Bulimia Nervosa: A Quest to Improve Intervention & Treatment

by James Mitchell, MD, University of North Dakota, Fargo, ND
Reprinted from Eating Disorders Review
January/February 2000 Volume 11, Number 1
©2000 Gürze Books

Approximately 20 years have passed since Gerald Russell’s seminal 1979 article described bulimia nervosa (BN) as a separate diagnostic entity. While descriptions of such patients had appeared in the literature before this, Russell’s article documented BN as a distinct syndrome and opened a whole new area of inquiry in eating disorders that continues to this day.

Upon reflection, one can interpret the available literature that has accumulated since 1979 as suggesting that considerable progress has been made. Indeed, the database on BN has grown dramatically over these two decades. However, serious questions remain, particularly questions related to prevention and treatment. These questions should lead us to refocus our efforts as we enter the new century.

Prevalence. BN is a fairly prevalent disorder that affects from 1% to 2% of young women, and usually appears in late adolescence or young adulthood (Becker et al, 1999; Walsh & Devlin, 1998). It occurs far more commonly among women, and appears to cluster in females in western industrialized societies, although there is some evidence that the disorder is becoming more prevalent in the Third World. We also know that the rates of both anorexia nervosa (AN) and BN are exaggerated in first-degree relatives of patients with BN, suggesting that risks for the two disorders are transmitted together (Strober et al, in press). Indeed, recent results suggest a substantial genetic risk for BN, with a heritability of perhaps 50%, although the results have been inconsistent (Bulik et al, 1998; Sullivan et al, 1997; Fairburn et al, 1999). While many BN patients are categorized as impulsive, obsessive-compulsive traits are also commonly seen and appear to persist in some after recovery (von Ranson et al, 1999).

Abnormalities of the serotonin system. From the neurobiological standpoint, abnormalities of the serotonin system have been reported, including increased levels of CSF 5-hydroxyindoleacetic acid at long-term follow-up, suggesting the possibility of ongoing–and perhaps predisposing– serotonergic dysfunction (Kaye et al, 1998). These results are particularly intriguing since we know that serotonin is involved in the modulation of various processes, including temperament and impulsivity, as well as feeding.

And, as has been well documented over the last 20 years, BN is associated with high rates of comorbidity, including affective disorders, anxiety disorders, and personality disorders (Wonderlich & Mitchell, 1997). It is also well known that at long-term follow-up many individuals with the disorder remain symptomatic even though they may not meet full syndromal criteria (Keel et al, 1999).

Treatment Advances

Much of the research in the last 10 years or so has focused on the development of various treatment strategies for BN. Two separate lines of research have found efficacy for certain psychosocial treatments and for pharmacotherapy. The pharmacologic agent best established for BN is fluoxetine (Peterson & Mitchell, 1999; Goldstein et al, 1996).

Psychotherapeutic approaches have focused on the use of cognitive behavioral therapy (CBT). CBT has been shown to be as effective or more effective than every other treatment to which it has been compared, although recent studies suggest equal efficacy for interpersonal therapy or IPT, an interesting observation given the fact that IPT does not directly address eating issues (Fairburn et al, 1995). Available research also suggests that psychosocial interventions are superior to pharmacological interventions when both are available (Bacaltchuk et al, 1999). However, considerable evidence indicates that problems remain with the efficacy of these treatments, in that many individuals do not respond or subsequently relapse (Wilson, 1999). Also, there is considerable evidence that empirically validated treatments are being underutilized, and that alternative means of training therapists or administering such treatments need to be developed (Arnow, 1999).

The cultural challenge. Headway has been made in our understanding of this disorder, including the underlying psychobiology, the longitudinal course, the comorbidity, and the treatment. Priorities in the 21st century will be identifying effective and practical preventative intervention strategies (Striegel-Moore & Steiner-Adair, 1998) and the improvement of our treatments, to decrease the rate of non-response and rate of relapse. Unfortunately, the cultural background surrounding this disorder, which places a high value on slimness as a model of attractiveness for women in western industrialized societies, continues unabated. Any means of alleviating the burden that this unfortunate cultural message places on young women in our society has remained elusive.

References

Arnow BA. Why are empirically supported treatments for bulimia nervosa underutilized and what can we do about it? J Clin Psychol 1999; 55: 769.

Bacaltchuk J, Trefiglio RP, de Oliveira IR, et al. Antidepressants versus psychotherapy for bulimia nervosa: A systematic review. J Clin Pharm Therapy, 1999; 24:23.

Becker AE, Grinspoon SK, Klibanski A, et al. Eating disorders. N Engl J Med, 1999; 340: 1092.

Bulik CM, Sullivan PF, Weltzin TE, et al. Temperament in eating disorders. Int J Eat Disord 1995; 17: 251.

Fairburn CG, Cowen PJ, Harrison PJ. Twin studies and the etiology of eating disorders. Int J Eat Disord 1999; 26: 349.

Fairburn CG, Norman PA, Welch SL, et al. A prospective study of outcome in bulimia nervosa and the long-term effects of three psychological treatments. Arch Gen Psychiatry 1995; 52: 304.

Goldstein DJ, Wilson MG, Thompson VL, et al. The Fluoxetine Bulimia Nervosa Collaborative Study Group. Long-term fluoxetine treatment of bulimia nervosa. Br J Psychiatry 1996;153: 660.

Kaye WH, Greeno CG, Moss H, et al. Alterations in serotonin activity and psychiatric symptoms after recovery from bulimia nervosa. Arch Gen Psychiatry 1998; 55: 927.

Keel PK, Mitchell JE, Miller KB, et al. Long-term outcome of bulimia nervosa. Arch Gen Psychiatry1999; 56: 63.

Peterson CB, Mitchell JE. Psychosocial and pharmacological treatment of eating disorders: A review of research findings. J Clin Psychol 1999; 55: 685.

Russell G. Bulimia nervosa: An ominous variant of anorexia nervosa. Psychol Med 1979; 9: 429.

Striegel-Moore RH, Steiner-Adair C. Primary prevention of eating disorders: Further considerations from a feminist perspective. In: Vandereycken & Noordenbos (eds.), The Prevention of Eating Disorders. London: Athlone Press, pp. 1-22, 1998.

Strober M, Freeman R, Lampert C, Diamond J, Kaye W. A controlled family study of anorexia nervosa and bulimia nervosa: Evidence of shared liability and transmission of partial syndromes. Am J Psychiatry ( in press).

Sullivan PF, Bulik CM, Kendler KS. The genetic epidemiology of binging and vomiting. Br J Psychiatry 1998; 173: 75.

von Ranson KM, Kaye WH, Weltzin TE, et al. Obsessive-compulsive disorder symptoms before and after recovery from bulimia nervosa. Am J Psychiatry 1999; 156: 1703.

Walsh BT & Devlin MJ. Eating disorders: Progress and problems. Science 1998; 280: 1387.

Wilson GT. Cognitive behavior therapy for eating disorders: Progress and problems. Behav Res Ther 1999; 37: S79.

Wonderlich SA & Mitchell JE. Eating disorders and comorbidity: Empirical, conceptual, and clinical implications. Psychopharmacol Bull 1997; 33: 3981.

No Comments Yet

Comments are closed