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Summary articles Anxiety and related disorders

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This is a summary of all the articles for the course Anxiety and related disorders for the Master clinical psychology. Every article is included EXCEPT: Menzies, R.G. & Clarke, J.C. (1995). The etiology of phobias: a non-associative account. Clinical Psychology Review, 15, 23-48.

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Articles summary – Anxiety and related disorders

Week 1- Emotion Theory:
Mineka & Zinbarg (2006). A contemporary learning theory perspective on the etiology of anxiety disorders. Am Psychol, 61, 10-26.
The authors describe how contemporary learning theory and research provide the basis for perspectives on the etiology and maintenance of
anxiety disorders that capture the complexity associated with individual differences in the development and course of these disorders. These
insights from modern research on learning overcome the shortcomings of earlier overly simplistic behavioral approaches, which sometimes
have been justifiably criticized.
Most of us know that anxiety disorders would typically develop during or following a frightening or traumatic event or during a period of
significant stress when many of us experience some anxiety. Yet not everyone undergoing traumas or highly stressful periods develops an
anxiety disorder. Any good etiological theory must be able to account for this and many other apparent mysteries involved in who does and
who does not develop an anxiety disorder.
Although behavioral/learning approaches were the dominant empirical perspective on anxiety disorders from the 1920s until the 1970s, these
approaches have been widely criticized since the early 1970s. Many of these criticisms stemmed from the inability of early learning approaches
to account for the diverse factors involved in the origins of people’s anxieties.
- We believe that a contemporary learning theory approach can account for complexity at least as well as the other two prominent
contemporary psychological approaches to anxiety disorders—that is, the cognitive and the psychodynamic approaches. Moreover, we
believe that these new contemporary learning approaches have several advantages over the other two approaches: The learning
approaches are better grounded in the theories and methods of experimental psychology, they provide more comprehensive
formulations of the etiology of anxiety disorders, and they provide a more explicit analysis of factors promoting or inhibiting the
development of different anxiety disorders.
Specific phobia 
Individuals with specific phobias show intense and irrational fears of certain objects or situations that they usually go to great lengths to avoid.
Watson and Rayner (1920) originally argued that phobias are simply intense classically conditioned fears that develop when a neutral stimulus
is paired with a traumatic event, such as occurred when their Little Albert acquired an intense fear of rats after hearing a frightening gong
paired with the presence of a rat several times. This straightforward view of phobia acquisition was later criticized for several reasons we will
discuss. However, each of the cited problems with such views generally reflects some ignorance of a wide variety of vulnerability and
invulnerability factors that are predicted by contemporary learning theory to strongly influence who develops phobias among all those who
have had the seemingly requisite conditioning experiences.
Vicarious Conditioning of Fears and Phobias:
One criticism of early conditioning approaches centered on the observation that many people with phobias do not appear to have had any
relevant history of classical conditioning. Clinicians have long speculated that simply observing others experiencing a trauma or behaving
fearfully could be sufficient for some phobias to develop. The strongest experimental evidence for the role of vicarious conditioning in phobia
acquisition stems from a primate model showing that strong and persistent phobic-like fears can indeed be learned rapidly through
observation alone. Traditional conditioning models erred in not attending to the important role that vicarious conditioning can play in the
origins of phobic fears.
Sources of Individual Differences in the Acquisition of Fears and Phobias:
Another problem with traditional views is how to explain why many individuals who do undergo traumatic experiences do not develop
phobias. The diathesis-stress perspective, shows why some people do and other people do not develop phobia. First, there seems to be a
modest genetically based vulnerability for phobias. This genetic vulnerability may well be mediated through genetic contributions to fear
conditioning, which may in turn be mediated through personality variables such as high trait anxiety that also seem to serve as vulnerability
factors, affecting the speed and strength of conditioning.
- Moreover, children categorized as behaviorally inhibited (excessively timid, shy, etc.) at 21 months of age have been found to be at higher
risk for the development of multiple specific phobias (an average of three to four per child) by seven to eight years of age than were
uninhibited children (32% vs. 5%, respectively).
Differences in life experiences among individuals can also strongly affect the outcome of conditioning experiences. Such experiential factors
may serve as vulnerability (or invulnerability) factors for the development of phobias. The relevant differences in life experiences may occur
before, during, or following a fear-conditioning experience, and they can act singly or in combination to affect how much fear is experienced,
acquired, or maintained over time.
