Assessment and treatment of bulimia nervosa

Author: Beth M. McGilley, Tamara L. Pryor
Date: June, 1998

Bulimia nervosa is a psychiatric syndrome with potentially serious consequences.[1,2] Relatively effective treatments for this disorder have been developed, and early intervention is more likely to facilitate eventual recovery.[2] Unfortunately, few health care professionals receive training in the assessment of bulimia nervosa. Therefore, they may be unable to identify and treat patients with the disorder.

Historically, patients with bulimia nervosa often were hospitalized until the most disruptive symptoms ceased. In today's health care environment, hospitalization for bulimia nervosa is infrequent and tends to take the form of brief admissions focused on crisis management.[3] Specialists in the field of eating disorders have responded to the present cost-containment measures by developing a combination of treatment modalities, including medication and individual and group psychotherapy, that can be used in the outpatient care of patients with bulimia nervosa. This article discusses the assessment and treatment of bulimia nervosa and considers how this disorder can best be handled in a managed care environment.

Definitions and Etiology

Bulimia nervosa is a multifaceted disorder with psychologic, physiologic, developmental and cultural components.[1,2] There may be a genetic predisposition for the disorder. Other predisposing factors include psychologic and personality factors, such as perfectionism, impaired self-concept, affective instability, poor impulse control and an absence of adaptive functioning to maturational tasks and developmental stressors (e.g., puberty; peer and parental relationships, sexuality, marriage and pregnancy).

Biologic researchers suggest that abnormalities of central nervous system neurotransmitters may also play a role in bulimia nervosa.[4] Furthermore, several familial factors may increase the risk of developing this disorder. For example, researchers have discovered that first- and second-degree relatives of individuals with bulimia nervosa have an increased incidence of depression and manic-depressive illnesses, eating disorders, and alcohol and substance abuse problems.[5-7]

Regardless of the cause, once bulimia nervosa is present, the physiologic effects of disordered eating appear to maintain the core features of the disorder, resulting in a self-perpetuating cycle.

Diagnostic Criteria

The diagnostic criteria for bulimia nervosa (Table 1) now include subtypes to distinguish patients who compensate for binge eating by purging (vomiting and/or the abuse of laxatives and diuretics) from those who use nonpurging behaviors (e.g., fasting or excessive exercising).[1]

TABLE 1 Diagnostic Criteria for Bulimia Nervosa

A. Recurrent episodes of binge eating. An episode of binge eating is characterized by both of the following:

1. Eating, in a discrete period of time (e.g., within a two-hour period), an amount of food that is definitely larger than most people would eat during a similar period of time and under similar circumstances.

2. A sense of lack of control over eating during the episode (e.g., a feeling that one cannot stop eating or control what or how much one is eating).

B. Recurrent inappropriate compensatory behavior in order to prevent weight gain, such as self-induced vomiting; misuse of laxatives, diuretics, enemas, or other medications; fasting or excessive exercise.

C. The binge eating and inappropriate compensatory behaviors both occur, on average, at least twice a week for three months.

D. Self-evaluation is unduly influenced by body shape and weight.

E. The disturbance does not occur exclusively during episodes of anorexia nervosa.

Specify type:

Purging type: during the current episode of bulimia nervosa, the person has regularly engaged in self-induced vomiting or the misuse of laxatives, diuretics, or enemas.

Nonpurging type: during the current episode of bulimia nervosa, the person has used other inappropriate compensatory behaviors, such as fasting or excessive exercise, but has not regularly engaged in self-induced vomiting or the misuse of laxatives, diuretics, or enemas.

Reprinted with permission from American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. Washington, D. C.: American Psychiatric Association, 1994:549-50.

A binge eating/purging subtype of anorexia nervosa also exists. Low body weight is the major factor that differentiates bulimia nervosa from this subtype of anorexia nervosa. Thus, according to the established diagnostic criteria,[1] patients who are 15 percent below natural bodyweight and binge eat or purge are considered to have anorexia nervosa. Patients can, and frequently do, move between diagnostic categories as their symptom pattern and weight change over the course of the illness.

Some patients do not meet the full criteria for bulimia nervosa or anorexia. nervosa. These patients may be classified as having an eating disorder "not otherwise specified" (Table 2).[1]

TABLE 2 Diagnostic Criteria for Eating Disorder Not Otherwise Specified

1. For females, all of the criteria for anorexia nervosa are met except that the individual has regular menses.

2. All of the criteria for anorexia nervosa are met except that, despite significant weight loss, the individual's current weight is in the normal range.

