Unraveling The Mysteries of Anxiety and Its Disorders From The Perspective - Impresso

Barlow, D. H. (1986).
The causes of sexual dysfunction:

The role of anxiety and cognitive interference. Journal of
Consulting and Clinical Psychology, 54, 140--148.
Barlow, D. H. (1988). Anxiety and its disorders." The nature
and treatment of anxiety and panic. New York: Guilford Press.
Barlow, D. H. (1991a). Disorders of emotion. Psychological
Inquiry, 2, 58-7l.
combination for panic disorder: A randomized controlled

trial. JAMA, 283, 2529-2536.
Barlow, D. H., Hayes, S. C., & Nelson, R. O. (1984). The
scientist-practitioner: Research and accountability in clinical and educational settings. New York: Pergamon Press.
Barlow, D. H., & Hersen, M. (1984). Single case experimental designs." Strategies for studying behavior change
(2nd ed.). New York: Pergamon Press.
This document is copyrighted by the American Psychological Association or one of its allied publishers.
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
Barlow, D. H. (1991b). Introduction to the special issue on

diagnosis, dimensions, and DSM-IV: The science of classification. Journal of Abnormal Psychology, 100, 243-244.
Barlow, D. H. (1994). Psychological interventions in the era
of managed competition. Clinical Psychology." Science and
Practice, 1, 109-122.
Barlow, D. H. (1996). Health care policy, psychotherapy
research, and the future of psychotherapy. American
Psychologist, 51, 1050-1058.
Barlow, D. H., Sakheim, D. K., & Beck, J. G. (1983).

Anxiety increases sexual arousal. Journal of Abnormal
Psychology, 92, 49-55.
Bouton, M. E., Mineka, S., & Barlow, D. H. (in press). A
modern learning-theory perspective on the etiology of panic
disorder. Psychological Review.
Chorpita, B. F., & Barlow, D. H. (1998). The development
of anxiety: The role of control in the early environment.
Psychological Bulletin, 124, 3-21.
Barlow, D. H. (Ed.). (in press). Clinical handbook of psychological disorders." A step-by-step treatment manual (3rd
ed.). New York: Guilford Press.
Barlow, A. D., Abel, G. G., & Blanchard, E. B. (1977).
Gender identity change in a transexual: An exorcism.
Archives of Sexual Behavior, 6, 387-395.
Barlow, D. H., Blanchard, E. B., Vermilyea, J. A.,
Vermilyea, B. B., & Di Nardo, P. A. (1986). Generalized
anxiety and generalized anxiety disorder: Description and
reconceptualization. American Journal of Psychiatry, 143,
40-44.
Barlow, D. H., Brown, T. A., & Craske, M. G. (1994).
Definitions of panic attack and panic disorder in DSM-IV:
Implications for research. Journal of Abnormal Psychology,
103, 553-564.
Barlow, D. H., Chorpita, B. E, & Turovsky, J. (1996). Fear,
panic, anxiety, and disorders of emotion. In D. A. Hope
(Ed.), Nebraska Symposium on Motivation: Vol. 43.
Perspectives on anxiety, panic and fear (pp. 251-328).
Lincoln: Nebraska University Press.
The ascendance of emotion theory, recent advances in cognitive

science and neuroscience, and increasingly importantfindings
from developmentalpsychology and learning make possible an
integrative account of the nature and etiology of anxiety and its
disorders. This model specifies an integrated set of triple vulnerabilities: a generalized biological (heritable) vulnerability, a generalized psychological vulnerability based on early experiences in
developing a sense of control over sal&nt events, and a more specific psychological vulnerability in which one learns tofocus anxiety
on specific objects or situations. The author recounts"the development
of anxiety and related disorders based on these triple vulnerabilities and discusses implicationsfor the classification of emotional
disorders.
Editor's Note
Barlow, D. H., & Craske, M. G. (2000). Mastery of your
anxiety and panic: Client workbook for anxiety and panic
(3rd ed.). San Antonio, TX: Graywind

Publications/Psychological Corporation.
Barlow, D. H., Gorman, J. M., Shear, M. K., & Woods, S. W.
(2000). Cognitive-behavioral therapy, imipramine or their
November 2000 American Psychologist
David H. Barlow received the Awardfor Distinguished Scientific

Applications of Psychology. Award winners are invited to deliver
an award address at the APA's annual convention. This award
address was delivered at the 108th annual meeting, held August
4-8, 2000, in Washington, DC. Articles based on award addresses
are not peer reviewed, as they are the expression of the winners'
reflections on the occasion of receiving an award.
1247
The phenomenon of anxiety, to some prominent philosophers and psychologists, is at the very root of what it means
to be human (Kierkegaard, 1844/1944; May, 1979). To the
well-known early psychologist Howard Liddell, anxiety was
the shadow of intelligence:
The planning function of the nervous system, in the course of
evolution, has culminated in the appearance of ideas, values,
and pleasures--the unique manifestations of man's social living. Man, alone, can plan for the distant future and can experience the retrospective pleasures of achievement. Man, alone,
can be happy. But man, alone, can be worried and anxious.
Sherrington once said that posture accompanies movement as a
shadow. I have come to believe that anxiety accompanies intellectual activity as its shadow and that the more we know of the
nature of anxiety, the more we will know of intellect. (Liddell,
1949, p. 185)
In this sense, anxiety reflects our important capabilities to
adapt and plan for the future (Barlow, 1988).
Yet, individuals spend billions of dollars yearly to rid
themselves of anxiety. The cost of visits to primary care
physicians and the use of health care services by individuals with anxiety disorders are double what they are for
those without anxiety disorders, even if the individuals
seeking treatment are physically ill (Simon, Ormel,
VonKorff, & Barlow, 1995). Many take away prescriptions
from their physicians for various drugs to treat anxiety,
making these drugs among the most widely used in the
world. In fact, over the past decade individual drugs introduced for the treatment of anxiety by the major pharmaceutical companies have routinely yielded billions of dollars
per year in revenue for each product (Greenberg et al.,
1999; Hofmann & Barlow, 1999). For individuals availing
themselves of these anxiolytics, anxiety is a curse--something they could live without.
Is anxiety the shadow of intelligence or a curse on
mankind'? Our greatest thinkers have pondered these
questions. Freud spent much of his life confronting the
mysteries of anxiety and concluded at one point, "One
thing is certain, that the problem of anxiety is a nodal
point, linking up all kinds of most important questions; a
riddle, of which the solution must cast a flood of light on
our whole mental life" (Freud, 1917/1963, p. 401). In
1950, the great psychologist O. Hobart Mowrer described
what is perhaps the fundamental contradiction of the
experience of severe anxiety:
[It is] the absolutely central problem in neurosis and therapy. Most simply formulated, it is a paradox--the paradox of
behavior which is at one and the same time self-perpetuating and self-defeating!... Common sense holds that a
normal, sensible man, or even a beast to the limits of his
intelligence, will weigh and balance the consequences of his
acts: if the net effect is favorable, the action producing it
1248
will be perpetuated; and if the net effect is unfavorable, the

