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Changes in Patients’ Beliefs About the Causes of their Depression Following

Successful Treatment

Article  in  Cognitive Therapy and Research · July 2007

DOI: 10.1007/s10608-007-9130-5

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Cogn Ther Res (2007) 31:437–449
DOI 10.1007/s10608-007-9130-5

ORIGINAL ARTICLE

Changes in Patients’ Beliefs About the Causes of their

Depression Following Successful Treatment

Yan Leykin Æ Robert J. DeRubeis Æ Richard C. Shelton Æ

Jay D. Amsterdam

Published online: 9 March 2007

Springer Science+Business Media, LLC 2007

Abstract Research suggests that depressed patients’ beliefs about the causes of their
depression affect the course and outcomes of treatment. However, changes in such
beliefs during treatment have not been investigated. Before and after treatment,
participants in a randomized control trial comparing cognitive therapy (CT) with
antidepressant medication (ADM) in the treatment of depression were asked about
their beliefs concerning the reasons for their depression. The reason clusters of interest
were: Characterological, conceptually related to CT; and Biological, conceptually
related to ADM. Contrary to predictions, endorsement of treatment-relevant reasons
did not increase after a successful treatment. Rather, endorsement of treatment-
irrelevant reasons decreased significantly. Thus, successful treatment may preserve
people’s beliefs in causes of depression most closely related to the treatment, and
diminish beliefs in unrelated causes.

Keywords Depression
Causes of depression
Patient’s beliefs
Treatment

There are widely varying accounts of etiology of depression, each based on a particular
theoretical orientation (e.g., biological, cognitive, psychodynamic), and most are
connected to a related therapy system (antidepressant medication, cognitive therapy,
psychodynamic therapy, respectively). The lay consumer of various therapies of

Y. Leykin (&)
R. J. DeRubeis

Department of Psychology, University of Pennsylvania, 3720 Walnut St.,
Philadelphia, PA 19104-6196, USA
e-mail: leykin@psych.upenn.edu

R. C. Shelton
Department of Psychiatry, Vanderbilt University, Nashville, TN, USA

J. D. Amsterdam
University of Pennsylvania Medical School, Philadelphia, PA, USA
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438 Cogn Ther Res (2007) 31:437–449

depression is likely to have his or her own preconceptions of the nature and the cause of
his or her depressed state, and these would presumably be more consistent with some
theoretical orientations than they would be with others.
Addis, Truax, and Jacobson (1995) developed a measure (Reasons for Depression;
RFD) to capture the types of beliefs people have about the cause of their depression.
They named the eight subscales they identified with factor analysis: Characterological,
Achievement, Interpersonal Conflict, Intimacy, Existential, Childhood, Physical, and
Relationship. Later work using the instrument incorporated a Biological factor, based
on consultation with the authors of the original scale (Fitzgerald & Richardson, 2002).
Addis and colleagues reasoned that a patient’s belief system about the etiology of his or
her depression would influence him or her to seek a treatment more consistent with that
system. They have shown that the outcome of treatment may be different depending on
the set of beliefs the person holds about the causes of depression. For instance, people
endorsing existential reasons for their depression (e.g., ‘‘I can’t decide what to do with
my life’’) fared better in cognitive therapy than in behavioral activation therapy. Those
who strongly endorsed Relationship reasons for their depression had poorer outcomes
in cognitive therapy (Addis & Jacobson, 1996) than did those who did not do so. They
also showed that the endorsement of Existential and Relationship reasons predicted
homework compliance in therapy (Addis & Jacobson, 1996). The endorsement of
Characterological, Achievement, Intimacy, Existential, Childhood, and Relationship
reasons was differentially associated with reactions to the treatment rationales of
activation-oriented and insight-oriented therapies (Addis & Carpenter, 1999). In short,
it appears that reasons individuals give for their depression may play a substantial role
in their perception of, participation in, and response to treatments. This work may lead
to the optimization of individual treatment, based on assessable pre-treatment
characteristics (Beutler et al., 1991; Calvert, Beutler, & Crago, 1988; Karno, Beutler,
& Harwood, 2002).
The two treatments in the present study were cognitive therapy and pharmacotherapy.
According to the cognitive theory of depression, depressed individuals tend to have a
generally negative pattern of cognitions and beliefs about themselves and about the state
of the world. These negative beliefs and the maladaptive schemas associated with them
are the cause of the disorder (Beck, Rush, Shaw, & Emery, 1979). A successful cognitive
therapy is assumed to work by teaching the individual to challenge these maladaptive and
erroneous cognitions, thus helping the person to build an alternate set of accurate,
adaptive cognitions and beliefs. This change is said to reverse the pattern of
depressogenic thoughts, leading to the amelioration of symptoms. There have been a
number of studies indicating that individuals exhibit change of attitudes, cognitions, or
beliefs about themselves and the world after undergoing cognitive therapy depression
(e.g., Barber & DeRubeis, 2001; Beevers, Keitner, & Ryan, 2003). However, the
direction of the causal relationship between cognitions and depression has not been fully
established (e.g., Burns & Spangler, 2000, 2001a, 2001b; Kazantzis, Ronan, & Deane,
2000)
Biological theories of depression hold that depression is the result of abnormalities in
brain neurochemistry (Mann, 1999; Rossi, Barraco, & Donda, 2004; Thase, 2003).
Pharmacotherapy for depression using serotonin selective reuptake inhibitors such as
paroxetine increases serotonin transmission in the synapse (Borup, Meidahl, Petersen,
Vangtorp, & Le Fevre, 1982). This, in turn, is thought to help normalize the
neurochemical abnormalities. There is nothing in the biological theory or the treatment
based on that theory that deals directly with thoughts or beliefs.
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Cogn Ther Res (2007) 31:437–449 439

