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The impact of prior substance abuse on treatment outcome for bulimia nervosa
.Iddii,ri~rBrila~iors. Vol. 17,pp. 387-395. Printed in the USA. All rights resewed.
THE IMPACT
OF PRIOR OUTCOME
1991 Copyright
SUBSTANCE ABUSE OX TREATlIENT FOR BULIMIA NERVOS.4
TRACEY J. STRASSER, KATHLEEN Columbia
0306~4603/9255.00 + .OO 5 1392 Pergamon Press Ltd.
University.
M. PIKE, and B. TIXlOTHY W’ALSH
College of Physicians
and Surgeons
Abstract - The present investigation examined the signiticance ofa past history of substance abuse on treatment outcome for bulimia nervosa. Seventy&s women with bulimia ncrvosa participated in a &week double-blind outpatient trial ofdesipramine: I9 patients had a history ofsubstance abuse and 56 did not. Although patients with a history ofsubstance abuse reported higher levels ofanxiety and depression at presentation for treatment than patients without such histories. the two groups reported a similar age of onset of their bulimia ncmosa and similar severity of eating pathology with regards to binge and vomit frequencies and measures of concern about body shape and weight. On all outcome measures, the improvement ofthe substance abuse group was equal to or greater than that in the group without a histon ofsubstance abuse. Results suggest that a past history of substance abuse has no implication regarding response to pharmacological treatment for bulimia nervosa.
A number of clinical and epidemiological studies indicate that patients in treatment for bulimia nervosa report more frequent problems with current or past alcohol and drug abuse than would be expected in the general population (Wilson. 199 1). Depending on diagnostic criteria and sampling procedures, estimates of lifetime prevalence rates for substance abuse among bulimic women range from approximately 10% (Schwalberg, 1990; Walsh, Roose, Glassman, Gladis, & Sadik, 1985) to approximately 50% (Beary, Lacey, & Merry, 1986; Bulik, 1987; Hudson, Pope, Wurtman, Yurgelin-Todd, Mark, & Rosenthal, 1988; Kasset, Gershon, Maxwell, Guroff, Kazuba, Smith. Brandt, & Jimerson, 1989). This is in contrast to lifetime prevalence rates for psychoactive substance abuse of less than 5% among women in the general population (Bulik, 1987; Helzer. Canino, Yeh, Bland, Lee, Hwu, & Newman, 1990). Some data suggest that women with both bulimia nervosa and a history of substance abuse are more likely to report greater impairment in other aspects of their lives (Johnson & Love, 1985). These women are more likely to abuse diuretics, report greater social impairment, report more suicidal and sociopathic behavior. and have more previous psychiatric hospitalizations than bulimic women without such histories (Hatsukami, Mitchell, Eckert, & Pyle, 1986). Perhaps for these reasons. it has been suggested that women with bulimia nervosa who also have histories of alcohol or drug abuse may not respond as well to standard forms of treatment for their eating disorder (Lacey, 1984; Lacey & Moureli, 1986) and therefore might need to be differentiated from patients without such histories for treatment purposes (Hatsukami et al.. 1986). In an effort to test formally how a history of substance abuse affects treatment outcome. Mitchell, Pyle, Eckert, and Hatsukami (1990) compared bulimic women with and without such histories on their response to an intensive outpatient group psychotherapy program for bulimia nervosa. Contrary to their expectations that the dual diagnosis group would be more difficult to treat, the two groups did not differ significantly in their response to treatment. They found that 62.5% of the women with bulimia nerPlease direct requests for reprints to K. M. Pike, Ph.D., Columbia University. College of Physicians 77 West 168th Street, Box ~98. New York. NY 10032. Surgeons. Department of Psychiatry, 7__ 387
and
38s
TRACE)’
J. STR.ASSER
et ~11
vosa and a history ofsubstance abuse compared to 67.5?h ofthe women without a comparable substance abuse history were free of bulimic symptoms at follow-up. Thus. it appears that a history ofsubstance abuse is not a poor prognostic indicator in outpatient group treatment of bulimia nervosa. To date, an investigation comparing the elhcack ofa pharmacological intervention for bulimic women with and without prior substance abuse has not been conducted. The present report describes the implications ofa history ofsubstance abuse on the outcome ofa 6-week double-blind trial ofdesipramine (DhlI) for the treatment of bulimia nervosa.
hl E T H 0
D S
Eighty women met criteria to be randomized into this study: however. 5 potential subjects did not attend the post-randomization session and therefore were not included in any ofthe data analyses. Ofthe 5 subjects who did not follow through with treatment. 2 had been randomized to placebo and 3 had been randomized to DMI. One of the placebo dropouts had a history of substance abuse, and 2 of the DMI dropouts had a history of substance abuse. No other subjects dropped out of treatment prior to Session 4. Thus, subjects in this study were 75 women with bulimia nervosa who participated in a controlled trial of DMI for the treatment of bulimia nervosa and attended a minimum of four sessions after randomization (Walsh, Hadigan, Devlin, Gladis, & Roose. 199 1). The DSM-III-R (American Psychiatric Association, 1987) diagnosis of bulimia nervosa was established using a structured clinical interview (SCID. Structured Clinical Interview for DSM-III-R: Spitzer. Williams, & Gibbon, 1987). Patients were between the ages of 18 and 45 years and weighed within 85 and 120% of their ideal body weight based on Metropolitan Life Tables (Metropolitan Life Foundation. 1983). Patients were excluded from the study if they: a) met DSM-III-R criteria for current (within the past 12 months) psychoactive substance abuse; b) reported explicit suicidal ideation and plan that warranted acute attention; c) were judged to be unwilling or unable to comply with the medication regimen: d) were currently psychotic: or e) were suffering from acute or chronic medical conditions. Patients were divided into the substance abuse or non-substance abuse group based on the presence or absence of a past history of substance abuse as determined by the SCID for all patients except one who was diagnosed based on a psychiatric interview. Of the 75 patients in the study, 19 met diagnostic criteria for past substance abuse. Procedure
Patients first entered a 2 week single-blind placebo washout phase. After this period. patients were randomized to either DMI or placebo for a 6 week double-blind trial. Patients were seen on a weekly basis by a psychiatrist who monitored the patient’s general health, eating behavior, level of mood disturbance, and side effects. Sessions lasted no more than 30 minutes and did not constitute any form of in-depth psychotherapy. This intervention was modelled after the medication only cell in the NIMH Treatment of Depression Collaborative Research Program (Elkin, Shea, Watkins, Imber. Sotsky. Collins, Glass. Pilkonis, Leber, Dochet-ty, Fiester, & Parloff. 1989). As indicated in their published manual (Fawcett, Epstein, Fiester, Elkin, & Autry, 1987). the psychiatrist’s primary goal in this intervention is to monitor drug compliance, assess target behavior, and offer emotional support.
