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The causes of sexual dysfunction: combination for panic disorder: A randomized controlled
The role of anxiety and cognitive interference. Journal of trial. JAMA, 283, 2529-2536.
Consulting and Clinical Psychology, 54, 140--148.
Barlow, D. H., Hayes, S. C., & Nelson, R. O. (1984). The
Barlow, D. H. (1988). Anxiety and its disorders." The nature scientist-practitioner: Research and accountability in clini-
and treatment of anxiety and panic. New York: Guilford Press. cal and educational settings. New York: Pergamon Press.
Barlow, D. H. (1991a). Disorders of emotion. Psychological Barlow, D. H., & Hersen, M. (1984). Single case experi-
Inquiry, 2, 58-7l. mental designs." Strategies for studying behavior change
(2nd ed.). New York: Pergamon Press.
Barlow, D. H. (1991b). Introduction to the special issue on
diagnosis, dimensions, and DSM-IV: The science of classi- Barlow, D. H., Sakheim, D. K., & Beck, J. G. (1983).
fication. Journal of Abnormal Psychology, 100, 243-244. Anxiety increases sexual arousal. Journal of Abnormal
Psychology, 92, 49-55.
Barlow, D. H. (1994). Psychological interventions in the era
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
of managed competition. Clinical Psychology." Science and Bouton, M. E., Mineka, S., & Barlow, D. H. (in press). A
This document is copyrighted by the American Psychological Association or one of its allied publishers.
nature of anxiety, the more we will know of intellect. (Liddell, condition, well-known among the Eskimo tribes of
This document is copyrighted by the American Psychological Association or one of its allied publishers.
clear that the experience of emotion (and the development of us to respond to present danger with instantaneous, some-
This document is copyrighted by the American Psychological Association or one of its allied publishers.
emotional disorders) cannot be reduced to dry cognitive attri- times superhuman efforts. To make the response system as
butions and appraisals on the one hand, or to specific actions rapid as possible, underlying neural circuits bypass the cor-
of neurotransmitters and the intricacies of cell physiology on tex in favor of direct connections from the retina to the emo-
the other (Barlow, 1991c). The growing recognition of the tional brain (LeDoux, 1996). The topic of fear is taken up
necessity of focusing on emotional experience and expres- below. The nature of anxiety is somewhat more complex.
sion as a scientific subject in its own fight is highlighted by
the appearance of the new APA journal Emotion. The model The Nature of Anxiety
of emotional disorders I presented in the 1980s and 1990s In 1988 and in recent updates (Barlow, 1988, in press;
(Barlow, 1988, 1991 a, 1991b; Barlow, Chorpita, & Turovsky, Barlow et al., 1996), I described anxiety as a unique and
1996) highlights the role of fundamental emotions in the coherent cognitive-affective structure within our defensive
great tradition of the emotion theorists (Darwin, 1872; motivational system, and I outlined a model of the interac-
Ekman & Davidson, 1994; Izard, 1994). tion of the various components of anxiety. At the heart of
The underlying premise of this approach is that emotions this structure is a sense of uncontrollability focused largely
are innate patterns of reaction and responding that have on possible future threats, danger, or other upcoming poten-
evolved in many life forms because of their functional sig- tially negative events, in contrast to fear, where the danger is
nificance. Although clearly modifiable by learning and mat- present and imminent. Thus, anxiety could be characterized
uration, these basic patterns of emotion are present in roughly as a state of helplessness, because of a perceived
humans and animals at birth and show a remarkable consis- inability to predict, control, or obtain desired results or out-
tency both within and across species. The primary function, comes in certain upcoming personally salient situations or
or adaptive value, of emotional behavior is not only prepa- contexts. Accompanying this negative affective state is a
ration for action, but also communication from one member strong physiological or somatic component that may reflect
of the species to another. As Ohman (1996; Ohman, activation of distinct brain circuits such as the corticotropin
Esteves, & Soares, in press) pointed out, the function of releasing factor system and Gray's behavioral inhibition sys-