Whereas there are studies, cited above, that have examined the effect of reasons
for depression on the process and outcome of particular therapies, no work has been
done to address the reverse: the effect of different therapies on patients’ beliefs about
the nature and cause of their depression. During the first sessions of cognitive
therapy, the patient learns about the cognitive model of depression, and the majority
of subsequent therapeutic work is performed within this framework. The therapists
thus ‘‘indoctrinate’’ patients into adopting a particular theory of depression, one that
primarily concerns itself with thoughts or beliefs. Patients, especially those who
benefit from that therapy, may be expected to change their personal theories in favor
of the treatment-related one. While prior to treatment their beliefs about causes for
depression may have been ambiguous, the experience of therapy provides a
framework for structuring the belief system about causes for depression. Similarly,
engaging in pharmacotherapy with a clinician who explains that depression is a
biochemical imbalance that needs to be corrected via medication may shift a patient’s
beliefs about the etiology of depression towards the biological end of the spectrum. A
possible implication of this change in the beliefs about causes of depression is the
potential development of a preference for one treatment over others, as will be
discussed.
Conceptually, because cognitive therapy is theorized to work by affecting the
individual’s cognitions and beliefs about the self and the world, it seems to be most
closely related to the Characterological subscale, which includes items such as ‘‘I see
things in a depressive way.’’ Pharmacotherapy is a biologically oriented intervention,
therefore it is conceptually related to the Biological scale (e.g., ‘‘I have a
biochemical imbalance’’). Given those associations, we hypothesized that greater
endorsement of Characterological beliefs will be related to a positive outcome in
cognitive therapy, and greater endorsement of Biological beliefs to positive
outcomes in pharmacotherapy. Further, we hypothesized that successful cognitive
therapy would increase the belief that Characterological-type reasons were respon-
sible for the person’s depression; an increase in the Characterological subscale of
Reasons for Depression questionnaire will therefore be observed. Likewise, a
successful treatment with antidepressant medication would promote a belief that
biology is responsible for depression onset, and the Biological subscale will have
increased.

Method

Participants

The participants were 240 outpatients enrolled in a randomized controlled trial funded
by the National Institute for Mental Health that took place at two sites: the University
of Pennsylvania and Vanderbilt University. On average, participants were middle-aged
(average age = 40.4, SD = 11.7), Caucasian (81.7%), with some college education
(average years of education = 14.6, SD = 2.4). Women slightly outnumbered men in this
sample (58.8% women), which is not inconsistent with the difference in prevalence of
depression between men and women.

