ngz.;.32 '7 ’2
Michigan Sit-tilt .
Umvcrsity F g

  
  

OVERDUE FINES:
25¢ per day per item

RETURNING LIBRARY MATERIALS:

P1ace in book return to remove
charge from circulation records

    
     
 

fl.l\fi:|\‘ A
.\ A 4.; .
“gag V
W

V 1‘

six" ’9’; Dana

:71 :1. b
5 1"

Alumna

 

 

 

 

EXPERIMENTAL TESTS OF THE CAUSAL DIRECTION BETWEEN
DEPRESSED AND ELATED MOODS AND ATTRIBUTIONAL STYLE

By

Howard Mark Erman

A DISSERTATION

Submitted to
Michigan State University
in partial fulfillment of the requirements
for the degree of

DOCTOR OF PHILOSOPHY

Department of Psychology

1980

ABSTRACT

EXPERIMENTAL TESTS OF THE CAUSAL DIRECTION BETWEEN
DEPRESSED AND ELATED MOODS AND ATTRIBUTIONAL STYLE

BY

Howard Mark Erman

Reviewing the psychological theories of depression revealed a
fundamental disagreement on the nature of the relationship between
depressed thoughts and depression. A set of cognitive theories says
depressions arise because of the interaction between depressogenic
thought styles and painful events. The depressogenic thought patterns
presumably precede the depression and are a central cause of the
subsequent depressions. 0n the other hand, a second set of theories
says these depressive thought styles arise out of the depression but do
not precede it and are thus not a cause of depression.

To test these alternate thought-first and affect-first models of
depression, two experiments were conducted. The subjects in the first
experiment were 62 Michigan State University undergraduate women; in the
second experiment, the subjects were 24 male and 23 female M.S.U.
undergraduates.

The two experiments followed a similar design: subjects
completed a set of questionnaires on their thought style, their level of
depression and their mood; they were then randomly assigned to either a
control condition or to an experimental condition designed to induce a

mood change; afterwards, the initial questionnaires were again

completed. The two experiments differed in the experimental induction
used to alter mood states and in the timing: in experiment one subjects
returned for a second session, while experiment two was entirely
completed at one sitting.

Experiment one used the Velten Mood Induction Procedure (or
VMIP) to create neutral, depressed and elated moods. This procedure
consists of having students sit alone in a room and read aloud a set: of
60 mood related statements. In experiment two, mood was altered by
watching the movie "Peege"; the control group saw a neutral science
movie.

The following instruments were used in both experiments to
measure depressed mood: the Beck Depression Inventory or BDI; the
Multiple Affect Adjective Check List or MAACL; and a Personal Feelings
Scale or PFS. The measure of depressive thought style was the
Attribution Style Questionnaire or ASQ.

The results supported two conclusions. First both inductions
successfully created depressed moods, although the procedures also
induced additional emotions, most noticeably increased anxiety. Second,
there was some support for the thought-first hypotheses of depression.
There were significant predicted differences on one of three depressixnn
comparisons in experiment one and on two of six comparisons in
experiment two. This support is stronger than it seems because sex
interactions in experiment two necessitated separate analyses by sex,
making the cells used for the comparison quite small in size. In
addition, no comarisons were ever significant in a direction opposite

to the predictions.

The affect-first hypotheses were not supported. Furthermore, no
relation was found between induced elation in experiment one and either
the affect-first model or the thoughtrfirst model.

The discussion suggested future avenues of research which might
use naturalistic studies rather than experimental studies. The failxxre
to find any support for the affect-first model was explained as being
partly due to the experiment’s failure to fully test the affect-first
model, most notably because informed consent procedures made it
impossible to alter mood without subjects being aware of the mood
change. Finally, the discussion raised the possibility that the two

models are actually alternate phases of a single feed-back loop process.

This dissertation is dedicated to the loving memory of my father
Max Ermann
who died this year before he could see me graduate.

ii

ACKNOWLEDGEMENTS

I would like to thank Professor Rabin, my dissertation committee
chairman, for his advice and support. His careful reading of the
dissertation made it a much better manuscript. His belief that the
basic research question I was considering was worth investigating
provided reassurance during the uncertain transition between early
conception and the final prOposal. His research advice moderated my
impetuosity; his insistence that I do a pilot study, for example,
enabled me to skirt some mistaken approaches. But most of all, I wish
to thank Dr. Rabin for his friendship and support throughout my graduate
school career. He was an excellent teacher, a model of professional
integrity and decorum, and the very exemplar of the scientist-
practitioner clinician he sought to create in his graduate students. In
saying he will always have my esteem and affection, I know I am only
joining a long line of like students.

Dr. Messe' was the methodologist on this dissertation, a
capacity he had previously served on my masters thesis. On this work,
as on the earlier work, most of the credit for the analysis belongs to
him; any errors are naturally my own. Clinicians, I suspect, generally
have a better conceptual understanding of research design than they have
a strict mathematical understanding, and I am no exception. The value
of the methodologist to peOple like me is directly prOportional to both

their knowledge and their patience, and in these regards, Dr. Messe’ is

iii

the methodologist par excellence. I take the knowledge for granted, but
the patience I know of first hand, since I sorely put it to the test
whenever I started my tortured explanations of the project. Such
clarity as may exist in my plan of analysis and results sections owe
much to his careful reading of an early draft. In addition, Dr. Messe'
has been a friend and source of encouragement in all my research
endeavors; I especially treasured this research encouragement as my most
severe doubts early in my graduate school career centered on my ability
to perform research.

Dr. Ferguson made a number of valuable suggestions which
improved the basic experiment of this dissertation. Her advice here, as
elsewhere during my graduate school career, was astute and sensible.
She has always been an excellent teacher, a fine clinical supervisor and
a friend throughout my graduate school career. One of my comprehensive
questions was written for her this year, and she gave me enough leeway
on the project so that it became the most exciting theoretical endeavor
I attempted while in graduate school and one which I expect will engage
my interest for some time to come. This is typical; looking back, I see
many of the areas which are of most interest to me started in various
classes of hers.

Dr. DeRath focused my attention back onto the clinical issues
raised by the theoretical question I was addressing. His ability to
bring me back to earth, as it were, continues a long pattern in our
relationship, for Dr. DeRath was one of my first clinical supervisors,
both at the M.S.U. Psychological Clinic and later during my first
internship at Ingham Community Mental Health Center, and supervisors for

novice clinicians must always see that their students do not lose the

iv

actual clinical data in a propensity for abstracting. Dr. DeRath has
always shown a personal interest in my career develoPment and has been
the source of quite useful career advice to me over the last six years;
I only regret that I did not follow even more of it.

My wife Mary was helpful in more ways than I can ennumerate, but
perhaps most of all for her support and c00peration in seeing this to
completion. She not only picked up the slack in family matters whenever
I was spending long days and nights collecting data or writing, but even
well before this year, she tolerated and reduced my bouts of anxiety
during the long stretches when I was afraid I might never find a
research topic, and, in what was surely the most torturous part of this
all for her, she patiently listened to me as I wove through and then
rejected dozens of research ideas, ranging from the ridiculous to the
impossible. My son, Sam, too, deserves some mention, if only because
his easy-going nature made it easier to forgive myself for those times
when my anxiety about this work left less of me available for him than
he deserved.

David Hayes deserves a special place in this list of
acknowledgements. I was in constant touch with David during the
germinal stages of this proposal and he read and commented on the
prOposal before I presented it to my committee. Most of all, he was an
ever-available sounding board for my ideas and my worries, and a touch-
stone of reassurance that I would eventually complete this project.
David and his wife Peggy also fed me supper and offered me a place to
sleep many a night when my data collection in East Lansing was

continuing too late for me to return to my home in Ann Arbor in time.

The food was always good, but the encouragement was even more
nourishing.

I deveIOped an interest in doing research on depression.<h1ring
discussions with Dr. Naomi Lohr of the University of Michigan, and I
'wish to thank her for her time and interest. Dr. Lohr also let:lne Ilse
her office for writing purposes; without that office, I think the
writing of my comprehensives and the dissertation might have taken
another half year. Three other University of Michigan professors took
the time to discuss my earliest prOposal, and as their labors (and
Dr. Lohr’s) for a student of another university earn them no credit
outside these pages, I wish to thank them. They are Dr. Hazel Markus,
Dr. Richard Nisbett and Dr. Camille WOrtman.

Two undergraduates, Denise Cameron and Chris Keenan, aided in
the data collection for both experiments and in coding some of the data.
They were both reliable, hard-working and conscientious; because both
experiments involved moving peOple from room to room or from floor to
floor, it might have been impossible to run the experiments without
their help.

Dr. Abeles and Mr. VanderJagt, the director and assistant
directors of the M.S.U. Psych Clinic, consented to my using the clinic
to collect data for the first experiment and I wish to thank them for
their c00peration. I hope I did not disrupt clinic activities too much,
and I apologize to any clinicians who might have been inconvenienced.

While I was collecting data, I was commuting some sixty miles
from Ann Arbor, so I often had to make many arrangements by phone.
Marge Curtis, Carol Fischer and especially Susan Pavicks, all

secretaries in the department, did more than duty called for to help me.

vi

They always seemed most calm, competent and helpful at exactly those
moments when I felt most harried and absent-minded, and I am grateful to
them. I also received technical assistance from Mr. Roger Halley and
David Anderson, the visual-aids assistant. Michael Nolte and Anne Lloyd
provided computer advice and assistance. My typist, Anita Ernst, amazed
me with her speed and reliability. I was invariably asking her to type
things at the last moment, and she just as invariably would get it done.
She also patiently taught me how to use a word processor system. I
thank her most gratefully.

Finally, this dissertation was written while I was supported CH1
a research fellowship from the National Institute of Mental Heatlth. I
wish to thank N.I.M.H and the M.S.U. Department of Psychology for their?

support.

vii

TABLE

LIST OF TABLES C O O O O C O O O 0

CHAPTER

CHAPTER

CHAPTER

CHAPTER

CHAPTER

CHAPTER

1

6

OF CONTENTS

INTRODUCTION AND REVIEW OF RELATED LITERATURE.

Cognitive Theories of

Depression .

Affect Theories of Depression. . .

Comparing the Two Models

Testing the Two Models
HYPOTHESES . . . . . .
METHODS. . . . . . . .
Experiment One . . . .
Experiment Two . . . .

Plan of Analysis . . .

RESULTS. . . . . . . .

Discriminant Validation. . . . . .

Convergent Validation.
Depression Hypotheses.
Elation Hypotheses . .
Summary of Results . .

DISCUSSION OF RESULTS.

Elation Models . . . .
Thought-First Model of
Affect-First Model of
Two Models or One? . .

Depression.
Depression .

SUMMARY AND CONCLUSIONS. . . . . .

LIST OF REFERENCES . . . . . . . .

APPENDIX 1

APPENDIX 2

APPENDIX 3

APPENDIX 4

APPENDIX 5

of Depression

VELTEN MOOD INDUCTION PROCEDURE (VMIP)

PERSONAL FEELINGS SCALE (PFS). . .

MULTIPLE AFFECT ADJECTIVE CHECK LIST(MAACL). .

BECK DEPRESSION INVENTORY (BDI). .

ATTRIBUTION STYLE QUESTIONNAIRE (ASQ).

viii

ix

20
25

31
32
32
39
41
44
44
49
52
55
58
61
61
62
65
67
69
72
77
86
88
91

94

TABLE 1

TABLE 2

TABLE 3

TABLE 4

TABLE 5

TABLE 6

TABLE 7

TABLE 8

TABLE 9

TABLE 10

LI ST OF TABLES

THOUGHT-FIRST AND AFFECT-FIRST MODELS OF DEPRESSION .
DESIGN OF EXPERIMENTS ONE AND TWO . . . . . . . . . .

EXPERIMENT ONE: DEPRESSION, ANXIETY, HOSTILITY AS A
FUNCTION OF TREATMENT CONDITIONS. . . . . . . . . . .

EXPERIMENT TWO: DEPRESSION, ANXIETY AND HOSTILITY AS
AFUNCTIONOF SEXANDTREATMENT . . . . . . . . . . .

EXPERIMENT ONE: ANALYSES OF COVARIANCE FOR
DEPRESSIVE ATTRIBUTIONAL STYLE SUBJECTS . . . . . . .

EXPERIMENT TWO: ANALYSES OF COVARIANCE FOR
DEPRESSIVE ATTRIBUTIONAL STYLE SUBJECTS . . . . . . .

EXPERIMENT ONE: ANALYSES OF VARIANCE FOR ELATION
ATTRIBUTIONAL STYLE SUBJECTS. . . . . . . . . . . . .

EXPERIMENT ONE: DEPRESSION SCORES FOR HIGH VS. LOW
DEPRESSIVE ATTRIBUTIONAL STYLE SUBJECTS IN DEPRESSIVE
TREATMENTS. O O C O C C O O C O O O O I O I O O O O O

EXPERIMENT TWO: DEPRESSION SCORES FOR HIGH VS. LOW
DEPRESSIVE ATTRIBUTIONAL STYLE SUBJECTS IN DEPRESSIVE
TREATMENT . O O O C O C O O O O O O O O O O O O O O O

'EXPERIMENT ONE: DEPRESSION-ELATION SCORES FOR HIGH

VS. LOW ELATION ATTRIBUTIONAL SUBJECTS IN ELATI ON
TREATWNT . C O O O O O O O O O O O O O O O I O O O 0

ix

23

4O

46

48

50

52

53

56

57

59

CHAPTER 1

INTRODUCTION AND REVIEW OF RELATED LITERATURE

Cognitive Theories of Depression

 

In the last two decades, psychological research on clinical
depression has increasingly focused on thought processes. While the
nature of depressed thinking is becoming clearer, the relation between
such thinking and the causes of depression remains obscure. Two
essential questions remain unanswered. First, is such thinking the
cause of depression or is it the result of the depression? Second, what
is the relationship between depressive thoughts, external events and the
depressive syndrome; more specifically, must an external precipitating
event remain in conscious awareness for depression to then follow? The
theories which stress the role of conscious thought patterns in the
etiology of depression include Beck’s theory (1967), the original
learned-helplessness theory (Seligman, 1975), and the latter’s revised
or attribution version (Abramson et al, 1978, Miller & Norman, 1979).

Although these theories have a similar emphasis on cognition,
these theories are distinct. Looking at these theories one by one
should reveal these differences and should describe the nature of
depressive thinking as well.

Beck’s (1967, 1974) theory was deveIOped when his attention was
turned to thought distortions unique to depressives as a group. Such

distortions included arbitrary inference, selective abstraction,

overgeneralization, and magnification and minimization. He calls these
distortions a "cognitive triad" because they fall into three categories,
namely a negative view of the world, of the self, and of the future.
The negative world view involves special sensitivity to failure: the
depressive not only consistently reads his actual performance as
evidence of failure (for example, by consistently under-estimating what
he actually performed) but also consistently exaggerates minor
difficulties as examples of major failure. Ambiguous or minor stimulii
get blown into large eXperiences of ridicule or emptiness. In the
negative view of self, the depressed person lays all blame for his
negative life experiences solely upon himself. Any situation-specific
failure is distorted into a personality flaw. Finally, the third
feature of the triad is a negative view of the future: the patient sees
the short-term and the long-term future as an endless continuation of
the negative present experiences, including failure, deprivation and
self-depreciation.

All other symptoms emerge from these depressed cognitions. Beck
argues that the depressed mood, the motivational deficits, the increased
suicidality, the increased dependency and many of the physical symptoms
come from the depressive’s cognitive triad. Consider affect and
cognition, for example. Real life rejection or loss can lead to
depression; so too can the thought that such rejection or loss has
occurred. Depressed patients consistently misinterpret external
information in a way that leads them to feel they have been rejected or
suffered a loss. It is not that they immerse themselves in more no-win
situations in real life, but rather that their internal cognitive

processing system consistently distorts the experiences they have, so

that they always see themselves in these no-win situations. Just as the
thoughts cause the depression, so too if the thoughts change, the
depression then lifts. A student depressed because he thinks he has
failed an exam will no longer be depressed if he learns the posted
grades were in error.

The second major cognitive theory is Seligman’s (1975) learned
helplessness theory. Since even Seligman has now abandoned the original
theory, I will only briefly describe it. This theory emerged from
laboratory experiments involving dogs in a shuttle box, where an
electric shock can be switched from side to side. To escape the shock,
the dog jumps over a low barrier dividing the box. If a dog is
initially given inescapable shocks, it appears unable to learn how to
avoid the shock and instead just lies down and whines. This phenomenon
was called learned helplessness: the dogs had generalized their initial
helplessness to all later situations.

To create learned helplessness, there must be an objective
situation in which environmental responses remain invariant no matter
how one behaves and this response independence must be known to the
individual. Later this information becomes an expectation of
helplessness. Finally, this expectation has cognitive, emotional and
behavioral consequences.

Seligman argues that since learned helplessness and depression
have the same symptoms and the same cause, therefore learned
helplessness is depression, and vice versa. Both are marked by
passivity, by similar negative cognitive sets, by a similar lack of

hostility, by similar physiological effects, including loss of weight,

sex drive, and appetite, and even by similar biochemical processes
(norepinepherine depletion).

Finally, with regard to the original question of how thoughts
relate to emotion, the theory is quite clear: people must be consciously
aware of the essential environmental features for any depression to
occur; should response independent contingencies exist but remain
outside of awareness, no depression will result. Second, depressive
affects come after this thought-environment interaction.

The outcome of the research generally shows the original theory
is unconfirmed. Depue & Monroe (1978) note that learned helplessness
ought to be a theory of reactive depression, but the physiological
symptoms it describes are closer to endogenous depression. Costello
(1978) argues that the experiments do not support the theory. An
important discrepancy in the research is that subjects often react witfll
anger instead of depression--something not predicted by the theory.

