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pproximately 29% of the U.S. population is estimated to have or to have had one or more diagnosable anxiety disorders at some point in their
lives, making anxiety disorders the most common category
of diagnoses in the fourth edition of the Diagnostic and
Statistical Manual of Mental Disorders (DSMIV; American Psychiatric Association, 1994; see Kessler, Berglund,
Demler, Jin, & Walters, 2005). Most of us might intuitively
guess 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 it is also obvious that 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. Consider the following examples, which illustrate
the kinds of issues we address in this article:
Emily and Marian both had had traumatic experiences with dogs.
Emily was hiking with her own dog when another dog attacked
her and bit her on the wrist. She was terrified. The wound became
badly infected and very painful, requiring medical treatment.
Marian was walking in the fields when she became terrified by
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three large, growling dogs that chased her to a fence. One began
tearing at her pant legs, but their owner fortunately intervened before
she was physically injured. Why did Marian but not Emily go on to
develop dog phobia when only Emily was actually bitten by a dog?1
Ahmet and Hasan were both male Turkish citizens in their 30s
who were arrested, imprisoned, and tortured. Ahmet was imprisoned for several years and experienced a great deal of torture;
Hasan was imprisoned for several weeks and experienced far less
torture (M. Basoglu, personal communication, 1997). Why did
Hasan but not Ahmet develop posttraumatic stress disorder? What
accounts for such individual differences?
Specific Phobia
Susan
Mineka
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Richard
Zinbarg
father vomit while dying; shortly thereafter the boy developed a strong and persistent vomiting phobia. Indeed, in
middle age he even contemplated suicide one time when he
was nauseous and feared vomiting.
The strongest experimental evidence for the role of
vicarious conditioning in phobia acquisition stems from a
primate model showing that strong and persistent phobiclike fears can indeed be learned rapidly through observation alone. In Mineka and Cooks series of experiments on
observational conditioning of snake fear (e.g., Cook,
Mineka, Wolkenstein, & Laitsch, 1985), laboratory-reared
young adult rhesus monkeys who initially were not afraid
of snakes served as observers who watched unrelated wildreared model monkeys reacting very fearfully in the presence of live and toy snakes. These lab-reared observer
monkeys showed rapid acquisition of an intense phobiclike fear of snakes that did not diminish over a three-month
follow-up period. This vicarious conditioning also occurred
simply through watching videotapes of models behaving
fearfully (Cook & Mineka, 1990), suggesting that humans
are also susceptible to acquiring fears vicariously simply
through watching movies and TV (as expected from numerous anecdotal observations). Thus, 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 (e.g., Mineka & Sutton, in
press; Mineka & Zinbarg, 1996; Rachman, 1990). For
example, in studies using retrospective recall, many non12
phobic parent behaving fearfully with heights. Using Marian and Emily as examples, we note that Emilys own
extensive prior exposure to dogs probably immunized her
from developing dog phobia.
A persons history of control over important aspects of
his or her environment is another important experiential
variable strongly affecting reactions to frightening situations. For example, Mineka, Gunnar, and Champoux
(1986) found that infant monkeys reared with a sense of
mastery and control over their environments for 710
months later adapted more readily to frightening events and
novel anxiety-provoking situations than did monkeys
reared in identical environments except without the experiences with control. This experimental evidence supports
claims long made by developmentalists using correlational
data that 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. Such research suggests that children reared with a stronger sense of mastery over their
environments should be more invulnerable to developing
phobias following traumatic experiences (see also Chorpita
& Barlow, 1998).
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 (e.g.,
Mineka, Cook, & Miller, 1984). Thus, consider our example of Marian, who was not able to end the dog attack
herself. Instead, the dogs owner pulled the dog off her.
Our perspective suggests that if she had instead been able
to escape on her own at the same point during the attack
that the dog owner pulled the dog off her, she would have
been less likely to have developed dog phobia, even though
the dog attack would have been of equal duration and
intensity.
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 (e.g., Rescorla, 1974; White &
Davey, 1989). 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 (Mineka, 1985;
Mineka & Zinbarg, 1996). Davey (1997) has also described
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, Davey and
January 2006 American Psychologist
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. For example, McCabe, Antony, Summerfeldt, Liss, and Swinson (2003) reported that 92% of
their adult sample with social phobia reported a history of
severe teasing in childhood, compared with only 50% and
35% in their panic disorder and obsessive compulsive
disorder groups, respectively. Another study found that
56% of those with specific social phobias recalled direct
traumatic conditioning experiences as having played a role
in the origins of their social phobia (Stemberger, Turner,
Beidel, & Calhoun, 1995). One relevant case involved a
young man who came home one day to find his fiancee in
bed with his best friend (a humiliating and traumatic experience for him). Over the next few months he developed
severe social phobia.