emotions in this sense can be understood as a clever means, tem (Chorpita & Barlow, 1998; Gray & McNaughton, 1996;
guided by evolution, to ensure that people do what they Sullivan, Kent, & Coplan, 2000). These systems may be the
have to do to successfully pass their genes to coming gener- physiological substrate of readiness, underlying a state of
ations. In other words, emotions are now conceptualized by preparation to counteract helplessness. Vigilance (hypervigi-
most theorists as fundamental action tendencies whose pur- lance) is another characteristic of anxiety that suggests
pose is to motivate behavior related to survival of the readiness and preparation to deal with potentially negative
species. A theory of the nature of emotional disorders based events. If one were to put anxiety into words, one might say,
on discrete emotion theory as applied to depression, anger "That terrible event could happen (again), and I might not
(stress), and excitement (mania) has been described else- be able to deal with it, but I've got to be ready to try." For
where (Barlow, 1988, 1991a, 1991b, in press; Barlow et al., these reasons, I have suggested that a better and more pre-
1996). The focus of this article is on the defensive emotions cise term for anxiety might be anxious apprehension. This
of fear and anxiety, and their pathological expression. conveys the notion that anxiety is a future-oriented mood
With this new focus on the study of emotion, the myster- state in which one is ready or prepared to attempt to cope
ies of anxiety are giving way, grudgingly, to a new apprecia- with upcoming negative events. Another term often paired
tion of the richness and complexity of behavioral and cogni- with anxiety is anticipatory. However, in the present defini-
tive patterns associated with defensive emotions. One of the tion, all anxiety is anticipatory, so this qualifying adjective is
in turn, is associated with a shift to a self-evaluative focus of ance. The process of anxiety is seldom pathological, even
attention (or a rapidly shifting focus of attention from an exter- when intense, until it becomes chronic.
nal potentially threatening context to an internal self-evaluative When this happens, one or both of two prominent conse-
content) in which evaluation of one's (inadequate) capabilities to quences of the process of anxiety ultimately develop in an
deal with the threat is prominent. Evidence suggests that this attempt to cope with negative affect and its triggers. First, a
shift to a self-focused attentional state further increases arousal tendency to avoid entering a state of anxious apprehension
and negative affect, thus forming its own small positive feed- is always present. This tendency becomes more pronounced
Figure 1
The Processof Anxious Apprehension
Note. CRF = corticotropinreleasingfactor. From "'SocialPhobia (SocialAnxietyDisorder)," by S. G. Hofmannand D. H. Barlow,in Anxiety and Its Disorders: The Nature
and Treatment of Anxiety and Panic (2nded.), by D. H. Barlow, in press, New York: GuilfordPress. Copyrightby GuilfordPress. Reprintedwith permission.
Association, 1994), lack of control over the worry process is In 1988, I described the phenomenon of false alarms
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a defining feature of generalized anxiety disorder (Brown, (Barlow, 1988). That is, spontaneous or uncued panic seems
Barlow, & Liebowitz, 1994). Worry, or concern over future phenomenologically nearly identical in all respects to fear,
events, is of course not problematic and may even be adap- except for the ability of the individual to specify an antecedent
tive under some circumstances, unless it is so driven by anx- (Carter & Barlow, 1995; Forsyth & Eifert, 1996). The very
iety that it becomes intense and uncontrollable. It is in this definition of panic, specifying as it does sudden feelings of
sense that worry can become chronic and maladaptive. marked apprehension and impending doom that are associated
Chronic anxiety also is characterized by persistent central with a wide range of distressing physical sensations, would
nervous system tension and arousal, autonomic inflexibility certainly qualify as a definition for fear in other contexts. How
(Thayer, Friedman, & Borkovec, 1996), and functional brain common are false alarms, and why do they occur?
asymmetry (Heller, Nitschke, Etienne, & Miller, 1997), False alarms or panic attacks seem to be far more preva-
which seem to reflect the consequences of a state of per- lent in the general population than was assumed previously.
