eMedicine Specialties > Psychiatry > Adult

Bulimia

Author: Raj K Kalapatapu, MD, Fellow, Addiction Psychiatry, Columbia University College of Physicians and Surgeons
Coauthor(s): Kelda Harris Walsh, MD, Assistant Professor of Clinical Psychiatry, Section of Child and Adolescent Psychiatry, Department of Psychiatry, Indiana University School of Medicine; Chief, Obsessive-Compulsive/Tourette/Anxiety Disorders Clinic, Riley Hospital for Children; Gabriel I Uwaifo, MBBS, Clinical and Research Attending, Assistant Professor of Medicine and Endocrinology, MedStar Clinical Research Center, MedStar Research Institute and Washington Hospital Center; Robert C Daly, MB, ChB, MPH, BCh, Senior Fellow, Department of Behavioral Endocrinology, National Institute of Mental Health, National Institutes of Health
Contributor Information and Disclosures

Updated: Aug 12, 2008

Introduction

Background

Bulimia nervosa (BN) is one of the eating disorders identified in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR).1 The word bulimia is derived from the Greek words bous (ox) and limos (hunger), indicating a state of excessive hunger. Bulimia nervosa is characterized by frequent episodes of binge eating associated with emotional distress and a sense of loss of control accompanied by compensatory behavioral patterns aimed at preventing weight gain.

Compensatory behaviors used by individuals with bulimia nervosa include excessive exercise, episodes of fasting or strict dieting, self-induced vomiting, diuretic abuse, laxative abuse, use of appetite suppressants, and/or medications intended to speed up the metabolism (eg, thyroid hormone). DSM-IV-TR diagnostic criteria require episodes of binge eating that occur at least twice weekly for 3 months. People with bulimia nervosa are also dissatisfied with their body shape, weight,or both.

Binge eating is defined as eating in a discrete period (eg, 1 h) an amount of food that is significantly larger than is typical for most people during the same defined period. This is associated with a perceived loss of control of eating during that same time. The mere consumption of an unusually large amount of food in a defined period without concomitant perception of loss of control is defined as an overeating episode. Similarly, the consumption of rather minimal amounts of food in a defined period with a perception of loss of control is referred to as a subjective bulimic episode.

Eating disorders (EDs) as a group are characterized by a fear of weight gain and a distorted body image with associated anomalies in mood, perception, response to physical and emotional cues, and eating behaviors. Within the syndromes of eating disorders, disordered eating and weight control efforts can manifest as dietary restriction, binge eating, or other compensatory behaviors intended to prevent weight gain, as noted above. Among the eating disorders, bulimia nervosa and anorexia nervosa (AN) are far more common in young females, while binge-eating disorder (BED) is the most common eating disorder overall, and is more common in adults, with a 2:1 female-to-male ratio.

Bulimia is considered distinct from the only recently recognized syndrome of binge-eating disorder, in which no regular or consistent compensatory behavior accompanies the bingeing episodes. The DSM-IV-TR recognizes 2 major variants of bulimia nervosa, as follows: purging and nonpurging (ie, bingeing with use of nonpurging compensatory measures such as excessive exercise, stimulant substances, or fasting).

Many reports suggest that people with bulimia often have a history of anorexia nervosa. Some reports have suggested this association in as many as 60% of cases. While people with uncomplicated binge-eating disorder tend to be obese, people with bulimia nervosa more typically are of normal weight. Overlap between nonpurging bulimia nervosa and binge-eating disorder is seen. The natural history of eating disorders is such that individuals may pass through several diagnoses over time, meeting criteria for anorexia nervosa, bulimia nervosa, and binge-eating disorder at various points. The development of anorexia nervosa in people who have bulimia nervosa is possible, although uncommon.2

Seasonal variation in birth month for patients diagnosed with bulimia is not evident3 ; however, in one study, among those with a history of anorexia, peak season of birth was in March.4

For more information, see Medscape's Eating Disorders Resource Center.

Pathophysiology

Among the identified metabolic derangements identified in bulimia are low plasma insulin, C peptide, triiodothyronine, and glucose values, as well as increased beta-hydroxybutyrate and free fatty acid levels. Both fasting and postbinge/postvomiting hypoglycemia are seen in some patients with bulimia. The findings regarding the hypothalamo-pituitary-adrenal axis are more inconsistent. Some studies suggest an increased amplitude in cortisol and adrenocorticotropic hormone (ACTH) during a 24-hour period among persons with bulimia compared to persons without bulimia, as well as a blunted response to corticotrophin-releasing hormone (CRH). However, other groups reported normal adrenocortical dynamics in these individuals.

Reports have also suggested abnormal dexamethasone suppression tests akin to those seen in peoples with anorexia nervosa, suggesting that bulimia may also be associated with a pseudo-Cushing state. These findings tend to be more apparent among individuals with significant dietary restriction. Some data suggest that the findings on the dexamethasone suppression test may be the result of impaired dexamethasone absorption, which has been demonstrated in some persons with bulimia. Similar to findings in people with anorexia nervosa, patients with bulimia tend to have higher growth hormone levels at night, while the nocturnal prolactin levels tend to be less than those in controls.

Episodes of amenorrhea may occur in as many as 50% of women with bulimia.5 About half of women with bulimia have anovulatory cycles, while about 20% have luteal phase defects. The persons with anovulatory bulimia generally have reduced luteinizing hormone pulsatile secretion frequency and associated reduced estradiol and progesterone pulse amplitudes.

Reports suggest involvement of the serotonin transporter,6,7,8 autoantibodies against neuropeptides,9 various chromosome regions,10 brain-derived neurotrophic factor,11,12,13 and peptides leptin and ghrelin.14,15,16,17 Cerebral hemispheric lesions may be involved in pathogenesis.18 Regional cerebral blood flow abnormalities have been noted.19 Endogenous opioids and beta-endorphins have been implicated in the maintenance of binge eating.

Frequency

United States

Bulimia nervosa is thought to be significantly underrecognized. In the United States, prevalence rates are estimated to be 1-3% in women of high school and college age. Even more common, although not meeting criteria for bulimia, is the trend of periodic combined binge eating and purging. Approximately 10-15% of those with bulimia are male, and the disorder is more common in men who are homosexual. Bulimia is also more common among those whose occupation or hobbies require gaining and/or losing weight rapidly, such as wrestlers and competitive bodybuilders.20

Athletes as a subgroup are particularly prone to eating disorders21,22 ; anorexia nervosa has received the greatest public attention. The female athlete triad of eating disorders, hypothalamic amenorrhea, and osteoporosis is now well recognized and is particularly common in sports where slimness and body shape are of great importance, such as gymnastics, diving, and figure skating. Eating disorders are also being recognized as a problem in sports such as long-distance running, cycling, weight lifting, and wrestling. The scope of eating disorders is more widely recognized as more high-profile athletes are identified as having this problem.

Certain occupations, such as acting, modeling, and ballet dancing,23 also appear to be associated with a higher than average risk for these disorders. The most comprehensive study to date suggests that among elite female athletes, the prevalence of eating disorders may be close to 4 times greater than that in the general population.

The rates of bulimia nervosa among patients seeking assistance with weight control are significant. The prevalence of bulimia nervosa and binge-eating disorder among clients of commercial weight loss programs is about 30-50%. Among patients presenting for bariatric surgery (surgery to reduce weight), the prevalence reaches 25-70% in some cohorts.

While overall secular trends are difficult to assess given the changes in diagnostic criteria over time, most studies report a progressive increase in the prevalence of bulimia nervosa and, particularly, anorexia nervosa. Whether this secular trend is the result of environmental pressures encouraging unrealistic body shapes and weights is unclear.

