self-induced vomiting may occur only occasionally and may be of little consequence, a long-term pattern may develop, leading to poor overall health, decreased muscle strength, dental erosion, serious electrolyte abnormalities, cardiac arrhythmias, and even death.

Electrolyte abnormalities due to vomiting may be compounded by laxative-induced diarrhea or diuretic use. Long-term laxative (phenolphthalein) overdose has been reported. Diet pills can cause hypertension and cerebral hemorrhage when taken in excess. Ipecac-related deaths have been reported and are probably caused by emetine cardiotoxicity in conjunction with electrolyte imbalances.

Menstrual irregularities as a result of bulimia nervosa may be caused by weight fluctuations, nutritional deficiency, or emotional stress, or may be associated with increased androgen levels.

Potentially life-threatening complications of gastric or esophageal rupture, Mallory-Weiss tear, pneumomediastinum, and postbinge pancreatitis have resulted from gorging and vomiting. Most deaths related to bulimia probably result from cardiac arrhythmia.

Frequency

United States

The lifetime prevalence of bulimia is reported to range from 0.5-3%. Bulimia nervosa affects about 6% of adolescent girls and 5% of college women. More than 5 million individuals are believed to experience an eating disorder (bulimia nervosa or anorexia nervosa) in this country alone. Symptoms of bulimia, such as isolated episodes of binge eating and purging, have been reported in up to 40% of college women. The incidence of anorexia and bulimia nervosa may be increasing, although greater medical and public awareness of eating disorders has probably resulted in increased reporting of eating disorder cases.

International

Eating disorders are believed to be more common in industrialized countries, but appropriate epidemiologic studies have not been conducted in developing countries. The lifetime prevalence of bulimia in women living in Tehran, Iran, has been reported as 3.2%. Body dissatisfaction and a desire to be thin are common in this culture. A point prevalence of 5.79 for bulimia has been reported in Japan for women aged 15-29 years.3 The prevalence rate of adverse eating behaviors and bulimia nervosa in Hungary has been found to be similar to the scores published in the Western countries.4

Mortality/Morbidity

  • Bulimia nervosa is a long-term disorder with a waxing and waning course. Mortality rates are not known. Comorbid medical and psychiatric conditions associated with bulimia nervosa include irritable bowel syndrome, fibromyalgia, mood disorders, personality disorders, anxiety disorders, substance abuse, and adverse events related to aggression or poor impulse control. Lifetime rates of affective illness in bulimia nervosa range from 52-97%. The rate of major depression in bulimia nervosa ranges from 38-63%. Of 59 patients with bulimia who participated in a drug treatment trial, 21 (36%) had a diagnosis of an anxiety disorder. Obsessive-compulsive disorder (OCD) is common in patients with bulimia; a dysfunction in the serotonin neurotransmitter system has been implicated in both diseases. Interestingly, body dysmorphic disorder has been noted to have important similarities with OCD.5
  • Bulimia is associated with personality disorders, particularly those featuring impulse control issues and rigid thinking (eg, borderline personality disorder). A disturbance in the neuropsychological domain of mental flexibility may underlie the spectrum of eating disorders.  
  • Rates of comorbid substance abuse seem to be higher among persons with bulimia who have a family history of alcoholism. Among patients exhibiting symptoms of bulimia, substance abuse has been related to an increased incidence of attempted suicide, stealing, and promiscuity. Several studies have reported high rates (65-67%) of kleptomania among patients with eating disorders.
  • The subgroup of people with bulimia who display multiple impulsive behaviors may have a worse outcome than those without comorbid impulse disorders.

Race

According to current research, eating disorders occur more commonly in whites than in other races. See Frequency.

Sex

  • Most (90-95%) patients with bulimia nervosa are women. The female-to-male ratio has been reported to be 1.5:1 in adolescents.6  
  • Among men with eating disorders, the incidence of comorbid psychiatric illness and substance abuse may be increased. The incidence of homosexuality and bisexuality may also be increased.
  • Eating disorders also occur more frequently in men who participate in sports with either a weight requirement (eg, wrestling, horse racing) or a low body fat requirement (eg, bodybuilders).