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440 Cogn Ther Res (2007) 31:437–449

Measures

The Structured Clinical Interview for DSM-IV (SCID, First, Spitzer, Miriam, &
Williams, 2001) is a standard clinician-administered comprehensive diagnostic interview
for various Axis I disorders based on the Diagnostic and Statistical Manual of Mental
Disorders, 4th edition (APA, 1994). A k coefficient of .80 was obtained for the
assessment of the reliability of diagnoses of Major Depressive Episode.
The Hamilton Rating Scale for Depression (HRSD, Hamilton, 1960) is a widely used
clinician-administered interview which assesses depression severity. For this study,
consistent with DeRubeis et al. (2005), the 17-item version was used, which was
modified to include atypical symptoms (Reimherr et al., 1998). The HRSD as well as the
SCID were administered by trained M.A.- or Ph.D.-level evaluators. For the HDRS
score, an intraclass correlation coefficient of .96 was obtained.
The Reasons for Depression questionnaire (RFD; Addis et al., 1995) is a self-report
measure designed to assess depressed individuals’ beliefs about causes of their
depression. The measure consists of a prompt (‘‘I am depressed because...’’) and a list
of potential reasons to be endorsed on a on a 4-point Likert Scale (0 = ‘‘Definitely not a
reason’’, 1 = ‘‘Probably not a reason’’, 2 = ‘‘Probably a reason’’, 3 = ‘‘Definitely a
reason’’). In order to reduce the patients’ questionnaire burden, the version used in the
present study was shortened, including only 13 items from the original 48-item measure.
The items chosen were deemed to correspond to the beliefs especially prevalent and
strong among depressed individuals. One item not in the original scale (‘‘I was born to
be depressed’’) was added to the measure. This item represents a belief often voiced by
depressed patients and not reflected in any similar items within the original scale. The
measure included five of the original eight subscales, with two or three items per
subscale. The subscales were: Characterological (the belief that depression is due to the
tendency to think depressing thoughts or to see the world in a depressive way),
Biological (the belief that depression is caused by genes or a biochemical imbalance),
Intimacy (the belief that depression is due to a lack of a sympathetic partner or
confidant), Childhood (the belief that depression is caused by negative events in
childhood), and Relationship (the belief that depression is due to problems in a
romantic relationship). Subscale scores were calculated by averaging the scores of the
items that comprise each subscale.
We also modified the RFD for use after the completion of treatment. Because this
‘‘Post-treatment Reasons for Depression’’ questionnaire (post-RFD) was administered
when symptoms of depression may have remitted, each item was modified to reflect past
depression. Present tense was retained in parentheses in case a person had not
responded to treatment, and his or her depression still persisted (e.g., ‘‘I was (am)
depressed because...’’, ‘‘I had (have) a biochemical imbalance’’).

Procedure

Participants were enrolled in the study if they met criteria for Major Depressive
Disorder as assessed by the Structured Clinical Interview for DSM-IV (First et al.,
2001), as well as a score of 20 or more on the Hamilton Rating Scale for Depression
(Hamilton, 1960) sustained over a 2-week period. Average pre-treatment HRSD scores
(with standard deviation in parentheses) were: 23.2 (2.9) for ADM, 23.5 (2.9) for CT,
and 23.4 (2.9) for the placebo group. The scores did not differ significantly between the
groups. Additionally, to be enrolled, participants had to be aged 18–70, English
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Cogn Ther Res (2007) 31:437–449 441