Substance abuse and bulimta nervosa
389
.Measures To assess bulimic symptomatology,
patients kept daily records of all binge and vomit episodes which were submitted weekly. Patients also completed the Eating Attitudes Test (EAT: Garner & Garfinkel, 1979) and the Body Shape Questionnaire (BSQ; Cooper, Taylor. Cooper, & Fairburn, 1987). Associated psychopathology was assessed by the Beck Depression Inventory (Beck, Ward, Mendelson. Mock, & Erbaugh, 196 l), the Spielberger State Anxiety Scale (SSAS; Speilberger, Vagg, Barker. Donham. & Westberry. 1980) and the Symptom Checklist-90-Revised (SCL-90-R; Derogatis, Lipman, Rickels. Uhlenhuth, & Covi, 1974). Finally, social adjustment was measured by the Social Adjustment Scale (SAS; Weissman & Bothwell. 1976). RESULTS
The resuhs from this study are based on an endpoint analysis of 75 women who completed a minimum of four sessions of treatment post-randomization. Clinical characteristics ixtion (Table 1)
ofsubstance
abuse and non-substance
abusegro~~ps at rarldom-
The substance abuse and non-substance abuse groups reported a similar age of onset of their bulimia nervosa. However, the substance abuse group was significantly older at presentation for treatment (t = 3.03, p < .003) and therefore also reported a significantly longer duration ofbulimia nervosa than the group Lvithout a history ofsubstance abuse (t = 2.04. p < .05). The two groups did not differ in terms of their current degree of illness as indicated by comparable weekly binge and vomit frequencies, EAT, and
Table I. Clinical characteristics of substance abuse and non-substance abuse groups at randomization Substance-abuse group n = 19mean (s.d.)
Beck
27.84 yrs (5.57) 17.89 yrs (5.32) 8.05 yrs (4.42) 8.45/wk (4.72) 13.50/wk ( 15.40) 45.63 (16.81) 148.33 (33.72) 2.31 (.41) 56.00 (14.84) 17.32
Current dysthymia or major depression(n) History of anoresia nervosa (n)
L%‘) 6.00
.Age
Age of onset of bulimia nervosa Duration of bulimia nervosa Binge frequency Vomit frequency EAT
BSQ SAS Spielberger state anxiety scale
Non-substance abuse group n = 56 mean (sd.) 24.14 yrs (4.42) 16.98 yn (3.62) 5.95 yrs (3.69) 8.09/wk (5.23) 9.9 I/wk (9.38) 42.85 (15.36) 137.90 (31.0) 2.17 (.44) 47.86 (12.12) 10.95 (8.7) 27.00 9.00
P ,003 ns .05 ns ns ns ns ns .03 .012 chi-sq: n.s. chi-sq: ns.
TR.%CEI’ J. STRASSER
390
Table 2. Clinical
description
at termination
Substance
DMI mean (s.d.)
33.1 I (19.06) 8.30 (7.5 I) 10.78 (12.67) 116.75 (34.34) I.75 (0.33)
EAT hIJy
binge frequsncl
Wkly vomit frequent)
BSQ SAS
of substance abuse and non-substance D\lI and placebo
abuse group
Placebo mean (s.d).
et al
19.75 (13.51) 3.12 (4.18) 9.56 ( 18.49) 78.22 (33.34) I .86 (0.39)
Non-substance group Placebo mean (s.d.) 39.88 (13.43) 8.93 (7.25) I I .oo (9.20) 121.90 (37.74) 1.1 I (0.62)
abuse groups
abuse
DMI mean (sd.) 33.43 (15.56) 4.79 (3.59) 7.14 (13.21) 112.65 (34.0’)
2.00
ANCOV.4’s F-prob.
gP
rx
,001
.004
ns.
.oo I
“.S.
,017
,002
.05
.06
ns.
