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Behavior Therapy 47 (2016) 776–784
www.elsevier.com/locate/bt
Cognitive Therapy: Nature and Relation to Behavior Therapy –
Republished Article
Aaron T. Beck
University of Pennsylvania
Recent innovations in behavior modification have, for the
most part, detoured around the role of cognitive processes in
the production and alleviation of symptomatology. Although
self-reports of private experiences are not verifiable by other
observers, these introspective data provide a wealth of testable
hypotheses. Repeated correlations of measures of inferred
constructs with observable behaviors have yielded consistent
findings in the predicted direction.
Systematic study of self-reports suggests that an individual’s
belief systems, expectancies, and assumptions exert a strong
influence on his state of well-being, as well as on his directly
observable behavior. Applying a cognitive model, the
clinician may usefully construe neurotic behavior in terms
of the patient’s idiosyncratic concepts of himself and of his
animate and inanimate environment. The individual’s belief
systems may be grossly contradictory; i.e., he may simulta-
neously attach credence to both realistic and unrealistic
conceptualizations of the same event or object. This inconsis-
tency in beliefs may explain, for example, why an individual
may react with fear to an innocuous situation even though he
may concomitantly acknowledge that this fear is unrealistic.

Cognitive therapy, based on cognitive theory, is designed
to modify the individual’s idiosyncratic, maladaptive
ideation. The basic cognitive technique consists of delineating
the individual’s specific misconceptions, distortions, and
maladaptive assumptions, and of testing their validity and
reasonableness. By loosening the grip of his perseverative,
distorted ideation, the patient is enabled to formulate his
The preparation of this report was supported by a grant from the
Marsh Foundation. Reprint requests should be sent to 202
Piersol,
Hospital of University of Pennsylvania.
This article is a reprint of a previously published article. For
citation purposes, please use the original publication details;
Behavior Therapy, 1 (1970), pp 184-200.
DOI of original item: http://dx.doi.org/10.1016/S0005-
7894(70)80030-2.
0005-7894/© 2016 Association for Behavioral and Cognitive
Therapies.
Published by Elsevier Ltd. All rights reserved.
experiences more realistically. Clinical experience, as well
as some experimental studies, indicate that such cognitive
restructuring leads to symptom relief.
TWO SYSTEMS OF PSYCHOTHERAPY that have recently
gained prominence have been the subject of a rapidly
increasing number of clinical and experimental
studies. Cognitive therapy,1 the more recent entry
into the field of psychotherapy, and behavior therapy
already show signs of becoming institutionalized.
Although behavior therapy has been publicized in
a large number of articles and monographs, cognitive
therapy has received much less recognition. Despite

the fact that behavior therapy is based primarily on
learning theory whereas cognitive therapy is rooted
more in cognitive theory, the two systems of
psychotherapy have much in common.
First, in both systems of psychotherapy the
therapeutic interview is more overtly structured
and the therapist more active than in other
psychotherapies. After the preliminary diagnostic
interviews in which a systematic and highly detailed
description of the patient’s problems is obtained,
both the cognitive and the behavior therapists
formulate the patient’s presenting symptoms (in
cognitive or behavioral terms, respectively) and
design specific sets of operations for the particular
problem areas.
After mapping out the areas for therapeutic
work, the therapist explicitly coaches the patient
regarding the kinds of responses and behaviors that
are useful with this particular form of therapy.
Detailed instructions are presented to the patient,
1 Ellis (1957) used the label “Rational Therapy” which he later
changed to “Rational-Emotive Therapy.”
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777c t : na t ur e an d r e l at i o n t o be ha vi o r t h e r ap y
for example, to stimulate pictorial fantasies (system-
atic desensitization) or to facilitate his awareness and
recognition of his cognitions (cognitive therapy). The
goals of these therapies are circumscribed, in contrast

to the evocative therapies whose goals are open
ended (Frank, 1961).
Second, both the cognitive and behavior therapists
aim theirtherapeutic techniquesat the overt symptom
or behavior problem, such as a particular phobia,
obsession, or hysterical symptom. However, the
target differs somewhat. The cognitive therapist
focuses more on the ideational content involved in
the symptom, viz., the irrational inferences and
premises. The behavior therapist focuses more on
the overt behavior, e.g., the maladaptive avoidance
responses. Both psychotherapeutic systems concep-
tualize symptom formation in termsof constructsthat
are accessible either to behavioral observation or to
introspection, in contrast to psychoanalysis, which
views most symptoms as the disguised derivatives of
unconscious conflicts.
Third,infurthercontrastto psychoanalytictherapy,
neither cognitive therapy nor behavior therapy draws
substantially on recollections or reconstructions of
the patient’s childhood experiences and early family
relationships. The emphasis on correlating present
problems with developmental events, furthermore, is
much less prominent than in psychoanalytic psycho-
therapy.
A fourth point in common between these two
systems is that their theoretical paradigms exclude
many traditional psychoanalytic assumptions such
as infantile sexuality, fixations, the unconscious, and
mechanisms of defense. The behavior and cognitive
therapists may devise their therapeutic strategies on
the basis of introspective data provided by the
patient; however, they generally take the patients’

self-reports at face value2 and do not make the kind
of high-level abstractions characteristic of psycho-
analytic formulations.
Finally, a major assumption of both cognitive
therapy and behavior therapy is that the patient has
acquired maladaptive reaction patterns that can be
“unlearned” without the absolute requirement that
he obtain insight into the origin of the symptom.
One of the major assets of behavior therapy has
been the large number of well-designed experiments
that support certain of its basic assumptions.
Although of more recent vintage, several systematic
studies supporting the underpinnings of cognitive
2 Although the patient may not be immediately aware of the
content of his maladaptive attitudes and patterns, this concept is
not “unconscious” in the psychoanalytic sense and is accessible
to
the patient’s introspection. Furthermore, unlike many psycho-
analytic formulations, the inferences can be tested by currently
available research techniques.
therapy have also been reported (Carlson, Travers,
& Schwab, 1969; Jones, 1968; Krippner, 1964;
Loeb, Beck, Diggory, & Tuthill, 1967; Rimm &
Litvak, 1969; Velten, 1968). The few controlled-
outcome studies of cognitive therapy (Ellis, 1957;
Trexler & Karst, 1969) provide preliminary evidence
of the effectiveness of this therapy.
There are obvious differences in the techniques
used in behavior therapy and cognitive therapy. In
systematic desensitization, for example, the behavior
therapist induces a predetermined sequence of picto-
rial images alternating with periods of relaxation. The
cognitive therapist, on the other hand, relies more on

the patient’s spontaneously experienced and reported
thoughts. These cognitions, whether in pictorial or
verbal form, are the target for therapeutic work. The
technical distinctions between the two systems of
psychotherapy are often blurred, however. For
example, the cognitive therapist uses induced images
to clarify problems (Beck, 1967; 1970), and the
behavior therapist uses verbal techniques such as
“thought-stoppage” (Wolpe & Lazarus, 1966).
The most striking theoretical difference between
cognitive and behavior therapy lies in the concepts
used to explain the dissolution of maladaptive
responses through therapy. Wolpe, for example,
utilizes behavioral or neurophysiological explanations
such as counterconditioning or reciprocal inhibition;
the cognitivists postulate the modification of con-
ceptual systems, i.e., changes in attitudes or modes of
thinking. As will be discussed later, many behavior
therapists implicitly or explicitly recognize the
importance of cognitive factors in therapy, although
they do not expand on these in detail (Davison, 1968;
Lazarus, 1968).
Techniques of Cognitive Therapy
Cognitive therapy may be defined in two ways: In a
broad sense, any technique whose major mode of
action is the modification of faulty patterns of
thinking can be regarded as cognitive therapy. This
definition embraces all therapeutic operations that
indirectly affect the cognitive patterns, as well as
those that directly affect them (Frank, 1961). An
individual’s distorted views of himself and his world,
for example, may be corrected through insight into
the historical antecedents of his misinterpretations
(as in dynamic psychotherapy), through greater

congruence between the concept of the self and the
ideal (as in Rogerian therapy), and through increas-
ingly sharp recognition of the unreality of fears (as in
systematic desensitization).
However, cognitive therapy may be defined
more narrowly as a set of operations focused on a
patient’s cognitions (verbal or pictorial) and on the
premises, assumptions, and attitudes underlying
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these cognitions. This section will describe the
specific techniques of cognitive therapy.
Recognizing Idiosyncratic Cognitions
One of the main cognitive techniques consists of
training the patient to recognize his idiosyncratic
cognitions or “automatic thoughts” (beck, 1963). ellis
(1962) refers to these cognitions as “internalized
statements” or “self-statements,” and explains them
to the patient as “things that you tell yourself.” these
cognitions are termed idiosyncratic because they
reflect a faulty appraisal, ranging from a mild
distortion to a complete misinterpretation, and
because they fall into a pattern that is peculiar to a
given individual or to a particular psychopathological
state.
In the acutely disturbed patient, the distorted
ideation is frequently in the center of the patient’s
phenomenal field. In such cases, the patient is very
much aware of these idiosyncratic thoughts and can
easily describe them. The acutely paranoid patient,
for instance, is bombarded with thoughts relevant

to his being persecuted, abused, or discriminated
against by other people. In the mild or moderate
neurotic, the distorted ideas are generally at the
periphery of awareness.3 It is therefore necessary to
motivate and to train the patient to attend to these
thoughts.
Many patients reporting unpleasant affects describe
a sequence consisting of a specific event (external
stimulus) leading to an unpleasant affect. For
instance, the patient may outline the sequence of
(a) seeing an old friend and then (b) experiencing a
feeling of sadness. Oftentimes, the sadness is inexpli-
cable to the patient. Another person (a) hears about
somebody having been killed in an automobile
accident and (b) feels anxiety. However, he cannot
make a direct connection between these two phe-
nomena; e.g., there is a missing link in the sequence.
In these instances of a particular event leading to
an unpleasant affect, it is possible to discern an
intervening variable, namely, a cognition, which
forms the bridge between the external stimulus and
the subjective feeling. Seeing an old friend stimulates
cognitions such as “It won’t be like old times,” or
“He won’t accept me as he used to.” The cognition
then generates the sadness. The report of an
automobile accident stimulates a pictorial image in
which the patient himself is the victim of an
automobile accident. The image then leads to the
anxiety.
This paradigm can be further illustrated by a
number of examples. A patient treated by the writer
3 In obsessional neurosis, of course, the idiosyncratic ideas are
central and the patient has difficulty in ignoring them.