speaking, and able to consent to participation. Patients were excluded if they had a
history of Bipolar Disorder, psychosis, another Axis I disorder deemed to be primary,
certain Axis II disorders (Antisocial PD, Borderline PD, Schizotypal PD), substantial
substance abuse, imminent risk of suicide, medical conditions precluding pharmaco-
therapy, or lack of response to paroxetine during the previous year.
The patients were randomly assigned to pharmacotherapy with paroxetine,
augmented with lithium or desipramine for patients failing to respond to paroxetine
alone after 8 weeks (ADM, n = 120), cognitive therapy (CT, n = 60), or pill placebo
(n = 60). The active treatments (ADM and CT) were administered for 16 weeks, at
which point response to treatment was assessed. CT was administered according to the
standard texts of cognitive therapy for depression (Beck, 1995; Beck et al., 1979).
Antidepressant management was provided according to the guidelines used in
Treatment of Depression Collaborative Research Program (Fawcett, Epstein, Fiester,
Elkin, & Autry, 1987). Any techniques associated with cognitive therapy were forbidden
in the ADM management, and all psychoeducation was intervention-specific. For
ethical reasons, the pill-placebo condition was administered for 8 weeks only, at which
point patients who still required treatment were offered paroxetine. Response criteria
for the 16-week assessment were based on an HRSD score of 12 or less over at least a
3-week period, however, safeguards were designed to prevent a transient exacerbation
of depressive symptoms from keeping a patient from meeting criteria for response. The
criteria were: (a) completion of the 16-week treatment phase; and (b) either: 16-week
HRSD £ 12 and either a 14-week HRSD £ 14 or a 10-week and 12-week HRSD £ 12;
or a 12-week, a 14-week, and an 18-week HRSD £ 12. Participants completed the RFD
prior to their assignment to treatment. After completing the active treatment,
participants completed the post-RFD.
A more detailed description of the study methods and procedures is provided in
DeRubeis et al. (2005).

Data analysis

Three sets of data analysis were performed. First, the pre-treatment RFD data from all
participants (N = 240, which includes those in the pill-placebo condition) were factor
analyzed to confirm the previously published assignment of items to subscales
(Fitzgerald & Richardson, 2002), as well as to establish the subscale assignment for
the item we added.
For all other analyses, patients in the pill-placebo condition were excluded. As the
pill-placebo condition lasted only 8 weeks, as opposed to 16 weeks of active treatments,
it is not possible to compare prediction of response of placebo and active treatment.
Moreover, the post-RFD was not obtained at the termination of placebo treatment;
therefore analyses of changes of reasons for depression are not possible for the placebo
group.
Second, we tested whether reasons for depression predicted response to the two
treatments. This was accomplished in two ways. First, for each subscale, we entered that
subscale score, treatment condition, and the subscale*treatment interaction in an
analysis of covariance (ANCOVA) model predicting the HRSD score at termination of
treatment (week 16), controlling for the intake HRSD score, site, and site*treatment
interaction. Because DeRubeis et al. (2005), found a significant site*treatment
interaction, it was covaried in all ANCOVA models. Second, in order to examine the
effects of differential prediction of the unique variance of each RFD subscale
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442 Cogn Ther Res (2007) 31:437–449

(accounting for the variance it has in common with the other RFD subscales) we also
used an ANCOVA predicting HRSD score at termination of treatment, again
controlling for the intake HRSD score, site and site*treatment interaction. For this
model, we entered all of the subscale scores, and all of the subscale*treatment
interaction terms in the omnibus ANCOVA model.
Third, we tested whether successful treatment is associated with change in the two
RFD subscales of interest—Characterological and biological. We tested Character-
ological and Biological subscales for each treatment separately for significance of the
change using one-sample t-tests. We also compared the two treatments (ADM and CT)
for differences in both the Characterological subscale and the Biological subscale
separately using ANCOVAs. For these models, the subscale score was the dependent
variable, controlling for site and site*treatment interaction, and covarying the intake
HRSD score to control for initial severity. For this set of analyses only data from those
who responded to active treatments (N = 99, with n = 34 in CT and n = 65 in ADM)
and for whom both pre- and post-treatment RFD data were available were used as we
were primarily interested in reason change after a successful treatment.