(0.38)
65 0
PLACEBO
ezd
DESIPRAMINE
(n=lO)
-!_
60
W
55
2
zl I 6
(n=24)
50
(n=27)
E
W 2 w
r
i
-I
(n=9)
T
45
%
40
35 No History of Substance Abuse Fig. I. Spielberger state anxiety scores at termination abuse groups receiving DMI and placebo
History Substance of substance
receiving
of Abuse abuse and non-substance
Substance abuse and bulimia
391
nrr\osa
(n=lO)
is Y
16 14
(n=25)
(n=28)
10
(n-9
T
8
I
6 : No History of Substance Abuse Figs. 2. Beck depression scores at termination groups receiving DMI and placebo
History Substance
of Abuse
of substance abuse and non-substance
abuse
BSQ scores. Also, groups did not differ significantly on the Social Adjustment Scale at pre-treatment. Chi-squared statistics indicated that groups did not differ in the frequency of current dysthymia or major depressive illness: 12 of the 19 (63%) patients with a history of substance abuse also had current dysthymia or major depressive illness compared to 27 of the 56 (48%) patients without such a history. Also, the two groups did not differ in the frequency of a history of anorexia nervosa: ofthe 19 patients with a history of substance abuse, 6 (32%) also had a history of anorexia nervosa, and of the 56 patients without a history of substance abuse, 9 ( 16%) had a history of anorexia nervosa. The ANOVA on the Spielberger State Anxiety Scale indicated that groups differed significantly at randomization. The group with a history of substance abuse reported a mean state anxiety score of 56 (s.d. = 14.84) compared to the non-substance abuse group which reported a mean of 47.86 (s.d. = 12.12; t = 2.38, p < .02). Also, the two groups differed significantly on the Beck Depression Inventory (t = 2.59, p < .012); the group with a history of substance abuse reported a mean of 17.32 (s.d. = 10.67) whereas the non-substance abuse group reported a mean of 10.95 (s.d. = 8.70). Patients with a history of substance abuse reported a significantly higher total SCL90-R score than the group without such a history (X, = 2.28 (s.d. = .83) vs. X,_, = 1.87 (s.d. = .54); t = 2.41, p -=z.02). Comparisons of the nine subscale scores on the
392
TRACE\’
J. STR.-\SSER et aI
SCL-90-R indicated that in all cases the substance abuse group means were higher than the non-substance abuse group. However. after applying a Bonferroni correction for multiple comparisons (.05/g), the tvvo groups differed significantly on just two subscales: anger ( Xy = 2.26 (s.d. = 1.03) vs. X,_, = 1.61 (s.d. = .66): t = 3.1 y < .003) and anxiety (X, = 2.33 (sd. = .97) vs. X,_, = 1.76 (sd. = .56): t = 3.07, p < .003).
To account for differences among groups at pre-treatment, we carried out ANCOVA’s using the baseline value ofthe dependent variable as the covariate. Table 2 includes means. standard deviations. and significance tests on post-treatment analyses. The ANCOVA of overall eating problems as measured by the EAT revealed significant main effects for group and treatment. The main effect for group indicated that the substance abuse group reported a significantly lower EAT score at the time of termination than the group without such a history (F( 1, 59) = 13.32, p < .OOl). The main effect for treatment indicated that the group receiving active medication reported significantly lower EAT scores at termination (F( 1, 59) = 9.00, p < .004). The two-way interaction effect approached significance (F( 1, 59) = 3.32, p < .074) suggesting that the substance abuse group was more responsive to treatment overall and responded more dramatically to DMI than the non-substance abuse group. ANCOVA’s for weekly binge and purge frequencies indicated that the substance abuse and non-substance abuse groups did not differ significantly in their binge or purge frequencies at the time of termination. However, these ANCOVA’s did reveal a main effect for treatment: Individuals on active medication reported significantly lower binge and purge frequencies than those on placebo (Fblnys(1, 70) = 15.05, p < .OOl: Fpurgs( 1. 70) = 5.97, p -c .017). The ANCOVA for termination scores on the BSQ revealed significant main effects for group and treatment. The main effect for group indicated that overall the substance abuse group had a significantly lower BSQ score at the time of termination than the non-substance abuse group (F( 1,45) = 10.59, p < .002). The main effect for treatment indicated that the group receiving active medication reported significantly lower BSQ scores at termination (F( 1, 45) = 4.15, p < .05). The ANCOVA for termination scores on the SAS revealed no main effect for treatment and a main effect for group that approached significance (F(1, 41) = 3.7. p -c .06). The substance abuse group reported lower SAS scores at termination than did the non-substance abuse group. The ANCOVA on the post-treatment total SCL-90-R revealed a main effect for treatment but not group (F( 1, 60) = 7.05, p < .Ol). ANCOVA comparisons of the posttreatment subscale scores resulted in no significant main effects for group after applying a Bonferroni correction for multiple comparisons (.05/g). However, there was a main effect for treatment on three of the subscales: obsessionality (X,, = 2.15 (sd. = .95) vs. Xdm, = 1.61 (s.d. = .63); F(l, 60) = 9.33, p < .003): depression (X,, = 2.52 (s.d. = .92) vs. x,,, = 1.93 (s.d. = .67); F( 1, 60) = 8.22, p < ,006); and psychoticism (X,, = 1.80 (s.d. = .65) VS. Xdm,= 1.41 (s.d. = .37): F(l, 60) = 9.30,~ < .003). As depicted in Figure 1, the ANCOVA on the Spielberger State Anxiety Scale revealed no significant main effects for group or treatment. However, the two-way interaction was significant (F( 1, 69) = 6.70, p < .012), which suggests that whereas the group with a history ofsubstance abuse reported greater anxiety while on placebo, those with a history of substance abuse responded to active medication with a greater reduction in their level of anxiety than the group without such a history.