Bulimic symptoms may vary across geographic regions in the United States. In one small study, women from North Carolina and Virgina (South Atlantic region) reported more bulimic symptoms than the women from Louisiana and Tennessee (South Central region) and Ohio and Missouri (Midwest region).24

International

The overall prevalence of bulimia certainly appears to have increased considerably after World War II, and some say this is primarily the result of changing sociocultural expectations for young women. However, bulimia specifically and eating disorders as a whole appear to be predominantly Western diseases and occur most often in developed countries. Typically, reports of eating disorders outside of this setting are anecdotal.

The suggestion that environmental factors play a significant role in the prevalence and incidence of eating disorders is also borne out by the fact that immigrants from underdeveloped countries have a much higher risk for developing eating disorders than do their genetically similar relatives still residing in the countries of origin. Most studies tend to identify bulimia and other eating disorders more frequently among the middle and upper socioeconomic strata of society. Although often described as modern diseases, close review of the older medical literature suggests that similar conditions have been described since antiquity.

Mortality/Morbidity

See Prognosis.

Race

Bulimia is a cosmopolitan disorder that has been described in all ethnic, racial, and socioeconomic groups. Literature is mixed regarding ethnic differences in eating disorder psychopathology. No apparent consensus exists about the relative prevalence of eating disorders and associated symptoms across ethnicities. Clinicians should remain alert for possible ethnic diversity in symptom presentation or distress that could obscure the diagnosis or need for intervention.25,26,27,28,29,30

Sex

As with other eating disorders, bulimia occurs predominantly in women. Most reports suggest a female-to-male ratio of 10:1. While some reports suggest the prevalence in men may be as low as 5%, others suggest that it may be as high as 15%.

Awareness that men may also may develop bulimia nervosa and other eating disorders and to maintain a high index of suspicion is critical. Although few data are available, little evidence suggests that men have any significant differences in clinical course, complications, or response to management modalities compared with women.

The prevalence of eating disorders in males appears to have increased in the 1990s compared with earlier decades. Whether this finding demonstrates a true change in prevalence or whether more males are now seeking care is unclear. The psychopathology and attitudes of males with eating disorders are, as a whole, similar to those of females with eating disorders; both are associated with a significant family history.

Age

The typical age of onset for bulimia is in the teenage years and early third decade of life. This is slightly older than the peak age of onset for anorexia nervosa but generally lower than the age of onset of binge-eating disorder. The prevalence of bulimia nervosa in children younger than 14 years appears to be less than 5%. Bulimia has also been reported in the elderly.31

Clinical

History

A common presenting scenario is a patient with a concern about weight and who seeks help with weight loss. Symptoms may include bloating, constipation, and menstrual irregularities. Far less often, people may also present with arrhythmias, which are often the result of electrolyte abnormalities. Bulimia is also characterized by an inappropriate premium placed on being slender and an associated distorted body image that exaggerates physical appearance, though less prominently than in anorexia nervosa.

A close dietary inventory may reveal that individuals attempt to control their weight by dieting and abstaining from high-calorie foods until the binge episode. Often, a morbid preoccupation with food and eating is present, and recurring cycles of extreme dieting and/or fasting may alternate with gorging behavior. Usually, bingeing episodes are well planned. Foods are generally selected as being easy to swallow, vomit, and regurgitate and tend to have a high caloric value. A person may rapidly ingest up to 10 times (or more) of the recommended daily calorie allowance in a single binge episode. Situations in which control over food intake may be lost are avoided (eg, parties, eating out).

The level of physical activity that people with bulimia engage in is often cyclical in a fashion similar to that of the bingeing episodes. While most persons with bulimia induce vomiting,32 a minority choose to chew the food and then regurgitate it without actually swallowing it. Vomiting is usually achieved by activating the gag reflex through digital stimulation or by ingestion of emetics (eg, ipecac).

  • People with bulimia may report the following symptoms
    • Gastrointestinal symptoms: Common gastrointestinal symptoms that occur in people with bulimia include abdominal pain (more common among persons who self-induce vomiting), bloating, flatulence, constipation, and obstipation.
    • Pulmonary symptoms: In those with bulimia, pulmonary symptoms may be due to aspiration pneumonitis or, more rarely, pneumomediastinum.
    • Amenorrhea: Amenorrhea occurs in about 50% of women with bulimia, while a significant proportion of remaining patients have irregular periods.
  • A high index of suspicion is required in identifying bulimia nervosa because patients often do not directly admit to the problem.
    • A set of screening questions, such as the SCOFF mnemonic questionnaire,33 is useful to obtain a quick impression as to the potential need for further in-depth questioning. The SCOFF questionnaire includes the following 5 questions:
      1. Do you make yourself S ick because you feel uncomfortably full?
      2. Do you worry you have lost C ontrol over how much you eat?
      3. Have you recently lost more than O ne stone (about 14 lbs or 6.35 kg) in a 3-month period?
      4. Do you believe yourself to be F at when others say you are too thin?
      5. Would you say that F ood dominates your life?
    • The Eating Disorder Screen for Primary Care (ESP) questionnaire is an alternative screening tool.34 It contains the following 5 questions:
      1. Are you satisfied with your eating patterns?
      2. Do you ever eat in secret?
      3. Does your weight affect the way you feel about yourself?
      4. Have family members suffered from an eating disorder?
      5. Do you currently suffer with or have you in the past suffered with an eating disorder?
  • The eating attitudes test (EAT) is a self-reporting instrument that can be included in the paperwork patients fill out while waiting to see their health care provider. EAT has also been extensively validated as a useful screening tool for identifying individuals with eating disorders.35 (See Psych Central for more information.)
  • While still the subject of debate, family psychopathology may play a significant role in the development of bulimia, based on the perspective of interviewed patients with bulimia.
    • Generally, patients with bulimia view their families as conflicted, badly organized, noncohesive, and lacking in nurturance and caring. Detailed psychologic evaluation of these patients generally suggests that they are angrily submissive to rather hostile and neglectful parents.
    • Perceptions of appearance-related teasing by family members may be present.36
    • For individuals still living with their parents, a careful professional evaluation of the family dynamics must be completed.

Comorbidity

  • Affective disorders: The rather common association of eating disorders with affective disorders suggests a possible relationship between them.37 Major depressive disorder (MDD) is particularly common in this regard. Whether the association is causative (primary), secondary to the bulimia itself, or represents a common set of risk factors for bulimia and MDD is still unclear. Depressive symptoms can occur during pregnancy and postpartum in women with bulimia.38 Bipolar II disorder appears to be more common in patients with bulimia than in non-eating-disordered patients.
  • Anxiety disorders: Obsessive-compulsive disorder (OCD) is more common in persons with bulimia than in those without bulimia. Panic disorder, social phobia, specific phobias, generalized anxiety disorder (GAD), and posttraumatic stress disorder (PTSD) significantly contribute to comorbidity. Lifetime prevalences run around 40% (OCD), 11% (panic disorder), 20% (social phobia), 15% (specific phobias), 10% (GAD), and 13% (PTSD).
  • Substance use disorders: Some evidence suggests a relationship between addictions and bulimia, including alcohol dependence,39,40 nicotine dependence,41 and drug dependence.42 Studies on caffeine intake are mixed.43
  • Impulse control disorders: In a study of lifetime prevalence of impulse control disorders in patients with bulimia, compulsive buying and intermittent explosive disorder were the most frequently reported disorders at 17.6% and 13.2%, respectively. Kleptomania, pathological gambling, and trichotillomania have also been reported in patients with bulimia.44
  • Suicidal behaviors: Bulimia is associated with suicide attempts and suicidal ideations.45
  • Other psychopathology: The role of sexual abuse in the development of eating disorders is controversial.46,47 Some reports suggest a strong association, while others detect no association. (See Medscape CME activity Childhood Sexual Abuse Linked With Bulimia Later in Life.) Borderline personality disorder is found frequently,48 and these patients usually have histories of trauma and abuse and may represent a distinct subgroup. Pathologic narcissism49,50 and identity impairment51 may be present. Attention deficit hyperactivity disorder may be associated with bulimia.52 (See Medscape CME activity ADHD and Comorbid Conditions.)