3. All of the criteria for bulimia nervosa are met, except that the binge eating and inappropriate compensatory mechanisms occur at a frequency of less than twice a week or for a duration of less than three months.

4. The regular use of inappropriate compensatory behavior by an individual of normal body weight after eating small amounts of food (e.g., self-induced vomiting after the consumption of two cookies).

5. Repeatedly chewing and spitting out, but not swallowing, large amounts of food.

6. Binge-eating disorder: recurrent episodes of binge eating in the absence of the regular use of inappropriate compensatory behaviors characteristic of bulimia nervosa.

Reprinted with permission from American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. Washington, D.C. American Psychiatric Association, 1994:550.

Prevalence and Prognosis

Bulimia nervosa appears to have become more prevalent during the past 30 years. The disorder is 10 times more common in females than in males and affects 1 to 3 percent of female adolescents and young adults.[6]

Both anorexia nervosa and bulimia nervosa have a peak onset between the ages of 13 and 20 years. The disorder appears to have a chronic, sometimes episodic course in which periods of remission alternate with recurrences of binge/purge cycles. Some patients have bulimia nervosa that persists for 30 years or more.[8] Recent data suggest that patients with subsyndromal bulimia nervosa may show morbidity comparable to that in patients with the full syndrome.

The long-term outcome of bulimia nervosa is not known. Available research indicates that 30 percent of patients with bulimia nervosa rapidly relapse and up to 40 percent remain chronically symptomatic.[9]

Psychiatric Comorbidity

Clinical and research reports[10-13] emphasize a frequent association between bulimia nervosa and other psychiatric conditions. Comorbid major depression is commonly noted (Table 3), although it is not clear if the mood disturbance is a function of bulimia nervosa or a separate phenomenon.[11]

TABLE 3 Psychiatric Conditions Commonly Coexisting with Bulimia Nervosa

Mood disorders Major depression Dysthymic disorder Bipolar disorder

Substance-related disorders Alcohol abuse Stimulant abuse Polysubstance abuse

Anxiety disorders Panic disorder Obsessive-compulsive disorder Generalized anxiety disorder Post-traumatic stress disorder

Personality disorders Borderline personality disorder Histrionic personality disorder Narcissistic personality disorder Antisocial personality disorder

Information concerning the comorbidity rates of bipolar disorders (e.g., manic depression, rapid cycling mood disorder) and bulimia nervosa is somewhat limited. However, recent epidemiologic data indicate an increased incidence of rapid cycling mood disorders in patients with more severe, chronic bulimia nervosa.[13]

The association between bulimia nervosa and other anxiety and substance-related disorders has been well documented.[7] For example, substance abuse or dependence, particularly involving alcohol and stimulants, occurs in one third of patients with bulimia nervosa. Thus, a comorbid substance-related disorder must be addressed before effective treatment for bulimia nervosa can be initiated.

Significant research has been devoted to the high frequency of personality disturbances in patients with bulimia nervosa. Overall, between 2 and 50 percent of women with bulimia nervosa have some type of personality disorder, most commonly borderline, antisocial, histrionic or narcissistic personality disorder.[10,14-16]

[15.] Herzog DB, Keller MB, Lavori PW, Kenny GM, Sacks NR. The prevalence of personality disorders in 210 women with eating disorders. J Clin Psychiatry 1992;53:147-52.

[16.] Wonderlich SA, Swift WJ, Slotnick HB, Goodman S. DSM-III-R personality disorders in eating disorder subtypes. Int J Eating Disord 1990;9:607-16.

[17.] Sansone RA, Sansone LA. Bulimia nervosa: medical complications. In: Alexander-Mott L, Lumsden DB, eds. Understanding eating disorders: anorexia nervosa, bulimia nervosa, and obesity. Washington, D.C.: Taylor & Francis, 1994:181-201.

[18.] Kaplan AS, Garfinkel PE, eds. Medical issues and the eating disorders: the interface. New York: Brunner/Mazel, 1993.

[19.] Fairburn CG. Overcoming binge eating. New York: Guilford, 1995.

[20.] Jacobs MB, Schneider JA. Medical complications of bulimia: a prospective evaluation. Q J Med 1985; 54:177-82.

[21.] Pope HG Jr, Hudson JI, Jonas JM, Yurgelun-Todd D. Bulimia treated with imipramine: a placebo-controlled, double-blind study, Am J Psychiatry 1983; 140:554-8.