action producing it will be inhibited, abandoned. In neurosis, however, one sees actions, which have predominantly
unfavorable consequences; yet they persist over a period of
months, years, or a lifetime. (Mowrer, 1950, p. 486)
This self-perpetuating and self-defeating paradox is a uni.
versal experience. At the beginning of this century,
Danish travelers to Greenland reported observing a condition in which Eskimo hunters, alone in kayaks on a perfectly still sea for hours on end waiting for seals to
emerge, would experience sudden difficulty breathing,
accompanied by a racing heart, trembling, and other
strange bodily sensations. Subsequently, these hunters
would be unable to venture far from their villages. This
condition, well-known among the Eskimo tribes of
Greenland, was referred to as kayak angst (Katschnig,
1999). In more recent times, Khmer refugees have presented in large numbers to clinics complaining of trembling, weakness, sudden dizziness, fatigue, and a "sore
neck." The Khmer attribute these symptoms to kyol geou,
or wind overload, a condition that, when occurring in the
neck and limbs, may signal impending death. Thus, a
selective attention and exquisite sensitivity develop to
sensations in the neck, followed by feelings of impending
doom and thoughts of possible death (Hinton, Ba, Peou,
& Urn, in press-a, in press-b). Kayak angst and Khmer
"sore neck" seem to be culturally diverse expressions of
panic disorder.
Phobias and, to a lesser extent, other anxiety disorders
have one additional mysterious characteristic: a selective
association with being female. For example, over 90% of
individuals suffering from a phobia of insects or small
animals severe enough to keep them from moving to rural
areas, or even visiting friends in places where small animals or insects might be present, are female. Data from a
large survey conducted by the World Health Organization
in primary care settings revealed a consistently high proportion of women with panic disorder with or without
agoraphobia (odds ratio 1.63; 95%, confidence intervals
1.18-2.20), and this is a consistent finding around the
world (Gater et al., 1998). Similarly, a large sample of
over 1,000 adolescents revealed a strong preponderance of
female participants among those experiencing an anxiety
disorder. This gender imbalance emerged early in life,
with retrospective data indicating that by the age of 6,
girls were already twice as likely as boys to have experienced anxiety (Lewinsohn, Gotlib, Lewinsohn, Seeley, &
Allen, 1998).
Anxiety disorders are shockingly common, far
exceeding the prevalence of affective disorders or substance use disorders (Kessler et al., 1994), and these
disorders may last for decades or even a lifetime in the
absence of effective treatment, making them among the
most chronic of the mental disorders (Goisman et al.,
1998; Hirschfeld, 1996; Keller & Baker, 1992; Marks &

Lader, 1973; Noyes, Clancy, Hoenk, & Slymen, 1980;
Pollack et al., 1990). In this article, I summarize my
own view of what research has uncovered in the past
decade about the nature of anxiety and panic and discuss
the classification and development of anxiety and related disorders.
The Ascendance of Emotion Theory

In the 1980s, I made the then somewhat radical proposal that
to understand emotional disorders in general and anxiety disorders in particular, it was necessary to more fully appreciate
the nature of emotion (Barlow, 1988), a subject that has long
been absent from psychology's curriculum. It now seems
clear that the experience of emotion (and the development of
emotional disorders) cannot be reduced to dry cognitive attributions and appraisals on the one hand, or to specific actions
of neurotransmitters and the intricacies of cell physiology on
the other (Barlow, 1991c). The growing recognition of the
necessity of focusing on emotional experience and expression as a scientific subject in its own fight is highlighted by
the appearance of the new APA journal Emotion. The model
of emotional disorders I presented in the 1980s and 1990s
(Barlow, 1988, 1991 a, 1991b; Barlow, Chorpita, & Turovsky,
1996) highlights the role of fundamental emotions in the
great tradition of the emotion theorists (Darwin, 1872;
Ekman & Davidson, 1994; Izard, 1994).
The underlying premise of this approach is that emotions
are innate patterns of reaction and responding that have
evolved in many life forms because of their functional significance. Although clearly modifiable by learning and maturation, these basic patterns of emotion are present in
humans and animals at birth and show a remarkable consistency both within and across species. The primary function,
or adaptive value, of emotional behavior is not only preparation for action, but also communication from one member
of the species to another. As Ohman (1996; Ohman,
Esteves, & Soares, in press) pointed out, the function of
emotions in this sense can be understood as a clever means,
guided by evolution, to ensure that people do what they
have to do to successfully pass their genes to coming generations. In other words, emotions are now conceptualized by
most theorists as fundamental action tendencies whose purpose is to motivate behavior related to survival of the
species. A theory of the nature of emotional disorders based
on discrete emotion theory as applied to depression, anger
(stress), and excitement (mania) has been described elsewhere (Barlow, 1988, 1991a, 1991b, in press; Barlow et al.,
1996). The focus of this article is on the defensive emotions
of fear and anxiety, and their pathological expression.
With this new focus on the study of emotion, the mysteries of anxiety are giving way, grudgingly, to a new appreciation of the richness and complexity of behavioral and cognitive patterns associated with defensive emotions. One of the
more important developments is the recognition of substantial and fundamental differences in the behavioral expression
of anxiety, on the one hand, and fear, on the other, which
have only recently come to light. Thus, on a phenomenological, behavioral expressive, psychometric, and neurobiological level, the emotions of fear and anxiety seem to be fundamentally different emotions (Barlow, in press; Barlow et al.,
1996; Bouton, Mineka, & Barlow, in press). On the other
hand, these emotions are closely related, and the intimate
dance of these two action tendencies within our defensive
motivational system (Lang, Cuthbert, & Bradley, 1998) can
be observed not only at the level of behavior and cognition,
but also in closely related but unique brain circuits underlying these action tendencies. Fear is our emergency defensive
reaction (Cannon, 1929), our flight-fight response, enabling
us to respond to present danger with instantaneous, sometimes superhuman efforts. To make the response system as
rapid as possible, underlying neural circuits bypass the cortex in favor of direct connections from the retina to the emotional brain (LeDoux, 1996). The topic of fear is taken up
below. The nature of anxiety is somewhat more complex.
The Nature of Anxiety