Substance abuse and bulimia
nrr~ow
393
As depicted in Figure 2. the ANCOVA on the Beck Depression Inventory revealed no significant main effects for group or treatment; however. the two-way interaction approached significance (F( 1. 67) = 3.22, p < .077). DISCUSSION
The results ofthe present study offer two important findings regarding the history and treatment of bulimia nervosa. First, consistent with Mitchell, Pyle, Eckert, & Hatsukami ( 1990). we found that patients with and without a history of substance abuse reported both a similar age of onset of their bulimia nervosa and similar severity of their eating pathology. The two groups did not differ significantly in their binge or vomit frequencies. Nor did groups differ on measures of concern regarding body shape and weight. Second. with regard to treatment, contrary to the expectation that a history of substance abuse would be a poor prognostic indicator in the treatment of bulimia nervosa. we found that the substance abuse and non-substance abuse groups responded equally well to treatment with antidepressant medication, and in some respects the substance abuse group responded even more dramatically to treatment than the non-substance abuse group. It is important to note that these findings are based on a comparison ofwomen with past substance abuse problems and that women who were identified as having current problems with substance abuse or dependency were excluded from our sample. We referred individuals with active substance abuse problems to treatment for their substance abuse rather than admitting them into treatment for their concurrent eating disorder. Thus, the findings from this study indicate that past substance abuse is not a poor prognostic indicator for treatment of bulimia but cannot be generalized to individuals who are actively abusing drugs or alcohol. Patients with a history of substance abuse were older at presentation and reported a longer duration of illness than did patients without such histories. While it is not certain why the groups differ on these dimensions, these differences have been observed previously (Hatsukami et al., 1986; Mitchell et al., 1990). There is some evidence to indicate that the bulimia nervosa precedes the alcohol abuse (Beary et al., 1986) which suggests that the younger bulimic patients who do not present with a history of substance abuse are nonetheless at risk for developing a substance abuse problem as they get older. It is also possible that, in an analogous fashion to the role ofdenial often associated with substance abuse. patients with a history of substance abuse may be prone to deny the importance of their eating disturbance and therefore may delay seeking treatment. Although behavioral and psychological symptoms ofbulimia nervosa were similar in the two groups. patients with histories of substance abuse reported significantly more general anxiety and depression than did patients without such histories at the time of presentation for treatment. These data are consistent with other reports (Bulik. 1987; Hatsukami et al.. 1986) in suggesting that patients with bulimia nervosa and histories ofsubstance abuse tend to be generally more symptomatic in other areas offunctioning. It may be that the greater degree of associated psychiatric symptomatology in the substance abuse group has contributed to the impression that this group would be less responsive to treatment. However, what is most noteworthy about our findings was that just the opposite effect occurred with regard to associated symptomatology. The group with a history of substance abuse who received active medication actually reported lower levels of anxiety and depression at termination than the non-substance abuse group on active medication.
_ TRACEI.
394
J. STR.ASSER
et al.
The comparison of the response to antidepressant treatment between the two groups is of particular relevance to clinical practice. On all outcome measures. the improvement of the substance abuse group was equal to or greater than that in the group without such histories. The present investigation examined response to desipramine. and it is possible that the findings concerning treatment response would be different in other forms of treatment. However. our findings are consistent with those of Mitchell et al. ( 1990) who found that the long-term outcome of a cognitive-behavioral group psychotherapy program was similar for bulimic patients with and without histories of substance abuse. Taken together. these results suggest that a past history of substance abuse has no implication regarding the response to psychotherapeutic or pharmacologic treatments for bulimia nervosa. Although it will be important to determine whether studies of other treatment interventions for bulimia nervosa corroborate our findings. existing data suggest that a past history of substance abuse should not be a significant factor in treatment disposition for individuals presenting for treatment of bulimia nervosa. Despite the fact that patients with bulimia nervosa and past histories ofsubstance abuse do differ from bulimic patients without such histories in certain respects. the similarity between these two groups is impressive. especially in their response to treatment. REFERENCES American Psychiatric Association. ( 1987). Ding~ostic und slatisrical mcm~tul ~~/‘menral disorders (3rd ed. revised). Washington, DC: Author. Bear-y, IM. D.. Lacey, J. H., & Merry, J. (1986). Alcoholism and eating disorders in women of fertile age. British Journalof.-!ddiction. 81. 685-689. Beck. A. T., Ward, C. H.. Mendelson, M.. Mock. M., & Erbaugh. J. (1961). An inventon for measuring depression. Archives yfCenrra1 Ps.tchiutry. 4, 56 l-57 I. Bulik, C. M. (1987). Alcohol use and depression in women with bulimia. .dmericat~ Jortrnctlol’Drccgnrfd.Ik,ohol.-!bllse.
13, 343-355.
Cooper. P. J.. Taylor, M. J., Cooper. Z., & Fairburn, C. G. (1987). The development and validation of the body shape questionnaire. Inrrrnarional Journal ofE&ing Disorders, 6,485--194. Derogatis. L. R., Lipman. R. S., Rickels, K., Uhlenhuth, E. H., & Covi, L. (197-l). The Hopkins Symptom Checklist (HSCL): A self-report symptom inventory. Behavioral Science. 19. 1-I 5. Elkin, I., Shea, M. T., Watkins, J. T., Imber, S. D., Sotsky, S. M., Collins, J. F., Glass, D. R.. Pilkonis. P. A.. Leber. W. R., Docherty, J. P.. Fiester, S. J., & Parloff, M. B. (1989). National Institute of hlental Health treatment of depression collaborative research program: General effectiveness of treatment. .Archives q/ General
Psychiaw),,
46.97
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Fawcett. J.. Epstein. P., Fiester. S.. Elkin, I., & Autry. J. ( 1987). Clinical management - Imipramine/placebo administration manual. Psychopharmacology Bulletin. 23, 309-324. Garner, D. IM., & Garfinkel, P. E. (1979). The eating attitudes test: An index of the symptoms of anorexia nervosa. Ps.vchologicali2ledicine. 9,273-279. Hatsukami, D., Mitchell, J. E., Eckert, E. E., & Pyle, R. (1986). Characteristics of patients with bulimia only, bulimia with affective disorder, and bulimia with substance abuse problems, Addicriw Behaviors. 11, 399-406. Helzer, J. E., Canino, G. J., Yeh, E. K., Bland, R. C., Lee, C. K.. Hwu, H. G.. R: Newman, S. (1990). Alcoholism - North America and Asia. Archives of General Ps)*chiatry. 47, 3 13-3 19. Hudson. J. I.. Pope. H. G.. Wurtman. J.. Yureelin-Todd. D., Mark. S., & Rosenthal. N. E. ( 1988). Bulimia in obese’ind~viduals: Relationship to normal weight bulimia. The Jownnl q/lVervous and .\fenfa/ Disease, 176, 144-152. Johnson, C. L.. & Love. S. Q. (1985). Bulimia: Multivariate predictors of life impairment, Jorrr!tol ofPq*chiatric Research, 19, 343-347. Kasset, J. A.. Gershon, E. S., Maxwell, M. E., Guroff, J. J., Kazuba, D. M., Smith. A. L., Brandt. H. A., & Jimerson. D. C. (1989). Psychiatric disorders in the first-degree relatives of probands with bulimia nervosa. American Journal of &ychiarry, 146, I468- I47 I _ Lacev, J. H. f 1984). Moderation of bulima. J. Psvchosomafic Research, 28. 397-402 Lace;‘. J. H.,‘& Moureli, E. (I 986). Bulimic alcoholics: Some features ofa clinical subgroup. Bruish Journa/ o/Addiction,
81, 389-393.