Physical

Eating disorders are often concealed and require a high index of suspicion to diagnose. Patients with bulimia are often unremarkable in general appearance and frequently have no signs of illness or anomalies on physical examination.

  • Physical findings may include the following: 
    • Bilateral parotid enlargement, largely consequent to noninflammatory stimulation of the salivary glands, may be seen.53,54,55 See parotid gland swelling in Figure 1 in the article Diagnosing bulimia nervosa with parotid gland swelling from the Journal of the American Dental Association.
    • In patients with significant self-induced vomiting, erosions of the lingual surface of the teeth, loss of enamel, periodontal disease, and extensive dental caries may be observed.56,57,58 See images from the School of Dental Hygiene at the University of Manitoba, Canada.
    • Russell sign (one of the few physical examination findings in psychiatry) manifests as callosities, scarring, and abrasions on the knuckles secondary to repeated self-induced vomiting.59,60 See Media file 1.
    • Other cutaneous manifestations can include telogen effluvium (sudden, diffuse hair loss), acne, xerosis (dry skin), nail dystrophy (degeneration), and self-induced trauma.61,62
    • Other nonspecific but suggestive findings that may reflect the severity of the disease include bradycardia, hypothermia, and hypotension. Edema, particularly of the feet (and less commonly the hands), is found more often among patients with a history of diuretic abuse, laxative abuse, or both or in patients with significant protein malnourishment causing hypoalbuminemia.
    • Some patients may be clinically obese, but morbid obesity is rare. Patients with bulimia who are overweight can have excessive fat folds that favor humidity and maceration with bacterial and fungal overgrowth, striae due to skin overextension, stasis pigmentation related to peripheral vascular disease, and plantar hyperkeratosis due to increased weight.61
  • The evaluation of these individuals is not complete without a comprehensive mental status examination. This is of considerable importance as bulimia often coexists with mood disorders, particularly depression. These patients also commonly have associated neuroses (particularly anxiety neuroses), the management of which may be vital to the adequate management of the bulimia. Close attention must be paid to the patient's affect—especially the patient's level of depression, anxiety, or both.
  • The mental status examination also helps to identify potential psychopathology known to accompany bulimia (and possibly predispose to its development), including alcoholism within the family, family history of eating disorders, and personality disorders. Other areas of concern during the course of the mental status examination include disturbed interpersonal relations and dynamics, difficulties with impulse control, and a history of prior or ongoing substance abuse.
  • A typical mental status examination for a patient with bulimia is detailed below. (The Folstein Mini-Mental Status Examination [MMSE] is often ineffective in the evaluation of patients with bulimia nervosa because cognitive deficits that are typical of dementing illness are not common in those with bulimia.) 
    • Orientation: Patients with bulimia are typically oriented to their surroundings.
    • Appearance: Patients are typically neat, well dressed, and show attention to detail. Grooming is often meticulous and may further demonstrate a patient's concern about personal appearance.
    • Eye contact: Patients generally avoid eye contact.
    • Affect and mood: Patients often demonstrate a depressed mood but may also have significant anxiety.
    • Suicidal ideation: Suicidal ideation is a significant consideration, especially in patients with depressed moods. However, on closer questioning, the suicidal ideation is often restricted to thoughts rather than concrete plans.
    • Homicidal ideation: Homicidal ideation is not typically associated with patients with bulimia.
    • Delusions and hallucinations: Delusions and hallucinations are typically absent in patients with bulimia.
    • Comprehension: Comprehension is typically normal.
    • Insight: Insight is variable. While patients typically admit to episodes of binge eating, they often do not appreciate their inappropriate fixation on eating or their distorted ideas of body image and weight.
    • Judgment: Patients with bulimia generally demonstrate poor judgment. Weight-reducing strategies, such as induced vomiting and laxative and diuretic ingestion, are perceived as legitimate and appropriate methods of weight management.
    • Thought: Thoughts tend to revolve around food and concerns regarding body image and weight.
    • Speech: Content and articulation are generally normal.
    • Auditory: Patients with bulimia generally show no auditory deficits.
    • Memory: Immediate memory is normal, as is recent and remote memory recall.
    • Reading, writing, and drawing: A patient's ability to read, write, and draw typically remains normal.
    • Reasoning: Basic reasoning and calculating skills, including the serial 7 and digit scan, are typically normal.
    • Motor abilities: Motor functioning and gait are typically normal with no significant deficits.
    • Intellect: Estimated intellectual ability is within normal limits. In some cases, demonstrated intellectual ability may be even better than average.

Causes

Among the potential precipitating events for a binge/purge cycle in those with bulimia are anxiety states, emotional tension, boredom, environmental cues about food and eating, alcohol use, substance abuse, and exhaustion. Hunger is a rather uncommon precipitant for the bulimic cycles. Although the exact cause for bulimia and other eating disorders is unclear, some factors identified as playing potentially important roles in its etiopathogenesis are as follows:

  • Psychological factors: Among those suggested are difficulties with self-esteem and affective self-regulation. However, it is difficult to determine the premorbid status that predisposes persons to later develop eating disorders such as bulimia.
  • Psychodynamic factors: Patients with bulimia lack the superego control and the ego strength compared to patients with anorexia. Many patients have histories of difficulties separating from caretakers. The struggle for separation from a maternal figure manifests in ambivalence toward food. Eating may represent a wish to fuse with their caretaker, and regurgitating may unconsciously express a wish for separation.63
  • Sociocultural factors: An inappropriate concern about body image and an excessive preoccupation with thinness seem central to both anorexia and bulimia nervosa. Some evidence suggests an association of bulimia (particularly the bingeing episodes) with disinhibition for food intake.
  • Genetics: Although no definitive inheritance patterns have been identified, a familial component appears to be involved in the development of eating disorders in general. The results of twin studies of both monozygotic and dizygotic twins suggest that the genetic component to the etiology of eating disorders is much greater in anorexia nervosa than in bulimia.
  • CNS and gastrointestinal peptide interactions: It appears that a complex dysfunctional interaction exists between orexigenic factors such as neuropeptide Y (NP-Y) and anorectic factors such as cholecystokinin (CCK) and beta-endorphin. The exact details of this interaction are under active investigation, but available data show that people with bulimia have normal NP-Y levels, which do increase after successful treatment. Furthermore, people with bulimia have reduced beta-endorphin, normal dynorphin, and low CCK levels. Reduced activity of the central serotonin system has been suggested to have a role in the development of bulimia.

More on Bulimia

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

References

  1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Text Revision. In: American Psychiatric Association. 4th ed. Washington, DC; 2000.

  2. Santonastaso P, Zanetti T, De Antoni C, Tenconi E, Favaro A. Anorexia nervosa patients with a prior history of bulimia nervosa. Comprehensive Psychiatry. November-December 2006;47(6):519-522. [Medline].

  3. Button E, Aldridge S. Season of birth and eating disorders: patterns across diagnoses in a specialized eating disorders service. International Journal of Eating Disorders. July 2007;40(5):468-471. [Medline][Full Text].

  4. Morgan JF, Lacey JH. Season of birth and bulimia nervosa. International Journal of Eating Disorders. May 2000;27(4):452-458. [Medline][Full Text].