complained that he experienced anxiety whenever
he saw a dog.4 He was puzzled by the fact that he
experienced anxiety even when the dog was chained
or caged or else was obviously harmless. The patient
was instructed: “Notice what thoughts go through
your mind the next time you see a dog—any dog.” At
the next interview, the patient reported that during
numerous encounters with dogs between appoint-
ments, he had recognized a phenomenon that he had
not noticed previously; namely, that each time he saw
the dog he had a thought such as “It’s going to bite
me.”
By being able to detect the intervening cognitions,
the patient was able to understand why he felt
anxious, namely, he indiscriminately regarded every
dog as dangerous. He stated, “I even got that thought
when I saw a small poodle. Then I realized how
ridiculous it was to think that a poodle could hurt
me.” He also recognized that when he saw a big dog
on a leash, he thought of the most deleterious
consequences: “The dog will jump up and bite out
one of my eyes,” or “It will jump up and bite my
jugular vein and kill me.” Within 2 or 3 weeks, the
patient was able to overcome completely his long-
standing dog phobia simply by recognizing his
cognitions when exposed to a dog.
Another example was provided by a college student
who experienced inexplicable anxiety in a social
situation. After being trained to examine and write
down his cognitions, he reported that in social
situations he would have thoughts such as, “They
think I look pathetic,” or “Nobody will want to talk
to me,” or “I’m just a misfit.” These thoughts were
followed by anxiety.

A patient complained that he was chronically angry
at practically everybody whom he saw, but could not
account for his angry response to these people. After
some training at recognizing his cognitions, he
reported having such thoughts as “He’s pushing me
around,” “He thinks I’m a pushover,” “He’s trying to
take advantage of me.” Immediately after experienc-
ing these thoughts, he would feel angry at the
individual towards whom they were directed. He
also realized that there was no realistic basis for his
appraising people in this negative way.
Sometimes, the cognition may take a pictorial form
instead of, or in addition to, the verbal form (Beck,
1970). A woman who experienced spurts of anxiety
when riding across a bridge was able to recognize
that the anxiety was preceded by a pictorial image of
her car breaking through the guard rail and falling off
the bridge. Another woman, with a fear of walking
alone, found that her spells of anxiety followed
images of her having a heart attack and being left
4 Ellis (1962) described a similar case.
helpless and dying on the street. A college student
discovered that his anxiety at leaving his dormitory
at night was triggered by visual fantasies of being
attacked.
The idiosyncratic cognitions (whether pictorial or
verbal) are very rapid and often may contain an
elaborate idea compressed into a very short period
of time, even into a split second. These cognitions

are experienced as though they are automatic;
i.e., they seem to arise as if by reflex rather than
through reasoning or deliberation. They also seem
to have an involuntary quality. A severely anxious
or depressed or paranoid person, for example, may
continually experience the idiosyncratic cognitions,
even though he may try to ward them off. Further-
more, these cognitions tend to appear completely
plausible to the patient.
Distancing
Even after a patient has learned to identify his
idiosyncratic ideas, he may have difficulty in
examining these ideas objectively. the thought
often has the same kind of salience as the perception
of an external stimulus. “distancing” refers to the
process of gaining objectivity towards these cogni-
tions. since the individual with a neurosis tends to
accept the validity of his idiosyncratic thoughts
without subjecting them to any kind of critical
evaluation, it is essential to train him to make a
distinction between thought and external reality,
between hypothesis and fact. patients are often
surprised to discover that they have been equating
an inference with reality and that theyhave attacheda
high degree of truth-value to their distorted concepts.
The therapeutic dictum communicated to the
patient is as follows:
Simply because he thinks something does not
necessarily mean that it is true. While such a dictum
may seem to be a platitude, the writer has found with
surprising regularity that patients have benefited
from the repeated reminder that thoughts are not
equivalent to external reality.

Once the patient is ableto “objectify” his thoughts,
he is ready for the later stages of reality testing:
applying rules of evidence and logic and considering
alternative explanations.
Correcting Cognitive Distortions and
Deficiencies
The writer has already indicated that patients show
faulty or disordered thinking in certain circumscribed
areas of experience. in these particular sectors, they
have a reduced ability to make fine discriminations
and tend to make global, undifferentiated judgments.
part of the task of cognitive therapy is to help the
patient to recognize faulty thinking and to make
appropriate corrections. it is often very useful for the
patient to specify the kind of fallacious thinking
involved in his cognitive responses.
Arbitrary inference refers to the process of drawing
a conclusion when evidence is lacking or is actually
contrary to the conclusion. This type of deviant
thinking usually takes the form of personalization (or
self-reference). A depressed patient, who saw a frown
on the face of a passerby, thought, “He is disgusted
with me.” A phobic girl of 21, reading about a
woman who had had a heart attack, got the thought,
“I probably have heart disease.” A depressed
woman, who was kept waiting for a few minutes
by the therapist, thought, “He has deliberately left in
order to avoid seeing me,”
Overgeneralization refers to the process of
making an unjustified generalization on the basis
of a single incident. This may take the form that was
described in the case of the man with the dog

phobia, who generalized from a particular dog that
might attack him to all dogs. Another example is a
patient who thinks, “I never succeed at anything”
when he has a single isolated failure.
Magnificationrefers to the propensity to exaggerate
the meaning or significance of a particular event. A
person with a fear of dying, for instance, interpreted
every unpleasant sensation or pain in his body as a
sign of some fatal disease such as cancer, heart attack,
or cerebral hemorrhage. Ellis (1962) applied the label
“castrophizing” to this kind of reaction.
As noted above, it is often helpful for the patient
to label the particular aberration involved in his
maladaptive cognition. Once the patient has firmly
established that a particular type of cognition, such
as “That dog is going to bite me,” is invalid, he will
be equipped to correct this cognition on subsequent
occasions. For example, his planned, rational
response to the stimulus of a toy poodle would
be, “Actually, it is just a harmless poodle and there
is only a remote chance that it would bite me. And
even if it did, it could not really injure me.”
Cognitive deficiency refers to the disregard for an
important aspect of a life situation. Patients with
this defect ignore, fail to integrate, or do not utilize
information derived from experience. Such a
patient, consequently, behaves as though he has a
defect in his system of expectations: He consistently
engages in behavior which he realizes, in retrospect,
is self-defeating. This class of patients includes those
who “act out,” e.g., psychopaths, as well as those
whose overt behavior sabotages important personal
goals. These individuals sacrifice long-range satisfac-

tion or expose themselves to later pain or danger
in favor of immediate satisfactions. This category
includes problems such as alcoholism, obesity,
drug addition, sexual deviation, and compulsion
gambling.
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The deficient-anticipation patients show two
major characteristics: First, when they yield to their
wishes to engage in self-defeating, dangerous, or
antisocial activities, they are oblivious of the
probable consequences of their actions. At these
times, they avoid thinking about the consequences by
concentrating only on the present activity. They may
fortify this modus operandi through an elaborate
system of self-deceptions, such as “It can’t do any
harm to cut loose, now.” Secondly, irrespective of
how often the individual is “burned” as a result of his
maladaptive actions, he does not seem to integrate
knowledge of the cause-and-effect relationships into
his behavior.
Therapy of such cases consists of training the
patient to think of the consequences as soon as
his self-defeating wish arises. Consideration of the
long-range loss must be forced into the interval
between impulse and action. A patient, for instance,
who continually operated his car beyond the speed
limit or drove through stoplights was surprised each
time he was stopped by a traffic officer. On interview,
it was discovered that the patient was generally
absorbed in a fantasy while driving—he imaged
himself as a famous racing-car driver engaged in a
race. Therapy at first consisted of trying to get him to

watch the odometer—but without success. The next
approach consisted of inducing fantasies of speeding,
getting caught, and receiving punishment. At first,
the patient had great difficulty in visualizing getting
caught even though, in general, he could fantasize
almost everything. However, after several sessions of
induced fantasies, he was able to incorporate a
negative outcome into his fantasy. Subsequently, he
stopped daydreaming while driving and was able to
observe traffic regulations.
In the following case report, several cognitive
techniques directed at modifying anxiety proneness
are illustrated.
Case Report5
Mrs. G. was an attractive 27-year-old mother of three
children. When first seen by the writer, she complained of
Dy
periods of anxiety lasting up to 6 or 7 hr a day and recurring
repeatedly over a 4-year period. She had consulted her
family physician, who had prescribed a variety of sedatives,
including Thorazine, without any apparent improvement.
In an analysis of the cause-and-effect sequence of her
anxiety, the following facts were elicited. The first anxiety
episode occurred about 2 weeks after she had had a
miscarriage. At that time she was bending over to bathe her
1-year-old son, and she suddenly began to feel faint.
Following this episode, she had her first anxiety attack
which lasted several hours. The patient could not find any
explanation for her anxiety. However, when the writer
5 This patient was treated in collaboration with Dr. William
son.
asked whether she had had any thought at the time she felt
dizzy, she recalled having had the thought, “Suppose I

should pass out and injure the baby.” It seemed plausible
that her dizziness, which was probably the result of a
postpartum anemia, led to the fear she might faint and drop
the baby. This fear then produced anxiety, which she
interpreted as a sign that she was “going to pieces.”
Until the time of her miscarriage, the patient had been
reasonably carefree and had not experienced any episodes of
anxiety. However, after her miscarriage, she periodically
had the thought, “Bad things can happen to me.”
Subsequently, when she heard of somebody’s becoming
sick, she often would have the thought, “This can happen to
me,” and she would begin to feel anxious.
The patient was instructed to try to pinpoint any thoughts
that preceded further episodes of anxiety. At the next
interview, she reported the following events:
1. One evening, she heard that the husband of one of her
friends was sick with a severe pulmonary infection.
She then had an anxiety attack lasting several hours.
In accordance with the instructions, she tried to recall
the preceding cognition, which was, “Tom could get
sick like that and maybe die.”
2. She had considerable anxiety just before starting a
trip to her sister’s house. She focused on her thoughts
and realized she had the repetitive thought that she
might get sick on the trip. She had had a serious
episode of gastroenteritis during a previous trip to her
sister’s house. She evidently believed that such a
sickness could happen to her again.
3. On another occasion, she was feeling uneasy and
objects seemed somewhat unreal to her. She then had
the thought that she might be losing her mind and
immediately experienced an anxiety attack.