In 1988 and in recent updates (Barlow, 1988, in press;
Barlow et al., 1996), I described anxiety as a unique and
coherent cognitive-affective structure within our defensive
motivational system, and I outlined a model of the interaction of the various components of anxiety. At the heart of
this structure is a sense of uncontrollability focused largely
on possible future threats, danger, or other upcoming potentially negative events, in contrast to fear, where the danger is
present and imminent. Thus, anxiety could be characterized
roughly as a state of helplessness, because of a perceived
inability to predict, control, or obtain desired results or outcomes in certain upcoming personally salient situations or
contexts. Accompanying this negative affective state is a
strong physiological or somatic component that may reflect
activation of distinct brain circuits such as the corticotropin
releasing factor system and Gray's behavioral inhibition system (Chorpita & Barlow, 1998; Gray & McNaughton, 1996;
Sullivan, Kent, & Coplan, 2000). These systems may be the
physiological substrate of readiness, underlying a state of
preparation to counteract helplessness. Vigilance (hypervigilance) is another characteristic of anxiety that suggests
readiness and preparation to deal with potentially negative
events. If one were to put anxiety into words, one might say,
"That terrible event could happen (again), and I might not
be able to deal with it, but I've got to be ready to try." For
these reasons, I have suggested that a better and more precise term for anxiety might be anxious apprehension. This
conveys the notion that anxiety is a future-oriented mood
state in which one is ready or prepared to attempt to cope
with upcoming negative events. Another term often paired
with anxiety is anticipatory. However, in the present definition, all anxiety is anticipatory, so this qualifying adjective is
1249
not necessary. The process of anxiety as described above is

presented in Figure 1.
In this model, a variety of cues or propositions, to use the
terms of Lang (1985, 1994a, 1994b), would be sufficient to
evoke anxious apprehension. It is important to note that this
process could occur without the necessity of a conscious, rational
appraisal (Bouton et al., in press; Ohman, 1997; Ohman, Hykt,
& Lundqvist, 2000). For example, one might experience anxiety
without realizing the specific trigger or cue, such as an object or
situation that represents an earlier trauma or an internal somatic
sensation. These cues may be broad based or very narrow. For
example, test anxiety and sexual dysfunction each have a narrow
set Of cues, which signal the necessity of imminent performance
and evoke a state of anxious apprehension with its associated
heightened tension and arousal and negative valence. This state,
in turn, is associated with a shift to a self-evaluative focus of
attention (or a rapidly shifting focus of attention from an external potentially threatening context to an internal self-evaluative
content) in which evaluation of one's (inadequate) capabilities to
deal with the threat is prominent. Evidence suggests that this
shift to a self-focused attentional state further increases arousal
and negative affect, thus forming its own small positive feed-
back loop (Barlow, 1988, in press). This subsystem is also represented in Figure 1.
Continuing on in the larger system or feedback loop,
attention narrows to sources of threat or danger, setting the
stage for additional distortions in the processing of information, either through attentional or interpretive biases, reflecting preexisting hypervalent cognitive schemata. In any case,
one becomes hypervigilant for cues or stimuli associated
with sources of anxious apprehension. This process in
humans is analogous to and may represent Gray's (1987;
Gray & McNaughton, 1996) stop, look, and listen state of
behavioral inhibition, although the actual state of inhibition
is not as readily apparent in clinical examples of human
anxiety as it is in animals. At sufficient intensity, this
process results in disruption of concentration and performance. The process of anxiety is seldom pathological, even
when intense, until it becomes chronic.
When this happens, one or both of two prominent consequences of the process of anxiety ultimately develop in an
attempt to cope with negative affect and its triggers. First, a
tendency to avoid entering a state of anxious apprehension
is always present. This tendency becomes more pronounced
Figure 1
The Processof Anxious Apprehension

Evocation of Anxious Propositions
(Situational contexts, unexplained arousal or other cues)
Negative Affect
f
Attentional Shift
A sense ofuncontrollability and unpredictability

~ to self-evaluativefocus
(perceived inability to influence personally salient events
(on physiological or other
and outcomes)
K , aspects of responding)
DysfunctionalPerformance
and/or lack of concentration on
task at hand
Preparatorycoping set accompanied by supportive

~
/,I]
physiology and activation of specific brain circuits
~
~
(e.g., CRF system, Gray's Behavioral Inhibition S y s t e m ) ~
Hypervigilance and Cognitive Biases

Attentional Biases: Enhanced Recognition of Threat
Attention Narrowing on Sources of Threat
Interpretative Biases
Memory Biases
[
1
[
Additional Increases
in Arousal
Attempts to Cope Characterized By:

(Possible) Avoidance
of situational context or other
aspects of negative affect (e.g.,
arousal) if feasible
Process of Worry
Heightened verbal-linguistic capabilities and
restricted autonomic activity to support
(often futile) attempts to plan and problem solve
Avoidance of Core Negative Affect
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.
1250
and observable, depending on the severity or intensity of the

state and the specificity of the contextual cues that set the
occasion for anxious apprehension. Thus, test-anxious individuals will avoid tests to the extent that this is possible, and
sexually dysfunctional individuals will eventually avoid sex.
However, this rather maladaptive coping skill may not be
available to individuals whose anxious apprehension has diffused to many different situational contexts (or across many
different networks in memory). In these individuals, subtle
avoidance behaviors, rituals, or superstitious behavior may
become established. Second, worry driven by the process of
anxiety, which (at intense levels) is very difficult to control
(Brown, Dowdall, C6t6, & Barlow, 1994), seems best construed as an additional, most often futile, attempt to cope
with chronic anxiety. In the DSM-IV (American Psychiatric
Association, 1994), lack of control over the worry process is
a defining feature of generalized anxiety disorder (Brown,
Barlow, & Liebowitz, 1994). Worry, or concern over future
events, is of course not problematic and may even be adaptive under some circumstances, unless it is so driven by anxiety that it becomes intense and uncontrollable. It is in this
sense that worry can become chronic and maladaptive.
Chronic anxiety also is characterized by persistent central
nervous system tension and arousal, autonomic inflexibility
(Thayer, Friedman, & Borkovec, 1996), and functional brain
asymmetry (Heller, Nitschke, Etienne, & Miller, 1997),
which seem to reflect the consequences of a state of perpetual readiness to confront danger.
The Nature of Fear and Panic: True Alarms, False