Impact of prior experience:
A phenomenon known as latent inhibition demonstrates that simple prior exposure to a conditioned stimulus (CS) before the conditioned and
unconditioned stimulus (US) are ever paired together reduces the amount of subsequent conditioning to the CS when paired with the US.
Consistent with this, several studies have shown that children who have had more previous nontraumatic encounters with a dentist are less
likely to develop dental anxiety if subsequently traumatized at the dentist’s office than are those with fewer prior encounters when they are
traumatized. Moreover, Mineka and Cook (1986) also showed that most monkeys who had initially simply watched a non-fearful model
monkey behaving non-fearfully with snakes were completely immunized against acquiring a fear of snakes when subsequently exposed to
fearful monkeys behaving fearfully with snakes.
A person’s history of control over important aspects of his or her environment is another important experiential variable strongly affecting
reactions to frightening situations. Infants and children raised in environments in which they gain a sense of control over their environment are
less frightened by (and better able to cope with) novel and frightening events. Thus, this suggests that children reared with a stronger sense of
mastery over their environments should be more invulnerable to developing phobias following traumatic experiences.
Impact of contextual variables during conditioning:
Several different features of conditioning events themselves also have a strong impact on how much fear is acquired. For example, having
control over a traumatic event (such as being able to escape it) has a major impact on how much fear is conditioned to CSs paired with that
trauma. Far less fear is conditioned when the aversive event is escapable than when it is inescapable.
Impact of postevent variables:
Different kinds of experiences that people can have following conditioning also affect the strength of the conditioned fear that is maintained
over time. For example, animal and human research suggests that a person who is exposed to a more intense traumatic experience (not paired
with the CS) after conditioning of a mild fear is likely to show an increase in fear of the CS. This so-called inflation effect suggests that a person

,who acquired a mild fear of automobiles following a minor crash might develop full-blown driving phobia if he or she were later physically
assaulted even though no automobile was present during the assault. Furthermore, there is a US reevaluation process that can occur when a
person receives verbally or socially transmitted information about the US being more dangerous than when she or he originally experienced it
paired with the US. This can result in an inflated level of fear to the CS. Finally, it was also found that simple mental rehearsal of CS–US
relationships can lead to enhanced strength of the conditioned fear response.
- In sum, a number of factors occurring before, during, and following potentially traumatic conditioning experiences (direct or vicarious)
affect the strength of fear that is experienced, conditioned, and maintained over time.
Selective Associations in the Conditioning of Fears and Phobias:
Early conditioning models predicted that fears and phobias would occur to any random group of objects associated with trauma. However,
clinical observations show that people are much more likely to have phobias of snakes, water, heights, and enclosed spaces than of bicycles,
guns, or cars, even though today the latter objects (not present in our early evolutionary history) may be at least as likely to be associated with
trauma. Seligman and Ohman argued that primates may be evolutionarily prepared to rapidly associate certain kinds of objects (such as
snakes, spiders, water, heights) with aversive events. This is because there may have been a selective advantage in the course of evolution for
primates who rapidly acquired fears of certain objects or situations that posed threats to humans’ early ancestors. Consistent with this, several
studies have shown that the content of most phobias is rated by independent raters as “prepared” in the sense that it was probably dangerous
to pretechnological humans. Thus, prepared fears are not seen as inborn or innate but rather as very easily acquired and/or especially resistant
to extinction.
Studies show, in both monkeys and humans, that evolutionary fear-relevant stimuli more readily enter into selective associations with aversive
events, and these same stimuli seem more likely than others to become the objects of human phobias. Moreover, the special characteristics of
fear learning seen with fear-relevant (but not fear-irrelevant) stimuli (e.g., its automaticity and its resistance to higher cognitive control)
suggest that the acquisition of phobias involves a primitive basic emotional level of learning that humans share with many other mammalian
species.
Social Phobia 
Individuals with social phobias show excessive fears of situations in which they might be evaluated or judged by others, and they either avoid
such situations or endure them with marked distress. Several theorists have suggested that social phobia can arise as a result of direct
traumatic conditioning, and several retrospective studies (with all their inherent limitations) have produced evidence consistent with this idea.