4. One of her friends was committed to a state hospital
because of a psychiatric illness. The patient had the
thought, “This could happen to me. I could lose my
mind.” When questioned about why she was afraid of
losing her mind, she stated that she was afraid that if
she went crazy, she would do something that would
harm either her children or herself.
It was evident that the patient’s crucial fear was the
anticipation of loss of control, whether by fainting or by
becoming psychotic. The patient was reassured that there were
no signs that she was going psychotic. She was also provided
with an explanation of the arousal of her anxiety and of her
secondary elaboration of the meaning of these attacks.
The major therapeutic thrust in this case was coaching the
patient to recall and reflect on the thoughts that preceded her
anxiety attacks. The realization that these attacks were initiated
by a cognition rather than by some vague mysterious force
convinced her she was neither totally vulnerable nor unable to
control her reactions. Furthermore, by learning to pinpoint the
anxiety-reducing thoughts, she was able to gain some detach-
ment and to subject them to reality testing. Consequently, she
was able to nullify the effects of those thoughts. During the
next
few weeks, her anxiety attacks became less frequent and less
intense and,by the end of4 weeks,they disappeared completely.
Differences in Conceptual Framework between
Behavior Therapy and Cognitive Therapy
Behavior therapists conceptualize disorders of
behavior and procedures for their amelioration

within a theoretical framework borrowed from the
field of psychological learning theory and especially
by means of concepts of classical and operant
conditioning. Since these concepts are derived mainly
from experiments with animals, they focus on the
observable behavior of the organism. In fact, most of
the published writings on behavior therapy tend to
eschew inferred or hypothesized psychological states
which cannot be directly observed and measured.
Concepts andprinciples basedonimmediate referents
in the organism’s environment have advantages of
parsimony, testability, quantifiability, and reliability.
However, this framework does not readily accom-
modate notions of internal psychological states such
as thoughts, attitudes, and the like, which we
commonly use to understand ourselves and other
people. Cognitive therapists are more willing to use
these inferred psychological states, collectively called
“cognitions,” as clinical data. Consequently, large
and useful sets of variables are directly taken into
account.
In recent years, several writers in the area of
behavior therapy have acknowledged the importance
of mediational constructs or cognitive processes in
behavior therapy (Brady, 1967; Davison, 1968;
Folkins, Lawson, Opton, & Lazarus, 1968; Lazarus,
1968; Leitenberg, Agras, Barlow, & Oliveau, 1969;
London, 1964; Mischel, 1968; Murray & Jacobson,
1969; Sloane, 1969; Valins & Ray, 1967; Weitzman,
1967). Their cognitive formulations, however, have
for the most part been brief. Substantial amplifica-
tion of the nature of cognitive processes is necessary
to account adequately for clinical phenomena
and for the effects of therapeutic intervention (see
Weitzman, 1967).

A greater emphasis on the individual’s descriptions
of internal events can lead to a more complete view of
human psychopathology and the mechanisms of
behavioral change. By using introspective data, the
cognitive theorist has access to the patient’s thoughts,
ideas, attitudes, dreams, and daydreams. These
ideational productions provide the cognitive theorist
with the raw materials with which he can form
concepts and models. Such concepts are also capable
of generating hypotheses amenable to controlled
experiments on psychiatric patients (Loeb et al.,
1967). Also, introspective data, such as dreams and
cognitions, have been adapted to systematic investi-
gation (Beck, 1967).
Study and analysis of the introspective data suggest
that the cognitive organization, far from being a mere
link in the stimulus response chain, is a quasi-
autonomous system in its own right. Although this
system generally interacts with the environment to
a large extent, it may at other times be relatively
independent of the environment; for example, when
the patient is daydreaming or in the grip of an
abnormal state such as depression.
By getting inside the psychological matrix, as it
were, the cognitive theorist gains a glimpse of
considerable activity. Introspective data indicate the
existence of complex organizations of cognitive
structures involved in the processes of screening
external stimuli, interpreting experiences, storing
and selectively recalling memories, and setting goals
and plans (Harvey, Hunt & Schroder, 1961). Data
suggest that cognitive organizations are highly active
and are much more than a simple conduit between

stimulus and response.
A Cognitive Model of Psychopathology
The total cognitive organization appears to be
composed of primitive systems consisting of relatively
crude cognitive structures (corresponding to Freud’s
notion of Primary Process), and of more mature
systems composed of refined and elastic structures
(corresponding to the Secondary Process). Some of the
conceptual elements may be predominantly verbal,
whereas others may be predominantly pictorial.
Many of the primitive concepts are idiosyncratic
and unrealistic. Under ordinary waking conditions,
these idiosyncratic concepts appear to exert only
minimal or sporadic effects on the integrated thinking
of the individual. Peculiar or irrational cognitions
emanating from the primitive system are generally
tested, authenticated, and rejected by the higher
centers. However, when the cognitive organization
is dislocated, as in depression, anxiety, or paranoid
states, these idiosyncratic concepts are hyperactive.
In such circumstances, the conceptual systems grind
out a powerful stream of depressing, frightening, or
paranoid thoughts. As these idiosyncratic ideas
become hyperactive, they tend to supersede the more
realistic conceptualizations and to become more
refractory to reality testing and judgment.
The form of psychiatric disorder is related to
the content of the predominant, perseverating
verbal cognitions or fantasies. Depressed patients,
for example, report a high frequency of themes of
deprivation or of self-debasement in their waking
thoughts, daydreams, and dreams. Anxious patients
are dominated by the concept of specific or general-

ized personal danger. Paranoidpatients are controlled
by patterns relevant to unjustified abuse or persecu-
tion. The phobic patient has a disproportionate or
unrealistic notion of personal danger in specific and
avoidable situations. (When forced into these situa-
tions, he experiences anxiety in much the same way as
does the anxiety neurotic.) The compulsive patient is
dominated by doubts or by fears of some danger to
himself or others and he seeks to put an end to the
doubts or fears through rituals.
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Explanation of Therapeutic Change
How does the cognitive model provide an explanation
for the therapeutic effects of cognitive or behavior
therapy in states such as depressions, anxiety reac-
tions, or phobias?
First, the therapeutic situation produces a quieting
down of the hyperactive organization (Rachman,
1968). The quieting down may be the result of either
the therapist’s empathy and acceptance (Truax &
Carkhuff, 1967), his specific relaxation instructions
(Wolpe & Lazarus, 1966), or his explicitly stated
verbal approval (Wagner & Cauthen, 1968). The
quieting effects may also be produced by automated
relaxation instructions (Lang, 1969). In the treatment
of phobias, the quieting effect is introduced after the
schemas relevant to the phobia have been artificially
stimulated by the imagery instruction. As Lader and
Mathews (1968) have pointed out, reducing the level
of arousal below a certain critical point tends to
facilitate habituation (or desensitization).

Second, the therapeutic session affords an
opportunity for the patient to experience and to
reality-test verbal or pictorial cognitions that are
causally connected to his depressed or anxious
affect.
This mode of operation may be illustrated by the
treatment of a phobia through systematic desensi-
tization. In this procedure, the patient reproduces
the phobic situation in his fantasies, and experi-
ences the same type of anxiety (but in lesser degree)
that would occur if he actually were in the phobic
situation. Whether he is actually in the phobic
situation or is simply fantasizing himself in that
situation, he believes to some degree that he is in
danger. The more he believes in the reality of the
danger, the greater is his anxiety. At times the
fantasy may be so strong that the patient may
lose cognizance of the fact that he is not actually in
the phobic situation, and he may even scream for
help.
Many patients report that their fantasy experi-
ences are almost identical with the actual situational
experiences. The patient may live through the
frightening event in much the same way that a
patient with a combat neurosis relives (abreacts) a
combat experience under hypnosis or Amytal.
In systematic desensitization, the patient can
experience the problem in graded doses. This process
enables him, first, to experience the unpleasant event
(via imagery) and, second, to reality test his reactions
in status nascendi. Since the anxiety is not allowed
to mount up, the patient is able to regard the event

objectively. Even when flooding or implosive tech-
nique (Stampfl and Levis, 1968) is employed, the
patient still has the opportunity, when the fantasy has
been completed, to examine his reaction, and he soon
realizes that he has been reacting to a fantasy and not
to a real danger.
Another way of viewing the process of desensi-
tization is that the patient is enabled to increase his
objectivity, i.e., to discriminate between a real
danger and a fantasied danger as he proceeds in a
stepwise progression upthe desensitization hierarchy.
With increasing objectivity, he is less prone to
misread the situation or to accept his unrealistic
conceptualization of a situation. His increased
objectivity is reflected in a reduction in his anxiety
arousal by the imaged or the real situation (London,
1964).
Patients who are questioned at the termination of
an induced fantasy generally construethe threatening
situation differently and more realistically than
previously (Beck, 1970). The operation of cognitive
factors in desensitization has also been illustrated in
case material cited by Brown (1967) and Weitzman
(1967).
It could be argued that the phobic patient really
knows that there is no danger. However, his belief
that his fear is irrational exists only when the patient
is “safely” removed from the phobic situation. When
he is in the situation, he believes to some degree that
he is in danger. Desensitization is effective because it
provides a practice session in which the patient is able
to experience his reactions to the feared situation,
label them as inappropriate, and gain some inner