Alarms, and Learned (Conditioned) Anxiety
Only in the mid-1980s did researchers begin to collect information on the nature of panic. The accumulating evidence
points to a complex biopsychosocial process. This process
involves the interaction of an ancient alarm system, crucial
for survival, with inappropriate and maladaptive learning
and subsequent cognitive and affective complications. First,
it is important to consider the alarm system most commonly
known as fear.
There is general agreement that fear occurs when people
are directly threatened with a dangerous, perhaps life-threatening, event. An impending attack from wild animals is
something few people experience today, but our ancestors
knew this threat well in millennia past. This history may
account for our somewhat greater susceptibility to becoming
alarmed in the presence of snakes and mountain lions
(Cook, Hodes, & Lang, 1986; Ohman et al., in press;
Seligman, 1971). Relevant threats today include speeding
vehicles, guns, drowning, or seeing the safety of our children threatened. Under these conditions, the emotion of fear
represents a true alarm that mobilizes us physically and cognitively for quick action and sometimes superhuman efforts.
Most typically, running away or escaping is the behavioral
manifestation of fear. Occasionally, directed action to counter
the threat is apparent, such as attacking a predator or singlehandedly lifting an automobile so that a child trapped underneath can escape. These reactions represent Cannon's (1929)
emergency reaction characterized by the compelling action
tendencies of fight orflight. Sometimes these actions are
counterproductive, as in the case of a drowning victim vainly
struggling when the rational response would be to lie still
and attempt to float. The ancient response of freezing (tonic
immobility) may be called forth if other action tendencies,
such as escape or aggression, are ineffective or not available
and one is under direct attack by a predator (e.g., Gallup,
1974; Suarez & Gallup, 1979). Most theorists would agree
that these basic responses are primitive alarm reactions
observed far down the phylogenetic scale. As such, they
have profound evolutionary significance.
In 1988, I described the phenomenon of false alarms
(Barlow, 1988). That is, spontaneous or uncued panic seems
phenomenologically nearly identical in all respects to fear,
except for the ability of the individual to specify an antecedent
(Carter & Barlow, 1995; Forsyth & Eifert, 1996). The very
definition of panic, specifying as it does sudden feelings of
marked apprehension and impending doom that are associated
with a wide range of distressing physical sensations, would
certainly qualify as a definition for fear in other contexts. How
common are false alarms, and why do they occur?
False alarms or panic attacks seem to be far more prevalent in the general population than was assumed previously.
For example, our own data (Rapee et al., 1988) and data
from epidemiological surveys (e.g., Wittchen & Essau,
1991) suggest that between 10% and 14% of the population
had experienced an unexpected, uncued panic attack during
the past year. Typically, attacks were less intense and less
frequent in these "nonclinical panickers" than in patients
with anxiety disorders. Panic attacks also occurred during
sleep in nonclinical panickers and aggregated more strongly
in the families of these individuals than in families of participants who had not experienced panic (Craske, 1999;
Norton, Dorward, & Cox, 1986). Researchers have made
progress in the search for the causes of false alarms, particularly initial false alarms, during the past decade. Ongoing
lines of investigation are targeting a complex web of preexisting biological and psychological vulnerabilities interacting with contemporaneous events (e.g., life stress) in the
genesis of initial false alarms (panic; Bouton et al., in press).
The Structure of Anxiety, Mood, and Related Emotional

Disorders and the Concept of Neurosis:
Back to the Future?
Before discussing the origins of anxiety disorders and the role
of anxiety and panic in this process, it is important to discuss
the structure of anxiety, mood, and related disorders and the
personality traits that may predispose individuals to the development of these disorders. The death of neurotic disorders in
1980, after almost a century of domination, resulted in a split-
1251
ting of neurotic disorders into a number of major classes, such

as anxiety, mood, and somatoform disorders, each containing
its own list of more specific disorders. Yet, neuroticism lives
on and continues to be a serious topic for study, mostly by personality and developmental psychologists interested in traits or
temperaments as possible vulnerabilities for the development
of anxiety and mood disorders. The major constructs in this
study have been given different labels including neuroticism
(Eysenck, 1967), trait anxiety (Gray, 1982), behavioral inhibition (Kagan, 1994), and negative affect (Tellegen, 1985), but I
have presented evidence elsewhere that the conceptual and
empirical overlap among these constructs seems to outweigh
any differences (Barlow, in press).
Much evidence suggests the contribution of a unitary
construct to these former neurotic disorders. This evidence
includes high rates of comorbidity among these disorders
(Brown et al., 1994) and the success of very similar treatments across this wide range of disorders, such as selective
serontonergic reuptake inhibitors and very similar cognitive-behavioral strategies (e.g., exposure to emotionally
salient cues and the prevention of avoidance; Barlow, in
press). There is also evidence that treating one disorder in a
comorbid spectrum often leads to the remission of the additional disorders (e.g., Brown, Antony, & Barlow, 1995). On
the other hand, the key defining features of anxiety, mood,
and related disorders may differ dramatically from each
other. This diversity includes such features as perceptual
derealization, intrusive thoughts, sensitivity to social evaluation, panic attacks, phobic avoidance of blood, flashbacks of
trauma, psychomotor retardation, and cognitive rituals. Yet,
all of these phenomena are subsumed under anxiety or mood
disorders. This leads to a major conundrum. How can one
reconcile the unitary nature of this construct, most often
referred to as neuroticism or negative affectivity, with the
variety of specific features that distinguish one disorder
from another. To address these questions, my colleagues and
I have explored the structure of anxiety and mood disorders.
Basically, a complex network of data supports a hierarchical model of anxiety and mood disorders with negative
affect representing a higher order factor common to anxiety
(and depression), whereas lower order factors may contribute uniqueness to specific disorders (Brown, Chorpita, &
Barlow, 1998; Zinbarg & Barlow, 1996). Some of this work
is an outgrowth of pioneering efforts by Tellegen (e.g.,
1985) and Clark and Watson (e.g., 1991), who developed
the tripartite model of anxiety and depression. The most
recent iteration of the model of the structure of mood disorders from our center (Brown et al., 1998), based on structural equation modeling, is presented in Figure 2. These data
suggest mood and anxiety disorders are closely related, with
substantial contributions from the higher order factor of negative affect (neuroticism) to all disorders, as well as contributions to both depression and social phobia from a higher
order factor of low positive affect. Thus, depression and
1252
anxiety, in this structural model, share negative affect, neurobiological processes (see below), and most likely, similar
diatheses, making these two constructs more alike than different. Specific anxiety disorders may be differentiated by
the cues that elicit anxious apprehension (the focus of anxiety). In this model, anxious arousal, to use the original term
in the tripartite model, is identified as a separate panic factoi
that contributes differentially to the disorders in an expected
fashion (Mineka, Watson, & Clark, 1998). Notice that generalized anxiety disorder and depression are particularly
closely related, with a high zero-order correlation. Nevertheless,
the best fitting model continues to treat generalized anxiety
disorder and depression as separate disorders because of some
differences in presenting characteristics.
What this structure suggests, pending further elaboration,
is that any future system of nosology (e.g., DSM-V) describing emotional disorders may better represent these disorders
in a dimensional framework in which overall severity of
negative affect and low levels of positive affect are clearly
articulated. In this context, key features of anxiety and mood
disorders, such as intrusive thoughts, panic attacks, sensitivity
to social evaluation, psychomotor retardation, and so forth,
could be arrayed as dimensions emerging out of the higher
order factor in a manner similar to a Minnesota Multiphasic
Personality Inventory profile. It may be that this organization would lead to a more descriptive, and therefore more
valid, approach to our nosology. With this structure in mind,
it becomes possible to outline the origins of anxiety and
related disorders.
The Origins of Anxiety and Related Emotional