  5. Poyastro Pinheiro A, Thornton LM, Plotonicov KH, Tozzi F, Klump KL, Berrettini WH, et al. Patterns of menstrual disturbance in eating disorders. International Journal of Eating Disorders. July 2007;40(5):424-434. [Medline][Full Text].

  6. Ribasés M, Fernández-Aranda F, Gratacòs M, Mercader JM, Casasnovas C, Núñez A, et al. Contribution of the serotoninergic system to anxious and depressive traits that may be partially responsible for the phenotypical variability of bulimia nervosa. Journal of Psychiatric Research. January 2008;42(1):50-57. [Medline].

  7. Monteleone P, Tortorella A, Martiadis V, Serino I, Di Filippo C, Maj M. Association between A218C polymorphism of the tryptophan-hydroxylase-1 gene, harm avoidance and binge eating behavior in bulimia nervosa. Neuroscience Letters. June 21, 2007;421(1):42-46. [Medline].

  8. Monteleone P, Santonastaso P, Mauri M, Bellodi L, Erzegovesi S, Fuschino A, et al. Investigation of the serotonin transporter regulatory region polymorphism in bulimia nervosa: relationships to harm avoidance, nutritional parameters, and psychiatric comorbidity. Psychosomatic Medicine. Jan-Feb 2006;68(1):99-103. [Medline][Full Text].

  9. Fetissov SO, Harro J, Jaanisk M, Järv A, Podar I, Allik J, et al. Autoantibodies against neuropeptides are associated with psychological traits in eating disorders. Proceedings of the National Academy of Sciences of the United States of America. October 11, 2005;102(41):14865-14870. [Medline][Full Text].

  10. Bacanu SA, Bulik CM, Klump KL, Fichter MM, Halmi KA, Keel P, et al. Linkage analysis of anorexia and bulimia nervosa cohorts using selected behavioral phenotypes as quantitative traits or covariates. American Journal of Medical Genetics Part B (Neuropsychiatric Genetics). November 5, 2005;139(1):61-68. [Medline][Full Text].

  11. Steiger H, Bruce KR. Phenotypes, endophenotypes, and genotypes in bulimia spectrum eating disorders. Canadian Journal of Psychiatry. April 2007;52(4):220-227. [Medline].

  12. Monteleone P, Zanardini R, Tortorella A, Gennarelli M, Castaldo E, Canestrelli B, et al. The 196G/A (val66met) polymorphism of the BDNF gene is significantly associated with binge eating behavior in women with bulimia nervosa or binge eating disorder. Neuroscience Letters. October 2, 2006;406(1-2):133-137. [Medline].

  13. Mercader JM, Ribasés M, Gratacòs M, González JR, Bayés M, de Cid R, et al. Altered brain-derived neurotrophic factor blood levels and gene variability are associated with anorexia and bulimia. Genes, Brain, and Behavior. November 2007;6(8):706-716. [Medline][Full Text].

  14. Torsello A, Brambilla F, Tamiazzo L, Bulgarelli I, Rapetti D, Bresciani E, et al. Central dysregulations in the control of energy homeostasis and endocrine alterations in anorexia and bulimia nervosa. Journal of Endocrinological Investigation. December 2007;30(11):962-976. [Medline].

  15. Miyasaka K, Hosoya H, Sekime A, Ohta M, Amono H, Matsushita S, et al. Association of ghrelin receptor gene polymorphism with bulimia nervosa in a Japanese population. Journal of Neural Transmission. September 2006;113(9):1279-1285. [Medline][Full Text].

  16. Monteleone P, Tortorella A, Castaldo E, Di Filippo C, Maj M. No association of the Arg51Gln and Leu72Met polymorphisms of the ghrelin gene with anorexia nervosa or bulimia nervosa. Neuroscience Letters. May 8, 2006;398(3):325-327. [Medline].

  17. Ando T, Komaki G, Naruo T, Okabe K, Takii M, Kawai K, et al. Possible role of preproghrelin gene polymorphisms in susceptibility to bulimia nervosa. American Journal of Medical Genetics part B (Neuropsychiatric Genetics). December 5, 2006;141(8):929-934. [Medline][Full Text].

  18. Uher R, Treasure J. Brain lesions and eating disorders. Journal of Neurology, Neurosurgery, and Psychiatry. June 2005;76(6):852-857. [Medline][Full Text].

  19. Frank GK, Bailer UF, Meltzer CC, Price JC, Mathis CA, Wagner A, et al. Regional cerebral blood flow after recovery from anorexia or bulimia nervosa. International Journal of Eating Disorders. September 2007;40(6):488-492. [Medline][Full Text].

  20. Goldfield GS, Blouin AG, Woodside DB. Body image, binge eating, and bulimia nervosa in male bodybuilders. Canadian Journal of Psychiatry. March 2006;51(3):160-168. [Medline].

  21. Johnson MD. Disordered eating in active and athletic women. Clin Sports Med. Apr 1994;13(2):355-69. [Medline].

  22. Leon GR. Eating disorders in female athletes. Sports Med. Oct 1991;12(4):219-27. [Medline].

  23. Ravaldi C, Vannacci A, Bolognesi E, Mancini S, Faravelli C, Ricca V. Gender role, eating disorder symptoms, and body image concern in ballet dancers. Journal of Psychosomatic Research. October 2006;61(4):529-535. [Medline].

  24. Perez M, Hernandez A, Clarke A, Joiner TE Jr. Analysis of bulimic symptomatology across age and geographic locations. Eating Behaviors. January 2007;8(1):136-142. [Medline].

  25. Chui W, Safer DL, Bryson SW, Agras WS, Wilson GT. A comparison of ethnic groups in the treatment of bulimia nervosa. Eating Behaviors. 2007;8:485-491. [Medline].

  26. Franko DL, Becker AE, Thomas JJ, Herzog DB. Cross-ethnic differences in eating disorder symptoms and related distress. International Journal of Eating Disorders. March 2007;40(2):156-164. [Medline][Full Text].

  27. Hrabosky JI, Grilo CM. Body image and eating disordered behavior in a community sample of Black and Hispanic women. Eating Behaviors. January 2007;8(1):106-114. [Medline].

  28. Mancilla-Diaz JM, Franco-Paredes K, Vazquez-Arevalo R, Lopez-Aguilar X, Alvarez-Rayon GL, Tellez-Giron MT. A two-stage epidemiologic study on prevalence of eating disorders in female university students in Mexico. European Eating Disorders Review. November 2007;15(6):463-470. [Medline][Full Text].

  29. Soh N, Surgenor LJ, Touyz S, Walter G. Eating disorders across two cultures: does the expression of psychological control vary?. The Australian and New Zealand Journal of Psychiatry. April 2007;41(4):351-358. [Medline].

  30. Tseng MM, Fang D, Lee MB, Chie WC, Liu JP, Chen WJ. Two-phase survey of eating disorders in gifted dance and non-dance high-school students in Taiwan. Psychological Medicine. August 2007;37(8):1085-1096. [Medline].

  31. Morgan CD, Marsh C. Bulimia nervosa in an elderly male: a case report. International Journal of Eating Disorders. March 2006;39(2):170-171. [Medline][Full Text].

  32. Ruiz MC, Soler-Gonzalez J. Images in clinical medicine. Unfortunate ingestion. New England Journal of Medicine. November 24, 2005;353:2270. [Medline][Full Text].

  33. 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].

  34. Cotton MA, Ball C, Robinson P. Four simple questions can help screen for eating disorders. J Gen Intern Med. Jan 2003;18(1):53-6. [Medline].

  35. Mintz LB, O''Halloran MS. The Eating Attitudes Test: validation with DSM-IV eating disorder criteria. J Pers Assess. Jun 2000;74(3):489-503. [Medline].