In the last two years, Miller & Norman (1979) and Abramson,
Seligman & Teasdale (1978) have independently arrived at quite similar
attribution theories of depression. These two theories combine an
attribution model (Heider, 1958; Kelly, 1967) with learned helplessness
in an attempt to correct for the criticisms directed at the latter. The
theories assume that if a person finds himself in a helpless situaticnm,
he asks why he is helpless; the nature of the causal attribution
determines whether he is depressed. The original learned helplessness
theory always had such a cognitive component in it relating to
expectancies about future outcomes, but the cognitive component had IHDt
been important; the new theories primarily focus on this cognitive

aspect.

Three attributional dimensions determine the nature of
depression: internal-external; stable-unstable; and global-specific.
Depressive experiences are likely to be chronic if helplessness is given
a stable attribution, and the depression will generalize over many areas
of life if the helplessness is given a global attribution. (The tflnird
attribution dimension, internal-external, is discussed separately
below.)

The following examples may clarify these attributions. This
theory states that if someone loses his job, he must explain to himsefilf
how this happened and he‘therefore attributes the job loss to some set
of factors. The nature of these attributions may then determine his
reaction to the job loss. One man makes external attributions: he might
say the entire economy is in recession (global) or he might say his
company alone is floundering (specific); he might think this is a short-
term recession (unstable) or that this is the beginning of national
economic ruin (stable). A man making internal attributions might
likewise vary on the other dimensions. He might say he was fired
because of a global trait ("I am always unreliable") or because Of a
specific personnel problem ("My new boss and I just don't hit it off.");
similarly he could say it was something stable about himself ("I am tCH)
dumb") or something unstable and changeable ("I need more education").

The two attribution theories differ on the role of the internal-
external dimension. Abramson et a1 (1978) argue that helplessness can
be experienced as personal helplessness or universal helplessness (the
latter being helplessness not contingent on the person, such as
helplessness during a tornado); internal attributions will lead to

personal helplessness and lowered self-esteem while external

attributions are tied to universal helplessness and no lowered self-
esteem. However both forms of helplessness lead to depression. Miller
&Norman (1979) would say internal attributions are needed for
depression. If external attributions are made, the person will just get
angry.

The revised theory differs from the old learned helplessness
theory in still other ways. According to the old theory, any
uncontrolled event, good or bad, was supposed to lead to depression; in
the new attribution theory, dysphoric depressive affect only results
when the uncontrollability expectations are in regard to a ”bad event"
(bad event expectancies being the probability of aversive outcomes or
the improbability of desired outcomes). The new model also has room for
how self-esteem enters into the depressive equation, which the old model
did not.

What the new theory gains in its accurate description of
depression it loses in its explanatory power. The strength of the
original learned helplessness theory was its very simplicity: depression
was purely a function of a given kind of environment. If someone was in
that environment, and knew it, they became depressed; conversely,if
someone was depressed, they had to have been in such an environment.
Overcomingdepression merely involved changing the environment or
learning that ways one thought about the environment no longer applied.

This simplicity is lost and the greater complexity of the
attribution theory raises as many questions as it answers. We now have
a theory in which two people can be placed in the same environment and
not react in the same way, since we only know the reactions if we know

the attributions, and each person may have his own style of making

attributions. But what determines their attributions? There is nothing
in the theory to explain how and why different peOple have different
kinds of attributions when in the same situation. Here we have a theory
which may explain the process of depression but tells us nothing about
w_h_y this process occurs in some peOple and not in others (Bowlby (1980)
raised a similar objection to the Beck (1967) theory). We have lost the
clear-cut relation between depression and environment and have not fully
replaced it with an explanation of the individual and depression.
Returning again to the Beck and the learned-helplessness
theories, in addition to the attribution theory; it is clear that all
three cognitive theories say that depression begins with a pathogenic
thought-pattern interacting with real events. Since all three theories
assume that all the other symptoms in the depression syndrome1 stem
from this thought pattern, all three theories are aptly described as

thought-first theories: the thinking determines the depression. In

 

addition, all three theories say that thinking is directed at an
external event. This event may be neutral or aversive, but it must
remain at the forefront of the depressive’s thinking. Depressogenic
thought patterns can only create depression if the external

precipitating event remains in consciousness.

Affect Theories of Depression

 

The psychological literature presents another and altogether
different way of thinking about depression. This alternative view is
that the conscious thought patterns in depression are mainly a result or
manifestation of the depression and not its cause. What is the cause?
Here the theories vary, but they generally start with the depression as

an affect--an affect that then creates the typical depressive thought

patterns. In addition these theories say that depression can arise in
the absence of any conscious awareness of an external precipitating
event. Like the cognitive theories, these various affect-first theories
do differ from each other and so they each need some further
elaboration.

In psychiatry, most current research has been directed at
biochemical theories of depression (Akiskal & McKinney, 1973, 1975;
Baldessarini, 1975; Fawcett, 1975). Depression is directly traced to
the biochemical processes which are presumed to control moods; since the
other features of depression, including its thought features, are
presumed to then come from the affect changes, these theories are all
affect-first theories.

The second major group of theories which comprise the affect-
first model are the various psychoanalytic theories. These theories all
assume that unconscious processes can set off depression and thus all
argue that depression can theoretically arise in the absence of any
conscious awareness of a precipitating event. Therefore the ways we
think about events cannot explain all the thought symptoms in all
depressions.

Since these theories have been summarized elsewhere
(e.g. Mendelson, 1974), this summary will focus on two issues of
depression and depressed thought: first, can depression begin without
conscious awareness of the precipitating event; and second, can
depression begin as an affective change which then creates the other
features of the depressive syndrome, including depressive thinking?

Some theories answer one or the other question; Freud’s (1917)

explanation of depression (an explanation still underlying most

psychoanalytic theory on depression) answers both questions. With
regard to external precipitants, Freud notes that in depression, as in
all mourning, loss is the central issue; however in some types of
depression the loss is hidden and indeed must be inferred from the
presence of the depression. In the more extreme of such cases, the
individual is unaware of the loss; in the less extreme, he knows who he
has lost but not what it is about the person that he has lost.

How can the link between the depression and the precipitating
event be severed? It comes from the strong ambivalence in the
depressive’s feelings. In grief, the detachment of the libido from the
lost object also begins primarily in the unconscious, but this process
then easily moves on into the preconscious and then into. the conscious
system. Ambivalent conflict in depression, unlike grief in bereavement,
does not readily leave the unconscious; it is blocked within the
unconscious and this very blockage actually creates the melancholy. The
libidinal cathexes do abandon the object (as in grief) but because of
the ambivalence this occurs (and is dissimilar from grief) via a
regression and object identification taking over part of the ego. Only
after this regression has occurred does the depressive conflict become
conscious, and the form it takes, as a conflict within the self between
ego and the super-ego, is not the essential part of the conflict. The
real original conflict, between self and external object, is hidden.2

The second question is whence arise these depressive thoughts?
In one of his most famous comparisons, Freud says that in grief the
world appears "impoverished" while in depression it is the ego which is
impoverished and experienced as a devalued self. This is the now common

observation that depressives suffer a loss of self-esteem. Freud

.10

stresses that the depressed patient is not aware that this change has
taken place within the self, or more accurately, does not recognize this
self-devaluation as a change. Instead this self-devaluation or
"delusional belittling" is extended backwards into the past, as if it
always existed. Naturally, there is some truth in these harsh
criticisms, but it is a part truth. The statements which are true refer
to the after-effects of this process. For example, the depressive
declares he is incapable of love--true, but only because depression
makes him so.

In other words, Freud’s paper clearly suggests that the thinking
in depression neither precedes depression nor causes depression but
instead is created by the depression process--a process which occurs
when anger over object loss is directed within instead of being
externalized.

The next major change in psycho-analytic theory comes from
Bibring (1953), who also addresses the relation of depression and
depressed thought. Bibring says all depressions "represent an affective
state, which indicates a state of the ego in terms of helplessness and
inhibitions of functions." Depression is thus the emotional state which
occurs when the ego experiences helplessness or powerlessness . Such a
state follows a narcissistic blow (Bibring is referring to secondary
narcissism) which lowers self-esteem. Bibring notes three essential
narcissistic goals: these are the wish to be loved; the wish to be great
and strong; and last, the wish to be a good and loving person. These
goals remain highly charged goals for the individual since they are
internalized in the ego ideal, and hence retain both conscious and

unconscious components; when the ego becomes aware that it is unable to

11

reach or maintain these narcissistic goals, extraordinary tensions
result, and depression follows. Depression is thus an "emotional
correlate of a partial or complete collapse of the self-esteem of the
ego since it fails to live up to its aspirations," even while these
internalized aspirations remain and exert a powerful pull.

Seligman (1975) quotes Bibring in support of his own learned
helplessness theory, but this attempt to find support in Bibring
represents a fundamental misunderstanding of Bibring which, if
clarified, will also explicate the essential differences between the
thought-first and the affect-first models.

There are two essential differences between Bibring’s theory and
Seligman’s learned helplessness theory, differences which Seligman
either ignores or misunderstands. The first is that Bibring says
depression follows narcissistic blows, not real external blows.
Seligman presents a theory in which a person faces a 3'31 (objective)
situation in which gal: behaviors aimed at an achievement are
consistently unrewarded by the outside world, leading to a mind set in
which the individual gives up attempting to gain real rewards from the
outside world. But Bibring repeatedly stresses that the most frequent
cause of the depression is excessively high narcissistic ambitions; this
need not have to do with lack of real abilities or real rewards.

Consider a talented music student who wins many awards but who
fails to win the annual Tschaikovsky award in Moscow and becomes
depressed. Given the earlier pattern of rewards, Seligman has no
explanation of this depression. For Bibring it is simple: the

narcissistic goals are excessive, failure follows despite an earlier

12

string of successes and, given the narcissistic blow to self-esteem,
depression begins.

In a similar fashion, for Seligman’s learned helplessness theory
depression ends when real changes occur, namely either the reward
pattern for old behaviors is now altered, or else the individual now
institutes a new set of behaviors which is more successful in elicitiru;
rewards. Bibring, on the other hand, suggests four possible ways
depression could lift: either the narcissistic goals now appear more
reachable; self-esteem is recovered aside from altering the goals; the
goals are altered or just given up; or else the depression is defended
against, as by hypomania. Notice that only the first two of these
possibilities are even tangentially related to changes in behaviors or
skills.

The second misunderstanding is in Seligman’s interpretation of
Bibring’s phrase, "The ego’s acute awareness of its helplessness."
Seligman reads this as if it means that a person is cognitively
conscious that he is indeed in an objective situation of helplessness.
But the ego is an internal structure of the mind and ego states are
internal states of the person. Perception of reality is only one ego
function. The ego might also feel helpless vis a vis purely internal
processes independent of external situations (e.g. a depression set (off
by a dream). Bibring cites the example of a successful professional man
who became depressed whenever he did routine work. Not only was
analysis needed to explain why doing routine work made him depressed,
but the fact that this routine work triggered the depression was unknown
to the man. Until he entered the analysis, he knew only that he

occasionally became depressed, for reasons unknown.

13

Much recent psycho-analytic thinking about depression is even
closer to the affect-first model, since these theories say many features
of depression, including depressed thinking, is a reaction to the affect
of depression. Edith Jacobson (1971) has written extensively on
depression, and her work on moods, and especially depressive moods , is
central to contrasting the affect-first depression model with the
thought-first model.

According to Jacobson, moods are ego states in which all ego
ftmctioning, including thoughts, feelings, actions, etc., take on a
"particular uniform coloring" for a shorter or longer time period. More
specifically, Jacobson calls moods a "temporary fixation of generalized
discharge modifications." For example, an affective tone of joy or
anger is temporarily seen everywhere-"within the self, in internalized
objects, and in the external world, and hence in all one’s thoughts and
actions too. Other affect states are always directed at and derived
from a specific object; moods lack specificity.

Moods often overtake us without our knowing whence they come.
There is usually an external experience which sets off the mood, but we
often lose track of the provocative event. For a mood change to result,
the initial event must set off a great deal of tension which cannot be
immediately relieved. In some cases, a major external change can lead
to a mood change, as when someone is left by a lover. In other cases,
however, it can be a rather minor event so long as the event activates
considerable tension in the unconscious. At these times, the evocative
event may even be forgotten.

All objects and indeed all stimulii are affected by moods.

Emerging moods alter our internal world for a time, modifying all our

14

self-conceptions and object world. These changes run in parallel during
a particular mood state, so in a joyful mood state I feel joyful and the
entire world seems joyful too, while in an angry mood, I am angry and
the entire world appears dark and brooding. As a result, we act in ways
that confirm our mood colored vision of the world. In an angry mood we
will see others as angry and will act angrily at them. Their quite
naturally responding with anger only confirms that the world is indeed
an angry arena.

vmen mood changes overtake us, Jacobson continues, our
evaluative abilities are temporarily curtailed. In a normal mood state,
peOple know this is time limited and the distortions will lift as the
mood lifts. Even depression can be a normal mood, so long as peOple
tell themselves, "I am thinking this way because of the depression, and
when the depression lifts my view of myself and the world will also
alter."

Pathology enters when people cannot work out of their mood.
Three difficulties make moods pathological. The first is ego weakness,
including flaws in basic reality testing or an inability to tolerate
stress or loss. The second is a weakness of the super-ego. One
function of the super-ego is to signal the presence of strivings which
are not permitted; impairment of this signal function can lead to rapid
mood swings. Finally, if a mood is tied to an unconscious conflict,
then the repetition compulsion from the infantile conflict can block any
effective use of reality testing. When reality testing is attempted,
the new experience is distorted by the unconscious conflict so that it
merely confirms the infantile distortion. The model Arieti & Benunarad

present (later this chapter) is a variant of this model.

15

The key to mood pathology is thus the ability or inability to
work one’s way out of the mood, rather than the mood itself.

Even depression can be a normal mood, Jacobson adds. A
depressed mood always involves aggressive conflict. Frustration creates
a conflict which is turned against the self-image, creating a ”conflxict
between the wishful self image and the image of the deflated falling
self." This internal conflict between self image and ego ideal creates
a narcissistic experience central to all depression: the experience of
failure. There are two avenues to depression. Sometimes the depression
is created by narcissistic conflict; at other times the super-ego is
involved. In these second cases, the failure experience is matched by a
moral judgement on the self as being bad.

Because the conflict in depression arises from an internal
narcissistic conflict (ego ideal vs. self-representation), the reality
testing must occur within the person too: in the end, it is the internal
super-ego standards which must be satisfied and not the external
standards of the world. Introspection about the self is difficult, but
if the gap between ego-ideal and self representation is excessive, due
to an unrealistically high ego-ideal, then even satisfactory encountuers
with reality may not alleviate the depression. If I feel depressed
because I fail an exam, I can overcome this by studying harder, IHJC if
my standards remain excessive, then even success on future exams may
appear inadequate.

Tmakey points in Jacobson’s theory of moods should be
reiterated. First, moods change the way we think, and not the reverse.
Second, we need not be conscious of any external event which alters (Mir

mood.

16

Arieti & Bemporad (1978) propose a model similar to Jacobson’s,
except that they start with an inability to end a sad mood, where
Jacobson started with an inability to end a depressed mood.

Arieti and Bemporad (1978) say depression is intimately tied to
sadness. All painful emotions are designed to create actions which will
cause them to disappear but sadness is unique because it slows us down
first, making direct action less likely. The slowdown is adaptive
because the function of sadness is to give peOple a chance to re-arrange
their thoughts and goals, as when they remake their life plans. Sadness
follows a cognitive appraisal of an event and then promotes a reparative
change in our relation to that event. It is similar to the work of
mourning.

Depression arises from deep thought patterns or schema which
block this resolution of sadness. All people can use affecto-cognitive
schema to evaluate external environments and then make the best possible
adjustments to life circumstances. In the case of depression, there
exist depressogenic cognitive patterns which may reside in the
unconscious or but dimly in the conscious. These patterns lead to
depression if they block the resolution of sadness.

Arieti & Bemporad may sound quite similar to Beck’s cognitive
theory, described earlier, so it is important to see how they differ.
Arieti (Arieti & Bemporad, 1978) contrasts his own theory of
depressogenic thought patterns with that of Beck and finds Beck wanting.
Beck’s patterns are too close to conscious thought, Arieti says, and the
kind of thinking Beck describes often occurs after the depression has
set in and is indeed caused by the depression. The patient may then use

these thoughts as a way of justifying the depression to him or herself.

17

By contrast, Arieti says the essential depressogenic thought patterns he
describes are unconscious or but dimly in conscious awareness.

I think Arieti misreads Beck. Beck introduces the notion of a
"schema" as a slightly more abstract thought pattern than the actual
verbalized thoughts of the patients. The schema itself may not be fully
within the awareness of the patient; instead it is a basic thought
pattern which distorts experience so that the patient experiences it as
the distortions he talks about. This usage of schema is quite close to
the depressogenic thought patterns Arieti talks about.

The difference between them (and between Beck and other
analysts, though especially Jacobson) lies elsewhere. Beck says an event
occurs and we then think about it and feel depressed. Sometimes this is
because the event itself is depressing--for example, a death in the
family. For depressives, however, the objective meaning of the event is
less clear; instead they carry with them a mind set that consistently
misreads external information in a way that makes them feel depressed.
The misreading is always of external events. The cognitive distortion
occurs after the event and before the depressed affect is created. Once
the depressed affect occurs, the theory has little to say.