petual readiness to confront danger. For example, our own data (Rapee et al., 1988) and data
from epidemiological surveys (e.g., Wittchen & Essau,
The Nature of Fear and Panic: True Alarms, False
1991) suggest that between 10% and 14% of the population
Alarms, and Learned (Conditioned) Anxiety
had experienced an unexpected, uncued panic attack during
Only in the mid-1980s did researchers begin to collect infor- the past year. Typically, attacks were less intense and less
mation on the nature of panic. The accumulating evidence frequent in these "nonclinical panickers" than in patients
points to a complex biopsychosocial process. This process with anxiety disorders. Panic attacks also occurred during
involves the interaction of an ancient alarm system, crucial sleep in nonclinical panickers and aggregated more strongly
for survival, with inappropriate and maladaptive learning in the families of these individuals than in families of partic-
and subsequent cognitive and affective complications. First, ipants who had not experienced panic (Craske, 1999;
it is important to consider the alarm system most commonly Norton, Dorward, & Cox, 1986). Researchers have made
known as fear. progress in the search for the causes of false alarms, particu-
There is general agreement that fear occurs when people larly initial false alarms, during the past decade. Ongoing
are directly threatened with a dangerous, perhaps life-threat- lines of investigation are targeting a complex web of preex-
ening, event. An impending attack from wild animals is isting biological and psychological vulnerabilities interact-
something few people experience today, but our ancestors ing with contemporaneous events (e.g., life stress) in the
knew this threat well in millennia past. This history may genesis of initial false alarms (panic; Bouton et al., in press).
account for our somewhat greater susceptibility to becoming
alarmed in the presence of snakes and mountain lions The Structure of Anxiety, Mood, and Related Emotional
(Cook, Hodes, & Lang, 1986; Ohman et al., in press; Disorders and the Concept of Neurosis:
Seligman, 1971). Relevant threats today include speeding Back to the Future?
vehicles, guns, drowning, or seeing the safety of our chil- Before discussing the origins of anxiety disorders and the role
dren threatened. Under these conditions, the emotion of fear of anxiety and panic in this process, it is important to discuss
represents a true alarm that mobilizes us physically and cog- the structure of anxiety, mood, and related disorders and the
nitively for quick action and sometimes superhuman efforts. personality traits that may predispose individuals to the devel-
Most typically, running away or escaping is the behavioral opment of these disorders. The death of neurotic disorders in
manifestation of fear. Occasionally, directed action to counter 1980, after almost a century of domination, resulted in a split-
includes high rates of comorbidity among these disorders is that any future system of nosology (e.g., DSM-V) describ-
(Brown et al., 1994) and the success of very similar treat- ing emotional disorders may better represent these disorders
ments across this wide range of disorders, such as selective in a dimensional framework in which overall severity of
serontonergic reuptake inhibitors and very similar cogni- negative affect and low levels of positive affect are clearly
tive-behavioral strategies (e.g., exposure to emotionally articulated. In this context, key features of anxiety and mood
salient cues and the prevention of avoidance; Barlow, in disorders, such as intrusive thoughts, panic attacks, sensitivity
press). There is also evidence that treating one disorder in a to social evaluation, psychomotor retardation, and so forth,
comorbid spectrum often leads to the remission of the addi- could be arrayed as dimensions emerging out of the higher
tional disorders (e.g., Brown, Antony, & Barlow, 1995). On order factor in a manner similar to a Minnesota Multiphasic
the other hand, the key defining features of anxiety, mood, Personality Inventory profile. It may be that this organiza-
and related disorders may differ dramatically from each tion would lead to a more descriptive, and therefore more
other. This diversity includes such features as perceptual valid, approach to our nosology. With this structure in mind,
derealization, intrusive thoughts, sensitivity to social evalua- it becomes possible to outline the origins of anxiety and
tion, panic attacks, phobic avoidance of blood, flashbacks of related disorders.
trauma, psychomotor retardation, and cognitive rituals. Yet,
all of these phenomena are subsumed under anxiety or mood The Origins of Anxiety and Related Emotional
disorders. This leads to a major conundrum. How can one Disorders: Triple VulnerabUities
reconcile the unitary nature of this construct, most often The experience of the past decade has strengthened earlier
referred to as neuroticism or negative affectivity, with the speculations (Barlow, 1988) on an interacting set of three vul-
variety of specific features that distinguish one disorder nerabilities or diatheses relevant to the development of anxi-
from another. To address these questions, my colleagues and ety, anxiety disorders, and related emotional disorders.