Disorders: Triple VulnerabUities
The experience of the past decade has strengthened earlier
speculations (Barlow, 1988) on an interacting set of three vulnerabilities or diatheses relevant to the development of anxiety, anxiety disorders, and related emotional disorders.
Genetic contributions to the development of anxiety and negative affect constitute a generalized biological vulnerability.
Evidence now suggests that specific early life experiences,
under certain conditions, contribute to a psychological vulnerability, or diathesis, to experience anxiety and related negative
affective states generally (a generalized psychological vulnerability). Although the unfortunate cooccurrence of generalized
biological and psychological vulnerabilities may be sufficient
to produce anxiety and related states, particularly generalized
anxiety disorder and depression, yet a third set of vulnerabilities seems necessary to account for the development of at
least some specific anxiety disorders. Thus, early learning
experiences in some instances seem to focus anxiety on certain life circumstances. That is, these circumstances or events,
such as social evaluation or the experience of certain somatic
sensations, become imbued with a heightened sense of threat
and danger. It is this specific psychological vulnerability that,
when coordinated with generalized biological and psychologi-
Figure 2
Structural Relationsof Anxiety Disordersand Depression

-.36*
Positive)
Affect
.50'
(Negative
Aflbct
-.29~
/' 6 7 " /
.31'
Z~
.18'
.33*(
1 45*/Generalized\ .5~( Panic "/ .8~( Obsessive ~ . 7 ~ (
'x4 Depression
~
Anx~W_ )
\A~oraohobia/Disrder/ \ CompulsiveDisorder
/
'
Social
Phobia
Autonomic I~
Arousal
From"StructuralRelationshipsAmongDimensionsof the DSM-lVAnxiety and MoodDisordersand Dimensionsof NegativeAffect,PositiveAffect,and Autonomic

Arousal," by T. A. Brown,B. E Chorpita, and D. H. Barlow, 1998,Journal of Abnormal Psychology, 107, p. 187.Copyright1998by the AmericanPsychologicalAssociation.
Adaptedwith permissionof the authors.
*p < .01.
Note.
cal vulnerabilities mentioned above, seems to contribute to

the development of specific anxiety disorders such as social
phobia or social anxiety disorder, obsessive-compulsive disorder, panic disorder, and specific phobias.
Generalized Biological Vulnerability:

Genetic Contributions
Evidence suggests that the fundamental trait of being high
strung, nervous, or emotional runs in families and has a
genetic component. More formal studies of traits, such as
anxiety, neuroticism, negative affect, or behavioral inhibition, also evidence a substantial genetic component (Clark,
Watson, & Mineka, 1994). As noted earlier, the relationships
among the closely related traits of neuroticism, negative
affect, behavioral inhibition, and so forth have yet to be
fully worked out, but it is likely that each represents variations on a theme underlying a biological vulnerability to
develop emotional disorders generally. Genetic contributions
to the expression of these generalized traits are most usually
estimated to run in the range of 30% to 50% of the variance.
More important, it has now been established that traits of
neuroticism or negative affectivity are positively related to
anxiety and anxiety disorders (Brown et al., 1998; Clark et
al., 1994; Trull & Sher, 1994; Zinbarg & Barlow, 1996).
Of course, many of these early studies are correlational,

but more satisfactory prospective designs detailing the relationship between neurotic temperaments and the later
development of anxiety are now appearing. For example,
Gershuny and Sher (1998) evaluated the extent to which
personality dimensions of neuroticism (as well as extroversion and psychoticism) predicted global anxiety ratings in
over 400 young adults. They found that an interaction of
neuroticism and extroversion predicted both global anxiety
and depression three years after initial assessment. They
concluded that personality variables, in particular the combination of high neuroticism and low extroversion, constitute an important vulnerability for the later development of
anxiety and its disorders (although the purpose of this study
was not to predict the occurrence of specific anxiety disorders). Furthermore, Gershuny and Sher found a lack of
specificity for predicting anxiety versus depression, in that
the personality variables measured seemed to provide a
common diathesis, a subject to which I return below.
Although some tantalizing evidence exists on more circumscribed genetic contributions to some disorders, particularly specific phobia (e.g., Fyer, Mannuzza, Chapman,
Martin, & Klein, 1995), the strong consensus is that anxiety
and related emotional disorders, such as depression, have a
1253
common genetic basis, and that specific differences in these

disorders are best accounted for by environmental factors
(e.g., Andrews, Stewart, Allen, & Henderson, 1990;
Kendler et al., 1995; Martin, Jardine, Andrews, & Heath,
1988). Furthermore, no reasonable evidence to date confirms the existence of a specific "anxious gene." Instead,
weak contributions from many genes in several different
areas on a number of chromosomes (a polygenic model)
seem to contribute to a generalized biological vulnerability
to becoming anxious (e.g., Plomin et al., 1997).
The one deviation from the consensual conclusion
regarding nonspecific genetic contributions to emotionality
is the evidence for a differential, if overlapping, heritability
for panic and perhaps related defensive reactions. That is,
certain defensive reactions, such as responding to stressful
situations with panic attacks, may have a separate genetic
component, much as fainting and freezing in response to
certain specific stimulus situations seem to evidence a
strong heritable tendency (Craske, 1999; Kendler et al.,
1995; Marks, 1986).
In the absence of concurrent psychological diatheses, discussed below, the individual with this nonspecific biological
vulnerability would presumably not develop anxiety or other
negative affective states later in life, but rather would manifest tendencies to emotionality or exaggerated responsiveness to stress that would be within normal limits. To activate
the specter of anxiety and related negative affectivity, this
normal personality trait must incubate in the fertile ground
of early experience. This nonspecific genetic vulnerability
could also influence the propensity to develop conditioned
emotional responses when experiencing panic and anxiety,
because it has been established that temperamental variables
with known genetic contributions influence other forms of
conditioning (Bouton et al., in press; Mineka & Zinbarg,
1996).
Generalized Psychological Vulnerability:

A Diminished Sense of Control
The development of a sense of control in animals. As
represented in Figure 1, I have suggested that a sense of
unpredictability and uncontrollability is at the heart of anxiety. Individuals suffering from anxiety and related disorders
process failures or perceived deficiencies as an indication of
a chronic inability to cope with unpredictable, uncontrollable, negative events, and this sense of uncontrollability is
associated with negatively valenced emotional responding.
Functional or "normal" individuals, on the other hand, seem
to manifest what has been described as an illusion of control
in which response deficiencies are attributed to passing
external causes or trivial and temporary internal states
(Barlow, 1988, in press).
A fundamental question concerns the origins of this sense
of uncontrollability. Although the study of etiology is
fraught with difficulties, excellent analogues have in fact
1254
emanated from the laboratories of experimental psychology,