  36. Keery H, Boutelle K, van den Berg P, Thompson JK. The impact of appearance-related teasing by family members. Journal of Adolescent Health. August 2005;37(2):120-127. [Medline].

  37. Godart NT, Perdereau F, Rein Z, Berthoz S, Wallier J, Jeammet P, et al. Comorbidity studies of eating disorders and mood disorders. Critical review of the literature. Journal of Affective Disorders. January 2007;97(1-3):37-49. [Medline].

  38. Mazzeo SE, Slof-Op't Landt MC, Jones I, Mitchell K, Kendler KS, Neale MC, et al. Associations among postpartum depression, eating disorders, and perfectionism in a population-based sample of adult women. Internation Journal of Eating Disorders. April 2006;39(3):202-211. [Medline][Full Text].

  39. Duncan AE, Neuman RJ, Kramer JR, Kuperman S, Hesselbrock VM, Bucholz KK. Lifetime psychiatric comorbidity of alcohol dependence and bulimia nervosa in women. Drug and Alcohol Dependence. September 1, 2006;84(1):122-132. [Medline].

  40. Luce KH, Engler PA, Crowther JH. Eating disorders and alcohol use: group differences in consumption rates and drinking motives. Eating Behaviors. April 2007;8(2):177-184. [Medline].

  41. Anzengruber D, Klump KL, Thornton L, Brandt H, Crawford S, Fichter MM, et al. Smoking in eating disorders. Eating Behaviors. November 2006;7(4):291-299. [Medline].

  42. Baker JH, Mazzeo SE, Kendler KS. Association between broadly defined bulimia nervosa and drug use disorders: common genetic and environmental influences. International Journal of Eating Disorders. December 2007;40(8):673-678. [Medline][Full Text].

  43. Striegel-Moore RH, Franko DL, Thompson D, Barton B, Schreiber GB, Daniels SR. Caffeine intake in eating disorders. International Journal of Eating Disorders. March 2006;39(2):162-165. [Medline][Full Text].

  44. Fernández-Aranda F, Jiménez-Murcia S, Alvarez-Moya EM, Granero R, Vallejo J, Bulik CM. Impulse control disorders in eating disorders: clinical and therapeutic implications. Comprehensive Psychiatry. November-December 2006;47(6):482-488. [Medline].

  45. 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. International Journal of Eating Disorders. November 2007;40(7):589-595. [Medline][Full Text].

  46. Feldman MB, Meyer IH. Childhood abuse and eating disorders in gay and bisexual men. International Journal of Eating Disorders. July 2007;40(5):418-423. [Medline][Full Text].

  47. Wonderlich SA, Rosenfeldt S, Crosby RD, Mitchell JE, Engel SG, Smyth J, et al. The effects of childhood trauma on daily mood lability and comorbid psychopathology in bulimia nervosa. Journal of Traumatic Stress. February 2007;20(1):77-87. [Medline][Full Text].

  48. Zeeck A, Birindelli E, Sandholz A, Joos A, Herzog T, Hartmann A. Symptom severity and treatment course of bulimic patients with and without a borderline personality disorder. European Eating Disorders Review. November 2007;15(6):430-438. [Medline][Full Text].

  49. Lehoux PM, Howe N. Perceived non-shared environment, personality traits, family factors and developmental experiences in bulimia nervosa. British Journal of Clinical Psychology. March 2007;46 (Part 1):47-66. [Medline].

  50. Waller G, Sines J, Meyer C, Foster E, Skelton A. Narcissism and narcissistic defences in the eating disorders. International Journal of Eating Disorders. March 2007;40(2):143-148. [Medline][Full Text].

  51. Stein KF, Corte C. Identity impairment and the eating disorders: content and organization of the self-concept in women with anorexia nervosa and bulimia nervosa. European Eating Disorders Review. January 2007;15(1):58-69. [Medline][Full Text].

  52. Surman CB, Randall ET, Biederman J. Association between attention-deficit/hyperactivity disorder and bulimia nervosa: analysis of 4 case-control studies. Journal of Clinical Psychiatry. March 2006;67(3):351-354. [Medline][Full Text].

  53. Mandel L, Abai S. Diagnosing bulimia nervosa with parotid gland swelling. The Journal of the American Dental Association. May 2004;135:613-616. [Medline][Full Text].

  54. Mandel L, Kaynar A. Bulimia and parotid swelling: a review and case report. J Oral Maxillofac Surg. Oct 1992;50(10):1122-5. [Medline].

  55. Vavrina J, Müller W, Gebbers JO. Enlargement of salivary glands in bulimia. The Journal of Laryngology & Otology. June 1994;108:516-518. [Medline].

  56. Burkhart N, Roberts M, Alexander M, Dodds A. Communicating effectively with patients suspected of having bulimia nervosa. The Journal of the American Dental Association. August 2005;136(8):1130-1137. [Medline][Full Text].

  57. Kavoura V, Kourtis SG, Zoidis P, Andritsakis DP, Doukoudakis A. Full-mouth rehabilitation of a patient with bulimia nervosa. A case report. Quintessence International. July-August 2005;36(7-8):501-510. [Medline].

  58. Zachariasen RD. Oral signs and symptoms of bulimia nervosa. J Gt Houst Dent Soc. Aug 1997;69(1):31-4. [Medline].

  59. Glorio R, Allevato M, De Pablo A, Abbruzzese M, Carmona L, Savarin M, et al. Prevalence of cutaneous manifestations in 200 patients with eating disorders. International Journal of Dermatology. May 2000;39:348-353. [Medline][Full Text].

  60. Daluiski A, Rahbar B, Meals RA. Russell''s sign. Subtle hand changes in patients with bulimia nervosa. Clin Orthop. Oct 1997;(343):107-9. [Medline].

  61. Strumia R. Dermatologic signs in patients with eating disorders. American Journal of Clinical Dermatology. 2005;6(3):165-173. [Medline].

  62. Mitchell JE, Crow S. Medical complications of anorexia nervosa and bulimia nervosa. Current Opinion in Psychiatry. July 2006;19(4):438-443. [Medline].

  63. Sadock, B.J., and Sadock, V.A. Eating Disorders. In: Grebb, J.A., Pataki, C.S., and Sussman, N. Synopsis of Psychiatry. 10th Edition. Lippincott, Williams, & Wilkins; 2007:Chapter 23.

  64. Kruger D. Bulimia nervosa: easy to hide but essential to recognize. Journal of the American Academy of Physician Assistants. January 2008;21(1):48-52. [Medline].

  65. Bosanac P, Kurlender S, Stojanovska L, Hallam K, Norman T, McGrath C, et al. Neuropsychological study of underweight and "weight-recovered" anorexia nervosa compared with bulimia nervosa and normal controls. International Journal of Eating Disorders. November 2007;40(7):613-621. [Medline][Full Text].

  66. Brand M, Franke-Sievert C, Jacoby GE, Markowitsch HJ, Tuschen-Caffier B. Neuropsychological correlates of decision making in patients with bulimia nervosa. Neuropsychology. November 2007;21(6):742-750. [Medline].

  67. American Psychiatric Association. Treatment of patients with eating disorders, third edition. American Journal of Psychiatry. July 2006;163 (7 supplement):4-54. [Medline][Full Text].

  68. Berkman ND, Bulik CM, Brownley KA, Lohr KN, Sedway JA, Rooks A, et al. Management of eating disorders. Evidence Report/Technology Assessment. April 2006;135:1-166. [Medline][Full Text].