Age

  • Eating disorders usually develop in adolescence, but about 5% of people develop the disorder when they are older than 25 years. Peak onset of bulimia nervosa occurs at 18 years. Binge-eating behavior may precede the onset of purging. The development of bulimic symptoms at an earlier age may correlate with more severe disease.

Clinical

History

  • Chief complaints associated with bulimia nervosa may include muscle weakness, cramps, dizziness, carpopedal spasm, hematemesis, abdominal pain, chest pain, heartburn, sore throat, or menstrual irregularity. Life-threatening tonsillar hyperplasia has been reported in association with bulimia. Sialoadenitis may be a presenting sign in bulimia because of the excessive salivary gland activity associated with repetitive vomiting. Unrecognized bulimia nervosa has been associated with perioperative cardiac dysrhythmias.
  • Patients with bulimia nervosa are characteristically young and female. Males with bulimia often have a history of participation in sports with a weight requirement.  
  • Patients often deny self-induced vomiting or laxative use; they may admit to the use of diuretics because of leg edema or "bloating." 
    • Caffeine, pseudoephedrine, phenylpropanolamine (recalled from US market because of hypertensive effects with subsequent risk of cerebrovascular accident), and thyroid replacement preparations may be used to try to increase metabolic rate and calorie loss. Inquiry into the use of natural medicines or herbal supplements is important because many natural medicines and herbal supplements contain substances that can increase blood pressure, promote electrolyte imbalance, or both. Ma huang (ie, ephedra) is an herb commonly used in diet preparations. (The US Food and Drug Administration [FDA] has banned ephedra in the United States.)
    • Other substances used to increase metabolism, to decrease appetite, or to cause weight loss include bitter orange, green tea extract, guarana, hoodia, yohimbine, flax oil, sesamin, cayenne, and rhodiola. Prescription medications, such as Meridia (sibutramine), phentolamine, and Xenical (orlistat), may be obtained without a prescription via the Internet. 
  • Laxatives may include bisacodyl, cascara, senna, and high fiber supplements. Abuse of stimulant laxatives can lead to severe constipation, secondary to damage to the myenteric plexus.

Physical

  • Weight is frequently normal or above normal.
  • Vital signs may be normal. Tachycardia and hypotension reflect volume depletion. Hypertension should raise suspicion of stimulant use.
  • Physical examination may reveal signs of dehydration, enlarged parotid glands or tonsils, and erosion of tooth enamel (perimolysis) with or without frank caries.
  • A callus resulting from repetitive contact with teeth during self-induced vomiting may be found on the dorsal surface of the index finger and the long finger on the patient's dominant hand (the Russell sign). Alopecia, xerosis, hypertrichosis, and nail fragility are other common skin findings.
  • The remainder of the physical examination findings are usually normal, although specific complications may be found on examination of the abdomen (eg, epigastric tenderness, guaiac-positive stools), chest (eg, the Hamman crunch of pneumomediastinum), or extremities (eg, edema). Volume depletion may induce hyperaldosteronism, which can lead to pedal edema.

Causes

Anorexia and bulimia nervosa are illnesses with a variety of predispositions, including sociocultural, familial, individual, and neurohumoral. Predisposing factors of bulimia nervosa include female gender, familial obesity, and a culture that emphasizes thinness. A consistent predisposing factor is dieting; bulimia almost always develops during or after an attempt to lose weight.