Arieti too would say that depressives misread events in a way
that makes them more likely to feel sad. However psycho-analysts would
add the following:

1. All misreading stems from unconscious dynamic issues and thus
reflects a neurotic need. This need is not only manifested passively in
response to external events, but actively insofar as the external events
are sometimes created out of this neurotic need. Thus some peOple are

prone to chose for relationships peOple who are especially likely to

18

leave them. The confirming external event is created from the internal
neurotic need.

2. Depressed moods can arise in the absence of external events
if related to unconscious issues. Hence external events are sometimes
mis-identified as the cause of a depression.

3. Some amount of cognitive distortion normally occurs as a
consequence of mood changes (rather than always the reverse). This
affect caused distortion occurs even in healthy peOple. Healthy people
can step back and think about these mood-caused distortions: they
recognize that their distortion is temporary and mood related.
Depressives are less able to work out of their moods because they fail
to recognize that these distortions are fleeting and mood related. This
is different from Beck’s cognitive distortion because it occurs after
any precipitating event and because it is related to mis-reading
internal states and feelings.

4. If depression only arises from cognitive distortions, it can
be eliminated. Psycho-analysis, on the other hand, says it is a normal
mood so the issue is not the elimination of depression but the capacity
to bear it (e.g. Zetzel, 1965).

Two other sets of theorists have focused on how clinical
depression--including the thought features of clinical depression-"are
responses to a basic depression affect.

Joffe and Sandler (1965, 1967; Sandler & Joffe, 1965) argue
that, like anxiety, depression is a basic affect, a built-in
psychological and biological response. Depression is the human affect
which follows being helpless when physical or psychic pain is suffered.

It is thus an affect which can occur as early as infancy when an infant

19

is understimulated or starved; it can also occur at any later time in
life. The depressive affect must be distinguished from the illness.
The more complex features of depressive illness are attempts to block
this painful affect either before it deveIOps or after it has started.
Using a similar starting point, Schmale and Engel (Schmale &
Engel, 1975; Schmale, 1964) assmne that there is a basic biological
system leading the individual to withdraw from excessively or
inadequately stimulating environments. This biological state is
experienced as two distinct affects of depression, depending on when it

occurs. The earlier affect is helplessness. This occurs in the first

 

year of life when the infant is totally dependent on the external
environment for satisfaction. The infant is helpless to effect a
change; if gratification is not forthcoming, it will withdraw into a
sleep-like or depressive stupor and only later once again attempt to
regain contact with the external environment. After these first two
years, but especially during the Oedipal years, three to six, the affect

is experienced as hopelessness. Here the failure to obtain

 

gratification from a parent figure (especially the opposite sex parent)
is explained as being due to one’s own inadequacies--hence hopelessness.

The depressive affects, helplessness and hOpelessness, are like
anxiety in that they can serve a signal function so as to avoid re-
experiencing the original affect. For constitutional or experiential
reasons, some peOple find even the signal depression is intolerable.
Clinical depression (including depressive thinking) is a neurotic
attempt to master the depression and prevent a traumatic re-experiencing

of it (analagous to how phobias are attempts to master anxiety).

20

Comparing the Two Models of Depression

 

Despite their differences, the various cognitive theories of
depression can be merged into a basic thought-first model. In the
thought-first model, the mind is seen as an information processor,
working like a "cool" computer. Drives, conflicts, motives--"hot"
issues--play no crucial role. The external events are processed
primarily to see if they are rewarding or unrewarding. These theories
are concerned with the nature of external events--are the events
rewarding or not?--and how these events are processed-“are they gfl as
rewarding or not? The theories also consider the interaction between
the real events and how they are mentally processed.

Depression begins when for some reason the computer begins to
misfunction, reaching a conclusion of non-reward before all the data are
in and analyzed. During a period of malfunctioning, the mind as
computer begins to mis-read events, even reading success as if it were
failure. In this model, the primary feature of depression is the
inability of the mind to correctly analyze the environment. The mind
places the burden of non-success upon itself either by being unable to
read success where it is evident or else by blaming itself for a failure
which might justifiably be blamed on something external to the self--
such as bad luck, situational factors, etc.

By correcting the self-defeating cognitive thoughts, the
depression is lifted. Often this involves placing the depressive in a
situation where he experiences some success and then forcing him to take
note of this success. The processing of self-success then alters how
future information is processed. It is a bit like changing a computer

program. The old program, which read failure everywhere, is ousted and

21

new program which correctly reads the environment is entered, so now the
person can recognize his success, leading to a lifting of the
depression.

For the depression to occur, the event must clearly be at the
forefront of the person’s mind. In addition, the way of thinking about
the event (e.g., depressive attributional style) must be present before
the event occurs and then remain stable afterwards.

In the alternative affect-first model the precipitating event is
either absent altogether or else present but not at all in the forefront
of the person’s thoughts; there the characteristically depressive
thought style does not precede the onset of depression but merely
accompanies it. In various psychoanalytic theories there are two ways
in which thelonset of depression is not preceded by a person’s full
awareness of the external precipitating event. In the first, and more
extreme case, the trigger for the depression can be in the unconscious
and thus outside the realm of subject awareness (see Table 1). For
example, unconscious conflict or unconscious loss or rejection by a
loved one are sometimes thought to precipitate a depression (Freud,
1917, Bibring, 1953). In the less extreme and more common variation
(see Table 1) the triggering event is within the person’s awareness but
is not easily tied by the person to the depression which follows. This
is because the unconscious meaning of the event is far greater in impact
and importance than the conscious meaning of the event. In such a case,
the individual probably does not tie the depression to a precipitating
event unless he or she is actively forced to look for a connection
between the onset of the depression and the external event. Likewise,

in some bio-chemical theories of depression, the changes in mood and

22

thought are caused by changes in body chemistry and are not necessarily
tied to a concomitant external event.

This affect-first model stresses that the failure of self as
agent in the world is a secondary feature of depression; what comes
first is a set of feelings. As a result of such feelings (or as a
defense against such feelings) we no longer wish to participate in the
world. The world, as it were, no longer draws us into it. It is as if
the overload of feelings breaks the circuits of our ties to world. We
then take note of this breakage and read it as reflecting our lack of
abilities in our retreat from the world. We may think we are
ineffective, which lowers our self-esteem, but it is the feelings which
have broken the circuit and not the thoughts.

The following example might clarify the affect-first model.
About a month before a therapist’s summer vacation, a patient starts to
report feelings of depression. There is no clear precipitant which the
patient can cite. The patient now feels so inadequate and unappreciated
at work that he begins to consider changing careers. Based on
derivatives in the material, the therapist suggests the patient’s
depression has been triggered by the therapist’s upcoming vacation
(i.e., "object-loss"). The patient vigorously denies this and claims
his downcast view of his career is based on a correct assessment of the
facts. Just prior to the therapist’s vacation, the patient cries in the
session. He is surprised by this, but recalls an old memory of father
threatening to leave the family. Patient now ties his depression to the
therapist’s upcoming vacation, and some of the depression lifts.

This is a complicated example, but I will stress the following.

First, the precipitating event is not recognized as such. Second, the

23

TABLE 1

THOUGHT-FIRST AND AFFECT-FIRST MODELS OF DEPRESSION

 

 

A. Thought-First Model

 

Depression

No Depression

 

Time 1. Depressive Attributional
Thought Style
(internal+global+stable)

+

Time 2. Adverse Event
(e.g., fired from job)

Depression
(including depressive
affect)

No Depressive Attributional
Thought Style
(e.g., external attributions)

+

Adverse Event
(e.g., fired from job)

No Depression

 

B. Affect-First Mbdels

 

l. Strict Affect-First Mbdel

2. Concommitant Affect-First Model

 

Time 1. Event Outside Consciousness
(e.g., biochemical change;
unconscious conflict or
object loss)
Time 2. Depressed Affect
together
these =
depression
Time 3. Depressed Thought
(including depressive

attributional style)

Time 1. Event Outside Conscious-
ness (e.g., biochemical
change; unconscious con-
flict or object loss)

Time 2. Depression

/

Depressed Depressed Thoughts
Affect (including thoughts
attributional style)

 

24

event creates the depressed mood. Third, while in the depression, there
arise typical depressive thoughts (in this case, depressive attributions
about why he is a failure at his job). Fourth, confirmation about the
real precipitant of the depression is later forthcoming, and it is not
tied to the thoughts about the job which the patient expresses while in
the depression. Last, the depressive thought style changes as the
actual precipitant of the depression is recognized and the depression
begins to lift.

The two models have different clinical implications. If the
thought-first model were correct, it would be useful for clinicians to
find peOple who are not depressed but who have a depressive thought
pattern. Clinicians might then prevent depression before it occurred.

On the other hand, if the affect-first model were correct and
there were no depressive attributional style in a non-depressed person,
then there is no value in attempting to change this style if it appeared
in a depressed person. The reason is simple: the depression may be
causing the depressive thought style, and the style might disappear when
the depression lifts. This is valuable information. It suggests that
whenever someone who is in a depression begins to show depressive
thoughts, a clinician might say "That is not you talking; it is the
depression talking. You should not be making any major life decision

(e.g., changing career) until the depression lifts.' For someone who
suffers from serious and cyclical depression, this may be vital
information. Even on an everyday level, the experiment would provide a

scientific basis for the therapeutic value in the old homily "Go to

sleep: everything will look different in the morning." If moods affect

25

our thinking and if transient moods lift overnight, then this homily now
becomes sound advice in addition to being comforting advice.

The key differences between the two models is summarized below:

1. The thought-first model says depressive thought precedes any
depressive episode and the depressed affect is a consequence of this
thought. The affect-first says depressed thought is caused by the
depression; depression is either a primary affect, like anxiety, or an
affect arising from conflict. In either case, conscious thought is not
needed for its creation.

2. Both models agree that external events can trigger a
depression. The thought-first model says such events must be
consciously known and available to the person. The affect-first model

says the triggering event can be forgotten or misidentified.

Testing the Two Models

 

Testing the two depression models could reduce the number of
theories or at least indicate the limitations of some theories. But
there are three fundamental difficulties in Operationalizing a test of
these alternative models. The first is the difficulty of experimentally
inducing a mood change in people while keeping the nature of the
procedure outside the realm of conscious awareness. The second is the
difficulty in minimizing risk to subjects. The third is whether a
change in mood equals depression or merely approximates it.

Sidestepping conscious awareness during a mood altering
procedure may be virtually impossible if the subject is simultaneously
to have informed consent about the procedure. In another era, there may
have been ways of surreptitiously slipping a subject a mood altering

drug; the subject would then not know the cause of his‘ or her mood

26

change, and it would be easy to gauge whether the onset of depressed
mood led to a change of cognitive style. Such a procedure raises
serious ethical problems under any circumstances; it is clearly
impossible given the informed consent necessities of current
experimental work. Subjects must know, at the very least, that the
procedure may alter their mood. Thus it is impossible to introduce a
mood altering procedure which remains totally outside of subject
awareness.

In addition to the informed consent requirements, current
research must demonstrate limited risk to the subjects. With the
research on depression this creates an insurmountable dilemma: any
procedure which creates real depression is almost by definition a risk
to the subject; yet any procedure which is risk free may be too mild to
allow for even analogue studies in depression.

There is but one way to circumvent these twin problems: find an
affect-first theory that begins with mood changes rather than clinical
depression and find a thought-first theory that identifies which healthy
people show pre-depressive thought patterns. Given this, an experiment
can be run with a mild induction on a normal pOpulation.

For the affect-first theory, the choice is Jacobson (1971) and
Arieti & Bemporad (1978); each describes a normal, mild mood (normal
depression and normal sadness, respectively) which both change our
thinking and which directly precede depression. For each of these
theories, depression is an escalation or prolongation of these normal
moods. Creating mood changes instead of clinical depression circumvents
the ethical problems but not the informed consent problem: since

subjects must know their moods are to be changed, the precipitating

27

event is not outside consciousness. Thus one premise of the affect
first model is not met. Any support or non-support of the affect first
model must therefore be considered weak evidence.

For the thought-first model, the recent attribution theory is
ideal, since it predicts which normal people are pre-depressive. Of
course, for the attribution theory, a sad mood or even a depressed mood
is not the same as depression itself, if for no other reason than that
depression is more stable than mood. However the attribution theory is
experimentally derived from normal subjects rather than being clinically
derived, so an experimental test using moods meets the theory on its own
experimental terms. Recall that according to attribution theory, some
peOple have a depressive attributional style prior to any depression.
This style consists of a tendency to make internal, stable and global
attributions about their life circumstances; when such depression-prone
people than actually encounter a set of adverse life circumstances, they
become depressed.

Seligman, Abramson, Semmel & von Baeyer (1979) cite indirect
support for this new theory in studies which show that depressed
students attribute failure to internal causes while non-depressed
students make external attributions (Rizley, 1978; Klein, Fencil-Morse,
& Seligman, 1976; and Kuiper, 1978). However, the only study directly
designed to test this reformulated learned helplessness theory is the
study by Seligman, Abramson, Semmel, & von Baeyer (1979). Students
completed a newly created attributional style questionnaire and then
completed two measures of depression. The results supported the
theoretical predictions: the more depressed college students, when

compared to non-depressed college students, tended to attribute bad

28

outcomes to stable, global, and internal causes and good outcomes to
external, unstable and specific causes. The authors also found moderate
to strong correlations between level of depression and overall level of
depressive attitudinal style: on the Beck Depression Inventory (BDI)
the correlation was .48, while on the Multiple Affect Adjective Check
List (MAACL) the correlation was .24. At the end of the article, the
authors say they plan a longitudinal follow-up study of individuals with
a high depressive attributional style. If they obtain their expected
results, they will provide rather strong evidence that their theory
accounts for some types of depression.

Their study is a correlation study and not an experiment, and
thus it is not able to specify the direction of effect. Wortman &
Dintzer (1978) have speculated that peOple do not necessarily make an
attribution about adverse circumstances and furthermore, that
attributions may be caused by mood changes rather than by the causal
agent of the mood swing. The strength of such a possibility is
increased when the alternative affect-first model is considered. This
affect-first model of depression could account for the very same results
which Seligman et a1 (1979) obtained. In other words, Seligman et a1
may merely be describing a depression rather than pinpointing a cause .
Instead of being a stable feature of personality which leaves peOple
especially vulnerable to depression, attributional style may itself be
merely the result of the depression.

A similar choice of models exists with regard to the relation
between the mood of elation and the thoughts which are characteristic of
an elated mood. Although Seligman does not explicitly deal with

elation, it is possible to extend his theory to cover it. One could

29

postulate the existence of an elation attributional style which leaves
peOple especially vulnerable to elation or joyous moods. Such an
attributional style would consist of a tendency to make internal, stable
and global attributions about good or pleasant outcome events. This
could be operationalized in the following manner, using tflne
Attributional Style Questionnaire developed by Seligman et al (1979):
Elation Attributional Style- (global + internal + stable scores) on
positive outcome events. Elation would thus again be explained by a
thought-first model.

Psychoanalytic theorists have explicitly speculated on elation
being related to, but the opposite of, depression (Freud, 1917,
Jacobson, 1971). Edith Jacobson in particular develops a theory of
elated mood which is close to the affect-first model. Here, as with
depression, the thought change follows the mood change rather than
preceding it. In other words, while in an elated mood, peOple think;:1n
a grandiose way, but this self-centered gradiosity is not necessarily an

stable feature of personality which precedes the elated mood.

Footnotes

1 The key symptoms of depression--and these symptoms are among
the few facts associated with depression that rival schools accept--ar12
as follows (Beck, 1967):

I. Emotional Manifestations
l) dejected mood
2) negative feelings toward the self
3) reduction in gratification (from food, or libido,
etc.)
4) loss of emotional attachments
5) crying spells
6) loss of mirth response

II. Cognitive Manifestations
1) low self-evaluation
2) negative expectations
3) self-blame and self-criticism

3O

4) indecisiveness
5) distortion of body image

III. Motivational Manifestations
1) paralysis of will
2) avoidance, escapist and withdrawal wishes
3) suicidal wishes
4) increased dependency (not necessarily actual
increased dependency, but rather a feeling of being
increasingly dependent)

IV. Delusions
1) delusions of worthlessness
2) crime and punishment: belief that one has committed
a crime and will be punished
3) nihilistic delusions
4) somatic delusions
5) delusions of poverty

Hence the differences in the way grief ends when compared to
depression. Grief ends when reality finally wins out and the object: is
accepted as dead. The work of depression involves denigrating or
killing the object to weaken the libidinal ties to it. The unconscixnis
work in depression ends either when the anger at the object has been
exhausted or when the object is seen as worthless and thus can be easily
abandoned. Either way, the ego at the end of depression feels supeznlor
to the object, and this superiority does not occur at the end of the
grief process.

CHAPTER 2

HYPOTHE S ES

Four hypotheses are derived from the alternative thought-first
and affect-first models.

These first two hypotheses are from the Abramson et a1 (1978)
thought-first model.

Hypothesis One: Subjects with an initial high score on
depressive attributional style will show higher depression following
depressive mood treatment than will those with lower scores in
attributional style.

Hypothesis No: Subjects with initial high scores on elation
attributional style will show higher elation following elation mood
treatment than will those with lower scores in elation attributional
style.

These two hypotheses are from the affect-first model:

Hypothesis Three: Subjects given a depression mood treatment
will show a greater depressive attributional style than will subjects
given other mood treatments.

Hypothesis Four: Subjects given an elation mood treatment will
show a greater elation attributional style than will subjects given

other mood treatments.