Results

Factor analysis

For these analyses data from all participants who completed the RFD questionnaire
(231 of the 240 who participated in the trial) were included. Only Time 1 RFD data
were analyzed in order to preserve consistency with prior findings (Addis et al., 1995;
Fitzgerald & Richardson, 2002). Maximum Likelihood factor analysis with Promax
rotation and a specified 5 factor structure produced an interpretable result, as shown in
Table 1. Five factors were specified on theoretical grounds, as items were chosen from

Table 1 Factor assignments of the questions from the RFD questionnaire (current and original [from
Addis et al. 1995]), and item factor scores

Question Factor assignments Factor scores

Current Original Char Bio Int Child Rel

1. I see the world the way it really is Char Char .35 –.13 –.06 .03 .00
2. No one really cares about me Int Int .24 –.12 .38 .08 .05
3. It is the way I learned to be Char Char .45 .12 –.02 .21 –.01
4. I have a biochemical imbalance Bio Bio .02 .66 –.12 –.10 .00
5. I have some unresolved issues with family Del Child .30 –.06 .05 .19 .13
6. I think about things in a depressing way Char Char .67 .11 .06 –.21 –.08
7. My spouse/partner treats poorly Rel Rel .03 –.04 –.04 –.03 .90
8. I was born to be this way Bio N/A .19 .45 –.02 .06 .05
9. Certain things happened to me as a child Child Child .08 –.03 –.03 .90 –.02
10. There is no one to share my innermost Int Int –.06 .01 1.03 –.03 –.02
thoughts and feelings with
11. I had a difficult childhood Child Child –.12 .05 .02 .86 –.03
12. I inherited it from my parents Bio Char –.17 .73 .09 .12 .00
13. I am stuck in a bad marriage or relationship Rel Rel –.04 .00 .00 .02 .88
14. My spouse/partner doesn’t understand me Rel Rel –.03 .07 .05 –.04 .87

Note: Char, Characterological; Bio, Biological; Int, Intimacy; Child, Childhood; Rel, Relationship

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Cogn Ther Res (2007) 31:437–449 443

Table 2 Correlations between factor scores of RFD questionnaire

Characterological Biological Intimacy Childhood Relationship

Characterological 1.00 .31* .26* .32* .12

Biological 1.00 .05 .37* .07
Intimacy 1.00 .27* .32*
Childhood 1.00 .04
Relationship 1.00

* p < .01

five subscales, and the new item was expected to load on one of the five. Consistent with
previously published literature (e.g., Lievens & Anseel, 2004; Shaik, Lowe, & Pinegar,
2006; Swisher, Beckstead, & Bebeau, 2004) the cut-off for assignment of an item to a
subscale was a factor loading of .35 or greater, with no less than a .10 difference between
the largest loading and second-largest loading. While .35 may be considered somewhat
low, we felt that it was justified given that scales would have only 2 or 3 items per factor.
Factor analysis resulted in the assignment of items comparable to the original factor
assignments (Table 1) reported by Addis et al. (1995). One exception was the item ‘‘I
inherited it from my parents,’’ which was in the Childhood subscale in the original scale
but loaded on the Biological subscale in this factor structure. Conceptually, this item
seemed a better fit for the Biological subscale, as it reflects belief in the importance of
genetic predisposition, not childhood events. The new item (‘‘I was born to be
depressed’’) also loaded onto the Biological subscale. One item from the original
questionnaire (‘‘I have unresolved issues with family’’) was dropped, as its factor scores
did not meet the criteria stated above for any of the factors. Promax rotation used in the
analysis allows oblique factors; the correlations between subscales produced by the
factors ranged from r = .04 to r = .37 (Table 2).
The Cronbach’s alphas for each subscale scale were as follows: Characterological
subscale (3 items) = .46, Biological (3 items) = .65, Intimacy (2 items) = .63, Childhood
(2 items) = .86, Relationship (3 items) = .91.

Predicting outcome from reasons

Only those patients in the active treatments were included in the following analyses
(N = 172, with n = 116 in ADM condition, and n = 56 in CT condition; 8 participants
were excluded due to failure to provide RFD data). There were no differences between
the two treatment arms in the pre-treatment RFD scores, depression levels, or
demographic characteristics. The subscale scores could range from 0 to 3. The means
(with standard deviations in parentheses) of pre-treatment RFD scores were: Charac-
terological = 1.55 (.65), Biological = 1.31 (.68), Intimacy = 1.27 (.76), Childhood = 1.41
(.93), Relationship = .78 (.92). Post-treatment HRSD scores for the participants in the
two active treatments, adjusted for intake HRSD, site, and site*treatment interaction,
with last observation carried forward for dropouts, were: M = 10.9 (SD = 7.6) for ADM,
and M = 10.8 (SD = 7.6) for CT. The difference between these means was not
significant.
In order to examine whether any of the RFD subscales predicted improvement either
across treatments, or differentially depending on the treatment, we conducted five
ANCOVA models (one per subscale), predicting the HRSD termination score from the
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Table 3 Prediction of treatment response based on the HRSD