conviction that the phobic reaction is irrational.
The same mode of operation described in relation
to systematic desensitization may be observed in the
techniques of cognitive therapy. In cognitive psycho-
therapy, the patient examines his distorted ideas
and is trained to discriminate between rational and
irrational ideas, between objective reality and internal
embroidery. He is enabled to bring his reality testing
to bear and to apply judgment. He is thus able to
realize with conviction that his idiosyncratic ideas are
irrational.Oftenthe ideationis in theform of pictorial
fantasy, and the patient is able to view the fantasy as a
product of his mind and not as a veridical represen-
tation of a reality situation.
According to this analysis, a crucial mechanism in
the psychotherapeutic chain is a modification or shift
in the patient’s ideational system. As his irrational
concept that he is paralyzed (hysteria), helpless and
hopeless (depression), in danger (anxiety or phobia),
persecuted (paranoid state), or superhuman (mania)
becomes deactivated, the abnormal clinical picture
recedes.
Mechanism of Transfer or Generalization
Transfer of the desensitization to the phobic
situation can be explained readily using cognitive
concepts. When the untreated patient is placed in
the phobic situation (for example, an elevator,
tunnel, or bridge), he reacts as if there were a clear
and present danger to his life. His emotional

reaction, namely anxiety, is the same that would
be aroused if such a highly probable danger actually
did exist.
For example, a woman with an elevator phobia
would get the idea whenever she entered the elevator,
“There won’t be enough air in here and I will
suffocate.” Sometimes she would have a visual image
of herself gasping for air and suffocating. In addition,
she would experience a feeling of shortness of breath.
This experience occurred even when she was the
only passenger in a large, airy elevator. (The fear of
elevators has a different content from patient to
patient. Other patients believe that the elevator
cables will break during the ascent or descent, or
that the elevator will get stuck and they will starve to
death, or that they will be attacked by other people in
the elevator.) When away from the elevator,
however, the patient believed that her expectation
of suffocation was highly unreasonable.
In the therapy session the patient imagines that he
is in a phobic situation. The patient with an elevator
phobia, for instance, started to gasp for breath when
she was asked to imagine herself in the elevator. It
appears, both from the patients’ descriptions and
from external observation, that during the fantasy
the patient actually relives the situation as though it
were actually happening. In other words, the woman
with the elevator phobia who is simply imagining
herself in the elevator to some degree gets carried
away by the fantasy and to some degree perceives
herself as in the elevator at that time. Hence the fear
of being suffocated is stimulated even though she is in
the safety of the consultation room.
As the patient experiences her inappropriate

reaction during the desensitization procedure, she is
able to practice viewing her fears more objectively.
The transfer or the generalization to the real-life
situation may be explained in two ways: (a) The
rehearsal effect: The patient gains experience in
attacking the frightening ideas and therefore, as a
result of this practice, is able to counteract the
irrational ideas in the phobic situation; and (b) The
desensitization procedure produces a significant
modification in the patient’s concept of the phobic
situation so that the latent fear of being suffocated,
etc., is obliterated.
Conclusions
A question could be legitimately raised whether
introducing another system of psychotherapy is
warranted. The justification is twofold. First, the
theoretical framework of cognitive therapy is broader
than that of behavior therapy and of some of the
more traditional psychotherapies. This theoretical
framework is congruent with many of the assump-
tions of behavior therapy, but provides a greater
range of concepts for explaining psychopathology as
well as the mode of action of therapy. Moreover, the
theoretical structure of cognitive therapy yields
hypotheses that can be (and have been) readily tested
through the experimental techniques currently
available.
Secondly, the cognitive theories provide a frame-
work for the development of a number of therapeutic
strategies that are not derivable from the predomi-
nantly extrinsic concepts of the conditioning model.
Since these cognitive techniques, as well as the

behavior techniques, are easily defined and have
demonstrated some preliminary evidence of their
efficacy in clinical practice, further exposition seems
warranted.
Ultimately, the strategies of psychological modifi-
cation may be usefully regrouped into the cognition-
oriented techniques and the behavior-oriented
techniques. The cognitive techniques would include
the methods making direct use of ideational material
such as systematic desensitization and other forms of
induced imagery and in the direct attempts to modify
idiosyncratic cognitions. The behavioral techniques
would include those operations of a nonintrospective
nature, such as in operant conditioning, exposure
therapy, graded task assignments, roleplaying, and
assertive training.
References
Beck, A. T. (1963). Thinking and depression; I. Idiosyncratic
content and cognitive distortions. Archives of General
Psychiatry, 9, 324–333.
Beck, A. T. (1967). Depression: Clinical, experimental, and
theoretical aspects. New York: Hoeber.
Beck, A. T. (1970). Role of fantasies in psychotherapy and
psychopathology. Journal of Nervous and Mental Disease,
150, 3–17.
Brady, J. P. (1967). Psychotherapy, learning theory, and insight.
Archives of General Psychiatry, 16, 304–311.
Brown, B. M. (1967). Cognitive aspects of Wolpe’s behavior
therapy. American Journal of Psychiatry, 124, 162–167.

Carlson, W. A., Travers, R. M. W., & Schwab, E. A., Jr. (March
1969). A laboratory approach to the cognitive control of
anxiety. Paper presented at the meeting of the American
Personnel and Guidance Association, Las Vegas.
Davison, G. C. (1968). Systematic desensitization as a counter-
conditioning process. Journal of Abnormal Psychology, 73,
91–99.
Ellis, A. (1957). Outcome of employing three techniques of
psychotherapy. Journal of Clinical Psychology, 13, 344–350.
Ellis, A. (1962). Reason and emotion in psychotherapy. New
York: Lyle Stuart.
Folkins, C. H., Lawson, K. D., Opton, E. M., & Lazarus, R. S.
(1968). Desensitization of the experimental reduction of
threat. Journal of Abnormal Psychology, 73, 100–113.
http://refhub.elsevier.com/S0005-7894(16)30091-0/rf0005

784 be ck
Frank, J. D. (1961). Persuasion and healing. Baltimore: Johns
Hopkins Press.
Harvey, O. J., Hunt, D. E., & Schroder, H. M. (1961).
Conceptual
systems and personality organization. New York: Wiley.
Jones, R. G. (1968). A factored measure of Ellis’ irrational
belief
system with personality and maladjustment correlates.
Doctoral dissertation. Lubbock, Texas: Texas Technological
College.
Krippner, S. (1964). Relationship between reading improvement
and ten selected variables. Perceptual and Motor Skills, 19,
15–20.
Lader, M. H., & Mathews, A. M. (1968). A physiological
model of phobic anxiety and desensitization. Behaviour
Research and Therapy, 6, 411–421.
Lang, P. J. (1969). The mechanics of desensitization and the
laboratory study of human fear. In C. M. Franks (Ed.),
Behavior therapy: appraisal and status (pp. 160–191). New
York: McGraw-Hill.

Lazarus, A. (1968). Variations in desensitization therapy.
Psychotherapy: Theory, research and practice, 5, 50–52.
Leitenberg, H., Agras, W. S., Barlow, D. H., & Oliveau, D. C.
(1969). Contribution of selective positive reinforcement and
therapeutic instructions to systematic desensitization therapy.
Journal of Abnormal Psychology, 74, 113–118.
Loeb, A., Beck, A. T., Djggory, J. C., & Tuthill, R. (1967).
Expectancy, level of aspiration, performance, and self-
evaluation in depression. Proceedings of the Annual Conven-
tion, American Psychological Association, 2, 193–194.
London, P. (1964). The modes and morals of psychotherapy.
New York: Holt, Rinehart & Winston.
Mischel, W. (1968). Personalityand assessment.New York:
Wiley.
Murray, E. J., & Jacobson, L. T. (1969). The nature of learning
in traditional and behavioral psychotherapy. In A. E. Bergin
& S.L. Garfield (Eds.), Handbook of psychotherapy and
behavior change. New York: Wiley.
Rachman, S. (1968). The role of muscular relaxation in
desensitization therapy. Behaviour Research and Therapy,
6, 159–166.
Rimm, D. C., & Litvak, S. B. (1969). Self-verbalization and
emotional arousal. Journal of Abnormal Psychology, 74,
181–187.
Sloane, R. B. (1969). Converging paths of behavior therapy and
psychotherapy.American Journal of Psychiatry, 125, 877–885.
Stampfl, T. G., & Levis, D. J. (1968). Implosive therapy: A

behavioral therapy? Behaviour Research and Therapy, 6,
31–36.
Trexler, L. D., & Karst, T. O. (April 1969). The use of
fixed-role and rational-emotive therapy in treating public-
speaking anxiety. Paper presented at the meeting of the
Eastern Psychological Association, Philadelphia.
Truax, C. B., & Carkhuff, R. R. (1967). Toward effective
counseling and psychotherapy: Training and practice.Chicago:
Aldine.
Valins, S., & Ray, A. (1967). Effects of cognitive
desensitization
on avoidance behavior. Journal of Personality and Social
Psychology, 7, 345–350.
Velten, E. (1968). A laboratory task for induction of mood
states. Behaviour Research and Therapy, 6, 473–482.
Wagner, M. K., & Cauthen, N. R. (1968). Case histories and
shorter communications. Behaviour Research and Therapy,
6, 225–227.
Weitzman, B. (1967). Behavior therapy and psychotherapy.
Psychological Review, 74, 300–317.
Wolpe, J., & Lazarus, A. A. (1966). Behavior
therapytechniques: A
guide to the treatment of neuroses. New York: Pergamon Press.
RECEIVED: October 12, 2016
ACCEPTED: November 4, 2016
AVAILABLE ONLINE: 10 November 2016

http://refhub.elsevier.com/S0005-7894(16)30091-
0/rf0165Cognitive Therapy: Nature and Relation to Behavior
Therapy – Republished ArticleTechniques of Cognitive
TherapyOutline placeholderRecognizing Idiosyncratic
CognitionsDistancingCorrecting Cognitive Distortions and
DeficienciesCase Report55This patient was treated in
collaboration with Dr. William Dyson.Differences in
Conceptual Framework between Behavior Therapy and
Cognitive TherapyA Cognitive Model of
PsychopathologyExplanation of Therapeutic ChangeMechanism
of Transfer or GeneralizationConclusionsReferences