31

CHAPTER 3

METHODS

The two experiments created to test the alternative affect-first
and thought-first models use the same basic paradigm: subjects complete
a set of questionnaires on their attribution thought style, their.1eved.
of depression and their mood; they are then randomly assigned to either
a control condition or to an experimental condition designed to induce a
mood change; afterwards, the initial questionnaires are again completed.
The two experiments differ in the experimental induction used to alter
mood states (reading versus film) and in the timing: in experiment «one
subjects must return for a second session, while experiment two is

entirely completed at one sitting.

Experiment One

 

Subjects

The subjects in this experiment were 62 female undergraduates at
Michigan State University. All but two participated to receive course

credits.

Instruments

 

a) Mbod Induction
All three experimental treatments (sad, happy, neutral moods)
are based on the Velten Mood Induction Procedure or VMIP, a procedure

which consists of having subjects read aloud some sixty mood related car

32

33

neutral statements. This procedure has been safely and successfully
used in a large number of studies (Aderman, 1977; Coleman, 1975; Gouaux
& Gauaux, 1971; Hale & Strickland, 1976; Matheny & Blue, 1977; Natale,
1977a, 1977b; Scheier & Carver, 1977; Strickland, Hale & Anderson, 1975;
Velten, 1968). 'No of these studies demonstrated that the procedure
worked even when experimenter demand was controlled (Velten, 1967, 1968;
Coleman, 1975). In most studies, the VMIP was not used to test a theory
of depression but to study some feature of the mild dysphoric state it
creates, features such as speech patterns (Natale, 1977a), gazing
(1977b), and activity level (Strickland et al, 1975). In the current
experiment too, the VMIP is used to create a mild dysphoric mood.

In a recent study, Frost, Graf & Becker (1979) observed that the
VMIP depression treatment actually consisted of two kinds of statements:
some self-evaluative statements which attack self-worth or self-esteem
(self-devaluative statements); and other statements which only describe
body sensations (somatic statements). Examples of self-devaluative
statements are these: "I’ve doubted that I am a worthwhile person" and
"I’m discouraged and unhappy about myself.” Examples of somatic
statements include ”I’m getting tired out. I can feel my body getting
exhausted and heavy” and ”I feel terribly weak.” Frost et al found that
each subgroup of statements worked at least as well as the original
VMIP, but the somatic statements were significantly better than the
self-devaluative statements, when these two sub-groups were directly
compared.

I use only the self-devaluation statements and not the somatic
statements. This choice is based on a pilot study I ran to test the

various induction procedures. I found that the somatic statements had

34

no effect on mood, while the self-devaluation statements created a
strong consistent increase in depressed mood. This failure of the
somatic statements is contrary to the findings of Professor Frost.
There are two possible explanations for my pilot study’s failure to
replicate the Frost et a1 finding: first, M.S.U. undergraduates may
systematically differ from Smith College undergraduates, and second,
Frost et a1 might have had much stronger experimenter demand
characteristics than they imagined.

The elation subjects read positive, self-referent statements
connoting self-confidence, Optimism and energy, such as "I feel cheerful
and lively" and "On the whole, I have very little difficulty thinking
clearly." In the neutral condition subjects read statements unrelated
to moods or feelings. The original VMIP neutral condition contained
only non-self-referent statements. To make it more comparable to the
control and the elation conditions, I made half the neutral statements
self-referent statements without an affective content--statements such
as "I am an undergraduate at M.S.U." or "I am taking part in a
psychology experiment." The other half are non-self-referent
statements, such as "There is a large rose-growing center near Tyler,
Texas." The two kinds of neutral statements are randomly mixed
together.

A complete list of all VMIP statements used in this experiment
is provided in Appendix 1.

b) Measures of Mood, Depression and Attributional Style

Two measures of mood are used in this study; these are the
Personal Feeling Scale or PFS, which consists of ten 9-point ratings of

immediate mood state (e.g., extremely optimistic-extremely pessimistic,

35

extremely happy-extremely sad) and the today form of the Multiple Affect
Adjective Check List or MAACL (Zukerman & Lubin, 1965). These two mood
questionnaires were chosen because they have been shown to be sensitive
to mood induction procedures in a variety of studies (including Coleman,
1975; Hale & Strickland, 1976; Natale, 1977a; Strickland, Hale &
Anderson, 1975; Velten, 1968); they are listed in Appendices 2 to 3. A
depression mood subscale is derived from the total PFS. The MAACL
(unlike the PFS) is a well-validated measure; insofar as the depression
treatment only creates a depressed mood rather than real depression,
this will be the most important measure.

In addition to depression, the Multiple Affect Adjective Check
List can be scored for anxiety and hostility. Having three different
scale scores allows for discriminant validation of the induction
procedures.

Experiment one also employs a Counting Task to test the
effectiveness of the depression treatment. Subjects count backwards
from 100; since depression ought to make them count more slowly, the
subjects in the depression condition ought to have reached a
significantly higher number (i.e. closer to 100) after one minute than
subjects in the other conditions. Since this task is started only after
all the other questionnaires have been completed, or some ten to twenty
minutes after the induction is over, it is best seen as a measure of of
the strength of the induction. Should the other measures demonstrate a
significant induction effect while this measure does not, it would
demonstrate that the induction is weak or that it is not long lasting .

This measure is not used to test the elation induction as it is less

36

clear what the relation between elation and speed of counting ought to
be.

The study also uses the Beck Depression Inventory or BDI (Becflt,
1974) which is frequently used in research to evaluate transient or
reactive depression; in addition, it was the measure of depression useui
by Seligman et a1 (1979) in their initial study of the Abramson et a1
(1978) theory. The BDI is in Appendix 4. By using the BDI, the current
experiment tests the attribution theory on its own terms. Matching test
instruments with those used in the Seligman et a1 study makes this a
fairer if more conservative test of the theory. In experimental
research, a BDI score of nine or higher is used to indicate clinical
depression. If the induction treatment subjects score lower than nine,
then the induction created a depressed mood, but not real depression.

The BDI is not a good measure of elation, since it ranges from
high depression to no depression (at zero) but does not cover the area
from absence of depression through elation. By contrast, the PFS and
the MAACL range from elation to no elation/no depression (at the mid-
point) to high depression; they are thus better indicators of elation.

The final measure used in this study is the Attribution Style
Questionnaire or ASQ (Seligman et al, 1979). This is the crucial
instrument for measuring attributional style; it appears in Appendix 55.
The ASQ consists of brief descriptions of hypothetical events; six are
good outcome events (e.g. "You get a raise.") and six are bad-outcome
events (e.g. "A date goes badly."). Subjects are asked to imagine trust
the events occur to them and then to write down one major cause for this
event happening to them. Subjects then use seven-point Likert type

scales to rate this cause as stable-unstable, internal-external, global-

37

specific, and important-unimportant. In this study, the six bad outcome
events are scored separately and comprise the ASQ-B scale, while the six
good outcome events form the ASQ-G scale. The scores are the sums of
the internal-external, stable-unstable, and global-specific ratings,
with high scores being more internal, global, and stable. A high
depressive attributional style is operationally defined as a high score
on the ASQ-B; likewise a high elation attributional style is
operationally defined as a high score on ASQ-G. The elation and
depression attribution styles are therefore independent of one another:

subjects who are high on ASQ-B could be either high or low on ASQ-G.

Procedure

At Time One, all subjects sit together in a large room. They
are given a general description of the experiment and are then asked t1)
sign a standard department subject consent form. (As noted in Chapter
One, informed consent means subjects must know the experiment may alter
their mood; this knowledge violates an assumption of the affect-first
model, making this a weak experimental test of that model). I then
warn subjects about possible experimenter demand bias; in particular} I
ask them to complete all mood and thought questionnaires based on what
they are actually thinking and feeling at the time they complete it,
rather than based on what they might think I might wish to hear them
say. All subjects are then given copies of the BDI and the ASQ and
asked to complete them. The order of the two questionnaires is
counterbalanced. While subjects complete these questionnaires, a sign-
up sheet will be passed around which lists all available time slots :for

the second part of the experiment, Time Two.

38

Subjects are assigned to their VMIP treatment condition (happy,
sad, neutral) by a stratified sampling procedure. The stratified sample
is high vs. low A.S.Q.-B score, using a median split of Time One A.S.Q.-
B scores. Subjects do not learn which group they have been assigned to
until the debriefing.

Time Two is at least one week later. At Time Two, each subject
is alone in a room and a tape recorder is turned on; this entire part of
the experiment is automated via the tape recording. In the room there
are also a set of 4 x 6 index cards, a manilla envelope (containing
questionnaires), a pencil, and two questionnaires atop the manilla
envelOpe. The tape recording initially instructs subjects to turn off
the machine, complete the two loose questionnaires, and then turn on the
machine. These two questionnaires are the PFS and the MAACL. The order
of these questionnaires is counterbalanced.

Tape-recorded instructions then ask subjects to read aloud and
think about a series of statements, which are typed on the 4 x 6 inch
index cards. At fifteen second intervals the tape recording tells the
subjects to move on to a new card. Each subject reads a total of
60 VMIP statements; statements differ depending on treatment condition.
Upon completion, they are instructed to open the manilla envelope, take
out the questionnaires, and complete them in the order presented; they
are again asked to turn off the tape recorder while they work, and turn
it on upon completion. These questionnaires are a second cOpy of all
questionnaires already once completed, namely a second BDI, PFS, MAACL
and ASQ; these are in counterbalanced order. When these questionnaires
are completed, subjects are instructed to find the blank paper and, on

signal, to begin writing numbers in descending order from 100. I

39

remained available throughout the experiments to monitor any
difficulties.

Subjects are then debriefed and dismissed. For the subjects in
the sad mood condition, part of the debriefing consists of reading
through a subset of elation statements to insure that no residual
negative moods remain at the end of the experiment; this technique has
been successfully used in most mood induction studies. In the unlikely
event that any subject had continued to feel very sad, I planned to
offer this subject a home phone number where I could be reached.

The design of Experiment One is summarized in Table 2-A.

Experiment Two

 

Subjects and Measures

 

Subjects for experiment two were 24 male and 23 female
undergraduate volunteers.
This experiment uses the same questionnaires employed in

Experiment One: BDI, MAACL, ASQ and PFS.

Procedure

The first part of the experiment is similar to the procedure
used in Time One of Experiment One. Subjects sign consent forms after a
brief explanation, subjects are warned about experimenter demand
characteristics, and subjects then complete the BDI and ASQ. Two
modifications are introduced: there is no sign-up sheet as there will
be no second time for this experiment, and subjects also complete the
PFS and the MAACL. The four questionnaires are distributed in a

counterbalanced order.

TABLE 2

4O

DESIGN OF EXPERIMENTS ONE AND TWO

 

 

Experiment One (N=62)

 

Time One (all subjects
together in one room)

Time Two (each subject alone in a
room; at least one week later)

 

. Subjects Sign Consent Forms

Subjects Warned of Experi-
menter Demand Characteristics

. Subjects Complete BDI & ASQ*

. Subjects Sign Up for Time

Two of Experiment

5.
6.

Subject is Randomly Assigned to
Happy, Sad or Neutral Condition
(Prior to Arrival)

. Subject Completes MAACL & PFS*

. Subject Reads VMIP Statements Aloud

(Happy, Neutral or Sad Statements)

. Subject Completes MAACL, PFS, BDI

& ASQ*
Subject Completes Counting Task
Subject Debriefed

 

Experiment Two (N=47)

 

Subjects Sign Consent Forms

Subjects Warned of Possible Experimenter Demand Characteristics
Subjects Complete BDI, ASQ, MAACL, PFS*
Subjects are Randomly Divided into Two Equal Groups and Sent to

Two Rooms

Subjects in One Room Watch the Mbvie "Peege" Designed to Create a Sad
MOod; Subjects in the Second Room Watch a Mood Neutral Science Mbvie

 

6. After the Mbvie, All Subjects Complete BDI, ASQ, MAACL, & PFS*
7. Subjects Debriefed

*

Order of questionnaires is counter-balanced.

ASQ = Attributional Style Questionnaire

BDI = Beck Depression Inventory

PFS = Personal Feelings Scale

MAACL = Multiple Affect Adjective Check List

41

Subjects are then randomly divided into two groups and sent to
different rooms. In each room they see a movie. In one room, they see
”Peege" a movie about a family visit to a dying grandmother in an old
age home. This movie is designed to elicit sad or depressed feelings.

In the second room they see "Triple Play,’ a neutral science movie about
hydraulics. Movies have frequently been used to induce mood changes
(e.g. Averill, 1969; Zuckerman, Lubin, Vogel, & Valerius, 1964). The
movies used in this experiment were chosen in consultation with the
Michigan State University film librarian. The last few minutes of
"Peege," which were slightly optimistic in tone, are cut out in the
showing. After the movie is shown, the BDI, ASQ, MAACL and PFS are

redistributed in counterbalanced order and subjects again complete them.

The design of Experiment Two appears in Table 2-B.

Plan of Analysis

 

The two experiments are related by the logic of multi-trait
nulti-method analysis. The VMIP induction of experiment one and the
movie induction of experiment two are two quite different methods of
creating mood change, so any hypotheses supported in both experiments
are clearly not just method specific. Each experiment uses various

measures of depression, which provide convergent validation of the

 

induction effect (and of the hypotheses). Finally, if various moods and
emotions are tested and the inductions only change the predicted mood,

then discriminant validation has been achieved for the inductions.

 

If (and only if) the inductions work, then the specific
hypotheses can be tested. The thought first hypotheses always turn on a
simple comparison of means: in a specific treatment condition

(e.g. depression) do subjects high in the relevant attributional style

42

(i.e. depressive attributional style) show higher mood levels than do
the lows? The rationale for this comparison as applied to depression is
as follows. The thought-first model assumes that certain situations
lead to depression; in the two experiments, these situations are
operationalized by the two inductions for depression. However the
thought first model also assumes some people vary in their
susceptibility to depression; the most susceptible are the people high
in depressive attributional style. Thus if the thought-first model were
correct, then in the depression inducing treatment, the most depression
ought to occur among those people initially high in a depressive
attributional style. By similar reasoning, the thought-first model of
elation is proven if in the elation treatment, people high in elation
attribution style show more elation than people low in this thought
style.

The affect first hypotheses depend on an equally simple but
quite different comparison: use attributional style as the dependent
measure and see if a given treatment (e.g. depression) were causing a
higher level of relevant attributional style (i.e. depressive
attributional style) than the other treatments. The rationale for this
analysis is as follows. The affect first model says that the relation
between depression and depressive attributional style arises from
depression causing a change in the way we think: thought style is not
stable but changes as level of depression changes. Since we already
know that the depressive treatment is causing more depression than the
other treatments, then if the affect-first model were correct, subjects
in this treatment should also show a significantly higher level in their

depressive attributional style too. By similar reasoning, the affect

43

first hypothesis on elation is confirmed if there were a main effect of
treatment on elation attributional style and if subjects in the elation
condition show the highest elation attribution style score.

Experiment one basically uses a 2 x 3 analysis of covariance
with two levels of attributional style (high, low) and three types of
treatment (depression, neutral, elation). In experiment two, the basic
analysis of covariance is a 2 x 2 x 2 analysis with two levels of
attributional style (high, low) two treatments (depression, neutral) and

sex (male , female).

CHAPTER 4

RESULTS

Discriminant Validation

 

Affirmative findings for any of the four hypotheses would be
further strengthened if it could be demonstrated that the various
inductions create only their predicted mood change and no other
emotional change. Consider, for example, hypothesis three, which claims
that changes in depressive attributional style are actually caused by
changes in depression. If the depressive induction does create more
than just depression-"perhaps also creating significantly more boredom
or more intensity--than one cannot be certain what caused the change 111
attributional style: was it change in depression, or was it the change
in boredom or intensity?

Clearly one cannot test every possible additional emotixna, but
the MAACL can be rescored for both hostility and anxiety in additior: to
depression. All three emotional states are tested separately. Finding
significant changes on hostility or anxiety would not vitiate earlier
support of the four hypotheses, since there is no theoretical reason for
these moods to change attributional style or depression, but lack of
such findings would strengthen the logic of the experiment.

In experiment one, Table 3 addresses the issue of discriminant
validation for the VMIP mood induction procedures. This table presents

the results of three different 1 x 3 analyses of covariance (one mood x

44

45

three treatments) for three different measures of mood on the MAACL;
each analysis controls for initial level of mood.

There was a significant treatment effect for MAACL depression.
An inspection of the means for MAACL-depression in Table 3 indicates the
depressed moods were in the predicted directions: the depressive
treatment created the highest level of depression, the neutral treatment
created a middle level of depression, and the lowest depression (or
highest elation) was in the elation treatment. Thus both the depression
treatment and the elation treatment worked as expected.

Unfortunately, Table 3 also indicates that the VMIP did more
than just change levels of depression. There were also significant main
effects for anxiety and hostility. In the case of anxiety, the means in
Table 3 indicate that change in anxiety level came solely from the
elation treatment. The depression treatments and neutral treatments
showed almost equal levels of anxiety, while the elation treatment was
only two-thirds as large. For anxiety to drop in the elation treatment
makes intuitive sense, although it was not predicted. After all, if the
elation treatment were working and the mood of subjects were improving,
these subjects may have found they were growing more confident and more
relaxed, and hence less anxious.