n Individual subscales Omnibus model

F-value p F-value p

Characterological 172 .09 .77 .12 .73

Characterological*treatment .09 .77 1.25 .27
Biological 172 1.84 .18 .67 .41
Biological*treatment .39 .53 2.97 .09
Intimacy 172 11.80 .001 13.35 .001
Intimacy*treatment .61 .44 1.82 .18
Childhood 172 1.25 .27 2.77 .10
Childhood*treatment .46 .50 3.53 .07
Relationship 169 .88 .35 .19 .67
Relationship*treatment 1.08 .30 .04 .85

subscale score, treatment, and subscale*treatment interaction, controlling for effects of

site, site*treatment interaction, and pre-treatment depression level (HRSD score at
intake). Whenever the subscale*treatment interaction was not significant, it was
removed from the model to examine the main effect of the subscale. The results of these
analyses can be seen in Table 3. The only significant result in this set of analyses was the
main effect of the Intimacy subscale (belief that the patient is depressed because no one
cares about him/her), such that higher Intimacy scores predicted a more negative
outcome, irrespective of treatment (F(1, 166) = 11.80, p < .001, p-eta2 = .07).
Additionally, to test whether the unique variance of any RFD subscale was able to
differentially predict the outcome depending on the treatment, we entered all five
subscales, as well as the five subscale*treatment interactions into an omnibus ANCOVA
model with final HRSD score as a dependent variable, controlling for the effects of site,
site*treatment interaction, and intake HRSD score. This allowed us to consider the
contribution of each subscale*treatment interaction uncontaminated by the variance it
shares with the other subscale and subscale*treatment interactions. (As can be seen
from Table 2, the subscales were moderately intercorrelated.) We then removed the
subscale*treatment interactions from the model to examine the main effects of
subscales. The results can also be seen in Table 3. As in the previous model, we found a
significant main effect for Intimacy subscale, such that higher scores predicted worse
outcome irrespective of treatment (F(1, 159) = 13.35, p < .001, p-eta2 = .08). However,
we also found a trend-level Childhood subscale-by-treatment interaction (F(1,
154) = 3.53, p < .07, p-eta2 = .02), such that higher scores on that subscale predicted
better outcome in ADM, and were not associated with outcome in CT. Additionally, we
found a trend-level Biological subscale-by-treatment interaction (F(1, 154) = 2.97,
p < .09, p-eta2 = .02), indicating that stronger pre-treatment belief that biology is
behind the depression is somewhat related to the decrease in improvement with the CT,
but not with ADM. The findings with the Intimacy and Childhood subscales were not
predicted, and will not be discussed further.

Reasons change

We were primarily interested in changes in Characterological and Biological subscales

of the RFD, as they are theoretically related to cognitive and pharmacological
treatments, respectively. Table 4 displays RFD and post-RFD subscale means and
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Cogn Ther Res (2007) 31:437–449 445

Table 4 Reason change from pre- to post-treatment, means and standard deviations

Responders and non-responders

Pre-treatment Post-treatment

ADM CT ADM CT
Mean (SD) Mean (SD) Mean (SD) Mean (SD)

Characterological 1.58 (.65) 1.49 (.66) 1.32 (.72) 1.64 (.58)

Biological 1.33 (.67) 1.26 (.71) 1.42 (.66) 1.19 (.68)
Reason change
Non-responders Responders
ADM ADM ADM ADM
Mean (SD) Mean (SD) Mean (SD) Mean (SD)
Characterological –.01 (.74) .15 (.55) –.36 (.73)** .14 (.56)
Biological .03 (.53) .17 (.59) .06 (.54) –.27 (.59)*