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used to produce them lead us to believe that the uncontrollable, unpredictable stress animal model is highly relevant
for understanding PTSD. Specifically, to aid in the understanding of the onset, severity, and course of PTSD symptoms, Basoglu and Mineka (1992) argued for the relevance
of animal research on variables occurring before, during, or
following exposure to unpredictable, uncontrollable stress,
the topic to which we now turn.
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. Results from
retrospective studies consistent with this prediction have
been reported (e.g., Bolstad & Zinbarg, 1997; Regehr,
Cadell, & Jansen, 1999). In addition, organisms differ in
how they respond to the experience of uncontrollable
stress, and such differences can strongly affect the outcome. For example, animal research on social defeat shows
that the analgesia induced by extensive attacks from a
conspecific (analgesia is a characteristic facet of learned
helplessness) is more highly correlated with the extent to
which the animal assumed the characteristic posture of
defeat than with the number of bites received from the
conspecific (e.g., Rodgers & Hendrie, 1983). Conversely,
Weiss, Glazer, and Pohorecky (1976) found that allowing
animals to express aggression during uncontrollable stress
attenuated the effects of the stress.
Such findings led Basoglu and Mineka (1992) 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 victims psychological state of resistance and fighting back versus giving up
and conceding defeat. Consistent with this, studies of political prisoners and assault survivors have shown that
survivors with PTSD were more likely than those without
PTSD to retrospectively report having experienced mental
defeat during their traumatization (e.g., Ehlers, Maercker,
& Boos, 2000). It is important to note that Dunmore, Clark,
and Ehlers (2001) also found that perceived mental defeat
measured within four months of an assault predicted PTSD
symptom severity at follow-up assessments six and nine
months after the assault.
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 (e.g., Moye, Hyson, Grau, &
Maier, 1983). 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. For
example, one retrospective study showed that a history of
repeated childhood abuse had an even greater sensitizing
effect than a single incident of child abuse (Bolstad &
January 2006 American Psychologist
Zinbarg, 1997). Moreover, the results of a recent metaanalysis support this prediction, although prior trauma was
more strongly related to PTSD when the prior trauma
involved interpersonal violence such as child abuse rather
than combat exposure or an accident (Ozer, Best, Lipsey, &
Weiss, 2003). We should also note that there are a few
studies supporting a moderate genetic contribution to liability for PTSD (e.g., True et al., 1993), which might
perhaps be mediated by sensitivity to uncontrollable and
unpredictable stress (an interesting question for future
research).
By contrast, a prior history of control over stressful
events can immunize against the harmful effects of subsequent uncontrollable stress (e.g., Williams & Maier, 1977).
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 (and the case
studies at the outset), there is suggestive evidence from a
study of torture survivors that psychological readiness prior
to being tortured (such as the psychological readiness Ahmet had because of his background as a political activist) is
associated with a decreased likelihood of subsequently
developing PTSD despite very high levels of torture (Basoglu, Mineka, et al., 1997). Psychological readiness was
measured by a questionnaire asking about the participants
knowledge of torture methods, their expectations of being
imprisoned and tortured, and their training in stoicism
techniques, among other things. By contrast, torture victims like Hasan, who were ordinary citizens arrested out
of the blue, were much less prepared for their torture
experiences. Therefore, despite the fact that they experienced far less torture, they were more likely to develop
PTSD and other forms of psychopathology than were the
torture victims who had been political activists. Given that
the psychological readiness measure used was multifaceted, the active ingredients responsible for this protective
effect are unclear. However, the protective effects of readiness were probably mediated at least in part by rendering
the subsequent torture more predictable. In addition, the
stoicism training may have led the torture to be perceived
as partially controllable and therefore less likely to produce
mental defeat; indeed the nonactivists reported less perceived control but more distress than the activists.
Posttrauma 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 (e.g., in one study,
0% of male assault victims and approximately 30% of female
assault victims developed PTSD; Riggs, Rothbaum, & Foa,
1995). 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 the
January 2006 American Psychologist
stress), the usual time course for at least some of the effects of
the uncontrollable stress is prolonged indefinitely (Maier,
2001, p. 763). 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.