Social Learning and Social Phobia:
Another potentially important pathway to the development of social phobia is through social learning. Vicarious conditioning—that is, simply
observing another being ridiculed or humiliated or behaving in a very anxious way in some social situation—is one potent form of social
learning that may be sufficient to make the observer develop social phobia of similar situations. It was found in a study that 13% of individuals
with social phobia recalled vicarious learning experiences as having played a role in the origins of their social phobia. Additionally, there is
evidence of modeling of social anxiety in families of those with social phobia. Retrospective studies show that adults with social phobia report
that their parents were more likely than the parents of those without social phobia to have been avoidant of social interactions. Direct social
reinforcement and verbal instruction are also likely to play a role. For example, a study found that parents of anxious children were more likely
than other parents to reciprocate their children’s proposals of avoidant solutions. Finally, culturally transmitted display rules and norms are
another form of social learning that is likely to exert powerful influences on the expression of social anxiety, as is illustrated by the Japanese
disorder taijin kyofusho, which is related to the Western diagnosis of social phobia. People with this disorder fear that they will do something
to embarrass or offend others.
Preparedness and Social Phobia:
Another fruitful perspective comes from Ohman et al.’s (1985) extension of preparedness theory to social anxiety. Ohman et al. proposed that
social anxiety is a by-product of the evolution of dominance hierarchies and therefore predicted that social stimuli signaling dominance and
intra-specific threat should be fear-relevant or prepared CSs for social anxiety. Because angry facial expressions are prominent signals during
dominance conflicts among primates, he tested whether angry facial expressions would function as fear-relevant CSs for social fears in
humans. They found superior conditioning when slides of angry faces were used as CSs, compared with slides of happy faces or neutral faces.
Furthermore, fear CRs can even be conditioned to subliminal presentations of angry faces—that is, to angry faces that cannot be consciously
perceived.
Behavioral Inhibition as a Temperamental Diathesis for Social Phobia:
Obviously not everyone who has experienced a socially traumatic episode or observed a socially anxious model will develop social phobia. As
for specific phobias, one source of individual differences involves the temperamental diathesis known as behavioral inhibition, which may
influence the outcome of exposure to socially traumatic experiences and/or socially anxious models. Early behavioral inhibition not only
predicts the onset of multiple specific phobias in childhood but also social phobias in adolescence.
Uncontrollability and Social Phobia:
Perceptions of uncontrollability are another likely source of individual differences in vulnerability to the effects of socially traumatic episodes
or exposure to socially anxious models. In summary, a model of social phobias based on contemporary learning principles can account for
many of the complexities involved in their etiology because it acknowledges both temperamental diatheses such as behavioral inhibition, and
experiential diatheses such as learning histories, including those that lead to perceptions of uncontrollability.
Panic Disorder With and Without Agoraphobia 
People with panic disorder (PD) experience recurrent unexpected panic attacks that occur without their being aware of any cues or triggers,
and they must also experience worry, anxiety, or behavioral change related to having another attack. Many, but not all, people with PD also go
on to develop some degree of agoraphobic avoidance of situations in which they perceive that escape might be either difficult or embarrassing
if they were to have a panic attack.
- An early conditioning approach to panic disorder with agoraphobia (PDA) was proposed by Goldstein and Chambless (1978), who argued,
that exteroceptive conditioning (where CSs impinge on the external sensory receptors like eyes and ears) is central to the development of
agoraphobia. But Goldstein and Chambless also described a process they termed “fear of fear” developing from interoceptive
conditioning. In interoceptive conditioning, the CSs are the body’s own internal sensations.
However, this was criticized and a contemporary learning theory perspective was presented.
This perspective also builds on growing evidence from two sources that anxiety and panic are at least partially unique emotional experiences.
First, psychometric analyses of panic- and anxiety-related symptomatology reveal two separable factors: Panic is accompanied by strong

,autonomic arousal, extreme fear, and fight-or-flight action tendencies, and anxiety is accompanied by apprehension, worry, and tension.
Second, neurobiological research supports the existence of these two partially distinct emotional states of panic and anxiety.
In what follows, it is important to keep this distinction between anxiety and panic in mind because both are central to PD and PDA.