  • Patients with a familial history of depressive disorders, alcoholism, or obesity are at an increased risk for development of an eating disorder. Interpersonal dynamics between parent and child may play a role. 
  • At the individual level, predisposing factors for eating disorders include a sense of personal helplessness, fear of losing control, self-esteem highly dependent on the opinions of others, and an all-or-nothing style of thinking.  
    • Interpersonal conflict and achievement challenge may be perceived as particularly stressful by individuals with bulimia.
    • In one study that measured subjective ratings of desire to binge, negative mood, and hunger during imagery exercises involving achievement challenge (mental arithmetic), patients with bulimia responded with increases in hunger and desire to binge.  
  • Significantly higher rates of sexual and aggravated assault among women with bulimia nervosa support the hypothesis that victimization may contribute to the development and/or maintenance of the disease. Childhood abuse, particularly sexual abuse of a female child by her father or another adult male, may also be associated with the development of bulimia nervosa. For a related CME activity, see Childhood Sexual Abuse Linked With Bulimia Later in Life. 
  • Twin studies suggest that bulimia nervosa is familial. The studies reveal significant contributions from additive genetic effects and unique environmental factors. The magnitude of the environmental contribution on bulimia nervosa is less clear, but, in studies with the greatest statistical power, environmental contribution appears to be less prominent than additive genetic factors.7   
  • Evidence is mounting to support the role of serotonin (5-hydroxytryptamine [5-HT]) in bulimia, with deficient central states contributing to or arising from repeated episodes of nutritional chaos and purging.  
    • A variety of indirect evidence, including low levels of 5-hydroxyindole (a precursor to serotonin) in cerebrospinal fluid, elevated platelet 5-HT, and blunted prolactin responses to serotonergic challenges, supports such a link. Given evidence for the role of 5-HT in inducing satiety, especially in regulation of carbohydrate-containing foods, a deficiency in persons with bulimia may perpetuate the binge-purge cycle. Successful treatment of patients with bulimia using drugs that increase serotonin levels or otherwise modulate the 5-HT system provides additional support for this theory.
    • Leptin, the protein of the OB gene, is thought to influence weight regulation by acting in the central nervous system to decrease food intake. 5-HT dose-dependently increases leptin levels in mice. Ghrelin, a hormone primarily produced by the stomach, increases food intake and is thought to block the appetite-reducing effect of leptin. Cholecystokinin, made in the duodenum, is a third hormonal signal that is thought to promote satiety. Regulation and levels of these endocrine signals in eating disorders and binge-eating behavior is as yet unclear. Theories and results on ghrelin, leptin, and CCK levels in bulimia nervosa are contradictory.
    • Once the binge-purge cycle is established, enlarged gastric capacity along with other factors that may contribute to disturbed satiety, such as 5-HT receptor changes, slowed gastric emptying, decreased cholecystokinin release, and altered vagal activity, may reinforce the pattern.
    • Research is ongoing regarding the potential roles of other chemical mediators in the pathogenesis of eating disorders. For example, multiple studies have shown that patients with eating disorders have higher levels of cortisol than control subjects.

More on Bulimia

Overview: Bulimia
Differential Diagnoses & Workup: Bulimia
Treatment & Medication: Bulimia
Follow-up: Bulimia
Multimedia: Bulimia
References
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Further Reading

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Keywords

bulimia, eating disorder, anorexia nervosa, AN, binge eating disorder, binge/purge, binge-purge, purging, self-induced vomiting, laxative abuse, BN, bulimic, bulimia nervosa, gastric rupture, Mallory-Weiss tear, eating disorder management

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Contributor Information and Disclosures

Author

Rebeka Barth, MD, Staff Physician, Stanford-Kaiser Emergency Medicine Residency, Stanford University School of Medicine
Rebeka Barth, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Emergency Medicine Residents Association
Disclosure: Nothing to disclose.

Coauthor(s)

Rebecca Smith-Coggins, MD, FACEP, Associate Professor, Department of Surgery/Emergency Medicine, Student Life Advisor, Stanford School of Medicine, Stanford University
Rebecca Smith-Coggins, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Sleep Medicine, and American College of Emergency Physicians
Disclosure: Nothing to disclose.

Medical Editor

Samuel M Keim, MD, Associate Professor, Department of Emergency Medicine, University of Arizona College of Medicine
Samuel M Keim, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Public Health Association, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Robert Harwood, MD, MPH, FACEP, FAAEM, Program Director, Department of Emergency Medicine, Advocate Christ Medical Center; Assistant Professor, Department of Emergency Medicine, University of Illinois at Chicago College of Medicine
Robert Harwood, MD, MPH, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Council of Emergency Medicine Residency Directors, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Jonathan Adler, MD, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital; Division of Emergency Medicine, Harvard Medical School
Jonathan Adler, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: eMedicine.com, Inc. Consulting fee Consulting

 
 
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