where it seems researchers have been producing severe anxiety for over 50 years. In experiment after experiment, most
of them now classic, investigators have produced behavior
characterized by extreme agitation, restlessness, distractibility,
hypersensitivity, increased autonomic responding, muscle
tension, and interference with ongoing behavior. The names
of the investigators associated with these experiments occupy
a prominent place in every textbook of introductory psychology: Pavlov, Masserman, Liddell, and Gant. The phenomenon they produced was commonly termed experimental neurosis. Mineka and Kihlstrom (1978), in an important
review, made a compelling case for the specification of one
causal factor running through all paradigms subsumed under
the name experimental neurosis. They suggested that the
cause of "anxiety" in these animals is that "environmental
events of vital importance to the organism become unpredictable, uncontrollable, or both" (Mineka & Kihlstrom,
1978, p. 257). These animal models of anxiety have been
extended in an important way to primates. For example,
Suomi and his colleagues have been studying anxiety in rhesus monkeys for years as a function of genetic vulnerability
and early experience (e.g., Suomi, 1986, 1999).
Some fascinating research from Mineka, Insel, and their
colleagues in the 1980s began to illustrate not only the
seeming importance of negative life events in the production
of anxiety in rhesus monkeys, but also their interaction with
uncontrollability or unpredictability (e.g., Insel, Champoux,
Scanlan, & Suomi, 1986; Mineka, Gunnar, & Champoux,
1986). For example, Mineka et al. (1986), in a sophisticated
experiment, assigned infant monkeys to one of three groups:
master, yoked, and standard reared. Monkeys in the master
group had control over the delivery of food, drink, and other
appetitive stimuli. Monkeys in the yoked group received
equal amounts of these reinforcers but did not have control
over their delivery. Monkeys in the standard reared group
were treated according to standard laboratory procedures.
Testing began when the monkeys were approximately seven
months of age. Results showed that master monkeys
engaged in significantly more exploring behavior and less
clinging than did the yoked monkeys. Master monkeys also
showed reduced fear of a toy robot compared with yoked
monkeys. Finally, when separated from peers, master monkeys used coping strategies more effectively to reduce distress. These findings are significant in that they demonstrate
the negative influence of experiences with uncontrollability
in the early environment. In addition, whereas experimental
neurosis paradigms suggest the importance of control over
aversive stimuli, this study suggests that control over appetitive stimuli may be equally important.
Important extensions of this work have been reported by
Sapolsky and colleagues (e.g., Sapolsky, 1992; Sapolsky,
Alberts, & Altmann, 1997; Sapolsky & Ray, 1989) and by
Coplan et al. (1996, 1998). These investigators also demon-
strated that the later manifestation of anxiety and stress

seemed to be a function of early experiences with unpredictability and uncontrollability in primates, whether rearing
occurred in a controlled environment or in the wild.
Furthermore, both investigators characterized a neurobiological process associated with these emotional states that
develops as a consequence of early experience with uncontrollability. This process involves increased corticotropin
releasing factor (CRF) production combined with diminished sensitivity of the pituitary gland, increased production
of stress hormones (particularly cortisol), reduced negative
feedback sensitivity with lessened ability to regulate cortisol
production, and ultimately, hippocampal degeneration. Thus,
these animals are afflicted with chronically high levels of
CRF secretion and, in many cases, high basal levels of cortisol. Ultimately, this neurobiological profile seems to result
in autonomic inflexibility characterized by low vagal tone.
This is the opposite psychophysiological profile of organisms that have developed resilience and physiological toughness as a function of early experience (Dienstbier, 1989).
Now there is additional evidence from the animal laboratories that early experience, particularly stressful experience,
may effect relatively permanent alterations in brain function,
particularly in CRF-containing neurons and receptors. Much
of this work has emerged from the laboratories of Charles
Nemeroff and his colleagues (Heim & Nemeroff, 1999;
Ladd et al., 2000) and builds on the pioneering efforts of
experimental psychologists such as Robert Ader (Ader &
Groter, 1969), Victor Denenberg (e.g., 1964), and Neil
Miller (1980). Nemeroff and his colleagues have demonstrated that early uncontrollable psychological stressors
result in seemingly chronic alterations in hypothalamic pituitary adrenocortical (HPA) axis functioning. It is interesting
that comparable physical stressors early in life, such as hemorrhage, do not produce this activation. As a mechanism,
these investigators suggested that sensitivity of the hippocampus and frontal cortex to circulating glucocorticoids is
attenuated by these experiences, thereby decreasing the efficacy of negative feedback inhibition over HPA axis activity.
This, in turn, increases CRF and argininevasopressin synthesis in the hypothalamic paraventricular nucleus and perhaps
increases expression of CRF in the central nucleus of the
amygdala (Ladd et al., 2000). What is important about these
findings, again, is that a psychological variable, early unpredictable and uncontrollable experiences, but not early physical trauma, seems to result in an alteration of neurobiological function that may underlie chronic emotionality and perhaps neuroticism.
Taken together, this evidence indicates that, in animals at
least, early stress--particularly uncontrollable and/or unpredictable life events--leads to increased HPA axis responding, negative emotionality (chronic anxious apprehension
and/or depression), and alarm reactions. Instillation of a
sense of mastery or control during development seems to
protect against the likelihood of an anxious response. Other

evidence indicates that monkeys receiving social support
from a monkey peer group will have fewer anxiety reactions
than will monkeys reared in isolation (Mineka, 1985a,
1985b). The development of coping responses that imply a
sense of control (whether real or apparent) also buffers anxiety (Coplan et al., 1996; Heim & Nemeroff, 1999; Suomi,
1999). With this suggestive evidence in mind, it becomes
possible to examine findings on the etiology of human anxious apprehension.
The development of a sense of control in humans.
These findings with robust animal models of anxiety make it
important to identify crucial early experiences in humans
that may predispose the development of chronic anxiety
(and depression). Building on important early psychological
work delineating the concept of locus of control (Nowicki &
Strickland, 1973; Rotter, 1954) and attachment theory
(Bowlby, 1980), Chorpita and Barlow (1998) have recently
reviewed evidence on the potential importance of early parenting styles to the development of a sense of control in
children. Basically, a web of evidence has emerged supporting two propositions. First, parents who are more contingently responsive foster a sense of control. They may
accomplish this by providing children with more opportunities to exercise control over their environment by influencing the parents' behavior, particularly the provision of attention, food, and so forth early in life in a consistent and predictable manner. Second, parents who are less intrusive and
protective and provide their children with more occasions to
explore their world and develop new skills to cope with
unexpected environmental occurrences enhance a healthy
sense of control in their children. Similar data have appeared
regarding the development of depression (Nolen-Hoeksema,
Wolfson, Mumme, & Guskin, 1995), reflecting once again
the similar and perhaps identical diatheses, both psychological and biological, for these two emotional states.
Recently, Chorpita, Brown, and Barlow (1998) attempted
to evaluate this particular model of the development of anxiety through structural equation modeling. Building on previous evidence with depression (Nolen-Hoeksema, Girgus, &
Seligman, 1992), Chorpita et al. used a cross-sectional
design to evaluate a variety of models describing the development of anxiety in children presenting with anxiety disorders. The major hypothesis evaluated the notion that an
overcontrolling family environment fostering a diminished
sense of personal control should in fact produce a sense of
uncontrollability, as reflected in a more external locus of
control. This external locus of control should in turn contribute to increased negative affect and ultimately to clinical
symptoms. We also evaluated the possibility, based on evidence from childhood depression studies, that attributional
style would function as a mediator in the model. Compared
with a number of alternative models, the model depicting a
diminished sense of personal control (external locus of con-
1255
trol) as a mediator between a family environment fostering