I have explored the structure of anxiety and mood disorders. Genetic contributions to the development of anxiety and neg-
Basically, a complex network of data supports a hierar- ative affect constitute a generalized biological vulnerability.
chical model of anxiety and mood disorders with negative Evidence now suggests that specific early life experiences,
affect representing a higher order factor common to anxiety under certain conditions, contribute to a psychological vulner-
(and depression), whereas lower order factors may con- ability, or diathesis, to experience anxiety and related negative
tribute uniqueness to specific disorders (Brown, Chorpita, & affective states generally (a generalized psychological vulner-
Barlow, 1998; Zinbarg & Barlow, 1996). Some of this work ability). Although the unfortunate cooccurrence of generalized
is an outgrowth of pioneering efforts by Tellegen (e.g., biological and psychological vulnerabilities may be sufficient
1985) and Clark and Watson (e.g., 1991), who developed to produce anxiety and related states, particularly generalized
the tripartite model of anxiety and depression. The most anxiety disorder and depression, yet a third set of vulnerabili-
recent iteration of the model of the structure of mood disor- ties seems necessary to account for the development of at
ders from our center (Brown et al., 1998), based on struc- least some specific anxiety disorders. Thus, early learning
tural equation modeling, is presented in Figure 2. These data experiences in some instances seem to focus anxiety on cer-
suggest mood and anxiety disorders are closely related, with tain life circumstances. That is, these circumstances or events,
substantial contributions from the higher order factor of neg- such as social evaluation or the experience of certain somatic
ative affect (neuroticism) to all disorders, as well as contri- sensations, become imbued with a heightened sense of threat
butions to both depression and social phobia from a higher and danger. It is this specific psychological vulnerability that,
order factor of low positive affect. Thus, depression and when coordinated with generalized biological and psychologi-
-.29~
.31'
/' 6 7 " / Z~
.18'
.33*( 1 45*/Generalized\ .5~( Panic "/ .8~( Obsessive ~ . 7 ~ ( Social
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Autonomic I~
' Arousal
cal vulnerabilities mentioned above, seems to contribute to Of course, many of these early studies are correlational,
the development of specific anxiety disorders such as social but more satisfactory prospective designs detailing the rela-
phobia or social anxiety disorder, obsessive-compulsive dis- tionship between neurotic temperaments and the later
order, panic disorder, and specific phobias. development of anxiety are now appearing. For example,
Gershuny and Sher (1998) evaluated the extent to which
Generalized Biological Vulnerability:
personality dimensions of neuroticism (as well as extrover-
Genetic Contributions
sion and psychoticism) predicted global anxiety ratings in
Evidence suggests that the fundamental trait of being high over 400 young adults. They found that an interaction of
strung, nervous, or emotional runs in families and has a neuroticism and extroversion predicted both global anxiety
genetic component. More formal studies of traits, such as and depression three years after initial assessment. They
anxiety, neuroticism, negative affect, or behavioral inhibi- concluded that personality variables, in particular the com-
tion, also evidence a substantial genetic component (Clark, bination of high neuroticism and low extroversion, consti-
Watson, & Mineka, 1994). As noted earlier, the relationships tute an important vulnerability for the later development of
among the closely related traits of neuroticism, negative anxiety and its disorders (although the purpose of this study
affect, behavioral inhibition, and so forth have yet to be was not to predict the occurrence of specific anxiety disor-
fully worked out, but it is likely that each represents varia- ders). Furthermore, Gershuny and Sher found a lack of
tions on a theme underlying a biological vulnerability to specificity for predicting anxiety versus depression, in that
develop emotional disorders generally. Genetic contributions the personality variables measured seemed to provide a
to the expression of these generalized traits are most usually common diathesis, a subject to which I return below.
estimated to run in the range of 30% to 50% of the variance. Although some tantalizing evidence exists on more cir-
More important, it has now been established that traits of cumscribed genetic contributions to some disorders, particu-
neuroticism or negative affectivity are positively related to larly specific phobia (e.g., Fyer, Mannuzza, Chapman,
anxiety and anxiety disorders (Brown et al., 1998; Clark et Martin, & Klein, 1995), the strong consensus is that anxiety
al., 1994; Trull & Sher, 1994; Zinbarg & Barlow, 1996). and related emotional disorders, such as depression, have a
situations with panic attacks, may have a separate genetic cause of "anxiety" in these animals is that "environmental
component, much as fainting and freezing in response to events of vital importance to the organism become unpre-
certain specific stimulus situations seem to evidence a dictable, uncontrollable, or both" (Mineka & Kihlstrom,
strong heritable tendency (Craske, 1999; Kendler et al., 1978, p. 257). These animal models of anxiety have been
1995; Marks, 1986). extended in an important way to primates. For example,
In the absence of concurrent psychological diatheses, dis- Suomi and his colleagues have been studying anxiety in rhe-
cussed below, the individual with this nonspecific biological sus monkeys for years as a function of genetic vulnerability
vulnerability would presumably not develop anxiety or other and early experience (e.g., Suomi, 1986, 1999).