Available online at www.sciencedirect.com
ScienceDirect
Behavior Therapy 47 (2016) 785–803
www.elsevier.com/locate/bt
Cognitive-Behavioral Therapy: Nature and Relation
to Non-Cognitive Behavioral Therapy
Lorenzo Lorenzo-Luaces
John R. Keefe
Robert J. DeRubeis
University of Pennsylvania
1
Since the introduction of Beck’s cognitive theory of emotional
disorders, and their treatment with psychotherapy, cognitive-
behavioral approaches have become the most extensively
researched psychological treatment for a wide variety of
disorders. Despite this, the relative contribution of cognitive to
behavioral approaches to treatment are poorly understood
and the mechanistic role of cognitive change in therapy is
widely debated. We critically review this literature, focusing
on the mechanistic role of cognitive change across cognitive
and behavioral therapies for depressive and anxiety disorders.
Keywords: cognitive-behavioral therapy; cognitive theory;
psychotherapy processes; depression; anxiety
THE ORIGIN OF COGNITIVE-BEHAVIORAL THERAPIES
(CBTs) as a family of interventions can be traced to
the advent of behavioral treatments for psychopa-
thology in the 1950s and, later, the so-called
“cognitive revolution” of the 1950–1960s (Dobson,

2009). Consequently, CBTs blend techniques that are
emphasized in behavioral therapies (BTs) and cogni-
tive therapies (CTs). However, there remains skepti-
cism regarding the relative contributions of CT
strategies to BT strategies in promoting symptom
change within the CBTs (Longmore & Worrell,
2007). Additionally, critics have asserted that changes
in thinking are not mechanisms of change in CBTs
(e.g., Kazdin, 2007), calling into question whether
Correspondence regarding this article should be addressed to
Lorenzo Lorenzo-Luaces, University of Pennsylvania,
Department
of Psychology, 3720 Walnut Street D20, Philadelphia PA
19104;
e-mail: [email protected]
0005-7894/© 2016 Association for Behavioral and Cognitive
Therapies.
Published by Elsevier Ltd. All rights reserved.
there is any kind of contribution of the “cognitive” in
cognitive-behavioral therapy.
Despite debate regarding their active treatment
components as well as working mechanisms, CBTs
continue to be the most widely studied forms of
therapy (Hofmann, Asmundson, & Beck, 2013). A
uniquely appealing aspect of CBTs is that their theo-
ries of therapeutic change comport well with most
modern conceptualizations of psychopathology. In
this review, we attempt to reconcile skepticism
regarding the relative contribution of CT strategies
to BT, as well as the mechanisms that account for their
efficacy. First, we provide a very brief historical over-
view of the origins of CBT and discuss the support for
the cognitive vulnerability models to depression and
anxiety disorders. We discuss methodological chal-
lenges in psychotherapy research that have impeded

a more thorough understanding of the relative con-
tributions of cognitive to behavioral techniques. We
then focus most of our discussion on research on the
cognitive mechanisms of change in CT, BT, and CBTs
for depression and anxiety disorders.
We use the terms cognitive therapy (CT) and
cognitive techniques to refer to behaviors therapists
engage in that are targeted towards changing the
content or process of thoughts, inferences, inter-
pretations, cognitive biases, and cognitive schemas.1
The terms “cognitive therapy” (CT) and “cognitive-behavioral
therapy” (CBT) are often used interchangeably. We believe this
is
somewhat unfortunate in that it might be informative to reserve
the
term CT to a set of interventions within the broader family of
CBTs
that are more “purely” cognitive in nature. However, throughout
the
article, when we refer to findings in studies of CT or CBT, we
are
adhering to the label the study authors use. Additionally, we use
CBTs,
in plural, to refer to the family of cognitive-behavioral
therapies.
http://dx.doi.org/
http://dx.doi.org/
http://dx.doi.org/
mailto:[email protected]
786 l o re n zo - l ua c e s et a l .
These interventions can include Socratic question-
ing, examining the evidence for and against beliefs,

cognitive restructuring, and adopting alternative
core beliefs. We use the terms behavior therapy
(BT) and behavioral techniques to refer to behav-
iors therapists engage in that are targeted towards
a change in observable behavior, including in vivo
exposure, imaginal exposure, and activity sched-
uling. We use cognitive-behavioral therapies in the
plural (CBTs) to refer to the family of interventions
to which CT and BT belong, and in the singular,
CBT, to refer to a treatment package that combines
cognitive and behavioral techniques. By cognitive
change, we refer to changes in the content of
thoughts, inferences, interpretations, and cognitive
biases. By behavioral change, we refer to changes
in behavior, such as increasing the frequency of
selected behaviors (e.g., approaching feared stimuli,
engaging with pleasurable activities) or decreasing
the frequency of other behaviors (e.g., safety
behaviors). We include in our paper a discussion of
issues related to the conceptualization and measure-
ment of cognitive vs. behavioral interventions as well
as cognitive vs. behavioral mechanisms of change
and conclude with a summary and with recommen-
dations for future research.
Cognitive Therapy: Nature and Relation to
Behavioral Therapy
Behavioral therapies emerged in the 1950s–1960s
(O’Donohue & Noll, 1995). The behavioral
models emphasized maladaptive learning and self-
sustaining behaviors as key to the maintenance of
psychopathology. This made behavioral change
the obvious target of treatment, an approach that
was in stark contrast to the previously dominant
psychoanalytic models. Under psychoanalysis,

pathological behavior was seen to reflect dysfunc-
tion in underlying psychic structures. Behavioral
change was thus seen as surface-level “symptom
reduction” that did not address underlying prob-
lems. BTs proved very effective, particularly in the
treatment of phobias and more circumscribed
states of anxiety. Principles of associative learning
were used to account for the efficacy of these
interventions. To the behaviorists, learning had
a specific meaning: an overt change in behavior
(e.g., approaching a previously avoided stimulus)
in the absence of symptoms (e.g., without display-
ing the fear reaction). This definition avoided
“mentalistic” terms. Although early behavioral
models featured theoretical accounts focused on
associative learning, nonassociative learning, in-
cluding habituation, was also seen as important.
Newer behavioral models also focus on inhibitory
learning (Craske et al., 2008).
CT emerged in the context of the so-called cogni-
tive revolution (Beck, 1991; O’Donohue, Ferguson,
& Naugle, 2003) from the writings of Ellis (1962),
who described a form of therapy known as rational-
emotive therapy, and Beck (1963). The cognitive
models of Ellis and Beck focused on inferential errors
leading to maladaptive views of one’s self, world,
and the future. According to Beck, cognitive biases
and maladaptive cognitive content are the product of
the activation of cognitive schemas that typically
develop early in life. Unlike BTs, which were initially
successful in specific phobias and circumscribed
anxieties, CTs were focused on depressotypic pre-
sentations and more generalized anxiety. Early in
his writing, Beck recognized that his cognitive theory
of psychopathology, which gave a central role to
cognition in the etiology of disorder, contrasted

with behavioral theories of psychopathology. In his
highly cited article, “Cognitive Therapy: Nature
and Relation to Behavioral Therapy,” Beck (1970)
described important differences between the theories
that underlie BT and CT while recognizing areas of
overlap in the performance of the therapies. Similar-
ities include that both therapies deal with issues in
the present, are symptom-focused, and require active
therapist contribution.
Beck (1970) recognized differences between
behavioral and cognitive approaches. He applied
the principles of his then nascent cognitive theory to
account for the mechanisms of action of systematic
desensitization, a BT. He concluded that the cog-
nitive model “provides a greater range of concepts
for explaining psychopathology as well as the
mode of action of therapy.” That is, Beck made a
distinction between the nature of the therapeutic
interventions (i.e., cognitive vs. behavioral) and
their working mechanisms in providing a cognitive
account of the effects of a behavioral intervention.
Beck’s paper would become one of the early reflec-
tions on the relative contributions of cognitive to
behavioral strategies and the relevant mechanisms
of change. Although Beck has provided two up-
dates to his cognitive model (Beck, 1996; Beck &
Haigh, 2014), its basic tenets remain largely intact:
that the distinction between different forms of psy-
chopathology can be traced to differences in the
locus of the cognitive pathology and that cognitive
change, regardless of how this change is achieved, is
integral to symptom change.
Cognitive Vulnerability to Depression
and Anxiety

Basic research supports the notion that cognitive
vulnerabilities confer risk to the onset and main-
tenance of psychopathology (see Mathews &
MacLeod, 2005). Attentional biases to threatening
787cb t: n at ur e an d r el at ion to non -c bt
stimuli, along with overestimation of threat, have
been implicated in the etiology of anxiety disor-
ders (Bar-Haim, Lamy, Pergamin, Bakermans-
Kranenburg, & Van Ijzendoorn, 2007). Biases
associated with depression include difficulties dis-
engaging from negative material, sustained or sym-
metrical attention to negative, relative to positive,
stimuli (Kircanski & Gotlib, 2015), negative biases
in the appraisal of life events (Mehu & Scherer,
2015), symmetric memory for negative vs. neutral
or positive information (Kircanski & Gotlib,
2015), and negative schemas about the self that
foster maladaptive and negative thinking (Beck &
Haigh, 2014).
Overall, existing research is supportive of cog-
nitive vulnerability models of affective disorders.
For example, cross-cultural research consistently
suggests that, on average, healthy individuals have
a bias towards optimistic thinking that is not
found in individuals who are depressed and who,
instead, have a bias towards more negative thinking
(Mezulis, Abramson, Hyde, & Hankin, 2004).
Similarly, in a meta-analytic review of 172 studies
examining biases towards threatening stimuli,
Bar-Haim et al. (2007) found that anxious partic-
ipants are biased to attend to threatening stimuli,

relative to nonanxious participants (d = 0.45). The
causal role of these cognitive vulnerabilities, par-
ticularly in depression, has been questioned partly
because most of the early research on this matter
was correlational in nature (see Ingram et al.,
2006). Findings from prospective studies, however,
also support cognitive models. For example, daily
fluctuations in negative automatic thoughts have
been found to predict subsequent negative mood,
even controlling for prior levelsof automatic thoughts
(Wenze, Gunthert, & Forand, 2007; Wenze et al.,
2010). Negative dysfunctional attitudes also pre-
dict depressed mood following a stressor (Hankin,
Abramson, Miller, & Haeffel, 2004). In one
study, participants who were classified as being at
high cognitive risk were almost 7 times more likely
to report a major depressive episode at 2.5 years
follow-up, relative to those at low risk (Alloy et al.,
2006).
Although prospective studies provide a stronger
level of evidence for causality than correlational
studies, findings from these studies are still subject
to third variable confounds, making experimental
designs preferable. Relatively few experiments
manipulating cognitions and assessing the effects
of the manipulation on mood have been conducted.
The results of these experiments, however, are
consistent with models of cognitive vulnerability
(see Mathews & MacLeod, 2005). For example, in
a series of experiments, Mathews and Mackintosh
(2000) reported that inducing bias in the interpre-
tation of ambiguous information as threatening
leads to increases in state anxiety. In another study,
MacLeod et al. (2002) manipulated attention to
emotionally negative information. After a stressor