The treatment effects on hostility are less easy to explain, as
the level of hostility seemed positively related to level of depression.
One possible explanation is that the hostility levels reflected how
enjoyable each treatment was: hostility went up most in subjects placed
in the depression treatment since they realized they had been placed in
an unpleasant experience; hostility went up slightly in the neutral

condition since it was not very interesting to recite factual

46

Ho.vq«««

 

 

 

unmaumoua doaumam unusumona Hmuusoz

uaoaumoua aowmmounon

mo.vm «a
.«An.m N _ Hm. oo.e _ Hm. m~.k _ a“. an.o _ suaaaumoa
“ u n “ aau<<z
.««wm.n N _ mm. ne.n _ mm. Ho.m _ as. as.» _ sumaxea
“ n n “ uaoa<z
.«ma.m N _ ow.H mm.oH _ ma.~ -.mH _ HR.H ma.sa _ aoammuuame
_ _ _ _ _ ugu<<z
_ mm x _ am 2 _ am 2 _
m up _ +| + _ ouusom
_ “omuzv _ Aomuzv _ Ammuzv _
_ _ _ _

 

 

Avoaaouuaoo mouoom unmaumouumumv
monHHQZOU HszH<MMH mo ZOHHUZDm < m< WHHAHHmom .VBMHNZ< .ZOHmmmmmmn umzo HszHmmNNm

m mqm<a

47

statements; and hostility remained unchanged or even decreased in the
elation treatment since subjects actually enjoyed reading aloud those
uplifting statements. But whatever the explanation, the VMIP depression
and elation conditions did more than just effect depression and elation,
respectively.

Experiment two only had a neutral and a depression treatment,
but because it used men and women, sex also had to be considered as a
factor. Table 4 presents MAACL depression, anxiety, and hostility as a
function of sex and treatment. Each mood was analysed by a 1 x 2 x 2
analysis of covariance, controlling for initial mood; the results
suggest subjects cannot be pooled across sex. There was a significant
main effect for treatment when depression was analyzed, and the
depression adjusted means in Table 4 clearly indicate that the treatment
effect was in the right direction: the depressive treatment created
higher depression scores than the the neutral treatment.

Hostility levels remained the same for both men and women in the
experiment two treatment, but in the case of anxiety, there were
significant effects for treatment, sex, and sex-treatment interaction.
The depressive treatment made subjects more anxious than the neutral
treatment; this effect was not predicted, but it is sensible given the
nature of the depression movie’s subject matter, namely death and dying.
Women were generally more anxious than men, and the interaction came
because women in the depressive treatment were especially anxious.
Again, women may have been more sensitive than men to this subject

matter.

48

mo.vm ««

 

 

 

 

uaoaumoue x NO xom uaoaumoufi

0H.va «
«em.~ H _ on.~ H_««ma.m H_Ho.~ ma.nH Hm.~ m~.oH_oo.~ oe.o~ on.~ mH.mH_aonmmuame
“ u n n " uHo<<z
«mm.~ H _««Ho.s H_«eHn.m H_HH.H mm.e oo.H em.e _oo.H ~.HH oo.H om.“ _ sHmecm
_ _ _ n “ saueez
_ _ _
mm.H H _ as. H_ so. H_eH.H mo.m No.H mH.m .mo.H -H.¢ Ho.H Ha.o _ AHHHHHmon
_ _ _ _ _ uHo<<z
_ _ _ _ _
_ _ _ am z am 2 _ am z am 2 _
a He _ a He_ a He_ + _
_ _ _HHHuzv case: ANH-zv amz_H~Huzv Emacs A~Huzv aux. oceans:
L1 A L+ + _
m_ _ _

uaoaumoua Houuamz _ uaoaumous cowmmounon

 

 

HeaHHouueoo museum uaoauwmuumumv ezmza<mma oz< xmm mo
oneuzns < m< wsHHHemom nz< samez< .onmmmmmma Hogs ezmzHammxm

e mqm<fi

49

Convergent Validation

 

Convergent validation was inspected on four measures of
depression; the Beck Depression Inventory (BDI); the Personal Feelings
Scale (PFS); the depression sub-scale of the Multiple Affect Adjective
Check List (MAACL-d); and the Counting Task. The latter only appeared
in experiment one. On the BDI, the PFS, and the MAACL, the dependent
measure was post-induction depression with pre-induction depression
controlled. All three were analysed using analysis of covariance. The
Counting Task was analysed by analysis of variance. These analyses
appear in Table SfiA for experiment one and Table 6mA for experiment two.
If the depression and elation treatments worked, there should have been
a significant main effect for treatment, along with the highest
depression score in the depression treatment and the lowest in the
elation treatment.

As column one of Table 5-A indicates, on experiment one three
measures of depression (the BDI, the PFS, and the MAACL) showed a
significant treatment effect. Inspection of the means indicates that on
all three measures, subjects in the depressive VMIP treatment showed the
highest post-induction levels of depression. These results provide
further evidence that the depression treatment successfully increased
depression more than the neutral or elation treatments.

The Counting Task alone did not show any significant treatment
effects in experiment one. There are at least two possible explanations
for this. The first explanation is that the VMIP depression treatment
changed the way subjects felt about themselves, and hence changed
various self-report measures, but was not strong enough to translate

into actual behavior. The second explanation has to do with the order

50

TABLE 5

EXPERIMENT ONE: ANALYSES OF COVARIANCE FOR
DEPRESSIVE ATTRIBUTIONAL STYLE SUBJECTS (ASQ-B)

 

 

 

I I IExperimental

I Experimental I ASQ-B I Treatment
Measures I Treatment I(High vs. Low)I X ASQ-B

l 4. e

Idf MS F Idf MS F Idf MS F

 

A. Depression Measures
(pre-score controlled)

 

MAACL-Depression I

Counting Task1 I I I
(N=62) I 2 7.86 .093 | 1 5.82 .07I 2 44.89 .53
I I l
BDI l | l
(N=62) | 2 53.21 2.40* | 1 17.21 .78| 2 26.05 1.18
l l I
PFS | I l
(N=6l) | 2 113.72 8.23****l 1 15.43 1.12| 2 10.18 .74
I l
l l
l l

 

 

 

(N=62) 2 247.11 3.89** 1 67.86 1.07I 2 72.91 1.15
B. Depressive Attributional Style Measure
(pre ASQ-B Controlled)

ASQ-B l l l

(N=62) I 2 131.65 1.22 I 1 6.95 .O7I 2 38.65 .36
* p<.10
** p<.05
****p<.OOl

1
No pre-induction score, so reported means are unadjusted.

of the Counting Task within the overall experiment: the Counting Task
began when all post-induction questionnaires had been completed. This
was usually some ten to twenty minutes after the induction had
concluded. It is thus possible that the treatment effects had worn ()ff
by the time subjects started the Counting Task. Either of these
explanations suggests that the generalizability from this induction to

real depression is limited, since either the induction effects were tcu:

51

weak to translate into behavior or else they were too transient to lxast
more than twenty minutes. Real depression affects behavior and lasts
more than a half hour.

MaTable 6-A, column one indicates, the experiment two
depression treatment also created significantly higher levels of
depression on all three measures of depression (Beck Depression
Inventory, Personal Feelings Scale, and Multiple Affect Adjective Check
List-depression subscale). The PFS also showed a significant main
effect of sex; inspection of the means indicates this was because women
showed more depression on the PFS than men. Finally, the MAACL-
depression showed a significant interaction of sex and treatment: within
the depression treatment, female depression scores were almost half
again as large as the male scores. Just why women would have reacted
more strongly than men to the treatment is unclear. Perhaps women were
more sensitive to issues of object loss or perhaps they were more
willing to admit such feelings; the difference might also be related t1)
the sex of the protagonist in the depression movie. The movie was about
an infirm and dying grandmother, so perhaps the women were more upset
because they could identify more clearly with the protagonist.

The results of the elation induction are presented in column 1
of Table 7-A: there were significant treatment effects on two of the
three measures (PFS and MAACL-D) in the 2 x 3 analysis of covariance,
(controlling for initial mood level). In this analysis, elation was
Operationally defined as low scores on the depression measures.
Inspection of the means shows that the mood change was in the expected
direction: elation treatment lowered depression. Only the BDI failed to

show a significant treatment effect on mood, and as noted in description

52

TABLE 6

EXPERIMENT TWO: ANALYSES OF COVARIANCE FOR DEPRESSIVE
ATTRIBUTIONAL STYLE SUBJECTS (Pre-score Controlled) (N=47)

 

 

IB. Depressive

 

 

 

l
I A. Depression Measures IAttributional
I (pre-score controlled) IStyle Measure
Measures I I
I BDI I PFS I MAACL-D I
I :— : I df F
Idf F Idf F Idf F l
Treatment I 1 3.01* I 1 3.10*I l 6.11**I l 1.0
I l I I
ASQ‘B (high vs. 10W)I 1 2.20 I 1 .78 I 1 2.35 I 1 2.05
I l l I
Sex I 1 1.66 I 1 4.79**I 1 2.36 I 1 6.30**
I l l l
Treatment x I I I I
ASQ-B I l 1.29 I 1 1.60 I 1 1.35 I l .08
I I l l
Treatment x I I I I
Sex I 1 .31 I 1 2.64 I 1 3.10* I 1 .14
l I I I
ASQéB x I I I I
Sex I 1 2.21 I 1 .84 I 1 .04 | 1 .31
I I I |
Treatment x I I I I
ASQ-B x Sex I 1 .01 I 1 .41 l 1 .84 I 1 1.23

 

1Pre- and post scores were not significantly related, so controls

for pre-scores were not entered.
* p<.10
** p<.05

of the measures (pg. 36), this measure is not as apprOpriate for

measuring elation as is the PFS or the MAACL.

Depression Hypotheses

 

The depression inductions clearly created some depression, so
the two depression hypotheses (one and three) could be tested.
Hypothesis three, the affect-first hypothesis on depression is

considered first. This hypothesis says that higher depression created

53

TABLE 7

EXPERIMENT ONE: ANALYSES OF VARIANCE FOR ELATION
ATTRIBUTIONAL STYLE SUBJECTS (ASQ-G)

 

 

 

 

 

 

 

 

 

I Experimental I ASQ-G IExperimental
I Treatment I (high vs. low) I Treatment
MEasures I +~ I X ASQ-G
l I I-
Idf MS F I df MS F Idf MS F
A. Depression Measures (pre-score controlled)
BDI I I l
(N=62) I 2 51.58 2.26 I 1 10.42 .46 I 2 9.81 .43
I I I
PFS l l I
(N-61) I 2 114.37 8.85****I 1 53.40 4.13**I 2 15.40 1.19
I I I
MAACL-Depressionl I I
(N=62) I 2 254.78 4.07** I 1 66.80 1.07 I 2 98.2 1.57
B. Elation Attributional Style (ASQ-G) Measures
(preéASQ-G controlled)
ASQ-G I 2 274.40 1.63 I1.63 1 141.53 .84 I 2 25.99 .154
** p<.05
****p<.001

higher depression attribution style. For this hypothesis to be
confirmed, subjects in the depression treatment would have to stun: the
highest post-induction levels of depression attribution style. In
experiments one and two, Tables 5-B and 6-B respectively indicate that
there were no significant effects of treatment on depressive attribution
style. Hypothesis three was not confirmed. There was no evidence tIuat
dqnessive attribution style levels were altered by levels of
depression.

h>test1wpothesis one (the thought-first hypothesis on
depression), subjects were sorted into high vs. low depressive

attributional style groups. In experiment one this occurred before tIue

54

second experimental session. Experiment two subjects had only one
session. They were therefore ranked according to their pre-induction
depressive attributional style score (ASQ-B) and a median split was
obtained. Subjects above the median were called "high depressive
attributional style" subjects while subjects below the median were the
low depressive attributional style subjects (low ASQéB).

Hypothesis one was tested in experiments one and two by
inspecting the subjects in the depression treatment: if high depressive
attributional style subjects showed significantly more depression than
the low ASQ-B subjects, the hypothesis was confirmed. The test for
significance is a simple, one-tailed comparison of the difference in
means (t test). In experiment two, separate analyses had to be
performed on the men and the women because there was a significant main
effect of sex and a significant interaction involving sex.

The experiment one results of the test of hypothesis one are
presented in Table 8; this table looks at subjects in the depression
treatment and compares adjusted and unadjusted mean depression scores of
high depressive attributional style subjects (high ASQ-B) with the means
of low ASQ-B subjects. When the unadjusted means are considered
(columns 2 and 3), then only one measure, the MAACL-D, showed that high
ASQ-B had higher depression scores, as predicted. But Table 8,
column 4, also indicates that pre-induction and post-induction
depression scores significantly covaried, so the apprOpriate comparison
should use the adjusted means, columns 5 and 6. With adjusted means,
the PFS high ASQ-B subjects also showed the predicted higher level of
depression. However this difference was not significant. The only

significant difference was on the MAACL-D; since this difference was

55

both significant and in the predicted direction, hypothesis one was
supported in experiment one.

Table 9 presents the critical test from experiment two of the
thought-first hypothesis regarding depression, hypothesis one. Men and
women were analyzed separately because of sex effects and interactions.
Since pre-induction depression scores always covaried significantly with
post-induction depression scores, the preferred comparison used adjusted
means, columns 5 and 6. Hypothesis one predicts that in the depressitn1
treatment high ASQ-B women would show more depression than low women and
this was true on two depression measures, the BDI and the MAACL.
However none of the differences in means were significant, so hypothesis
one was not supported.

For men, all three depression measures showed differences in
adjusted means occurring in the predicted direction. In addition, the
size of these differences was significant on the BDI and the MAACL.
Thus hypothesis one was supported for men although it was not supported
for the women. Why there should be a difference by sex is not fully
clear, but the lack of results for women may in part arise because the
N’s in each cell became quite small when we divided both by sex and by
ASQ-B level. Indeed the N’s were so small that getting results for"the

men was more surprising than getting no results for the women.

Elation Hypotheses

 

Since the elation treatment created elation, the elation
hypotheses (two and four) were tested. The affect first hypothesis on
elation, hypothesis four, was considered first. This hypothesis says
higher elation creates a higher elation attributional style (ASQ-G). As

Table 7-B indicates, there was no main effect for treatment when elation

56

neon eeHHeuueeo .mo.veee

 

 

 

 

Aaowumfl>on vumcamum voumsfiv<v
aowwmouaoa voumnmo<

oowmmoumoa

_ Ame.~v Hoe.~v _ oooo.ue _ _
«.me.Hnu _ ne.eH Hm.ow _ oH.me-e _ eH.HH oo.H~ _ eIHueez
_ _ _ _
_ AwH.HV HNH.HV _ oooo.ue _ _
eeeOHeHewHeeH _ w~.~H H~.mH _ om.HoH-e _ ao.wH me.HH _ wee
_ _ _ _
_ Hee.HV H~3.HV _ Nooo.ue _ _
HeeOHHHemeeH _ Ne.e ee.H _ Ne.mHue _ Hw.H we.“ _ Hem
_ muom< 36H maom< eme _ _ HHanv AHHqu
memo: aw _ _ mouoom umom was Ioum _ miom< sou mlomd swam
monouOMMHQ _ _ mo oocmwum>oo _ ouammmz
_ _ _
_ _ _

 

 

mHzmzH<mme m>HmmmMmma zH nmI0m<v mfiumhmam mqwhm A<ZOHHDmHMHH<
m>Hmmmmmma 304 .m> ZOHm mom mmmoum onmmmmmmo "mzo HszHMmmNm

w m4m<fi

57

Home eoHHeuuoee .mo.veee
umou voaamuloao .o~.vn «

 

 

 

 

 

 

«me.Hne _ Hee.mv Ame.no _ _ _ eeHeeoeeue
_ me.mH e~.- _ _ oo.~H mm.n~ _ uHo<<z
_ _ _ _
_ HeH.HV Hom.Hv _ _ _
HeEOHHHewHeeH . oH.eH no.eH _ _ HH.eH He.o~ _ mes
_ _ _ _
«sum.alu _ Ann.Hv Ann.av _ _ _
_ e~.m Ho.n _ _ n.~ n.n _ Ham
ea: .HH
_ H~e.mo Awe.mv _ Hoo.ne _ _
HeeOHHHewHeeH _ He.e~ n~.e~ _ om.mne _ oo.m~ mm.Hn _eeHee0eeeeIHo<<z
_ _ _ _
_ HoH.HV HNH.HV _ Hooo.ue _ _
HeeOHeHemHeeH _ se.- em.o~ _ ee.mH-m _ oo.m~ HH.- _ men
_ _ _ _
_ Hem.Ho Hem.Ho _ ooo.ue _ _
HeeueeeemHeeH _ Hn.n n.e _ NH.meue _ o.e on.» _ Hem
am:— 03 e H
_ evome 6H ewom< Hm _ _ Aenzv euzv
mama: aw monouowmqn- museum:

_HeeHueH>ee eeeeeeum eeueene<v_
nowmmmuamn woumafin<

mo ooamaum>oo

 

_
I_mouoom umom was loam—mlam< on mTom< «m—
_
_

noummoumon

 

 

azmza<mma u>Hmmmmema zH Amuomev meomnmam mawam H<ona=mHmea<

gHmmmMmmo g..— .m> MUHm mom wumoum ZOHmmmEm—n

m m4m<fi

“one Hzmszmmxm

58

attributional style was the dependent measure. This meant that subjects
in the elation treatment received no higher ASQ-G scores after the
induction than did subjects in the other treatments. There was thus TH)
evidence that elation thought style was changing as elation mood was
boosted, and hypothesis four was not confirmed.1

Table 10 addresses the thought-first hypothesis on elation,
hypothesis three, which predicts that subjects high in elation
attribution style would show more elation following elation mood
treatment than would subjects low in ASQ-G. Only subjects placed in the
elation treatment in experiment one were considered in this table, and
theeflation moods of subjects initially high in their elation
attribution style (high ASQ-G) were compared with the moods of low ASQ-G
subjects. Subjects were ranked by elation attribution style level and a
median split was obtained to create the high and low ASQ-G groups. High
ASQ-G subjects always showed more elation than low ASQ-G subjects. 'The
pre-induction and post-induction scores of elation always significantdjr
co-varied, so the adjusted means were used for comparison. Even when
initial levels of elation were thus controlled, the high ASQ-G subjects
always responded to the elation treatment by obtaining higher elation
than the low ASQ-G subjects. This pattern, predicted by hypothesis
three, was consistent across the three measures of elation. However
none of these differences were significant, so hypothesis three could
not be confirmed. Since experiment two had no elation treatment, therwa

was no test of the elation hypotheses in experiment two.