Exteroceptive and Interoceptive Conditioning in Panic Disorder:
Bouton et al. (2001) argued that the conditioning that may occur in vulnerable individuals during initial panic attacks sets the stage for the
development of PD and PDA. The initial attacks become associated with initially neutral interoceptive and exteroceptive CSs through
conditioning. Specifically, because of their status as terrifying emotional events, replete with strong interoceptive stimuli, panic attacks are
capable of supporting conditioning. Prototypic CSs during initial (as well as later) panic attacks include heart palpitations and dizziness
(interoceptive CSs), as well as escalators and malls (exteroceptive CSs). Bouton et al. proposed that the primary effect of this conditioning is
that anxiety becomes conditioned to these CSs, but another effect is that panic attacks themselves are also likely to be conditioned to certain
internal cues. Bouton et al. (2001) also noted that different CSs paired with the very same US often result in qualitatively different CRs to the
different CSs. Some internal and external cues present before and during panic attacks may become conditioned to elicit anxiety (different
from the panic UR), and others may become conditioned to elicit panic itself. Interoceptive cues in close proximity to panic (as opposed to
more distal external cues) may serve as “prepared” or fear-relevant CSs and may be especially likely to elicit panic, just as other fear-relevant
CSs seem especially likely to condition CRs that strongly resemble URs. Interoceptive conditioning is robust and stable.
The Development of Agoraphobia:
Many people who develop panic attacks and panic disorder go on to develop some degree of agoraphobic avoidance of situations in which
they fear or expect they may have a panic attack in the future. Many of these situations are the commonly observed ones such as shopping
malls, driving, standing in line, sitting in a theater, and so forth. Anxiety and avoidance of such situations have long been thought to develop as
a result of exteroceptive conditioning of anxiety to these situations when panic attacks have occurred there in the past, followed by learned
avoidance of these situations to minimize anxiety. Moreover, as the disorder develops, these agoraphobic fears and avoidance often
generalize to other similar situations, as would be expected on the basis of the principles of classical conditioning.
- Two major risk factors are gender and employment: Women are far more likely to than men to develop agoraphobia, and people who
must leave the house to work are less likely than those who do not work or who work from home to develop agoraphobia. The learning
theory approach can explain both of these factors because in each case the person is allowed to avoid his or her feared situations rather
than be exposed to them, which would extinguish his or her anxiety.
Further Complexities of the Role of Conditioning in Panic Disorder and Agoraphobia:
Conditioned stimuli not only come to elicit conditioned responses but also to facilitate or inhibit responses controlled by other events.
- For example, for individuals with PD or PDA, inhibitory CSs for safety (such as the presence of a trusted companion) can attenuate panic
symptoms ordinarily elicited by carbon dioxide inhalation (a US which is widely used as a panic provocation agent). By contrast, CSs for
anxiety (e.g., a warning about facing a stressful day at work) can strengthen ongoing avoidance behavior (such as agoraphobic avoidance
like calling in sick) or engaging in “safety behaviors” (such as carrying talismans).
Baseline levels of anxiety strongly predict who will experience panic in response to various panic provocation agents as USs. Moreover, several
prospective monitoring studies have shown that anxiety is very often a precursor to (and may potentiate) panic attacks. Finally, because the
same CR (anxiety) elicited from two different sources can summate (e.g., baseline anxiety and anxiety elicited by a shopping mall), one would
also expect that baseline anxiety could potentiate agoraphobic anxiety and avoidance.
Vulnerability Factors for Panic Disorder:
Far more people experience panic attacks than go on to develop panic disorder. Among those individuals who experience panic attacks, what
determines who will develop PD or PDA? Bouton et al. (2001) considered three types of vulnerability factors that seem likely to predispose
some people who experience panic attacks to develop PD or PDA.
First, they discussed a moderate nonspecific genetic vulnerability for PD and PDA (that overlaps especially with the genetic vulnerability for
phobias) that may well be mediated by temperamental or personality vulnerability factors like neuroticism or trait anxiety.
A second set of nonspecific vulnerability factors discussed by Bouton et al. (2001) are prior learning experiences that lead to perceptions of
lack of control and helplessness and that may serve as psychological vulnerability factors influencing the development of panic, agoraphobia,
and other emotional disorders. Early experience with uncontrollable stressful life events such as death and divorce can enhance vulnerability
to PD and depression.
Finally, Bouton et al. (2001) also reviewed some more specific learning experiences that may play a more unique role in creating risk for
developing PD and PDA per se.