less autonomy and subsequent negative affect and clinical
symptoms was the best fit for the data. The results are
reflected in Figure 3. Thus, these findings once again suggest that a family environment characterized by limited
opportunity for personal control is associated with the
development of anxiety. This relationship is mediated by
low perceived control in young children, which appears to
be a more robust mediator than attributional style.
In summary, the evidence has begun to support a model
of the development of anxiety (and depression) characterized
by a sense of relative uncontrollability, as a mediator
between negative life events and the emergence of anxiety
and depression early in development. It is interesting that this
mediational model in early childhood stands in contrast to a
moderational model that seems operative in late childhood
and adulthood (Chorpita et al., 1998; Cole & Turner, 1993;
Hammen, Adrian, & Hiroto, 1988; Nolen-Hoeksema et al.,
1992). These findings suggest an important developmental
progression in the formation of this generalized psychological vulnerability. That is, the environment may help foster a
(cognitive) template, with early experience contributing to
the formation of a vulnerability (i.e., mediational model).
Later in development, this vulnerability may begin to operate
as an amplifier for stressful environmental events (i.e., moderational model). This development structure seems to be
consistent across models of anxiety and depression.
Figure 3
A StructuralModel of the Relationof PerceivedControl to

Family Environment,Negative Affect, and Clinical Symptoms
Thus, genetic contributions to the development of anxiet3

seem to account for approximately 30% to 50% of the variance. However, neurobiological processes underlying anxious apprehension that may emerge from this biological
(genetic) diathesis seem to be influenced substantially by
early psychological processes, contributing to a generalized
psychological vulnerability. This early experience with controllability and predictability, based in part but certainly not
exclusively on interactions with caregivers,
contributes to something of a psychological template, which at
some point becomes relatively fixed and diathetic. Stated
another way, this psychological dimension of a sense of control
is possibly a mediator between stressful experience and anxiety, and over time this sense becomes a somewhat stable moderator of the expression of anxiety. (Chorpita & Barlow, 1998,
p. 16)
A preliminary conceptual model outlining these operations
is presented in Figure 4.
A synergism of generalized biological (genetic) and generalized psychological (early experience) vulnerabilities
would be likely to lead to the clinical syndromes of generalized anxiety disorder and the depressive disorders triggered
by a stressful life event as outlined in Figure 5. Notice that
false alarms (panic attacks) may occur as a function of
stressful life events, may be facilitated by high levels of
baseline anxiety, and may emerge as a function of these synergistic generalized vulnerabilities. However, these false
alarms would not in themselves be implicated in a clinical
disorder. For that to occur, an additional layer of more specific psychological vulnerabilities must be considered.
Specific Psychological Vulnerabilities:

Learning WhatIs Dangerous
Note.
FES-C = Family Environment Control Scale, child report; FES-P = Family

Environment Control Scale, parent report; LOC = Nowicki-Strickland Locus of
Control Scale; RCMAS = Revised Children's Manifest Anxiety Scale; CDI =
Children's Depression Inventory; CBCL = Child Behavior Checklist, Internalizing
Scale; CSR-C = Clinical Severity Rating, Child Interview; CSR-P = Clinical
Severity Rating, Parent Interview. From "Perceived Control as a Mediator of Family
Environment in Etiological Models of Childhood Anxiety," by B. E Chorpita, T. A.
Brown, and D. H. Barlow, 1998, Behavior Therapy, 29, p. 468. Copyright 1998 by
the Association for Advancement of Behavior Therapy. Adapted with permission.
*p < .05.
1256
I have also described a third set of psychological vulnerabilities that predisposes the individual to focus anxiety on some
specific object or event (Barlow, 1988, in press; Bouton et
al., in press). This particular psychological vulnerability, also
a function of early learning experiences, becomes relevant
for certain anxiety disorders where anxious apprehension is
focused on potentially dangerous specific objects or events.
In panic disorder (Ehlers, 1993; McNally & Eke, 1996), this
would be somatic (interoceptive) sensations and other cues
signaling the possible occurrence of the next panic attack.
This vulnerability seems to arise when individuals learn early
on from caregivers, through modeling or information transmission, that unexplained somatic sensations are dangerous
and could signal possible illness or death. In specific phobias, this set of vulnerabilities contributes substantially to
determining the particular object or situation that becomes
the focus of fear (Antony & Barlow, in press). In social phobia, there is evidence that individuals have been differentially
subjected to early experiences in which the potential danger
of social evaluation was clearly communicated by parents or
other important caregivers or friends (e.g., Barrett, Rapee,
Figure 4
Model of the Developmentof Vulnerability for Anxiety and Depression

Early Development
Later Development
storedinfooation
(ie memory)
' "'
"~
r-\
control
//'~11
(mis)interpreted
as uncontrollable
intensification of
temperamental stability of hypothalamic

and limbic structures (BIS)
~
//
undifferentiated somatic outputs
/!
incre od
and.PA ac.vity
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.
Note.
Figure 5
Figure 6
Diatheses-StressModel of the Developmentof Generalized
Triple Vulnerabilities in the Development of Certain

Anxiety Disorders
Anxiety and Depression Specifying Synergistic Biological

and Psychological Vulnerabilities
Synergistic Vulnerabilities
Biological Vulnerabilities
Synergistic Vulnerabilities
Generalized Psychological Vulnerability
Biological Vulnerabilities
-=
~5
Generalized Psychological Vulnerability
.............................
.......
t .........................................
[Stress
I
]------*[
Specific Psychological Vulnerability

(Focus of anxiety: e.g., physical sensations are dangerous;
social evaluation is dangerous; bad thoughts are dangerous)
...................................
False Alarms
(Panic)
l ...................................
Stress
E ~
J
Generalized Anxiety
False Alarms
(Panic)
Panic Disorder
Social Phobia
OCD
Depression
OCD = obsessive-compulsive disorder. From "Social Phobia (Social

Anxiety Disorder)," by S. G. Hofmann and D. H. Barlow, in Anxiety and lts
Disorders: The Nature and Treatment of Anxiety and Panic (2nd ed.), by D. H.
Barlow, in press, New York: GuilfordPress. Copyrightby GuilfordPress. Reprinted
with permission.
Note.
From"Social Phobia (Social Anxiety Disorder)," by S. G. Hofmannand