Summary of Results

 

1) The elation and the two depression treatments created their expected

mood changes, but they also created additional emotional changes.

59

 

 

 

 

HeeuHHHewHeeH_ HHm.~v HNn.NV _ oooo.ue _ _
_ em.m H¢.HH _ mm.~elm _ oo.m oo.a _:owmmouaonlqo<<z

_ _ _ _

HeeuHHHewHeeH_ Ao~.Hv AeH.HV _ oooo.ne _ _
_ wo.qH NN.¢H _ Na.~oHlm _ NN.~ oq.~ _ mam

_ _ _ _

HeeuHeHemHeeH_ AHn.HV HNm.Hv _ eooo.ne _ _
_ Hm.n mn.m _ mm.mH|m _ om.n o~.o _ Ham

_ ouome 36H oucm< eme _ _ HoHuzv AoHuzv _
memo: cw _ n_ mouoow umom mam _UIOm< 30A 0I0m< :wwm_ museum:

mucoumwman _Aaoaumw>mn vumvcmum woumsfip<v_loum mo oocmwum>oo_ _

_ cowmmoumon\=owumam wouwsfiv< _ _ coaumam\aowmmoumoa _

 

 

HZMEH<MMH ZOHH<AM zH Aulom<v mHUMHmDm A<ZOHHDmHMHH< ZOHH<AM
30A .w> mUHm mom mmmoom ZOHH<AMIonmmmmme umzo Hzmszmmxm

OH mqm<H

2)

3)

4)

60

The thought-first hypothesis on depression was significantly
supported on one of three depression measures in experiment one and
on two of three depression measures for the men in experiment two.
Low attribution style subjects in the apprOpriate treatment were
never significantly higher than high attribution style subjects,. so
whenever the difference in means was significant, it was in the
predicted direction.

There was no support for the affect first hypothesis of depression.
There was no support for either the affect-first or the thought-

first models of elation.

Footnote

1Furthermore, introducing a second covariate to control for

initial depression level made no appreciable difference. The following
covariates were attempted, and none made the results significant: pre
BDI; z score for pre PFS + pre MAACL; z scores for pre PFS + pre MAACL +
pre BDI.

 

 

 

CHAPTER 5

DISCUSSION OF RESULTS

This conclusion section will first discuss the elation
hypotheses. It will then consider the thought-first model of depression

and follow this by a discussion of the affect-first model.

Elation Models

 

The hypotheses of this experiment were derived from two models
of human depression. The elation hypotheses were not based on empirical
research about elation nor were they based on a separate theory of
elation; instead they were derived by extending the logic behind the
depression models to cover elation, a related but different mood. In
particular, the attribution theory of depression related depression to a
way of processing information about unpleasant events: people who laid
the blame for these events outside of themselves escaped depression,
while peOple who attributed these unpleasant outcomes to some feature of
their own personality became depressed. It seemed logical that a
similar situation might exist with regard to good events: some peOple
might be especially apt to take personal credit for good events and feel
terrific about themselves while other people are less apt to take credit
for these pleasant events and thus would be less apt to reap the
dividend of good or elated feelings. And just as the causal direction
between depression and depressive attributions lay open to question,

especially given the alternative affect-first model of depression, so

61

62

too the causal direction between elated mood and elated thought style
was unclear.

The results of this experiment cannot be used to support either
the thought-first of the affect-first models of elation. In part the
failure of the results to distinguish between the two models may arise
because the paradigms derived from depression may not be directly
transferable to elation. In addition, the measures in this experiment
were measures initially derived from theories of and research with
depression, and these measures may not be suitable to elation. Thus the
Attribution Style Questionnaire may not be measuring the essential
thought processes conducive to elation. The dependent measures of
depression may likewise not work as measures of elation: in this
experiment, elation was operationally defined as the absence of
depression, whereas in reality elation might be a singular mood,
unrelated or perhaps more than the mere absence of depression. Thus any
future studies specifically aimed at investigating the thought-first or
affect-first models of elation should begin with measures both

specifically designed to measure elation and validated with elation.

Thought-First Model of Depression

 

The thought-first model, as represented by the attribution
theory of depression, was supported by this experiment. The critical
test of this theory was whether the depressive treatment created more
depression in the high depressive attributional style subjects (high
ASQ-B) than in the low ASQ-B subjects. There were nine of these
critical tests: three depression measures were tested in experiment one,

and three each were tested for men and for women separately in

63

experiment two. Of these nine tests, three were significant in the
predicted direction and the other six were insignificant. Thus where
the difference in means did reach a level of significance, the direction
was always in the predicted direction. When additional factors are
considered-mamely the very small N’s in each box of the critical tests
(N’s-six per box on the six critical tests in experiment two) and that
support was not method specific, occurring in two quite different
treatments--then the support for the attribution theory is all the more
striking.

But before considering any clinical applications of this theory,
the limitations of the experiment must also be considered. The primary
question is whether this is a study of an analogue of depression or a
study of a real (albeit induced) depression. There are two pieces of
evidence which shed light on this issue. The first is the failure in
experiment one of the Counting Task even when all self-report measures
showed a significant depressed mood in the treatment condition. Two
explanations were offered for this failure of the Counting Task to be
affected by the induction: either the induction was too weak to change
behavior (as opposed to changing self-reported feelings) or else the
induction had worn off in the ten to twenty minutes between the end of
the induction and the completion of the questionnaires, when the
Counting Task started. Either explanation suggests the induction
created a depressed mood rather than real clinical depression.

The second piece of evidence on this issue is more clear-cut.
On one of the three depression measures, the BDI, there exist normative
data which compare clinical depression with levels in the normal

population. We can thus see if the levels of depression created by the

64

inductions reached the levels of clinical depression. On the BDI,
clinical depression for experimental purposes begins at a score of 9.
In experiment one, the experimental treatment created a mean BDI score
of 8.4; on this measure in experiment two, the men have a score of five
and the women of six. This means that neither induction created
clinical depression.

If the inductions were only creating mood changes and not
clinical depression, then the direction of future research is clear.
The relation found in this experiment between attribution style and
depressed mood must now be repeated in a naturalistic experiment, and
this relationship must also be demonstrated to exist at levels of
clinical depression. These two research directions will be discussed in
turn.

Experimental studies are powerful research tools but somewhat
artificial. NOw that we have experimentally demonstrated how depressive
attribution style predicts later depression, this relationship must also
be explored outside the laboratory, in the real world. It should be
possible to measure depressive attributional style in a group of peOple
and to follow them over time to see if the high depressive attributional
style peOple were more prone to depression following bad events.
Seligman et a1 (1979) say they are currently Imdertaking such a study.
One possible way to conduct this study would be as follows: use the
attributional style questionnaire to obtain a measure of depressive
attributional style on a large group of incoming undergraduates before
they arrive at college, and later see if their depressive attribution
score predicts a depressive response to either leaving home or to any

failure experiences when the first set of grades are returned. To

65

accurately test the theory, students would have to be controlled on
their levels of intelligence and previous academic success. Some
measure of ambition (or an ambition/ability ratio) might be obtained
too, as some alternative theories of depression say that depression will
arise if ambition exceeds ability (i.e. excessively high narcissistic
goals), presumably independent of depressive attributional style.
Finally the dependent variables measuring later depression will have to
be inspected to see if results indicate only depressive mood or the more
serious and higher scores of clinical depression.

A similar study could be undertaken in a clinical pOpulation.
People who obtained clinical help for their depression could be tested
upon discharge (from hospital or from out-patient clinic) for their
level of depressive attributional style (controlled for level of
depression at discharge). Follow-up studies could then be attempted to
see if peOple with high depressive attributional styles were more likely

to later suffer a recurrence of depressive episodes.

Affect-First Model of Depression

 

The affect-first model suggests that the thought-first features
of depression such as attributional style are not the causes of
depression but merely the result of depression, and likely to go up as
levels of depression increase. This study provides no support for the
affect-first model: in both experiments, treatments which significantly
increased depression had no significant effect on changing depressive
attributional style.

Does this mean the affect first model should be dismissed? And
if not, what future research should be attempted to test the affect-

first model?

66

The first question is easier to answer than the second. An
accurate test of the affect-first model would change moods without
subjects being aware of what had caused this change. As noted in
Chapter One, current informed consent procedures make this impossible.
Since the experiment only partially tests the affect-first model, the
results are more suggestive than conclusive. It is too soon, pending
further studies, to dismiss the affect-first model.

What these further studies could be remains a difficult
question. In the last year there has been a renewal of interest in how
information and especially affect can be processed outside of conscious
awareness (Shevrin & Dickman, 1980; Zajonc, 1980). For example, Wilson
1979) found that during a dichotomous listening task, people given
information at below threshhold levels showed an affective response to
this information--a liking response--even when they could not identify
the information. Such dichotomous listening experiments might
eventually be used to see if affective information is unconsciously
'processed in a different way during depression.

A second, albeit indirect approach, would derive from affect-
first theories those personality types thought to be prone to
depression. The key to such an approach is obtaining a personality
criterion not related to the processing of external information. If the
criterion could be operationalized, a new set of depression-prone
subjects could be identified. If they showed a wide range of
attributional styles, then they could be studied in a fashion similar to
the future research proposed for the thought-first model: such people
could be followed over time to see if they were more depression prone

than controls (with levels of depressive at tributional style being

67

controlled). An example of this approach is provided by Blatt (1974)
who has extended psychoanalytic object relations theory to depression.
He has recently started to devise ways of empirically identifying
various depression-prone personality types based on his theoretical

extension (Blatt, S., D’Afflitti, J. P., & Quinlan, D. M., 1976).

Two Models or One?

 

A basic premise of this study was that there are two
fundamentally different models of depression. Before these models are
set aside, one last possibility must be considered in passing: these
models, however different, may be alternate aspects of a single on-going
process in which affect alters thought which alters affect which alters
thought, etc. In reality, perhaps, the relation between depressed
thought and depressed affect may be closer to a feed-back 100p.

In part this feed-back possibility arises from an inadequacy of
the cognitive theories noted earlier. These theories do not explain
whence there arise the differences in thought-style that the cognitive
theories describe so well. After all, why should one person develop a
depressive attributional thought-style while another develops a less
pathogenic cognitive pattern? Bowlby (1980) has suggested that the
cognitive theories are incomplete because they omit any etiological
explanation, and he suggests Beck’s theory can be subsumed under his own
theory of early attachment difficulties (most especially loss) creating
depressogenic thought patterns.

However there is another body of deveIOpmental research which
suggests that there exist temperamental differences from birth, and that
among these temperamental differences are mood variations (Buss, A. ,

Plomin, R., & Willerman, L., 1973; Scarr, S., 1969; Thomas, A.,

68

Chess, 3. & Birch, H., 1968). The work of Thomas et al in particular
suggests that there are some infants whose emotional temperament leaves
them especially vulnerable to behavior disorders. Perhaps the origin of
depressive thinking likewise arises out of the interaction between
inherited mood characteristics and particular environments (e.g., earJJr
loss experiences). This line of reasoning can only be investigated by

careful developmental research.

CHAPTER 6

SUMMARY AND CONCLUS ION S

Reviewing the psychological theories of depression revealed a
fundamental disagreement on the nature of the relationship between
depressed thoughts and depression. A set of cognitive theories says
depressions arise because of the interaction between depressogenic
thought styles and painful events. The depressogenic thought patterns
presumably precede the depression and are a central cause of the
subsequent depressions. On the other hand, a second set of theories
says these depressive thought styles arise out of the depression but (10
not precede it and are thus not a cause of depression.

To test these alternate thought-first and affect-first models of
depression, two experiments were conducted. The subjects in the first
experiment were 62 Michigan State University undergraduate women; in the
second experiment, the subjects were 24 male and 23 female M.S.U.
undergraduates.

The two experiments followed a similar design: subjects
completed a set of questionnaires on their thought style, their level of
depression and their mood; they were then randomly assigned to eithe1:.a
control condition or to an experimental condition designed to induce a
mood change; afterwards, the initial questionnaires were again
CMpleted. The two experiments differed in the experimental induction

used to alter mood states and in the timing: in experiment one subjects

69

70

returned for a second session, while experiment two was entirely
completed at one sitting.

Experiment one used the Velten Mood Induction Procedure (or
VMIP) to create neutral, depressed and elated moods. This procedure
consists of having students sit alone in a room and read aloud a set <3f
6O mood related statements. In experiment two, mood was altered by
watching the movie "Peege"; the control group saw a neutral science
movie.

The following instruments were used in both experiments to
measure depressed mood: the Beck Depression Inventory or BDI; the
Multiple Affect Adjective Check List or MAACL; and a Personal Feelings
Scale or PFS. The measure of depressive thought style was the
Attribution Style Questionnaire or ASQ.

The results supported two conclusions. First both inductions
successfully created depressed moods, although the procedures also
induced additional emotions, most noticeably increased anxiety. Second,
there was some support for the thought-first hypotheses of depression.
There were significant predicted differences on one of three depressitnm
comparisons in experiment one and on two of six comparisons in
experiment two. This support is stronger than it seems because sex
interactions in experiment two necessitated separate analyses by sex,
making the cells used for the comparison quite small in size. In
addition, no comparisons were ever significant in a direction Opposite
to the predictions.

The affect-first hypotheses were not supported. Furthermore, no
relation was found between induced elation in experiment one and either

the affect-first model or the thought-first model.

71

The discussion suggested future avenues of research which might
use naturalistic studies rather than experimental studies. The failarre
to find any support for the affect-first model was explained as being
partly due to the experiment’s failure to fully test the affect-first
model, most notably because informed consent procedures made it
impossible to alter mood without subjects being aware of the mood
change. Finally, the discussion raised the possibility that the two

models are actually alternate phases of a single feed-back 100p process.

LIST OF REFERENCES

 

 

LIST OF REFERENCES

Abramson, L., & Sackeim, H. A paradox in depression: Uncontrollability
and self-blame. Psychological Bulletin. 1977, 84, 838-851.

 

Abramson, L., Seligman, M., & Teasdale, J. Learned helplessness in
humans: Critique and reformulation. Journal of Abnormal

 

 

Aderman, D. Elation, depression and helping behavior. Journal of
Personalityand Social Psychology. 1972, _24_, 91-101.

 

 

Akiskal, H., & McKinney W. Depressive disorders: Toward a unified
theory. Science. 1973, 182, 20-29.

Akiskal, H., & McKinney, W. Overview of recent research in depression.
Archives of General Psychiatg. 1975, 3_2, 285-305.

 

Arieti, S. & Bemporad, J. Severe and mild depression. New York: Basic
Books, Inc., 1978.

 

Averill, J. R. Autonomic response patterns. during sadness and mirth.
Psychophysiology. 1969, 5 (4), 399-413.

 

Baldessarini, R. J. The basis for the amine hypothesis in affective
disorders. Archives of General Psychiatry. 1975, 32, 1087.

 

Beck, A. Depression: Clinical, experimental and theoretical aspects.
New York: Harper and Row, 1967.

Beck, A. The development of depression: A cognitive model. In R. J.
Friedman & M. M. Katz (Eds.) The psychology of depression.
washington: Winston‘Wiley, 1974.

Bibring, E. The mechanisms of depression. In P. Greenacre
(Ed.) Affective Disorders. New York: International Universities

Press, 1953.

 

Blaney, P. Contemporary theories of depression: Critique and
comparison. Journal of Abnormal Psychology. 1977, 86 (3),

 

Blatt, S. Levels of object representation in anaclitic and introjective
depression. The Psychoanalytic Study of the Child. 1974, 29,

 

72

73

Blatt, S., D’Afflitti, J. P., & Quinlan, D. M. Experiences of
depression in normal young adults. Journal of Abnormal
Psychology. 1976, 8_5, 383-389.

 

 

Bowlby, J. Attachment and loss volume III: Loss. New York: Basic
Books, 1980.

 

Buss, A. H., Plomin, R., & Willerman, L. The inheritance of
temperament. Journal of Personality, 1973 41_ (4), 513-524.

 

Coleman, R. Manipulation of self-esteem as a determinant of mood of
elated and depressed women. Journal of Abnormal Psychology.
1975, 84, 693-700.

 

Costelo, C. A critical review of Seligman’s laboratory experiments on
learned helplessness and depression in humans. Journal of
Abnormal Psychology. 1978, 7_8 (1), 21-32.

 

 

Depue, R. & Monroe, S. Learned helplessness in the perspective of the
depressive disorders. Journal of Abnormal Psychology. 1978,
87, 3-21.

 

Fawcett, J. Biochemical and neurOpharmacological research on the
affective disorders. In E. J. Anthony & T. Benedek
(Eds.) Depression and human existance. Little Brown & Co. ,
1975.

 

Freud, S. Mourning and melancholia (1917). In P. Rieff (Ed.) General
psychological theory: papers on metapsychology. New York:
Collier Books, 1972.

 

Frost, R., Graf, M., & Becker, J. Self-devaluation and depressed mood.
Journal of Consulting and Clinical Psychology. 1979, 4_7_ (5),
958-62.

 

Goldberg, A. The evolution of psychoanalytic concepts of depression.
In E. J. Anthony & T. Benedek (Eds.) Depression and human
existance. Boston: Little Brown & Co., 1975.