Note: * = p < .05; ** = p < .001

standard deviations. The reason change from Time 1 (T1) to Time 2 (T2) was computed
as the post-RFD subscale mean minus the RFD subscale mean. Thus, a positive number
indicates an increase in the subscale, and negative number indicates a reduction.
Participants’ change scores could range from –3 (a change from fully endorsing a belief
cluster to not endorsing it at all) to 3 (a change from not endorsing a belief cluster at all
to endorsing it fully). The means of reason change (ranging from –.25 to .14) and
standard deviations of the changes in the two subscales can be found in Table 4.
Contrary to our hypothesis, one sample t-tests revealed that among responders, the
scores for scales that were concordant with treatments did not increase significantly
after treatment, but rather remained almost the same (Table 4; Characterological
subscale in the CT group, t(33) = 1.42, p < .17, d = .22, Biological in the ADM group,
t(65) = .91, p < .37, d = .07). However, the subscale discordant with the patient’s
treatment decreased significantly and substantially (see Fig. 1). Biological subscale
scores decreased after CT treatment (t(33) = –2.61, p < .05, d = –.36); Characterological
subscale scores decreased after ADM (t(65) = –4.01, p < .001, d = –.54). Among non-
responders, neither of the two subscales in either treatment changed significantly (for
those receiving CT, Characterological reason change: t(16) = 1.17, p < .26, d = .20,
Biological reason change: t(16) = 1.23, p < .24, d = .26; for those receiving ADM,
Characterological reason change: t(29) = –.08, p < .94, d = –.02, Biological reason
change: t(29) = .35, p > .73, d = .05).
We also used ANCOVAs to compare the two treatments on Characterological
reason change and on Biological reason change separately, covarying the effects of site
and the site-by-treatment interaction, as well as pre-treatment HRSD. Among
responders, with the Characterological reasons change as the dependent variable, we
found a significant difference between the treatments (F(1, 95) = 12.61, p < .001,
d = .75). Similarly, with Biological reasons change as the dependent variable, the
difference between the two treatments was significant (F(1, 95) = 9.31, p < .003,
d = .64). However, for non-responders the difference between the two treatments was
not significant with either Characterological reason change (F(1, 42) = .75, p < .39,
d = .27) or with Biological reason change (F(1, 42) = .67, p < .42, d = .26). From these
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Characterological
Biological
0.3

0.2

0.1 0.14
0.06
Reason change 0

-0.1 CT ADM

-0.2
-0.27
-0.3
-0.36

-0.4

-0.5
Treatment received
Fig. 1 Mean Change (and SE) in Characterological and Biological subscales of the Reasons for
Depression inventory after undergoing cognitive therapy and pharmacotherapy (responders only)

analyses it appears that treatments have a differential effect on both Characterological

and Biological reason change, but only among responders.