  69. Shapiro JR, Berkman ND, Brownley KA, Sedway JA, Lohr KN, Bulik CM. Bulimia nervosa treatment: a systematic review of randomized controlled trials. International Journal of Eating Disorders. May 2007;40(4):321-336. [Medline][Full Text].

  70. Schembri C, Evans L. Adverse relationship processes: the attempts of women with bulimia nervosa symptoms to fit the perceived ideal of intimate partners. European Eating Disorders Review. January 2008;16(1):59-66. [Medline][Full Text].

  71. Self-help and guided self-help for eating disorders, Volume 4 [database online]. The Cochrane Database of Systematic Reviews: The Cochrane Library, The Cochrane Collaboration; 2002. Updated 2007.

  72. American Psychiatric Association. Treatment of Patients with Eating Disorders, Third Edition. American Journal of Psychiatry. July 2006;163 (7 Suppl):4-54. [Medline][Full Text].

  73. Mitchell JE, Agras S, Wonderlich S. Treatment of bulimia nervosa: where are we and where are we going?. International Journal of Eating Disorders. March 2007;40(2):95-101. [Medline][Full Text].

  74. Adson DE, Mitchell JE, Trenkner SW. The superior mesenteric artery syndrome and acute gastric dilatation in eating disorders: a report of two cases and a review of the literature. Int J Eat Disord. Mar 1997;21(2):103-14. [Medline].

  75. DeBate RD, Shuman D, Tedesco LA. Eating disorders in the oral health curriculum. Journal of Dental Education. May 2007;71(5):655-663. [Medline][Full Text].

  76. Mayer LE, Walsh BT. The use of selective serotonin reuptake inhibitors in eating disorders. J Clin Psychiatry. 1998;59 Suppl 15:28-34. [Medline].

  77. Milano W, Siano C, Putrella C, Capasso A. Treatment of bulimia nervosa with fluvoxamine: a randomized controlled trial. Advances in Therapy. May-June 2005;22(3):278-283. [Medline].

  78. Leombruni P, Amianto F, Delsedime N, Gramaglia C, Abbate-Daga G, Fassino S. Citalopram versus fluoxetine for the treatment of patients with bulimia nervosa: a single-blind randomized controlled trial. Advances in Therapy. May-June 2006;23(3):481-494. [Medline].

  79. Walsh BT, Sysko R, Parides MK. Early response to desipramine among women with bulimia nervosa. International Journal of Eating Disorders. January 2006;39(1):72-75. [Medline][Full Text].

  80. McElroy SL, Arnold LM, Shapira NA, et al. Topiramate in the treatment of binge eating disorder associated with obesity: a randomized, placebo-controlled trial. Am J Psychiatry. Feb 2003;160(2):255-61. [Medline].

  81. Hsu LK, Clement L, Santhouse R, Ju ES. Treatment of bulimia nervosa with lithium carbonate. A controlled study. J Nerv Ment Dis. Jun 1991;179(6):351-5. [Medline].

  82. Faris PL, Kim SW, Meller WH, et al. Effect of decreasing afferent vagal activity with ondansetron on symptoms of bulimia nervosa: a randomised, double-blind trial. Lancet. Mar 4 2000;355(9206):792-7. [Medline].

  83. Broft AI, Spanos A, Corwin RL, Mayer L, Steinglass J, Devlin MJ, et al. Baclofen for binge eating: an open-label trial. International Journal of Eating Disorders. December 2007;40(8):687-691. [Medline][Full Text].

  84. Naessén S, Carlström K, Byström B, Pierre Y, Hirschberg AL. Effects of an antiandrogenic oral contraceptive on appetite and eating behavior in bulimic women. Psychoneuroendocrinology. June 2007;32(5):548-554. [Medline].

  85. Antidepressants versus placebo for people with bulimia nervosa, Volume 1 [database online]. The Cochrane Database of Systematic Reviews: The Cochrane Library, The Cochrane Collaboration; 1999. Updated 2002.

  86. Psychotherapy for bulimia nervosa and binging, Volume 1 [database online]. The Cochrane Database of Systematic Reviews: The Cochrane Library, The Cochrane Collaboration; 1998. Updated 2005.

  87. Antidepressants versus psychological treatments and their combination for bulimia nervosa [database online]. The Cochrane Database of Systematic Reviews: The Cochrane Library, The Cochrane Collaboration; 1997. Updated 2005.

  88. Grunwald M, Wesemann D. Special online consulting for patients with eating disorders and their relatives: analysis of user characteristics and E-mail content. Cyberpsychology & Behavior. February 2007;10:57-63. [Medline][Full Text].

  89. Jacobi C, Morris L, Beckers C, Bronisch-Holtze J, Winter J, Winzelberg AJ, et al. Maintenance of internet-based prevention: a randomized controlled trial. International Journal of Eating Disorders. March 2007;40:114-119. [Medline][Full Text].

  90. Ljotsson B, Lundin C, Mitsell K, Carlbring P, Ramklint M, Ghaderi A. Remote treatment of bulimia nervosa and binge eating disorder: a randomized trial of Internet-assisted cognitive behavioural therapy. Behaviour Research and Therapy. April 2007;45:649-661. [Medline].

  91. Robinson S, Perkins S, Bauer S, Hammond N, Treasure J, Schmidt U. Aftercare intervention through text messaging in the treatment of bulimia nervosa--feasibility pilot. International Journal of Eating Disorders. December 2006;39:633-638. [Medline][Full Text].

  92. Fichter MM, Quadflieg N. Long-term stability of eating disorder diagnoses. International Journal of Eating Disorders. November 2007;40 Supplement:S61-S66. [Medline][Full Text].

  93. Milos G, Spindler A, Schnyder U, Fairburn CG. Instability of eating disorder diagnoses: prospective study. British Journal of Psychiatry. December 2005;187:573-578. [Medline][Full Text].

  94. Grilo CM, Pagano ME, Skodol AE, Sanislow CA, McGlashan TH, Gunderson JG, et al. Natural course of bulimia nervosa and of eating disorder not otherwise specified: 5-year prospective study of remissions, relapses, and the effects of personality disorder psychopathology. Journal of Clinical Psychiatry. May 2007;68(5):738-746. [Medline][Full Text].

  95. Björck C, Clinton D, Sohlberg S, Norring C. Negative self-image and outcome in eating disorders: results at 3-year follow-up. Eating Behaviors. August 2007;8(3):398-406. [Medline].

  96. Fosse GK, Holen A. Childhood maltreatment in adult female psychiatric outpatients with eating disorders. Eating Behaviors. November 2006;7(4):404-409. [Medline].

  97. Micali N, Holliday J, Karwautz A, Haidvogl M, Wagner G, Fernandez-Aranda F, et al. Childhood eating and weight in eating disorders: a multi-centre European study of affected women and their unaffected sisters. Psychotherapy and Psychosomatics. 2007;76(4):234-241. [Medline].

  98. Fernández-Aranda F, Krug I, Granero R, Ramón JM, Badia A, Giménez L, et al. Individual and family eating patterns during childhood and early adolescence: an analysis of associated eating disorder factors. Appetite. September 2007;49(2):476-485. [Medline].

  99. Mikami AY, Hinshaw SP, Patterson KA, Lee JC. Eating pathology among adolescent girls with attention-deficit/hyperactivity disorder. Journal of Abnormal Psychology. February 2008;117(1):225-235. [Medline].

  100. 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. International Journal of Eating Disorders. November 2007;40 Supplement:S67-S71. [Medline][Full Text].

  101. Woodside BD, Staab R. Management of psychiatric comorbidity in anorexia nervosa and bulimia nervosa. CNS Drugs. 2006;20(8):655-663. [Medline].