 

 

Gouaux, C. & Gouaux, S. The influence of induced affective states on
the effectiveness of social and nonsocial reinforcers in an

instrumental learning task. Psychonomic Science. 1971, 22,

 

Hale, W., & Strickland, B. The induction of mood states on cognitive

and social behavior. Journal of Consulting and Clinical
Psychology. 1976, E, 155.

 

 

Hamilton, M. A rating scale of depression. Journal of Neurology,
Nerosurgery, and Psychiatry. 1960, 23, 56-62.

 

 

Heider, F. The psychology of interpersonal relations. New York: Wiley,
1958.

 

74

Jacobson, E. Depression. New York: International University Press,
Inc., 1971.

 

Joffe, W. & Sandler, J. Notes on pain, depression and individuation.
Psychoanalytic Stug of the Child. 1965, 29, 294-424.

 

Joffe, W. & Sandler, J. On the concept of pain, with special reference
to depression and psychogenic pain. Journal of Psychosomatic
Research. 1967, _1_1_, 69-75.

 

Kelly, C. Attribution theory in social psychology. In D. Levine
(Ed.) Nebraska Symposium on Motivation (Volume 15). Lincoln:
University of Nebraska Press, 1967.

 

Klein, D., Pencil-Morse, E., & Seligman, M. Depression, learned
helplessness and the attribution of failure. Journal of
Personality and Social Psychology. 1976, 85_, 11-26.

 

 

Kuiper, N. A. Depression and causal attributions for success and
failure. Journal of Personality and Social Psychology. 1978,
i, 236-246.

 

Mandell, A. & Segal, D. Neurochemical aspects of adaptive regulation in
depression: Failure and treatment. In E. J. Anthony &
T. Benedek (Eds.) Depression and Human Existance. Little Br own
& Co., 1975.

 

Matheny, K., & Blue, F. The effects of self-induced mood states on

behavior and physiological arousal. Journal of Clinical
Psychology. 1977, £2 936-40.

 

 

Mendelson, M. Psychoanalytic concepts of depression. New York:
Spectrum Publications, Inc., 1974.

 

Miller, I. W. & Norman, W. H. Learned helplessness in humans: A review
and attribution theory model. Psychological Bulletin. 1979,

 

Natale, M. Effects of induced elation-depression on speech in the
initial interview. Journal of Consulting and Clinical
Psychology. 1977, 4_5, 45-52 (a).

 

 

Natale, M. Induction of mood states and their effect on gaze behaviors.
Journal of Consulting and Clinical Psychology. 1977, 4_5_, 960
(b)-

 

Rizley, R. Depression and distortion in the attribution of causality.
Journal of Abnormal Psychology. 1978, 81, 32-48.

 

Sandler, J. & Joffe, W. G. Notes on childhood depression.
International Journal of Psychoanalysis. 1965, _4_§_, 88-96.

 

Scarr, S. Social introversion-extroversion as a heritable response.
Child Development, 1969, 40, 823-823.

 

75

Scheier, M. & Carver, C. Self-focused attention and the experience of
emotion: Attraction, repulsion, elation and depression. Journal
of Personality and Social Psychology. 1977, 88, 625-36.

 

Schmale, A. A genetic view of affects. The Psychoanalytic Study of the

 

Child. 1964, 13, 287-310.

Schmale, A. & Engel, G. The role of conservation-withdrawal in
depressive reactions. In E. J. Anthony & T. Benedek Depression
and human existance. Boston: Little, Brown & Co., 1975.

 

 

Seligman, M. Helplessness: 0n depression, development and death. San
Francisco: W. H. Freeman, 1975.

 

Seligman, M. Comment and integration. Journal of Abnormal Psychology.
1978, 81, 165-180.

 

Seligman, M., Abramson, L., Semmel, A., & Baeyer, C. Depressive
attributional style. Journal of Abnormal Psychology. 1979, 88
(3), 242-7.

 

Shevrin, H. & Dickman, S. The psychological unconscious: A necessary

assumption for psychological theory? American Psycholggist.
1980, I_3_5_ (5), 421-434.

 

Strickland, B. Hale, W., & Anderson, L. Effect of induced mood states
on activity and self-reported affect. Journal of Consulting and
Clinical Psychology. 1975, 4_3, 587.

 

 

Teasdale, J. & Fogarty, S. Differential effects of induced mood on
retrieval of pleasant and unpleasant events from episodic
memory. Journal of Abnormal Psychology. 1979, 88 (3), 242-7.

 

Thomas, A., Chess, 8., & Birch, H. G. Temperament and behavior
disorders in children. New York: New York University Press,
1968.

 

 

Velten, E. The induction of elation and depression through the reading
of structured sets of mood statements. Unpublished doctoral
dissertation, U.S.C. 1967.

Velten, E. A laboratory task for induction of mood states. Behavior
Research & Therapy. 1968, 8, 473-82.

 

Wilson, W. P. Feeling more than we can know: Exposure effects without
learning. Journal of Personalityand Social Psychology. 1979,
8_7_, 811-821.

 

Wortman, C. & Dintzer, L. Is an attributional analysis of the learned
helplessness model phenomenon viable? A critique of the

Abramson-Seligman-Teasdale reformulation. Journal of Abnormal
Psychology. 1978, 8_7_, 75-90.

 

 

76

Zajonc, R. B. Feeling and thinking: Preferences need no inferences.
American Psychologist. 1980, 88 (5), 421-434.

Zetzel, E. Depression and the incapacity to bear it. In Schur,
M. (Ed.) Drives, affects, behavior volume 2. New York:
International Universities Press, 1965.

Zuckerman, M. & Lubin, B. Manual for the Multiple Affect Adjective

Check List. San Diego: Education and Industrial Testing
Service, 1965.

Zuckerman, M., Lubin, 3., Vogel, L., & Valerius, E. Measurement of
experimentally induced affects. Journal of Consulting
Psychology. 1964, 88, 418-425.

 

 

APPENDICES

APPENDIX 1

VELTEN MOOD INDUCTION PROCEDURE (VMIP)

VMIP: Elation Statements

 

Please read each of the following statements out loud. As you look at
each statement, focus your observation only on that one. The tape
recording will tell you when to move on to the next card.

These statements are intended to create a certain mood. YOur success at
coming to experience this mood will largely depend on your willingness
to accept and respond to the idea in each statement and to allow each
suggestion to act upon you without resistance.

Attempt to respond to the feeling suggested by each statement. Then try
to think of yourself as definitely being and moving into that mood
state.

 

If it is natural for you to do so, try to visualize a scene in which you
have had such a feeling.

If you feel the urge to laugh, it will probably be because humor is a
good way to counteract unwanted feelings or it might be because you feel
yourself going into that mood. Try to avoid laughing.

TOday is neither better nor worse than any other day.

I 88_feel pretty good, though.

I feel light-hearted.

This might turn out to be one of my good days.

If your attitude is good, then things are good, and my attitude is good.
I’ve certainly got energy and self-confidence to spare.

I feel cheerful and lively.

0n the whole I have very little difficulty in thinking clearly.

77

78

My parents are pretty proud of me most of the time.

I’m glad I’m in college--it’s the key to success nowadays.
For the rest of the days, I bet things will go really well.
I’m pleased that most peOple are so friendly to me.

My judgement about most things is good.

Ig’s encouraging that as I get further into my major, it’s going to take
less study to get good grades.

I’m full of energy and ambition--I feel I could go a long time without
sleep.

This is one of those days I can grind out school work with practically
no effort at all.

My judgment is keen and precise today. Just let someone try to put
something over on me.

When I want to, I can make things turn out fine.

I feel enthusiastic and confident now.

There should be Opportunity for a lot of good times coming along.
My favorite song keeps running through my head.

Some of my friends are so lively and optimistic.

I feel talkative--I feel like talking to almost anybody.

I’m full of energy and am ready to get to like the things I am doing CH1
campus.

I’m able to do things accurately and efficiently.
I know good and well that I can achieve the goals I set.

Now that it occurs to me, most of the things that have depressed me
wouldn’t have if I just had the right attitude.

I have a sense of power and vigor.
I feel so vivacious and efficient today--sitting on tOp of the world.
It would really take something to stop me now.

In the long run, it’s obvious that things have gotten better and bettuer
during my life.

I know that in the future I won’t over-emphasize so-called_’problems.’

79
I’m optimistic that I can get along very well with most of the peoplma I
meet.
I’m too absorbed in things to have time for worry.
I’m feeling amazingly good today!
Things look good; things look great!
I feel that many of my friendships will stick with me in the future.
I can find the good in almost anything.
I am particularly inventive and resourceful in this mood.
I feel superb! I think I can work to the best of my ability.

I feel so gay and playful today I feel like surprising someone by
telling a silly joke.

I feel an exhilirating animation in all I do.
I feel highly perceptive and refreshed.
My memory is in rare form today.

In a buoyant mood like this one, I can work fast and do it right the
first time.

I can concentrate hard on anything I do.

I feel industrious as heck--I want something to do!

Life is firmly in my control.

I wish somebody would play some good loud music!

This is great--I really do feel good. I gg_elated about things.
I’m really feeling sharp now.

This is just one of those days when I’m ready to go.

I feel like I’m bursting with laughter--I wish somebody would tell me E!
joke or give me an excuse!

I’m full of energy.

God, I feel great.

80

VMIP: Neutral Statements

 

Please read each of the following statements out loud. As you look at
each statement, focus your observation only on that one. The tape
recording will tell you when to move on to the next card.

These statements are intended to create a certain mood. Your success at
coming to experience this mood will largely depend on your willingness
to accept and respond to the idea in each statement and to allow each
suggestion to act upon you without resistance.

Attempt to respond to the feeling suggested by each statement. Then try
to think of yourself as definitely being and moving into that mood
state.

 

If it is natural for you to do so, try to visualize a scene in which you
have had such a feeling.

If 37% feel the urge to laugh, it will probably be because humor is a
good way to counteract unwanted feelings or it might be because you feel
yourself going into that mood. Try to avoid laughing.

I am a woman.

Japan was elected to the United Nations almost fourteen years after
Pearl Harbor.

This quarter I am enrolled in a psychology course.

Oklahoma City is the largest city in the world in area, with 631. 161
square miles.

Right now I am reading this statement aloud.
At the end appears a section entitled "Bibliography notes."
Michigan is where I now reside.

We have two kinds of nouns denoting physical things: individual nouns
and mass nouns.

I attend Michigan State University.

There is a large rose-growing center near Tyler, Texas.

deay I have had to walk up some stairs.

I am sitting by myself in a room.

This book or any part thereof must not be reproduced in any form.

Agricultural products comprise seventy percent of the income.

81

While I read these statements I am also listening to a tape recording.
I attend a university located in East Lansing.

Saturn is sometimes in conjunction, beyond the sun from the earifl1, arui
is not visible.

I am a high school graduate.

Some streets were still said to be listed under their old names.
I dressed myself today.

I am participating in the second part of this experiment.

I am a female undergraduate.

The system is supervised by its Board of Regents.

When the plant bent down under its own weight, its branches began to
take root.

By participating in this experiment, I am helping advance knowledge.
There isn’t a scientific explanation for every U.F.O. sighting.
Completing this experiment gains me credit in my psychology course.
During high school, I took mathematics courses.

The Hope Diamond was shipped from South Africa to London through the
regular mail service.

The review is concerned with the first three volumes.

I can hear my own voice while I talk.

The ship was ancient and would as soon be retired from the fleet.

I have heard a number of different college lectures at this university.
Two men dressed as repairmen will appear shortly after the van pulls up.
The wood was discolored as if it had been held in a fire.

This is not the only building I have entered.

At different times in my life I have taken exams.

A light was noticed in the dark outside and it moved eerily towards tine
house.

During the first part of this experiment, I sat in a room with many
other people.

82

Painting in a few other non-European countries is treated in a sepatnite

volume.

A recent study revealed that one half of all college students were

unable to find summer jobs.

The school I attend is a co-ed school.

The map would prove useless as a beginning guide.

The speaker outlined a plan whereby the deficit could be eliminated.
I am seated in a chair.

In my hand I am holding an index card.

Black and white pictures are arranged in ten sections.

The voices are only at night, and whisper words, terrible words.
The papers had been front-paging it for days.

I have already completed some questionnaires in this experiment.
The organization depended on the people for support.

I sometimes use a pencil when I write.

In 1965, Elizabeth made the first state visit by a British monarch
Germany in 56 years.

The foods I eat vary in taste.

It was their sixth consecutive best-seller.

t0

83

VMIP: Depression Statements

 

Please read each of the following statements out loud. As you look at
each statement,focus your observation only on that one. The tape
recording will tell you when to move on to the next card.

These statements are intended to create a certain mood. Your success at
coming to experience this mood will largely depend on your willingness
to accept and respond to the idea in each statement and to allow each
suggestion to act upon you without resistance.

Attempt to respond to the feeling suggested by each statement. Then try
to think of yourself as definitely being and moving into that mood
state.

 

If it is natural for you to do so, try to visualize a scene in which you
have had such a feeling.

If you feel the urge to laugh, it will probably be because humor is a
good way to counteract unwanted feelings or it might be because you feel
yourself going into that mood. Try to avoid laughing.

Today is neither better nor worse than any other day.

However, I feel a little low today.

I’m too tired and gloomy to care about anything.

Sometimes I wonder whether school is all that worthwhile.

It has occurred to me more than once that study is basically useless,
because you forget almost everything you learn anyway.

I don’t concentrate anymore. I just want to forget about everything.

I’ve had daydreams in which my mistakes kept occurring to me--sometiuues
I wish I could start over again.

I just can't make up my mind; it’s so hard to make simple decisions.
I just don’t care about anything. Life just isn’t any fun.

It takes too much effort to convince peOple of anything. There’s no
point in trying.

I couldn’t remember things well right now if I had to.
It's so discouraging the way people don't really listen to me.
I’ve doubted that I’m a worthwhile person.

It often seems that no matter how hard I try, things still go wrong.

84

Things are easier and better for other people than for me. I feel like
there’s no use in trying again.

I’ve noticed that no one seems to really understand or care when I
complain or feel unhappy.

I’m not very alert; I feel listless and vaguely sad.
I’m uncertain about my future.

Too often I have found myself staring into the distance, my mind a
blank, when I definitely should have been studying.

I’m discouraged and unhappy about myself.

Things are worse now than when I was younger.

I’ve lain awake at night worrying so long that I’ve hated myself.
I'm not sure school is helping me very much.

I’m so tired.

Some very important decisions are almost impossible for me to make.
The way I feel now, the future looks boring and hOpeless.

I fail in communicating with peOple about my problem.

My thoughts are so slow and downcast--I don’t want to think or talk.

Things are easier and better for other peOple than for me. I feel like
there’s no use in trying again.

There have been days when everything went miserably wrong.

I just can't make up my mind; it’s so hard to make simple decisions.
I feel terribly weak.

Often peOple make me very upset. I don’t like to be around them.

I fail in communication with peOple about my problems.

It’s so discouraging the way peOple don’t really listen to me.

I can’t get people to understand me.

I’ve felt so alone before that I could have cried.

Everything seems to take so much effort.

I get so discouraged because I can’t solve my problems.

85

Sometimes I’ve wished I could die.
I just don’t care about anything. Life just isn’t any fun.

Too often I have found myself staring listlessly into the distance, my
mind a blank.

I just can't seem to do things right very often.

Even the simplest decisions are almost impossible for me.

I have too many bad things in my life.

I can't seem to get peOple to like me.

I don't concentrate or move. I just want to forget about everything.
I often feel there is something terribly wrong with me.

I feel terribly tired and indifferent to things today.

Everything seems utterly futile and empty.

My future seems bleak and hOpeless.

Every now and then I feel so tired and gloomy that I'd rather just sit
than do anything.

I want to go to sleep and never wake up.
All of the unhappiness of my past life is taking possession of me.

Life seems too much for me anyhow. My efforts are wasted.

APPENDIX 2

PERSONAL FEELINGS SCALE (PFS)

(Note: PFS Depression subscale 8 optimistic/pessimistic + energetic/
listless + reversed scores for (sad/happy + hopeless/hopeful)
Maximum score - 36

Please Indicate the Way YOu Are Feeling RIGHT NOW

 

 

 

 

 

 

 

 

extremely extremely
optimistic pessimistic

1 2 3 4 5 6 7 8 9
extremely extremely
sad happy

1 2 3 4 5 6 7 8 9
extremely extremely
nervous calm

I’ 2’ 3’ 4 5' 6' 7 8 9
extremely extremely
open closed

I’ 2 ’3 4 5 6 7 8 9
extremely extremely
steady unsteady

’I 2’ 3 4 5’ 6' 7 8 9
extremely extremely
confident unconfident

1 2 3 4 5 6 7 8 9
extremely extremely
hopeless hOpeful

1 2 3 4 5 6 7 8 9
extremely extremely
angry serene

1 2 3 4 5 6 7 8 9

86

87

 

extremely extremely

inspired uninspired
1 2 3 4 5 6 7 8 9

extremely extremely

energetic listless

 

l 2 3 4 5 6 7 8 9

APPENDIX 3

MULTIPLE AFFECT ADJECTIVE CHECK LIST(MAACL)

I+III>U

- depression sub-scale (Note:
- anxiety sub-scale (Note:
- hostility sub-scale (Note:

Maximum score = 40)
Maximum score 8 21)

Maximum score - 28)

item must be checked to be counted on sub-scale
item must not be checked to be counted on sub-scale

Directions: On these pages you will find words which describe

different kinds of moods and feelings.
words which describe how you feel now - today.