In summary, Bouton et al.’s (2001) perspective on PD and PDA argues that initial panic attacks set the stage for conditioning of anxiety to
external and internal cues associated with panic, thus explaining the origins of anticipatory and agoraphobic anxiety. Moreover, the process of
interoceptive conditioning also allows certain bodily sensations to become conditioned to elicit panic itself such that, for example, heart
palpitations occurring early in an attack become predictors of the rest of the attack and acquire the capacity to provoke panic. Finally, people
with certain genetic/temperamental and/or experiential vulnerabilities will show stronger conditioning of anxiety and panic, explaining why
only a subset of those who have panic attacks develop PD or PDA.
Posttraumatic Stress Disorder 
The symptoms of posttraumatic stress disorder (PTSD) include reexperiencing the trauma, passively avoiding reminders of the trauma,
numbing of affect, and heightened general arousal. Although a traumatic event is necessary for the diagnosis of PTSD, there are many puzzles
in the development of PTSD that require explanation.
Regarding symptoms, animals exposed to uncontrollable and/or unpredictable stress, like individuals with PTSD, show heightened generalized
anxiety and arousal. They also show enhanced passive avoidance behavior resembling the avoidance symptoms of PTSD. In addition, the
opioid-mediated analgesia (relative insensitivity to pain) produced by cues associated with uncontrollable stress in animals may resemble
certain numbing symptoms seen in PTSD. Finally, the reexperiencing symptoms of PTSD include fear and distress at exposure to reminders of
trauma (as well as nightmares and flashbacks), and these emotional reactions can be seen as conditioned emotional responses elicited by
reminder cues (CSs previously paired with trauma). In addition, the intense physical stressors typically used in animal studies of the effects of
uncontrollable and unpredictable stress (e.g., electric shocks, defeats in physical fighting) are similar to several forms of human trauma often
associated with PTSD—torture (e.g., electric shocks, beatings), child abuse, and assault.
Considered together, the symptom similarities and resemblance of physical stressors used to produce them lead us to believe that the
uncontrollable, unpredictable stress animal model is highly relevant for understanding PTSD.
Trauma phase:

, The most obvious prediction from the animal model is that traumas that are perceived to be uncontrollable and unpredictable are more likely
to result in PTSD. In addition, organisms differ in how they respond to the experience of uncontrollable stress, and such differences can
strongly affect the outcome. This led to hypothesize that the amount of trauma inflicted during torture (or assault) may be less predictive of
the long-term emotional effects of the torture than is the victim’s psychological state of resistance and fighting back versus giving up and
conceding defeat.
Pretrauma Phase:
The effects of prior experiences with control or lack of control on reactions to subsequent uncontrollable trauma are complex. Sometimes
prior uncontrollable stress sensitizes an organism to the harmful effects of subsequent exposure to such trauma. This means that as repeated
exposures to trauma occur, the adverse effects get larger rather than smaller (as in habituation). Thus, a history of prior trauma (especially
repeated trauma, which is more likely to be perceived as uncontrollable) should be associated with increased risk of developing PTSD to a
recent trauma.
By contrast, a prior history of control over stressful events can immunize against the harmful effects of subsequent uncontrollable stress.
Hence, we also predict that a prior history of control over stress can immunize against the development of PTSD to a recent trauma. Consistent
with this prediction there is suggestive evidence from a study of torture survivors that psychological readiness prior to being tortured is
associated with a decreased likelihood of subsequently developing PTSD despite very high levels of torture.
Post trauma Phase:
One potential discrepancy between the effects of uncontrollable, unpredictable stress and the symptoms of human PTSD is that at least some
of the effects of uncontrollable, unpredictable stress in animals are short-lived (usually dissipating over several days), in contrast to the
sometimes chronic nature of PTSD, which often lasts many years. However, this discrepancy may be more apparent than real. First, only a
small number of individuals who develop initial signs of PTSD go on to develop chronic PTSD. Second, if rats are simply exposed at two- to
three-day intervals to the context in which they had previously experienced uncontrollable stress (without actually experiencing stress), the
usual time course for at least some of the effects of the uncontrollable stress is prolonged “indefinitely”. Such contexts associated with stress
become CSs for anxiety, and we consider such exposure to anxiety CSs as eliciting conditioned emotional responses that are analogous to the
anxiety-provoking aspects of the reexperiencing symptoms in PTSD.
