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Psychiatric Times. Vol. 19 No. 7
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Integrating Treatment in Eating Disorders

By Phillipa J. Hay, M.D.
| July 1, 2002
Dr. Hay is a senior lecturer with University of Adelaide in Australia and senior consultant psychiatrist to Royal Adelaide Hospital. She has longstanding research and clinical interests in eating disorders, in particular, their epidemiology and evidence for their treatments.

Bulimia Nervosa

In contrast, for bulimia nervosa, the use of medication--most commonly antidepressants--in combination with psychotherapy is often useful, and there are now several published randomized, controlled trials. A recent meta-analysis (summarized in Table 2) found that where antidepressants are combined with focused psychotherapies and compared with either antidepressants alone or with psychotherapy alone, the combination is favored (Bacaltchuk et al., 2001).

How medications and psychotherapies--biological and psychological--act together to give a better outcome is unknown, but it is a phenomena not confined to eating disorders. For example, in obsessive-compulsive disorder, brain imaging changes have been reported to occur following psychological treatments (Schwartz et al., 1996). Whether similar effects occur in the treatment of patients with bulimia nervosa is speculative, but reports by Hirano and colleagues (1999) and Kaye and colleagues (2001) support further exploration of the biological mechanisms in treatment and the mode of synergy of combination therapies. In addition, the effect of antidepressants has been found across a number of trials in study subjects most often without comorbid severe depression (Bacaltchuk et al., 2000). This supports there being a specific effect in bulimia nervosa, not merely a general effect on depressive symptoms.

In these meta-analyses, however, non-completion rates are high in the groups where medications are included compared to those that have psychotherapy alone. This suggests that patients find antidepressants less acceptable than psychotherapy. Why this should be so has not been rigorously explored in treatment studies. One possibility is because of greater side effects, but it could also be because taking tablets lacks credibility for patients. It is known that a range of important personal and social-cultural factors are likely to contribute to the etiology of bulimia nervosa and similar disorders (e.g., Fairburn et al., 1998; Fairburn et al., 1997). Thus, treatments (such as CBT or interpersonal psychotherapy) that appear to address these issues are easy to explain to patients with respect to their theoretical underpinnings. Similarly, however, as already noted, there is evidence that biological mechanisms such as possible serotonin depletion (Kaye et al., 2001) are likely to also be important. Whether these changes are a cause or consequence of bulimia nervosa is unclear, but they do provide some rationale for the use of, for example, the SSRIs in the treatment of bulimia nervosa.

There are several instances where I have found it most useful to integrate an antidepressant and psychotherapy, which accords with other opinion (Garfinkel and Walsh, 1997). (I commonly use the staged and manualized form of CBT as described by Wilson et al., 1997). The first is in cases of very frequent and severe binge-eating and the antidepressant aids reduction in bingeing to a point where the patient has a greater capacity to engage in psychotherapy. This is similar to the second instance, in which the patient suffers moderate to severe depressive symptoms. The third most common situation in which I use antidepressants is when patients have made some improvement with CBT but moderate eating disorder symptoms remain. Finally, when specialized psychotherapeutic help is difficult for patients to access, primary care physicians often may commence antidepressants while awaiting a specialist opinion.

Conclusion

While the evidence for integrating treatments in eating disorders is not strong, there is sufficient evidence to support combining antidepressant and psychotherapies in the active treatment of bulimia nervosa. This may, however, be at the cost of people withdrawing from treatment, due possibly to side effects or the lack of treatment credibility.

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References

Aalto-Setala T, Marttunen M, Tuulio-Henriksson A et al. (2001), One-month prevalence of depression and other DSM-IV disorders among young adults. Psychol Med 31(5):791-801.

APA (1994), Diagnostic and Statistical Manual of Mental Disorders, 4th Ed. Washington, D.C.: American Psychiatric Association, p550.

Bacaltchuk J, Hay P, Mari JJ (2000), Antidepressants versus placebo for the treatment of bulimia nervosa: a systematic review. Aust N Z J Psychiatry 34(2):310-317.

Bacaltchuk J, Hay P, Trefiglio R (2001), Antidepressants versus psychological treatments and their combination for bulimia nervosa (Cochrane Review). In: The Cochrane Library, Issue 4. Oxford, England: Update Software.

Bushnell JA, Wells JE, Hornblow AR et al. (1990), Prevalence of three bulimia syndromes in the general population. Psychol Med 20(3):671-680.

Fairburn CG, Doll HA, Welch SL et al. (1998), Risk factors for binge eating disorder: a community-based case-control study. Arch Gen Psychiatry 55(5):425-432.

Fairburn CG, Welch SL, Doll HA et al. (1997), Risk factors for bulimia nervosa. A community-based case-control study. Arch Gen Psychiatry 54(6):509-517.

Garfinkel PE, Walsh BT (1997), Drug therapies. In: Handbook of Treatment for Eating Disorders, 2nd Edition, Garner DM, Garfinkel PE, eds. New York: Guilford Press, pp372-380.

Garner DM, Garfinkel PE, eds. (1997), Handbook of Treatment for Eating Disorders, 2nd Edition. New York: Guilford Press.

Goldberg SC, Casper RC, Eckert ED et al. (1980), Effects of cyproheptadine in anorexia nervosa. Psychopharmacology Bulletin 16(2):29-30.

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Halmi KA, Eckert E, LaDu TJ, Cohen J (1986), Anorexia nervosa. Treatment efficacy of cyproheptadine and amitriptyline. Arch Gen Psychiatry 43(2):177-181.

Hay P (1998), The epidemiology of eating disorder behaviors: an Australian community-based survey. Int J Eat Disord 23(4):371-382.

Hay P, Ben-Tovim D, Walker K (2001), The quantity and quality of the evidence base for treatments used in anorexia nervosa: a matter for concern. P-157. Presented at the Ninth International Cochrane Colloquium. Lyon, France; Oct. 12-13.

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Hirano H, Tomura N, Okane K et al. (1999), Changes in cerebral blood flow in bulimia nervosa. J Comput Assist Tomogr 23(2):280-282.

Kaye WH, Nagata T, Weltzin TE et al. (2001), Double-blind placebo-controlled administration of fluoxetine in restricting- and restricting-purging-type anorexia nervosa. Biol Psychiatry 49(7):644-652.

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Russell G (1979), Bulimia nervosa: an ominous variant of anorexia nervosa. Psychol Med 9(3):429-448.

Schwartz JM, Stoessel PW, Baxter LR et al. (1996), Systematic changes in cerebral glucose metabolic rate after successful behavior modification treatment of obsessive-compulsive disorder. Arch Gen Psychiatry 53(2):109-113.

Treasure J, Schmidt U (2001), Anorexia nervosa. Clinical Evidence 5:0-12.

Wilson GT, Fairburn CG, Agras WS (1997), Cognitive-behavioral therapy for bulimia nervosa. In: Handbook of Treatment for Eating Disorders, 2nd Edition, Garner DM, Garfinkel PE, eds. New York: Guilford Press, pp67-93.


 
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