 

Mark an §_beside the
Some of the

words may sound alike, but we want you to check all the words
that describe your feelings.

 

Work rapidly.

 

 

 

1. ___active(D-)
4. ___afraid(A+)
7. __ aggressive
10. amiable(H-)
13. annoyed

16. bitter(H+)
19. calm(A-)
22. clean

25. contrary

2.

5.

8.

11.

14.

17.

20.

23.

26.

___adventurous
.__ agitated
___alive(D-)
___amused
___awfu1(D+)

-__ blue(D+)

cautious

___complaining

cool

88

3.

___affectionate

6.___ agreeable(H-)

9.

12.

15.

18.

21.

24.

27.

___ alone(D+)

__ angry(H+)
___bashful
___bored
___cheerful(A-)

contented(A-)

c00perative

89

 

 

 

28.

31.

34.

37.

40.

43.

46.

49.

52.

55.

58.

61.

64.

67.

70.

73.

76.

79.

82.

85.

88.

91.

critical
daring

devoted

discouraged(D+)

energetic
fearful(A+)
forlorn(D+)
friendly(H-)
gay(D-)
gloomy(D+)
grim
hopeless(D+)

incensed

interested(D-)

joyful(A-)
lost(D+)
1ucky(D-)
meek
miserable(D+)
offended(H+)
patient

p1easant(A-)

41.
44.
47.
50.
53.
56.
59.
62.
65.
68.
71.
74.
77.
80.
83.
86.
89.

92.

cross
desperate(A+)
disagreeable(H+)
disgusted(H+)
enraged(H+)
fine(D-)
frank
frightened(A+)
gentle
good(D-)
happy(A-)
hostile
indignant
irritated(H+)
kindly(H-)
loving(A-)
mad(H+)
merry(D-)
nervous(A+)
outraged(H+)
peaceful(D-)

polite(H-)

42.

45.

48.

51.

54.

57.

60.

63.

66.

69.

72.

75.

78.

81.

84.

87.

90.

93.

cruel(H+)
destroyed(D+)
discontented(H+)
displeased
enthusiastic(D-)
fit(D-)

free(D-)
furious(H+)
glad(D-)
good-natured(H-)
healthy(D-)
impatient
inspired(D-)
jealous
lonely(D+)
low(D+)
mean(H+)

mild

obliging
panicky(A+)
pleased

powerful

9O

 

 

 

94. __ quiet
97. __ rough
100. satisfied

103.

106.

109.

112.

115.

118.

1210-—

124.

shy
stubborn

suffering(D+)

sympathetic(H-)

tense(A+)

___thoughtful(A-)
understanding(H-)

___upset(A+)

127. ___whole(D-)

130.

___wilted(D+)

95.

98.

101.

104.

107.

110.

113.

116.

119.

122.

125.

128.

131.

___reckless
___sad(D+)

___secure(A-)

soothed
stormy(H+)
sullen

tame(H-)

96.

99.

102.

105.

108.

111.

114.

terrible(D+) 117.

timid
unhappy(D+)
vexed(H+)

wild

120.

123.

126.

129.

worrying(A+) 132.

'__ rejected(D+)

___safe(D-)

shaky(A+)
steady(A-)
strong(D-)
sunk(D+)
tender
terrified(A+)
tormented(D+)
unsociable
warm

willful(H-)

young(D-)

(Note:

APPENDIX 4

BECK DEPRESSION INVENTORY (BDI)

Maximum score - 63)

INSTRUCTIONS: In each of the following groups of statements, circle the
one statement which best describes how you feel RIGHT NOW.

1.

1)
2)
3)
4)
5)

1)

1)
2)
3)
4)

5)

do not feel sad

feel blue or sad.

am blue or sad all the time and I can’t snap out of it.
am so sad or unhappy that it is quite painful.

am so sad or unhappy that I can’t stand it.

hihihihdh!

I am not particularly pessimistic or discouraged about the
future.

I feel discouraged about the future.

I feel I have nothing to look forward to.

I feel that I won’t ever get over my troubles.

I feel that the future is hOpeless and that things cannot
improve.

I do not feel like a failure.

I feel that I have failed more than the average person.

I feel I have accomplished very little that is worthwhile or
that means anything.

As I look back on my life all I can see is a lot of
failures.

I feel I am a complete failure as a person (parent, wife,
daughter, etc.)

I am not particularly dissatisfied.

I feel bored most of the time.

I don’t enjoy things the way I used to.

I don’t get satisfaction out of anything any more.

I am dissatisfied with everything.

I don't feel particularly guilty.

I feel bad or unworthy a good part of the time.

I feel quite guilty.

I feel bad or unworthy practically all the time now.
I feel as though I am very bad or worthless.

91

10.

11.

12.

13.

1)
2)
3)
4)

1)
2)

4)

1)

3)
4)

HHHHH HHHHH

HHHH

I
I

92

don’t feel I am being punished.

have a feeling that something bad may happen to me.
feel I am being punished or will be punished.

feel I deserve to be punished.

want to be punished.

don’t feel disappointed in myself.
am disappointed in myself.

don't like myself.

am disgusted with myself.

hate myself.

don’t feel I am any worse than anybody else.

am critical of myself for my weaknesses or mistakes.
blame myself for my faults.

blame myself for everything bad that happens.

don’t have any thoughts of harming myself.
have thoughts of harming myself but I would not carry

out.

I

I
I
I
I
t

I
I
I
I

feel I would be better off dead.
feel my family would be better off if I were dead.

have definite plans about committing suicide.
would kill myself if I could.

don’t cry any more than usual.
cry now more than I used to.
cry all the time now. I can’t stop it.

used to be able to cry but now I can’t cry at all even
hough I want to.

am no more irritated now than I ever am.

get annoyed or irritated more easily than I used to.
feel irritated all the time.

don’t get irritated at all at the things that used to

irritate me.

I

have not lost interest in other people

them

I am less interested in other peOple now than I used to be.

I have lost most of my interest in other peOple and have

little feeling for them.
have lost all my interest in other people and don’t care
about them at all.

I

I
I
I
I

make decisions about as well as ever.

try to put off making decisions.

have great difficulty in making decisions.
can’t make any decisions at all any more.

14.

15.

16.

17.

18.

19.

20.

21.

1)
3)
4)

1)
2)
3)
4)
5)

1)
2)
3)

4)

1)
2)
3)
4)

1)
2)
3)

1)
2)
3)
4)

1)
2)

3)
4)
1)
2)

3)
4)

93

I don’t feel I look any worse than I used to.

I am worried that I am looking old or unattractive.

I feel that there are permanent changes in my appearance and
they make me look unattractive.

I feel that I am ugly or repulsive looking.

I can work about as well as before.

It takes extra effort to get started at doing something.
I don’t work as well as I used to.

I have to push myself very hard to do anything.

I can’t do any work at all.

I can sleep as well as usual.

I wake up more tired in the morning than I used to.

I wake up 1-2 hours earlier than usual and find it hard to
get back to sleep.

I wake up early every day and can’t get more than 5 hours
sleep.

I don’t get any more tired than usual.
I get tired more easily than I used to.
I get tired from doing anything.

I get too tired to do anything.

My appetite is no worse than usual.

My appetite is not as good as it used to be.
My appetite is much worse now.

I have no appetite at all any more.

haven’t lost much weight, if any, lately.
have lost more than 5 pounds.
have lost more than 10 pounds.
have lost more than 15 pounds.

HHHH

I am no more concerned about my health than usual.

I am concerned about aches and pains or upset stomach or
constipation.

I am so concerned with how I feel or what I feel that it’s
hard to think of much else.

I am completely absorbed in what I feel.

I have not noticed any recent changes in my interest in sex.
I am less interested in sex than I used to be.

I am much less interested in sex now.

I have lost interest in sex completely.

APPENDIX 5

ATTRIBUTION STYLE QUESTIONNAIRE (ASQ)

Directions

 

Please try to vividly imagine yourself in the situations that
follow. If such a situation happened to you, what would you feel would
have caused it? While events may have many causes, we want you to pick
only one--the major cause if this event happened to you. Please write
this cause in the blank provided after each event. NEEt we want you to
answer some questions about the cause and a final question about the
situation. To summarize, we want you to:

 

1) Read each situation and vividly imagine it happening to you.

2) Decide what you feel would be the major cause of the situation if it
happened to you.

3) Write one cause in the blank provided.
4) Answer three questions about the cause.
5) Answer one question about the situation.

6) Go on to the next situation.

YOU MEET A FRIEND WHO COMPLIMENTS YOU ON YOUR APPEARANCE.

1) Write down the one major cause

 

2) Is the cause of your friend’s compliment due to something about you
or something about the other person or circumstances? (Circle one
number)

Totally due

to the other

person or Totally due
circumstances 1 2 3 4 5 6 7 to me

94

95

3) In the future when you are with your friends, will this cause again
be present? (Circle one number)

Will never
again be Will always
present 1 2 3 4 5 6 7 be present

4) Is the cause something that just affects interacting with friends or
does it also influence other areas of your life? (Circle one

number)
Influences
just this Influences
particular all situations
situation 1 2 3 4 5 6 7 in my life

5) How important would this situation be if it happened to you?
(Circle one number)

N0t at all Extremely
important 1 2 3 4 5 6 7 important

YOU HAVE BEEN LOOKING FOR A JOB UNSUCCESSFULLY FOR SOME TIME.

6) Write down the one major cause

 

7) Is the cause of your unsuccessful job search due to something about
you or something about other people or circumstances? (Circle one
number)

Totally due to
other people Totally due
or circumstances 1 2 3 4 5 6 7 to me

8) In the future when looking for a job, will this cause again be
present? (Circle one number)

Will never
again be Will always
present 1 2 3 4 5 6 7 be present

9) Is the cause something that just influences looking for a job or
does it also influence other areas of your life? (Circle one

nwmber)
Influences
just this Influences
particular all situations

situation 1 2 3 4 5 6 7 in my life

96

10) How important would this situation be if it happened to you?
(Circle one number)

N0t at all Extremely
important 1 2 3 4 5 6 7 important

YOU BECOME VERY RICH.

11) Write down the one major cause

 

12) Is the cause of your becoming rich due to something about you or
something about other people or circumstances?

Tbtally due
to other peOple Tbtally due

or circumstances 1 2 3 4 5 6 7 to me

13) In your financial future, will this cause again be present?

Will never
again be Will always
present 1 2 3 4 5 6 7 be present

14) Is the cause something that just affects obtaining money or does it
also influence other areas of your life?

Influences

just this Influences all
particular situations in
situation 1 2 3 4 5 6 7 my life

15) How important would this situation be if it happened to you?

NOt at all Extremely
important 1 2 3 4 5 6 7 important

A FRIEND COMES TO YOU WITH A PROBLEM AND YOU DON’T TRY TO HELP THEM.

16) Write down the one major cause

 

17) Is the cause of your not helping your friend due to something about
you or something about other peOple or circumstances? (Circle one
number)

Tbtally due
to other peOple Totally due
or circumstances 1 2 3 4 5 6 7 to me

97

18) In the future when a friend comes to you with a problem, will this
cause again be present? (Circle one number)

Will never
again be Will always
present 1 2 3 4 5 6 7 be present

19) Is the cause something that just affects what happens when a friend
comes to you with a problem or does it also influence other areas
of your life? (Circle one number)

Influences

just this Influences
particular all situations
situation 1 2 3 4 5 6 7 in my life

20) How important would this situation be if it happened to you?
(Circle one number)

Not at all Extremely
important 1 2 3 4 5 6 7 important
YOU GIVE AN IMPORTANT TALK IN FRONT OF A GROUP AND THE AUDIENCE REACTS

NEGATIVELY.

21) Write down the one major cause

 

22) Is the cause of the audience reacting negatively due to something
about you or something about other peOple or circumstances?
(Circle one number)

Totally due to
other people Totally due
or circumstances 1 2 3 4 5 6 7 to me

23) In the future when giving talks, will this cause again be present?
(Circle one number)

Will never
again be Will always
present 1 2 3 4 5 6 7 be present

24) Is this cause something that just influences giving talks or does
it also influence other areas of your life? (Circle one number)

Influences
just this Influences
particular all situations

situation 1 2 3 4 5 6 7 in my life

98

25) How important would this situation be if it happened to you?
(Circle one number)

NOt at all Extremely

important 1 2 3 4 5 6 7 important

YOU DO A PROJECT WHICH IS HIGHLY PRAISED.

26) Write down the one major cause

 

27) Is the cause of being praised due to something about you or
something about the other people or circumstances?

Totally due to
other peOple Totally due

or circumstances 1 2 3 4 5 6 7 to me

28) In the future when doing a project, will this cause again be

present?
Will never
again be Will always
present 1 2 3 4 5 6 7 be present

29) Is this cause something that just affects doing projects or does it
also influence other areas of your life?

Influences

just this Influences
particular all situations
situation 1 2 3 4 5 6 7 in my life

30) How important would this situation be if it happened to you?

NOt at all Extremely
important 1 2 3 4 5 6 7 important

YOU MEET A FRIEND WHO ACTS HOSTILELY TOWARD YOU.

31) write down the one major cause

 

32) Is the cause of your friend acting hostile due to something about
you or something about other people or circumstances? (Circle one

number)

TOtally due to
other people Totally due
or circumstances 1 2 3 4 5 6 7 to me

99

33) In the future when interacting with friends, will this cause again
be present? (Circle one number)

Will never
again be Will always
present 1 2 3 4 5 6 7 be present

34) Is the cause something that just influences interacting with
friends or does it also influence other areas of your life?
(Circle one number)

Influences

just this Influences
particular all situations
situation 1 2 3 4 5 6 7 in my life

35) How important would this situation be if it happened to you?
(Circle one number)

Nor at all Extremely
important 1 2 3 4 5 6 7 important

YOU CAN‘T GET ALL THE WORK DONE THAT OTHERS EXPECT OF YOU.

36) Write down the one major cause

 

37) Is the cause of your not getting the work done due to something
about you or something about the other peOple or circumstances?
(Circle one number)

Totally due
to other people Totally due
or circumstances 1 2 3 4 5 6 7 to me

38) In the future when doing the work that others expect, will this
cause be present? (Circle one number)

Will never
again be Will always
present 1 2 3 4 5 6 7 be present

39) Is the cause something that just affects doing work that others
expect of you or does it also influence other areas of your life?
(Circle one number)

Influences
just this Influences
particular all situations

situation 1 2 3 4 5 6 7 in my life

100

40) How important would this situation be if it happened to you?
(Circle one number)

NCt at all Extremely

important 1 2 3 4 5 6 7 important

YOUR SPOUSE (BOYFRIEND/GIRLFRIEND) HAS BEEN TREATING YOU MORE LOVINGLY.

41) write down the one major cause

 

42) Is the cause of your spouse (boyfriend/girlfriend) treating you
more lovingly due to something about you or something about other
peOple or circumstances?

Tbtally due to
other people Totally due
or circumstances 1 2 3 4 5 6 7 to me

43) In future interactions with your spouse (boyfriend/girlfriend) will
this cause again be present?

Will never
again be Will always
present 1 2 3 4 5 6 7 be present

44) Is this cause something that just affects how your spouse
(boyfriend/girlfriend) treats you or does it also influence other
areas of your life?

Influences

just this Influences
particular all situations
situation 1 2 3 4 5 6 7 in my life

45) How important would this situation be if it happened to you?

N0t at all Extremely
important 1 2 3 4 5 6 7 important

YOU APPLY FOR A POSITION THAT YOU WANT VERY BADLY (E.G., IMPORTANT JOB,
GRADUATE SCHOOL ADMISSION, ETC.) AND YOU GET IT.

46) Write down the one major cause

 

47) Is the cause of your getting the position due to something about
you or something about other people or circumstances? (Circle one
number)

Tbtally due to
other peOple Totally due
or circumstances 1 2 3 4 5 6 7 to me

101

48) In the future when applying for a position, will this cause again
be present? (Circle one number)

Will never
again be Will always
present 1 2 3 4 5 6 7 be present

49) Is the cause something that just influences applying for a position
or does it also influence other areas of your life? (Circle one

number)
Influences
just this Influences
particular all situations
situation 1 2 3 4 5 6 7 in my life

50) How important would this situation be if it happened to you?
(Circle one number)

N0t at all Extremely
important 1 2 3 4 5 6 7 important

YOU GO OUT ON A DATE AND IT GOES BADLY.

51) Write down the one major cause

 

52) Is the cause of the date going badly due to something about you or
something about other peOple or circumstances? (Circle one number)

Totally due to
other people Totally due
or circumstances 1 2 3 4 5 6 7 to me

53) In the future when dating, will this cause again be present?
(Circle one number)

Will never
again be Will always
present 1 2 3 4 5 6 7 be present

54) Is the cause something that just influences dating or does it also
influence other areas of your life? (Circle one number)

Influences

just this Influences
particular all situations
situation 1 2 3 4 5 6 7 in my life

55) How important would this situation be if it happened to you?
(Circle one number)

Not at all Extremely
important 1 2 3 4 5 6 7 important

 

102

YOU GET A RAISE.

56) Write down the one major cause

 

57) Is the cause of your getting a raise due to something about you or
something about other people or circumstances?

Totally due to
other people Totally due

or circumstances 1 2 3 4 5 6 7 to me

58) In the future on your job, will this cause again be present?

Will never
again be Will always
present 1 2 3 4 5 6 7 be present

59) Is this cause something that just affects getting a raise or does
it also influence other areas of your life?

Influences

just this Influences all
particular situations in
situation 1 2 3 4 5 6 7 my life

60) How important would this situation be if it happened to you?

N0t at all Extremely
important 1 2 3 4 5 6 7 important