D Colin Drummond John Strang

BULIMIA NERVOSA Since 1980, bulimia nervosa has been recognized by the American Psychiatric Association as an autonomous eating disorder. The term bulimia means ''an extreme hunger,'' but the word is most commonly understood to refer to Bulimia Nervosa. It is characterized by recurrent episodes of binge eating followed by such regular activities as self-induced vomiting, excessive use of laxatives and/or diuretics, fasting or dieting, and vigorous exercise—all of which are directed at weight control. A characteristic feature in the bulimic patient is a persistent concern with weight and body shape. Other psychiatric disorders can accompany bulimia, particularly major depression. The full syndrome affects 1 to 3 percent of the adolescent and young adult female population, but many more experience subclinical variants of the disorder. Bulimia nervosa does occur in males, but such incidence is rare.

This disturbance in eating affects mostly young women—usually women of normal weight—and is often preceded by ANOREXIA nervosa (restricted eating). The bulimic symptoms may continue for many years with exacerbations and remissions. From the mid-1970s to the mid-1990s, the prevalence of eating disorders appeared to be increasing in industrialized countries. The etiology of bulimia is unknown, although psychological, sociocultural, and biological theories have been proposed. Many consider Western societies' increasing emphasis on thinness, especially among women, to be a contributing influence.

Parallels between bulimia nervosa and substance abuse have been drawn based on an ADDICTION model, a self-psychology model, and a psycho-biological model. According to the addiction model, food is the ''substance'' that is abused in bulimia nervosa. Although there are superficial similarities in phenomenology between binge eating and substance abuse, these similarities are selective and rely on a loose definition of addiction. The self-psychology perspective is that both bulimia nervosa and substance abuse arise from a common deficit in psychological functioning. Difficulties regulating affect and tension generate a need for the external distraction provided by food or psychoactive substances, respectively. This model may have some heuristic value but it has not, as of the mid-1990s, received empirical validation. The psychobiologi-cal view regards eating and drinking as consummately behaviors with the potential for dysregulation. One possibility is a shared disturbance in the brain neurochemical functioning that regulates drives of appetite. There is some evidence that brain SEROTONIN function may be disrupted in both bulimia nervosa and ALCOHOL abuse; however, research in this area has just begun and the validity of this model is unknown as of the mid-1990s.

Among women receiving treatment for substance abuse, estimates of the prevalence of bulimia nervosa range from 8 to 17 percent, and estimates of the prevalence of some eating disorder range from 26 to 47 percent. Similarly, estimates of alcohol abuse among women seeking treatment for bulimia nervosa range from 27 to 49 percent. Thus, substance abuse and bulimia nervosa occur together in young women much more frequently than would be expected for independent disorders. One potential source of this comorbidity lies in genetic risk. Several studies have indicated an overrepre-sentation of alcohol abuse in the families of women with eating disorders. Another possibility is that certain psychological factors place certain women at risk for the development of either bulimia nervosa or substance abuse. There is some limited evidence for an underlying ADDICTIVE PERSONALITY in both disorders. As well, women with both disorders seem to have more difficulties, generally, with impulsive behaviors.

The treatment of bulimia nervosa depends on its severity. Many cases of the eating disturbance resolve on their own. Specific interventions that may be tried include psychodynamic (individual, family, group) therapies as well as cognitive and be-haviorally oriented therapies and pharmacological treatments. Modest improvements have been reported with the use of ANTIDEPRESSANT medication. Studies conducted in the late 1990s have shown that ondansetron (a drug commonly used for patients with vomiting associated with chemo-theraphy) could be an effective treatment for those with bulimia; this drug was not shown to treat the psychological aspects of the disorder though (Kiss, 2000).

BIBLIOGRAPHY

FAIRBURN, Christopher G., ET AL. (2000). The natural course of bulimia nervosa and binge eating disorders in young women. Archives of General Psychiatry, 57, 659.

Goldbloom, D. S. (1993). Alcohol abuse and eating disorders: Aspects of an association. Alcohol and Alcoholism.

Kiss, Alexander (2000). Treatment of chronic bulimic symptoms: new answers, more questions. The Lancet, 355, 769.

Mitchell, J. E. (1990). Bulimia nervosa. Minneapolis:

University of Minnesota Press. Peveler, R., & Fairburn, C. (1990). Eating disorders in women who abuse alcohol. British Journal of Addiction, 85, 1633-1638. Vandereycken, W. (1990). The addiction model in eating disorders: some critical remarks and a selected bibliography. International Journal of Eating Disorders, 9, 95-101. Wilson, G. T. (1991). The addiction model of eating disorders: a critical analysis. Advances in Behaviour Research and Therapy, 12, 27-72.

Marion Olmsted David Goldbloom Miroslava Romach Karen Parker Revised by Rebecca Marlow-Ferguson

BUPRENORPHINE Buprenorphine is a semisynthetic OPIATE which is produced from thebaine, a naturally occurring ALKALOID present in the ripe pods of the opium poppy (Papaner somniferum). Buprenorphine has an ANALGESIC potency twenty-five to fifty times greater than MORPHINE on a weight basis. However, the analgesic actions of buprenorphine are quite similar to those of morphine and the other opiates after taking into consideration its greater potency. It is assumed that these effects are dependent upon its ability to act at mu (morphine) receptors in the brain. Once bound to the receptor, however, buprenorphine only produces a limited effect, and thus it is termed a partial Agonist. This ability to produce only a partial response may explain why buprenorphine lowers breathing (respiratory depression) less than drugs such as morphine. Because it is a partial agonist, buprenorphine administration to morphine-dependent patients does not elicit significant withdrawal symptoms and can therefore be used as a metha-done-like opiate substitute in treatment programs. Another reason for the use of the agent in this respect is its particularly long duration of action. Single doses of buprenorphine can attenuate or prevent many of the actions of morphine for up to thirty hours. Thus, buprenorphine maintenance programs have been proposed to treat opiate addiction.

The interactions of buprenorphine with ANTAGONISTS are interesting. Buprenorphine actions can be readily prevented by antagonists such as NALOXONE, when the antagonist is administered prior to buprenorphine. However, antagonists given after buprenorphine do not readily reverse the opioid actions. This unique pharmacology distinguishes it from traditional opiates such as mor

Figure 1

Buprenorphine phine. Many believe that this observation is due to the prolonged occupation of the receptor by buprenorphine. Once it is bound, other drugs can no longer get to the receptor.

In the early 1990s, it was proposed that buprenorphine might also prove effective in lowering COCAINE use. Some studies in primates showed that buprenorphine lowered the amounts of cocaine taken. Although some small clinical studies in people also suggested a similar effect, more controlled studies did not show a special effect on cocaine use. More extensive work will be needed to determine whether buprenorphine can be useful in the treatment of cocaine abusers.

(SEE ALSO: Heroin; Treatment/Treatment Types)

BIBLIOGRAPHY

JAFFE, J. H., & MARTIN, W. R. (1990). Opioid analgesics and antagonists. In A. G. Gilman et al. (Eds.), Goodman and Gilman's the pharmacological basis of therapeutics, 8th ed. New York: Pergamon.

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