[22.] Mitchell JE, Groat R. A placebo-controlled, double-blind trial of amitriptyline in bulimia. J Clin Psychopharmacol 1984;4:186-93.

[23.] Hughes PL, Wells LA, Cunningham CJ, Ilstrup DM. Treating bulimia with desipramine. A double-blind, placebo-controlled study Arch Gen Psychiatry 1986;43:182-6.

[24.] Agras W, Dorian B, Kirkely B, Arnow B, Bachman J. Imipramine in the treatment of bulimia: a double-blind controlled study. Int J Eating Disord 1987; 6:29-38.

[25.] Barlow J, Blouin J, Blouin A, Perez E. Treatment of bulimia with desipramine: a double-blind crossover study. Can J Psychiatry 1988;33:129-33.

[26.] Blouin AG, Blouin JH, Perez EL, Bushnik T, Zuro C, Mulder E. Treatment of bulimia with fenfluramine and desipramine. J Clin Psychopharmacol 1988;8: 261-9.

[27.] Walsh BT, Hadigan CM, Devlin MJ, Gladis M, Roose SP. Long-term outcome of antidepressant treatment for bulimia nervosa. Am J Psychiatry 1991;148:1206-12.

[28.] Walsh BT, Gladis M, Roose SP, Stewart JW, Stetner F, Glassman AH. Phenelzine vs placebo in 50 patients with bulimia. Arch Gen Psychiatry 1988; 45:471-5.

[29.] Kennedy SH, Piran N, Warsh JJ, Prendergast P, Mainprize E, Whynot C, et al. A trial of isocarboxazid in the treatment of bulimia nervosa. J Clin Psychopharmacol 1988;8:391-6 [Published erratum appears in J Clin Psychopharmacol 1989;9:3].

[30.] Horne RL, Ferguson JM, Pope HG Jr, Hudson JI, Lineberry CG, Ascher J, et al. Treatment of bulimia with bulpropion: a multicenter controlled trial, J Clin Psychiatry 1988;49:262-6.

[31.] Pope HG Jr, Keck PE Jr, McElroy SL, Hudson JI. A placebo-controlled study of trazodone in bulimia nervosa. J Clin Psychopharmacol 1989;9:254-9.

[32.] Goldstein DJ, Wilson MG, Thompson VL, Potvin JH, Rampey AH Jr. Long-term fluoxetine treatment of bulimia nervosa. Br J Psychiatry 1995;166:660-6.

[33.] Fluoxetine Bulimia Nervosa Collaborative Study Group. Fluoxetine in the treatment of bulimia nervosa. A multicenter, placebo-controlled, double-blind trial. Arch Gen Psychiatry 1992;49:139-47.

[34.] Mitchell JE, Christenson G, Jennings J, Huber M, Thomas B, Pomeroy C, et al. A placebo-controlled, double-blind crossover study of naltrexone hydrochloride in outpatients with normal weight bulimia. J Clin Psychopharmacol 1989;9:94-7.

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

[36.] Fairburn C, Marcus M, Wilson G. Cognitive behavior therapy for binge eating and bulimia nervosa: a treatment manual. In: Fairburn CG, Wilson GT, eds. Binge eating: nature, assessment, and treatment, New York: Guilford, 1993.

[37.] Wilson GT. Treatment of bulimia nervosa: when CBT fails. Behav Res Ther 1996;34:197-212.

[38.] Agras WS, Telch CF, Arnow B, Eldredge K, Wilfley D, Raeburn SD, et al. Weight loss, cognitive-behavioral, and desipramine treatments in binge eating disorder: an additive design. Behav Ther 1994; 25:225-38.

BETH M. MCGILLEY, PH.D., is a nationally recognized specialist in eating disorders and maintains a private practice. She codirects the eating disorders clinic at the University of Kansas School of Medicine--Wichita, where she is a volunteer faculty member. Dr. McGilley is a member of the Managed Care Task Force of the Academy of Eating Disorders.

TAMARA L. PRYOR, PH.D., is clinical associate professor in the Department of Psychiatry and Behavioral Sciences at the University of Kansas School of Medicine--Wichita, where she founded and currently codirects the eating disorders clinic. Dr. Pryor also developed one of the few postdoctoral internship and fellowship programs in eating disorders accredited by the American Psychological Association. She is a member of the Managed Care Task Force of the Academy of Eating Disorders.

Address correspondence to Tamara L. Pryor Ph.D., University of Kansas School of Medicine-Wichita, 1010 N. Kansas, Wichita, KS 67214-3199. Reprints are not available from the authors.

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