D. H. Barlow,in Anxiety and Its Disorders: The Nature and Treatment of Anxiety and
Panic (2rided.), by D. H. Barlow,in press, New York: GuilfordPress. Copyrightby
GuilfordPress. Reprintedwith permission.
Note.
N o v e m b e r 2000 A m e r i c a n Psychologist
1257
Figure 7
The Development of Social Phobia (Social Anxiely Disorder)
Jl
r PsychologicalVulnerability
)
Stressors
Bi'
icalv'nerabi'ity l
(including heritablecomponent
of behavioral inhibition)
I~
DirectExperience
[ Anxiousapprehension, including t
increased self-focusedattention
I SpecificVulnerability
(social evaluation is dangerous)
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,

Heimberg, Berger, & Collins, 1987; Rapee, 1997). In obsessive-compulsive disorder, where obsessional thoughts,
images, or urges themselves become the focus of anxiety,
there is evidence that at least some of these individuals had
previously learned to equate dangerous thoughts with dangerous actions (thought-action fusion; Steketee & Barlow,
in press).
In summary, vicarious learning of potential threat emanating from objects or situations seems to serve as a specific
psychological vulnerability for the development of individual
anxiety disorders. Once again, these experiences in isolation
would not be sufficient to produce a clinical disorder. For
example, someone vicariously learning that physical sensations are potentially dangerous may well develop hypochondriacal tendencies as an adult or may differentially attend to
illness-related behaviors in their children, but would be
unlikely to develop a clinical disorder such as panic disorder
or hypochondriasis in the absence of more generalized biological and psychological vulnerabilities. The synergism of
these triple vulnerabilities is detailed in Figure 6.
To take one example, social phobia is often characterized by
false alarms occurring after stressful events in social evaluative
1258
situations (or by true alarms occurring after traumatic, humiliating direct social experiences). The socially phobic individual
then focuses anxiety on upcoming social and evaluative situations on the basis of having learned that these contexts are
potentially threatening ones that may lead to undue anxiety and
possibly a panic attack, resulting in social failure and ridicule.
Alternatively, severe anxious apprehension, particularly associated with deficient social skills, may be sufficient to reach the
threshold for social phobia in the absence of alarms, but chronic
social anxiety would be unlikely to develop, even following a
difficult social situation, in the absence of synergistic triple vulnerabilities. This arrangement is depicted in Figure 7.
Conclusions
I have broadly outlined a theory of the development of anxiety

and related emotional disorders, as well as the structure of
these disorders. This theory draws heavily on emotion theory
and on scientific findings from the laboratories of experimental psychology, specifically, cognitive science, neuroscience,
developmental psychology, and learning theory. The applicability of the science of psychology to clinical disorders has
become possible only in the past several decades, but seems
essential to an understanding of the development, treatment,
and ultimately, prevention of anxiety and related disorders.

The existence of the triple vulnerabilities consisting of generalized biological, generalized psychological, and specific psychological vulnerabilities is a hypothetical structure that
requires further confirmation, although data supporting each
vulnerability in isolation are increasingly robust. However, this
effort is only a beginning, and the individual components
recounted in this review, as well as the structure of their relationship to each other, must continue to be subject to the slow
but inexorable process of science.
Author's Note
David H. Barlow, Center for Anxiety and Related Disorders
and Department of Psychology, Boston University.
This address includes modified excerpts from a forthcoming book: Barlow, D. H. (in press). Anxiety and Its
Disorders: The Nature and Treatment of Anxiety and Panic
(2nd ed.). New York: Guilford Press.
Correspondence concerning this address should be
addressed to David H. Barlow, Center for Anxiety and
Related Disorders, Boston University, 648 Beacon Street,
6th Floor, Boston, MA 02215-2013.
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Barlow, D. H. (1986).

The causes of sexual dysfunction:

combination for panic disorder: A randomized controlled

Barlow, D. H. (1991b). Introduction to the special issue on

Barlow, D. H., Sakheim, D. K., & Beck, J. G. (1983).

The ascendance of emotion theory, recent advances in cognitive

(3rd ed.). San Antonio, TX: Graywind

November 2000 American Psychologist

David H. Barlow received the Awardfor Distinguished Scientific

will be perpetuated; and if the net effect is unfavorable, the

November 2000 American Psychologist

1998; Hirschfeld, 1996; Keller & Baker, 1992; Marks &

The Ascendance of Emotion Theory

The Nature of Anxiety

not necessary. The process of anxiety as described above is

The Processof Anxious Apprehension

A sense ofuncontrollability and unpredictability

Preparatorycoping set accompanied by supportive

Hypervigilance and Cognitive Biases

Attempts to Cope Characterized By:

November 2000 American Psychologist

and observable, depending on the severity or intensity of the

The Nature of Fear and Panic: True Alarms, False

November 2000 American Psychologist

The Structure of Anxiety, Mood, and Related Emotional

ting of neurotic disorders into a number of major classes, such

The Origins of Anxiety and Related Emotional

November 2000 American Psychologist

Structural Relationsof Anxiety Disordersand Depression

From"StructuralRelationshipsAmongDimensionsof the DSM-lVAnxiety and MoodDisordersand Dimensionsof NegativeAffect,PositiveAffect,and Autonomic

cal vulnerabilities mentioned above, seems to contribute to

Generalized Biological Vulnerability:

November 2000 American Psychologist

Of course, many of these early studies are correlational,

common genetic basis, and that specific differences in these

Generalized Psychological Vulnerability:

emanated from the laboratories of experimental psychology,

November 2000 American Psychologist

strated that the later manifestation of anxiety and stress

November 2000 American Psychologist

protect against the likelihood of an anxious response. Other

trol) as a mediator between a family environment fostering

A StructuralModel of the Relationof PerceivedControl to

Thus, genetic contributions to the development of anxiet3

Specific Psychological Vulnerabilities:

FES-C = Family Environment Control Scale, child report; FES-P = Family

November 2000 American Psychologist

Model of the Developmentof Vulnerability for Anxiety and Depression

temperamental stability of hypothalamic

undifferentiated somatic outputs

BIS = behavioralinhibitionsystem;CRF = corticotropinreleasingfactor; HPA = hypothalamicpituitaryadrenocortical.From "The Developmentof Anxiety:The Role

Diatheses-StressModel of the Developmentof Generalized

Triple Vulnerabilities in the Development of Certain

Anxiety and Depression Specifying Synergistic Biological

Generalized Psychological Vulnerability

Generalized Psychological Vulnerability

Specific Psychological Vulnerability

OCD = obsessive-compulsive disorder. From "Social Phobia (Social

From"Social Phobia (Social Anxiety Disorder)," by S. G. Hofmannand

The Development of Social Phobia (Social Anxiely Disorder)

Dadds, & Ryan, 1996; Bruch & Heimberg, 1994; Bruch,

I have broadly outlined a theory of the development of anxiety

November 2000 American Psychologist