task, participants who had had their attention
manipulated towards negatively valenced stimuli
showed greater anxiety and depression than par-
ticipants in the control group.
If cognitive biases increase the risk for depression
and anxiety states, it follows that strategies that
address these biases should result in a reduction of
risk. This hypothesis has support in basic research
on emotion regulation. Webb, Miles, and Sheeran
(2012) conducted a meta-analysis of 306 compar-
isons of emotion regulation strategies. Strategies
that focused on cognitive change were estimated to
be the most consistently effective ways of regulating
emotions (d = 0.36). Strategies aimed at helping
individuals adopt more rational perspectives, as is
encouraged in CT, were associated with the largest
effect (d = 0.45). Providing even more support for
cognitive theories, studies that examine the bio-
logical vulnerabilities to negative emotional states
suggest that, at the phenomenological level, biolog-
ical vulnerabilities render individuals more likely to
experience negative emotional states by interfering
with their abilities to engage in cognitive reapprais-
al strategies (Firk, Siep, & Markus, 2013; Lemogne
et al., 2011).
More research is needed that characterizes more
precisely the nature of the cognitive biases impli-
cated in depression and anxiety, especially research
that is experimental. The relationship between
affective disorders and cognition is bidirectional,
which must also be accounted for in theories of
psychopathology. However, given the amount of
evidence and the dearth of competing explanations,
it can be safely asserted that the cognitive model is

a valid characterization of the etiology of affective
disorders. Thus, one would expect considerable
support for the hypothesis that change in cognition
mediates symptom change in the context of psy-
chotherapy. Instead, the literature contains ques-
tions about whether “we need to challenge thoughts
in cognitive behavior therapy?” (Longmore &
Worrell, 2007) and assertions such as “whatever
may be the basis of changes with CT, it does not
seem to be the cognitions as originally proposed”
(Kazdin, 2007). Why is this so?
It’s Complicated
Previously, we (Lorenzo-Luaces, German, &
DeRubeis, 2015) have argued that disagreement
among commentators (e.g., Kazdin, 2007; Longmore
& Worrell, 2007) regarding the role of cognitive
change in promoting symptom change in psycho-
therapy for depression emerges from different
assumptions regarding the inferences that can be
drawn from treatment studies. Below we review
some of these issues in psychotherapies for depres-
sion and anxiety.
experimental designs: additive and
dismantling studies
When two treatment packages are very different
(e.g., psychoanalysis vs. exposure and response-
prevention), it is easy and perhaps even appropriate
to interpret findings from studies comparing treat-
ment packages to reflect the relative efficacy of
specific therapy procedures (e.g., analyzing trans-

ference vs. engaging in exposure). However, when
assessing treatments, such as CBT or eye-movement
desensitization and reprocessing (EMDR), which
combine multiple active and overlapping elements,
in this case exposure and cognitive restructuring
(Tolin, 2014), it becomes more difficult to extrap-
olate conclusions about therapy procedures from
outcome data.
In lieu of tightly controlled basic research, such
as the research on emotion regulation strategies
(Webb et al., 2012), researchers have used compo-
nent studies as a way of addressing questions about
the differential utility of treatment elements. These
component studies are often referred to as if they
represent a single class of study design, but there are
at least two different types of study designs, additive
and dismantling designs, that fall under this rubric.
As described by Bell, Marcus, and Goodlad (2013),
they address different kinds of questions. In additive
component studies, in one condition a component
is added to and compared with an already-existing,
simpler treatment. Butler, Cullington, Munby,
Amies, and Gelder (1984) provide an early example
of such a study. They examined the value of adding
anxiety management to exposure for social anxiety
by comparing the combined treatment to exposure
only as well as to exposure plus a nonspecific filler.
Their findings suggested that adding anxiety man-
agement to exposure improved treatment outcomes.
In dismantling designs, at least one component of a
multicomponent treatment package is removed from
the treatment and compared to the full treatment
package or to the other components. For example,
Foa, Steketee, Grayson, Turner, and Latimer (1984)
dismantled exposure and response-prevention (ERP)

and compared its effects with the effects of exposure
only and response prevention only. Their findings
suggested that ERP was superior to either of its single
components and that, for contamination fears, ex-
posure alone may be more effective than response-
prevention alone. Bell et al. (2013) conducted a
meta-analytic review of components studies and
concluded that it is uncommon, in studies that have
used dismantling designs, for one component of
a treatment to outperform another. However, in
studies that have used additive designs, adding one
treatment component to another enhances positive
therapeutic outcomes, particularly in the longer
term.
A meta-analysis by Adams et al. (2015) addressed
the contribution of CT to BT and did not find an
added benefit of CT to BT and CBT packages.
However, this meta-analysis did not differentiate
between additive and dismantling designs. Al-
though, on the face of it the component studies in
the meta-analysis by Adams et al. seem like they
provide very conclusive answers about the superi-
ority or equipotency of CT and BT, component
studies, as they have been conducted and inter-
preted, have been extremely problematic. Summar-
ily reviewing some of the limitations of component
studies, Bell et al. (2013) stated:
… Null results [in component studies] do not directly
address the issue of specific versus common factors because
there is no group that received only common treatment
components. [...] Component designs may also under-
estimate the contributions of the component. Rehm (2009)
suggested that because much improvement typically occurs
in the early stages of therapy, whichever component is

presented first will appear to be the most effective. Thus, the
dismantled component (which is never introduced) is likely
to appear unnecessary. Component studies are also likely to
be statistically underpowered (Kazdin & Whitley, 2003) to
detect the relatively small effect sizes that are likely to occur
with these types of designs. […]. [A] two-group component
study with a presumed effect size of .24 (half the treatment
vs. placebo effect size) would require over 250 patients
in each condition to have a power of .80. Even Kazdin
and Whitley’s (2003) higher estimate of an effect size of
.45 for additive design studies would require 78 patients
in each condition. In contrast, the average sample size for
the studies included in the present meta-analysis was 23
participants in each condition, which would require a large
effect size of .84 to have a power of .80.
The component methodology evidenced a surge
in popularity following a landmark study by
Jacobson et al. (1996). Jacobson et al. conjectured
that the full CBT for depression package could be
divided into three components: (1) behavioral
activation (BA); (2) challenging automatic thoughts
(ATs); and (3) modifying core beliefs (CBs). To
compare the relative efficacy of these procedures,
and perceiving limitations in prior work suggesting
that CT for depression was superior to BT (Shaw
1977), Jacobson et al. randomized participants to
three conditions lasting a maximum of 20 sessions:
(1) 100% BA; (2) a condition that could use all
the elements of BA and could include AT work; and
(3) a condition that could use all of the elements of
BA, work on ATs, with a required minimum of 8

sessions devoted to CB work. In this study, across
various metrics, no statistically significant between-
conditon differences in outcome were reported.
These findings have generally been misinterepreted
as indicating that BA is the active component in
CBT for depression and that the interventions
provided in the cognitive components were inert,
thus presenting a major challenge to Beck’s cogni-
tive theory (Longmore & Worrell, 2007).
Data from assessments of therapists’ adherence
speak to the construct validity of the experiment
by Jacobson et al. (1996). Although, in terms of
the absolute frequency with which techniques were
conducted, behavioral work was nearly as frequent
in the CB condition as they were in BA, the relative
frequency of BA procedures was greater in BA than
in AT and CB. In the follow-up analysis of the trial,
Jacobson and colleagues went on further to note:
... by definition, participants in the BA condition received
more BA than did those in the other treatment conditions.
Although one might be tempted to infer from this study that
cognitive interventions are nonessential, our study does not
directly address the validity of such an interpretation. All we
can conclude is that adding cognitive interventions to BA is
no more effective than using that time to add more BA.
(Gortner, Gollan, Dobson, & Jacobson, 1998, p. 381,
emphasis added)
In other words, if the findings from Jacobson
et al. (1996) are taken to mean that CT procedures
are inert, a corollary emerges that was not tested in
their design: that a BA condition that allowed only
6 or 7 sessions (one-third of the 20 sessions) should
yield outcomes equivalent to a 20-session course

of BA. Thus, per Gortner et al. (1998), the only
hypotheses regarding behavioral treatment of de-
pression that could have been tested with the study
design were that BA is: (a) superior to, or (b) not
inferior to, a cognitive-behavioral treatment. As
there were no significant differences between the
treatments, the most that can be said is that the BA
condition, in the context of a study with low power,
was not shown to be inferior to treatments that
divided time between cognitive components and
behavioral ones.
Very few dismantling studies have directly
compared “pure” cognitive and behavioral inter-
ventions. The handful of studies that have com-
pared purely behavioral (e.g., activity scheduling)
to purely cognitive (e.g., cognitive restructuring)
treatments for depression have tended to find little
if any difference in the acute effects of cognitive
versus behavioral treatments (Mazzucchelli, Kane,
& Rees, 2009). In one study comparing BA to CT
(Dimidjian et al., 2006), although there were no
statistically significant differences between the two
treatments, BA was more effective than CT or
medications for individuals who were severely
depressed. In the BA condition, 76% of more
severely depressed participants met criteria for re-
sponse or remission, compared to 48% of patients in
CT and 49% in antidepressant medications. Among
the less severely depressed patients, response rates
on the BDI were 56% in CT, 60% in BA, and 40%
in ADM. Coffman et al. (2007) identified patients
from the Dimidjian et al. trial who exhibited a
pattern of “extreme non-response” (ENR) in CT
(approximately one-fourth of those assigned to CT)
and noted that none of the patients assigned to BA

evidenced an ENR. At baseline, the CT ENR patients
were more severely depressed, evidenced more
functional impairment, and reported more problems
with their primary support group. They interpreted
these findings to suggest that, relative to CT and
medications, BA may be particularly effective for
patients with severe depression that is accompanied
by interpersonal dysfunction. However, it should be
noted that the advantage of BA over CT dissipated
entirely across the trial’s 2-year follow-up (Dobson
et al., 2008). Moreover, to our knowledge, the
findings of Dimidjian et al. (2006) have not been
replicated. An attempt to replicate Coffman et al.’s
ENR findings in a separate sample of depressed
patients (Koenig, Jarrett, Gallop, Barrett, & Thase,
2014) treated with CT found a low (6%) rate of
nonresponse, and severity, functional impairment,
and interpersonal problems were not good predictors
of nonresponse. Finally, Webb et al. (2013) found
that the therapists in the Dimidjian et al. (2006) trial
implemented CT with a relatively more behavioral
than cognitive focus, compared to therapists from
other CT trials.
The effect of cognitive change strategies in Beck’s
C(B)T for depression has also been questioned, on
the basis that much of symptom change occurs early
in treatment (Ilardi & Craighead, 1994). However,
it has been shown in several studies that CBT
therapists use cognitive change techniques as early
as session one (Braun, Strunk, Sasso, & Cooper,
2015; Conklin & Strunk, 2015; Strunk, Brotman,
& DeRubeis, 2010). In fact, at least one therapy
manual (i.e., Muñoz & Miranda, 1986) addresses
cognitive change exclusively for several sessions
before addressing behavior.