negative affective states later in life, but rather would mani- Some fascinating research from Mineka, Insel, and their
fest tendencies to emotionality or exaggerated responsive- colleagues in the 1980s began to illustrate not only the
ness to stress that would be within normal limits. To activate seeming importance of negative life events in the production
the specter of anxiety and related negative affectivity, this of anxiety in rhesus monkeys, but also their interaction with
normal personality trait must incubate in the fertile ground uncontrollability or unpredictability (e.g., Insel, Champoux,
of early experience. This nonspecific genetic vulnerability Scanlan, & Suomi, 1986; Mineka, Gunnar, & Champoux,
could also influence the propensity to develop conditioned 1986). For example, Mineka et al. (1986), in a sophisticated
emotional responses when experiencing panic and anxiety, experiment, assigned infant monkeys to one of three groups:
because it has been established that temperamental variables master, yoked, and standard reared. Monkeys in the master
with known genetic contributions influence other forms of group had control over the delivery of food, drink, and other
conditioning (Bouton et al., in press; Mineka & Zinbarg, appetitive stimuli. Monkeys in the yoked group received
1996). equal amounts of these reinforcers but did not have control
Generalized Psychological Vulnerability: over their delivery. Monkeys in the standard reared group
A Diminished Sense of Control were treated according to standard laboratory procedures.
Testing began when the monkeys were approximately seven
The development of a sense of control in animals. As months of age. Results showed that master monkeys
represented in Figure 1, I have suggested that a sense of engaged in significantly more exploring behavior and less
unpredictability and uncontrollability is at the heart of anxi- clinging than did the yoked monkeys. Master monkeys also
ety. Individuals suffering from anxiety and related disorders showed reduced fear of a toy robot compared with yoked
process failures or perceived deficiencies as an indication of monkeys. Finally, when separated from peers, master mon-
a chronic inability to cope with unpredictable, uncontrol- keys used coping strategies more effectively to reduce dis-
lable, negative events, and this sense of uncontrollability is tress. These findings are significant in that they demonstrate
associated with negatively valenced emotional responding. the negative influence of experiences with uncontrollability
Functional or "normal" individuals, on the other hand, seem in the early environment. In addition, whereas experimental
to manifest what has been described as an illusion of control neurosis paradigms suggest the importance of control over
in which response deficiencies are attributed to passing aversive stimuli, this study suggests that control over appeti-
external causes or trivial and temporary internal states tive stimuli may be equally important.
(Barlow, 1988, in press). Important extensions of this work have been reported by
A fundamental question concerns the origins of this sense Sapolsky and colleagues (e.g., Sapolsky, 1992; Sapolsky,
of uncontrollability. Although the study of etiology is Alberts, & Altmann, 1997; Sapolsky & Ray, 1989) and by
fraught with difficulties, excellent analogues have in fact Coplan et al. (1996, 1998). These investigators also demon-
sol. Ultimately, this neurobiological profile seems to result work delineating the concept of locus of control (Nowicki &
This document is copyrighted by the American Psychological Association or one of its allied publishers.