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Xtetropoiitan Life Foundation. (I 983). S/otirtkul B~dlefin. 64. -7-9. Xlitchell. 1. E.. Pyle. R.. Eckert. E. D., & Hatsukami. D. (1990). The intluenceofprioralcohol problems on bulimia nervosa treatment outcome. .-lddic,/irr Behiors. 15. l69- 173.
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Schualberg. ht. D. ( 1990). .4 comparison of bulin~iclv. obese birrge rulers. social phobit,s. nnd iru~ividuzls rc.ilh panic disorder on an.\-itq. depression, chenrictrl abuse. and bordt~rlinepersonul;l~, disorder. Unpublished doctoral dissenation, State University of New York at Albany. Alban?. NY.
Spielberger. C. D.. Vagg. P. R.. Barker, L. R.. Donham, G. W., & Westbem. L. G. ( 19SO).The factorstructure ofthe state-trait anxiety inventory. In 1. G. Sarason & C. D. Spielberger (Eds.). .Srress and.4rrriety(Volume 7. pp. 95-109). New York: Hempshire/Wiley. Spitzer. R. L.. Williams, J. B.. & Gibbon, M. (1987). Sfrucfured Clinical Inleniwfir D.S.\f-III-R ~SCID). New York: New York State Psychiatric Institute, Biometrics Research. Ii’alsh. B. T.. Hadigan. C. M.. Devlin, M. J., Gladis. M.. & Roose. S. P. ( 199 I). Long-term outcome of antidepressant treatment for bulimia nervosa. .-lmericon Jownnl ojPgchio/r): 148. 1206-12 12. IValsh. B. T.. Roose. S. P., Glassman. A. H.. Gladis, M., & Sadik, C. (1985). Bulimia and depression. Psrc+wsot~icltic.Ift~dicirw, 47, l23- I3 I. 14’eissman. ht. bl.. & Bothwell. S. (1976). Assessment ofsocial adjustment by patient self-report. .4rc/liws q/ Gentwl Psjvhicmy. 33. I I I I- I I 15. Wilson, G. T. (199 I). The addiction model of eating disorders: A critical analysis. .4dvances in Behnrior Rtwrmlr
und Thertip~:
13. 27-72.
THE IMPACT
OF PRIOR OUTCOME
1991 Copyright
SUBSTANCE ABUSE OX TREATlIENT FOR BULIMIA NERVOS.4
TRACEY J. STRASSER, KATHLEEN Columbia
0306~4603/9255.00 + .OO 5 1392 Pergamon Press Ltd.
University.
M. PIKE, and B. TIXlOTHY W’ALSH
College of Physicians
and Surgeons
Abstract - The present investigation examined the signiticance ofa past history of substance abuse on treatment outcome for bulimia nervosa. Seventy&s women with bulimia ncrvosa participated in a &week double-blind outpatient trial ofdesipramine: I9 patients had a history ofsubstance abuse and 56 did not. Although patients with a history ofsubstance abuse reported higher levels ofanxiety and depression at presentation for treatment than patients without such histories. the two groups reported a similar age of onset of their bulimia ncmosa and similar severity of eating pathology with regards to binge and vomit frequencies and measures of concern about body shape and weight. On all outcome measures, the improvement ofthe substance abuse group was equal to or greater than that in the group without a histon ofsubstance abuse. Results suggest that a past history of substance abuse has no implication regarding response to pharmacological treatment for bulimia nervosa.
A number of clinical and epidemiological studies indicate that patients in treatment for bulimia nervosa report more frequent problems with current or past alcohol and drug abuse than would be expected in the general population (Wilson. 199 1). Depending on diagnostic criteria and sampling procedures, estimates of lifetime prevalence rates for substance abuse among bulimic women range from approximately 10% (Schwalberg, 1990; Walsh, Roose, Glassman, Gladis, & Sadik, 1985) to approximately 50% (Beary, Lacey, & Merry, 1986; Bulik, 1987; Hudson, Pope, Wurtman, Yurgelin-Todd, Mark, & Rosenthal, 1988; Kasset, Gershon, Maxwell, Guroff, Kazuba, Smith. Brandt, & Jimerson, 1989). This is in contrast to lifetime prevalence rates for psychoactive substance abuse of less than 5% among women in the general population (Bulik, 1987; Helzer. Canino, Yeh, Bland, Lee, Hwu, & Newman, 1990). Some data suggest that women with both bulimia nervosa and a history of substance abuse are more likely to report greater impairment in other aspects of their lives (Johnson & Love, 1985). These women are more likely to abuse diuretics, report greater social impairment, report more suicidal and sociopathic behavior. and have more previous psychiatric hospitalizations than bulimic women without such histories (Hatsukami, Mitchell, Eckert, & Pyle, 1986). Perhaps for these reasons. it has been suggested that women with bulimia nervosa who also have histories of alcohol or drug abuse may not respond as well to standard forms of treatment for their eating disorder (Lacey, 1984; Lacey & Moureli, 1986) and therefore might need to be differentiated from patients without such histories for treatment purposes (Hatsukami et al.. 1986). In an effort to test formally how a history of substance abuse affects treatment outcome. Mitchell, Pyle, Eckert, and Hatsukami (1990) compared bulimic women with and without such histories on their response to an intensive outpatient group psychotherapy program for bulimia nervosa. Contrary to their expectations that the dual diagnosis group would be more difficult to treat, the two groups did not differ significantly in their response to treatment. They found that 62.5% of the women with bulimia nerPlease direct requests for reprints to K. M. Pike, Ph.D., Columbia University. College of Physicians 77 West 168th Street, Box ~98. New York. NY 10032. Surgeons. Department of Psychiatry, 7__ 387
and
38s
TRACE)’
J. STR.ASSER
et ~11
vosa and a history ofsubstance abuse compared to 67.5?h ofthe women without a comparable substance abuse history were free of bulimic symptoms at follow-up. Thus. it appears that a history ofsubstance abuse is not a poor prognostic indicator in outpatient group treatment of bulimia nervosa. To date, an investigation comparing the elhcack ofa pharmacological intervention for bulimic women with and without prior substance abuse has not been conducted. The present report describes the implications ofa history ofsubstance abuse on the outcome ofa 6-week double-blind trial ofdesipramine (DhlI) for the treatment of bulimia nervosa.