  102. Micali N, Treasure J, Simonoff E. Eating disorders symptoms in pregnancy: a longitudinal study of women with recent and past eating disorders and obesity. Journal of Psychosomatic Research. September 2007;63(3):297-303. [Medline].

  103. [Best Evidence] Micali N, Simonoff E, Treasure J. Risk of major adverse perinatal outcomes in women with eating disorders. British Journal of Psychiatry. March 2007;190:255-259. [Medline][Full Text].

  104. Chizawsky LL, Newton MS. Eating disorders: identification and treatment in obstetrical patients. Association of Women's Health, Obstetric and Neonatal Nurses. December 2006 - January 2007;10(6):482-488. [Medline][Full Text].

  105. Morgan JF, Lacey JH, Chung E. Risk of postnatal depression, miscarriage, and preterm birth in bulimia nervosa: retrospective controlled study. Psychosomatic Medicine. May/June 2006;68(3):487-492. [Medline].

  106. Marsden P, Karagianni E, Morgan JF. Spirituality and clinical care in eating disorders: a qualitative study. International Journal of Eating Disorders. January 2007;40:7-12. [Medline][Full Text].

  107. Richards PS, Berrett ME, Hardman RK, Eggett DL. Comparative efficacy of spirituality, cognitive, and emotional support groups for treating eating disorder inpatients. Eating Disorders. October-December 2006;14:401-415. [Medline].

  108. Graap H, Bleich S, Herbst F, Trostmann Y, Wancata J, de Zwaan M. The needs of carers of patients with anorexia and bulimia nervosa. European Eating Disorders Review. January 2008;16(1):21-29. [Medline][Full Text].

  109. Agras WS. Pharmacotherapy of bulimia nervosa and binge eating disorder: longer- term outcomes. Psychopharmacol Bull. 1997;33(3):433-6. [Medline].

  110. American Psychiatric Association. Practice guideline for eating disorders. American Journal of Psychiatry. 1993;150:212-228.

  111. American Psychiatric Association. Practice guideline for the treatment of patients with eating disorders (revision). American Journal of Psychiatry. 2000;157 (supplement):1-39.

  112. Andersen AE. Eating disorders in males. in Brownell KD and Fairburn CG. Eating disorders and Obesity. 1995;177-182.

  113. Arnow BA. Why are empirically supported treatments for bulimia nervosa underutilized and what can we do about it?. J Clin Psychol. Jun 1999;55(6):769-79. [Medline].

  114. Becker AE, Grinspoon SK, Klibanski A, Herzog DB. Eating disorders. N Engl J Med. Apr 8 1999;340(14):1092-8. [Medline].

  115. Beumont PJV. The clinical presentation of anorexia and bulimia nervosa. In: Brownell KD, Fairburn CG, eds. Eating Disorders and Obesity. 1995;151-158.

  116. Beumont PJV, Touyz SW. The clinical presentation of anorexia and bulimia nervosa. In: Brownell KD, Fairburn CG, eds. Eating Disorders and Obesity. 1995;306-312.

  117. Braun DL, Sunday SR, Huang A, Halmi KA. More males seek treatment for eating disorders. Int J Eat Disord. May 1999;25(4):415-24. [Medline].

  118. Brownell KD. Eating disorders in athletes. In: Brownell KD, Fairburn CG, eds. Eating disorders and Obesity. 1995;191-198.

  119. Bryant-Waugh R, Lask B. Childhood onset eating disorders. In: Brownell KD, Fairburn CG, eds. Eating disorders and Obesity. 1995;183-187.

  120. Bulik CM, Sullivan PF, Wade TD, Kendler KS. Twin studies of eating disorders: a review. Int J Eat Disord. Jan 2000;27(1):1-20. [Medline].

  121. Carlat DJ, Camargo CA Jr. Review of bulimia nervosa in males. Am J Psychiatry. Jul 1991;148(7):831-43. [Medline].

  122. Carmichael KA, Carmichael DH. Bone metabolism and osteopenia in eating disorders. In: Medicine. Baltimore. 1995;74:254-267.

  123. Caruso D, Klein H. Diagnosis and treatment of bulimia nervosa. Semin Gastrointest Dis. Oct 1998;9(4):176-82. [Medline].

  124. Comerci GD. Medical complications of anorexia nervosa and bulimia nervosa. Med Clin North Am. Sep 1990;74(5):1293-310. [Medline].

  125. Crago M, Shisslak CM, Estes LS. Eating disturbances among American minority groups: a review. Int J Eat Disord. Apr 1996;19(3):239-48. [Medline].

  126. Crow SJ, Mitchell JE. Integrating cognitive therapy and medications in treating bulimia nervosa. Psychiatr Clin North Am. Dec 1996;19(4):755-60. [Medline].

  127. Fairburn CG. Bulimia nervosa. BMJ. Feb 24 1990;300(6723):485-7. [Medline].

  128. Fairburn CG. Short term psychological treatments for bulimia nervosa. In: Brownell KD, Fairburn CG, eds. Eating Disorders and Obesity. 1995;344-348.

  129. Fairburn CG, Walsh BT. Atypical eating disorders. In: Brownell KD, Fairburn CG, eds. Eating Disorders and Obesity. 1995;135-140.

  130. Farrow JA. The adolescent male with an eating disorder. Pediatr Ann. Nov 1992;21(11):769-74. [Medline].

  131. Fisher M, Golden NH, Katzman DK, et al. Eating disorders in adolescents: a background paper. J Adolesc Health. Jun 1995;16(6):420-37. [Medline].

  132. Garfinkel PE. Classification and diagnosis of eating disorders. In: Brownell KD, Fairburn CG, eds. Eating Disorders and Obesity. 1995;125-134.

  133. Hetherington MM. Eating disorders: diagnosis, etiology, and prevention. Nutrition. Jul-Aug 2000;16(7-8):547-51. [Medline].

  134. Hoek HW. The distribution of eating disorders. In: Brownell KD, Fairburn CG, eds. Eating Disorders and Obesity. 1995;207-211.

  135. Hofland SL, Dardis PO. Bulimia nervosa. Associated physical problems. J Psychosoc Nurs Ment Health Serv. Feb 1992;30(2):23-7. [Medline].

  136. Holden RJ, Pakula IS. The role of tumor necrosis factor-alpha in the pathogenesis of anorexia and bulimia nervosa, cancer cachexia and obesity. Med Hypotheses. Dec 1996;47(6):423-38. [Medline].

  137. Hsu LK. Epidemiology of the eating disorders. Psychiatr Clin North Am. Dec 1996;19(4):681-700. [Medline].

  138. Hsu LKG. Outcome of bulimia nervosa. In: Brownell KD, Fairburn, CG eds. Eating Disorders and Obesity. 1995;238-246.

  139. Johnson C. Psychodynamic treatment of bulimia nervosa. In: Brownell KD, Fairburn CG, eds. Eating Disorders and Obesity. 1995;349-353.

  140. Kaltiala-Heino R, Rissanen A, Rimpelä M, Rantanen P. Bulimia and bulimic behaviour in middle adolescence: more common than thought?. Acta Psychiatr Scand. Jul 1999;100(1):33-9. [Medline].

  141. Katz JL. Eating disorders: a primer for the substance abuse specialist: 1. Clinical features. J Subst Abuse Treat. 1990;7(3):143-9. [Medline].

  142. Kaye W, Strober M, Stein D, Gendall K. New directions in treatment research of anorexia and bulimia nervosa. Biol Psychiatry. May 15 1999;45(10):1285-92. [Medline].