Discussion

The purpose of this study was two-fold. First, we wanted to understand whether
endorsing beliefs consistent with the treatment rationale prior to commencing the
treatment translates into better treatment outcome. In answering this question, our
hypothesis was not supported, such that neither characterological nor biological reasons
for depression predicted outcome. Only the Intimacy scale yielded a significant
prediction. The meaning of this association should be explored if future investigations
replicate this predictive relationship. Second, we wished to characterize the ways in
which two different effective treatments for depression change patients’ beliefs about
the causes of their depressions. We expected that these beliefs would change depending
on the nature of the treatment, such that the belief in characterological causes of
depression would increase for those patients who improved in cognitive therapy, and the
belief in biological causes would increase for those who improved on pharmacotherapy.
The major finding of this study is that, contrary to our hypothesis, there was no
evidence that belief in treatment-relevant causes increased after successful treatment.
Although the scores changed in the predicted direction, the increases were very small,
and not significantly greater than zero. However, beliefs in the treatment-irrelevant
causes (Biological for CT, Characterological for ADM) showed significant decreases.
This suggests that treatments, instead of augmenting concordant beliefs about causes of
depression, result in ‘‘weeding out’’ of reasons that are not related to the theory behind
the treatment that led to symptom improvement, perhaps because patients see
characterological and biological reasons for depression as competing.
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One reason for this shift may be the actual success of the treatment. For instance, a
person in a pharmacotherapy condition may think that because he or she was helped by
medicine that corrected the biological condition, then all other reasons s/he attributed to
the cause of his or her depression were relatively inconsequential. Likewise, a person in
the CT condition may conclude that because talking about thoughts helped with the
depression, his or her thoughts must have been the cause of depression, and that the
importance of other reasons or causes will be diminished. This explanation is supported
by our data. We found that after undergoing pharmacotherapy or cognitive therapy, the
beliefs about causes for depression changed, but only if the treatment was successful.
An alternative explanation of the ‘‘weeding out’’ finding is that a person’s depression
level itself may influence the perception of his or her environment. The Reasons for
Depression questionnaire and the post-treatment Reasons for Depression questionnaire
were taken in different states vis-à-vis depressive symptoms—the first time while
depressed, the second time while remitted. It may be that when completing the
pre-treatment questionnaire in a depressed state, a person would tend to rate all causes
for his or her depression as very salient. The same person, completing a different (post-
treatment) form from the non-depressed perspective, would tend to give lower ratings
across the various reasons for depression. However, in this scenario, one would expect
all ratings to decrease uniformly, and our data show a different pattern: some ratings
remained high, while others decreased.
Several limitations of this investigation should be noted. First, the sample under
investigation consisted of individuals with moderate-to-high levels of depression. The
results thus may not fully generalize to the overall population of depressed individuals.
However, because the majority of participants in this study had chronic and recurrent
depression, as reported in DeRubeis et al. (2005), it is likely that they may have already
been treated for their depression, and thus were already ‘‘indoctrinated’’ in the beliefs
about depression etiology. In that sense, the results obtained in this study may in fact be
weaker than what could be expected from treatment-naı̈ve participants. Second, the
alpha for the Characterological subscale was fairly low. However, a low Cronbach’s
alpha would raise the likelihood of type II error, thus making it less likely to obtain
significant results. That we were able to detect significant results despite low alpha may
speak to the strength of the effect found in our study. Finally, post-treatment RFD
scores were not available for those participants who dropped out. The change in the
belief of participants, many of whom could be presumed to be sufficiently dissatisfied
with treatments to drop out, was not examined. Future studies should address belief
change in those with milder depression, as well as those who were dissatisfied with their
treatment. Similarly, future studies should address the longevity of the belief change, as
well as the precise nature of its mechanism.
Our findings have two implications. First, it appears that effective treatments for
depression lead not only to symptom change, but also to changes in patients’ beliefs
about the reasons they were depressed in the first place. What seemed to be the cause of
the person’s depression at the beginning of treatment may lose its causative importance,
depending on the treatment that led to the improvement. One can speculate that if
responding to a treatment changes a person’s beliefs about the etiology of depression, a
popular treatment, even if it is not more effective than other treatments, might
potentially have an effect on beliefs in patients, perhaps their families and, ultimately,
on how society views the nature and causes of depression.
Second, if patients change their views as a consequence of responding to an
antidepressant treatment, such changes could be expected to affect how they
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interpret future episodes of depression, and thus which treatment(s) they seek. A
CT-treated patient who dismisses his or her beliefs in biological causes (and
consequently, in the benefits of antidepressant medications) will be less likely to turn
to medication in the future, thus limiting his/her options for effective treatment.
Likewise, medication-treated patients may come to believe that their thoughts and
actions do not have a bearing on their depression. Such patients may thus have a
reduced sense of personal control. Not only might this make them less likely to seek
character-changing or belief-changing treatments in the future, but it may also affect
the likelihood of their using these techniques on their own. For example, if treating
one’s negative thoughts with skepticism was once a viable coping strategy, an
ADM-treated patient may ignore it, and choose to pursue a course of pharmaco-
therapy instead. Knowing that in treating a patient he or she may alter the nature of
patient’s beliefs about depression, a conscientious clinician should provide the patient
with complete and up-to-date psychoeducational advice, informing the patient of the
multi-faceted nature of depression and the various efficacious treatment options at
the patient’s disposal.

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