hl E T H 0
D S
Eighty women met criteria to be randomized into this study: however. 5 potential subjects did not attend the post-randomization session and therefore were not included in any ofthe data analyses. Ofthe 5 subjects who did not follow through with treatment. 2 had been randomized to placebo and 3 had been randomized to DMI. One of the placebo dropouts had a history of substance abuse, and 2 of the DMI dropouts had a history of substance abuse. No other subjects dropped out of treatment prior to Session 4. Thus, subjects in this study were 75 women with bulimia nervosa who participated in a controlled trial of DMI for the treatment of bulimia nervosa and attended a minimum of four sessions after randomization (Walsh, Hadigan, Devlin, Gladis, & Roose. 199 1). The DSM-III-R (American Psychiatric Association, 1987) diagnosis of bulimia nervosa was established using a structured clinical interview (SCID. Structured Clinical Interview for DSM-III-R: Spitzer. Williams, & Gibbon, 1987). Patients were between the ages of 18 and 45 years and weighed within 85 and 120% of their ideal body weight based on Metropolitan Life Tables (Metropolitan Life Foundation. 1983). Patients were excluded from the study if they: a) met DSM-III-R criteria for current (within the past 12 months) psychoactive substance abuse; b) reported explicit suicidal ideation and plan that warranted acute attention; c) were judged to be unwilling or unable to comply with the medication regimen: d) were currently psychotic: or e) were suffering from acute or chronic medical conditions. Patients were divided into the substance abuse or non-substance abuse group based on the presence or absence of a past history of substance abuse as determined by the SCID for all patients except one who was diagnosed based on a psychiatric interview. Of the 75 patients in the study, 19 met diagnostic criteria for past substance abuse. Procedure
Patients first entered a 2 week single-blind placebo washout phase. After this period. patients were randomized to either DMI or placebo for a 6 week double-blind trial. Patients were seen on a weekly basis by a psychiatrist who monitored the patient’s general health, eating behavior, level of mood disturbance, and side effects. Sessions lasted no more than 30 minutes and did not constitute any form of in-depth psychotherapy. This intervention was modelled after the medication only cell in the NIMH Treatment of Depression Collaborative Research Program (Elkin, Shea, Watkins, Imber. Sotsky. Collins, Glass. Pilkonis, Leber, Dochet-ty, Fiester, & Parloff. 1989). As indicated in their published manual (Fawcett, Epstein, Fiester, Elkin, & Autry, 1987). the psychiatrist’s primary goal in this intervention is to monitor drug compliance, assess target behavior, and offer emotional support.
Substance abuse and bulimta nervosa
389
.Measures To assess bulimic symptomatology,
patients kept daily records of all binge and vomit episodes which were submitted weekly. Patients also completed the Eating Attitudes Test (EAT: Garner & Garfinkel, 1979) and the Body Shape Questionnaire (BSQ; Cooper, Taylor. Cooper, & Fairburn, 1987). Associated psychopathology was assessed by the Beck Depression Inventory (Beck, Ward, Mendelson. Mock, & Erbaugh, 196 l), the Spielberger State Anxiety Scale (SSAS; Speilberger, Vagg, Barker. Donham. & Westberry. 1980) and the Symptom Checklist-90-Revised (SCL-90-R; Derogatis, Lipman, Rickels. Uhlenhuth, & Covi, 1974). Finally, social adjustment was measured by the Social Adjustment Scale (SAS; Weissman & Bothwell. 1976). RESULTS
The resuhs from this study are based on an endpoint analysis of 75 women who completed a minimum of four sessions of treatment post-randomization. Clinical characteristics ixtion (Table 1)
ofsubstance
abuse and non-substance
abusegro~~ps at rarldom-
The substance abuse and non-substance abuse groups reported a similar age of onset of their bulimia nervosa. However, the substance abuse group was significantly older at presentation for treatment (t = 3.03, p < .003) and therefore also reported a significantly longer duration ofbulimia nervosa than the group Lvithout a history ofsubstance abuse (t = 2.04. p < .05). The two groups did not differ in terms of their current degree of illness as indicated by comparable weekly binge and vomit frequencies, EAT, and
Table I. Clinical characteristics of substance abuse and non-substance abuse groups at randomization Substance-abuse group n = 19mean (s.d.)
Beck
27.84 yrs (5.57) 17.89 yrs (5.32) 8.05 yrs (4.42) 8.45/wk (4.72) 13.50/wk ( 15.40) 45.63 (16.81) 148.33 (33.72) 2.31 (.41) 56.00 (14.84) 17.32
Current dysthymia or major depression(n) History of anoresia nervosa (n)
L%‘) 6.00
.Age
Age of onset of bulimia nervosa Duration of bulimia nervosa Binge frequency Vomit frequency EAT
BSQ SAS Spielberger state anxiety scale
Non-substance abuse group n = 56 mean (sd.) 24.14 yrs (4.42) 16.98 yn (3.62) 5.95 yrs (3.69) 8.09/wk (5.23) 9.9 I/wk (9.38) 42.85 (15.36) 137.90 (31.0) 2.17 (.44) 47.86 (12.12) 10.95 (8.7) 27.00 9.00
P ,003 ns .05 ns ns ns ns ns .03 .012 chi-sq: n.s. chi-sq: ns.