In anxiety disorders, among the studies included
in the meta-analyses of Adams et al. (2015) and Bell
et al. (2013), only eight studies (Barlow, Rapee,
Brown, 1992; Borkovec, Newman, Pincus, & Lytle,
2002; Emmelkamp & Beens, 1991; Marks, Lovell,
Noshirvani, Livanou, & Thrasher, 1998; Mattick,
Peters, & Clarke, 1989, Szymanski, & O’Donohue,
1995; White, Keenan, & Brooks, 1992; Williams,
& Falbo, 1996) compared a purely cognitive
treatment condition to a purely behavioral condi-
tion. Among these eight studies, we conducted a
random effects meta-analysis (settings as per
IntHout, Ioannidis, & Borm, 2014). There was no
statistically significant difference in end-state pri-
mary outcomes between “pure” CT and “pure”
BT (higher values indicate superiority for CT; g =
0.010 [95% CI: -0.203 to 0.222], SE = 0.090, t =
0.106, p = 0.919; see Fig. 1). There was minimal
heterogeneity between effect sizes included in the
meta-analysis (Cochrane’s Q = 3.371, df = 7, p =
0.849; 14.90% heterogeneity), consistent with an
account that trial-level findings were generally
equivocal, with few meaningful between-trial dif-
ferences in effects. The results of these studies
suggest that CTs can be as effective as BTs in the
treatment of anxiety disorders. Although exposur-
e-based treatments are considered the mainstay
of CBTs for anxiety, other meta-analytic reviews
also suggest that ERP, CBT, and CT are about
equally effective across a range of anxiety disorders
(Norton & Price, 2007; Ougrin, 2011). This led

Arch and Craske (2008) to propose that cognitive
restructuring is a form of exposure whose effects
are possibly cognitively mediated. One exception to
the pattern of equivalence in CT and BT is that, for
OCD, ERP appears to be more effective than CT
FIGURE 1 Meta-analytic plot of the comparative efficacy of
“pure” C
Adams et al. (2015) and Bell et al. (2013). Positive values
indicate a super
effect size of the end-scores of a trial primary outcome measure,
sele
prepared by LLL. No notable changes in effect size or statistical
significanc
meta-regressing the Hedge’s g of the pre-treatment score
differences bet
not detect the presence of a significantly asymmetrical funnel
plot pot
Copas’ (2010) test of publication bias proffered a similar
between-grou
(Fisher & Wells, 2005; McLean et al., 2001; but see
Öst, Havnen, Hansen, & Kvale, 2015). Another
exception is that, in social anxiety, the CT com-
ponent appears to add to the efficacy of exposure
(Hofmann, 2004; Mayo-Wilson et al., 2014;
Ougrin, 2011; but see Chambless & Gillis, 1993).
It has been suggested that, because with some
anxiety disorders cognitive techniques may add little
or nothing to the efficacy of BTs, exposure and other
BTs are best conducted without the questioning
of beliefs or the provision of other CT procedures
(e.g., Arch & Craske, 2008). Indeed, a favored
approach to the treatment of simple phobias has
been and continues to be one that relies primarily or
only on BT techniques (Wolitzky-Taylor, Horowitz,
Powers, & Telch, 2008; but see Choy, Fyer, &

Lipsitz, 2007). Some BTs, like the ones focused on
relaxation, do not even directly address feared
stimuli which may be taken to call into question
the need to engage in cognitive work. There are at
least two things to keep in mind regarding these
comparisons. First, there is no evidence that these
therapies lead to greater symptom reduction than
CT (e.g., Borkevec et al., 2002; Mayo-Wilson et al.,
2014). Second, the fact that these therapies, which
do not directly address thinking, are effective does
not directly inform about their mechanisms. Recall
that Beck (1970) accounted for the efficacy of
T compared to “pure” BT in anxiety disorder RCTs identified by
iority of CT over BT. Hedge’s g was calculated as a between-
groups
cted by RJD and JRK from a results-blinded list of trial
outcomes
e resulted from controlling for pre-treatment severity
differences by
ween treatments (analyses available upon request). Egger’s test
did
entially indicative of publication bias (p = 0.169), and Henmi
and
ps effect estimate (g = 0.017).
behavioral therapies, giving the specific example of
desensitization, in cognitive terms.
techniques vs. mechanisms
It appears to be a frequent misunderstanding of
comparative psychotherapy research, including com-
ponent trials, that outcome studies inform about
the mechanisms of treatments. Various authors have

cautioned against conflating the efficacy of thera-
peutic procedures with their mechanisms of action
(e.g., Hofmann, 2008; Lorenzo-Luaces et al., 2015),
and the separation between therapeutic procedures
and mechanisms has long been recognized (e.g., Beck,
1970; Foa & Rauch, 2004). Jacobson et al. (1996)
explained it this way:
Of course, it is also possible that BA-focused treatments are
more effective ways of changing the way people think than
treatments that explicitly attempt to alter thinking. Perhaps
the exposure to naturally reinforcing contingencies produces
changes in thinking more effectively than the explicitly
cognitive interventions do. (p. 303)
Although it may be tempting to assume that BT
and CT produce symptom change via different
theorized mechanisms (see DeRubeis, Brotman, &
Gibbons, 2005), they may also do so by the same
mechanisms (Hofmann, 2008). It is possible that
both treatments work because they change think-
ing. A pattern of findings that would be consistent
with this hypothesis is that both therapies change
cognition and that the cognitive changes lead to
symptom change irrespective of how the cognitive
changes are achieved. This latter point is one of
contention in the research literature because some
have erroneously assumed that a cognitive theory
of change implies that change in cognition leads to
symptom change uniquely in CBTs (see Hollon,
DeRubeis, & Evans, 1987). To the contrary, cogni-
tive theories highlight the mechanistic role of cog-
nition in psychopathology (Lorenzo-Luaces et al.,
2015).
Given that findings from comparative outcome

studies can, at best, provide food for thought about
mechanisms of change, what is needed is more
research on the psychological changes that account
for symptom change in psychotherapy. In the con-
text of component designs (e.g., Hofmann, 2004),
as well as in other kinds of randomized compari-
sons, investigations of the mediation of the effects
of psychotherapy promise to advance the under-
standing of the workings of psychotherapy.
temporality
One of the greatest challenge to our understanding
of how BT and CT work is that most studies that
explore these questions have been unable to rule out
reverse causality. Inferences about causality rest on
the ascertainment of the correct temporal relation
of the criterion and predictor variables. One must
have confidence that change on the predictor
variable preceded the change in the criterion. This
has sometimes been interpreted to mean that pre-
post changes in an outcome measure, regressed on
an index of early change, establishes temporal
precedence. However, it frequently is the case that
substantial portions of pre to post changes in both
proposed mediator and the outcome occur early in
treatment, making early measurement of the medi-
ator variable a crucial step in establishing causality.
Changes in the criterion variable must be assessed
subsequent to the assessment of change in the
mediator if the aim is to rule out reverse causality.
Only a small minority of tests of relations between
symptom changes and proposed mediators of those
changes has conformed to this pattern.
third variable confounds
Even in studies with the temporal features that allow

reverse causality to be ruled out, third variable con-
founds can limit the inferences that can be made.
Third variable confounds can never be entirely ruled
out because the multitude of variables that may
be confounding the relation between a therapeutic
procedure, a mechanism, and symptom change are
unknown and potentially unknowable. With obser-
vational studies the best one can do is to test for the
most plausible confounds, using the best available
measures of the potentially confounding construct.
Experimental designs can protect against many of
the third variable confounds, but unobserved vari-
ables may still act as proxies for the purported
mediating construct. Yet, as noted by Kazdin (2007),
most of the experimental designs in psychotherapy
are manipulations of the therapy, not of the proposed
mediator.
In the study of change in psychotherapy, the
domains most commonly hypothesized to account
for symptom change have been: common factors,
especially the therapeutic alliance; cognitive change;
and behavioral changes. Ideally, a study that was
attempting to address questions about causality in
psychotherapy would include measures or manipu-
lations of these phenomena. Given that the literature
is replete with studies that measure only one or two
of these variables, any conclusion that can be drawn
about common factors, cognitive change, and be-
havioral change is necessarily tentative.
statistics and mediation
Another conceptual hurdle in the understanding of
the relationship between therapeutic procedures,