in autonomic inflexibility characterized by low vagal tone. Strickland, 1973; Rotter, 1954) and attachment theory
This is the opposite psychophysiological profile of organ- (Bowlby, 1980), Chorpita and Barlow (1998) have recently
isms that have developed resilience and physiological tough- reviewed evidence on the potential importance of early par-
ness as a function of early experience (Dienstbier, 1989). enting styles to the development of a sense of control in
Now there is additional evidence from the animal labora- children. Basically, a web of evidence has emerged support-
tories that early experience, particularly stressful experience, ing two propositions. First, parents who are more contin-
may effect relatively permanent alterations in brain function, gently responsive foster a sense of control. They may
particularly in CRF-containing neurons and receptors. Much accomplish this by providing children with more opportuni-
of this work has emerged from the laboratories of Charles ties to exercise control over their environment by influenc-
Nemeroff and his colleagues (Heim & Nemeroff, 1999; ing the parents' behavior, particularly the provision of atten-
Ladd et al., 2000) and builds on the pioneering efforts of tion, food, and so forth early in life in a consistent and pre-
experimental psychologists such as Robert Ader (Ader & dictable manner. Second, parents who are less intrusive and
Groter, 1969), Victor Denenberg (e.g., 1964), and Neil protective and provide their children with more occasions to
Miller (1980). Nemeroff and his colleagues have demon- explore their world and develop new skills to cope with
strated that early uncontrollable psychological stressors unexpected environmental occurrences enhance a healthy
result in seemingly chronic alterations in hypothalamic pitu- sense of control in their children. Similar data have appeared
itary adrenocortical (HPA) axis functioning. It is interesting regarding the development of depression (Nolen-Hoeksema,
that comparable physical stressors early in life, such as hem- Wolfson, Mumme, & Guskin, 1995), reflecting once again
orrhage, do not produce this activation. As a mechanism, the similar and perhaps identical diatheses, both psychologi-
these investigators suggested that sensitivity of the hip- cal and biological, for these two emotional states.
pocampus and frontal cortex to circulating glucocorticoids is Recently, Chorpita, Brown, and Barlow (1998) attempted
attenuated by these experiences, thereby decreasing the effi- to evaluate this particular model of the development of anxi-
cacy of negative feedback inhibition over HPA axis activity. ety through structural equation modeling. Building on previ-
This, in turn, increases CRF and argininevasopressin synthe- ous evidence with depression (Nolen-Hoeksema, Girgus, &
sis in the hypothalamic paraventricular nucleus and perhaps Seligman, 1992), Chorpita et al. used a cross-sectional
increases expression of CRF in the central nucleus of the design to evaluate a variety of models describing the devel-
amygdala (Ladd et al., 2000). What is important about these opment of anxiety in children presenting with anxiety disor-
findings, again, is that a psychological variable, early unpre- ders. The major hypothesis evaluated the notion that an
dictable and uncontrollable experiences, but not early physi- overcontrolling family environment fostering a diminished
cal trauma, seems to result in an alteration of neurobiologi- sense of personal control should in fact produce a sense of
cal function that may underlie chronic emotionality and per- uncontrollability, as reflected in a more external locus of
haps neuroticism. control. This external locus of control should in turn con-
Taken together, this evidence indicates that, in animals at tribute to increased negative affect and ultimately to clinical
least, early stress--particularly uncontrollable and/or unpre- symptoms. We also evaluated the possibility, based on evi-
dictable life events--leads to increased HPA axis respond- dence from childhood depression studies, that attributional
ing, negative emotionality (chronic anxious apprehension style would function as a mediator in the model. Compared
and/or depression), and alarm reactions. Instillation of a with a number of alternative models, the model depicting a
sense of mastery or control during development seems to diminished sense of personal control (external locus of con-
storedinfooation
• "~ intensification of
Note. BIS = behavioralinhibitionsystem;CRF = corticotropinreleasingfactor; HPA = hypothalamicpituitaryadrenocortical.From "The Developmentof Anxiety:The Role
of Control in the Early Environment,"by B. F. Chorpita and D. H. Barlow,Psychological Bulletin, 124, p. 16. Copyright 1998 by the AmericanPsychologicalAssociation.
Adapted with permissionof the authors.
Figure 5 Figure 6
Diatheses-StressModel of the Developmentof Generalized Triple Vulnerabilities in the Development of Certain
Anxiety and Depression Specifying Synergistic Biological Anxiety Disorders
and Psychological Vulnerabilities
Synergistic Vulnerabilities
Biological Vulnerabilities
Synergistic Vulnerabilities
I Generalized Psychological Vulnerability
Biological Vulnerabilities J
-= I ~5 Specific Psychological Vulnerability
Generalized Psychological Vulnerability j (Focus of anxiety: e.g., physical sensations are dangerous;
/ social evaluation is dangerous; bad thoughts are dangerous)
............................. ....... t ......................................... 7 ................................... l ...................................
[Stress ]------*[ False Alarms Stress
I (Panic)
E ~ False Alarms
J (Panic)
Generalized Anxiety
Panic Disorder
Social Phobia
Depression OCD
) Stressors I~
i
~ DirectExperience
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
This document is copyrighted by the American Psychological Association or one of its allied publishers.