TR.%CEI’ J. STRASSER
390
Table 2. Clinical
description
at termination
Substance
DMI mean (s.d.)
33.1 I (19.06) 8.30 (7.5 I) 10.78 (12.67) 116.75 (34.34) I.75 (0.33)
EAT hIJy
binge frequsncl
Wkly vomit frequent)
BSQ SAS
of substance abuse and non-substance D\lI and placebo
abuse group
Placebo mean (s.d).
et al
19.75 (13.51) 3.12 (4.18) 9.56 ( 18.49) 78.22 (33.34) I .86 (0.39)
Non-substance group Placebo mean (s.d.) 39.88 (13.43) 8.93 (7.25) I I .oo (9.20) 121.90 (37.74) 1.1 I (0.62)
abuse groups
abuse
DMI mean (sd.) 33.43 (15.56) 4.79 (3.59) 7.14 (13.21) 112.65 (34.0’)
2.00
ANCOV.4’s F-prob.
gP
rx
,001
.004
ns.
.oo I
“.S.
,017
,002
.05
.06
ns.
(0.38)
65 0
PLACEBO
ezd
DESIPRAMINE
(n=lO)
-!_
60
W
55
2
zl I 6
(n=24)
50
(n=27)
E
W 2 w
r
i
-I
(n=9)
T
45
%
40
35 No History of Substance Abuse Fig. I. Spielberger state anxiety scores at termination abuse groups receiving DMI and placebo
History Substance of substance
receiving
of Abuse abuse and non-substance
Substance abuse and bulimia
391
nrr\osa
(n=lO)
is Y
16 14
(n=25)
(n=28)
10
(n-9
T
8
I
6 : No History of Substance Abuse Figs. 2. Beck depression scores at termination groups receiving DMI and placebo
History Substance
of Abuse
of substance abuse and non-substance
abuse
BSQ scores. Also, groups did not differ significantly on the Social Adjustment Scale at pre-treatment. Chi-squared statistics indicated that groups did not differ in the frequency of current dysthymia or major depressive illness: 12 of the 19 (63%) patients with a history of substance abuse also had current dysthymia or major depressive illness compared to 27 of the 56 (48%) patients without such a history. Also, the two groups did not differ in the frequency of a history of anorexia nervosa: ofthe 19 patients with a history of substance abuse, 6 (32%) also had a history of anorexia nervosa, and of the 56 patients without a history of substance abuse, 9 ( 16%) had a history of anorexia nervosa. The ANOVA on the Spielberger State Anxiety Scale indicated that groups differed significantly at randomization. The group with a history of substance abuse reported a mean state anxiety score of 56 (s.d. = 14.84) compared to the non-substance abuse group which reported a mean of 47.86 (s.d. = 12.12; t = 2.38, p < .02). Also, the two groups differed significantly on the Beck Depression Inventory (t = 2.59, p < .012); the group with a history of substance abuse reported a mean of 17.32 (s.d. = 10.67) whereas the non-substance abuse group reported a mean of 10.95 (s.d. = 8.70). Patients with a history of substance abuse reported a significantly higher total SCL90-R score than the group without such a history (X, = 2.28 (s.d. = .83) vs. X,_, = 1.87 (s.d. = .54); t = 2.41, p -=z.02). Comparisons of the nine subscale scores on the
392
TRACE\’
J. STR.-\SSER et aI
SCL-90-R indicated that in all cases the substance abuse group means were higher than the non-substance abuse group. However. after applying a Bonferroni correction for multiple comparisons (.05/g), the tvvo groups differed significantly on just two subscales: anger ( Xy = 2.26 (s.d. = 1.03) vs. X,_, = 1.61 (s.d. = .66): t = 3.1 y < .003) and anxiety (X, = 2.33 (sd. = .97) vs. X,_, = 1.76 (sd. = .56): t = 3.07, p < .003).
To account for differences among groups at pre-treatment, we carried out ANCOVA’s using the baseline value ofthe dependent variable as the covariate. Table 2 includes means. standard deviations. and significance tests on post-treatment analyses. The ANCOVA of overall eating problems as measured by the EAT revealed significant main effects for group and treatment. The main effect for group indicated that the substance abuse group reported a significantly lower EAT score at the time of termination than the group without such a history (F( 1, 59) = 13.32, p < .OOl). The main effect for treatment indicated that the group receiving active medication reported significantly lower EAT scores at termination (F( 1, 59) = 9.00, p < .004). The two-way interaction effect approached significance (F( 1, 59) = 3.32, p < .074) suggesting that the substance abuse group was more responsive to treatment overall and responded more dramatically to DMI than the non-substance abuse group. ANCOVA’s for weekly binge and purge frequencies indicated that the substance abuse and non-substance abuse groups did not differ significantly in their binge or purge frequencies at the time of termination. However, these ANCOVA’s did reveal a main effect for treatment: Individuals on active medication reported significantly lower binge and purge frequencies than those on placebo (Fblnys(1, 70) = 15.05, p < .OOl: Fpurgs( 1. 70) = 5.97, p -c .017). The ANCOVA for termination scores on the BSQ revealed significant main effects for group and treatment. The main effect for group indicated that overall the substance abuse group had a significantly lower BSQ score at the time of termination than the non-substance abuse group (F( 1,45) = 10.59, p < .002). The main effect for treatment indicated that the group receiving active medication reported significantly lower BSQ scores at termination (F( 1, 45) = 4.15, p < .05). The ANCOVA for termination scores on the SAS revealed no main effect for treatment and a main effect for group that approached significance (F(1, 41) = 3.7. p -c .06). The substance abuse group reported lower SAS scores at termination than did the non-substance abuse group. The ANCOVA on the post-treatment total SCL-90-R revealed a main effect for treatment but not group (F( 1, 60) = 7.05, p < .Ol). ANCOVA comparisons of the posttreatment subscale scores resulted in no significant main effects for group after applying a Bonferroni correction for multiple comparisons (.05/g). However, there was a main effect for treatment on three of the subscales: obsessionality (X,, = 2.15 (sd. = .95) vs. Xdm, = 1.61 (s.d. = .63); F(l, 60) = 9.33, p < .003): depression (X,, = 2.52 (s.d. = .92) vs. x,,, = 1.93 (s.d. = .67); F( 1, 60) = 8.22, p < ,006); and psychoticism (X,, = 1.80 (s.d. = .65) VS. Xdm,= 1.41 (s.d. = .37): F(l, 60) = 9.30,~ < .003). As depicted in Figure 1, the ANCOVA on the Spielberger State Anxiety Scale revealed no significant main effects for group or treatment. However, the two-way interaction was significant (F( 1, 69) = 6.70, p < .012), which suggests that whereas the group with a history ofsubstance abuse reported greater anxiety while on placebo, those with a history of substance abuse responded to active medication with a greater reduction in their level of anxiety than the group without such a history.