cognitive change, and symptom change regards the
role of statistical analyses. Statistical tests cannot
determine causality. It does not matter how robust
the test’s statistic is or whether the test is conducted
in the context of so-called “causal modeling.” The
crucial matter is whether the structure of the data,
which is dependent on the assessment schedule,
meets the assumptions of causal models. In addi-
tion, plausible third variables confounds must be
ruled out. Thus, a series of carefully planned single-
case studies, in which mediators are experimentally
manipulated, and temporal order and third variable
issues are addressed, may provide stronger evidence
concerning the causal status of a mediator than
would the use of more seemingly sophisticated
data analyses developed in a large sample (if there
is overlap in the time periods referenced in the
mediator and outcome assessments).
Furthermore, an assumption in the writing of
several commentators is that mediational tests
are the sine qua non for establishing causality (see
Hundt, Mignogna, Underhill, & Cully, 2013;
Kazdin, 2007). As it relates to cognitive change
procedures and cognitive change, in the mediation
framework proposed by Baron and Kenny (1986),
evidence concerning cognitive change as a mediator
of symptom change is given by answers to the
following questions:
1. Are cognitive change procedures more effica-
cious than (at least some) other procedures?
2. Do cognitive change procedures generate

more cognitive change than those other
procedures?
3. Does superiority in cognitive change account
for superior symptom change in the context
of cognitive change procedures vs. those other
procedures?
This framework for conducting tests of media-
tion is widely accepted, but can easily be mis-
applied. Two change procedures can result in
equivalent magnitudes of changes both on the
outcome variable and on a putative mediator
variable. For example, when cognitive and be-
havioral techniques produce equivalent outcomes,
they may do so because they are equally effective
at changing cognitions (or behavior). A study may
find that cognitive and behavioral techniques are
equally effective in changing symptoms, cogni-
tion, and behavior. However, a traditional medi-
ational analysis will not be informative unless a
condition is included in the design and analysis
that produces less change in the mediator(s) and
the symptoms because there would be no effect to
mediate. As regards the role of cognitive change in
producing symptom change, there are four guid-
ing questions:
1. Are cognitive change procedures more effica-
cious in reducing symptoms than other
procedures?
2. Do cognitive change procedures generate more
cognitive change than other procedures?
3. Does cognitive change lead to symptom

change?
4. Is cognitive change a specific predictor of
symptom change only in the context of cog-
nitive change interventions?
Although some writers have assumed that the
cognitive change model implies that the answer to
all of these questions should be affirmative (e.g.,
Longmore & Worrell, 2007), we have argued that
only the third question is a test of the cognitive
theory of change (Lorenzo-Luaces et al., 2015). In
agreement with Jacobson et al. (1996) it is even
possible that a noncognitive procedure will produce
more cognitive change than an explicit cognitive
focus. The question is whether cognitive change, once
it has been produced, leads to symptom change.
Behavioral Change Strategies, Cognitive
Change, and Symptom Change
Existing evidence largely supports cognitive chang-
es as mechanisms of change in cognitive, behavior-
al, and cognitive behavioral therapies. Most of this
research has been conducted in the context of social
anxiety, panic disorder (Smits et al., 2012), and
depression (Lorenzo-Luaces et al., 2015). Below,
we review evidence for the role of cognitive change
in symptom change in CT, BT, and CBT.
social anxiety
Cognitive models of social anxiety highlight the
etiological role of cognitive biases in the perceived
likelihood that negative social events will occur
(Smits, Rosenfield, McDonald, & Telch, 2006), as
well as in the overestimation of costs associated

with these events (Clark & Wells, 1995). Moreover,
it has been suggested that individuals with social
anxiety tend to believe they are less socially desirable
than they actually are (Moscovitch, 2009).
The proposed cognitive mediators of outcomes in
social anxiety co-vary with symptom change in
CBTs (Hofmann, 2008; Wilson & Rapee, 2005).
For example, Boden et al. (2012) reported that
changes in maladaptive interpersonal beliefs fully
accounted for changes in social anxiety over the
course of CBT for social anxiety. Hoffart, Borge,
Sexton, and Clark (2009) explored four cognitive-
behavioral and four interpersonal processes of
change in CBT and interpersonal psychotherapy
(IPT) for social phobia. The lone IPT variable that
predicted symptom change, perceived acceptance by
others, is arguably a cognitive construct. By con-
trast, change in each of the four cognitive-behavioral
variables—self-focus, estimated probability of nega-
tive social events, estimated cost of negative social
events, and safety behaviors—predicted changes in
social anxiety. Changes in positive, but not negative,
self-view have been reported to co-vary with the
reduction of social anxiety symptoms following
acute CBT and over a 1-year follow-up (Goldin
et al., 2013). Changes in self-focused attention have
also been reported to account for treatment out-
comes in individual CT and in group-based CBT
(Hedman et al., 2013), whereas change in negative
and positive self-statements predict outcomes in ACT
and CBT (Niles et al., 2014).

Thus, a variety of cognitive constructs have shown
associations with symptom improvement in CT,
CBT, IPT, and ACT. An issue with many of these
studies, however, is that the measurement of the
predictor and criterion variables is contemporane-
ous. In one study that accounted for the temporal
order of change in a mediator and change in out-
come, Goldin et al. (2014) reported that the success
(but not the frequency of use) of cognitive reappraisal
strategies predicted subsequent decreases in social
anxiety symptom. Decreases in social anxiety did
not predict the successful use of cognitive reappraisal
strategies. This study is encouraging in suggesting
that cognitive process variables predict symptom
change in social anxiety. However, given the large
number of cognitive constructs that have been
reported to co-vary with outcomes in social anxiety,
it is likely that at least some of them are products
rather than predictors of symptom change. Illustrat-
ing this point, Smits et al. (2006) found that
changes in probability biases for negative social
events predicted changes in social anxiety. However,
after symptoms improved, there was a reduction in
patients’ estimates of the costs attributed to negative
social events. This pattern of results suggests that
whereas changes in probability biases were causally
related to symptom change, changes in cost estimates
were the consequence of symptom change. These
findings were replicated successfully and tested
against the therapeutic alliance as a competing
predictor of change (Calamaras, Tully, Tone, Price,
& Anderson, 2015). In this study, the alliance was
not found to predict symptom change.
panic

In cognitive models of panic disorder, catastrophic
misinterpretations of interoceptive cues are implicat-
ed in the etiology and maintenance of the pathology
(Clark, 1986). Anxiety sensitivity, the attribution of
negative somatic, cognitive, and social consequences
to anxiety, has been specifically reported to render
individuals vulnerable to panic disorder (Reiss,
1991). Additionally, panic self-efficacy, the percep-
tion of one’s ability to cope with panic attacks, has
also been implicated in the maintenance of the
disorder (Casey, Oei, & Newcombe, 2004).
In one study, fear of bodily sensations and anxiety
sensitivity, jointly “fear of fear,” were reported
to mediate the superiority of exposure relative to
a wait-list control (Smits, Powers, Cho, & Telch,
2004). Casey, Oei, Newcombe, and Kenardy (2004)
reported that changes in catastrophic misinterpreta-
tions, as well as changes in self-efficacy, co-varied
with symptom change in CBT. Others, however,
have reported that changes in self-efficacy, but not in
catastrophic beliefs, correlate with symptom change
(Fentz et al., 2013; Hoffart, 1995).
Attending to the temporal order of cognitive and
symptom change, Teachman, Marker, and col-
leagues have reported that cognitive change pre-
cedes and predicts symptom change in CBT for
panic (Teachman, Marker, & Clerkin, 2010;
Teachman, Marker, & Smith-Janik, 2008). In one
study, changes in automatic panic associations
predicted changes in symptom severity (Teachman
et al., 2008). In another study, changes in cata-
strophic misinterpretations predicted subsequent
change in overall symptom severity, panic attack
frequency, panic apprehension, and avoidance

behavior (Teachman et al., 2010). Gallagher et al.
(2013) also provided evidence for the temporal
precedence of changes in anxiety sensitivity and also
found changes in self-efficacy to precede symptom
change. These authors observed that overall change
in anxiety sensitivity was greater than change in
self-efficacy, and that changes in self-efficacy oc-
curred later in treatment than changes in anxiety
sensitivity. Taken together, these studies support the
mediational roles of anxiety sensitivity, catastrophic
misinterpretations, and panic self-efficacy as cogni-
tive mediators of treatment effects in CBTs for panic
disorder (Sandin et al., 2015).
ptsd
Current theories of posttraumatic disorder (PTSD)
highlight the causal role of associations between
threatening (unconditioned fear stimuli) and non-
threatening (i.e., conditioned) stimuli in fear struc-
tures of traumatic memories (Cahill & Foa, 2007).
Additionally, trauma-related cognitions about the
self, others, and the world—most commonly mea-
sured with the Post-Traumatic Cognitions Inventory
(PCTI; Foa, Ehlers, Clark, Tolin, & Orsillo, 1999)—
have also been implicated in the etiology and main-
tenance of the disorder.
In prolonged exposure (PE), changes in negative
cognitions about the self have been reported to
co-vary with changes in PTSD symptoms, whether
or not the intervention includes cognitive restruc-
turing (Foa & Rauch, 2004). In a sample of patients

with a severe mental illness comorbid with PTSD,
changes in posttraumatic cognitions were found to
mediate the superiority of CBT relative to treatment
as usual (Mueser et al., 2008). Research attending
to the temporality of cognitive change and symp-
tom change suggests that these findings do not
reflect an epiphenomenal status for the cognitive
changes. In patients who received trauma-focused
CT for PTSD, weekly changes in trauma-related
cognitions predicted subsequent reduction in symp-
toms (Kleim et al., 2013). Similarly, using data from
a sample of patients who received PE, Zalta et al.
(2014) reported that session-to-session changes in
trauma-related cognitions predicted subsequent
changes in PTSD symptoms, but not the other
way around. Thus, there is support for the cognitive
model of symptom change in treatments for PTSD,
although more research, with tests of additional
measures of trauma-relevant cognition, would help
advance our understanding of how treatments for
PTSD work.
ocd
Cognitive theories of obsessive–compulsive disor-
der (OCD) highlight the role of various cognitive
variables. Overly attaching significance to one’s
thoughts is central to Rachman’s influential cogni-
tive theory (Rachman, 1997). Intolerance of uncer-
tainty, overestimation of threat, the belief that
thoughts should be controlled, inflated sense of
responsibility, and perfectionism have also been
implicated (Obsessive Compulsive Cognitions
Working Group, 2003), with disagreement among
the authors as to which cognitions are key to the
etiology of OCD (Grayson, 2010; Gwilliam, Wells,
& Cartwright-Hatton, 2004).

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