What other kinds of post-trauma events can affect the course and intensity of PTSD symptoms? The inflation and US reevaluation effects,
described earlier, can also affect the course of PTSD. Thus, mild PTSD symptoms could become full-blown PTSD when there is reason to
reevaluate the danger posed by the original trauma. In addition, reinstatement of fear is the term for the phenomenon in which after a CS has
extinguished, the CS can regain its ability to elicit a CR by simply exposing the animal to the US.
Generalized Anxiety Disorder
People with generalized anxiety disorder (GAD) are primarily characterized by chronic excessive worry about a number of events or activities
for at least six months, and the worry must be experienced as difficult to control. Several theorists have suggested that uncontrollable and
unpredictable aversive events may play an important role in the development of GAD. Conversely, there is evidence relevant to individual
differences suggesting that people with extensive experience controlling important aspects of their lives may be immunized against developing
GAD. Moreover, because neuroticism and trait anxiety are known risk factors for anxiety disorders, it is possible that people high on
neuroticism or trait anxiety may be especially susceptible to the effects of uncontrollable and unpredictable aversive events.
- In recent years worry has increasingly come to be seen as the central feature of GAD.
Borkovec et al., (1994) have incorporated ideas from learning theory to help explain why worry is such a persistent process. They have
investigated both the perceived benefits of worry as well as what actual functions worry serves. Most of the perceived benefits of worry center
around people’s beliefs that worry helps avoid catastrophe (either superstitiously or in reality) and deeper emotional topics that they do not
want to think about. Investigations of how worry actually functions help reveal why the worry process can become so self-sustaining. First,
when people with GAD worry, their emotional and physiological responses to aversive imagery are actually suppressed. Borkovec et al. argued
that this suppression of emotional and physiological responses serves to reinforce the process of worry (i.e., increases its probability). Because
worry suppresses physiological responding, this also prevents the person from fully experiencing or processing the topic that is being worried
about; such processing is necessary if extinction of anxiety is to occur. Thus, the threatening meaning of the topic will be maintained. Finally,
Borkovec et al. noted that worry may also be reinforced superstitiously because the vast majority of things people worry about never happen.
The theory thus proposes that worry serves as a cognitive avoidance response.
Worry is not an enjoyable activity and can actually lead to a greater sense of danger and anxiety because of all the catastrophic outcomes the
worrier envisions. Moreover, it can actually lead to more negative intrusive thoughts, and for these and other reasons people sometimes try to
suppress or control their worrying. But research has also shown that attempting to control thoughts and worry may paradoxically lead to
increased experience of intrusive thoughts and enhanced perception of being unable to control them.
In summary, people who have a history of uncontrollable and unpredictable life stress may be especially prone to developing GAD. Worry
about possible bad outcomes or dangerous events, the central characteristic of GAD, seems to serve as a cognitive avoidance response that is
reinforced because it suppresses emotional and physiological responding. Because attempts to suppress or control worry may lead to more
negative intrusive thoughts, perceptions of uncontrollability over worry may develop, which is in turn associated with greater anxiety, leading
to a vicious cycle.
Obsessive–Compulsive Disorder
The central features of obsessive– compulsive disorder (OCD) are unwanted and intrusive thoughts, impulses, or images that cause marked
anxiety or distress; these are usually accompanied by compulsive behaviors or mental rituals that are performed to neutralize or prevent the
distressing thoughts or images. Even “normal” people experience occasional cognitive intrusions that do not differ in content from those seen
in OCD. What distinguishes people with OCD is that clinical intrusions/obsessions are (a) associated with greater distress, (b) more frequent,
and (c) more strongly resisted. Thus, one critical question regarding the development of OCD is why intrusions are more distressing, frequent,
and strongly resisted in certain people.
Verbal Conditioning and Social Learning:
Although research thus far has failed to find good evidence that a traumatic conditioning history is involved in the origins of many cases of
OCD, verbal transmission of dangerous thoughts (as discussed for specific phobias) may occur in addition, direct verbal conditioning may also
occur in which a neutral idea is paired with some scary idea that a person may have (e.g., “I saw that filthy person use the toilet and wash her
hands before me so I should be very careful in all bathrooms”). In addition, there is some evidence to suggest that social learning factors may
play a role in the greater levels of distress and resistance associated with clinical intrusions.

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