On the basis of earlier reports of Maiers (2001)
findings with rats, Mineka and Zinbarg (1996) predicted
that the severity of reexperiencing symptoms after a trauma
should influence the course of the symptoms of PTSD;
greater reexperiencing would be associated with a more
persistent course. At least six prospective studies of trauma
survivors now support this prediction (e.g., Ehlers, Mayou,
& Bryant, 1998). Moreover, in several studies, early reexperiencing symptoms significantly predicted later PTSD,
but early avoidance (e.g., McFarlane, 1992) or numbing
symptoms (e.g., Rothbaum, Foa, Riggs, Murdock, &
Walsh, 1992) did not, suggesting some degree of specificity
between early reexperiencing symptoms and later PTSD.
What other kinds of posttrauma 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 (e.g., finding
out weeks after an assault that ones assailant was in fact a
convicted murderer). 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 (not paired with the
CS) (cf. Rescorla & Heth, 1975). Thus, a posttherapy
trauma not linked with any of the cues associated with the
original trauma could lead to a reinstatement of the original
trauma symptoms.
In summary, there are compelling parallels between
the literature on uncontrollable, unpredictable stress in animals and human PTSD. These include striking similarities
in the symptoms of each as well as significant resemblance
between the kinds of stressors. These parallels suggest that
perceptions of uncontrollability and unpredictability play a
role in the development and course of PTSD. Moreover,
striking parallels have been observed between the trauma
and pre- and posttrauma variables affecting the outcome of
exposure to unpredictable, uncontrollable stress in animals
and several forms of human trauma associated with PTSD.
ObsessiveCompulsive 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 (e.g., Rachman & de Silva,
1978). 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 (Mineka & Zinbarg, 1996;
Rachman & Hodgson, 1980), verbal transmission of dangerous thoughts (as discussed for specific phobias) may
occur (e.g., my mother told me that dirt and contamination
may be on doorknobs or toilet seats). In addition, direct
January 2006 American Psychologist
fluctuations in frequency of occurrence of compulsive rituals as a person goes through varying levels of stress.
Preparedness and OCD
Finally, the preparedness concept discussed earlier in the
context of specific and social phobias is also relevant to
understanding OCD in an evolutionary context. As demonstrated years ago by De Silva, Rachman, and Seligman
(1977), the contents of most obsessions and the forms of
most compulsive rituals are nonrandom (thoughts about
dirt, contamination, and danger are the most common obsessions; cleaning and checking for danger are the most
common rituals). Indeed, humans obsessions with dirt,
contamination, and danger have deep evolutionary roots
(Mineka, 1985; Mineka & Zinbarg, 1996). Moreover, the
displacement activities that many animal species engage in
under situations of conflict or high arousal (such as grooming, nesting, or tidying) bear a significant resemblance to
the compulsive rituals seen in OCD. Whether these fears
are based on nontraumatic conditioning (verbal or vicarious
verbal conditioning) or on social learning, the idea is that
people with OCD do not typically obsess about random
scary thoughts and do not show arbitrary ritualistic behaviors; rather, their thoughts and behaviors have deep evolutionary roots.
In summary, we have argued that verbal learning and
social learning factors are involved in the acquisition of
beliefs that lead to heightened levels of distress and resistance to intrusions; these beliefs tend to center on a few
evolutionarily relevant themes. Moreover, once compulsive rituals have developed as methods to neutralize or
prevent obsessive thoughts, they show the same high resistance to extinction seen in learned avoidance responses
in animals.
Conclusions
The influence of early, rather simplistic learning approaches to understanding the etiology and course of anxiety disorders had begun to wane around the mid-1970s
following some forceful criticisms of such models for
phobias. However, contemporary learning theory and research provide a foundation for the development of models
of the anxiety disorders that can capture the richness and
complexity associated with the development and course of
these disorders (see Figure 1). Not only do contemporary
learning models of the etiology of anxiety disorders have a
great deal of explanatory power but they are also testable.
We have outlined several falsifiable predictions derived
from these models here and elsewhere (e.g., Basoglu &
Mineka, 1992; Bouton et al., 2001; Foa et al., 1992;
Mineka, 1985; Mineka & Zinbarg, 1996). Some of these
predictions have already been tested and supported. Only
time and additional research will tell if the remaining
predictions are also supported or refuted.
Whereas some of the predictions derived from learning theory models of the etiology of anxiety disorders
overlap with predictions made by models emanating from
other theoretical perspectives, we believe that the learning
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Figure 1
Overview of Major Elements Incorporated in Contemporary Learning Models of the Etiology of the Anxiety
Disorders
Note.
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