Substance abuse and bulimia
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393
As depicted in Figure 2. the ANCOVA on the Beck Depression Inventory revealed no significant main effects for group or treatment; however. the two-way interaction approached significance (F( 1. 67) = 3.22, p < .077). DISCUSSION
The results ofthe present study offer two important findings regarding the history and treatment of bulimia nervosa. First, consistent with Mitchell, Pyle, Eckert, & Hatsukami ( 1990). we found that patients with and without a history of substance abuse reported both a similar age of onset of their bulimia nervosa and similar severity of their eating pathology. The two groups did not differ significantly in their binge or vomit frequencies. Nor did groups differ on measures of concern regarding body shape and weight. Second. with regard to treatment, contrary to the expectation that a history of substance abuse would be a poor prognostic indicator in the treatment of bulimia nervosa. we found that the substance abuse and non-substance abuse groups responded equally well to treatment with antidepressant medication, and in some respects the substance abuse group responded even more dramatically to treatment than the non-substance abuse group. It is important to note that these findings are based on a comparison ofwomen with past substance abuse problems and that women who were identified as having current problems with substance abuse or dependency were excluded from our sample. We referred individuals with active substance abuse problems to treatment for their substance abuse rather than admitting them into treatment for their concurrent eating disorder. Thus, the findings from this study indicate that past substance abuse is not a poor prognostic indicator for treatment of bulimia but cannot be generalized to individuals who are actively abusing drugs or alcohol. Patients with a history of substance abuse were older at presentation and reported a longer duration of illness than did patients without such histories. While it is not certain why the groups differ on these dimensions, these differences have been observed previously (Hatsukami et al., 1986; Mitchell et al., 1990). There is some evidence to indicate that the bulimia nervosa precedes the alcohol abuse (Beary et al., 1986) which suggests that the younger bulimic patients who do not present with a history of substance abuse are nonetheless at risk for developing a substance abuse problem as they get older. It is also possible that, in an analogous fashion to the role ofdenial often associated with substance abuse. patients with a history of substance abuse may be prone to deny the importance of their eating disturbance and therefore may delay seeking treatment. Although behavioral and psychological symptoms ofbulimia nervosa were similar in the two groups. patients with histories of substance abuse reported significantly more general anxiety and depression than did patients without such histories at the time of presentation for treatment. These data are consistent with other reports (Bulik. 1987; Hatsukami et al.. 1986) in suggesting that patients with bulimia nervosa and histories ofsubstance abuse tend to be generally more symptomatic in other areas offunctioning. It may be that the greater degree of associated psychiatric symptomatology in the substance abuse group has contributed to the impression that this group would be less responsive to treatment. However, what is most noteworthy about our findings was that just the opposite effect occurred with regard to associated symptomatology. The group with a history of substance abuse who received active medication actually reported lower levels of anxiety and depression at termination than the non-substance abuse group on active medication.
_ TRACEI.
394
J. STR.ASSER
et al.
The comparison of the response to antidepressant treatment between the two groups is of particular relevance to clinical practice. On all outcome measures. the improvement of the substance abuse group was equal to or greater than that in the group without such histories. The present investigation examined response to desipramine. and it is possible that the findings concerning treatment response would be different in other forms of treatment. However. our findings are consistent with those of Mitchell et al. ( 1990) who found that the long-term outcome of a cognitive-behavioral group psychotherapy program was similar for bulimic patients with and without histories of substance abuse. Taken together. these results suggest that a past history of substance abuse has no implication regarding the response to psychotherapeutic or pharmacologic treatments for bulimia nervosa. Although it will be important to determine whether studies of other treatment interventions for bulimia nervosa corroborate our findings. existing data suggest that a past history of substance abuse should not be a significant factor in treatment disposition for individuals presenting for treatment of bulimia nervosa. Despite the fact that patients with bulimia nervosa and past histories ofsubstance abuse do differ from bulimic patients without such histories in certain respects. the similarity between these two groups is impressive. especially in their response to treatment. REFERENCES American Psychiatric Association. ( 1987). Ding~ostic und slatisrical mcm~tul ~~/‘menral disorders (3rd ed. revised). Washington, DC: Author. Bear-y, IM. D.. Lacey, J. H., & Merry, J. (1986). Alcoholism and eating disorders in women of fertile age. British Journalof.-!ddiction. 81. 685-689. Beck. A. T., Ward, C. H.. Mendelson, M.. Mock. M., & Erbaugh. J. (1961). An inventon for measuring depression. Archives yfCenrra1 Ps.tchiutry. 4, 56 l-57 I. Bulik, C. M. (1987). Alcohol use and depression in women with bulimia. .dmericat~ Jortrnctlol’Drccgnrfd.Ik,ohol.-!bllse.
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