[ Anxiousapprehension, including t
increased self-focusedattention
¢
I SpecificVulnerability
(social evaluation is dangerous) I
¢
I Social Phobia /
Note. From "Social Phobia (Social Anxiety Disorder)," by S. G. Hofmann and D. H. Barlow, in Anxiety and Its Disorders: The Nature and Treatment of Anxiety and Panic
(2nd ed.), by D. H. Barlow, in press, New York: Guilford Press. Copyright by Guilford Press. Reprinted with permission.
Dadds, & Ryan, 1996; Bruch & Heimberg, 1994; Bruch, situations (or by true alarms occurring after traumatic, humiliat-
Heimberg, Berger, & Collins, 1987; Rapee, 1997). In obses- ing direct social experiences). The socially phobic individual
sive-compulsive disorder, where obsessional thoughts, then focuses anxiety on upcoming social and evaluative situa-
images, or urges themselves become the focus of anxiety, tions on the basis of having learned that these contexts are
there is evidence that at least some of these individuals had potentially threatening ones that may lead to undue anxiety and
previously learned to equate dangerous thoughts with dan- possibly a panic attack, resulting in social failure and ridicule.
gerous actions (thought-action fusion; Steketee & Barlow, Alternatively, severe anxious apprehension, particularly associ-
in press). ated with deficient social skills, may be sufficient to reach the
In summary, vicarious learning of potential threat emanat- threshold for social phobia in the absence of alarms, but chronic
ing from objects or situations seems to serve as a specific social anxiety would be unlikely to develop, even following a
psychological vulnerability for the development of individual difficult social situation, in the absence of synergistic triple vul-
anxiety disorders. Once again, these experiences in isolation nerabilities. This arrangement is depicted in Figure 7.
would not be sufficient to produce a clinical disorder. For
Conclusions
example, someone vicariously learning that physical sensa-
tions are potentially dangerous may well develop hypochon- I have broadly outlined a theory of the development of anxiety
driacal tendencies as an adult or may differentially attend to and related emotional disorders, as well as the structure of
illness-related behaviors in their children, but would be these disorders. This theory draws heavily on emotion theory
unlikely to develop a clinical disorder such as panic disorder and on scientific findings from the laboratories of experimen-
or hypochondriasis in the absence of more generalized bio- tal psychology, specifically, cognitive science, neuroscience,
logical and psychological vulnerabilities. The synergism of developmental psychology, and learning theory. The applica-
these triple vulnerabilities is detailed in Figure 6. bility of the science of psychology to clinical disorders has
To take one example, social phobia is often characterized by become possible only in the past several decades, but seems
false alarms occurring after stressful events in social evaluative essential to an understanding of the development, treatment,
Darwin, C. R. (1872). The expression of emotions in man Gray, J. A. (1982). The neuropsychology of anxiety. New
and animals. London: John Murray. York: Oxford University Press.
Greenberg, P. E,, Sisitsky, T., Kessler, R. C., Finkelstein, S. N., Kagan, J. (1994). Galen's prophecy: Temperament in human
Berndt, E. R., Davidson, J. R. T., Ballenger, J. C., & Fyer, A. J. nature. New York: Basic Books.
(1999). The economic burden of anxiety disorders in the
1990s. Journal of Clinical Psychiatry, 60, 427435. Katschnig, H. (1999). Anxiety neurosis, panic disorder or
what? In D. J. Nutt, C. Ballenger, & J.-R L6pine (Eds.),
Hammen, C., Adrian, C., & Hiroto, D. (1988). A longitudi- Panic disorder: Clinical diagnosis, management and mecha-
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
nal test of the attributional vulnerability model in children at nisms (pp. 1-8). London: Dunitz.
This document is copyrighted by the American Psychological Association or one of its allied publishers.
Hinton, D., Ba, E, Peou, S., &Um, K. (in press-a). Kyol Kessler, R. C., McGonagle, K. A., Zhao, S., & Nelson, C. B.,
goeu ("wind overload"): Part I. Cultural syndromes, cata- Hughes, M., Eshkeman, S., Wittchen, H. U., & Kendler, K. S.
strophic cognitions, and the generation of panic; or, kyol (1994). Lifetime and 12 month prevalence of DSM-III-R psy-
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