  143. Kaye WH, Klump KL, Frank GK, Strober M. Anorexia and bulimia nervosa. Annu Rev Med. 2000;51:299-313. [Medline].

  144. Kaye WH, Weltzin TE. Neurochemistry of bulimia nervosa. J Clin Psychiatry. Oct 1991;52 Suppl:21-8. [Medline].

  145. Kreipe RE, Birndorf SA. Eating disorders in adolescents and young adults. Med Clin North Am. Jul 2000;84(4):1027-49, viii-ix. [Medline].

  146. Lacey JH. Inpatient treatment of multi-impulsive bulimia nervosa. In: Brownell KD, Fairburn CG, eds. Eating Disorders and Obesity. 1995;361-368.

  147. Laue L, Gold PW, Richmond A, Chrousos GP. The hypothalamic-pituitary-adrenal axis in anorexia nervosa and bulimia nervosa: pathophysiologic implications. Adv Pediatr. 1991;38:287-316. [Medline].

  148. Mcgilley BM, Pryor TL. Assessment and treatment of bulimia nervosa. Am Fam Physician. Jun 1998;57(11):2743-50. [Medline].

  149. Mitchell JE. Medical complications of bulimia nervosa. In: Brownell KD, Fairburn CG, eds. Eating Disorders and Obesity. 1995;271-277.

  150. Muscari ME. Thin line: managing care for adolescents with anorexia and bulimia. MCN Am J Matern Child Nurs. May-Jun 1998;23(3):130-40; quiz 141. [Medline].

  151. Parry-Jones B, Parry-Jones WL. History of Bulimia and Bulimia nervosa. In: Brownell KD, Fairburn CG, eds. Eating Disorders and Obesity. 1995;145-150.

  152. Patel DR, Phillips EL, Pratt HD. Eating disorders. Indian J Pediatr. Jul-Aug 1998;65(4):487-94. [Medline].

  153. Pirke KM. Physiology of bulimia nervosa. In: Brownell KD, Fairburn CG, eds. Eating Disorders and Obesity. 1995;261-265.

  154. Robinson PH. Review article: recognition and treatment of eating disorders in primary and secondary care. Aliment Pharmacol Ther. Apr 2000;14(4):367-77. [Medline].

  155. Sokol MS, Steinberg D, Zerbe KJ. Childhood eating disorders. Curr Opin Pediatr. Aug 1998;10(4):369-77. [Medline].

  156. Strober M. Family-genetic perspectives on anorexia nervosa and bulimia nervosa. In: Brownell KD, Fairburn CG, eds. Eating Disorders and Obesity. 1995;212-218.

  157. Strober M, Freeman R, Morrell W. The long-term course of severe anorexia nervosa in adolescents: survival analysis of recovery, relapse, and outcome predictors over 10-15 years in a prospective study. Int J Eat Disord. Dec 1997;22(4):339-60. [Medline].

  158. Stunkard A. Eating disorders: the last 25 years. Appetite. Oct 1997;29(2):181-90. [Medline].

  159. Thomas MA, Rebar RW. The endocrinology of anorexia nervosa and bulimia nervosa. Curr Opin Obstet Gynecol. Dec 1990;2(6):831-6. [Medline].

  160. Tuschen B, Bents H. Intensive brief inpatient treatment of bulimia nervosa. In: Brownell KD, Fairburn CG, eds. Eating Disorders and Obesity. 1995;354-360.

  161. Vaz FJ. Outcome of bulimia nervosa: prognostic indicators. J Psychosom Res. Nov 1998;45(5):391-400. [Medline].

  162. Walsh BT. Pharmacotherapy of eating disorders. In: Brownell KD, Fairburn CG, eds. Eating Disorders and Obesity. 1995;313-317.

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

  164. Wilson GT. Treatment of bulimia nervosa: when CBT fails. Behav Res Ther. Mar 1996;34(3):197-212. [Medline].

  165. Wilson GT, Vitousek KM, Loeb KL. Stepped care treatment for eating disorders. J Consult Clin Psychol. Aug 2000;68(4):564-72. [Medline].

  166. Yanovski SZ. Biological correlates of binge eating. Addict Behav. Nov-Dec 1995;20(6):705-12. [Medline].

  167. Yanovski SZ. Obesity and eating disorders. In: Bray GA, Bouchard C, James WPT, eds. Handbook of Obesity. 1997:115-128.

  168. Ziolko HU. Bulimia: a historical outline. Int J Eat Disord. Dec 1996;20(4):345-58. [Medline].

Keywords

bulimia nervosa, BN, binge-eating/purging eating disorder, binge-eating disorder, BED, binging and purging, pathological voracity, cynorexia, kynorexia, morbid hunger, eating disorder, ED, excessive exercise, fasting, dieting, self-induced vomiting, diuretic abuse, laxative abuse, use of appetite suppressants, thyroid hormone, subjective bulimic episode

Contributor Information and Disclosures

Author

Raj K Kalapatapu, MD, Fellow, Addiction Psychiatry, Columbia University College of Physicians and Surgeons
Raj K Kalapatapu, MD is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, American Association for Geriatric Psychiatry, American Medical Association, and American Psychiatric Association
Disclosure: Nothing to disclose.

Coauthor(s)

Kelda Harris Walsh, MD, Assistant Professor of Clinical Psychiatry, Section of Child and Adolescent Psychiatry, Department of Psychiatry, Indiana University School of Medicine; Chief, Obsessive-Compulsive/Tourette/Anxiety Disorders Clinic, Riley Hospital for Children
Kelda Harris Walsh, MD is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry and American Psychiatric Association
Disclosure: Nothing to disclose.

Gabriel I Uwaifo, MBBS, Clinical and Research Attending, Assistant Professor of Medicine and Endocrinology, MedStar Clinical Research Center, MedStar Research Institute and Washington Hospital Center
Gabriel I Uwaifo, MBBS is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians-American Society of Internal Medicine, American Diabetes Association, American Medical Association, American Society of Hypertension, and Endocrine Society
Disclosure: Nothing to disclose.

Robert C Daly, MB, ChB, MPH, BCh, Senior Fellow, Department of Behavioral Endocrinology, National Institute of Mental Health, National Institutes of Health
Disclosure: Nothing to disclose.

Medical Editor

Sarah C Aronson, MD, Associate Professor, Departments of Psychiatry and Medicine, Case Western Reserve School of Medicine/University Hospitals of Cleveland
Sarah C Aronson, MD is a member of the following medical societies: American Academy of Family Physicians, American Medical Association, and American Psychiatric Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

David Bienenfeld, MD, Vice-Chair, Program Director, Professor, Department of Psychiatry, Wright State University School of Medicine
David Bienenfeld, MD is a member of the following medical societies: American Medical Association, American Psychiatric Association, and Association for Academic Psychiatry
Disclosure: Nothing to disclose.

CME Editor

Harold H Harsch, MD, Program Director of Geropsychiatry, Department of Geriatrics/Gerontology, Associate Professor, Department of Psychiatry and Department of Medicine, Froedtert Hospital, Medical College of Wisconsin
Harold H Harsch, MD is a member of the following medical societies: American Psychiatric Association
Disclosure: lilly Honoraria Speaking and teaching; Forest Labs Honoraria Speaking and teaching; AstraZeneca Honoraria Speaking and teaching; Pfizer Grant/research funds Speaking and teaching; Northstar Grant/research funds Research; Novartis Grant/research funds research; Pfizer  Speaking and teaching; Sanofi-avetis Grant/research funds research; Otsuke Grant/research funds reseach; GlaxoSmithKline Grant/research funds research

Chief Editor

Stephen Soreff, MD, President of Education Initiatives, Nottingham, NH; Faculty, Metropolitan College of Boston University, Boston, MA
Stephen Soreff, MD is a member of the following medical societies: American College of Mental Health Administration and American Psychosomatic Society
Disclosure: Nothing to disclose.

 
 
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.